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+{"text":" \n## Thyroid For Dummies, 2nd Edition\n\nby Alan L. Rubin, MD\n\nThyroid For Dummies, 2nd Edition\u00ae\n\nPublished by  \n **Wiley Publishing, Inc.**  \n111 River St.  \nHoboken, NJ 07030-5774  \nwww.wiley.com\n\nCopyright \u00a9 2006 by Wiley Publishing, Inc., Indianapolis, Indiana\n\nPublished simultaneously in Canada\n\nNo part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, electronic, mechanical, photocopying, recording, scanning, or otherwise, except as permitted under Sections 107 or 108 of the 1976 United States Copyright Act, without either the prior written permission of the Publisher, or authorization through payment of the appropriate per-copy fee to the Copyright Clearance Center, 222 Rosewood Drive, Danvers, MA 01923, 978-750-8400, fax 978-646-8600. Requests to the Publisher for permission should be addressed to the Legal Department, Wiley Publishing, Inc., 10475 Crosspoint Blvd., Indianapolis, IN 46256, 317-572-3447, fax 317-572-4355, or online at http:\/\/www.wiley.com\/go\/permissions.\n\nTrademarks: Wiley, the Wiley Publishing logo, For Dummies, the Dummies Man logo, A Reference for the Rest of Us!, The Dummies Way, Dummies Daily, The Fun and Easy Way, Dummies.com and related trade dress are trademarks or registered trademarks of John Wiley & Sons, Inc. and\/or its affiliates in the United States and other countries, and may not be used without written permission. All other trademarks are the property of their respective owners. Wiley Publishing, Inc., is not associated with any product or vendor mentioned in this book.\n\nLIMIT OF LIABILITY\/DISCLAIMER OF WARRANTY: The contents of this work are intended to further general scientific research, understanding, and discussion only and are not intended and should not be relied upon as recommending or promoting a specific method, diagnosis, or treatment by physicians for any particular patient. The publisher and the author make no representations or warranties with respect to the accuracy or completeness of the contents of this work and specifically disclaim all warranties, including without limitation any implied warranties of fitness for a particular purpose. In view of ongoing research, equipment modifications, changes in governmental regulations, and the constant flow of information relating to the use of medicines, equipment, and devices, the reader is urged to review and evaluate the information provided in the package insert or instructions for each medicine, equipment, or device for, among other things, any changes in the instructions or indication of usage and for added warnings and precautions. Readers should consult with a specialist where appropriate. The fact that an organization or Website is referred to in this work as a citation and\/or a potential source of further information does not mean that the author or the publisher endorses the information the organization or Website may provide or recommendations it may make. Further, readers should be aware that Internet Websites listed in this work may have changed or disappeared between when this work was written and when it is read. No warranty may be created or extended by any promotional statements for this work. Neither the publisher nor the author shall be liable for any damages arising herefrom.\n\nFor general information on our other products and services, please contact our Customer Care Department within the U.S. at 800-762-2974, outside the U.S. at 317-572-3993, or fax 317-572-4002.\n\nFor technical support, please visit www.wiley.com\/techsupport.\n\nWiley also publishes its books in a variety of electronic formats. Some content that appears in print may not be available in electronic books.\n\nLibrary of Congress Control Number: 2006920628\n\nISBN-13: 978-0-471-78755-6\n\nISBN-10: 0-471-78755-8\n\nManufactured in the United States of America\n\n10 9 8 7 6 5 4\n\n2B\/SY\/QS\/QY\/IN\n\n## About the Author\n\n**Alan L. Rubin, MD,** is one of the nation's foremost experts on the thyroid gland in health and disease. He is a member of the Endocrine Society and has been in private practice specializing in thyroid disease and diabetes for over 28 years. Dr. Rubin was Assistant Clinical Professor of Medicine at UC Medical Center in San Francisco for 20 years. He has spoken about the thyroid to professional medical audiences and nonmedical audiences around the world. He is a consultant to many pharmaceutical companies and companies that make thyroid products.\n\nDr. Rubin has written extensively on the thyroid gland as well as diabetes mellitus. As a result, he has been on numerous radio and television programs talking about the cause, the prevention, and the treatment of conditions of the thyroid. He is also the best-selling author of _Diabetes For Dummies_ and _Diabetes Cookbook For Dummies,_ both now in second editions and translated into multiple languages including Chinese, Spanish, French, and Russian. His __ latest book is _High Blood Pressure For Dummies._\n\n##\n\n## Dedication\n\nThe second edition of this book is again dedicated to my wife, Enid. She smilingly let me do my work, sometimes into the wee hours of the morning, and missed many an opportunity to go out to dinner or a movie so that I could produce this book for you. If you have a fraction of the support in your life that she has given me, you are a lucky person, indeed.\n\n##\n\n## Author's Acknowledgments\n\nThe great publisher and midwife, Kathy Nebenhaus, deserves enormous appreciation for helping me to deliver yet another bright-eyed baby. Her optimism and her enthusiasm actually made this book possible. Acquisitions editor Michael Lewis played a huge role in ironing out the inevitable problems that arise when book publishing and medicine meet.\n\nMy editor, Michael Baker, did a magnificent job turning my sometimes incomprehensible prose into words that you can understand. He also conducted a whole orchestra of other editors who contributed to the book, including Melissa Wiley. My thanks to Dr. Kathleen Bethin for the technical editing of the book.\n\nLibrarian Karen O'Grady at St. Francis Memorial Hospital was tremendously helpful in providing the articles and books upon which the information in this book is based.\n\nMy teachers are too numerous to mention, but one person deserves special attention. Dr. Francis Greenspan at the University of California Medical Center gave me the sound foundation in thyroid function and disease upon which this book is based.\n\nFinally, there are my patients over the last 28 years, the people whose trials and tribulations caused me to seek the knowledge that you will find in this book. This book is written on the shoulders of thousands of men and women who made the discoveries, tried the medications, and held the committee meetings. Their accomplishments cannot possibly be given adequate acclaim. We owe them big time.\n\n## Publisher's Acknowledgments\n\nWe're proud of this book; please send us your comments through our Dummies online registration form located at www.dummies.com\/register\/.\n\nSome of the people who helped bring this book to market include the following:\n\nAcquisitions, Editorial, and Media Development\n\n**Project Editor:** Mike Baker\n\n_(Previous Edition: Joan Friedman)_\n\n**Acquisitions Editor:** Michael Lewis\n\n**Copy Editor:** Melissa Wiley\n\n**Editorial Program Coordinator:** Hanna K. Scott\n\n**Technical Editor:** Kathleen Bethin, MD\n\n**Editorial Manager:** Christine Meloy Beck\n\n**Editorial Assistants:** Erin Calligan, David Lutton\n\n**Cartoons:** Rich Tennant (www.the5thwave.com)\n\nComposition Services\n\n**Project Coordinator:** Adrienne Martinez\n\n**Layout and Graphics:** Carl Byers, Andrea Dahl, Stephanie Jumper, Barbara Moore, Heather Ryan\n\n**Special Art:** Kathryn Born\n\n**Proofreaders:** Laura Albert, Leeann Harney, Jessica Kramer, Aptara\n\n**Indexer:** Aptara **__ **\n\n**Publishing and Editorial for Consumer Dummies**\n\n**Diane Graves Steele,** Vice President and Publisher, Consumer Dummies\n\n**Joyce Pepple,** Acquisitions Director, Consumer Dummies\n\n**Kristin A. Cocks,** Product Development Director, Consumer Dummies\n\n**Michael Spring,** Vice President and Publisher, Travel\n\n**Kelly Regan,** Editorial Director, Travel\n\n**Publishing for Technology Dummies**\n\n**Andy Cummings,** Vice President and Publisher, Dummies Technology\/General User\n\n**Composition Services**\n\n**Gerry Fahey,** Vice President of Production Services\n\n**Debbie Stailey,** Director of Composition Services\n\n## Contents\n\nTitle\n\nIntroduction\n\n About This Book\n\n Conventions Used in This Book\n\n Assumptions\n\n How This Book Is Organized\n\n Icons Used in This Book\n\n Where to Go from Here\n\nPart I : Examining the Thyroid\n\nChapter 1: The Big Role of a Little Gland\n\n Discovering the Extent of the Problem\n\n Identifying an Unhappy Thyroid\n\n Recognizing Who's at Risk\n\n Realizing the Importance of a Healthy Thyroid\n\n Treating What Ails You\n\n Examining Additional Contributors to Thyroid Ailments\n\n Realizing the Consequences of Delaying Treatment\n\n Paying Attention to Special Groups and Considerations\n\n Keeping the Rest of Your Body Healthy\n\n Staying Informed\n\nChapter 2: How the Thyroid Works\n\n Picturing Your Thyroid\n\n Examining the Production of Thyroid Hormones\n\n Understanding the Function of Thyroid Hormones\n\nChapter 3: Finding a Thyroid Doctor\n\n Asking the Right Questions\n\n Consulting Possible Sources\n\n Questions for and Observations about the Doctor on First Meeting\n\n Reviewing Special Considerations When Choosing a Thyroid or Eye Surgeon\n\nChapter 4: Testing Your Thyroid\n\n Checking Thyroid-Hormone Levels with Older Tests\n\n Checking Your Levels with the Best Tests\n\n Taking Nonhormonal Blood Tests\n\n Determining the Size, Shape, and Content of Your Thyroid\n\nPart II : Diagnosing and Treating Thyroid Conditions\n\nChapter 5: Dealing with Decreased Thyroid Function\n\n Living with Autoimmune Thyroiditis\n\n Identifying Hypothyroidism\n\n Pinpointing the Causes of Hypothyroidism\n\n Diagnosing Severe Hypothyroidism\n\n Treating Hypothyroidism with Hormones\n\n Treating Myxedema Coma\n\n Managing Subclinical Hypothyroidism\n\n Understanding the Nonthyroidal Illness Syndrome\n\nChapter 6: Taming the Hyperactive Thyroid\n\n Detecting the Signs and Symptoms of Hyperthyroidism\n\n Confirming a Diagnosis of Hyperthyroidism\n\n Determining Whether Graves' Disease Is the Culprit\n\n Recognizing Other Causes of Hyperthyroidism\n\n Choosing the Best Treatment for Graves' Disease\n\n Treating Other Causes of Hyperthyroidism\n\n Surviving Thyroid Storm\n\nChapter 7: Thyroid Nodules\n\n What's a Thyroid Nodule?\n\n Evaluating Cancer Risks\n\n Securing a Diagnosis\n\n Treating Cancerous Nodules\n\n Dealing with Nodules That Aren't Cancer\n\nChapter 8: Thyroid Cancer\n\n Determining What Causes Thyroid Cancer\n\n Identifying the Types of Thyroid Cancer\n\n The Stages of Thyroid Cancer and the Treatment Options\n\n Following up on Cancer Treatment\n\nChapter 9: Multinodular Goiters: Thyroids with Many Nodules\n\n A Multinodular Goiter Grows Up\n\n Making a Diagnosis\n\n Choosing to Treat It or Ignore It\n\n Treating a Multinodular Goiter\n\n Dealing with a Goiter Behind the Sternum\n\nChapter 10: Drugs That Impact Your Thyroid\n\n Revealing the Drug-Food-Thyroid Connection\n\n Identifying the Effects of Specific Substances\n\n Looking At the New Drugs\n\n Discovering Whether You're at Risk\n\nChapter 11: Thyroid Infections and Inflammation\n\n Putting a Face on Subacute Thyroiditis\n\n Coping with Postpartum and Silent Thyroiditis\n\n Identifying Acute Thyroiditis\n\n A Rare Form of Thyroiditis\n\nChapter 12: Iodine Deficiency and Excess Disease\n\n Consuming Iodine in the U.S., Canada, and the U.K.\n\n Realizing the Vastness of the Problem\n\n Facing the Consequences of Iodine Lack\n\n Managing the Problem of Iodine Deficiency\n\n Delineating the Drawbacks of Iodization\n\nChapter 13: Surgery of the Thyroid\n\n Deciding If Surgery Is Necessary\n\n Finding Your Surgeon\n\n Making Final Preparations Before Surgery\n\n What Happens During Surgery\n\n Considering a New Approach\n\n Recuperating After the Operation\n\nPart III : Reviewing Special Considerations in Thyroid Health\n\nChapter 14: The Genetic Link to Thyroid Disease\n\n Taking Genetics 101\n\n Probing the Origins of Genetic Thyroid Diseases\n\n Viewing the Future of Managing Hereditary Thyroid Disease\n\nChapter 15: The Thyroid and Your Mental Health\n\n The Underactive Thyroid and Your Mood\n\n Overactivity of the Thyroid and Your Mind\n\n Fighting Depression\n\nChapter 16: What's New in Thyroid Treatment?\n\n Treating Subclinical Hypothyroidism\n\n Finding the Right Dose of Hormone\n\n Dealing with Hyperthyroidism\n\n Assessing Goiters and Nodules\n\n Using Antithyroid Drugs Properly\n\n Handling Thyrotoxic Periodic Paralysis\n\n Taking New Approaches to Thyroid Cancer\n\n Tackling Iodine-Deficiency Disease\n\nChapter 17: The Thyroid and Pregnancy\n\n The Normal Thyroid During Pregnancy\n\n Pregnancy and Hypothyroidism\n\n Hyperthyroidism in Pregnancy\n\n New Thyroid Nodules in Pregnancy\n\nChapter 18: Thyroid Conditions and Children\n\n Understanding the Onset and Development of Thyroid Function\n\n Screening the Newborn\n\n Coping with Hypothyroidism in Children\n\n Dealing with Hyperthyroidism in Children\n\n Diagnosing Goiters in Children\n\n Finding Nodules and Cancer in Children\n\nChapter 19: Thyroid Disease and the Elderly\n\n Thyroid Changes in the Elderly Due to Aging and Nonthyroidal Disease\n\n Real Thyroid Disease in the Elderly\n\n Sources of Confusion in Diagnosis\n\n Discovering Hypothyroidism in the Elderly\n\n Hyperthyroidism in the Elderly\n\n Thyroid Nodules in the Elderly\n\nChapter 20: Diet, Exercise, and Your Thyroid\n\n Guaranteeing Your Best Nutrition\n\n Clarifying the Thyroid-Weight Connection\n\n Getting Enough Iodine in a Vegetarian Diet\n\n Exercising for Your Thyroid\n\n Uncovering a New Hormone: Connecting Leptin to Weight Loss and the Thyroid\n\nPart IV : The Part of Tens\n\nChapter 21: Ten Myths about Thyroid Health\n\n I'm Hypothyroid, so I Can't Lose Weight\n\n I'm Hyperthyroid, so I Can't Gain Weight\n\n Breastfeeding and Antithyroid Pills Don't Mix\n\n Brand-Name Thyroid Hormone Pills Are Best\n\n I Have to Take Thyroid Medication for Life\n\n Natural Thyroid Hormones Are Better Than Synthetic Hormones\n\n Thyroid Disease Is Contagious\n\n Iodine Deficiency Is a Medical Problem\n\n The Higher My Autoantibody Levels, the Worse My Thyroid Disease\n\n Clinical Symptoms Are More Reliable Than Blood Tests\n\nChapter 22: Ten Ways to Maximize Thyroid Health\n\n Screening at Appropriate Intervals\n\n Checking Thyroid Function As Your Body Changes\n\n Performing a \"Neck Check\"\n\n Getting Enough Iodine to Satisfy Your Thyroid\n\n Stopping Thyroid Medication, If Possible\n\n Using Both Types of Thyroid Hormone\n\n Preventing the Regrowth of Thyroid Cancer\n\n Using the Same Thyroid Preparation\n\n Anticipating Drug Interactions\n\n Protecting Your Thyroid from Radiation\n\n Keeping Up-to-Date with Thyroid Discoveries\n\nChapter 23: Ten Questions Readers Have Posed\n\n Basing Doses of Methimazole on TSH\n\n Reversing Cold Sensitivity\n\n Treating a Teenager for Hyperthyroidism\n\n Taking Methimazole All at Once\n\n Insisting on Radioactive Iodine Treatment\n\n Treating with Thyroid after Pregnancy\n\n Explaining Joint Problems\n\n Taking Antithyroid Drugs Long Term\n\n Reversing Chronic Thyroiditis\n\n Changing Thyroid Dosage\n\nPart V : Appendixes\n\nAppendix A: A Glossary of Key Terms\n\nAppendix B: Sources of More Information\n\n## Introduction\n\nWhen the first edition of this book was published more than four years ago, I knew that knowledge of the thyroid and its diseases was minimal among the general public, but I had no idea of the burning desire of that same public to know more. Judging by the many thousands of copies that have been sold and the hundreds of e-mails that I have received, this book filled a huge gap. So many of you have written to thank me for helping you to understand what the thyroid does when it's working normally and how to tell when it isn't working normally.\n\nThe purpose of this second edition is to educate you about the newest developments since the previous edition and to fill in the areas that you tell me need more discussion and explanation. I thank you for your praise, your suggestions, and for allowing us specialists to study and understand you for the benefit of others.\n\nAs I entered the psychiatric medical unit at Bellevue Hospital the first day of my internship in 1966, I noticed a loud woman with penetrating eyes. I looked closely at her and saw that her neck was very enlarged. Because I was the new doctor on the unit, I picked up her chart and discovered that she had a case of Graves' disease, a form of excessive thyroid production. For the next few months, I became intimately involved with her problems. She taught me a great deal about thyroid disease and probably represents the explanation for my lifelong interest in this subject. I've taken care of many such patients over the years (though never again in a psychiatric unit), but she stands out in my memory like a first love.\n\nFor hundreds of years, people have understood that a connection exists between a strange-looking growth in the neck and certain diseases. Until about 60 years ago, confusion reigned because people with similar growths in their necks often had opposite conditions. One group would show excessive excitement, nervousness, and shakiness; the other would show depression, sleepiness, and general loss of interest. What the two groups had in common was that they consisted mostly of women.\n\nAround 60 years ago, measuring the chemicals that were coming from those growths (enlarged thyroid glands) became possible, and suddenly the whole picture began to make sense. Since then, a vast amount has been learned about the thyroid, the chemicals (hormones) made in that gland, and the purpose of those hormones.\n\nIn this book, you benefit from the hard work of doctors and other scientists over the last few hundred years. You find that, with very rare exceptions, thyroid diseases, including thyroid cancer, are some of the most easily treated of all disorders (which is why many thyroid specialists say, \"If I have to have a cancer, let it be thyroid cancer.\")\n\nAfter you read this book, I hope you're a lot less confused than the poor thyroid itself, which doesn't know where it is. I once heard the left side of a thyroid say to the right, \"We must be in Capistrano. Here comes another swallow.\" If you've read any of my previous books, _Diabetes For Dummies,_ _Diabetes Cookbook For Dummies,_ and _High Blood Pressure For Dummies,_ you know that I use humor to get my ideas across, a technique that characterizes the _For Dummies_ series. I want to emphasize that I'm not trying to trivialize anyone's suffering by being comic. The work of Norman Cousins and others has shown that humor has healing properties. A positive attitude is far more conducive to a positive outcome than is a negative attitude.\n\n## About This Book\n\nI don't expect you to read this book from cover to cover. Because the first few chapters are a general introduction to the thyroid, you may want to start in Part I, but if you prefer to go right to information about the thyroid condition that affects you, by all means do so. If you run across any terms that you don't understand, look for them in the glossary of terms in Appendix A.\n\nI've written this book as a sort of medical biography of the Dummy family \u2014 Tami Dummy, Stacy Dummy, Linda Dummy, Ken Dummy, and other members of the clan whom you meet during your reading. These folks illustrate the fact that thyroid disease often runs in families. (Exceptions do exist to this fact, which I explain.) You meet members of the Dummy family, as well as some other fine fictional folks, at the beginning of each chapter that describes a thyroid disease so that you have a good picture of the condition I cover in that chapter.\n\nOne very big difference between thyroid disease and the other diseases that I wrote about in _Diabetes For Dummies_ and _High Blood Pressure For Dummies_ is that thyroid disease isn't a lifestyle disease. You can't cure any disease of the thyroid that I know of by changing your diet, exercising more, drinking less alcohol, or smoking fewer cigarettes. Although those changes are good for your health in general, you can't cure thyroid disease on your own. You need your doctor's help and sometimes the help of a specialist. What I hope you gain from this book is a good general knowledge of the thyroid gland and an understanding of the correct approach to thyroid disease. At the least, you should be able to ask much more informed questions and even decide for yourself how you want the doctor to approach your disease in some situations.\n\nMany \"facts\" in the treatment of thyroid disease aren't so factual when you look at the medical research literature. For instance, one \"fact\" dictates that doctors always start with a low dose of thyroid hormone when treating an older person who has low thyroid function in order to avoid overstressing the older person's heart. But research doesn't support this rule. This book points out many such examples of incorrect \"facts\" that doctors often believe with no evidence to support them.\n\n## Conventions Used in This Book\n\nTo help you navigate this book, I use the following conventions:\n\n  _Italic_ text is used for emphasis and to highlight new words and terms that we define in the text.\n\n  **Boldfaced** text is used to indicate keywords in bulleted lists or the action parts of numbered steps.\n\n  Monofont is used for Web addresses. If you find that a specific address in this book has been changed, try scaling it back by going to the main site \u2014 the part of the address that ends in .com, .org, or .edu.\n\n  Sidebars are shaded gray boxes that contain text that's interesting to know but not necessarily critical to your understanding of the chapter or topic.\n\nAnd as much as I'd love to use all nonscientific terms in this book, if I did so, you and your doctor would be speaking two different languages. Therefore, I do use scientific terms, but I explain them in everyday English the first time you run across them. Plus, those difficult terms are defined in the glossary at the back of the book.\n\nThree scientific terms come up over and over again in this book: _thyroxine, triiodothyronine,_ and _thyroid-stimulating hormone_ (also known as _thyrotropin_ ). I explain these terms in detail in Chapter 3. For these three words, I often use abbreviations: Thyroxine is T4, triiodothyronine is T3, and thyroid- stimulating hormone is TSH.\n\n## Assumptions\n\nI make the assumption in this book that you or someone you care about has a thyroid condition that hasn't been treated or perhaps isn't being treated to your satisfaction. If this assumption doesn't apply to you, perhaps you suspect that you have a thyroid condition and want to determine whether you should see a doctor, or you can't get your doctor to run the necessary tests to determine whether a thyroid problem exists. Regardless of your individual situation, this book has valuable information for you.\n\nI try to make no assumptions about what you know related to the thyroid. I don't introduce any new terms without explaining what they are. If you already know a lot about the thyroid and its functions, you can still find new information that adds to your knowledge.\n\n## How This Book Is Organized\n\nThe book is divided into five parts to help you find out all you want to know about the thyroid gland.\n\n## Part I: Examining the Thyroid\n\nHere is where you gain an understanding of the function of the thyroid and its location in your body. You're able to tell if the gland is working the way it should. In this part, you learn about the medical tests that help us determine if something is wrong with your thyroid. Your doctor orders these tests, but you need to understand their meaning and which ones are appropriate for the condition you have. This understanding helps you know the severity of your condition and when it's under control. A test that works in some situations isn't always valid in others. I try to let you know when exceptions occur. Be careful not to frighten your doctor with the extent of your knowledge.\n\nBecause you can't cure your thyroid disease without your doctor's help, and often without the help of a specialist, I tell you how to find a good specialist in this part. Although far too many patients with thyroid disease exist for each one to see one of the limited numbers of specialists, in some cases a specialist is essential, and you need to know how to fine a good one in your area.\n\n## Part II: Diagnosing and Treating Thyroid Conditions\n\nThis part explains each of the conditions that affect the thyroid and how they affect you. By the time you finish with this part of the book, I may be able to retire, because you will know just about everything I know about thyroid disease: how to identify it and how to treat it. External factors also influence your thyroid, particularly drugs you may take and irradiation that you may have had. I discuss these factors in this part of the book.\n\nMany people who wrote to me asked if certain of their symptoms were found in one of the thyroid diseases I discuss. Many people who were already diagnosed with the disease asked me if a particular symptom was part of the disease process. I add a number of minor symptoms to the lists to be more inclusive. The question also arises as to whether the presence of certain symptoms after the disease has been cured means the disease is back. I clear up that issue as well.\n\n## Part III: Reviewing Special Considerations in Thyroid Health\n\nThyroid conditions can have a profound effect on your mental health. You understand what's happening in your brain along with the rest of your body when your thyroid gland is overactive or underactive. Unfortunately, such conditions impair your ability to think, so understanding this book may be more difficult for the person who hasn't received treatment for his or her thyroid condition, which gives me more reason to be as clear as possible. Let me know if I'm not completely successful in doing this.\n\nThroughout the book are many mentions about the hereditary nature of many of the thyroid diseases. A chapter in this part explains how people inherit thyroid diseases. You can do little to alter your genes unless you know a way to choose your parents. In that case, you wouldn't be the same you anyway.\n\nThree groups of people deserve special consideration in this book: pregnant women, children, and the elderly. Thyroid conditions take unusual directions in these groups, so the chapters in this part address their unique difficulties. The final chapter here offers suggestions for ways to improve your thyroid health \u2014 and your health in general \u2014 through diet, exercise, and lifestyle choices.\n\n## Part IV: The Part of Tens\n\nMisinformation about the thyroid is rampant. In this part, I clear up some of that misinformation (though not all, because it accumulates faster than I can address it). I also show you how you can maximize your thyroid health. Thanks to all your questions, I have a new chapter in this part that answers the ten questions that recurred most often in your e-mails and seemed most important to clear up. Many things that seem so obvious to a person who has studied the thyroid and its diseases for thirty years may not be obvious for the person newly diagnosed with a thyroid disease. Keep those questions coming to me at thyroid@drrubin.com, and who knows \u2014 your question may appear in the next edition of this book.\n\n## Part V: Appendixes\n\nIn Appendix A, you find a glossary of medical terms that relate to the thyroid; you may want to bookmark the glossary so you can go back and forth with ease as you read other chapters. In Appendix B, I direct you to the best-of-the-best Web sites, where you can get dependable facts to fill in any blank spots that remain after you read this book. Remember that Web sites are in flux. Some begin, and some close. If you want to be aware of the latest and most reliable Web sites, check at my Web site, www.drrubin.com, every so often. At my Web site, you're able to click on a choice of one of three lists of \"Related Websites\" about diabetes, thyroid, and high blood pressure. They're the most up-to-date and reliable resources on these subjects. And when you're there, you may listen to my healthcasts (podcasts), several of which are about the thyroid gland.\n\n## Icons Used in This Book\n\nBooks in the _For Dummies_ series feature icons in the margins, which direct you toward information that may be of particular interest or importance.\n\nThis icon means the information is essential. You want to be sure you understand it.\n\nThis icon points out important information that can save you time and energy.\n\nThis icon alerts you to situations in which you may need to dial up your doctor for some help.\n\n .jpg)\n\nThis icon warns against potential problems you can encounter, such as the side effects of mixing medications.\n\nThis icon alerts you to information that, while informative, may provide a little more detail than you're looking for.\n\n## Where to Go from Here\n\nWhere you go from here depends on your needs. If you want to understand how the thyroid works, head to Part I. If you or someone you know has a thyroid condition, you may want to pay particular attention to Part II. For help in maintaining good thyroid health, turn to Part III. If you're pregnant or have a child or parent with a thyroid disorder, Part IV is your next stop. In any case, as my mother used to say when she gave me a present, use this book in good health.\n\nIf you've had an unusual or even a humorous thyroid experience you'd like to share, by all means, let me know about it by e-mailing me at thyroid@drrubin.com. Who knows \u2014 I may share it with the world in a future edition of this book.\n\n##### Part I\n\n## Examining the Thyroid\n\nIn this part . . .\n\nW hat exactly is the thyroid gland, and what does it do? In this part, you discover how important this little gland in your neck really is, what function it plays in your body, and how to determine if it is functioning properly. I also help you find a specialist who can help you fight thyroid disease.\n\n##### Chapter 1\n\n## The Big Role of a Little Gland\n\n### In This Chapter\n\n  Crunching numbers: The incidence of thyroid disease\n\n  Recognizing signs, symptoms, and risk factors\n\n  Appreciating your thyroid's hard work\n\n  Giving a sick thyroid some TLC\n\n  Pinpointing times of life that pose special risks\n\nThe thyroid is a little like Rodney Dangerfield: It doesn't get the respect it deserves. Anyone who watches those primetime TV news shows knows about the importance of other body parts \u2014 the heart and lungs sure get a lot of press time. But unless you come face to face with a thyroid problem, chances are that you don't hear much about what this little gland does and how important it is to your good health.\n\nThe fact that you're reading these words tells me that you've encountered a thyroid problem personally. (I suppose you could have just picked this book up off the shelf out of curiosity \u2014 or because you belong to the Dr. Rubin fan club \u2014 but I'm betting that a thyroid problem is the more likely impetus.) Maybe you've recently been diagnosed with a thyroid condition. Or maybe your husband, wife, mother, or friend is receiving treatment for a thyroid problem. You've probably found out at least a little about this mysterious gland. Now you're looking for answers to the questions that keep popping up in your mind:\n\n  What causes this thyroid condition?\n\n  What types of symptoms are related to this thyroid problem?\n\n  How is this thyroid condition treated?\n\n  What are the consequences of leaving it untreated?\n\n  Does treatment end the problem forever?\n\n  What can I (or my husband, wife, mother, or friend) do to help get back to optimal health?\n\nI can't promise that this book will give you every possible answer to your questions. After all, doctors and researchers are constantly discovering new things about the thyroid \u2014 the information here is only as complete as our current knowledge. But if you're looking for concrete information about how the thyroid functions, what makes it malfunction, and what to do when a problem occurs, you're holding the right book.\n\n## Discovering the Extent of the Problem\n\nThyroid disease may be one of the most common diseases in the world. Research indicates that thyroid disease affects more than 200 million people worldwide. Table 1-1 shows the approximate incidence, or number of new cases a year, in 2004 of various types of thyroid disease in the United States, which has a population of more than 275 million.\n\nTable 1-1 Incidence of Thyroid Disorders in the U.S. Hypothyroidism (low thyroid function)  | 1.5 million  \n---|---  \nHyperthyroidism (excessive thyroid function)  | 375,000  \nThyroid cancer  | 37,500  \nDeath due to thyroid cancer  | 2,250\n\nThe incidence of thyroid disease becomes even higher when you factor in careful autopsies done on people who didn't die of a thyroid condition. As many as 60 percent of these people show growths on the thyroid, and 17 percent have small areas of cancer that weren't detected during life.\n\nThese numbers are statistics, but thyroid disease affects individuals. Realizing that many people in the public eye have gone on to great accomplishments after receiving successful treatment for thyroid conditions may help you. Some of the people you may recognize include the following:\n\n  Model Kim Alexis had hypothyroidism.\n\n  Author Isaac Asimov had thyroid cancer.\n\n  Golfers Pat Bradley and Ben Crenshaw both had hyperthyroidism.\n\n  Former President George Bush, former first lady Barbara Bush, and even their dog Millie had hyperthyroidism.\n\n  Runner Gail Devers had hyperthyroidism, while runner Carl Lewis had hypothyroidism.\n\n  Supreme Court Chief Justice William Renquist had the very rare and most aggressive form of thyroid cancer.\n\n  Roger Ebert, the movie critic, had thyroid cancer.\n\n  Former second lady Tipper Gore received treatment for a thyroid growth, as did singer Rod Stewart.\n\nI particularly enjoy the story of Isaac Asimov. He had thyroid cancer at age 52, and he died of unrelated causes at age 72. After his cancer surgery, he wrote about how he'd paid $1,500 for the surgery and then wrote an article about the experience, for which he received $2,000. Asimov said that he had the last laugh on the medical profession and was glad that he didn't finish medical school.\n\nThis list is far from exhaustive, but it should help drive home the point that if diagnosed and treated, thyroid conditions don't need to put a damper on your lifestyle, except in very rare cases.\n\n## Identifying an Unhappy Thyroid\n\nLet's tackle some basics: Where is the thyroid, and how do you know when it needs some tender loving care? Chapter 2 gives you a detailed explanation of how to locate your thyroid, but for now, suffice it to say that it's just below your Adam's apple, at the front of your neck. If your thyroid becomes visible in your neck, if that area of your neck is tender, or if you have some trouble swallowing or breathing, consider visiting your doctor so that he or she can examine your thyroid. Any change in the size or shape of your thyroid can indicate that it's not functioning correctly or that you have growths on your thyroid, called _nodules,_ which should be tested to rule out cancer (see Chapter 7). Soreness or tenderness in the area of your thyroid may indicate that you have an infection or inflammation, which I discuss in Chapter 11.\n\nIn addition to changes in the size and shape of the gland, some very common problems occur when your thyroid malfunctions. If your thyroid function is low, meaning that you aren't producing enough thyroid hormone, (you have _hypothyroidism_ ), you feel cold, tired, and maybe even a little depressed. I know that description doesn't sound very specific \u2014 those symptoms could indicate any number of other physical problems. But low thyroid function is so prevalent that asking your doctor to check it out is worth it if you experience such symptoms, especially if you're over age 35. Chapter 5 gives you the specifics about the causes and symptoms of hypothyroidism.\n\nWhen your thyroid function is too high, meaning that you're producing too much thyroid hormone, (you have _hyperthyroidism_ ), you feel hyper and warm, and your heart races. You may have trouble sitting still, and your emotions may change very rapidly for no clear reason. These symptoms are a little more specific than those for low thyroid function, but again, they could easily result from some cause unrelated to your thyroid. The best way to determine whether a thyroid problem exists is to ask your doctor to check your thyroid function. Chapter 6 offers a detailed look at hyperthyroidism.\n\n## Recognizing Who's at Risk\n\nA few key facts help doctors determine whether thyroid disease is a strong probability:\n\n  Women experience thyroid problems much more frequently than men, as much as 10 to 15 times as often, depending on the condition.\n\n  Thyroid conditions tend to run in families.\n\n  Thyroid problems often arise after the age of 30.\n\nThese facts don't mean that a 20-year-old man with no family history of thyroid problems can't develop a thyroid condition. They simply mean that a 35-year-old woman whose mother was diagnosed with low thyroid function 20 years ago is at greater risk of having a thyroid problem than the young man. With this in mind, the young woman should be sure to tell her doctor about her family history. And she should definitely be tested periodically to make sure her thyroid function is normal.\n\nAbout half (perhaps even more) of all the people with thyroid disorders are undiagnosed. The American Thyroid Association and other experts recommend that thyroid testing begin at age 35 and continue every five years thereafter. Women with family histories of thyroid disease may benefit from even more frequent testing.\n\n## Realizing the Importance of a Healthy Thyroid\n\nYour thyroid gland influences almost every cell and organ in your body, because its general function is to control your metabolism. If your thyroid is functioning correctly, your metabolism should be normal. If your thyroid is working too hard (making too much hormone), your metabolism is too high. The result can be anything from an increased body temperature to an elevated heart rate. When your thyroid function drops below normal and you make too little hormone, so does your metabolism \u2014 you may gain weight, feel tired, and experience digestive problems.\n\nChapter 2 details how your thyroid affects various parts of your body, including your muscles, heart, lungs, stomach, intestines, skin, hair, nails, brain, bones, and sexual organs. (That's quite a list!)\n\n## Treating What Ails You\n\nDepending on the specific thyroid problem, treatment options can range from taking a daily pill to having surgery to remove part or all of the thyroid. I discuss the details of treatment options and offer my opinions about which options are generally best throughout Part II of this book. But keep in mind that no matter what you read here (or anywhere else), you should always discuss your specific situation with your doctor. This book can help you have a more productive conversation with your doctor by explaining the pros and cons of each type of treatment and by suggesting questions to ask your doctor if a treatment doesn't seem to be working for you. It can't, however, act as a substitute for your doctor, because I don't know the ins and outs of your particular case.\n\nHowever, following are the general approaches for treating the most common thyroid conditions:\n\n  **Hypothyroidism:** In general, if you experience hypothyroidism (low thyroid function), your doctor prescribes a daily pill to replace the thyroid hormone that your body is lacking. Many people take this type of pill for the rest of their lives, but some people are able to stop taking it after a few years if lab tests prove that the condition has righted itself. See Chapter 5 for a detailed discussion of treating hypothyroidism.\n\n  **Hyperthyroidism:** Three types of treatment options exist for someone with hyperthyroidism (an overactive thyroid). A patient with this condition may be placed on antithyroid drugs, may be receive a dose of radioactive iodine in a pill in order to destroy part of the thyroid tissue, or may undergo surgery to remove some or all of the thyroid gland. In the United States, most doctors recommend the radioactive iodine treatment for this condition, but I've seen antithyroid drugs work very well for many patients. Doctors generally perform surgery only when a patient can't have one of the other two treatments. Chapter 6 goes into the specifics about each treatment and explains why your doctor may suggest one treatment over the others, depending on your specific situation.\n\n  **Thyroid cancer:** For patients with thyroid cancer, surgery is often required. Doctors may also use radioactive iodine to destroy any thyroid tissue that remains after the surgery. Chapter 8 discusses the treatment of various types of thyroid cancer.\n\n  **Nodules:** Someone whose thyroid has _nodules_ (bumps) may need surgery, may not need treatment at all, or may need a type of treatment that falls between those extremes, such as thyroid hormone replacement or radioactive iodine. See Chapters 7 and 9 for all the details about how your doctor may deal with thyroid bumps and lumps.\n\nSometimes the complications surrounding your thyroid condition are too much for the general physician to handle. At that point, you need a specialist. But how do you go about finding one that you know is competent? To answer this question, I've inserted Chapter 3 into this edition of the book. It tells you what to look for in a thyroid specialist and how to go about finding one. As much as I'd love to personally take care of all of you, considerations of time require that I send you to some other physicians. I give you directions in Chapter 3 to find the best qualified doctor to help you.\n\nOnce you have your specialist, he or she can help you to understand the various tests that doctors run to determine the severity of your thyroid condition and to follow the condition as it improves. These tests range from blood tests to various ways of visualizing the thyroid to biopsies. Chapter 4 provides a basic introduction to these tests and which tests your doctor should order and when. Some old-fashioned doctors are still ordering old-fashioned tests, and I explain these tests in Chapter 4 so you know their meaning. Don't hesitate to tell your doctor that you think a newer test is more appropriate. Refer the doctor to this book if he or she disagrees.\n\nAnd as you can see from the preceding list of treatments, in the course of treatment for thyroid ailments, many people undergo surgery of the thyroid. I want you to understand what to expect if you have surgery, which is why I conclude the chapters on thyroid disease and its treatment with a chapter on surgery of the thyroid, Chapter 13. The most important aspect of such surgery is finding a highly competent surgeon, and I tell you how to do this.\n\n## Examining Additional Contributors to Thyroid Ailments\n\nMany drugs have an effect on the thyroid, and Chapter 10 explains the most important of these effects: whether they're increasing thyroid function or blocking thyroid hormone production. The drugs that can impact your thyroid have all sorts of primary actions, but they also change thyroid function. If you're already on thyroid hormone, you need to understand that these drugs can change your dosage. You may need more or less thyroid hormone. Understanding what you need to do to maintain normal thyroid function while you take a drug for some other reason is important. Make sure you ask your doctor if a new medication interferes with your thyroid medicine.\n\nViruses and bacteria can also invade the thyroid. You may have a mild condition with a little pain in your neck or a severe illness with high fever, severe weakness, chills, and so much neck pain that you need a strong painkiller. Chapter 11 explains viral or bacterial forms of \"thyroiditis,\" which are very different from other forms of thyroiditis, which I explain in Chapters 5 and 11.\n\nBecause thyroid hormones contain a lot of iodine, situations where too little iodine is in your body or too much iodine is in your body also change your thyroid function. Outside the industrialized nations, iodine deficiency causes major disease and even death for millions of people. Theoretically, death from iodine deficiency could be overcome without a great deal of difficulty, but the practical considerations of race and politics have made this very hard to do. In more industrialized nations, too much iodine is a greater problem, and Chapter 12 explains the consequences of both of these situations.\n\n## Realizing the Consequences of Delaying Treatment\n\nEarlier in the chapter, I mention that at least half of all people with thyroid conditions are undiagnosed. Many people die of other causes without ever discovering their thyroid problem, which may lead you to wonder whether the diagnosis and treatment of thyroid problems is really necessary.\n\nIn some situations, a thyroid condition may be so benign that you don't even notice it. For example, many people with thyroid nodules never have any problems except for a little bump on the neck. In those cases, treatment may be unnecessary. Some patients have no symptoms at all, yet the laboratory tests of thyroid function indicate that they have low thyroid hormone production. Debate exists about whether such patients need treatment. I discuss this issue extensively in Chapter 5.\n\nBut for many other people, thyroid conditions are much more serious, having a significant impact on overall health and quality of life. The section \"Realizing the Importance of a Healthy Thyroid,\" earlier in this chapter, gives you a sense of some of the consequences of delaying treatment. If you leave a low-functioning thyroid untreated, you could become so fatigued and depressed that you have trouble just doing your daily activities. With an overactive thyroid, you could experience heart trouble and extreme nervousness. A cancerous thyroid could be life threatening if untreated, depending on the type of cancer. And a thyroid with many nodules could become so enlarged or misshapen that it impacts your ability to swallow or breathe.\n\nUnless your symptoms are already extreme, only lab tests can determine whether treatment for your thyroid condition is necessary. Given how important this little gland is to your health, both physical and mental, I can't imagine not asking your doctor to determine whether you need treatment.\n\n## Paying Attention to Special Groups and Considerations\n\nI believe that everyone should have thyroid tests periodically, especially after age 30, to ensure that their thyroids are working as they should. But certain groups of people need to pay special attention to their thyroid function. Pregnant women, children, and the elderly have even more at stake than other folks when it comes to monitoring thyroid function. For this reason, I devote much of Part III of this book to these three groups of people, as well as to some other important considerations that you need to know about.\n\nDoctors first discover that many patients have a thyroid condition when they have a breakdown in their mental health. They may be depressed, or they may be thought to be manic, unable to sit still and complaining that their heart is racing \u2014 situations where medication and other treatments can cure a disease that appears to be mental in origin if the thyroid is at fault. Chapter 15 shows you how your thyroid affects your mind and how your mind can return to health through treating the underlying thyroid condition. If I accomplish just one thing with this book, I hope I can raise your awareness of the mental consequences of thyroid disease, which can have such devastating effects if left undiagnosed and untreated.\n\nA lot is new in our understanding of the thyroid in health and disease, which is the main reason that you're now reading the second edition of this book. I explore the most important of these advances in Chapter 16, so don't miss it. Nevertheless, science keeps finding even more valuable information, so be sure to go to my Web site at www.drrubin.com and click on \"Thyroid\" under the topic \"Related Websites\" to find the information that comes out even after this book is published, the stuff that will make it into the third edition.\n\nPregnancy can have a big impact on a woman's thyroid, whether she had a thyroid condition prior to the pregnancy or not. If she does have a known thyroid condition, her doctor monitors it closely during pregnancy, because her treatment may need altering. But if she doesn't have a thyroid condition, she and her doctor should watch carefully for signs and symptoms of thyroid problems, which the physiological changes she's experiencing can trigger.\n\nNot only is a healthy thyroid crucial for the mother during pregnancy, but it's essential for the development of the fetus as well. For details about what to watch for during pregnancy and the types of problems a thyroid condition can create for mother and child, see Chapter 17. You also find information about the thyroid problems that can arise even after the pregnancy, which can be very devastating to the new mother.\n\nChapter 18 discusses the importance of thyroid screening after the baby is born. Screening is mandatory by law, because a healthy thyroid is necessary for proper mental and physical development. If you're a parent of an infant or young child, be sure to take a look at Chapter 18 so you understand what the screening is for, what risks children of parents with thyroid disease face, and how you and your doctor can reduce those risks.\n\nThe third group that should pay special attention to thyroid health is the elderly (for purposes of this discussion, people age 70 and over). The reason they're at such risk for thyroid disease is because the symptoms of a thyroid condition so often mirror symptoms of other ailments. If an elderly person is known to have a heart or blood pressure problem, a doctor may overlook a possible diagnosis of thyroid disease and attribute his or her symptoms to another condition. To confuse the issue even more, elderly people often experience symptoms that are _opposite_ of what we expect to see with a certain thyroid condition. For example, an elderly person with a low-functioning thyroid may actually lose weight (instead of gaining weight, which would be expected), because he or she is depressed and loses interest in food. Chapter 19 helps you to understand how thyroid disease affects you if you're elderly or if you have an elderly relative.\n\n## Keeping the Rest of Your Body Healthy\n\nSo you or a loved one has received a diagnosis of a thyroid problem \u2014 what next? You start taking a prescription, or you undergo another type of treatment, and you wonder what else you should be doing to help yourself along toward better health. Did you do something that led to this problem in the first place? Can you make some change in your lifestyle that will lead to a cure?\n\nI wish I could just tell you that if you ate more lima beans and got eight hours of sleep each night, your thyroid would return to perfect health. I could stop writing right now if that were the case. Unfortunately, the line between lifestyle choices and thyroid health isn't quite so straight. Your lifestyle definitely plays a role in your thyroid health, but lifestyle doesn't seem to cause thyroid conditions in the first place. If you receive a diagnosis of a hyperactive thyroid, for example, you most likely have the condition because you inherited a certain gene (or group of genes), as I discuss in Chapter 14. But if your life is full of stress, if you sleep only five hours a night, and if you drink lots of caffeine to get through the day, you definitely aren't doing your thyroid any favors. You may be aggravating the symptoms of your thyroid condition through your lifestyle choices. If you make some positive changes to your eating, sleeping, and exercise habits, your thyroid will definitely benefit.\n\nIn Chapter 20, I suggest ways that you can take a proactive role in upgrading your thyroid health by improving your diet, reducing your stress, exercising on a regular basis, and keeping a close eye on other aspects of your lifestyle.\n\nYour thyroid gland doesn't exist in a vacuum. Your diet, the exercise you do, and your lifestyle in general all affect it. Although I've said that poor lifestyle choices don't cause thyroid disease, a healthy lifestyle will help to make any thyroid treatment work to its greatest extent, which is why I go into the basics of achieving a healthy lifestyle in Chapter 20. Chapter 20 informs you how the thyroid affects your weight. You may be surprised.\n\nFinally, in the traditional Part of Tens, I offer ten or more things you need to know about myths surrounding the thyroid (Chapter 21) and about maximizing thyroid health (Chapter 22). You also find a new chapter that you've helped me to write in a way. In Chapter 23, I try to answer the major questions that you've asked me over the past few years since the first edition of the book was published. I hope you keep writing to me at thyroid@drrubin.com so I can continue to address your concerns about the thyroid gland. Many aspects of the thyroid that I take for granted may be unclear to you. I need you to let me know about them. If I can't put them into the next edition of this book, I can at least reply to your questions immediately through e-mail.\n\nMy goal is to help you preserve and defend your thyroid by knowing what to look for no matter what stage of life you're in. The more you know about the signs and symptoms of thyroid disease, the earlier you're able to alert your doctor that thyroid function tests may be a good idea.\n\n## Staying Informed\n\nDoctors don't know everything. We do, however, tend to have an insatiable curiosity that drives us to always seek more information about the conditions we encounter. For this reason, new discoveries and treatment breakthroughs are popping up all the time. By the time this book is printed, doctors will have conducted hundreds of new studies that suggest or prove something new about thyroid diseases and their treatment.\n\nI can't update this book every time I discover something new, but you can still stay on top of the latest discoveries thanks to the speed of the Internet. In Appendix B, I direct you to electronic resources that you can use to stay up to date on thyroid health. If you use only one of these resources, I hope that it's my own Web page, www.drrubin.com, which can link you to all the other sites I recommend, as I describe in the section \"Paying Special Attention.\" And I promise a new edition of this book in a few years will gather together all the newest information so you can always be on the cutting edge of thyroid knowledge.\n\n##### Chapter 2\n\n## How the Thyroid Works\n\n### In This Chapter\n\n  Identifying the thyroid in your body\n\n  Understanding the production of thyroid hormones\n\n  Carrying thyroid hormones around your body\n\n  Recognizing the functions of thyroid hormones\n\n  Knowing when your thyroid is abnormal\n\nThe thyroid is a unique organ (or gland) that affects every part of your body by making hormones and sending them into your bloodstream, which carries them to every other cell and organ. ( _Hormones_ are substances made in one organ and carried by body fluids to another organ, where they produce an effect.) These hormones perform many different functions depending upon the particular organ your thyroid sends them to.\n\nIn this chapter, I show you how to locate your thyroid. If you're really perceptive and your thyroid is on the larger side, you may even be able to feel it. I describe the names of the various hormones that control your thyroid and that your thyroid produces. I show you what happens to your body when you produce thyroid hormones in excessive or insufficient amounts. And because your body contains many organs that perform various functions, I explain what thyroid hormones do in each organ to make that organ work more efficiently. This chapter also shows you how to recognize when the thyroid is abnormal in size and shape.\n\nIf you read this whole chapter, you'll know so much about thyroid function that you'll never suffer from _hamburger hyperthyroidism,_ a real disease that results from eating cuts of meat that include the thyroid gland of the cow. When you finish this chapter, I expect that you'll have a much greater appreciation for your thyroid gland.\n\n## Picturing Your Thyroid\n\nHave you ever seen one of those wonderful anatomy books where you can peel the layers away, starting from the skin and moving down, to see all the inner structures of the body? If you did that with the neck, as soon as you peeled away the skin, you'd find a bony, V-shaped notch created by the connection of the inside edges of the collar bones. The tissue that surrounds the front and sides of the _trachea_ (windpipe) between the V and your Adam's apple is the _thyroid gland._ You can see the gland in Figure 2-1 with some of the more important surrounding structures.\n\n**Figure 2-1:** The thyroid gland and surrounding anatomy.\n\n|     \n---|---\n\nIf you want to find your thyroid (without peeling away your skin), place your index finger at the bony notch below your Adam's apple and push your finger toward the back of your neck. If you then swallow, you may feel something push up against your finger. You're feeling your thyroid gland!\n\nIn Figure 2-1, you see that the thyroid has the shape of a butterfly. The wings of the butterfly are called the _left_ and _right lobes_ of the thyroid. Connecting the lobes is the _isthmus,_ a narrow strip of tissue between the two larger parts. Sometimes you can see a third thyroid lobe called the _pyramidal lobe,_ another narrow strip of thyroid tissue rising up from the isthmus.\n\nIf you look at the thyroid under a microscope, you can see that it consists of rings of cells one cell deep with a clear center that contains the thyroid hormones. The rings are called _follicles_ and are shown in Figure 2-2.\n\n**Figure 2-2:** A micro- scopic view of the thyroid gland.\n\n|     \n---|---\n\nWhen the thyroid is normal in size, it weighs between 10 and 20 grams, or somewhere between one-fiftieth and one-twenty-fifth of a pound \u2014 not terribly large considering everything it does. Each lobe of the thyroid is only about the size of the last bone of your thumb underneath your nail. Even so, the thyroid is one of the largest hormone-producing glands in your body.\n\n## Examining the Production of Thyroid Hormones\n\nThe production of thyroid hormones actually begins in the brain, as shown in Figure 2-3. A structure called the _hypothalamus_ (part of the brain that regulates many basic functions, such as body temperature) produces a hormone called _thyrotrophin-releasing hormone_ (TRH). This hormone is carried a short distance in the brain to the pituitary gland, where it promotes the release of _thyroid-stimulating hormone_ (TSH).\n\n**Figure 2-3:** Your brain stimulates thyroid hormone production.\n\n|     \n---|---\n\nTSH leaves the pituitary gland and travels in the bloodstream to the thyroid. When TSH reaches the thyroid, it prompts two reactions:\n\n  It causes the release of existing thyroid hormone into the blood.\n\n  It prompts the production of more thyroid hormones, which collect in the space inside the follicles (see the section \"Picturing Your Thyroid\" earlier in this chapter), awaiting future release.\n\n## Meeting the hormones\n\nThe two thyroid hormones are thyroxine (T4) and triiodothyronine (T3). T3 is the active form of thyroid hormone. T4 is considered a _prohormone,_ a much weaker chemical that gains its potency only after it's converted to T3 by the thyroid or another organ of the body (wherever thyroid hormones do their work).\n\nThe thyroid gland normally releases about 13 times as much T4 as T3. However, your body as a whole produces only about three times as much T4 as T3. That T3 production gap is closed by organs such as the liver, kidneys, and muscles, which produce most (80 percent) of the T3 in your body through T4 conversion. The thyroid gland itself releases only 20 percent of the T3 it produces every day.\n\nThese production facts have profound importance for the treatment of thyroid hormone deficiencies. Most patients with _hypothyroidism_ (low thyroid function) are deficient in T3 and T4, but during treatment, they receive only T4 (by ingesting daily doses of replacement thyroid hormone). Their bodies must get the T3 they need by converting the T4. Despite the conversion, some patients are still somewhat deficient in T3. I discuss this problem and possible solutions in Chapter 5.\n\n### The birth of thyroid hormones\n\nThyroid hormones are actually made in the follicular cells (see Figure 2-2). Enzymes in the cells add iodine to a compound called _tyrosine_ to produce _monoiodotyrosine_ (one iodine plus tyrosine) and _diiodotyrosine_ (two iodines plus tyrosine). A monoiodotyrosine and a diiodotyrosine are combined to produce triiodotyrosine, or T3. Two diiodotyrosines are combined to produce thyroxine, or T4. These are combined together in a long chain called _thyroglobulin,_ which is sent into the area of colloid in the center of the follicle. When thyroid hormones are needed in your body, thyroglobulin is broken down, and thyroid hormones flow into your bloodstream. The parafollicular cells, or C cells, another type of cell found in the thyroid, are important because they can form a tumor called medullary thyroid cancer (see Chapter 8).\n\n## Identifying the importance of iodine\n\nAnother substance that has a major effect on the production of thyroid hormones is iodine. When iodine is present in large amounts in the blood, it reduces the production of the hormones by blocking the stimulating effect of TSH. Doctors use this function, for example, when a patient is extremely hyperthyroid (see Chapter 6) to bring the patient under control rapidly. Iodine may also be used before surgery to remove large, overactive thyroid glands to quickly reduce the blood flow to the thyroid to reduce bleeding.\n\nInterestingly, because much of the thyroid hormone _is_ iodine, a lack of iodine also reduces the production of thyroid hormone. A large part of the world suffers from thyroid disease due to lack of iodine, which I discuss in Chapter 12.\n\nBoth thyroid hormones, T3 and T4, contain iodine (T4 contains four parts of iodine, which make up 65 percent of its weight; T3 has three parts of iodine, which make up 58 percent of its weight; see the sidebar \"The birth of thyroid hormones\" for more information), which means that the thyroid gland must trap iodine to make the hormones. Therefore, doctors can study the workings of the thyroid by substituting radioactive iodine for regular iodine. They can detect and measure radioactive iodine with a refined version of a Geiger counter (see Chapter 4) to perform a study called a _thyroid scan and uptake._\n\nOther organs, such as the breasts, the stomach, and the salivary glands, also trap iodine. However, no other organ in the human body besides the thyroid gland uses iodine for any important purpose. Thyroid hormones are the only significant chemicals that contain iodine in the human body.\n\n### All aboard! Proteins carry your thyroid hormones\n\nExactly why proteins carry thyroid hormones isn't clear. Among the theories is that by having so much thyroid hormone bound to proteins and therefore inactive, large changes in the thyroid gland's output of thyroid hormones don't result in large changes in thyroid activity. Another theory is that the combination of the hormone and the protein produces a large molecule, which can't escape from the body through the urine, thus preserving iodine.\n\nThree different proteins carry thyroid hormones. By far the most important is _thyroxine-binding globulin,_ responsible for carrying 75 percent of the hormone in the blood. _Transthyretin,_ which used to be called _thyroxine-binding prealbumin,_ carries 20 percent of the thyroid hormones. _Thyroxine-binding albumin_ carries the other 5 percent.\n\n## Moving thyroid hormones around\n\nAfter your thyroid releases T3 and T4, the hormones don't just travel loosely in the blood to their targets. Proteins in your bloodstream carry them.\n\nOnly _free_ thyroid hormones can leave your blood and enter your cells. The rest are solidly bound to proteins, which means they're not available to perform the actions of thyroid hormone. Because 99.97 percent of thyroid hormone is attached to proteins, only 0.03 percent is free and active. When a doctor measures the _total_ thyroid hormone in your blood, he or she measures bound hormone along with the unbound hormone. If the doctor knows only the total T4 amount in your blood, he or she needs to order a second test to determine the unbound T4 \u2014 the fraction of the total hormone free in your blood.\n\nKnowing the distinction between free and bound hormones is important because many drugs and diseases alter the blood levels of _thyroxine-binding proteins_ \u2014 one of the proteins that thyroid hormones bind to (see the following sidebar). If a drug like estrogen, for example, increases the amount of thyroxine-binding proteins in your body, your thyroid makes more thyroid hormone to bind to these proteins, keeping the unbound thyroid hormone constant and normal. Yet, the results of a total T4 blood test (see Chapter 4) will be elevated. Conversely, testosterone, the male hormone, causes a decrease in the thyroxine-binding proteins. If your testosterone level rises, your thyroid makes less thyroxine, and a measurement of total T4 shows a decrease (while the unbound T4 again remains normal). In both these situations, the measurement of total thyroxine will suggest that your thyroid function is not normal when, in fact, it is normal.\n\n## Regulating thyroid hormones with TSH\n\nThe released T3 and T4 circulate throughout your body, reaching, among other places, the pituitary gland. If the pituitary gland detects enough thyroid hormone, it continues to release the same amount of TSH. If your thyroid hormone levels drop for any reason, the pituitary releases more TSH to stimulate the thyroid to make and release more thyroid hormone, if it can. (If your TSH levels are elevated, it can also stimulate overall growth of your thyroid that can lead to an enlarged thyroid, called a _goiter._ ) If your thyroid hormone levels are excessive, TSH release falls. (This is called the _negative feedback for TSH release._ )\n\nIn short, as thyroid hormone falls, TSH rises, and as thyroid hormone rises, TSH falls. Because T3, T4, and TSH can all be measured in the blood, it's simple to determine the state of your thyroid function (see Chapter 4).\n\nTSH is also regulated by the release of thyrotrophin-releasing hormone (TRH) from the hypothalamus. Between TRH and thyroid hormones, the level of TSH in your blood remains very stable throughout life, and abnormal levels usually mean some disease is present.\n\n## Understanding the Function of Thyroid Hormones\n\nThyroid hormones are active in just about every cell and organ of your body. They perform general functions that increase the efficiency of each organ's specific functions, whatever they may be. The following sections tell you all about those functions of thyroid hormones and explain what too much or too little of the hormones would do to a healthy person.\n\nMany bodily changes may be caused by other factors besides too little or too much thyroid hormone. For example, an infection can raise your body temperature, just as too much thyroid hormone can. Also, if you have a condition like menopause that tends to be associated with dry skin, this symptom may predominate even if you have hyperthyroidism that tends to cause moist skin. The information in this section shows you what classic symptoms of thyroid problems look like, but each case can have individual variations.\n\n### How thyroid hormone works\n\nThyroid hormone attaches to compounds called _receptors_ in the membranes' surrounding cells and enters the cells with these receptors. Once inside the cells, the combination of hormone and receptor interacts with the DNA, the material that makes up the genetic code. The end result is the activity of thyroid hormone in that particular cell. This way of affecting your cells explains why it takes weeks to feel the effect of thyroid hormone. Changes in the DNA take a long time both to do and undo, so when you stop taking thyroid, it takes weeks before your body realizes that it is not getting thyroid any longer and you begin to feel low thyroid function. On the other hand, when you give antithyroid drugs that block the production of thyroid hormone, there is a large store of thyroid hormone in the follicles of the gland that must be used up before the concentration of thyroid hormone falls in the blood.\n\nFor example, in heart muscle, thyroid hormone and its receptor act to stimulate the formation of the proteins of muscle cells that increase contraction of heart muscle while suppressing the proteins of these same muscle cells that reduce contraction. The ratio of proteins changes in favor of more contraction, and the muscle cell contracts harder as it is exposed to more thyroid hormone.\n\nAnother example is that the combination of thyroid hormone and receptor stimulates metabolic activities in all cells throughout the body by increasing the activity of genes that produce enzymes, the proteins that are necessary for chemical reactions in the body. As these chemical reactions are revved up, much like increasing the fuel entering an engine, the body heats up, and this is translated into an increased body temperature. If thyroid hormone is reduced, metabolism declines, less heat is produced, and the body temperature falls.\n\n## General functions\n\nIn every cell, thyroid hormones cause that cell to make more _protein enzymes,_ the chemicals that promote your _metabolism,_ the sum total of all the chemical reactions going on in your body to form more tissue and to create energy. Think of your body as a machine. Adding extra thyroid hormone is like adding a richer fuel to it. The result is usually a revving up of the machine \u2014 like going from 2,000 revolutions per minute to 4,000 or more revolutions per minute, depending upon the amount of hormone added. Thus, when more thyroid hormone is present in your body, more chemical reactions are taking place.\n\n### Metabolism\n\nThe _basal metabolic rate_ (BMR) is an overall measure of the amount of metabolism that's taking place in your body. Increased thyroid hormone may increase your BMR by as much as 60 to 100 percent. Any machine that increases its activity heats up; likewise, your body heats up with more thyroid hormone, and the result is a higher body temperature. At the other end of the spectrum, not enough thyroid hormone results in an abnormally low body temperature as your \"machine\" cools down.\n\nAs more metabolism takes place, your body burns more of your food intake for energy, so less is left to be stored. Your body detects the need for more energy and you get hungrier, but your faster metabolism usually more than offsets any increase in food intake. The net result is that you lose weight. However, if you take in too much extra food, you can actually gain weight. Check out Chapter 20 for more information on the relationship between your metabolism, your thyroid, diet, exercise, and weight loss.\n\n### Development\n\nNormal development requires sufficient thyroid hormone. In one of the early thyroid experiments that showed this fact, researchers deprived tadpoles of thyroid hormone. The result was that they didn't develop into frogs. People deprived of thyroid hormone don't develop normally, either. In particular, the human brain fails to develop, and mental retardation is the result.\n\n### Muscle function\n\nYour muscles need thyroid hormone for proper functioning, but too much isn't a good thing. An excess of thyroid hormone results in muscle wasting, as your body consumes muscle tissue for energy. As you lose muscle, you become weaker. If too much thyroid hormone is present, the nerves going to the muscles also show increased excitability, resulting in increased reflexes and tremor in the muscles.\n\n .jpg)\n\nDon't use thyroid hormone in an attempt to lose weight. Many diet programs, recognizing that increased thyroid hormone results in weight loss, use thyroid hormones. An overabundance of thyroid hormone results in muscle loss, so the weight that you lose isn't just fat, but also muscle, the so-called lean tissue of your body. You don't want to lose lean tissue.\n\n### Energy sources\n\nIn addition to the protein found in your muscles, thyroid hormone affects the other sources of energy in your body, namely _carbohydrates_ and _fats._ Carbohy- drates are the main sources of immediate energy in the body, so your body uses them up faster than normal when thyroid hormone levels rise, resulting in more heat production. Your body also uses up fat faster than normal. The result is a lowering of the different kinds of fat in your body, namely _cholesterol_ and _triglycerides._ On the other hand, when thyroid hormone levels drop, the fats accumulate in your liver, and the level of cholesterol in your blood rises.\n\nBecause chemical reactions require vitamins, your need for vitamins increases when your body produces more thyroid hormone. Increased thyroid hormones cause a more rapid breakdown of the vitamins. Vitamins have little effect on the thyroid gland itself, except for those that contain iodine (often in the form of kelp or seaweed).\n\n .jpg)\n\nAvoid vitamins that contain iodine when you're being treated for hyperthyroidism or have a condition like multinodular goiter (see Chapter 9), where the iodine maybe used to make too much thyroid hormone.\n\n## Organ-specific functions\n\nEvery organ in your body requires thyroid hormone to function normally. When that hormone is lacking, the organs tend to do less of their usual functions. When too much thyroid hormone is present, the organs do more than they should. In this section, you find the most important changes brought on by abnormal amounts of thyroid hormone in your body. By no means is this discussion complete; that would require a large book by itself, and many of the changes that occur are too subtle to result in signs or symptoms that you can detect.\n\n### The heart and blood vessels\n\nYour heart needs thyroid hormone for proper pumping. If an insufficient amount of thyroid hormone is present, the heart slows down and its pumping action decreases. If thyroid hormone is severely lacking, heart failure can result. Conversely, when thyroid hormone levels rise, your heart rate becomes too rapid. Your heart pumps out more blood at first, but if this increased pumping is allowed to go on for too long, the end result may be decreased heart strength because excessive thyroid hormone causes muscle wasting. (The heart is made of muscle.)\n\nDepending upon the level of your physical activity, your normal resting heart rate should be between 60 and 80. (If you're in good physical condition, your heart rate should be around 60.) People with too much T4 often have a heart rate of 120 or faster.\n\nThyroid hormone also stimulates blood vessels to open up more, which increases blood flow in many organs of the body. One of the main objects of this increased blood flow is the thyroid gland itself. So much blood is flowing through the gland that you can actually feel the movement of the blood when you place a hand over your thyroid gland, and you can hear the whoosing sound of increased blood flow when you place a stethoscope over the gland.\n\n### The lungs\n\nThyroid hormone is necessary for proper formation of the lungs, because lung cells require thyroid hormone to grow properly. When animals are deprived of thyroid hormone during their development, their lung weight is decreased compared to animals that have enough thyroid hormone.\n\nAs you increase your metabolism, you need more oxygen for the chemical reactions in your body to take place. Oxygen comes into the body through your lungs. Your respiration rate, normally about 16 times per minute, speeds up to bring in more oxygen. However, even an increased respiration rate may fail to provide the body with enough oxygen if the muscular diaphragm and chest muscles are wasting from excess thyroid hormone.\n\n### The stomach, intestines, and liver\n\nThyroid hormone is required for the muscles of the stomach and intestines to push food along for digestion and excretion. When an insufficient amount of thyroid hormone is present, intestinal movement slows, as well as the absorption of food. The common complaint is constipation. On the other hand, too much thyroid hormone speeds up the bowels. Loose bowel movements, more frequent bowel movements, or diarrhea may be the result.\n\nThyroid hormone also permits normal development of the liver and the enzymes that the liver uses to break down many substances in the blood and to form sugar from other substances. Thyroid hormone is needed for the liver to form bile and handle cholesterol properly.\n\n### The skin, hair, and nails\n\nThyroid hormone is necessary to maintain your skin, hair and nails. Skin temperature is controlled by the flow of blood to the skin, which is maintained by your thyroid.\n\nThe increase in blood flow with increased thyroid hormone is especially prominent in your skin. The skin often feels warm, and perspiration may increase, so it also feels moist. When thyroid hormone levels fall, the skin often becomes dry and may scale, and it feels cold to the touch. The nails can't achieve their proper toughness without enough thyroid hormone and may break easily. The hair, likewise, is fragile, dry, and brittle, and excessive hair loss is a common complaint when an insufficient amount of thyroid hormone is present.\n\n### The brain and cerebral functioning\n\nAs the brain develops, it requires thyroid hormone to form its cells. Absence of thyroid hormone can lead to mental retardation. Even after birth, the brain is still developing and requires thyroid hormone to develop properly for up to three years. The right amount of thyroid hormone is necessary for normal mental function later in life.\n\nChapter 15 details the changes in mood that occur with too much or too little thyroid hormone. A person with excessive thyroid hormone may feel as if his or her brain is racing, which can result in extreme nervousness. The person may feel anxious without knowing why and become worried about minor things. In extreme cases, the result may be paranoia. Not enough thyroid hormone can lead to mental dullness and depression.\n\n### Sexual functioning and menstruation\n\nNormal sexual development requires thyroid hormone, especially in women. Without it, sexual development is delayed, and the onset of menstrual function comes later. Proper development of the uterus requires thyroid hormone as well.\n\nThyroid hormone is also needed for normal sexual function. Both men and women lose interest in sex when an insufficient amount of thyroid hormone is present. They don't necessarily have increased interest in sex when thyroid hormone levels rise, because so many psychological and physical problems result from the increase.\n\nThe menstrual cycle depends on adequate thyroid hormone to proceed normally. Women with a lack of thyroid hormone may have trouble conceiving a baby. They tend to have increased menstrual flow and may become anemic (resulting from losing too much blood). Too much thyroid hormone often decreases the menstrual flow or causes missed periods.\n\n### The bones and teeth\n\nThyroid hormones help keep bone growth normal. When too little thyroid hormone is present in early life, your bones show delayed development and don't grow to their correct length. The result is a dwarf with short arms and legs and a larger trunk. If thyroid hormone is lacking after growth has stopped, your bones appear more dense than normal because of decreased bone turnover.\n\nWith an overabundance of thyroid hormone, due to taking too much thyroid hormone or inadequate treatment of hyperthyroidism, bone turnover and loss increases. The result may have the appearance of osteoporosis, the kind of bone loss that occurs in women after menopause. However, it rarely results in bone fractures if the increased thyroid hormone is controlled with treatment (because the bone loss stops).\n\nYour teeth require thyroid hormone to erupt at the proper time and to grow to the proper size. When thyroid hormone is lacking, the roots of your teeth grow more slowly, your dental enamel is thinner, and you lose your \"baby teeth\" much later.\n\n##### Chapter 3\n\n## Finding a Thyroid Doctor\n\n### In This Chapter\n\n  Asking the right questions\n\n  Searching your insurance plan\n\n  Checking with your doctor, friends and family\n\n  Approaching major medical centers\n\n  Looking at magazines\n\n  Making use of the Internet\n\nYou may have a good idea that your thyroid gland is the cause of your medical problem but don't know much about it. You do know that you need the help of an expert, because your regular doctor doesn't know much about thyroid disease. How do you go about finding the specialist who can help you? As much as I'd like to schedule you for an appointment with me, my schedule is stretched to the breaking point. Instead, this chapter will provide you with everything you need to find a qualified thyroid doctor in your area. Plenty of qualified specialists are out there whom I would go to if I had a problem.\n\nI do, however, make the time to answer general questions about thyroid disease, which I receive all the time by e-mail. You can write me at thyroid@drrubin.com. But I have an unbreakable rule: I never answer specific questions about your case without the opportunity to ask you questions directly and examine you with my own hands. Any doctor who answers your specific questions without examining you personally breaks one of the basic rules of our profession.\n\nIn this chapter, I tell you the process that I use to find a good doctor, and you can apply this process not only to finding a thyroid doctor but a doctor for any special and unusual medical problem that you feel your general physician isn't adequately addressing. Although some of my recommendations don't apply exactly to physicians other than thyroid doctors, as you can see, most of them do.\n\nYou're fortunate, because your options for finding an excellent doctor are vast, especially if you possess the essential tool for conducting your search \u2014 a computer with an Internet connection. As this chapter shows you, you may find a doctor long before you need to search the Internet, but even if you do, you can still use the Internet to verify your doctor's qualifications. Qualifications may not be the first thing you research about your doctor, but as I explain below, they should definitely be the last.\n\n## Asking the Right Questions\n\nYou may think that I'm starting at the end by telling you the right questions to ask potential specialists before even signing on with them. First, you're probably thinking, I've got to find a doctor. But most of these questions can and should be answered \u2014 correctly \u2014 before you get to the doctor's office. A few of the following questions do require a face-to-face meeting with the doctor; so wait to ask those questions at your first appointment. But if your candidate fits in with the criteria I list here, feel pretty confident that you've found the right office. As you read through this material, you also get an introduction to the doctors who work with thyroid patients.\n\nIf the answer to either of the following first two questions is no, you probably don't want to go to that doctor.\n\n## Is the doctor board certified in endocrinology?\n\nThe medical profession is very careful to permit only the most qualified doctors to take care of complicated medical problems. The U.S. system of medical education ensures that doctors don't graduate before they are fully qualified to manage the problems they want to treat. Early in their education, medical students choose to pursue one path of medicine, surgery, pediatrics, or psychiatry. After that, they're observed by other doctors who already possess the qualifications they are trying to obtain. After young doctors have gone through the years of training thought necessary to achieve expertise in their specialty, they take an examination, called a \"board\" examination because one of the educational organizations accepted by all physicians \u2014 the American Board of Internal Medicine, the American Board of Surgery, the American Board of Pediatrics, or the American Board of Psychiatry \u2014 administers it.\n\nIf the doctor passes a board examination, he or she is said to be qualified to practice in the general specialty of internal medicine, surgery, pediatrics, or psychiatry the doctor has chosen. The doctor who wants to be able to call himself a subspecialist, isn't done yet. After enough years of training in that subspecialty, whether it is _endocrinology,_ which mainly treats people with diabetes and thyroid disease (but covers diseases of many other glands that happen to occur less commonly), or _nephrology,_ which treats people with kidney disease or _cardiology,_ which treats diseases of the heart, the doctor must take and pass another examination. This examination emphasizes the skills that someone in that subspecialty must possess, and only when the doctor passes it can he call himself a board-certified subspecialist in that particular field, and he must have a certificate to prove it.\n\nAfter he or she picks a subspecialty, the doctor can choose to take care of all the various components of that subspecialty or focus on one of them. For example, endocrinologists can further specialize in diabetes, thyroid disease, adrenal disease, parathyroid disease, and so forth or work in only one of them as a kind of \"sub-subspecialist.\" There's no examination that a sub- subspecialist takes. Doctors who choose only one area, like thyroid disease, are often found at medical centers, while doctors who take care of all areas are often found in the community, but this isn't always the case.\n\nAny doctor can call himself a specialist in anything and can even have some certificate that seems to confirm it, but you can check for yourself by searching for a doctor's name on the Web site of a particular specialty board. For the internal medicine specialties, you can go to www.abim.org and click on \"Who is Certified.\" By filling in the name of the doctor, you can find out whether that doctor is certified and in what specialty and subspecialty. Your potential thyroid doctor should be board certified in the specialty of internal medicine and the subspecialty of endocrinology and metabolism.\n\nFinding out if a doctor who is a surgeon is board certified isn't quite so easy. You have to call the American Board of Surgery at 215-568-4000 to verify the board status of the doctor you name. For written confirmation, you must provide a written request. You can write them at: The American Board of Surgery, 1617 John F. Kennedy Blvd., Suite 860, Philadelphia, PA 19103.\n\nIf the doctor is board certified, you know she possesses a very good knowledge of her specialty and has trained for enough years to be allowed to take the test. However, she may have taken the test 25 years ago and trained before that. The boards offer re-certification examinations, so if she has passed a re-certification examination in the last few years, that's an excellent sign of a doctor who wants to keep up to date. You can't pass these examinations without a strong knowledge of your subject.\n\n## Does the doctor belong to a specialty society?\n\nTo further medical education, the medical profession has organized itself into specialty societies that hold meetings at least annually and usually publish a monthly journal containing articles about their specialty. Your potential doctor should belong to one of these specialty societies and, hopefully, even attend meetings regularly.\n\nHow can you answer this question? You can go to the Web site of one of the societies and see if your potential doctor is listed as a member. The societies for thyroid disease and their corresponding Web sites are\n\n  American Thyroid Association at www.thyroid.org\n\n  American Association of Clinical Endocrinologists at www.aace.com\n\n  American Association of Endocrine Surgeons at www.endocrinesurgery.org\n\n  Endocrine Society at www.endo-society.org\n\n  Lawson Wilkins Pediatric Endocrine Society at www.lwpes.org\n\nIf you need a specialist, such as an eye doctor for thyroid eye disease, you can find a clickable list of doctors participating in specialty societies at the following Web site, maintained by the National Institutes of Health: www.nlm.nih.gov\/medlineplus\/directories.html.\n\nTo find out whether your potential doctor attends a specialty society's meetings, you have to ask the doctor. Unfortunately, knowing a doctor attends a meeting still doesn't tell you if he spends his time at the educational programs or the roulette table.\n\n## Where was the doctor trained?\n\nIf the answers to the previous two questions are yes, you don't need to ask where your doctor was trained. If the answer to either one of them is no, you probably don't want to go to this doctor. But if you still do for other reasons, like your mother-in-law swears by him, find out where he did his medical-school and post-graduate training.\n\nThe states license doctors. To receive a license, doctors must prove they are qualified to practice, but some medical schools aren't as good as others, particularly schools outside the United States on small islands. Plenty of great medical schools exist outside the United States. Just make sure your potential doctor went to one of them if she was not educated here.\n\nCompetent thyroid specialists should have done their post-graduate specialty training in a hospital that is known for its division of endocrinology with endocrine fellows. _Fellows_ are doctors who have completed their general training in internal medicine and are now devoting their time to their subspecialty of endocrinology. Even some American hospitals fail this test.\n\nAsk doctors' nurses or receptionists where doctors trained. Find out where the doctor did her fellowship in endocrinology. Any unwillingness to provide this information should lead you to seek a doctor elsewhere.\n\n## Has the doctor been disciplined for any infraction?\n\nThe licensing department of the state in which the doctor practices can tell you whether a doctor has been disciplined. States often make accessing doctors' infractions very easy by providing a Web site that lists pertinent information after you type in the doctor's name.\n\nBe wary of doctors who have been disciplined. By the time the state licensing department disciplines a doctor, that doctor has already taken every possible route to avoid discipline. The fact that discipline took place anyway suggests that there's definite substance to the infraction. Examples of infractions include using illegal drugs or excessive amounts of alcohol, failure to answer licensing questions truthfully, sexual contact with patients, and a host of other possibilities.\n\n## Consulting Possible Sources\n\nYou may be limited to certain doctors in your insurance plan, you may have total trust in your personal physician, or you may feel that your family and friends are the best source for information about doctors. This section discusses how you use these various resources to find the best possible medical care.\n\n## Searching your insurance plan\n\nAll insurance plans, in order to be competitive, offer a number of doctors in each medical specialty and subspecialty. Your plan may mandate that you can go to only doctors who have a contract with your plan. Sometimes a plan pays almost all the cost of seeing a doctor within the plan and less for seeing a doctor outside the plan. If you don't want to end up with a big financial burden, find out your plan's stipulations before you go.\n\nMost plans now offer a Web site where you can find the names of the specialists who belong to it and whether the specialists are accepting new patients. The fact that a health plan lists a doctor is reassuring because it shows the plan has done a certain amount of checking on a doctor's credentials. But you still need to ask the hard questions I discuss in the preceding section, \"Asking the Right Questions.\" If you have a choice of several specialists, then the questions I give you can separate them out so you choose the one who looks the best.\n\n## Checking with your doctor\n\nIf you trust your general doctor, he or she may be the best source for finding a specialist. Your doctor usually knows the other physicians in the community, refers patients to many of them, and has an idea of the quality of the work that other doctors do. You can always ask your doctor that old standby question, \"Would you send your mother to this physician?\" Of course, you don't know if your doctor particularly cares for his mother. But I don't recommend following up with \"Do you love your mother?\"\n\nEven if your doctor recommends the specialist, still use the information I provide in the \"Asking the Right Questions\" section of this chapter to evaluate the specialist. You have to weigh the value of a specialist who, for example, fails the tests of board certification and membership in a specialty society but holds the respect of your primary doctor.\n\nSome insurance plans actually require that you have authorization from your primary physician before you can see a specialist, and then only one that is within your plan. If you don't get this authorization, you have to pay out of your own pocket.\n\nNo doctor has the right to tell you not to see another doctor, in any specialty. If you feel you need different advice, are not satisfied with the advice you are getting, or just want to talk to someone else, feel free to do so.\n\n## Turning to family and friends\n\nSecond to your doctor's advice, you may find the advice of family and friends helpful. Because thyroid disease is often hereditary (found in multiple members of the same family, who have many similar genes), chances are that your mother, sister, or aunt has seen a thyroid specialist at one time or another and can happily offer you a recommendation. (Thyroid disease is much more common among women than men.) And because thyroid disease is so common, as I discuss in Chapter 2, one or another of your friends has likely seen a thyroid specialist. You can first judge the quality of their health before listening to their advice. Then you have to decide how much respect you have for their opinion.\n\nDon't fail to use the key criteria I discuss in the first sections of this chapter for doctors your family and friends recommend as well. Your aunt or college roommate probably has a good idea of how much time the doctor spends with her patients and whether she listens to them. But unless your aunt has read this book or a similar resource, she doesn't know how to judge the doctor's knowledge of endocrinology.\n\nFinding the perfect physician is hard. You may have to make compromises, but if you do, for the sake of your health, give up a little of the art of medicine in favor of the science of medicine. A doctor who doesn't keep you waiting but gives you the wrong advice isn't for you. A full waiting room is also a poor reason for choosing a doctor. I wrote this book because the general knowledge of thyroid disease is very sparse. Most people don't even know the thyroid exists, much less how knowledgeable their specialist happens to be.\n\n## Approaching major medical centers\n\nYou can't go far wrong if you seek a specialist in a major medical center. Places like the Mayo Clinic and the Cleveland Clinic or university centers like New York University or the University of California\u2013San Francisco Medical Center are bound to have experts on your condition. The benefits of seeing a specialist in a major medical center are numerous:\n\n  **Specialization:** Major medical centers usually have a division of endocrinology. Within their endocrinology division, they have subdivisions devoted to thyroid disease, diabetes, pituitary disease, and all the other sub-subspecialties that make up endocrinology, leaving little doubt of the quality of the physicians working in such medical centers.\n\n  **Credentials:** Medical centers do all the research on doctors for you by checking their references and following their skills carefully before promoting them to the position of assistant professor or professor. Your task is to find the right doctor within a center's massive structure.\n\n  **Experience:** In addition, doctors at major medical centers have seen multiple examples of complicated medical cases and have much more experience than doctors in private practice. This depth of experience is particularly significant if your condition is especially complicated.\n\n  **Shared knowledge:** Major medical centers usually have multiple specialists in each division. Your task is to select from among the many specialists. Your own doctor may know the reputation of one or another of them, or you can take a chance. If your problem is complicated, the chances are good that you get to meet all members of the group at one time or another and benefit from the accumulated knowledge of the whole group.\n\nMake sure that your professor is a clinical professor, not a research professor. In medical institutions, the production of research papers, which may have little to do with intact human beings, often earns people promotions. Make sure that your potential doctor regularly sees patients and doesn't spend all of his or her time in a laboratory.\n\nMajor medical centers need new patients constantly, just like any doctor who isn't retiring. So they make it relatively easy for you to get a handle on who's who within the organization. Most centers have a book that lists all their subdivisions and the names of the doctors within them. You can find a copy of a center's book of doctors in its medical library. Often, medical centers send copies to local doctors so doctors know how to refer their patients. Most major medical centers also have a large representation on the Internet, where you can find their list of doctors and the specialist that you need.\n\n## Looking at magazines\n\nMany publications take it upon themselves to rate doctors. The good ones rate doctors by their level of knowledge and the efficiency of their office. When you run across a publication that rates doctors, don't simply take it at face value. Read the small print and ascertain how the ratings were put together. Make sure that you can answer \"yes\" to the following questions:\n\n  Does the publication ask doctors in the community for the names of the best specialists in their opinion?\n\n  Does the publication send out questionnaires to its subscribers, asking them to rate their doctors like they rate their car repair shops?\n\n  Does the publication check with nurses to see which doctors they feel are most qualified?\n\n_Consumer Checkbook,_ an offshoot of _Consumer Reports Magazine,_ which has been providing highly reliable information for the consumer for over 50 years, __ publishes one of the best examples of a trustworthy rating of doctors. _Consumer Checkbook_ asked about 260,000 physicians to name the physicians they would send their loved ones to for care. The result was 20,000 doctors around the country. At the present time, _Consumer Checkbook_ publishes local versions of the magazine for seven areas around the country: Boston, Chicago, Delaware Valley, Puget Sound, San Francisco\/Oakland\/San Jose, Twin Cities, and Washington, DC. _Consumer Checkbook_ has also posted the results for those areas in past issues of its national magazine. However, to help you locate the best doctors as well as the best hospitals, it publishes the national guides _Consumers' Guide to Top Doctors_ and _Consumers' Guide to Hospitals._\n\nYour local city magazine may also have a guide to the best doctors in your area. For example, my local magazine, _San Francisco Magazine,_ in its January 2005 issue published \"520 Best Doctors, Top Bay Area Physicians.\" Similar to _Consumer Checkbook,_ the magazine featured the opinions of other doctors in the community _._ Check back issues of your local publication or call the office of the magazine to find out if it has published such a guide.\n\n## Making use of the Internet\n\nIf you want a list of the doctors who are specialists in thyroid disease in your area, you can use the following Web resources to find a specialist. Start at my Web site, www.drrubin.com, and click on \"Thyroid\" under \"Related Web sites\" on the left side of the page. You then come to a list of the best resources on the Web for thyroid disease, including links to the following societies for thyroid disease.\n\n### American Thyroid Association\n\nStart by clicking on the address for the American Thyroid Association (www.thyroid.org). If you click on \"Public and Patients,\" you come to a page where you can click on \"Find a Specialist,\" which takes you to a map of the United States. Now click on your state, select a state from the drop-down list, or select another country from the non-U.S. residents list. After you click on a state, you see a list of thyroid specialists from that state.\n\nThe listing of specialists on the American Thyroid Association Web site isn't an endorsement by the American Thyroid Association, which the association makes clear on the page with the map on it. The specialists on the listing are simply members of this organization who have agreed to take new patients. Their membership in this organization suggests that they are knowledgeable in this field but doesn't prove it.\n\n### American Association of Clinical Endocrinologists\n\nGo back to the list of thyroid addresses on my Web site and click on the American Association of Clinical Endocrinologists link (www.aace.com). On the first page, find \"Services\" on the left side. By clicking on it you can choose \"Find an Endocrinologist.\" On the page that pops up, choose the U.S. or your country of residence. By choosing the U.S., you bring up a box where you fill in your city, state, zip, distance you are willing to travel, and the particular specialty you are seeking a doctor in. Choose \"Search,\" and up pops the names of the members of this organization in your chosen specialty who are practicing in your area and want to be listed. Again, the list isn't an endorsement.\n\n### Endocrine Society\n\nReturn to the list of thyroid addresses on my Web site and click on the address for the Endocrine Society (www.endo-society.org). On the page that comes up, click on \"Information for Patients,\" found at the top under \"The Hormone Foundation.\" On the top, left-hand side of the next page, click the \"Find an Endocrinologist\" link. Type in your zip code, the distance from that zip code you are willing to travel, and the specialty you are seeking a doctor in, and a list of lots of names appears. The same caveat applies: The list isn't an endorsement, simply a list of members of the Endocrine Society who are willing to see new patients.\n\n### American Association of Endocrine Surgeons\n\nThe lists for the previously discussed societies contain the names of highly qualified thyroid surgeons. But if you want to go to the site that contains surgeons in their own society, find the American Association of Endocrine Surgeons (www.edocrinesurgery.org) on my thyroid addresses page. On the association's home page, choose the \"Members\" link on the left-hand side of the page. Then choose \"Membership List\" on the top of the next page that appears. To access the list, you need to have Adobe Acrobat installed on your computer, which you can download free of charge. Doctors' names appear under their resident state and city. If you page down to California, for example, you find a large number of names that I know include some of the best thyroid surgeons in the country.\n\n### National Institutes of Health\n\nThe National Institutes of Health maintains a list of all the specialty societies for doctors that can help you find a specialist in any field that may have to do with thyroid disease. For example, you may need an eye doctor if you have the eye disease associated with hyperthyroidism (see Chapter 6) or a skin doctor if you have the skin disease also associated with this condition. Check out the \"Does the doctor belong to a specialty society?\" section earlier in the chapter for the Web site.\n\n## Questions for and Observations about the Doctor on First Meeting\n\nAsking your potential doctor the following questions gives you a chance to find out if the doctor practices the art as well as the science of medicine. You receive little benefit from the most highly trained doctor if you can't communicate with her. Some key questions to ask the doctor are:\n\n  Will you call or e-mail me or permit me to call you about test results within a few days, or do I have to wait until our next appointment? (Appointments may be months apart, while test abnormalities sit in the doctor's file until you show up again.)\n\n  May I e-mail you with questions and expect to hear from you soon after?\n\nSome key questions to ask yourself as you observe your potential doctor, his staff, and surroundings are as follows:\n\n  Does the doctor look at you when she talks to and examines you?\n\n  Does the doctor listen to you and respond to your questions?\n\n  Do you feel you are getting enough time or being rushed?\n\n  Are the doctor's staff members helpful and happy? Their positive attitude suggests they feel good about working for this caregiver.\n\n  Does the doctor's office appear clean and well maintained?\n\n  Do other patients in the waiting room seem to be happy to be in this office?\n\nA white lab jacket doesn't confer godliness or special knowledge. Some of the best physicians (I humbly include myself in this category, at least with respect to my clothes) never wear white coats.\n\n## Reviewing Special Considerations When Choosing a Thyroid or Eye Surgeon\n\nSurgery of the thyroid gland is fairly complicated. Despite the fact that the thyroid is so close to the surface of the skin, it is intimately associated with many nerves, blood vessels, other glands, the trachea, and esophagus. You want a surgeon who has a lot of experience with thyroid surgery. The consequence of making an error may be permanent hoarseness, loss of function of the parathyroid glands, which control calcium, and even more severe damage.\n\nTry to find out how many thyroid surgeries the doctor does annually. If the number is less than ten, you probably want to find another surgeon. If it is between ten and fifty, this is a surgeon who can do most thyroid operations in which the gland is located in the neck and the operation involves removal of part or all of a thyroid that has not been operated upon previously. When the thyroid is under the breastbone, is being operated upon for a second time, or is involved with rapidly spreading cancer, you need a highly trained surgeon who does at least fifty operations on the thyroid per year. You probably have to go to a medical center, as described earlier in this chapter, to find one. Check out Chapter 13 for more information on surgeons and thyroid surgery.\n\nMost of the time, a regular ophthalmologist can handle 95 percent of the eye problems that thyroid patients, especially those with hyperthyroidism, experience (see Chapter 6). For the other 5 percent or less, an eye surgeon who has done surgery on the bony orbit of the eye is essential. The biggest complication may be blindness if the surgery isn't done right and sometimes may still result even though it is. You can find such a super specialist only at medical centers. Preserving your vision is definitely worth a trip to such a center. If you are in that exceedingly rare group of patients that requires such surgery, make sure the surgeon has successfully done this operation in the past and what his or her success rate is.\n\n##### Chapter 4\n\n## Testing Your Thyroid\n\n### In This Chapter\n\n  Determining your thyroid hormone levels\n\n  Using blood chemicals other than hormones to make a diagnosis\n\n  Checking the size and shape of your gland\n\n  Investigating abnormal lumps and bumps on the thyroid\n\nThese days, we take for granted our ability to precisely measure thyroid function. Yet only 60 years ago measurements were so primitive that we depended more on a patient's physical and emotional state than the lab tests to make a diagnosis. Past limitations were unfortunate because the patients with obvious signs and symptoms of thyroid disease are just the tip of a huge iceberg of those folks facing thyroid abnormalities.\n\nToday, the tests that measure thyroid function are getting more and more sensitive. Tests now enable doctors to identify many people with _subclinical_ thyroid disease (thyroid disease in which symptoms aren't yet apparent to the patient or the doctor), which may be slowly damaging the patient and will become clinical sooner or later. Thyroid tests' increasing sensitivity is especially useful with our aging population, whose symptoms of aging are so similar to the symptoms of mild hypothyroidism. Although you can't order the tests I describe in this chapter for yourself, the information I provide can increase your understanding of what various tests involve and what their results mean. The information in this chapter can help you have better discussions with your doctor about your diagnosis.\n\n## Checking Thyroid-Hormone Levels with Older Tests\n\nMany doctors practicing today learned about thyroid disease when only older tests were available to measure the amount of thyroid hormone in our blood, and some doctors still use the older tests. Inn case your doctor orders such tests or you have copies of old test results you want to understand, in this section I explain how some of the older blood tests work (although the sooner they're dropped from the list of tests that labs do, the better for patients). The _total thyroxine_ and _resin T3 uptake_ tests, as I discuss in the following sections, should be used in combination to determine your _free thyroxine index._ (For information on more accurate tests, skip ahead to the \"Checking Your Levels with the Best Tests\" section.)\n\n## Total thyroxine\n\nThyroxine (T4) is considered a _prohormone,_ a weaker thyroid hormone that gains its potency only after it's converted to T3, the other thyroid hormone (see Chapter 2). The _total thyroxine test_ (sometimes called the _T4 immunoassay_ ) measures all the T4 thyroid hormone in a given quantity of blood. (Total thyroxin is often abbreviated as TT4.) But most of the hormone measured in a total thyroxin test is bound to protein, so it doesn't get into cells where it does its job (see Chapter 2). By itself, the total thyroxine test doesn't tell you how much thyroid is available to get into the cells. To give a more accurate picture of your available thyroid hormone function, your doctor should combine the total thyroxine test with a test that measures what percent of the total thyroxine is bound and what percent is free.\n\nThe TT4 test can also be deceiving because many drugs and clinical states raise the level of TT4 in your blood (because they raise the amount of thyroxine- binding protein in your system) yet don't impact your amount of free thyroxine.\n\nSome of the drugs that can raise the level of TT4 in your blood include\n\n  Estrogenic hormones taken for hormone replacement or birth control\n\n  _Amiodarone,_ a drug used for the heart\n\n  Amphetamines\n\n  Methadone\n\nSome clinical states that can raise TT4 levels include\n\n  High estrogen states, such as pregnancy\n\n  Acute illness, such as AIDS or hepatitis\n\n  Acute psychiatric problems\n\nConversely, some drugs and physical conditions tend to lower the results of a TT4 test (because they depress the amount of thyroxine-binding protein) while not impacting the amount of free thyroxine.\n\nThe drugs that can lower TT4 levels include\n\n  _Androgens,_ male hormones taken to build muscle\n\n  _Steroids,_ usually given to reduce inflammation\n\n  _Nicotinic acid,_ given to lower harmful blood fats\n\n  Aspirin in high doses (more than 3,000 milligrams daily)\n\nPhysical conditions that can lower TT4 levels include\n\n  Severe chronic illness, such as kidney failure or liver failure\n\n  Starvation\n\nA normal range of TT4 is 5 to 11 micrograms per deciliter of blood.\n\nDifferent laboratories may use different techniques to perform the same test, resulting in slightly different normal values. Even when different labs use the same technique, slight variations in the normal values may occur from lab to lab because values originate from each lab's own group of people without thyroid disease.\n\nIf your doctor chooses to use the total thyroxine test to monitor your thyroid function, he or she must make certain you aren't taking any of the drugs or experiencing any of the physical conditions I list in the preceding section. In addition, your doctor must also order the next test, the resin T3 uptake, to get a complete picture of your condition.\n\nThe total T4 test is actually a better measure than the free T4 test that I describe below in one important situation \u2014 pregnancy. Because of the method almost all labs use to measure free T4, the free T4 test gives an incorrect level when a woman is pregnant. During pregnancy, the total T4 is used instead, and should be one and a half times the normal total T4 when the woman isn't pregnant. The TSH may not give a correct reading until the end of pregnancy, so the total T4 is the measurement of choice. (See Chapter 17 for more information on the thyroid during pregnancy.)\n\n## Resin T3 uptake\n\nThe _resin T3 uptake_ measures how many sites on thyroxine-binding proteins are available for T3 hormone (active thyroid hormone) to bind to. Lots of sites are available when the TT4 is low (and therefore takes up very few of the sites) or the binding protein levels are very high.\n\nThe usual result of a resin T3 uptake is 25 to 35 percent, depending on the lab. Here's the explanation for results that vary from this range:\n\n  **Higher results:** Anything that reduces the binding sites leaves very few binding sites for any more thyroid hormone to bind to. If T3 is added to a sample of that blood, little T3 will be bound, leaving a lot of measurable free T3. The resin T3 uptake will be high.\n\n  **Lower results:** Anything that raises the binding sites also leaves a lot of binding sites available for added T3. The amount of free T3 measured is low, giving a decreased resin T3 uptake.\n\n## Free thyroxine index\n\nAs I indicate in the previous sections, your doctor must use the total thyroxine (TT4) test and the resin T3 uptake together to be valuable. In the \"Total thyroxine\" section, I note several drugs and physical conditions that can alter the results of the TT4 test (and that also alter the resin T3 uptake results). The impact of such drugs and physical conditions always affects the TT4 and resin T3 uptake results in opposite directions: If the TT4 is depressed, then the resin T3 uptake is high; if the TT4 is elevated, then the resin T3 uptake is low.\n\nTake, for example, the effect of estrogen pills. As I note in the \"Total thyroxine\" section earlier in the chapter, estrogen pills tend to raise the amount of thyroid-binding protein, resulting in many more binding sites for thyroid hormone. Free thyroid hormone is taken up from the blood, so the total thyroxine, which measures all the thyroid hormone in the blood, is higher. If radioactive T3 is added to the same blood, so many binding sites for the T3 still remain that little T3 is left in the free state, and the resin T3 uptake is low.\n\nLikewise, as I note in \"Total thyroxine,\" pregnancy raises the number of thyroid-binding proteins. If the doctor only measures the total thyroxine, the measurement is high, and the doctor thinks the patient has hyperthyroidism (see Chapter 6). The patient receives treatment, inappropriately, for hyperthyroidism with antithyroid drugs and possibly becomes hypothyroid, which isn't good for the mother or the baby. However, if the doctor measures resin T3 uptake as well, the doctor finds the product of total thyroxine and resin T3 uptake to be normal.\n\nConversely, androgens lower the amount of thyroid-binding protein. T4 releases from binding sites to become free T4. As soon as your body detects an excess of free T4, it reduces the release of T4 from the thyroid so the level of free T4 remains normal. The total measured T4 is lower than normal, because far fewer binding sites containing T4 exist. If radioactive T3 is added to this blood, it has fewer binding sites to attach to, and most of it remains free. All this free T3 attaches to the resin, giving you an elevated resin T3 uptake. Again, when you multiply the low total T4 by the high resin T3 uptake, the product is normal. And when you take steroids for an inflammatory condition like arthritis, for example, they reduce the number of thyroid-binding proteins. If your doctor measures only total T4, it is low and the doctor may incorrectly prescribe thyroid hormone, making the patient hyperthyroid. By measuring the resin T3 uptake, the doctor can find the correct state of normal thyroid function by multiplying the low total T4 and the high resin T3 uptake.\n\nTo determine a useful test result, doctors multiply the TT4 level by the resin T3 uptake. The result, the _free thyroxine index,_ is an indicator of thyroid function and usually falls between 1.25 and 3.85. A free thyroxine index below 1.25 indicates low thyroid function, and a result above 3.85 indicates increased thyroid function.\n\nEven if you're taking one of the drugs or experiencing one of the physical conditions I list in the \"Total thyroxine\" section, your free thyroxine index should be within the normal range if your thyroid is functioning normally.\n\n## Checking Your Levels with the Best Tests\n\nNumerous blood tests can measure thyroid function, but the most accurate and sensitive tests for determining thyroid function are the _free thyroxine_ (FT4) and the _thyroid-stimulating hormone_ (TSH) tests, both of which I describe in this section. (Free thyroxine is the tiny portion of thyroid hormone in the blood that's free to get into cells; see Chapter 2.) The vast majority of people who take FT4 and TSH tests receive accurate diagnoses. If your doctor is screening you for thyroid function and wants to order just one test, that test should be the TSH test because of its accuracy and the fact that it's a simple blood test.\n\n## Free thyroxine (FT4)\n\nThe _free thyroxine_ (FT4) _test_ is the best way to measure the amount of free thyroid hormone in your blood. The FT4 test measures the 0.03 percent of T4 that's not bound to protein \u2014 the T4 that's free to interact with your cells (see Chapter 2). All the factors that can change the amount of total thyroxine in your system, such as the drugs and physical conditions I list in the \"Total thyroxine\" section earlier in the chapter, don't affect the amount of FT4 in your blood. Depending on the test method your particular laboratory uses, the usual FT4 level is around 1 to 3 ng\/dl (that's nanograms per deciliter).\n\nThe level of FT4 in your blood is high if you have hyperthyroidism and low if you have hypothyroidism. (As I explain in more detail in Chapter 6, in rare cases a patient with hyperthyroidism has too much T3 rather than too much T4 in her blood, and her FT4 test can come back normal or even low.)\n\nThe FT4 isn't a perfect test, because certain conditions make the FT4 level appear abnormal when the patient actually has normal thyroid function. Fortunately, your doctor can easily recognize these conditions, which include the following:\n\n  Patients with severe chronic illness (not thyroid disease) may have slight decreases in FT4.\n\n  People producing or eating large amounts of T3 have decreased FT4.\n\n  The rare patient with resistance to T4 has high levels of FT4 yet isn't hyperthyroid, possibly due to a hereditary condition.\n\n  Patients on heparin to prevent blood clotting may have slight increases in FT4.\n\n  Patients with an acute illness may briefly have elevated FT4 as binding proteins suddenly fall.\n\nSometimes the FT4 test may be the only useful way of knowing if thyroid function is normal. When a hyperthyroid patient receives treatment, the FT4 result falls. But the TSH level, the other highly sensitive test that I describe as the best screening test for abnormalities of thyroid function, may remain low for months and finally return to normal. Your doctor can't and shouldn't use the TSH test to determine thyroid function in hyperthyroidism that is under treatment. Similarly, many patients have a low TSH and a normal FT4 score. If the TSH is the only test a doctor looks at, the doctor incorrectly labels the patient hyperthyroid. Patients with a low TSH and normal FT4 score actually have pre-hyperthyroidism (euthyroid Graves' disease) and don't need treatment as long as their free T4 remains normal.\n\n### Free triiodothyronine (FT3)\n\nThe free triiodothyronine (FT3) test measures the free T3 hormone in the blood. The FT3 test is rarely necessary, except when a patient is hyperthyroid yet has a normal FT4 test result. The usual level of FT3 is 0.25 to 0.65 ng\/dl (nanograms per deciliter). A hyperthyroid patient has a high FT3 result. A hypothyroid patient has a low FT3 result.\n\nThyroid-binding proteins affect T3 in a similar way to T4. As thyroid-binding proteins rise, the proteins absorb more T3, and the thyroid gland makes more T3 to take its place. As thyroid-binding proteins fall, the proteins absorb less T3, and the thyroid reduces its production of T3. The total T3 doesn't give an accurate measurement of active T3, and a measurement of resin T3 uptake must accompany it to accurately measure thyroid function.\n\n## Thyroid-stimulating hormone (TSH)\n\nThe _thyroid-stimulating hormone_ (TSH) test is the most sensitive test of thyroid function in most circumstances. The TSH rises when the T4 level in the blood falls, and the TSH falls when the T4 rises (see Chapter 2). The chemical tests that measure TSH are the most accurate assays currently being done, so the TSH test is an excellent test to measure thyroid function. If you have hyperthyroidism, your TSH level is low (because the high level of T4 in your blood is suppressing TSH production). If you have hypothyroidism, your TSH level is high (because your body is trying to stimulate the production of more T4). As always, depending on the particular laboratory doing the test, the TSH is usually 0.5 to 5 mU\/ml (that's microunits per milliliter).\n\nMany experts, myself included, don't agree with the standard normal range of TSH and believe it should be narrower because of the many people who aren't thought to have thyroid disease yet have elevated levels of thyroid autoantibodies (see section below on thyroid autoantibodies). We believe that such patients have chronic thyroiditis with subclinical hypothyroidism. The patients have a normal free T4 but an elevated TSH. So we feel that the upper part of the \"normal\" range is actually abnormal for patients with chronic thyroiditis. The normal range in adults, after taking patients with chronic thyroiditis with subclinical hypothyroidism into account, is probably 0.5 to 2.5 mU\/ml (microunits per milliliter).\n\nA low TSH doesn't necessarily mean you have hyperthyroidism. Some of the many conditions and factors that can decrease your TSH include\n\n  Excessive treatment with T3 or T4 hormone\n\n  Thyroid nodules that make excessive T3 or T4 (see Chapter 7)\n\n  The first trimester of pregnancy (A woman's body produces a hormone called _chorionic gonadotrophin_ during the first trimester, which has TSH-like properties and stimulates the production of T4, thereby suppressing TSH.)\n\n  The cancer _choriocarcinoma_ or molar pregnancy, both of which are associated with the production of large amounts of the hormone chorionic gonadotrophin\n\n  A pituitary tumor that destroys TSH-producing cells\n\n  Euthyroid Grave's disease, where hyperthyroidism is present in the thyroid but the thyroid isn't making excessive levels of T4 (see Chapter 6)\n\n  Acute depression\n\nSeveral conditions can cause an increase in your TSH level, even if your thyroid isn't underactive. The following conditions require consideration when your doctor discovers a high TSH:\n\n  A pituitary tumor involving the cells that make TSH\n\n  Recovery from a severe illness\n\n  Insufficient dietary iodine\n\n  Resistance to the action of T4\n\n  Failure of the adrenal gland to make adrenal hormone\n\n  Psychiatric illness\n\nMany of the conditions I list in this section are temporary, meaning that a patient's TSH level will return to normal if she just waits. Other conditions, such as a pituitary tumor, require action (such as the removal of the tumor) to restore the TSH to its normal level.\n\nSometimes a condition that suppresses production of TSH, such as hyperthyroidism, produces a low TSH level for some time even after you've returned to a normal metabolic state with treatment. If your FT4 is normal but your TSH remains low, your doctor can't use the TSH as a reliable guide to thyroid function and has to rely on the FT4 instead.\n\nAfter your doctor establishes a diagnosis for a thyroid problem, you may have repeated TSH tests during the course of your treatment to monitor your progress. If you're receiving treatment for hyperthyroidism, however, repeated TSH tests may not be the most effective way to monitor progress, because your TSH may not recover for a long time after your metabolism returns to normal.\n\n## Taking Nonhormonal Blood Tests\n\nHaving thyroid disease doesn't necessarily mean that your thyroid is functioning too much or too little. For example, a patient who has thyroid inflammation or thyroid cancer could have normal levels of FT4 and TSH. In this situation, blood tests other than the ones I describe in the preceding sections may be helpful in making the correct diagnosis. In this section, I help you understand when nonhormonal blood tests are necessary and how you interpret their results.\n\n## Thyroid autoantibodies\n\nMany thyroid conditions, which I explain in detail in later chapters, are called _autoimmune diseases_ because they appear to result from the body rejecting its own tissue. If you look at diseased thyroid tissue under a microscope, it contains many of the same cells you'd find if a foreign invader were present in the body, such as if an organ were transplanted from one person to another. An _antigen_ is the tissue, cell, or chemical that the body is trying to reject. An _antibody_ is the chemical (usually a protein) that the body manufactures to reject an antigen. An _autoantibody_ is an antibody directed against yourself, or your own tissue.\n\nMany autoantibodies play a role in autoimmune thyroid disease, but the two principal ones are _antithyroglobulin_ _autoantibodies_ and _thyroid peroxidase_ _autoantibodies_ (sometimes referred to by their older name, _antimicrosomal autoantibodies_ ). Doctors find thyroid peroxidase autoantibodies more often than antithyroglobulin autoantibodies. (Bet you can't say that three times fast.)\n\nIf your doctor wants to confirm a diagnosis of autoimmune thyroid disease, he or she orders tests of your antithyroglobulin autoantibodies and thyroid peroxidase autoantibodies. If either test returns at a level of over 100 international units per milliliter, the test confirms the diagnosis.\n\nAntithyroglobulin and thyroid peroxidase autoantibodies are found at the highest levels in patients with a condition called _Hashimoto's thyroiditis_ (which I explain in Chapter 5), but they are also found in patients with Graves' disease, a form of hyperthyroidism (see Chapter 6). Autoantibodies are found at lower levels in up to 10 percent of normal people (the percentage increases with age). As noted above, some thyroid specialists believe that people with low levels of autoantibodies actually have subclinical (nonsymptomatic) thyroid disease \u2014 if this is true, the population with thyroid disease is far greater than previously thought.\n\nIf autoantibodies aren't present in abnormal amounts, a doctor can't make a diagnosis of Hashimoto's thyroiditis.\n\nAlthough I discuss each autoimmune thyroid disease in its own chapter, these diseases are actually different clinical presentations of the same underlying condition. The evidence for this is based upon the following facts:\n\n  The thyroid tissue appears the same in the different autoimmune diseases.\n\n  Autoimmune thyroid disease runs in families.\n\n  One person may pass through Graves' disease, Hashimoto's disease, and hypothyroidism at different times.\n\n  The same types of autoantibodies are present in all three groups.\n\nFinding autoantibodies may be a clue that thyroid disease will occur in the future. Relatives of people with autoimmune thyroid disease often have autoantibodies, and many of them develop thyroid disease at some point in life.\n\nSome autoantibodies stimulate the thyroid, while others suppress the thyroid by blocking the activity of thyroid-stimulating hormone. At any given time, the condition of a patient with an autoimmune thyroid disease depends on which group of antibodies is present at the highest levels. If more suppression than stimulation is occurring, the patient will have low thyroid function. If more stimulation than suppression is occurring, hyperthyroidism will result. The patient may start with high function, go back to normal, and end up with low thyroid function. Treatment sometimes does nothing more than speed up this natural process of going from high thyroid function to normal thyroid function to low thyroid function.\n\nIn up to 25 percent of patients, an autoimmune thyroid disease goes away after a time. A higher concentration of autoantibodies doesn't mean that a patient is sicker than someone who has a lower concentration. A higher concentration of autoantibodies may simply mean that the illness is less likely to go away. However, the rate of miscarriages is greater in women who have high levels of thyroid peroxidase autoantibodies compared with low or no autoantibodies.\n\nOne other autoantibody may be especially important in patients who have hyperthyroidism \u2014 _thyroid-stimulating immunoglobulin_ (TSI). TSI acts like TSH in stimulating the thyroid to make and release more hormones. Its importance lies in that it can pass through the placenta from the hyperthyroid mother to her growing baby. The baby may then become hyperthyroid as well, but when the connection between the mother and her fetus is broken at birth, the baby's hyperthyroidism goes away. The risk of the baby becoming hyperthyroid during the pregnancy is greatest for the babies of mothers with the most severe hyperthyroidism. And a hyperthyroid baby doesn't develop normally in its mother's body.\n\n## Serum thyroglobulin\n\n_Thyroglobulin_ is the form in which thyroid hormones are packaged and stored within the thyroid follicle (see Chapter 2). Thyroglobulin is present in the blood of normal individuals, but its levels are much higher when thyroid damage exists (for example, with cancer of the thyroid or inflammation of the thyroid). A normal level of thyroglobulin is between 3 and 42 nanograms per milliliter.\n\nDoctors won't test the level of thyroglobulin in your blood for the purpose of making a diagnosis of thyroid disease, because several different conditions cause thyroglobulin elevations. Rather, a thyroglobulin test follows the course of a patient already diagnosed with a thyroid condition \u2014 especially a thyroid cancer patient, who shows an increase in thyroglobulin if the cancer grows and spreads. Immediately after surgery for thyroid cancer, the thyroglobulin level is very low, but if the cancer remains present and spreads, the thyroglobulin increases.\n\n## Determining the Size, Shape, and Content of Your Thyroid\n\nAs I mention earlier in their respective sections, free thyroxine (FT4) and thyroid-stimulating hormone (TSH) levels are normal in patients who have thyroid conditions in which hormone activity is normal. Therefore, other types of tests may be necessary to gather information about the size, shape, and content of the thyroid gland. Even when a doctor has already diagnosed an abnormal thyroid activity, one or more of the following studies may help to differentiate the causes. Each test is easy and painless and provides information that a doctor can obtain no other way.\n\n### Theories explaining autoantibody production\n\nExactly why the body forms antibodies against its own tissue isn't known, but several theories exist. Ordinarily, certain cells in the body prevent production of antibodies against parts of your own body. People who form thyroid autoantibodies may be deficient in protective cells at some point early in life. Another possibility is that a foreign invader (like a virus) with antigens similar to antigens in thyroid tissue attacks the body at some point. In making antibodies to fight the foreign antigens, the body makes antibodies that fight its own tissue as well.\n\n## Radioactive iodine uptake and scan\n\nThe thyroid concentrates iodine from the blood in order to make thyroid hormones (see Chapter 2), a fact used for decades to perform a study of the dynamic activity of the thyroid. The procedure is performed in the hospital in the nuclear medicine laboratory. If a patient takes radioactive iodine (in the form of a capsule the patient swallows), a device like a Geiger counter can be passed over the thyroid to count the radioactivity. This count is done 6 and 24 hours after the radioactive iodine is swallowed to measure the speed with which the thyroid takes up the iodine.\n\nA normal thyroid appears like a butterfly (see Chapter 2) at the lower end of the neck. The counts of radioactivity are uniform throughout. On paper, the counts register as dots. If the gland is normal, dots in every part of the gland are uniform, and the picture on paper shows the shape and two-dimensional size of the gland.\n\nWhen one thyroid nodule is overactive, most of the radioactive iodine concentrates in that nodule, giving it a darker appearance on paper. The overactivity suppresses production of TSH so the rest of the thyroid isn't stimulated to take up iodine. Because of its appearance, the dark spot of overactivity on the thyroid is called a _hot nodule._ The rest of the gland is suppressed and appears lighter and is therefore said to be \"cold.\" A _cold nodule_ is a nodule that doesn't concentrate as much iodine as the rest of the gland _._ Thyroid cancers are generally \"cold,\" because cancerous parts of the thyroid don't produce thyroid hormone in the usual way. However, most cold nodules aren't cancer.\n\nIn addition to showing the size and shape of the gland, a radioactive scan and uptake measures how active the thyroid is. When the thyroid is overactive, it takes up more iodine than normal. When it's underactive, it takes up less than normal. The maximum uptake of radioactivity usually occurs about 24 hours after swallowing the iodine. At this point, a normal thyroid has taken up between 5 and 25 percent of the administered dose of iodine. An overactive thyroid takes up 35 percent or more. Uptake between 25 and 35 percent is borderline.\n\nFigure 4-1 shows the appearance of a normal thyroid scan and a scan that indicates hyperthyroidism. The second scan is much darker and shows a larger thyroid gland, which is consistent with the increased uptake and growth of the thyroid in hyperthyroidism.\n\n**Figure 4-1:** A normal thyroid and a hyperactive thyroid as shown in a radioactive iodine scan.\n\n|     \n---|---\n\nA few situations prevent obtaining a thyroid scan and uptake. If a patient takes in large amounts of iodine, the iodine then both blocks iodine uptake by the thyroid and dilutes the administered dose. If you take thyroid replacement hormone, the hormone blocks thyroid activity and reduces the uptake of radioactive iodine. Diseases such as silent thyroiditis (see Chapter 11), where the iodine leaves the thyroid rapidly, also prevent a proper study.\n\nIn the past, doctors generally did the radioactive iodine scan and uptake to make a diagnosis of an overactive thyroid. Doctors don't do these tests as much anymore, because the blood levels of T4 and TSH are usually definitive along with the physical examination. Doctors use the scan and uptake more often for a thyroid that's abnormal in shape to establish whether multiple nodules are present (see Chapter 9) and to determine whether a nodule is overactive. The thyroid scan also assists in the management of thyroid cancer (see Chapter 8). It helps to determine if any thyroid tissue is left after the thyroid is removed by surgery and later to find new growths of cancer that have developed in the neck or elsewhere in the body.\n\n### Deciphering ultrasound\n\nA beam of sound from an ultrasound device consists of high-frequency sound waves. The frequency is far higher than anything the human ear can hear. Such a beam can be focused and directed just like a beam of light. When the beam strikes tissue, the tissue reflects a certain amount of sound back \u2014 the amount depends on how dense the tissue is. Air hardly reflects back any of the sound beam at all, while tissue, which consists of many layers and contains water, sends plenty of sound back. Different tissues absorb the sound differently, reflecting the sound to a different extent. A cancer appears differently on an ultrasound than normal thyroid tissue or a cyst filled with fluid. When the reflection returns, the sound energy is converted to light energy and electrical energy. The electrical energy can be displayed on a cathode ray tube or made into a permanent record by exposing a film to the light energy.\n\n## Thyroid ultrasound\n\nThe _thyroid ultrasound,_ also known as an _echogram_ or _sonogram,_ is a study that uses sound to measure the size, shape, and consistency of thyroid tissue. An ultrasound study uses no radiation. To get a thyroid ultrasound, you go to the testing facility and lie on your back on a table with your neck hyperextended. A gel is placed on your neck to assist in the transmission of the sound. A device called a _transducer_ passes over the area of the thyroid, sending out high-pitched sound waves that tissue reflects back and a microphone collects. Tissue that contains water gives the best reflections, while solid tissue like bone gives poor reflections.\n\nA thyroid ultrasound can measure the size of the thyroid or nodules very precisely. It can be used to follow treatment for an enlarged thyroid or nodule to see whether it's shrinking. It can tell the difference between a cyst filled with fluid (which is almost never a cancer) and a solid nodule that may be a cancer. Ultrasound is much better than a physical examination in detecting thyroid cancer spread into the neck. Therefore, your physician should find any possible site of cancer in the neck before thyroid cancer surgery so the surgeon can remove it.\n\nThis test is often used after a radioactive iodine scan detects an area that's cold. But is it cold because it contains no thyroid tissue, which is how a cyst appears, or is it cold because it contains cancerous thyroid tissue that's solid? The ultrasound can differentiate a cyst from a solid mass but can't tell you whether the mass is cancer. (Most of the time, the mass isn't cancer.)\n\nFigure 4-2 shows a normal ultrasound study of the thyroid and one in which a prominent nodule is solid.\n\n## Fine needle aspiration biopsy (FNAB)\n\nWhen a doctor has a question about the type of tissue making up a growth on the thyroid, the _fine needle aspiration biopsy_ (FNAB) may be the definitive test. It's just about painless and free of complications. It is done in your doctor's office with no anesthesia. After cleaning the area with alcohol, a small needle is introduced into the growth and, pulling back on the plunger to create a vacuum, removes tiny bits of tissue. The needle is moved to a few different places. You don't usually have to stay to be observed, because complications from the FNAB are so rare.\n\nUltrasound of the thyroid can guide the needle into the questionable thyroid tissue. You can see both the end of the needle and the tissue at the same time to make sure that you're getting the specimen you want and not some normal tissue next to it.\n\nThe tissue is sprayed on a fixative, stained, and examined for signs of cancer. Most of the time, FNAB can rule cancer out or in. Occasionally, the tissue won't provide a clear diagnosis, and your doctor does a core needle biopsy or removes the lobe (side) of the thyroid that contains the lump.\n\nFNAB has saved thousands of patients from surgery and is often the first test performed to check for cancer, skipping the thyroid scan and the ultrasound. The Willie Sutton theory is the basis for using an FNAB first to check for thyroid cancer. Willie was a bank robber, and someone once asked him why he robbed banks. His answer was \"You go where the money is.\"\n\n## Core needle biopsy of the thyroid\n\nIf the FNAB doesn't provide an accurate diagnosis, the next step may be a core needle biopsy. The needle in a core needle biopsy is significantly larger than in a fine needle aspiration biopsy. The nodule needs to be at least three-fourths of an inch in diameter to do a core needle biopsy, which you usually receive in the outpatient department of your hospital. The biopsy takes about 30 minutes, and you need to stay at the hospital for an additional 30 minutes to be observed for bleeding.\n\nThe skin over the area of the thyroid to be biopsied is cleaned with alcohol and is injected with a local anesthetic. A needle is inserted into the suspected tissue several times to obtain a sample of thyroid tissue. Unlike the fine needle biopsy, the suspected tissue maintains its structure so the pathologist can get a good view of it. The technique can be even more valuable if an ultrasound study guides the needle, allowing it to go exactly where the abnormal tissue is.\n\nSometimes you experience a little tenderness after a core needle biopsy. You can take Tylenol but nothing that prolongs your bleeding time, such as aspirin.\n\n##### Part II\n\n## Diagnosing and Treating Thyroid Conditions\n\nIn this part . . .\n\nT he thyroid can be overactive or underactive. It can be too large or too small. It can be bumpy or smooth. The chapters in this part introduce you to all kinds of thyroid abnormalities. You discover how to recognize them and how to differentiate one from another. For those of you with thyroid disorders, I explain how they occur, which of the common signs and symptoms you have, how a particular disorder damages your body, and what you can do to cure it so no damage occurs.\n\n##### Chapter 5\n\n## Dealing with Decreased Thyroid Function\n\n### In This Chapter\n\n  Understanding thyroiditis and hypothyroidism\n\n  Determining the cause of low thyroid function\n\n  Checking for other autoimmune conditions\n\n  Treating hypothyroidism\n\n  Reviewing another cause for falling thyroid hormone levels\n\nThe most common form of thyroid disease throughout the world is _hypothyroidism,_ or low thyroid function (also known as _myxedema_ ). Hypothyroidism has numerous causes, but worldwide, iodine deficiency probably leads the list (see Chapter 12). In the United States and Europe, however, iodine deficiency is rare, and the leading cause of hypothyroidism is autoimmune thyroid disease.\n\nIn this chapter, I introduce you to the immensity of hypothyroidism, show you how hypothyroidism affects the body, and explain the proper treatment for the various forms of hypothyroidism. In the last few years, some key changes in our understanding of hypothyroidism have developed. I include new medical information here so you can be up to date when you talk with your doctor about your symptoms and treatment.\n\n## Living with Autoimmune Thyroiditis\n\nStacy Dummy is a 46-year-old woman who is the cousin of Sarah and Margaret Dummy, whom you meet in Chapter 15. She has generally been healthy but recently noticed some swelling in the lower part of her neck. The swelling seemed to develop very slowly, and she didn't notice it until she tried to button a collar over her neck. Other than the swelling, she really doesn't have any physical problems. She isn't gaining weight. She sleeps well at night and isn't overly tired. She isn't feeling unusually hot or cold. Her appetite is normal, as are her bowel movements. She has no discomfort associated with the growth in her neck.\n\nStacy's cousin Sarah, who recently received a diagnosis of hypothyroidism, tells Stacy that she knows a good thyroid specialist who told her that other members of her family may have thyroid disease. Stacy goes to see Dr. Rubin, who examines her and finds that her thyroid gland is twice as large as normal. He finds no other significant abnormalities. He sends Stacy to the laboratory for two tests \u2014 a thyroid-stimulating hormone (TSH) test and a free thyroxine (FT4) test \u2014 both of which return within the normal range (see Chapter 4). Because of his clinical suspicion, Dr. Rubin also obtains thyroid autoantibody tests. Stacy's autoantibodies are very elevated, particularly her thyroid peroxidase autoantibodies _,_ but also her antithyroglobulin __ autoantibodies (see Chapter 4).\n\nDr. Rubin tells Stacy that she has a condition called autoimmune thyroiditis, also known as chronic thyroiditis. He tells her that treatment is optional for the present. If she's unhappy with the tissue sticking out on her neck, she can take thyroid hormone to shrink it. If not, she need only return in six months or a year to check to see whether the disease progresses to hypothyroidism.\n\nStacy's condition is a typical illustration of chronic thyroiditis, also called _Hashimoto's thyroiditis,_ _autoimmune thyroiditis,_ or _autoimmune thyroid disease._ She is currently free of symptoms of hypothyroidism such as coldness and fatigue, and her only abnormality is a _goiter,_ an enlargement of the thyroid. The blood tests that reflect her thyroid function are normal. The high levels of thyroid autoantibodies in her system determine her diagnosis.\n\nMost studies indicate that 10 percent of the world's population tests positive for elevated thyroid autoantibodies (see Chapter 4). If the U.S. has a population of approximately 296 million people, about 29.6 million of them would test positive. Many experts (including me) believe that these 29.6 million people have chronic thyroiditis. The good news: Chronic thyroiditis will never bother the vast majority of folks who have it.\n\nOnly about 1 in 1,000 people who test positive for elevated thyroid autoantibodies develop symptomatic chronic thyroiditis, which means that about 29,600 new cases of symptomatic chronic thyroiditis occur in the United States each year. A woman is 20 times more likely to have symptomatic chronic thyroiditis than a man. The typical patient is 30 to 50 years old, but chronic thyroiditis also affects children.\n\nChronic thyroiditis is a familial disease that mothers usually transmit to their daughters (see Chapter 14). Even members of a family who show no symptoms of chronic thyroiditis often have thyroid autoantibodies in their blood (especially the females) and may develop hypothyroidism later on.\n\n## Signs and symptoms\n\nThe classic picture of chronic thyroiditis is a very gradual, painless swelling of the entire thyroid gland in a woman between 30 and 50 years of age. Over time, destruction of thyroid cells may occur, and if it does, the end stage of chronic thyroiditis is hypothyroidism (see the following section, \"Approach to treatment\"). Alternately, hypothyroidism may develop from chronic thyroiditis when autoantibodies that block thyroid-stimulating hormone (TSH) prevent TSH from reaching the thyroid. In this case, the hypothyroidism can reverse itself when the antibodies that block TSH decline, a reversal that occurs for up to 25 percent of patients with chronic thyroiditis.\n\nOther autoantibodies form in chronic thyroiditis that may stimulate the thyroid in a way similar to thyroid-stimulating hormone. If such autoantibodies predominate, the chronic thyroiditis leads to hyperthyroidism rather than hypothyroidism. Some patients can alternate between hypothyroidism and hyperthyroidism, depending on which autoantibodies are most active. (Turn to Chapter 6 for more information on hyperthyroidism.)\n\nSome people with chronic thyroiditis do have symptoms, even when their thyroid function tests are normal. In addition to neck swelling, symptoms include\n\n  Pain in the neck (which is unusual)\n\n  Chest pain (which occurs in about 25 percent of patients)\n\n  Trouble swallowing or a sensation of fullness in the neck\n\nChronic thyroiditis is one of several autoimmune conditions that can affect an individual. If you have chronic thyroiditis, you have a greater chance of contracting other autoimmune conditions, including type 1 diabetes, rheumatoid arthritis, celiac disease, adrenal insufficiency, and pernicious anemia (see the \"Coexisting autoimmune diseases\" section, later in the chapter).\n\n## Approach to treatment\n\nBecause it's so benign, doctors usually don't treat chronic thyroiditis that hasn't progressed to hypothyroidism. If you have neck pain because of chronic thyroiditis, aspirin can generally control it. In rare cases, the neck pain responds to nothing but removal of the thyroid gland.\n\nIf the swelling in your neck is unsightly or you have difficulty swallowing, your doctor will prescribe thyroid hormone to block the production of thyroid-stimulating hormone (TSH). Your thyroid gland then shrinks. Thyroid hormone works better to shrink the thyroid in younger people with chronic thyroiditis because permanent changes like scarring may occur as the patient gets older. The shrinkage may take place within two to four weeks after starting thyroid. Usually, you should stop the hormone treatment after a few years, because up to one quarter of patients with chronic thyroiditis have a remission and no longer need thyroid treatment.\n\nTransient symptoms of hyperthyroidism as a result of chronic thyroiditis usually require no treatment either. The symptoms usually last a few weeks, and then you return to normal. In especially severe cases, you can take drugs that block the action of thyroid hormones (see Chapter 6).\n\n## Coexisting autoimmune diseases\n\nOccasionally, a patient with autoimmune thyroid disease has other autoimmune diseases, many of which involve other glands of the body. For example, diabetes mellitus type 1 sometimes occurs together with autoimmune thyroid disease. The cause is the autoimmune destruction of the insulin-producing cells of the pancreas. Another example is Addison's disease, the autoimmune destruction of the adrenal gland. Addison's disease is associated with severe fatigue and low blood pressure and is especially important to identify because giving thyroid hormone without adrenal hormone to a patient who is hypothyroid and has Addison's disease can be dangerous.\n\nAutoimmune destruction of the ovaries in women or the testicles in men may also occur when a patient has autoimmune thyroiditis. The result for women is failure to menstruate; for men it is infertility and impotency.\n\nAnother gland that autoimmune disease may affect is the _parathyroid_ (which actually consists of four parathyroid glands), sitting behind the thyroid in the neck. Loss of parathyroid function results in low blood calcium and the possibility of severe muscle spasms and psychological changes.\n\nSome autoimmune diseases that affect the joints of the body occur together with autoimmune thyroiditis. Rheumatoid arthritis is the most common example, but other diseases with names like _Sjogren's syndrome_ and _systemic lupus erythematosis_ may also be present.\n\nLastly, be aware of a blood disease called _pernicious anemia,_ an autoimmune disease that accompanies autoimmune thyroiditis on occasion. In pernicious anemia, autoimmunity destroys cells of the stomach that produce acid. The patient is unable to absorb vitamin B12 and develops anemia along with symptoms in the nervous system.\n\nOn occasion, when different autoimmune diseases occur together, treatment of one of them treats the other at the same time. For example, treating your hypothyroidism with thyroid hormone may greatly improve your diabetes.\n\n## Identifying Hypothyroidism\n\nKaren Dummy is Stacy's younger sister. Over the last few years, she has noticed the gradual enlargement of her neck \u2014 a symptom similar to the one Stacy experienced. But Karen has a number of other problems as well. She has gained a few pounds, and her legs appear swollen but don't retain an indentation when she presses on them. She feels cold when her husband feels comfortable and is constantly asking for more heat. Her skin is dry, and her nails are brittle. She has dry hair and notices that she is losing more hair than before. The outer third of her eyelashes seems to have disappeared. She used to love to sing in her choir, but her voice is husky lately. She has trouble seeing to drive at night and notices trouble hearing as well. When her periods occur, the amount of bleeding is much greater than it used to be. She and her husband are trying to become pregnant without much success.\n\nDr. Rubin, who is rapidly becoming the Dummy family doctor, examines her in his office. He finds that in addition to all the symptoms Karen explains to him, she also has a slow pulse and an enlarged thyroid gland. He sends her for thyroid function tests (TSH and FT4) as well as thyroid autoantibody tests.\n\nKaren's tests show that she has a low FT4 and a high TSH. Her autoantibody levels are elevated. Dr. Rubin makes a diagnosis of hypothyroidism due to chronic thyroiditis. He starts her on thyroid-hormone replacement. Within six weeks, Karen is her old self. Full of gratitude, she puts Dr. Rubin in her will.\n\nThe preceding stories of Stacy and Karen illustrate that although thyroid disease runs in families, especially the female members of a family, it doesn't have to manifest itself the same way in each person.\n\nAlthough Stacy doesn't show evidence of hypothyroidism, Karen is clearly hypothyroid.\n\n## Signs and symptoms of hypothyroidism\n\nThe classic signs and symptoms of hypothyroidism include\n\n  A slow pulse and enlarged heart\n\n  An enlarged thyroid _(goiter),_ unless prior removal of the thyroid gland is the cause of hypothyroidism\n\n  Dry, cool skin that's puffy, pale, and yellowish\n\n  White patches of skin where pigment is lost (a condition called _vitiligo_ )\n\n  Brittle nails and dry, brittle hair that tends to fall out excessively\n\n  Swelling that doesn't retain an indentation, especially of the legs\n\n  Hoarseness and slow speech with a thickened tongue\n\n  An expressionless face\n\n  Slow reflexes\n\nPatients with hypothyroidism complain of many different symptoms, and each patient has unique complaints. Among the most common are\n\n  Intolerance to cold\n\n  Weight gain\n\n  Tiredness and a need to sleep\n\n  Weakness\n\n  Pain and stiffness in the joints and muscles\n\n  Constipation\n\n  Increased menstrual flow\n\n  Trouble with memory and decreased concentration\n\n  Trouble hearing and a ringing in the ears\n\n  Trouble seeing at night\n\nThe symptoms of hypothyroidism develop over many years and are so gradual that most folks don't recognize the fact that the same disease causes them all. Plus, the signs and symptoms of hypothyroidism are fairly nonspecific, and you can easily confuse them with signs and symptoms of other common conditions. The three major sources of confusion are menopause, normal aging, and stress. All three are common occurrences for women, and men experience at least two out of the three (some people are now arguing that male menopause exists). You can see how a person with low thyroid function could easily neglect to check for hypothyroidism, which is a major reason why doctors, including me, advise routine thyroid testing starting at age 35 and continuing every five years thereafter, especially for women.\n\nPeople who smoke cigarettes suffer much worse degrees of the symptoms of hypothyroidism than people who don't. Older people experience much less severity of symptoms than younger people.\n\n## Diagnosing the disease\n\nThe physician who sees a patient with the signs and symptoms of hypothyroidism obtains several tests to confirm the diagnosis. As I cover in Chapter 4, the two tests essential to the diagnosis are\n\n  **Free thyroxine (FT4) level:** Lower than normal\n\n  **Thyroid-stimulating hormone (TSH) level:** Higher than normal\n\nIf central hypothyroidism is present (see the \"Absence of brain hormones,\" section, later in the chapter), the TSH is low when the FT4 is low. If you have subclinical hypothyroidism (see the \"Managing Subclinical Hypothyroidism\" section, later in the chapter) or nonthyroidal illness (see \"Understanding the Nonthyroidal Illness Syndrome,\" later in the chapter), your TSH is slightly elevated but FT4 is normal.\n\nOther tests that support the diagnosis include\n\n  **Red blood cell counts:** A mild anemia (decrease in red blood cells)\n\n  **Cholesterol count:** An increased cholesterol count\n\n  **Thyroid autoantibody levels:** Elevated levels of thyroid autoantibodies (if the patient has autoimmune hypothyroidism)\n\n  **Blood glucose level:** A blood glucose level that's lower than normal\n\nAfter your doctor makes the diagnosis of hypothyroidism, he or she needs to check the various causes of your hypothyroidism (see the \"Pinpointing the Causes of Hypothyroidism\" section, later in the chapter) because many of them are reversible without treating the thyroid directly.\n\n## Related conditions\n\nHypothyroidism leads to a number of consequences that aren't good for the patient. This section describes the most important of them.\n\n### Fat abnormalities\n\nAs a result of the metabolic changes in hypothyroidism, the blood contains levels of total cholesterol and \"bad\" (LDL) cholesterol that lead to _atherosclerosis,_ hardening of the arteries. The changes your doctor may find include the following:\n\n  Increased total cholesterol\n\n  Increased LDL, or \"bad cholesterol\"\n\n  Decreased HDL, or \"good cholesterol\"\n\n  Increased triglycerides\n\nThe result of hypothyroidism is an increased tendency toward heart attacks or strokes, which reverses when you receive proper treatment for your hypothyroidism.\n\n### Changes in reproductive function\n\nBoth men and women have major changes in their reproductive function due to lack of thyroid hormone. Their libido is reduced. Men may be impotent but can have normal semen production and make their partner pregnant. Hypothyroid women can get pregnant, but their rate of miscarriage increases. They tend to have high blood pressure with their pregnancy at a much higher rate. If hypothyroid pregnant women don't receive adequate treatment, their babies have a reduction in IQ.\n\nUsually, hypothyroid women who are premenopausal suffer from increased bleeding during menstruation but occasionally have no menstrual flow at all. Both conditions reverse with treatment.\n\n## Pinpointing the Causes of Hypothyroidism\n\nThe two most common causes of hypothyroidism are iodine deficiency and autoimmune (chronic) thyroiditis. Iodine deficiency is rare in the United States and Europe but very common throughout the rest of the world. I discuss iodine deficiency in detail in Chapter 12. As I discuss earlier in this chapter, chronic thyroiditis is an inherited condition your doctor diagnoses by checking the levels of thyroid autoantibodies in your blood.\n\nIn addition to iodine deficiency and chronic thyroiditis, people become hypothyroid for many other reasons. Your doctor should rule out the causes I detail in the following sections before starting to treat your condition with thyroid-hormone replacement.\n\n## Removal of the thyroid\n\nIf you've had your thyroid removed because of cancer or an infection or in the course of treatment for hyperthyroidism (see Chapter 6), you are probably hypothyroid. Only if some tissue remains can the thyroid possibly continue to function.\n\n## Absence of brain hormones\n\nAnything that destroys the _hypothalamus_ (the part of the brain that secretes _thyrotrophin-releasing hormone_ ) or the _pituitary gland_ (the part of the brain that secretes thyroid-stimulating hormone) produces _central hypothyroidism_ \u2014 hypothyroidism originating in the control center of the body, the brain. A trauma, infection, or infiltration (a replacement of brain tissue with other tissue, which can occur when a patient has cancer) can cause this type of destruction. The same result can also occur if the pituitary is involved with a destructive lesion, such as radiation treatment to the area of the pituitary gland, that prevents the production and release of TSH.\n\nIf a problem with the hypothalamus or pituitary causes your hypothyroidism, your doctor won't be able to find some of the signs and symptoms associated with chronic (autoimmune) thyroiditis. In particular, hoarseness and a thickened tongue occur in autoimmune hypothyroidism but not in hypothyroidism associated with a lack of brain hormones. In addition, in hypothyroidism caused by the absence of brain hormones, the thyroid isn't usually enlarged because TSH isn't stimulating it. Also, the patient's hair and skin aren't coarse (as they are if the patient has autoimmune hypothyroidism).\n\nSymptoms that result from a lack of other pituitary hormones also help to differentiate central hypothyroidism from failure of the thyroid gland. Symptoms include fine wrinkling of the skin of the face and a more pronounced loss of underarm, pubic, and facial hair.\n\n## Foods that cause hypothyroidism\n\nMany common foods can cause hypothyroidism if you eat them in sufficient quantities, especially if you have an iodine deficiency or are already mildly hypothyroid. Foods that can cause hypothyroidism are called _goitrogens,_ because they can trigger the enlargement of the thyroid (a goiter) as well as hypothyroidism. They block the conversion of T4 hormone to T3, the active form of thyroid hormone (see Chapter 2). They also prevent the formation of thyroid hormone by binding iodine so your body can't use it. Among the more common foods that may cause hypothyroidism are\n\n  Almond seeds\n\n  Brussels sprouts\n\n  Cabbage\n\n  Cauliflower\n\n  Corn\n\n  Kale\n\n  Turnips\n\nSoybeans can increase the need for thyroxine by increasing the loss of T4 in bowel movements. Soybeans also may contain a substance that blocks thyroid hormone production.\n\nIf consuming the preceding foods is the cause of your hypothyroidism, you can cure your hypothyroidism by simply removing them from your diet. It takes between three and six weeks for your thyroid to return to normal after you stop eating these foods.\n\n## Drugs that cause hypothyroidism\n\nMany different medications cause hypothyroidism in the same way as the goitrogens I list in the previous section: They block the conversion of T4 to T3. The drugs you are most likely to run into include\n\n  Adrenal steroids like prednisone and hydrocortisone, which treat inflammation\n\n  Amiodarone, a heart drug\n\n  Antithyroid drugs like propylthiouricil and methimazole (see Chapter 6)\n\n  Lithium, for psychiatric treatment\n\n  Propranolol, a beta blocker (see Chapter 6)\n\n## Diagnosing Severe Hypothyroidism\n\nThe United States rarely sees hypothyroidism in its severest form within its borders, but if the disease goes untreated and total thyroid failure occurs, the patient may die. The clinical picture that develops is one of extreme worsening of the signs and symptoms I describe earlier in the chapter. The skin becomes extremely dry and coarse, and the patient's hair falls out. The patient may lose all of his or her eyelashes, and body temperature may fall to a low level, 92 degrees or lower. The patient is less and less active and may lapse into a coma called _myxedema coma,_ which can last for many days until the patient dies of heart failure or infection. (An infection or heart disease may precipitate the myxedema coma in the first place in an elderly person with very low thyroid function.)\n\nBecause a patient with the severest form of hypothyroidism may not be taking in food or, if the patient is, absorbing the food extremely slowly, treatment may require injections of thyroid hormones (which I describe in the following section).\n\n## Treating Hypothyroidism with Hormones\n\nThe treatment of hypothyroidism, once thought to be very complicated, is now fairly simple after a doctor makes a diagnosis. However, a number of newer thoughts on the subject are worth considering as you and your doctor discuss treatment.\n\nPatients with hypothyroidism caused by chronic thyroiditis or removal of the thyroid take daily thyroid-hormone replacement pills. If the cause of your hypothyroidism is something other than autoimmune failure of the thyroid or removal of the thyroid, your physician must address the cause of your hypothyroidism along with replacing the thyroid hormone that's deficient.\n\nFor example, if you have a pituitary tumor responsible for a loss of TSH, your doctor must treat the tumor and replace other hormones in addition to thyroid hormones. If a drug or food is causing your hypothyroidism, removal of the responsible drug or food usually cures the condition. Sometimes you can't quit taking the drug causing your hypothyroidism, in which case you receive thyroid-hormone replacement to alleviate your hypothyroidism.\n\n## Turning to the right hormones\n\nThe first treatment to replace absent thyroid hormone came from the thyroids of animals and was called _desiccated thyroid._ For many decades, it was the only treatment available. When it became possible to make T4 hormone in the laboratory, T4 (also called _L-thyroxine_ ) replaced desiccated thyroid. Several reasons were behind the change. First, the amount of hormone in a given animal's thyroid differs from animal to animal, so the dose delivered could never be standardized. Second, desiccated thyroid contained both T4 and T3 in amounts significantly different from the way the normal thyroid gland secretes it. No logical reason now justifies using desiccated thyroid for the treatment of hypothyroidism.\n\nBecause 80 percent of the T3 thyroid hormone in your body comes from the conversion of T4 into T3 (at sites other than the thyroid), doctors believe that you can take T4 alone, and the body takes care of producing the T3 it needs. A number of recent studies confirm that you can safely take T4 alone. For example, a study reported in _The Journal of Clinical Endocrinology and Metabolism_ in May 2005 reviewed nine controlled clinical trials that compared T4 alone to combinations of T4 and T3. No difference in mood, quality of life, or mental functioning existed between the two groups.\n\nAlmost all people in the world who are currently receiving replacement thyroid hormone to treat hypothyroidism are taking T4 alone.\n\n## Determining the right amount\n\nLifelong treatment with thyroxine subjects you to no medical complications if you're on the correct dose. A TSH test determines the amount of thyroid hormone you receive (assuming that central hypothyroidism isn't the diagnosis). The normal blood level of TSH is 0.5 to 5.0 mU\/ml (microunits per milliliter) in most laboratories.\n\nKeep in mind that some doctors question whether 0.5 to 5.0 mU\/ml is actually the normal range for TSH. We know that 10 percent of the population tests positive for thyroid autoantibodies and probably has autoimmune thyroid disease. Most of these 10 percent don't receive the diagnosis of hypothyroidism. When a laboratory creates a normal range, it tests several hundred or more people considered free of thyroid disease, usually because they have no signs or symptoms. The laboratory measures their TSH and produces the range for TSH in the normal population. But is the laboratory really measuring a normal population when one in every ten people tested may have a subclinical thyroid disease (see the \"Managing Subclinical Hypothyroidism\" section, later in the chapter)?\n\nIn my practice, I've had several patients who didn't feel normal with a TSH between 3 and 5. I've given these patients enough thyroid hormone to lower their TSH to under 3 with gratifying results. I believe that future studies will indicate that the normal range for TSH is more like 0.5 to 2.5.\n\nIf you're receiving treatment for hypothyroidism and don't feel right on your current dose of replacement thyroid hormone, ask your doctor to check your TSH. If it's above 3, ask your doctor to prescribe more thyroid hormone to lower it below 3.\n\nAnother important point is that hypothyroidism isn't necessarily permanent. Up to 25 percent of patients with autoimmune hypothyroidism may return to normal thyroid function at a later date. The reason is that the autoantibodies that block the action of TSH may decline over time.\n\nIf you've been receiving treatment for several years for autoimmune hypothyroidism, ask your doctor if you can stop the thyroid-hormone replacement for four to six weeks to see whether your TSH remains low. (Don't stop taking your hormone replacement without your doctor's supervision, however.)\n\nOn the other hand, a thyroid gland that's failing due to autoimmune thyroiditis goes through several levels of failure. At first, you may need little thyroid hormone to replace what you're missing. With time, more of your thyroid tissue may fail, or the antibodies that block TSH may increase, and you need more thyroid hormone. Seeing your doctor on a regular basis to check for the increasing (or decreasing) failure of your thyroid is important. Making routine appointments to check your thyroid function is especially important if your hypothyroidism develops as a result of radioactive iodine treatment for a hyperactive thyroid gland \u2014 in which case your thyroid gland gradually loses its function, and your dose of thyroid may not stabilize for several years.\n\nAfter your thyroid function stabilizes, see your physician every six months or every year to check your TSH level and alter your dosage of thyroid hormone if necessary. Checkups are important, because you may not feel different even if your thyroid function gradually declines.\n\n## Filling your prescription and taking your medication\n\nThe various brands of thyroxine aren't necessarily biologically equivalent. You therefore need to get the same brand every time you renew your prescription. For example, if you're on Levoxyl, make sure your pharmacy gives you Levoxyl every time you get more pills. Small differences in dosage may result in overtreatment or undertreatment. If your pharmacy switches your brand for any reason, your doctor must be retest you in 8 to12 weeks on the new preparation.\n\nThyroxine (T4) comes in many different dose sizes so doctors can tailor it to the patient. The sizes include 25, 50, 75, 88, 100, 112, 125, 137, 150, 175, 200, and 300 micrograms. The correct dosage for you should be among the many choices I list.\n\n_Take thyroid hormone on an empty stomach._\n\nDoctors have long recommended that people over 60 who have to start taking thyroid hormone start with a very low dose and build up to the correct dose. No evidence in the medical literature supports this assertion. A recent study published in the _Archives of Internal Medicine_ in January 2005 shows that building seniors' dosage of thyroid hormone isn't necessary. The study gave 25 patients over 60 half the starting dose of another group of 25 patients over 60. None of the patients had symptomatic cardiac disease, and no one in the group given the larger dose voiced cardiac complaints. Therefore, doctors should start most patients on the full dose.\n\nFor many years, doctors suspected that generic forms of thyroid-hormone replacement pills didn't consistently provide a known level of the hormone, so doctors recommended brand-name products. Recent studies, however, show that generic thyroid hormone has the same potency as brand-name thyroid hormone and is, of course, much cheaper.\n\n## Testing hormone levels\n\nAbout four to six weeks must elapse for a change in your dose of replacement thyroid hormone to make a difference in your lab tests. If your doctor changes your dose, he or she should retest you in about four to six weeks to make sure you're on the correct dose.\n\n## Treating Myxedema Coma\n\nMxedema coma, the severest form of hypothyroidism, is a medical emergency. Mxedema coma isn't something you can manage outside a hospital. Large medical centers may see one case a year, so no one has much experience treating it. About 20 percent of cases don't survive.\n\nThe person with myxedema coma may be unarousable. Her body temperature may be extremely low even though she has an infection. Usually some event, such as an infection, a drug overdose, some trauma, a stroke, or a heart attack, trips the patient over from severe hypothyroidism to coma. When doctors test the TSH, it may be 100 or 200, and the free T4 may not be measurable. However, the patient receives treatment for myxedema coma before the results of blood tests return.\n\nThe doctor checks all aspects of the patient, including respiration, blood glucose, body temperature, presence of a precipitating event, and so forth, and treats all aspects at the same time. The key treatment is thyroid hormone given by injection.\n\n## Managing Subclinical Hypothyroidism\n\nIn a way, subclinical hypothyroidism is one extreme of hypothyroidism, and myxedema coma is the other. In _subclinical hypothyroidism,_ the free T4 is normal while the TSH is only slightly elevated. A value of 6 for the TSH is common. Knowing whether the slight fatigue or dry skin the patient complains about (if she complains about anything) has anything to do with her thyroid function is very difficult.\n\nWhen doctors follow patients with subclinical hypothyroidism without treating them, very few of the patients, less than 20 percent, develop overt hypothyroidism later on. If they receive treatment, proving that they have improved in any way is difficult because they're mostly not symptomatic. Even if they do improve with treatment, saying whether their improvement is because of the thyroid hormone or a placebo effect is similarly difficult.\n\nThough less than 20 percent of folks with subclinical hypothyroidism develop overt hypothyroidism later, the fact is that the presence of thyroid autoantibodies makes patients with subclinical hypothyroidism more likely than people without autoantibodies to go on to develop overt hypothyroidism.\n\nAlthough the current consensus is that people with subclinical hypothyroidism don't need treatment because the consequences of the condition are minimal, the newest studies appear to reverse this assessment. See Chapter 19 for more information on recent studies that show that subclinical hypothyroidism should be treated. Thyroid doctors will be reviewing this new information over the next several months.\n\nI believe that patients with subclinical hypothyroidism should generally be treated with thyroid hormone to make the TSH normal. Selected patients with more symptoms should definitely undergo a trial of six months of thyroxine therapy with a review of their clinical response after that.\n\n## Understanding the Nonthyroidal Illness Syndrome\n\nFalling thyroid hormone levels aren't always due to hypothyroidism. Nonthyroidal illness syndrome may be to blame. The syndrome can cause confusion with hypothyroidism, so it requires understanding. A number of conditions cause nonthyroidal illness syndrome:\n\n  Starvation\n\n  Severe infection\n\n  Severe trauma\n\n  Severe illness\n\nThe first change in thyroid blood levels in a patient with nonthyroidal illness syndrome is a fall in the serum free T3. The fall is due, at least in part, to a failure of conversion of T4 to T3. As the condition gets worse, the free T4 falls as well. The fact that the free T4 falls is a very bad prognostic sign. Most people die when their free T4 is below a certain level. The TSH is usually normal in people with nonthyroidal illness syndrome.\n\nWhen a doctor examines a patient with nonthyroidal illness syndrome for signs of hypothyroidism, the doctor usually can't find any, but the patient is so sick that the syndrome may be masking signs like low body temperature; plus, the signs of nonthyroidal illness syndrome usually take weeks to develop. However, a patient with the syndrome does have low tissue levels of T3 and T4 in addition to the low blood level of T3. The question is whether the low T3 and T4 tissue levels are beneficial for the very sick individual or need treatment.\n\nWhen patients with nonthyroidal illness syndrome are givenT4, they show no improvement in their clinical condition or their mortality compared to patients with the syndrome who are not given T4, even though the measured T4 in their body increases. However, the measured T3 doesn't increase. When T3 is given, it does seem to improve the clinical situation to a mild degree and doesn't seem to make it any worse.\n\nMuch more study of this unique syndrome is required, but for now, the recommended treatment consists in giving the patient T3 while treating all the other features of the particular illness, such as infection, at the same time.\n\n##### Chapter 6\n\n## Taming the Hyperactive Thyroid\n\n### In This Chapter\n\n  Recognizing the symptoms of hyperthyroidism\n\n  Linking hyperthyroidism and Graves' disease\n\n  Deciding on treatment\n\n  Battling severe hyperthyroidism\n\nH _yperthyroidism_ refers to the excessive production of thyroid hormones, which leads to many signs and symptoms that suggest your body is, in effect, speeding up. Hyperthyroidism is fairly common. Each year, about 100 per 100,000 people receive a diagnosis, which adds up to more than 296,000 new cases in the United States every year.\n\nMost people with hyperthyroidism (about 80 percent) have an autoimmune disorder called _Graves' disease,_ which I discuss in detail in this chapter. In addition to causing signs and symptoms of hyperthyroidism, Graves' disease also causes eye disease and skin disease. Hyperthyroidism and eye and skin disease are all the result of _autoimmunity_ (your body, in essence, rejecting your own tissue; see Chapter 4). In some circumstances, a patient has hyperthyroidism but no eye disease or skin disease, and blood tests show no evidence of autoimmunity. Such patients don't have an autoimmune disorder, but the medical picture their hyperthyroid state produces is the same as if they had Graves'.\n\nIn this chapter, I show you how to recognize hyperthyroidism, what the treatment options are, and what possible complications may occur as a result of your treatment or the disease itself. You also discover how I would treat you if you came to me with Graves' disease. Hyperthyroidism has special features in various physical states and at different ages. Therefore, I devote more space to hypothyroidism during pregnancy (Chapter 17), in children (Chapter 18), and in the elderly (Chapter 19) later in this book. If this coverage applies to you, check out these chapters when you're finished here.\n\nMany people believe that if you have hyperthyroidism, you're lucky because it makes weight control or weight loss easier. By the time you finish this chapter, I hope you realize why that thinking is flawed.\n\n## Detecting the Signs and Symptoms of Hyperthyroidism\n\nTami Dummy is the mother of Stacy and Karen. Stacy has recently received a diagnosis of autoimmune (chronic) thyroiditis and Karen a diagnosis of hypothyroidism (see Chapter 5). Tami has always been a very active person, but lately she has noticed a lot of things wrong with her, and they're getting worse.\n\nTami feels warm all the time, and her skin is moist. A few months ago, she lost some weight without trying and was delighted, but the weight loss has continued despite the fact that she has a strong appetite and is eating more than usual. She often feels her heart racing, which makes her very nervous. She notices that her hands shake when she just sits quietly. She goes to the bathroom more frequently than usual, both to urinate and to move her bowels.\n\nThe changes in Tami aren't lost on her husband, Patrick, or her daughters. They notice that she's constantly staring at them, though when they question her, she denies it. Patrick, in the course of giving her a massage, notices a bump on the front of her neck that wasn't there before. Tami's family insists that she see their favorite doctor, none other than (did you guess?) Dr. Rubin.\n\nDr. Rubin asks a number of questions and does a physical examination. He discovers that Tami's thyroid is enlarged, and he finds a skin abnormality on her lower legs. He tells the family that Tami almost certainly has hyperthyroidism due to Graves' disease. The final diagnosis requires only some confirmatory blood tests, and the outcome of the tests is so certain that Dr. Rubin gives Tami a prescription for antithyroid pills at the first office visit.\n\nThe tests confirm the diagnosis. Tami immediately starts taking a pill three times a day. After three weeks, she feels better, and after eight weeks she's her old self. She's a bit disappointed when the pounds start coming back, but she feels so good that she returns to her health club and sheds several of them in no time. Patrick is delighted to have his wife back at moderate rather than high speed. He has been wanting to go to the Oregon Shakespeare Festival, and he knew that she wouldn't sit through a play in her previous condition.\n\nTami continues taking the pills for the next year, with monthly visits with Dr. Rubin to confirm that she remains healthy. Blood tests show that her production of thyroid hormone is declining, and Dr. Rubin reduces her dose to two pills daily, which she can take all at once after three months. A few months later, he reduces her dose to one pill daily.\n\nThe abnormality on her lower legs doesn't get any worse but doesn't get much better either. Tami isn't particularly bothered by it, so no treatment is given. At the end of the year, Tami stops taking the medication entirely. Tami comes in for follow-up visits every six weeks, then every two months, and then every three months. She has now gone four years without taking the antithyroid drug and remains in good health.\n\nHyperthyroidism, whether caused by Graves' disease or another condition, produces consistent signs and symptoms that affect every part of your body. In the following sections I describe the major abnormalities, grouped according to the organ system of the body hyperthyroidism is affecting.\n\n## The body generally\n\nAlthough the signs and symptoms of hyperthyroidism seem distinctive, most occur in people who don't have hyperthyroidism as well. For example, although palpitations occur in 75 percent of people with hyperthyroidism, they also occur in 26 percent of people who don't have hyperthyroidism. While 73 percent of people with hyperthyroidism prefer the cold, so do 41 percent of people without hyperthyroidism. Therefore, you must use laboratory tests to confirm a diagnosis of hyperthyroidism.\n\nHyperthyroidism can cause your body temperature to be persistently high. As a result, you may prefer wearing fewer clothes and sleeping with no covers at night. You may prefer to take your vacations in Alaska rather than Mexico. You may sweat when everyone else is comfortable.\n\nYou may lose weight despite an increased appetite. The weight loss is due to the loss of lean body tissue like muscle, not a loss of fat. In rare cases, a patient gains weight because she's eating so many calories. Hyperthyroidism can cause you to feel weak. You may feel lymph glands all over your body, because Graves' disease is an autoimmune disease and the lymph system is a key player in autoimmunity. Your tonsils, which are part of the lymph system, also enlarge.\n\nYour face may appear to be anxious or frightened. If you lose a lot of weight, your face may be thin or emaciated. But you may also have fairly severe hyperthyroidism without any obvious change in facial appearance. Your elbows may be red.\n\nOther possible reasons, which are more serious than Graves' disease, such as cancer in the lymph glands, may explain the enlargement of your lymph glands, so if you experience enlarged lymph glands, see your doctor.\n\n## The thyroid\n\nWhen Graves' disease is the cause of hyperthyroidism, your thyroid is enlarged in a symmetrical way and the entire gland is firm. When a single overactive _nodule_ (a bump on your thyroid) is to blame for hyperthyroidism, the nodule is large, but it often causes the rest of the gland to shrink. (See Chapter 7 for a discussion of nodules.) When a multinodular goiter is responsible (see Chapter 9), you can feel many lumps and bumps on your thyroid. Figure 6-1 shows a comparison of the size of the thyroid gland before treatment with antithyroid drugs and six weeks after beginning treatment in one of my hyperthyroid patients. This figure also shows the before and after affects of treatment on the appearance of your eyes, which you can read about later in the chapter.\n\n**Figure 6-1:** The enlarged thyroid gland before and after treatment.\n\n|     \n---|---\n\nIf you put your hand over an enlarged thyroid, you can often feel a buzz, or _thrill,_ that results from the great increase in blood flow in the overactive thyroid. You can hear the thrill with a stethoscope; the sound is called a _bruit._ You may also have trouble swallowing and the sensation of a lump in your throat if your thyroid is large enough.\n\n## The eyes\n\nAny form of hyperthyroidism results in reversible changes to your eyes. Your eyes appear more prominent than usual. Figure 6-1 shows an example. Your upper eyelids may be higher so that more of the white above your pupil is visible, which makes you appear as if you're staring and pop-eyed. When someone asks you to look down, your upper eyelid may not follow your eye, which exposes even more white, a phenomenon called _lid lag._ Graves' disease can cause more serious eye problems, which I discuss later in the \"Thyroid eye disease\" section of this chapter.\n\n## The skin and hair\n\nThe sweat glands depend upon thyroid hormone. Too much of the hormone causes them to work excessively so that the skin all over the body is moist. Because the blood vessels in the skin are widened in hyperthyroidism, the skin also feels warm. Moist and warm skin are often most notable in the hands and feet, which may appear red. You may experience a loss of skin pigmentation (a condition called _vitiligo_ ) in places, which is another sign of autoimmunity. Other areas of your skin may appear darker.\n\nYour hair may be fine, straight, and unable to hold a curl. Hair growth also depends on thyroid hormone. Therefore, some loss of hair is common as the disease loses its grip. The same autoimmune process that affects the eyes and the skin affects the hair follicles.\n\nSometimes the nails of the fingers and toes undergo a distinctive change called Plummer's nails \u2014 a rising up of the end of the nails so that dirt and other substances can get underneath them, which makes keeping your nails clean very difficult. Plummer's nails begins on the fourth finger of each hand and spreads to the rest of the fingers and toes.\n\n## The heart\n\nHyperthyroidism can cause a rapid pulse, which you feel as heart palpitations. You may feel your heart beat very vigorously and may find it very uncomfortable, especially when trying to sleep. The first sign of Graves' disease is sometimes _atrial fibrillation,_ an irregular heart rhythm. If a patient is older and already has heart disease, hyperthyroidism can induce heart failure. Heart pain (angina) may appear or worsen because the heart beats too rapidly. You may experience shortness of breath.\n\nEven very mild increases in thyroid hormone may cause a decreased ability to exercise, because the heart is less able to respond to exercise. Make sure your dose of thyroid is correct if you're receiving treatment for hypothyroidism.\n\n## The nervous system and muscles\n\nIf you have hyperthyroidism, your fingers have a fine tremor when you hold your hands out. The loss of muscle tissue leads to weakness, especially in the muscles that are closer to the center of the body. Your reflexes increase; some patients can't sit still. In Chapter 15, I discuss the psychological changes associated with hyperthyroidism. Basically, if you're hyperthyroid, most likely you're nervous, you don't sleep as much as you used to, and you have rapidly changing emotions, from exhilaration to depression.\n\nYou may find that you can't perform mentally at the high level that you did before you developed hyperthyroidism. Several of my patients, law students and medical students, couldn't take examinations successfully and had to take several months off of school to recover before they could return to their studies. You may also tire much earlier than you used to.\n\n## The reproductive system\n\nHyperthyroidism can cause a decrease in fertility, because it interferes with ovulation. However, pregnancy can occur. Miscarriage is more common, especially if the hyperthyroidism goes uncontrolled. Menstrual flow decreases as well and may cease. I discuss more about hyperthyroidism and pregnancy in Chapter 17.\n\nMales with hyperthyroidism have trouble having an erection in half the cases. They often experience infertility with reduced sperm count. The sperm appear abnormal when looked at under a microscope. All changes in the reproductive system disappear with successful treatment.\n\n## The stomach, intestines, and liver\n\nIf you're hyperthyroid, food moves more quickly through your intestines than it used to, and you have more frequent bowel movements or even diarrhea. You may experience nausea and vomiting. Your appetite greatly increases, and you eat more but don't gain weight. Your doctor may tell you that your liver is enlarged. Blood tests of the liver suggest a picture of hepatitis, but when the thyroid is under control, the liver returns to normal.\n\n## The bones\n\nYour bones lose calcium and become less dense, especially if you're past menopause and aren't taking estrogen. Despite loss of bone density and calcium, bone fractures aren't common in hyperthyroid patients. When your doctor measures your blood calcium, it's elevated, but kidney stones don't occur. All bone changes return to normal with treatment of your hyperthyroidism.\n\n## The urinary system\n\nAs more blood flows, your kidneys filter more, and your body produces more urine, so you go to the bathroom more frequently. In turn, you feel thirstier than usual.\n\n## Confirming a Diagnosis of Hyperthyroidism\n\nThe signs and symptoms I describe in the previous section usually lead to a conclusive diagnosis of hyperthyroidism, which blood tests confirm. The definitive tests for hyperthyroidism are as follows:\n\n  **Free thyroxine (FT4) level:** The levels of free T4 in your blood are elevated.\n\n  **Thyroid-stimulating hormone (TSH) level:** The thyroid-stimulating hormone (TSH) level is suppressed (see Chapter 4).\n\nOther tests that support the diagnosis include\n\n  **Total T3 and Free T3 levels:** Less than 5 percent of patients with hyperthyroidism have a normal free T4 but an elevated total T3 and free T3, a condition called _T3 thyrotoxicosis,_ which behaves just like T4 thyrotoxicosis. T3 thyrotoxicosis can be a source of confusion when the patient has all the symptoms of hyperthyroidism but has a normal T4. The TSH is still low in cases of T3 thyrotoxicosis.\n\n  **Thyroid autoantibody levels:** If Graves' disease is the cause of hyperthyroidism, the levels of peroxidase autoantibody and antithyroglobulin autoantibody are elevated (see Chapter 4). They decline when the treatment is antithyroid drugs (see the \"Antithyroid pills\" section later in the chapter) but not when the patient receives radioactive iodine.\n\n  **Blood glucose level:** Your blood glucose (sugar) level is elevated, because your body is absorbing food so rapidly. You may have insulin resistance, and your doctor may find that you have diabetes or that it's worsening if insulin resistance is already present. (Diabetes improves after you receive treatment for your hyperthyroidism.)\n\n  **Liver function tests:** Blood tests of your liver function (such as the alkaline phosphatase and bilirubin levels in your blood) may be elevated.\n\n  **Cholesterol count:** Blood tests for cholesterol and other fats may be lower than normal.\n\nThe radioactive iodine uptake and scan study (see Chapter 4) used to be a common test in the diagnosis of hyperthyroidism, but the free T4 and TSH results generally make radioactive iodine uptake unnecessary.\n\n## Determining Whether Graves' Disease Is the Culprit\n\nMost cases of hyperthyroidism result from Graves' disease, an autoimmune condition. Graves' disease is most common in women; it occurs 10 to 20 times more often in women than in men. Symptoms tend to start between the ages of 30 and 60, but they can occur at any age. Graves' disease consists of any one or all of three parts: hyperthyroidism, eye disease, and skin disease.\n\nMost of the signs and symptoms of Graves' disease are the result of hyperthyroidism, which in turn results from the excessive production of thyroid hormones. Doctors can distinguish Graves' disease from other forms of hyperthyroidism because blood tests identify autoimmunity. In addition to the symptoms of hyperthyroidism I detail earlier in the chapter, autoimmunity can lead to eye disease and skin disease.\n\n## Causes of Graves' disease\n\nIn Chapter 5, I explain that about 10 percent of the world's population has thyroid autoantibodies, and these autoantibodies can lead to both hypothyroidism (underactive thyroid function) and hyperthyroidism. Some autoantibodies suppress the thyroid, and others stimulate it. If you have Graves' disease, the stimulating antibodies are in control in your body. Just why a person develops Graves' disease isn't clear, but doctors and researchers have a number of theories:\n\n  Your body makes many cells to prevent foreign tissue from invading and other cells that recognize your body's own tissue. When you have an autoimmune disorder, your body may have lost the cells meant to prevent other cells from reacting against the body's own tissue.\n\n  Invading organisms such as viruses may share characteristics of normal body tissue. When your body creates antibodies to fight the invaders, the antibodies may react against normal tissue as well.\n\n  Certain drugs can change the immunity of your body so that your body's immune system reacts against itself. The class of drugs that does this is called the _cytokines._ Doctors use cytokines to treat hepatitis and leukemia, for example. Their effect is to activate or increase immunity. As a side effect, they may activate thyroid-stimulating immunity.\n\n  Women, especially, may have genes that promote autoimmunity. The frequent occurrence of Graves' disease in mothers, daughters, and sisters confirms the genetic association (see Chapter 14).\n\n  When your thyroid suffers an injury, for example by a viral illness, it releases chemicals into your blood that aren't normally found there. The protective immunity cells may make antibodies against the chemicals, which then act to stimulate the thyroid.\n\n  Iodine, given to a person with a large thyroid gland not making enough thyroid hormone (such as a person with a multinodular goiter; see Chapter 9), can cause a sudden production of a lot of thyroid hormone, leading to hyperthyroidism.\n\n  Stress can produce a rapid heart rate, sweating, and other signs similar to hyperthyroidism. Its role in the onset of hyperthyroidism is unclear.\n\n## Symptoms specific to Graves' disease\n\nEye disease and skin disease associated with Graves' disease may be apparent even when a person has no overt symptoms of hyperthyroidism. Eye disease may be present long before the hyperthyroidism begins. Sometimes eye and skin problems progress even after hyperthyroidism is under control. Severe forms of thyroid eye and skin disease are rare, but thyroid eye disease can lead to blindness.\n\n### Thyroid eye disease\n\nThyroid eye disease, called _infiltrative ophthalmopathy_ or _exopthalmus,_ is present in almost all patients with Graves' disease. An ultrasound or MRI of the eye area can determine whether a patient has thyroid eye disease. Usually the condition is mild and doesn't progress after hyperthyroidism comes under control. Sometimes \u2014 in no more than 5 percent of Graves' patients \u2014 it does progress despite controlling the hyperthyroidism.\n\nAlthough Graves' disease is much more common in women than in men, the ratio of women to men decreases as the eye disease worsens. About nine women for every man has mild thyroid eye disease, but the ratio of women to men is almost equal in cases of severe eye disease.\n\nA strong association exists between eye disease in Graves' disease and cigarette smoking. Smokers have larger thyroid glands and higher levels of autoantibodies than nonsmokers, so thyroid damage may be the cause of this association.\n\nThyroid eye disease presents a clear-cut clinical picture. The eye, with its muscles and coverings, sits in a bony part of the skull called the _orbit._ When eye disease is present, the skin covering the eye and the muscles within the orbit are swelled and puffy. The limited room within the orbit forces the swollen skin and muscles to push forward. Usually thyroid eye disease affects both eyes, but the disease can start or progress more rapidly on one side. If your eye is pushed forward far enough, your eyelids cannot close fully. The result is irritation and redness of the eyeball.\n\nThyroid eye disease stretches and sometimes damages the optic nerve that carries the visual signal to your brain as well as the back of the eye, the _retina,_ where your eye focuses what it sees. Eye disease may compromise the blood supply to the optic nerve and retinal tissues.\n\nWith eye disease, your eye muscles don't function properly, so your eyes don't move together; you may experience double vision as a result. Occasionally, blindness may be the end result of all the damage.\n\nAs a result of the abnormalities thyroid eye disease causes, the person with thyroid eye disease has the following complaints:\n\n  **Injection:** The eye appears red much of the time.\n\n  **Tearing:** Tears form without provocation.\n\n  **Foreign-body sensation:** Pain like a dust particle in the eye.\n\n  **Photophobia:** Sensitivity to bright light.\n\nWhen a doctor examines the eye muscles of a patient with thyroid eye disease under a microscope, large numbers of autoimmune cells appear (similar to what appears in the thyroid itself).\n\nStudies show that thyroid eye disease progresses more often when treatment is by radioactive iodine rather than antithyroid drugs (see the \"Radioactive iodine treatment\" section later in the chapter). In one typical study in the _New England Journal of Medicine_ in January 1998, a group of 150 patients received radioactive iodine as treatment, and 148 patients took antithyroid drugs. After treatment, the eye disease was worse in 15 percent of the radioiodine patients but in only 2.7 percent of the antithyroid patients.\n\nTreatment of thyroid eye disease usually occurs in steps; doctors apply severe measures only when milder measures fail. First, you receive local measures like methylcellulose-containing eye drops to treat the inflammation. Sunglasses manage your sensitivity to light. Prisms correct the double vision that sometimes occurs. If all these treatments fail to cure the problem, you take oral steroids to reduce your immunity. Doctors can also prescribe other drugs that suppress immunity.\n\nIf you've taken radioactive iodine for hyperthyroidism (see the \"Radioactive iodine treatment\" section) and are now taking thyroid hormone, adjusting the level of the thyroid hormone won't affect your eye disease.\n\nSevere cases of thyroid eye disease usually respond to irradiation of the muscles in the orbit. If irradiation doesn't work or the case is severe enough, a surgeon can remove bone from the orbit, thus decompressing the tissues.\n\nWhile the eye doctor is removing bone from the orbit, another surgeon also attempts to remove all your thyroid tissue to eliminate antigens against which antibodies can be made, and the immune cells decline. After a doctor removes your thyroid, you need to take thyroid hormone replacement pills. In theory, it would be helpful for you to take an antithyroid drug (which I describe later in \"Antithyroid pills\") along with thyroid hormone replacement, because the antithyroid drugs decrease immunity. But the effect of taking antithyroid drugs in conjunction with thyroid hormone hasn't received enough careful study to warrant a recommendation.\n\n### Thyroid skin disease\n\nThyroid skin disease, called _pretibial myxedema_ and _thyroid acropachy,_ occurs even less often than thyroid eye disease and is very severe in only 1 to 2 percent of patients with Graves' disease.\n\n_Pretibial myxedema_ is an abnormal thickening of the skin, usually in the front of the lower leg. Raised patches of skin are pink in appearance. Rarely, thyroid skin disease affects other parts of the body, such as the thighs, shoulders, and forearms. The skin problems may last for several months or longer, then gradually improve. If they become severe, they may respond to steroids applied under tight dressings. A study in the _Journal of Clinical Endocrinology_ in February 2002 suggests that people who don't receive steroids as treatment have about the same clinical course as those who do, so steroids may not be of much value in treating skin disease.\n\nWith _thyroid acropachy,_ a patient's fingers become wider, and she may experience arthritic damage to the joints of her fingers. Fortunately, arthritic lesions usually cause only unsightly fingers and no symptoms. Patients with these finger changes don't receive any particular treatment.\n\n## Recognizing Other Causes of Hyperthyroidism\n\nAlthough the vast majority of patients with hyperthyroidism have Graves' disease, about 20 percent don't. Hyperthyroid patients without Graves' disease may have one of several other conditions that lead to the increased production of free T4 and T3 (thyroid hormones). The treatment of these conditions may differ from the treatment of Graves' disease, so recognizing them is important.\n\n_Factitious_ (false) _hyperthyroidism_ occurs when a patient is consuming large amounts of thyroid hormone without a doctor's knowledge. Usually some kind of psychological disturbance causes this behavior. The way to distinguish between factitious hyperthyroidism and other causes of hyperthyroidism is to check the size of the thyroid gland; someone with factitious hyperthyroidism has a small thyroid gland. The large amount of thyroid hormone suppresses the gland. If a doctor does a radioactive iodine uptake (see Chapter 4), this patient's thyroid gland won't absorb a great deal of the iodine.\n\nA large thyroid with many nodules that's exposed to a lot of iodine may become hyperthyroid (see Chapter 9). Sometimes a single nodule may produce excessive amounts of thyroid hormone and cause the rest of the thyroid to shrink. A doctor can feel whether nodules are present on the thyroid, which an ultrasound study or a thyroid scan can confirm (see Chapter 4). A number of situations exist in which consuming iodine may precipitate \"iodine-induced hyperthyroidism\":\n\n  You take iodine for a goiter caused by iodine deficiency (see Chapter 12).\n\n  You take iodine after being hyperthyroid but are normal after taking antithyroid pills.\n\n  You take iodine and have multiple nodules but aren't hyperthyroid (see Chapter 9).\n\n  You take iodine without having iodine deficiency, aren't hyperthyroid, but have a large thyroid.\n\nOccasionally the thyroid produces large amounts of T3 but normal or even low levels of T4, a condition called T3 _thyrotoxicosis._ T3 thyrotoxicosis is an autoimmune condition and produces the same signs and symptoms as Graves' disease. If you have T3 thyrotoxicosis, you receive exactly the same treatment as people with Graves' disease (which is associated with a high free T4 level). T3 thyrotoxicosis is really just Graves' disease with a predominance of T3. Doctors don't yet know why T3 is elevated in these cases rather than T4. If you have the signs and symptoms of hyperthyroidism but your free T4 level is normal or even low, your doctor should measure your T3 level.\n\n_Subacute thyroiditis_ (see Chapter 11) may cause the release of a lot of thyroid hormone from the thyroid and briefly cause hyperthyroidism. It results from the breakdown of thyroid cells rather than overproduction of thyroid hormone. The thyroid is usually tender, and the hyperthyroidism doesn't last because the disease is usually brief in duration and the cells stop breaking down. In fact, a period of hypothyroidism may also occur as thyroid hormone stores in the thyroid gland build up again.\n\nCertain (not very common) tumors called _choriocarcinomas,_ which arise from the placental tissue between a fetus and its mother, produce a lot of the _human chorionic gonadotrophin_ hormone, which stimulates the thyroid. Your doctor can measure this hormone in your blood.\n\nFinally, _central hyperthyroidism_ may also cause hyperthyroidism, although it occurs much less frequently than Graves' disease. Central hyperthyroidism has two causes: too much thyrotrophin-releasing hormone from the hypothalamus in the brain and too much thyroid-stimulating hormone (TSH) from the pituitary gland in the brain (often as a result of a tumor). In this condition, the patient's TSH level is high (whereas with Graves' disease, TSH level is low). The patient may experience symptoms of a brain tumor, such as headaches or loss of part of the visual field.\n\nYour doctor shouldn't have difficulty differentiating any of the conditions I discuss in this section from Graves' disease, especially if he or she looks for signs that your eyes and skin are changing and orders tests that check for thyroid autoantibodies.\n\n## Choosing the Best Treatment for Graves' Disease\n\nThe treatment of Graves' disease has evolved over the years as doctors and researchers have come to understand it better and additional tools have become available. As soon as doctors understood that the thyroid was responsible for the excessive production of thyroid hormones, their obvious response was to cut out the offending tissue \u2014 a practice that produced an era of great thyroid surgeons, along with a lot of unexpected problems, which I describe in the next section, \"Thyroid surgery.\" Around 1950, the administration of radioactive iodine began to replace surgery, which cured many patients but brought its own difficulties. Finally, antithyroid drugs became available.\n\nEach form of treatment has its pros and cons. I find it interesting that doctors in Europe generally prefer antithyroid pills, while doctors in the U.S. choose radioactive iodine more often. In the following sections, I explain the advantages and disadvantages of each treatment, and I share with you my own bias regarding the best treatment options.\n\nNo useful or proven homeopathic methods exist for the treatment of Graves' disease; none withstand scientific investigation. A certain number of patients go into remission without any treatment, which may be the reason that some have thought that certain treatments besides surgery, RAI, and antithyroid drugs can cure hyperthyroidism.\n\n## Thyroid surgery\n\nThyroid surgery involves the removal of part of the thyroid gland. Surgery quickly reduces the symptoms of hyperthyroidism by removing the source of those symptoms: the thyroid that was producing too much hormone. With the availability of nonsurgical treatments, patients rarely undergo surgery today for hyperthyroidism. Some situations, however, leave surgery as the only choice:\n\n  You refuse to take radioactive iodine and develop an allergy or a bad reaction to antithyroid pills (or simply fail to take them).\n\n  Your thyroid gland is extremely large, which means that radioactive iodine or antithyroid pills may not be effective.\n\n  You receive a diagnosis of hyperthyroidism during pregnancy that antithyroid drugs cannot control, causing problems for you or the fetus. (Women can have surgery safely any time in the second trimester of pregnancy.)\n\n  Your thyroid has a nodule that suggests a possible cancer. Ultrasound and other studies I describe in Chapter 7 can evaluate you if you have nodules indicating cancer.\n\n .jpg)\n\nOne reason doctors rarely perform surgery to treat thyroid conditions these days is that surgery carries certain risks. I list them here in no particular order:\n\n  Any surgical operation requiring anesthesia involves risk.\n\n  A person with severe heart or lung disease can't undergo surgery.\n\n  Women in their third trimester of pregnancy can't undergo surgery, because it can induce labor.\n\n  Surgery can damage one or both _recurrent_ _laryngeal nerves,_ which can lead to hoarseness or permanent damage to your voice with vocal cord paralysis.\n\n  Surgery can damage the _parathyroid glands,_ which lie behind the thyroid, leading to a severe drop in blood calcium.\n\n  Although a surgeon's goal is to leave enough thyroid tissue to keep your thyroid function normal, low thyroid function may begin immediately after surgery or develop during the next few years.\n\n  If you've had previous neck surgery, attempting another operation is risky because there's so much scar tissue from the previous surgery and the nerves, glands, and blood vessels are no longer in their usual positions.\n\n  The surgery is intricate, and a highly experienced surgeon isn't always available. See Chapter 3 for help finding a highly competent thyroid surgeon.\n\nSome specialists believe that surgery releases thyroid _antigens_ (tissue or chemicals that the body isn't normally exposed to) into the blood stream and leaves a lot of thyroid tissue intact, which can worsen the autoimmune condition, possibly resulting in worse eye disease. Whether this is true is unclear.\n\nThyroid surgery controls hyperthyroidism in 90 percent of patients. The rest have a recurrence, usually due to the fact that doctors didn't remove enough thyroid tissue. Just as determining the exact dose of radioactive iodine to eliminate hyperthyroidism but avoid hypothyroidism (see \"Radioactive iodine treatment\" below) is impossible, determining the exact amount of thyroid tissue to remove is also impossible. The fact that thyroid tissue can regrow further complicates the question of how much thyroid tissue to remove.\n\nFor more information about thyroid surgery, see Chapter 13.\n\n## Radioactive iodine treatment\n\nIn radioactive iodine treatment, a patient swallows a capsule containing radioactive iodine (RAI). Because the thyroid uses more iodine than any other organ or gland in your body, the RAI concentrates in your thyroid and slowly destroys the overactive thyroid cells. Radioactive iodine may seem like an ideal solution to the problem of hyperthyroidism. Decades of experience with radioactive iodine have lain to rest a number of the fears surrounding this treatment. Here are some of its benefits:\n\n  Adults who receive RAI experience no increase in thyroid cancer.\n\n  After RAI, no increase in cases of leukemia occurs.\n\n  RAI doesn't affect reproductive ability.\n\n  RAI is effective and safe for small children and adolescents with hyperthyroidism.\n\n  Children of mothers who previously received RAI have normal thyroid function and no congenital defects at birth (though doctors never give RAI to women during a pregnancy or during breast feeding). Children of mothers who received RAI can, however, still develop Graves' disease later in life because it's hereditary.\n\nIn addition, RAI is inexpensive and avoids the risks of surgery.\n\n .jpg)\n\nBut RAI does have its share of drawbacks:\n\n  Pregnant women can't take RAI, because it crosses the placenta and enters the baby's thyroid, possibly destroying it.\n\n  RAI should not be used in babies because of the possible incidence of thyroid cancer when babies are exposed to it. (For example, thyroid cancer was rampant among children exposed to RAI outside the Russian nuclear plant at Chernobyl.)\n\n  Finding the exact dose to cure your hyperthyroidism but leave you with normal thyroid function is impossible. If you take too little RAI, you need another treatment. Most patients who receive enough RAI to cure their hyperthyroidism eventually become hypothyroid and need to take thyroid hormone replacement (possibly for life). You can receive even a third treatment with RAI if necessary.\n\nHypothyroidism caused by RAI may feature three unusual symptoms doctors don't find in other causes of hypothyroidism: joint aches, stiffness, and headaches. The headaches may be due to swelling of the pituitary gland.\n\n  By slowly destroying the thyroid, RAI releases a large amount of thyroid antigens into the patient's circulation, similar to what occurs in surgery, which may greatly increase autoimmunity and make eye disease worse.\n\n  A patient must have follow-up blood tests for years to monitor for the development of hypothyroidism.\n\nYou must take some precautions after RAI:\n\n  Because some iodine appears in saliva, you shouldn't kiss someone for two or three days after receiving RAI.\n\n  Stay away from very close contact with your baby or spouse for two days, including sleeping in the same bed, dancing, and other very close interactions.\n\nAfter you receive RAI, it takes about three weeks to begin to have an effect, and it has its maximal effect about two months after treatment. (Timeframes can vary depending on how large the gland is when the treatment occurs.)\n\n## Antithyroid pills\n\nDoctors use two antithyroid pills in the United States to control hyperthyroidism, _propylthiouricil_ (PTU) and _methimazole._ In other countries, doctors also use a third drug, _carbimizole._ All three pills block the production of thyroid hormones, but propylthiouricil also blocks the conversion of T4 to T3, giving it a theoretical advantage over methimazole. (The advantage doesn't seem to matter so much in practice unless you're trying to control the hyperthyroidism very rapidly.)\n\nA major advantage of antithyroid pills is that, unlike surgery or radioactive iodine, they help to treat all complications of Graves' disease, including eye disease, by reducing autoimmunity. Very soon after you start taking the pills, levels of thyroid-peroxidase autoantibody and thyroid-stimulating antibody (see Chapter 4) begin to fall and stay down after you stop taking the drug. Also, taken in correct dosages, they don't lead to hypothyroidism.\n\nWhen these drugs are given, you usually begin to feel better after three weeks, and the hyperthyroidism comes under control within six weeks. Then monitoring your free T4 level at least every six to eight weeks becomes important, because treatment can lower the T4 into the hypothyroid range. This may be detected if your thyroid starts to enlarge even though you have no more symptoms of hyperthyroidism.\n\nFollow-up should continue for years after successful treatment, because your thyroid gland is unstable once you've had hyperthyroidism, especially if you're under severe stress. In the absence of symptoms, a visit to your doctor every six months to a year is appropriate.\n\n .jpg)\n\nThe TSH can't be used to monitor the effect of treatment with antithyroid drugs. It will remain suppressed for many weeks to months after normal thyroid function is restored.\n\nOne way to speed up your return to normal \u2014 by as much as one to two weeks \u2014 is to use the drug cholestyramine. This drug has been used to lower cholesterol by binding the cholesterol in the intestine so it can't be absorbed into the blood stream. Thyroxine circulates between the liver and the intestine in a similar way. Cholestyramine can bind thyroxine and keep it in the intestine so it doesn't get absorbed, just like cholesterol. The dose (in case any doctors might be reading this) is 4 milligrams twice daily for the first four weeks of treatment.\n\nMost patients start taking 5 milligrams of methimazole three times daily or 50 milligrams of propylthiouricil three times daily. The major advantage of methimazole is that doctors can prescribe it in a once-a-day regimen from the very beginning, because it lasts longer in the body. As your T4 level falls, your doctor can reduce the dose to two pills or even one pill daily. The current standard is to keep the drug going for a year and then to stop it to see whether the disease recurs.\n\nThe hyperthyroidism of about 50 percent of patients taking antithyroid pills remains under control after they stop taking the propylthiouricil or methimazole. For the others, the symptoms recur after they stop taking the pills, usually within three to six months of stopping the drug. These patients can continue on antithyroid drugs or undergo surgery or take RAI. A study in the _European Journal of Endocrinology_ in May 2005 shows that methimazole is a safe and effective treatment for more than ten years for patients with hyperthyroidism caused by Graves' disease.\n\n .jpg)\n\nLike surgery and RAI, antithyroid drugs carry some risks. The major risk is that they can cause a reduction in white blood cells and, very rarely, a complete lack of white blood cell production _(agranulocytosis)_. Although this usually occurs early in treatment when patients take especially large doses of medication, diminished white blood cell production occasionally occurs later on and in patients taking low doses. This problem goes away when the patient stops taking the antithyroid drug. Some patients develop a rash when using one of the antithyroid drugs. You can try one of the other antithyroid drugs if you develop a rash. Rarely, the pills affect the liver, and blood tests become abnormal. Make sure your doctor checks your liver function every few visits when you take antithyroid drugs. Once your liver function remains normal for several tests, this problem will likely not recur. These abnormalities in your liver also respond to withdrawal of the offending drug.\n\nIf you're on methimazole or propylthiouricil and develop a cold, sore throat, or other illness usually associated with a virus, contact your doctor, who should do a white blood cell count. One way to avoid severe loss of white blood cell production is to have white cell count done each time you visit your doctor while you're on the antithyroid pills.\n\n### My choice of treatment\n\nFor most patients with Graves' disease, methimazole is my first choice of treatment (or propylthiouricil for pregnant women). Although not all (about 70 to 80 percent) patients have a permanent remission after taking antithyroid drugs, the fact that antithyroid drugs suppress the immune reaction (thus helping to reduce eye disease in hyperthyroidism) is an important reason for my choice. Methimazole and propylthiouricil (plus carbamizole in Europe) are the only choices of treatment that may be truly curative and not simply destructive. The largest thyroids I've seen have eventually responded to antithyroid drugs.\n\nMany doctors cite the need to take a pill every day as a reason not to recommend antithyroid drugs. Most of these doctors give their patients radioactive iodine, and the patients often end up hypothyroid and needing to take daily thyroid hormone replacement pills, so I don't agree with this argument.\n\nFor other chronic illnesses, such as diabetes or hypertension, patients take pills for a lifetime. I've never understood the reluctance to do the same thing with Graves' disease to avoid surgery and radioactive destruction of the thyroid gland. No rule says that a patient can't take pills for more than a year. Patient can also stop taking the pills on a yearly basis and not start them again until the disease recurs, if it does.\n\nI have a number of patients in my practice who've gone more than five years with normal thyroid function after a course of antithyroid therapy. They haven't had to take any pill. Many of them are in the 30-to-50 age group and are quite happy to be free of medications.\n\nIf a patient is very symptomatic at the beginning of treatment, I use the beta blocker propranolol to control her symptoms until methimazole takes effect (in three to four weeks).\n\nI can see a patient who is stable on pills every few months, as long as she knows that she should contact me if she experiences any symptoms of a virus, which may mean a reduction in her white blood cell count that the medication causes.\n\nI've had occasion to use radioactive iodine on only a few patients in the last ten years, who were generally elderly patients with other severe complicating conditions. The vast majority I treated with antithyroid medication. A few of them required a second treatment with antithyroid drugs or needed treatment for longer than one year because their thyroid gland took a long time to shrink. Several patients have gone five years or longer with no further treatment and are doing fine.\n\n## Other helpful considerations and medications\n\nYou need to take into account two further general considerations in the treatment of your hyperthyroidism:\n\n  **Rest:** As a result of the hypermetabolism of hyperthyroidism, you may be exhausted both mentally and physically. You're certainly unable to do an eight-hour job while you're still hyperthyroid and for some time thereafter. Your doctor should provide you with a note for your employer or your school asking for time for you to rest or to delay test taking until you're functioning more normally. Don't try to continue any heavy exercise routine until your thyroid tests are normal and you regain your muscle strength.\n\n  **Nutrition:** In terms of nutrition, hyperthyroidism is a state of catabolism, which means you're losing muscle, bone, and even some fat while the disease is still active. Your lost muscle, bone, and fat needs restoring, which happens fairly quickly, especially if you continue to eat when your thyroid function is normal as you did when you were hyperthyroid. During hyperthyroidism, everything in your body is used up, including your vitamins and minerals. You may have to pay special attention to restore your body's levels of vitamins and minerals. You can read a lot more about this topic in Chapter 20.\n\nCertain pills can reduce the symptoms of hyperthyroidism without treating the condition. They're valuable for controlling the disease while antithyroid pills or radioactive iodine has a chance to work. They don't affect the underlying disease, and you shouldn't take them alone in treatment. The major class of drugs is called _beta blockers,_ and the most commonly used drug is _propranolol._ When taken in a dose of 20 to 40 milligrams three to four times a day, propranolol slows the heart, decreases anxiety, and reduces tremors. You can continue taking it for a few weeks until the other medications take effect or it can be used as preparation for surgery. Preparations of iodine temporarily block thyroid hormone production and reduce the blood flowing to the thyroid in preparation for surgery.\n\n## Treating Other Causes of Hyperthyroidism\n\nPeople who have hyperthyroidism not caused by Graves' disease may need other treatment options:\n\n  Factitious hyperthyroidism is treated by removing the thyroid pills from the patient and starting some form of psychotherapy.\n\n  A thyroid with one or more nodules that produce too much thyroid hormone responds best to radioactive iodine because an autoimmune condition doesn't cause the nodules, so no concern exists about thyroid eye disease lingering after the treatment. In the case of a single nodule causing the hyperthyroidism, after RAI eliminates the nodule, the rest of the thyroid often functions normally. When single or multiple overactive nodules are present, antithyroid drugs almost never cause a permanent remission.\n\n  T3 thyrotoxicosis responds to antithyroid medication just like Graves' disease caused by excess T4.\n\n  The hyperthyroid phase of subacute thyroiditis doesn't last very long. If necessary, the beta blocker propranolol can control symptoms until the hyperthyroidism subsides.\n\n  A surgeon must remove a choriocarcinoma-that is making hormones that stimulate the thyroid.\n\n  Surgery or radiation therapy is the treatment for a tumor in the brain causing excessive production of thyroid-stimulating hormone.\n\n## Surviving Thyroid Storm\n\nFortunately, _thyroid storm_ is rare, because doctors almost always diagnose hyperthyroidism at a much earlier stage. However, the condition may be fatal. It is primarily a disease of the elderly, so as the population ages, doctors will see more cases. The clinical picture is one of extreme signs and symptoms of hyperthyroidism. The patient has a high fever, as high as 103 to 104 degrees Fahrenheit, and a very rapid heart rate, 130 beats per minute or more. She may be vomiting, have diarrhea, and become dehydrated. She may be in heart failure and have an uncontrollable heart rhythm. She can be delirious and lapse into a coma.\n\nJust as in myxedema coma (see Chapter 5), a precipitating event usually produces thyroid storm in someone who already has hyperthyroidism. The most important such events are:\n\n  Heart failure\n\n  Diabetic ketoacidosis\n\n  Bowel loss due to loss of circulation\n\n  Surgery or labor and delivery\n\n  Trauma\n\n  Clot in the lung\n\n  Infection\n\n  Mental disturbance\n\nThe preceding kinds of events are already dangerous and often fatal to an elderly patient. When thyroid storm adds to the illness, the outlook is grim, with a mortality rate of between 25 and 60 percent.\n\n .jpg)\n\nThyroid storm is a true medical emergency that should be managed by a physician who is very aware of the treatment of severe hyperthyroidism.\n\nThe doctor usually starts a number of treatments all at once. The patient is given fluids, one of the antithyroid drugs (such as propylthiouricil), potassium iodide, steroids, and a beta blocker like propranolol. This can lower the level of T3 hormone to normal in a day, although the patient takes many more days to fully recover.\n\n##### Chapter 7\n\n## Thyroid Nodules\n\n### In This Chapter\n\n  Defining the thyroid nodule\n\n  Determining whether a nodule is cancer\n\n  Performing thyroid surgery\n\n  Treating benign nodules\n\nIn some ways, the thyroid is really an annoying gland. If it weren't so important to our health, there would be good reason to get rid of it, just like doctors used to get rid of tonsils. The thyroid is forever forming bumps and growths that turn out to be of little or no significance but that doctors have to evaluate on the outside chance that they're cancerous. Even if a thyroid growth turns out to be cancerous (see Chapter 8), it's rarely fatal.\n\nThe reason doctors pay so much attention to bumps on the thyroid is the same reason a piece of property is valuable: location, location, location. If the thyroid gland weren't located so prominently in the front of the neck, you wouldn't notice all its little growths, and most people would be no worse off for it. Instead, your thyroid got put right up front, thus providing a lifetime source of work and income for specialists who call themselves thyroidologists (like me).\n\nThis chapter tells you what you need to know about all your thyroid's bumps and lumps. I explain whether you should be concerned about or just ignore a nodule on your thyroid, as well as what to do if you must get rid of it. By the end of the chapter, I think you'll appreciate that most thyroid nodules are minor inconveniences and that knowing what to do about them keeps them that way.\n\n## What's a Thyroid Nodule?\n\nKenneth Fine is a 35-year-old man in excellent health. While shaving one day, he notices a bump on the front of his neck that he hasn't seen before. He ignores it for several months but finally decides that he ought to have someone check it out. He goes to his doctor, who does thyroid function tests. His free T4 and thyroid-stimulating hormone (TSH) levels are normal (see Chapter 4). His doctor then sends him to a thyroid doctor for evaluation.\n\nThe thyroid doctor asks Kenneth if the lump has grown noticeably and if it causes any trouble swallowing or breathing. Kenneth answers \"no\" to these questions. The specialist then proposes that Kenneth have a fine needle aspiration biopsy (see Chapter 4). When this test is done, the report comes back affirming Kenneth has a _benign thyroid adenoma,_ which means that the lump isn't cancerous. The doctor tells Kenneth to come back in a year for a reexamination.\n\nA year later, no change in the lump has occurred, and the specialist asks him to return a year after that. Kenneth forgets about his appointment, and the doctor's receptionist has a poor bookkeeping system, so Kenneth lives happily ever after.\n\nKenneth is a very good example of the typical case history of a person with a thyroid nodule. He illustrates the unexpected finding of a bump, the tendency to ignore it, and the fact that it generally isn't a problem in the long run.\n\n .jpg)\n\nKenneth's story isn't meant to minimize the fact that some nodules, about 5 percent, do turn out to be cancerous and that doctors must deal with them in the proper way. Kenneth's example simply illustrates the most common course of events.\n\nThe thyroid is ordinarily a smooth, butterfly-shaped gland (see Chapter 2). Whenever something grows that alters its smoothness, the growth is considered a _nodule._ Nodules can be _benign,_ that is, free of cancer, in which case they're called _adenomas,_ or they can be _malignant._ When ultrasounds are done routinely on a group of people, as many as 20 percent of them have nodules. That 20 percent represents 60 million people in the United States alone. Picking out the few who have cancer provides full-time work for a lot of people.\n\nExactly why nodules form isn't clear, but a number of theories exist:\n\n  Because they're most common in women, some people think that hormonal changes, especially through the menstrual cycle or during pregnancy, cause alternate growth and shrinkage of thyroid tissue. When shrinkage isn't complete, thyroid nodules result.\n\n  Another cause of thyroid nodules is the growth of thyroid tissue that occurs when you have part of your thyroid removed.\n\n  Chronic thyroiditis (see Chapter 5) may enlarge the thyroid in an irregular fashion, leading to nodules.\n\n  The condition called subacute thyroiditis (see Chapter 11) may also enlarge the thyroid irregularly.\n\nA _neoplasm_ is any new growth on the thyroid. Despite its harsh-sounding name, the term simply means \"new growth.\" A person's thyroid may have one or several growths, and multiple explanations exist for why they appear. Physicians identify the various possibilities according to the appearance of the nodule tissue under a microscope. This is known as the _pathological appearance_ of the tissue. For our purposes, we just want to know whether the nodule is benign (not cancerous) or malignant (cancerous).\n\nMost thyroid nodules \u2014 _more than 95 percent_ \u2014 are benign.\n\n## Evaluating Cancer Risks\n\nA number of facts about a patient's history, signs, and symptoms can help sway the balance toward or away from a diagnosis of cancer:\n\n  **Gender:** Doctors find nodules less often in men than women, but nodules are cancerous more often in men.\n\n  **Age:** Nodules found in children are cancerous more frequently than they are in adults. However, a nodule in a child is still benign more often than it's malignant.\n\nA nodule in a person over age 70 is also highly suspicious for cancer. Whether a person over 70 should have surgery for such a generally nonaggressive cancer is another issue.\n\n  **Number of nodules:** If a patient has many nodules, this suggests that a cancer isn't present. Most multinodular thyroids are benign.\n\n  **Growth rate:** A nodule that grows rapidly is probably a cancer, but if it pops up suddenly and is tender, it may be a hemorrhage. A hemorrhage that suddenly occurs isn't usually a serious problem, but it does cause discomfort.\n\n  **Additional growths:** Finding growths in the neck away from the thyroid suggests cancer that has spread, and those growths must be evaluated by a biopsy.\n\n  **Hoarseness and trouble swallowing:** These symptoms suggest cancer, especially if they're of recent onset.\n\n  **Movement:** If the thyroid doesn't move freely, it's a sign of fixation, which suggests cancer.\n\n  **Previous exposure to irradiation:** (This doesn't include the use of radioactive iodine in the treatment of hyperthyroidism \u2014 see Chapter 6.) A significant increase in reports of thyroid cancer occurred among children exposed to the radiation from the Chernobyl nuclear plant in Russia. In this case, multiple nodules don't rule out cancer. Almost half the nodules in an irradiated gland turn out to be cancer. Doctors may find the cancer 10 to 30 years after the irradiation. Even today, doctors use radiation to treat tumors in the head and neck, which will result in a certain amount of cases of thyroid cancer.\n\nVirtually no family or hereditary connection pertains to nodules, either benign or cancerous. The exception is a condition called _multiple endocrine neoplasia,_ in which many members of a family have nodules on several different glands, such as the thyroid, the pancreas, the parathyroids, and the adrenal glands. When such a family history is present, doctors should perform a blood test for calcitonin levels because the tumor that is found in the thyroid, medullary thyroid cancer (see Chapter 8), produces a lot of calicitonin. Although the thyroid tumor is malignant, the tumors in the other glands may be malignant or benign.\n\n## Securing a Diagnosis\n\nIf the factors in the previous section don't provide enough evidence suggesting whether a nodule is cancerous, your doctor can use several tests to make a diagnosis.\n\n## Thyroid function tests\n\nThyroid function tests that suggest hyperthyroidism (see Chapter 6) or hypothyroidism (see Chapter 5) usually mean that a thyroid nodule is benign. However, the possibility exists for two different conditions to be present in the thyroid at the same time. Therefore, your doctor should examine the nodule occasionally to guarantee that it isn't growing.\n\n## The thyroid scan\n\nA thyroid scan (see Chapter 4) distinguishes a nodule that takes up radioactive iodine from one that doesn't. A nodule may be actively concentrating the iodine even though the thyroid function tests are normal. A \"warm\" nodule takes up radioactive iodine like the rest of the gland. If the nodule concentrates most of the iodine (while the rest of the gland is less active) and the thyroid function tests are elevated, it's a \"hot\" nodule. Cancerous nodules are usually \"cold,\" meaning they don't concentrate the radioactivity. However, most cold nodules aren't cancerous.\n\nFigure 7-1 shows the typical appearance of a cold nodule and a hot nodule.\n\n**Figure 7-1:** A hot nodule and a cold nodule.\n\n|     \n---|---\n\nIn addition, the thyroid scan sometimes shows multiple nodules when a doctor sees or feels only one. Multiple nodules argue against a cancer.\n\n## The thyroid ultrasound study\n\n_The thyroid ultrasound study_ (see Chapter 4) also gives a picture of the entire thyroid and demonstrates if more than one nodule is present. More helpful than that, the ultrasound can distinguish between a solid mass and a cyst. A _cyst_ is a nodule that is either filled with fluid or contains some solid tissue. A cyst filled with fluid is generally believed to be a benign growth. A cyst that contains some solid tissue may be a cancer.\n\nThe thyroid ultrasound can also be performed on several occasions to provide a continuous picture of the status of the nodule \u2014 whether it's shrinking, growing, or remaining the same. A nodule that shrinks or remains the same is less likely to be a cancer. Because thyroid cancer doesn't tend to be aggressive, an ultrasound every few months to follow the growth of a nodule is reasonable, particularly if the patient doesn't want a biopsy.\n\nAbnormalities may be seen in an ultrasound study that helps to identify cancers, including tiny bits of calcium and greatly increased blood flow in the nodule, but these abnormalities aren't total proof of cancer. They simply help doctors in choosing which nodule to biopsy first when several nodules are present in a thyroid gland.\n\nAnother important use for thyroid ultrasound is guiding the needle when doctors perform a fine needle biopsy. Doctors can place the tip of the needle so accurately that no doubt exists whether the tissue of interest is being biopsied.\n\n## The fine needle aspiration biopsy\n\nThe fine needle aspiration biopsy is the gold standard for the diagnosis of a thyroid nodule. Often specialists skip the other steps and go right to this simple, painless, and very specific procedure. The test involves sticking a tiny needle into the nodule and removing bits of tissue from it. Doctors believe that this test gives the correct diagnosis 98 percent of the time, especially when an ultrasound guides it, as I explain in the preceding section.\n\nWhen a person has a fine needle aspiration biopsy, the organization of the tissue as it exists in the body is lost. Cells that would've been found next to other cells in the intact tissue are broken apart. The pathologist is looking for the presence of certain cells and the appearance of the cells to make a diagnosis. A hallmark of cancer, which is invasion of surrounding tissues, isn't visible during a fine needle aspiration biopsy, but usually it doesn't matter.\n\nEver since doctors have used the fine needle aspiration biopsy, the number of surgeries for possible thyroid cancer has dropped dramatically. Fine needle aspiration biopsies allow doctors to place their diagnosis of a nodule into one of four possible categories and then take the appropriate actions:\n\n  **Benign adenoma (about 65 percent of the time):** Benign nodules require no further treatment. They don't turn into cancers at a later date.\n\n  **Suspicious nodule (about 15 percent of the time):** Suspicious nodules are probably the most difficult of the categories to deal with. They evince no definite sign of cancer but exhibit changes that are sometimes observable in cancer but also observable when cancer isn't present. Doctors usually remove a suspicious nodule and examine it in a more intact state under a microscope. However, you can avoid surgery if you have a thyroid scan with radioactive iodine and the nodule demonstrates it's active by concentrating iodine. Active nodules are generally not malignant.\n\n  **Malignant nodule (about 10 percent of the time):** Doctors must remove malignant nodules (cancers) along with the rest of the thyroid gland, because cancer is often in other parts of the gland, especially if you have a history of irradiation.\n\n  **Nondiagnostic (about 10 percent of the time):** Doctors find nondiagnostic nodules when the tissue consists of follicular cells (see Chapter 2). In order to know if they're cancerous, invasion of surrounding tissues must be visible. As I note above, the normal architecture of the tissue is lost with fine needle aspiration biopsies, so doctors can't detect invasion with this technique. If the nodule is nondiagnostic, the patient will usually go to surgery so the nodule can be examined in a more intact state. If cancerous, the thyroid is removed.\n\nThyroid cancers tend to grow either very slowly or so fast that they're obvious. If they grow fast, you have the biopsy done immediately. If they grow slowly, you can have the fine needle aspiration biopsy done a year or more after you discover a slowly growing nodule, still leaving plenty of time to treat a newly discovered cancer. Of course, your doctor must check for evidence of changes in the key findings I discuss previously (see the \"Evaluating Cancer Risks\" section) each time he sees you, such as the development of hoarseness, the finding of a new growth away from the thyroid in the neck, or fixation of a thyroid that previously moved freely.\n\nYou can also have a fine needle aspiration biopsy if you have any lymph nodes that are suspicious in the area of the nodule. Finding thyroid cancer in a lymph node verifies a diagnosis of thyroid cancer in the thyroid gland, even if the nodule is negative.\n\n## Treating Cancerous Nodules\n\nEvery so often, one of the anonymous nodules turns out to be a cancer (see Chapter 8), and treatment becomes necessary. (Sometimes all the tests available to a doctor don't provide a definitive diagnosis, in which case I believe treating the nodule as if it were cancer is wise.) The treatment of choice for a cancerous thyroid nodule is surgery. (Even benign nodules may some- times require surgery if they're unsightly or cause compression or trouble swallowing.)\n\nWhen you and your doctor determine that surgery is necessary, you need to find two additional competent and experienced physicians:\n\n  **Surgeon:** A surgeon with plenty of experience in thyroid surgery must be available. I discuss the potential complications of thyroid surgery in Chapter 13. No general surgeon who does only occasional thyroid cases should undertake thyroid surgery for potential cancer, because the cancer may be very extensive. Furthermore, a surgeon must do the right procedure the first time around, because a second surgery is much more difficult and complicated.\n\nIf you need to have thyroid surgery, check the qualifications of the surgeon. Don't accept a referral without checking the surgeon's experience and rate of complications. See Chapter 3 for help in finding a good thyroid surgeon.\n\n  **Pathologist:** A _pathologist_ is a doctor trained to diagnose disease by looking at the abnormal tissue under a microscope. The hospital where you're having your surgery must have an experienced pathologist because the pathologist gives a diagnosis of the tissue that the surgeon removes as surgery proceeds. The pathologist's opinion determines whether the surgeon does a complete removal of the thyroid (called a _total thyroidectomy_ ) and then goes on to remove lymph nodes in the neck around the thyroid to see if the cancer has spread. Your surgeon should not perform this extensive (and expensive) operation unless the pathologist gives the surgeon a precise diagnosis. Ideally, the final diagnosis of the tissue, made after surgery is complete, won't contradict the diagnosis made during the operation.\n\nYou probably won't find highly experienced pathologists at community hospitals, even though doctors discover many thyroid cancers at these hospitals. Do yourself or your loved one a major favor and go to a referral center to get this special care.\n\nA few thyroid specialists argue that even if a doctor diagnoses your nodule as cancerous, you're better off leaving the nodule alone. They base this argument on the fact that although doctors detect about 15,000 new cases of thyroid cancer in the United States each year, only 1,500 to 2,000 people in the U.S. die from thyroid cancer each year. Furthermore, the 15,000 new cases of thyroid cancer derive from as many as 15 million people with nodules of one kind or another. Because death from thyroid cancer is such a rare event, some specialists reason that treatment may not matter. Most evidence doesn't support not treating cancerous nodules, however.\n\nI believe that surgical removal should be the treatment for nodules that contain thyroid cancer.\n\n## Dealing with Nodules That Aren't Cancer\n\nHot nodules and benign cysts may require some treatment but not necessarily surgery.\n\nDealing with the thyroid nonsurgically is almost always preferable if the results will be satisfactory because of the potential for surgical complications, not to mention the cost and the trauma that surgery brings with it.\n\nFortunately, other treatment choices are available for nodules that aren't cancerous, and specialists are discovering new ones regularly.\n\n## Hot nodules\n\nA hot nodule produces hyperthyroidism, so it must be treated. Hot nodules represent about 10 percent of the nodules doctors find. One choice of treatment is to take radioactive iodine (RAI), as patients with Graves' disease do (see Chapter 6). However, up to 40 percent of the patients who receive RAI develop hypothyroidism (underactive thyroid) later in life. Those who don't develop hypothyroidism usually return to normal thyroid function.\n\nA second choice of treatment for a hot nodule is surgical removal of the lobe of the thyroid in which the nodule is found. Surgeons perform a surgical removal on younger individuals and those who refuse radioactive iodine. Antithyroid drugs help prepare patients for surgery. When thyroid function is normal, patients undergo surgery. In the hands of a good surgeon, you experience few problems with the surgical approach. However, about half the patients who have this kind of surgery become hypothyroid later on.\n\nA newer treatment that eliminates the hot nodule while not destroying the rest of the thyroid gland is the injection of ethanol into the nodule. Injections take place several times over several days. Complications include pain in the thyroid area and fever. Doctors may use this treatment more and more often in the future as they gain experience with it. Doctors can inject ethanol into the nodule very precisely using guidance by ultrasound. One big advantage is that patients who receive these injections don't develop hypothyroidism later. Doctors in Europe first used this treatment. Although it is done in the United States, it is not the treatment of first choice here. My own opinion is that it can be successful at a medical center with experience in the technique and that it will become the treatment of first choice as more and more doctors gain that experience.\n\n## Benign cysts\n\nA nodule filled with fluid shrinks when a doctor inserts a needle and removes the fluid. Unfortunately, the cyst often fills right up again. Repeated removal of the fluid sometimes cures the problem. Doctors can inject ethanol into a cyst just as into a solid nodule; they then remove the ethanol by the same needle they use to inject it. The cyst often shrinks after one ethanol treatment.\n\nThen again, you can leave the cyst alone if you're willing to live with it.\n\n## Warm or cold nodules\n\nDoctors sometimes treat nodules that don't produce excessive thyroid hormone and aren't cancer by giving you thyroid hormone in an attempt to shrink the nodule. Little evidence supports that this treatment actually works. Very rarely have I found these nodules to respond to thyroid hormone. The risk involved is that giving too much thyroid hormone can cause bone loss or abnormal heart beats.\n\nSometimes, when even a fine needle biopsy doesn't produce a definite diagnosis, a doctor suggests using _thyroid hormone suppression,_ having patients take thyroid pills to shrink the nodule _._ If a patient consumes thyroid hormone and the nodule shrinks, then the doctor assumes that the nodule isn't a cancer. If the nodule doesn't shrink, the suspicion of a cancer is greater. I disagree with this method, because most nodules don't respond to thyroid hormone, yet most nodules aren't cancer.\n\nYour doctor should examine your warm and cold nodules every six months or every year. Should your nodule grow, you have a fine needle biopsy done again. Otherwise, a nodule can be left alone.\n\n## Ignoring small nodules\n\nEvery so often a study, such as an ultrasound of the neck, reveals one or more very small nodules on the thyroid. The best specialists probably can't feel a nodule that's less than one centimeter in size. The ultrasound may detect a half-centimeter or smaller nodule. My advice is to ignore a bump this small, which has been termed an _incidentaloma_ (a thyroid specialist's agonizing attempt at humor).\n\n##### Chapter 8\n\n## Thyroid Cancer\n\n### In This Chapter\n\n  Understanding how thyroid cancer starts\n\n  Recognizing the types of thyroid cancer\n\n  Knowing and treating the stages of cancer\n\n  Ensuring proper long-term follow-up\n\nFor me, this chapter is probably the hardest one to write. The word _cancer_ evokes a number of images, and none of them are particularly positive. The fact is that people do die of thyroid cancer. For this reason, you must know what thyroid cancer is, how it grows, how you treat it, and how you follow up after treatment if you or a loved one has thyroid cancer. Putting thyroid cancer into perspective is also important.\n\nResearchers estimate that as much as 6 percent of the world's population has cancer in the thyroid gland. Based on this percentage, about 16.5 million people in the United States may have evidence of thyroid cancer. Yet in the U.S., doctors find only 15,000 new cases each year, and the total deaths due to thyroid cancer each year are 1,500 to 2,000. The vast majority of people with thyroid cancer live and die without ever knowing they had it. Only when doctors carefully examine the thyroid under a microscope can they detect the cancer.\n\nThyroid cancer doesn't appear among the top 75 causes of death in the United States. Among cancers, thyroid cancer isn't in the top 15 causes of death, which suggests that compared to most other cancers, thyroid cancer is one of the least dangerous. If you have to have a cancer, this may be the one to choose.\n\nThe relatively benign course of most thyroid cancers makes it difficult to say which treatment is best. Perhaps certain treatments are very effective, or perhaps any number of treatments works just as well because the disease itself is so mild. For this reason, much difference of opinion prevails among thyroid specialists. If you ask two thyroid specialists how to treat a certain type of thyroid cancer, you may get three opinions. In this chapter, I give you my recommendations based on the best and most recent investigations of thyroid cancer treatment.\n\n## Determining What Causes Thyroid Cancer\n\nJohn D'Mee is 40 years of age and has noticed that he has a lump in the front of his neck on the left side. His family has no history of thyroid cancer. The lump is painless and moves when he swallows. He doesn't know how long it has been there. John goes to see his doctor, who does thyroid function tests and finds that John's TSH and free T4 are normal. The doctor does a thyroid scan and finds that the area of the nodule on John's thyroid doesn't take up any radioactivity \u2014 it's a _cold nodule._ John's doctor sends him to see Dr. Rubin, who does a fine needle aspiration biopsy (see Chapter 4). The pathologist diagnoses a _papillary carcinoma,_ the most common type of thyroid cancer. Dr. Rubin sends John to a head and neck surgeon who has done more than 2,000 thyroid surgeries.\n\nThe surgeon, Dr. Stark, recommends removing the thyroid gland while carefully retaining the tissue around the parathyroid glands and the recurrent laryngeal nerves that pass along the thyroid. Dr. Stark performs the surgery successfully, and no other suspicious nodes or nodules appear during the procedure.\n\nJohn has no other treatment initially. He returns to Dr. Rubin, and three weeks after surgery he has a TSH test. The result is very high \u2014 45 \u2014 indicating that little thyroid tissue remains in his body. He has another scan that shows no uptake of radioactive iodine except for in a small area of the thyroid tissue the surgeon left intact. Dr. Rubin gives John a large dose of radioactive iodine to eliminate that small bit of tissue. A follow-up scan shows that all the thyroid tissue is gone. Dr. Rubin places John on thyroid-hormone replacement and continues to monitor him. John will probably live a normal life span with no further trouble associated with the thyroid cancer other than the periodic visits for follow-up.\n\nJohn is representative of the majority of people who develop thyroid cancer. The cancer shows itself as a thyroid nodule (see Chapter 7). Keep in mind that the vast majority of thyroid nodules aren't cancerous.\n\nOur understanding of why cancer occurs is becoming clearer and clearer. We know that genes (part of our hereditary makeup) called _oncogenes_ cause a cell to grow and divide without control. Oncogenes exist in all our cells. Just exactly what permits certain oncogenes to begin to be active isn't clear, but a mistake in cell division (a _mutation_ ) or some chemical or radiation in the environment could be to blame. Scientists have found other genes called _tumor suppressor genes_ in the human chromosome (the _DNA_ ). Some people lack tumor suppressor genes and can develop tumors. Doctors have actually found loss of the tumor suppressor gene in some thyroid cancers.\n\nThe best-known initiator of thyroid cancer is irradiation, which has been the source of many cancers in children who lived in the area of Chernobyl in Russia during the nuclear disaster. The children drank milk from cows that ate the grass upon which radioactive substances (including radioactive iodine) fell. Within a few years, many of the children had multiple sites of cancer in their thyroid glands. Adults exposed to radioactive iodine also developed thyroid cancer, though not as often as children, who seem to be more sensitive.\n\nChildren who have received neck and face irradiation for benign conditions such as acne or enlarged tonsils have also developed thyroid cancer \u2014 as many as 40 years after the irradiation. The size of these cancers isn't different from cancers that have no association with radiation, but they usually exist in multiple places in the thyroid, and often the thyroid shows several benign adenomas as well.\n\nDoctors who analyze the chromosomal content of thyroid tumor cells find that all cells in one tumor have exactly the same genetic makeup. This uniformity indicates that thyroid cancers start in one cell, which multiplies over time to form the thyroid cancer that you can feel.\n\nExactly why radioactive iodine treatment for hyperthyroidism doesn't cause thyroid cancer isn't clear. It may be that the very high dose used destroys the thyroid cells before they can develop cancer.\n\nSome cancers of the thyroid run in families, especially _medullary thyroid cancer._ I discuss this hereditary connection later in the \"Medullary thyroid cancer\" section. In some places like Hawaii and Iceland, thyroid cancer occurs at an unusually high rate. In Hawaii, it's especially high among Chinese males and Filipino females, much higher than in their country of origin. Many believe that something in the environment is the cause, though no one knows exactly what.\n\n### Experimental thyroid cancer\n\nTwo conditions are necessary for scientists to successfully produce thyroid cancer in animals. The first is some abnormal change in the chromosomes, the nuclear material in the thyroid cells. Exactly what kind of damage is necessary isn't clear. As a result of the change in the chromosomes, the cells aren't able to produce enough thyroid hormone, provoking the second condition, which is overstimulation of the thyroid cells. Scientists have caused an abnormal change in the chromosomes with radiation to the thyroid. By giving the animals goitrogens, the chemicals that further block thyroid hormone production, scientists cause increased thyroid-stimulating hormone, resulting in the second condition. In human children, irradiation of the neck for acne, enlarged tonsils or adenoids, or other reasons results in a hundredfold increase in the occurrence of thyroid cancer. The higher the dose of radiation, the greater the number of cases of thyroid cancer. Adults who received radiation in Hiroshima or Nagasaki also developed thyroid cancer, but their incidence wasn't as high as in children who also received radiation.\n\n## Identifying the Types of Thyroid Cancer\n\nAlthough it can be discovered in different ways and follow several different courses, most thyroid cancer can be expected to approach the following history:\n\n  Discovery occurs by accident by the female patient who notices a lump in her neck or the male patient who notices a lump in his neck while shaving. Or an ultrasound performed for other reasons detects the lump as an unexpected finding.\n\n  Occasionally a cancerous thyroid lump may appear as an enlarging mass with hoarseness, trouble swallowing, or trouble speaking.\n\n  When your doctor examines your neck, she finds a painless lump on one side of your thyroid.\n\n  If you find a cancerous lump before the age of 45, it takes a more benign course than if you find a lump later on.\n\nThe rest of the course depends on the particular type of tumor.\n\nA pathologist identifies thyroid cancer according to the appearance of the tissue that she examines. If she diagnoses a nodule as cancer, identifying the particular cancer is important because each one follows a different course. Treatments that work for one type of thyroid cancer may not work at all for a different type.\n\nAs a patient, you don't need to know how to identify types of thyroid cancer \u2014 that's the pathologist's job. But a basic understanding of the types of cancer helps you know what the future holds if your doctor identifies a thyroid cancer. When your doctor tells you the name of the cancer, you then have an idea of what to expect.\n\nThe descriptions for each type of thyroid cancer are true for most patients with that type of cancer, but exceptions exist. Occasionally, people with the most aggressive type of thyroid cancer find that their cancer isn't as aggressive as expected. By the same token, once in a while, a more benign form of thyroid cancer (based upon its appearance) takes a more aggressive turn. Medicine isn't an exact science.\n\n### How a pathologist identifies a cancer\n\nPathologists look for a number of abnormalities that separate normal tissue from cancerous tissue. They study thousands of tissue slides and know the difference in appearance between tissue that suggests cancer and tissue that's benign. The key elements that pathologists look for are as follows:\n\n  A malignant appearance to the tissue \u2014 very large, abnormal-looking cells containing abnormal-looking parts.\n\n  The presence of even normal-looking tissue in an area where it doesn't belong, which suggests that it has invaded the area. Examples are thyroid cells in a lymph gland, in bone, or in the lung.\n\n## Papillary thyroid cancer\n\n_Papillary thyroid cancer_ is the most common form that thyroid cancer takes, accounting for more than 70 percent of thyroid cancers in both adults and children. Fortunately, this form of thyroid cancer also tends to take a benign course, meaning it's not very aggressive. Although it spreads to the local lymph glands in the neck as often as half the time, the spread doesn't seem to make the cancer more aggressive. The following are the most important characteristics of papillary thyroid cancer:\n\n  It rarely spreads away from the neck. Spread to lymph nodes in the neck may even be protective in younger patients, while it's a bad sign in patients over 45. Why this is so is not known.\n\n  Diagnosis occurs most commonly between the ages of 30 and 50.\n\n  Females have papillary cancer three times as often as males.\n\n  It's the thyroid cancer most often associated with radiation exposure.\n\n  It may be present for decades without harming you.\n\n  It can also spread to bone and the lungs, but without causing problems for years.\n\n  It concentrates radioactive iodine, which doctors can use to destroy it.\n\n  Patients over age 45 may have a more aggressive course, especially if the tumor is larger than 1 centimeter.\n\n  It's especially mild in younger patients, very rarely causing death.\n\n## Follicular thyroid cancer\n\n_Follicular thyroid cancer_ makes up another 20 percent of all thyroid cancers. It's a little more aggressive than papillary cancer but still usually takes a benign course. It doesn't tend to spread locally to lymph glands but goes to bone and the lungs more often than papillary cancer. The following are its central features:\n\n  Diagnosis occurs most often between the ages of 40 and 60.\n\n  It affects females three times as often as males.\n\n  Local spread to lymph nodes is uncommon.\n\n  It concentrates radioactive iodine, which makes treatment easier.\n\n  It invades blood vessels, accounting for its tendency to go to distant sites, especially bone and lung.\n\n  When it's more aggressive, it invades local structures like the trachea and nearby muscles, blocking the airway.\n\n  It tends to be more aggressive in older patients.\n\nAnother cancer follows a course similar to follicular cancer but has a different appearance under the microscope: _Hurthle cell tumor._ It doesn't tend to concentrate radioactive iodine, so doctors can't use radioactive iodine in treatment. Despite not being able to use radioactive iodine, patients with Hurthle cell tumors survive the cancer at a rate almost identical to people with follicular thyroid cancer.\n\n## Medullary thyroid cancer\n\nMedullary thyroid cancer makes up only about 5 percent of all cancers of the thyroid gland. This cancer doesn't arise in the cells that produce thyroid hormones; rather, it arises in another type of cell found in the thyroid, the _C cell._ The C cell produces a chemical (a hormone) called _calcitonin,_ which doesn't affect metabolism. After doctors treat this cancer by completely removing the thyroid, they can measure the calcitonin level. If calcitonin levels are measured at regular intervals, a recurrence of cancer can be diagnosed easily.\n\nMedullary thyroid cancer differs from the other thyroid cancers in its occasional tendency to run in families. Eighty percent of the time no other family member has it. Twenty percent of the time it's hereditary. Either another member of the family also has medullary thyroid cancer or the patient has medullary thyroid cancer as part of a condition called _Multiple Endocrine Neoplasia_ (MEN) _Syndrome._ Two different types of MEN exist:\n\n  Patients with MEN type II-A have tumors of the adrenal medulla (called _pheochromocytoma_ ) and the parathyroid glands in the neck. The adrenal medulla makes a hormone called _epinephrine,_ so these patients have high blood pressure. They also have elevated levels of calcium as a result of the parathyroid tumor.\n\n  MEN type II-B also includes the adrenal tumor that produces excessive amounts of epinephrine but not the parathyroid tumor. People with MEN II-B also have tumors in the mouth.\n\n .jpg)\n\nIf your diagnosis is medullary cancer of the thyroid, a doctor must check to see if you have tumors in the adrenal medulla, because medication must control such tumors before surgery. Otherwise, your blood pressure can be high, making surgery on your neck extremely dangerous.\n\nThe important characteristics of medullary thyroid cancer include the following:\n\n  It occurs in women more often than in men, but the difference between the sexes is smaller than for other tumors that begin in the thyroid.\n\n  It's not associated with exposure to radiation.\n\n  It's more aggressive than papillary or follicular thyroid cancers, especially if it spreads to the lymph glands in the neck or to the bone and liver. More than 50 percent of people with medullary thyroid cancer have local or distant spread at the time of their diagnosis.\n\n  The medullary thyroid tumors secrete other hormones besides calcitonin. While calcitonin can cause diarrhea, the other hormones can cause constipation.\n\n  Drinking alcohol may cause secretion of calcitonin by the tumor, and the patient may have flushing and diarrhea.\n\n  If one family member receives a diagnosis of medullary thyroid cancer, other family members should have their calcitonin levels checked. If a family member's calcitonin is elevated, he or she should have the thyroid removed; elevated calcitonin almost always indicates cancer is present or, if not yet present, will develop later.\n\n  Even when the calcitonin isn't elevated in a family member, genetic testing can determine whether the family member may eventually get a medullary thyroid cancer (see Chapter 14).\n\n  Measuring calcitonin levels reveals whether a tumor has spread or recurred after the removal of the thyroid.\n\nSome thyroid specialists advocate measuring calcitonin as a screening test for all nodules suspected to contain thyroid cancer. So far, doctors aren't practicing this kind of screening.\n\nAfter ten years, about 70 percent of patients with medullary thyroid cancer who receive treatment are still alive.\n\n## Undifferentiated (anaplastic) cancer\n\nFortunately, _undifferentiated cancer_ is very rare, accounting for about only 2 percent of all thyroid cancers. This type of cancer is very aggressive and rarely cured. Although 95 percent or more of patients with papillary or follicular thyroid cancer will be alive and doing well after ten years, less than 10 percent of patients with undifferentiated thyroid cancer will be alive after three years.\n\nThis cancer is aggressive and invasive. Although lymph node invasion by papillary cancer isn't a bad sign, lymph node invasion by undifferentiated cancer predicts a bad outcome.\n\nThe cancer tends to attach to local structures like the nearby muscles, the trachea, the esophagus, and the blood vessels, making surgery very difficult, if not impossible. The outlook is so bad that little justification exists for extensive surgery that just mutilates the patient without accomplishing a cure.\n\nImportant features of undifferentiated cancer include the following:\n\n  The ratio of people with undifferentiated cancer is 60 percent female and 40 percent male.\n\n  It presents itself most often with a rapidly enlarging neck mass.\n\n  It usually occurs in patients over the age of 65.\n\n  It may occur in patients with a distant history of radiation to the neck or face.\n\n  By the time a person receives a diagnosis, the cancer has already spread to local nodes and distant structures like the lungs, bone, brain, and liver.\n\n  The average survival period following diagnosis is three months, and most people die of this cancer within six months or a year of diagnosis.\n\nUndifferentiated cancer is most probably the kind of thyroid cancer that Chief Justice William Rehnquist suffered from beginning in October 2004. The fact that he needed a tracheotomy, an opening from the outside into his windpipe, very early suggests a very aggressive tumor that had spread into his trachea. The fact that he was able to continue his work to the extent that he did while being treated for this disease is surprising. He lived about one year with the tumor, which is the most that you can expect under current methods of treatment.\n\n## The Stages of Thyroid Cancer and the Treatment Options\n\nFor purposes of treatment, thyroid cancers are _staged_ (divided into stages). Cancers divide up by whether the cancer remains within the thyroid, whether and where spread has taken place, and whether the tumor moves or is attached to surrounding tissues. Knowing which stage a cancer is in is important, because a follicular cancer in the same stage as a papillary cancer responds to treatment in the same way, while two follicular cancers at very different stages respond differently.\n\n  **Stage I:** The tumor is entirely within the thyroid gland with no spread to other areas.\n\n  **Stage II:** A tumor is in the thyroid but also has spread to the local lymph nodes. Both the thyroid and the lymph nodes are freely movable. The tumor hasn't become attached to surrounding tissues.\n\n  **Stage III:** The tumor and\/or lymph nodes are attached to the surrounding tissues.\n\n  **Stage IV:** The tumor has spread outside the neck.\n\nMost treatment of thyroid cancer initially involves surgery. The experience and competence of the surgeon is extremely important, no matter what stage of cancer you're in.\n\nThe most controversial treatment involves stage I of thyroid cancer, because knowing if the treatment itself or the benign course of the disease is responsible for a good outcome is difficult. General agreement exists about the best way to treat the other stages, but even there some disagreement exists. In the following sections, I try to offer the most generally accepted treatment recommendations, but of course anyone facing treatment must talk with an internist and surgeon to get their perspective.\n\n## Stage I\n\nBecause the size of the tumor plays a role in the prognosis, doctors recommend different levels of surgery depending on whether the tumor is less than or greater than 1 centimeter.\n\nSurgeons treat a tumor smaller than 1 centimeter by removing the lobe of the thyroid in which it's found, plus partially removing the other lobe, leaving some tissue intact (including the tissue next to the parathyroid glands and the recurrent laryngeal nerve). Surgeons usually treat a tumor larger than 1 centimeter by removing the entire thyroid, with the exception of the tissue adjacent to the parathyroid glands and recurrent laryngeal nerve. Both operations are intended to ensure that the patient's parathyroid glands continue to function and that his or her speech won't be damaged after surgery. The difference between the two is that the first operation leaves part of the thyroid intact because the chance that the cancer has spread to the other lobe is small.\n\nSome thyroid specialists recommend the smaller operation for any stage I thyroid tumor, regardless of size, due to the generally good prognosis of any stage I tumor. No one has proved that more surgery is better for stage 1 tumors.\n\nIf even a small tumor has developed as a result of receiving radiation to the thyroid, you should have the larger operation (removal of the entire thyroid) because usually cancer is present in both lobes.\n\nIn the previous edition of this book, I suggested that a patient who has most of his or her thyroid removed (the larger operation) is kept off thyroid hormone treatment in order to prepare him for evaluation of remaining tissue. If any thyroid cancer remains, a radioactive iodine scan detects it, which a large dose of radioactive iodine can treat. The radioactive iodine destroys all remaining thyroid tissue, which a subsequent scan can prove, and makes it easier to diagnose and treat a recurrence of the thyroid cancer in the future.\n\nHowever, more recent evaluation of patients with stage I thyroid cancer suggests that doing post-operative radiation treatment to ablate (remove) the remaining thyroid isn't necessary. Patients who don't have post-operative ablation with radioactive iodine do just as well as those who do. In a publication in the _World Journal of Surgery_ in August 2002, the 25-year survival rate of 636 low-risk thyroid cancer patients at the Mayo Clinic who didn't take radioactive iodine after surgery was 100 percent. No difference existed between the survival of patients not given radioiodine therapy in the 1940s and those given radiotherapy in later decades when the cancer was stage I or II. Radioactive iodine treatment can't improve on that.\n\nGiving large doses of radioactive iodine isn't completely free of side effects, especially if metastases (cancerous spread away from the original site of the cancer) of the thyroid cancer are in critical places, which concentrate the iodine and expose the tissue to a lot of radioactivity. Some of the possible damage from radioactive iodine includes the following:\n\n  Radiation sickness\n\n  Pain in the tissues surrounding the radioactivity\n\n  Damage to the salivary glands with decreased saliva and loss of teeth\n\n  Suppression of ovulation or even sterilization if metastases are in the ovaries\n\n  Suppression of sperm formation\n\n  Fibrosis of the lung with severe difficulty breathing\n\n  Decreased white blood cells, platelets, and red blood cells\n\n  Suppression of the bone marrow and even bone marrow failure\n\nI highly advise using radioactive iodine only when definite proof supports that it will be beneficial.\n\n## Stage II\n\nThyroid doctors generally agree about the correct treatment for stage II thyroid cancer: An experienced surgeon should remove as much of the thyroid as possible, preserving the parathyroid glands and the recurrent laryngeal nerves. The surgeon also looks for enlarged nodes in the neck, which he removes. If the surgeon finds cancer in these nodes, he removes as many of the nodes in the local area of the neck as he can find. Doing a neck ultrasound, which can detect enlarged, suspicious nodes, before surgery makes detecting cancerous lymph nodes easier.\n\nAfter surgery, the doctor keeps a patient off thyroid hormone treatment for three weeks and then measures the level of TSH. If it's above 20, the doctor does a thyroid scan to look for any residual thyroid tissue. A large dose of radioactive iodine removes any tissue found. The doctor then places a patient on enough thyroid hormone to keep the TSH at the bottom of the normal range (around 0.3). The patient takes thyroid hormone, because even thyroid cancer responds to TSH stimulation, and the object is to prevent further growth of the cancer.\n\n## Stage III\n\nBecause the tumor has invaded the local structures, treating stage III thyroid cancer requires more extensive surgery. The need for a highly experienced surgeon is even greater. An invasion of the tumor into the wall of the _trachea_ (windpipe) may have occurred, and a surgeon must remove part of the trachea. If a tumor is in the muscle, the surgeon removes the involved muscle. The surgeon must remove as much of the tumor as possible without disfiguring the patient. Because the cells of this stage III tumor are so abnormal, they often don't take up radioactive iodine, so radioactive iodine can't treat patients in stage III. Instead, patients often receive external irradiation if much of a tumor has to be left in the neck during the surgery.\n\n## Stage IV\n\nIf possible, the surgeon removes any distinct areas where the tumor has spread away from the thyroid outside the neck. In addition, the surgeon completely removes the thyroid as well as the lymph glands in the neck. If the spread of cancer is very wide, the doctor makes an attempt to get the distant tumor to take up radioactive iodine after removing the thyroid. If the tumor doesn't take up radioactive iodine, doctors use external irradiation to treat it.\n\nOnly about 5 to 10 percent of stage IV patients have successful removal of all the tissue in the neck that contains the thyroid tumor. For these patients, their survival is longer. The rest, unfortunately, won't survive more than a year.\n\nIf the tumor is more like normal thyroid tissue in appearance but has distant metastases or is of the anaplastic variety, chemotherapy can also be a treatment. For chemotherapy, you need the help of an oncologist, a specialist in cancer chemotherapy who should be aware of the various protocols developed for aggressive thyroid cancer treatment.\n\n## Medullary thyroid cancer\n\nThis type of cancer isn't a tumor that originates in thyroid-producing cells, so its treatment is a little different. A surgeon removes the entire thyroid, because the fact that medullary thyroid cancer, or medullary carcinoma, doesn't concentrate iodine means radioactive iodine can't eliminate thyroid tissue. The surgeon also removes lymph nodes in the neck that contain the tumor. External irradiation may be a treatment for medullary thyroid cancer. The doctor measures a patient's calcitonin level at intervals to check for any regrowth of the tumor.\n\nFamily members of a patient with medullary carcinoma should have their calcitonin levels checked, and if their levels are high, they should seek treatment as well. Genetic testing can also rule out medullary thyroid cancer in other family members.\n\n## Following up on Cancer Treatment\n\nAny patient who has most or all of her thyroid removed must start taking a thyroid-hormone replacement after surgery and needs to continue that treatment for the rest of her life. As I discuss in Chapter 5, thyroid-hormone replacement simply involves taking a daily pill. The current technique is to give enough thyroid hormone to keep the TSH between 0.1 and 0.3, which is supposed to suppress the growth of new thyroid tissue, including cancer.\n\nPatients who receive treatment for stage I or II thyroid cancer should have their blood levels of thyroglobulin (see Chapter 2) checked regularly after surgery. If their levels start to rise, their doctors stop thyroid-hormone replacement for several weeks. The doctor does a full body scan with radioactive iodine, looking for any evidence of thyroid tissue. If the body scan finds thyroid tissue, the patient receives a much larger treatment dose of radioactive iodine, which destroys the remaining thyroid tissue. The patient resumes replacement thyroid hormone a few days later.\n\nStopping the thyroid hormone allows the body to produce thyroid-stimulating hormone (TSH), which stimulates uptake of radioactive iodine by thyroid tissue. Instead of stopping thyroid-hormone replacement, your doctor can give you synthetic TSH injections for several days prior to a thyroid scan with almost as good a result. Another approach that works is to reduce your usual dose of thyroid hormone to half of the daily dose for several weeks. If the TSH rises above 20, you can do the radioactive treatment.\n\nPatients with stage III or IV thyroid cancer probably show regrowth of their tumor. Their tumor may respond to more external irradiation or to chemicals known to kill the tumor. The outlook is poor for patients who have recurrent stage III or IV thyroid cancer.\n\n##### Chapter 9\n\n## Multinodular Goiters: Thyroids with Many Nodules\n\n### In This Chapter\n\n  Knowing what causes a multinodular goiter\n\n  Diagnosing and treating the problem\n\n  Dealing with unexpected complications\n\nM _ultinodular goiters_ \u2014 large thyroids with many nodules \u2014 may well be the most common of all thyroid disorders. In various studies of thyroid glands of people who died of any cause, between 30 and 60 percent of the glands had multiple nodules. This means as many as 165 million people in the United States alone have multinodular goiters. What a bonanza for thyroid specialists! (With numbers like that, you have to wonder whose idea it was to place the thyroid gland so prominently in the front of the neck, near so many vital structures, and to make it so important. I call it bad planning.)\n\nFortunately (or unfortunately, depending on which side of the desk you're sitting on), doctors never see or treat most people with multinodular goiters for their thyroid nodules. Only a small fraction of people with multinodular goiters develop the signs and symptoms I discuss in this chapter and need an evaluation.\n\n## A Multinodular Goiter Grows Up\n\nRyan Fine (a distant cousin of Kenneth from Chapter 7) is 46 years old. He goes to his doctor for a routine physical examination, and the doctor tells him that his thyroid feels bumpy. He has no symptoms of pain or difficulty swallowing in his neck. His doctor obtains thyroid function tests, which are normal, and thyroid autoantibody tests, which are negative. His doctor refers him to the specialist, the venerable Dr. Rubin.\n\nDr. Rubin examines Ryan and tells him that he can feel several distinct nodules, all of them soft and freely movable. He sends Ryan for a thyroid scan, which shows that all the nodules can concentrate radioactive iodine (none of them are \"cold\"; see Chapter 7). Dr. Rubin assures Ryan that he has a multinodular goiter and that he needs no treatment as long as he is free of symptoms. He asks Ryan to return in six months so that he can examine the thyroid again.\n\nFour months later, Ryan suddenly feels pain in his neck and notices that one area has gotten larger. He goes to see Dr. Rubin, who inserts a needle in that area and removes a small amount of blood. He tells Ryan that a hemorrhage has occurred in one of the nodules, forming a _cyst_ (a fluid-filled nodule) that requires no more treatment than evacuation of the blood. A hemorrhage occurs once more, and then it stops. Ryan returns every six months thereafter and experiences no further change.\n\nRyan is an excellent illustration of the way that someone typically discovers a multinodular goiter, how a specialist evaluates it, and the most common outcome of the condition. Doctors believe that multinodular goiters result from some or all of the following circumstances:\n\n  Starting around puberty, sometimes related to a deficiency of iodine (see Chapter 12), the thyroid is stimulated to grow. It grows a certain amount and then enters a resting state. This growth-resting cycle repeats itself many times.\n\n  The cells in the thyroid, though they almost all perform the same task of making thyroid hormone, aren't identical and grow at different rates.\n\n  Some thyroid cells develop and multiply that aren't under the control of thyroid-stimulating hormone (TSH). They form the autonomous nodules that are often found in a multinodular goiter and can lead to hyperthyroidism.\n\n  Certain stresses to the body, such as a pregnancy, increase the need for iodine, leading to more stimulation of the thyroid.\n\n  Some foods called _goitrogens_ (see Chapter 5) prevent the production of thyroid hormone and lead to more stimulation of the thyroid.\n\n  Certain drugs, such as amiodarone (taken for heart rhythm irregularities), block production of thyroid hormone, which leads to more growth of the thyroid to compensate.\n\n  Genetic connections may cause multinodular goiters to occur more often in some families than in others.\n\nFigure 9-1 shows what a multinodular goiter looks like in comparison to a normal thyroid.\n\nRyan illustrates one way you can discover a goiter, but you may find goiters in many ways, including the following:\n\n  Your neck suddenly gets much larger, leading to a visit to the doctor.\n\n  You feel a sudden pain in your neck, and one side of your neck becomes larger because of bleeding in a nodule.\n\n  A doctor feels a large thyroid with many nodules during a routine examination.\n\n  Symptoms develop, such as a cough, difficulty swallowing, a feeling of pressure in the neck, or a lump in the throat.\n\n  Your doctor discovers the goiter incidentally when you have other testing done, like an ultrasound study of the neck or an X-ray of the chest.\n\n  Occasionally, particularly in older people, the patient has a heart irregularity or signs and symptoms of hyperthyroidism (see Chapter 6). Rarely if ever do patients with a multinodular goiter become hypothyroid. When they do, the diagnosis is probably Hashimoto's thyroiditis (see Chapter 5).\n\n**Figure 9-1:** A multi-nodular goiter compared to a normal thyroid.\n\n|     \n---|---\n\nMultinodular goiters are very common throughout the world, but they're especially common in places where iodine is deficient in the diet.\n\n## Making a Diagnosis\n\nDepending on how you discover a multinodular goiter, a doctor does a number of studies to determine exactly what is going on in the thyroid gland. A good pair of expert hands can feel the presence of many nodules (although no one can feel nodules smaller than a centimeter). An examination by a specialist is very important, because it serves as a baseline for future thyroid exams. The doctor notes the size of the thyroid so he can compare what he feels during future examinations to determine if the thyroid is growing.\n\nThe first study of a multinodular goiter consists of thyroid function tests to see whether your thyroid is making enough thyroid hormone. These test results are usually normal, but occasionally they show excess production of thyroid hormone. You should always have thyroid function tests done if you have a multinodular goiter. Depending on the stress you feel from the growth in your neck and how much the doctor values leaving no stone unturned, your doctor may do many, all, or none of the following tests.\n\n  **Thyroid autoantibody tests:** Your doctor sometimes does these tests, especially if you have a family history of goiters. These test results are usually negative unless autoimmune thyroiditis is present (see Chapter 5).\n\n  **Fine needle aspiration biopsy:** When one nodule stands out or is harder than the others, the doctor often does a fine needle aspiration biopsy to rule out cancer, even though the study has a poor sensitivity in this situation. But the test is so benign that it's worth doing despite the rare positive finding of cancer. A thyroid scan may precede the biopsy to see whether the nodule is functional (warm or hot) or if it's cold (see Chapter 7). Cancers are usually cold. However, keep in mind that the majority of cold nodules aren't cancer. If cancer isn't present, the fine needle biopsy doesn't add any information that points to a diagnosis of the multinodular goiter.\n\n  **Thyroid scan:** A thyroid scan gives a general picture of the thyroid, showing the size of the gland, the many nodules, and the position of the gland, which is particularly important if it's below the sternum (as I explain in the previous section).\n\n  **Thyroid ultrasound:** A thyroid ultrasound picks up very small nodules. This test can show whether a tender nodule is a cyst (a fluid-filled nodule).\n\n  **Barium swallow:** If you feel significant pressure in your neck or have trouble swallowing, your doctor may order a _barium swallow:_ You swallow barium, and your doctor takes X-rays as it passes down. This test may show that the thyroid gland is putting pressure on the _esophagus,_ the swallowing tube from the mouth to the stomach. A plain film (without barium) of the neck reveals if the mass of the thyroid is deviating the trachea.\n\nIf thyroid function tests indicate hyperthyroidism, your doctor looks for other signs of hyperthyroidism due to Graves' disease. Thyroid eye and skin disease, which I describe in Chapter 6, support a diagnosis of Graves' disease. A patient who has hyperthyroidism in a multinodular goiter may instead have a condition called _toxic multinodular goiter,_ also known as _Plummer's disease._ Plummer's disease doesn't involve eye disease. A thyroid scan can differentiate the two conditions (see Chapter 4). Graves' disease shows increased activity throughout the gland, while Plummer's disease shows a few hyperactive nodules.\n\n## Choosing to Treat It or Ignore It\n\nMultinodular goiters generally proceed along the same path in most patients. When thyroid function tests are done, the results are either normal or the thyroid hormone levels are possibly elevated, suggesting hyperthyroidism; the thyroid hormone levels are rarely low. If a patient experiences sudden pain in one area of the thyroid, the doctor performs a _fine needle aspiration biopsy_ (see Chapter 4). Usually that area of the thyroid contains blood as a result of a hemorrhage in one of the nodules. When a doctor removes the blood, the nodule shrinks.\n\nIf a particular nodule stands out or is harder than the others, it is biopsied and usually found to be benign. If the nodule is cancerous, treatment for cancer is begun (see Chapter 8). The problem is that a fine needle biopsy of a dominant nodule in a multinodular gland rarely discovers a cancer, even when cancer is present.\n\nIf the only problem is the large gland, most of the time the doctor doesn't treat it. If you experience other symptoms in the neck, or if the thyroid gland is particularly unsightly, the doctor treats the gland.\n\nSometimes the thyroid, instead of growing up and out, grows downward behind the chest bone (the _sternum_ ) and is said to be _substernal._ In a substernal position, where the goiter has little room to grow, it can squeeze other organs like the _trachea,_ the air pipe from the nose to the lungs. Treatment may be necessary to reduce symptoms that arise from substernal goiters.\n\nMost people with a multinodular goiter don't realize they have it, and even if they're aware that it exists, they don't find treating it necessary. Even very large goiters don't seem to disturb patients other than the cosmetic abnormality. Goiters that compress the trachea and push it sideways don't seem to cause any problem in breathing.\n\n## Treating a Multinodular Goiter\n\nTherapy for a multinodular goiter differs somewhat depending on whether the goiter is toxic and causing hyperthyroidism.\n\n## The nontoxic goiter\n\nIf the nodules of a multinodular goiter aren't causing symptoms of hyperthyroidism and don't contain cancer, and if you have no symptoms, your doctor usually leaves the multinodular goiter alone. Doctors used to think that you could shrink a multinodular goiter with thyroid hormone. This hasn't proven to be the case. In fact, thyroid hormone may be dangerous for an elderly patient, who may become overtreated.\n\nIf you dislike the appearance of your neck, or if you're hyperthyroid, your doctor uses radioactive iodine to destroy some of the thyroid tissue (see Chapter 6). This treatment works even for large goiters but sometimes results in hypothyroidism. Also, in the course of destroying thyroid tissue, a lot of thyroid hormone flows into the bloodstream, inducing temporary hyperthyroidism if it isn't present already. Older people, especially, need to receive antithyroid drugs before using radioactive iodine (see Chapter 6).\n\nSome people (less than 10 percent) who take radioactive iodine to shrink a large multinodular goiter develop Graves' disease, which I discuss in Chapter 6. Graves' disease happens because thyroid tissue is released into the bloodstream, and the body forms antibodies against it.\n\nDoctors rarely perform surgery for a multinodular goiter unless they find a cancer. Radioactive iodine is able to treat most thyroid glands, even the large ones that grow in a downward direction. Some reasons to do surgery include the following:\n\n  Sudden growth of the goiter\n\n  Bleeding in the goiter with compression of vital tissues\n\n  One very firm nodule suspicious for cancer\n\n  Paralysis of the vocal cords, suggesting cancer\n\n  Suspicious lymph nodes, again suggesting cancer\n\nIf you have surgery for a benign multinodular goiter, you have enough thyroid tissue left to keep functionally normal. You don't take thyroid hormone pills. Even if you did take them, they wouldn't prevent a multinodular goiter from growing again. If more growth of the goiter occurs, then you can have radioactive iodine.\n\nIf you have a multinodular goiter, you should return to your doctor at least annually to have an examination of your thyroid. Visit your doctor earlier when you see new growth or pain develops.\n\n## The toxic goiter\n\nDoctors treat hyperthyroid multinodular goiters in a similar fashion to nonhyperthyroid glands. But hyperthyroid multinodular goiters usually require more radioactive iodine to control the hyperthyroidism, which generally leads to hypothyroidism later on.\n\nSome patients have a worsening of their hyperthyroidism when they take radioactive iodine. This is because the thyroid cells are breaking down and release a large amount of the hormone stored in the thyroid. To avoid worsening hyperthyroidism, patients can take antithyroid drugs to make them normal and diminish the amount of stored thyroid hormone for several weeks before their doctor administers radioactive iodine.\n\n## Dealing with a Goiter Behind the Sternum\n\nA goiter behind the sternum occurs when the nodules form at the lower part of the thyroid and grow in a downward direction. Because little room exists in this area for further growth, the thyroid begins to compress vital structures like the trachea and the swallowing tube, the esophagus. The symptoms come from this compression, but hyperthyroidism can also occur.\n\nSome of the complaints of people with goiters behind the sternum include the following:\n\n  A severe choking sensation\n\n  Severe shortness of breath during a respiratory infection\n\n  Sudden increase in symptoms due to bleeding in a nodule\n\n  A cough and hoarseness\n\nA doctor can make the diagnosis just by a chest X-ray that shows the large goiter behind the sternum. A thyroid scan also reveals a lot of thyroid tissue below the neck, where it doesn't belong.\n\nThe treatment is like that for a multinodular goiter above the sternum \u2014 radioactive iodine. The radioactive iodine shrinks the thyroid and sometimes permits it to return to the neck position when the large amount of thyroid that prevents upward movement is gone.\n\nOccasionally, doctors perform surgery if the patient doesn't want radioactive iodine or the gland is in a particularly difficult position. Antithyroid drugs prepare the patient for surgery. Surgery is more complicated than radioactive iodine, but the surgeon can raise up the thyroid fairly easily once it's separated from the tissues surrounding it.\n\n##### Chapter 10\n\n## Drugs That Impact Your Thyroid\n\n### In This Chapter\n\n  Realizing the impact of food and drugs on your thyroid\n\n  Knowing the effects of specific drugs\n\n  Avoiding drug interactions\n\n  Determining whether you are taking one of these drugs\n\nIt should come as no surprise that a ton of drugs are going to have some effect on your thyroid, because thyroid hormones affect every cell in your body. Drug scientists haven't yet reached the stage where they can produce a drug that hits only the target they're aiming at without banging a few other, unexpected targets along the way. These undesired hits are _side effects._ You must understand side effects so that you don't draw wrong conclusions about the state of your thyroid health from changes in your thyroid hormone levels or your metabolism that result from using the drugs I discuss in this chapter. Certain drugs in our food and in the environment also change thyroid function. You need to understand and perhaps avoid these substances, too.\n\nWhether you have high blood pressure or a headache or heart failure, at some point you're bound to run into drugs that impact your thyroid function. In this chapter, you meet most of the important drugs that interact with your thyroid in one way or another. By absorbing the information in this chapter, you can probably tell your doctor a thing or two. Just try not to embarrass your doctor.\n\nWith so many drugs effecting thyroid function in one way or another, avoiding drug interactions is difficult, particularly if one of the drugs you're taking is thyroid hormone. If you're taking thyroid hormone, your body isn't able to make the subtle changes in thyroid function necessary to compensate for the other drug you're taking, which is most likely reducing the thyroid hormone available to your system. The best solution is to ask either your doctor or druggist to run a computer program that looks at multiple drugs and determines interactions. If your doctor doesn't have the capability to do this check, she can ask her hospital pharmacy to do it.\n\n## Revealing the Drug-Food-Thyroid Connection\n\nThe following cases illustrate the broad spectrum of effects that various drugs and foods can have on thyroid function. Some drugs affect thyroid function tests while the thyroid itself is still normal. Other drugs can create hypothyroidism or hyperthyroidism. As if these effects aren't confusing enough, the same drug given to two different people may cause opposite effects, depending on their particular clinical situation.\n\nNatasha Smart is a 36-year-old woman who is healthy and wants to avoid having any more children. She asks her gynecologist to put her on oral contraceptive tablets. One day, while browsing in a bookstore, she comes upon Dr. Rubin's __ book _Thyroid For Dummies, 2nd Edition_ (Wiley). (She can't miss it; the \"Must Read\" section of the bookstore features it.) She opens it and reads on the Cheat Sheet at the front of the book that thyroid testing is advised for people over age 35 every five years. After buying several copies of the book for herself and her friends, she returns to her gynecologist and asks to be tested. Her gynecologist, unfortunately, hasn't read the book and still tests thyroid function with a total thyroxine test (see Chapter 4). The result is high. He tells Natasha that she may have hyperthyroidism. Natasha reads further in the book and finds that the estrogen in oral contraceptive pills raises the amount of thyroid-binding protein in her system. Meanwhile, the _free thyroxine,_ the form of the thyroid hormone that can enter cells and therefore actually have an effect, remains normal. She informs her (embarrassed) gynecologist, who does a free thyroxin test and a TSH (thyroid-stimulating hormone) test, both of which are normal. Nothing further is done.\n\nLeonard Bright is a 72-year-old man who is having trouble with a very irregular heartbeat. His physician places him on a relatively new drug called _amiodarone_ that is used to correct irregular heartbeats _._\n\nAbout two months later, Leonard's heartbeat has become regular, but he is beginning to feel cold and sleepy. He has gained a few pounds and notices that his skin is dry. His doctor recognizes the symptoms of hypothyroidism (see Chapter 5), sometimes associated with amiodarone. The doctor orders thyroid function tests to confirm the diagnosis and starts Leonard on thyroid hormone. In a month, he returns to his normal state of health.\n\nDr. Rubin has followed Kathy Brilliant for many years because of a multinodular goiter. No treatment has been necessary. At the age of 68, she develops a rapid heartbeat and sees a cardiologist, who places her on amiodarone (the same medication that Mr. Bright takes), and her heart problem resolves itself. However, after six weeks she notices that her heart is beating rapidly again. Not only that, she is losing weight and having trouble sleeping. She feels warm all the time, though she is well past her menopause.\n\nKathy returns to the cardiologist, who recognizes that her symptoms are a side effect of amiodarone and sends her back to Dr. Rubin. He tells Kathy that she has hyperthyroidism due to the effect of amiodarone on her multinodular goiter. He suggests that she take pills to control the thyroid and stop taking the amiodarone if the cardiologist can substitute another drug.\n\nKathy stops the amiodarone and takes pills called _methimazole,_ but her condition doesn't improve. After two months, Dr. Rubin recommends thyroid surgery. When the surgery is done, Kathy improves dramatically. She is now able to take the amiodarone and feels fine.\n\nGeorge Shrub absolutely loves broccoli and consumes prodigious quantities, even at breakfast. He finds that he is often sleepy and cold. He has trouble thinking and making appropriate decisions. He goes to his doctor, who runs blood tests that show a high TSH. The doctor tells George that he is hypothyroid and puts him on thyroid medication.\n\nOne night, George and his wife invite Natasha Smart and her husband to dinner. As Natasha watches George consume huge quantities of broccoli, she remarks that she has read in Dr. Rubin's book that broccoli contains a substance that reduces thyroid function. George is very surprised to hear this news, but he sharply reduces his broccoli intake after that night. After talking the situation over with his doctor, he also gradually reduces his thyroid-hormone replacement. After he's been off broccoli for a month, George's thyroid tests are normal.\n\nEach year, all the various drug companies get together to produce a huge book called the _Physicians' Desk Reference_ (PDR). The purpose of this book is to provide, in one convenient place, current information about all the drugs that require prescriptions (a separate book covers nonprescription drugs). Every physician receives a copy of the PDR annually. The edition for the year 2005 contains more than 3,400 pages, describing more than 2,000 drugs. To say that most of these drugs affect the thyroid in one way or another isn't an exaggeration. Fortunately, in most cases, the effect is nothing to worry about. But plenty of drugs are a source of concern.\n\nDo I know all the details about how each of these 2,000-plus drugs affect the thyroid? No way, Renee! But I know about the ones that folks use most frequently and the ones that have the greatest effect on thyroid function or thyroid function tests. These are the products I discuss in this chapter. I deal with them in terms of how they affect thyroid function.\n\nAt the end of the chapter, I group these drugs according to their main clinical purpose so that you can check if you need to be concerned about your blood pressure pill or the pill you take for diabetes or fluid retention. Although I use only the generic (nontrademarked) name in the earlier sections, I give you all the various drug company names at the end of the chapter so you can recognize the particular drug you're taking. For example, _nifedipine_ is the generic name for Adalat, Procardia, and Nifedipine capsules, all the same drug made by different manufacturers. Pretty confusing, huh?\n\nYou should know that new medications come on the market at least hourly. These products get better and better at curing the latest diseases, but initially, drug companies rarely know their other effects from the few thousand people who test them before they come to market. The side effects of many drugs don't become clear until hundreds of thousands of people take them. Many if not all new drugs affect the thyroid in one way or another. The people who must pay particular attention to the side effects of new drugs are those who have some underlying thyroid disease to begin with. For example:\n\n  If you've had hyperthyroidism (see Chapter 6) and it's under control with antithyroid drugs, a drug containing a lot of iodine will probably cause a recurrence of your disease.\n\n  If you've had a multinodular goiter (see Chapter 9), iodine will possibly bring on hyperthyroidism.\n\n  If you're borderline hypothyroid (see Chapter 5), iodine or one of the drugs that block thyroid hormone production will bring on clinical hypothyroidism.\n\n  If you have mild subacute thyroiditis (see Chapter 11), some drugs make it worse to the point that you experience more severe symptoms of thyroiditis.\n\n### How drugs affect your thyroid hormones\n\nChapter 2 explains how your body makes and releases thyroid hormones, how they're carried around the body, how cells take them up, where they do their work, and how they work within the cells. Drugs can affect thyroid function at any one or more of these levels.\n\n  **Thyroid hormone production:** Thyroid hormone forms when iodine is added to a compound called _thyronine._ When four iodine molecules are attached to this compound, the result is _thyroxine_ (T4). When three molecules of iodine are attached, the resulting compound is _triiodothyronine_ (T3). Removing one iodine molecule from thyroxine can also produce T3. Many drugs and food substances block the production of both T4 and T3.\n\n  **Amount of thyroid-binding proteins present:** After your body produces T3 and T4, they must travel in the body to get to their site of action. Thyroid-binding proteins carry them in the bloodstream (see Chapter 2). Drugs can affect thyroid function by increasing or decreasing the amount of binding protein in the blood. Drugs can affect thyroid test results even while the thyroid function remains normal. This occurs because the _free thyroid hormone_ (hormone not bound to protein) is active in the body, not the hormone that is attached to protein.\n\n  **Cell receptor sites:** The free hormone arrives at the cell where it needs to do its work. It must get into the cell by attaching to a substance called a receptor on the membrane of the cell. The receptor is another place where certain drugs can prevent thyroid hormone from doing its job. They can block the receptors so that no hormone can enter. The situation may be almost like diabetes, in which plenty of glucose (sugar) is available in the bloodstream for energy, but it can't enter the cell where it does its work.\n\n  **Hormones' effects inside of cells:** Once inside the cell, the thyroid hormone attaches to the nucleus, where the genetic material is stored. Thyroid hormone then encourages a certain action to take place within the cell. Here, various drugs block the hormone's attachment to the nucleus or alter it so that it doesn't produce the desired effect.\n\n## Identifying the Effects of Specific Substances\n\nIn this section, you encounter particular drugs that affect the thyroid. I group them together according to their potential impact on your thyroid. I don't provide brand names of medications here \u2014 only generic names. If you're wondering whether your specific brand of medication is something that may affect your thyroid, check out the listings in the \"Discovering Whether You're at Risk\" section later in the chapter, where I group these drugs according to their primary purpose.\n\n## Initiating or aggravating hypothyroidism\n\nMany drugs have the potential to cause or intensify hypothyroidism. In the following sections, I introduce you to the most commonly prescribed medications that have these potential side effects.\n\n### Drugs and chemicals that compete with iodine\n\nIf iodine can't enter the thyroid, your body can't make thyroid hormone, and you experience hypothyroidism. Some drugs compete with iodine for entry into the thyroid. Usually the effect is mild, and hypothyroidism doesn't occur. But if your diet is limited in iodine, these drugs can cause low thyroid function. The most important drugs in this category include:\n\n  **Lithium,** for the treatment of manic-depressive psychosis. In one study, as many as 10 percent of patients who took lithium became hypothyroid. This effect is much more common in women than in men and occurs within the first two years of treatment. Most likely, the large population of women with autoimmune thyroid disease (see Chapter 5) is most susceptible to the antithyroid effect of lithium. Not only does lithium block the uptake of iodine, but it also inhibits the production and release of thyroid hormone. Some people being treated with lithium develop a goiter. Curiously (and rarely), lithium can cause hyperthyroidism rather than hypothyroidism.\n\n  **Ethionamide,** for the treatment of tuberculosis. A goiter may or may not accompany the hypothyroidism that results.\n\nMinerals such as **fluorine,** which is found in the diet (especially in fluoridated water), have a similar effect on the thyroid. If you consume substantial amounts of fluorine, your thyroid decreases its production of T4. Your pituitary gland then makes more TSH to stimulate the thyroid, and you can end up with a goiter.\n\n### Drugs and chemicals that prevent the addition of iodine to form thyroid hormones\n\nAnother large group of medications blocks the production of thyroid hormones in a slightly different way. They keep iodine from combining with thyronine to form either T4 or T3, the two thyroid hormones. This group of medications includes the following:\n\n  **Aminoglutethimide,** for the treatment of breast and prostate cancer. As many as one-third of patients treated with this medication develop hypothyroidism.\n\n  **Ketoconazole,** used as an antifungal drug. Hypothyroidism is a rare side effect of this agent.\n\n  **Para-aminosalicylic acid,** for the long-term treatment of tuberculosis.\n\n  **Sulfonamide drugs,** which eliminate excess water from the body and act as antibiotics. These include **sulfadiazine, sulfasoxazole,** and **acetazoleamide.** If you use these diuretics and antibiotics for prolonged periods of time, they can cause hypothyroidism.\n\n  Certain **sulfonylureas,** used in the treatment of diabetes, such as **tolbutamide** and **chlorpropamide.** Doctors rarely prescribe these drugs today.\n\n  The **thionamide** drugs, including **propylthiouricil, methimazole,** and **carbimazole.** With the exception of carbimazole, I discuss these drugs extensively in Chapter 6, because they're the primary drugs used to treat hyperthyroidism. Carbimazole is used in the United Kingdom especially.\n\nTwo chemicals found in food have an impact similar to the medications in the preceding list. They are\n\n  **Isoflavins,** found in soybeans. Children who eat large amounts of soy products may develop a goiter.\n\n  **Thiocyanate,** which is in many common foods like Brussels sprouts, cauliflower, cabbage, horseradish, kale, kohlrabi, mustard, rutabaga, and turnips. If cattle consume foods like these and you drink milk from those cattle, thyiocyanate can affect your thyroid as well.\n\n### Drugs that affect the transport of thyroid hormone\n\nMany drugs affect how thyroid hormones are transported in your bloodstream. Chances are you'll take one of these drugs at some point in your life. If you have normal thyroid function, your thyroid simply makes more or less thyroid hormone to compensate for the effects of these drugs. But if you're hypothyroid and taking a thyroid-hormone replacement, your doctor may need to increase or decrease your dose if you have to take one of these drugs.\n\nThe following drugs increase thyroid-binding protein, resulting in an increase in total (but not free) thyroxine, unless you get your thyroid hormone as a medication:\n\n  **Estrogens** are the most commonly used drugs in this category. For years, estrogens caused confusion about thyroid function, because doctors used to measure how much total thyroxine was in your system, not just the amount of free thyroxine (see Chapter 4). Estrogens are found in birth control pills and hormone replacement therapy. Some animals are fed estrogens to fatten them up, so as you consume those animals, you get estrogen that way as well. The list of medications that contain estrogens is huge.\n\n  **Clofibrate** is a drug used for lowering blood fats, especially cholesterol and triglycerides. There are now better drugs for this purpose, but some doctors still use this one. Not only does it increase thyroid-binding protein, but it may act like thyroid hormone, attaching to proteins that thyroid hormone normally attaches to, and stimulating thyroid function. It can lead to muscle breakdown.\n\n  **Perphenazine** is a treatment for psychotic disorders in the group of drugs called _phenothiazines._ This group includes a number of well-known medications, such as **prochlorperazine, trifluoperazine,** and **chlorpromazine.** Perphenazine is the main ingredient in a number of different preparations and can also treat nausea and vomiting.\n\nThe following drugs decrease thyroid-binding protein, resulting in a decrease in total (but not free) thyroxin, unless you get your thyroid hormone as a medication:\n\n  **Anabolic steroids** promote weight gain after extensive surgery or severe illness, as well as assist in the treatment of anemia. Doctors rarely use them, because they frequently cause liver abnormalities.\n\n  **Androgens** substitute for the male hormone, testosterone, when the patient can't make his own. They permit muscle growth and normal sexual function.\n\n  **Glucocorticoids** are used very extensively to treat inflammation and to reduce immunity when the inflammation and autoimmunity are damaging to the body, such as in rheumatoid arthritis and many other illnesses. The list of glucocorticoids is a long one.\n\n  **Nicotinic acid** is a vitamin used for the treatment of elevated fats in the blood.\n\nIf you're hypothyroid and your doctor puts you on one of the agents that decreases thyroid-binding protein for a long time, have your doctor check your thyroid function with a TSH test periodically.\n\nThe opiates **heroin** and **methadone** also impact the movement of thyroid hormones in the bloodstream.\n\n### Amiodarone\n\n**Amiodarone** treats disturbances of the heart rhythm. This drug may cause hypothyroidism in up to 10 percent of the people who take it. The drug is also associated with a number of other side effects, including skin and corneal discoloration and fibrosis of the lungs. It may cause hepatitis and bone marrow suppression. Despite all these negatives, it's very useful in treating heart rhythm disturbances.\n\nAmiodarone has received a great deal of study because doctors prescribe it so extensively. It contains a large amount of iodine and acts like other large sources of iodine. It blocks the production of the thyroid hormone T3 from T4 (see Chapter 2). It also has a structural resemblance to thyroid hormone and causes a reduction of thyroid hormone entering tissues where it does its work.\n\nWhen amiodarone releases iodine, the iodine may block thyroid hormone production, causing hypothyroidism in areas of the world that are already iodine sufficient. Or it may form large amounts of thyroid hormone, causing hyperthyroidism in areas that are deficient in iodine.\n\nThe best way to determine the clinical state of the patient is to do a thyroid-stimulating hormone test. If you're hypothyroid, your TSH should be high. If you're hyperthyroid, your TSH should be low.\n\nIf amiodarone causes hypothyroidism, you require an unusually large amount of thyroid hormone to overcome the situation or, if possible, you stop taking the amiodarone. Radioactive iodine can't treat amiodarone-induced hyperthyroidism, because the large amount of iodine suppresses the iodine uptake of the thyroid. Therefore, you either have surgery or take antithyroid drugs if stopping the amiodarone is impossible.\n\n### Drugs that treat severe hyperthyroidism\n\nThe drugs in this group are very useful when a patient has severe hyperthyroidism and needs to reduce the T3 hormone level as soon as possible. However, these drugs have other primary purposes, and when doctors prescribe them for those other purposes (to patients who aren't hyperthyroid), they can create hypothyroidism.\n\n  **Glucocorticoids** I discuss in the preceding \"Drugs that affect the transport of thyroid hormone\" section.\n\n  **Iodinated contrast agents** assist in achieving better X-ray studies. Doctors have used such agents as **ipodate** and **iopanoic acid** in the treatment of hyperthyroidism. A single dose can last for ten days.\n\n  **Propranolol** slows a rapid heartbeat, but doctors also use it to treat hyperthyroidism because it controls many of the symptoms, such as palpitations, shakiness, and nervousness.\n\n  **Propylthiouricil** is one of the standard drugs for the treatment of hyperthyroidism.\n\n### Growth hormone\n\nWhen the body doesn't make its own growth hormone, an injectable growth hormone restores growth. Doctors administer growth hormone to children who aren't growing properly because they lack this hormone. If someone is borderline hypothyroid, this hormone may push her into hypothyroidism by reducing the T4 hormone to abnormally low levels.\n\n### Drugs that remove thyroid hormone from your system\n\nA number of drugs act upon the liver to speed up the metabolism of thyroid hormones into products that aren't active. Other drugs pull thyroid hormones out of the body with bowel movements. These drugs are very common.\n\nIf you're taking a thyroid-replacement hormone and you use one of the following drugs, you may develop hypothyroidism. Ask your doctor to check your thyroid hormone levels about a month after you start to take one of the following drugs:\n\n  **Aluminum hydroxide** neutralizes the acid in patients with peptic ulcers.\n\n  **Carbamazepine** and **diphenylhydantoin** treat convulsions.\n\n  **Cholestyramine** and **colestipol** reduce fats.\n\n  **Ferrous sulfate** is given to people who are deficient in iron and have anemia. At some point, the doctor stops the ferrous sulfate treatment when the patient's iron reserves are full. The patient may actually become hyperthyroid when she stops taking the ferrous sulfate if her doctor increased her thyroid hormone dose due to the initial effects of the drug.\n\n  **Phenobarbital** treats convulsions as well as mild anxiety.\n\n  **Rifampin** is one of the treatments for tuberculosis. This drug very rarely causes hypothyroidism in a person who takes thyroid hormone.\n\n  **Sucralfate** treats peptic ulcer disease. It may result in hypothyroidism if you take it chronically.\n\nMonitoring your thyroid function is important both during and after use of a short-term medication that lowers the levels of thyroid hormone in your blood, especially if you're taking oral thyroid medication.\n\n### Drugs that decrease your TSH\n\nThe following drugs can lower the level of thyroid-stimulating hormone in your system, potentially leading to lower thyroid function:\n\n  **Acetylsalicylic acid** is commonly known as aspirin. People taking more than 8 or 10 aspirin daily may suffer a lower level of TSH.\n\n  **Bromergocryptine** prevents lactation (milk production) and shrinks prolactin-secreting pituitary tumors.\n\n  **Clofibrate** lowers the fat particles that contain triglycerides. It also lowers the TSH but doesn't seem to cause clinical problems.\n\n  **Dopamine** lowers blood pressure, especially in an emergency setting. It lowers TSH, but patients usually don't use it long enough to cause problems with hypothyroidism.\n\n  **Glucocorticoids** treat inflammation and reduce immunity.\n\n  **Octreotide** treats certain tumors that produce hormones, especially _acromegaly,_ which produces excessive growth hormone, and _carcinoid tumors,_ which produce a chemical that causes severe diarrhea and flushing.\n\n  **Opiates,** including morphine and heroin, control pain if taken legally and are taken illegally for a chemical high.\n\n  **Pamidronate** (brand name Aredia) may cause hypothyroidism. Doctors prescribe it for building bone when a person has diminished bone formation.\n\n  **Phentolamine** controls blood pressure in patients who have a tumor of the adrenal gland called a _pheochromocytoma._ This drug reduces TSH, but patients generally don't take it long enough to make a difference in thyroid function.\n\n  **Pyridoxine** is vitamin B6. Doctors prescribe it to women during pregnancy and when evidence suggests that someone has a B6 vitamin deficiency.\n\n  **Thyroid hormones** replace a deficiency or suppress thyroid cancer or a goiter. They suppress the production of TSH.\n\n## Creating false test results\n\nCertain drugs can alter the thyroid hormone (T3 and T4) tests that measure total thyroid hormones (but not free thyroid hormones, which remain normal). If you're taking one of the drugs I list here, you and your doctor should keep that fact in mind if your total T4 test shows hypothyroidism but you aren't experiencing any symptoms of the condition.\n\n  **Salicylates** such as aspirin are the most commonly used drugs in this group.\n\n  **Diphenylhydantoin** and **carbamazepine** treat convulsions.\n\n  **Furosemide** causes the loss of excess water through the kidneys.\n\n  **Heparin** prevents blood clots. It doesn't change your thyroid function, but if you receive an injection of _low molecular weight heparin,_ a measurement of free T4 taken within 10 hours of the injection will be falsely elevated.\n\n  **Orphenadrine** relieves muscle spasms in a number of drug preparations. It isn't a muscle relaxant but may reduce pain.\n\n## Initiating hyperthyroidism\n\nThe following drugs increase the production of TSH, which can result in hyperthyroidism:\n\n  **Amphetamine** reduces congestion, and some people also use it (inappropriately) as a weight-loss agent.\n\n  **Cimetidine** and **ranitidine** reduce acid secretion to treat peptic ulcers. Both can raise the TSH, but studies don't show a change in thyroid function with these drugs.\n\n  **Clomiphene** brings on ovulation to promote pregnancy. It has effects on several of the hormones in the pituitary gland, including TSH.\n\n  **L-dopa inhibitors** such as **chlorpromazine** and **haloperidol** help to manage psychotic disorders. They raise TSH, although people who take them don't generally become hyperthyroid.\n\n  **Metoclopramide** and **domperidone** control nausea and vomiting, especially after surgery. Metoclopramide also treats gastrointestinal disorders in diabetes mellitus.\n\n  **Iodine** can raise TSH levels as it blocks the release of thyroid hormones.\n\n  **Lithium** raises TSH, in addition to all its other effects on thyroid function. In very rare cases it causes hyperthyroidism. (It causes hypothyroidism much more frequently.)\n\n## Looking At the New Drugs\n\nSince the first edition of this book, thousands of drugs have come on the market. The vast majority are drugs that have been around for years and have reached the point that the original drug company that made the drug no longer has the exclusive right to sell it. Any company can manufacture and sell it. Another large group of drugs are the \"me-too\" drugs. Me-too drugs are slightly different chemically from other drugs with exactly the same action, but because of the slight difference, the food and drug administration permits companies to sell them.\n\nI've looked at most of these \"new\" drugs for the possibility that they interact with the thyroid and thyroid hormone. Doctors prescribe most of them so rarely that they aren't worth discussing. The new me-too drugs that affect the thyroid belong to classes of drugs that I cover in the previous \"Identifying the Effects of Specific Substances\" section.\n\nA few new drugs deserve discussion, because doctors prescribe them very often, and they interact with thyroid hormone. Curiously, several of them are drugs used in type 2 diabetes mellitus (see my book _Diabetes For Dummies, 2nd Edition_ [Wiley]). __ The drugs are as follows:\n\n  **Rosiglitazone** (brand name Avandia), of the class of drugs called glitazones, interacts with thyroid hormone. The thyroid hormone reduces the effect of rosiglitazone. The glitazone drugs increase the activity of insulin in the body. They sensitize the body to insulin.\n\n  **Pioglitazone** (brand name Actos) belongs to the same class of drugs as roziglitazone and has the same interaction with thyroid hormone.\n\n  **Miglitol** (brand name Glyset) is affected in the same way as the two preceding drugs by thyroid hormone. Thyroid hormone reduces its effect. It is used to slow the digestion of carbohydrates, thereby reducing the blood glucose. Thyroid hormone interferes with this action.\n\n  **Repaglinide** (brand name Prandin) also is affected by thyroid hormone, which reduces its effect. Repaglinide lowers glucose by stimulating insulin.\n\n  **Nateglinide** (brand name Starlix) has the same effect as repaglinide.\n\n## Discovering Whether You're at Risk\n\nYou may not recognize many of the drugs I name in the previous sections, because I use their generic names. The generic name is the official name of the drug regardless of the name the manufacturer gives it. In this section, I list brand names of drugs that may affect your thyroid, and I group them according to their usage. If you have a specific medical problem that requires one or another of a class of drugs \u2014 for example, anemia drugs \u2014 go to the section below that refers to your problem, look at the drugs I list, and see whether the brand name is the same as the one you're using.\n\nIf one of the drugs I list below is something you take, asking your doctor to run thyroid function tests may be a good idea.\n\n## Anemia drugs\n\n**Ferrous sulfate:** Feosol elixer and tablets, Fero-Folic 500 Filmtab tablets, Fero-Grad 500 Filmtab tablets, Iberet-500 liquid and tablets, Irospan capsules and tablets, Slow Fe tablets, Fe-50 caplets, Vi-Daylin\/F multivitamin and iron drops with floride\n\n## Antiaddiction agents\n\n**Methadone:** Dolophine Hydrochloride tablets, Methadone HCl powder, Methadose dispersible tablets, Methadose oral tablets\n\n## Antibiotics\n\n**Ethionamide:** Trecator-SC tablets\n\n**Ketoconazole:** Nizoral tablets, Ketoconazole tablets\n\n**Para-aminosalicylic acid:** Paser granules\n\n**Sulfonamide drugs:** Bactrim tablets, Septra tablets\n\n**Rifampin:** Rifadin capsules, Rifater\n\n## Anti-inflammatory drugs\n\n**Glucocorticoids:** Celestone, Decadron, Depo-Medrol, Hydrocortone tablets, Solu-medrol sterile powder\n\n**Aspirin:** Darvon compound, Ecotrin Enteric coated aspirin, Excedrin, Fiorinal Halprin tablets, Norgesic tablets, Percodan tablets, Robaxisal tablets, Soma compound, Fiortal capsules, Gelpirin tablets, Propoxyphene compound, Roxiprin tablets\n\n## Antithyroid drugs\n\n**Propylthiouricil:** Propylthiouricil tablets\n\n**Methimazole:** Tapazol tablets, Methimazole tablets\n\n## Diabetes drugs\n\n**Tolbutamide:** Orinase\n\n**Chlorpropamide:** Diabinase\n\n## Diuretics (reduce body water)\n\n**Furosemide:** Lasix, Furosemide tablets\n\n## Drugs to improve alertness\n\n**Amphetamine:** Adderall tablets\n\n## Fat-lowering drugs\n\n**Clofibrate:** Atromid-S capsules\n\n**Cholestyramine:** LoCholest powder, Questran Light for oral suspension, Prevalite for oral suspension\n\n**Colestipol:** Colestid tablets\n\n## Growth-hormone controlling drugs\n\n**Octreotide:** Sandostatin\n\n## Heart rhythm drugs\n\n**Amiodarone:** Cardarone tablets, Pacerone tablets\n\n**Propranolol:** Inderal tablets, Propranolol HCl tablets\n\n**Phentolamine:** Regitine vials\n\n## Hormone replacement\n\n**Estrogens** **(female hormones):** Estinyl tablets, Estrace vaginal cream, Estratab tablets, Menest tablets, Ogen tablets, Premarin tablets, Vagifem tablets\n\n**Estrogen and progestin combinations:** Activella tablets, Brevicon 28-day tablets, Demulen (many strengths), Desogen tablets, Estrostep 21 tablets, Levora tablets, Lo\/Ovral tablets, Mircette tablets, Modicon tablets, Necon tablets (many strengths), Norinyl tablets (many strengths), Ortho Tri-Cyclen tablets (many strengths), Ortho-Cyclen tablets (many strengths), Ortho-Novum tablets (many strengths), Ovcon tablets, Premphase tablets, Prempro tablets, Trinorinyl-28 tablets, Triphasil tablets, Trivora tablets, Zovia tablets\n\n**Anabolic steroids:** Anandrol-50 tablets, Oxandrin tablets, Winstrol tablets\n\n**Androgens (male hormones):** Androderm transdermal system, AndroGel, Android capsules, Delatestryl injection, Testoderm transdermal systems, Testred capsules\n\n**Growth hormone:** Geref for injection, Humatrope, Nutropin, Protropin, Saizen for injection\n\n**Clomiphene:** Clomid tablets, Serophene tablets, Clomiphene Citrate tablets\n\n**Thyroid hormones:** Synthroid, Levothroid, Levoxyl tablets\n\n## Nausea-controlling drugs\n\n**Metoclopramide:** Reglan, Metoclopramide tablets\n\n## Pain medication\n\n**Morphine:** Astramorph\/PF injection, Duramorpf injection, Kadian capsules, MS Contin tablets, MSIR oral capsules, Oramorph SR tablets, Roxanol 100 concentrated oral solution, Morphine Sulfate, OMS concentrate CII, RMS suppositories CII\n\n## Peptic ulcer drugs\n\n**Aluminum hydroxide:** Amphogel, Maalox, Mylanta, Alu-Cap capsules, Alumina and Magnesia oral suspension\n\n**Sucralfate:** Carafate suspension and tablets, Sucralfate tablets\n\n**Cimetidine:** Tagamet, Cimetidine tablets\n\n**Ranitidine:** Zantac, Ranitidine HCl\n\n## Prolactin controlling drugs\n\n**Bromergocryptine:** Parlodel capsules, Bromocryptine Mesylate tablets\n\n## Psychoactive drugs\n\n**Lithium:** Eskalith capsules, Eskalith CR controlled-release tablets, Lithium Carbonate capsules, Lithobid slow-release tablets\n\n**Perphenazine:** Estrafon 2\u201310 tablets, Estrafon tablets, Estrafon-Forte tablets, Trilafon tablets, Perphenazine tablets\n\n**Chlorpromazine:** Thorazine, Chlorpromazine HCl\n\n**Haloperidol:** Haldol\n\n##### Chapter 11\n\n## Thyroid Infections and Inflammation\n\n### In This Chapter\n\n  Encountering subacute thyroiditis\n\n  Dealing with postpartum and silent thyroiditis\n\n  Suffering from acute thyroiditis\n\n  Finding out about more rare forms of thyroiditis\n\nI use the term _thyroiditis_ in this book (see Chapter 5) to denote Hashimoto's thyroiditis and chronic thyroiditis. In this chapter, I introduce you to causes of thyroiditis that are less common than autoimmune disorders but just as important to know about. Usually, but not always, non-autoimmune thyroiditis is associated with infection.\n\nFortunately, infection of the thyroid is rare, perhaps because of all the iodine and hydrogen peroxide in the thyroid gland. If you ever had a cut or boo-boo when you were young, your mother probably covered it with a solution containing iodine or hydrogen peroxide, both of which kill bugs.\n\nDespite all the thyroid's natural protection, every so often people develop an infected thyroid. In this chapter, you discover how doctors tell one form of infection from another, as well as the method of treatment and the prognosis for each illness.\n\n## Putting a Face on Subacute Thyroiditis\n\n_Subacute thyroiditis_ has gone by many names in the past, including _de Quervain's thyroiditis,_ _giant cell thyroiditis,_ and _subacute painful thyroiditis._ It's called _subacute_ to differentiate it from the condition I discuss later in the chapter, _acute_ thyroiditis, which is usually much more painful and associated with more symptoms that make the patient sick. Subacute thyroiditis isn't very common. In my practice, which is about 60 percent diabetes mellitus and 40 percent thyroid disease, I see perhaps two cases per year.\n\nJoan Sharp is a 40-year-old woman who has been suffering from a cold and a cough with a low-grade fever for about a week. One morning, she awakens and notices that her neck hurts. She can tell that the pain is located in the center of her neck beneath her Adam's apple. She goes to her doctor, Dr. Hammerbe, who notes that her thyroid is enlarged and tender. The doctor also finds that Joan is nervous, and her fingers are shaking slightly.\n\nDr. Hammerbe sends Joan to the lab for some tests. The lab results show that her free T4 is elevated, while her TSH is depressed (see Chapter 4), suggesting hyperthyroidism. The doctor does a test for inflammation called an _erythrocyte sedimentation rate,_ and the result is elevated. Knowing that neck pain is unusual in hyperthyroidism due to Grave's disease (see Chapter 6), Dr. Hammerbe calls Dr. Rubin about what to do next.\n\nDr. Rubin suggests that she do a blood test for _serum thyroglobulin,_ which comes back high, and a thyroid uptake (see Chapter 4), which comes back low. Joan finds out that she has subacute thyroiditis. Dr. Hammerbe starts her on aspirin, and Joan rapidly improves. The swelling of her neck declines, and the tenderness rapidly decreases.\n\nAs you can tell from the case of Joan Sharp, this condition often begins with an infection that suggests a virus. The person may have muscle aches and fever and then begins to feel neck pain in the area of the thyroid. This pain may be severe. The neck pain usually brings the patient to the doctor. When the doctor examines the patient, the thyroid isn't only painful but enlarged as well.\n\n## Causes and effects\n\nSubacute thyroiditis has four stages in the more severe cases:\n\n  **Stage 1** lasts one to three months, during which the thyroid is painful and tender. You experience fever and muscle aches and pains.\n\nAs a result of the inflammation, the thyroid releases much of its stored hormone along with the stored thyroglobulin (see Chapter 4). The virus seems to temporarily damage thyroid cells at this point. The large quantity of released thyroid hormone produces hyperthyroidism. Because the thyroid cells are damaged and the production of thyroid hormone isn't ongoing, the hyperthyroidism lasts only a brief time, sometimes a few days, until the thyroid gland is depleted of hormone.\n\n  **Stage 2** lasts one to two weeks. You experience a state of normal thyroid function as thyroid hormone levels fall. The acute infection releases thyroid hormone that clears from the body.\n\n  **Stage 3** can last for months and is the stage of hypothyroidism because the thyroid suffers such severe damage that the gland is depleted of hormone.\n\n  **Stage 4** occurs when you return to a state of normal thyroid function. Because a viral illness usually doesn't last, the thyroid gland returns to normal, the pain goes away, and the thyroid function returns to normal. However, 5 percent of people with subacute thyroiditis remain permanently hypothyroid.\n\nEvidence exists that a virus may cause subacute thyroiditis: Cases of this condition tend to be seasonal, and they sometimes occur in outbreaks like any infectious disease. Over the years, doctors have looked for a particular virus that may be the cause of all cases of subacute thyroiditis, but they've never been able to isolate any one virus in all cases. The only virus doctors have found with some frequency is the mumps virus. Subacute thyroiditis seems to occur more often in people who have decreased immunity from infection, such as AIDS patients or people who are getting bone marrow transplants for leukemia.\n\nLike most thyroid conditions, subacute thyroiditis is more common in women than in men; the ratio of cases is three to one. This condition appears to have some genetic basis, because the same genetic marker \u2014 an antigen on human white blood cells \u2014 is present in about 75 percent of cases, suggesting that these patients are more susceptible to the disease because of their genetic makeup. In fact, scientists have described two different genetic markers for subacute thyroiditis. Each marker seems to be associated with the disease occurring at a particular time of the year, although in either case subacute thyroiditis generally occurs in a person's forties or fifties.\n\nIf you have subacute thyroiditis, you have a small (about 2 percent) but definite possibility of a recurrence some years later. A recurrence is generally milder than the original attack. Occasionally, a patient may experience repeated attacks of pain. Thyroid hormone helps to prevent such recurrences, but if you continue to have recurrences, removing the thyroid with surgery or radioactive iodine becomes necessary.\n\n## Laboratory findings\n\nLab tests are very helpful in pinning down a diagnosis of subacute thyroiditis. Some of the findings from lab tests are as follows:\n\n  The _erythrocyte sedimentation rate,_ a general blood test for inflammation, is often unusually high considering the relative mildness of the symptoms, sometimes reaching a value of over 100, when the normal is about 20.\n\n  Shortly after the thyroid becomes infected, up to 50 percent of patients experience hyperthyroidism, so TSH level are low while FT4 levels are elevated.\n\n  The inflammation causes the release of a large quantity of both T4 and T3. Because the thyroid contains so much more T4 than T3 compared to the blood, a drop in the ratio of T4 to T3 occurs as T4 and T3 escape into the bloodstream.\n\n  Liver tests often reveal an elevated level of _alkaline phosphatase._ The infection appears to affect the liver in addition to the thyroid, though the impact on the liver is mild.\n\n  Blood tests show that a lot of thyroglobulin is present in the blood.\n\n  The test for thyroid autoantibodies (see Chapter 4) is negative.\n\n  Some specialists suggest that a thyroid ultrasound study (see Chapter 4) is distinctive in subacute thyroiditis, but doctors usually don't run this test.\n\n  The key test, the thyroid uptake of radioactive iodine, is very low, which differentiates subacute thyroiditis from other causes of hyperthyroidism.\n\nWhen your doctor puts the results of all these tests and the clinical picture together, the diagnosis is fairly certain, although no one test proves that subacute thyroiditis is present. To prove the diagnosis, a biopsy of the gland is necessary, but the mildness of the disease means that your doctor rarely needs to do a biopsy.\n\nThe presence of generalized thyroid pain differentiates subacute thyroiditis from other forms of thyroiditis, though sometimes the pain may occur on one side of the thyroid only. Another cause of a painful thyroid is bleeding, producing a hemorrhagic thyroid cyst. This pain usually occurs on one side of the thyroid, and a viral illness doesn't precede it. Lab tests help to secure a diagnosis, particularly a radioactive uptake, which is normal for the cystic thyroid but low for subacute thyroiditis. In rare cases, chronic thyroiditis is painful (see Chapter 5). With chronic thyroiditis, levels of thyroid autoantibodies are high.\n\n## Treatment options\n\nAt the beginning of subacute thyroiditis, when you're hyperthyroid, a drug such as propranolol can reverse the symptoms of excessive thyroid hormone. _Propranolol_ is a beta blocker that slows the heart, decreases anxiety, and reduces tremor. Antithyroid drugs like propylthiouricil and methimazole have no place in this treatment, because the thyroid isn't chronically making excessive hormones.\n\nAspirin or a nonsteroidal anti-inflammatory agent can manage thyroid pain. Once in a while, using a steroid like prednisone is necessary for a week or two. When the uptake of radioactive iodine returns to normal, the inflammation is finished, and you can stop taking steroids.\n\nWith the end of symptoms, the patient is back to normal permanently in almost every case. Like so much in medicine, rare exceptions exist where the disease goes away and then returns, or the pain is persistent. Patients who experience persistent pain or a return of the disease may need to have their thyroids removed to finally control the disease.\n\n## Coping with Postpartum and Silent Thyroiditis\n\nMichelle Clever is a 29-year-old woman who gave birth to a healthy boy about five months ago. Recently she has noticed that her neck is larger than before, but it's not painful. She is feeling nervous, and her hands shake. She has trouble going to sleep, which makes her situation tough because the baby wakes her up at night. She can feel her heart beating rapidly at times.\n\nMichelle goes to her obstetrician, who examines her and tells her that she is probably hyperthyroid. Her obstetrician sends her to see Dr. Rubin, who notes that she was pregnant recently. He obtains thyroid function tests, which are elevated. Dr. Rubin tells Michelle that he believes she probably has postpartum thyroiditis. He places her on the beta blocker propranolol, which controls her symptoms well. He also explains that she will probably go through a phase of low thyroid function before she returns to normal. A few weeks later she appears to be better.\n\nSeveral weeks after that, Michelle notices that she is feeling cold and having trouble keeping awake. Dr. Rubin reassures her that this is the hypothyroid phase of postpartum thyroiditis. Within a few weeks, she feels normal. Two years later, after a second pregnancy, the problem recurs.\n\nDoctors consider postpartum and silent thyroiditis to be variations of the same disease. Postpartum thyroiditis occurs usually three to six months after a pregnancy, while silent thyroiditis can happen to anyone at any time.\n\n## Understanding the disease\n\nDoctors consider postpartum thyroiditis to be an autoimmune disorder, because high levels of peroxidase autoantibodies are present in the blood (see Chapter 4). In this condition, the antibodies seem to damage thyroid cells, causing a release of thyroid hormone that leads to temporary hyperthyroidism. So far, no one has found a single gene associated with postpartum thyroiditis.\n\nPostpartum thyroiditis is very common; it occurs after 5 to 10 percent of all pregnancies. With this condition, unlike subacute thyroiditis, a patient has no symptoms of fever or weakness, although she may complain of feeling warm. A rapid heartbeat and palpitations are part of the condition. The thyroid itself isn't painful, although it's often abnormally large. However, the changes that occur in thyroid function are similar to those that occur with subacute thyroiditis. Postpartum thyroiditis usually occurs in the following stages:\n\n**1.** **Hyperthyroidism for the first one to three months after giving birth.**\n\n**2.** **Normal thyroid function for a month or two.**\n\n**3.** **Hypothyroidism at four to six months after delivery.**\n\n**4.** **The hypothyroidism may resolve, but the patient is at high risk for permanent hypothyroidism.**\n\nWomen who develop postpartum thyroiditis show a high rate of recurrence in later pregnancies, and 25 percent of them are permanently hypothyroid after three to five years. As many as 50 percent are hypothyroid after seven to nine years. The recurrence rate of silent thyroiditis is also very high.\n\nDoctors used to think that postpartum thyroiditis was associated with depression in women who had given birth. Recent investigation has shown, however, that the depression occurs just as often when women don't have postpartum thyroiditis as when they do.\n\n## Interpreting lab results\n\nThe lab test that best distinguishes a patient with subacute thyroiditis from a patient with postpartum or silent thyroiditis is the test of _erythrocyte sedimentation rate._ With subacute thyroiditis, the rate is high, but with postpartum or silent thyroiditis, the rate is normal.\n\nThyroid function tests from patients with postpartum or silent thyroiditis are initially high, then normal, then low. As in subacute thyroiditis, the hyperthyroid phase of the disease is due to leakage from the thyroid. Because the ratio of T4 to T3 is much higher in the thyroid than it is in the blood, the ratio of T4 to T3 temporarily becomes high in the blood as well. The TSH and the radioactive uptake of iodine are also on the low side during the hyperthyroid phase.\n\nIf the hyperthyroidism is severe, it may mimic Graves' disease. But the hyperthyroidism is the result of damage to thyroid cells and release of thyroid hormone, so the uptake of radioactive iodine is low rather than high, as it is in Graves' disease.\n\n## Getting treatment\n\nTreatment for postpartum and silent thyroiditis depends on the stage at which your doctor diagnoses the disease. If your doctor diagnoses you during the hyperthyroid phase, you take the beta blocker propranolol, which helps to control the symptoms of hyperthyroidism. Antithyroid drugs aren't useful, because they won't prevent hyperthyroidism caused by a leakage of thyroid hormone. When the hypothyroidism phase occurs, you take thyroid-hormone replacement with the understanding that you may not need it on a permanent basis.\n\n## Identifying Acute Thyroiditis\n\nPatrick Clever is a 45-year-old man who has suddenly developed severe pain in his neck, fever, and chills. The pain is so severe that he has to bend his neck forward to cope with it. He can't swallow without pain. He also feels weak.\n\nPatrick goes off to see his doctor, who notes that he is very sick. His thyroid gland is exquisitely tender, and he has a fever. The doctor sends him to his thyroid specialist friend, Dr. Rubin, who notes that the tender area is somewhat soft. He puts a fine needle into it and removes a quantity of pus. Dr. Rubin sends the pus for culture and for staining to determine the bug causing the infection and places Patrick on an antibiotic along with aspirin.\n\nIn a few days, Patrick is feeling much better. The pus grows out a bug that's sensitive to the antibiotic, which Patrick continues taking for ten days. Patrick recovers fully.\n\nAcute thyroiditis is much rarer than subacute thyroiditis, but doctors can confuse the two, depending on the way the disease appears in the patient. In my 33 years in practice, I've seen only four cases of acute thyroiditis. However, because many more people have lost their immunity to infection as a result of the AIDS epidemic, doctors will probably see more cases in the near future.\n\n## Describing the disease\n\nDoctors have found many different organisms in the thyroid glands of patients with acute thyroiditis. Bacteria are present about 70 percent of the time. The type of bacteria varies from _pneumococcus_ (which often causes pneumonia) to _streptococcus_ (associated with strep throat) to _staphylococcus_ (which causes skin infections). About 15 percent of the time, a fungus is the infecting organism; tuberculosis is the cause 10 percent of the time, and various other bugs are the culprits much less frequently.\n\nBesides the tender thyroid, nearby structures such as the trachea (voice box) and esophagus (swallowing tube) are inflamed, and local lymph glands in the neck are tender. In many patients, doctors find a connection from the outside (such as the throat) to the thyroid tissue, through which the infection invades. This connection is called a _fistula_ and is a result of abnormal development from birth. It acts as an open pipe to the thyroid for the passage of the infection. If a doctor discovers a fistula in association with acute thyroiditis, a surgeon must remove it, or infection will recur. Acute infection of the thyroid is so rare that doctors should look for a fistula in every case.\n\nIf you have acute thyroiditis, you look obviously sick. You complain of the pain in your neck and may have to bend your neck forward to decrease it. You have a fever and chills. Your thyroid is enlarged (usually on one side), hot, and tender. Depending on how large your thyroid gets, you may have trouble swallowing or even breathing. Lymph nodes are often enlarged, swollen, and tender as well.\n\n## Confirming the diagnosis with lab tests\n\nIn a patient with acute thyroiditis, general blood tests for infection, such as the white blood count and the erythrocyte sedimentation rate, are abnormally high. These results confirm that an infection or inflammation is present.\n\nWhen your doctor does thyroid tests such as the free T4 and the TSH, the results are generally normal, although once in a while the destruction of the thyroid is so great that enough hormone leaks to cause hyperthyroidism. Thyroid uptake of radioactive iodine is normal. Thyroid autoantibodies are negative.\n\nThe best test for acute thyroiditis is a needle biopsy. Usually the biopsy shows inflammation and the infecting organism, but occasionally no inflammation appears. Then the diagnosis is much more difficult. Sometimes the thyroid has an abscess, which the needle drains.\n\n## Treating acute thyroiditis\n\nThe treatment for acute thyroiditis is to give the appropriate antibiotic based on the suspected organism. The biopsy can provide a good idea of what type of organism is causing the infection, which a culture of the biopsy tissue can confirm. The right antibiotic generally cures the infection and restores normal thyroid function. Sometimes the infection doesn't respond, and surgery to remove the infected part of the thyroid or the whole thyroid is necessary.\n\nWhen acute thyroiditis recurs, a doctor should suspect that a fistula is allowing bugs to get into the thyroid from the outside. In this situation, the patient does a barium swallow, which shows a trail of barium going from the throat into the thyroid gland. Surgery is necessary to eliminate a fistula.\n\nOccasionally, acute thyroiditis causes such damage to the thyroid tissue that the patient needs to take replacement thyroid hormone.\n\n## A Rare Form of Thyroiditis\n\nChristopher Dull is a 42-year-old man who comes to his doctor complaining of gaining weight and feeling tired, weak, cold, and sleepy. He also says that his neck feels very tight. He has trouble swallowing and breathing.\n\nHis doctor examines him and notes that his neck feels very dense. His thyroid barely moves when he swallows. The doctor doesn't feel swelling in the lymph nodes in his neck.\n\nThe doctor runs thyroid function tests, which show a low free T4 and a high TSH. At the same time, he obtains a calcium level, and this test result is low as well. The doctor runs a test of the hormone made by the parathyroid glands, called _parathyroid hormone,_ and the result of the test is low. The doctor sends Chris for a barium swallow, which shows compression on the esophagus. He refers Chris to Dr. Rubin.\n\nDr. Rubin attempts to do a fine needle biopsy of Chris's thyroid but is unable to get tissue. Dr. Rubin makes a presumptive diagnosis of _Riedel's thyroiditis._ He starts Chris on steroids, thyroid hormone, and calcium. Chris's symptoms gradually decrease, but the hypothyroidism and the _hypoparathyroidism_ (low parathyroid function resulting in low calcium) remain. Chris continues to take thyroid hormone replacement and vitamin D for the rest of his life.\n\nTo be thorough, I feel that I need to discuss this final form of thyroiditis even though I've seen only one case in my career. The disease is called Riedel's thyroiditis. The cause isn't known. Reidel's thyroiditis is associated with elevated levels of antithyroid autoantibodies, so autoimmunity probably plays some role, especially in view of the good response of people with the disease to steroids. Some specialists believe that Riedel's thyroiditis is a variant of chronic autoimmune thyroiditis (see Chapter 5). Both conditions are associated with autoantibodies, and both can coexist with other autoimmune diseases in the same person.\n\nSome say Riedel's thyroiditis is twice as frequent in men as in women, but so few cases are recorded that it's hard to tell. It tends to occur between ages 30 and 60.\n\nIn Riedel's thyroiditis, the thyroid experiences a _fibrosis_ \u2014 the replacement of thyroid tissue by hard fibers that can be so dense that the patient loses thyroid function and becomes hypothyroid. The fibrous tissue firmly attaches the thyroid to the trachea and the nearby muscles so that it doesn't move in the neck. A small needle can't penetrate the fibrous thyroid.\n\nIf the fibrosis continues, it involves the parathyroid glands, which sit behind the thyroid. The fibrosis can destroy them, and the patient develops hypoparathyroidism. Because the parathyroid glands are important for maintaining calcium levels, the result of this disease is a fall in calcium. Symptoms of tingling and numbness in the hands and feet and tingling around the mouth begin to occur. As the calcium falls, it can result in severe muscle spasms.\n\nSometimes the fibrosis stops, and the patient remains stable. Other times it continues, and the patient has trouble breathing, swallowing, and even talking. The fibrosis can extend into the chest, the eyes, the gall bladder, and other parts of the body.\n\nWhen the doctor does thyroid function tests early in the disease, they may be normal. Later the patient becomes hypothyroid. The erythrocyte sedimentation rate is normal as well.\n\nBecause the fibrosis can be so invasive, people sometimes confuse Reidel's thyroiditis with anaplastic carcinoma, an extremely rapidly growing, invasive form of thyroid cancer that's usually fatal (see Chapter 8). A biopsy generally shows the difference. Sometimes doctors don't recognize the condition until the patient is in the operating room about to have surgery for what doctors think to be cancer.\n\nIf severe neck symptoms occur, surgery may be necessary to free the tissues. Sometimes so much fibrosis is present that surgery isn't successful in removing the tissue. A trial of steroids often slows or stops progression of the disease. The other agent that has shown some success is the drug tamoxifen.\n\n##### Chapter 12\n\n## Iodine Deficiency and Excess Disease\n\n### In This Chapter\n\n  Grasping the extent of the problem\n\n  Understanding iodine's place in mental and physical development\n\n  Identifying endemic cretinism\n\n  Dealing with the crisis\n\nIn the movie _Love and Death,_ Woody Allen describes a convention of village idiots in Russia. If such a convention actually occurred, sadly, most of the people in attendance would probably be suffering from iodine deficiency disease.\n\nThis chapter gives you a greater appreciation of the major role of thyroid hormone in the growth and development of the human body, particularly mental development. As you discover in this chapter, iodine deficiency disease is the world's most common and preventable cause of mental retardation. What stops its elimination is more often politics than medicine. The situation is very similar to the problem of infectious diseases that immunization can prevent. Doctors clearly understand the science of the condition, including the treatment. Only the means to transfer that knowledge into action is missing.\n\nA case in point is the story of the former East Germany. Prior to 1980, 50 percent of East German adolescents developed goiters. In 1980, the country began a program of adding minute amounts of iodine to common table salt, and the percentage of adolescents with goiters dropped to less than 1 percent. With the reunification of Germany, iodization became voluntary, and the goiter rate began to rise again.\n\nWhen you finish this chapter, you won't have any chance of getting invited to that convention in Russia.\n\n## Consuming Iodine in the U.S., Canada, and the U.K.\n\nThe recommended intake of iodine daily is 150 to 200 micrograms. One teaspoon of salt contains about 400 micrograms of iodine, and a slice of bread contains about 150 micrograms of iodine. A recent study in _Thyroid_ in July 2005 shows that the intake of iodine by the American population has stabilized at an acceptable level. In other words, most folks in the United States get a daily amount of iodine that is sufficient for the needs of the thyroid. But this hasn't always been the case \u2014 even in the recent past.\n\nIn Canada, all table salt is iodized, so there's no problem with deficiency. In fact, Canada has been a leading advocate for iodinization of salt throughout the world. In the U.K., there's no policy of iodizing table salt, and the soil contains little salt, but people in the U.K. get their iodine from cow's milk. The cows are fed iodine-enriched feed. There's no deficiency of iodine in the U.K. either.\n\nWith iodized salt and the addition of iodine to bread, there were no recognized cases of hypothyroidism due to lack of iodine in the U.S. for some time. In the 1970s and 1980s, in fact, doctors were concerned more about the overuse of iodine than the underuse. A study by the Michigan State Department of Health provided dramatic evidence of the benefit of the iodization of salt. The study indicated that in 1924, 39 percent of all children in several counties in Michigan were found to have a _goiter,_ an enlarged thyroid. After salt was iodized, the numbers dropped to 10 percent by 1928 and 0.5 percent by 1951.\n\nBut a study in the _Journal of Clinical Endocrinology and Metabolism_ in October 1998 showed that the urinary excretion of iodine, a well-established method for monitoring sufficient iodine intake, had fallen by half compared to earlier times in the United States. Twelve percent of Americans had low iodine concentration in their urine compared to 1974, when the percentage was less than 1. Europe has also seen an increase in cases of iodine deficiency that has resulted in adding more iodine to table salt and monitoring more carefully the population's iodine intake. The problem in Europe is now improving as well. The major reasons for the decline seem to be a reduction in the addition of iodine to salt as well as a reduction of amounts of iodine in bread.\n\nVegetarians are at risk if they eat vegetables grown in soil that has little iodine, which is the case in the U.K. They must be sure to use salt that has been iodized or eat iodine-rich seaweed. (Check out Chapter 20 for more information.)\n\n## Realizing the Vastness of the Problem\n\nMore than one-quarter of the world's population, or 1.6 billion people, suffer from some level of iodine deficiency disease. Of these people, 655 million have a goiter, an enlargement of the thyroid that can sometimes be debilitating. Twenty-six million people have brain damage, and 11 million of those 26 million are _cretins,_ individuals so handicapped by their thyroid conditions that they're completely dependent on those around them to live. Some researchers believe that for each day we delay treating this vast problem, 50,000 infants are born with decreased mental capacity caused by an iodine deficiency.\n\nThe numbers of people affected with iodine deficiency are even more startling when you look at certain areas of the globe. For example, 99 percent of the people of Eastern Europe and Southeast Asia are iodine deficient, while 98 percent of the people of China and the Far East and 91 percent of the people of the Americas are iodine sufficient. (For more details on how many people iodine deficiency disease affects on each continent, go to the Web page of the International Council for the Control of Iodine Deficiency Disorders at <http:\/\/indorgs.virginia.edu\/iccidd>.)\n\nThe reason so many people suffer from iodine deficiency is that the food they eat or the ground their food comes from contains little or no iodine. Chapter 2 explains that iodine is necessary to form _thyroxine_ (T4) and _triiodothyronine_ (T3), the two major thyroid hormones. Table 11-1 shows the usual sources of iodine in our diet.\n\nTable 11-1 Where Our Iodine Comes From Dietary Iodine  | Daily Intake in Micrograms |   \n---|---|---  \nDairy products  | 52 |   \nGrains  | 78 |   \nMeat  | 31 |   \nVegetables  | 20 |   \nEggs  | 10 |   \nIodized salt  | 380 |\n\nAll soil on earth used to contain iodine. However, over hundreds of thousands of years, the iodine has been leached out of the soil in two major areas of the earth: the high mountains and the plains. Far from oceans, water covered the plains in the past. Glaciers once covered the high mountains. As the glaciers melted, they carried iodine out of the soil, back to the ocean. In the same way, the flooded plains leached iodine from the soil and carried it back to the ocean as the water flowed away. As a result, high mountains and plains far from oceans are the areas where iodine deficiency disease occurs most often.\n\nCrops that grow in soil low in iodine are iodine deficient. Animals that feed on crops grown in soil low in iodine become iodine deficient. If cows that provide milk feed on these crops, children who drink their milk may be iodine deficient. The meat from those cows is also iodine deficient. The result is a huge public health problem. Even pets such as dogs become iodine deficient.\n\nIf you look at a map of the world that shows the areas where iodine deficiency disease is most prevalent, you see that vast areas of China, Russia, Mexico, South America, and Africa are rife with the disease. Surprisingly, the United States isn't spared. At one time, the iodization of salt and the addition of iodine to bread seemed to solve the problem in the U.S. More recently, as a study in the _Journal of Clinical Endocrinology and Metabolism_ in October 1998 shows, Americans have decreased their iodine intake. Nearly 12 percent of Americans studied had insufficient iodine in their urine. (The urine test is a reliable measurement of daily iodine intake.) This percentage compares with only 3 percent of people with insufficient iodine intake 20 years earlier.\n\nFood manufacturers added iodine to salt and bread not for health reasons but because they needed it in the production process. As other substances have replaced iodine in the production process, the daily iodine intake of Americans has fallen. Although I advocate taking iodine in iodized salt in this book, I recommend limiting your salt intake to lower blood pressure in my book _High Blood Pressure For Dummies_ (Wiley). __ Reduction in salt intake has become standard practice in the last few decades to combat the growing prevalence of high blood pressure and is another reason for the fall in total iodine in our diets.\n\nWestern Europe also used to be virtually free from iodine deficiency, but recent studies among Europeans have shown decreases in iodine intake as well.\n\n### Measuring iodine deficiency\n\nIn order to determine whether iodine deficiency is present in large populations, developing simple tools to measure a lack of iodine became necessary. One simple technique is a measurement of iodine in the urine. In areas where iodine isn't deficient, the iodine in the urine is 100 micrograms per day or more.\n\nIf a country or population undertakes an iodization program, the population takes a urine test before it receives iodine and at intervals afterward to see whether the program is working. (If it is, a much higher level of iodine appears in the urine after iodization begins.)\n\nThe second important measure of iodine deficiency is the frequency of goiters. A goiter is present if the lobes of the thyroid are larger than the end parts, or _terminal phalanges,_ of the thumbs. Unfortunately, such a measurement of the thyroid is very hard to make in practice, especially in small children, where a measurement is most important. To overcome this difficulty, doctors use a portable ultrasound device (see Chapter 4), which produces a measurement that's highly accurate and reproducible.\n\nFinally, measurement of thyroid hormones and TSH in the blood can evaluate the production of thyroid hormones.\n\n## Facing the Consequences of Iodine Lack\n\nIf your body lacks iodine, it can't produce sufficient thyroid hormone. Iodine deficiency has severe consequences at every stage of life. This section discusses the price your body pays in bad health and abnormal function at every stage of life, beginning with the pregnant woman and her fetus.\n\nDoctors divide iodine deficiency into four categories: _none_ when iodine intake is greater than 150 micrograms (ug) per day, _mild_ between 75 to 149 ug per day, _moderate_ between 30 to 74 ug per day, and _severe_ when less than 30 ug per day. The occurrence of goiters in a population increases as the intake falls, from less than 5 percent of the population with goiters when no deficiency exists to greater than 30 percent when iodine is severely reduced.\n\n## From pregnancy to adulthood\n\nThe entire body's formation is dependent on adequate T4. If sufficient hormone isn't available, congenital anomalies may occur. The infant may not survive much past birth. If it does, it may not live more than a few years.\n\nAs you can see in the following sections, the costs of iodine deficiency disorder are enormous both for the individual and for society. A village filled with people like those I describe here wouldn't be able to govern itself, provide an economic base to help better the condition of the people, or take the steps necessary to overcome the problem, including using iodine.\n\n### Pregnancy\n\nThyroid hormone, T4, has iodine in its basic structure. Even before pregnancy, a lack of T4 hormone has a harmful effect. Women who are hypothyroid have greater difficulties becoming pregnant, and they have more miscarriages and stillbirths than women with normal thyroid function. The recommendation for iodine intake for pregnant women is 200 ug per day.\n\nA fetus doesn't begin to make thyroid hormone until the 24th week of pregnancy. Until then, it's dependent on the mother's T4. During this time, the fetal brain is developing, and the entire chain of events that produces a normal brain requires T4 at every stage. If this hormone is lacking, the consequences are severe.\n\nIf a fetus is deficient in T4, its brain triggers an increase in the amount of the enzyme that converts T4 to T3 within the brain. This form of the enzyme isn't in other tissues, so the brain may experience protection from hypothyroidism while the rest of the body doesn't.\n\nIn this nuclear age, realizing that a thyroid gland that isn't making enough thyroid hormone will take up large amounts of iodine from whatever source it can is important. In a nuclear accident where radioactive iodine is released, a hypothyroid mother concentrates the iodine and passes it on to her growing fetus. If radioactive iodine doesn't completely destroy the fetal thyroid, that thyroid will at least be very prone to developing thyroid cancer.\n\n### Infancy\n\nA new baby deprived of iodine will have a goiter and show signs of hypothyroidism. Depending on the severity of the lack, the baby may be a cretin, which I explain later in this chapter in \"Defining the problem: Endemic cretinism.\" The brain of a newborn continues to develop up to age 2, so providing iodine starting immediately after birth may prevent retardation. A baby lacking in iodine also shows increased susceptibility to radioactive iodine (or any iodine). Infants should take at least 110 ug of iodine up to six months of age and 130 ug from 7 to 12 months of age per day.\n\n### Childhood\n\nIodine-deficient children often have goiters. They show reduced intelligence and poor motor function, and they may be deaf. Like infants, these children have a tendency to accumulate iodine from any source and are at greater risk in the case of a nuclear accident. Children should consume 90 to 120 ug of iodine daily.\n\n### Adulthood\n\nAfter the iodine-deficient child grows up, a goiter is often present in an iodine-deficient adult, though not always. He or she is intellectually retarded and may have movement difficulties. This person's thyroid gland is highly susceptible to radioactivity. Adults should eat at least 100 to150 ug of iodine every day.\n\n## Changes brought on by iodine deficiency\n\nYour body goes through a series of changes as your iodine level falls:\n\n**1.** **Your serum T4 level falls.**\n\n**2.** **Your pituitary releases more thyroid-stimulating hormone (TSH).**\n\n**3.** **TSH causes the thyroid to enlarge.**\n\n**4.** **The production of T3 increases within the thyroid relative to T4, because T3 is 100 times more biologically active than T4 and requires only three iodine atoms rather than four.**\n\n**5.** **Your body produces a goiter that's smooth at first but nodular later.**\n\n**6.** **You become hypothyroid.**\n\n## Defining the problem: Endemic cretinism\n\nShabmir is a 46-year-old woman living in Pakistan. Since she can remember, she has had a huge growth on the front of her neck that the doctors tell her is a goiter. She isn't alone, because more than 70 percent of the villagers around her suffer from the same condition.\n\nShabmir attended the local school but seems to have no aptitude for learning. Because of the unsightly growth on her neck, she has been discriminated against by those who don't have the same problem (perhaps because they come from an area with sufficient iodine in the food). The goiter is so large that she has difficulty moving her head and neck, which makes it hard for her to earn a living. She didn't marry until she found another person who had a severe goiter.\n\nFor years, Shabmir was unable to become pregnant. When she did, the baby was stillborn. She hasn't been pregnant again.\n\nShe appears swollen and lethargic. She has very little interest in her neighbors or her surroundings, and she tends to sleep a lot.\n\nShabmir's story is typical of the way that iodine deficiency disease affects the lives of millions of people. It's a worldwide plague that can render whole populations unable to function. The shame is that this condition is completely preventable!\n\nIn this section, I show you the different ways that iodine deficiency disease appears in people. The manifestations of iodine deficiency disease that I describe here are far worse than the hypothyroidism commonly found in the United States (see Chapter 5), because the hypothyroidism in iodine deficiency states begins when babies are conceived. Their mothers were already hypothyroid. Unless and until providing sufficient iodine breaks the chain of iodine deficiency, the disease will continue to disrupt the lives of a quarter of the world's population.\n\n_Endemic cretinism_ is the term used to describe the group of signs and symptoms in severe iodine deficiency disease. The Pan American Health Organization has defined endemic cretinism. It consists of several features:\n\n  **An association with endemic goiter and severe iodine deficiency.** _Endemic goiter_ means that more than 5 percent of children in a population age 6 to 12 have enlarged thyroid glands.\n\n  **Mental deficiency.** Patients also show one of the following:\n\n\u2022 **Nervous cretinism:** Predominantly nervous system symptoms (like defects of hearing and speech) as well as defects when they stand and walk\n\n\u2022 **Myxedematous cretinism:** Symptoms of hypothyroidism and stunted growth\n\nWhere iodine has been adequately replaced, cretinism doesn't occur.\n\nFigure 12-1 shows a typical goiter on a person living in an area of endemic cretinism.\n\n**Figure 12-1:** A typical goiter for a person living in an area of endemic cretinism.\n\n|     \n---|---\n\n### Goiter: The body's defense\n\nThe thyroid and the rest of the body do what they can to prevent hypothyroidism. The body's first response is a fall in the production of T4. When this drop occurs, the pituitary gland doesn't sense sufficient T3 in the brain, and it responds by secreting more TSH (see Chapter 2). The thyroid reacts by getting larger, thus forming a goiter, and by making more of the active hormone T3 (relative to the amount of T4). At the same time, the body converts more T4 into T3 away from the thyroid.\n\nIf a person's intake of iodine is severely limited, T3 production starts to fall. The consequence is severe hypothyroidism, which is particularly damaging in the brain.\n\n### Neurologic cretinism\n\nScientists believe that neurologic cretinism results from a lack of thyroid hormone from the mother during the third to the sixth month of pregnancy. The severe iodine lack means that the growing fetus is unable to contribute thyroid hormone either. During this time period, the brain should be achieving the ability to hear as well as perform important motor functions, so neurologic cretinism affects hearing and motor abilities most.\n\nNeurologic cretinism has three major characteristics:\n\n  Mental deficiency or retardation, although memory and social functions are unaffected.\n\n  Deafness and often loss of speech.\n\n  Stiffness of the arms and legs and an increase in the reflexes (both sets of symptoms opposite to those in hypothyroidism). The result is that a person with neurologic cretinism has a shuffling gait or may not be able to walk at all.\n\nNeurologic cretins may not be hypothyroid later in life. If they receive sufficient iodine, they can have a thyroid that makes sufficient thyroid hormone. But the damage done by the lack of thyroid hormone during development of the brain is irreversible.\n\n### Myxedematous cretinism\n\nPeople with myxedematous cretinism aren't as mentally retarded as those with neurologic cretinism. They don't tend to be deaf or mute as a result of their cretinism. Instead, they demonstrate the signs and symptoms of severe hypothyroidism from birth, including the following:\n\n  Very dry, scaly, and thickened skin\n\n  Retarded growth\n\n  Thin hair, eyelashes, and eyebrows\n\n  Puffy features\n\n  Delayed sexual maturation\n\nPeople with myxedematous cretinism don't have enlarged thyroids, but scar tissue often replaces their thyroids. As a result, their uptake of radioactive iodine is reduced despite having very high TSH levels. The levels of T4 and T3 hormones are very low. Many individuals have a combination of neurologic and myxedematous cretinism.\n\nJust why such a difference exists between neurologic and myxedematous cretinism isn't clear. The difference may have to do with social forces in various cultures. In the Andes, where neurologic cretins are more widely present, a tradition of taking extraordinary care of these very handicapped individuals endures. This tradition of caring may not be present in places where neurologic cretins are more sparse; in these places, they haven't received the kind of care required and therefore have died. Or the environments of some areas may be too severe for neurologic cretins to survive in.\n\nA study done by Dr. Stephen Boyages and published in the _Journal of Clinical Endocrinology and Metabolism_ in 1988 sheds some light on this subject. Dr. Boyages studied a group of cretins in Qinghai Province in China and found both neurological and myxedematous cretins along with a mixed group. The length of time that they were hypothyroid after birth explained the difference between the types of cretins, the myxedematous cretins having suffered for a longer time than the neurologic cretins. The neurologic cretins, after suffering mental retardation from a lack of thyroid hormone during brain development, experienced normal thyroid function after birth by getting enough iodine for the production of normal amounts of thyroid hormone. Myxedematous cretins had thyroid destruction, while neurologic cretins had normal thyroid function. The conclusion of the researchers was that myxedematous and neurologic cretinism are actually the same disorder, only modified by the amount of hypothyroidism after birth.\n\n## Looking at the geographic distribution\n\nEndemic cretinism is present in the mountainous regions of the world, as I explain earlier in the chapter. It's most common in the Andes and the Himalayas. It was present in the Alps until iodine replacement began several decades ago, but areas in the Alps still exist where people don't get sufficient iodine. It's present in mountainous regions of China, the Pacific, and the Middle East, as well as in lowlands away from the ocean where heavy rains wash iodine out of the soil. It's present in central Africa, in central Brazil, and even in Holland.\n\n  **Africa:** In Africa, endemic cretinism is present in Cameroon, the Central African Republic, Nigeria, Uganda, Rwanda, the Sudan, Tanzania, Zaire, and Zimbabwe.\n\n  **Australia:** Australia has iodine deficiency in its mountainous regions, especially Tasmania.\n\n  **Europe:** Iodine deficiency disease remains a significant problem in numerous countries, including Austria, Belgium, Bulgaria, the Commonwealth of Independent States (including Russia), Croatia, Germany, Greece, Holland, Hungary, Ireland, Portugal, Romania, Spain, and Turkey.\n\n  **Latin and South America:** In Latin and South America, large populations lack iodine in Bolivia, Brazil, Chile, Ecuador, Mexico, Peru, and Venezuela \u2014 mostly in the Andes Mountains and the mountains of Mexico.\n\n  **South Asia:** In South Asia, iodine deficiency disease is common in Bangladesh, India, Nepal, Tibet, and Pakistan.\n\n  **Southeast Asia:** In Southeast Asia, large populations of people with goiters exist in Myanmar, Vietnam, Thailand, and New Guinea.\n\n## Contributing factors\n\nLack of iodine is, without a doubt, the main factor in endemic cretinism, but other issues definitely play a role in different areas of the world.\n\n### Dietary factors\n\nDietary factors other than iodine consumption are a major aspect of iodine deficiency disease. A number of foods contribute to the problem:\n\n  **Cassava:** In some areas of iodine deficiency disease, the normal diet includes substances that are harmful to the thyroid. In Africa, for example, cassava is a major part of the diet. Cassava contains cyanide, which you can destroy only by properly preparing the food. If not, the cyanide converts to thiocyanate in the body. Thiocyanate competes with iodine for uptake by the thyroid, thus decreasing even further the tiny amount of iodine that gets into the thyroid. (If someone consumes sufficient iodine, it overcomes any block from thiocyanate.)\n\n  **Soybeans:** Soybeans also interfere with thyroid function, preventing the production of thyroid hormone in the thyroid gland (see Chapter 10). Again, sufficient iodine can overcome the block and permit normal production of thyroid hormone, but when iodine is scarce, the extra loss of thyroid hormone can make a huge difference.\n\n  **Broccoli and cauliflower:** A third group of foods that may contribute to endemic cretinism is the Brassica group of vegetables, which includes foods such as broccoli and cauliflower. Hypothyroidism is more common in areas where these vegetables make up a large part of the diet and the diet is deficient in iodine.\n\n  **Others:** Other foods that impair thyroid hormone production and are significant sources of food calories in certain areas of the world are bamboo shoots, sweet potatoes, corn, and lima beans.\n\n### Lack of selenium\n\nAnother important contributing factor in the development of iodine deficiency disease is the absence of selenium in the diet in certain areas, especially in China, Siberia, Korea, Tibet, and central Africa \u2014 places where iodine deficiency is already present. _Selenium_ is a mineral that the body needs in order to create the enzyme that turns T4 into the more potent T3.\n\nSelenium may play a role in reducing the number of goiters associated with iodine deficiency. The enzyme in the thyroid that selenium helps to produce also has the function of disposing of hydrogen peroxide, a side product of thyroid hormone production. A buildup of hydrogen peroxide may destroy thyroid cells, leading to a small thyroid. But the small thyroid is still not healthy, despite the lack of a goiter.\n\nWhen both selenium and iodine are absent from the diet, a disease called _Kashin\u2013Beck disease_ develops. This disease can lead to short stature as a result of the destruction of the growth plates of bones, the _cartilage._ The damage is different than that in the short stature associated with myxedematous cretinism, which I describe later in the chapter. Scientists previously thought that Kashin\u2013Beck disease resulted from selenium deficiency alone, but the combination of deficiencies makes the disease even worse.\n\n## Managing the Problem of Iodine Deficiency\n\nYou may think that managing the problem of iodine deficiency disease \u2014 preventing all goiters, cretinism, thyroid-related retardation, and hypothyroidism \u2014 should be easy. The trick is just to get everyone to eat a sufficient amount of iodine. The daily requirement is less than a pinhead of iodine. An individual requires only a teaspoon of iodine over a lifetime. But consuming enough iodine is much easier said than done. And sufficient iodine consumption must occur prior to the conception of a baby to prevent cretinism.\n\n## A sprinkle of salt\n\nAs far as food sources of iodine, the highest content is present in fish and, to a lesser extent, milk, eggs, and meat. Fruits and vegetables contain very little iodine. Using iodine-rich foods to solve the problem isn't likely to be globally successful, though, because diets and tastes differ throughout the world, and the logistics of transporting sufficient daily amounts of fish, milk, eggs, or meat to everyone in the world are overwhelming.\n\nBecause virtually every culture in the world uses salt, which is cheap and simple to iodize, iodized salt has been the standard way of overcoming the problem of iodine deficiency disease. The amount of salt needed to carry the daily requirement of 200 to 300 micrograms of iodine is very small and easily consumed.\n\nIn many countries, salt iodization has worked well, but some of its success has been less than glowing. Numerous international meetings have set goals and dates to eliminate iodine deficiency by. Charitable organizations, particularly the Kiwanis Clubs, have made the elimination of iodine deficiency disease a major goal. Some areas have achieved the goal of elimination of iodine deficiency, but in many other areas, the problem continues to exist.\n\nOne major organization, the International Council for the Control of Iodine Deficiency Disorders (ICCIDD), serves as the central organization for coordination of these efforts. This organization has created the _global iodized salt logo,_ which appears on packages of salt that have been properly iodized (see Figure 12-2).\n\n**Figure 12-2:** The global iodized salt logo.\n\n|     \n---|---\n\nThe history of efforts to overcome iodine deficiency disease in Bangladesh serves as an excellent illustration of the problems of eliminating iodine deficiency disease. The UNICEF statistical summary for Bangladesh says that only 55 percent of households consume iodized salt, despite international efforts to rid the nation of iodine deficiency.\n\nBangladesh is subject to annual flooding with monsoon rains that have effectively washed all iodine out of the soil. The iodine has washed into the Bay of Bengal, which means that the fish caught there contain plenty of iodine. However, most of the population of the country lives in rural areas far from the supply of iodine. More than 50 million people in Bangladesh have goiters.\n\nThe Law of Iodination in Bangladesh has made it illegal since 1984 to sell salt in Bangladesh without iodizing it. However, no penalties were established until 1992. The cost of iodized salt in Bangladesh is 25 cents per kilogram, and noniodized salt is 14 cents per kilogram. The poorest families buy the cheaper salt.\n\nThe cost of iodizing salt is only 5 cents per person per year. Iodization is a simple process that can take place in a salt factory. But tests of iodine in salt show that as many as half the factories in Bangladesh are producing salt with insufficient iodine. In a country with a population the size of Bangladesh, this represents inadequate iodine intake for millions of people.\n\nSome of the so-called iodized salt isn't iodized at all in Bangladesh so that the provider can make an extra profit. Bangladesh sometimes imports salt from other countries, which is mislabeled as iodized and sells for a cheaper price than Bangladesh iodized salt. The country borders on Myanmar (formerly Burma) and India, which don't enforce iodization as strictly as Bangladesh. So smuggling contributes to iodine deficiency disease in Bangladesh as well.\n\nOne step in the right direction is the development of a simple kit by UNICEF that can detect whether salt contains iodine. A drop of liquid solution added to salt turns the salt blue if iodine is present. UNICEF distributes these kits to school children, who test their salt at home.\n\nAnother example of a successful iodization program is the situation in Tasmania, Australia. A paper in the _Journal of Clinical Endocrinology and Metabolism_ described the situation in June 2002. The authors tell us that before 1950 a great deal of goiter in Tasmania led to the detection of iodine deficiency. At that time, children began to receive potassium iodide pills; iodine was also added to bread and was present in a disinfectant used for cattle. The problem seemed to disappear, but then the government stepped in and established an upper limit of iodine in milk, while the addition of iodine to bread ceased. As a result, many children in this study were in the moderate group of iodine deficient people and had thyroid enlargement. The children of Tasmania are again getting supplements to insure that they have sufficient iodine in their diets.\n\nYou can see that a successful iodization program involves much more than passing a law and setting up salt iodization programs in salt factories. A mountain of barriers can block such a simple solution.\n\n## An injection of oil\n\nA highly effective way of managing iodine deficiency disorder is to inject iodized oil, called _lipiodol,_ into the muscle of iodine deficient people. A single injection provides enough iodine to last four years or longer. People can also take lipiodol by mouth, although it lasts only a little more than a year when consumed orally. Iodine given through lipiodol has resulted in significant shrinkage of goiters in just a few months. However, giving iodine injections also has its problems.\n\nIodine deficiency is present in rural areas, where giving sterile injections isn't always possible. Qualified people aren't always available to give the injections. Sufficient supplies of sterile needles and the iodized oil must be available. Also, in this age of AIDS, many people are reluctant to accept an injection. The oral form of lipiodol, of course, solves all these problems.\n\n## A slice of bread or cup of water\n\nOther ways of managing iodine deficiency that have proven effective in some areas include the iodization of bread and the addition of iodine to the water supply. The problem with the iodization of bread is that bread consumption varies widely, and so this method works only in limited areas. Adding iodine to water doesn't work in areas with no public water supply, as is the case in most areas of the world where iodine deficiency disease is most prevalent.\n\n## Delineating the Drawbacks of Iodization\n\nOne major problem of iodization programs is the occurrence of hyperthyroidism when a person whose thyroid is under hyperstimulation with TSH receives a lot of iodine. Hyperthyroidism happens with iodine injections and even with iodized salt that contains excessive iodine. The tools for managing hyperthyroidism (see Chapter 6) in a rural environment may not be readily available, especially if a large number of cases exist. This is another issue that is most important in the less developed nations of the world.\n\nPeople commonly take a number of drugs that provide iodine in fairly large amounts. Among the most important are the following:\n\n  Amiodarone with 75 mg of iodine per tablet\n\n  Calcium iodide with 26 mg of iodine per milliliter (ml)\n\n  Iodine-containing vitamins with .15 mg per tablet\n\n  Kelp with .15 mg per tablet\n\n  Lugol's solution containing 6.3 mg per drop\n\n  Supersaturated potassium iodide solution with 38 mg per drop\n\n  Tincture of iodine with 40 mg\/ml\n\n  Radiology contrast agents\n\n\u2022 Telepaque with 333 mg per tablet\n\n\u2022 Ipodate with 308 mg per capsule\n\n\u2022 Visipaque with up to 320 mg\/ml\n\n  Vioform with 12 mg\/gram\n\nThe preceding drugs and other sources of high levels of iodine can cause either hypothyroidism or hyperthyroidism, depending on the clinical state of the patient. Patients who become hypothyroid may have no underlying disease. Hypothyroidism occurs in newborns, infants, and adults who take large amounts of iodine, which blocks production of thyroid hormone.\n\nA group of people with some thyroid condition already present develop hypothyroidism when they take iodine in large amounts. Some of the patients in this category include the following:\n\n  Patients with chronic thyroiditis (see Chapter 5)\n\n  Patients with controlled Graves' disease (see Chapter 6)\n\n  Patients with subclinical hypothyroidism (see Chapter 5)\n\n  Patients with subacute thyroiditis (see Chapter 11)\n\n  Patients on lithium\n\nOn the other side are patients who become hyperthyroid as a result of too much iodine. The people in this category include the following:\n\n  Patients with nontoxic nodular goiter (see Chapter 9)\n\n  Patients with one nodule that's autonomous, or not under the control of TSH\n\n  Patients with nontoxic diffuse goiter, a large thyroid with normal function\n\n  Patients without any thyroid disorder who live where mild iodine sufficiency exists\n\n##### Chapter 13\n\n## Surgery of the Thyroid\n\n### In This Chapter\n\n  Determining whether you need surgery\n\n  Picking the surgeon\n\n  Preparing for surgery\n\n  Understanding the procedure\n\n  Managing after surgery\n\nIf you need to have a thyroid operation, the good news is that the thyroid is in a very convenient location \u2014 a few millimeters under the skin of the neck \u2014 so surgeons easily find it. Except in rare circumstances in which the gland is matted down and can't be freed up, thyroid surgery isn't difficult in the hands of a skilled surgeon. Complications are few and infrequent, and the result is usually very satisfactory. If you're about to have surgery, you need to know a few things to make the experience as benign as possible. Revealing those things is the purpose of this chapter. You probably won't be able to perform thyroid surgery after reading it, but you will have a good idea of what to expect so that you won't get any surprises.\n\n## Deciding If Surgery Is Necessary\n\nOrlo Blunt is a 45-year-old man who has a solitary thyroid nodule \u2014 a lump on the thyroid. His doctor performs a fine needle biopsy, which shows a _follicular lesion,_ tissue that looks like normal thyroid follicles (the circles of cells that make thyroid hormone). The pathologist is uncertain whether the nodule is cancerous. Orlo's doctor refers him to Dr. Allen, a thyroid surgeon with extensive experience, for thyroid surgery. After examining Orlo, Dr. Allen tells him that he needs a _lobectomy_ (removal of one lobe of the thyroid). During the surgery, a pathologist examines the tissue that the surgeon removes. If the lobectomy shows that Orlo has follicular cancer, Dr. Allen will do a total _thyroidectomy_ \u2014 he will remove the entire thyroid.\n\nOrlo undergoes blood studies before the surgery, including thyroid function tests, which come back normal. Orlo doesn't eat the morning of surgery, which is supposed to start at 7 a.m., but due to various glitches, the operation begins at 9 a.m. Dr. Allen puts him under general anesthesia. The operation goes smoothly. The lesion proves to be a follicular _carcinoma_ (cancer), so Dr. Allen performs a total thyroidectomy. Dr. Allen feels no nodes on the side of the thyroid but removes nodes in the central neck to look for cancer there. The pathologist determines that these nodes aren't cancerous.\n\nAfter the surgery, Orlo feels some soreness in his neck but isn't hoarse. A clear plastic bandage covers the incision on his neck. Orlo has a chest X-ray and bone scan to make certain that cancer hasn't spread to those areas. These tests come back negative, indicating no cancer spread.\n\nSeveral weeks after surgery, Orlo receives a dose of radioactive iodine (see Chapter 6) to destroy any remaining thyroid tissue. For the next several years, Orlo sees his doctor every six months with no evidence of recurrence.\n\nA number of reasons may bring you to the thyroid surgeon. Orlo's situation is one of the most serious \u2014 thyroid cancer (see Chapter 8). But surgery is the best way to handle several other thyroid situations as well.\n\n  If you're hyperthyroid, antithyroid pills don't successfully treat your condition (or you're allergic to them), and you don't want to have treatment with radioactive iodine, surgery is your only other choice (see Chapter 6).\n\n  If you're pregnant and develop hyperthyroidism (see Chapter 17), and you're unable to take the antithyroid pills because of allergies, surgery is your only option. (You can't receive radioactive iodine during pregnancy.)\n\n  If you have a large thyroid that's causing local symptoms in your neck, such as trouble swallowing or breathing, or if the goiter is especially unattractive, (see Chapter 5) surgery is necessary, though you may also try radioactive iodine.\n\n## Finding Your Surgeon\n\nUsually, your doctor picks your surgeon for you and you agree, assuming that your doctor has your best interest at heart. In most cases, your doctor does have your best interest at heart, so this is a good method to follow. But sometimes other factors determine the doctor's choice as well. Perhaps the surgeon is an old friend and colleague your doctor has been working with for years. Or perhaps your doctor wants to keep your case within the confines of a particular hospital. (Occasionally, your insurance mandates that you can go to only certain surgeons.)\n\nThe three most important criteria for a surgeon are experience, experience, and experience. If a surgeon does an operation once a month, that isn't experience. If he or she does it several times a week, that's experience. But how do you find a surgeon with the kind of experience you need? I devote an entire chapter (Chapter 3) to the subject of finding a doctor to treat your thyroid condition. And much of the research I suggest that you do there is applicable to finding an experienced thyroid surgeon, including checking out the following organizations on the Web:\n\n  American Association of Endocrine Surgeons (<http:\/\/endocrinesurgery.org>)\n\n  American Association of Clinical Endocrinologists (www.aace.com)\n\nAnother good resource is www.thyroid.org.\n\nSimply because a doctor is an endocrine surgeon doesn't mean that he or she specializes in thyroid surgery. Many endocrine organs \u2014 the pancreas, the adrenals, the ovaries, and so forth \u2014 require a surgery that's entirely different from thyroid surgery. Be sure you find a _thyroid_ surgeon.\n\nDon't go to a surgeon unless you're certain that you're ready for surgery. The job of the surgeon is to cut, and he or she probably won't try to talk you out of having surgery. You and your thyroid specialist should agree on the need for surgery before you arrive in the surgeon's office.\n\nAfter you find a potential surgeon, your responsibility to your neck isn't over. You need to ask the surgeon some hard questions before you give him or her the privilege of cutting into you. The most important questions are the following:\n\n  How often do you perform this surgery? (The answer should be more than three times a month, at least.)\n\n  Have you had any deaths in the last five years while doing this surgery? (The answer had better be \"no.\")\n\n  Have your patients had any serious and permanent complications from your surgery? (Keep reading for information about specific complications.)\n\nIf you're happy with the surgeon's answers to these questions, go ahead and sign up.\n\n## Making Final Preparations Before Surgery\n\nIn the weeks before you head in for surgery, you may have to juggle some medications, depending on your condition.\n\n  If you're having an operation for hyperthyroidism, you'll probably take antithyroid pills for four to six weeks prior to surgery to get your thyroid function to be normal, which a free T4 test shows. (If you can't take antithyroid pills because of an allergy, obviously you skip this step.) You often get iodine for ten days before surgery to reduce the size and blood vessels of the thyroid. Your doctor may also place you on _propranolol,_ a beta blocker, to control symptoms such as a rapid heartbeat or shakiness.\n\n  If you have hypothyroidism, you need to take thyroid hormone replacement pills prior to surgery so that your thyroid function is normal. Anesthesia is risky if a patient is very hypothyroid.\n\n  If you're taking aspirin or other medications like coumadin that thin the blood (and therefore prolong bleeding), stop taking them a week before surgery.\n\nA few days prior to surgery, you have blood tests to confirm that your organs, such as your liver and kidneys, are performing satisfactorily. The doctor also wants to confirm that you don't have anemia, although you won't lose much blood during thyroid surgery.\n\nYou should eat nothing after supper the night before surgery. The anxiety, the trauma of surgery, and the anesthesia all make you more prone to vomit, and you don't want to have anything in your stomach in case you do.\n\n## What Happens During Surgery\n\nYou generally come to the hospital on the morning of surgery. A staff member wheels you into the operating room, where the anesthesiologist gives you general anesthesia. (Rarely, local anesthesia is used.) Two hours later, you awaken minus some or all your thyroid. (But thyroid surgery isn't the greatest way to lose weight.)\n\n## Making the initial incisions\n\nThe anesthesia may be local (an injection in the area of the surgery that doesn't put you to sleep) or general (a medication that causes you to sleep through the operation). Most patients prefer the latter. After all the preparations of cleaning and covering the area of the operation, the surgeon makes an incision about 3 inches (8 centimeters) long horizontally over the area of the thyroid. The surgeon minimizes the scar by carefully placing the incision over the normal skin fold (the place where your skin folds when you bend your head forward) and by making the smallest possible incision. If the surgeon has to remove lymph nodes (as can be the case with thyroid cancer), the surgeon may carry the incision up in the direction of the ear at one or both ends of the incision. The incision cuts through the fat underneath the skin and a thin muscle called the _platysma._ The surgeon pulls the skin and the muscle overlying the thyroid back to reveal the thyroid gland.\n\nThe surgeon then sees what he or she will be dealing with in the next hour or so. The thyroid is shaped like a butterfly, with an _isthmus_ (a narrow strip) of thyroid tissue connecting the two \"wings\" of the butterfly (check out the illustration in Chapter 2). Above the isthmus, the surgeon may see a projection of thyroid tissue called the _pyramidal lobe._ Surgeons usually remove the pyramidal lobe during any partial thyroid operation so that it won't regrow as a large bump on the front of the neck when the gland grows to restore thyroid hormone production.\n\nThe surgeon knows that the thyroid is firmly fixed to the trachea and larynx in back, so any operation has to free it up before the surgeon can remove the thyroid tissue. He or she sees two _superior thyroid arteries_ entering the thyroid from above and two _inferior thyroid arteries_ entering the thyroid from below. A fifth artery sometimes enters the thyroid in its central portion from below. The surgeon may have to tie and cut one or all of these arteries, depending on how much of the thyroid he or she is removing.\n\nThe surgeon must also deal with the thyroid veins. The _middle thyroid veins_ connect to the thyroid from the side. The surgeon must tie and cut them. The surgeon also ties and cuts the veins connecting to the top of the thyroid, called the _superior thyroid veins,_ if the plan is to remove the entire lobe.\n\n## Dealing with surgical obstacles\n\nBetween three and six parathyroid glands, as well as the recurrent laryngeal nerves (one on each side), are found on the back of the thyroid, and the surgeon must carefully preserve them if possible. In any thyroid surgery, the main obstacles to easy surgery are the parathyroid glands and the recurrent laryngeal nerves.\n\n### Parathyroid glands\n\nThe _parathyroid glands_ sit on the back of the thyroid and share blood supply with it. There are usually four of these tiny glands, but there may be more or less, and surgeons find them in many locations. They weigh only 30 to 40 milligrams each and may be accidentally removed, damaged, or lose their blood supply during surgery because they're so tiny.\n\nThe parathyroids are responsible for managing the calcium level in the blood. If they aren't functioning, the calcium level falls. Sometimes the trauma of surgery causes the parathyroids to shut off temporarily, but they recover in a few days.\n\nWhen you have a total thyroidectomy, preserving the parathyroid glands often isn't possible. In this case, the surgeon cuts them into small pieces and injects them back into a muscle, for example in the shoulder, where they seem to function just fine.\n\nIf a patient has symptoms of low calcium after surgery, oral calcium supplements can usually manage the problem. The symptoms that may occur include:\n\n  Feelings of numbness, tingling, and prickling along the extremities, as well as loss of sensation in those areas\n\n  Increased irritability\n\n  Fatigue\n\n  Mood swings\n\n  Hoarseness\n\n  Muscle cramps\n\nRarely, a person needs intravenous calcium. If, by chance, the parathyroids don't recover their function after surgery, the patient takes vitamin D and calcium for life \u2014 a rare occurrence associated with only 1 in 300 surgeries of the thyroid.\n\n### Recurrent laryngeal nerves\n\nThe two recurrent laryngeal nerves, one behind each thyroid lobe, can be major obstacles to the surgeon. Each nerve controls the vocal cord on its side. Both nerves lie close to the thyroid; a surgeon can easily cut them accidentally or include them in a knot that's tying off a blood vessel. If the diagnosis is thyroid cancer, one or both of the recurrent laryngeal nerves may already be included in the cancer, and the patient may have to sacrifice them at the time of surgery.\n\nThe trauma of surgery may temporarily damage recurrent laryngeal nerves. If so, the patient has a hoarse voice for a few days after surgery. If surgery damages both nerves, the situation is more serious, and the patient may need a _tracheostomy_ (an opening from the neck into the breathing tube) to breathe. The damage and the hoarseness may be permanent. Damage to a recurrent laryngeal nerve should be very rare. In good hands, it doesn't happen more often than once every 250 operations on the thyroid.\n\nThe superior laryngeal nerve may suffer an injury during surgery as well. Damage to this nerve produces milder symptoms than those of recurrent laryngeal loss. Loss of this nerve produces voice fatigue and a decrease in the range of the voice.\n\n## Determining the extent of surgery\n\nThe purpose of the surgery determines what happens next. If the surgeon is removing a hot nodule (see Chapter 7), the surgeon locates any blood supply to it, cuts and ties off the blood supply, and removes the nodule. If hyperthyroidism is the reason for surgery, the surgeon performs a _subtotal thyroidectomy,_ leaving a few grams of the part of the thyroid nearest the trachea to avoid damaging the parathyroid glands.\n\nA debate rages about how much thyroid to remove when a cancer is present in the thyroid. Most of the debate concerns small thyroid cancers \u2014 the ones that measure less than 1.5 centimeters (0.6 inches) in diameter. The survival rate for this size of cancer seems to be just as good whether you have a total thyroidectomy or less than a total thyroidectomy. Less than a total thyroidectomy leaves thyroid tissue in the area of the recurrent laryngeal nerve in order to avoid damaging it.\n\nA _total thyroidectomy_ is an attempt to remove all visible thyroid tissue. It's an extensive surgery that's more difficult than partial removal of the thyroid. A total thyroidectomy results in more frequent damage to parathyroids and nerves. Therefore, many surgeons do a _subtotal thyroidectomy,_ leaving a small piece of one lobe of the thyroid intact, when the tumor has a diameter less than 1.5 centimeters.\n\nOther surgeons elect to do a total thyroidectomy on all thyroid cancer patients. They offer fairly convincing arguments:\n\n  The morbidity and mortality rate of this surgery in their hands is very low.\n\n  Thyroid cancer is often _bilateral_ \u2014 it affects both lobes of the thyroid. If radiation is the cause of cancer, the cancer is almost always bilateral.\n\n  Scanning for evidence of new tumors and treating any new tumors is much easier when no thyroid gland remains to take up radioactive iodine.\n\n  After surgery, levels of thyroglobulin in the blood fall to zero. Therefore, if blood tests later show that a patient's thyroglobulin levels are rising, that's a strong indicator that a tumor is recurring.\n\nIf cancer brings you to the surgeon, a very important part of your history is whether you've had radiation therapy to your neck. If you have, then a total thyroidectomy is the correct operation because cancers tend to be in both lobes in this situation. Most surgeons remove the entire thyroid even if the tissue that was suspicious turns out to be free of cancer, because cancer in the rest of the thyroid is so likely.\n\nAfter the surgeon removes all or part of the thyroid, the question arises whether to remove lymph nodes, especially if none are enlarged. Many surgeons remove nodes over the trachea because cancer often spreads there first. They biopsy nodes to the side of the thyroid if they're enlarged, and they remove most of those nodes if the tissue has cancer \u2014 a procedure called a _modified radical neck dissection._ A more extensive form of this surgery is called an _unmodified radical neck dissection,_ which involves removing muscles and other tissues. No study shows that this extensive surgery improves mortality; it leaves the patient disfigured for no reason.\n\nStudies show that if a surgeon injects a dye into the thyroid, it goes to the chain of lymph nodes on the trachea behind the isthmus. The surgeon knows that this chain is where to look first for the spread of cancer.\n\nThe following outlines surgical treatment approaches particular to each of the types of thyroid cancer (which I discuss in Chapter 8):\n\n  **Papillary or follicular cancer:** After surgery, doctors put patients with papillary or follicular carcinoma on suppressive doses of thyroid hormone for life. A suppressive dose is a dose that keeps the TSH between 0.1 and 0.5. This is a value below the normal range, which means that the patient has slightly too much thyroid hormone in her system, but the dose seems to prevent growth of new thyroid tissue without causing damage to the patient.\n\n  **Medullary cancer:** A tumor of the medullary type (see Chapter 8) is managed with a total thyroidectomy and the removal of the central nodes around the trachea; a surgeon removes lateral nodes to the side of the thyroid only if they're visibly enlarged. Medullary tumors often secrete hormones that cause diarrhea or stimulate the adrenal gland, so removing as much tissue as possible prevents or reverses these complications.\n\nA medullary tumor may be part of a hereditary condition known as _multiple endocrine neoplasia_ (MEN). MEN patients have tumors of their adrenal glands and occasionally their parathyroids. Some experts recommend removal of the thyroid before age 5, because the likelihood of cancer is so great. If an adrenal tumor is present, a surgeon should remove it first, because surgery on the thyroid may be dangerous when a malignant adrenal is making large amounts of adrenal hormones as surgery is occurring.\n\n  **Undifferentiated cancer:** The surgeon attempts to remove as much cancer and thyroid as possible if the tumor is the undifferentiated type. By the time surgery occurs, these tumors usually have spread, and doctors can do little. But surgery can slow the inevitable local spread of this aggressive type of tumor.\n\nIf a surgeon has any concern about bleeding after surgery, or if the surgeon has removed so much tissue that a large space is left in the neck, the surgeon leaves a drain in the wound. A drain is necessary only rarely, and the surgeon usually removes it after a day or two in any case. The drain helps prevent fluid accumulation and results in a better cosmetic outcome.\n\n### Dealing with a tumor in the thorax\n\nSometimes most of the cancerous tumor is located in the thorax, under the sternum, the breast bone. The surgeon can usually bring the thyroid up through the neck and remove it, in the process of the standard surgical procedure I outline in the \"What Happens During Surgery\" section. Occasionally the thyroid surgeon has to go into the chest by splitting the sternum if the mass is especially large and the surgeon can't remove it through the neck, if the blood supply to the thyroid in the chest is especially great in the chest, or if the large mass is a cancer.\n\n## Considering a New Approach\n\nRecently, surgeons have been trying a less invasive approach to thyroid surgery called _endoscopic thyroid surgery._ Surgeons perform this surgery when a diagnosis of cancer is uncertain and a nodule needs to be removed. The surgeon inserts a tiny tube in the neck, and a stream of carbon dioxide gas opens up the area. The surgeon uses high magnification to see the area in excellent anatomical detail. Another tube inserted into the area has a cutting edge that allows for removal of the nodule. The result is a less unsightly scar and a quicker return to activity for most patients, although the amount of pain that patients feel is about the same as those who have a conventional operation.\n\nEndoscopic thyroid surgery may take a little longer than an open operation. If the surgeon finds cancer during the endoscopic surgery, the surgeon usually opens the neck to proceed with an open, total thyroidectomy. However, endoscopic thyroid surgery is promising as a way to avoid large scars and shorten the time between surgery and returning to work. As surgeons gain more experience with this method, it may start to replace the open operation.\n\n## Recuperating After the Operation\n\nYou'll have a permanent scar after surgery, but it may not be very visible. Most people leave the hospital the same day of the surgery if no complications develop, which is usually the case. But as I note later in this section, the possibility of hemorrhage is rare but present. You must stay in the hospital for 24 hours after surgery to deal with this complication. Don't let the hospital staff kick you out early.\n\n## Getting back on your feet\n\nA week is usually necessary to recover from thyroid surgery. During that time, you feel some neck stiffness and tenderness. Your throat is sore, and your voice is hoarse. You have a cough for a few days and feel some pain when you swallow, but pain killer medicine usually manages it. The scar becomes hard initially and then softens over the next month. An occasional patient forms a very thick scar called a _keloid,_ which will be permanent because attempts to remove keloids with plastic surgery often result in new keloid formation.\n\nThe only postoperative restriction is that you shouldn't submerge yourself in water for the first day or two (no swimming). You can drive a car as soon as your head can turn without difficulty. You can resume most of your usual activities after a week, building up to them slowly. Many people are back at work in two weeks. The surgeon often wants to see you again about three weeks to check on your results.\n\nAny patient who has had extensive removal of the thyroid needs to take thyroid hormone replacement for life. If the operation is for thyroid cancer, you receive enough thyroid hormone to mildly suppress your thyroid-stimulating hormone.\n\n## Dealing with complications\n\nIn the hands of an experienced thyroid surgeon, complications should be rare and insignificant. Death is a very rare occurrence after thyroid surgery. Seven problems exist that you may need to manage after surgery:\n\n  **Hypothyroidism** is normal after removal of most of the thyroid, and doctors treat it by giving the proper amount of thyroid hormone. Usually T4 is all that's needed. If the surgery is for benign disease, then the patient receives enough T4 to make the TSH normal. If the surgery is for cancer, the patient receives T4 in a sufficient amount to suppress the TSH, as I describe in the preceding section, \"Getting back on your feet.\"\n\n  **Thyroid storm** occurs when the patient who is having surgery for hyperthyroidism isn't prepared properly with antithyroid drugs and propranolol before surgery (see Chapter 6 for more on this condition). Thyroid storm should never occur when the patient is made ready for surgery properly.\n\n  **Wound infection** occurs in less than 1 percent of thyroid surgeries, and antibiotics and drainage treat it.\n\n  **Wound hemorrhage** is also rare. It occurs in less than 1 percent of operations. It begins with swelling of the neck in the first 12 hours after surgery. Often, the patient has some bandage placed over the site of the operation. If the bandage is too tight and bleeding occurs, the bleeding can compress the trachea and cause breathing difficulties. Sometimes the patient has to have the wound opened at the bedside in an emergency.\n\n  **Injury to the recurrent laryngeal nerve** is often temporary. The voice becoming hoarse or husky allows doctors to discover it. This injury is the result of one side of the vocal cord being paralyzed. The situation is much worse if recurrent laryngeal nerves on both sides of the thyroid are injured. Then the patient may be unable to breathe and has to have a tracheostomy.\n\n  **Hypoparathyroidism** sometimes occurs for a brief time after surgery, but the glands recover. Permanent hypoparathyroidism is a very rare event when experienced surgeons are doing the operation. A low serum calcium plus the symptoms I describe in the \"Parathyroid glands\" section such as a feeling of numbness in the extremities, mood swings, hoarseness and muscle cramps allow doctors to easily diagnose it.\n\n  **Tracheomalacia** is a softening of the trachea due to pressure from a large goiter. Every time the patient breathes in, the trachea narrows and may even collapse. Sometimes a tracheostomy is necessary to allow a person to breathe.\n\n##### Part III\n\n## Reviewing Special Considerations in Thyroid Health\n\nIn this part . . .\n\nT hese chapters clue you into some special situations that can affect your thyroid, such as medications you take for other conditions. You discover the genetic link to thyroid diseases and what scientists are doing to try to prevent their transmission from one generation to the next. I also synthesize the latest findings in thyroid treatment to help you stay informed and up to date.\n\nCertain groups of people are affected differently from the rest of us by thyroid disease. These include pregnant women, children, and elderly people. Their special needs are taken up in this part. Plus, there is plenty you can do to keep your thyroid happy and making those essential hormones in the right quantities. The last chapter in this part discusses some ways you can manage your body so that thyroid function takes place in a healthy environment.\n\n##### Chapter 14\n\n## The Genetic Link to Thyroid Disease\n\n### In This Chapter\n\n  Grasping the basics of genetics\n\n  Discovering how your genes impact your thyroid\n\n  Planning for the prevention of hereditary thyroid disease\n\nThroughout this book, I introduce you to several members of the Dummy family: Sarah, Stacy, Karen, and Tami. The reason these five women, who come from the same prestigious family, all suffer from thyroid conditions is that thyroid diseases often run in families. Many (though not all) thyroid diseases are hereditary.\n\nIn this chapter, I discuss the various hereditary thyroid diseases and how they're passed from one generation to the next. The progress that scientists have made in the last decade alone in understanding the inheritance of thyroid disease is nothing short of amazing. But all this new information has made the subject pretty complicated.\n\nI try to clear up some of the complications of _genetics,_ the science of heredity, in this chapter, but I'll be honest: This subject isn't for the fainthearted. If you're interested in knowing how genetics program your body to experience a certain disease, this chapter definitely tickles your intellect. If you're reading this book solely to determine how to treat your present thyroid condition, you may want to head over to the chapter that details your specific condition instead.\n\nBut even if the term _genetics_ strikes fear in your heart, you may want to jump to the end of the chapter (the section called \"Viewing the Future of Managing Hereditary Thyroid Disease\") to discover some of the exciting ways that scientists are attempting to prevent people from inheriting thyroid disease and many other genetic diseases in the future.\n\n## Taking Genetics 101\n\nTo understand how genetic disease affects the thyroid, you need a basic understanding of genetics. This section provides the background that you need. This book isn't about genetics, so I've made this section as brief as possible while still giving you the essentials.\n\n## Pouring over pea plants\n\nGregor Mendel, an Austrian monk, is the starting point for all the great discoveries in genetics, although he never got credit for his pioneering efforts in his lifetime. Mendel studied pea plants, looking at the ways that various characteristics of the plants were inherited, such as height, the texture of the seeds, the plumpness of the pods, and so forth.\n\nMendel knew that pea plants form new seeds when the _pollen_ (which functions the same as sperm) in the male part of the plant called the _anther_ manages to attach to the _stigma,_ the female part, and get down to the _ovary_ (the egg), which the pollen fertilizes. The result is a seed, which grows into a plant.\n\nMendel carefully controlled the fertilization of his pea plants so that he knew which plant provided the pollen and which plant provided the ovary. He took, for example, the pollen of short pea plants that had never produced anything but short pea plants, and used that pollen to fertilize the ovaries of tall pea plants that had never produced anything but tall pea plants. Then he took the pollen from tall pea plants and fertilized the ovaries of short pea plants. Much to his surprise, the result in both cases was always tall pea plants (he expected the short and tall plants to combine to form a medium-sized plant).\n\nMendel then crossed the tall offspring from this first fertilization (called the _first cross_ ) with each other. The offspring of the second cross weren't all tall: Three-fourths were tall, and one-fourth was short. When Mendel crossed the short plants from the second cross with other short plants from the second cross, the result was plants that were always short. But if he crossed short and tall plants from the second cross, the new plants were usually, but not always, tall. The same pattern held true for the other characteristics that Mendel studied.\n\nOn the basis of these studies, Mendel made the following observations of the pea plant:\n\n  A feature of the pollen and the egg determines whether a plant is tall or short. (This feature is now called a _gene;_ Mendel didn't use this term.)\n\n  When the gene (what he called an _atom of inheritance_ ) from the tall plant combines with the gene from the short plant, the genes don't mix to form an average-sized plant.\n\n  If a plant has two characteristics for the same gene, such as tallness and shortness, one tends to appear more often than the other when they're crossed. (The gene that produces the trait that appears more often is the _dominant_ gene, and the gene producing the trait that appears less often is the _recessive_ gene.)\n\n  Two different genes can exist for a trait. (Two genes that determine the same trait are called _alleles._ )\n\n  Genes follow the principle of _independent assortment:_ Plants inherit each trait separately from all other traits. When plants are crossed that have two different traits, such as height and texture of the seed, these traits are passed to the offspring independently of one another. For example, a tall plant doesn't always have a smooth seed or always have a wrinkled seed.\n\nMendel's work received little attention when he announced it in 1865, but scientists rediscovered it in 1900. He got posthumous credit for his discoveries (for what that was worth).\n\n## Talking the genetics talk\n\nUsing Mendel's research, scientists later began to create the new language of genetics so that you and I couldn't possibly understand what they were talking about. I'm going to test my interpretation skills here to walk you through the maze they've created.\n\nIf a person (or a plant, dog, or chimpanzee) has two copies of the same allele, he or she is said to be _homozygous_ for that gene. If he or she has one of each allele, the person is _heterozygous_ for that gene. (We now know that, within an entire population, more than two different alleles can exist for each gene. However, any given person, animal, or plant has only two alleles for each gene because a single individual has only two copies, while others in the population may have two different copies.)\n\nThe appearance of the trait controlled by a gene is called the _phenotype,_ while the genes that make up that phenotype are called the _genotype._ For instance, two tall pea plants may have the same appearance (phenotype), while their genotype may be different. One plant may have only tall genes and is tall, while the other has a tall gene and a short gene and is still tall \u2014 because tallness is the dominant gene.\n\nA quick quiz: Based on your in-depth knowledge of genetics, can two short pea plants have different genotypes? The answer is no, because shortness is the recessive gene. If you throw a tallness gene into the mix, the plant is tall. Therefore, all short pea plants must have only the genes for shortness.\n\n## Observing the great divide\n\nAt the same time that the world was ignoring Mendel's work, great things were happening under the microscope. Scientists were seeing that tissues are made up of cells and that new cells come from the division of old cells. As two new cells form, the old cell produces two copies of everything so that each new cell has exactly what the old cell had. _Mitosis_ is the whole process by which one cell becomes two.\n\nOne particular area of the cell, which looks like a cell within the cell, was especially intriguing to scientists. This area is called the _nucleus_ of the cell. As two new cells are being formed, some substances in the nucleus double and separate so that each new cell gets a complete set of these substances, called _chromosomes._\n\nOver the years, scientists discovered that each plant and animal has a set of chromosomes, but the numbers of chromosomes may differ between species. For instance, humans have 23 pairs, or 46, chromosomes, while chimpanzees have 24 pairs, or 48, chromosomes. (But chimpanzee chromosomes look more like human chromosomes than ape chromosomes, so don't be thinking that you're so smart.)\n\nExamining the division of egg cells and sperm cells (the so-called _germ cells_ ), scientists discovered that each of these cells contains only half the normal number of chromosomes. In humans, for example, each egg cell and each sperm cell has one set of 23 chromosomes (while other human cells have 46 chromosomes). When these cells divide to form more sperm or egg cells through a process called _meiosis,_ the result is again 23 chromosomes per cell. When the egg and the sperm join together in fertilization, the combination, called a _zygote,_ has the normal number of 46 (23 pairs) chromosomes.\n\nWhen a zygote forms, one set of its chromosomes comes from the female, and one set of chromosomes comes from the male; these sets pair up two by two. The members of each chromosome pair are called _homologous_ chromosomes.\n\nAs is always the case, the rule that all chromosome pairs have identical sets of genes has an exception. But like the French say, _vive le difference._ Loosely translated, that means \"thank goodness for this particular set of chromosomes.\" I'm referring to the sex chromosomes that determine whether you're a boy or a girl. All other pairs of chromosomes have matched genes; if a gene exists for a given characteristic on one of the chromosomes of the pair, the other chromosome has a gene for that same characteristic. A female has two matched sex chromosomes (called _X chromosomes_ ), and a male has two different sex chromosomes (called an _X chromosome_ and a _Y chromosome_ ).\n\n## Mapping traits with genes and chromosomes\n\nAny given plant, animal, or human has far more traits than its number of chromosomes. Recognizing this fact, scientists realized that each chromosome must contain many genes.\n\nEach chromosome is passed down to its _daughter cells_ \u2014 the cells created when a cell divides. Therefore, some genes (and the traits they create) get passed down together from generation to generation. (They don't follow the principle of independent assortment.) Genes on the same chromosome are _linked._\n\nEven though some genes are linked, they sometimes do get inherited independently, just as Mendel predicted, which happens because _crossing over_ takes place. What is crossing over? During the process of meiosis, which produces sperm and egg cells, as the sets of chromosomes line up close together, genes on one chromosome can cross over to the other while their alleles cross over in the other direction. In this way, _recombinant_ chromosomes are formed \u2014 new combinations that help to make your offspring different from you.\n\nThe discovery of crossing over meant that scientists could start to _map_ chromosomes. That is, scientists could determine which genes are on which chromosomes and where, because the closer two genes are, the less likely they're separated by a cross-over. The farther genes are from one another, the more likely they are to separate.\n\nAnother way that a new trait replaces an old one is when a _mutation_ takes place. In a mutation, a new gene replaces as old one as a result of faulty copying of the chromosome or an outside influence, such as radiation, chemicals, or the sun. Usually mutation isn't noticed, either because the gene is recessive or because the mutation may kill the individual so that it isn't reproduced. Once in a while, a mutation is good for the animal or plant in which it occurs, producing a useful trait.\n\n## Getting down to the DNA\n\nGenes consist of long, long, long chains of _nucleic acids._ Nucleic acids have three components: a sugar called _deoxyribose,_ a _phosphate_ attached at one end of the sugar, and a _base,_ which may be adenine, cytosine, guanine, or thymine, attached to the sugar at another point. The genes contain _deoxyribonucleic acid,_ or DNA.\n\nWithin the DNA, the number of adenine molecules is always equal to the number of thymine molecules, while the amount of cytosine equals that of guanine. In 1952, biochemists James D. Watson and Francis H. C. Crick showed that this equality is because each gene contains two chains of nucleic acids. The adenine on one chain is always paired with the thymine on the other, while cytosine on one chain is always paired with guanine on the other. Other researchers had shown that DNA has a helical structure, so Watson and Crick called the structure a _double helix_ \u2014 a shape that looks like a spiral staircase.\n\nOne of the best outcomes of the identification of the double helix was that scientists understood how the genes copy themselves, or _replicate._ The helix can break apart into two strands. The two individual strands then each act as a template so that a new strand forms on each in the only way it can, by connecting to the only nucleic acid it can combine with \u2014 namely, a nucleic acid containing adenine connects to a nucleic acid containing thymine, and a nucleic acid containing cytosine connects with a nucleic acid containing guanine. The result is two new double helixes.\n\nThe DNA has to somehow control the creation of the animal or plant and the ongoing processes that allow it to live. The DNA does so by producing _ribonucleic acid,_ or RNA. RNA comprises nucleic acids just like DNA. But the sugar in RNA is ribose, and the bases are adenine, cytosine, and guanine, with uricil replacing thymine.\n\nIn the same way that the double helix can break apart to reproduce itself, it can break apart and construct a complementary RNA molecule. This process is called _transcription._ The RNA remains a single strand, not a double helix. The RNA is called _messenger RNA_ because it carries the message from the DNA to the next level of control, the _enzyme._ An enzyme is a protein that acts as a facilitator for a chemical reaction \u2014 for example, the breakdown of a complex carbohydrate like glycogen (the storage form of glucose \u2014 the body's source of immediate energy) into small glucose molecules that the body can instantly use.\n\nThe messenger RNA accomplishes its task by acting as a template in its turn for the production of the enzyme or protein in the process of _translation._ Proteins consist of amino acids. Every three bases in the messenger RNA, called a _triplet,_ causes one particular amino acid to line up opposite them. Each group of three is a _codon,_ because it codes for a specific amino acid. By making up artificial messenger RNA that contained the same codon again and again, determining which amino acid each codon selected became possible.\n\nWith 4 different bases in sets of 3, the maximum number of codons is 64, but only 20 amino acids exist. Different codons select the same amino acid, and some codons act as the code for the end of a protein without selecting an amino acid.\n\nJust to complicate the issue a little further, the amino acids don't actually line up opposite the codons but are carried at one end of another RNA molecule, called _transfer RNA._ At its other end, transfer RNA has the bases that are complementary to the codon. So the transfer RNA lines up neatly against the messenger RNA, while the amino acids line up next to one another at the other end. A series of other steps that you don't need to know to understand hereditary thyroid disease bind the amino acids into a protein that may be an enzyme or a muscle or whatever.\n\nGenes also contain large segments of bases that don't code anything and, in fact, have to be cut out from their complementary RNA before the RNA can produce a protein. These sequences are called _introns,_ and scientists don't know what their function is.\n\n## Determining whether to be a liver or a heart\n\nA fertilized egg reproduces itself by the process of mitosis, creating two identical cells. But how can each identical cell transform itself into a thyroid cell or a liver cell or even a brain cell?\n\nThe gene uses a number of techniques to turn gene action on and off. Short sequences of bases called _promoters_ precede the active gene. When various factors bind to a promoter, it turns on the action of the gene to begin transcription. Other sequences of elements called _enhancers_ increase the activity of the gene further, while _silencers_ tend to shut down the activity of the gene. The process of transcription from DNA to messenger RNA comes to a halt when certain sequences of bases are reached.\n\nBecause all cells contain the same genetic information, a thyroid cell differs from a brain cell as a result of the particular genes that are _expressed_ (active) in each cell. Many different factors determine whether a gene is expressed. Promoters and enhancers increase their activity in response to various hormones or growth factors that may be present in one cell but not another.\n\nThe expression of a gene may be controlled at the level of the gene itself, or it may be controlled after transcription has taken place so that the messenger RNA never makes the protein.\n\nIn these and in many other ways scientists have yet to discover, cells use only the genes they need to function within their environment.\n\n## Probing the Origins of Genetic Thyroid Diseases\n\nNow that you have a basic understanding of genetics, you can apply your knowledge to thyroid diseases that are transmitted through inheritance. A child inherits a thyroid disease in one of three basic ways:\n\n  A single gene from a parent transmits a dominant or recessive trait to the child. This method goes back to Mendel and his peas.\n\n  The child inherits all of the many genes involved in the inheritance of a disease.\n\n  An entire chromosome is abnormal. For example, if a female ends up with only one X chromosome, that lack can produce a condition known as _Turner's syndrome,_ which often includes a thyroid disorder.\n\n## Inheriting a disease through a single gene\n\nPeople inherit many diseases through a single gene, often as a result of a gene mutation, in one of three ways:\n\n  **As a recessive gene:** Both parents must supply the same gene in order for the disease to appear.\n\n  **As a dominant gene:** Only one parent supplies the gene necessary to cause the disease.\n\n  **With the X chromosome in a recessive form:** A male gets the disease (because he has only one X chromosome), but a female is spared unless both her X chromosomes have the gene.\n\nYou can find the entire list of diseases transmitted by single-gene inheritance at www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?db=OMIM, the homepage of Online Mendelian Inheritance in Man (OMIM), a huge database compiled by Dr. Victor McKusick at Johns Hopkins University and others. If you search the term \"thyroid\" from the homepage, 554 different thyroid diseases appear (at the time of this writing). A full description accompanies each one, with citations of all the research that has been done to define the defect and a complete bibliography at the end of each description.\n\nInherited thyroid diseases can affect every step in thyroid hormone production, transportation, and action. The ones I list in the following sections are only 14 of the 554 currently listed in the OMIM database. Scientists are discovering new conditions all the time. These 14 are the best understood.\n\n### Recessive inheritance\n\nMany conditions where the body doesn't make thyroid hormone properly fall into the category of recessive inheritance. Two \"bad\" genes are necessary to develop one of these conditions. If you have just one bad gene, you're a carrier of the disease, but you don't experience it yourself. The phenotype (the way this gene makes itself known) is usually a large thyroid that doesn't produce sufficient thyroid hormone. Note that several of the conditions appear to be the same because the final result of the condition is absence of thyroid hormone, but each condition involves a defect in a different step in the production of thyroid hormone. Among the conditions inherited this way are the following:\n\n  **A defect in the creation of the enzyme that produces thyroid hormone:** (see Chapter 4): Patients with this condition are hypothyroid (see Chapter 5) and have goiters.\n\n  **Thyroid hormone unresponsiveness:** If you inherit a bad gene instead of the gene that makes the receptor protein for thyroid hormone, your end organs aren't responsive to the thyroid hormone your body produces. This condition causes patients to be deaf and have goiters. With this condition, the T3, T4, and TSH levels are all elevated (see Chapter 4).\n\n  **Pendred syndrome:** Patients with this disease are deaf and have goiters, but their thyroid function is normal. The disease also causes mental retardation and an increased tendency to develop thyroid cancer. The defect is in the production of thyroid hormone, but at some point it improves so that hypothyroidism isn't present later on.\n\n  **Thyroid transcription\u2013factor defect:** Patients have goiters and decreased levels of thyroglobulin. If you remember that _transcription_ is the term for the production of messenger RNA from DNA, you understand that this defect arises from a failure to produce the enzyme necessary to make thyroid hormone.\n\n  **Defect in thyroid production:** This disease is different from thyroid transcription\u2013factor defect. Patients are hypothyroid, have goiters, and experience mental retardation. Lab tests show a defect in the formation of thyroid hormone. Normally, two molecules of tyrosine with iodine attached couple to form thyroid hormone, but this process fails in this particular inherited condition.\n\n### Dominant inheritance\n\nMany inherited thyroid conditions pass from parents to children through dominant inheritance: One \"bad\" gene produces the disease. These diseases tend to be more common than those inherited by recessive genes. Examples of diseases inherited this way are as follows:\n\n  **Thyroid hormone\u2013receptor defects:** A number of receptor defects are possible. With one of these conditions, your body is resistant to the action of thyroid hormones. At the same time, you experience mild hyperthyroidism. Patients with this condition have short stature, learning disabilities, deafness, and goiters. Lab tests show high levels of T3, T4, and TSH. These conditions are rare, resulting from a mutation in the gene responsible for the thyroid receptor. Another type of receptor defect produces a child with severe cretinism of the neurologic form (see Chapter 12).\n\n  **Papillary thyroid carcinoma** (see Chapter 8). This type of cancer usually occurs at an earlier age than thyroid cancer that's not inherited.\n\n  **Thyroid hormone resistance** (also found in a recessive form). Patients with this condition have a goiter and begin to speak at a later than expected age but have normal thyroid function. Lab tests show that T3 and T4 levels are high, but the TSH level is normal.\n\n  **Multiple endocrine neoplasia, type II:** This condition causes tumors on multiple organs, including the thyroid (see Chapter 8), the adrenal gland, and the parathyroid glands. Lab tests show increased levels of epinephrine and calcitonin in the blood.\n\n  **Medullary carcinoma of the thyroid, familial:** Patients with this condition have medullary cancer (see Chapter 8).\n\n### X-linked inheritance\n\nX-linked inheritance presents fewer examples of thyroid disease because men have only one X chromosome, and women have two, compared to 44 other chromosomes that can produce a disease by recessive or dominant inheritance. If a disease passed on by the X chromosome is recessive, both parents must give the gene to a daughter in order for the disease to appear. But a son gets the disease if only one parent passes along the gene. Because Y chromosomes are only present in males, Y-linked inheritance is only found in males, and it's rare because the Y chromosome is so small. Some examples of diseases inherited this way include\n\n  **Immunodeficiency and polyendocrinopathy:** A baby with this condition has unmanageable diarrhea, diabetes, and thyroid autoimmune disease and usually dies very young.\n\n  **Thyroid-binding globulin abnormality:** This condition produces retardation. Lab tests show that patients with this disease have decreased thyroid-binding globulin (see Chapter 3).\n\n  **Multinodular goiter:** The thyroid is larger than normal and multinodular (see Chapter 9).\n\n## Inheriting a disease through multiple genes\n\nThe major thyroid disease inherited as a result of abnormalities of multiple genes is _autoimmune thyroiditis._ This disease is much more common in women than in men, so you may assume that the inheritance is linked to the X chromosome somehow. But if this is the case, scientists don't know the method by which the X chromosome passes the disease along. One idea is that the female sex hormone influences the occurrence of this disease, but scientists don't understand just how this may happen.\n\nAutoimmune thyroiditis is easy to diagnose because lab tests show that a person has autoantibodies (see Chapter 5) that damage the thyroid. Many genes are involved in the production of autoantibodies. The substance (such as thyroid tissue) that provokes antibodies is called an _antigen._ The antigen is broken into small pieces that proteins called _major histocompatibility molecules_ bind to cells. This combination of cells and antigens leads to the activation of another cell called the _T cell._ The T cell helps yet another cell, the _B cell,_ recognize the antigen and produce antibodies against it. All these steps involve multiple genes.\n\nThe major histocompatibility region of the chromosomes is on the short arm of chromosome six. It is a set of genes that determines which antigens are found on white blood cells. These antigens are the _human leukocyte antigens_ (HLA). Scientists can identify the antigens chemically. In this way, scientists have shown that in whites, HLA-B8 and HLA-DR3 are the antigens associated with Graves' disease (see Chapter 6), while in Koreans, the DR5 and DR8 are most common. In Japanese, the antigen most associated with Graves' disease is DR5, and in Chinese, the DR9. All of this knowledge is important because doctors can test for these antigens in relatives of affected individuals. If the antigens are present, they're more likely to get the disease.\n\nAutoimmune thyroid disease really comprises three different conditions:\n\n  **Graves' disease:** This disease consists of hyperthyroidism, eye disease, and skin disease (see Chapter 6).\n\n  **Chronic thyroiditis:** This condition consists of goiter in a person with normal thyroid function or hypothyroidism (see Chapter 5).\n\n  **Myxedema:** This condition is severe hypothyroidism.\n\nWhen scientists examine the thyroid glands of patients with the preceding conditions, the appearance is amazingly similar despite the completely different clinical outcome. In addition, as the Dummy family shows throughout this book, different members of the same family can have one or the other of these conditions. And the same person can have one or the other of these conditions at different times. Which type of antibody a person's body is producing determines which condition is present. If an antibody that stimulates the thyroid is predominant, then Graves' disease is present. If antibodies that block thyroid-stimulating hormone are predominant, then chronic thyroiditis or myxedema is present.\n\nThe greater occurrence of other autoimmune conditions in people with autoimmune thyroiditis strengthens their autoimmune basis for this disease. These other autoimmune conditions include the following:\n\n  **Myasthenia gravis:** A disease of muscle weakness that activity worsens and rest improves, resulting from an autoimmune attack at the place where nerves and muscles come together.\n\n  **Pernicious anemia:** A reduction in red blood cells caused by a lack of _intrinsic factor,_ a substance made in the parietal cells of the stomach that's essential for absorbing vitamin B12 into the body. An autoimmune attack destroys the parietal cells.\n\n  **Vitiligo:** A loss of pigmentation of the skin caused by autoimmune destruction of _melanocytes,_ the cells that produce pigmentation.\n\n  **Type 1 diabetes mellitus:** (See my book _Diabetes For Dummies,_ 2nd Edition __ [Wiley].) __ A disease caused by excessive levels of glucose in the blood as a result of an autoimmune attack on the pancreas, which makes insulin, the chemical that controls the blood glucose.\n\n  **Addison's disease:** Failure of the adrenal gland to produce hydrocortisone as a result of an autoimmune attack on the hydrocortisone- producing adrenal cells.\n\n  **Alopecia areata:** Patchy loss of hair in any part of the body, caused by an autoimmune attack on hair follicles.\n\n  **Ovarian failure:** Loss of function of the ovaries, resulting in infertility on account of an autoimmune attack on the ovarian follicles, the structures that nurture the eggs.\n\n  **Testicular failure:** Loss of fertility as a result of autoimmune attack on the sperm in the testicles.\n\n  **Pituitary failure:** Loss of function of the pituitary gland with failure to make the hormones that stimulate other glands, including the thyroid, the adrenal gland, and the ovaries and testicles, as a result of autoimmune attack on pituitary cells.\n\n  **Rheumatoid arthritis:** Systemic lupus erythematosis and Sjorgren's syndrome, all examples of autoimmune attacks on the joints of the body.\n\nWhew! That's really quite a list. But don't worry. The chances that you'll get any of the preceding conditions in combination with your autoimmune thyroid disease are quite small, though greater than if you don't have the thyroid condition.\n\nThyroid autoantibodies are also present in several other clinical conditions, but whether they're the cause of these conditions or represent a marker for a disturbance in autoimmunity that's to blame isn't clear. These clinical conditions are as follows:\n\n  Increased risk of miscarriage in women attempting to become pregnant by in-vitro fertilization\n\n  Breast cancer\n\n  Depression in middle-aged women\n\nAnother disease that's found more often in people with certain human leukocyte antigens is postpartum thyroiditis (see Chapter 11). In whites, the antigens are HLA, DR3, DR4, or DR5, while in Chinese, the antigen is DR9. The antigens are not certain for other ethnic groups.\n\n### Antigens in autoimmune thyroiditis\n\nA number of antigens are present in autoimmune thyroiditis against which antibodies are formed, but three antigens are most important.\n\n  **Thyroglobulin** is the substance within the thyroid that contains thyroid hormones T4 and T3. Not just one kind of thyroglobulin exists, but different kinds in different people. Thyroglobulin is also present in tissue in the eye. Some of the eye disease of Graves' disease may be due to the reaction of antibodies against thyroglobulin in the eyes.\n\n  **TSH receptor,** the second antigen, is the substance on the thyroid cell to which TSH binds in order to stimulate the thyroid. Antibodies to TSH receptor bind to it and cause hyperthyroidism by acting like TSH.\n\n  **Thyroid peroxidase,** which used to be called antimicrosomal antigen, is the third important antigen. As its previous name implies, scientists found it in a part of the thyroid cell called the microsome. Its antibody is the most easily measured thyroid antibody and is most often positive in autoimmune thyroiditis.\n\n## Inheriting a chromosome abnormality\n\nDuring the creation of a zygote, as new cells are being formed, a mistake can occur in the division of the chromosomes into the two new cells \u2014 one cell ends up with an extra chromosome, and the other ends up with one less chromosome. The most well-known conditions associated with this kind of chromosome mistake are Turner's syndrome and Down's syndrome. Both conditions are associated with hypothyroidism, but Down's syndrome is also associated with hyperthyroidism on occasion.\n\nDown's syndrome results when the new cells have an extra chromosome \u2014 they have three copies of the 21st chromosome instead of two. People with this condition have a typical physical appearance with characteristic facial features that are recognizable at birth. Children with Down's syndrome have palms that have a single crease, and their muscles lack tone. Reduced intelligence and other abnormalities are part of this syndrome.\n\nTurner's syndrome results when an X chromosome is left behind so that a female is born with a single sex chromosome. The woman has distinctive facial features, including low-set ears, folds of skin in the inner corner of the eye, and drooping eyelids. The woman also may have diabetes mellitus, cataracts, rheumatoid arthritis, and cardiac abnormalities in addition to chronic thyroiditis.\n\n## Viewing the Future of Managing Hereditary Thyroid Disease\n\nUp to now, scientists haven't been successful in their attempts to remove a \"bad\" gene from a human and replace it with a healthy gene \u2014 a process known as _genetic engineering._ The problem is that they don't yet know how to insert the new gene successfully. If scientists can determine how to do so, they can open the door to preventing diseases that people inherit through a single gene.\n\n## Genetic engineering\n\nIf a recessive gene causes a disease, replacing that gene with its dominant form in sufficient amounts should be enough to cure the condition. Usually in a recessive-gene disorder, the disease occurs because that particular gene isn't functioning at all, so providing even a small level of function may cure the condition.\n\nThe disorders that may most easily respond to genetic engineering are disorders of the blood system, because doctors and scientists may easily remove blood. A new gene can be spliced into the cells and the blood reintroduced to the patient. The first trial of gene therapy, performed in 1990, was for a disorder that resulted in severe loss of immunity so that the patient was very susceptible to any infection, as well as a cancer. Scientists were able to introduce the necessary gene into the blood cells of the patient by connecting the gene to a virus, which infected the cells and added the gene to their DNA. The cells were grown to increase their number and reinserted. Unfortunately, the trial didn't work, probably because the efficiency of splicing the gene into the cells was low.\n\nOther genetic disorders for which trials of gene therapy have taken place include\n\n  **Familial hypercholesterolemia:** Excessive production of cholesterol leads to early death by heart attack.\n\n  **Cystic fibrosis:** Lack of a certain gene leads to excessive production of a thick mucous in the lungs, resulting in chronic lung infection.\n\n  **Duchenne muscular dystrophy:** Severe muscle deterioration leads to the individual dying by the third decade of life.\n\nA trial of gene replacement in all three of these conditions has been unsuccessful.\n\nAnother novel way of managing diseases caused by defective genes is to find a gene that's active during fetal life (but becomes dormant later on) and that can replace the activity of the defective gene if it can be made to express itself. A prime candidate for this treatment is sickle cell disease. In this disease, abnormal hemoglobin (hemoglobin is the chemical in red cells that carries oxygen to the tissues of the body) leads to the early loss of red blood cells, which become sickled (crescent shaped) in appearance and can block blood flow to tissues, causing great pain. A gene active during fetal life produces fetal hemoglobin, which doesn't sickle. If this gene can be turned on during adult life, it can replace the defective hemoglobin made by the patient. Scientists are looking for the drug that may be able to turn this gene on.\n\nCancer treatment has seen a lot of activity in the area of gene therapy. Gene therapy can treat cancer of the thyroid in a number of ways, including the following:\n\n  Inserting a gene that increases the sensitivity of the cancer to a drug, or inserting a poison into cells that are injected directly into the tumor.\n\n  Inserting a gene that increases the activity of the patient's immune system.\n\n  Inserting a new gene into blood cells to restore tumor-suppressor activity. This treatment works because some tumors arise when the activity of tumor suppressors (chemicals in the body that suppress the growth of tumors) declines.\n\n  Using a virus to introduce a gene into a thyroid cancer cell. The virus causes the DNA to change so that the cell takes up radioactive iodine, which can kill the cell. (This approach is the newest cancer treatment and is outlined in a paper in _Thyroid_ in June 2004.)\n\nAll these treatments have seen some success, but no one has yet been cured of cancer with gene therapy.\n\nScientists are also attempting to increase a tumor's immune response by modifying the tumor so that it provokes body cells against it. Scientists perform this technique by inserting genes into the tumor that cause it to produce new antigens that the body can fight against. Tumors like malignant melanoma and colon cancer have been the target of this type of therapy. A similar technique involves inserting a gene directly into a tumor that activates a cancer-killing agent, which is subsequently injected. These techniques have led to some decrease in tumor size but, so far, no cures of cancer. Interestingly, gene therapy isn't limited to tumors brought on by faulty genes but can be directed at any tumor, genetic or not.\n\n## Exploring the ethics of germline gene therapy\n\nYou can see that the range of techniques for using genetic engineering to cure disease is enormous. Scientists are discovering new methods of delivering healthy genes to replace disease-conferring genes as you read this book. This approach would certainly be the simplest and most successful way of treating the diseases provoked by inheritance of a single dominant gene. However, this type of treatment would cure only the particular individual without affecting the transmission of the disease to his offspring. To eliminate the disease from future generations, genetic engineering has to take place in the sperm and\/or the egg, the _germline_ of the individual.\n\nGermline gene therapy raises tremendous ethical questions. If we have the tools for eliminating the recessively inherited Pendred syndrome by replacing a Pendred gene with a normal gene, don't we also have the tools for changing skin color, height, or any other body characteristic in future generations? An entire field of genetics concerns _ELSI,_ the ethical, legal, and social implications of genetic science.\n\nSo far, germline gene therapy has actually been successful in some animals, but hasn't been done on humans for several reasons:\n\n  The methods used so far are very imprecise, so the final product is uncertain, including the possible introduction of harmful genes.\n\n  Many people fear that germline gene therapy may lead to germline enhancement, an attempt to produce a \"superior\" human being.\n\n  Whether germline gene therapy is even needed is uncertain, because a harmful recessive trait requires mating with another human with the same trait to express itself, while dominant traits are present in only half of a germline. Identifying the sperm or egg with the normal gene and using that gene in fertilization makes more sense than trying to modify the sperm or egg with the abnormal gene. Scientists should perform genetic testing of the germline if they are to eliminate these diseases.\n\nClearly, genetics is the current frontier in medical science. Genetics promises to prevent or cure many of the diseases that plague humans, including hereditary thyroid disease and nonhereditary tumors. But the road to those cures and preventions is full of cracks and bumps that assure a very uneven ride.\n\n##### Chapter 15\n\n## The Thyroid and Your Mental Health\n\n### In This Chapter\n\n  Discovering that you're not alone\n\n  Coping with an underactive thyroid\n\n  Understanding the psychology of an overactive thyroid\n\n  Finding thyroid problems in depressed people\n\n  Using thyroid drugs to treat depression\n\nThe term _myxedema_ _madness_ may not be familiar to you, but it was popular when it was introduced in 1949 and for many years thereafter. _Myxedema_ refers to low thyroid function, or hypothyroidism. The term _myxedema madness_ resulted in the unfortunate association that all people with low thyroid function were somehow mad. My goal in this chapter is to clear up this misconception.\n\nThe abnormal production of thyroid hormones, which I explain in Chapter 3, can cause changes in the mood of a patient, and these changes can be severe in rare instances. But for most patients, simply treating their overactive or underactive thyroid allows them to live psychologically and physically normal lives.\n\nIn this chapter, I share what doctors currently understand about how changes in the production of thyroid hormones (both overproduction and underproduction) affect your personality. You discover how often personality or mood disorders are associated with thyroid abnormalities and why thyroid hormones play a role in the treatment of depression, even when no thyroid problem exists. Because the emphasis in this chapter is on the psychology of thyroid abnormalities, I don't discuss physical signs and symptoms here; those discussions occur elsewhere in the book, especially in Chapters 5 and 6.\n\n## The Underactive Thyroid and Your Mood\n\nSarah Dummy is a 44-year-old woman who hasn't been herself for several months. Her husband, Milton, notices that she is much less talkative than before. She often forgets to pick up the food that they need at the supermarket or to stop at the dry cleaner's to pick up clothes she dropped off.\n\nMilton wants to discuss a vacation with Sarah, but she doesn't seem to care. Sarah is usually the one responsible for making plans with their friends, but she hasn't made any for months. Everything she does seems to take more time than it used to, like preparing dinner or getting ready to go to bed. When she finally gets in bed, she isn't particularly interested in having sex anymore. The most serious change is that Sarah, usually a happy person, seems sad a lot of the time.\n\nWorried about these changes, Milton encourages Sarah to see Dr. Rubin, who examines her and sends her for some lab tests. A few days later, Dr. Rubin tells Sarah that she has hypothyroidism \u2014 her thyroid gland isn't making enough thyroid hormone. He gives her a prescription for replacement thyroid hormone, and about a month later Sarah is well on her way to becoming her old self. Milton is happy because he has clean underwear again.\n\nSarah is an excellent example of the changes in personality that occur when the body doesn't produce enough thyroid hormone. Depending on the level of the deficiency, the changes are more or less severe and include the following:\n\n  Decreased talking\n\n  Memory loss, especially for recent events at first, and for remote events later on\n\n  General loss of interest\n\n  Inability to concentrate\n\n  Withdrawal from society\n\n  A general slowing of movement and thought\n\n  Depression, generally mild but sometimes severe (see the \"Fighting Depression\" section, later in the chapter)\n\n  Loss of interest in sex\n\n  In severe cases, a kind of ironic sense of humor\n\nPatients and doctors can easily confuse many of the preceding complaints, which are nonspecific and poorly defined, with depression. For this reason, both patients and doctors can easily miss their significance.\n\nNo one or group of the preceding mental changes means that you definitely have low thyroid function, but they certainly suggest that you need testing to find out.\n\nIf your doctor determines that lack of thyroid hormone is the cause of your symptoms, then the right dose of hormone replacement should reverse them. If it doesn't, then you and your doctor need to look elsewhere for the cause, which may be underlying depression. See Chapter 5 for a thorough discussion of hypothyroidism.\n\nAny person over the age of 60 who has a psychosis and reduced mental ability should receive testing for possible thyroid disease.\n\nAnd keep in mind the following additional hypothyroid\u2013mental illness related issues:\n\n  Occasionally, a patient who has schizophrenia has hypothyroidism. Giving thyroid pills may not completely cure the patient, because some changes may be irreversible.\n\n .jpg)\n\n  If a patient with manic-depressive psychosis caused by hypothyroidism receives lithium, the lithium may make the problem worse because it causes hypothyroidism as well.\n\n### The most severe mental symptoms \u2014 historical notes\n\nYears ago \u2014 I'm talking about more than 50 years ago \u2014 doctors saw patients with much more severe and longstanding cases of hypothyroidism and hyperthyroidism than we see today.\n\nAt one time, doctors saw many more hypothyroid individuals with decreased accuracy of perception that led to visual and other hallucinations. Still later, bizarre behavior appeared. Patients showed increasing drowsiness, difficulty in arousal, sleeping for long periods, and finally coma followed by death if they didn't receive treatment for their hypothyroidism.\n\nDoctors found hyperthyroid patients with huge thyroid glands who were visibly shaky and nervous, unable to sit still for more than a few moments, resembling mania. Such severe hyperthyroidism very rarely happens now, because doctors usually diagnose the condition earlier, but rare cases of severe, prolonged hyperthyroidism may result in hallucinations, both in vision and hearing. In fact, a severely hyperthyroid patient first caused me to become very interested in thyroid disease. She had a large goiter, and I saw her in the medical psychiatric ward during my training days at Bellevue Hospital Medical Center at New York University School of Medicine.\n\nBut doctors rarely see patients suffering from such severe symptoms today, and the medical literature and descriptions of such cases relies on the observations of people living in a very different society fifty or more years ago.\n\n## Overactivity of the Thyroid and Your Mind\n\nSarah Dummy's sister, Margaret, who is five years younger, began showing some big personality changes a few years ago. Previously a fairly even- tempered person, she now becomes easily excited and loses her temper after fairly mild provocation. Her small children never know when their mother is going to yell at them. She sometimes has a crying spell but, if asked, can't give a reason why.\n\nAt other times, Margaret is extremely happy, but she can't explain the reason for that either. When she tries to do a task, she often loses interest rapidly and gets distracted. She can't sit still for very long and seems to be always moving. Her memory of recent events is poor.\n\nMargaret and her husband, Fred, go to see Dr. Rubin about her condition after a few months of absolute chaos in their home. During an examination, Dr. Rubin discovers a number of physical findings, including a rapid pulse, a large thyroid gland, and a fine tremor of Margaret's fingers. He confirms his findings with lab tests (see Chapter 4). Two days later, he tells the concerned pair that Margaret is suffering from hyperthyroidism \u2014 her body is producing too much thyroid hormone. He begins treatment with medication, and in three weeks a definite change begins to occur. After six weeks, Margaret is just about back to normal. Margaret and Fred take the kids to Lollipop Land to make up for all the yelling.\n\nMargaret is an excellent example of the psychological changes that occur when the body produces excessive levels of thyroid hormone. Some of these changes are\n\n  Increased excitability and agitation\n\n  Anxiety\n\n  Impaired concentration\n\n  Insomnia\n\n  An emotional roller coaster of moods\n\n  Outbursts of anger for no reason\n\n  Crying spells\n\n  A tendency to get easily distracted\n\nPsychiatric illness is present in about 10 percent of patients with hyperthyroidism.\n\nOther conditions seem to be indicators of hyperthyroidism but turn out not to be when doctors perform thyroid function tests. They include\n\n  **An anxiety state or neurosis:** A compulsion to do something continuously like washing the hands, cleaning the windows, or making certain sounds or an extreme and unrealistic fear are examples.\n\n  **Panic attacks:** Panic attacks are associated with rapid heart rates that mimic hyperthyroidism.\n\n  **Thyrotoxicosis factitia:** This is a condition of false hyperthyroidism brought on by secret ingestion of thyroid hormone, usually by nurses. This is a psychiatric disorder.\n\n  **Mania:** Characterized by extreme excitability and excessive activity.\n\nWhen hyperthyroidism affects elderly people (who I define as anyone older than I am), the condition may actually look like hypothyroidism. An elderly patient with hyperthyroidism may feel sad and depressed, apathetic, and withdrawn from society. I explain how thyroid problems affect the elderly in Chapter 19.\n\nThe treatments for hyperthyroidism, which I describe in Chapter 6, are very effective in reversing all the mental and physical symptoms, particularly in younger people who often get the disease. If the mental symptoms are present long enough, however, curing the hyperthyroidism may not cure the manic state.\n\nStress is sometimes blamed for bringing on hyperthyroidism, but little objective evidence supports this claim. Hyperthyroidism may precede stress. Most people who live through severe stress don't develop hyperthyroidism. However, some evidence suggests that patients with established hyperthyroidism may do better if they're able to handle stresses that come along while they're receiving treatment and afterward. If they're able to handle the stress, then relapse is less likely.\n\n## Fighting Depression\n\nDepression may be a symptom of a lack of thyroid hormone. On the other hand, thyroid hormone may help in the treatment of depression, even when tests indicate that the patient has enough thyroid hormone. The following sections explain the role that thyroid hormone plays in depression.\n\n## Determining if the thyroid is the cause\n\nDepression is a prominent symptom of thyroid disease, especially hypothyroidism. Therefore, when someone receives a diagnosis of depression, determining whether a thyroid disease is the cause is important.\n\nStudies show that most depressed people don't have hypothyroidism. How- ever, the condition may be present in a mild form in as many as 20 percent of depressed people, more often in women than in men. If a person receives a diagnosis of hypothyroidism, a doctor should determine whether the patient is taking a drug for treatment of depression that may actually be causing hypothyroidism (see Chapter 10). Two such drugs are lithium and carbamazepine.\n\nIf a drug is responsible for hypothyroidism, a person has two options. The patient can stop taking the drug, in which case its contribution to the depression disappears, but the patient may still be depressed for other reasons. Alternately, the patient can receive thyroid hormone as treatment if the doctor feels that the drug is helping the depression a great deal and no substitute exists.\n\nIf you're receiving treatment for depression and haven't had thyroid function tests, ask your doctor to perform them.\n\n### TSH, autoantibodies, and depression\n\nThyroid abnormalities are often associated with other chemical changes in the blood besides too much or too little thyroid hormone. A patient with hypothyroidism, for example, may have too much thyroid-stimulating hormone (TSH) or high levels of thyroid autoantibodies, both of which I explain in Chapter 3. Could these other chemical changes promote depression in some patients?\n\nDoctors haven't yet found a correlation between levels of TSH and thyroid autoantibodies and depression. Patients may sometimes have high autoantibodies while their thyroid function is normal, in which case they don't experience thyroid-related depression. The level of TSH in the blood doesn't seem to impact depression either.\n\nCurrent research indicates that the level of the thyroid hormones themselves affects mood, and the levels of TSH and thyroid autoantibodies don't.\n\n## Using thyroid hormone to treat depression\n\nMany doctors believe that replacement thyroid hormone has a role in the treatment of depression, even when no thyroid abnormality is present.\n\nGiven by itself, thyroid hormone doesn't seem to reverse depression in a patient who doesn't have a thyroid disease. However, when a patient takes the thyroid hormone _triiodothyronine_ (see Chapter 3) together with antidepressants, it can improve the effectiveness of the treatment. This is especially true when a patient is taking a class of drugs called _tricyclic antidepressants,_ which have brand names like Elavil, Tofranil, Etrafon, Norpramin, and Sinequan. The thyroid hormone is particularly effective in turning people who don't respond to tricyclic antidepressants into responders. It also increases the effectiveness of those drugs when they do work.\n\nWhen used to help treat depression in patients who don't have thyroid disease, the patient can stop taking the thyroid hormone after a few weeks or months, and the positive effect persists.\n\n##### Chapter 16\n\n## What's New in Thyroid Treatment?\n\n### In This Chapter\n\n  Managing hypothyroidism\n\n  Zeroing in on the right dose of hormone\n\n  Treating hyperthyroidism\n\n  Shrinking nodules and goiters\n\n  Understanding antithyroid drugs\n\n  Dealing with thyrotoxic periodic paralysis\n\n  Overcoming thyroid cancer\n\n  Correcting iodine deficiency\n\nIn November 2005, I visited PubMed, an online search page of the National Library of Medicine (www.pubmed.gov), and did a search for \"thyroid disease.\" The result was more than 9,500 citations to studies done by thousands of scientists that were published in medical journals since the first edition of this book. (Thousands more studies were offered for publication but didn't get into the journals for one reason or another.) This research represents the cutting edge of medicine. But how do you stay on the cutting edge without slipping and getting sliced up? One of the reasons you bought this book is so I can do the work of sifting through the research for you.\n\nIn this chapter, you find a selection of the most important discoveries in thyroid medicine during the last couple years. Some discoveries are single studies of a subject that a similar study can revise or even overturn. You have to keep an open mind when new (and not necessarily validated) material presents itself in the future.\n\nKnowing something about the observer is equally important as knowing what someone is observing. For instance, one of the studies about whether thyroid nodules shrink when a doctor gives a patient thyroid hormone points out that two different observers differ by as much as 50 percent in their observation of the size of the same thyroid nodule. So any change less than 50 percent can be observer \"error\" as much as it can be true change.\n\nFurthermore, some observers have a self-interest in what they're observing. Unfortunately, the drug or equipment companies pay for most studies of new drugs and techniques that require special equipment. Is it likely that these companies will continue to fund researchers who constantly come up with negative findings? The best studies are those that aren't connected to specific companies, but knowing which studies don't have such connections is sometimes hard. So don't be surprised if today's magic cure-all turns out to be tomorrow's source of major side effects.\n\nEven with no observer bias, results that are excellent when a drug is tested on a few hundred or thousand people may be very different when hundreds of thousands of people begin to use the drug.\n\nAs I write this chapter, researchers are studying just about every aspect of thyroid disease, with articles in every medical journal andnew findings that are getting ready to join the thousands of studies before them. Being up to the minute in a book isn't possible given the constraints of a publishing deadline and the amount of information coming out. If you have a particular problem that concerns you or a loved one, don't hesitate to use the enormous amount of free resources at your disposal. Go to the PubMed Web site (www.pubmed.gov), or check out your local bookstore and hospital library. And be sure to utilize the references you find in Appendix B of this book.\n\n## Treating Subclinical Hypothyroidism\n\nOne of the great debates in thyroid management is what to do about _subclinical hypothyroidism,_ condition in which the patient's TSH level is slightly elevated (say to 6 or 7), the free T4 level is normal, and the patient has some nonspecific symptoms that can be the result of hypothyroidism or something else. Doctors have been studying these patients, looking for signs of low thyroid function or a response to thyroid medication, because they aren't sure whether treatment is necessary.\n\nOne study from Italy, published in the _Journal of Clinical Endocrinology and Metabolism_ in March 2001, looked at the function of the heart in 20 people with subclinical hypothyroidism, all of whom showed some abnormality in heart activity. Half of the study participants were given thyroid treatment, and the other half were given a placebo. The study found that people given the thyroid-treatment drug showed an improvement in heart function, while those given a placebo showed no change. The study concluded that people with subclinical hypothyroidism have measurable abnormalities that thyroid treatment improves.\n\nAnother study from Germany, published in _Thyroid_ in August 2000, looked at heart disease and heart attacks in patients with subclinical hypothyroidism. The author of the study found that these patients sustained a definite increase in heart disease and heart attacks over patients without the condition. Various tests of normal heart function, such as changes in heart rate with exercise, indicated that those functions were impaired in people with subclinical hypothyroidism. The most at-risk people were women over age 50 who smoked and had TSH levels greater than ten. Giving the study patients thyroid medication improved these functions and also improved the levels of fats in the blood. The author of this study felt that these changes justified the use of thyroid treatment in subclinical hypothyroidism. He noted, however, that giving a patient thyroid-replacement hormone tends to speed up the heart rate and may worsen chest pain, which doctors must consider when treating someone with this condition.\n\nA more recent study in the _Annals of Family Medicine_ in July 2004 provides further evidence that patients with subclinical hypothyroidism probably don't need treatment. The authors of the study looked at people who didn't have a diagnosis of hypothyroidism and weren't taking thyroid pills. They found that a subgroup of those people had subclinical hypothyroidism, which they defined as a TSH between 6.7 and 14.9 with a normal thyroxine (T4). The authors looked at the fat levels of these patients and found that although they had slightly more total cholesterol, their levels of HDL cholesterol (good cholesterol) and LDL cholesterol (bad cholesterol) as well as triglyceride were no different from people with normal TSH levels. Even the levels of total cholesterol weren't different in the two groups when adjusted for age and sex. The authors' conclusion was that subclinical hypothyroidism doesn't need to be treated, as least as far as treating to benefit fat levels in the body. They raised the possibility that other abnormalities may benefit from treatment.\n\nThis remains a very controversial topic. At this time, my bias is to treat subclinical hypothyroidism since on balance the evidence suggests that these patients suffer heart abnormalities that are improved by thyroid hormone treatment.\n\nIf you have subclinical hypothyroidism, you and your doctor should look carefully for subtle evidence of low thyroid function and treat the condition with thyroid-replacement hormone if you find such evidence. Then determining whether thyroid hormone makes a difference in those subtle findings becomes important.\n\n## Finding the Right Dose of Hormone\n\nA question that keeps coming up among doctors who treat hypothyroidism is \"What is the correct dose of thyroid medication?\" Some physicians believe that lowering a patient's level of thyroid-stimulating hormone (TSH) to under five is sufficient to eliminate signs and symptoms of low thyroid function, but many patients are still symptomatic at that level. In a study published in the _Medical Journal of Australia_ in February 2001, the authors show that lowering the TSH to between 1\/3 and 2 may be beneficial.\n\nRecent examinations have taken place of the question of whether combined T4 and T3 is better treatment for hypothyroidism than T4 alone. A report in the _Journal of Clinical Endocrinology and Metabolism_ in May 2005 evaluated all the carefully controlled studies comparing treatment with T4 and T3 to T4 alone. Nine studies met the authors' of the report's criteria, which was that the studies were double-blind (neither the patient nor the doctor knew what the patient was getting). Only one study found that the patients given both hormones had improved mood, quality of life, and psychological measurements compared with T4 alone. Later studies didn't confirm this study. The authors conclude that no evidence supports that combined T4 and T3 have advantages over T4 alone in treating hypothyroidism.\n\nIf you're being treated for hypothyroidism and still have symptoms when your TSH level is between three and five, ask your doctor to treat you to lower that level. I believe that doing so will improve your health.\n\n## Dealing with Hyperthyroidism\n\nDespite the availability of several treatments for hyperthyroidism (see Chapter 6), specialists aren't satisfied with any of them. Each treatment is associated with either frequent failure or undesirable side effects like hypothyroidism. The search for better therapy continues.\n\nA study published in January 2001 in the _Journal of Clinical Endocrinology and Metabolism_ emphasizes the importance of measuring calcium levels of patients with thyroid conditions, especially hyperthyroidism. This German study shows that after thyroid surgery, _hypoparathyroidism_ \u2014 the loss of parathyroid function \u2014 frequently occurs and leads to low calcium levels. (A high calcium level, on the other hand, may be caused by _hyperparathyroidism_ \u2014 excess parathyroid function. In this study, excess parathyroid function was also relatively common in association with thyroid disease.)\n\nBoth decreased and increased parathyroid function occur at a higher rate in patients with hyperthyroidism than in people who don't have thyroid disease. If you have hyperthyroidism, be sure to have your calcium level checked regularly.\n\n## Connecting hyperthyroidism and the heart\n\nPeople with hyperthyroidism have an increase in heart disease and death. The main types of heart disease are heart failure and blood clots from the heart. Thyroid hormone has many effects on the heart, including the following:\n\n  Increased heart rate\n\n  Increased force of the heart\n\n  Increased flow of blood from the heart\n\n  Increased consumption of oxygen by the heart muscle\n\n  Enlarged heart\n\n  Decreased diastolic blood pressure\n\n  Decreased blood-vessel resistance\n\nBecause of the preceding effects, especially in patients who have other heart problems, diagnosing and treating hyperthyroidism as early as possible is important. These abnormalities lead to a number of symptoms and signs. The most important are as follows:\n\n  Feeling that the heart is beating rapidly\n\n  Intolerance to exercise\n\n  Shortness of breath on exertion\n\n  Rapid heart rate\n\n  Atrial fibrillation (a very irregular rhythm of the heart)\n\nIn the elderly, atrial fibrillation may be the only sign of hyperthyroidism. An elderly person with atrial fibrillation should always be tested for hyperthyroidism.\n\nBlood clots are a major complication of atrial fibrillation and should be prevented by _anticoagulation,_ administration of a drug that prevents clots.\n\nSubclinical hyperthyroidism, where the T4 is normal but the TSH is low, is also associated with heart problems, including a rapid heart rate, reduced tolerance to exercise, and atrial fibrillation. Subclinlical hyperthyroid patients, especially those over 60 with other heart problems, need to receive treatment to make the TSH normal. But atrial fibrillation, if present, won't always return to a normal heart rhythm after treatment.\n\nAmiodarone, as I note in Chapter 12, can also induce hyperthyroidism, increasing the blood-iodine level 40 times. If the patient was previously deficient in iodine, the result may be hyperthyroidism. As a result of its other properties, amiodarone can conceal hyperthyroidism. Amiodarone also stays in the body long after it's stopped, so hyperthyroidism can occur months later.\n\nThe best treatment for amiodarone-induced hyperthyroidism is to stop the amiodarone. Other treatments may be more helpful for maintaining a normal heart rhythm and can replace the amiodarone. Scientists are investigating other compounds that work as well as amiodarone but don't contain iodine.\n\n## Exploring hyperthyroid eye disease\n\nSevere hyperthyroid eye disease, though rare, can lead to blindness. Just exactly why hyperthyroid eye disease occurs isn't clear, but researchers generally believe that it has a basis as an autoimmune disorder (see Chapter 4). One suggestion is that thyroglobulin enters the muscles of the eyes, and antibodies react against it. A study from Italy in the journal _Thyroid_ in 2001 showed that thyroglobulin can, indeed, be found in the muscle tissue of the eyes. The study demonstrated that the thyroglobulin originated in the thyroid gland, which confirms that the autoimmune reaction in the thyroid is very similar to the autoimmune reaction in the eyes. The findings of the study help bolster the argument in favor of using anti-immunity therapy for hyperthyroid eye disease, as I discuss in Chapter 6.\n\nHyperthyroid eye disease has a very negative impact on quality of life, even when it's moderate, which is usually the case. Severe eye disease occurs less than 5 percent of the time, but treatment works in only two-thirds of patients. The eye disease goes through three phases:\n\n  **First phase:** High activity with redness of the eye, pain, tearing, and sensitivity to light.\n\n  **Second phase:** Stabilization of the signs and symptoms.\n\n  **Final phase:** Improvement of the eye disease, which becomes inactive.\n\nThe duration of these phases varies, but the eye disease burns out within a couple of years. Steroids are helpful during the first active phase.\n\nSteroids given intravenously are more effective than steroids by mouth for thyroid eye disease. Steroids can be injected right into the muscles around the eye and are effective there. Doctors give IV steroids in very high amounts, which can cause liver damage. IV steroids are effective about 90 percent of the time, while liver damage occurs only 1 percent of the time.\n\nIf steroids aren't successful, then doctors perform orbital radiation therapy. This therapy is successful about 60 percent of the time. Using both steroids and orbital radiation at the same time is even better than either alone.\n\nRecent studies of other therapies, including drugs called somatostatin analogs and antioxidants, haven't shown that these therapies are effective. Antioxidants may be useful for mild eye disease but not moderate or severe forms.\n\nThree factors are definitely important in the progression of hyperthyroid eye disease, and should be managed as strongly as possible:\n\n  **Cigarette smoking:** Cigarette smoking not only promotes the development of eye disease but blocks the effectiveness of steroid and orbital\u2013 radiation therapy treatments. Quitting smoking is probably the most important preventive measure in this disease.\n\n  **Active thyroid dysfunction:** Active thyroid dysfunction, whether hyperthyroidism or hypothyroidism, promotes the progression of eye disease. Both conditions need to be corrected as soon as possible.\n\n  **Radiation therapy:** This hyperthyroidism treatment causes progression of the eye disease as well. A course of steroids can prevent this progression.\n\n## Assessing Goiters and Nodules\n\nGoiters and nodules remain a very common problem in thyroid medicine. Newer studies are changing how doctors manage patients with these conditions. Ultrasound studies pick up nodules in the necks of as many as 67 percent of people who don't have a nodule by physical examination.\n\n## Differentiating benign from malignant nodules\n\nThe fine-needle biopsy remains the best way to diagnose a thyroid nodule, but it's much more effective when guided by ultrasound, especially when the nodule is very small (less than 1.5 centimeters in size). The fine-needle biopsy guided by ultrasound permits a correct diagnosis of cancer 60 percent of the time compared to 40 percent when not guided by ultrasound.\n\nIt's not possible to make a definite diagnosis about 10 percent of the time with fine-needle biopsy. Of these 10 percent, only 15 percent turn out to be cancers. The problem is how to pick out that 15 percent that will need surgery; the other 85 percent can be followed medically. Two chemical markers have recently shown some promise in telling the difference. Doctors can assess both of these chemical markers in the clinical laboratory. They may become generally available if they prove their success in further studies. The two chemical markers are as follows:\n\n  **Human bone marrow endothelial cell-1:** This chemical is an antibody that seems to be specific for thyroid malignancy. When cells are exposed to this antibody attached to a substance that causes staining, strongly positive staining occurs for the papillary and follicular cancers, but little or no staining for benign tissues.\n\n  **Galectin-3:** Galectin-3 is found in tissues of patients with thyroid cancer but not in those with nonmalignant thyroid tissue. Cancerous tissues stain positive for galectin-3, and those that aren't don't stain. Ninety-five percent of tumors stain positive. Very few malignant thyroid glands don't have this marker.\n\nDoctors can watch and restudy small thyroid nodules less than 1.5 centimeters (0.6 inches) that high-resolution ultrasound discovers. Most of the nodules are \"incidentalomas,\" with no clinical significance. The decision as to whether they should be biopsied is still controversial. My opinion is that careful monitoring with high-resolution ultrasound is sufficient because most of the nodules, even if they turn out to be microcancers, don't change in size over five years.\n\nRecent studies have taken up the question of whether to measure calcitonin routinely to diagnose medullary thyroid cancer. This cancer makes up only 5 percent of thyroid cancers. Calculations suggest that screening routinely costs $20,000 to pick up one malignancy. If the level of the calcitonin isn't high enough to make a definite diagnosis, the cost for more testing is even greater. Therefore doctors don't recommend it.\n\n## Performing surgery after ethanol injections\n\nOne of the newer techniques for eliminating nodules in the thyroid is the injection of ethanol directly into the nodules (see Chapter 7). When this technique was brand new, it raised the question of whether surgeons would face complications if they had to operate on patients who had ethanol injections. For example, a surgeon may need to operate if the ethanol fails to eliminate a nodule, if a doctor suspects that a nodule is malignant, or if a nodule is compressing the trachea. A 2000 study in the periodical _Thyroid_ reported that surgeons didn't encounter any special surgical problems while operating on the thyroids of 13 people who had received injections.\n\nOne suggestion for improving this technique of injecting ethanol directly into the nodules is to remove the fluid with a second puncture in an attempt to reduce pain. In a study reported in the _American Journal of Neuroradiology_ in September 2005, the authors wrote that the second puncture greatly prolonged the procedure, wasn't appreciated by the patients, and didn't result in reduced pain or more frequent success in destroying the nodule. The authors recommended against it.\n\nAnother study in the _Endocrine Journal_ in August 2005 evaluated the long-term effects of ethanol injections in three types of nodules: benign cystic nodules (which contain fluid), toxic nodules (which make the patient hyperthyroid), and solitary nodules (which aren't overactive). The authors of the study found that they were successful in partially or completely eliminating cystic nodules and solitary nodules but were successful in treating toxic nodules only 1 in 24 times, so this technique may not work for a toxic nodule.\n\nSerious complications of ethanol injections are extremely rare. As more and more physicians become skilled in using them, ethanol injections may become the treatment of choice for cystic nodules and nontoxic solitary thyroid nodules.\n\nThe best assurance that ethanol injections don't cause problems down the road is to do your research and make certain that the person giving you an injection is highly skilled and experienced. You should always receive ethanol injections under ultrasound observation.\n\n## Shrinking goiters and nodules\n\nDoctors have used thyroid hormone for decades to treat goiters; the hope has always been that the hormone will help to shrink the goiter. Most recent studies have shown that goiters respond little if at all to thyroid hormone.\n\nIn a study published in 2001 in the _Journal of Clinical Endocrinology and Metabolism_ from the Netherlands, the authors compared thyroid hormone to radioactive iodine in the treatment of goiters. They used ultrasound to measure goiter size, and they measured the thyroid function of all test patients.\n\nThe researchers found that patients who received radioactive iodine had, on average, a 44 percent reduction in goiter size, while those patients who took thyroid hormone had a reduction of 1 percent. Only 1 of 29 patients didn't respond to radioactive iodine, while 16 of 28 had no response to thyroid hormone. Almost half the patients who got radioactive iodine developed hypothyroidism, while 10 of 28 taking thyroid hormone had symptoms of hyperthyroidism. In addition, those patients on thyroid hormone developed increased bone turnover and a loss of bone mineral density. The conclusion of this study is that radioactive iodine is more effective and better tolerated than thyroid hormone in the treatment of goiters.\n\nIf you have a goiter and want to get rid of it, you're much better off with radioactive iodine than thyroid hormone. The days of using thyroid hormone for this condition may be numbered.\n\nOn the other hand, benign thyroid nodules respond to thyroid hormone by shrinking, according to studies that looked at large numbers of studies of this question. One of the problems in interpreting whether shrinkage occurs is the difference between different observers. In a study done in Germany and reported in _Thyroid_ in October 2005, three different observers evaluated the size of the nodules in a group of patients. A variability of 49 percent existed between observers of the same thyroid nodule. This variability means that any change less than 50 percent is as likely to be due to the observer as to actual shrinkage. This study brings into question all those reports that thyroid hormone shrinks nodules when the shrinkage noted is less than 50 percent.\n\nUnless a change of 50 percent or greater occurs, saying a true change in the size of at thyroid nodule has occurred isn't possible. Until we have a definitive answer to the question of whether thyroid hormone can shrink benign thyroid nodules, using thyroid hormone in an attempt to shrink benign nodules is worthwhile.\n\n## Using Antithyroid Drugs Properly\n\nThe two antithyroid drugs available in the United States, propylthiouricil (PTU) and methimazole (tapazole), are thought to have slightly different actions, but their clinical effectiveness is about the same. PTU not only blocks the formation of the thyroid hormones within the thyroid but also blocks the conversion of T4 into T3. Methimazole has the former but not the latter activity. In clinical practice, patients do just as well with either drug.\n\nStudies show that these drugs block the autoimmune reaction from taking place and restore the body to its more normal state. This effect makes them more useful in treatment than surgery or radioactive iodine (RAI), both of which may worsen the autoimmunity. However, the rate at which the hyperthyroidism returns is up to 50 percent, while surgery and RAI usually accomplish a permanent cure.\n\nNo change you can measure tells you whether a patient will eventually remain normal or have a return of hyperthyroidism. Neither the size of the thyroid, the level of thyroid hormone, nor the level of antibodies can predict the eventual outcome.\n\nPTU and methimazole can cause some serious side effects, the principal one being _agranulocytosis_ \u2014 failure of production of white blood cells, which usually occurs within the first 90 days of treatment. Switching from one drug to the other may not help because the drugs have similar properties, so that a reaction to one may occur with the other (a _cross-reaction_ ). Cross-reacting occurs in about 1 in 300 patients.\n\n .jpg)\n\nIf you have a sore throat or fever when taking an antithyroid drug, stop taking it and notify your physician. Sudden onset of high fever, chills, and severe weakness is especially worrisome. A drug called granulocyte colony-stimulating factor may help to reverse this serious problem. Minor side effects include rashes, pain in the joints, a slight reduction in white blood cells, and stomach upset in about 5 percent of the people who take these drugs.\n\nIn pregnancy, PTU is the preferred drug because women have reported abnormalities of the fetus with methimazole. Both drugs cross the placenta and should be used at the smallest possible dose to protect the fetus. Doctors find both drugs in the mother's breast milk but in very tiny amounts. Babies of women taking these drugs aren't physically or mentally abnormal.\n\n## Handling Thyrotoxic Periodic Paralysis\n\n_Thyrotoxic periodic paralysis_ is a disorder that occurs when a patient, especially an Asian patient, has hyperthyroidism of any cause, including Graves' disease, toxic nodular goiter, excessive thyroxine use, or a solitary toxic thyroid nodule. Some new information has been discovered about periodic paralysis in the last few years. Thyrotoxic periodic paralysis has the following characteristics:\n\n  Thyrotoxic periodic paralysis occurs between the ages of 20 and 40.\n\n  Thyrotoxic periodic paralysis is much more common in men (20:1) compared to women, despite the greater frequency of all types of hyperthyroidism in women.\n\n  Two percent of Asians but 0.2 percent of Caucasians suffer from it.\n\n  Patients have muscle aches, cramps, and muscle stiffness before an attack.\n\n  The attack consists of severe weakness, sometimes progressing to paralysis.\n\n  Serum potassium levels during an attack are below the normal range but not always.\n\n  Hard exercise or eating a lot of carbohydrates can bring on an attack.\n\n  Patients may not know they have hyperthyroidism.\n\n  Spontaneous improvement occurs within hours to two days, but abnormal heart rhythms and respiratory failure may kill the patient.\n\n  Between attacks, patients are free of symptoms.\n\nThe condition results from a sudden shift of potassium from the bloodstream into cells. Exactly why this shift happens isn't clear. The total potassium in the body of these patients is normal, so immediate treatment is directed to restore the potassium in the bloodstream without overloading the patient. When this treatment is done, rapid improvement takes place. The danger is that the potassium in the cells will be released, leading to the patient having too much potassium in the blood \u2014 which happens in up to 70 percent of patients given potassium, unless the dose is kept fairly low. Lower doses work just as well and avoid excess potassium.\n\nPermanent treatment consists of bringing the hyperthyroidism under control with antithyroid drugs, radioactive iodine, or surgery. Propranolol also works to reverse the movement of potassium. Giving potassium between attacks doesn't work.\n\nWhile waiting for definitive treatment, patients should avoid precipitating activities, such as\n\n  Heavy exercise\n\n  Trauma\n\n  Cold exposure\n\n  Infection\n\n  Emotional stress\n\nThyrotoxic periodic paralysis isn't hard to treat. The key is recognizing the condition, especially when the patient has previously had hyperthyroidism.\n\n## Taking New Approaches to Thyroid Cancer\n\nNot surprisingly, much of the research concerning advances in thyroid disease centers around thyroid cancer. The following sections provide you with some of the more provocative and important studies of the last year or two. Undoubtedly, many more studies are to come.\n\n## Understanding the impact of radioactive iodine exposure\n\nMore than 15 years after the nuclear disaster in Chernobyl, researchers still follow up with the children who were exposed to excessive radioactive iodine. In the _World Journal of Surgery_ in 2000, a group of Russian scientists published the results of surgery on 330 children who had thyroid cancer after Chernobyl. The cancers tended to develop rapidly after exposure, were more aggressive than typical thyroid cancers, and spread early to distant sites in the body. The patients were treated by _total thyroidectomy_ (removal of the entire thyroid), followed by radioactive iodine treatment and suppression of TSH. The authors of the study emphasize that doctors will find many more cases of thyroid cancer among the children of Chernobyl, who need to be monitored over the next several decades.\n\nAre any environmental factors protective in the situation of radioactive-iodine exposure? A study in _Environmental Health_ in 2000 looked at people in Germany who were exposed to radioactive iodine. The study confirmed that drinking coffee and eating cruciferous vegetables like broccoli reduce the risk of developing cancer in people exposed to radioactive iodine. If a patient had a goiter prior to the exposure, or if he consumed decaffeinated coffee instead of caffeinated, he was at increased risk for malignant or benign tumors.\n\nThese researchers also found that tomato consumption was a risk factor for malignant disease. They suggest that off-season tomatoes coming from areas where the farmers are careless about the use of chemicals may promote the development of thyroid cancer.\n\nThere are a number of recent reports of the children exposed to radioactive iodine at Chernobyl. The best was in May 2005 in the _Journal of the National Cancer Institute._ The authors reported several new and important findings:\n\n  Diets deficient in iodine increase the chance of radiation-induced thyroid cancer occurring.\n\n  The more radiation exposure, the more thyroid cancer.\n\n  Boys and girls have the same risk of developing thyroid cancer.\n\n  Use of dietary supplements rich in iodine reduces the chance of getting thyroid cancer.\n\n  Children who were iodine deficient but were given iodine supplements after exposure to radioactive iodine were one-third as likely to get thyroid cancer as those not given iodine after exposure.\n\nThe effect of iodine supplements may be good news for populations where no iodine deficiency exists. This could not be studied in Russia because all exposed areas were iodine deficient. But if there is sufficient iodine in the diet, the occurrence of thyroid cancer after exposure may be low, and giving iodine even weeks to months after exposure may reduce the instances of thyroid cancer even more.\n\n## Blocking estrogen to slow tumor growth\n\nOne source of bewilderment about thyroid cancer is that it occurs more often in women than in men. One study suggests that the reason may lie with the fact that women make estrogen as their primary sex hormone, and estrogen may stimulate thyroid tumor-cell growth. The authors of a study in the March 2001 _Journal of Clinical Endocrinology and Metabolism_ describe an experiment in which estrogen was shown to stimulate tumor cells and, to a lesser extent, benign cells. (Estrogen activates a metabolic pathway that leads to much greater growth activity in both malignant and benign cells.) When patients received a drug that blocks estrogen action, the tumor cells were no longer stimulated.\n\n## Predicting thyroid cancer\n\nIs it possible to predict the future occurrence of thyroid cancer? The authors of a study from Iceland present an analysis of blood taken many years before the diagnosis of thyroid cancer was made in 164 patients. Their study was published in _Acta Oncologica_ in 2000. The authors report that levels of _thyroglobulin,_ the chemical that resides in the thyroid and that doctors monitor when following thyroid-cancer patients, can also be found in much elevated levels up to 15 years before the diagnosis of thyroid cancer is made. In contrast, the authors found no difference in the blood levels of TSH or thyroid hormone in the thyroid-cancer patients compared to patients who never had thyroid cancer.\n\n## Detecting residual thyroid cancer\n\nAnother important recent advance is in the ability to detect thyroid cancer that remains after surgery. Thyroglobulin plays a major role in detecting remaining cancer. Another important tool that doctors often use is the whole\u2013body radioactive iodine scan, which can locate active thyroid tissue. The limitation of the scan is that it can't locate thyroid tissue that isn't making thyroid hormone. Sometimes a thyroglobulin level is high, indicating that active thyroid tissue is present, but the body scan is negative.\n\nA newer type of scan called a _PET scan_ is able to localize thyroid tissue that isn't functioning well as thyroid tissue but is very metabolically active. A study in _Advances in Internal Medicine_ in 2001 reviews the successful use of the PET scan for this purpose. The study points out that the need still exists for new agents that attack these tumor tissues when they don't concentrate radioactive iodine.\n\nIf you've had thyroid cancer and discover a new growth that doesn't concentrate radioactive iodine on a thyroid scan, ask your doctor about the possibility of having a PET scan.\n\n## Following up on thyroid-cancer treatment\n\nDoes the thyroid-cancer patient need to be followed for life, or does the patient reach a point at which she can be considered cured of the disease? The authors of a study in _Annales Chirurgiae_ in 2000 attempt to answer this question.\n\nThe study's authors contend that studying patients for seven months after thyroid surgery is necessary. At that time, patients can be divided into groups:\n\n  **Group I:** Patients with microcancers\n\n  **Group II:** Patients with no lymph-node involvement or metastases and normal thyroglobulin\n\n\u2022 **A:** Younger than age 45\n\n\u2022 **B:** Age 45 or older\n\n  **Group III:** Patients with cancer with lymph-node involvement but a normal thyroglobulin level\n\n  **Group IV:** Patients who have extension of the cancer beyond local lymph nodes or an elevated thyroglobulin level\n\nTable 16-1 shows the survival rates for these groups.\n\nTable 16-1 Survival Rates for Thyroid-Cancer Patients Length of Time after Surgery  | 10 Years  |  | 15 Years |   \n---|---|---|---|---  \nGroup I  | 100%  |  | 100% |   \nGroup II A  | 100%  |  | 100% |   \nGroup II B  | 96%  |  |  | 92%  \nGroup III  | 100%  |  | 100% |   \nGroup IV  | 86%  |  |  | 73%\n\nThe latest time of a recurrence in groups I and II A was at 12 years. For groups II B, III, and IV, tumors were discovered as late as 16 years after treatment. The study emphasizes that patients must have thyroglobulin tests and whole-body scanning every five years. Doctors need to follow patients in groups I and II A for up to 15 years; they should follow other patients for 20 years before saying with certainty that the disease is eliminated. If a recurrence happens, then the doctor needs to follow the patient another ten years with no more cancer before declaring that she is cancer-free.\n\n## Knowing what to expect from medullary thyroid cancer\n\nMedullary thyroid cancer (MTC) is different from thyroid cell cancers like follicular or papillary cancer (see Chapter 8). MTC arises from the C-cells in the thyroid, and doctors can't detect it with radioactive iodine.\n\nA study from Finland in the _Annales Chiarurgiae Gynecologica_ in 2000 provides helpful information about the prognosis of medullary thyroid cancer. The authors divided their cases into hereditary (inherited) MTC and sporadic (not inherited) MTC. They found that sporadic MTC is a much deadlier disease than hereditary MTC.\n\nBoth groups were treated with total thyroidectomy and lymph-node dissection. The group with sporadic MTC had a ten-year survival rate of 57.9 percent. Within the group of patients with sporadic MTC, those who had recurrent cancer in their lymph nodes that doctors found and removed had a survival rate of only 51.4 percent at ten years. More important predictors of survival than lymph nodes were distant metastases and local spread of the cancer in the neck.\n\n## Using recombinant TSH with thyroid-cancer patients\n\nRecombinant TSH is a valuable tool both for the detection and treatment of residual thyroid cancer. Before recombinant TSH, in order to be tested for residual cancer with a total body scan, patients had to be taken off thyroid-replacement hormone for four weeks or longer to allow their tissues to become hypothyroid. Going off hormone replacement greatly enhances the uptake of radioactive iodine, allowing for a more accurate scan of thyroid tissue.\n\nDoctors have always been concerned that this time off the thyroid hormone allows cancer to grow more rapidly. For this reason, they use recombinant TSH to stimulate uptake and identify cancer recurrences without needing patients to stop taking thyroid hormone.\n\nA group in Massachusetts, writing in the _Journal of Clinical Endocrinology and Metabolism_ in 2001, explored the dosages of recombinant TSH required for optimal effect. The group looked at patients' thyroglobulin levels as well as TSH, T4, and T3. The group found that a dose of 0.3 milligrams of recombinant TSH produced the maximal increase in thyroglobulin and radioactive-iodine uptake. Going higher than 0.3 milligrams didn't increase the effect of treatment.\n\nAnother group from New York showed in the _European Journal of Endocrinology_ in 2001 that using recombinant TSH was just as good as taking patients off thyroid medication in stimulating thyroglobulin secretion and radioactive-iodine uptake. The group concluded that, in terms of diagnostic accuracy, preparing patients for a scan with recombinant TSH is equivalent to taking patients off thyroid hormone.\n\nFinally, doctors can use recombinant TSH to stimulate thyroid cancer to take up radioactive iodine in order to destroy it. In a study published in 2001 in the _European Journal of Endocrinology,_ scientists used recombinant TSH to increase uptake. They noted that the recombinant TSH was free of side effects other than mild nausea. The results were excellent. The thyroid-cancer treatment was as effective as with patients who were taken off thyroid hormone therapy prior to treatment. By using recombinant TSH, patients avoid the discomfort of being without thyroid hormone for weeks and avoid becoming hypothyroid.\n\n## Checking testicular function after radiation therapy\n\nScientists don't know whether radiation therapy to ablate remaining thyroid tissue after surgery for thyroid cancer or for treatment of recurring cancer leads to damage to the production of sperm. The authors of a study in the _Annals of Andrology_ in May\u2013June 2005 showed a reduction in sperm production and evidence of damage to the testes, especially after more than one treatment with radioactive iodine. Levels of a hormone called FSH rose after radiation treatment and declined over time, indicating that the testicles were damaged but recovered. Patients who got several radiation treatments didn't show this recovery.\n\nIf you require several treatments with large-dose radioactive iodine, protect your future as a father by banking sperm before you receive the treatments.\n\n## Testing calcium levels after cancer surgery\n\nIn the process of removing the thyroid gland because of thyroid cancer, patients inevitably experience some trauma to the parathyroid glands that lie on the back of the thyroid lobes. Most of the time, these glands recover, but sometimes the trauma results in permanent hypoparathyroidism, which causes a patient to have low calcium levels.\n\nIn a study published in the _Journal of the European Society of Surgery and Oncology_ in 2000, researchers wanted to establish how long cancer patients take to recover their normal calcium levels. The researchers also wanted to determine how often treatment is necessary. The study showed that if a patient had just one lobe of the thyroid removed, even though two of the parathyroid glands weren't touched, the patient experienced a 10-percent drop in the level of calcium. Thirty-four percent of patients with this type of surgery required some calcium treatment because the level fell too low. Their calcium levels returned to normal within one week after surgery and remained normal.\n\nWhen patients had both sides of the thyroid operated on, as expected, the operation had more effect on the parathyroids and the calcium. Calcium levels decreased 15 percent on average; some patients experienced severely low levels early in their recovery. The calcium decline was greater if the number of preserved parathyroid glands was fewer. Fifteen percent of these patients needed calcium treatment for 2 to 7 days, 26 percent for 8 to 180 days, and 9 percent for longer than a year. Only 1 patient of 82 required permanent treatment for low calcium after a single thyroid surgery on both sides. One of four patients who had several thyroid surgeries needed permanent calcium treatment.\n\n## Understanding familial papillary thyroid cancer\n\nIn the last few years, specialists have recognized an inherited familial form of papillary thyroid cancer. The familial form differs from sporadic thyroid cancer in a number of ways:\n\n  The age of onset is younger (age 38 rather than age 45 to 50).\n\n  Females are only twice as likely to get it.\n\n  Many locations in the thyroid tend to be involved.\n\n  Benign nodules are present more often.\n\n  The cancer recurs a little more often.\n\nAt present, identifying carriers of the abnormal gene who don't have symptoms isn't possible. Removal of the thyroid in advance of the development of thyroid cancer isn't recommended because carriers can't be found, and the tumor grows very slowly.\n\n## Tackling Iodine-Deficiency Disease\n\nWhen you consider the numbers of people affected by iodine-deficiency disease (see Chapter 12), you may think that most of the articles on thyroid disease concern themselves with this topic. But iodine-deficiency disease isn't a common problem in the United States, so American scientists, who make up the majority of the world's investigators, don't tend to write about it. Still, plenty is going on in this area. This section describes the more important recent studies on iodine-deficiency disease.\n\n## Recognizing the importance of selenium\n\nSelenium is an element that plays a role in thyroid-hormone production because it's part of an enzyme responsible for converting T4 into T3. Until now, researchers and doctors have generally believed that selenium deficiency alone doesn't cause hypothyroidism; only when an iodine deficiency exists does selenium deficiency contribute to the disease. However, a study from the journal _Biological Trace Element Research_ in 2000 contradicts this belief. The study's authors describe three girls who had hypothyroidism due to lack of selenium alone. When given replacement selenium, all returned to normal thyroid function. This study is the first description of hypothyroidism due to lack of selenium alone.\n\nWriting in _Endocrine Reviews_ in September 2005, the authors provided further information about the importance of selenium in the thyroid and other endocrine tissues. In the thyroid, selenium protects thyroid cells from damage from hydrogen peroxide produced when the body makes thyroid hormone. Selenium is also present in higher amounts in endocrine tissues compared to other tissues. When selenium deficiency exists in the rest of the body, selenium is maintained in normal amounts in the thyroid and these other endocrine tissues. Although tiny quantities of selenium are necessary, selenium plays an important role in the body.\n\nSelenium received further approval in a paper in the _Journal of Endocrinology_ in March 2005. Selenium in an enzyme controls the amount of the T3 by removing iodine from the hormone. Men who are deficient in selenium have low sperm production and poor sperm quality, leading to infertility. Selenium also helps to reduce blood glucose and prevents the negative effects of diabetes on the heart and the kidneys.\n\nAlthough selenium deficiency reduces the response of iodine-deficient patients to lipiodol (a type of iodized oil; see the following section for more), overall it doesn't prevent iodine from restoring thyroid function.\n\n## Using iodized oil for goiters\n\nDoctors commonly use iodized oil injection to treat iodine deficiency and prevent goiter formation in areas of the world where iodine deficiency persists (see Chapter 12). The authors of a study in _Medicine_ in 2001 wanted to consider any potential problems associated with lipiodol, a type of iodized oil. When lipiodol was given to a person who already had a multinodular goiter, that person sometimes became hyperthyroid. The hyperthyroidism tended to be mild and didn't last long. If the patient was a pregnant woman, the iodine sometimes entered the bloodstream of the fetus but didn't affect the fetus. The study confirms that using iodized oil for the replacement of iodine is a safe, cheap, and effective way to treat iodine deficiency.\n\nIodine deficiency and hypothyroidism also contribute to hearing difficulties in children. A study in the _Journal of Endocrinological Investigation_ in July 2005 showed that supplementation of iodine with iodized oil can greatly reduce the hearing loss that these children suffer. That the supplementation be continuous is important. Ten years of giving iodine improved hearing almost to normal in a large group of iodine-deficient children.\n\nDoctors usually give lipiodol by injection, which requires all kinds of precautions and equipment that may not be available in rural areas where it's needed most. The authors of a study in the _Journal of Endocrinological Investigation_ in 2003 showed that oral lipiodol once a year gives prolonged protection from iodine deficiency just as effectively as intramuscular lipiodol, as shown by increased urinary iodine. Intramuscular lipiodol lasts for two to three years in the body, while oral lipiodol must be renewed once a year. But the ease of administration and lack of a need for special equipment may make oral lipiodol the preferred route of administration.\n\nIn some areas of the world, people aren't only iodine deficient but iron deficient as well. A Swiss group studied whether iodine supplementation would be successful despite iron deficiency. The group reported in the _American Journal of Clinical Nutrition_ in July 2000 that iodine would eliminate goiters in children who were iron deficient. Restoring iron stores is necessary before using iodine.\n\nIodized oil does have some side effects associated with it. Iodized oil causes a rash in a small percentage of people who get it, but the rash doesn't last long. Iodized oil can bring on hyperthyroidism in some patients, but the incidence is less than 1 percent. The hyperthyroidism is mild and doesn't last long but may require the use of antithyroid medication for a period of time. Iodized oil can also bring on hypothyroidism, again with a very low incidence of less than 1 percent, which is treated with thyroid hormone.\n\n## Increasing the intelligence of babies born to hypothyroid mothers\n\nBabies born to hypothyroid mothers tend to have low intelligence. In a study done in Taiwan and published in the _Journal of the Formosa Medical Association_ in 2001, researchers looked at the level of intelligence of 62 babies of hypothyroid mothers and sought an early screening to avoid retardation. They found that the level of T4 at the time of diagnosis was a good predictor of the future intelligence of the baby. By measuring T4 at birth and giving thyroid-replacement hormone, the researchers improved the outlook of these babies in terms of their intelligence.\n\nThe screening of babies with TSH tests doesn't always discover newborn hypothyroidism, especially when the baby has very low birth weight. In a study in the _Journal of Pediatrics_ in November 2003, the authors found that some babies with very low birth weight, especially those with heart disease, had normal TSH values at birth but elevated values when tested weeks or months later. The authors recommended TSH tests for all babies with very low birth weight.\n\nIn another paper, this time in the journal _Clinical Biochemistry_ in September 2004, the authors looked at the TSH at different times after birth. TSH taken within the first 24 hours wasn't reliable for making a diagnosis of hypothyroidism. The best time to do a TSH test is at 48 hours after birth. If it is taken earlier, the cutoff value for an abnormal TSH has to be set too high, and some truly hypothyroid babies will be missed.\n\n##### Chapter 17\n\n## The Thyroid and Pregnancy\n\n### In This Chapter\n\n  Understanding normal thyroid function in pregnancy\n\n  Dealing with hypothyroidism during pregnancy\n\n  Managing hyperthyroidism in pregnancy\n\n  Treating new thyroid nodules\n\nIn the last ten years, doctors have learned a lot about how the thyroid functions during pregnancy. This new level of understanding makes a tremendous difference in your ability to have a healthy baby, even if you have a thyroid disorder. If you and your doctor keep up with the latest information available, thyroid disease shouldn't seriously impact your ability to have a healthy baby.\n\nThis chapter is about the wonderful state of pregnancy, with particular reference to how it changes thyroid function and how abnormalities of thyroid function affect the pregnancy. As I explain in earlier chapters, thyroid disease is very common among women. Many women come into a pregnancy with a thyroid condition, whether they know it or not. Others develop a thyroid condition during pregnancy. For the health of both the mother and the fetus, detecting the condition and treating it appropriately are important. This chapter explains how you and your doctor should monitor your thyroid function during pregnancy and describes some of the consequences that could occur from not managing a thyroid condition.\n\n## The Normal Thyroid During Pregnancy\n\nThree important changes occur in a woman's body during pregnancy, leading to a much greater need for iodine:\n\n  Early in pregnancy, the flow of blood to a woman's kidneys increases, resulting in more clearing of iodine and a greater loss of iodine through the urine.\n\n  Because the fetus can't make thyroid hormone at first, it takes thyroid hormone from the mother through the placenta.\n\n  The growing fetus starts to make its own thyroid hormone after a while and needs iodine to do so.\n\nAt the same time, as a result of increases in hormones, particularly estrogen, the mother makes much more thyroxine-binding globulin \u2014 a protein that transports thyroid hormone through the blood \u2014 than she used to. (In fact, the concentration doubles.) She also makes a form of thyroxine-binding globulin that leaves the circulation much more slowly. This substance takes up a lot of the thyroid hormone that the mother's body is making, which leads to an even greater need for iodine to make more.\n\nThe daily requirement for iodine in pregnancy is at least 250 micrograms per day, a figure recommended at a meeting of the World Health Organization in 2005. In much of the United States, Canada, and Western Europe, this requirement is generally met. However, in other parts of the world, getting this increased amount of iodine can be a problem (check out Chapter 12 for more on iodine deficiency).\n\nThe increased need for iodine has important consequences for pregnant women in iodine-deficient areas:\n\n  If the woman is depending on iodized salt for her iodine needs and has to be salt-restricted, she may quickly become iodine deficient.\n\n  Some areas thought to be iodine sufficient are discovered to be low in iodine when the greater needs of pregnancy must be taken into account, even in areas of the United States.\n\n  Different areas of the same country may differ greatly in the amount of iodine in the diet.\n\nIodine levels must be constantly monitored in areas where iodine is deficient, even though supplemental iodine is being given.\n\nIf you're hypothyroid and take thyroid hormone pills, understanding all these changes is important. To maintain normal thyroid function, you probably need to increase your dose of thyroid-hormone replacement early in pregnancy, based on your level of thyroid-stimulating hormone (TSH).\n\nWhile all these changes are happening, the placenta \u2014 the tissue that connects the fetus to the mother \u2014 is making a lot of a hormone called _human chorionic gonadotrophin_ (HCG). HCG has some parts that look very much like TSH. It reaches the mother's thyroid and starts to stimulate it into making more thyroid hormone, just as TSH does. As a result, the mother's level of free T4 rises, causing a fall in the amount of TSH her body produces. If she is having twins, her HCG level can be especially high and can persist for weeks. As I show you in the section \"Hyperthyroidism in Pregnancy,\" later in this chapter, the result may be a form of hyperthyroidism.\n\nA condition called _hyperemesis gravidarum_ occurs early in pregnancy. The symptoms are severe nausea, vomiting, and dehydration, which may require hospitalization. Doctors believe that the temporary increase in thyroid hormone stimulated by HCG along with the significant increase of estrogen that results from the same HCG stimulation cause this condition. Morning sickness may be a milder form of the same condition. The amount of vomiting is directly proportional to the level of HCG and T4 and inversely proportional to the level of TSH.\n\nThese changes in levels of thyroid hormone and TSH mean that the usual way of defining normal thyroid function, a normal free T4 and a normal TSH, doesn't apply in pregnancy. TSH is actually below the lower level of the normal range in one-fifth of healthy pregnant women. So far, no ranges for normal for these tests during pregnancy have been established, but doctors agree that a temporary rise in free T4 occurs in the first trimester and a decrease to normal from that level in the second and third trimesters.\n\nThe need for more thyroid hormone as well as the increased stimulation of the thyroid gland by the HCG causes the thyroid to enlarge, especially in areas where iodine is deficient. A goiter is one consequence of the pregnancy. The thyroid may enlarge symmetrically, or it may form nodules. The enlarged gland and the nodules don't necessarily shrink away when the pregnancy ends, which may be one explanation for the great increase in thyroid disease in women compared to men.\n\nOne of the confusing aspects of pregnancy with respect to thyroid disease is that many signs and symptoms of a normal pregnancy are similar to the findings in hyperthyroidism. These signs and symptoms include\n\n  A rapid heart rate\n\n  Intolerance to heat\n\n  Tiredness\n\n  Anxiety\n\n  Trouble sleeping\n\n  Sweating\n\nYour weight is the biggest clue as to whether hyperthyroidism is an issue. Most pregnant women gain weight throughout their pregnancy (although some women lose a few pounds initially if they experience vomiting). A hyperthyroid woman often doesn't gain weight and sometimes loses weight during pregnancy.\n\n## Pregnancy and Hypothyroidism\n\nThe fact that a mother's body doesn't reject a fetus as a foreign intruder just as it would reject any foreign invasion is a miracle. (Even a few foreign cells injected inside your body wouldn't last long.) The fact that the mother's body doesn't reject the fetus is evidence that a general decline in immunity takes place during pregnancy.\n\nAs a result, women who have autoimmune diseases prior to pregnancy often discover that they improve during a pregnancy, with their condition returning to its original state again after delivery. This is true for women with either hypothyroidism or hyperthyroidism that results from an autoimmune condition \u2014 the most common cause of both hypothyroidism and hyperthyroidism in the United States and Europe (see Chapters 5 and 6). If levels of antibodies are measured, they are found to fall throughout the pregnancy. Along with this is a general fall in the inflammation that is found in most autoimmune diseases.\n\n .jpg)\n\nAfter the pregnancy, a woman may experience a rebound in levels of autoantibodies, and the diseases that they represent may worsen.\n\n## Decreased fertility\n\nIf a woman has hypothyroidism that goes untreated, she will probably have a difficult time becoming pregnant because the hypothyroidism decreases her fertility. In a study of infertile women in Finland published in _Gynecological Endocrinology_ in 2000, 5 percent were hypothyroid. If the hypothyroid woman does become pregnant, the risk of a miscarriage is much higher than if she didn't have a thyroid condition.\n\nAntithyroid antibodies, which are present in women with autoimmune thyroid disease, are associated with an increased risk of miscarriage. They may not be the cause of the miscarriage, but they are present much more often in women who miscarry than in the general population of women.\n\nIf you suffer one or more miscarriages, be sure to have your doctor check your thyroid function.\n\nIf you're hypothyroid and aren't receiving thyroid-hormone replacement, you may suffer from a number of obstetric complications if you become pregnant. Complications may include high blood pressure, problems with the placental connection to the fetus, and problems with delivery. You can avoid all these complications with proper treatment of the thyroid.\n\n## Iodine deficiency\n\nA mother with an iodine deficiency during pregnancy can't make sufficient thyroid hormone for herself and her fetus. (The fetus gets the thyroid hormone it needs from its mother up until the 20th week of the pregnancy.) As a result, the mother is chronically stimulated by TSH to make more thyroid hormone, and she develops a goiter.\n\nA goiter doesn't develop in the mother during a normal pregnancy. If a mother develops a goiter, she is experiencing iodine deficiency, hypothyroidism, or hyperthyroidism.\n\nThe mother's goiter may not fully shrink after delivery, when her iodine needs are reduced. This may partly explain the much greater incidence of thyroid enlargement in women when compared with men.\n\nIodine deficiency also strongly affects the fetus. It may develop a goiter as well, and it may suffer from abnormal brain development (see Chapter 12). A goiter in the fetus can result in problems during delivery.\n\nLaboratory tests show that iodine-deficient pregnant women have\n\n  Reduced T4 and, if severe, reduced T3 hormone levels\n\n  Increased TSH\n\n  Increased ratios of T3 to T4, because the thyroid begins to prefer making T3\n\n  Increased thyroglobulin\n\n## Autoimmune hypothyroidism\n\nAutoimmune thyroid disease is much more common in iodine-rich countries than in iodine-deficient countries. Most cases of hypothyroidism in pregnancy result from this disease. Autoimmune hypothyroidism probably affects between 2 percent and 4 percent of pregnant women at some time during their pregnancy. Pregnant women with type 1 diabetes have an even higher incidence of chronic autoimmune thyroiditis and hypothyroidism.\n\n### Understanding the risks to the mother and fetus\n\nIf lab tests show that a woman has thyroid autoantibodies \u2014 even if her doctor doesn't diagnose her as hypothyroid because her thyroid function tests are normal \u2014 she is at an increased risk for a miscarriage. Doctors aren't clear why this is so. One suggestion is that these women really have mild hypothyroidism despite the normal test results. Another is that the autoantibodies are just a marker for other autoimmune diseases that may be responsible for the miscarriage. A third hypothesis is that miscarriage in these autoimmune mothers is meant to prevent the transmission of autoimmune diseases to the next generation.\n\nThe thyroid autoantibodies can be transmitted to the fetus through the placenta, causing hypothyroidism in the fetus. Usually if the mother is hypothyroid and is receiving adequate treatment with thyroid hormone, enough thyroid hormone gets to the fetus to prevent hypothyroidism. If the baby is born with hypothyroidism, the pediatrician places the baby on thyroid-hormone replacement until the autoantibodies are cleared from the baby's circulation, usually in three or four months. The baby doesn't need treatment after that.\n\n### Knowing when to treat the mother\n\nAt what point do women who have autoimmune hypothyroidism in pregnancy need treatment? If a mother's TSH level is greater than 4, treatment is appropriate. She needs to have thyroid function tests during every trimester of pregnancy to confirm that she is receiving the right amount of thyroid medication.\n\nIf the mother's TSH level is between 2 and 4 and she tests positive for thyroid autoantibodies, her doctor should probably treat her and should check the fetus for goiter or other signs of a thyroid abnormality. Fortunately, recent studies show that if the mother has very mild hypothyroidism in early pregnancy, the hypothyroidism has no negative effect on the newborn's hearing or physical activity.\n\nSeveral obstetrical complications are associated with a mother who is hypothyroid. These complications include\n\n  Anemia, when a woman has decreased red blood cells\n\n  Bleeding after delivery\n\n  Preeclampsia, where a woman has high blood pressure, headache, weight gain, and blurred vision\n\n  Rupture of the placenta\n\nMaking the thyroid hormone levels normal can prevent the preceding complications.\n\nAlthough autoimmune hypothyroidism generally improves during pregnancy, after the baby is born, the mother's hypothyroidism may become worse, and her T4 level may decrease further. Her doctor should check her TSH every six to eight weeks after delivery.\n\nThe experts make no general recommendation for screening for hypothyroidism in pregnancy despite the high incidence and the severe consequences if maternal hypothyroidism is present. Women who are at high risk should certainly be tested. Make sure you're tested if any of the following apply to you:\n\n  Members of your family have chronic thyroiditis or hypothyroidism.\n\n  You already take thyroid hormone.\n\n  You have type 1 diabetes mellitus or another autoimmune disease.\n\n  You have diminished thyroid reserve as a result of surgery or a history of neck irradiation.\n\nIf you have hypothyroidism during pregnancy, have thyroid function tests done about two months after delivery to verify that you're taking the right dose of thyroid hormone.\n\nTreatment of newly diagnosed hypothyroidism in pregnancy is with levothyroxine. In an effort to make the mother normal rapidly, doctors often give a large dose for several days followed by the usual dose. Women have to undergo retesting in six weeks to make sure the dose is correct.\n\nCertain drugs that women commonly take during pregnancy, such as iron, sucralfate, and aluminum hydroxide (see Chapter 10), can block the absorption of thyroid hormone. Pregnant women should take these drugs several hours before or after taking the thyroid hormone.\n\n## Hyperthyroidism in Pregnancy\n\nHyperthyroidism occurring in pregnancy is much less common than hypothyroidism. It occurs in about 2 in 1,000 pregnancies. If doctors don't recognize it, the baby will be premature at birth and have a low birth weight, not to mention possible hyperthyroidism.\n\nHyperthyroid women who wish to become pregnant should make sure that their disease is under control before they do so. It is important that women have normal thyroid function when they conceive their baby. The miscarriage rate for babies conceived by a hyperthyroid mother is greater than normal, just like the situation I describe in the preceding section for hypothyroidism.\n\nWomen who have previously received treatment for Graves' disease and are now normal, with or without thyroid medication, also have to be aware that hyperthyroidism can still occur in their baby during the pregnancy. If the treatment was antithyroid drugs, the risk is much less. But if surgery or radioactive iodine were the treatments, the mother may still have thyroid-stimulating autoantibodies that she passes to the baby. Doctors can measure these autoantibodies in the mother's blood. If they're not present, then hyperthyroidism in the baby is unlikely.\n\nSome women with Graves' disease who are already pregnant but don't realize it receive radioactive iodine in treatment. Most radiation therapists ask the woman if she may possibly be pregnant. Occasionally she is unaware of a pregnancy and denies it. Whether damage to the fetal thyroid results depends on the stage of the pregnancy.\n\nThe following considerations determine whether radioactive iodine mistakenly given to the pregnant woman will cause damage to the fetal thyroid:\n\n  The fetal thyroid begins to concentrate iodine after the 10th to the 12th week of gestation.\n\n  The fetal thyroid takes in iodine more avidly than the maternal thyroid.\n\n  Fetal tissues are more radio sensitive than maternal tissues.\n\n  Radioactive iodine given to a pregnant woman up to the tenth week isn't an indication for termination of the pregnancy.\n\nAt birth, sampling the umbilical cord blood for thyroid hormone levels should determine the possibility of fetal hyperthyroidism. Such babies have a higher incidence of malformations, which doctors have to carefully look for.\n\nDoctors once believed that most hyperthyroidism in pregnancy was due exclusively to Graves' disease. Recently doctors have become aware of another cause for hyperthyroidism in pregnancy that's actually more frequent than Graves' disease \u2014 a condition called _gestational transient thyrotoxicosis._ I discuss both conditions in this section.\n\nRegardless of the cause, the symptoms of hyperthyroidism in pregnancy are those I mention earlier in this chapter: rapid heart rate, sweating, trouble sleeping, anxiety, heat intolerance, and fatigue. These symptoms are all fairly common for any pregnant woman. One way to determine whether the mother is hyperthyroid is that if she has Graves' disease, she usually won't gain a great deal of weight during pregnancy; she may even lose weight.\n\nLab tests show that a hyperthyroid mother has high levels of free T4 and low levels of TSH. In this situation, doing a total T4 test (see Chapter 4) isn't helpful at all, because the total T4 will always be elevated in view of the increase in thyroid-binding globulin in the mother's system.\n\nDoctors need to control hyperthyroidism during pregnancy. If it's not controlled, some of the consequences may include\n\n  Premature delivery\n\n  Fetal malformations\n\n  Low birth weight\n\n  Hyperthyroidism in the infant\n\n  High blood pressure and other problems in the mother\n\n## Graves' disease\n\nAlice Dummy is a cousin of Stacy, Karen, Sarah, and Margaret \u2014 our friends from earlier chapters. She is married, but \u2014 conveniently for us \u2014 she kept her maiden name. She became pregnant about a month ago. She notices that her heart is beating very fast all the time and that she is feeling very warm. She has actually lost a few pounds. Her husband notices that her neck seems enlarged.\n\nAlice and her husband go to their obstetrician, Dr. Ufbaum, who obtains thyroid blood tests to rule out hyperthyroidism. To her surprise, Dr. Ufbaum rules in the possibility of hyperthyroidism when she finds that the free T4 level in Alice's blood is elevated while the TSH level is suppressed. The doctor immediately refers Alice to her favorite endocrinologist, Dr. Rubin.\n\nDr. Rubin sends Alice for a blood test for thyroid-stimulating hormone\u2013 receptor-stimulating antibodies. The test result is very positive. He starts Alice on the antithyroid medication propylthiouricil. Within three weeks, Alice begins to feel better. By six weeks, she is gaining weight, and her heart slows noticeably. Alice can stop taking the propylthiouricil during the second half of her pregnancy, which proceeds normally. Dr. Rubin instructs Dr. Ufbaum to check carefully for hyperthyroidism in the fetus; fortunately, hyperthyroidism doesn't develop.\n\nAfter the delivery, Alice again needs antithyroid medication, which she takes for a year. She does well.\n\nAutoimmune hyperthyroidism is associated with antibodies that stimulate the TSH receptors on thyroid cells and trigger the production of more thyroid hormone. In some cases, the mother may have had Graves' disease prior to pregnancy and received successful treatment with radioactive iodine, surgery, or antithyroid drugs. She may have normal thyroid function, but she still has the antibodies that can be transferred through the placenta to the fetus, giving the fetus hyperthyroidism and a probable goiter.\n\n### Finding hyperthyroidism in the fetus\n\nA number of signs indicate that the fetus has hyperthyroidism, most of which are determined by an ultrasound study of the developing fetus. They include\n\n  Fetal goiter\n\n  Very rapid fetal heart rate (over 160 beats per minute)\n\n  Increased movement of the fetus\n\n  Acceleration in the bone maturity of the fetus\n\n  Fetal growth retardation\n\n .jpg)\n\nIf you become pregnant after successful treatment for Graves' disease, your fetus can become hyperthyroid because you still have thyroid-stimulating antibodies that can pass through the placenta. It is important for your doctor to monitor the fetus for signs of hyperthyroidism and check you for TSH-receptor antibodies early in pregnancy . If your TSH receptor antibodies are elevated, but no signs of fetal hyperthyroidism appear, your doctor should check both again in six months.\n\nDoctors give antithyroid drugs to the mother to treat hyperthyroidism in the fetus; the medication passes through the placenta to decrease the thyroid function of the fetus. The mother may need to also take thyroid hormone replacement, because the antithyroid drugs will reduce her thyroid function as well.\n\nThe fetus may also show hyperthyroidism at birth if the mother has Graves' disease that hasn't been well controlled or has a lot of TSH receptor\u2013stimulating antibodies. A mother who has previously had a baby with neonatal hyperthyroidism is at especially high risk to have another baby with neonatal hyperthyroidism in a subsequent pregnancy.\n\nHyperthyroidism in the newborn may not appear until the antithyroid drugs, obtained through the placenta, clear out of the baby's system. The baby then has the usual signs of hyperthyroidism plus signs specific to a newborn, such as failure to thrive, increase in the yellow color of the skin (due to increased bilirubin), and increased irritability. After the mother's thyroid-stimulating antibodies are cleared from the baby's blood, the baby has normal thyroid function.\n\n### Treating the mother during pregnancy\n\nAs I mention earlier in the chapter, autoimmune hyperthyroidism tends to improve through the course of a pregnancy because of a general decline in the mother's autoimmunity. Other factors aiding the improvement of autoimmune hyperthyroidism include an increase in thyroxine-binding globulin, an increased loss of iodine in the urine, and an increase in TSH receptor\u2013blocking antibodies as the TSH receptor\u2013stimulating antibodies decline.\n\nThe usual treatment for Graves' disease during pregnancy is the use of antithyroid drugs. At one time, doctors preferred propylthiouricil because they thought that it didn't cross the placenta, while methimazole did. However, pregnant women use methimazole in Europe and Asia without any problem, so most specialists feel that using either one is fine.\n\nThe dose of antithyroid drug that doctors use is the least amount that can keep the free T4 in the upper part of the normal range (see Chapter 4). When this is done, the fetus receives the right amount of T4 from the mother.\n\nA study of goiters in babies at birth found that 8 of 11 goiters were due to hypothyroidism in the baby, while 3 were due to hyperthyroidism. Of the eight hypothyroid babies, five of the goiters were a result of excessive amounts of antithyroid drugs that doctors gave to the mother during pregnancy. The results of this study emphasize how important it is to give the least amount of antithyroid drug that can make the mother normal.\n\nA few circumstances require surgery rather than antithyroid drugs, including the following:\n\n  The patient fails to take the antithyroid drug.\n\n  The mother needs exceptionally high doses of medication \u2014 more than 300 milligrams of propylthiouricil or 20 milligrams of methimazole daily.\n\n  A slow fetal heart rate indicates that the fetus may be hypothyroid due to the antithyroid drug the mother is taking.\n\n  The mother has extremely severe hyperthyroid symptoms.\n\n  The mother experiences side effects, like a fall in white blood cells, from the drug.\n\nIf a woman must have surgery, it's best done in the second trimester of the pregnancy, when it's least harmful to the fetus and the mother.\n\n .jpg)\n\nTo prepare for surgery, doctors sometimes give the mother iodine. Iodine passes easily through the placenta to the fetus, where it can cause goiter and hypothyroidism. Iodine is also found in topical compounds and dyes used for better observation of the growing fetus. The use of iodine is necessary in these situations, but be aware of (and talk with your doctor about) the consequences of its use.\n\n### Checking mother and child after birth\n\nThe easiest way to check the thyroid status of a newborn is to check the levels of free T4 and TSH in the umbilical cord serum. Treatment depends on the findings.\n\nAfter you deliver your baby, if your Graves' disease was under control during the pregnancy, you can expect a worsening of symptoms as the autoimmunity becomes severe again. Checking your thyroid function with blood tests after the delivery is important.\n\nPostpartum Graves' disease isn't the same as postpartum thyroiditis (see Chapter 11). The treatment for these two conditions is entirely different. Postpartum thyroiditis is a condition associated with a low uptake of radioactive iodine and results when a damaged thyroid spills thyroid hormone (rather than from stimulation by TSH receptor\u2013stimulating antibodies). Thyroglobulin also spills into the blood in postpartum thyroiditis but not in postpartum Graves' disease.\n\nPostpartum thyroiditis is associated with a finding of thyroid autoantibodies. Some specialists recommend that all pregnant women have tests for thyroid autoantibodies early in pregnancy, because about 50 percent of those with positive tests develop postpartum thyroiditis.\n\n### Breastfeeding with Graves' disease\n\nFor many years, doctors believed that mothers who were taking antithyroid drugs for Graves' disease shouldn't breastfeed because the drugs would enter the mothers' milk and pass to the babies. Recent studies have proved that this isn't the case.\n\nOne study shows no effect on breastfed infants when mothers take up to 750 milligrams of propylthiouricil (PTU) daily. In another study, no effect on breastfed infants was found when the mothers were taking up to 20 milligrams of methimazole daily. (For more information on related studies, see Chapter 21.)\n\nYou can breastfeed safely if you're taking antithyroid drugs for hyperthyroidism. Use the guidelines in the previous paragraph for the maximum dosage of drugs. Doctors should never give radioactive iodine for treatment to the mother with hyperthyroidism who is breastfeeding.\n\n## Gestational transient thyrotoxicosis\n\nHolly Bright is a 27-year-old woman who has become pregnant for the first time. She has had a lot of morning sickness during the first several weeks of her pregnancy. She notices that she has lost some weight, but she believes that it's due to the morning sickness. However, in the last few days, she has had symptoms of a rapid heartbeat, fatigue, trouble sleeping, and a feeling of warmth all the time. She checks with her obstetrician, Dr. Ufbaum. As a result of her recent experience with Alice Dummy, Dr. Ufbaum is convinced that Holly has Graves' disease. Thyroid function tests seem to confirm this. She refers Holly to Dr. Rubin.\n\nDr. Rubin isn't as convinced. He notices that her thyroid isn't enlarged. He is concerned about the extent of the vomiting that Holly describes. He sends her to be tested for TSH receptor\u2013stimulating autoantibodies. The result is negative. Dr. Rubin tells Holly that she probably has a condition called _gestational transient thyrotoxicosis._ He is able to reassure her that the condition will be brief. He gives her a low dose of propranolol, a drug that relieves her symptoms, along with a drug for her vomiting. Over the next few weeks, Holly returns to normal and has no further trouble with hyperthyroid symptoms. The thyroid function tests also return to normal.\n\nGestational transient thyrotoxicosis (GTT) is actually more common than Graves' disease in pregnancy, occurring as often as two to three times in 100 pregnancies. Fortunately, it's generally mild. But it's sometimes more serious, and doctors can confuse it with Graves' disease, leading to incorrect treatment.\n\nThe hormone human chorionic gonadotrophin (HCG), which I discuss in the section \"The Normal Thyroid During Pregnancy,\" earlier in the chapter, causes GTT. HCG is at its highest level in the mother's circulation at around ten weeks of pregnancy, but it continues to be elevated above normal throughout. It may appear in a form that's cleared very slowly from the circulation of the mother. It can act as a stimulant on the thyroid, leading to increased free T4 and decreased TSH, which produces a diagnosis of hyperthyroidism. No TSH receptor\u2013stimulating antibodies are found in GTT.\n\nAbout half of GTT patients show the typical symptoms of hyperthyroidism. In addition, many patients experience a significant increase in vomiting associated with this condition, sometimes called _hyperemesis gravidarum,_ as I mention previously _._ A goiter isn't usually present in patients with GTT.\n\nMost patients need no more treatment than beta blockers like propranolol (see Chapter 6). Sometimes the mother has to be given fluids to replenish what she loses from vomiting. Occasionally, she needs to take antithyroid drugs for a short time, until levels of HCG begin to fall (usually after ten weeks of pregnancy). However, in twin pregnancies, HCG levels may be particularly high and sustained for a longer time period. Some studies don't show a difference in the level of HCG between pregnant women who vomit a lot and those who don't. This suggests that women who experience a lot of vomiting may be making a form of HCG that's especially stimulating to the thyroid.\n\nThe most severe vomiting associated with GTT occurs when the level of thyroid hormone, the level of HCG, and the level of estrogen in the pregnant mother are all at a maximum.\n\n .jpg)\n\nIf you have symptoms of hyperthyroidism accompanied by vomiting early in pregnancy, your doctor should consider GTT as the diagnosis rather than Graves' disease. You can expect GTT to pass after several weeks, while Graves' disease requires treatment throughout the pregnancy in many cases.\n\n## Hydatidiform mole and choriocarcinoma\n\nOccasionally, as a result of some abnormality of the mother's egg or in fertilization, the placenta forms a series of grapelike clusters called a _hydatidiform mole._ No viable fetus can result from this mole, but in about 10 percent of cases it can secrete large amounts of HCG and cause hyperthyroidism. The mother often experiences vaginal bleeding, and her uterus isn't the correct size for the stage of the pregnancy (it's usually too large).\n\nDoctors often perform an ultrasound study in this situation, showing the mole very clearly. Because no viable fetus is present, the pregnancy is terminated.\n\nVery rarely \u2014 about 2 percent of the time \u2014 the mole changes into a cancer called a _choriocarcinoma,_ which also can make a large amount of HCG. Fortunately, this cancer is very treatable, and the patient may even be able to preserve the ability to have children.\n\n## New Thyroid Nodules in Pregnancy\n\nBecause pregnant women have frequent exams and their doctors follow them carefully, doctors sometimes discover thyroid nodules during pregnancy. In addition, pregnancy is a time of thyroid growth due to the need for increased iodine. Doctors find nodules in as many as 10 percent of pregnant women. Treatment depends on the tissue found in the nodule and the stage of the pregnancy.\n\nThe first step is to do a fine needle aspiration biopsy of the nodule (see Chapter 7). If the biopsy shows that a nodule is definitely cancer, and the patient hasn't yet reached her third trimester, she should have surgery of the thyroid at that time. The second trimester is the best time for this surgery, because it offers the least chance of interfering with the development of the baby or causing premature labor.\n\nIf the biopsy doesn't definitely show cancer, waiting until after the delivery, when a radioactive iodine scan is done (see Chapter 4), is safe. Keep in mind that after a woman has a radioactive scan, she can't breastfeed her baby. If the scan shows that the iodine uptake is high, the nodule probably isn't cancer. If the scan shows that the nodule remains cold, and the diagnosis remains uncertain, then the woman has surgery to obtain a final diagnosis and determine the appropriate treatment.\n\nSome evidence exists that pregnancy and breastfeeding tend to stimulate the development of a new thyroid cancer if the woman is less than 45 years of age. No association exists between the number of births, the age of the mother during the first birth, or her age during the last birth and the incidence of thyroid cancer if the woman is over 45, according to one study.\n\nPregnancy doesn't make the cancer worse in terms of spread of the tumor or recurrence. A woman who has received treatment for thyroid cancer previously is permitted to become pregnant after the treatment. Even if she had received radioactive iodine, it doesn't put her or her baby at risk in a later pregnancy.\n\n##### Chapter 18\n\n## Thyroid Conditions and Children\n\n### In This Chapter\n\n  Understanding thyroid function in newborns and infants\n\n  Screening for thyroid disease in babies\n\n  Dealing with hypothyroidism and hyperthyroidism in kids\n\n  Concentrating on goiters\n\n  Treating thyroid nodules in the young\n\nNewborns and children who have thyroid abnormalities present special problems because their brains and bodies are developing at the same time that their thyroids aren't functioning properly. Thyroid hormones are a critical part of their development. The hormones must be available in the right amount at the right time in order for a child to have normal mental function and normal growth.\n\nChildren can experience all the kinds of thyroid diseases that are found in adults. This chapter discusses normal thyroid development and the impact of thyroid diseases on a developing human being. As a parent, you can do little to treat these conditions, but your early recognition of a problem, your understanding of the consequences if the problem isn't treated, and your continued support of your child through treatment and recovery can have a major impact on the way your child handles the challenges of thyroid disease.\n\n## Understanding the Onset and Development of Thyroid Function\n\nThe body produces thyroid hormones (T3 and T4) when _thyroid-stimulating hormone_ (TSH) stimulates the thyroid to make them. TSH is released from the pituitary gland when the hypothalamus produces _thyrotrophin-releasing hormone_ (TRH). (For an expanded discussion of thyroid hormones, see Chapter 2.) All these structures and their hormones are in place when a baby is born. Much recent research has established how this process comes about.\n\n### Keeping fetal T3 normal in the brain\n\nThree chemicals in the fetus called enzymes affect the production of T3. The major enzyme, iodothyronine deiodinase 1 (D1), which con- verts T4 to T3 in the adult, is reduced in the fetus so blood levels of T3 are lower in the fetus than in the adult. The second enzyme, iodothronine deiodinase 2 (D2), which also converts T4 to T3, is found in the brain by seven weeks of gestation. The third enzyme, iodothyronine deiodinase 3 (D3), which converts T4 into inactive chemicals, is also found in the brain by seven weeks and protects the fetus from too much T4 from the mother. When T4 is too low, D2 increases its activity while D3 decreases it. Therefore, the brain always has enough T3, except in the most severe cases of lack of maternal T4.\n\n## Focusing on the fetus\n\nAfter just 15 weeks of development, the fetus shows function in its pituitary gland, and TRH is detectable. TSH and the other pituitary hormones start to appear between weeks 10 and 17. The thyroid is functioning by the 10th week, and its production of thyroid hormone becomes significant around the 20th week. The ability of thyroid hormone to shut off TSH production matures toward the end of the pregnancy and in the first two months after delivery.\n\nThe placenta acts as a barrier, preventing the mother's TSH from reaching the circulation of the fetus throughout the pregnancy. The placenta also contains an enzyme that breaks down the mother's thyroid hormones before they can reach the fetus. In breaking down the hormones, the enzyme releases iodine from the mother's hormones so the fetus can use the iodine to make thyroid hormone for itself. At the same time, the placenta is producing _human chorionic gonadotrophin (HCG),_ a hormone that stimulates the thyroid (see Chapter 17).\n\nAs the pregnancy progresses, the enzyme in the placenta that breaks down the mother's thyroid hormones stops working as much, and other enzymes take over to convert T4 into the active hormone, T3. By not working so much, the placental enzyme no longer prevents the mother's T4 from getting to the fetus. This is very important, because the fetus needs the T4 for normal development, especially of its brain, at a time when it can't make much T4 for itself.\n\nOne enzyme, which converts T4 to T3, works in the liver, the kidneys, and the thyroid. Another enzyme works mainly in the pituitary gland. If the fetus isn't getting enough T4, the enzyme in the pituitary increases, and the other enzyme decreases so the fetal brain gets enough T3.\n\n## Bringing a baby into the world\n\nWhen the baby is born, leaving the warmth of the uterus for the colder temperatures of the outside world, the baby's pituitary releases a large amount of TSH. This increased flow of TSH stimulates the thyroid to release a large amount of T3 and T4, causing the temperature of the baby's body to rise. (The T4 concentration in the baby increases by 50 percent, and the T3 concentration increases three or four times.) This process is known as the _TSH surge._ The TSH surge peaks after only 30 minutes but continues to stimulate extra thyroid hormone for the next 24 hours. A large increase in the enzyme that converts T4 to T3 is also responsible for the great increase in T3. Babies also produce T4 at a much higher rate than adults.\n\nA premature baby has similar hormone changes to a normal-term baby, but to a lesser extent. A premature baby doesn't have as much of a TSH surge and doesn't produce as much thyroid hormone. The T3 doesn't increase as much either, because the converting enzymes aren't yet as active. A premature baby can't defend its body temperature the way that a normal-term baby can.\n\nAs the baby grows, it stores more thyroid hormones in its thyroid along with thyroglobulin (see Chapter 2), and it produces more thyroid hormone. The thyroid gland grows so that the lobes are normally about the same size as the part of the baby's thumbs after the last joint (the _terminal phalanx_ ).\n\nA lack of thyroid hormone during fetal growth has important consequences (see Chapter 12). Thyroid hormone is particularly important in the development of hearing, but many other body organs also need it for proper development. Some of the damage that results from lack of thyroid hormone includes the following:\n\n  Immature bones\n\n  Immature liver\n\n  Reduced mental function\n\n  Increased sleepiness\n\nThe brain is dependent on thyroid hormone for development for the first two to three years after birth. For every month that a hypothyroid newborn doesn't receive thyroid hormone, the baby suffers a loss of five IQ points.\n\nDuring the first 20 years of life, the free T3 and free T4 slowly decline, as do the total T3 and total T4 (see Chapter 2 for an explanation of the difference between _free_ and _total_ ). As estrogen levels begin to rise during puberty in the female, her body makes more thyroid-binding globulin, and she has more total T3 and total T4. The decrease in the free T3 and free T4 is probably because of a gradual decline in TSH.\n\n## Screening the Newborn\n\nNoah Stern is the newborn son of Barry and Sally Stern. Sally finds that Noah feeds very poorly. He seems to be cold to the touch. Otherwise he appears fine.\n\nAccording to law, Noah is screened for hypothyroidism a couple days after birth. The TSH level comes back elevated at 35. The pediatrician notifies the Sterns and asks them to bring Noah in for testing. A blood test confirms that his TSH is elevated, and the free T4 is low. The pediatrician diagnoses Noah with congenital hypothyroidism.\n\nA thyroid scan is performed on Noah, which shows little active thyroid tissue. Noah is given thyroid hormone, and his feeding and his body temperature rapidly improve. Sally notices that Noah looks less puffy as well. The doctor measures thyroid functions frequently until Noah stabilizes. Noah grows and feeds normally. He doesn't appear to have any deficits in his intellectual development.\n\nThe major reason for screening for thyroid disease is to diagnose congenital hypothyroidism as early as possible. _Congenital hypothyroidism_ means hypothyroidism that is present when the baby is born (see the next section, \"Coping with Hypothyroidism in Children\").\n\nBecause the consequences of not treating hypothyroidism in newborns are so great and the response to early treatment is so successful, screening for thyroid disease is essential in the newborn. In a study of 800 children who had congenital hypothyroidism before the era of screening began in 1974, the average IQ was 80, which is low. Some of these babies were noted to have signs of hypothyroidism and were tested. Children who testing confirmed to have hypothyroidism and who received any treatment experienced no lowering of the IQ. Within that group, some children didn't receive adequate treatment. Even these children had normal IQs, though somewhat lower than the fully treated children.\n\nScreening is a simple process. A drop of blood is placed on filter paper. (This filter paper is the same type used for screening tests for other diseases as well.) Then the filter paper is tested for TSH (sometimes for total T4 instead). If the TSH is above 40, the baby has a regular blood test for TSH and free T4, and the doctor begins treating the baby with thyroid hormone while waiting for the result. If the TSH is between 20 and 39, the doctor performs blood tests but begins no treatment until the diagnosis is confirmed. The reason for this delay is that up to 75 percent of babies with a TSH at this level during screening test normal when they have a regular blood test.\n\nA TSH surge occurs immediately after birth. Screening on the first day may result in a false positive test.\n\nThe screening test isn't perfect. Screening fails to diagnose children who have _secondary hypothyroidism,_ which results from the body's failure to secrete TSH. Screening also won't identify children who have a normal TSH and a low T4 (which the screening doesn't measure) at birth, whose TSH becomes abnormal a week later. Premature babies, especially, may show this pattern. Babies who fail to secrete TSH often have failure of other hormones as well, which leads to many signs and symptoms that point to disease. It is the occurrence of these signs and symptoms that leads the doctor to do further testing.\n\nDoctors can misdiagnose infants with low birth weight because these babies tend to be born with low levels of hormones that soon rise to normal.\n\nScreening has shown that congenital hypothyroidism is more common than was previously thought, affecting about 1 in 3,750 babies. Doctors now do screening, by law, throughout the United States and in Western Europe, Japan, Australia, New Zealand, and Israel. A major campaign is under way to promote neonatal screening for thyroid disease throughout the world.\n\nNot only does screening make excellent medical sense, but it makes excellent economic sense as well. A study in Denmark found that the future medical costs for the babies who were found to be positive at screening, had they not been discovered and treated, would have been 28 times the cost of screening all the babies in Denmark.\n\n## Coping with Hypothyroidism in Children\n\nA number of conditions can cause hypothyroidism in the newborn and in the older child. You find out about these conditions in this section.\n\nSpecialists disagree as to whether pregnant mothers should be routinely tested for hypothyroidism to protect their babies from a hypothyroid environment. The incidence of hypothyroidism in the mothers is up to ten times as frequent as in the babies. Yet screening of the mothers very early in pregnancy isn't mandatory as it is for the babies, despite the great dependency of the fetus on the mother's T4, which is a strong argument for screening of all newly pregnant women. A study in the _New England Journal of Medicine_ in August 1999 showed that babies experienced some slight loss of IQ if their mothers were hypothyroid and untreated during pregnancy.\n\nMy own bias is that every pregnant woman should be screened for hypothyroidism with a TSH test. For more on the thyroid and pregnancy, see Chapter 17.\n\n## Transient congenital hypothyroidism\n\nDoctors diagnose some babies with hypothyroidism at birth because their TSH levels are found to be high, but these levels fall to normal shortly after birth. This condition is called _transient congenital hypothyroidism_ because it doesn't last. One common cause of this condition is iodine deficiency in the mother.\n\nThis condition is especially prevalent in very low-birth-weight infants, who should be screened for thyroid disease not only at birth, but also at two and six weeks of age.\n\nBecause this condition is so common in premature infants, the question is whether premature babies need thyroid supplementation for a short time at birth. A study in the _Texas Medical Journal_ in 2000 suggests that babies who have more than 27 weeks gestation at the time of birth don't need supplemental thyroid hormone at birth and that such treatment may actually harm them. Whereas babies who spend less than 27 weeks in the uterus may benefit from supplementation.\n\nSometimes, determining whether the hypothyroidism is transient or permanent isn't possible. In this case, the doctor treats the baby with thyroid hormone until the age of 4 and then stops treatment for a short time to see if the child can make her own thyroid hormone. This short pause in treatment doesn't damage the child's brain.\n\n## Congenital hypothyroidism\n\nBabies who are born with hypothyroidism that doesn't correct itself shortly after birth have _congenital hypothyroidism._ This condition used to be a significant cause of mental retardation, but since neonatal thyroid screening began in the 1970s, doctors are able to prevent mental retardation from occurring.\n\n### Causes\n\nMany causes lead to congenital hypothyroidism, but 80 percent of cases result from _thyroid dysgenesis_ \u2014 a failure of the thyroid to grow or to end up in its proper place in the neck. The following are common causes of thyroid dysgenesis:\n\n  No thyroid at all (a condition called _thyroid agenesis_ )\n\n  A small thyroid gland that can't make enough thyroid hormone _(thyroid hypoplasia)_\n\n  A thyroid gland that grows in the wrong place, often at the base of the tongue _(ectopic thyroid)_\n\nSome of the other far less frequent causes of congenital hypothyroidism include the following:\n\n  The baby's thyroid doesn't respond to TSH.\n\n  The mother is exposed to radioactive iodine that destroys the baby's thyroid.\n\n  The hypothalamus doesn't release TRH (a condition called _hypothalamic hypothyroidism_ ).\n\n  Some step of the synthesis of thyroid hormone is defective.\n\nWith the exception of maternal exposure to radioactive iodine, the conditions in the preceding list are all genetic diseases (see Chapter 14). In the United States, these diseases are rare among African Americans and more frequent among Hispanics.\n\n### Signs and symptoms\n\nMany babies with congenital hypothyroidism have few signs or symptoms of hypothyroidism at birth. Screening discovers this condition (see \"Screening the Newborn,\" earlier in the chapter). If the condition is severe, the baby shows some or all of the following signs:\n\n  Low body temperature\n\n  Slow heart rate\n\n  Poor feeding\n\n  Umbilical hernia (an outward protrusion of the umbilicus \u2014 the belly button \u2014 that may contain intestine)\n\nOnce doctors recognize and confirm the condition, treatment should begin immediately. Doing a thyroid scan just before treating the baby may help detect any functioning thyroid tissue, a lack of which indicates the need for lifelong treatment. Doctors may not see tissue or may find it in an unusual site. If no tissue is seen on the thyroid scan, a thyroid ultrasound shows whether tissue exists and whether it's unable to take up iodine, possibly due to a genetic abnormality. This information can be helpful in counseling the parents about hypothyroidism in future children.\n\n### Treatment\n\nBabies with congenital hypothyroidism are usually given a relatively high dose of thyroxine (T4) hormone replacement for the first week to restore their thyroid hormone levels. The daily dose administered after that initial dose must be individualized.\n\nDoctors should check the baby's thyroid function at 7, 14, and 28 days. In view of all the changes taking place in thyroid function soon after birth, the stabilization of thyroid function may take time. Once the tests are normal and stable, the tests are measured every three months until two years of age and then every year until the child shows normal and stable thyroid function three years in a row.\n\nDoctors determine proper dosing of thyroid hormone not only by performing thyroid function tests but also by making sure that the baby is growing properly. Doctors check the height and weight of the baby regularly to verify the hormone dosage.\n\nIf thyroid hormone treatment is delayed more than four to eight weeks after birth, a child with congenital hypothyroidism will almost certainly have some decrease in intellectual function.\n\n## Acquired hypothyroidism\n\nChildren may acquire hypothyroidism at any time after birth. When hypothyroidism occurs in a child over the age of 2, it doesn't damage brain function, but it does greatly affect growth and development.\n\n### Causes\n\nChildren may develop hypothyroidism for all the same reasons that adults become hypothyroid. Iodine deficiency is, by far, the most common cause throughout the world. Where iodine is sufficient, autoimmune thyroiditis (see Chapter 5) is the leading cause. Less common reasons for acquired hypothyroidism include\n\n  Drugs like iodine or lithium\n\n  Irradiation \u2014 externally (for a tumor, for example) or internally, in treatment of hyperthyroidism with radioactive iodine\n\n  Removal of the thyroid for any reason\n\n  Abnormal production of thyroid hormone\n\n  Resistance to thyroid hormone\n\n  Central or secondary hypothyroidism due to a tumor in the pituitary or hypothalamus or a lack of production of TSH or TRH\n\n### Signs and symptoms\n\nThe signs and symptoms of acquired hypothyroidism in children are similar to the signs and symptoms found in adults, except that a growing, developing child experiences the consequences of poor growth. Constipation and dry skin are features of any hypothyroid person. The child, in addition, doesn't keep up with height and weight guidelines for growing children.\n\nThe child who becomes hypothyroid after he enters school starts to have trouble with schoolwork or keeping up with the physical activity of the other children. Lack of energy is a major complaint at this time.\n\nInterestingly, some hypothyroid kids appear unusually muscular despite being weak. This is because they have swelling of their muscle fibers, called _pseudohypertrophy_ of muscles.\n\nThe growth of the skeleton and the teeth is delayed. Other signs of acquired hypothyroidism include\n\n  Enlarged thyroid (goiter), unless it has been removed\n\n  Dry, cool skin that's puffy, pale, and yellowish\n\n  Brittle nails and dry, brittle hair that tends to fall out excessively\n\n  Swelling that doesn't retain an indentation, especially of the legs\n\n  Hoarseness and slow speech with a thickened tongue\n\n  An expressionless face\n\n  A slow pulse\n\n  Early sexual development (occasionally)\n\nEarly sexual development is thought to be the result of the large amount of TSH in these children's bodies. TSH has a structure that shares some features with _follicle-stimulating hormone_ (FSH). The TSH activates cells that normally respond to FSH, so girls may have early vaginal bleeding, and boys may have large testicles for their age. The boys don't have a lot of male hormone, which is the result of stimulation by another hormone, _luteinizing hormone_ (LH). TSH doesn't share features with LH. The girls, however, do have increased estrogen for their age because their ovaries can respond to the FSH-like properties of TSH; LH-like stimulation isn't necessary to accomplish increased estrogen production.\n\nThe adolescent who develops hypothyroidism has signs and symptoms that parallel the symptoms in a hypothyroid adult, with a few differences. If the child has begun puberty, puberty may stop unless the child receives thyroid hormone treatment. Also, a delay in the growth of permanent teeth may occur, and the child doesn't gain height as quickly as normal.\n\nWhen central or secondary hypothyroidism (a lack of TRH or TSH; see Chapter 5) is the cause, the signs and symptoms of hypothyroidism tend to be milder. The main symptoms are due to the underlying cause, which may be a brain tumor, for example. The child complains of headaches or trouble with vision.\n\n### Laboratory confirmation\n\nA TSH and free-T4 test confirm the diagnosis of hypothyroidism. In order to make a diagnosis of chronic (autoimmune) thyroiditis, doctors test the child for the presence of thyroid autoantibodies. X-rays that evaluate any growth abnormalities determine the child's bone age.\n\nIf central hypothyroidism is responsible, the free T4 and the TSH are low, as are the other hormones the pituitary gland makes. An X-ray of the pituitary is necessary to look for a tumor.\n\n### Treatment\n\nThe current treatment for hypothyroidism is thyroxine (T4) hormone replacement. However, recent studies suggest that giving both T3 and T4 replacement in the same proportions the normal thyroid makes may be more appropriate (see Chapter 5). This conclusion is based on studies in adults. Similar studies in children haven't been published.\n\nIn most cases, doctors change the dose of replacement hormone until the TSH is normal. However, if the cause is central hypothyroidism, doctors can't use the TSH as a guide because the pituitary isn't making any TSH.\n\nIn some cases, starting the child at a low dose of the replacement hormone and gradually increasing to the full therapeutic dose may be necessary. Some children show more symptoms when they suddenly go from no thyroid hormone to full replacement. They experience trouble sleeping, restlessness, and deterioration in their school performance. The rare patient has headaches due to increased pressure in the brain. Lowering the dose and gradually building it back up manages this situation.\n\nIf the child's growth has been delayed, she usually catches up when she takes thyroid hormone.\n\n .jpg)\n\nGiving too much thyroid hormone may cause early bone closure, resulting in stunted growth and a decrease in the mineral content of the bone.\n\n## Dealing with Hyperthyroidism in Children\n\nHyperthyroidism rarely occurs in babies and is less common in children and adolescents than in adults. Almost always, kids with hyperthyroidism have Graves' disease (see Chapter 6). When a newborn is hyperthyroid, usually the mother is also hyperthyroid (see Chapter 16), and the mother's thyroid-stimulating antibodies have passed to the fetus. When these antibodies are cleared from the fetus after is born, the hyperthyroidism subsides about 3 to 12 weeks after birth.\n\n## Signs and symptoms\n\nWhen a mother with hyperthyroidism passes a large amount of thyroid- stimulating antibodies to the fetus through the placenta, the fetus develops hyperthyroidism. The signs of the hyperthyroidism in the fetus include\n\n  Rapid heart rate\n\n  Increased fetal movements\n\n  Poor fetal body growth\n\n  Abnormally rapid bone growth\n\nAfter the baby is born, the baby shows a number of signs and symptoms of hyperthyroidism. They're the result of excessive metabolism in a baby who should be growing and developing normally. These signs and symptoms include\n\n  Low birth weight and failure to gain weight\n\n  Increased appetite\n\n  Irritability\n\n  Rapid heart rate\n\n  Enlarged thyroid\n\n  Prominent eyes\n\nHyperthyroidism is rare in children under the age of 5, and Graves' disease is usually the cause. Once in a while, the cause may be a functioning thyroid adenoma, a new growth of tissue on or within the thyroid that's making excessive amounts of thyroid hormone. Girls are more often affected than boys by thyroid adenomas. A family history of other autoimmune diseases may exist if the cause is Graves' disease.\n\nIn children under the age of 5, the signs and symptoms of hyperthyroidism are like those seen in adults (see Chapter 6). But the needs of a growing child who has reached school age temper these signs and symptoms. Unique signs at this age include the following:\n\n  Poor school performance\n\n  Trouble sleeping\n\n  Poor athletic performance related to muscle weakness\n\n  Tiredness\n\n  More rapid growth in height but early closure of bone growth\n\n  Irritability\n\nHyperthyroid children are hungry all the time but don't gain weight despite eating. They generally have mild eye disease. They have goiters and also have bowel movements more frequently than they should.\n\nHyperthyroidism in children before they reach puberty tends to be more severe than in children after puberty. They need longer treatment and go into remission less often than the older children, which is particularly true if the child is less than 5 years old.\n\nChildren with Graves' disease have a greater tendency to develop other autoimmune diseases (see Chapter 14), such as Addison's disease, type 1 diabetes mellitus, and so forth.\n\n## Laboratory confirmation\n\nObtaining a free T4 and a TSH level confirms the diagnosis of hyperthyroidism. If doctors suspect fetal hyperthyroidism, they can determine these levels from umbilical cord blood at birth. If hyperthyroidism is present, the free T4 is high and the TSH low. Rarely, if the hyperthyroidism is due to excessive TSH secretion from the pituitary, the TSH is high. In that case, the doctor should be on the lookout for a pituitary tumor. Doctors rarely do a thyroid scan and uptake unless they suspect that the child has subacute thyroiditis (see Chapter 11), which shows a low uptake, the opposite of Graves' disease.\n\n## Treatment\n\nIf your child has hyperthyroidism, you have many treatment options. The important point to remember is that your scrutiny doesn't end with treatment, because the recurrence of hyperthyroidism or the development of hypothyroidism can accompany all forms of treatment.\n\nBe sure that you follow up with your child's condition regularly after treatment, because the disease process is ongoing. Regularly means every six months or yearly, as your doctor recommends.\n\nIf the fetus is hyperthyroid, the doctor gives antithyroid drugs to the mother. The drugs pass through the placenta to affect the fetus's thyroid hormone production. The goal is to have a fetal heart rate less than 140 beats per minute. Sometimes, the mother takes a beta blocker (such as propranolol) to control severe symptoms.\n\nAntithyroid drugs are another treatment for hyperthyroidism in babies. Once the baby receives treatment, the baby rapidly improves. In a few months, the pediatrician withdraws the antithyroid drugs because the thyroid-stimulating antibodies that were passed from mother to baby disappear from the baby.\n\n### Radioactive iodine\n\nAt one time, doctors resisted using radioactive iodine to treat hyperthyroidism in children. However, doctors commonly use this treatment today because long-term studies have shown no negative effects upon the child. Specifically, radioactive iodine causes no increase in cancer, no loss of fertility, and has no negative effect on the offspring of children treated with radioactive iodine.\n\nThe problem with radioactive iodine is that most children become hypothyroid after some time. (The same is true of adults; see Chapter 6.) In addition, thyroid eye disease may get worse with radioactive iodine because of the release of a lot of antigen from the thyroid.\n\n### Antithyroid drugs\n\nAntithyroid drugs, such as propylthiouricil (PTU) and methimazole, are the preferred treatment for hyperthyroidism in children. They take three to six weeks to work, but they control the disease in at least 85 percent of children. If the medication doesn't work, the child either has a very large goiter or doesn't take the medication as prescribed. In most cases, doctors continue the treatment for two to four years.\n\nHow does the doctor choose which of these drugs to use? PTU has the advantage of blocking the conversion of T4 to T3, whereas methimazole lasts longer after taking it. In practice, these differences don't seem to matter much. I tend to use methimazole only because I have more experience with it, not because I believe it's better.\n\nIf the disease recurs after the child stops taking the pills, the child usually has measurable amounts of TSH receptor\u2013stimulating antibodies. Doctors do this test at the time they stop treatment to help to predict a recurrence. The drugs may fail to produce a permanent remission in up to half the patients treated, even though 85 percent can be controlled temporarily.\n\nJust as in adults, antithyroid medications cause side effects in children. The most important is the halting of the production of white blood cells. The doctor should monitor white blood cells, and if the white blood cell count is less than 1,000, must stop the drug. If the doctor uses PTU initially, the child is not switched to methimazole and vice versa. The child receives a totally different treatment. Sometimes the white blood cell count falls a little, but it returns to normal after some weeks. Another important side effect is the development of a rash, which the doctor can treat without needing to stop the drug.\n\n### Surgery of the thyroid\n\nSometimes antithyroid drugs cause serious side effects, or the child doesn't take the pills correctly, and radioactive iodine isn't an option (usually because the parents are concerned about giving radioactivity to their child). In these cases, surgery is a safe and rapid form of treatment when done by a competent surgeon who has experience with children. If possible, the antithyroid drugs should secure normal thyroid function before the child undergoes surgery. The doctor gives the child iodine for two weeks prior to surgery to block the thyroid gland and reduce blood flow into it. The usual operation is a near total thyroidectomy (see Chapter 13).\n\nLeaving enough thyroid tissue to retain thyroid function while eliminating hyperthyroidism may be possible, but the doctor must check the child at least every six months to a year to detect a recurrence or loss of thyroid function and the need for thyroid medication.\n\n## Diagnosing Goiters in Children\n\nAn enlarged thyroid gland (a goiter) is actually the most common thyroid abnormality doctors find in children. It occurs in about 5 percent of all children. A child with an enlarged thyroid usually has normal thyroid function.\n\nThe most common cause of thyroid enlargement in children is autoimmune thyroiditis (see Chapter 5). The second most common cause is a multinodular goiter (see Chapter 9).\n\nDifferentiating between these causes is important because autoimmune thyroiditis can lead to hypothyroidism (or sometimes hyperthyroidism), whereas a multinodular goiter doesn't. Thyroid autoantibody studies tell the difference, pointing to autoimmune thyroiditis if the results are positive. Testing the child's levels of free T4 and TSH verifies that her thyroid function is normal.\n\nChildren with autoimmune thyroiditis may have a negative thyroid antibody test the first time but develop the antibodies later. Therefore, doctors should perform testing more than once to find these children, especially if a family history of autoimmune thyroiditis exists.\n\nThese goiters sometimes get smaller and then larger again, sometimes growing at different rates in different parts of the thyroid, leading to a multinodular thyroid gland.\n\nDoctors apply treatment if the large thyroid is pressing on nearby structures like the esophagus and trachea or is disfiguring. The treatment is either surgery or radioactive iodine. Doctors check the thyroid every six months for a few visits and then yearly.\n\nIf the goiter is painful, the diagnosis is more likely subacute or acute thyroiditis (see Chapter 11). These diseases cause similar signs and symptoms in children as they cause in adults. Subacute thyroiditis generally makes a child less sick than acute thyroiditis. Subacute thyroiditis affects the whole gland, whereas acute thyroiditis may swell only part of the gland. If acute thyroiditis occurs several times, a malformation may exist in the thyroid that will probably require surgery.\n\n## Finding Nodules and Cancer in Children\n\nAlthough a functioning nodule or a cystic nodule (see Chapter 7) is rarely cancer in an adult, this isn't true in children. Children rarely get thyroid nodules, but when they do, the nodules indicate cancer more frequently than they do in adults. The incidence of nodules in children by examination is about 1 percent. But young adults who are autopsied have an incidence of 13 percent, and older adults are found to have nodules 50 percent of the time, so the true incidence in children may be higher. The signs that make a nodule particularly suspicious for cancer are the same as in adults: rapid growth, painlessness, firmness and fixation, and nodes felt in the neck.\n\nA number of risk factors exist for nodules in children, which include\n\n  Female sex\n\n  Family history of thyroid disease\n\n  Previous thyroid disease\n\n  Onset of puberty\n\nA very important clue that a child's nodule may be cancerous is past exposure to irradiation. Exposure leads to nodules and cancer in multiple places in the thyroid. (The leading type of thyroid cancer in both children and adults is _papillary_ \u2014 the type of cancer most closely associated with irradiation exposure.) Exposure to X-rays isn't limited to people living in the area around a nuclear power plant. In the United States, in the not-so-distant past, doctors used X-rays to treat acne and enlarged thymus glands (which lie near the thyroid). Children with Hodgkin's disease also receive X-ray treatment, which may result in cancer later.\n\nChildren with a history of exposure to irradiation need to be followed regularly with thyroid function tests and thyroid ultrasound studies. Make sure your child's doctor does these tests every six months to a year.\n\nA doctor does a fine needle biopsy of the nodule if she suspects cancer; the false negative result is only about 4 percent. Doctors should perform the biopsy under ultrasound guidance because the tumors in children tend to be smaller than adult tumors. Solid nodules are cancerous much more often than cystic nodules.\n\nIn children, thyroid cancer presents itself as a painless mass about 90 percent of the time. Of all diagnosed thyroid cancer cases in children, 25 percent already have lymph nodes in the neck that can be felt. A thyroid mass that's hard or a thyroid that's fixed and doesn't move with swallowing is more suggestive of thyroid cancer. Thyroid function tests (free T4 and TSH) are usually normal.\n\nThyroid cancer is the most common malignancy of the endocrine glands in children. Thyroid cancer is the papillary form (see Chapter 8) in 75 percent of cases. The rest are follicular and medullary cancers. Children tend to have more cancer spread in the neck and into the lungs at the time of diagnosis than adults do, but this doesn't make their prognosis worse. The cancer can be managed just like adult cancer with a total thyroidectomy (see Chapter 13), preserving the parathyroid glands and the recurrent laryngeal nerves. Radioactive ablation of the remaining thyroid tissue follows the thyroidectomy. Doctors place the patient on thyroid hormone to replace the thyroid hormone and to suppress growth of new thyroid tissue.\n\nDoctors monitor children with thyroid cancer with thyroglobulin blood tests; this test should read close to 0 shortly after surgery. Doctors do the blood tests every six months to a year. If the level of thyroglobulin rises, a whole body scan is done, looking for tissue that takes up iodine. Doctors can do the scan using the new recombinant TSH (see Chapter 8), so the patient doesn't have to stop taking thyroid hormone to perform this study. If doctors find all the iodine in the neck, local surgery may be enough to eliminate the additional thyroid cancer tissue. If the tissue is spread around the body, a large dose of radioactive iodine destroys it.\n\n##### Chapter 19\n\n## Thyroid Disease and the Elderly\n\n### In This Chapter\n\n  Discovering how many elderly people have thyroid disease\n\n  Recognizing the difficulty of diagnosis\n\n  Dealing with hypothyroidism and hyperthyroidism\n\n  Treating thyroid nodules in the elderly\n\nBefore we start talking thyroids, let's get our definitions straight. Who is \"elderly\"? The answer to this question becomes more and more important to me as I get older. For the sake of the information in this chapter, let's accept the definition used in most studies, namely, a person age 65 or older.\n\nThyroid disease often afflicts elderly people. The trouble with thyroid disease in the elderly, and the reason that I devote an entire chapter to it, is that doctors so often miss it. Doctors miss it for two key reasons. First, when elderly people go to a doctor, hospital, or nursing home, the illness or condition that prompts them to seek care is, naturally, the doctor's primary focus. Second, symptoms of thyroid disease often mirror symptoms of other conditions, so even if the doctor looks for other conditions in the patient, the doctor can easily misdiagnose thyroid disease in an elderly patient.\n\nWhen doctors are taught about disease, they learn a set of signs and symptoms that are characteristic of the disease. Elderly patients with thyroid disease may have none of the symptoms typical of the disease, or their symptoms may be almost opposite of what doctors expect. The only way doctors are going to discover thyroid disease in many elderly patients is with screening \u2014 obtaining thyroid function tests from a person who appears to be healthy.\n\nScreening for thyroid disease in the elderly has its own problems. The main problem is that screening picks up a lot of _subclinical disease_ \u2014 a situation where one blood test isn't normal but another is, and the patient has no symptoms of the disease. Tremendous controversy exists concerning what to do with subclinical thyroid disease. As a community, doctors haven't yet made any final decisions about whether to treat subclinical thyroid disease, wait for symptoms to develop, or wait for both thyroid blood tests to become abnormal. In this chapter, I share my own biases as I discuss the various diseases.\n\n## Thyroid Changes in the Elderly Due to Aging and Nonthyroidal Disease\n\nThe blood levels of thyroid hormones differ in the elderly compared to younger individuals. Also, chronic illness, common in the elderly, causes changes in thyroid hormone levels that need to be understood so they will not be thought to be thyroid disease and treated.\n\n## Normal aging changes\n\nThere are normal changes in thyroid function in the elderly that should not be confused with disease of the thyroid. Among the more important are the following:\n\n  The baseline TSH levels in older people are higher.\n\n  Baseline free T4 and free T3 levels are lower.\n\n  Production of T3 from the thyroid and from removal of iodine from T4 is diminished.\n\n  Uptake of iodine by the thyroid is diminished.\n\nHowever, the size of the thyroid correlates more with body weight and less with aging.\n\n## Changes due to chronic illness or drugs\n\nThyroid function tests also change in response to nonthyroidal chronic illness and a poor nutritional state, neither very uncommon in the elderly. Drugs (see Chapter 10) may alter thyroid tests as well. The changes, which need to be understood so the person isn't treated as though he has a thyroid condition, include the following:\n\n  A fall in free T3\n\n  A fall in serum TSH\n\n  Later on, a fall in free T4\n\nKnowing whether thyroid disease is present is difficult when doctors find the preceding changes. But if free T3 falls, TSH should rise unless failure of the pituitary to make TSH (secondary hypothyroidism) occurs. If the patient overcomes the chronic illness, these changes return to normal.\n\nWhen these changes in thyroid hormone levels are found, whether they're the body's way of adjusting to aging or illness in a way that helps the body or are part of the disease and need to be reversed with thyroid hormone isn't clear. Giving patients with these changes thyroid hormone doesn't seem to make a difference.\n\n## Real Thyroid Disease in the Elderly\n\nTo determine how many elderly people thyroid disease affects, we need yet another definition. How do we define \"thyroid disease\"? Is having an abnormal TSH level sufficient to make a diagnosis, or must the free T4 level be abnormal as well? (See Chapter 4 for information about these tests.) This is difficult to answer in the elderly, because they often have so many symptoms; many of these symptoms are symptoms of other conditions as well as thyroid disease.\n\n## Looking at current definitions of thyroid disease\n\nSome doctors consider an abnormal TSH to be insufficient evidence of thyroid disease; they use the term _subclinical_ to describe the situation where the TSH is abnormal but the free T4 is normal. They advocate against treating a patient with subclinical thyroid disease. Yet many studies show that treatment reduces or eliminates many of the symptoms. On the other hand, treating an elderly person, particularly with thyroid hormone, for hypothyroidism may not be entirely benign and helpful, as I discuss later in this chapter in the section on hypothyroidism in the elderly.\n\nThe most recent clinical studies in 2005 indicate that subclinical hypothyroidism is associated with damage to the heart and that treatment prevents that damage. Studies from two different groups published in the _Archives of Internal Medicine_ in November 2005 showed that heart failure and heart attacks occurred more often in patients with subclinical hypothyroidism than in normal people. Thyroid specialists may reconsider their refusal to treat subclinical hypothyroidism as a result of these findings.\n\nIn one study from the United Kingdom, published in the _Archives of Internal Medicine_ in January 2001, doctors tested all patients age 65 or older for thyroid disease when they entered the hospital. Out of 280 patients (leaving out those who already were known to have thyroid disease), 9 had hypothyroidism, and 5 had hyperthyroidism. Doctors had previously suspected none of these 14 cases. An additional 21 patients had subclinical hypothyroidism (high TSH, normal free T4), and 12 had subclinical hyperthyroidism (low TSH, normal free T4). The authors stated that overall, nearly 40 percent of the elderly people not thought to have thyroid disease had some evidence of it. Should all these people receive some treatment?\n\nWriting in rebuttal to this study, other authors suggested that many of the people with subclinical disease actually have temporary abnormalities caused by other diseases.\n\nIn another study of elderly people who weren't hospitalized, researchers discovered unsuspected hyperthyroidism in 1 percent and unsuspected hypothyroidism in 2 percent of participants. So 3 of 100 elderly people are walking around with clinical thyroid disease. That may not seem like a lot, but in the population of the United States, it means that almost one million elderly people are walking around with undetected and highly treatable thyroid disease. (That number doesn't even account for the age group 35 to 65, which contains many more cases of undiagnosed thyroid disease.)\n\nLarge population studies have shown that 10 percent of women over age 65 have elevated TSH levels. Most of them don't have symptoms of thyroid disease.\n\nI find it interesting that no argument exists about screening babies for thyroid disease (when the occurrence of abnormal tests is 1 in 3,750), yet the debate continues about screening the elderly (when doctors may find 3 in 100 cases of clinical thyroid disease).\n\nMy own bias is that everyone should be screened for thyroid disease beginning at age 35 and every five years thereafter. Doctors easily perform screening with a TSH test. If this test is abnormal, then the doctor does a free T4 test. If both tests are abnormal, the patient is treated for thyroid disease. If only the TSH is abnormal, taking a careful history and doing a physical examination is reasonable. Then the doctor decides on treatment based on that evaluation. Doctors can take other factors into consideration when making the decision whether to treat; later in the chapter, I discuss these factors in relation to specific diseases.\n\n## Trying thyroid hormone for subclinical patients\n\nDoctors find that more than 10 percent of elderly women and 3 percent of elderly men have abnormally high TSH when tested. Among elderly patients with subclinical thyroid disease whose TSH level is less than 10, only half show some clinical improvement after receiving thyroxine (T4 hormone replacement). Such patients should probably not receive treatment if they complain of anginal heart pain. Every patient whose TSH level is over 20 improves with treatment.\n\nAn important study, whose results indicate that doctors should treat subclinical hypothyroidism in the elderly, was published in _Clinical Endocrinology_ in 2000. It was a study of 1,843 people ages 55 and over. Researchers evaluated all patients for the presence of hypothyroidism and followed the patients for as short a time as just two years. Of those individuals in the study who had an elevated TSH but a normal free T4, the risk of dementia and Alzheimer's disease was three times greater than the risk of those with normal TSH and free T4. The lower the free T4 (though still in the normal range), the higher the incidence of dementia and Alzheimer's. Those individuals who had positive antiperoxidase antibodies also had a higher incidence of dementia. The authors' conclusion was, \"This is the first prospective study to suggest that subclinical hypothyroidism in the elderly increases the risk of dementia and Alzheimer's disease.\"\n\nAnother factor that influences treatment decisions is that an elderly patient who has subclinical hypothyroidism along with another autoimmune disorder \u2014 such as type 1 diabetes, pernicious anemia, rheumatoid arthritis, or premature graying of the hair \u2014 is likely to eventually become clinically hypothyroid. In addition, certain other disorders, such as high blood pressure and nonpernicious anemia, may be associated with hypothyroidism and may reverse with thyroid hormone treatment. The anemia and high blood pressure, in turn, may be damaging to the heart, the brain, and the kidneys.\n\nMake sure your doctor tests you for hypothyroidism if you have recent onset of high blood pressure or anemia.\n\nIf you have subclinical thyroid disease and your doctor starts you on thyroid-hormone replacement, there are several reasons why you may want to continue that treatment. If you test positive for thyroid autoantibodies and you have a high TSH, chances are very good that you'll develop clinical hypothyroidism in the future. Also, your cholesterol level may benefit from the thyroid hormone; a measurement of cholesterol before and after taking the pills may show that it has been lowered significantly. The thyroid hormone also often lowers a chemical in the blood called _homocysteine,_ which can contribute to heart disease.\n\n## Sources of Confusion in Diagnosis\n\nThe natural consequences of aging, the many complicating diseases found in the elderly, and medications can all confuse a diagnosis of thyroid disease. Aging and other diseases can cause symptoms that may be identical to those found in thyroid disease. Medications cause changes in laboratory tests that confuse the diagnosis (see Chapter 10).\n\n## Other chronic illnesses, conditions, and diseases\n\nNonthyroidal chronic illness and certain diseases common in the elderly also cause changes in thyroid hormone levels that doctors need to understand so they won't mistake them for thyroid disease. The more common conditions and diseases that confuse thyroid testing are\n\n  Poor nutrition\n\n  Poorly controlled diabetes mellitus\n\n  Liver disease\n\n  Heart failure\n\nSevere illness causes a temporary fall in T4 that doctors may misdiagnose as hypothyroidism.\n\n## Medications\n\nDrugs the elderly often take that can alter thyroid function tests include the following:\n\n  **Epilepsy drugs:** Epilepsy drugs such as carbamazine and diphenylhydantoin cause the rapid breakdown of thyroid hormones by the liver, which lowers thyroid hormone levels in the blood.\n\n  **Aspirin:** Aspirin decreases the binding of thyroid hormones to thyroid-binding globulin, thereby lowering the total (but not the free) T4.\n\n  **Arthritis drugs:** Arthritis drugs such as prednisone decrease thyroxine-binding globulin levels.\n\n  **Drugs for abnormal heart rhythm:** These drugs, particularly amiodarone, can cause both hypothyroidism and hyperthyroidism.\n\n  **Heparin:** Heparin, used for anticoagulation, can cause a temporary rise in T4 by displacing it from binding proteins.\n\nFor a complete discussion on medications and their effect on the thyroid, please see Chapter 10.\n\n## Discovering Hypothyroidism in the Elderly\n\nVictor Brooklyn is a 68-year-old man who has been feeling a bit fatigued lately. He has put on a few pounds, and he feels cold when others seem comfortable. He also notices that he is more constipated than before. Victor thinks that all these changes are the natural effects of aging. He had been constipated for years, but it has recently become a serious problem, and this is what brings him to his doctor. The doctor observes that Victor's pulse is slow and that he has lost some of his eyelashes. He tells Victor that he believes this may be hypothyroidism and sends him for thyroid function tests.\n\nThe TSH level comes back high at 9, but the free T4 is within the normal range. Because his doctor is unsure of what to do, he sends Victor to Dr. Rubin. Dr. Rubin tells Victor that he appears to have subclinical hypothyroidism, although he thinks that his thyroid is causing the symptoms that Victor describes. He puts Victor on thyroid-hormone replacement pills.\n\nAfter two weeks, Victor notices that his bowel movements improve. He is less tired and less cold. He returns to Dr. Rubin for repeat thyroid function tests. The TSH is now 6, so Dr. Rubin increases the dose of thyroid hormone. A month later, the TSH test is down in the normal range, and Victor states that he is now just his mildly constipated self.\n\n## Deciphering signs and symptoms\n\nDoctors so easily miss the diagnosis of hypothyroidism in the elderly that I have to admit I've missed it myself on occasion (very rare occasions, of course). The principal reason is that so many of the changes our bodies experience as we grow older are typical findings in hypothyroidism. Some of the most important are the following:\n\n  Slowing of mental function\n\n  Slowing of physical function\n\n  Tendency to have a lower body temperature\n\n  Intolerance of cold\n\n  Constipation\n\n  Hardening of the arteries\n\n  Elevation of blood fats (especially cholesterol)\n\n  Weight gain\n\n  Elevation of blood pressure\n\n  Anemia\n\n  Muscle cramps\n\n  Dry skin\n\nAll the above changes are common effects of aging but are also signs and symptoms of hypothyroidism.\n\nOn the other hand, some signs found in the elderly tend to point away from a diagnosis of hypothyroidism, making an accurate diagnosis even less likely. For example, the elderly get Parkinson's disease, which results in tremors, or they simply develop senile tremors. Many elderly people lose weight because of poor nutrition; they may also be nervous. These symptoms may point to an overactive thyroid, but they definitely don't neatly fit into the list of symptoms of hypothyroidism.\n\nMany elderly people with hypothyroidism don't have goiters. Just as in younger patients, the most common reasons for hypothyroidism in the elderly are chronic thyroiditis and previous removal of the thyroid for cancer or hyperthyroidism (see Chapter 5).\n\n## Getting laboratory confirmation\n\nThe only way to know for sure that an elderly person doesn't have hypothyroidism is to obtain thyroid function tests. If hypothyroidism is present, the free T4 should be low, and the TSH should be high (see Chapter 5). Often the TSH is high, but the free T4 is normal \u2014 the situation known as _subclinical hypothyroidism._ The only way to determine whether hypothyroidism is having an effect on the patient is to give a trial of thyroid hormone. I am very much in favor of doing this, although, as I explain in the next section, the patient may not feel much different on medication.\n\n## Taking treatment slowly\n\nAs far as treatment is concerned, it has been thought that it's most important that the doctor go slowly. The doctor should start the patient with a very low dose of thyroxine (for example, 25 micrograms), increasing it every four to six weeks until the TSH is at the upper limit of normal. You don't want excessive treatment, because it can possibly worsen heart pain and increase shortness of breath, palpitations, and rapid heartbeats, as well as nervousness and heat intolerance. Even the first exposure to a small dose of thyroxine may bring on anginal chest pain. An excessive dose causes osteoporosis, a thinning of the bones. These problems may be more theoretical than real. No careful study has shown that older people have more trouble with thyroid hormone than younger ones.\n\nThe major problem doctors have when treating elderly patients with hypothyroidism may be one of adherence \u2014 ensuring that a patient is taking his or her medication. If you have a parent who must take medication, putting the pills into a case with daily slots may help. Ultimately, only someone standing beside the patient, observing him or her taking the drug, can be sure.\n\nThe dose of thyroid that provides normal thyroid function in these elderly patients is usually lower than that of younger patients.\n\nTesting thyroid function on a regular basis is important to ensure that the TSH and free-T4 levels remain normal. Testing every six months should be adequate.\n\nThe elderly with hypothyroidism are especially at risk of developing myxedema coma (see Chapter 5). With all their other diseases, myxedema coma is particularly dangerous for this age group.\n\n## Hyperthyroidism in the Elderly\n\nToby Dummy is the 76-year-old aunt of Stacy and Karen Dummy. Her husband has noticed that she seems depressed lately. Although she used to love to cook, she seems to have lost interest. She sits on her couch most of the day, not doing much of anything. She has gained several pounds and seems fatigued most of the time. Toby's doctor suggests that perhaps she is hypothyroid. He obtains thyroid function tests. To his surprise, the free T4 is elevated, and the TSH is suppressed, suggesting a diagnosis of hyperthyroidism. He sends Toby to see Dr. Rubin.\n\nDr. Rubin, whose practice is filled with members of the Dummy family by this time, examines Toby and finds that she doesn't have a goiter. However, her pulse is somewhat fast. He makes a diagnosis of _apathetic hyperthyroidism_ and explains to Toby's husband that this type of hyperthyroidism isn't uncommon in the elderly population. He starts Toby on the antithyroid drug methimazole. After six weeks, Toby's thyroid function tests are normal. Dr. Rubin stops the methimazole and gives Toby radioactive iodine several days later.\n\nToby is feeling so much better that she invites Dr. Rubin and his wife, Enid, to a delicious dinner in a lovely dining room recently remodeled by Toby's husband.\n\n## Sorting through confusing signs and symptoms\n\nHyperthyroidism is less common than hypothyroidism, but it's still a significant problem among the elderly. As with hypothyroidism, doctors can easily confuse the symptoms of an overactive thyroid with the normal signs of aging. The following characteristics are among the similarities between normal aging and hyperthyroidism:\n\n  Shaking of the hands and fingers\n\n  Weight loss\n\n  Irregular heart rhythms\n\n  Increased threat of congestive heart failure\n\n  Intolerance to heat\n\n  Profuse sweating\n\n  Fatigue and weakness\n\nAt the same time, the elderly may have signs that aren't consistent with hyperthyroidism at all. They may appear entirely apathetic, sitting very quietly, acting depressed, and showing fatigue and weight gain. This is the picture of apathetic hyperthyroidism that Toby Dummy illustrates.\n\nMany elderly patients with hyperthyroidism don't have goiters.\n\nSometimes the first sign of hyperthyroidism is the finding of _atrial fibrillation,_ an irregular heartbeat. (If you're diagnosed with atrial fibrillation, you may need to take an anticoagulant to prevent _pulmonary emboli,_ blood clots that form in the irregularly beating heart and flow to the lungs, cutting off blood flow when they become stuck. After your heart rhythm is restored to normal, you can stop taking the anticoagulant.)\n\nIf your heart rhythm suddenly becomes very irregular, and your doctor tells you that it's atrial fibrillation, ask him or her to order thyroid function tests.\n\nLoss of bone is another important consequence of hyperthyroidism. The elderly, particularly women who already have much diminished bone, can't afford to lose more bone. One study published in the _Journal of Clinical Investigation_ in 2000 showed that elderly people with hyperthyroidism had significant reduction in bone density when compared with elderly people without hyperthyroidism. After hyperthyroid patients were successfully treated, their bone mineral density showed improvement within six months. Other studies show a definite increase in bone fracture risk in people with hyperthyroidism.\n\nGraves' disease is the most common cause of hyperthyroidism in the elderly, just as it is in younger people (see Chapter 6). However, two causes of hyperthyroidism are more common at this age than earlier in life: a toxic nodule, a nodule that produces too much thyroid hormone, and iodine-induced hyperthyroidism, hyperthyroidism that occurs in a person who had previously been deficient in iodine and suddenly takes a large amount of it. Less frequently, thyroiditis may provoke hyperthyroidism temporarily (see Chapter 11).\n\n## Securing a diagnosis\n\nThyroid function tests remain the key method for making a diagnosis of hyperthyroidism in the elderly. If hyperthyroidism is present, the free T4 should be high, and the TSH should be suppressed. Occasionally, the T4 is normal, but the free T3 is elevated, a condition called _T3 thyrotoxicosis_ (see Chapter 6). This condition is especially common if a hyperactive nodule is the source of the hyperthyroidism.\n\nWhen confusion exists about the cause of hyperthyroidism, a thyroid uptake and scan can help to clarify the situation. It shows a high uptake if the hyperthyroidism is due to Graves' disease but a low uptake if autoimmune (chronic) thyroiditis is the cause. Generally this study isn't necessary.\n\nJust as a subclinical form of hypothyroidism exists, a subclinical form of hyperthyroidism exists that doctors find more often in the elderly than younger patients. However, it is a much less common problem. A normal free T4 but a low level of TSH defines subclinical hyperthyroidism. These patients don't have the florid symptoms that patients with high free-T4 levels show, which is why it's called _subclinical._ And just as subclinical hypothyroidism is associated with heart disease that improves with treatment, subclinical hyperthyroidism is also associated with heart disease that improves with treatment. Elderly patients with subclinical hyperthyroidism who don't receive treatment have a higher rate of death from heart disease than those who do receive treatment.\n\nThe use of the word _subclinical_ is unfortunate. Subclinical patients have a disease, whether hypothyroidism or hyperthyroidism, and need treatment. Doctors have to be more careful in their selection and application of treatment and of all their patients' other medical conditions, but doctors do their elderly patients no favor by ignoring their thyroid condition.\n\n## Treating hyperthyroidism in the elderly\n\nThe treatment of choice for hyperthyroidism in the elderly is _radioactive iodine_ (RAI). A single treatment brings the disease under control in four to six weeks. RAI avoids the problems associated with taking the daily antithyroid pills. However, many people who take RAI develop hypothyroidism and need to be on a daily thyroid hormone pill for the rest of their lives.\n\nThe problem with antithyroid drugs in the elderly is one of adherence to daily drugs for at least a year. However, antithyroid drugs are a very acceptable alternative to RAI. Elderly people are actually more sensitive to them than younger people and have a higher remission rate. This may be the treatment of choice in an older individual with few or no complicating diseases who is alert and can be depended on to take her medicine.\n\nAnother problem with antithyroid drugs is that agranulocytosis, the loss of white blood cell production, is more common in elderly people treated with antithyroid drugs than younger people. White blood cells protect the body from infection. Using methimazole at a dose of less than 30 milligrams can avoid agranulocytosis. Most elderly patients never need that much to treat their hyperthyroidism.\n\nA beta blocker such as propranolol is also useful in controlling symptoms of hyperthyroidism (such as tremor, nervousness, sweating, and rapid heart rate).\n\nIf a doctor gives RAI to a person with a hyperactive thyroid, a sudden release of thyroid hormones may occur as the thyroid tissues break down. This may be dangerous for an elderly person, who could have a sudden worsening of heart failure and a very rapid heart rate, as well as much worse chest pain. To avoid this complication, doctors give antithyroid drugs for six weeks before administering the RAI. When the patient has normal thyroid function on the drugs, the risk of a sudden release of thyroid hormones is eliminated.\n\nMost heart symptoms associated with hyperthyroidism disappear after successful treatment. However, sometimes the atrial fibrillation doesn't reverse. The reason is that the elderly have other damage to the heart, usually from hardening of the arteries, or arteriosclerosis. Reversing the hyperthyroidism doesn't correct arteriosclerosis.\n\n .jpg)\n\nThe elderly person with hyperthyroidism is also a more likely candidate to develop thyroid storm (see Chapter 6). It occurs when the hyperthyroidism isn't treated or treated inadequately and the patient develops a complicating illness like pneumonia or suffers some kind of trauma or needs surgery. Even the taking of radioactive iodine to treat the hyperthyroidism in the first place may cause thyroid storm because of the sudden release of so much thyroid hormone. This is a medical emergency. Unfortunately, elderly people with multiple medical problems who develop thyroid storm have a high death rate.\n\n## Thyroid Nodules in the Elderly\n\nNodules are very common in the elderly, but doctors find thyroid cancer less often in elderly people than in younger people. Doctors can study the nodules with a radioactive iodine scan to see whether they're active and with an ultrasound to see whether they're filled with fluid _(cystic)._ Both of these characteristics point the diagnosis to a benign nodule rather than a cancer. Thyroid function tests can show whether the nodule is hyperfunctioning and needs treatment.\n\nPeople who have had neck irradiation even 50 years ago are still at risk for developing thyroid cancer. Thyroid specialists are seeing less and less thyroid cancer associated with neck irradiation as the population that was irradiated before 1950 is dying out. Neck radiation is more dangerous to people who have been irradiated before age 15, which makes them 70 years of age or older at this time.\n\nMost of the cancers in the elderly (80 percent) are papillary thyroid cancers (see Chapter 8), especially if patients have a history of irradiation to the neck. The next group is follicular cancer, which is more dangerous in the elderly than in younger patients. Follicular cancer spreads to bone and can cause fractures in an older person who already has much loss of bone.\n\nAn even less common kind of thyroid cancer in the elderly is medullary thyroid cancer. It has a worse prognosis in the elderly and is often detected at a late stage, especially because most medullary thyroid cancers are sporadic, occurring only in the one individual and not their relatives (familial medullary thyroid cancer). Doctors don't test the sporadic cases early as they do familial cases.\n\nRarely (1 or 2 in 100 tumors) does an elderly person have anaplastic thyroid cancer. It has a terrible prognosis, and most patients are dead within a year. This is a cancer that almost never appears before the age of 60. Neither surgery nor radiation therapy nor chemotherapy has much use in this cancer.\n\nAs doctors do more ultrasound of the neck, they find more small masses in the thyroid. The masses can be biopsied under ultrasound control and may be cancer. Should doctors treat these small tumors in elderly patients the same way as they treat them in younger patients? The current consensus is that they should, especially if the patient belongs to the growing group of healthy elderly.\n\nIn the final analysis, a fine needle aspiration biopsy remains the best single test to rule out cancer in a nodule. If this test is positive for cancer, surgery is the treatment of choice, with follow-up similar to any thyroid cancer patient (see Chapter 8). Obviously, surgery is more risky in this patient population. Use of radioactive iodine to ablate remaining thyroid tissue is also a problem because many of these tumors don't take up the radioactive iodine.\n\nDoctors consider patients who can't take up RAI for treatment with chemotherapy. These patients tolerate chemotherapy very poorly, so doctors don't often give it to them.\n\n##### Chapter 20\n\n## Diet, Exercise, and Your Thyroid\n\n### In This Chapter\n\n  Working to assure your best nutrition\n\n  Evaluating your thyroid and weight loss\n\n  Getting enough iodine in a vegetarian diet\n\n  Using exercise to maintain thyroid and body health\n\n  Understanding leptin and your thyroid\n\nThis chapter answers important questions you may have about how best to maintain your thyroid health and offers further evidence of the starring role that the thyroid gland plays in your body. Remember that your thyroid gland functions at its best if it finds itself in a healthy body whose tissues are fed by the right nutrients and whose muscles and bones are strengthened by an appropriate level of exercise. For this reason, I give you some basic ideas about diet and exercise here. For a more complete guide to diet, see my book _Diabetes Cookbook For Dummies,_ which contains dietary suggestions not just for people with diabetes, but for all people who want to eat healthy food. To learn more about exercise in your lifestyle, see _Diabetes For Dummies,_ which presents an exercise program for everyone who wants to feel good in their body. Wiley publishes both these titles.\n\n## Guaranteeing Your Best Nutrition\n\nTwo friends run into each other, and the first friend asks how the second one feels. The second friend answers, \"Lousy \u2014 I've got arthritis and a bad back. I'm always tense, and I have insomnia. Miserable. I'm miserable.\" \"And what kind of work are you doing?\" the first friend asks. \"The same thing \u2014 I'm still selling health foods.\"\n\nThis story is good for a chuckle, but the truth is that what you eat (and drink and smoke) has more influence on your health than all the diseases in a medical textbook. In the United States, we spend more than $100 billion on health each year. (That goes a long way toward explaining all the healthy doctors in this country.) The U.S. government is aware of these health costs and knows that its citizens function best when they eat right and exercise. For this reason, the government has long published a list of dietary recommendations, the _Dietary Guidelines for Americans._\n\nThe _Dietary Guidelines for Americans,_ updated every five years, is a great place for you to start to turn your body into a suitable \"container\" for a healthy thyroid gland. You can check them out at www.healthierus.gov\/dietaryguidelines. The 2005 version of the guidelines is divided into ten chapters that cover issues such as weight management, physical activity, healthful eating habits, and food safety. Basically they concern your level of fitness, a healthy diet, your alcohol intake, and the safe consumption of food. The following section gets more specific about these recommendations.\n\n## Maintaining a healthy weight\n\nIf you go online and check out a message board about thyroid disease, you'll probably find that lots of people have lots of questions about how the thyroid affects weight gain and loss. This section helps set the record straight.\n\nA very simple calculation allows you to determine your ideal weight; the calculation differs slightly for men and women:\n\n  **Men:** Calculate your height in inches. Give yourself 106 pounds for the first 60 inches (5 feet) of height and 6 pounds for each inch above 60. For example, a 5'6\" man should weigh 106 plus 6 times 6, or 142 pounds. This is his ideal weight. However, there really is a weight range that is appropriate for each height, because each of us has a different body shape.\n\nTo calculate the range, take 10 percent of the number you calculate as your ideal weight, and add that number to and subtract it from the ideal weight number. For example, the man who is 5'6\" would determine that 10 percent of 142 is 14 pounds. He'd add 14 to 142 and subtract 14 from 142 to get his weight range. The range for a 5'6\" man is 128 to 156 pounds.\n\n  **Women:** Calculate your height in inches and give yourself 100 pounds for the first 60 inches (5 feet) and then 5 pounds for each inch over 60. A 5'4\" woman has an ideal weight of 120 pounds. Using the same technique I describe for men, the 5'4\" woman would calculate that her proper weight range is 108 to 132 pounds.\n\nNow that you know how much you should weigh, do you have to achieve that goal? The answer is no. Are you shocked?\n\nThe simple fact is that I, your kindly and wise doctor, want you to achieve a weight at which you'll have no risk of disease. If that weight is 10 or 15 pounds above the top of your \"ideal\" weight range, I'm telling you that's okay. If you gain much more than that, chances are you'll suffer some medical consequence, but even that isn't certain. If you want to look like a fashion model, that's up to you.\n\n## Using the Food Guide Pyramid to make your food choices\n\nIn 2005, the government reorganized its Food Guide Pyramid and individualized it. This means that each person has his or her own specific pyramid. Instead of horizontal divisions, the divisions are now vertical, with each one having a thickness that corresponds to the amount of that food group that you should be eating. Your amount depends on your age, sex, and level of physical activity. If you go to www.mypyramid.gov\/pyramid\/index.html, you can plug in a few numbers and get specific recommendations for your personalized Food Guide Pyramid, along with a host of additional nutrition information.\n\nThe old recommendations for servings are gone from this Pyramid. They were confusing. People can relate to amounts like ounces and cups much more easily. The new pyramid consists of the following food groups, which I present below in the recommended order of consumption, more to less:\n\n  **Grains:** The health benefits of grains include reduction in heart disease, constipation, diabetes, and cancer. They also help with weight management. The government wants you to eat plenty of grains, which they help you to calculate, the amount depending on your calorie needs. You should be eating whole grains, grains that contain the whole grain kernel, such as whole-wheat flour, bulgur (cracked wheat), oatmeal, whole cornmeal, and brown rice. The government wants you to eat less refined grain, such as white flour, white bread, and white rice.\n\n  **Vegetables:** You should be eating more dark green vegetables, more orange vegetables, and more dry beans and peas. The health benefits of vegetables are reductions in strokes, diabetes, weight, and loss of bone. The amount you need to consume varies from 1 cup to 3 cups a day based on your age, sex, and level of activity.\n\n  **Fruits:** You need to eat a variety of different fruits, and the amount varies from 1 to 2 cups a day. They can be fresh, canned, frozen, or dried. Fruits benefit you by reducing heart disease, diabetes, high blood pressure, and cancer.\n\n  **Milk and dairy products:** This group includes dairy and cheese. You get the benefit of larger bone mass and reduction of osteoporosis from this group. Consume 2 to 3 cups of milk or something else from this group each day.\n\n  **Proteins:** Meat and beans fit the bill here. The instruction is to \"go lean on protein,\" and you should eat no more than 2 to 6 1\/2 ounces of protein daily. Proteins give you vitamins, iron, magnesium, and zinc. They are also the building blocks for bones, muscles, cartilage, skin, and blood. Fish, nuts, and seeds, which provide fat in a better form (unsaturated fat), are preferred to beef, which contains more saturated fat and cholesterol, the fats that lead to arteriosclerosis. Beans are also a good source of protein.\n\n## Counting calories\n\nThe guidelines I explain in the previous section offer a range of ounces of each food group rather than a fixed number of ounces. The reason for this is that your intake of the various food groups depends on your ideal weight. Also, because no two people are exactly alike in their metabolism and in their activity level, a daily calorie level for two people of the same height and weight is different, particularly if they're male and female. But you can get a general idea of how many calories you should be consuming to maintain your ideal weight, and then make adjustments if you find that you need fewer or more calories.\n\nI talk about \"ideal weight\" just to give you a reference from which to calculate your daily caloric needs. What I want you to achieve is a healthy weight.\n\nHere's a relatively simple formula to use to figure out how many calories you need. Start with the figure for your ideal weight (see the previous section, \"Maintaining a healthy weight\"). Multiply that number by ten. If you should weigh 140 pounds, for example, your calculation comes to 1,400 kilocalories, which is your basal calorie need. Now you add more depending on your activity level. A person who doesn't exercise much at all increases the basal calorie number by 10 percent to arrive at a daily kilocalorie level of 1,540. A person who does moderate exercise, for example a daily walk for 25 minutes, adds 20 percent to that total to arrive at 1,680 kilocalories. The very active person, who digs ditches all day, for example, needs 40 percent more or even higher to arrive at a daily need of 1,960 kilocalories or greater.\n\nThe government has made it easy for you to figure out how much to eat on a daily basis. Go to the Web site www.mypyramid.gov\/mypyramid\/index. aspx and put in your age, sex, and level of physical activity. For example, I put in a male age 50 who does about 1 hour of physical activity a day. The chart told me that I should eat 8 ounces of grains, 3 cups of vegetables, 2 cups of fruit, 3 cups of milk, and 61\/2 ounces of protein and beans daily. It told me to aim for four whole grains a day, a variety of vegetables throughout the week, 7 teaspoons of oils a day, and to limit my sugar and fat kilocalories to 360. Then came the caveat, \"This calorie level is only an estimate of your needs. Monitor your body weight to see if you need to adjust your calorie intake.\"\n\nTo give you an idea of the difference that age makes, the chart instructs a male age 10 who does the same amount of physical activity to eat 6 ounces of grains, 21\/2 cups of vegetables, 11\/2 cups of fruits, 3 cups of milk, and 5 ounces of protein and beans. The chart instructs this boy to eat 6 teaspoons of oil and only 195 kilocalories of additional food from sweets and fats.\n\nIf you adhere to these guidelines, you are well on your way to hitting the target of a healthy weight. The next sections fine-tune this information by discussing individual nutrients and why you ought to choose a variety of grains, fruits, and vegetables.\n\n## Selecting a variety of foods\n\nChoosing among the many foods that make up each group has many benefits. Most important, when you eat a variety of foods, you ensure that you get all the nutrients your body (including your thyroid) needs. In particular, some foods contain certain vitamins and minerals that aren't present in other foods. Only a variety of foods gives you all the vitamins and minerals that you need. In addition, your meals are more interesting when you eat a variety of foods rather than the same meal again and again.\n\nKeep in mind that despite their differences in color and appearance, most fruits and vegetables share about the same energy sources as other members of their group (see the following \"Energy sources\" section). The different colors and appearances indicate that they differ in their vitamins and minerals.\n\n### Energy sources\n\nThe energy that we use to move our bodies comes from one of three sources:\n\n  **Protein:** Protein is necessary to build muscles and the organs of the body. Proteins also make up certain hormones. The backbone of the thyroid hormone is an amino acid, one of the several amino acids that combine to make up protein.\n\nYou get your protein when you eat animal foods, such as meat, fish, poultry, and milk. These are sources of complete protein. Each of these foods contains all the amino acids that the human body needs to manufacture its own protein, including certain amino acids that the human body can't manufacture called _essential amino acids._ Plants, especially beans and peas, also contain protein, but a single source of vegetable protein doesn't have all the essential amino acids in one food source. Therefore, vegetarians must eat a variety of protein sources.\n\n  **Carbohydrates:** Carbohydrates are mainly found in the bread, cereal, rice, and pasta food group, as well as in fruits and some vegetables. When carbohydrates are broken down in the intestine, they're absorbed into the body as sugars, which give you the immediate energy you need to move your muscles. Your body can also store them in your muscles and your liver to provide energy if you need it later on.\n\n  **Fats:** Your body needs fats in very small quantities to provide the backbone for certain essential hormones, such as estrogen and testosterone. Fats also store energy in the fat tissues of your body, but when they're present in excessive amounts, they can accumulate in places where they do damage, especially the arteries of the heart. The worst offenders are the _saturated fats,_ the kind that are solid at room temperature. Butter and the fat attached to a steak are examples. The calories in this type of fat should make up no more than 10 percent of your total calories. Most of the fats of vegetable origin (like canola oil and olive oil) are _unsatu_ Vegetable fats that are saturated are coconut and palm oils, so use them sparingly. Check out the \"Choosing your fats properly\" section later in the chapter for more information on this important subject.\n\n### Vitamins\n\nAlthough you only need vitamins in tiny amounts, they're essential for a healthy body. They change the stored energy in the energy sources into energy that the body can use. Your body uses them in many of the chemical reactions that take place in your cells. You need to eat a number of vitamins, because your body can't make them. The various vitamins, their function, and their sources in food include\n\n  **Vitamin A,** used for vision and growth of bone and teeth, is found in liver, carrots, and spinach.\n\n  **Vitamin B1,** used for digestion and nervous system function, comes from whole-grain cereals, peas, and nuts.\n\n  **Vitamin B2,** which helps to release energy and maintain the skin and eyes, comes from liver, milk, eggs, and leafy vegetables.\n\n  **Vitamin B3,** used for maintenance of the skin and nerves, comes from chicken, salmon, and peanuts.\n\n  **Vitamin B6** is necessary to make red blood cells and to release energy from the energy sources. It comes from meat, fish, poultry, and peanuts.\n\n  **Vitamin B12** is essential for the nervous system and red blood cells. It's found in all foods coming from animals, including meat and milk; a person who eats nothing but vegetables won't get this vitamin.\n\n  **Vitamin C** helps with healing and prevention of infections and is found in citrus fruits, strawberries, and broccoli.\n\n  **Vitamin D** is necessary for the proper use of calcium and comes in milk, fish, and the yolk of eggs. Fortunately, this is a vitamin that the body can make when the skin is exposed to sunlight.\n\n  **Vitamin E** has many functions, including prevention of cholesterol buildup and production of red blood cells and muscles. You get it in vegetable oils, peas, and nuts.\n\n  **Vitamin K** is essential for clotting of the blood so that you don't continue to bleed when you're cut. It comes from broccoli and leafy vegetables.\n\n  **Folic acid** is another vitamin needed to produce red blood cells and protein. It's found in leafy vegetables, oranges, and peanuts.\n\n### Minerals\n\nThe minerals aren't _organic_ \u2014 they aren't of animal or vegetable origin. They come from the earth and are taken up by vegetables, which animals then eat. Minerals consist of the major minerals, which are present in relatively large\n\n_rated fats,_ although they're still a source of concentrated calories. Vegetable fats that are saturated are coconut and palm oils, so use them sparingly. Check out the \"Choosing your fats properly\" section later in the chapter for more information on this important subject.\n\n### Vitamins\n\nAlthough you only need vitamins in tiny amounts, they're essential for a healthy body. They change the stored energy in the energy sources into energy that the body can use. Your body uses them in many of the chemical reactions that take place in your cells. You need to eat a number of vitamins, because your body can't make them. The various vitamins, their function, and their sources in food include\n\n  **Vitamin A,** used for vision and growth of bone and teeth, is found in liver, carrots, and spinach.\n\n  **Vitamin B1,** used for digestion and nervous system function, comes from whole-grain cereals, peas, and nuts.\n\n  **Vitamin B2,** which helps to release energy and maintain the skin and eyes, comes from liver, milk, eggs, and leafy vegetables.\n\n  **Vitamin B3,** used for maintenance of the skin and nerves, comes from chicken, salmon, and peanuts.\n\n  **Vitamin B6** is necessary to make red blood cells and to release energy from the energy sources. It comes from meat, fish, poultry, and peanuts.\n\n  **Vitamin B12** is essential for the nervous system and red blood cells. It's found in all foods coming from animals, including meat and milk; a person who eats nothing but vegetables won't get this vitamin.\n\n  **Vitamin C** helps with healing and prevention of infections and is found in citrus fruits, strawberries, and broccoli.\n\n  **Vitamin D** is necessary for the proper use of calcium and comes in milk, fish, and the yolk of eggs. Fortunately, this is a vitamin that the body can make when the skin is exposed to sunlight.\n\n  **Vitamin E** has many functions, including prevention of cholesterol buildup and production of red blood cells and muscles. You get it in vegetable oils, peas, and nuts.\n\n  **Vitamin K** is essential for clotting of the blood so that you don't continue to bleed when you're cut. It comes from broccoli and leafy vegetables.\n\n  **Folic acid** is another vitamin needed to produce red blood cells and protein. It's found in leafy vegetables, oranges, and peanuts.\n\n### Minerals\n\nThe minerals aren't _organic_ \u2014 they aren't of animal or vegetable origin. They come from the earth and are taken up by vegetables, which animals then eat. Minerals consist of the major minerals, which are present in relatively large amounts in the body, and trace elements that are essential but present in only tiny amounts.\n\nThe major minerals consist of the following:\n\n  **Calcium** for strong bones and teeth, for blood clotting, and for muscle function is found in dairy products, almonds, broccoli, and other green vegetables.\n\n  **Magnesium** for nerve and muscle function is found in milk, seafood, bananas, and green leafy vegetables.\n\n  **Phosphorus** for the bones and teeth comes from milk, hamburger, and cheese.\n\nThe trace elements include the following:\n\n  **Chromium,** for using carbohydrates properly, is found in organ meats, mushrooms, and broccoli.\n\n  **Iodine,** the key mineral for the production of thyroid hormones, is found in seafood and iodized salt and bread.\n\n  **Iron,** for red blood cell hemoglobin, comes from meat, poultry, fish, and raisins.\n\n  **Selenium,** also used in enzymes that affect thyroid hormones, is found in seafood and whole grains.\n\n  **Zinc,** needed in the production of insulin, is found in red meat, shellfish, and eggs.\n\nNow you know what these nutrients are, what they do, and where you find them. No discussion of proper nutrition can leave out a discussion of fats, so keep reading.\n\n## Choosing your fats properly\n\nYou want to limit your fat intake to no more than 30 percent of your total daily calories while limiting your intake of saturated fat to no more than one third of that amount. Eating your calories according to the Food Guide Pyramid keeps you within those limitations if you choose your fats wisely. Select foods that contain unsaturated fat, like vegetable oils (not coconut or palm oils).\n\nYou can keep your fats down by looking for low-fat foods, which are plentiful in the supermarkets these days. Just remember not to substitute foods rich in carbohydrates. Food labels can tell you what you need to know about the energy sources in the food as well as the amounts of the vitamins and minerals.\n\n### Measuring your cholesterol\n\nThe fat that most people think about is cholesterol. You should know your level of cholesterol. Ask your doctor to check your cholesterol level if you don't know it yet. The recommendation is that your total cholesterol should be less than 200. However, a particle in your blood called _high density lipoprotein_ (HDL) carries cholesterol away from the arteries back to the liver, where it's broken down. That's why HDL is commonly referred to as \"good\" cholesterol. You can do a simple calculation to see if your level of cholesterol is dangerous. If you divide the total cholesterol by the HDL cholesterol and the result is less than 4.5, you're at lower risk to have a heart attack. The higher that number, the greater your risk.\n\nYou can do something to raise your HDL. The best way is exercise. The more you do (within reason), the higher your HDL and the lower your risk of a heart attack.\n\n### High cholesterol and hypothyroidism\n\nHigh cholesterol is also a well-known effect of hypothyroidism. Moreover, high cholesterol isn't only associated with coronary artery disease and heart attacks, but with peripheral vascular disease (leading to blocked blood flow to the arms and legs) and cerebral artery disease, which can lead to strokes.\n\nThe number of people with high cholesterol is far greater than the number of people who have hypothyroidism. Most abnormalities in cholesterol are due to excessive fat in the diet and lack of exercise.\n\nMany cases of undiagnosed hypothyroidism may result in high cholesterol. Studies show that more than 10 percent of people with high cholesterol (levels over 200) have hypothyroidism. Most people with high cholesterol have never been tested for hypothyroidism, and most people don't know that hypothyroidism and high cholesterol have a connection in the first place.\n\nWhen a patient with high cholesterol receives a diagnosis of hypothyroidism, the treatment is, of course, thyroid hormone. The results can be pretty dramatic, with a major improvement in the fats in the blood. (This result may not be true for people with _subclinical hypothyroidism,_ who have an elevated TSH level but a normal free T4.) Reduction in cholesterol by as much as 30 to 40 percent may follow the use of thyroid hormone in a person with hypothyroidism.\n\nThe explanation for the increase in cholesterol in hypothyroidism is that the metabolism (or breakdown) of cholesterol declines with hypothyroidism just as the metabolism of everything else in the body declines. However, the production of cholesterol remains the same, leading to a rise in the blood cholesterol.\n\nIf your cholesterol is elevated above 200, ask your doctor to check your thyroid function.\n\n## Moderating your sugar intake\n\nThe U.S. government guidelines recommend choosing beverages and foods to moderate your intake of sugars. Many reasons support this recommendation:\n\n  Sugary foods promote tooth decay.\n\n  Sugary foods often contain few essential nutrients and replace those foods that have these nutrients.\n\n  Sugary foods are the source of many calories. People often eat them in an effort to avoid fatty foods but still end up with too many calories.\n\nYou can avoid these problems by keeping your portions of sugary foods like pies, cakes, candies, and cookies small. Substituting fruit for these sugary desserts reduces sugar intake, provides a certain amount of sweetness for your sweet tooth, and provides you with other important nutrients all at once.\n\n .jpg)\n\nThe biggest offender when it comes to eating lots of sugar with no nutrition is a bottle of soda. Unless it's diet soda, prepared with noncaloric sweeteners, the typical bottle of soda gives you a huge amount of sugar and nothing else. Twelve ounces of soda has between 100 and 200 unhealthy kilocalories of sugar. Drink one a day for 15 days, and you gain a pound. Even the flavored fruit sodas have this problem. Do yourself a favor and switch to water with lemon or lime or the diet sodas that have no sugar. Be sure to read the label to find out what you're drinking.\n\n## Choosing and preparing foods with less salt\n\nThe guideline regarding salt intake is meant to protect you from developing high blood pressure. The recommended amount of salt is a teaspoon, or 6 grams, daily. Most people eat twice as much as that or more. One problem is that food manufacturers typically add a lot of salt to their foods. Avoid this by choosing low-salt foods as well as less processed foods and more whole fruits and vegetables.\n\nAnother problem is that people are so used to picking up the salt shaker and heavily spraying their food with salt. The result is food that tastes like salt and not much else. Try your food without salt for a change. At first it may taste bland, but then you begin to notice the subtle flavors of the food coming through. When you do, you may never want to go back to eating so much salt again.\n\nMost recipes, especially in older cookbooks, recommend more salt than is necessary for proper preparation of the food. Try reducing the salt in the recipe by half. The food will probably cook just as well, and the taste may even be superior. If you don't tell your family that you're reducing the salt, they'll probably never know.\n\nIn the United States and many other countries, iodized salt is the major source of iodine. That teaspoon of salt a day contains twice as much iodine as you are required to eat each day, so you can reduce your salt intake to a half teaspoon and still be assured of getting enough. If you eat one piece of bread, it contains just about your daily requirement of iodine. You don't need to eat excess salt to assure yourself of getting enough iodine.\n\n## Drinking alcohol in moderation\n\nMen who consume more than two drinks of alcohol a day or more than ten in a week and women who consume more than one drink a day or five a week should work to reduce those amounts. Like cigarettes, alcohol can damage your body in many ways. It raises your blood pressure, causes liver destruction, and promotes certain cancers. It provides no nutrition and often causes you to eat less of the foods you need for good nutrition. Severe alcoholism results in damage to the nervous system, vitamin deficiency diseases, anemia, and skin damage.\n\nAlcohol also destroys families. When one or more members of a family are alcoholics, the incidence of divorce, accidents, suicide, loss of employment, and disease within that family is much greater than in families that don't have an alcoholic member. Alcoholism can also lead to impotency, making sexual relations impossible.\n\nKeep in mind that alcohol in moderation (as specified by the numbers I've provided) can raise the level of HDL, or \"good cholesterol,\" in your body. Alcohol can also be a pleasant part of a meal and a key element in certain social scenes. Clearly, alcohol isn't going to go away, but you must control its use.\n\n## Keeping foods safe to eat\n\nTo protect yourself from the chemicals that are sprayed on foods as they're grown and the chemicals present in the soil that fruits and vegetables are grown in, wash all fruits and vegetables before eating them. (Obviously, this doesn't eliminate chemicals inside the food.)\n\nProper refrigeration of foods that can spoil is essential. You must keep raw meat, fish, and poultry in the refrigerator before cooking them thoroughly. Keep your hands clean when you handle these foods. And make sure that you clean cutting boards and knives well after you use them for cutting raw meats. The use of a mild bleach solution to cleanse cutting boards is also recommended.\n\nAfter you cook food, if you want to save it for a later time, keep it in the refrigerator. Leaving it at room temperature allows bacteria to grow that may be present when you eat the food again, even if you reheat it.\n\nFor more information on food safety, visit www.foodsafety.gov. Clicking on the \"Consumer Advice\" link is a great place to start for information on food handling, product-specific advice, and information targeted to various groups of people.\n\n## Making good food choices\n\nYou can easily choose to eat foods that contribute to better health and weight control over those that lead to illness and obesity. You just need to know how to substitute one for the other. In Table 20-1, I show you the wiser choices that you can make every day. By making these choices, you notice a little loss of taste but a definite improvement in your health and your ability to lose weight.\n\nTable 20-1 Choosing Healthier Foods Food Group  | Better Choice  | Worse Choice  \n---|---|---  \nBreads  | Whole-grain breads, whole-  | Refined-flour breads and cakes,   \n| grain and bran cereals,  | croissants, cookies, pastries   \n| rice, pasta |   \nVegetables  | Dark green, leafy vegetables;  | Avocados, vegetables in butter or   \n| yellow-orange vegetables;  | cream sauce   \n| cabbage; broccoli |   \nFruits  | Citrus fruits, berries,  | Coconut, fruit pies, or pastries   \n| apples, pears |   \nDairy  | Low-fat cheese, low-fat or  | Whole milk, butter, sweet cream,   \n| nonfat milk, sherbet  | ice cream, cream cheese, hard   \n|  | cheeses  \nMeats  | Lean meats, chicken, fresh  | Fatty meats, lunch meats, tuna in   \n| fish, cooked dry beans and  | oil, egg yolks (or whole eggs),   \n| peas, egg whites  | sausages\n\n## Clarifying the Thyroid-Weight Connection\n\nCertain misconceptions exist about how your thyroid reacts to weight loss and how your weight reacts to a change in your thyroid function. In this section, I hope to dispel these misconceptions by showing you how your thyroid and your weight really interact.\n\n## Does my metabolism slow when I lose weight?\n\nPeople who lose weight on a diet often regain the weight after a time. If you've had this experience, maybe you've heard that the reason you can't keep the weight off is that your thyroid and metabolism slow down after you lose some pounds, so the weight comes back on more easily. This reasoning implies that your body establishes a \"set-point\" weight and tries to maintain it by changing your thyroid function and your metabolism whenever you move away from that weight. The idea is that if you lose weight, your metabolic rate falls because your thyroid function declines. Researchers have studied this idea to determine its validity.\n\nIn a study in the _American Journal of Clinical Nutrition_ in November 2000, researchers tested thyroid function and metabolic rates for 24 overweight women in the process of losing weight. When they were actively losing weight, the women's resting metabolic rates and free T3 hormone levels declined. But after they reached their ideal weight, their free T3 levels and resting metabolic rate were normal as well. This study contradicts the idea of a \"set-point\" weight.\n\nIf you're having trouble keeping off the weight you lose and your thyroid is functioning normally, this study shows that you can't blame your thyroid. You may want to take a closer look at your exercise and eating habits instead.\n\n### The thyroid and celiac disease\n\n_Celiac disease_ is an autoimmune disease of the small intestine that results in poor absorption of fat, protein, carbohydrates, iron, and vitamins A, D, and K. The consequences of celiac disease are diarrhea, _osteomalacia_ (poorly mineralized bone), signs of vitamin deficiency, and anemia. Studies show that as high as 21 percent of patients with celiac disease also have autoimmune hypothyroidism, and 3 percent of people with thyroid disease have celiac disease.\n\nThe treatment for celiac disease is to remove gluten from the patient's diet. Gluten is present in wheat, barley, oats, rye, and as a filler in many prepared foods and medications. When gluten is removed from the diet, not only does the celiac disease disappear, but the patient's thyroid disease is cured as well.\n\nA study in the _American Journal of Gastroen- terology_ in March 2001 found that out of 241 patients with celiac disease, 31 (13 percent) also had hypothyroidism. Of the 31, 29 had subclinical hypothyroidism with an elevation in TSH but a normal T4. When they received treatment for a year by avoiding gluten in their diet and the celiac disease was cured, the thyroid abnormalities disappeared in all of them as well.\n\nThyroid disease is so commonly associated with celiac disease that everyone with celiac disease should be tested for thyroid disease. If present, both the celiac disease and the thyroid disorder may respond to gluten withdrawal.\n\n## If I'm treated for hyperthyroidism, am I doomed to gain weight?\n\nMany people who receive treatment for hyperthyroidism with radioactive iodine complain that they can't lose weight after they become hypothyroid and are placed on thyroid-hormone replacement. If this describes your situation, you should consider a number of possible explanations:\n\n  You may not be taking enough thyroid hormones to replace your deficit. Checking that your thyroid-stimulating hormone (TSH) is in the normal range and ideally less than 2.5 is important.\n\n  You may need to take T3 hormone replacement as well as T4, even if your TSH is normal (see Chapter 4).\n\n  You may be eating some food that interferes with thyroid hormone absorption, such as soy protein, around the time you take the thyroid hormone.\n\nThen again, maybe none of the above explain your weight gain.\n\nA study in the _Journal of the American College of Nutrition_ in 1999 attempted to address this issue. The authors studied ten people who received radioactive iodine for hyperthyroidism. The researchers looked at the participants' total food energy intake; their T4, T3, and TSH levels; and their height and weight at the time of treatment and at one, two, three, six, and twelve months afterward. The participants' thyroid hormone levels declined in the first months of treatment but increased later. Even when thyroid hormone levels increased, the participants continued to gain weight. Interestingly, the average weight of the participants before the development of hyperthyroidism was about 170 pounds; at the time of treatment, 148 pounds; and after a year, about 168 pounds. Their final average weight was actually _lower_ than their average weight before hyperthyroidism developed. The study concluded that weight gain after treatment of hyperthyroidism was initially due to a fall in the metabolic rate that accompanied the drop in thyroid hormone but later was due to food intake or lifestyle choices.\n\nAnother study in the _Journal of Clinical Endocrinology and Metabolism_ in 1998 showed where the weight gain occurs in the body when you receive treatment for hyperthyroidism. The researchers showed that most of the weight gain in the first three months occurred as fat in the waist area and in muscle tissue, whereas weight gain later on was in the fat under the skin. This study shows very clearly that the weight loss that occurred before treatment for hyperthyroidism was loss of lean tissue, the muscle mass \u2014 further proof that using excess thyroid hormone for weight loss leads to loss of muscle.\n\nMany people treated for hyperthyroidism gain more weight than they want to after treatment. In most cases, this occurs either because their thyroid hormone levels aren't in the range they should be or because they don't alter their eating and exercise habits after treatment. If you're in this situation, keep in mind that you probably increased your food intake and decreased your activity level when your body was hyperthyroid. You need to make lifestyle adjustments after treatment in order to bring your body back to its healthy weight.\n\n### Avoiding iodine before thyroid studies\n\nThe results of thyroid uptake studies are more valuable if the subjects avoid foods that contain iodine for a time before the test. The purpose of most such studies is to determine the size and shape of the thyroid and whether a given abnormality of the thyroid takes up iodine.\n\nIf your doctor is testing you for hyperthyroidism, you don't have to avoid iodine. In fact, avoiding iodine may confuse the diagnosis, because you're looking for abnormally high uptake of the iodine, and you don't want to artificially enhance the test results by following a low-iodine diet.\n\nIf you're having a thyroid scan done for reasons other than hyperthyroidism, follow a low-iodine diet for several days:\n\n  Use only noniodized salt.\n\n  Avoid milk or milk products.\n\n  Avoid commercial vitamin preparations unless they definitely don't contain iodine.\n\n  Steer clear of eggs.\n\n  Don't eat seafood, fish, shellfish, seaweed, or kelp.\n\n  Avoid cured or corned foods.\n\n  Don't use bread products made with iodine dough conditioners.\n\n  Avoid foods that contain Red Dye #3, chocolate, molasses, or soy.\n\n## Getting Enough Iodine in a Vegetarian Diet\n\nBecause iodine is a key element of thyroid hormones, iodine is a necessary part of your daily diet.\n\nVegetarians avoid eating the key foods that contain iodine, such as fish, seafood, eggs, meat, and milk. You must have sufficient iodine in your diet to have good thyroid health. A study of vegetarians in the _British Journal of Medicine_ in December 1998 found that 63 percent of the females and 36 percent of the males had inadequate iodine intake.\n\nIf you follow a vegetarian diet, you may want to take iodized salt or iodine supplements. If you have any doubt about whether you're getting enough iodine, ask your doctor to check your iodine level (with a urine test). A teaspoon of salt a day or a piece or two of bread takes care of your iodine needs as a vegetarian.\n\n## Exercising for Your Thyroid\n\nIf you're being successfully treated for a thyroid condition and tests show that you have normal thyroid function, you can exercise as much as you want. (Just be sure to listen to your body and slow down if you feel like you're overextending yourself.) You should be doing aerobic exercise, which forces your heart to beat faster, to keep your heart healthy and your body fat under control. You should also be doing strength training to retain and build muscle.\n\nThe amount of exercise that you do determines its effect on your body. If you do 30 minutes of aerobic exercise daily, you achieve aerobic fitness. If you do 60 minutes of aerobic exercise daily, you're able to maintain weight loss. If you do 90 minutes of aerobic exercise daily, you lose weight.\n\nA study in the November 2005 issue of the _Archives of Internal Medicine_ looked at the long-term effects of exercise at different levels of intensity for different durations. The study divided 500 people into four exercise groups: a moderate, intensity-low frequency group; a moderate, intensity-high frequency group; a hard, intensity-low frequency group; and a hard, intensity-high frequency group. The heart rate during exercise determined the intensity of the exercise. Low frequency was three to four days per week, while high frequency was five to seven days per week. All groups showed significant improvement in cardiorespiratory fitness by six months and maintained that fitness over two years. However, only the group that combined hard exercise with high frequency showed improvement in blood fats.\n\nIf you have a thyroid condition that hasn't yet been treated, you need to be aware of some special considerations regarding exercise. In this section, I discuss these situations and talk about how to use exercise to maximize your health in general.\n\nIf you are older than 35 and starting an exercise program, especially a vigorous one, talk to your doctor first.\n\n## Recognizing the natural consequences of aging\n\nDon't confuse the natural effects of aging with the consequences of having thyroid disease. As you get older, your ability to do aerobic exercise decreases, as does your strength. If you go to the gym for the first time in years and find that you can't last as long on the treadmill as you used to, chances are that your thyroid isn't the culprit.\n\nYour ability to take in oxygen is a measure of your physical condition. Your oxygen uptake peaks around age 25, and after that, it steadily declines no matter what you do to prevent it. Your strength also seems to peak around the same time, but it remains more or less the same until around age 40, when it starts to decline steadily. We all lose about 25 percent of our maximum strength by age 65. We also lose flexibility with aging \u2014 our tendons, ligaments, and joint capsules become stiffer.\n\nYou've certainly heard the old saying, \"You will only be young once.\" Take my word for it: It's true.\n\nAt any age, you can maximize your strength, your stamina, and your flexibility by doing plenty of exercise. By plenty, I mean at least 30 minutes, four or more times per week, preferably every day.\n\n## Working out with hypothyroidism\n\nWhen you have an underactive thyroid, the fatigue that accompanies this condition limits your ability to exercise. After you begin taking the proper replacement dose of thyroid hormone, you should be able to exercise normally. But if you still can't exercise because of fatigue, consider the two common reasons:\n\n  You may not be receiving sufficient thyroid hormone, so your TSH is between 0.5 and 2.5. If your symptoms linger even after taking the hormone replacement, don't settle for a TSH of 3 or higher.\n\n  You may need to take T3 hormone in addition to T4 to fully replace your missing thyroid function.\n\nHypothyroidism does affect the functioning of your heart, which can become apparent during exercise. If you're receiving treatment with thyroid hormone, your heart function should return to normal (assuming that you don't have any other heart conditions).\n\nHeart function during exercise may actually be a greater issue for patients with _subclinical hypothyroidism_ (where your TSH is elevated, but your free T4 is normal), because these patients aren't necessarily treated with thyroid hormone. (See Chapter 19 for a detailed discussion of the debate over treatment.) Subclinical hypothyroidism is associated with mild abnormalities in the heart, which aren't measurable when you're resting but are detectable when you exercise. The normal heart's adaptation to effort is diminished in subclinical hypothyroidism. Subclinical hypothyroidism also results in a rise in the form of cholesterol that leads to heart attacks and a fall in the form that's protective against heart attacks. Some thyroid specialists believe that these subtle changes are reason enough to treat subclinical hypothyroidism with thyroid hormone.\n\nThe muscles of a person with subclinical hypothyroidism show abnormal energy metabolism that leads to early fatigue, which thyroid hormone also corrects. Subclinical hypothyroidism also impairs the ability of blood vessels to open up to allow more blood flow, which is further evidence of the need for treatment, particularly before the condition worsens.\n\n## Exercising with hyperthyroidism\n\nIf you're hyperthyroid, your heart rate and the amount of blood pumped per heartbeat are both elevated when you're resting, but they don't respond to exercise in a normal fashion. After you achieve normal thyroid function through treatment, these abnormalities disappear.\n\nCareful study of the hearts of hyperthyroid patients shows that their resting heart rates are abnormally high, as are the frequent occurrences of abnormal heart rhythms. Abnormal thickening of the heart muscle increases the size of the heart.\n\nWith exercise, the hyperthyroid heart can't increase its workload the way that a normal heart can. The result is that the hyperthyroid person can't exercise as long as she used to, and her peak level of exercise is reduced. This is true even in subclinical hyperthyroidism, where the TSH is suppressed below the normal range, but the free T4 remains normal. When a person takes the beta blocker propranolol to slow the heart, the patient feels an improvement in exercise capacity.\n\nAn elderly person with hyperthyroidism must be especially careful with exercise, because she has an increased risk of heart failure and may experience abnormal heart rhythms (which may not improve even when the hyperthyroidism is brought under control). Chest pain can get worse as hyperthyroidism continues.\n\nNot only heart muscle but also skeletal (arm, leg, and trunk) muscles are abnormal in hyperthyroidism. Hyperthyroid skeletal muscle requires more energy to perform the same amount of work as healthy muscle. As a result, it can be fatigued much earlier.\n\n## Meeting your minimal exercise needs\n\nWhile you're recovering from hypothyroidism or hyperthyroidism, you may not be able to do much exercise and certainly not the amount necessary for good health. After you're cured, however, you want to get up to speed. You want to do two types of exercise, which I describe in the following sections.\n\n### Aerobic exercise\n\nAerobic exercise is used to improve heart and lung function and raise the healthy cholesterol. Any exercise that gets the heart beating faster for a sustained period is aerobic exercise. Doctors used to recommend a formula for determining the ideal heart rate during exercise: Subtract your age from 220, and your ideal heart rate is 60 to 75 percent of that number. Now we know that many people can sustain aerobic exercise at higher heart rates. Perhaps the best way to know whether you're meeting your exercise goals is to rank the exercise as follows: very, very light; very light; fairly light; somewhat hard; very hard; and very, very hard. If you stay at the level of _somewhat hard_ while you get into shape, you're doing the right amount of aerobic exercise.\n\nYou should sustain aerobic exercise for 20 to 30 minutes every day. By doing this, despite the normal loss of exercise capacity with aging, you're maximizing what you have and adding significant time to your life.\n\nOne way of insuring that you get enough exercise is to get yourself a pedometer, a little device you wear on your belt that counts your steps. If you count your daily steps for a week, you likely find that you average around 3,000 to 4,000 a day. Your ultimate goal is to average 10,000 steps a day, and you can achieve this rapidly or more slowly. Setting some athletic event in the future as your reason for building up your walking ability is often a good idea. That gives you a goal to work toward and permits you to compare your time over the years to see how fit you're becoming (or not).\n\n### Anaerobic exercise\n\nDon't forget to do muscle strengthening anaerobic exercises as well. Anaerobic exercise strengthens muscles and increases stamina. Using light weights of 10 to 15 pounds, three times a week, you want to do at least three or four different exercises to work your arms and legs and strengthen your back. I recommend the following exercises for strengthening your muscles:\n\n  Bicep curls\n\n  Shoulder presses\n\n  Lateral raises\n\n  Bent-over rowing\n\n  Good mornings\n\n  Flys\n\n  Pullovers\n\nYou can find the details for performing these exercises in my book _Diabetes For Dummies,_ 2nd Edition as well as in _Weight Training For Dummies_ (both published by Wiley, Inc.). You should do each exercise 15 times and repeat the whole set twice. Doing this every few days greatly increases your strength.\n\n## Uncovering a New Hormone: Connecting Leptin to Weight Loss and the Thyroid\n\nLeptin is a relatively new hormone that has an important role in normal thyroid function. First described in 1994, _leptin_ is a hormone made by fat cells that's a major regulator of body weight. As your body fat goes up, the leptin in your body increases.\n\nWhen a person fasts, he or she has a fall in T3 and TSH. A fall in leptin may be responsible for this, which could explain a decline in weight loss that occurs over time in a fasting individual. In the future, the use of leptin during a diet may promote increased weight loss. This section explains the brief history of our knowledge of leptin and what we know so far about its relationship with thyroid hormone.\n\n## Learning the functions of leptin\n\nResearchers conducted the first studies of this hormone on a strain of obese rats, which they found to have a genetic mutation that resulted in failure of leptin production. Administering leptin to these mice resulted in weight loss \u2014 the mice reduced their food intake and had increased energy. The same thing was found when leptin was given to normal-weight mice \u2014 they lost fat mass. Researchers then discovered leptin in human beings, which was hailed as the obesity gene. Unfortunately, injections of leptin in human beings didn't lead to substantial weight loss.\n\nObesity isn't the result of a genetic mutation in the leptin gene. However, several families have been found to have a mutation of the leptin gene that leads to severe obesity at a young age. This gene is a recessive trait, meaning that family members who have only one abnormal leptin gene instead of two don't show the disease. When people with the disease take leptin, they experience significant weight loss and the reversal of metabolic abnormalities.\n\nFurther studies showed that leptin was doing more than just signaling to the body that it had too much fat. When researchers compared body-fat percentages and leptin levels of women and men, they found that women's leptin levels were as much as two to three times that of men. But even though women typically have more fat mass than men, this result doesn't fully explain the difference. Studies now show that the female sex hormone, estrogen, stimulates leptin production, while the male sex hormone, testosterone, suppresses leptin.\n\nResearchers know that girls go into puberty when they reach a certain weight. Puberty begins when a hormone from the _hypothalamus,_ a part of the brain, begins to be released. This hormone is called _gonadotrophin-releasing hormone_ (GnRH). The question arose, what was the signal to release GnRH? The presence of leptin proved to be the answer to that question, because it clearly indicates when the fat mass is sufficient for puberty to begin.\n\n## Interacting with thyroid hormone\n\nResearchers have now shown that leptin interacts with several other hormones in the body, especially insulin, which appears to have an important place in regulating leptin secretion. Leptin interacts with the adrenal gland and growth hormone as well. Because thyroid hormone increases the metabolic rate, which increases the body temperature, researchers thought that leptin (which also regulates metabolism and body temperature) may interact with thyroid hormone.\n\nResearchers have now shown that leptin helps to regulate the part of the brain that releases _thyrotrophin-releasing hormone_ (TRH), and it also regulates the release of thyroid-stimulating hormone. When a person fasts, both the thyroid hormone and leptin concentrations fall. If leptin is given to the fasting individual, the TSH and the T4 hormone return to normal.\n\nOn the other hand, researchers have found that thyroid hormone controls leptin production to some extent. In animals without thyroids, leptin is increased, but when thyroid hormone is replaced, leptin is suppressed. So far in humans, researchers haven't shown that thyroid hormone causes either a rise or a fall in leptin concentration.\n\nThe understanding of the role of leptin is at an early stage. Much more will be learned in the next few years. Doctors and scientists are just starting to clarify leptin's place in thyroid disease; stay tuned.\n\n##### Part IV\n\n## The Part of Tens\n\nIn this part . . .\n\nA s you would expect, a part of your body as important as the thyroid prompts all sorts of myths and mistaken ideas. Here you find the ones I consider the most important (and possibly the most damaging if you believe them). I show you what you can do to make sure that you maximize your thyroid health in ten easy steps. And finally, I answer ten representative questions that I've received from readers since the first edition of this book was published.\n\n##### Chapter 21\n\n## Ten Myths about Thyroid Health\n\n### In This Chapter\n\n  Getting the facts about weight loss and gain\n\n  Learning the truth about hormone replacement\n\n  Understanding how thyroid disease occurs\n\n  Trusting your symptoms\n\nThanks to the Internet, you have access to incredible amounts of information about your thyroid. Unfortunately, much (perhaps most) of it isn't accurate. Much of what you read online is based on the experiences and opinions of one or a few people who took this or that medicine or herb and got better in two weeks. Maintaining a healthy degree of skepticism is important.\n\nIn this chapter, I try to clear up some commonly held myths concerning the thyroid and its diseases.\n\n## I'm Hypothyroid, so I Can't Lose Weight\n\nIf you have hypothyroidism, or if you've received treatment for a thyroid condition and the cure resulted in your becoming hypothyroid, you may find that you have a hard time losing weight. The myth is that you _can't_ lose weight if you have hypothyroidism, even when you receive proper treatment.\n\nA large percentage of people who are receiving successful treatment for hypothyroidism weigh almost the same after treatment as they did before they developed the disease.\n\nI've occasionally seen hypothyroid patients \u2014 mostly elderly people \u2014 who actually lose weight rather than gain it after they receive replacement thyroid hormone. This occurs when a patient is receiving poor nutrition, which the complacency that can accompany hypothyroidism makes worse, because he or she may not take in enough calories.\n\nKeep in mind that hypothyroidism is associated with fatigue. Many patients with hypothyroidism reduce their physical activity as a result. They may not restore their previous level of activity after they receive proper treatment for their hypothyroidism. Therefore, first look to whether your level of activity is sufficient (I provide suggestions for determining the answer in Chapter 20).\n\nIf you struggle to lose the weight that you've gained after becoming hypothyroid, and if your activity level has remained the same, your thyroid treatment may be inadequate (which a TSH test can determine), or you may need to take T3 replacement hormone in addition to T4 (see Chapter 5).\n\nYou may also have another autoimmune condition. Because the most common cause of hypothyroidism is autoimmune thyroiditis (see Chapter 5), your doctor should look for diabetes mellitus type 1 or autoimmune adrenal insufficiency (Addison's disease \u2014 failure to make the hormone cortisol), among other conditions. A blood glucose test for diabetes or a serum cortisol level for autoimmune adrenal insufficiency easily determines whether you have one of these conditions.\n\nThe bottom line is that we all follow the principle of conservation of energy. If we take in too much energy compared to what we need, we gain weight. If we take in too little energy compared to what we need, we lose weight.\n\nAnother truth is that our metabolic rate declines, as does our tendency to move around, as we age. Both changes tend to make weight loss more difficult, but it's still possible.\n\nIf you've had hypothyroidism and are on the proper dose of thyroid hormone, you're able to lose weight with sufficient diet and exercise.\n\n### Your thyroid health and the Internet\n\nYou're not completely on your own when it comes to reading thyroid sites on the Net. If you're lucky enough to find a statement on a Web site indicating that it adheres to the Health on the Net Foundation Code of Conduct (HONcode), you can feel sure that the information is accurate. The Health on the Net Foundation has established a set of principles that any site on the Internet can adhere to. A site that follows the HONcode principles agrees to the following:\n\n**Principle 1:** Medical advice will be given by qualified professionals (or the site will state that this is not the case).\n\n**Principle 2:** The information supports, but does not replace, the patient\/physician relationship.\n\n**Principle 3:** Confidentiality of visitors to the site is respected.\n\n**Principle 4:** Information is supported by references.\n\n**Principle 5:** Claims about the benefits of specific treatments are supported by references.\n\n**Principle 6:** Information is provided in the clearest possible manner, with contacts provided for more information \u2014 including the Webmaster's e-mail address.\n\n**Principle 7:** Support for the site is clearly identified (especially commercial support).\n\n**Principle 8:** If a site is supported by advertising, it's clearly stated, along with the advertising policy. Advertising is clearly differentiated from nonadvertising material.\n\nIn addition, at the back of this book in Appendix B and on my Web site (www.drrubin.com), I list sites that I consider authoritative and accurate. Just go to my site, click on \"Useful Addresses\" on the home page, select \"Thyroid Sites\" on the next page, and read to your heart's content.\n\n## I'm Hyperthyroid, so I Can't Gain Weight\n\nThe myth that weight loss always accompanies hyperthyroidism is a source of confusion in making an accurate diagnosis. Although the majority of patients do lose weight when they become hyperthyroid, some patients actually gain weight \u2014 the elderly, in particular.\n\nA study published in the _Journal of the American Geriatric Society_ in 1996 compared 19 classical signs of hyperthyroidism in older patients and younger patients. Researchers found three signs in more than 50 percent of older patients: rapid heartbeat, fatigue, and weight loss. However, some people experienced no weight loss or weight gain. Researchers found seven signs less frequently in older patients than in younger patients. Researchers found only two signs \u2014 loss of appetite and an irregular heart rhythm \u2014more often in the older patients. Overall, of the 19 classical clinical signs, older people had only six of them on average, while younger people had 11.\n\nAnother study published in _Thyroidology_ in 1992 showed very similar results. It also emphasized the importance of checking levels of thyroid hormones and TSH in the elderly population before making a diagnosis of hyperthyroidism.\n\nWeight loss, as well as other symptoms of hyperthyroidism, may not always be present in hyperthyroid patients, especially in the elderly population. The best way to rule out thyroid disease is to get thyroid blood tests every five years, beginning at age 35.\n\n## Breastfeeding and Antithyroid Pills Don't Mix\n\nFor years, doctors advised women who took antithyroid pills for hyperthyroidism during pregnancy not to breastfeed. The fear was that the medication would enter the baby's circulation through the breast milk and make the baby hypothyroid. Doctors now know this is a myth.\n\nTwo important studies have shown that this belief is incorrect. In one study published in the _Journal of Clinical Endocrinology and Metabolism,_ researchers gave 88 mothers one of the two major antithyroid drugs, methimazole, for 12 months. Researchers then measured the levels of methimazole in the babies' blood. In addition, they tested the babies for thyroid function, urinary iodine, thyroid autoantibodies, intelligence quotient (IQ), and verbal and functional ability. All of the babies of treated mothers had normal thyroid function. They grew normally, and their IQ, verbal, and functional tests were identical to children who breastfed from mothers without hyperthyroidism. In a second study, researchers gave the other major antithyroid drug, propylthiouricil (PTU), to breastfeeding mothers; some took as much as 750 milligrams of PTU daily. Again the thyroid function tests of the babies were entirely normal, as were the babies' development.\n\nA hyperthyroid mother taking methimazole or propylthiouricil to control her hyperthyroidism may safely breastfeed her new baby.\n\n## Brand-Name Thyroid Hormone Pills Are Best\n\nBecause the number of people taking thyroid-replacement hormone in the United States and throughout the world is enormous, the amount of money people spend on thyroid-hormone replacement pills is also huge. The company that captures the largest share of the market makes its stockholders very happy.\n\nThe myth is that generic preparations of thyroxine (T4 hormone) aren't equal in potency to brand-name thyroxine, aren't standardized over time, and shouldn't be used in the treatment of hypothyroidism.\n\nThis myth began, as so many do, with research that was correct at the time but is now outdated. In 1980, an article appeared in the _Journal of the American Medical Association_ showing that generic preparations weren't equal to brand-name thyroxine. Sometimes the generic preparations were weaker, and sometimes they were stronger; they weren't uniform from lot to lot. This type of information continued to appear in medical literature as late as 1995.\n\nHowever, a study completed in 1990 \u2014 but didn't appear until 1997 in the _Journal of the American Medical Association_ \u2014 looked at the problem again. Twenty women who were receiving successful treatment for hypothyroidism were put on four different preparations at the same dosage for six weeks at a time. Blood tests taken during this study showed absolutely no difference in any of the preparations. All the preparations met the Food and Drug Administration criterion for equivalent activity. The conclusion was that the preparations, including two brand names and two generics, were sufficiently equal in their activity, and that no reason supported choosing any one over the others. I'm happy to add that my great thyroid mentor, Dr. Francis Greenspan, among others, performed this study.\n\nSome allege that one of the brand-name companies making thyroid-hormone replacement originally paid for the preceding study, and that when the study didn't show that its product was better, the company suppressed the study's results.\n\nGeneric thyroid preparations save you money, and you can use them interchangeably with brand-name thyroxine. Because hypothyroidism may not be a stable condition, you still want to have your doctor check your thyroid function regularly (perhaps yearly).\n\n## I Have to Take Thyroid Medication for Life\n\nDoctors tell many patients that once they're on thyroid-hormone replacement, they must take it for life. For many people, this is true. Any treatment that removes or destroys much of the thyroid (such as surgery or radioactive iodine) requires treatment with thyroxine (T4 hormone) for life. However, in certain situations, hypothyroidism is temporary; you may need thyroxine for a time, but you later stop taking it. Sometimes the fact that you no longer need the medication may be obvious, but other times you and your doctor may need to attempt a trial period off thyroid for four to six weeks to see if you still need it.\n\nThe following are some of the conditions that require thyroid-hormone replacement for a limited amount of time. I explain each in detail in Chapter 11:\n\n  _Subacute thyroiditis_ causes the temporary breakdown of thyroid cells and the release of thyroxine from the thyroid. As this condition improves, your thyroid begins to make and store thyroxine again, and oral thyroxine is no longer necessary.\n\n  _Silent_ and _postpartum thyroiditis_ also cause temporary loss of thyroxine, which the body restores with time.\n\n  _Acute thyroiditis_ occasionally requires temporary treatment with thyroid hormone.\n\nThe most common diagnosis that requires thyroid hormone treatment but may later subside so you don't need thyroid hormone pills for life is chronic thyroiditis (see Chapter 5). This condition is the result of antibodies that block TSH from sufficiently stimulating the thyroid to produce enough thyroid hormone. Occasionally, levels of blocking antibodies fall. The only way you know if this happens is by measuring the antibodies (which isn't well standardized) or stopping the thyroid hormone and testing thyroid function four to six weeks later. If your thyroid function remains normal, you may not have to take thyroxine any longer.\n\nDepending on your diagnosis, you may be able to stop thyroid hormone treatment at some point. Checking is well worth it, particularly if you're under 40.\n\n## Natural Thyroid Hormones Are Better Than Synthetic Hormones\n\nScientist extracted the first thyroid hormones used to treat people with low thyroid function from the thyroids of animals and called them _desiccated thyroid_ (see Chapter 5). After decades of use, synthetic thyroid hormones made in the laboratory replaced desiccated thyroid. Some holdouts still believe that desiccated thyroid is superior to synthetic thyroxine (T4 hormone) for treating hypothyroidism.\n\nAs long ago as 1978, an article appeared in the _American Journal of Medicine_ titled \"Why does anyone still use desiccated thyroid USP?\" The article declared desiccated thyroid an obsolete therapy. The hormone extracted from animals has plenty of problems:\n\n  Desiccated thyroid can't be standardized from dose to dose, because one animal has a different amount of the thyroid hormones in its thyroid than the next animal.\n\n  Desiccated thyroid has impurities that may cause immune reactions.\n\n  The use of desiccated thyroid confuses the thyroid testing. If doctors measure only the total T4 hormone, that result is often low because of the large amount of T3 in the medication. The patient may receive even more thyroid hormone and actually become hyperthyroid.\n\n  The dose of T4 and T3 that desiccated thyroid supplies doesn't provide the same levels as what the normal thyroid releases.\n\nThese problems have had their consequences in the past. Patients have been undertreated or overtreated by different preparations of desiccated thyroid. Doctors have found some patients to be hyperthyroid for a few hours a day due to the large amount of T3 in some desiccated thyroid pills.\n\nOne thing to be said for desiccated thyroid is that it does contain some T3, which most synthetic hormone replacements don't have. However, a synthetic preparation of T3 does exist, and it's far superior to the mixture in desiccated thyroid.\n\nSynthetic thyroxine is currently the medication of choice in the treatment of hypothyroidism. In the future, a combination of T4 and T3 in the exact ratio that it leaves the thyroid may replace T4 alone.\n\n### Conducting proper medical studies\n\nScientists who conducted studies using control groups (people who didn't get active medicine or treatment but thought they did) and treatment groups (people who got the active medicine or treatment but weren't certain that they did) have found the myths in this chapter to be just that \u2014 myths. In studies using control and treatment groups, even the doctors administering the treatment or medicine don't know who is getting real treatment and who isn't. Only by conducting studies this way can scientists make a fair comparison between groups. This is the famous _double blind placebo\u2013controlled study,_ and scientists arrange it in the following manner:\n\n  No patient knows what he or she is getting, nor does the doctor, but all patients get something \u2014 either real treatment or a placebo.\n\n  The benefits for the patient getting the real treatment must be significantly better than those for the patient getting a placebo to prove the treatment's value.\n\n  The side effects for each group should be about equal so the patient with the disease isn't having many more side effects than the person serving as a control.\n\n## Thyroid Disease Is Contagious\n\nUnderstanding why this myth has become so entrenched in the minds of the public isn't hard. Most thyroid disease is hereditary; so the likelihood of finding the same disease in two sisters or a mother and her daughter is relatively high, potentially suggesting that their physical closeness to one another causes them to have the same disease. Furthermore, in areas where people don't consume enough iodine, practically everyone has thyroid disease \u2014 again seeming to suggest that it may be catching.\n\nAnother situation that seems to suggest that thyroid disease is catching is the occurrence of thyroid disease after large-scale radiation exposure. Just about everyone comes down with some illness in this situation. Children, especially, often develop goiters, nodules, and thyroid cancers.\n\nAn understanding of the way these diseases develop quickly clarifies the situation:\n\n  The hereditary thyroid diseases affect the females of a family, usually sparing the males.\n\n  The incidence of thyroid disease rapidly declines in iodine-deficient areas after iodine is supplied to the population.\n\n  Children who take iodine pills or avoid exposure to radioactive iodine generally won't get thyroid diseases, while those who don't do.\n\nYou can't catch thyroid disease, nor can you give it to someone else in the way that germs pass from person to person.\n\n## Iodine Deficiency Is a Medical Problem\n\nBecause iodine deficiency (see Chapter 12) causes hypothyroidism, goiter, and cretinism (when severe), you may think that it's a clear-cut disease that should respond to medical treatment with iodine. If this were so, the disease would have disappeared years ago.\n\nAs with any major medical problem (like AIDS, breast cancer, and prostate cancer), iodine deficiency is a social, economic, and political problem as much as, or more than, a medical problem.\n\nTo begin with, an understanding about the cause of hypothyroidism in iodine-deficient areas is often lacking. The people are poor, work very hard, and have little time for the intricacies of the cause of disease. Their poverty means that they can't afford to pay for nurses to give them medication or inject them with iodized oil. They don't understand that certain foods, like cassava, worsen the problem, so they continue to consume large quantities of them.\n\nOften the local or federal government pumps in lots of money to improve the situation by providing iodine supplementation. But it provides no punishment for those who don't follow the regulations. Manufacturers may fail to put any iodine into their so-called \"iodized\" salt and claim the subsidies for it anyway. Much of that money disappears after it leaves government control.\n\nSometimes attempts to solve the problem run up against the realities of salt production. This has been the case in Indonesia, for example, where numerous salt farmers rather than a centralized salt-production facility make salt (as salt is made in China). Consequently, altering salt production to make enough iodized salt was easier and more productive in China than in Indonesia.\n\nWhen a tremendous need for a substance like iodine exists, the cheats try to profit from people's misery. They charge more for iodized salt and then fail to actually iodize the salt. They also underprice the government's iodized salt so that people buy their salt rather than true iodized salt from the government.\n\nThe instability of poor governments also plays a role. For example, when Communist East Germany recognized the problem of iodine deficiency, the government provided iodine and brought the disease under fairly good control. After the reunification of East and West Germany, the combined government neglected the problem, and iodine deficiency began to reappear.\n\nThe solution to a clearly medical problem like iodine deficiency may have to involve social, cultural, and economic changes that populations often resist, making a cure exceedingly difficult.\n\n## The Higher My Autoantibody Levels, the Worse My Thyroid Disease\n\nThis myth derives from a phenomenon that seems obvious: The more you have of something that denotes a disease, the worse that disease must be. For example, if your temperature is 102 degrees Fahrenheit, you're probably sicker than someone whose temperature is only 99 degrees Fahrenheit. When it comes to thyroid autoantibodies, however, this isn't the case.\n\nWhen doctors measure and compare the levels of autoantibodies with the severity of a patient's thyroid disease, they find no correlation. Some of the sickest patients with hyperthyroidism due to Graves' disease have relatively low levels of autoantibodies, while people with milder cases of Graves' may have high levels.\n\nAdding to the confusion is the fact that the disappearance of thyroid autoantibodies after treatment with antithyroid drugs is a marker for improvement and suggests that the disease won't recur.\n\nVery low levels of autoantibodies are often present in elderly women. But unless those women have abnormal thyroid function tests, the autoantibodies have little importance. Although people with low levels of autoantibodies should be retested occasionally, they don't require treatment unless a thyroid condition develops.\n\nDoctors shouldn't compare autoantibody levels between laboratories. Laboratories practice little consistency in the methods they use in their tests, so a level of a thousand at one laboratory means something very different from a level of a thousand at another laboratory.\n\nVery high thyroid autoantibody levels don't indicate that you have a bad case of autoimmune thyroiditis. They simply confirm the diagnosis if other signs and symptoms exist.\n\n## Clinical Symptoms Are More Reliable Than Blood Tests\n\nThyroid disease can be very confusing. In certain age groups, particularly the elderly, the expected signs and symptoms may not exist. Sometimes doctors find opposite symptoms. For example, some people gain weight as a result of hyperthyroidism.\n\nMany people, including some physicians, believe that clinical signs and symptoms are more accurate than laboratory tests when diagnosing thyroid conditions.\n\nWhat would a doctor who relies on symptoms do with an elderly woman who is apathetic, doesn't have an enlarged thyroid, and is depressed but has a free T4 level of 3.5 and a TSH of less than 0.3? Her clinical signs and symptoms point to hypothyroidism, but her tests show hyperthyroidism. Relying on symptoms alone, a doctor may give this patient thyroid-hormone replacement. Lots of luck.\n\nI've relied upon thyroid-function tests to diagnose disorders of thyroid function for 33 years. Especially in the last decade, as the TSH test has become more accurate and the free T4 and free T3 have become available, I've felt extremely confident that I have the right diagnosis.\n\nThe proof of the pudding is in the eating. When I treat patients with confusing clinical signs according to their lab test results rather than their clinical findings, they invariably get better.\n\nSigns and symptoms of hypothyroidism can be very subtle, just like many other diseases. The signs and symptoms mimic those of diseases like depression, menopause, and aging.\n\nThe placebo effect of any drug is another problem. If you give a group of patients a pill that's not supposed to have any effect on the disease in question, a few of them get better. This doesn't mean that the pill is the reason they improve.\n\nA good physician bases his or her treatment on evidence-based medicine. This means that single instances of improvement don't prove that a treatment is correct; they can just as easily mean that the original diagnosis is wrong.\n\nDon't allow a doctor to treat you for a thyroid disease, such as hyperthyroidism or hypothyroidism, unless the thyroid function tests confirm the diagnosis.\n\n##### Chapter 22\n\n## Ten Ways to Maximize Thyroid Health\n\n### In This Chapter\n\n  Keeping an eye out for thyroid disease\n\n  Getting enough iodine\n\n  Managing hyperthyroidism and cancer\n\n  Avoiding drug interactions and radiation\n\n  Staying up-to-date\n\nIf you've been reading this book from beginning to end, we've come a long way together. Now the time has come to put the icing on the cake or perhaps the exclamation point at the end of the sentence. In this chapter, I discuss the steps you can take to ensure your best thyroid function. You may have thought that there was little you could do \u2014 that your thyroid, like the Mississippi River, would just keep rolling along. As I show you here, you can do a lot to maximize thyroid health (so much, in fact, that I've included 11 ways to maximize your thyroid health in this edition, instead of just 10).\n\nYou can make sure that you have thyroid testing done at the right intervals. You can do some self-examination to determine whether the shape of your thyroid is normal. You can make sure that you're getting the proper nutrients so that your thyroid can make its hormones in sufficient quantities. And perhaps most important of all, you can be knowledgeable about all the new discoveries concerning thyroid health and disease that appear on an almost daily basis.\n\nBy doing these things, you're doing all that you can to take care of that little gland that weighs less than an ounce but plays such an important role in your life and your health. And don't forget to take care of all those cells, tissues, and organs that surround that 20-gram gland. It won't be of much use if all the rest of you is falling apart.\n\n## Screening at Appropriate Intervals\n\nMany symptoms of hypothyroidism are subtle or are similar to symptoms of aging or menopause (see Chapters 5 and 19). Hyperthyroidism can also be tricky because symptoms may not be prominent (especially in elderly people), and sometimes symptoms appear to point toward an underactive thyroid even though the thyroid is overactive (see Chapter 19).\n\nThe most common form of thyroid disease is autoimmune thyroiditis. It probably affects 10 percent of the population of the United States, although only a small fraction of people with this disease actually develop hypothyroidism.\n\nHypothyroidism often begins when a woman is in her 30s. For this reason, and because of the confusion that can exist between the diagnosis and the signs and symptoms a patient experiences, doctors recommend that you start screening for abnormal thyroid function at age 35 and continue at five-year intervals for the rest of your life. This applies to both sexes. Of course, if tests reveal a thyroid condition, your doctor will perform testing much more frequently.\n\nYour doctor uses a blood test, the TSH (thyroid-stimulating hormone) test, to screen for abnormal thyroid function. Although the normal range is usually given as 0.5 to 5, the true normal range may be narrower, 0.5 to 2.5 (see Chapter 5). If your doctor tells you that your screening test is normal, but you still have symptoms consistent with hypothyroidism, ask the doctor for the exact number of your TSH. If it's above 2.5, ask your doctor to consider giving you a trial of treatment with thyroid-hormone replacement.\n\n## Checking Thyroid Function As Your Body Changes\n\nIf you're taking thyroid hormone treatment, you're on a fixed dose of medication. However, many physical states, particularly pregnancy (see Chapter 17), create chemical changes in your body that can alter the amount of thyroid hormone that you need to maintain normal function. The same is true as you get older.\n\nChemical changes that cause you to make more thyroid-binding proteins (see Chapter 4) require you to take an increased dose of thyroid medication. Any condition that increases your estrogen is an example, such as pregnancy and taking oral contraceptive pills. As your body makes more thyroid-binding proteins, more of your dose of thyroid is bound to the proteins and less is available to enter your cells. You must increase your dose of thyroid hormone. Blood tests determine when you again have enough.\n\nChemical changes that cause you to make less thyroid-binding proteins require a decreased dose of thyroid hormone. If you take androgens (see Chapter 10) or have a disease that causes your body to produce androgens excessively, you may need your dosage of thyroid hormone reduced. Less thyroid-binding protein means less binding of your thyroid dose so more is available to enter cells. If you don't reduce your dose of thyroid hormone in this circumstance, you can become hyperthyroid.\n\nAnother situation that occurs in pregnancy is the reduction in autoimmunity (see Chapter 17). If you're being treated for hyperthyroidism with antithyroid pills, you may need a lower dose or none at all until the pregnancy is completed. Then you need treatment again.\n\nDuring times of major body change such as pregnancy or illness, your need for thyroid hormone or antithyroid medication may change. The only way to be sure you are on the right dose is to have thyroid function tests at regular intervals, usually every three months.\n\n## Performing a \"Neck Check\"\n\nThe American Association of Clinical Endocrinologists (AACE), recognizing that many people have thyroid disease that's not diagnosed, proposes that everyone perform the thyroid \"neck check.\" You can find details at their Web site, www.aace.com. Under \"Awareness Campaigns,\" click on \"Patient Awareness Campaigns.\" On the page that comes up, click on \"Thyroid Awareness 2005.\" At the next page, scroll down to \"When the Blues Hit\" and click on that. The page that comes up has a choice that you can click on called \"Neck Check.\"\n\nYou can detect abnormalities in the size and shape of your thyroid gland. If you think you have an enlarged thyroid, seek your doctor's help to determine whether you have any problem.\n\nAACE urges everyone to \"think thyroid.\"\n\nYou need to follow five steps to do a neck check. You need a hand-held mirror and a glass of water. The steps are as follows:\n\n**1.** **Hold the mirror in your hand, focusing on the area of your neck just below the Adam's apple and immediately above the collarbone.** Your thyroid is located in this area of your neck.\n\n**2.** **While focusing on this area in the mirror, tip your head back.**\n\n**3.** **Take a drink of water and swallow.**\n\n**4.** **As you swallow, look at your neck. Check for any bulges or protrusions in this area when you swallow.** _Reminder:_ Don't confuse the Adam's apple with the thyroid gland. The thyroid gland is located farther down on your neck, closer to the collarbone. You may want to repeat this process several times.\n\n**5.** **If you do see any bulges or protrusions in this area, see your physician.** You may have an enlarged thyroid gland or a thyroid nodule, and your doctor should check to determine whether cancer is present or if you need treatment for thyroid disease.\n\n## Getting Enough Iodine to Satisfy Your Thyroid\n\nThough iodine deficiency isn't as vast a problem in the United States, Canada, and Western Europe as in other parts of the world, a few considerations still need addressing.\n\nIf you're a vegetarian, you may not eat the foods that are the major sources of iodine in the diet, namely fish, and, to a lesser extent, meat, eggs, and milk. Little iodine is present in fruits and vegetables.\n\nBecause high blood pressure is such a concern these days, your doctor may urge you not to add salt to your food because salt raises the blood pressure. However, the American Heart Association's nutritional recommendations are to limit salt intake to less than 6 grams daily, slightly more than a teaspoon. This amount contains plenty of iodine for your diet.\n\nHow do you act when you receive contradictory recommendations from health professionals? (\"You need sufficient iodine.\" \"Don't eat salt!\") You can certainly use a small quantity of salt daily, and this contains enough iodine for your needs because 1 teaspoon of salt contains about 400 micrograms of iodine. Or you can eat a couple slices of bread each day. Each slice of bread contains about 150 micrograms of iodine. The recommended intake of iodine daily is 150 to 200 micrograms.\n\n## Stopping Thyroid Medication, If Possible\n\nYou're always better off if you let your normal body thyroid physiology work for you than if you try to replace it with an external source of thyroid hormones.\n\nDuring my many years of medical practice, I've seen numerous people who were taking thyroid hormone who had never been tested with thyroid function tests. They had developed symptoms of fatigue or had gained a few pounds and had been put on medication. Most of these patients, when taken off thyroid hormone, proved to have normal thyroid function on their own. Often, if questioned about whether the thyroid hormone had made a difference, they admitted that they were still fatigued and still had trouble losing weight, even on the medication. These people should never have been placed on thyroid hormone in the first place but should certainly have had a trial off of thyroid hormone replacement over the years.\n\nAnother group of patients who have been put on thyroid hormone replacement because of laboratory evidence of low thyroid function may also get off thyroid hormone at some point. These are patients who have hypothyroidism due to chronic thyroiditis (see Chapter 5). Their hypothyroidism is the result of antibodies that block the action of thyroid-stimulating hormone. Up to 25 percent of these patients may be able to come off treatment. The level of these blocking antibodies may possibly fall to the point that the thyroid gland is able to make its own thyroid hormone. Stopping the thyroid hormone after a few years of treatment to see if the thyroid can function on its own is certainly worthwhile.\n\nIf you have hypothyroidism due to chronic thyroiditis and have been taking thyroid hormone pills for a few years, ask your doctor if you can stop the thyroid hormone replacement for a month and check your thyroid function tests.\n\n## Using Both Types of Thyroid Hormone\n\nThe thyroid gland makes two different thyroid hormones: T4, the major component, and T3, considered to be the active form of thyroid hormone but made in much lower amounts by the gland (see Chapter 2).\n\nBecause drug manufacturers have had the ability to synthesize it, T4 is the only treatment doctors give when patients need thyroid hormone. Doctors give it so that a patient's TSH level returns to normal, as does the free T4 in the blood. This suggests that most people who receive treatment for hypothyroidism may have a deficiency of T3.\n\nIn practical terms, over the years a deficiency of T3 hasn't proven to be a significant problem. However, I've noted in my thyroid practice, as have other specialists, that a few patients continue to complain of symptoms of low thyroid function despite normal laboratory test results. These patients may improve if their doctors add T3 to their treatment.\n\nMeasuring this kind of improvement objectively is difficult, because the test results remain in the normal range. This is a case where I've been willing to accept the subjective symptoms of the patient indicating that he or she feels better on the combination therapy compared to T4 alone.\n\nThis is still a gray area in medicine. I've seen a handful of patients who didn't feel better regardless of how much T3 I added, even though their thyroid tests were normal. And the latest studies, which I quote in Chapter 5, suggest that additional T3 makes no difference in treatment.\n\nI hope that in the future doctors will have some objective test that will tell them that thyroid function is perfectly normal by a measurement separate from thyroid function tests \u2014 for example, a new blood test measuring a chemical that we don't even know about yet or a nonblood test.\n\nIf you have symptoms of hypothyroidism and are taking T4 hormone replacement alone, ask your doctor to prescribe a small dose of T3. You may do better on the combination.\n\n## Preventing the Regrowth of Thyroid Cancer\n\nIf you've had thyroid cancer, you have probably had thyroid surgery followed by irradiation to eliminate the remaining thyroid tissue. Now you want to prevent any regrowth of thyroid cancer. You prevent regrowth by taking sufficient thyroid hormone to suppress the production of thyroid-stimulating hormone. The goal is for your TSH level to drop below the normal range. The lower level of the normal range is about 0.5, so you want a reading of 0.3 or below to be sure your thyroid isn't being stimulated.\n\nBut how low is too low? If a reading of 0.3 is good, would a reading of 0.1 be better? A study published in _Thyroid_ in 1999 addressed this issue. The researchers had two groups of cancer patients: One group's TSH levels were suppressed to below 0.1; the other group's TSH levels were kept between 0.4 and 0.1. The study found that residual thyroid tissue was no more suppressed when the TSH was less than 0.1 than when it was between 0.4 and 0.1. The researchers concluded that thyroid cancer patients should receive suppressive doses of T4, but that greater suppression is no better than lesser degrees of suppression.\n\nExcessive suppression of thyroid hormone runs the risk of causing osteoporosis, heart problems, and loss of muscle tissue. The advantage of taking the least suppressive dose of thyroid hormone possible is that you have less risk of developing osteoporosis or rapid heartbeats, particularly if you're middle aged or older.\n\n## Using the Same Thyroid Preparation\n\nThe American Association of Clinical Endocrinologists' campaign for Thyroid Awareness Month in 2005 (Thyroid Awareness Month is January of each year) was \"A Healthy Thyroid: You Make the Difference.\" The focus of this year's theme was that fact that \"the body is sensitive to even small changes in thyroid hormone levels,\" along with \"the importance of knowing the brand and dose of your thyroid medication.\" But you, you genius, already know all about it because you're reading this book.\n\nAlthough it would be wonderful if a dose of 0.125 mg of Levoxyl, 0.125 mg of Synthroid, and 0.125 mg of levothyroxine were interchangeable, the fact is that they aren't. Despite the best efforts of the Food and Drug Administration, these medications are made slightly differently, and their potency is slightly different. That means if you get on one of these preparations, staying with the same preparation is important to be sure you experience no change in your thyroid function.\n\nWhat conditions may cause your preparation to change? If you change pharmacies, the new pharmacy will likely use a different source for its medications. The pharmacy you use, even if you don't change, may change its source. If you change health plans, your new health plan may use a different manufacturer. If you buy your drugs from Canada or Mexico, you can bet you're getting a different potency. If you change doctors, the same thing can happen.\n\nWill you realize you're on a new preparation? Probably not, because the changes in your body may be too subtle for you to notice. But the different strength may cause damage to your body, depending on whether it's too much or too little.\n\nHow can you prevent this from happening?\n\n  Check the name of the medication on your new bottle each time you get a refill of your thyroid medication.\n\n  Ask your pharmacist if he or she is using the same source each time you refill.\n\n  Try to use the same pharmacy or drug program each time you refill.\n\n  Avoid discounted sources of thyroid medication. It should be a very inexpensive drug.\n\nIf all else fails and you have to change the source of your thyroid medication, get thyroid function tests four to six weeks after you make the change.\n\n## Anticipating Drug Interactions\n\nSo many drugs interact with thyroid hormones that you must check with your doctor whenever he or she places you on a new medication or takes you off an old medication (see Chapter 10).\n\nYour thyroid function can be affected not only when you start a new medication but also if your doctor takes you off an old medication or changes the dosage significantly.\n\nThe way to avoid a problem is to perform (or have your doctor perform) a search for interactions between thyroid hormone and the drugs you'll be taking.\n\nDrugs can affect thyroid function at any level. They can increase or decrease the release of thyrotrophin-releasing hormone, which affects how much thyroid-stimulating hormone (TSH) your body creates. They can increase or decrease the release of thyroid hormone from the thyroid. They can change the ratio of T4 hormone versus T3. They can affect the uptake of thyroid hormone by cells. They can increase or decrease the action of thyroid hormone within the cells.\n\nThe major drugs that you should be concerned about are the following, which I discuss in Chapter 10:\n\n  Lithium\n\n  Amiodarone\n\n  Estrogen\n\n  Steroids\n\n  Aspirin (in doses greater than 3,000 milligrams)\n\n  Iron tablets\n\n  Iodine\n\n  Propranolol\n\nChances are that you'll take one or more of these drugs in your lifetime.\n\nJust about every drug affects thyroid function in one way or another. Fortunately, your thyroid gland makes some adjustment to overcome most of the effects. But if you're on a fixed treatment dose of thyroid hormone, your thyroid can't adjust as it would normally. Having your thyroid function tested four to six weeks after you start a new medication or stop an old one is wise.\n\n## Protecting Your Thyroid from Radiation\n\nOne million or more Americans received neck irradiation for various conditions in the years between 1920 and 1960, and they're at higher risk for thyroid cancer. Close to 10 percent of people who were so treated have developed thyroid cancer to date.\n\nIf you received irradiation to your neck area as a child because of enlarged tonsils, acne, an enlarged thymus, or some other condition, you're at increased risk for thyroid cancer and should inform your doctor.\n\nIf you've had any kind of radiation treatment to your head, chest, or neck in the past, you should perform the \"neck check\" I describe earlier in the \"Performing a 'Neck Check'\" section of this chapter. If you feel something unusual in shape or size, see your doctor. If you don't, see your doctor anyway, because changes may be very subtle, and the incidence of thyroid cancer is definitely higher if you've been irradiated. The exception here is that radiation treatment for hyperthyroidism doesn't increase your risk of cancer.\n\nA thyroid scan or a thyroid ultrasound (see Chapter 4) should find any significant abnormality that exists. If one is found, the usual next step is a fine needle biopsy of the thyroid.\n\nWhat about follow-up if nothing is found? Having an examination of your thyroid on at least an annual basis is probably a good idea if you have a history of thyroid exposure to radiation.\n\nEven those of us who were never exposed to radiation as part of a medical treatment need to be aware of the risks of radiation. That's because as sources of fossil fuel for energy are used up, like it or not, energy companies will probably turn more and more to nuclear energy.\n\nYou want to be prepared to avoid taking in a lot of radioactive iodine if a nuclear accident occurs at the power plant near you. Fortunately, the Nuclear Regulatory Commission takes this threat seriously. It has arranged to have stockpiles of iodine available to take in the event of a nuclear accident. By taking a large dose of iodine daily for several days, you block the uptake of iodine into the thyroid.\n\nThe other thing you can do to protect yourself is to stay indoors. The radiation can't affect you if you don't come in contact with it.\n\nExposure of your thyroid to radiation in the past (other than for treatment for hyperthyroidism) definitely increases your risk of thyroid cancer. However, should cancer occur, it's no more dangerous than thyroid cancer not associated with radiation as long as you receive proper treatment.\n\n## Keeping Up-to-Date with Thyroid Discoveries\n\nThis book is an excellent start in your quest for knowledge about the thyroid gland and how it affects you. Most of the information here will be useful for at least ten years or so. Given the pace of research, however, a book can't keep you completely up-to-date with new findings about thyroid physiology and pathology. You need to seek them out for yourself. Where do you look?\n\nAn obvious start is to wait for an updated version of this book, which will generally have all the important information since the last publication. You can also try the Internet.\n\nIn Appendix B, you find the Internet sites that I believe are most accurate and reliable with respect to thyroid function and disease. I list the Web sites of large organizations like the American Association of Clinical Endocrinologists, the American Thyroid Association, the American Association of Endocrine Surgeons, and the American Association of Thyroid Surgeons.\n\nYou also find smaller sites belonging to individuals and groups who have various thyroid conditions or are advocates for those conditions. You can learn a great deal about the experience of having a particular thyroid disease by reading their comments.\n\nSeveral government sites provide a ton of free information about the thyroid. Likewise, many institutions of higher learning want to provide information with the hope that you seek out their specialists for your ongoing care.\n\nThe various drug companies that make thyroid medications have Web sites that contain information, especially about their products, and often general information about the thyroid as well.\n\nIf you speak French, go to the site of the Thyroid Foundation of Canada, where you can find everything you want to know in a French version. This site also has an International Directory of Thyroid-related Organizations. Among the countries the site lists are Denmark, Germany, Italy, Japan, and the Netherlands.\n\nSo many different organizations provide the same information about the thyroid that I often wonder why some of them don't pool their resources to provide one major source. I suppose too many egos are involved to take this logical step, but I still think it's a good idea. Perhaps you're thinking, \"Why, Dr. Rubin, with all this information available, did you bother to write this book?\" My answer is, of course, that this book is unique. No other one out there is quite like it, believe me.\n\n##### Chapter 23\n\n## Ten Questions Readers Have Posed\n\n### In This Chapter\n\n  Basing the dose of methimazole on the TSH\n\n  Treating a teenager with radioactive iodine or tapazole\n\n  Taking all the tapazole at one time\n\n  Managing hypothyroidism during pregnancy\n\n  Considering side effects of long-term thyroid hormone\n\nThe number of e-mails that I've received from my readers has been very gratifying. You've thanked me for writing this book with comments like the following:\n\n  I just finished reading your _Thyroid For Dummies_ book, and I have to tell you, I thoroughly enjoyed reading it!\n\n  I want to thank you for your _Thyroid For Dummies_ book.\n\n  I just want to tell you that your book has been extremely helpful to me.\n\n  I read your wonderful book _Thyroid For Dummies_ and was so impressed.\n\n  I've recently read your book and thoroughly enjoyed it.\n\nAt the same time, you've posed a lot of excellent questions that apply not just to you but to many of my readers. The purpose of this chapter is to answer the ten most common questions you've sent me. I'm sorry if I don't answer your particular question here. However, I try to answer all questions that are general in nature by return e-mail, so don't hesitate to write me at thyroid@ drrubin.com; I promise to reply. If your question applies to enough people, it will probably get into the next edition of this book. I can't answer specific questions about your case, however, without the opportunity to talk to you and examine you myself. To do so would be unethical.\n\nI can't pose your questions better than you do, so this chapter basically replicates your questions. I've tried to omit any information that can identify you, because I consider your privacy extremely important. Thank you again for all your support and interest.\n\nTaken as a whole, your questions have led me to consider a number of interesting issues. I have listed some of the conclusions I've drawn here so you can benefit from the insights that your questions have provoked.\n\n  Not all so-called \"specialists\" know what they're talking about.\n\n  You're the one who should make the final decision about your treatment with the help of your doctor.\n\n  No doctor has the right to demand that you take a certain treatment.\n\n  Even the best treatments change over time, because they too are subject to new research.\n\n  We as doctors don't have the answers to all your questions, but we keep trying.\n\n## Basing Doses of Methimazole on TSH\n\n_On 8\/23\/05, follow-up lab work indicated normal FT3 and FT4 levels again, but TSH had dropped to 0.19. Endocrinologist increased dosage of methimazole to 20 mg. twice daily, and patient is to return in 6 weeks for follow-up and lab work. I have read conflicting reports that dosing for Graves' should not be based upon the TSH alone, especially when FT3 and FT4 are normal. However, I don't want to be \"under-medicated\" and have my eyes worsen or go into a thyroid storm either. Do you think my endocrinologist is right on track?_\n\nThe answer is a definite _no_! Your endocrinologist doesn't seem to be aware that the TSH can remain low for months after the free T4 returns to normal, which doesn't mean you still have active hyperthyroidism. Once the free T4 returns to normal, your doctor should gradually lower your dose of the antithyroid drug to keep the free T4 normal for at least a year. Then your doctor can consider stopping the antithyroid drug, depending on your clinical situation. For example, if the thyroid gland is still large after a year, I would keep the patient on the drug a longer time.\n\nSometimes, even when taking the lowest dose of an antithyroid drug, your free T4 falls below normal and your TSH rises above normal, indicating you're now hypothyroid. Should you stop the drug at this point? My answer is no, because I believe you need to give your thyroid at least a year of medication to reverse the hyperthyroidism. Instead of stopping the antithyroid drug, I recommend adding thyroid hormone to the antithyroid medication to keep your thyroid function normal.\n\nIf your doctor's advise doesn't agree with what you read in this book or some other reliable source, go find another opinion.\n\n## Reversing Cold Sensitivity\n\n_Two years ago, months before my 40th birthday, I was diagnosed with hypothyroidism. My doctor put me on 50mcg of Synthyroid medication. Within several months, most of my previous symptoms such as low energy, hair fall etc. were reversed and I was feeling pretty good. That is with the exception of my sensitivity to cold and insensitivity to heat. After I started taking Synthyroid, this issue has completely reversed itself to the point of being a real bother to me._\n\nYou're saying that, although you had cold sensitivity before taking the Synthroid, you're now sensitive to heat as well. My opinion is that you are probably now getting too much thyroid hormone. People who are hypothyroid are sensitive to cold, but people who are hyperthyroid, whatever the reason, are sensitive to heat, which is one example of many ways the two conditions are the reverse of one another. Table 23-1shows other examples:\n\nTable 23-1 Comparisons of Signs of Hypothyroidism versus Hyperthyroidism  Hypothyroidism  | Hyperthyroidism |   \n---|---|---  \nGain weight  | Lose weight |   \nSlow pulse  | Fast pulse |   \nDry skin  | Moist skin |   \nIncreased menstrual flow  | Decreased menstrual flow |   \nHigh cholesterol  | Low cholesterol |   \nDecreased body temperature  | Increased body temperature |\n\nI could list many more opposites. But keep in mind that some people don't exhibit the classic signs of hypothyroidism or hyperthyroidism. The elderly, for example, may have hypothyroidism but lose weight because they eat so little.\n\nIf you have hypothyroidism or hyperthyroidism, receive treatment, and begin having symptoms opposite to what you had before, your doctor may have overtreated you. Have your thyroid blood tests done to find out.\n\n## Treating a Teenager for Hyperthyroidism\n\n_We have seen a pediatric endocrinologist who recommended both the meds: PTU (temporarily) and then the radiation treatment. As parents we are leaning towards the RAI treatment and planning on getting it scheduled in a week or two. But we still have questions... Won't her body still be making the antibody for the thyroid? How does this treatment deal with that? How can we get rid of the antibody attack? Does this RAI treatment do that? What about her eyes? \u2013 Does the replacement hormone take care of that risk? In general, what is the best treatment for a 16-year-old?_\n\nI believe that antithyroid medication is the best treatment for a 16 year old with hyperthyroidism or almost anyone at any age with the condition. As far as I know, radioactive iodine and surgery don't reverse the underlying pathology, the autoimmune reaction. Antithyroid drugs do. Studies of patients who've been on antithyroid drugs for more than ten years demonstrate the drugs' excellent control of hyperthyroidism without side effects. In my own practice, I have patients who, after initial treatment with antithyroid drugs, have gone more than ten years without taking any medication and enjoy normal thyroid function.\n\nIf you elect radioactive iodine (or surgery), your 16 year old will likely be hypothyroid for the rest of her life, needing to take a pill every day. In addition, some evidence suggests that the eye disease of hyperthyroidism continues to progress after radioactive iodine or surgery but not after taking antithyroid drugs.\n\nSurgery is probably the best choice for a person with obstruction due to a large thyroid around the esophagus and trachea. Radioactive iodine may be better for a person who can't be depended upon to take antithyroid drugs regularly or has a reaction to the drugs. The same person, however, probably won't take the thyroid pill necessary after radioactive iodine.\n\nSome doctors say that a very large thyroid gland doesn't respond well to antithyroid drugs, but this hasn't been my experience.\n\nMy preferred treatment for Graves' disease (hyperthyroidism) is antithyroid medication, for patients of any age and in almost all circumstances.\n\n## Taking Methimazole All at Once\n\n_I wanted to ask you something. I've been on methimazole 10mg 4x per day (40mg total per day) for 4 weeks. I just went to my doctor who said my levels had dropped by 1\/2 and I was doing very well. I do feel 100% better. He now wants me to take all 40mg at once for the next month. I checked with my pharmacist and she said that's not the way it's usually done. You mention this spaced out dosing in your book also. Have you ever heard of this dosing schedule. I asked my doctor and he said that first it's taken spaced out, then it's taken all at once, then the dosage is reduced._\n\nYour doctor is correct. Doctors usually begin prescribing methimazole in divided doses but prescribe a single dosage once the thyroid is under control. As you know, methimazole and the other antithyroid drug, propylthiouricil, take three to six weeks to bring the thyroid under control. Methimazole isn't like penicillin or allergy medications, which begin to work within minutes of taking them. Because a dose of methimazole takes weeks to work, you might as well take your daily dosage all at once. You may even question why we start with multiple daily doses. As Tevya says in _Fiddler on the Roof,_ it's tradition.\n\nTaking several pills at one time often helps you remember to take the medication. You can more easily remember to take your pills once instead of multiple times a day.\n\nI usually give more medication to the person who has a higher free T4 and less to the person with a close to normal free T4. But I suspect that the lower dose works just as well in both cases.\n\n## Insisting on Radioactive Iodine Treatment\n\n_At my insistence I was placed on PTU and Inderal. ( **Author's note:** This is the same as propranolol.) My endocrinologist never even suggested it, they wanted me to do radioactive iodine and I refused, insisting I wanted to try the anti-thyroid drug first. Anyway, I have done great on a block and replace regimen and my endocrinologist is now wanting me to stop the PTU to see if I obtain remission. I am more than willing to do that, however, my endocrinologist has made it clear that if remission is not obtained he is insisting on RAI and stated he \"would discharge me as a patient\" if I did not agree to the RAI. I feel that I am being bullied into this treatment and I am very concerned as I have some eye involvement. I have called around and thus far all the endo's that I have contacted all have the same mindset . . . RAI or nothing!!!_\n\nYou must find some doctors near you who will listen! As I note above, my preferred treatment is antithyroid drugs. If you can't find a doctor who will go along with your wishes, check Chapter 3 and find a doctor according to the ways I suggest. You don't have to take any treatment that you don't want, even if (although it's not the case here) the treatment is life-saving. You may consider a trip to Europe, where all the doctors use antithyroid drugs in preference to radioactive iodine. If you figure out the cost of office visits and medicine in the United States, you may find out you save money.\n\nI've received a large number of e-mails exactly like this one. Doctors tell their patients they have to take radioactive iodine, which is ridiculous and very unsatisfactory. No doctor has the right to tell patients they have to do anything.\n\nYou have the final decision about how you want to be treated. If a doctor insists on something you don't want, find another physician.\n\n## Treating with Thyroid after Pregnancy\n\n_I was diagnosed at around age 6 with a goiter and hypothyroidism due to Hashimoto's. When I was twenty I had a baby and ever since then I don't seem to be able to get my thyroid 'under control'. Does it seem that having a baby can literally make things worse for my condition? My son (my only child) will be ten this year. Over the past few years I have had trouble maintaining a constant TSH. Recently I quit my meds and my TSH shot up to 23. I started back on meds at .150 mg and went back to the doctor. I went down to .125 mg\/Levoxyl and my TSH is within range (around 3) but I still have symptoms of hypothyroid. Does adding T3 really help some people with symptoms?_\n\nWhen you have a baby, your body undergoes major changes. One of them is a significant reduction in autoimmunity. If you have chronic thyroiditis (Hashimoto's thyroiditis), you may stop producing as much blocking autoantibody and may not need as much or any thyroid for the duration of the pregnancy. (Similarly, people with hyperthyroidism may stop making stimulating antibodies, decreasing their hyperthyroidism in severity during the pregnancy.) Usually both hypothyroidism and hyperthyroidism come back like before once the pregnancy is over.\n\nIf you were last pregnant ten years ago, the pregnancy probably isn't playing a role in your current thyroid function. Antibody levels can rise and fall, and your disease may worsen, requiring more thyroid hormone, or improve, requiring less thyroid hormone, as your antibodies rise and fall. In addition, be careful of changing your type of thyroid from one brand to another; the brands may not be biologically equivalent. Your TSH and free T4 need to be tested six to eight weeks after starting a new brand.\n\nTry never to stop thyroid on your own without consulting your doctor. Thyroid takes weeks to build back up in your body, leaving you hypothyroid as it does. Additionally, as I mention in Chapter 5, a TSH of 3 may not mean you have normal thyroid function, even though a TSH of 3 is within the normal range.\n\nThe severity of autoimmune thyroiditis can wax and wane, and different brands of thyroxine have different potencies, so stabilizing your thyroid function may be difficult.\n\n## Explaining Joint Problems\n\n_I was wondering if you can tell me (and I have found little research on this) why thyroid troubles can result in tendon troubles and trigger fingers. ( **Author's note:** Trigger finger is a catching feeling in a finger due to obstruction of the free movement of the tendon that moves the finger) I have had a huge flare-up of deQuervains Tendinitis, and a few triggerfingers develop, and have found other women with the same problems (or fibromyalgia.)_\n\nIn Chapter 5, I discuss the other autoimmune conditions that may accompany autoimmune thyroiditis. Among them are arthritis and other joint conditions. Although the \"thyroid troubles\" aren't to blame for the tendon troubles and trigger finger, they suggest that you may be prone to other diseases. The main ones besides arthritis are celiac disease, hypoadrenalism, diabetes type 1, and pernicious anemia. Each of these conditions has its own set of symptoms. The fact that you have thyroid troubles along with arthritic problems suggests that you're suffering from another disease as well.\n\nIdeally, you may be able to cure your other troubles by curing your thyroid disease. Unfortunately, other conditions run their own course, so you may suffer from other symptoms even if your thyroid condition becomes normal.\n\nIf you have autoimmune thyroiditis (chronic thyroiditis), you have a tendency to suffer from other autoimmune diseases. Although you're still unlikely to experience them, your chances of getting one are greater than someone who doesn't have autoimmune thyroiditis.\n\n## Taking Antithyroid Drugs Long Term\n\n_My husband bought_ Thyroid For Dummies _so that we could learn more about my hyperthyroidism. I was stunned to read that no rule says that antithyroid pills cannot be given for more than a year, because I was led to believe otherwise. I was told that I could only take methimazole for 1 1\/2 to 2 years after which I would have to take radioactive iodine if my thyroid did not go into remission. About 3 months after ending methimazole, tests showed I was again hyperthyroid and I was advised to take radioactive iodine._\n\nAs I've noted previously, no reason exists not to take antithyroid drugs for as long as you need them. About 50 percent of the patients who take antithyroid drugs go into remission. If you don't fall into this lucky group, you can still go back on the antithyroid drugs for another trial. Many of my patients have gone into remission after a year on antithyroid drugs, but some have required two or even three years. I eventually try to take all of them off of methimazole, because I don't like to use drugs as a general rule. But if a patient has a recurrence and is willing to continue to try drugs, I don't hesitate to put her on antithyroid drugs again.\n\nHowever, some people are allergic to antithyroid medication, while others experience a fall in white blood cell count when taking the drug, which reverses when they stop taking it. In such cases, I first try the other common antithyroid drug. If that too is a problem, I go on to radioactive iodine.\n\nPatients have been on antithyroid drugs for 10 years and longer with no harmful effect. I am frankly at a loss to explain the reluctance of many endocrinologists to use these drugs for as long as it takes to accomplish a remission.\n\nAntithyroid drugs are safe and effective. They may be a better form of treatment than radioactive iodine and surgery, except in certain circumstances I describe here and in Chapter 6. No reason exists for not using them for years if necessary.\n\n## Reversing Chronic Thyroiditis\n\n_I am a 41-year-old practicing surgeon. I obtained your book which stated up to 25 percent of the chronic thyroiditis patients have reversal. I stopped taking the meds on my own and I feel pretty darn good after only 7 days. Of course, I will check my TSH in 5 weeks from now to see if the disease is in remission. I am now bench pressing 365 lbs which I have not done since 1982, this is only after 7 days. I asked the internist and the endocrinologist can the chronic thyroiditis go away and they both said never. I showed them your book and they are now reviewing all their patients with Hashimoto's. Myself as well as the other physicians are wondering 3 things: 1) Do anabolic steroids trigger Hashimoto's? 2) After reversal how long does it take before the body is normalized (arthralgias, weakness, etc.)? and 3) What is the chance of the Hashimoto's returning?_\n\nI don't recommend stopping your antithyroid drugs to improve your weight lifting. I think it's a coincidence that you're stronger seven days after stopping your medication, because the effect of antithyroid drugs lasts four to six weeks or longer. As for your questions, as far as I know, anabolic steroids don't trigger Hashimoto's, and I found nothing in the thyroid literature that suggests this could happen. Chronic thyroiditis (Hashimoto's) is an autoimmune disease passed down in the family. Anabolic steroids do reduce the blood levels of thyroid-binding globulins, but thyroid function remains normal.\n\nAs chronic thyroiditis reverses, a gradual reduction in the levels of blocking autoantibodies occurs, which may take years. A gradual reduction in the need for thyroid hormone may accompany the reduction in the blocking autoantibodies, although this may be very subtle. Your other symptoms may be due to another autoimmune disease that doesn't reverse, explaining why your symptoms may continue.\n\nIf the autoantibodies have fallen, they probably won't return, so the lucky 25 percent who have reversal of the Hashimoto's are probably free from the disease from now on.\n\nChronic thyroiditis goes into remission in about 25 percent of patients. After you've been on thyroid for several years, I recommend discussing with your doctor the possibility of coming off the thyroid medication for four to six weeks to test for a return of normal thyroid function.\n\n## Changing Thyroid Dosage\n\n_I'm a 20+ year hypothyroid patient, and I enjoyed reading your book. Most of my questions concern dosage changes over time \u2014 for example, over the 20+ years of treatment, my optimal dosage of thyroid hormone has significantly decreased (from .2mcg to .125mcg). This drop in dosage took place quickly \u2014 over a two to three year period. I have never come across any literature thoroughly explaining why this decreased tolerance occurred in such a sort time period. Another dosage question I have is whether dosage varies depending upon patient's weight \u2014 do heavier patients require a higher dosage than thin patients of the same height? Does a heavy patient who looses substantial weight normally remain at the same dosage?_\n\nYour questions are excellent. You say that your thyroid dosage declined over a two- to three-year period. Your decline in dosage was probably due to what I described in the previous question, a fall-off in your thyroid autoantibodies. No one knows how slowly or quickly a fall-off in thyroid autoantibodies can take place, so your situation may not be unusual. It suggests that you may eventually be able to come off the thyroid completely. You should discuss this with your doctor.\n\nThe next question is whether the dosage varies according to the patient's weight. Because patients with more blocking antibodies need more thyroid than those with fewer antibodies, weight is one consideration that determines the amount of thyroid needed. However, all things being equal, lean body mass, which is the size of the muscles and bones regardless of how much fat a person has, determines how much thyroid a person needs. In a study from the _Journal of Clinical Endocrinology and Metabolism_ from March 2005, doctors evaluated patients with thyroid cancer who had all their thyroid removed to see how much thyroid patients needed to bring their TSH down to a certain value. The best correlation was with the lean body mass, which means that a heavy person who loses substantial weight remains at the same dosage because the fat loss doesn't change the lean body mass.\n\nYour muscle and bone mass determines how much thyroid you have to take, not the amount of fat in your body. A tall person who is thin probably needs more thyroid than a small person who is fat, because the tall person has much more lean body mass.\n\n##### Part V\n\n## Appendixes\n\nIn this part . . .\n\nA ppendix A is a glossary of the terms you encounter as you read and hear about the thyroid gland, its function, and its diseases. All the strange words you meet for the first time in the text of the book are listed here and defined. Appendix B shows you where to look for more information as well as the latest research findings on the thyroid. There is a huge amount of research focusing on every aspect of normal thyroid function and abnormal thyroid conditions. This book gives you a good working knowledge of the subject, but there is always more to know, and these Web sites are where to find it.\n\n##### Appendix A\n\n## A Glossary of Key Terms\n\n**Acute thyroiditis:** A bacterial infection of the thyroid.\n\n**Allele:** One of two or more genes that determine which enzyme will be made or which body characteristic will prevail.\n\n**Antigen:** A foreign protein that prompts the production of antibodies to destroy it.\n\n**Autoimmune thyroiditis:** Inflammation of the thyroid associated with the production of antibodies against thyroid tissue.\n\n**Beta blocking agent:** One of a group of drugs given to block some of the adverse effects of excess thyroid hormone.\n\n**Chorionic gonadotrophin:** A hormone made by the placenta, which shares some properties with thyroid-stimulating hormone.\n\n**Chromosome:** One of 23 pairs in the nucleus of every human cell that carry all the genes that determine the characteristics of the body.\n\n**Chronic thyroiditis:** Another name for _autoimmune thyroiditis._\n\n**Cretinism:** A syndrome affecting children; its most outstanding feature is mental retardation that results from a lack of iodine during pregnancy.\n\n**Cyst:** A saclike structure containing fluid.\n\n**Cytomel:** A brand name for T3 medication.\n\n**Dominant gene:** The gene that determines which particular enzyme or body characteristic will be expressed when two different genes are present.\n\n**Ectopic thyroid:** Thyroid tissue found in an abnormal site, such as the base of the tongue.\n\n**Exopthalmus:** Eye disease associated with Graves' disease.\n\n**Fine needle aspiration biopsy (FNAB):** The process of putting a tiny needle into tissue, in this case the thyroid, for the purpose of determining the nature of that tissue. This process is particularly helpful for identifying thyroid cancer.\n\n**Free thyroxine (FT4):** The tiny fraction of the T4 hormone that isn't bound to protein and is therefore available to enter cells.\n\n**Free thyroxine index (FTI):** An obsolete test once used for determining thyroid function. The product of multiplying the total T4 by the T3 resin uptake.\n\n**Free triiodothyronine (FT3):** The tiny fraction of the T3 hormone that isn't bound to protein and is therefore available to enter cells.\n\n**Gestational transient thyrotoxicosis:** A brief period of hyperthyroidism during pregnancy that results from the large production of human chorionic gonadotrophin (which acts as a thyroid stimulator).\n\n**Goiter:** An enlarged thyroid gland.\n\n**Graves' disease:** An autoimmune condition that combines hyperthyroidism, eye disease, and skin disease.\n\n**Hashimoto's thyroiditis:** Another name for autoimmune or chronic thyroiditis.\n\n**Heterozygous:** Possessing two different genes for an enzyme or trait.\n\n**Homozygous:** Possessing two of the same gene for an enzyme or trait.\n\n**Hyperthyroidism:** A hyperactive state caused by the excessive production or taking of thyroid hormone.\n\n**Hypothyroidism:** A hypoactive state produced by the diminished production or intake of thyroid hormone.\n\n**Isthmus of the thyroid:** The thyroid tissue that connects both lobes of the thyroid.\n\n**Leptin:** A hormone produced by fat cells that signals the brain that the intake of calories is excessive.\n\n**Levothroid:** A brand name for synthetic thyroxine (T4).\n\n**Levoxyl:** A brand name for synthetic thyroxine (T4).\n\n**Liothyronine:** A generic name for T3 medication.\n\n**Liotrix:** The generic name for the combination of T3 and T4 medication.\n\n**Medullary thyroid cancer:** A cancer in the thyroid associated with cells called _parafollicular,_ or _C-cells,_ which make a hormone called _calcitonin._\n\n**Multinodular goiter:** An enlargement of the thyroid associated with many nodules, or outgrowths.\n\n**Multiple endocrine neoplasia:** Hereditary production of tumors in several endocrine glands \u2014 one of the tumors may be a medullary thyroid cancer.\n\n**Mutation:** An unexpected change in the enzyme or body characteristic produced by an alteration in a particular gene.\n\n**Myxedema:** Another name for hypothyroidism.\n\n**Myxemeda coma:** A severe form of hypothyroidism usually found in elderly people usually brought on by a complicating factor, such as infection or trauma, which may result in coma and death.\n\n**Postpartum thyroiditis:** Inflammation of the thyroid after a pregnancy that is associated with thyroid autoantibodies and may go through stages of hyperthyroidism, normal thyroid function, and hypothyroidism. It may resolve or end in hypothyroidism.\n\n**Pyramidal lobe of the thyroid:** An accessory lobe rising from the isthmus of the thyroid.\n\n**Recessive gene:** A gene that will determine an enzyme or body characteristic only when it's present on both chromosomes. (Otherwise, the dominant gene prevails.)\n\n**Resin T3 uptake:** A test of thyroid function (now obsolete) that provides an assessment of the amount of T4 bound to protein compared to the free T4.\n\n**Riedel's thyroiditis:** A rare form of thyroid inflammation that is often associated with thyroid antibodies. It results in fibrosis of thyroid tissue, and sometimes parathyroid tissue, with tight adherence to the trachea.\n\n**Silent thyroiditis:** A form of thyroiditis that's identical to postpartum thyroiditis but can occur at any time of life.\n\n**Subacute thyroiditis:** A viral inflammation of the thyroid that's associated with pain in the thyroid.\n\n**Subclinical hypothyroidism:** An elevation of the TSH, with a normal free-T4 level and minimal to no symptoms of hypothyroidism.\n\n**Synthroid:** A brand name for synthetic thyroxine (T4).\n\n**Thiocyanate:** A chemical found in some foods that may interfere with thyroid function.\n\n**Thyroglobulin:** Material in the follicle of the thyroid in which thyroid hormones are stored.\n\n**Thyroid agenesis:** Failure to produce a thyroid gland.\n\n**Thyroid autoantibodies:** Proteins that react against the thyroid, sometimes to suppress or destroy it and sometimes to stimulate it.\n\n**Thyroid dysgenesis:** Failure of the thyroid to grow or move into its proper place in the neck, attached to the trachea below the Adam's apple.\n\n**Thyroid hypoplasia:** Production of a thyroid gland that's inadequate for the needs of the body.\n\n**Thyroid scan and uptake:** Use of radioactive iodine to outline the thyroid, determine if tissue is actively producing thyroid hormone, and determine the level of activity of the gland.\n\n**Thyroid-stimulating hormone (TSH):** A hormone from the pituitary gland that stimulates the thyroid to produce more thyroid hormone.\n\n**Thyroid storm:** A very severe form of hyperthyroidism with high fever and severe sickness \u2014 a medical emergency.\n\n**Thyroid ultrasound:** Use of sound waves to outline the thyroid and determine if growths are solid or cystic.\n\n**Thyrolar:** Brand name for combined synthetic T3 and T4 medication.\n\n**Thyrotrophin-releasing hormone (TRH):** A hormone from the hypothalamus in the brain that stimulates the production and release of thyroid hormone through thyroid-stimulating hormone (TSH).\n\n**Thyroxine (T4):** The major thyroid hormone.\n\n**Thyroxine-binding protein:** Several proteins that bind the T3 and T4 hormones, making them unavailable to enter cells.\n\n**Total thyroxine:** The sum of the thyroxine bound and unbound to thyroid-binding proteins.\n\n**Transient congenital hypothyroidism:** Temporary hypothyroidism in newborns that often results from prematurity.\n\n**Triiodothyronine (T3):** The active form of thyroid hormone.\n\n**Unithroid:** Brand name for synthetic thyroxine (T4).\n\n**Vitiligo:** Patchy loss of skin pigment sometimes occurring in autoimmune diseases.\n\n##### Appendix B\n\n## Sources of More Information\n\nThe Web sites I describe in this appendix offer a vast array of information on thyroid disease, thyroid research, specialists in the field of thyroid health and disease, and companies that make thyroid products. If you can't find what you're looking for here, it probably doesn't exist. Many of the sites point to other links that provide still more information. You can access all these sites from my Web page: www.drrubin.com. On the left-hand side of the page, under \"Related Websites,\" select \"Thyroid,\" and you can click on all the addresses that follow.\n\nYou can generally depend on the information in these sites (although some of them may point you toward other sites where the information is less reliable). But no matter what you read online, never make changes in your thyroid care without consulting your physician.\n\n**American Association of Clinical Endocrinologists** www.aace.com\n\nThis organization was founded in 1992 to serve as the voice of clinical endocrinologists, those actually seeing patients. The site provides practice guidelines, a calendar of important events in endocrinology, and a place both to find an endocrinologist and for endocrinologists to find a position.\n\n**American Association of Endocrine Surgeons** <http:\/\/endocrinesurgery.org>\n\nThis organization is dedicated to the advancement of endocrine surgery, and the site is a place to find a thyroid surgeon.\n\nIf you live outside the United States, go to the site of the **International Association of Endocrine Surgeons** (www.iaes-endocrine-surgeons.com) and select your home area.\n\n**American Thyroid Association** www.thyroid.org\n\nThis organization was founded in 1923 to promote research in thyroid disease, to spread new knowledge of thyroid disease, and to guide public policy on issues related to thyroid disease. On this important site, you find patient information and guidelines for physicians.\n\n**Asia and Oceania Thyroid Association** www.aota.or.kr\n\nThis organization was founded to promote thyroid research and education throughout Asia and Oceania.\n\n**Endocrine Society** www.endo-society.org\n\nThis organization, founded in 1916, is a leading source for research and information on all branches of _endocrinology,_ the study of the glands that produce hormones.\n\n**European Thyroid Association** www.eurothyroid.com\n\nThis organization of European thyroid specialists promotes research and education about thyroid disease.\n\n**Latin American Thyroid Society** www.lats.org\n\nThis site is dedicated to thyroid research and knowledge in Latin America.\n\n**The Mayo Clinic** www.mayoclinic.com\n\nThis site is an excellent source of patient information on major thyroid conditions.\n\n**Medline Plus Thyroid Diseases** www.nlm.nih.gov\/medlineplus\/thyroiddiseases.html\n\nThis service of the National Library of Medicine provides information about thyroid disease management and research.\n\n**Merck Thyrolink** www.thyrolink.com\/servlet\/PB\/menu\/1247710\/index.html\n\nThis service of Merck Pharmaceutical Company offers patient information in English, German, and French.\n\n**National Graves' Disease Foundation** www.ngdf.org\n\nThis support group, now more than ten years old, is dedicated exclusively to Graves' patients.\n\n**Online Mendelian Inheritance in Man** www.ncbi.nlm.nih.gov\/entrez\/query.fcgi?db=OMIM\n\nThis site is a huge database of diseases that are inherited by getting a single gene. If you search by \"thyroid,\" you find all the currently known thyroid disorders in this database.\n\n**Synthroid Information Network** www.synthroid.com\n\nThis site was founded by Abbott Laboratories, the makers of Synthroid (a form of thyroxine hormone replacement), to provide information concerning their drug.\n\n**Thyroid Disease Manager** www.thyroidmanager.org\n\nThis is an excellent source for authoritative information on all aspects of thyroid disease. It may be a little technical, but check it out. It's constantly updated and revised.\n\n**Thyroid Federation International** www.thyroid-fed.org\n\nThis organization was founded in 1995 to deal with the problems of thyroid disease on a global basis. It's mainly involved in helping people start a thyroid patient organization in their country or locale.\n","meta":{"redpajama_set_name":"RedPajamaBook"}}
+{"text":"\nPRAISE FOR\n\nMOST WANTED PARTICLE\n\nAn _**Observer**_ Top Ten Science and Technology book\n\n\"Most of the existing popular accounts of the events leading up to the July 2012 discovery claim at CERN are written from a theoretical perspective by outsiders. Jon Butterworth is an experimentalist and is **the first to give a vivid account of what the process of discovery was really like for an insider**.\"\n\n\u2014 **Peter Higgs,** Winner of the Nobel Prize in Physics\n\n\"The story of the search for the Higgs boson is so **edge-of-your-seat exciting** that it practically tells itself\u2014but still, why not get **the story from someone who was there for every step along the way**? Jon Butterworth is a talented writer and a world expert in the physics, and his book is hard to put down.\"\n\n\u2014 **Sean Carroll** , physicist at Caltech and author of _The Particle at the End of the Universe_\n\n\"This is **a unique book** , which captures the highs and lows of the last 20 years of particle physics, culminating with the discovery of the Higgs Boson. I've known Jon for most of my career\u2014he's an insightful, creative, diplomatic and occasionally outspoken physicist, and every facet of his character is on display in this beautifully written book. **If you want to know what being a professional scientist is really like, read it!** \"\n\n\u2014 **Brian Cox** , author of _Why Does E=mc 2_ _?_ and _The Quantum Universe_\n\n\"If you met Jon Butterworth in a pub\u2014which, judging from the many anecdotes in Most Wanted Particle, is a non-trivial probability\u2014his is the voice you'd like to hear, this is the tale you'd want him to tell: a breezy recounting of the discovery of the Higgs boson that turns out to be both **an accessible primer on particle physics and a lively look at behind-the-scenes Big Science**.\"\n\n\u2014 **Richard Panek** , author of _The 4% Universe: Dark Matter, Dark Energy, and the Race to Discover the Rest of Reality_\n\n\"[A] **charming, enlightening** bulletin from one of the most exciting fields of human endeavor.\"\n\n\u2014 _Guardian_\n\n\"The book contains a **fascinating inside perspective of the discovery of the Higgs boson**. It offers an insight into the intense, bewildering and intimidating media scrutiny that physicists aren't used to, combined with intimate details about the life of a high-powered physicist and some lovely explanations of the physics behind the discovery.\"\n\n\u2014 _New Scientist_\n\n\"This is more than just another telling of the story of the hunt for the Higgs at the LHC\u2014 **the reader here is utterly immersed in the politics, excitement and sheer intellectual adventure of discovery . . . from someone who was actually there!** The process of scientific research is laid bare in all its glory, warts and all, and emerges as a delightful example of what is best about human intellectual endeavor.\"\n\n\u2014 **Jim Al-Khalili** , author of _Quantum: A Guide for the Perplexed_\n\n\"Like _The Lord of the Rings, Most Wanted Particle_ takes readers on a long path with many moments of peril and uncertainty to reach the triumphant discovery of the Higgs Boson. It is **a great chronicle** of a part of the endless chain of progress in science at the LHC.\"\n\n\u2014 **Jim Gates** , University System of Maryland Regents Professor of Physics\n\n\"A smashing journey.\"\n\n\u2014 _Physics World_\n\n\" **An excellent, accessible guide to one of science's greatest discoveries** . . . vivid insights into the doing of science, including the customs of various scientific tribes at CERN.\"\n\n\u2014 _Sunday Times_\n\n\"The mix of technical description, anecdote and humour works brilliantly and feels completely fresh in my experience of science writing\u2014it really **unlocks the holy grail of combining entertainment and understanding**.\"\n\n\u2014 _PFILM_\n\n\" **Riveting!** Gonzo journalism but in the entrails of experimental particle physics.\"\n\n\u2014 **Pedro G. Ferreira** , author of _The Perfect Theory_\n\n\"A great read if you're curious about the Higgs boson, the work done at the LHC, what it's like to be a physicist or how life as a research scientist has to dovetail with the 'real' world in terms of politics, economics and justifying to the public why science is important and should be funded. **If you're remotely curious about the universe, read this**.\"\n\n\u2014 **Steven Thompson** of Physics Steve, a theoretical physics blog\n\nMOST WANTED PARTICLE: _The Inside Story of the Hunt for the Higgs, the Heart of the Future of Physics_\n\nCopyright \u00a9 Jon Butterworth 2014  \nForeword \u00a9 Lisa Randall 2014\n\nFirst published in the UK as _Smashing Physics_ by Headline Publishing Group, 2014\n\nAll rights reserved. Except for brief passages quoted in newspaper, magazine, radio, television, or online reviews, no portion of this book may be reproduced, distributed, or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or information storage or retrieval system, without the prior written permission of the publisher.\n\nMany of the designations used by manufacturers and sellers to distinguish their products are claimed as trademarks. Where those designations appear in this book and The Experiment was aware of a trademark claim, the designations have been capitalized.\n\nThe Experiment, LLC  \n220 East 23rd Street, Suite 301  \nNew York, NY 10010-4674  \nwww.theexperimentpublishing.com\n\nThe Experiment's books are available at special discounts when purchased in bulk for premiums and sales promotions as well as for fund-raising or educational use. For details, contact us at info@theexperimentpublishing.com.\n\nLibrary of Congress Cataloging-in-Publication Data\n\nButterworth, Jon. [Smashing physics]  \nMost wanted particle : the inside story of the hunt for the Higgs, the heart of the future of physics \/ Jon Butterworth.  \npages cm  \nFirst published in Great Britain in 2014 as Smashing physics, by Headline Publishing Group. Includes index.  \nISBN 978-1-61519-245-8 (hardcover) -- ISBN 978-1-61519-246-5 (ebook)  \n1. Butterworth, Jon--Career in physics. 2. European Organization for Nuclear Research. 3. Large Hadron Collider (France and Switzerland) 4. Higgs bosons. I. Title.  \nQC16.B88A3 2015  \n539.7092--dc23  \n[B]  \n2014036045\n\nISBN 978-1-61519-245-8  \nEbook ISBN 978-1-61519-246-5\n\nJacket design by Catherine Casalino  \nCover graphic depicting ATLAS experiment particle collisions courtesy of CERN  \nAuthor photograph \u00a9 Claudia Marcelloni 2014  \nTypeset in Berkeley by Avon DataSet Ltd., Bidford-on-Avon, Warwickshire\n\nManufactured in the United States of America  \nDistributed by Workman Publishing Company, Inc.  \nDistributed simultaneously in Canada by Thomas Allen & Son Ltd.\n\nFirst printing January 2015  \n10 9 8 7 6 5 4 3 2 1\nTo Susanna, Leon, Felix and Edie\n\n## Contents\n\nForeword by Lisa Randall\n\nIntroduction\n\nChapter 1. Before the Data\n\nChapter 2. Restart\n\nChapter 3. High Energy\n\nChapter 4. Standard Model\n\nChapter 5. Rumours and Limits\n\nChapter 6. First Higgs Hints and Some Crazy Neutrinos\n\nChapter 7. Closing In\n\nChapter 8. Discovery\n\nChapter 9. What Next?\n\nAcknowledgements\n\nIndex\n\nAbout the Author\nA science is any discipline in which the fool of this generation can go beyond the point reached by the genius of the last generation.\n\nMax Gluckman\n\n## Foreword\n\nOn July 4, 2012, two large groups of physicists working at the Large Hadron Collider, the enormous machine near Geneva that smashes together two very energetic beams of protons in the hopes of creating matter never before observed on Earth, announced a momentous discovery. They had found the particle known as the Higgs boson.\n\nOn that day in 2012, the world that we particle physicists know and study changed forever. A prediction that Peter Higgs had made about fifty years earlier was confirmed, as was the theory of the mechanism that Higgs, the team of Robert Brout and Fran\u00e7ois Englert, and several others had developed. This discovery helped physicists not only more fully understand the Standard Model of particle physics\u2014the theory of matter's most basic elements and interactions\u2014but it provided theoretical physicists like me with essential information about how to grapple with the physics that underlies the Standard Model in the hopes of advancing beyond the status quo.\n\nBut for experimenters like Jon Butterworth, the Higgs discovery changed the world in a more immediate fashion. The many physicists working on the two major general-purpose LHC experiments, ATLAS and CMS, had successfully completed their first major LHC goal: to find this particle, show it did not exist, or demonstrate that a more complicated or subtle model was at work. The discovery accomplished the first of these possibilities, but also meant that the experimenters who had been so successful in this first mission now had even more work cut out for them. They could now perform the detailed measurements that would determine the new particle's properties sufficiently well to either confirm theoretical predictions or determine that they did not precisely conform to expectations, paving the way for something new.\n\nAt the time of discovery, I was overwhelmed by what it meant for science\u2014and also by the many questions I was being asked. As a response to this wonderful excitement and curiosity, I wrote a short book about the Higgs as a coda to _Knocking on Heaven's Door_ , which I'd written while anticipating results from the LHC. _Higgs Discovery: The Power of Empty Space_ was an opportunity for me to explain both the discovery and what it meant for theoretical physicists like myself, who predict and respond to experimental results in an attempt to piece together their implications.\n\nBut Jon Butterworth has a different story to tell. He is not a theorist but an experimenter who was actively working at CERN (the facility where the LHC is located) on the ATLAS experiment and who was privy to many of the internal discussions and activities that led to that thrilling moment in July when the results were announced. Jon is the ideal experimenter to tell the story of the anticipation and preparation, the team's experiences at the time of discovery, and the implications of the discovery for his colleagues and him. He is the rare scientist who can actively engage in research while also clearly explaining to the public what he is doing and why it is important. He participates in groundbreaking physics research, but he is also getting the word out through his blog and his writings for the _Guardian_ newspaper in Britain and elsewhere.\n\nIn fact, I think I first heard Jon Butterworth's name from his public writing. Experimental collaborations at the LHC have a few thousand people, so theorists don't immediately know them all. He also shares my fondness for Twitter as a means of communicating scientific results, so we can learn some science from each other that way, too. We are not alone in this. I was amused when, while we were out for drinks, Jon introduced me to Mark, one of his colleagues, who then promptly informed me that I knew him already from his informative ATLAS tweets. He was right. Indeed without thinking I spouted off Mark Tibbetts' full name.\n\nBut one day in a conversation about analysis methods, I heard about some interesting analysis tools and learned that Jon was working on these, too, meaning he is not solely an excellent communicator but a true experimenter in the best sense of the word. Jon is someone who can talk to theorists and who also knows ATLAS inside and out. Most importantly for this book, he is someone who can successfully translate the process and the physics for the public while providing a sense of the experience of a physicist who is heavily involved in the cutting edge of the field.\n\nIn this book, Jon, with his delightfully nerdy self-referential humor that physicists\u2014well, at least some of the better ones\u2014often have, captures the wonder and elation that I and others experienced when first witnessing the machine and the experiments. Jon tells us what the LHC is, what it is designed to study, and why people work there. And his first-person account reveals what life was really like as a physicist at the LHC before, during, and after the discovery, from the initial circulating protons in 2008, the disaster that ensued nine days later that delayed the actual physics run for a year, the following year's hard work of fixing the machine and properly readying the experiments, and finally the completion of the actual physics run.\n\nIt is a great story, and Jon's telling of it not only gives readers a visceral feel for what it was like to be there as an experimenter participating in this enormous collaboration, but teaches a lot of physics along the way. Jon conveys the excitement, the anxiety, the sleep-deprivation, and the sense of satisfaction that went into the results. He describes how the LHC, twenty-five years into its history, was responsible for the discovery of an actual new particle in the universe\u2014one that was predicted on purely theoretical grounds and found through the hard work of scientists and engineers.\n\nFinding the Higgs boson was one of the most amazing experimental results of my lifetime. My colleagues and I still discuss over lunch the bizarreness of its actual existence. When first contemplated, it was a theory. The model could have taken many forms. The Higgs boson was part of the simplest versions of that theory\u2014one that doesn't even seem to fully make sense when taken in the full context. Yet it was a precise model with specific predictions that could be searched for. In fact, by the time the LHC turned on\u2014despite the theoretical misgivings\u2014experimental results seemed to indicate that indeed the particle did exist and should be just barely accessible to the first major LHC implementation\u2014even before the upgrade to higher energy that is now underway. And with the extended LHC run that finished in 2012, the anticipation culminated in the now-famous uncovering of the actual particle\u2014buried in the mountains of data the experimenters had collected.\n\nThis book shares the joy of that discovery as well as the joy of science more generally. It also describes the challenges that science faces in the precarious political and economic climate of today. Jon's tales from the front lines of the debates over the role of science in Britain impart lessons that apply to all of us around the world. I hope Jon's book encourages people to value the amazing insights into nature that discoveries like the Higgs boson reveal, as well as inspires future generations to learn more about how our world really works.\n\n**Lisa Randall,** Harvard University theoretical physicist and author of _Warped Passages_ , _Higgs Discovery_ , and _Knocking on Heaven's Door_\n\n## Introduction\n\nThere is a kebab restaurant in the Meyrin suburb of Geneva that has half a dozen pool tables. In early July 2012, I found myself playing pool with Tom Clarke, the science correspondent of Channel 4 News, one of the UK's major TV news bulletins, by way of trying to explain to him and his viewers the significance of the discovery we had just made at the Large Hadron Collider.\n\nI still find that last sentence amazing \u2013 both the discovery and the huge public interest demonstrated by the fact that Tom, along with many other journalists, came out for a day and spoke to dozens of physicists. His report was the lead item on the 4 July bulletin.\n\nThe discovery we announced that day was a huge step forward in physics. The public interest was a significant milestone in people's increasing engagement with the science that lies behind our civilisation. I really mean the science, not just the technology but the processes of science \u2013 to what extent it is self-correcting, and what constitutes scientific certainty (very little!) and scientific knowledge (a lot!).\n\nMeyrin is significant here because CERN, the European laboratory for particle physics, is just five minutes up the road. Meyrin village is quite picturesque, but the part Tom and I were in, Cit\u00e9 Meyrin, is a series of blocks of flats that would be a urine-smelling, graffiti-ridden concrete jungle pretty much anywhere else in the world. However, because this is Switzerland (just \u2013 by about 100m) it is a clean, orderly concrete jungle. It is also where many of the scientists working at CERN stay.\n\nI work for University College London (UCL), but, along with many particle physicists from all over the world, I do most of my research at CERN. The UCL commuter flat is in Meyrin, and my colleagues and I spend a lot of time there. In particular, I ran a working group on the ATLAS experiment at CERN from October 2010 to October 2012, the period during which we got our first flood of high-energy data. During that time, I was there more or less every week.\n\nThis book is not a physics textbook; it is not a historical account of the discovery of the Higgs boson; it is not a diary; and it is not a manifesto for greater engagement between scientists and the general public. It does contain elements of all these things, however. You will learn a lot about particle physics and what it is like to be a particle physicist, about how science works (and occasionally doesn't), about how research sometimes struggles to thrive and survive, and about the people who do it, including a bunch of personal opinions from me. I hope it will also explain why Tom Clarke and much of the world's media descended on Meyrin that July.\n\nTo get that far, though, I need to introduce a number of interconnected and probably unfamiliar pieces of information. Some of them won't seem very relevant the first time they appear, like isolated pieces of a jigsaw puzzle, but as you collect them through the book, hopefully they will start to reinforce each other and in the end the full picture will emerge. And if I succeed, you'll have fun as you follow the story collecting the pieces \u2013 and gain a sense of excitement. Because fun and excitement are the two impressions that dominate my memory of the first high-energy run of the biggest scientific apparatus ever constructed: the Large Hadron Collider.\nONE\n\n## Before the Data\n\n#### 1.1 Why So Big?\n\nThe Large Hadron Collider (LHC) sits in a tunnel 27km (nearly 17 miles) long and about 100m (almost 330 feet) underground. If you know London, it might help you to know that 27km is about as long as the Circle Line on the Underground, and the tunnel itself is similar in size to the Northern Line. If that doesn't help, then try this.\n\nImagine setting off from Meyrin, on the Swiss\u2013French border near the airport, and driving towards the French countryside. The Jura Mountains are in front of you, Geneva Airport is behind. As you pass the border, you also pass the main site of the CERN laboratory on your left, and if you look to the right you will see a big wooden globe that looks like a sort of eco-nuclear reactor (it's not, it's an exhibition space, though it is eco-friendly, apparently), and you might catch a glimpse of the building housing the control room of the ATLAS experiment. You will know it if you see it, because it has a huge mural of the ATLAS detector itself on the wall.\n\nBig though it is, the mural is painted to only one-third scale. ATLAS is very large, and is hidden underground, positioned at one of the interaction points of the LHC. These are the points where the two highest-energy particle beams in the world are brought into head-on collision. ATLAS is one of the two big general-purpose particle detectors designed to measure the results of these collisions.\n\nContinue driving. You may imagine yourself in a nerdy little white van with a CERN logo on the side if this helps.\n\nPass through the village of St-Genis and continue into the Pays de Gex, in the foothills of the Jura Mountains. You are now surrounded by the LHC. If you are imagining yourself in winter, you might see the lifts of Crozet, the little Monts Jura ski resort, chugging away ahead of you. (Mont Blanc is behind you on the horizon, but keep your eyes on the road.) Keep driving, bear right towards Gex, maybe pass through the villages of Pregnin, V\u00e9raz and Br\u00e9tigny. After about 25 minutes' driving through the French countryside \u2013 longer if you get stuck behind a tractor \u2013 you will get to the village of Cessy, near Gex. Here you will find the top of the shaft that leads down to CMS, the other big general-purpose detector on the LHC ring. ATLAS and CMS are independent rivals, designed differently by different collaborations of physicists, but with the same goal: to measure as well as possible the particles produced when protons collide in the LHC. They were designed to cross-check each other's observations, and to compete head-to-head for the quickest and best results.\n\nAll this time, on your journey from ATLAS to CMS, you have been inside the circumference of the world's biggest physics experiment. You entered it at the border when you passed ATLAS, and have now crossed its diameter.\n\nThe LHC is designed to collide subatomic particles at the highest energies ever achieved in a particle accelerator. We do this to study the fabric of the universe at the smallest distances possible, which for reasons to be described later also implies the highest energies possible. Given that the experiment is designed to look at very small things, it might be a surprise that it is so big. Building a long tunnel is very expensive, so why not make a smaller one?\n\nIn fact, it is the length of the tunnel that limits the energy of the colliding beams. If you accept the fact that to study small stuff you need high energies (please do, for now at least), you can understand why the LHC needs to be so big just from an understanding of fairly everyday physics.\n\nParticles travel in a straight line at a constant speed, unless a force acts on them. This is one of Newton's laws of motion. In everyday life it isn't completely obvious (Newton was quite clever to work it out), but once you are aware of it, it is easy to see it in action.\n\nThe reason it is not completely obvious in everyday experience is that on Earth practically everything that moves has forces due to friction and air resistance acting on it, and everything experiences gravity. This is why if you set a ball rolling, it will eventually stop. Friction and air resistance act on it to slow it down. And if you throw a ball in the air, gravity will slow it down and eventually drag it back.\n\nBut in situations where friction or gravity can be ignored, things are clearer. Driving a fast car, or even a nerdy CERN van, you clearly have to apply a force, via the brakes, to slow it down. And more relevantly in the context of the LHC, if you want to change direction, to turn a corner at speed, this can only be done if there is sufficient friction between the tyres of the van and the road. Otherwise, you skid.\n\nThe driver and passengers experience a rapid turn of a corner as a sort of 'pseudo-force'. The van is turning, but your body wants to carry on in a straight line, so you feel as though you are being pressed against the sides of the van. It would be more true to our understanding of physics to think of the sides of the van as pushing against you, to force you to change direction, pushing you round the corner along with the vehicle.\n\nThe combination of speed and direction is called velocity. And if you combine the velocity and the mass of the object (the van, for example, or the passenger), you get the momentum. The bigger the mass, or the velocity, the bigger the momentum, and if you want to change the momentum of something, you need to apply a force to it.\n\nI am being deliberately vague about how the velocity and mass combine to give momentum. At speeds much lower than the speed of light, it is good enough to just multiply \u2013 momentum is mass times velocity \u2013 and this is probably the right answer if you are taking a school course in physics. However, the exact expression is a little different, and the difference gets more and more important as speeds approach the speed of light. Then you need Einstein and relativity (of which more later), rather than Newtonian mechanics. But don't try this in a van.\n\nRegardless of that, the larger the desired change in momentum, the bigger the force has to be. Hence the brakes on a lorry need to be able to exert more force than the brakes on a van, because even if the velocity is the same, the mass of the lorry is bigger so the change in momentum involved in making it stop is bigger.\n\nThis is the situation of the protons in the LHC tunnel. These are the highest-energy, and highest-momentum, subatomic particles ever accelerated in a laboratory. Even though the mass of a proton is tiny, their speed is tremendously high. They are really, really determined to travel in a straight line. So, to make the two beams of protons bend around the LHC and come into collision requires a huge force. The force is provided by the most powerful bending magnets we could build.\n\nGiven this maximum force, there is then a trade-off between how sharp the bend in the accelerator is and how high the proton momentum can be. Back to the van: this is exactly equivalent to the fact that there is a maximum speed at which you can take a given corner without skidding. If the corner is sharp, the speed has to be low, but for a gentle curve you can go faster. This, then, is why the LHC is so big. A big ring has more gentle curvature than a small one, and so the protons can get to a higher momentum without 'skidding'. Or, in their case, 'catastrophically escaping the LHC and vaporising expensive pieces of magnet or detector'. Something to be avoided.\n\nThe maximum bending power of magnets is thus the reason that proton accelerators need to be large if they are to get to high energies. For the other commonly collided particle, the electron, there is another reason that is worth looking at.\n\nBefore the LHC was installed, another machine occupied the 27km tunnel under the Swiss\u2013French border. This was LEP \u2013 the Large Electron\u2013 Positron Collider. (Positrons are the antiparticle of the electron, carrying positive charge, in contrast to the electron's negative. LEP collided electrons and positrons together. Incidentally, people occasionally accuse particle physicists of hyping-up their equipment, but these are very descriptive, even dull, names.) LEP was turned off in the year 2000 because it had explored most of the physics within its reach and could not increase its energy further. The reason it could not go higher was, as with all the protons, also connected to the size of the tunnel, but in a different way.\n\nThis is to do with the fact that electrons have a mass about 1800 times smaller than the proton. Now, at the highest energies that doesn't make any significant difference to the force required to bend them round a corner. This is because, whether they are electrons or protons, they are moving very close to the speed of light, so you need the full special relativity expression for momentum, and the net result is that the mass they have when they are at rest is irrelevant for calculating the required force. So that wasn't the problem.\n\nThe problem was synchrotron radiation. This is the energy radiated by charged particles when they are accelerated. It is a universal phenomenon, roughly analogous to the wave a speedboat makes when it turns in the water. As a charged particle accelerates round a corner, photons fly off and carry away energy.\n\nThe effect is actually much more pronounced for particles with low mass. The amount of synchrotron radiation given off when a particle accelerates depends very strongly on the mass: if the particle mass drops, the energy loss increases by the mass-drop to the fourth power. So, as the proton mass is 1800 times bigger, the energy lost on the bends for electrons is (1800 x 1800 x 1800 x 1800) or about 11 trillion times larger than it is for protons.\n\nAs the electrons and positrons squealed round the corners of LEP, photons were radiated this way, and with every revolution of the beam around the ring, more energy had to be pumped in to compensate. This is done by radio-frequency electromagnetic waves confined in big metal structures at intervals around the ring. Electric and magnetic fields oscillate in these structures precisely in time with the passing of the bunches of electrons, so that every time a bunch arrives it gets a kick from the field. This is true in all such machines. But at some point you reach a beam energy where so much is lost in synchrotron radiation that the electromagnetic waves in those structures cannot replace it. That's your maximum collision energy. LEP hit that wall.\n\nThis is where the size of the tunnel comes in again, of course. A 27km tunnel has a rather gentle curve. If it were smaller, the bends would be sharper, the acceleration would need to be bigger, so the energy lost through synchrotron radiation would be greater, and the maximum collision energy would be lower.\n\nAs an aside, this synchrotron radiation is very useful in other contexts. The Diamond Light Source at Harwell in Oxfordshire, in South East England, for example, was built to produce it intentionally. The radiated beams of photons are used to study atoms, crystals, molecules, materials and surfaces. Many machines and laboratories originally built to study particle physics have been converted to become light sources once they have been superseded in the quest for higher energies. I have reason to be grateful for this personally, in fact. I did my doctoral work in Hamburg, at the DESY (Deutsches Elektronen-Synchrotron) laboratory. The particle physics of interest there at the time was the HERA electron\u2013proton collider, where I worked in the ZEUS collaboration, the team of physicists responsible for one of the main particle detectors at the laboratory. But my then girlfriend was a crystallographer, using synchrotron light to work out the structure of proteins and other stuff. Because of the symbiotic relationship between particle-physics accelerators and synchrotron light sources, there is a branch of the European Molecular Biology Lab at DESY, and after a high-level discussion in the crowd at a St Pauli football match, Susanna managed to get her PhD supervisor to send her to Hamburg for most of her research. We've been married 20 years now, and it's all very fine and romantic. But synchrotron radiation is still a pain in the arse if you want a high-energy electron beam.\n\nSo, LEP was shut down in 2000 and dismantled, and installation of the LHC began. The LHC can get to higher energies because it collides protons with 11 trillion times less of a synchrotron radiation problem, but it requires the most powerful bending magnets you can make if you want to get to the highest possible momentum.\n\nThe formal approval for construction of ATLAS and CMS was given on 1 July 1997 by the then Director General of CERN, Chris Llewellyn Smith.1\n\nLEP had been good, but the protons promised more.\n\n1. Incidentally, a man who previously, as head of physics at Oxford and afterwards as provost of UCL, seems to have had a period of following me around and being my boss.\n\nGlossary: The Standard Model Particles and Forces\n\nIf you just want to crack on with the story and don't mind the odd unfamiliar word, you can skip these 'Glossary' bits. But without knowing something about the Standard Model, some of it might not make much sense.\n\nThe Standard Model of particle physics is our current best answer to the question 'What is stuff made of, if you break it down into its smallest components?'\n\nStart with anything \u2013 a rock, the air, this book, your head \u2013 and pull it into its component parts (I recommend this remains a thought experiment). You will find fascinating layers of structure, micro- and nano-scale bits and pieces: fibres, cells, mitochondria.\n\nYou will eventually find molecules. With enough energy you can break them apart into component atoms. Atoms consist of a dense nucleus surrounded by electrons.\n\nWith a bit more energy, you can separate the electrons from the nucleus. With more energy still, the nucleus can be broken into protons and neutrons. With still more energy (and now you do need a big collider!), you can see quarks inside those protons and neutrons.\n\nWe have never managed to see anything inside a quark, or break one into pieces.\n\nIf, at the 'atom-smashing' stage, we had ignored the nucleus and tried breaking up the electron, we'd have reached that point earlier. We have never managed to see anything inside an electron, or break one into pieces. This \u2013 the fact that we haven't managed to break one yet \u2013 is our working definition of what it means for a particle to be 'fundamental'.\n\nAnd a key point is that wherever we had started, with whatever material, we would have ended up with electrons and quarks. In the Standard Model, they are the stuff that everything is made of, and they themselves are not made of other stuff.\n\nYou will come across a lot of particles in this book, but remember, there aren't many different kinds of fundamental ones when you get right down to it.\n\nElectrons are an example of a class of particles called leptons. There are also muons and taus, which are just like electrons only heavier. The only other leptons are the three kinds of neutrino. Neutrinos do not interact much with other matter, but there are lots of them around. More than a trillion neutrinos pass through you from the Sun every second.\n\nThe other class of fundamental-matter particles consists of the quarks. There are six of them, too, just as there are six lepton types. They are called up, down, strange, charm, bottom and top, becoming more massive as you go (but peaking on whimsy in the middle).\n\nProtons and neutrons are made of up and down quarks. Quarks are never found out on their own, they are always stuck together in bigger particles. These particles, the ones made of quarks, are generically called hadrons (hence the Large Hadron Collider, which mostly collides protons but occasionally collides atomic nuclei, which also have neutrons inside).\n\nThose are all the matter particles we know of. They all have anti-particle partners, and they all interact with each other \u2013 attracting, repelling, scattering \u2013 via forces, which are carried by another kind of particle \u2013 vector bosons.\n\nThe electromagnetic force is carried by photons (quanta of light) and is experienced by all charged particles. That is, everything except the neutrinos.\n\nThe strong force, which holds protons, neutrons, and atomic nuclei together, is carried by gluons, and is only experienced by the quarks.\n\nThe weak force is carried by W and Z bosons, and all particles experience this. The weak force is responsible for radioactive beta decay, amongst other things, but because it is weak, it does not feature much in everyday life. Even so, it is crucial to how the Sun works.\n\nTo make the Standard Model work, and in particular to allow the fundamental particles to have mass, another unique and completely new object is also required \u2013 a Higgs boson. The hunt for this is, of course, the main topic of this story and I'll say much more about it later.\n\nGravity doesn't fit into the Standard Model. It is described by Einstein's theory of general relativity, but we do not know how to make a working quantum theory of that.\n\nThose are the actors on the stage of the universe. There are lots of open questions in physics, but an astonishingly wide array of data \u2013 most of physics, chemistry and biology \u2013 from very large to very small distance scales, can be described astonishingly accurately by just these elements: quarks, leptons and the four forces between them, and the Higgs boson.\n\n#### 1.2 The 'No Lose' Theorem\n\nI didn't begin working seriously on the LHC until around 2001. That was about nine years before we got our first high-energy collisions. Believe it or not, this makes me a bit of a Johnny-come-lately to the experiment. Options for a large hadron collider had already been considered in the design of the 27km tunnel for LEP, and were mentioned in the LEP design report in 1984, when I was just finishing secondary school and moving to sixth-form college. There would be many years of scientific, technical, financial and political discussions, followed by R & D, simulation and more politics, before the LHC gained approval in 1997.\n\nBack in 1997, I had just moved to London from Hamburg and was still completely absorbed in work at HERA. It is a feature of big collaborations that you accumulate responsibilities along with a bank of experience and expert knowledge that can make it hard to disengage. It is difficult to climb a new learning curve on another experiment, with its confusing software and hardware and unfamiliar physics. Sometimes you need a bit of a shove to really start doing something else.\n\nFor me, bizarrely, the shove was the birth of my first child. This was such an overriding priority that I managed to say no to a whole bunch of managerial and technical roles within the ZEUS collaboration. I wanted no responsibilities that would conflict with the terrifying challenges of looking after Susanna during her pregnancy and of being a dad after it.\n\nAs it turned out, the whole thing went very smoothly and was generally wonderful. So, as a bonus, I had lots of free time to think creatively about physics. One of the things I'd long been wanting to do was read enough and think enough to get my head around physics at the LHC, which was by then under construction at CERN. This holiday from HERA heat was the opportunity. With a couple of friends, Jeff and Brian, also HERA physicists,2 I'd been thinking about what we might do \u2013 what the most exciting things to study would be. We were all very sceptical about new 'Beyond the Standard Model' physics and were keen to work on measurements of real things that would actually happen, rather than seeking evidence for speculative ideas to which we accorded little credibility. I think this may have been because we all came from a HERA background, where precision measurement was the main goal. Although to be honest, the main legacy of LEP was also precision measurement, so maybe it made no difference.\n\n2. Jeff Forshaw and Brian Cox, who amongst other things have also written physics books, though not about this yet.\n\nAnyhow. Not only did we not believe in such things as supersymmetry, or large extra dimensions, or Technicolor, all of them speculative extensions of the Standard Model designed to solve some of the problems with it. We didn't even believe in the Higgs boson \u2013 an integral part of the Standard Model, but one lacking experimental verification. So we asked ourselves, 'What is the most important and interesting thing to measure if there are no new particles?' A pessimist's approach, perhaps, but still fun.\n\nThe answer we came up with3 was vector-boson scattering. This is a peculiar and rare scattering process that is expected to happen occasionally in very high-energy collisions, and it lay behind what was called the 'no lose' theorem at the LHC. It is very deeply connected to the reasons why the Higgs boson is so important. So it wasn't a bad choice for a first bit of LHC physics for us to look at, and it's worth spending a bit of time on now.\n\n3. After some reading around \u2013 I'm not claiming we were the first to think of this!\n\nVector bosons are force carriers. The photon, which is the quantum of light and carries the electromagnetic force, is a vector boson. Of more interest here, though, are the W, and to some extent the Z, bosons. These carry the weak force, and one of the oddest things about them is that, unlike the photon, they have mass.\n\nIn a proton\u2013proton collision at the LHC, you have to picture two quarks, one from a proton in each beam, zooming towards each other. There is a small but non-zero chance that, as they do this, each will radiate a W boson. There's an even smaller, but still non-zero, chance that these W bosons will hit each other. That is vector-boson scattering \u2013 WW scattering in this case. It could happen with Zs or photons too. There are a bunch of different ways the bosons can bounce off each other, or fuse together and break up again. As is always the case in quantum mechanics, all the possibilities have to be taken into account and combined4 \u2013 sometimes they add up, sometimes they subtract from each other. Put the whole thing together and you get the probability of the WW scattering occurring.\n\n4. This includes taking into account time orderings other than the quarks-emit-Ws-that-then-collide one I gave here.\n\nThe 'no lose' theorem came from this calculation. Some of those scattering possibilities include a Higgs boson, and at the time there was no direct evidence for such a beast. However, if you do the sum and do not include a Higgs boson, then as you go to higher and higher energies, the probability of WW scattering grows and grows.5 At some point you get nonsense answers involving probabilities bigger than one, or infinities. That is just a sign that your theory is broken \u2013 there won't be infinities in nature \u2013 but what it meant was that either a Higgs boson would be discovered at the LHC, or some other new physics would come into play and keep the calculation sane.\n\n5. The possibilities involving the Higgs would contribute with a negative sign, and so they would stop this happening.\n\nSo in the pessimist's scenario of no Higgs boson, no black holes, whatever, measuring WW scattering might well be the only, or best, clue as to what was going on. It certainly had to involve either a Higgs boson or something else new \u2013 hence the 'no lose' theorem. By studying these scatterings we were certain we would discover some interesting physics.\n\nMeasuring WW scattering properly would be difficult, and we found lots of fun challenges. The Universtiy of Manchester had done a deal with Apple and had a big new farm of Macs that had just started running Unix (OSX), making them useful to us (if still more expensive than the Linux boxes everyone else had). I have fond memories of sitting in a flat in Saddleworth, feeding the farm with lots of simulation jobs to test our ideas, then popping over the road to the pub for beer and dinner to argue about newer ideas. This was still before my son was born, but I had already divested myself of lots of other responsibilities. We submitted the paper in January 2002 and it was more or less ignored for six years, though it later became more fashionable and I'm very proud of it. One of the ideas we used turned out to be quite widely useful and would feature in the Higgs search itself.\n\n#### 1.3 People Are Going to Be Interested in This . . .\n\nWhile work was going on at CERN and around the world to construct the LHC and its detectors, it became increasingly obvious that quite a lot of people were going to be interested in the project, for all kinds of reasons. For the engineering and science, of course. But also because of the sheer scale, including the cost of the thing. The international collaboration and the sociology of several thousand physicists working together were intriguing to quite a few people, including academics in social sciences. Plus, of course, there were the two or three delusional publicity-seekers who thought, or claimed to think, that we were about to destroy Switzerland. Or the world. Or the entire universe.\n\nThe last bunch \u2013 the delusionists and conspiracy theorists \u2013 were bound to get lots of media coverage, 'because of balance'.6 The only way to deal with that is to get real information out there. Also, since the European taxpayer had been investing something like the equivalent of a billion euros in CERN every year, we really owed it to people to explain what we'd done with the cash, and why.\n\n6. To quote David Shiffman: 'World's leading experts say there's a problem with false balance in environmental journalism, but Steve disagrees.'\n\nThoughts like these were passing through the minds of many people involved, including, I am sure, James Gillies, the head of communications at CERN, and many good science journalists. This is presumably why, in 2008, the doors of CERN were flung open to the world's media for 'Big Bang Day', when we switched on the machine.\n\nSuch thinking was certainly one reason why I agreed to be part of a series of short documentary films called _Colliding Particles_. These were a sort of 'fly on the wall' affair that started in the summer of 2008. Mike Paterson was the cameraman, producer, interviewer and director \u2013 everything, in fact, except animator and occasionally soundman. He won some support from the Science and Technology Facilities Council (STFC), the research council that funds particle physics in the UK, to make the films. They were aimed at schools, specifically at a then new part of the curriculum based on learning how science works. Apparently pupils would learn this by watching some physicists from behind Mike's camera.\n\nActually, it worked out very well. Amongst other things, Mike has some sort of genius for cutting and matching a long ramble by me to amazing pictures that make me appear coherent. There is roughly five minutes in the first film where I speak without ever finishing a sentence properly, while shots of the LHC and of the ATLAS detector being assembled fill the screen, imparting to the viewer a sense of the vision and wisdom I am pouring forth. Well, that's how it looked to me and my mum, anyway. The films also featured Adam Davison, who at the start was my PhD student, later a postdoc, and Gavin Salam, a theorist in Paris, and were (at least to start with) loosely based around a paper we'd written in 2007 with Gavin's student, Mathieu Rubin.\n\nI mention all this now to show that, despite strong reservations from some particle physicists, we were taking public engagement quite seriously. The film was one of several initiatives at the time, a level of activity unprecedented in particle physics. Mike, Adam, Gavin and the films will pop up from time to time as we progress towards discovery.\n\nAnyway, here we were, after many years of R & D and eight years of construction, at the switch-on.\n\nIt was 10 September 2008. In CERN, the control room was packed with journalists and Brian Cox. BBC Radio 4, the UK's major news and current affairs channel, made a day out of it \u2013 'Big Bang Day'. I had come back from CERN and was in Westminster, in a big hall with the minister ( John Denham, the UK's Secretary of State for Innovation, Universities and Skills), many other of the great and occasionally good, and more journalists. This was all very exciting and totally new territory for us in terms of engagement with the media and politicians, but still the most terrifying and exciting thing was the fact that after so many years of preparation we were finally about to switch on our experiment.\n\nThe switch-on was pretty closely choreographed, with Lyn Evans, the LHC project leader, the ringmaster in the LHC control room. The beams were to be sent into the LHC octant by octant. That is to say, initially the beams would go an eighth of the way around the 27km tunnel and hit a beam blocker. Then a quarter, three-eighths, and so on until hopefully they got all the way around and came back again, registering two dots (one on the way in, one on the way back) on a scintillation counter that was the centre of attention for thousands of physicists and a significant chunk of the world's media.\n\nOne nice thing was that when the beam hit a blocker in front of one of the detectors, a spray of particles would be produced that would register in the detector \u2013 the first beam activity we'd seen in these highly complex and sensitive pieces of kit. Less nice from my point of view was that because Lyn chose to send the clockwise beam around first, ATLAS was the last in line, and therefore the last to see particles. Still, the next step after us was a full circuit. Lyn counted down: 3 . . . 2 . . . 1. A moment of nerves when nothing appeared . . . then bingo! Two dots. The most exciting two dots I've seen before or since. For the first time, a beam had successfully completed a circuit of the LHC.\n\nAs the day progressed, beams were sent round in both directions and stored successfully. Sheer exhaustion at Westminster led us to the pub next door, though the accelerator teams at CERN were still hard at work. I will never forget drinking a beer at lunchtime and seeing progress updates of my own physics experiment on the BBC news ticker at the bottom of the pub TV screen. It was hard not to be triumphalist about it all. The headlines the day after, declaring that we hadn't destroyed the world, were fun if a bit premature (we hadn't yet collided the beams, after all), but we had got ourselves a working experiment and we had managed to share our excitement with the people who were paying partners in the enterprise. I was looking forward to welcoming the new PhD students to UCL with the promise of imminent data.\n\nNine days later, it had all gone catastrophically wrong.\n\n#### 1.4 Breakdown\n\nAs I have already described, the limiting factor on the maximum energy the protons can get to in the LHC is the centripetal force \u2013 the force needed to bend them round the corners so that they stay in the ring. This force is provided by huge magnets. Imagine whirling a brick round your head on a thin piece of string. If you whirl it too fast, the string will break. The protons are the brick, our magnets are the string. We really do not want them to break.\n\nIn days after the start-up, many tests were performed on the LHC. In particular, when the beams were circulated on 10 September, the magnets had not been running at full strength.\n\nThe magnets are electromagnets, meaning that the magnetic field is generated by circulating electric currents. As well as the impressive engineering and industrial know-how that goes into making them (there are 1232 dipole magnets to bend the beam, each of them is 15m long and has a mass of 35 tonnes), there is a lot of physics here.\n\nThe facts that electric currents create magnetic fields and that magnetic fields bend electric currents were observed and measured by Michael Faraday in the 19th century, and built into the theory of electromagnetism by James Clerk Maxwell. Maxwell's equations are one of the highlights of a physics degree, and are arguably the first expression of a mathematical unification of two apparently different forces (electrostatics and magnetism), setting a trend that physics has followed ever since.\n\nTo produce the force required to bend the proton beams at the LHC, very high currents are needed. At full power the magnets need to carry a current of nearly 12,000 amps (A). This is about half a million times bigger than the current drawn by a typical incandescent household light bulb.\n\nWhen an electric current flows through a normal material (such as the light-bulb filament), the electrons carrying the current collide with the vibrating atoms of the material. This makes the electrons lose energy and the atoms vibrate more vigorously, heating up the material. This is electrical resistance, and it is a big problem if you want a current of 12,000 A. Essentially, any normal material will vaporise.\n\nThe discovery of superconductivity changed this. Superconducting materials offer zero resistance to the flow of an electric current. This is a rather amazing quantum mechanical effect, understood in the Bardeen, Cooper and Schrieffer theory. At low temperatures, the electrons form pairs and start to behave like bosons.7 This allows them all to sink into the same quantum state \u2013 a condensate \u2013 and overlap with each other. At that point, it takes quite a lot of energy to have any effect on a pair, because that would mean changing the whole condensate, which is in a coherent quantum state. In general, the collisions with the material don't have enough energy to do this \u2013 at least not when the material is very cold, when the atoms in the material are hardly vibrating at all. So the pairs of electrons flow on unimpeded, losing no energy and experiencing no resistance.\n\nThe magnets in the LHC are superconducting. They are cooled to a temperature of 1.9 kelvins (-271.3\u00b0C), using pressurised liquid helium.8\n\n7. See Glossary: Bosons and Fermions. 8. This is, as is frequently pointed out, colder than outer space. The cosmic microwave background has a temperature of 2.7 kelvins. However, it is not, as is sometimes said, the coldest place in the universe. Apparently the Boomerang Nebula is at 1 kelvin. I have no idea why.\n\nOn 19 September, the LHC team were testing the magnets up to full electric current \u2013 the current at which they could bend beams around the LHC at full energy. The LHC operates as eight independent sections, which can be powered, warmed or cooled separately. They had commissioned seven of these octants to full current and were on the eighth and last, almost ready for first collisions.\n\nAt this point, all information from the monitors and sensors in that sector suddenly ceased.\n\nWatching the dashboard remotely in London, I just saw a note that 'first collisions' had been delayed for at least a few days. But the reality was much worse. There had been a catastrophic explosion. Several of the huge magnets had been ripped out of their concrete moorings. We were not going to get our first proton\u2013proton collisions for more than a year.\n\nI had to explain to various journalists, including a live phone call to breakfast TV, what had happened. To tell the truth, other than that it was very bad, we didn't completely know at that stage. By far the worst experience was having to stand up in front of the PhD students and tell them they wouldn't be getting any collision data for a while longer. I phrased it as 'two steps forward, one step back', but the step backwards felt enormous.\n\nThe full story gradually emerged days and weeks later. There had been a fault in one of the connectors between two magnets. This was due to a flaw in the welding. The connector developed a small electrical resistance. On its own that would have been a serious but not catastrophic problem. Part of a superconducting system suddenly developing a resistance is an occupational hazard of the technology; it leads to what is called a 'quench', and the superconducting magnets have elaborate protection against quenches, meaning that the enormous energy in the electric currents is safely dissipated before it heats up and damages the magnet.\n\nUnfortunately, the quench protection didn't extend to the connectors. The current was not safely dissipated, and the connector was vaporised.\n\nAgain, on its own this would have been a big problem, leading to months of delay, but not a catastrophic one. However, the huge current now had nowhere to go and sparked across the gap left by the vaporised connector. The spark punctured the liquid-helium containment vessel and suddenly tonnes of pressurised liquid helium became a gas. Very quickly. This was the explosion, powerful enough to tear some of those 35 tonne magnets from their concrete moorings. Several of them were destroyed or damaged, and the precision instrumentation and delicate cryogenics were turned into a mess of twisted metal. It all meant that we had a very long wait, and a lot of work to do, before the machine would deliver physics results.\n\n#### 1.5 While We Were Waiting . . .\n\nThe aftermath of this disaster was quite instructive.\n\nAs with any big project, there are people who object to the amount of resources spent. There are people who resent the huge public and media interest that is denied to lots of other good science. Also, apparently, particle physicists are sometimes perceived as arrogant, though I can't think why. For whatever reason, while there was much genuine sympathy for us disappointed LHC physicists, there was also _Schadenfreude_.\n\nAnd remember, a substantial section of the particle-physics community thought the whole media- and public-engagement exercise around the start-up a big mistake. Many colleagues saw it as at best a hostage to fortune, and at worst unscientific media hype. The failure of the machine nine days after such a high-profile public event must have seemed a massive opportunity to say 'I told you so'. I was mainly just miserable about the delay, and did indeed have moments when I felt we'd made massive idiots of ourselves in a very public fashion and should have kept quiet until we had the results.\n\nIn October 2008, very soon after the catastrophe, we had the 'inauguration' of the LHC. This was a very odd event. It was a formal celebration, planned before the disaster. It was held in the huge magnet-testing hall, soon to be reopened to test (re-test) the repaired and refurbished magnets, which would be needed to repair the wounded machine below our feet. Despite being very interested in CERN and the LHC, Lord Drayson, the UK science minister, didn't show up. To be honest, I don't blame him. Frankly, it was a depressing affair.\n\nBut these feelings gradually changed.\n\nThe embarrassment became almost a source of pride. The failures in the magnet connector should not have happened, of course. But listening to accelerator physicists and engineers diagnose and discuss the systems involved just emphasised the amazing complexity of the LHC and the amount of new technology that had been integrated, on an industrial scale, into this huge machine. Not only were we on the edge of physics, we were on the edge of engineering, too. Also, no one had been hurt. In fact the whole LEP and LHC civil-engineering project, which was on the scale of the Eurotunnel construction, was carried out with remarkably few casualties.\n\nResearch carries risks. As the project leader Lyn Evans said, many times in many interviews, the LHC was its own prototype. Nothing like it had been done before. A notable feature of the wide-eyed physicists staring into multiple cameras on 10 September was that we were more nervous and excited about the possibility our experiment might, or might not, work than we were about our live-TV debut. The nearest equivalent is the visible nervousness on the faces of space scientists when a precisely engineered satellite they have built is making its way into orbit on top of a plume of flame.9\n\n9. In a display cabinet at UCL's Mullard Space Science Laboratory, they have the twisted remnants of delicate electronics from the first version of the Cluster mission, fished out of the Kourou swamps in French Guiana after the Ariane launch failed in 1996. Chastening stuff. But Cluster flew again, as Cluster II, and did the science it was built for.\n\nThis was really doing science in public, and the reality is that science is not a seamless progression of triumphant advances. Two steps forward, one step back, indeed.\n\nFrom the point of view of the media, this twist just prolonged a good story, and they were remarkably reasonable in the way they treated us, despite (or including, really) a certain amount of mocking on the occasional game show.\n\nAs for the misery . . . well that was harder to shake, but there were some important things to be getting on with. We'd locked ourselves into an obsolete version of the Linux operating system, fearing to upgrade with data imminent. We could fix that \u2013 and a lot of other bugs frozen into our software because we didn't have time to fix them properly. One of the most significant things we did was to get rid of an obsolete jet finder. But I realise that's going to take some explaining.\n\nGlossary: Quarks, Gluons and Jets\n\nJets are what quarks and gluons make when they try to escape.\n\nEvery proton (in fact, every hadron) is made up of quarks stuck together by gluons. As already mentioned, these gluons are the force carriers of the strong force, just as photons carry the electromagnetic force, and the W and Z bosons carry the weak force. The role played by the electric charge in electromagnetism is played by a quantity called 'color' in the case of the strong force. This color has nothing to do with the colour we perceive with our eyes, and I'll use the US spelling to distinguish between them, since the physicist who introduced it, Oscar W. Greenberg, is an American. However, there is an analogy in there.\n\nFor electric charges, there is only one way to get a neutral charge \u2013 you have exactly as many anti-charges (negative charges) as positive charges. So an atom is neutral because the number of protons in the nucleus (carrying one positive charge each) is exactly equal to the number of electrons in the cloud around the nucleus (each carrying a negative charge). The result of adding up all the positive and negative charges is zero \u2013 they cancel each other out, and the atom is neutral.\n\nFor color, the same thing can happen. If we (arbitrarily) name one of the colors 'red', then there is also an 'anti-red' color (which you might want to call cyan since it's the complementary colour, though personally I think that pushes the analogy between the quanta of charge for the strong force and visible colours a bit too far). Color-neutral objects called mesons can be made by combining a color with its anti-color.10 But one difference between electromagnetism (more correctly known in its quantum version as quantum electrodynamics, QED) and the strong force (known as quantum chromodynamics, QCD) is that there is an additional possible way of getting a color-neutral object.\n\n10. The name meson comes from the Greek _meso_ , meaning 'medium', because its mass is lighter than that of protons and neutrons but heavier than an electron's. A meson contains a quark and an antiquark, and it is color-neutral because these will have, for example, red and anti-red color respectively, which cancel each other out. Or, if you prefer, red and cyan, making white.\n\nThere are three possible colors, often (still arbitrarily) called red, green and blue. If you have one of each, you also get a color-neutral object. This is where the analogy with mixing three primary colours to get white comes in. Protons and neutrons are made this way. They contain three quarks, one of each color, and so also end up being colorless. Particles made of three quarks like this are called baryons (from the Greek, meaning 'heavy') and protons and neutrons are the most common examples. Mesons and baryons are both subclasses of hadrons, of course, since anything made of quarks is a hadron.\n\nAn odd feature of all this is that quarks are never observed on their own, a long way away from other quarks. They are always confined inside color-neutral hadrons of one kind or another, due to another peculiarity of the strong force.\n\nMost of the fundamental forces get weaker with distance \u2013 the attractive force between a positive and a negative electric charge, for example, is weaker the further away from each other the charges are (it falls off as the inverse of the separation squared \u2013 1\/r2). But the strong nuclear force is different. The force between two quarks actually gets stronger as you pull them apart. It is as though they are attached to each other by an elastic band or a piece of string. As they move apart, the string becomes taut, and a large amount of energy is stored in the string tension.\n\nInside the LHC, when two quarks inside protons bounce off each other, they head away from each other at practically the speed of light and with an enormous amount of energy. Initially, the 'string' is slack and they feel very little force. This phenomenon is called 'asymptotic freedom', and the 2004 Nobel Prize in Physics was awarded jointly to David J. Gross, H. David Politzer and Frank Wilczek 'for the discovery of asymptotic freedom in the theory of the strong interaction'. It means that when quarks are inside the proton, you can for some purposes and to some approximation treat them as though they are free, as though they aren't bound together at all.\n\nHowever, that apparent freedom ends rather quickly when you try to remove a quark from a proton \u2013 for instance by hitting it with another quark from another proton going the opposite way around the LHC. Though they fly away from each other initially (and even radiate more gluons and quarks as they accelerate), the string gets taut almost immediately, and the quarks and gluons know they aren't really free.\n\nWhat happens next is intriguing, though. There is so much energy stored in the tension of the string between two quarks, as the force pulling them back together doesn't fall off with distance, that it becomes energetically possible, and indeed favourable, to make a new quark and an antiquark. The cost of doing this in terms of energy ( _E_ ) is the mass of the quark plus the mass of the antiquark, multiplied by the speed of light squared ( _E_ = _mc_ 2, but you probably knew that). But the benefit is that you can have much shorter strings and so much less potential energy stored in the string tension.\n\nYou can think of the quarks as being the ends of the string. They fly away from each other until at some point the string snaps and two new ends (new quarks) are produced.\n\nEventually, we see a spray of hadrons. You might think that this is a bit useless if we really want to see what is going on with the fundamental particles \u2013 the quarks and the gluons and so on. But all is not lost. Because the initial quarks get kicked so hard, the sprays of hadrons are shaped into narrow jets. All the splitting and production of new quarks and gluons shuffles energy around, but the amounts of energy shuffled that way are much smaller than the initial kick the quarks get from the collision. So in the end, the direction of the jet reflects pretty closely the initial direction of the quark.\n\nOf course, 'pretty closely' is not a very scientific term. We need to quantify that and be as precise as possible about it. Jet algorithms are the tools that let us do that. They give a recipe of how to combine the observed hadrons produced in a collision, to get objects (jets) with energy and momenta that can be compared to a theoretical prediction. You can imagine many ways of doing that, but some ways are definitely better than others.\n\nOne issue in designing (or choosing) a good jet algorithm is the fact that the theory really doesn't know how to predict what happens at low energies. These low energies correspond to (relatively) long distances, where the strings are snapping, hadrons are being formed and lots of low-energy gluons get thrown around. Since you can't predict how many of these low-energy gluons might be produced \u2013 and since anyway that is not something we can measure, or want to measure, and it will fluctuate a lot \u2013 having a jet finder that is insensitive to the number of low-energy gluons seems like a good idea. In fact it is essential. The jargon for this insensitivity is 'infrared safety'. One of the things we did while the LHC was under repair was switch to an infrared-safe jet algorithm.\n\n#### 1.6 Names, Inertia and the Media\n\nIn 2008, the main jet algorithm used in ATLAS (and CMS) analysis code was not infrared safe. After the breakdown, we managed to change this to a newer, better, infrared-safe algorithm. This would make a huge difference to the quality of the physics we could do later.\n\nYou might wonder why, if it made such a big difference, we didn't change earlier. It's an interesting question, and the answer tells you something about doing science in very large collaborations (as well as something about physics).\n\nBack when I was still in Hamburg working on HERA, LEP was still running at CERN and the Tevatron in Chicago was finding the top quark, proto-collaborations had formed to design and propose possible detectors for the coming LHC. ATLAS was formed out of two of these \u2013 EAGLE and ASCOT. This kind of thing often happens. It is very important not to use up your best collaboration name on the first proposal, since you will almost certainly have to merge with some other proposal and therefore have to pick a new name at some point. I can only presume CMS made this mistake. Probably their proto-collaborations were called cool things like TITAN or JOR-EL11 but they had to merge so often they ran out of ideas and ended up as CMS.\n\n11. They weren't.\n\nAnyway, ATLAS is a good name, so well done, Peter Jenni et al.\n\nMarginally more important than choosing the name is showing that the detector will be able to do the physics required. Will it have a good enough resolution? Will there be enough bandwidth to read out the data? Will there be enough detectors in the right places to measure everything you want to see? And will you be able to afford it? To answer these questions convincingly, you have to write a technical design report. To do this and persuade people that you should be allowed actually to build your ideas, you need lots of results from test beams, where you fire particles into prototypes to show you understand them. But you also need huge amounts of software, some of it to simulate what the physics and the detector might look like, and some of it to reconstruct from the simulated data (or from test-beam data) what the measurement might eventually look like.\n\nThis means that by the time first data seem imminent, there are people who have been working on the experiment for ten or more years, and they have grown used to using the tools that were available ten years earlier. Attempts to change this will be met with huge inertia, even when there are much better tools available and when physics has moved on a lot due to data from elsewhere during those ten years. When the priority is to get everything ready for first data, the reluctance to change or reinvent anything is understandable. This is the state we were in on ATLAS in 2007.\n\nThe jet algorithm is just such a tool. The understanding of jets and the strong interaction, QCD, improved greatly in the 1990s and 2000s, due to a lot of work by theorists and a lot of data, mainly from HERA and LEP. The problems with infrared safety were understood and a new generation of jet finders was proposed. Unfortunately, ATLAS (and also, to a large extent, the Tevatron experiments) had already started using the old jet algorithms. And the new algorithms had problems: some of them were too slow, and lots of them made jets with irregular shapes, which made understanding the experimental resolutions and efficiencies harder. The HERA, LEP and Tevatron experiments did make measurements with the new algorithms (in fact HERA and LEP eventually moved over to them completely), but there were doubts about whether they could really be used at the LHC, and these doubts, combined with both inertia and the pressure of time, meant we did not change in time for 2008.\n\nOf course, everyone knew that once we'd taken some data with the old algorithms it would only get more difficult to change to the new ones. So once we had an unlooked-for extra year before data arrived, it was a golden opportunity to switch, once and for all, to the new, better technology. Crucial, too, was the fact that the problems with speed and irregular-shaped jets seemed to have been solved.12 Coordinated by our jet conveners, dozens of postdocs and students began checking whether the new algorithm really worked, not just theoretically but in the software ATLAS would use to select and analyse the data. Some of those people were working at UCL, and I edited the enormous internal note that, taken as a whole, finally persuaded everyone to make the switch. I think this was time very well spent. It certainly cheered me up a lot.\n\n12. For those who want to know the specific science, the best solution turned out to be the so-called anti-k-T algorithm by Matteo Cacciari, Gavin Salam and Gregory Soyez (<http:\/\/arxiv.org\/abs\/0802.1189>).\n\nFor me, another galvanising event, not directly related to the LHC, was a meeting on 18 May of the Skeptics in the Pub at Penderel's Oak in Holborn, London, just down the road from UCL. This was the first Skeptics in the Pub meeting I'd been to. It's a bit of a random thing to throw into a more-or-less chronological run-through of the LHC story, but it does connect, trust me.\n\nSimon Singh, a well-known science writer with a PhD in particle physics \u2013 he worked on LEP at Cambridge with some of my present ATLAS colleagues \u2013 was being sued by the British Chiropractic Association (BCA) for writing that it was happily promoting what he felt were 'bogus treatments' without taking account of the lack of reliable evidence showing the treatments worked. Since Singh clearly believed the treatments were bogus and since the BCA was obviously promoting them, you might have thought the argument would hinge on how happy the association was. Unfortunately, British libel law was a complete ass and it looked as though Singh, in order to defend an honestly made comment, was going to have to prove that the BCA was knowingly lying; that meant that so long as they could show that they didn't believe the treatments were bogus they would be home and dry. Finally, Singh persuaded the court of appeal that he didn't have to prove the BCA knew the treatments to be bogus, just that _he_ had good reasons for contending that they were. The BCA withdrew its legal action at that point.\n\nI went along to the meeting partly out of a sense of outrage that the law could be used to effectively silence a science-based critique, and partly just to have a beer with some friends who were going. Holborn is very near the UCL campus in Bloomsbury. I got a lot more out of this than beer. I met a whole bunch of intelligent, diligent and well-informed journalists working in newspapers and broadcasting, and I have to say this came as a bit of a shock. I met several excellent writers who wrote blogs and other online stuff. And I became aware of a set of people who knew and cared more about science and rationality than I, in my arrogance and ignorance, had expected to find outside the world of scientific academia I knew. This was as heartening, and as exciting, as the libel situation was depressing and dangerous. This wasn't just about Singh. Dr Peter Wilmshurst was being sued for analysing the health outcomes of a heart implant, and others have written better than I can about the chilling effect bad libel laws can have on scientific discussion when exploited by rich people or big companies. When Singh announced he was going to fight on, he appeared brave but unlikely to succeed. However, there was to be a campaign not just to help him, but to get the law changed, and there was at least some hope that it would be successful.\n\nSome of the writers became good friends, and the campaign led to a measure of success in reforming the law \u2013 the new libel laws, which included some specific protections for peer-reviewed science, came into effect at the start of 2014. And Singh saw off the BCA. All of that was good, but looking back on this period, there was an additional and important benefit for me.\n\nThe campaign helped to break down some of the barriers that exist between the world of science, the world of academia (which overlaps with but is very different from the world of science) and other worlds, including those of the media, comedy and politics. This was a new experience for me, and proved rather important in influencing how I talked to people about what we were doing at CERN. Brian Cox, who was a friend and collaborator before he stormed those barricades with huge success, made it easier for us all by showing that if you present things well, people will be interested, but there was more to it than that. While I only participated in the libel-reform campaign in a very small way by writing letters and attending meetings, select committees and the like, I still made connections and gained an understanding of those other worlds in the process.\n\nThis removed a lot of my fear and suspicion of the media and politics, and also showed how lobbying could be done effectively. Along with a 'Science Blogging Talkfest' organised in 2010 by Alice Bell (then at Imperial, the large technical university in South West London) and Beck Smith of the Biochemistry Society, the libel-reform process did a huge amount to make me more comfortable with discussing science in public and via the media.\n\nThis permeability between different worlds seems essential to me, and while it requires some face-to-face interaction (and for me, at least, alcohol helps with this), online tools such as blogs and social media also have a very positive impact. It was after Alice and Beck's talkfest that Alok Jha, who was one of the panellists, asked me to join a new _Guardian_ science-blogging initiative.\n\nExchanging ideas on Twitter in particular is something that has helped me a lot. Having a blog and a Twitter account that are read by a fairly large number of my colleagues in science and by contacts in the media turned out to be invaluable for my confidence when talking to bigger audiences elsewhere. Months later, I was sitting in a taxi on the way to be interviewed by John Humphrys on BBC Radio 4's _Today_ programme about why the Higgs search was a waste of time. Knowing that if I said something stupid, or was misrepresented, I could at least tweet or blog about what I had really meant to say was a great comfort. As a scientist, it is a daunting thing to pop up briefly in the media and be given a few minutes, more or less at the mercy of professionals, to describe your work and why it is worthwhile. To have the means to reach people directly makes a big difference.\n\nIt turned out for me that in the particular example of the _Today_ programme, John Humphrys was great and I didn't need to apologise for anything. But I still love that the tool invented by Tim Berners-Lee in the office downstairs from mine at CERN is supporting, amongst many other things, improved engagement between the science of CERN and the rest of the world.\n\nGlossary: Bosons and Fermions\n\nThe word boson causes no end of trouble when people report on the search for the Higgs boson. It regularly gets spelled or pronounced 'bosun', and once, while being interviewed on TV and reading the autocue over the presenter's shoulder, I saw it spelled as 'bosom'. Like a true professional, Krishnan Guru-Murthy, the urbane Channel 4 News presenter, said 'boson' without blinking.\n\nBoson is the name for a generic class of particles. The Higgs boson is one, but so are many other particles. In the Standard Model, all the particles that carry forces \u2013 gluons, the W and the Z, photons, plus the graviton, if there is one \u2013 are bosons.\n\nQuarks, electrons and neutrinos, on the other hand, are fermions. The difference between them is just spin. But in this context, spin is a quantum of angular momentum. It is a bit like the particle is spinning, but that is really just an analogy, since point-like fundamental particles could not spin, and anyway fermions have a spin such that in a classical analogy they would have to go round twice to get back to where they started. Quantum mechanics is full of semi-misleading analogies like this.\n\nRegardless, spin is important. Bosons have, by definition, integer spin. The Higgs has zero, the gluon, photon, W and Z all have one, and the postulated graviton has two units of spin. Quarks, electrons and neutrinos are fermions and all have a half unit of spin. This causes a huge difference in their behaviour.\n\nThe best way we have of understanding fundamental particles is quantum field theory. In quantum field theory, a 'state' is a configuration describing all the particles in a system (say, a hydrogen atom). The maths is such that if you swap the places of two identical fermions, with identical energies (say, two electrons), then you introduce a negative sign in the state. If you swap two bosons, there is no negative sign.\n\nSince swapping two identical particles of the same energy makes no physical difference to the overall state, you have to add up the two different cases (swapped and unswapped) when calculating the actual probability of a physical state occurring. Adding the plus and the minus in the fermion case gives zero, but in the boson case they really do add up. This means any state containing two identical fermions of the same energy has zero probability of occurring. Whereas a state with two identical bosons of the same energy has an enhanced probability.\n\nThis fairly simple bit of maths is responsible for the periodic table and the behaviour of all the elements. Chemical elements consist of an atomic nucleus surrounded by electrons. Because electrons are fermions, not all the electrons can be sucked into the lowest energy level around the nucleus. If they were, the probability of that 'state' happening would be zero, by the argument above. So as more electrons are added around a nucleus, they have to sit in higher and higher energy levels \u2013 less and less tightly bound to the nucleus. The behaviour of a chemical element \u2013 how it reacts with other elements and binds to form molecules, and where it sits in the periodic table \u2013 is driven by how tightly bound its outermost electrons are.\n\nWhen bosons clump together they do some fascinating stuff too. The condensate that is responsible for the superconductivity in the LHC magnets, for instance. But it's hard to beat being responsible for the whole of chemistry, and therefore biology. And the rest.\n\nSome theories extend the Standard Model by relating force-carrying bosons to matter-particle fermions. They do this by introducing a new symmetry between them. This symmetry is so mathematically compelling that it is called 'super' \u2013 supersymmetry \u2013 but that's another story.\n\n#### 1.7 Boost One\n\nSomething else that we had time for, while the LHC was being fixed, was a lot more study with simulated data.\n\nTo be honest, by now a lot of us were pretty sick of this. I'd left the analysis of real data when I left the ZEUS experiment in 2005, and had been doing little but simulation studies since. There's a joy in a well-written program, and a lot you can learn from modelling things in computer code. But without actual experimental results it all begins to feel a bit self-referential.\n\nWe did now have better software tools, some of which had been improved using information gleaned from the few 'beam splash' events we had recorded before the LHC broke down, and also by studying cosmic-ray data taken with the full ATLAS detector. Cosmic rays are particles from space that bombard the Earth constantly.13\n\n13. See 2.2 Minimum Bias and 4.2 Science Board for more about them.\n\nAnd, very specifically, Adam and I could do some more work on our fancy boosted Higgs analysis. I mentioned this in section 1.3; now may be a good time to expand on it.\n\nThe _Colliding Particles_ films I mentioned, made by Mike Paterson and featuring Gavin, Adam, me and a cast of dozens, were popular with teachers. They show a lot about how particle physics is done. As intended, they seemed to be doing a decent job of hitting the UK's ever-changing National Curriculum on 'how science works'. But even though they are partly based around our scientific paper about one way we might find the Higgs boson,14 they do not contain much actual physics. There was a review of the films in _Physics World_ , the magazine of the Institute of Physics, the UK professional body for physicists, which gently pointed this out.\n\n14. Referred to in the films as the 'Eurostar paper', as a sort of code for an initially underground London\/Paris collaboration.\n\nFair comment, which I felt ought to be addressed. So I wrote my first ever blog post in an attempt to explain the physics behind the paper. Here is a rewritten version of that, which concentrates on explaining the new ideas in the paper rather than giving a summary of why the Higgs is interesting, which will come later . . .\n\nWhat we knew at the point the paper was written was that if the Higgs boson existed, and if its mass was what seemed to be the most likely value (around 120 GeV15), then lots of Higgs bosons would be produced at the LHC. The difficult trick would be to pick them out from all the other things that would be going on.\n\n15. GeV stands for gigaelectronvolts, the particle physicist's preferred unit of both mass and energy. I will say more about what they mean in section 2.1.\n\nThe Standard-Model Higgs boson is a wave, or, more correctly, an excitation, in a quantum field16 that fills the universe. Interacting with this field is what gives the other particles mass. Particles get different amounts of mass depending on the way they 'couple', or stick, to the field. This meant that the Higgs boson itself would couple to the mass of every particle, and would therefore be very likely to decay into the heaviest particle it could. These decays would happen super-quickly, so all we would see would be the things into which it had decayed. We would have to work out from them whether or not there was, briefly, a Higgs boson produced by the LHC.\n\n16. See Glossary: Fields, Quantum and Otherwise.\n\nFor a 120 GeV Higgs, the heaviest thing it could decay into would be a pair of bottom (b) quarks. Quarks come in pairs. Down and up quarks are all you really need to make protons and neutrons, but for some not fully understood reason we also have strange and charm quarks (similar to the down and up respectively, but more massive) and bottom and top. The strange quark was so named because the first evidence for it was particles with strange properties (basically living longer than expected and decaying oddly) seen in cosmic-ray interactions. 'Charm' seems a very whimsical name, but I guess the quark was quite charming when it turned up because it solved some tricky issues with the weak interaction. When the last two quarks were discovered, the names beauty and truth were proposed, I guess extrapolating from 'charm'. This shows you how unreliable extrapolation can be . . . Anyway, everyone calls them top and bottom now. Top only showed up at Fermilab, the US national particle physics laboratory in Chicago, and home to the Tevatron, in 1995. This was a great relief as it finally laid to rest the theoretical models in which the bottom quark had no partner, usually giving rise to tediously suggestive names \u2013 bare-bottom models, topless models, you get the idea . . .\n\nI digress. The Higgs, if it were to have a mass of around 120\u2013130 GeV, would not have enough energy to decay to top quarks, or to W and Z bosons, and so would mostly decay to bottom.\n\nBottom quarks also then decay (after travelling a few 100 microns or so) and each one gives a spray, or jet, of hadrons. We could see some of these particles in our detectors, and would be able to reconstruct the fact that two bottom quarks decayed, and that they came from a Higgs decay.\n\nSo: if a Higgs boson were to be produced, it would decay to two b quarks, and they would give two jets of hadrons.\n\nThe problem is, lots and lots of b quarks and jets of hadrons are produced at the LHC, and most of them have nothing to do with a Higgs. Before our paper, it looked like this background noise would completely swamp the signal and we would have to rely on other, rarer, Higgs decays to find it. Not only did this make finding the Higgs harder, but even if you found the Higgs some other way, seeing the decays to b quarks is actually pretty important in proving that whatever you might have found really was a Standard Model Higgs boson.\n\nThe idea we had in the paper was to look at those collision events where a Higgs is not just made, but is made and given a lot of kinetic energy \u2013 i.e. it is moving very fast, at speeds that are a substantial fraction of the speed of light. This happens in about 5 per cent of the Higgs production events we were simulating (assuming the LHC design beam energy of 14 TeV), so we would miss a lot of Higgs bosons by only looking at the fast ones. In fact, with the LHC starting at lower energies we would waste even more of them. But the advantage of this approach would be that we would lose still more of the backgrounds, the non-Higgs events, because the background jets usually have a lower energy.\n\nSomething happens when you look at these fast-moving Higgs decays. The faster the Higgs moves, the smaller the opening angle between the two b quarks it produces when it decays. In fact, very often the jets from the two quarks merge into a single jet.\n\nThis is a problem if, as had been done in all the studies until then, you look for two b-quark jets as your telltale signature that a Higgs boson was there. In our paper we turned this problem into an advantage. By looking at the internal structure of this single jet, at its substructure, we could see evidence for the two b quarks and the Higgs decay, get rid of even more background, and measure the mass of the Higgs boson well enough to make it stand out over the remaining background. What had looked like a hopeless case was recovered as a promising way of finding the Higgs at the LHC.\n\nThe idea of looking at jet substructure to find the decays of fast-moving particles had been put forward earlier by Mike Seymour,17 and again in the paper18 I mentioned in 1.2, which I wrote with Brian and Jeff. But Gavin had a better way of doing it. And together with Adam and Mathieu we were the first to apply these ideas to the Higgs boson.\n\n17. See <http:\/\/inspirehep.net\/record\/359650?ln=en>. 18. See <http:\/\/arxiv.org\/abs\/hep-ph\/0201098>.\n\nThe unexpected delay of a year meant that \u2013 with Erkcan Ozcan, a UCL postdoc, and a group from Freiburg \u2013 Adam and I could try it out on a fully simulated ATLAS detector. We found it should still work pretty well even with a more realistic estimate of the experimental errors and a more complete study of the backgrounds.\n\nA sign that these ideas were picking up fans was that out of the blue, Gavin and I received an invitation to go to the SLAC National Accelerator Laboratory to talk about them at a meeting called 'Giving New Physics a Boost'. Or just 'Boost'. This was July 2009, and there were by now quite a few papers coming out developing new ways of finding the decays of boosted particles and highlighting applications at the LHC. If you have enough energy in your collider, boosted heavy particles turn up quite often. So, even though London to SLAC is a long way to travel for a two-day meeting, it was worth the trip.\n\nSLAC is in Menlo Park, California, about 40km from San Francisco. I'm not good at long-haul flights and the two days passed in a bit of a daze, to be honest, though from the discussions it was clear that exciting physics was happening, to the extent that a longer, follow-up meeting was already planned for 2010 in Oxford. I remember sitting on the seafront in San Francisco eating clam chowder from a bread bowl, waiting for the flight home and wondering what had just happened. Whatever it was, it was good.\n\nAnyway, by the autumn of 2009 the LHC was repaired, at least to the extent that CERN was confident it could get the beams up to half the design energy \u2013 still a factor of 3.5 higher than any previous experiment. Slightly chastened but wiser, we were ready to try again for real data.\nTWO\n\n## Restart\n\n### December 2009\u2013March 2010\n\n#### 2.1 Low-Energy Collisions and Electronvolts\n\nThe LHC officially became a collider on 23 November 2009, when it began smashing together beams of protons with 450 gigaelectronvolts (GeV) of energy.\n\nThis is not a particularly high energy. For comparison, the Tevatron in Chicago was running at an energy of 1000 GeV. But it was the first time that we could measure real collisions in our detectors. The ATLAS detector recorded particles produced by a collision for the first time at 2:22 in the afternoon. All the experiments recorded data that day, and from that moment on, the LHC was a real physics experiment.\n\nThose units of energy (GeV) probably aren't very familiar if you aren't a physicist. An eV is an electronvolt, and a volt is a measure of electric potential. So a standard domestic battery might provide a potential of 12 volts. If you allow a single electron to fall through this potential (that is, be repelled from the negative terminal and attracted to the positive terminal of the battery, because electrons have negative charge and like charges repel, opposites attract), it will pick up some speed.\n\nThings that are travelling at speed have energy because of that speed, which we call 'kinetic energy'. The kinetic energy this electron will have gained due to the speed it acquires accelerating through the voltage provided by the battery will be 12 eV (12 electronvolts). That is how an eV is defined \u2013 the kinetic energy picked up by an electron as it falls through an electrical potential of 1 volt.\n\nSince an electron is a very tiny thing with a tiny electrical charge, 1 eV isn't very much energy at all. The standard unit of energy is a joule, which is 1 kilogram (metre per second) squared (kg m2s-2). The approximate expression for kinetic energy in terms of mass and speed is \u00bd mv2, so if you have a kilogram mass (m) travelling at a speed (v) of 1 metre per second, it will have a kinetic energy of \u00bd x 1 x 12 = \u00bd a joule. It takes a lot of electrons to make a kilogram, so 1 joule is 6.24 x 1018 eV, that is, 6.24 million million million electronvolts.19\n\n19. If food calories mean anything to you, 1 calorie is about 4200 joules or about 2700 million million million eV.\n\nClearly the eV isn't a very useful unit for everyday life (though you would lose weight very quickly, possibly terminally, on the electronvolt diet). It is handy for physics and chemistry, though, where we are often discussing the amount of energy needed to move individual electrons around. Chemical bonds often involve transfers of electrons with energies of a few eV, though it can be much more. To break up a water molecule, for example, you need to give an electron about 500 eV of energy. Also, when electrons move between energy levels in an atom or a molecule, they absorb or emit photons \u2013 quanta of light. In a sodium lamp, for example, electrons jump between levels separated by about 2 eV in energy, and give off the distinctive yellow light of sodium street lamps.20\n\n20. This behaviour is at the heart of spectroscopy, which I get to again in section 7.3.\n\nSo a yellow photon has an energy of about 2 eV.\n\nX-ray photons have energies of a few thousand eV (kilo-electronvolts, keV). These can knock even the most tightly bound electrons away from the atomic nucleus. To break up the nucleus itself, you need even more energy \u2013 millions of eV (mega-electronvolts, MeV). This is the energy domain of nuclear physics.\n\nI said that unless you were a physicist, you might not be familiar with this. To be honest, unless you are an astro- or particle physicist, you probably aren't used to GeV (giga-, or billion, electronvolts) or TeV (tera-, or thousand billion, electronvolts). Single particles with this kind of energy only really occur either in high-energy cosmic rays or in big accelerators such as the Tevatron (you can probably work out where the name comes from now) or the LHC. With particles at these energies, you can not only break up the nucleus, you can shatter the protons and neutrons inside it. And, if nature works that way, maybe even shatter the quarks and gluons inside them.\n\nSo, a TeV is a lot of energy for one particle to have. But these particles are very small. If you took all the kinetic energy in a 1 TeV proton (say from the Tevatron) and gave it to a 1kg mass, the kilogram would barely move.21 However, a proton with the same kinetic energy would travel at nearly the speed of light.\n\n21. From the example above, 1 TeV is 1012 eV, so 1 joule is 6.24 x 106 TeV, so you'd be giving the kilogram about 0.17 millionths of a joule. Invert the kinetic energy formula to calculate the speed and you can work out that the speed of the kilogram would be about 0.5mm per second.\n\nEnough about units. Something fun happened on Tuesday, 8 December 2009.\n\nThe disaster of 2008 had occurred when the magnet currents were ramped up high enough to bend 7 TeV proton beams. After the repairs, caution ruled and the plan was to take them up gradually to a level that could cope with 3.5 TeV beams. At 450 GeV (0.45 TeV) we had a long way to go. We would be watching carefully, and quite nervously, as the accelerator teams took the beams up in steps.\n\nIn the run-up to 8 December, the LHC team were edging the beams up in energy and got above the Tevatron record of 1 TeV per beam. So the LHC was now providing the highest-energy beams in the world, but had not yet brought them into collision at those energies. That Tuesday, there was obviously something going on with the beams, and the ATLAS shift crew were watching carefully. They even had parts of the detector switched on, though no plan for collisions had been announced. By coincidence there were a number of UCL people around \u2013 one student (Catrin Bernius) on shift in the control room, plus Adam Davison and Nikos Konstantinidis looking at the 'event display', the graphic program used to display the results of a collision.\n\nAt 21:40 the two beams crossed and there were a few collisions, almost by accident it seemed. But ATLAS was ready \u2013 the shift crew recorded them, sent them through to the event-display people, who sent them on to Fabiola Gianotti, the head of the experiment. The first proton\u2013proton collision to go above the maximum energy of the Tevatron! Not that it was any use for physics \u2013 the detector magnets weren't even on \u2013 but you could see particles produced from the highest-energy particle collision ever made in a laboratory, and that was the moment the LHC became the highest-energy collider ever. It was on the web page the morning after. A bit silly, but fun.\n\n#### 2.2 Minimum Bias\n\nIn March 2010 the first physics papers based on LHC collisions came out. They addressed the first thing we needed to do, which was to measure the properties of the average, or 'minimum bias', collision.\n\nIt is surprisingly difficult to define a collision.\n\nTwo protons approaching each other in the LHC will repel each other because they both carry positive electric charge and things that have the same charge repel each other. This electromagnetic force falls off with the inverse square of the distance,22 so if the distance between the protons doubles, the force decreases by a factor of four. But it never goes to zero. So even two protons that miss each other by miles (OK, microns inside the LHC beam pipe) will repel each other slightly and bounce away from each other a tiny amount, and so could be said to have 'collided'.\n\n22. That is, 1\/r2 if the distance between them is r.\n\nIn practice, we would not detect such glancing collisions. The protons would carry on down the LHC beam pipe and would never make it into the ATLAS detector.\n\nProtons that come closer to each other, however, can undergo much stronger scattering, and of course in many cases they smash each other to pieces. At such short distances and at such high energies, the electromagnetic force is, in fact, not the main effect; most interactions between the protons are carried by the strong nuclear force \u2013 QCD, the theory of quarks and gluons.\n\nThe strong force really is short-range. It barely reaches beyond the size of an atomic nucleus. But where it reaches, it is _strong_. It is strong enough to overcome the huge electromagnetic repulsion between the two positively charged up quarks inside a proton, for example.\n\nMany of the strong collisions are still glancing blows, though. And in most of them the protons hardly get broken up, or don't break up at all, and mostly they don't register in ATLAS. These are called diffractive collisions. There are some specialised detectors, tens or hundreds of metres away from ATLAS or CMS down the LHC beam pipe, that can pick up some small fraction of the unbroken protons from these events in special LHC runs, but most of them get overwhelmed in normal LHC running.\n\nSo when do you say there has been a real collision? How do you define that? It matters, because we try to measure things like the average particle distributions in so-called 'minimum bias' events. What are we averaging over? On the face of it we would try for an unbiased selection of collisions. But we can't _possibly_ be truly unbiased; since the vast majority of glancing collisions don't leave any trace in the detector, we can't select them, whatever we do. In practice we will see most of the non-diffractive events \u2013 where the protons are smashed up and some of the bits hit the detector \u2013 and only see a few of the diffractive events.\n\nHere's an analogy. Say you want to measure the average height of people in the UK.\n\nYou go out at lunchtime every day and pick a random selection of people off the street and measure their height. You add up all the heights and divide by the number of people you measured, and you have the average height. Just like us counting how many particles are produced in all the collisions we see, and dividing by the number of events seen. Simple. And wrong.\n\nThe problem in both cases is that the people (or collisions) we see constitute a biased sample. In the collisions, we miss the diffractive events, in which fewer particles are produced, so we will overestimate the average number of particles produced in a collision. In the height case . . . well, you are measuring at a time when most children are in school.23 And children are shorter than most people. So you will overestimate the average height because you haven't accounted for them.\n\n23. Unless you are measuring in the school holidays. Or on a weekend. I am a bit disturbed that I feel compelled to add this footnote.\n\nYou could do one of a few things here to try and improve matters.\n\n  1. You could, for example, make an estimate of how many children there are in school, so how many you would have seen if you had had a chance of measuring their height; you could model (estimate, guess) what their distribution of heights might be, and you can put all that together to apply a correction to the data. Or,\n  2. you could say, I'm just going to measure the average height of adults. So in my random sampling, I will not measure the height of any of the children I meet who happen to be bunking off school. Or,\n  3. you could say, I'm going to measure the average height of people on the street at lunchtime. This way, by definition you've got the right answer already, so long as you had no other biases in there.\n\nHistorically, experiments have used theoretical models, either to add in the missing diffractive events (the kids in school \u2013 first option) or to remove the small remaining diffractive contamination and produce measurements of what they call non-diffractive events (adults only \u2013 second option).\n\nThe trouble is, this means that what they measured is only defined within a particular theory. 'Diffractive' and 'non-diffractive' are really just words. There's no clear, unambiguous definition of the separation between the two. In the UK, we choose the 18th birthday as the somewhat arbitrary but universally accepted dividing line between children and adults. There is no such widely accepted division for the separation between diffractive and non-diffractive in physics.\n\nIf you use a model to correct for diffractive events, you buy into a particular theoretical definition of them, and a set of assumptions as to what they look like. You are no longer just reporting what happens. I think it is very important that, having gone to the enormous trouble of building the LHC and the detectors, we first just measure what happens, with the minimum of theoretical input. The next step is of course to confront the data with theory as part of the process of exploration and understanding. But the first, reporting, step is essential.\n\nFortunately my collaborators agreed. So instead of measuring the particle distributions in 'non-diffractive' events, or averaging over all events, ATLAS measured the distributions for all events that have at least one charged particle in a given region, regardless of whether a particular model would call the event 'diffractive' or not. This is like option three above: measuring everyone you meet, adult or not, but stating the sample bias explicitly. The charged-particle requirement is a physical criterion that can be reproduced regardless of any model (it is the equivalent of 'meet them on the street'). The difference is significant (up to about 20 per cent). But the difference in _principle_ is huge, and comparisons to models become much less ambiguous.\n\nThis approach was surprisingly new, and in some quarters controversial. Partly because of conservatism \u2013 'That's not how we did minimum bias on my experiment' \u2013 and also perhaps because 'average height of people I met' is not such a useful number as 'average height of people in the UK'. But it's the only thing we can actually measure \u2013 the rest is interpretation.\n\nThese measurements, and more like them since then, have told us various things. One of the main things was that the detectors were working well. But more than that, they tell us about QCD and the proton. We know the proton is full of quarks, stuck together by gluons, the force carriers of QCD. But while we can write down what we think is the fundamental equation governing this, we have not solved that equation for the proton, and neither had we measured its behaviour at these energies before. Because the fundamental equation is not solved, there are lots of models, based on various approximations, with various free parameters in them. The new data allowed some of these models to be rejected, and allowed the parameters of some of the others to be constrained and improved.\n\nApart from the intrinsic interest of understanding these things, we need this better understanding of 'average' events in order to more effectively find rarer events amongst them. Events in which photons, W or Z bosons or top quarks were produced, for instance. Or even Higgs bosons.\n\nAnother place these improved models are needed is in understanding the showers of particles produced when a proton, or some other particle, hits the upper atmosphere. Super-high-energy particles, with energies much higher than the LHC, bombard the Earth all the time.24 They collide with atoms in the upper atmosphere, smash them to pieces, and the result is a spray of particles that can be detected at the Earth's surface by experiments such as the Pierre Auger Observatory in Argentina. The more we understand about the processes involved in these high-energy collisions, the more confident we can be in using such detections to work out the energy, direction and composition of the initiating particles, and hence where they come from and what violent stuff is going on out there in space to produce them.25\n\n24. This is perhaps the most compelling evidence that such collisions don't cause black-hole\/death\/horror catastrophes, since we are all still here at time of writing. 25. I like to think they are crossfire from interstellar space battles at the fall of the First Galactic Empire.\n\nNone of these first papers were the really exciting new physics the LHC had been built for, but it was interesting and important for firming up our knowledge as we stepped into the unknown. And it was great to have real data at last!\n\n#### 2.3 Energy and Mass\n\nDuring this time I was also teaching a course to first-year undergraduate physicists at UCL. It was a lot of fun (for me, anyway) being able to drop the latest news from the LHC into the start of a pretty dry lecture on differential equations or matrices.\n\nThe course is fairly typical of first-year physics degree courses; the main goal is to provide students with the mathematical tools they need to do degree-level physics. It contains some techniques for solving differential equations and for doing multidimensional integrals, matrix manipulation and coordinate transformations. The sweetener at the end is that we do Einstein's special relativity.\n\nWhen I was talking about the energy of the LHC beams at the start of this chapter, I didn't give the speeds, apart from to say 'nearly the speed of light'. That's because I can never remember how many nines to put after the decimal point. This is clearly a great failing of mine. I was asked the speed of the protons in the LHC by an audience member after a talk at the headquarters of the huge Wellcome Trust medical charity once, and they seemed very miffed that I didn't know the exact answer.26\n\n26. I did get gingerbread Daleks (for fans of Doctor Who), though, which was a bonus.\n\nThe answer is 'nearly the speed of light', of course, and that has been the case for every high-energy accelerator for decades. The more precise answer was 0.999999964 times the speed of light in 2010, and on reaching full energy this will be 0.999999991 times the speed of light. In the first case this is 299792447 metres per second and in the second 299792455 metres per second. So all the effort in 2013\u20132014 to get up to full energy buys us another 8 metres per second in speed; about as fast as I cycle to work.\n\nThis illustrates the fact that it is actually the energy that matters. Special relativity means that protons can never reach the speed of light, even though they can keep on getting more energy and momentum. In everyday physics, where speeds are small fractions of the speed of light, momentum is mass multiplied by velocity. In special relativity there is a gamma factor (that's \u03b3) that goes in front of this, which is nearly one at low speeds, but gets very large as the speed gets close to the speed of light.27 The gamma factor is a consequence of Einstein's fundamental postulate in special relativity, that the speed of light is the same for all observers. So the momentum gets very big even though the speed only gradually approaches the speed of light. The same thing happens with energy; the total energy of a particle is actually _E_ = \u03b3 _mc_ 2. When the speed is zero, \u03b3 = 1 and this is just the famous _E_ = _mc_ 2. When the speed, _v_ , is much less than the speed of light, _c_ , this is approximately _E_ = _mc_ 2 \\+ \u00bd _mv_ 2, where the second term is the kinetic energy. But at speeds near _c_ , \u03b3 gets huge and that approximation doesn't work any more. The energy can keep on increasing but _v_ can never quite reach _c_. It's all a bit odd, but it works.\n\n27. This isn't a textbook, but I can't resist giving the actual expression for \u03b3, which is \u03b32 = 1\/(1- _v 2\/c2_), where _v_ is the speed of the particle and _c_ is the speed of light. You can see from this that as _v_ gets close to _c_ , \u03b3 approaches 1\/0 (one divided by zero), which is infinite.\n\nParticle physicists very often talk about masses and momenta in units of GeV or MeV. Strictly speaking this is wrong. Energy is in GeV, momentum is GeV\/ _c_ and mass is GeV\/ _c_ 2. We avoid having to scatter factors of _c_ all around the place by using what we call 'natural' units, where _c_ is defined to be 1. In these units, Einstein's equation is even easier: _E_ = _m_.\n\nThe mass of a proton is about a GeV.28 So a proton in the LHC travelling with an energy of 4000 GeV is very highly relativistic, by which I mean that its kinetic energy is more than 4000 times bigger than its rest mass energy. This implies that when we collide two of these protons head-on, the energy that is in principle available to make new particles is 8000 GeV. This is enough to make more than 8000 new protons out of the collision of just two. And of course this energy might make something much more interesting, and newer, than that . . .\n\n28. 0.938272046 +\/- 0.000000021 GeV, actually.\n\n#### 2.4 'Is There Any Chance You are Going to Destroy the World?'\n\nThat's one of those tricky questions scientists hate being asked.\n\nIt is very hard to prove a zero probability, especially if you take quantum mechanics seriously, which I do, of course. So conversations can often go like this . . .\n\n'Is there any chance you are going to destroy Geneva\/the world\/the universe?'\n\n'No significant chance, no.'\n\n'No significant chance? You mean there is a chance, then?'\n\n'Well, possibly an insignificant one. But\u2014'\n\n'You evil bastard! Any chance at all is too much! I like their chocolate!\/ I have kids you know!\/Wow that's kinda cool, but . . . !'\n\n'Wait. I said\u2014'\n\n'You people must be stopped!'\n\nNo one leaves that discussion feeling good. The next interview is likely to go:\n\n'Is there any chance you are going to destroy Geneva\/the world\/the universe?'\n\n'No.'\n\n'Are you really sure?'\n\n'Yes. Shut up, you scaremongering idiot.'\n\nWhich doesn't really advance the public understanding of science, and may in fact be less reassuring than the first approach. Some way down that route lies: 'Of course there's no risk from mad cow disease. Look, I'm feeding a burger to my child . . .'\n\nThe problem is a misunderstanding of probabilities and, possibly, of significance.\n\nOnce upon a time I went to a festival (the Secret Garden Party) to give a talk about the LHC for a group called Guerilla Science that arranges such things. I took with me my son, who was then aged seven. We saw some bands, bought some hats and camped overnight. Then we got up and listened to some talks in the 'Science and Rationality' tent, which was where I was going to give my own show. One of the speakers was David Spiegelhalter, Winton Professor of the Public Understanding of Risk in the Statistical Laboratory, University of Cambridge, and very good at explaining risk and probability.\n\nSpiegelhalter described the idea of a micromort: a term invented by Ronald Howard for a one-in-a-million chance of death due to a given choice or action. Eating a burger, smoking a joint, crossing a road . . . any given action can, given enough data, be assigned a risk of death in terms of micromorts. Getting up in the morning carries micromorts. So does staying in bed. Part of the context was the so-called 'Equasy' affair, in which the British Government's drug adviser Professor David Nutt had pointed out that taking the drug ecstasy carried about the same risk as horse riding (about 0.5 micromorts a hit).\n\nMicromorts and balance of risk made a great impression on my son. More than a year later, he had to discuss for his homework the question 'Why do people take risks?' His answer was: 'They have no choice. All you can do is decide which risk to take.'\n\nNow my son is an utter genius, of course, as is David Spiegelhalter. But the rest of us can still learn to understand risk better than we do. Perhaps some scenarios will help.\n\nImagine doing something for the first time. Say a new experiment. Say, oh I don't know, the LHC, or RHIC,29 or the Tevatron, or one of the previous machines some people have got agitated about. Then take the worst consequence imaginable, even if it is in contradiction to all experimental evidence, theory and even logic. As science has a hard time proving a negative, you might conclude that there is an infinitesimally small chance of the bad thing happening and be inclined not to go ahead. But before deciding, you have a duty to consider also the risk of not doing it.\n\n29. Relativistic Heavy Ion Collider, Brookhaven, NY, USA.\n\n##### Scenario 1\n\nThe year is AD 2125 and the Earth has a serious problem. A rogue planet, drifting through the spiral arm of our galaxy, has just been detected via several innovative astronomical techniques involving gravitational wave detectors and observations from our deep-space telescope system. The planet is on course to enter the solar system and is massive enough to seriously disrupt the orbits of the other planets. Many-body quantum gravity calculations, using the detailed knowledge we have accumulated of the masses and trajectories of our 'local' environment, indicate a near certainty that one result of this disruption will be to send the Earth crashing into the Sun within two decades. Fortunately these observations and calculations have given the inhabitants of Earth enough warning. Using the latest antimatter fuel cells, a small robot ship is sent to the planet. Once on the planet, nanobots assemble a mini-black-hole factory that is used to provide a small but steady and powerful warp drive, diverting the planet away from the solar system into a cosmological near miss. Party time.\n\n##### Scenario 2\n\nThe year is AD 2145 and the Earth has a serious problem. There's no one to help it because its most intelligent species wiped itself out in a nuclear armageddon\/global climate catastrophe\/whatever the next one is. The Earth mostly bounced back from this and is still a marvellous cradle of life, until a rogue planet sends it spiralling into the Sun in the mother of all environmental catastrophes.\n\n##### Scenario 3\n\nThe year is AD 2135 and the Earth has a serious problem. A rogue planet, drifting through the spiral arm of our galaxy, has just been detected. The planet is on course to enter the solar system and is massive enough to seriously disrupt the orbits of the planets. Calculations using all the knowledge we have of the masses and trajectories of our 'local' environment indicate a significant probability that one result of this disruption will be to send the Earth crashing into the Sun within a few years. Unfortunately, many commentators and politicians refuse to believe this and claim the whole thing is a left-wing (or right-wing, according to taste) conspiracy. Anyway, there's not a lot we can do about it. The warning has come a bit late, and we still do not even know whether there is a Higgs or extra dimensions or mini black holes, so we have no suitable power sources to get us to the planet and no way of dealing with the threat even if we did. We spend five years moping about the foolishness of the 'safety first' legal ruling that made us turn off the LHC back in 2010, as well as the similar rulings that followed on new experimentation across many fields of physical and life sciences. Then we crash into the Sun.\n\nThe above scenarios are of course three amongst an infinite number of tiny possibilities. However, anyone who advocates stopping research because of imagined doomsday scenarios should also be made to estimate the risks associated with stopping the research and the doomsday scenarios we might thereby be exposed to.\n\n#### 2.5 Impact\n\nImplicit in the scenarios just described is an assumption that knowledge practically always turns out to be useful, often in unpredictable ways. Or, if you prefer, knowledge is power.30\n\n30. Often attributed to Sir Francis Bacon. It sounds even better for my purposes in Latin \u2013 ' _scientia potential est_ ' \u2013 though what Bacon actually wrote was ' _ipsa scientia potestas etc_ ' (1597), meaning 'knowledge itself is power'. Which is also a good thought, but now the Bacon and potato thing is making me want tartiflette, which serves me right for spending too much time on Wikipedia.\n\nFor the whole of my career as a scientist, there have been arguments about whether research, and research funding, should be directed towards known benefits (economic, medical or others) or somehow 'purely' for the joy of finding stuff out. These arguments sometimes degenerate into partisan battles between various interest groups, but usually they are between two sides, both of whom believe strongly that scientific research is a societal good, even a necessity. The disagreement is over the best strategy to optimise the benefits.\n\nMost participants in the debate agree, for example, that encouraging more young people to study physics is a good thing, because physicists are economically beneficial things to have around.\n\nYou might think \u2013 I do \u2013 that the excitement of the LHC and the wonder of reaching further into the heart of matter than ever before would be a major positive in that regard. Physics stories don't often get into the news on the scale that we did on 10 September 2008, for example. But Sir David King, former Government Chief Scientist and at the time President of the British Association for the Advancement of Science (BAAS, now the British Science Association), felt so strongly that research should be directed at urgent practical problems and applications that he went on _Newsnight_ , on the evening of the biggest physics story in decades, to accuse us particle physicists of 'navel-gazing'.\n\nLuckily for physics, Brian Cox was on hand. He wasn't then as well known as he is now, and was quite nervous and wound-up after what had been an amazing day of high-stress physics in public.31 Even so, he was thankfully more confident with the media than any other member of an LHC collaboration, so we did not have to end the most exciting day of physics for years with a smug, unchallenged takedown on prime-time television. After a moment's unfeigned total astonishment at the 'navel-gazing' accusation, Brian managed to make some effective arguments about the benefits of particle-physics research in terms of both its direct spin-off technologies and its inspirational effects, which were obvious on that day of all days. The objectives of the BAAS \u2013 'promoting science, directing general attention to scientific matters, and facilitating interaction between scientific workers' \u2013 were in the end served, though I don't think much credit went to its president.\n\n31. Initially, when Brian was on the way back from CERN for the programme, _Newsnight_ 's planned opponent for the ritual confrontation had been the right-leaning lobby group the TaxPayers' Alliance. Sir David was probably more interesting.\n\nAnyway (and you can probably tell the sense of betrayal still rankles . . .), although that moment was spectacularly poorly chosen, the argument has not gone away, and nor should it. The conflict between applied and 'other' science is so artificial and damaging that I have trouble deciding what the 'other' should be called. Not 'fundamental', definitely not 'pure' (there's no such animal). 'Curiosity-led' is about the best I can reach for. I think that when we study far-off galaxies or the Higgs boson we are mostly motivated by curiosity as to how the universe works. When we study new materials, or climate, we may be primarily motivated by trying to solve a pressing problem or develop a cool new technology. But the boundaries are fuzzy: the vast majority of scientists working on the LHC would be overjoyed if applications were found for our discoveries, and many of the software, detector or accelerator developments lead physicists off at highly applicable tangents. Likewise, while the desire to cure disease or save the world from climate change is a serious and rational priority for many, most scientists I know in such areas have a deep intellectual curiosity about the fundamental mechanisms they are studying.\n\nAt the moment I am head of the Department of Physics and Astronomy at UCL. Actually, while I am working on this chapter right now, we are going through an exercise known as the Research Excellence Framework (REF32). I am the 'unit of assessment lead' for three departments: mine, the Mullard Space Science Laboratory, and the London Centre for Nanotechnology. The range of science and engineering done in these departments covers cosmology, quantum computing, particle physics, materials science, the physics of biological systems and much more. We have been required to collect evidence of how our work has affected society beyond academia, and the case studies come from all these areas.\n\n32. Personally I expect this clunky name is another acronym-driven contrivance, as in the cries of 'Oi, Ref!' heard both in universities and football grounds all over the UK. One of those making the big jump is precision-lens manufacturing (for astrophysical projects such as the Dark Energy Survey, very 'curiosity-led' cosmology), which is now at the heart of a company started by Professor David Walker in North Wales, selling machines and expertise to a wide range of manufacturing and engineering companies. The technology they have developed is used to grind and polish everything from precision components for the space industry to replacement hip and knee joints for health care.\n\nThe purpose of the above paragraph is not to bang the drum for UCL. Any major physics department could paint a similar picture (and in the UK they all are, at the moment, thanks to the REF). The point is that for people like Sir David King to pick out a part of this ecosystem as useless (which is what I take 'navel-gazing' to mean) is dangerous nonsense. Even though the lead times from basic research to application can be very long, there are already examples of technology developed for the LHC that are being deployed in practical situations. Novel detectors developed for the LHC are being used to monitor radiation doses for hospital patients undergoing radiotherapy, and are also being developed for retinal implants. The worldwide computing grid technology, put in place primarily to analyse LHC data, has been used to run structural analysis for antimalarial drugs.33 Physics is useful and interesting all over the place, and this is why many very bright young people want to study it, many of whom take their degrees and go and do amazing things outside of academia or physics. But I do not ever want to be in the position as a senior physicist of having to tell the new students at induction that they should 'learn all this stuff because it's useful, but don't get carried away trying to do new fundamental physics, we don't do that here'. Any more than I would be happy telling them that string theory is the top of the pile and they should avoid getting their hands dirty with data and applications.\n\n33. See 'Particle Physics, It Matters', Institute of Physics, 2009, <http:\/\/www.iop.org\/publications\/iop\/2009\/page_38211.html>.\n\n#### 2.6 From Liquid Argon to M-Theory\n\nFinally, before moving on to the first high-energy running of the LHC, I want to say something about the relationship between experiment and the multidimensional fringes of theoretical particle physics. Those fringes include string theory, in which fundamental particles are tiny vibrating strings, brane theories, in which they are higher-dimensional objects, still vibrating, and M-theory, which is a rather vague attempt to unify these approaches. In general, such highly mathematical frameworks strive to bring together quantum field theory and general relativity and grope towards a theory of everything.\n\nTowards the end of a series of interviews with would-be undergraduate physicists who all want to be string theorists, I sometimes find myself sympathising more with the David Kings of this world. I do occasionally breathe a sigh of impatience and resist the urge to say, 'But I thought you wanted to be a real physicist?'\n\nSuch a slur on my theory colleagues would, of course, be unworthy. In the ecosystem I described in the previous section, theoretical physics is a vital component, and string theory and its relations are a legitimate part of that. Our observation and understanding of nature have led us to a number of beautiful and highly mathematical underlying principles. Using what are effectively thought experiments to see where these principles lead us, where they break down and what might replace them, is thrilling science. But for me, at least, it has to retain a connection with data.\n\nI care much more about the ability of a theory to stand up to experimental testing than I do about its mathematical beauty. M-theory, string theory and so on have a long way to go in this regard. Even supersymmetry, a necessary prerequisite for string theory, struggles, although subspecies of supersymmetry are at least in contact (indeed, often conflict) with data, and will be discussed later in this story.\n\nThe LHC experiments may discover supersymmetry, and (or) find evidence for extra dimensions. This is really exciting, and either discovery would certainly add credibility to M-theory, as well as revolutionising our understanding of fundamental physics. But finding such evidence is the main thing, and the search tends to keep your feet on the ground even if the goals are highly abstract. Not only do we need the accelerator, we need our detectors to record what happens when protons collide. We also need to know how to interpret what our detectors are telling us.\n\nMost high-energy particle-physics detectors surround the point at which the particle beams collide, and consist of concentric layers of different technologies, each designed to tell us something different about the collision. In one of the world's least helpful analogies, I have often described this as like 'a sort of high-tech cylindrical onion'. Various layers of this onion will crop up during the story, but one of the most important is the calorimeter.\n\nThis measures energy \u2013 calories. As discussed,34 food carries energy, and particles carry energy when they are produced in a proton\u2013proton collision at the LHC. We want to know, as precisely as possible, how much energy they carry, as this is vital for working out what actually happens in the collisions.\n\n34. See 2.1 Low-Energy Collisions and Electronvolts.\n\nThe basic idea of a calorimeter, whatever technology it uses, is to stop the particles with some very dense material. They hit the material, slow down, and as they do so they give off electromagnetic radiation (photons \u2013 light, basically). The amount of light given off has a correspondence with the energy the particle had in the first place. So the trick is to measure the light, work out the correspondence, and so measure the energy. Working out the correspondence is called calibration. It's difficult.\n\nThe main calorimeter technology in the ATLAS detector uses liquid argon interleaved with lead or copper to stop the particles. Liquid argon may sound exotic, but we use it because it gives out light in a very nice way, proportional to the energy going in. It is actually quite cheap, too: less per litre than a well-known brown fizzy drink. Plus it's very stable \u2013 the amount of light it gives out per GeV doesn't change with time \u2013 and it is resistant to radiation.\n\nEven so, it does give off a different amount of light when it is hit by an electron compared with when it is hit by, for example, a pion (a commonly produced hadron made up of a quark and an antiquark). And the mix of pions and electrons hitting the calorimeter is not something we know in advance. There are many such subtleties you have to calibrate for before you really believe what you see.\n\nThe whole calibration process is equivalent to checking your experimental set-up in any small science experiment on a laboratory bench. It consists of many, many 'control' studies \u2013 measuring stuff you already know, in order to understand your apparatus. Without such procedures, we cannot believe any particle measurement we make, whether it's a couple of particles produced in a hospital scanner, or a spray of particles indicating extra dimensions at the LHC.\n\nIf and when the experiments start seeing well-understood signals over and over again, for supersymmetric particles or extra dimensions, that's when those theories win. And that's when, maybe, I'll start taking M-theory more seriously.\n\nGlossary: Fields, Quantum and Otherwise\n\nCommonly used words are often appropriated by areas of specialism and used to refer to something more specific and technical than their everyday meanings. An example in physics is 'work'. If a constant force acts on a particle and pushes it through some distance, the work done is defined as the force (in the direction of movement) multiplied by the distance travelled. It is a very specific quantity, and in fact is a form of energy. The energy of the particle will increase by the amount of work done. There is clearly a relationship between the everyday idea of work \u2013 making an effort to get something done, often for some financial reward \u2013 but the physics usage is precise and limited whereas the everyday usage is a bit fuzzy and very general.\n\nMomentum seems to be a word that went the other way. In physics it is \u03b3 _mv_ (the relativistic gamma factor multiplied by the rest mass multiplied by the velocity), and is a way of quantifying the tendency of a particle to keep moving at a given speed in a given direction. And for speeds much lower than the speed of light, \u03b3 is very close to 1 so can be ignored. In more general usage momentum is used to describe the impetus behind a political campaign or some other social or political process or policy, with the same implied meaning that the more momentum something has, the harder it is to stop, but with no precise definition of what the momentum is in each case.\n\nOne of the words I have so far tried to use infrequently, but which I will really need to use more often in the following chapters, is 'field'. In general usage a field is a flatish bit of land with stuff growing on it, probably looked after by a farmer and possibly containing cows. It can also mean an area of study or expertise, and looking back I see I have already used it in this sense too. These meanings can also be mixed up \u2013 as in the reason the scarecrow got tenure.35\n\n35. He was outstanding in his field.\n\nIn physics, 'field' has a more technical, but related, definition. A field in physics is simply a quantity that has a value at all points over a certain region of space. So if you are in a room, there are various fields you might use to describe your environment. As a physicist you might do it this way:\n\nFirst you need a way of specifying any given point in the room. A good way of doing this would be to choose the floor level at one corner of the room to define an 'origin'. Any point on the floor can be reached by going a distance (call it _x_ ) along the floor parallel to one of the walls that meets at the corner you chose, then another distance (call it _y_ ) along the floor parallel to the other. Then any point in the room can be reached by going up some distance (call it _z_ ). Three numbers, _x_ , _y_ and _z_ , are all you need.\n\nYou can now talk about various useful fields. The temperature, for example, has a value at every point in the room. Say on average it is the nominal 21\u00b0C room temperature. If it were really this temperature everywhere, then you would have a constant field, with no dependence on position in the room, so no dependence on _x_ , _y_ or _z_.\n\nHowever, it is quite likely that the temperature is slightly higher near the ceiling than at the floor, since hot air is less dense than cold, so will rise to the ceiling. We could describe such a dependence with a field like _T_ ( _z_ ), that is a value _T_ depending only on the height, _z_. _T_ would be a function36 of _z_ , maybe something like _T_ ( _z_ ) = 20.5 + 0.5 _z_ , with _z_ given in metres and temperature in degrees Celsius, for example. For a 2m high room, the floor temperature would be 20.5 + 0.5 x 0 = 20.5\u00b0C, and the ceiling temperature would be 20.5 + 0.5 x 2 = 21.5\u00b0C. And the temperature at every point in between can be worked out from the expression for the field. Other fields could be used to describe the air density, for example, or even the amount of noise.\n\n36. 'Function' \u2013 there's another common word, appropriated by mathematics this time.\n\nAll of those are fields that are described by a single number at any point. They have a size, but they have no direction. We call them 'scalar fields'. A 'scalar' is just a word for a thing that has size but no direction.\n\nThere are other kinds of fields that have direction, too, and we call these 'vector fields'. I have already used examples of these \u2013 electric and magnetic fields such as those in the LHC magnets, for example. In the room there will be a gravitational field. It has a size at every point (a force of about 9.81 newtons per kilogram) and a direction (it points downwards).\n\nAlthough the fact can be ignored for most everyday purposes, the electric and magnetic fields are in fact quantum fields.37 This means that if you study them at very short distances, you will see that the field does not have a continuum of possible values, but is described by the sum (superposition) of a series of discrete38 quanta, or excitations,39 of the underlying quantum field. These excitations are a bit like waves and a bit like particles. The quantum field theory of electromagnetism, QED, has two fields \u2013 the photon field and the electron field. What we measure as electromagnetic waves, or as individual photons or electrons, are excitations in these fields.\n\n37. Gravity may be too, but we don't know the theory yet. 38. Discrete meaning discontinuous and distinct, rather than politely done in pastel shades. 39. Another appropriation, with an obvious relation to everyday usage, since quantum field theory is very exciting.\n\nQuantum or not, the idea of a field remains the same. It is a physical quantity that has some value, or superposition of values, at all the points in space over some region you are interested in.\nTHREE\n\n## High Energy\n\n### March\u2013September 2010\n\n#### 3.1 Seven TeV\n\nOn the morning of Tuesday, 30 March 2010, the LHC really became the highest-energy particle collider in the world.\n\nIt began to accelerate protons to an energy of 3.5 TeV (3500 GeV), three and a half times higher than the previous record held by the Tevatron at Fermilab in Chicago, thereby breaking new ground in fundamental physics and accelerator technology. We were also breaking new ground in terms of doing science live and in public, or so it felt, at least.\n\nWe had hoped for collisions for breakfast, but it didn't work out that way. Although the false starts reminded me of frustrating night shifts on the ZEUS experiment in Hamburg where I did my PhD, they aren't unusual on a new collider. Given the major accident in 2008, however, plus the huge public interest, it was a very nerve-wracking morning. I guess this is how space scientists feel when launch delays happen in mid-countdown. Injecting and ramping the beam energy feels like the initiation of a countdown sequence and we had to go through it three times before we finally launched the high-energy physics program of the LHC. In time for lunch. Good enough. Fantastic, in fact.\n\nI was in London, not CERN, and seeing how crowded the ATLAS control room looked, that seemed a good choice. Up to a hundred people really had something vital to do in the early running of the ATLAS detector at any one time, but there are 3000 people on the collaboration, contributing skills ranging from software and electronic and mechanical engineering to theoretical physics. Trying to cram everyone into the control room for the first collisions would have been impossible. A good thing, therefore, that CERN had invented the web, so there was a live feed and the results were available instantaneously. There was also a flood of emails, phone calls and tweets.\n\nThe storage and acceleration up to 3.5 TeV of the hair-thin proton beams in the LHC was achieved as planned. The beams were then brought into head-on collision and the results were recorded. We were at only half the design energy of the LHC, but this was still more than enough to break into the territory of unknown physics. The plan then was to do this routinely for a couple of years, collecting enough data to explore the new landscape thoroughly, with a particular focus on searching for signs of the Higgs boson. If the boson was there to be found, it might possess any one of a range of different masses, and might decay to a number of possible less-massive particles. Those decays would be relatively rare, and the signs that they had occurred would have to be sifted out from a range of different background processes that threatened to swamp them. So we needed to collect many collisions before anything was likely to be clear. Then we planned to pause, upgrade, and redouble the energy.\n\nI seemed to spend much of the day on radio and TV news. After my nerves watching the LHC operators coax the beams into collision, and hoping ATLAS would successfully record the collisions, being interviewed on live TV was (almost) a breeze.\n\nI remember hoping at the time that seeing a science story like the LHC develop in public over a few years would help people gain a clearer view of scientists, and also of the erratic but real process of science. The experience of the 2008 start and failure had given me some reason to hope. Scientists periodically pop up in the headlines of some story or other as either angels or demons and without much context,40 then vanish again. 'It's a breakthrough!' \u2013 but then it proves a bit more complicated than that and no one can be bothered to follow it up. The LHC story, however, seemed to be big enough that a subset of the media and the public were ready to stick with it through several twists. That could be good for particle physics, and maybe even helpful for other big science stories, including the more controversial ones, as well as those with a more immediate impact on our well-being.\n\n40. Not even so much as a turgid thriller about blowing up the Vatican.\n\n#### 3.2 This Is Not a Drill\n\nIn 2010, the UK general election was approaching. We'd had a terrible time with science funding around 2007\u201308 when, after a longish period of stability, the government used a merger of two research councils to make massive cuts in astronomy and particle physics. Then the global financial crisis began and science funding had been cut across the board.\n\nIn 2010 the financial crisis hadn't stopped and banking malpractice stories were still emerging regularly, but in the world of the research councils (the main bodies responsible for distributing taxpayer funds into research projects) things had settled into some kind of stand-off, with funding slowly declining but with enough resources around that we could still be major players in the LHC. The LHC was of course much more interesting than political lobbying, so I wasn't always paying as much attention to science policy in the election as I should have been.\n\nThis is fairly typical scientist behaviour, by the way. We just get the data and are happy. However, in many discussions with civil servants and those who work with them, I've heard that our big mistake was that in the economic good times, when science was getting some share of the growth (and particle physics was getting somewhat less, but not being cut), we had just shut up and got on with the science. The argument was that we should have been aggressively pushing for more and more cash, just so that there was more fat to cut when the bad times came. Sadly, this illustrates one of the gulfs in understanding between the worlds of science and politics, and it's an issue that impedes funding of science programs around the world, not just in the UK.\n\nResearch is about finding good questions to ask, then answering them. Good questions that can actually be addressed don't come along too often, and the capacity to identify and answer them grows slowly \u2013 you can't just go out and double the size of a good research group overnight. There are some big, wonderful and expensive things we could do if we had the money, but unless such an injection comes on the back of sustained, long-term investment, it would not take us long to run out of the skilled people to deliver them. In a world where business and other interests continually lobby, it's not always easy for politicians to place the right value on stability and the strategic planning of research capacity.\n\nScientists, on the other hand, mostly want to do science, and many of us only get noisy and politicised when our capacity to do science is under imminent threat. As well as being a huge tactical mistake, this is an insult to the interested and intelligent public who foot the bill and deserve to hear what we are up to. It is also a recipe for political and social disaster \u2013 public life needs science, and scientists who engage consistently. We should have been more engaged \u2013 at least saying thanks for the resources and reporting the good things they were funding.\n\nBut oh, the temptation of real data! Shortly after the high-energy start-up, Oxford University hosted the second 'Boost' meeting. This took the topic of jet substructure a lot further,41 but the results were still all based on simulation, and the tension induced by the knowledge that real data were already arriving pervaded the conference.\n\n41. Unusually, the conference proceedings became a highly cited paper. <http:\/\/arxiv.org\/abs\/1012.5412>.\n\nI had lived through this transition from simulation to reality during my doctoral research in the early 1990s. I wrote an emulation42 for part of the 'trigger' system built to select data from electron\u2013proton collisions in ZEUS and spent two years checking that code to death. The idea had been to feed simulated data into both the real trigger43 and my emulation, and check that we had identical results.\n\n42. In FORTRAN 77. 43. Which was in the Occam language and running on a network of transputers, if you care about such things. This was very cutting edge at the time.\n\nIt had worked perfectly until we got our first real data. At that point the trigger _and_ the emulation both began producing nonsense. It was not a good moment. All that careful preparation, and yet we couldn't make head nor tail of the real data. The only glimmer of hope was that the emulation and the trigger were producing identical nonsense, so I could use my code to investigate. After a few stressful hours, I had it. The wires in the detector were arranged in a pattern of little cells, each cell being a row of eight wires,44 and each wire received an electrical pulse if a charged particle passed nearby. In the simulated data, the pulse had come out in order of wire number, 1\u20138. In the real data they came out in order of arrival time, which depended on where the particle was! Once we took it into account properly, all the crazy numbers lined up again. Obvious in retrospect, but somehow not anticipated. These things happen. We practise on simulations for so long, and it helps, but it can't fully prepare you. On the LHC, things were now very real, and nervous tension was everywhere.\n\n44. Numbered 1\u20138 rather than 0\u20137 because this was FORTRAN.\n\n#### 3.3 Copenhagen\n\nWithin a couple of weeks, a steady stream of head-on proton\u2013proton collisions was being delivered at a collision energy of 7 TeV (that is, two beams of 3.5 TeV each), allowing us to search for new particles, forces and dimensions in completely new territory.\n\nIn some optimistic scenarios, new particles or other exotica could simply have poured out of the collisions the moment they began. Like many physicists, I never quite believed that would happen, but we had to be prepared for the possibility. I suspected it was always going to be a long haul involving several years of hard, sometimes tedious, work. The LHC would be producing new physics for at least a decade. We weren't going to find the Higgs boson (if there was one) on day two, but the work had begun.\n\nEven so, we had the big conference45 coming up in Paris in July, and we were all hoping to get some preliminary, relatively simple results ready in time for that. In late June, we all headed off to our collaboration meeting in Copenhagen to prepare.\n\n45. The International Conference on High Energy Physics, ICHEP. Like the LHC, a name designed for accuracy rather than inspiration.\n\nATLAS is a big international collaboration. There are about 3000 of us, from 38 different countries. We have three big meetings a year, and more-or-less continuous smaller ones. We are the meeting on which the sun never sets. Of the three big annual meetings, two are typically in CERN while the other is in one of the collaborating institutes. That year it was Copenhagen's turn.\n\nMuch of the meeting was dedicated to results on how well the detector was working: did we understand what it was telling us? How good were the calibrations? Most of the rest of the time was for the discussion \u2013 and hopefully the approval \u2013 of preliminary results to be shown in Paris. The main result I was involved in was trying to understand and measure the jets46 formed from quarks and gluons smashed out of the protons. We wanted to get a preliminary result written up in a 'conference note', which is the way ATLAS provides backup information about a result that has been shown in public but isn't quite ready to be submitted to a journal. (You'll hear more about these during the Higgs search.) This would have to be followed up by a paper as quickly as possible.\n\n46. See Glossary: Quarks, Gluons and Jets.\n\nATLAS, like most big collaborations, has a pretty intricate review process. It evolves, but basically goes something like this:\n\n  1. Have an idea for a measurement you would like to publish.\n  2. Do some work and present it in the relevant group. ATLAS has several physics groups, for 'Higgs' or 'Top Physics' or 'Standard Model', for example. You need to persuade the group, and particularly the group conveners, that your idea is a good one that ATLAS should publish.\n  3. They will request that an 'editorial board' be appointed. The ATLAS publications committee will appoint one.\n  4. Have meetings with your editorial board until they are happy with your analysis.\n  5. Present the analysis for approval in the physics group.\n  6. If it's not approved, go back two steps (this applies to most of these steps).\n  7. Now agree on the paper draft with the group leaders and the editorial board.\n  8. Distribute the draft to the whole of ATLAS. Wait for comments.\n  9. Present the result to ATLAS, addressing all the comments in a new draft.\n  10. Circulate the new draft to the whole of ATLAS again. Wait for comments.\n  11. Final presentation to ATLAS. Get approved.\n  12. Send draft for 'final sign-off' by some senior physicists on ATLAS (usually the spokesperson or deputies). If everything has gone well, this should be almost a formality. But it is the last chance for ATLAS to catch any mistakes. Also, if you are unlucky, you get a senior physicist who hasn't been paying attention to the first 11 steps, and wants to start all over again.\n  13. Send to journal, and to the arXiv (pronounced 'archive'. This is the place all good particle physics and astronomy papers are released, stored and freely accessible). The result is now public. Wait for comments from the referees.\n  14. Address referees' comments.\n  15. Journal acceptance. Now smile.\n\nIt is a lot of work, but generally it functions, as long as you have reasonable and diligent people involved in each step. At every step, confidence in the result increases, though mistakes do get found up to, including and unfortunately sometimes even after step 15. Journal publication is an important badge of quality for a scientific result, but it is not infallible. It will be useful to refer to these steps when discussing some of the rumours and leaks about the Higgs that emerged over the months that followed.\n\nFor a conference note, rather than a journal paper, steps 10 and 11 can be skipped, and 13, 14 and 15 don't happen. In Copenhagen many notes were passing steps 5 to 9. The note I was writing passed steps 5 to 8. Step 9 happened on 12 July, and step 12 went smoothly soon after. On 16 July, the jet cross-section note was released47 in time for ICHEP, which started on 21 July.\n\n47. <http:\/\/atlas.web.cern.ch\/Atlas\/GROUPS\/PHYSICS\/CONFNOTES\/ATLAS-CONF-2010-050\/>\n\nI realise I haven't actually said what a cross section is. As it's an important and common concept in physics, it has its own section together with luminosity \u2013 see Glossary: Cross Sections and Luminosity. Sufficient to say here that a 'jet cross section' is a measure of how likely we are to see hadronic jets when we fire two protons at each other.\n\nWhen we collide protons, we really care most about the collisions between the proton's constituents \u2013 quarks and gluons. Unfortunately, the quarks and gluons only carry a fraction of the energy of the proton, and we have no way of choosing how much. If the fraction were a half, for example, then we would have jets with 1750 GeV of energy (half of 3.5 TeV). But most of the quarks and gluons carry much smaller fractions; our jet cross sections ran out of statistics at about 600 GeV. Still, since jets are the most commonly produced high-energy objects in proton collisions, this was a higher energy than anything else seen so far from the LHC, and it in fact had already reached the point where the Tevatron measurements had run out of steam. To have a real measurement of this, and to be able to show that the predictions of QCD agreed with the data, felt like a real achievement. Dozens of people were directly involved, and hundreds less directly. Like the minimum bias results, it was an important part of finding our feet in the new energy regime of the LHC. This is what we presented at the Copenhagen conference.\n\nDespite this triumph, Copenhagen remains more famous for the role it played in the development of quantum mechanics, especially in the work of Niels Bohr and in the 'Copenhagen interpretation' of quantum mechanics. This is arguably the most flaky aspect of current physics, and unfortunately it's one that the LHC seems extremely unlikely to help us with.\n\nIn the Copenhagen interpretation, quantum mechanics only allows us to calculate the probability of something happening. All possible ways that the 'something' could occur have a number \u2013 an 'amplitude' \u2013 associated with them. You add up all the amplitudes, square the result and you get the probability. This is a very accurate way of making predictions if you have a large number of 'somethings'. In particular, amplitudes do not have to be positive numbers, so contributions can cancel each other out rather than build each other up, and this means that the probability of particles travelling from one place to another can exhibit interference effects.48 Depending on the possible routes, there are regions of high probability and regions of zero probability, where everything cancels. This is behaviour we are used to seeing in waves, and the maths behind it is basically the resolution of wave\u2013particle duality. Is an electron a wave or a particle? Well, it's a discrete quantum object, an excitation in a quantum field, a lot like a particle, but since we need to use amplitudes to calculate its behaviour, it can behave like a wave sometimes.\n\n48. This is the physics at play in the WW scattering processes I discussed in 1.2. The 'No Lose' Theorem, for example.\n\nNone of the above is the problem many of us have with the Copenhagen interpretation. That all works. The problem is, how do you move from a 'probability' that we have calculated to an actual occurrence. I can calculate the probability of an electron taking a particular route between an emitter and my detector, but what decides which route it will actually take? Even worse, what decides when the decision will be made? It doesn't bother me so much that there is an indeterminacy in there, what bothers me is that at some point a particular outcome happens, and the transition between a superposition of amplitudes and a single result is not understood.\n\nIn the Copenhagen interpretation this decision point is called 'wave function collapse' and it is the point at which you put away the amplitudes and the quantum stuff and treat everything as definite. If you like, it's the point you open Schr\u00f6dinger's box and give him the news about his cat. It is a very uncomfortable thing to have in physics because it seems to separate the observer from the observed, and we would like physics to explain both of them together as a single system. Cosmologists explicitly talk about the 'wave function of the universe', where the universe includes all physicists and their detectors, and their cats. How does that get collapsed, then?\n\nIt seems that as a quantum system gets bigger and more complex, the wave function does tend to collapse. Building large uncollapsed, or 'coherent', quantum systems is very difficult. There are rooms full of people in my department at UCL trying to do this, both to try and understand how it works and because if you can do it there are many applications, starting with quantum computing.\n\nThere are other interpretations, such as the many-worlds one, where all the possibilities are realised in a multiverse. (How did your consciousness end up in this one, then?) Several good physicists have spent time trying to develop hidden variables, but these make predictions that fail experimental tests, or at least the hidden variables must be very weird \u2013 they must be 'non-local', involving what Einstein disparagingly called ' _spukhafte Fernwirkung_ ' or 'spooky action at a distance'.\n\nI get invited to quite a lot of science-influenced art shows and exhibitions, of varying quality. Science is undeniably the source of some wonderful images. But speaking generally, the art that has most impact on me usually hints at, and shows back to me, something I have some knowledge of already, and leads me into a different way of thinking about it. This happens with art that is not specifically about science. It may refer to love, distance, location, parenthood, fear . . . almost anything. This sets off all kinds of echoes in my thoughts and deepens the experience and understanding.\n\nThe only piece of art about science that has had this effect on me is related to this business of hidden variables and wave functions. It is _Copenhagen_ , the play by Michael Frayn, which I saw years ago at the South Bank theatre in London and which still surfaces in my mind at random intervals, especially when I am working with or teaching quantum mechanics. Frayn brilliantly explores a meeting between Niels Bohr, his wife Margrethe, and Werner Heisenberg in Copenhagen during the Second World War. Bohr and Heisenberg, giants in the development of quantum mechanics, were long-standing colleagues, but on opposite sides during the war. No one really knows what was said, but afterwards the Bohrs fled Denmark to the UK and from there went to the USA (not a moment too soon). Heisenberg led German efforts to develop an atomic bomb. Bohr collaborated on the Los Alamos project.\n\nWhy exactly Heisenberg visited, whether he warned Bohr, whether key physics information, or misinformation, was exchanged, and what impact this had on the fact that Los Alamos succeeded and the Nazis failed, has been the subject of much speculation, and alternative versions are presented in the play.\n\nAll that is fascinating, but there is another layer to it. There is an unstated but to me very clear analogy between, on the one hand, known facts of history (the meeting definitely happened) and the unknown motivations and conversations that may have been behind them, and, on the other hand, the idea of measurable quantities in quantum physics (for example, the position at which an electron hits a screen) and the indeterminate states, the amplitudes, in between that lead to it. To calculate the final position of an electron you have to consider all possible paths it could take, and it makes no sense to say it took a particular one. This is more than just lack of knowledge, it is in principle unknowable. For me, this is reflected in the personality of Heisenberg, in that he probably had very mixed motivations and was probably not even clear to himself what they were, or which were dominant. So in a sense only the actions taken are real. The motivations are potentially unknowable and perhaps you have to consider all of them to understand the deeds.\n\nBohr left for safety, and Nazi Germany did not develop the atomic bomb. In happier times, the ATLAS collaboration left Copenhagen with a lot of new results to show in the big Paris conference.\n\nGlossary: Cross Sections and Luminosity\n\n'Cross section' is a common concept in particle physics, but a potentially confusing one. In this context it is basically a measurement of probability, except that probabilities have no units and are all between zero (never happens) and one (definitely happens), whereas a cross section has units of area and can take any (positive) value.\n\nTo see how this works and why, imagine trying to score a penalty in football without a goalkeeper present. If your skills are anything like mine (or if you are an England player in a shoot-out against Germany), there's a non-negligible chance you will miss. There are many factors to take into consideration, but the chance you will actually score will depend on the cross-sectional area of the goal. The bigger the area, the bigger the chance.\n\nThis (or equivalent experiments with nuclear beams fired at targets, such as Rutherford's experiment firing alpha particles at gold foil) is why when we calculate whether a particle interaction will take place, say between two protons at the LHC, we can express it as a cross section, with units of area.\n\nIf I were firing randomly at a wall with goalposts painted on it, the actual probability of me scoring with a given kick would be the area of the goal divided by the area of the wall, assuming I always at least hit the wall. If the goal is about 18m2, and the wall is about 100m2, and I scatter my shots evenly over the wall (OK, I'm not really that bad, see below), then the probability of any one shot going in would be 18\/100 = 0.18. This is really a probability. It ranges from zero (goal of zero area!) to one (goal as big as the wall).\n\nParticle and nuclear physicists measure cross sections in barns. A barn is just a unit of area. It was supposed to be something big and easy to hit (as in 'barn door') and is roughly the cross-sectional area of a uranium nucleus. It is small by everyday standards \u2013 10-28 square metres, or one ten billion billion billionth of a square metre. This is a nonsense number, I know, and it gets worse. A femtobarn, which is the type of cross section we measure at the LHC, is a million billionth of a barn. We just have to deal with the fact that nature operates on a variety of distance scales and not all of them are easy to imagine, I guess.\n\nAs I hinted above, something else that affects the probability (of a scored goal, or a particle collision) is the number of attempts I make per unit area. In the penalty-shooting example above, if I scatter my shots across the wall equally with an area density of one per square metre, then I will probably score 18 goals. If I scatter them at two per metre, then most likely I'll score 36 goals.\n\nThe 'shots per square metre' number is the 'luminosity'. It has units of inverse area, or 'per square metre'. A particle collider like the LHC can increase the luminosity by either firing more particles (like me still shooting randomly but shooting twice as often) or firing them more accurately (like me shooting the same number of balls but concentrating on the 50m2 of wall nearest the goal, something of which I believe myself to be fully capable).\n\nAt the LHC we now measure luminosity in inverse nano- pico- or femtobarns. These are useful units for luminosity, because the cross section for a proton\u2013proton scattering at the LHC to produce a Higgs, for example, is expected to be about 10,000 femtobarns. If you multiply femtobarns by inverse femtobarns (like multiplying the number of shots per square metre by the number of square metres for the football), you get the number of collision events. At the point that we had one inverse picobarn, or a thousandth of an inverse femtobarn, of luminosity, we might well have made ten Higgs bosons already. Unfortunately, most of them would have decayed in ways impossible for us to distinguish from other kinds of events, so we would have missed them. We needed more.\n\n#### 3.4 Paris in the Summertime\n\nAnd so to Paris. The world was waiting. Some of it, anyway \u2013 that fraction of the world with at least a passing interest in particle physics, which seemed to be a bigger fraction than we were used to. Even President Sarkozy was going to turn up. Not only would the first results from the LHC be shown, but the last major update from the Tevatron was expected (with more rumours than usual circulating that they might have seen something Higgs-like or otherwise surprising), and on top of all that there was action in the world of neutrinos and the usual potential for surprises from anywhere else in the field.\n\nThe ICHEP is split into two, with a series of small sessions running in parallel for the first three days on fairly focused topics, then a day off, followed by three days of plenary talks, where ideally the details are pulled together and we see how physics has moved on.\n\nI registered, acquiring yet another geeky backpack, a pen and a map of Paris. Plus a dog tag with my name and 'ICHEP 2010' on it so that security wouldn't throw me out \u2013 more of a worry than usual given the President of the Republic's pending presence.\n\nIn one of the parallel talk sessions the audience were hearing how well the LHC detectors were working. I already knew that the answer from ATLAS was 'very well indeed', and the same turned out to be true for CMS, a major achievement and further evidence that neither of us had wasted the unwelcome extra year of preparation we'd had due to the failure in 2008.\n\nBeing a bit LHC-saturated, and partly for old times' sake, I went to another very crowded session where the latest HERA and Tevatron measurements of the W and Z bosons were being shown, along with the very first measurements of these particles from ATLAS and CMS. I got a curious feeling from this. To observe the W and Z bosons was by no means a surprise. They have been well measured in previous experiments. Rubbia and van der Meer won the Nobel Prize for their discovery at CERN in the 1980s. The LEP machine, which had preceded the LHC in its 27km tunnel, had made enormously precise measurements of the Z boson, and the Tevatron experiments had measured the W mass to better than one part in a thousand. Yet somehow, seeing them again, now in 7 TeV collisions, brought home to me in a surprisingly powerful way the anchor that experiments provide for our understanding.\n\nThe W and Z lead very fleeting lives, decaying almost immediately into other particles. They are gauge bosons generated by the symmetries of the Standard Model of physics,49 and according to this model their masses come directly from the Higgs boson (or, more correctly, the field associated with it). In a sense they are partly made up of the Higgs. This is all very weird stuff. But there are also very definite predictions. For example, when you plot the distribution of electron\u2013positron pairs in our collisions, you should see a big bump. And there it is. It works. Don't let anyone tell you quantum mechanics is only about uncertainty.\n\n49. See Glossary: Gauge Theories.\n\nIn fact, quantum mechanics, when used in conjunction with precision measurements of the properties of the Standard Model particles, allowed us to set some constraints on the mass of the Standard Model Higgs boson itself. This is because within the Standard Model, quantum corrections to some of the things we measure involve the Higgs boson indirectly,50 and they depend on its mass. By this stage, the least well-known, most important parameters to measure in order to constrain the Higgs mass were the masses of the W boson and the top quark, both of which the Tevatron experiments were reporting on. By the end of ICHEP, these constraints told us that if the Standard Model Higgs boson existed, there was a 95 per cent chance that its mass lay between 42 and 159 GeV. When the limits from the Higgs searches were included (from LEP and Tevatron) this became 114\u2013157 GeV.51 Of course these calculations were all made assuming that the Higgs existed and that the Standard Model was correct, so they were no substitute for actually finding the boson. But it illustrates again how predictive the Standard Model was, and how confident we were that we would either find the Higgs boson, or falsify the Standard Model, once we had enough data from the LHC.\n\n50. Via little loops in the Feynman diagrams, see Glossary: Feynman Diagrams. 51. These results were reported by Martin Goebel http:\/\/indico.cern.ch\/contributionDisplay.py?confId=73513&contribId=313.\n\nFloating significantly more freely from the anchors of experiment in the hard-core theory session was Erik Verlinde of the Institute for Theoretical Physics in Amsterdam, discussing the idea that gravity and general relativity may not be fundamental, but instead may emerge from the bulk behaviour of smaller things. If I understand it right, this would make gravitational waves essentially no more fundamental than sound waves. Fascinating, possibly a new direction, but as the speaker himself said, the theory needs to make some experimentally testable predictions.\n\nIn the final session of the first day we had presentations on the Higgs searches at the Tevatron particle collider at Fermilab in Chicago. The room was packed and I ended up hanging around outside, peering through the doorway and chatting with Gavin and Mike Paterson from the _Colliding Particles_ films. What we saw were the component parts of a number of different searches for the Higgs, carried out independently at the CDF (Collider Detector at Fermilab) and D0 (D-Zero) experiments. What became quickly obvious was that no one was going to announce a clear-cut observation of the Standard Model Higgs at this conference. What was not yet clear was how close we were, how much room the Higgs would have left to hide in (meaning what mass values would still be allowed for it), and whether there would be any hints of its presence. We'd have to wait for the combined results in the plenary sessions for that.\n\nI loved Saturday's session on jet measurements. There were talks from HERA, the Tevatron and the LHC, with the last including the jet cross sections I was involved with. Even though it switched the machine off in 2007, the HERA collaboration was still analysing its data and presented some really beautiful, precise measurements. The Tevatron also presented very good measurements. Of particular interest to me was its first measurement of the mass of a jet. Measuring jet mass is a good way to learn about QCD, but it is also important if you want to search for boosted particles using jet substructure, as I described in section 1.7. The CDF results showed that for 'normal' jets from quarks and gluons, the theory described the data quite well, to within a few per cent, which was good news.\n\nOne of the busiest sections of the conference was the session on neutrinos, an area of particle physics quite independent of the LHC that was making a lot of progress. I'll come back to what was happening there in later chapters.\n\nAs ICHEP moved from the parallel to the plenary sessions, some people left, some arrived, some, like me, stayed on. Sunday was a day off and featured the final stage of the Tour de France. The plenary sessions began with a grand opening by President Sarkozy, followed by the LHC summaries, a press conference, and the presentation of the combined, updated Higgs search results from the Tevatron by Ben Kilminster of Fermilab.\n\nDoing the femtobarns\/inverse femtobarns calculation for the Tevatron, it was possible to work out that if the Standard Model Higgs existed, about a thousand of them would have already been created at the Tevatron, with the exact number depending on the mass of the Higgs. But, as at the LHC, so at the Tevatron: they are incredibly difficult to dig out of the data. The CDF and D0 collaborations had now closed off a section of the possible Higgs mass range (158\u2013175 GeV), leaving the boson less room to hide. This raised the stakes, both for the Standard Model and for supersymmetry (of which more soon). Both prefer lower Higgs masses than this, so ruling out high masses strengthens their case. But both need the Higgs to be there, so ruling out some mass range threatens them.\n\nThe statement was that if the Tevatron could run until about 2013, and if the analyses kept improving, it would be able to rule out the whole mass range for the Higgs at some level, or find a hint of its existence if it was there. This would have set up some kind of race over those years between the Tevatron and the LHC. It wasn't to work out quite that way.\n\nSarkozy's speech gave a strong endorsement to the place of fundamental science in our society and economy, and powerful statements on the need to make sure that current economic 'urgencies and emergencies' would not harm its long-term future. This was a refreshing change from the edgy situation in the UK, where the new coalition government was planning its first budget in the middle of the economic crisis, and the Royal Academy of Engineers had just released a policy document urging that 'The overriding consideration for BIS [the Department for Business, Innovation and Skills] should be the impact of research on the economy in the short to medium term,' with a heavy not-even-subtext that pulling out of CERN would be a great idea. Given the long-term symbiosis of great engineering and science at CERN (where the LHC was led by a Welshman and then a Northern Irishman), this felt like a massive betrayal, or as one might put it more diplomatically, a 'missed opportunity'. The battle over science funding would continue in the run-up to the budget. And for ever, I suspect.\n\nThe week of ICHEP was followed by a small add-on meeting at LAL Orsay, the French national physics laboratory to the south of Paris, so I ended up spending the best part of ten days in Paris (one day was spent in unlovely Swindon, back in England, at research council meetings, so I do mean the _best_ part). I like Paris a lot, and Susanna came out for the weekend in the middle, so even better. My hotel was pretty dumpy but functional, and since it served breakfast in a nicotine-stained dungeon I went to a caf\u00e9 every morning, where the waiters were friendly and the view was better.\n\nThe _Colliding Particles_ crew (Mike and his soundman) were around most of the time filming, in part also for the _Guardian_ newspaper. They had also been to the previous ICHEP in 2008 in Philadelphia. One of my colleagues had actually seen the Philadelphia film and thought it was made in Paris. Of course Philadelphia and Paris are not so similar, so it is disorientating when they suddenly show commonalities. We had a meal in a small bistro in Paris, apparently off the beaten track but it must have featured prominently in some key guidebook since it turned out to be full of American couples plus their children, all drinking water. I became so culturally disorientated I spilled my wine all over the table.\n\nEnough tourism. ICHEP overall was a good reminder that older experiments can still throw up interesting stuff, even though new experiments may surpass them in many ways. The trade-off between old and new means the best physics from an experiment often comes close to the end of its lifetime.\n\nAll that said, the next two years would belong to the new kid on the block \u2013 the Large Hadron Collider.\n\n#### 3.5 Super Symmetry\n\nI realise this is in danger of reading like a travelogue, but I sort of have to mention that a couple of weeks after ICHEP I gave a talk at the SUSY 2010 conference in Bonn, because it is about time to bring supersymmetry (SUSY) into the story. For a variety of reasons it is not possible to discuss LHC physics for long without talking about SUSY.\n\nIt is a bit weird that there have been _21_ annual SUSY meetings, even though there is as yet no experimental evidence for SUSY playing any role in actual particle physics. Perhaps it's excusable. At least before the LHC switched on, SUSY was arguably the best way to improve the Standard Model of particle physics.\n\nAs you'll know if you read the Glossary on the Standard Model particles and forces, all the matter particles (quarks and leptons) are fermions, and all the forces are carried by bosons. You might (especially if you are a physicist) ask whether this is really a rule of nature, or a coincidence. What if you swapped all the bosons and fermions over, would the world be very different or not?\n\nThis is a very good question, by which I mean that asking questions similar to this has led us over the years to some very important and interesting answers. It is a symmetry question. Symmetry is probably the single most important concept in physics. One of the most important theorems we have, which applies to the classical and quantum regimes of physics, is Noether's theorem. This states (with some formal caveats that I am not going to go into here) that for every continuous symmetry in nature, there is a conservation law.\n\nThat may not leap out at you as being quite as profound and important as it is. But consider this:\n\n  1. Emmy Noether was a mathematician. She proved this. This is not just an opinion.\n  2. It means that because the laws of physics don't depend on where you are, momentum is conserved. Because the laws of physics don't depend on what angle you look at them, angular momentum is conserved. Because the laws of physics don't depend on when you look at them, energy is conserved.\n\nThat is a lot to get to grips with. But bear with me, it's worth it.\n\nBy the 'laws of physics' here, I mean the equations we use to describe the way physical systems behave. They are derived from a combination of observation and mathematics, they're provisional, this is not a religion (or a judiciary), and they work. When Noether talks about a continuous symmetry, she means, for example, there is a variable \u2013 call it _x_ , why not? \u2013 in my equation meaning 'distance from my house', and if everywhere in the equation I replace ' _x_ ' by ' _x_ plus _y_ ', where y can be any distance \u2013 a nanometre, a mile, the distance to the nearest chemist's \u2013 the equation still works. That's a continuous symmetry. It's called translational symmetry. If my equation (with _x_ in it) is the equation describing the motion of some object, the equation really will look the same whatever value of _y_ I choose. This symmetry leads directly to conservation of momentum, which is basically Newton's first law: An object will remain at rest or moving with a constant velocity unless acted on by an external force.\n\nStep back and think about that (I'm doing so myself as I write this). Noether's theorem connects the idea that there is no privileged position in space \u2013 that the physical rules that the universe obeys don't care where you are \u2013 with Newton's first law. It's really pretty stunning.\n\nContinuous, universal symmetries like that are very powerful. In fact, rotational and translational symmetries combined are part of a bigger symmetry called the Poincar\u00e9 symmetry group, which seems to be the symmetry group of space and time. As well as translations and rotations, it includes the symmetry that physics is the same whatever velocity you are travelling with, which is basically the principle that underlies Einstein's special relativity. And if you think by bringing Einstein into this I am appealing to authority, I'm not. I'm just saying it works, and it's amazing.\n\nThere's another class of symmetry that is also quite amazing. This is the class of 'internal' symmetries, related to the quantum numbers a particle can have. A 'quantum number' is a property that is intrinsic to a particle, such as the charge of an electron, or the color charge of quarks. If you invert the charge of all charged particles at once \u2013 so all electrons become positively charged and all protons become negatively charged \u2013 the electromagnetic force will look just the same. You won't be able to tell the difference.52 So 'charge inversion' is a symmetry of the electromagnetic force. These kinds of symmetries are also crucially important, and in fact all the forces of the Standard Model are derived from internal symmetries like these.53\n\n52. You will if you use the weak force, however. 53. See Glossary: Gauge Theories.\n\nSo symmetry is a really vital element of physics. This applies to fundamental particles, but also to other areas of physics. It is one of the most powerful mathematical tools in our toolbox, and appears in the natural world all over the place. It is, in general, pretty super.\n\n'Supersymmetry', or SUSY, is an extension of these ideas, and as I said before being diverted by Emmy Noether, it postulates a symmetry between bosons and fermions. In a perfectly supersymmetric universe, everything would look the same if you swapped bosons for fermions and vice versa. This is obviously not true \u2013 there is no boson around with the same mass as the electron, for instance \u2013 so supersymmetry can't be exact. But it could be a symmetry that is present in the underlying theory, but broken in everyday life. This could manifest itself as the fact that the bosonic partner of the electron (which we would call a selectron, for 'supersymmetric electron') has a mass much higher than the electron. But this mass might be low enough for selectrons (or other superpartners of Standard-Model particles) to be found at the LHC.\n\nSo while symmetry is firmly established as a useful principle in physics \u2013 and in particle physics in particular \u2013 supersymmetry has yet to prove itself. Why, then, have there been (at the time of writing) 21 conferences on the topic? As far as I can see there are three big arguments in its favour:\n\n  1. It helps with an important problem in the Standard Model.\n  2. It sort of predicts dark matter.\n  3. It looks nice.\n\nThe first of these is to do with the Higgs boson. Now, like SUSY, the Higgs boson had not shown up at this point. However, unlike SUSY, the Higgs boson is an integral part of the Standard Model, without which it doesn't work. There is a subtle problem with this, though. Because the Higgs boson, uniquely amongst all Standard Model particles, has no spin, its mass picks up a particular kind of quantum correction. If left alone to do their thing 'naturally', these quantum corrections tend to make the Higgs boson millions of times heavier than it has to be in the Standard Model. This was (and is) a real worry for the credibility of the theory. From one point of view, it makes the Standard Model look like a coincidence on the level of one in ten thousand million million (1016). This is about _a hundred times less likely_ than winning the lottery jackpot two weeks running if you buy a single ticket each week. SUSY gets around this because fermions give negative corrections and bosons give positive ones, so if there is an (even approximate) symmetry between the two, most of the corrections cancel each other out and the Higgs mass can be sensible without fine-tuning things to achieve such a crazy coincidence.\n\nThe second argument is to me the most compelling. Astronomical observations tell us there is probably some dark matter out there (or else we really do not understand gravity). Many SUSY models predict a particle that would be an ideal candidate for dark matter. It may be right behind you. When two different branches of science have problems that seem to converge on the same solution, look out for progress.\n\nThe third argument is essentially the fact that, as discussed, SUSY is a way of pushing ideas about symmetry, which have already been shown to be a great way of understanding nature, even further. Going back to the two types of symmetries (the Poincar\u00e9 group of external, space\u2013time symmetries, and the internal symmetries like charge), there is a theorem54 that states that external and internal symmetries cannot mix up amongst each other. Internal symmetry operations turn one kind of particle into another (for example, the matter\u2013antimatter symmetry operation turns electrons into positrons), whereas external symmetry operations move you around in space\u2013time (for example, the translation symmetry operation just moves an electron to a different place). But swapping a boson for a fermion does both, because while it obviously turns one kind of particle into another, it also involves a space\u2013time transformation, because spin is actually angular momentum. Angular momentum is a space\u2013time property, conserved because of rotational symmetry. So SUSY is a special loophole in the theorem that says internal and external symmetries can't mix.55 In fact it is the _only_ such loophole in a four-dimensional theory like the one we need to describe our universe. Since all the other available symmetries are exploited in nature, with elegant and far-reaching consequences, it is very attractive to suppose this last available symmetry should appear too.\n\n54. Coleman and Mandula, _Physical Review_ 159 (5): 1251\u20136 (1967). 55. Which was therefore generalised to the Haag-Lopuszanski-Sohnius theorem, if you really want to know. _Nuclear Physics_ , _B_ 88: 257\u201374 (1975).\n\nThose are three quite strong reasons for taking SUSY seriously. But they all have their weaknesses too. For the first one, maybe the universe just got lucky? Some string theorists might say we should be glad the odds were better than one in a 'landscape' of 10500. Or maybe we're missing something subtle in the Standard Model that might force these cancellations, so they happen without that fine-tuning, a bit like cheating on the lottery. For the second of those reasons, well, there are other theories that can also produce dark-matter candidates. And for the third, we know that many beautifully symmetric mathematical ideas have wrecked themselves on the rocks of data. We shall have to wait and see.\n\nMore prosaically, and from the point of view of an experimentalist more practically, another important feature of SUSY is its flexibility. It can appear in many different guises in an experiment, to the extent that almost any weird event we see could (and will, I bet you) be interpreted as a 'hint of SUSY'.\n\nFor example, a big part of my doctoral thesis involved simulating a SUSY process that we might have seen at the electron\u2013proton collider, HERA. When you whack protons and electrons together, one thing that might happen is that the quarks in the proton stick to the electron. This would be a 'leptoquark' (because electrons are leptons) and would be a sign of the unification of the strong, weak and electromagnetic interactions \u2013 so-called 'Grand Unification'. Very exciting stuff.\n\nJust before we switched on, JoAnne Hewitt, a theorist at Stanford, realised that the signature of a leptoquark also looked like a particular form of SUSY. Herbi Dreiner, then a postdoc at Oxford (and later organiser of SUSY 2010), had realised that if so, there would be other ways it could decay, and he calculated them.\n\nI remember his calculation being given to me on a napkin, but my memory may be embellishing here. Anyway, I wrote a program predicting how the events might show up in our detector, so we could search for them. Sadly, they never showed up, though we did have a bit of a false alarm at one point.\n\nOf course, SUSY is one of the things we might find at the LHC. In fact I have even written a couple of papers on some possible signatures. (Which is one reason I was talking at SUSY 2010.) Basically the 'boosted, jet substructure' type ideas I was trying to spread have some application to SUSY searches as well as to Higgs searches.\n\nThis flexibility makes SUSY a good test case for experimentalists to make sure we aren't missing anything. If we are alert to all possible SUSY processes, we are alert to a very wide range of weird stuff. However, when weird stuff doesn't show up, as so far it has not, that unfortunately does not disprove SUSY, it just rules out a given subset of SUSY models. This can be frustrating.\n\nStill, to its credit, if there were no low-mass Higgs, SUSY would lose much of its attraction. It would not quite be ruled out, but it would certainly be relegated down the ranks of speculative theories. Conversely, therefore, if we were to find a low-mass Higgs, the search for SUSY would become much more compelling.\n\nI can't really give an account of the meeting because I could only be there for one day. But even on that day you could see the change of mood now that people were finally showing real LHC data rather than simulations. So far the data hadn't broken new ground in the search for SUSY, but it was obvious it would not be long before they would. At the time of the meeting we had about three inverse picobarns of data.56\n\n56. See Glossary: Cross Sections and Luminosity.\n\nAfter about 50 inverse picobarns we would pass the Tevatron in the search for SUSY \u2013 and within a year, we were expecting to have collected about 1000 inverse picobarns \u2013 that is, one inverse femtobarn. Not only were we accumulating a lot of data, we were doing so at an increasing pace.\n\n#### 3.6 Names, Fame and Citations\n\nA citation is when one scientific publication refers to another. The number of citations a paper receives tells you something, but it is often quite hard to work out exactly what. In experimental particle physics this is even trickier than some other fields, partly because the author lists are so long. The reasons they are so long are tied up with the challenges of how such a big collaboration actually works.\n\nCounting how often your papers are cited is one way to estimate how much influence your work is having, and it's very tempting to keep watching them. Especially when assessments by funding bodies, or promotions, hang in the balance.\n\nBefore ATLAS started publishing, my most highly cited papers were measurements of proton structure from ZEUS. These were important measurements, and I helped build and run the experiment, but I made no direct input into some of those papers. ZEUS had about 400 physicists signing the papers. About 3000 people signed the first LHC papers.\n\nThis is common practice in particle physics, for good reasons. But people do ask how it is possible for individual scientists to make a reputation, even a career, in these circumstances. It is a good question. Funding agencies and interview panels ask it too. Mostly, the answer is that 3000 people is a big peer group. People in there will know who does what, who really contributes and who doesn't. References count, as does authorship of important internal notes often accompanying the collaboration publications. The ability to work hard and well in a collaborative environment is at a premium \u2013 this is part of what makes particle physicists employable outside of the area, according to friends in industry \u2013 and prima donnas and time-wasters get quite widely known as such.\n\nOur author lists are long and alphabetical. We discuss trimming or ordering them every now and then, and have always concluded that to do so would at best waste even more time, and at worst break the experiment. We already have far too many meetings, rivalries and resentments, and arguing about author lists, or the ordering of author lists, would likely make this much worse. The current practice is not perfect, but it works, and we haven't thought of a better way yet. The author list is a tangible expression of the fact that we are, all 3000-odd (yes, odd) egos, in it together. We need that kind of solidarity when things go wrong. And they do go wrong.\n\nThe man who headed the UCL high-energy physics group when I was appointed to the faculty was Tegid Jones. He is a fount of wonderful stories (many involving opera singers) and responsible for several new particle-physics words in the Welsh dictionary. His stories include an account of the water-filled proton-decay detector he worked on in a salt mine \u2013 the IMB (Irvine\u2013Michigan\u2013Brookhaven) experiment. When first filled with water, the experiment leaked, dissolving quite a lot of the mine and almost drowning the PhD hopes of a future congressman, amongst others. On the next attempt, it somehow achieved a 490m siphon effect with a cesspit on the surface, which was very bad for the optical purity of the water. After the third filling, it worked, but they failed to find proton decay. Not due to incompetence, but because protons don't decay, it seems.\n\nSticking together under such duress requires that everyone is in it together, and for scientists that means the author list. In the end, as well as setting limits on the time taken for some proton decays at about 1023 times the age of the universe, IMB did observe neutrinos from Supernova 1987a. This event (in 1987, as the name suggests) was the first observation of neutrinos from outside the solar system. IMB also developed a lot of the techniques taken forward by Super-Kamiokande, the experiment in Japan that eventually made the first measurement of neutrino oscillations.57\n\n57. See 5.5 Meanwhile in the Neutrino Sector.\n\nWith ZEUS and ATLAS, I'm lucky to have been involved in the start of two major particle-physics colliders. In the first year of my doctorate research on ZEUS, data-taking seemed a long, long way away. Life consisted of unintelligible code, meetings full of acronyms, and schedules that slipped by a month every few weeks. Like (I am told) war, the ZEUS UK software meetings consisted of long periods of boredom followed by sudden violent conflict. While some senior colleagues got all excited about obscure software, the ZEUS Central Tracking Detector (the main UK contribution to ZEUS and _essential for all the physics_ \u2013 a phrase we all had tattooed on our foreheads to impress the grant panels) was leaking gas and looking like it might never work. HERA started late, and more slowly than planned, and the ZEUS tracker was missing a lot of electronics when we began. However, the leaks were fixed, the electronics arrived, and in the end the tracker worked brilliantly for 15 years. ZEUS (along with our rivals H1) produced the best information we have on the internal structure of the proton, and made major advances in our understanding of the strong interaction (QCD).\n\nThe LHC also had a very public failure at the start, of course. Throughout all these tribulations, the collaborations, and their unfeasibly long author lists, stuck together.\n\nSo, I have hundreds of scientific papers to my name, and my degree of direct involvement in them varies wildly. I have my favourites, of course, the papers in which I recognise my own words, plots and ideas, as well as the results of my experiment.\n\nEven amongst these, the top two at the start of the LHC were funny ones. The top 'paper', which I actually partly wrote and edited, contains no real data and no original theoretical ideas, and is not even published in a journal. It's an 1852-page tome containing preparatory studies for using the ATLAS detector. It was useful (though now obsolete) and the fact that it was cited a lot showed the level of interest in ATLAS, so it's fair in that sense.\n\nNext down was a real paper from ZEUS. We reported the mass we measured when two types of particles produced in our collisions were combined: neutral kaons and protons. The neutral kaon is (like the pion) a meson \u2013 that is, it consists of a quark and an antiquark bound together, in this case a mixture of strange quarks and down quarks.\n\nWe made this measurement because some other experiments had seen a bump in the mass distribution they got when they combined neutrons with charged kaons, which might have been the first observation of a hadron made of five quarks. In the Standard Model, all the hadrons we know of are made of either one quark and one antiquark (mesons) or three quarks (baryons). If it really was a five-quark thing \u2013 a pentaquark \u2013 this would mean:\n\n  1. Big physics news, and\n  2. There should be a similar bump in our mass distribution.\n\nWe indeed saw a bump, though it was not completely compelling statistically and not necessarily in exactly the right place. Anyway, we did our job, we reported what we saw, and this was during a flurry of excitement so we got cited a lot. Sadly it looks like that particular pentaquark thing was a false alarm. Our bump may have been real, but something else, less interesting. Anyway.\n\nFurther down were lots of papers I'm more pleased with, some of which I've already mentioned. But the point is to illustrate how dangerous citation counts can be as an indicator of merit. I'd happily lose the top two papers before most of the next ten, because the next ten contain more data or more original ideas. They advance knowledge more.\n\nThe idea that the planets orbit the Sun dates back at least to Aristarchus of ancient Greece. Even the work of Copernicus, who is credited now with the first accepted heliocentric model of the solar system, was ignored for many years. Copernicus and Aristarchus would have struggled for promotion and grants based on citation counts during their lifetimes.\n\nIt is sometimes hard to fathom why some good ideas or important measurements languish in obscurity for ages while others have a rapid impact. I often wonder how much the name of a project influences this. Maybe having a catchy, memorable name helps. But then what constitutes a good name? Particle-physics project names seem to come in two types: the fancy names and the simple acronyms. Sometimes (rarely) they are both.\n\nThe LHC is obviously in the second category. Large. Hadron. Collider. Does what it says on the tin, as long as you realise the collider is big, the hadrons are small, and you spell them correctly.\n\nCMS too. Compact Muon Solenoid. Actually it's 21m long and 15m by 15m thick, but compared to ATLAS it's compact.\n\nATLAS is a fancy-name type, really, though it makes a stab at being an acronym with 'A Toroidal LHC ApparatuS'. Flaky, if you ask me. Just be out and proud with your big strong classical allusions, I say.\n\nOn HERA (Hadron Electron Ring Anlage. Nice \u2013 classical, catchy and a proper acronym) there was an experiment called H1. Logic demanded that the other would be H2, but I guess someone rebelled and called it ZEUS. All very erudite, if a little Freudian. It had a novel calorimeter, made of scintillators and depleted uranium borrowed from the US (we sent it back when we had finished with it). The wits of H1 decided ZEUS was an acronym for 'Zero Experience with Uranium Scintillator'. How we laughed. But the calorimeter worked very well, so who cares.\n\nIt does go to show that you can make almost any name into an acronym if you try hard enough. Even ALICE is A Large Ion Collider Experiment (not bad, actually). There are limits, though. One of my most often cited papers, which I do like, illustrates this.\n\nBack in 1993, Jeff Forshaw and I put some cosmic-ray calculations together into a program to generate multiple quark and gluon scatters. We couldn't think of an acronym right off, but we needed to call our terrible FORTRAN 77 code something, so we operated under the working title of Jimmy Generator because it was mildly amusing and easy to say. We were confident we would eventually either work out what Jimmy could stand for or find a better name. The program lives on (after some help from Mike Seymour and a paper published with him in 1996). It was one of the main programs used to simulate the hadronic environment at the LHC during the first three years of running, and I have sat through many serious presentations with 'JIMMY' appearing on important plots. The paper with Mike and Jeff is now one of my highest-cited papers, and the program is still called Jimmy Generator. And I still don't know what it stands for.\n\n#### 3.7 Another Layer of the Onion\n\nI wrote in section 2.6 about the calorimeters, which constitute one or two layers of the 'cylindrical onion' of detector technologies with which ATLAS and CMS surround the proton\u2013proton collision point at the LHC. Each layer tells us something distinct and important about the particles produced in the collisions, thus allowing us to work out the underlying physics.\n\nThe calorimeters measure the energy deposited by particles that stop in them \u2013 and by design that is as many particles as possible. The lead tungstate crystals and liquid argon of CMS and ATLAS respectively are chosen to be as dense as possible in order to achieve this. The lead crystals of CMS are wonderful objects. They are as clear as glass, but many times heavier.58 They also, as an aside, absorb X-rays very efficiently: Dave Britton, who is now an ATLAS colleague but used to be at Imperial on CMS, told me of a time he took some crystals in his hand luggage from CERN to London for testing. They showed up in the scanner like lead bricks would. When his bag was searched, the security officer took an awful lot of convincing that the glass block he could see in the bag was the lead brick he had seen on the scanner.\n\n58. At the CMS experiment visitor centre they have pairs of crystals, one glass, one lead tungstate. They look identical but you can pick them up and feel the difference in weight. Even when you know what to expect, it is remarkable.\n\nBut it was. Lead tungstate, like any good calorimeter material, is very dense. Hadrons, photons, electrons \u2013 all the particles stop. The two known exceptions are muons, which leave some energy behind but do not stop, and neutrinos, which leave no trace. Muons we can follow later, but neutrinos we can do nothing about, except deduce that they were probably there from the momentum imbalance in a collision.\n\nHowever, even for the vast majority of particles, where the calorimeter can tell us their energy, we need more information. This is where the inner layer of tracking detectors comes in. They allow us get precise information on the actual path a particle takes from its creation in a collision to its impact at the calorimeter.\n\nThere are several reasons we need this information. For example, while it is usually a safe assumption that the particles came roughly from where the LHC proton beams cross, this is not a very tight constraint. We would really like to know very precisely \u2013 within a few tens of microns if possible \u2013 where they came from. This information can be combined with the information from the calorimeter to obtain a good measure of a particle's direction as well as its energy.\n\nAlso, there are usually several proton\u2013proton collisions happening at the same time, a phenomenon we call 'pile-up'. This happens because the beams are dense, which is good for increasing the luminosity. However, pile-up is bad and confusing, since we really want to measure particles from an individual collision. If we can track a particle back to an individual collision vertex we can throw away the pile-up particles and focus on the ones we really want.\n\nWe can also see if a particle came directly from the collision vertex, or if some other particle was produced that travelled a little way and then decayed, giving a 'secondary vertex'. Tau leptons, and hadrons containing b quarks, generally do this, and detecting them is important for lots of measurements. For example, these are the two heaviest fermions the Standard Model Higgs boson could decay to (unless its mass was very high so that it could decay to top quarks). For some possible values of the Higgs mass, detecting taus and b quarks would be essential for a discovery.\n\nFinally, if we apply a magnetic field, which we do, then the curvature of the path of a charged particle will allow us to measure its momentum. High-momentum particles will travel in a nearly straight line, while lower-momentum particles will bend a lot. The lowest momentum of all will go in circles.\n\nSo, for all those reasons and more, we build an inner onion layer of tracking detectors. The main technology used is silicon. Silicon is a semiconductor.\n\nIn an isolated atom, electrons are bound to the atomic nuclei. They are in discrete energy levels. We know this because we see electrons jump between different energy levels, emitting and absorbing photons with distinct energies as they do. Each photon's energy corresponds to the distance between two levels. In fact, by observing the emission and absorption of photons we can actually work out which atoms are present in a material. This is the field of spectroscopy, and it is how we know what stars are made of, even though we have never visited them.\n\nThese energy levels are the quantum-mechanical solutions behind the discrete electron orbits that Niels Bohr proposed in his model of the atom. This was the first model of an atom to have the nucleus and the electrons in essentially the correct relationship, and understanding it was a key point in the development of quantum mechanics as a theory.\n\nAnyway, in an individual atom the electrons are stuck. What happens to this situation when you bring lots of atoms closer together to make a material?\n\nIn the case of an electrical insulator, nothing much. The electrons remain stuck to their individual atoms.\n\nHowever, in some materials, metals for example, the upper electron energy levels of neighbouring atoms merge. This means that the electrons are free to move, without changing energy, throughout the material. Thus they can carry an electric current. This is an electrical conductor.\n\nA semiconductor is, as you might guess, the borderline case. In fact, in its pure form, a semiconductor such as silicon is an insulator. Some energy levels have merged, but they have no electrons in them, so no current can flow. However, if there is a small impurity or fault in the material, a few electrons can escape into the merged energy levels and can then carry a current. By careful introduction of impurities, this effect can be controlled very precisely. This is the physics that lies behind the whole of the computing industry. Silicon chips are semiconductors with impurities that define exquisitely intricate circuitry, responsible for the words appearing on the screen as I type this sentence right now.\n\nA semiconductor detector in particle physics exploits the same effect. When a charged particle passes through a semiconductor, it can knock into some of the electrons, giving them the tiny amount of energy they need in order to escape into the merged energy band. By applying voltages across the detector, we can make these electrons flow as a current, count them and work out where they were released. This tells us a particle passed close by, and from many of these 'hits' we can work out the path \u2013 track \u2013 of the particle.\n\nThis is the latest in a long line of particle-tracking technologies, and it is the best we have so far because it is very fast (important given the rapid collision rate at the LHC), very precise (we can tell to within a few tens of microns where a particle passed by) and also it takes very little energy to release an electron.\n\nThe last point is important because we want to measure the original energy of a particle produced in a collision. Every time it collides with a piece of material in our detector, its energy changes, and the original energy and direction are obscured a little. Every time it gives some energy to an electron and releases it, the original energy and direction of the particle are obscured further. And remember, this all happens before the particle reaches the calorimeter where its energy will be measured. With a semiconductor, the production of electrons is very efficient, so the amounts of material can be rather small and measurements of the original energy and momentum remain precise.\n\nEven though these scatterings and energy losses are, hopefully, small, it is an important part of understanding and calibrating your detector to measure what they are. When constructing the detectors, we keep a record of how much material is in there and where it is \u2013 not just the semiconductor sensors themselves, but the data cables, the mechanical supporting structure, the high-voltage cables. The detectors also have to be kept cool (otherwise thermal energy can release electrons and give spurious signals) and so there is a whole infrastructure for doing this \u2013 in ATLAS we use C3F8 (octafluoropropane, a CFC) gas as a coolant.59\n\n59. We do not let it get anywhere near the ozone layer.\n\nAll the information from the construction is coded up into a computing model of the detector. There's an open-source software project called GEANT, initiated at CERN but now with many collaborators, which provides a toolkit for putting together materials and geometries and simulating how various particles interact with them and with electric and magnetic fields. GEANT is now widely used in applications from space science to medicine. While we were using it to understand ATLAS events, Lewis Dartnell was down the corridor at UCL using it to see how deep underground on Mars any bugs would have to hide to escape cosmic radiation.\n\nThese semiconductor detectors only register particles that have electric charge. For example, neutrons and photons do not show up. However, photons are rather useful for working out whether our GEANT map of the detector is in fact accurate.\n\nOccasionally a photon will interact with the material (if there is a lot of a material it definitely will, of course \u2013 this is what happens in the denser calorimeter). One of the things that can happen in this case is that the photon converts into an electron\u2013positron pair. These particles are now charged and we can track them as they spiral away from each other. We can therefore see where they were produced. If you bathe the detector in enough photons (which the LHC certainly does!) then you can build up a map of the material from these production vertices, since the density of vertices will be proportional to the density of the material. The more material in a particular region, the higher the chance of an interaction, and so the more vertices.\n\nThis allows amazing maps to be made, where in the pattern of dots (one dot per vertex) you can see the silicon detector modules, the cooling pipes, the cables and the carbon-fibre supporting structures. We can make the same maps for our simulated detector, and check that we really do know what we are doing \u2013 and correct our simulation if we don't!\n\nI presented all this stuff at a meeting at the Rutherford Appleton Laboratory in September 2010. The day ended with Jeff Forshaw arguing about what a particle _really_ is, when you get right down to it. At 3 a.m. in the bar. I missed most of that, since I went to bed at 1 a.m., so possibly I still don't know.\n\nBut it's something to do with all those dots.\n\n#### 3.8 Into the Unknown\n\nThe first LHC paper really to probe for new physics was submitted by ATLAS to the preprint server60 and to _Physical Review Letters_ on 13 August 2010.\n\n60. <http:\/\/arxiv.org\/abs\/1008.2461>.\n\nThere had already been one paper (by CMS) on minimum bias results in 7 TeV collisions.61 That was the first paper from the high-energy collisions. There were also numerous preliminary results from all the LHC experiments. But this ATLAS paper had got to step 13 of the approval process62 and was therefore considered 'final' by ATLAS. It was the first paper to contain results from collisions between quarks and gluons at energies beyond the reach of the Tevatron. This was the point that we were really, confidently, reaching out into new territory.\n\n61. See 2.1 Low-Energy Collisions and Electronvolts. 62. See 3.2 This Is Not a Drill.\n\nThe paper set exclusion limits. This means we hadn't seen anything unexpected, but we had pushed the boundaries of our knowledge of fundamental physics up a notch in energy. More data were still coming in and the measurements were getting more precise. The exploration had really begun in earnest.\n\nGlossary: Gauge Theories\n\nThe concept of 'gauge symmetry' is at the heart of the Standard Model, and so I want to try and explain it. But to be honest, while I do understand the mathematics behind it, it is something I struggle to hold an intuitive picture of in my mind. Most of the things I talk about in this book I do have such a picture for \u2013 that's how I understand physics \u2013 but this one I don't, right now. So here I am trying to make it up as I go along.\n\nConsider a snooker table (if you are American, consider a pool table). Consider the way the balls on the table interact with each other and how they move. They will obey Newtonian mechanics, trundling along at a constant speed in a constant direction until they bounce off another ball or a cushion. Eventually they will slow down and stop as they lose their energy of motion due to friction.\n\nThere is a symmetry within the physical equations describing how the balls behave. Actually there are several, but consider one of them. Imagine if the table is raised by 50cm. While this would make it harder to play snooker, it will not affect in the slightest how the balls move and interact with each other, as long as the table is raised by the same amount everywhere \u2013 that is, it stays flat and level.\n\nThis is an example of a 'global symmetry'. Some variable (the height of the table) changes everywhere at once (i.e. globally) and it has no observable effect on the physical system (the snooker balls).\n\nNow, there are such symmetries in what we currently think are the underlying physical laws of the universe. I will give a real example shortly. But carry on with this case study for now. If the snooker table is the whole universe, it is a bit weird to think of it all changing at once. What, in fact, does 'at once' even mean? Since nothing travels faster than the speed of light, there is no absolute definition of everything happening 'at once'. Time depends upon speed, so what appears 'at once' to one observer will be a change that gradually moves across the table to another. The laws governing the interactions between the snooker balls should not depend on the speed of the observer, so this is all highly suspect. Put it another way \u2013 if the snooker table is 100 light years across and I raise one end of it, the soonest the far end can even know that the other end has been raised is 100 years later, since nothing travels faster than light.\n\nSo let's try making the symmetry bigger. Let's say the laws of physics have to be the same, have to be symmetric, under _local_ changes in height, not just global ones. If the snooker table is being raised, to some observers it might all happen at once, but to others there will be moments when one part is higher than another. But for all of them, the physical laws must look the same. What are the consequences?\n\nWell, obviously we will see some balls running downhill, or slowing down as they try to go uphill. If there is a dip in the table, balls will speed up as they run down it and collect at the bottom. If there is a hill, the balls will be repelled from it. These are observable differences, and they break the requirement that physics should look the same to all observers. To make the motion of the balls consistent for everyone, you have to introduce some kind of effective force acting on the snooker balls to get them over the hills and through the valleys \u2013 this is the gauge force.\n\nThis is not a perfect analogy, no analogy ever is. But the business of taking a global symmetry and making it local is what is called (for reasons that remain obscure to me) 'gauging' the symmetry. This really, really works and is very powerful. Here is a real-world example. It involves particles behaving like waves, so it's trickier than snooker balls, but it is no longer an analogy, it is a description of what actually happens in the theory, and the theory describes real life very, very accurately.\n\nElectrons behave like waves. So they have peaks and troughs, and they have a phase that tells you when a peak (or a trough) is coming at you. If two electrons have peaks and troughs lined up, then the chance of finding an electron there is doubled. If the peak lines up with a trough, they will cancel out and you won't find any electrons.\n\nThe important fact here is that the only thing that makes any difference is the _relative_ phase \u2013 are they lined up or not? If you change the phase of all electrons at the same time all over the universe by the same amount, absolutely nothing happens. This is like raising the snooker table while keeping it level and flat. It is another global symmetry. In group theory, this phase shift even has a name, it is the symmetry group called U(1). Actually, as I mentioned63 when talking about Noether's theorem, this symmetry imposes a conservation law, which in this case turns out, remarkably, to be conservation of electric charge.\n\n63. In 3.5 Supersymmetry.\n\nLike the snooker table, it is unrealistic, meaningless even, to think of changing the phase of every electron everywhere in the universe at the same time. So we should consider the possibility of it changing by different amounts in different places. And we should see what we need to do in order to make sure that the physical laws look the same even if this happens. Just as with the snooker table, what we have to do to achieve that is introduce a force. In fact, if you require that nature respects this U(1) gauge symmetry, you must introduce a very specific force: the electromagnetic force. In terms of quantum field theory, you have introduced a gauge boson \u2013 the photon.\n\nThose words describe the maths; they aren't an analogy, they are a description in English of what happens in the equations. It is a beautiful thing to see.\n\nThere are other symmetry groups possible, not just U(1). Imposing a gauge symmetry based on the group called SU(2) gives rise to the W and Z. Using SU(3) gives you the gluon. This is why the photon, W, Z and gluon are called gauge bosons (and the Higgs boson is not, because uniquely it is not derived this way). This is why the Standard Model is referred to in the literature as a U(1) x SU(2) x SU(3) gauge theory. And this is why physicists sometimes seem obsessed with symmetry \u2013 it is beautiful, powerful, and it works.\n\nThe thing to take away from this, even if my pictures didn't work for you, is that all the forces in the Standard Model have to be based on these local \u2013 gauge \u2013 symmetries, and the bosons that carry them are therefore gauge bosons.\nFOUR\n\n## Standard Model\n\n### October 2010\u2013April 2011\n\n#### 4.1 Science is Vital\n\nIn October 2010 I went on a demo for the first time in more than 20 years. The previous occasion had been to shout either for the abolition of Margaret Thatcher's poll tax or for the retention of student grants. Averaging over both would give me a 50 per cent success rate. Probably there should have been others in between. Oh well. This one was for science.\n\nTo the extent that scientists form a community, it has rarely been mobilised in an overtly political way. Some individual scientists are very politically engaged, some are scientific advisers to the government, and certainly there have been lobby groups to protect research funding before. But I can't think of another time when such a broad-based coalition of scientists ever got together to voice a single message and hold a public demonstration in Whitehall, London, outside the Treasury.\n\nThe circumstances were unusual. The mobilisation for the Science is Vital demo was begun by Jenny Rohn, then a researcher in life sciences at UCL and a writer, along with CASE (the Campaign for Science and Engineering) and many other fellow travellers. Some of them (for example the former Liberal Democrat MP Evan Harris and Ben Goldacre of _Bad Science_ fame) were longtime pro-science campaigners whom I had met during the libel-law campaign (still ongoing, though without demonstrations). I was a participant rather than any kind of organiser, but from my point of view the message of the campaign was extremely well chosen.\n\nWe were in the middle of an economic crisis and we had a new government. Everyone knew cuts in government spending were on the way. The previous government had said lots of good things about science and under Lord Sainsbury as Minister of Science and Innovation these words had largely been matched by action. However, when he had stepped down in 2006 the wheels seemed to come off. In particular, massive cuts had hit particle physics and astronomy when two research councils were merged to form the Science and Technology Facilities Council, or STFC (presumably to the annoyance of neighbouring Swindon Town Football Club). Two subsequent science ministers had seemed either not to care or to be unable to do anything about it.\n\nI had watched and participated in this long and very painful process as both a particle physicist and a member of various STFC committees. One high point had been a visit to see the Secretary of State responsible, John Denham, in July 2008, when I'd got to meet Peter Higgs for the first time. Peter Higgs was rather eloquent about the importance of fundamental physics, and John Denham and his then Science Minister, Ian Pearson, had listened and discussed it with us politely. But there had been many low points. In the end, after years of damage, Lord Drayson, the third science minister in the three years since the formation of the STFC, had set up a structure that, while it did not fix the damage that had been done already, did resolve some of the organisational issues that had contributed to the crisis.\n\nAfter that nightmare, the particle-physics and astronomy communities were anxious to point out that they had already been severely cut, even before the financial crisis, and we were anxious that the good work done in the end by Lord Drayson should not be undone. The rest of the science community had not had to suffer all the problems of the STFC, but were also very worried that basic science might be seen as an unaffordable luxury in tough times rather than a critical investment for helping make times less tough.\n\nThe whole process had taught me that there are many different politically useful ways of making an argument. Winning an intellectual argument, or establishing the truth through evidence-based discussion, is one thing. Getting anyone to pay attention and act on the conclusions is another. Hence my presence at the demo. We had to tell the public and the politicians that the UK has something precious (as in valuable _and_ vulnerable) in its scientific capability, and in fact in its research and education more generally. And it was not enough just to tell politicians behind closed doors, no matter how eminent the attendees at the meeting. The public needed to know and the politicians needed to know that the public knew. We could not afford to keep quiet.\n\nWhen I was a PhD student, I did 'safety shift' on the ZEUS detector on one of its very first nights of data-taking (sometime in 1991). ZEUS was a massive particle detector, about 20m high and mostly hidden behind concrete shielding. Safety shift was a good one for inexperienced graduate students. Just plod around every hour reading dials and ticking a list, and report anything strange to the shift leader.\n\nAt some point during the shift, someone saw water dripping out of the bottom of the concrete shielding around ZEUS. This was very bad. A leak could do horrendous damage to the delicate instrument we'd spent years building.\n\nPeople rushed around. The water was turned off, the procedure for opening the detector began, and various senior physicists appeared and went into a huddle with the shift leader.\n\nWell below the level of this activity, I plodded on with my safety round. I noticed in the 'rucksack' (three floors of high-speed electronics in a metal box) that one or two of the temperature dials were slightly outside their allowed range. I went down to the control room again. Strictly speaking, I should report this. But everyone was so busy with important stuff. What to do?\n\nFor science funded via the STFC, the water had begun dripping in 2007. In the years between then and the Science is Vital demonstration in 2010, cuts in research grants of around 40 per cent had been imposed. I had been sitting on various committees, trying to decide which great science to kill in order to try and save the rest. Stressful, unpleasant work in which the 'best' outcome is still dreadful.\n\nThere had been petitions, select committee reports and more. All through this, various important people in science policy were buttonholing scientists behind the scenes, saying things along the lines of 'Don't make a fuss, we see the problem and we'll sort it out. All this noise is counterproductive.' Sometimes some of us had believed them, not realising that often their only goal was to keep a lid on things while the policy was implemented. It's true that shouting, on its own, won't solve anything, and abuse is usually counterproductive. There need to be serious, sensible arguments based on strong evidence. But keeping quiet is a sure way to be ignored.\n\nThere had also been an undercurrent of 'Do you really want the public to know how much money we spend on stuff like astronomy and particle physics? Sure, _we_ know it's not useless, but _they_ won't understand, and if you make a fuss you'll get _no_ support.' Thankfully, on that one we hadn't believed them. And at the demo we didn't just have our woe about cuts to tell the public. There was exciting science being done. The LHC was a big story, but there were plenty of others: the Planck satellite had been launched in 2009, for example, and there were great images from Cassini when it arrived at Saturn's moon. Somewhat to our surprise and relief, the public response had been overwhelmingly positive, even after the breakdown of the LHC in 2008. We also received a lot of support from fellow scientists who were sadly now in danger of being in the same boat and who were all represented at the demo.\n\nBack at ZEUS, I nervously tapped the shift leader on the shoulder and showed him the reading. The effect was dramatic. He leapt out of the room, ran up the stairs and pressed the emergency power cut-off for the entire rucksack. They had turned off the cooling water but not the electronics. A few more minutes and the delicate, expensive electronics, the product of years of work, would have fried.\n\nCarrying on doing science, if you are lucky enough still to be able to, can sometimes be the best way of influencing the outcome. But keeping quiet, no matter what the appearances, will get you nowhere and may be terminal. Scientists have to be part of the political debate about both their own funding and the relationship between science and the society that supports it and benefits from it.\n\nWhen the budget settlement did come out, there was a cut for science, but less than most areas of government spending, and much less severe than some of the scenarios that had been proposed, which would have meant the loss of hundreds of research posts and studentships, and would most likely have forced us to close major scientific facilities in the UK or renege on some international commitments. Science is Vital was credited by some with being a significant factor in this relatively benign result. It is impossible to be certain how influential it really was, but it was our duty and we did it.\n\n#### 4.2 Science Board\n\nComplaining about science-funding decisions is an occupational hazard of being a scientist. Rather than complain from the sidelines, I prefer to get involved (and then still complain). That's one of the reasons I spend quite a lot of my time on various research council committees, a job that can be both stressful and dull \u2013 a peculiarly unpleasant combination. On the other hand, you learn quite a lot about how things work, meet quite a lot of interesting and smart people, and get to see quite a lot of good science. Sometimes you are even able to fund it.\n\nIn October 2010 I was a member of the STFC's Science Board and we visited the Harwell campus in Oxfordshire. We saw the Diamond Light Source,64 a bunch of really very big lasers, and ISIS. ISIS is a storage ring that provides beams of neutrons for lots of science applications. It is one of the things we were able to fund, at least partially, over this period.\n\n64. See 1.1 Why So Big?\n\nNeutrons are hadrons; like protons they are made of three quarks, but because they have two downs and an up they have no electric charge.65 The neutron was discovered by James Chadwick in 1932. Without it, atomic nuclei would not hold together. Neutrons can also break up nuclei \u2013 depending upon what one does with them this can be explosive, or can run a power station. Because they are neutral, you cannot use electric fields to steer or accelerate them. They do have a magnetic dipole moment, but it is very small, making it much more difficult to guide them with magnetic fields. At ISIS, a beam of protons is smashed into a target and the neutrons fly off \u2013 produced when the protons hit atomic nuclei in the target.\n\n65. \u2013 \u2153 \u2013 \u2153 + \u2154 = 0.\n\nYou can put various things in front of a beam of neutrons. Again, because they carry no electric charge, they ignore the cloud of electrons around atoms and molecules, and just 'see' the nuclei. How strongly they see them depends on the kind of nucleus. For instance, water molecules consist of two hydrogen atoms and an oxygen atom (H2O), and neutrons scatter very strongly off the hydrogen \u2013 they can transfer energy to it very efficiently, largely because a hydrogen nucleus is simply a proton, which has almost the same mass as a neutron. (Just as in a head-on collision between snooker balls with the same mass, the incoming ball can stop dead, transferring all its energy to the ball that it hits.) This means that, studied with a beam of neutrons, water shows up very clearly. However, aluminium (along with many other metals) is almost transparent to neutrons (neutron-nucleus-scattering cross sections vary wildly with the mass, spin and internal structure of the nucleus). This was illustrated to us with a cute video of coffee being made _inside_ an aluminium espresso percolator, seen through the walls by neutron scattering. More serious applications include watching liquid flow around inside a high-tech engine in order to study obstructions and optimise the design.\n\nThere are several other applications. Scientists and engineers come from all over the world to use neutrons from ISIS. Another major commercial application is the investigation of the effect on electronics of the cosmic-ray air showers caused by high-energy particles from space hitting the atmosphere.\n\nElectronic devices rely on semiconductors. Like the tracking detectors in ATLAS and CMS, the electrons in semiconductors need only a little nudge and they can carry an electrical current. This is why they are good for tracking particles, and it is also why we can use them to build complex solid-state devices by arranging exactly how and when any current will flow. Every electronic chip in the world is made like this, including some quite critical ones, such as those steering aeroplanes. Unfortunately, the electronics in these complex chips can still get a nudge from a passing particle. Not from the LHC, in general (though this does happen for the electronics we have near the collision point), but certainly from the particles in cosmic-ray air showers. This can turn a one to a zero in a computer's memory, which is not too bad if it just means your MP3 player skips a beat, but is terrible if the autopilot goes haywire.\n\nImagine a high-energy particle from outer space approaching the Earth. It will hit an atom in the upper atmosphere, very likely shattering it into hadrons, electrons and photons all travelling rather fast. They in turn will shatter other atoms and the fragments will shatter others, so that a shower of fast-moving particles develops, heading for the surface of the planet, with the number of particles growing as it gets lower. At some point \u2013 the shower maximum \u2013 the energy is shared out over so many particles that many of them no longer have enough energy to shatter atoms. At this point the number of particles in the shower starts to shrink as particles gradually slow and stop and do not set off any more showers of fragmented atoms. That shower maximum just happens to be about 10,000m on average, which is the typical cruising altitude for a passenger jet, meaning aeroplanes get a significantly heavier bombardment from cosmic rays than we do at ground level.\n\nSo you need to be _very sure_ that any critical electronics controlling the plane can cope. The same applies to a lesser degree even at ground level, especially as electronic systems get smaller and faster. Putting your electronics in a neutron beam is a good way to test how likely they are to fail under cosmic-ray bombardments when they are at 10,000m. The neutrons fake the most dangerous cosmic rays.\n\nI was particularly pleased to learn all this as in October 2010 I also became convener of the ATLAS Standard Model group, which meant a dramatic increase in air travel, essentially to the level of a weekly London\u2013Geneva commute. We use teleconferencing and the web, but chats over coffees are still essential for proper coordination of what was by then a huge production machine for scientific papers.\n\nTravel has always fascinated me. To be honest, it was part of the attraction of particle physics when I was applying for research student-ships. At the time, I had never been on an aeroplane and my total experience of 'abroad' consisted of a couple of trips to Wales and one day in Normandy. Despite the fact that travel is now a regular part of my work, the fascination remains.\n\nHaving a routine, and a job to do at the other end of the journey, makes the whole thing different from holiday travel. Conference travel is not routine \u2013 often the place is new and exciting. But big labs such as CERN (Geneva), DESY (Hamburg), KEK (Tsukuba, near Tokyo) and Fermilab (Chicago) just become another place of work. I'm glad I have never had a regular long-haul commute like many particle physicists do. At least when I read my kids bedtime stories by teleconference, my evenings coincide with theirs.\n\nA strange feature of routine travel is the way disconnected bits of the world become as familiar as your street back home, but are separated by huge expanses of the unknown. This seems weird to me and reminds me of the way I treated the Tube map when I first moved to London: I'd pop out of a station and have no idea how to get to another except by going back down underground again. When I finally merged my Kentish Town and Trafalgar Square islands of knowledge, via Camden Town and Bloomsbury, I felt a strange sense of security that I hadn't even realised I was missing before.\n\nI'll never walk from London to Geneva, not even for charity. Commuting over such distances is only made possible by technology. Technology also helps us cope with the disconnects though, especially the Internet and the social networking it carries. Perhaps this applies to islands of cultural and social knowledge as well. There are people I know well, whom I trust and would go to for help if needed and a drink if not, scattered all over the world. I often wonder whether the combination of travel and remote two-way communication \u2013 person-to-person via public communication like social media, rather than broadcast media \u2013 is eventually going to make a real global civilisation. By that I mean one where most people's social network is way more geographically diffuse than ever before. The decisions we make, or which are made on our behalf by companies and governments, have been having global consequences for many years. Powerful people have been able to broadcast their points of view globally for ages. The fact that two-way, small-scale relationships are also possibly becoming global and routine represents a big opportunity to correct an imbalance. I wonder what we'll do with it?\n\n#### 4.3 Prospecting and Surveying\n\nIn those first couple of years of LHC data-taking, the Standard Model group on ATLAS was responsible for making many of the first measurements. Everything from the average number of particles produced in a collision,66 to some of the rarest events, such as those in which two W or Z bosons were produced. By this stage we had millions of 'minimum bias' events, and only a few dozen containing a pair of Z bosons.\n\n66. See 2.2 Minimum Bias.\n\n'Standard Model group' is a bit of a misnomer really. Some bits of the Standard Model \u2013 the top quark, b-quark decays, and most notably the search for the Higgs boson \u2013 had their own separate groups. Also, calling it the Standard Model group sort of implies that we already knew the answer \u2013 that we would measure the Standard Model. Of course we didn't really know that, at least not for everything we were measuring. Some things were being measured for the first time, and all of it was being measured at a higher energy than ever before. The key thing was that we were in general measuring processes for which the Standard Model made predictions. Often the theory made rather precise predictions, so it was a challenge to make precision measurements to compare to them.\n\nIn all cases, agreement would be a confirmation that the Standard Model worked in a new process, and a disagreement would mean either that the Standard Model was wrong or that there was a mistake in the calculation or (perish the thought) in our measurement. Convening this group as the first LHC data came in was essentially my dream job: helping ATLAS digest, understand and publish the vast amount of first-time physics information buried in the millions of proton\u2013proton collisions the Large Hadron Collider was giving us.\n\nThe publications from ATLAS could be pretty much divided into two types. There are the searches for new stuff, and there are the measurements of new stuff.\n\nThe first type is made up of the 'prospecting' papers. Prospectors zoom into the new landscape of physics to which the LHC has given us access and look for quick wins, for really unusual and surprising features. If they don't see them, we have learned something about the new land \u2013 'Hey, no gold volcanoes yet!' (Or no supersymmetry yet, or no black holes yet . . .). Of course, if anyone finds a gold volcano, they've got it made. And those things seriously might be out there; similar surprises have turned up before, many times. We were only in the foothills so far.\n\nSort of alongside but often slightly behind the prospectors come the surveyors. They study the new land, measure it, see whether it really complies with our best understanding of geology and suchlike. If it does \u2013 'Success!' We have extended the validity of our current theories. If it doesn't \u2013 'Success!' We have found what might be a gold volcano hidden under something else, and we and the prospectors can dig a deep mine together to get at it. Examples include measuring jets, isolated photons or W bosons produced in the highest-energy quark and gluon collisions ever seen.\n\nThere was a third type of result on the way, of course. This would come from the Higgs group, and from that part of the landscape where our understanding of the way things work meant that there had to be a gold volcano (OK, a Higgs boson in this case); otherwise the Standard Model would have failed. Those searches were starting in earnest around this time. Nothing was published by this stage, but there were enough collisions collected that staring at the plots and trying to guess if there was a Higgs boson hidden in them was starting to become a pastime, for me as much as for everyone else at the LHC.\n\nWhen it runs, the LHC runs around the clock, seven days a week. The pre-accelerators accumulate and accelerate enough protons to fill the LHC, the LHC then accelerates them the last bit (from 450 GeV up to 3500 GeV at that time) and will then store the two counter-circulating beams for several hours, some of the protons colliding on each revolution. The shift crews on the experiments struggle to keep the detectors recording data, and to keep our eyes open. Every time the LHC is filled with protons, more landscape is opened up. The pressure was on to study it quickly, but even though it's a frontier, no one wants to be a cowboy. It has got to be done right. If we get it wrong, no one would die, and it wouldn't destroy the world, but it would waste time, could send us down blind alleys and, since the data would continue to flow, the truth would come out in the end and mistakes would be found out. That could range from mildly embarrassing to career-endingly awful, depending on the circumstances. Even the prospectors have to be careful.\n\n#### 4.4 Antarctic Interlude\n\nAway from the LHC, other physics was going on. Ryan Nichol, who works upstairs from me at UCL, gets together with NASA every now and then and flies a balloon around the Antarctic. He even gets to visit the continent occasionally, which is both better and worse than Geneva. The balloon is very large, bigger than Wembley Stadium which seats 90,000, when fully inflated, and it carries an experiment called ANITA (Antarctic Impulsive Transient Antenna. An experiment name that is almost, apart from the appropriated N, both fancy and an acronym).\n\nANITA is looking for clues to one of the great questions in astrophysics: Where do cosmic rays come from, and how are they produced? We know that there are really, really high-energy particles hitting the Earth (and sometimes aeroplanes) all the time from outer space. The energy spectrum of these particles extends up to enormously high energies \u2013 more than 1020 electronvolts. Remember the LHC beams are at a few thousand GeV, or a few trillion (1012) eV. The highest-energy cosmic-ray particles have energies a billion times higher than that! Imagine what kind of accelerator produces those. Actually, people have tried to imagine. Spinning neutron stars, black holes in the centre of galaxies, and supernova shock waves are some of the more prosaic proposals. Decays of super-heavy dark-matter particles and 'topological defects' \u2013 boundaries between bits of the universe that cooled down differently after the big bang and could manifest themselves as cosmic strings or magnetic monopoles \u2013 are some of the more exotic. In general, the relative number of neutrinos and other particles produced will be different depending on which, if any, of these models operate.\n\nThere is another source of neutrinos. The universe is filled with a bath of very low-energy photons left over from the big bang \u2013 the cosmic microwave background. Protons travelling through the universe will interact with these photons, and if their energy is high enough they can collide with these very low-energy photons and produce a new kind of particle (called a Delta \u2013 a particle like the proton but with a higher mass). Because this becomes possible, the probability of the collision goes up, and that means the cosmic-ray protons at high energy are attenuated. However, the Deltas will decay producing pions, and the pions then decay producing neutrinos.67\n\n67. So-called GZK neutrinos: Kenneth Greisen, Georgiy Zatsepin and Vadim Kuzmin (1966).\n\nIt is also true that there could be some very interesting physics going on in the collisions between these particles and the atoms in the atmosphere. The fact that they hit the stationary atmosphere, rather than another particle with just the same energy coming the other way, means the amount of energy available to make new particles is reduced, but it is still 100 times more than the LHC. Again, the presence of such collisions throughout the universe is one of the main reasons we knew the LHC would not cause a catastrophe.\n\nWe would really like to know where they are coming from, and what kind of extreme conditions produce them. The aim of ANITA is to address this by looking for neutrinos. This might not seem an obvious choice, since neutrinos are famously hard to find. But that same property means they are not affected by all the material and magnetic fields in the universe between wherever they started and ANITA, so they should, if we can measure their direction, point straight back to the source.\n\nWhat ANITA actually detects is short radio bursts, using them to build up an image of the continent. Another \u2013 along with coffee seen by neutrons \u2013 in a series of weird ways to look at the world, I guess. They can measure the polarisation of the radio waves \u2013 which direction the electromagnetic field oscillates in as the waves travel. Neutrino interactions produce vertically polarised pulses. In the first ANITA flight, though, they didn't find any of these, and so, no neutrinos. But they found something else. They saw 16 pulses of horizontally polarised radio waves.\n\nThese turned out to be the signature of cosmic-ray air showers. In these showers, electron\u2013positron pairs are produced and they spiral around the Earth's magnetic field lines, giving a characteristic radio signal seen by ANITA. As Ryan put it:\n\nThe cosmic-ray air-shower radio signals were really unexpected and we only found them by checking a 'background' event sample for the neutrino search. It took us a long time to understand their significance to the point that for the second ANITA we removed the horizontal polarisation from the trigger to maximise neutrino efficiency. Whoops! Needless to say we will be reinstating it for the third flight.\n\nThese showers have been seen before, for example by the Auger experiment in Argentina. But new ways of seeing them, and measuring where they come from, are valuable. ANITA had, serendipitously, demonstrated an important new technique with a lot of potential.\n\nNeutrinos from the Sun, and those produced in cosmic-ray air showers, reactors and accelerators, have taught us a lot about particle physics. The hunting for neutrinos from beyond the solar system could tell us a lot, too, about particle and astrophysics. As well as ANITA, the giant IceCube array was looking for them. IceCube is a cubic kilometre of Antarctic ice instrumented with photomultiplier tubes to detect the light produced when neutrinos interact with the results. It would see the first high-energy neutrinos three years later.\n\n#### 4.5 Inside a Proton\n\nMost of the time (though not all), the LHC collides protons, which are not fundamental but are made of quarks, bound together by gluons. When doing physics with proton collisions, it is important to know this, and to know as much as you can about how the quarks and gluons are distributed inside the proton.\n\nAt some level a proton is a nuclear family of two up quarks and a down quark, but if you look inside you see all kinds of mess. First of all, the quarks are exchanging gluons between each other, which is why they are bound together inside a proton. But even looking (or trying to look) at a single quark, surprising physics emerges.\n\nIf the proton were made of homogeneous mush, the smaller the wavelength of photon you use to probe it, the less of the mush you would see. But if you are probing quarks inside protons, once you have enough resolution to see them, you would expect things to look pretty much the same no matter how much you increase the resolution. This is because if quarks are fundamental, it doesn't make much difference how closely you look, they look like tiny points. This prediction is called 'scaling'. It was observed in experiments at SLAC at the end of the 1960s, and was compelling evidence that the quarks Murray Gell-Mann had postulated to explain the patterns of hadron masses and quantum numbers were actual physics objects. The observation of scaling won the Nobel Prize in 1990 for Jerome Friedman, Henry Kendall and Richard Taylor.\n\nBut theorists noticed that if quarks can radiate gluons, the scaling doesn't quite hold. And according to QCD, they are rather likely to do this. If you try to observe a quark, for example by hitting it with a photon, you are likely to see it after it has undergone some of these radiations. Since there are three quarks inside a proton, you might think that on average they would be observed to carry about a third of the proton's momentum each. However, the fractions (usually called, imaginatively enough, x) that we see them carrying are typically much less than this, because radiated gluons carry the rest.\n\nIf we are looking at a quark by hitting it with a photon, then the wavelength of the photon sets the resolution \u2013 basically, how closely are we looking? Photons with a short wavelength can see shorter distances, and so can tell whether a quark has radiated a gluon or not, even if the gluon is still very close to the quark. Longer wavelength photons will not be able to resolve such a gluon from the quark and will see what looks like a single quark, with a momentum that is the sum of the quark and the radiated gluon. Short wavelength corresponds to high momentum,68 and so high-momentum photons will see more quarks in the proton, at lower x, than will photons of lower energy.\n\n68. We'll return for more on this in 7.3 Waves.\n\nThere is an awful lot of physics in this. It's one of those stories of more precision revealing more. To put it the other way round, the closer you look at a quark, the more of the gluon radiations you can resolve, and therefore the lower the momentum fraction, _x_ , carried by the quark, that you see. This violates scaling, and the amount by which scaling doesn't quite hold can be calculated in QCD. These 'scaling violations' also agree with what is now much more precise data, mainly from the experiments at HERA. This is one of the cornerstones of evidence that QCD is the right theory for the strong interaction.\n\nIt is fairly amazing that such a complex object as the proton, with all of this going on inside it, will, left on its own, last practically for ever without falling apart. 'For ever' isn't something we can measure, but we do know that they last for at least 1029 or so years on average. We know this because experiments like IMB,69 and now Super-Kamiokande, have watched lots and lots of protons very, very carefully for a very long time, and none of them decayed. Given the universe seems to be about 1.4 x 1010 years old, the limits set on proton decay mean the current limit on the lifetime of your average proton is 7,000,000,000,000,000,000 longer than the age of the universe.\n\n69. See 3.6 Names, Fame and Citations.\n\nApart from being a mess of quarks, a proton is also a hydrogen ion. Hydrogen, the most common element in the universe, is just a proton with an electron stuck to it. Along with helium, most hydrogen was made very shortly after the big bang, and everything else came from fusing these two elements together in stars much later. In this process, some protons are transformed into neutrons. However, the vast majority of protons in hydrogen have been that way for about 13.8 billion years.\n\nSo, left to themselves protons are OK. Of course, we don't leave them alone, and we smash some of them up in the LHC. Smashing things up is a time-honoured particle-physicist method of finding out about them. When I worked in Hamburg on ZEUS, we were smashing up protons with a beam of electrons. Smashing stuff works sometimes. A friend of mine bought a melon from the Fischmarkt on a Sunday morning (after a long Saturday night) and in the taxi home became convinced that he had bought a pumpkin by mistake. It was only when he threw it away in disgust and it smashed on the pavement that it was confirmed as an actual melon.\n\nOne thing we can learn from smashing protons at HERA, and the LHC, is how the quarks are distributed inside the protons. For example at the LHC when W bosons are produced, a positively charged W (W+) can be made by an up quark annihilating with an anti-down quark, and a negatively charged W (W-) can be made by an anti-up quark annihilating with a down quark. The anti-up and anti-down quarks are part of the scaling-violation business in the proton. Not only can the quarks radiate gluons, those gluons can split into quark\u2013antiquark pairs. In other words, a proton contains gluons, but it also contains many more than three quarks, and lots of antiquarks too. But if you cancel every antiquark off against a quark, you are still left with a net total of three quarks. And since of these there are twice as many ups as downs, the relative rates and distributions of W+ and W- production give information on where these quarks usually are inside the proton. Towards the end of 2010 the ATLAS and CMS experiments both published measurements of this, followed up by increasingly precise measurements later. Combined with data from HERA and other experiments, this improved our knowledge of the internal content and workings of the amazing proton.\n\nI find it extraordinary how rich the phenomenology of QCD is. The equations for QCD (what we would call the Lagrangian,70 the bit that gets written on souvenir mugs and T-shirts for the CERN gift shop) fit on one line, and to me at least give no real clue that things like hadron masses, and scaling violations, are implicit in their structure. Many people have spent their careers studying, calculating and measuring the implications of this equation.\n\n70. After Joseph-Louis Lagrange, or Guiseppe Lodovico Lagrangia as he was born. It is a function that describes a physical system. Actually, it is just the kinetic energy minus the potential energy, but it still manages to be way too convoluted to show here.\n\nThis \u2013 studying QCD \u2013 was what I was doing when I was working at HERA. This is not what most people assumed I was doing when they heard I was working in Hamburg. Usually the first thing they would say was, 'Are you in the army, then?' (Presumably this would be in some role not involving haircuts or heavy lifting.) The second thing they were likely to say was something like, 'Reeperbahn, eh? Phwoar!'\n\nI did like the Reeperbahn, the city's red-light district. It is sort of a more explicit version of Blackpool, really. Actually I haven't been to Blackpool for ages, maybe it too is explicit now. When I had visitors, an evening on the Reeperbahn was pretty much obligatory. These evenings kind of blur into each other, except for one particularly bizarre all-nighter that culminated in the most surreal experience.\n\nUsually we'd sit in various pubs, then go dancing. The sex-industry stuff was really only part of the scene; there was some actual good nightlife there too. However, one night three of us decided to thoroughly visit some of the strip bars and pole-dancing dives. (Not the brothels, though.) We chose carefully, making sure of a 'free' drink with the entry fee so that we didn't lose out even if we had to leave in a hurry. Some of the dives were enjoyable, but the last one wasn't. It was about 4:30 on Sunday morning by then, it had been a long night and I expect no one involved really wanted to be there. This was a large number of 'free' drinks later, so I wasn't looking around very carefully when a rather large, naked foot appeared way too close to our noses. I put the almost full bottle of lager in the inside pocket of my jacket, and we left in a hurry.\n\nOne great thing about a Saturday night in Hamburg is the Fischmarkt (the source of the melon\/pumpkin confusion earlier) that follows on Sunday morning. Opening at about 5 a.m., it's an invigorating mix of very proper Sunday-morning shoppers and the dazed-and-confused remnants of the night before. Like us. There are fish, plants, bad bands, melons, coffee, beer and, most importantly, Bratkartoffeln mit Spiegelei \u2013 an enormous mound of fried potatoes with three fried eggs on top. Just the ticket.\n\nAnnoyingly, when I got to our table, having negotiated my way unsteadily across the cobbles from the big pan with the potatoes, I was one egg down. Looking back, I saw it lying on the cobbles, glistening, still whole and unsullied, yolk-side up. Of course, I went back for it. Unfortunately, as I bent down to get it, some git poured beer on the floor right next to it. I stood up and looked around, but they'd gone. I bent down again. More beer!\n\nEventually I gave up and made my way with my two remaining eggs back to my by now hysterical companions, who had been watching the whole thing. I complained to them about the beer, and when they could speak, they explained that the bottle in my jacket pocket had been responsible.\n\nThis wasn't the surreal thing.\n\nThat came about eight hours later when, after an eel curry and not enough sleep, I went swimming. (I was a lot younger then.) Having swum, I was sitting beside the pool, drinking hair of the dog in the civilised way you can in Germany, when the lights suddenly dimmed, everyone got out of the pool and some strange music started. A line of small children, aged between five and ten and wearing odd hats, trooped in. They climbed into the pool one by one, and as they did so, an adult lit the candle that was mounted right on top of each child's head. They swam round the pool (there were about 40 of them, if I remember right), the little ones barely keeping the candles above water. Then they climbed out. As they did so, the adult snuffed out each candle in turn. The children trooped out, the music stopped, the lights came on, and everyone carried on as though nothing had happened. I still have no explanation. I blame the eels.\n\nI digress. Back in 2010, Christmas was coming, and the LHC had a new treat in store for us.\n\n#### 4.6 Heavy Ions for Christmas\n\nThe Large Hadron Collider is called that because it is large and it collides hadrons. Up until November 2010 it had been colliding one type of hadron \u2013 protons \u2013 so it might as well have been called the Large Proton Collider. At the end of the 2010 run, however, it showed its versatility. Lead ions, containing both protons and neutrons, were loaded into the tunnel and smashed into each other. The LHC became a heavy ion collider for a few days.\n\nAlthough the beam energies for the lead nuclei were much higher than the proton-beam energies (575 TeV compared to 7 TeV) the energy per nucleon (nucleon being a generic term for protons and neutrons) was lower, only about 1.43 TeV. Thus the average energy per quark or per gluon was even lower. When it runs in this mode, the LHC is not really an 'energy frontier' machine.\n\nEven so, you can legitimately describe both the proton and heavy-ion physics programmes as 'probing the first moments of the big bang', and it is worth examining why that is the case, and why they are different.\n\nIf you start from the present day and observe that the universe is expanding, then it is reasonable to suppose that in the past it was smaller. Now it is tempting71 to reason along the lines that, since energy is conserved, this smaller universe contained the same energy as the present universe, but in a smaller space. Thus the energy density, which is essentially the temperature, was higher. There is a potential flaw in this argument, however. Remember that Noether's theorem72 connects conservation of energy with the fact that the laws of physics do not change with time, effectively saying that all times are the same as far as physics is concerned. However, if we are considering cosmology, clearly all times are not the same. There is now a zero time \u2013 the big bang \u2013 which all observers agree on. We can measure absolute times relative to this; that's what we call the age of the universe! This implies that physics does not necessarily have to look the same \u2013 all times are not the same, and there is a universally agreed 'zero time'. So can we really rely on energy conservation when we are talking about the whole universe?\n\n71. And I've done it myself sometimes. Sorry. 72. See 3.5 Super Symmetry.\n\nIn a sense, yes. The master equations of cosmology, in general relativity, do not change, so they remain the same even if you choose a different origin. Therefore there is some definition of energy you could take that would be conserved. But this would have to include the energy stored in the gravitational field, which in general relativity means the curvature of space\u2013time. Some cosmologists choose to do this and rescue conservation of energy, and some do not. Either way, the physics remains the same \u2013 it is just a matter of different interpretations of the same equations.\n\nIt turns out that when doing the cosmology properly, the main conclusion is the same. The average temperature of the early universe was higher than the current average. This is because the early universe was dominated by matter and, even earlier, by photons. This in turn means that all the particles in it were, on average, moving faster, and therefore colliding with each other at high energies \u2013 energies that increase as you approach the big bang from the present day.\n\nAs particles collide at higher and higher energies, different physical effects occur. For example, if atoms collide with high enough energy, they knock electrons off each other \u2013 they ionise. While the temperature was high enough for this to happen often, therefore, the universe was filled with plasma \u2013 a mix of ionised atoms and electrons. Light cannot travel through this; it keeps getting scattered by all the charged particles.\n\nAt some point the universe cooled to the extent that the typical collision energy was too low for ionisation. This meant that atoms and molecules with no net electric charge could form, and stay together. In turn, this meant that light could travel much more easily, since the photons were not continually interacting with charged particles. These photons, which were all over the universe at this point, are still travelling. They are much cooler now \u2013 about 2.7 kelvins, or -270\u00b0C \u2013 and they were spotted in the 1960s by Penzias and Wilson (who initially mistook them for bird poo).\n\nExperiments mapping the cosmic microwave background, such as COBE (Cosmic Background Explorer), WMAP (Wilkinson Microwave Anisotropy Probe) and most recently the Planck satellite, look at the physics from this moment, about 400,000 years after the big bang, when the first atoms formed. From the fluctuations and frequencies of these photons it is possible to get clues as to what happened before, during those 400,000 years. But the collision energies at the LHC allow us to directly study the physical processes that must have dominated the universe then.\n\nA few minutes after the big bang, the collisions were so violent that even atomic nuclei could not hold together. At this point, protons and neutrons were everywhere. These are the kinds of energies you need for nuclear fusion, as is being attempted at the International Thermonuclear Experimental Reactor (ITER).\n\nBack a big step further (to about a millionth of a second after the big bang) and the protons and neutrons can't even stay whole. The quarks and gluons that they are made of spread over the whole universe (which is quite small at this point). This is a new form of matter we refer to as 'quark\u2013gluon plasma', though experiments at the Relativistic Heavy Ion Collider (RHIC) at Brookhaven National Laboratory indicate it may actually behave more like a quark\u2013gluon liquid. This is the stuff that the LHC could reproduce in November 2010 by colliding lead nuclei. (RHIC used gold nuclei rather than lead. It's flashier, but makes no difference to the physics.) ATLAS and CMS can make some measurements, and the ALICE detector (which we in ATLAS are living next door to) was optimised for precisely this purpose.\n\nThe concentrations of energy the LHC produces in proton\u2013proton collisions are even higher. They take us back to energies above another threshold \u2013 the electroweak symmetry-breaking scale \u2013 above which the weak nuclear force is as strong as the electromagnetic force. This would be about 10\u201311 seconds after the start of the big bang. That is about ten zeros between the decimal point and the one. Before this, energies are even higher and frankly no one knows, though there are plenty of theories and a few constraints from data.\n\nMore about electroweak symmetry-breaking shortly, but back now to the quark\u2013gluon plasma.\n\nWe managed to analyse and publish the data from the heavy-ion collisions remarkably quickly. On a Tuesday in November I was in the ATLAS control room doing my first shifts, monitoring and controlling some of the detector while we took more and more data from lead\u2013lead collisions. During the quiet moments I was trying to write two talks, but more importantly I was trying to keep up with the collaboration review of a paper based on lead\u2013lead data taken only days before.\n\nThese results were released and published a few days later.73 They were a measurement of hadronic jets, again, but this time jets produced in heavy-ion collisions. And the interesting thing about them was actually the jets that weren't there.\n\n73. <http:\/\/arxiv.org\/abs\/arXiv:1011.6182>.\n\nRemember, hadronic jet is a spray of particles caused by a pair of quarks or gluons colliding, leading to quarks or gluons being knocked out of a proton, or in this case possibly a neutron, in the lead nucleus. Normally at least two jets would appear in such a collision, balancing each other so that momentum is conserved. A jet heads off in one direction, and an equal and opposite jet heads off in the other.\n\nWe had recorded some events where this happened, but we had recorded a lot of events where only one jet was visible. Momentum was still conserved, but rather than a second jet balancing the first one, a much more diffuse spray of lower-energy particles did the job instead.\n\nWhat seemed to be happening is that, as intended, two lead nuclei were colliding and producing a brief soup of quarks and gluons. This is indeed the form of matter that filled the universe about a millionth of a second after the big bang. And it is within this soup that a single pair of quarks or gluons, one from each nucleus, were colliding with a very high energy.\n\nIn general, if such a collision happens near the edge of the soup, one quark only has to pass through a bit of soup to escape \u2013 that's the big jet. But in that case the other, going in the opposite direction, has to travel through lots of hot dense exotic matter. It gets scattered around and loses lots of energy into the medium it is passing through. That's the 'missing' second jet.\n\nHints of this behaviour had been seen before, at RHIC, but at ATLAS we had for the first time really measured it. And not only in a few events. We were actually getting a measure of how much 'soup' was being created in a given collision (more is made in collisions where the lead nuclei hit each other centrally, less if it is a glancing collision). We could see that in the events where more soup was created, more energy was being lost by the second jet, as one would expect. This meant we had a really good measurement of the nature of this soup. We were effectively using the quarks to study it, firing a quark through the material the early universe was made of.\n\nSince those first results, ALICE, ATLAS and CMS have produced lots of results studying the effect in more detail, and also using other methods to study this weird new state of matter where quarks and gluons are no longer confined inside hadrons. The details of how much energy quarks lose as they travel, and how they lose it, have now started to tell us an enormous amount about the strong force, about this new form of matter, and about the early universe.\n\n#### 4.7 Putting the Higgs in its Place\n\nOn 31 January 2011, it was decided that rather than stop in the summer of 2012 as previously planned, the LHC would run all the way through to the end of the year. This made a lot sense. We hadn't yet published any results on searching for the Higgs, but we had learned a lot about the physics of 7 TeV proton collisions, the performance of our detectors, and the ability of the LHC itself to deliver data. Things were looking good, and from the projections we could now make, it seemed clear that if we extended the run until the end of 2012 we would have a very good chance of either finding the Higgs boson or proving that it didn't exist. So this is a good time to say more about why this would be such a big deal.\n\nAs already described symmetries are very important in physics, and the fundamental forces in the Standard Model are all gauge theories, generated by local symmetries.74 The importance of the Higgs boson is connected to this, but in fact it is to do with breaking \u2013 or at least hiding \u2013 a symmetry rather than adding one. There are a few steps to go through to understand how this works.\n\n74. See 3.5 Super Symmetry and Glossary: Gauge Theories.\n\nBack in the mid-20th century, the first part of the Standard Model to be put in place was the relativistic quantum field theory of electromagnetic interactions, quantum electrodynamics (QED). Paul Dirac wrote down an equation that could describe electrons in a way that was consistent with special relativity, and eventually Richard Feynman, Julian Schwinger and Sin-Itiro Tomonaga proved that the theory was internally consistent. This internal consistency was in particular to do with a property called 'renormalisability'. The theory was plagued with infinities, coming from quantum corrections to the electron mass and charge.\n\nThe infinities arise, for example, from the fact that an electron travelling along can emit a photon, then reabsorb it. This makes a little closed loop. To calculate the probability of this happening in quantum field theory, you have to sum over all possible energies of that photon. The only condition is that the electron has to be the same after the loop as it was before. Unfortunately, because it is a closed loop, the energy that goes into the loop gets paid back, or cancelled out, at the end of the loop, so this condition isn't much of a constraint. In fact _any_ amount of energy can flow around that loop! This is a disaster, because the energy in these loops gives a kind of infinite 'self energy' for the electron and ( _E_ = _mc_ 2 again) this means the electron mass comes out as infinite. You do not have to be an experimental genius to notice that this is not the case for real electrons. In fact, we have measured the electron mass, and it is just over half an MeV.75\n\n75. 0.510998910 +\/- 0.000000013 to be precise.\n\nThe obvious thing to do is replace the infinities by the measured value.\n\nFeynman, Schwinger and Tomonaga proved76 that if you do this \u2013 replace the infinite electron mass by the measured electron mass, and the infinite electron charge by the measured electron charge \u2013 then _all_ the infinities in the theory disappear, and the theory (with those two experimental inputs) could make very precise predictions for all kinds of electromagnetic processes. This replacement of infinite mass and charge by finite, measured mass and charge is called 'renormalisation'. Feynman didn't like it much. He called it 'simply a way to sweep the difficulties of the divergences of electrodynamics under the rug'. But that is a direct quote from his Nobel lecture,77 so it can't be all bad. This property of renormalisability is obviously quite important. Nobody wants infinities hanging around in predictions for real physical processes.\n\n76. Independently and in different ways, which Freeman Dyson later showed to be equivalent. 77. He won the prize for this with Schwinger and Tomonaga in 1965.\n\nThe same applies for the other fundamental forces. Several models for the strong and weak forces were proposed, but showing whether or not they were renormalisable was very difficult. Some of them clearly were not. Then Gerardus 't Hooft and Martinus Veltman showed that if a force is generated by a gauge symmetry, this is a necessary and sufficient condition for it to be renormalisable. This is important because it means that the trick of generating forces from symmetries is not just a neat way of getting a predictive theory, it is the _only_ way. And it means that the sweeping of difficulties under the rug that Feynman grumbled about is not just a sneaky trick, it is built into the symmetries of the theory.\n\nThis was a big breakthrough and they duly won the Nobel Prize for it in 1999. But the Standard Model was not out of the woods yet. The problem is that the bosons generated by gauge symmetries were always massless. This is not a problem for QED, because the photon has no mass. It is also not a problem for the QCD, since gluons are massless. But it is a big problem for any theory of the weak force, since the W and Z bosons have a large mass. So, on the face of it, if you write down a gauge theory for the weak interaction, you have massless bosons, and if you add in the mass by hand to agree with observations, you break the gauge symmetry and end up with a non-renormalisable theory.\n\nNow, it is possible to hide symmetries. By this, I mean that you can have a completely symmetric theory that nevertheless gives rise to asymmetric situations. A favourite example is a marble78 in a wine bottle.\n\n78. Actually, having broken my wine bottle when using it as an example at the Royal Institution, I recommend a plastic ball rather than a glass marble.\n\nIf you look at a wine bottle from above, there is a circular symmetry around the centre of the bottle. That is, turning the bottle around an axis joining the centre of the neck to the centre of the base changes nothing.\n\nNow imagine a marble in the wine bottle, but imagine the marble is bouncing around, perhaps because the wine bottle is being shaken (carefully). This is a representation of the early universe and the marble is a high-energy particle shortly after the big bang. Averaged over time the system is still symmetric because the marble could be anywhere in the bottle and is no more likely to be in one place than another.\n\nNow place the wine bottle on a table and let the marble settle down. Because there is a bump in the base of the wine bottle, the marble cannot stop in the middle and has to roll off to one side. Once it has done this and come to rest, the situation is no longer symmetric.\n\nThis is an example of a hidden symmetry. All the physical principles governing the system \u2013 gravity, the kinetic energy of the marble and the shape of the wine bottle \u2013 are symmetric around the central axis. But the final configuration of the system once the kinetic energy has dissipated is not symmetric. The final configuration is the lowest-energy state of the system, what physicists call the vacuum or ground state, which just means the state with the minimum energy.\n\nThis trick can be deployed to evade the problem associated with having massive particles while preserving the necessary symmetries of the Standard Model. Keep the equations of system symmetric, but set them up so that they generate an asymmetric ground state \u2013 and that is the ground state in which the universe currently finds itself. In this ground state, fundamental particles, and especially the W and Z bosons, can have mass, but the weak interaction can still be a gauge theory.\n\nThere is one more step to this, and since this is the crucial step made by the 'gang of six' (Brout and Englert; Higgs; and Guralnik, Hagen and Kibble) in 1964, we had better finish with it.\n\nThis idea of 'spontaneous' symmetry breaking had been tried before, and had worked in other contexts. But it came with a catch known as the 'Goldstone theorem', after Jeffrey Goldstone. This theorem states that when a symmetry like this is spontaneously broken, new massless scalar particles (i.e. particles with no spin) appear, as possible excitations of the quantum field.79\n\n79. See Glossary: Fields, Quantum and Otherwise.\n\nTo see what this might mean in the wine-bottle analogy, imagine giving the marble, which has settled on one side of the bottle, a push, putting a tiny bit of energy into the system. If you push the marble towards the centre of the base of the bottle, up the hump in the middle, it will roll back. There is an 'excitation' of the marble possible here, where it rolls up and down the sides of the trough around the base. On the quantum scale, there's a minimum amount of energy you have to put in to make it do that, and for a quantum field, that minimum amount would be the mass. This oscillation corresponds to a massive particle.\n\nBut if you had pushed the marble along the trough so that it went around the base of the bottle, it would not roll back, it would keep right on rolling. In fact, precisely because of the hidden symmetry, all points around the base have the same energy, and you can make this marble roll around the bottom by putting an arbitrarily small amount of energy into it. The fact that there is no minimum amount of energy means this corresponds to a massless excitation \u2013 a massless particle. It is there because of the broken, or hidden, symmetry of the system, and Goldstone's theorem said this would always happen.\n\nThis is a big problem, because these massless scalar particles don't exist in nature. In fact, Yoichiro Nambu had already shown that spontaneously broken symmetry could allow hadrons (such as the proton and neutron) to have mass. But because of Goldstone's theorem, it also predicted a massless scalar particle. Which just wasn't there.\n\nWhat Brout, Englert, Higgs and the others did was show that when you have a gauge symmetry _and_ a spontaneously broken symmetry present together, the massless scalar particle (from the broken symmetry) becomes incorporated into the gauge bosons (from the local symmetry). This simultaneously allows the gauge bosons to have mass, and eliminates the awkward massless scalar particle.\n\nThis was a big breakthrough, though it wasn't universally recognised as such at the time. This was probably at least in part because the idea found its place in the Standard Model in a way not really anticipated at the time.\n\nWhen the 'gang of six' did this work, they were mainly thinking, like Nambu, of the masses of hadrons. This was back in the early 1960s, before the W and Z had been discovered and before the Standard Model was at all established. We now know that hadrons acquire their mass a different way. They are not fundamental, and their mass comes from the binding energy of their constituent quarks. Because of this, the Higgs boson is only responsible for about 1 per cent of the mass of everyday stuff. QCD is responsible for the rest.\n\nBut this 1 per cent is crucial, because it is the mass of the fundamental particles, and in particular, the mass of the W and the Z. Which, remember, seemed to be incompatible with them being gauge bosons.\n\nIn April 2011 I was in Edinburgh, home to Peter Higgs (since he left UCL in 1960), at the Science Festival. I love Edinburgh, right from the moment the train pulls in to Waverley Station. I love the fact that it has a daffodil-filled valley with a railway in the middle where most cities would have a river. I was visiting to take part in a discussion on 'Engineering the Large Hadron Collider', chaired by the comedian Robin Ince and with a talk from Lyn Evans, the project leader for LHC construction and the man who had counted us down to the great switch-on in 2008. My job was to be on at the beginning to try and explain _why_ we had built it.\n\nHunting for the Higgs boson isn't really why we built the LHC. Actually, what we wanted to do was to understand why the electromagnetic force and the weak force have the same strength at high energies whilst being very different at everyday energies.80 We knew that the difference in strength is caused by the fact that the W and Z boson have mass and the photon does not. Because they are massless, it is relatively easy to radiate and exchange photons, and they do not decay, so they can travel long distances (across the universe for billions of years, even). On the other hand, it takes a lot of energy to make a W or a Z, and even when you have one, it will very rapidly decay to other particles, meaning the weak force is short-range and, indeed, weak. But once the energy in an interaction is high enough that you can ignore the mass difference between the photon and the Z, the strength of the two forces is very similar. The energy scale at which they come together (if you are going up in energy) or diverge (if, like the universe, you are cooling down) is called the 'electroweak symmetry-breaking scale'.\n\n80. Which does connect back to the Higgs in the end, bear with me.\n\nThis cooling down of the universe is like the marble settling in the bottom of the bottle. In the Standard Model, it is the quantum field equivalent of the bump in the bottom of the bottle that breaks the symmetry and introduces the masses of the W and Z, and in doing so introduces the difference in strength between the two forces. This is the Higgs field or, more correctly, the Brout\u2013Englert\u2013Higgs (BEH) field. It puts the universe into an asymmetric ground state, even though the underlying theory is symmetric.\n\nEven if this model were wrong, the fact that the W and Z have mass would still be true, and with the LHC we would be able for the first time to do physics at energies well above the electroweak symmetry-breaking scale. Without the BEH field, the Standard Model would not work at these energies, so we would truly be in unknown territory and would hopefully get some clues as to the origin of mass, Higgs boson or not.\n\nOn the Sunday after the Edinburgh event with Evans and Ince, I chaired a talk with the _Guardian_ science correspondent Ian Sample on his book _Massive_ , about the history of hunting the Higgs. One audience question after Ian's talk was along the lines of 'If it is so important, ubiquitous and fundamental, why is the Higgs so hard to find?'\n\nThis is a really good question. The answer is that in a sense it's not the boson that matters. It is the BEH _field_ that fills the universe, giving mass to the W, Z and other fundamental particles, that is the really important thing. If you think this BEH mechanism is correct, then every time you measure the mass of something you are seeing evidence for it.\n\nOn the other hand, this becomes simply a matter of interpretation, since the BEH theory has explained the mass, but has made no unique prediction for any new phenomena that you can test experimentally. Maybe some other theory could also explain the mass. In fact, this is pretty much why the draft of Peter Higgs' second paper on the matter was initially rejected by the journal _Physics Letters_.\n\nHe then went and added an equation that essentially says something along the lines of 'Well, if this field is there, you can also make waves in it and this will appear as a new scalar, i.e. spinless, particle.' These waves, or, again, quantum excitations, are not the massless scalar boson that Goldstone's theorem would have, but they are the leftovers from spontaneous symmetry breaking after the gauge bosons have had the rest. They still make a scalar boson, but one with mass. That is the famous Higgs boson, and that is why we have to see whether it is there or not. It was this prediction that made it possible to experimentally demonstrate whether the BEH mechanism was just a neat piece of mathematics or whether it really operates in nature.\n\nOn 22 April 2011, the LHC collided beams with a luminosity that passed the previous world record set by the Tevatron collider in 2010.81\n\n81. The LHC reached 4.67 x 1032 cm-2s-1, compared to 4.024 x 1032 cm-2 s-1 from the Tevatron.\n\nThe intensity, or luminosity, is a measure of how many proton collisions per second are happening in the LHC.82 The units here are protons per unit area per second. So we were getting them at a faster rate than anyone ever had before.\n\n82. See Glossary: Cross Sections and Luminosity. This record of 4.67 x 1032 cm-2 s-1 corresponds to 4.67 x 10-7 inverse femtobarns per second, or (very roughly, depending on how long the machine could maintain this value and how quickly the team could refill the beams with protons after a run) 0.03 inverse femtobarns per day.\n\nIf the Higgs boson existed, we were rapidly closing in on it. Data from the LHC collisions were streaming through our analysis software, and the tension was mounting day by day as we struggled to see what they might be telling us.\nFIVE\n\n## Rumours and Limits\n\n### April\u2013August 2011\n\n#### 5.1 Why Would a Bump Be a Boson?\n\nBy this time the LHC had been running at high energy for just over a year and we were deeply involved in analysing the data while greedily collecting more as fast as possible. It is about time I introduced some of the data distributions we were all obsessing over at this point. And indeed to unpack a bit what it means to measure something in a collider experiment like ATLAS.\n\nThe basis of measuring a distribution typically goes something like this . . .\n\nFirst, you record as many interesting collision events as possible. A 'collision event', which we would usually just call 'an event', means in this context all the data we can get associated with a certain time-window in which a pair of proton bunches83 passed through each other in the centre of the ATLAS detector. In LHC running to date, this has happened every 50 nanoseconds while the beams are on. So there are 20 million potential 'events' happening every second during LHC operation.\n\n83. 'Bunch' is not a colloquialism, as in 'Hey what a crazy bunch of protons.' Bunch is technical jargon, as in 'The LHC is now operating with 1404 bunches.' The beams are not a continuous, uniform stream of protons, but a series of bunches, matched to the time structure of the radio-frequency accelerating fields of the LHC. Each bunch is a few centimetres long and contains 100 billion or so protons.\n\nMost of these events are not 'interesting', that is either no protons actually collided with each other as the bunches passed through each other, or, much more likely, all the collisions were of a type that we have measured extensively already. We have sophisticated online selection algorithms (collectively called 'the trigger') to try and pick out the rare few interesting events. Some of these algorithms reside in hardware (application-specific integrated circuits \u2013 ASICs \u2013 and field programmable gate arrays \u2013 FPGAs \u2013 are the terms to bandy about here) and some in software running on a huge computing farm just next to the detector.\n\nData from a single bunch crossing arrive from the detector at a range of different times, not least because the detector is so large that a particle travelling at the speed of light takes up to 80 nanoseconds to travel from the collision point to the edge of ATLAS. So even before the particles from one bunch crossing have left the detector, the next lot are on their way. Then there is the time taken to read the information out of the detector and send it along cables to the computing farm. All the data have to be time-stamped84 and all those time stamps have to be correct so that we end up building a picture of a single event: all the particles produced in a single bunch crossing. Of the 20 million possibilities every second, about 200 will be saved.\n\n84. Incidentally, the 'Timing Interface Module' that keeps the tracking and some other components of ATLAS in time with each other and in time with the LHC was one of the contributions of the UCL group.\n\nNext you have to 'reconstruct' the event. The events are stored at CERN, and also transmitted around the world to a network of computers (the LHC Computing Grid) to be reconstructed.\n\nReconstruction includes, for example, identifying the points where a particle passed through the silicon of a tracking detector, and performing pattern recognition to join the dots and make a particle track. These tracks are fitted to curves to extract the momentum that the particle had and extrapolated backwards to see where they started.\n\nAnother part of the reconstruction code will identify pulses of energy in the calorimeter, where particles have stopped. These will be analysed to see whether they look like hadrons (which will have a long, deep shower of energy) or photons or electrons (where the shower will be more compact). What is the energy? And is there a track pointing to the energy? Photons should not have one since they are neutral, electrons should. And so on.\n\nSome basic reconstruction will have been done already by the online selection algorithms, but here we do a more complete job, using the best calibrations and taking the time we need.\n\nNext, you have to clean up the sample of events you have recorded and reconstructed. By this stage you really ought to have had a good think about what sort of events you want to measure for this particular analysis. With the trigger selection, anything not selected is lost for ever, so we err on the side of caution. By this stage, however, all the events are saved, so you can try different selections, optimise and re-optimise. Let's say that we are searching for the Higgs boson decaying to two photons. This is a rare decay for the Higgs (the Standard Model Higgs will do this much less than 1 per cent of the time \u2013 the exact number depends on the Higgs mass), but we can select for photons very efficiently, with a high degree of confidence, and measure them very accurately, which more than compensates for that.\n\nSo we want to identify photons. The results of the reconstruction will tell us whether there are any likely-looking candidates in our collisions. But the photons from Higgs decays would be higher energy than most \u2013 photons are the quanta of light, but the ones we measure here are about a billion times more energetic than the photons of visible light. They are also 'isolated', meaning that there aren't any other particles near to them in the detector. This is important, because photons can also be produced from the decays of a very commonly produced hadron, the neutral pion. These are just background noise if you are looking for the Higgs boson, but luckily they will most often occur in a hadronic jet, so surrounded by other hadrons, and they can be rejected.\n\nOne thing we have to worry about is that when the proton bunches collide, it is very likely (almost a certainty) that more than one pair of protons hit each other. The particles from all the pairs in a bunch that collided will be stored together, but we are only interested in the proton\u2013proton collision that produced our photon candidates. We can generally remove the other stuff, either on a statistical basis (because we have measured the properties of the extra collisions, which will generally be minimum bias events, see section 2.2) or because we can see that some particles come from a different collision vertex from others. This is tricky for photons, however, since being neutral they leave no tracks and often can't be identified with a particular vertex.\n\nAnyway, after selecting events with two isolated photons in them, and calibrating the measurement of the photon energy and direction, what next?\n\nOne can hypothesise that the photons were the exclusive product of the decay of a new particle of unknown mass. Under this assumption, we can calculate what the mass of that particle would be. The photons themselves each have zero mass, but their combined mass is not zero because they are moving away from each other very fast, so have a lot of energy whichever way you look at them. This is relativity in action. If they travelled in the same direction as each other, then you could in principle try to catch them up and their energy would get smaller the faster you moved in their direction.85 But if they move away from each other, trying to catch one of them up increases the energy of the other one, and you can't get rid of the energy of the pair no matter how fast you go. And since energy is equal to mass times the speed of light squared, this means the pair has a mass too. Often this is called the 'invariant mass', because it is a quantity you can measure, or calculate, which does not vary depending upon how fast you are moving. The invariant mass of the photon pair does not depend at all on whether you try catching one of them up or just sit there in the control room drinking coffee. And, if they came from the decay of a new particle, this invariant mass of the photon pair will be the invariant mass of the new particle, since energy is conserved.\n\n85. This is the Doppler shift. The energy and wavelength of the photon change, although the speed of course remains the same \u2013 the speed of light.\n\nThen we can make a histogram of the data, that is a graph where we have the mass of the photon pair along a horizontal axis, and we divide it into 'bins', with each bin covering a small range of masses. Every time an event comes along, we put it into a bin along this axis according to the invariant mass of each photon pair we find. This way you get a graphical distribution displaying the number of events recorded at each mass value.\n\nEven if there were to be a Higgs boson in there, most of the photon pairs will come from other sources. There are processes other than a Higgs that can produce two pairs of photons (for example, they could just be radiated off quarks). There will also be some fake photons in the sample. But these sources will generally have a smooth distribution of masses \u2013 there's no reason for them to cluster around a particular mass. Any photons from a Higgs boson decay, on the other hand, would be concentrated around a single mass, and so would show up as a bump in a smoothly falling distribution.\n\nAs time passed, we were collecting more and more photon pairs. There were fake, statistically insignificant 'bumps' in the distribution everywhere. This is where we just had to keep calm and carry on, despite the tension and the pressure for news \u2013 not just from particle physicists around the world but, bizarrely for a physics experiment, from the media.\n\nWhile we collected more data, we were trying all kinds of tricks to make sure we were measuring the mass of the photon pairs correctly \u2013 calibrating and recalibrating the detector. If we saw a real bump, how sure would we be that we had the energy right? Or would we miss it, maybe wash it out by scattering the photon pairs around at wrong masses? White-knuckle time, really.\n\n#### 5.2 Crying Wolf\n\nThe Large Electron\u2013Positron Collider (LEP) ran from 1989 to 2000 in the tunnel now occupied by the LHC. The LEP experiments made many of the measurements that established the Standard Model as a precise theory; amongst these were measurements that, when fed through the precise calculation framework of the Standard Model, indicated roughly what the Standard Model Higgs boson mass had to be (if it existed). Towards the end of the run, there was one of those heated decision points in particle physics: should the machine be turned off as planned, to start construction of the LHC, or should it run a bit longer at maximum energy to see if the Higgs boson popped up, right about the limit of sensitivity?\n\nExtending the run would have cost a lot of money and would have delayed the LHC. But there were hints (how I hate hints) that the Higgs boson might be there, at a mass of about 115 GeV. The hints were just a few suggestive collision events, but a one-month extension was granted to see if more showed up. None did, so the machine was turned off. Several LEP physicists remained utterly convinced they had seen the Higgs and that its mass was 115 GeV. I have a colleague who bet several bottles of champagne on this, and another who gave a talk a year later in which he claimed they really had seen the Higgs already \u2013 and wasn't _entirely_ joking.86 Passions ran high.\n\n86. He later became a leading Higgs physicist at the LHC, so obviously \u2013 and very sensibly \u2013 recanted.\n\nPerhaps it shouldn't have been a surprise, then, that as the data were accumulating and we were all obsessing about the latest distributions (especially the two-photon mass I talked about in the previous section), a group of ATLAS physicists, amongst them some of the leading proponents of the 115 GeV 'LEP Higgs', got a rush of blood to the head \u2013 or some part of their anatomy \u2013 when for a while the data showed a small excess around the 115 GeV mass bin. An internal note making extravagant claims was distributed very widely within the ATLAS collaboration. It was clearly an overstated claim and in my opinion showed a lack of objectivity.\n\nThese are easy mistakes to make, but not so easy to email to thousands of colleagues. It should still have remained a slip-up between friends, part of the internal process by which ATLAS discusses such things and filters out those that aren't robust. Unfortunately, someone chose to breach collaboration confidentiality and post the title and abstract (and the internal author list, naming those would-be Nobel Prize winners who had beaten all their colleagues to the punch) on a blog . . .\n\nThe upshot was that many of us on the ATLAS experiment at CERN were a little busier than we anticipated over the Easter break.\n\nThe level of public and media interest in the Higgs search was high. The fear was that if too many false claims made the headlines, the interest would dissipate into cynicism, and if and when we actually had something to say, people would be too jaded to listen. On the other hand, to ignore the story would be to fail to engage, would risk us looking secretive, and would leave communication channels open to people who didn't really get the context. Having tried to ignore it as long as possible, when Channel 4 News called up I felt the story was already widespread enough that I had better help ATLAS respond.\n\nI talked to Krishnan Guru-Murthy about it. I tried to explain that it really wasn't a hoax, but that the rumours were based on an analysis that had not passed the many levels of scientific scrutiny87 required before anyone should get at all excited by it. It could fail at any stage, and given the manner of its release I expected it to do that, frankly. If it passed, it would be released by ATLAS and submitted to a journal.\n\n87. See 3.3 Copenhagen.\n\nAt the time, all we really knew was that the results were overstated. The boson could have been at 115 GeV, but even if it was, the data at the time showed no significant sign of it. Apart from the embarrassment to the authors and the hopefully troubled conscience of the leaker, I think the whole episode was probably useful in educating the media and public about the difference between 'official results' and 'rumours'. Either can be right or wrong, of course, but stamping something as an 'official result' doesn't mean it has had policy approval, or commercial approval, or whatever else it might mean in the context of a political party or a company. What it means is that the collaboration of many physicists have done their absolute best to make sure it is correct, and correctly stated, and are all prepared to stand behind it. This is a real test for a complex result; it's the application of scientific method. It's not infallible, but it's a hell of a lot more reliable than a rumour . . .\n\nI think we also gained some further confidence in dealing with the media on this. Scientists are sometimes too harsh in their judgement of journalists. The thing is, CERN is an exciting place now, as it was then. New data are coming in all the time. There are lots of levels of collaboration and competition. Retaining a detached scientific approach is sometimes difficult. And if we ourselves can't always keep clear heads, it's not surprising that people outside get excited too. I suspect we should be more forgiving of some of the excitable headlines \u2013 without, of course, encouraging them when they are misleading.\n\nReviewing is an occupational hazard of life in a big collaboration. The path from the first idea through to final publication of a result is arduous and full of potholes, trapdoors and mind-sapping disputes about commas and hyphens, often conducted at volume by a group of tired, angry people, none of whom have English as their first language. Even so, and the comma-and-hyphen element notwithstanding, reviewing is vital.\n\nMeanwhile, in May there was another 'Boost' meeting, this time in Princeton. All good, but the best thing was that we had lots of data by then. We'd made the first measurements of some of the new jet substructure variables. Adam Davison and Lily Asquith, a postdoc at Argonne National Lab, showed the first ATLAS results. Miguel Villaplana, a PhD student at Valencia, actually showed pictures of the first highly-boosted heavy-particle candidates \u2013 two top quarks.\n\nGlossary: Sigmas, Probabilities and Confidence\n\nThe business of trying to decide objectively whether or not to take seriously a bump in your data requires statistical analysis and agreed criteria. In particle physics we tend to talk about 'sigmas' as a way of quantifying this.\n\nIn this context, sigma (\u03c3) is a parameter determining the width of a Gaussian, or normal, distribution. This is a bell-shaped curve that appears an awful lot in experiments because measurements often contain several independent possible sources of error. If you repeat a measurement many times, then the distribution of the results, with those independent and random errors in, will follow a Gaussian distribution,88 with a particular width set by sigma, also called the 'standard deviation'.\n\n88. This is the 'central limit theorem'.\n\nNow, take a theoretical model \u2013 of, say, the two-photon mass distribution discussed in the previous sections \u2013 and a measurement scattered around the model, the actual data. If there is a visible bump in the distribution, we can use the 'sigma' idea to quantify how significant the bump is. In the Gaussian curve, made of many measurements, 68 per cent of the measurements are within 1 sigma of the central value, 95 per cent of them are within 2 sigma, and 99.7 per cent are within 3 sigma. So if we have estimated the sigma \u2013 the width of our error distribution \u2013 and we see a data point that is 3 sigma away from the background model, then on the face of it, if the data point really is just a background fluctuation, it must be one of the 0.3 per cent not lying within 3 sigma of the mean. Put it another way, there is only a three in a thousand chance that the background model alone describes the data.\n\nThis might sound like enough to get excited, and indeed conventionally '3 sigma' is deemed a sufficiently significant effect to be officially called evidence. But you have to be cautious. If you make a thousand measurements, the chances are three of them will show a 3 sigma effect, even if there is nothing but background noise in your data. This so-called 'look elsewhere' effect can also be estimated and factored into your confidence level. More crudely, the convention is that 5 sigma is what you really need to have to declare a discovery. This would correspond to one chance in nearly two million that your 'discovery' is just a background fluctuation.\n\nIn some areas of science it is more common just to quote the probabilities, or 'p-values'. We do that, too, often. But particle physicists do seem attached to their sigmas.\n\n#### 5.3 The Tevatron Goes Bump\n\nThe LHC was not the only game in town when it came to looking for bumps in distributions. The CDF experiment at the Tevatron proton\u2013 antiproton collider had a bump, which they actually reviewed and released89 and which was published in a journal. This caused a stir and a special seminar. This is a more common situation in scientific research than unauthorised leaking. The result was (a) really important if confirmed, and (b) in need of confirmation before everyone could be certain of it.\n\n89. <http:\/\/arxiv.org\/abs\/1104.0699>.\n\nWhat they had done was measure events in which a W boson was produced \u2013 subsequently decaying to an electron or muon, and a neutrino \u2013 and two hadronic jets were also produced. They then calculated the invariant mass of the pair of jets. At masses of about 150 GeV, there were more events than expected in the Standard Model.\n\nA bump like this could be a sign that a new particle (a bit like the W boson but nearly twice as massive) was being made and decaying to two jets. There is no such particle known to science. It would be wonderful. It didn't fit very neatly into any expected theory, but within a day there were already several new theoretical papers eager to explain it. It would represent a massive breakthrough in our understanding of fundamental physics, though it would take quite some time to actually understand it!\n\nThere were plenty of reasons for caution, too. Firstly, there was the chance that it was just a statistical fluke. The paper quoted a one-in-ten-thousand (0.0001) chance that the bump was a fluke. That's pretty small. However, lots of distributions like this get plotted. If you plot 1000 different distributions, the chances become about one in ten (0.1) that you'll see something this odd in one of them. Still, that's pretty small. And it's not clear to me that there really are 1000 different distributions as interesting as this one.\n\nAnother worry is that, quite apart from the statistical uncertainties, neither the data nor the predictions were exact. The energies of the jets were only known to within 3 per cent on average, for example. This is a systematic uncertainty. Systematic uncertainties are harder to evaluate probabilistically than statistical ones. If the energy scale of the jets is known to within 3 per cent, this means there is some reasonable probability that all the jet energies are wrong by 3 per cent.\n\nIf this was a statistical uncertainty, the 3 per cent would probably be the '1 sigma' uncertainty, meaning 68.2 per cent of the measured values would be expected to lie within 3 per cent of the correct value.90 For a systematic uncertainty this won't necessarily be the case, though. They could all be uniformly too high by 3 per cent, for example. It is also hard to guess how probable that is. As with statistical uncertainties, if the '3 per cent' number is '1 sigma', there is a 68.2 per cent chance that the result is within 3 per cent of the right answer. If the errors are distributed normally, the 2 sigma point, which is the 95 per cent band, would be at twice 1 sigma, i.e. 6 per cent. But with a systematic uncertainty, the errors are unlikely to be normally distributed and it is very hard to assign probabilities to outcomes. CDF considered a lot of factors like this, and estimated that the probability of the bump being a false alarm is raised by a factor of eight (still only 0.0008, of course).\n\n90. See Glossary: Sigmas, Probabilities and Confidence.\n\nThe other Tevatron experiment, D0 (D-Zero), followed this up later, and saw nothing, as did ATLAS and CMS. CDF also eventually performed a new analysis with more data, and also saw nothing. So like those Higgs rumours, it looks like this was a mistake of some kind. The Higgs rumour hadn't been reviewed by the experimenters concerned (me and my colleagues on ATLAS), and failed miserably when it was. The CDF result was reviewed by the collaboration, and by a journal, and was a much higher-quality analysis. But even so, it was not reproducible and seems already to have found its place in the 'false alarm' folder.\n\nIt's worth going over some of these false starts, though. I think it gives a feel for how tense we all were, and of the pressures. It also gives flavour and weight to the kinds of cross-checks and studies that were going on within ATLAS and CMS all the time to try to make sure that if and when we did announce any progress on the Higgs search, it would not be retracted or contradicted later. But perhaps most important is the wider point about openness and reproducibility.\n\nA second or third independent person looking over your results can see things you can't. Errors can be of omission, wishful thinking or just rubbish coding. In particle physics there is little commercial involvement (though careers are certainly at stake in these things). But when it comes to other areas of science, such as studying the effectiveness of a new treatment or a drug on people, it can be a matter of life and death. It is frankly astonishing that many health-care decisions (for instance whether to license a new drug) are based on data that are never released. Conclusions, even those based on good, honestly analysed data, can be wrong and can't be trusted unreservedly. They need to be reviewed by independent scientists and, ideally, reproduced. This is not even because they might be lying (though when big money is at stake it would be naive not to consider that possibility), but because if they haven't exposed their analysis to external review, they might be honestly wrong and we would never find out. Similar concerns or worse occur when libel laws are misused to silence criticism of analyses and conclusions. Either way, money is wasted and people suffer.\n\nReviewers are also good protectors of a night's sleep. One of the first papers I wrote was a measurement of the rate of production of jets of hadrons in photon\u2013proton collisions, using data collected with the ZEUS detector. I made the plots in the paper myself, with my own code, and I became very aware of the enormous number of steps between the raw data and my result. I was also very, very aware of the fact that people on another experiment (H1) would likely repeat the result, and that physicists coming after me would measure it more precisely once we got more data. So any mistakes I made would eventually be exposed. But we were the first. No one knew the answer until we measured it.\n\nIn the early stages of the analysis, I would regularly find mistakes that would change the result by large factors. Things eventually settled down. The room for error got smaller. It got to the stage where I was tracking down tiny inconsistencies in the error bars, very minor things that, while some of them were still genuine mistakes, had essentially no impact on the conclusions of the analysis.\n\nEven so, in the last week or two before publication, I woke up several times in the middle of the night in a panic, worrying about something I hadn't checked. The only thing that kept me (relatively) calm was the knowledge that the final plots had been made independently by someone else as well as me. In ZEUS we had a rule that required at least two independent analyses of any result for publication. In fact the 'second analyser' and I found several bugs in each other's analysis by comparing things at different stages. The chances of us both having made an identical massive blunder that would significantly change the final answer were pretty small. So I would go back to sleep \u2013 but still check when I got up.\n\nAnyway, we were right and I am still very proud of that paper,91 which was a significant step in understanding photons, protons and the strong interaction.\n\n91. <http:\/\/arxiv.org\/abs\/hep-ex\/9502008>.\n\nAt the core of this behaviour is whether we want to know the answer, or whether we want to impose our view on the universe. In any science, and even more so in engineering, you'd better get the right answer. Nature won't pay any attention to a mistake and people may die. Finding an unwelcome right answer may appear to be a setback, but proceeding on the basis of a welcome but wrong result can be fatal.\n\nI think one of the fault lines between science and politics is that this dynamic is less clear in politics. No matter their prejudices, politicians cannot change the science behind the consequences of carbon emissions, rape or vaccination. But when it comes to economic and social consequences, maybe they can. Persuade people to save, or spend, more money, you change the economy. Persuade people to support, or denigrate, universal health care, you change society. You can see why politicians, lobbyists or indeed drug-company executives may sometimes get confused about where the lines are.\n\nEven where justified, using persuasion to change reality meets with varying success. But it has more chance of working in politics than it does in physics. Whatever worries you might have about quantum mechanics and the effect of the observer, don't try persuading gravity to give you a day off.\n\nGlossary: Feynman Diagrams\n\nA Feynman diagram is a particle physicist's best friend and worst enemy. As I have been describing physics processes in this book, most of the time I have had pictures of Feynman diagrams in my mind. Pretty soon (the next section, in fact) I am going to have to start actually drawing some diagrams and discussing them. So it is time to describe why they are so wonderful \u2013 and also why they should be treated with caution.\n\nFeynman diagrams are cartoon representations of the actual equation you would use to calculate a quantum mechanical amplitude92 for a particle, or several particles, starting in one state and finishing up in another. The initial state could be a pair of quarks inside protons in the LHC, the final state could be practically anything. As a simple demonstration, I'll use an initial state of an electron and a positron colliding in LEP, the accelerator that was in the same tunnel as the LHC but a decade earlier. And I will use as a final state a muon and an antimuon.\n\n92. See 3.3 Copenhagen.\n\nHere come the electron and the positron (time is running from left to right):\n\nFor each incoming particle there is a line in the Feynman diagram, and (though I won't write them down here) there is a corresponding term in the equation for calculating this. Now we let the electron and positron collide, and annihilate to give a photon:\n\nThis vertex, where three particles meet, also has a corresponding term in the equation. In this case it is a very simple one \u2013 it is a number, the electron charge. The vertex is an electromagnetic interaction, and the probability of such an interaction occurring depends on the charge.\n\nThe photon continues for a while, and then decays, via another vertex, this time depending on the charge of the muon (which happens to be the same as the charge of the electron):\n\nThere is a term in the equation for each of the final-state particles (the muon and the antimuon), and for the wiggly photon line. This internal photon line is known as a 'propagator', and it is what we call a 'virtual' particle since while it is an important factor in calculating the amplitude, it can never be observed directly in the final state, so in a sense it is not real. The fact that it is virtual means that it can behave somewhat oddly. For instance, virtual particles do not have to have the same mass as their real-particle equivalents. This photon does not have to have mass zero \u2013 in fact in LEP it cannot have mass zero, because it has to be at rest, and it has to carry a lot of energy, so good old _E_ = _mc_ 2 means it has a mass that is bigger than zero.\n\nTo calculate the probability of this process happening one simply squares amplitude and combines this with a term describing how many electrons and positrons are incoming (the flux) and how many different final configurations are possible (the phase space). Not too tricky really, and the Feynman diagram gives a really intuitive, snooker-ball-style representation of the process.\n\nAnd STOP, because that's where the caution is needed.\n\nFeynman diagrams are amplitudes, and before squaring them to get the probability, you have to add up all the possible amplitudes. And there is another possibility we have neglected. As well as a virtual photon in the middle there, we might also have drawn a Z boson, like this:\n\nThe initial and final states are the same, so the amplitude for this possibility has to be added to the previous one involving the photon to get the total amplitude. In fact, at LEP, because the collision energy was designed to be the mass of the Z boson \u2013 and therefore the Z propagator can have the correct mass \u2013 the Z amplitude was much bigger than the photon one.\n\nTo get the final answer we square the sum of these two amplitudes. The ordering (add first, then square, rather than the other way round) is crucial, because this is where the wave-like aspect of quantum mechanics is built in. Call the first amplitude, with the photon, _P_ , and the second with the Z boson, _Z_. Add them to get the total _T_ , so _P_ \\+ _Z_ = _T_. The probability, _T_ 2, is then equal to ( _P_ \\+ _Z_ )2. This is different from the result I would get if I went in the wrong order, that is, first square the two amplitudes separately and then add: _T_ 2 = _P_ 2 \\+ _Z_ 2. You can see the difference matters immediately when you realise that amplitudes do not have to be positive numbers. Imagine the case where _P_ = 2 and _Z_ = -2. In the correct calculation, I get _T_ 2 = (2-2)2 = 0. This is an example of destructive interference between two amplitudes. If I do it wrong, I get _T_ 2 = 22 \\+ 22 = 8.\n\nIf you think of Feynman diagrams as real snooker-ball-like pictures of what is happening, you would never get interference effects, you would never get zero for the answer. You are neglecting the quantum nature of the interaction, and you will not describe the data.\n\nA final twist on these wonderful diagrams . . . There are other amplitudes that one should add as well. For instance, there is no reason why two photons couldn't be exchanged, like this:\n\nSo we should add this amplitude too. And in fact an infinitely large stack of increasingly complicated diagrams is possible and should in principle be included. The fact that saves us from this, and means we just have to calculate a few diagrams, is that the number that comes into the equations with every new vertex \u2013 where three or four particle lines meet \u2013 is small. So every time a diagram gets more complicated, it also gets less important. This means that by calculating the first few diagrams, you can get a very precise answer, and the more complicated diagrams would just be a small correction to this.93\n\n93. This is perturbation theory, see 6.2 Perturbation Theory: Are We Covering Up New Physics? And it doesn't always work.\n\nThere you have them. Feynman diagrams: a beautiful and essential tool, very intuitive and helpful, but potentially deceptive if not treated carefully. Even the best physicists can be misled by Feynman diagrams occasionally.\n\n#### 5.4 W and Double W\n\nIn the summer of 2011, the data from the LHC started to show an effect that might, or might not, be the first indication of the presence of a Higgs boson. Most of this effect was due to the number of pairs of W bosons that were being produced in the proton\u2013proton collisions. These extra W boson pairs could have been the result of a Higgs boson entering into the production process, like this:\n\nDiagram showing a Higgs boson decaying to a W+ and a W-, which then decay to leptons. (See Glossary: Feynman Diagrams.)\n\nIt was tantalising to think this might be happening, but of course lots of caveats applied, both statistical and systematic.\n\nIf the Higgs boson were to have enough mass (that is, since _E_ = _mc_ 2, enough energy at rest), it would decay very quickly into a pair of W bosons. So if the Higgs was there, extra pairs of W bosons were one way we might first see it.\n\nIn contrast to the Higgs decay to two photons, however, a decay to W bosons will not lead to a bump. Generally, if you can measure the energy and momentum of the decay products you can reconstruct the mass of the original (in this case the Higgs boson). Unfortunately, the W bosons in question decay to an electron, or muon, plus a neutrino. The electrons and muons can be measured well (in the inner tracking detectors, the calorimeter and the muon system), but the neutrinos cannot. Neutrinos do not interact much at all with anything, including our detectors. To see any neutrinos, you need a detector much bigger and denser than ATLAS, and billions of neutrinos. So we don't see them. The missing momentum they carry away gives a clue, but it doesn't allow us to reconstruct a Higgs mass bump.\n\nThis is one reason the excess we were seeing was so susceptible to theoretical uncertainty. You don't need much of a theory to tell you whether or not there's a bump in your distribution. If the distribution has a significant bump in it, there's probably something there, whatever the theorists say. But we can't reconstruct a bump, so we just have to count WW pairs and see whether there are more than we expect. The theory tells us what to expect, but comes with errors.\n\nAbout midnight on 14 June, the ATLAS and CMS experiments passed a major milestone six months early. The target at the start of the year, set for themselves by the people running the accelerator, was to deliver one inverse femtobarn of integrated luminosity to the experiments in 2011. The integrated luminosity determines how many proton\u2013proton collisions the experiments can record. In line with the presentational sensibilities of the average particle physicist, this led to a Clip Art bottle of champagne featuring in the status reports the day after.\n\nThe round number was a largely arbitrary milestone. However, lots of the studies and projections done over the previous year used an inverse femtobarn as their 'baseline projection', so everyone knew very well that a lot of physics could be done with that amount of data, and that the accelerator was continuing to deliver at a great rate.\n\nBy coincidence, the first ATLAS paper on the search for the Higgs94 was submitted on the same day; there was no sign of the Higgs, but it was easy to see that we would be closing in soon, and that the WW decay mode would be playing an important role.\n\n94. <http:\/\/arxiv.org\/abs\/1106.2748>.\n\n#### 5.5 Meanwhile in the Neutrino Sector\n\nEven in 2011, particle physics was not all about hadron colliders.\n\nTwo major particle-physics labs are a couple of hundred kilometres south of Sendai in Japan. The J-PARC facility is right on the coast, in Tokai, and an accelerator there sends a beam of neutrinos to the Super- Kamiokande experiment, 295km away in Kamioka. This is the T2K long-baseline neutrino experiment.\n\nThe neutrino beam is measured in J-PARC, very close to the target in which it is produced. (You produce neutrinos by hammering protons into a lump of stuff. There's a bit more to it than that, but those are the basics.) Then the beam travels 295km, mostly unimpeded by the rock it travels through, to the Super-Kamiokande experiment. This is an enormous underground bubble filled with 50,000 tons of water and surrounded by 13,000 photon detectors. Some of the neutrinos interact here.\n\nIn the Standard Model, neutrinos are produced at the same time as an antilepton. This can be either an antineutrino, or a charged antilepton \u2013 a positron, an antimuon or an antitau. When they are produced along with a charged antilepton, they are labelled accordingly as an electron-, muon- or tau-neutrino. This label is called 'flavour'. Likewise, if and when they interact with the Super-Kamiokande detector, they mostly produce an electron-, muon- or tau-lepton, so you can label them by this at the end of their journey too.\n\nHowever, neutrinos also have mass. And as they travel along, the mass is actually what is important, since it fixes the relationship between their energy and momentum. If you think of them as waves, which is the right thing to do in this case, the mass fixes their wavelength.\n\nThe odd thing is that the mass labels (call them masses m1, m2 and m3) do not match up with the flavour labels (electron, muon and tau). Because each lepton label is made of a mixture of mass labels, the neutrinos oscillate between lepton labels as they travel, because the different wavelengths go in and out of synchronisation as they travel. So the labels you see in Super-Kamiokande are not necessarily the same as the labels you see at J-PARC.\n\nThis phenomenon of neutrino oscillation has been measured before; it is the reason we know that neutrinos do have non-zero mass. In the old Standard Model, as it existed up until 1998, they had zero mass. There was an outstanding problem in physics called the 'solar neutrino problem', dating from the 1960s and stemming from pioneering measurements by the Homestake experiment led by Ray Davis and John Bahcall. This detector, in a mine in South Dakota, USA, measured the rate of neutrinos coming from the Sun and compared it to predictions based on what we know of the nuclear processes taking place there. The result was that there were not enough neutrinos. Various explanations for this were floated, including the possibility that the experiment was wrong (so it was repeated with independent techniques several times) or that our understanding of the Sun was wrong. No one could find a problem with Bahcall's model, but there was one rather terrifying possibility. Neutrinos and photons are both produced inside the Sun, and the number produced depends upon the rate of the nuclear reactions in the heart of the Sun. Photons produced inside the Sun scatter and re-scatter from the solar plasma and take thousands of years to escape, whereas neutrinos, because they only interact weakly, escape immediately. So a possible explanation for the deficit of neutrinos was that the core of the Sun was running down, and the sunlight we could see was the result of nuclear processes thousands of years ago, which had now slowed or stopped. If so, the Sun would be unstable, and we would be living on borrowed time.\n\nSomething of a relief, then, that another explanation turned out to be correct instead. The Homestake experiment only measured electron-neutrinos. If neutrinos oscillated to muon- or tau-neutrinos on their journey between the Sun and the Earth, then some of those that started off as electron-neutrinos would arrive as muon- or tau-neutrinos, would not be detected, and would therefore explain the deficit. This oscillation can only happen if at least some of the neutrinos have mass. So Davis and Bahcall were right, solar physics was right, but the Standard Model was wrong.\n\nThe breakthrough came in 1998 when Super-Kamiokande measured neutrino oscillations in neutrinos produced by cosmic rays hitting the upper atmosphere. An even more direct confirmation came when the Sudbury Neutrino Observatory, a big tank of heavy water in Ontario, Canada, used a different technique to measure all the neutrinos from the Sun regardless of their flavour, showing that it agreed with the expectations of the solar model.\n\nSince then, neutrino oscillations have been measured more precisely using beams produced at accelerators and reactors. The first accelerator experiment to do this was the Main Injector Neutrino Oscillation Search, or MINOS. (A good name that doubles as the Minnesota\u2013Illinois Neutrino Oscillation Search, given that the beam is fired from Fermilab in Illinois to the Soudan mine in Minnesota.) T2K was part of the next generation of these experiments.\n\nBack at ICHEP in Paris, Eric Zimmerman from the University of Colorado had shown some of the first neutrino events from the T2K experiment. These were being analysed as more data were collected, and the result had been eagerly anticipated. However, a catastrophic earthquake struck Sendai in March 2011, just before a planned seminar to announce the first T2K results on neutrino oscillations. In fact, a series of seminars around the world had been planned. The lab suffered serious damage and for a worrying period all the websites and email addresses at the big high-energy physics labs, KEK and J-PARC, went offline. Though everyone in the neutrino experiment hall of T2K was evacuated safely, the seminars were postponed until the results could be announced in Japan first. In June, finally, the results were made public. T2K had seen indications of muon-neutrinos turning into electron-neutrinos.\n\nThe Standard Model can be modified, and has been, to accommodate neutrino masses, but this is a major change. It's a case of 'The Standard Model is dead \u2013 long live the Standard Model.' But it is a profound change, and has taken a long time to absorb properly. I still find myself examining PhD theses where the introduction states that 'In the Standard Model, neutrinos are massless . . .'\n\nIn the post-1998 Standard Model, the way neutrinos oscillate can be defined using a matrix containing three angles. By 2011, two of these had already been measured by several experiments, including MINOS. But the third was unknown, and could have been zero, in fact. T2K was seeing indications (at the level of a couple of sigma) that it was not zero. That would be quite profound news, if confirmed.\n\nApart from the fact that neutrinos themselves are important \u2013 they are fundamental and they are everywhere, and their presence affects how the universe formed and developed \u2013 this question goes way beyond neutrinos alone. In nature, all the fundamental matter particles come in three copies, or generations. Like the neutrinos, quarks also have these three copies. The mass of each generation is heavier, so muons are basically heavier copies of electrons, and tau leptons are heavier still. Likewise, top quarks are heavier than charm quarks, which are heavier than up quarks.\n\nAlso we know (from measurements of the decays of the Z boson at LEP) that if there are any more generations out there, they are much, much heavier \u2013 even the neutrinos. Or else they are weirdly different in other ways. It looks like the fundamental particles of nature come in three and only three copies. The Standard Model does not predict this should be so, it just seems to be that way.\n\nThis is pretty odd, and is connected to one of the big open questions in physics \u2013 where did all the antimatter go? Since everyday matter, every atom, is basically made of the first generation alone (up and down quarks, and electrons), the other two copies, or generations, seem a bit superfluous. But there is a really intriguing hint in this of some deeper theory. Three copies are _just_ enough to allow matter to be different from antimatter. The effect can occur when you mix up three or more copies, but mixing up two, or only having one, is no good. Experiments have shown that such mixing, and matter\u2013antimatter differences, do occur between quarks. What was unclear was whether this might also happen with neutrinos. Going back to the mixing angles: if the third mixing angle were zero, then it couldn't happen, because we would only have two-way mixing. If, and only if, the third angle is non-zero, then matter\u2013antimatter differences could happen amongst leptons as well as quarks. Given that we are made of matter, not antimatter, such differences are important. How the universe, at least as far as we can see it, got to be made of matter and not antimatter is one of the outstanding questions of physics and cosmology. The matter\u2013antimatter differences we do see in the interactions of quarks seem to be too small to explain it all. So if the neutrinos also show some differences, that would not only be a big new piece of physics in its own right, but it might be a clue as to what is missing in our understanding of the whole relationship between matter and antimatter.\n\nAnyhow, the first step is to see whether the neutrinos mix three ways or just in pairs, because that's a necessary condition for the kind of matter\u2013antimatter asymmetry we would expect in the Standard Model. At this point, T2K was saying most likely they are, though the uncertainties were still too large to be sure. Meanwhile, physicists in China and Korea were working on it with nuclear reactors . . . of which, more later.\n\n#### 5.6 Quantum Fields and Missing Quotes\n\nI was asked to give a CERN seminar on 7 June about ATLAS measurements of jets. I always learn something when I have to give a seminar, even if the audience don't. One of the things I learned this time is that not everything is on the Internet yet. Of course I knew this really, but I needed reminding.\n\nJet measurements tell us a lot about the strong nuclear force, QCD, which holds the atomic nucleus together. We talk a lot about how the LHC may find 'new physics', by which we often mean new particles or new forces, or even wilder stuff like extra dimensions of space\u2013time. However, we also have a lot of new physics to learn about the forces we already know of, especially the strong force.\n\nStrong forces in general are tricky. They can lead to consequences that are impossible (or at least very difficult) to predict with current techniques. Things like the masses of hadrons, and the way quarks and gluons are distributed inside them, can be understood to a very large extent using different approaches to calculating with QCD, but all of them need some experimental inputs, even though in principle it should be possible to derive them from the theory alone. This derivation is tricky exactly because the interaction is strong. The emergent properties of strongly interacting quantum field theories are complex, fascinating and worthy of study.\n\nAnyway, I remembered a quote I had used in a talk nearly ten years before from Martinus Veltman, who won the Nobel Prize in 1999 with Gerardus 't Hooft for work on fundamental forces. The quote was something like:\n\nIf the Large Hadron Collider finds a Higgs boson and supersymmetry, nature will have missed a golden opportunity to force us to understand strongly interacting quantum field theories.\n\n_Nobel Prize winner Martinus Veltman (possibly)_\n\nWhat he meant was, if there is a Higgs boson and supersymmetry within reach of the LHC, our current techniques for solving quantum field theories will be 'good enough' to understand them. But if there were no Higgs, a very likely outcome is that even the weak and electromagnetic forces become strong, and therefore badly understood, at LHC energies. In this scenario, if we want to understand anything, improving our understanding of strong forces in general would be essential.\n\nOf course, my point in the talk was that we should do this anyway, since we know one of the fundamental forces is strong.\n\nI wanted to use the quote again, so I went searching for the source on the Internet, like you do. I knew the words might not be exact, so I tried the usual tricks of different combinations in Google and so on. No joy.\n\nIn desperation, I went searching for my own talk, in which I knew I had used the quote. I had to dig out an old password to get into the site, but in the end I tracked down my slides. Only to find in there the approximate quote, with the words:\n\n(Paraphrased . . . couldn't find the exact quote this morning.)\n\n_Jon Butterworth (being sloppy ten years ago)_\n\nDamn.\n\nI know I met Veltman at Nikhef, the Dutch national subatomic physics lab in Amsterdam, a few months before that talk. He was associated with the lab so they were celebrating his Nobel, and by coincidence I was giving a seminar there, and Susanna had come along for a weekend break. We got invited to the party. We drank quite a bit of champagne and, a bit star-struck and urged on by Susanna, I got the great man to sign my _Rough Guide to Amsterdam_. I suppose it is remotely possible that I actually got the quote direct from him at this party. If so, I hope the paraphrase is accurate. Either way, the sentiment is still correct, and I used it again in the CERN seminar.\n\n#### 5.7 Exclusion Limits: The Boson Fights Back\n\nAs the conference season rolled on in the summer of 2011, the Large Hadron Collider continued to deliver shedloads of data (or inverse barnloads, perhaps). We continued telling people that unauthorised leaks should be ignored because the results had not been reviewed. But this of course just meant that the pressure mounted to get the real, official results reviewed and approved as soon as possible. An organised chaos of analysis, cross-checks, comments and approvals continued around the clock (literally, since ATLAS is a collaboration crossing many time zones). This was not just about the Higgs results, but also searches for other stuff that might happen, and measurements of what was actually happening in our collisions. The last of these took up most of my time, since that was the job of the group I was coordinating.\n\nAbsorbed in those measurements as I was, I couldn't ignore what was happening in the Higgs searches. In fact, some of the measurements my group was making (for example the measurements of WW production) were essential cross-checks and inputs for the search. Eventually we had our results ready for the next big conference \u2013 in this case the European Physics Society (EPS) meeting in Grenoble.\n\nAs is usual for scientists, I worry a lot about bias. The prospect of going to all the effort of building an experiment to find an answer, but getting the wrong answer because of subjective bias, is a nightmare. This is true of any experiment, but it's very stark for one the size of the LHC and for a question as important as whether there is a Higgs boson or not.\n\nOnce I knew the ATLAS results, but before they were public, I wrote an article about them. Of course, I didn't publish it until after the results were released, but at the point of release we would also have the independent results from CMS, and I wanted to put down my thoughts about our data without using the CMS data as a cheat sheet that might bias me. Here's what I said:\n\nIt is Wednesday evening, after a day of sitting in discussions where the last batch of ATLAS results were approved to be shown at EPS. These included our Higgs searches. I can only reveal the results on Friday, which is why you aren't reading this before then. But I am writing it beforehand for a good reason, which I'll explain at the end.\n\n. . . With the amount of data we have analysed, we should have ruled out possible Higgs bosons with masses between about 130 GeV and 200 GeV, and also between about 320 GeV and 460 GeV. If we had done this, it would be a big extension of the previous exclusion limits and would really be squeezing the possible hiding places for the Higgs . . . All this, of course, is if there is no Higgs boson.\n\n. . . What the data actually say [is] we have excluded at 95% confidence a Standard Model Higgs with a mass between 155 GeV and 190 GeV, and similarly between 295 GeV and 450 GeV. Some of this range was already excluded by the Tevatron experiments, but this is still a big advance. In fact around 290 GeV we are doing 'better' than expected, which could of course just be to do with fluctuations in the data.\n\nBut it gets even more interesting about 155 GeV. Below here, we are not doing as well as we should.\n\nThis means one of three things:\n\n1) We were unlucky, and an upward random fluctuation in the background messed up our sensitivity.\n\n2) We did something wrong and failed to find it yet (these are still preliminary results, though they have been reviewed by the ATLAS collaboration).\n\n3) A Higgs boson, or something very much like it, is lurking in there somewhere below 155 GeV and is starting to emerge, blinking, into the light.\n\nI am writing this now because I want to say what I think about our own data before I see what the Tevatron experiments, or our friends across the LHC, CMS, are going to say. By the time you read this, I will probably know. But here you get my judgement of what our stuff means, independent of any bias from other experiments.\n\nIf [at EPS the other experiments] show exclusion limits going down below 155 GeV, this means ATLAS was unlucky (or wrong) and the Higgs has less room to breathe.\n\nIf they show exclusion limits which they didn't expect to go below 155 GeV, this means they are not sensitive enough to say anything about the ATLAS result in this region.\n\nIf they show exclusion limits which, like us, they _expected_ to go below 155 GeV but which _don't_ , then the chances that this is the first sign of the Higgs boson emerging into the light are increased.\n\nIt's not decisive, but from the ATLAS data alone the odds have shifted in favour of the Higgs being around. When CMS and the Tevatron show their data, the odds will either shift back again, or shift further in favour of the Higgs. I don't know yet. But in contrast to some previous occasions, it's now getting really interesting.\n\nThe ATLAS Higgs results are being reported by Kyle Cranmer (New York University) at 15:00 CEST (after which I will post this article), just before CMS. All the Higgs results from the Large Hadron Collider will be summarised in the plenary later by Bill Murray (STFC Rutherford Appleton Laboratory). They are the result of a massive amount of work by hundreds of people on the LHC machine and on ATLAS.\n\nI am putting this in here because I think it gives a sense of the real uncertainty at the time \u2013 the caution, but also the excitement.\n\nAs I've mentioned, and whatever the lunatic black-hole-armageddon fringe might say, when it comes to particle-physics results lives don't generally hang in the balance. But many of the same issues \u2013 statistical confidence, systematic bias, blinding of experiments \u2013 apply to medical trials, or climate research, where lives are at stake. In all cases there are usually plenty of massive egos and vested interests involved. Real knowledge about how things work emerges from rumour, claim, counterclaim and honest doubt.\n\nRegarding those results I wrote about before the EPS \u2013 what actually happened? Which of those three options turned up? Well, the Tevatron experiments were not sensitive to the standard-model Higgs in the relevant mass range. Their sensitivity stopped at 148 GeV, at the time. However, CMS were indeed sensitive, and saw something similar to ATLAS (without having seen our results first, just like we had not seen theirs). So that improved the odds further.\n\nNext we needed to reduce the uncertainties.\n\nFirstly, the statistical ones. The excess could have been just a random upward fluctuation. Imagine tossing a coin to see if it was fair. If the first four throws all came up heads you might become suspicious, since you would have expected two heads and two tails. But this is not a very significant result. The chances of getting four heads even with a fair coin are one in two to the power of four, or one in 2 x 2 x 2 x 2 = 16. And the chances of getting four the same (either four heads or four tails) are twice this (one in eight). So you would have to carry on tossing the coin a lot longer before you were more convinced (to, say, one in a thousand, or 99.9 per cent confidence) that it was biased. This is an example of statistical uncertainty on the confidence with which you can say something \u2013 in this case, 'the coin is biased'. The uncertainty shrinks as you take more data \u2013 toss the coin longer. So obviously we would continue to collect data from more proton\u2013proton collisions at the LHC and to analyse them \u2013 the equivalent of tossing coins \u2013 so that we could see whether the Higgs was in there, biasing the result.\n\nThe second type of uncertainty is systematic. These uncertainties can come from how well (or how badly) we understand our detectors. For example, if an electron hits it, how often do we actually see it? And how well do we really measure its energy?\n\nATLAS and CMS are completely independent detectors. So not only do they double the statistics (shrinking the first kind of uncertainty), they also have independent, and very different, systematic uncertainties arising from how the different detector technologies are understood. So seeing things in both experiments really builds confidence. Also, the more data we get, the more control experiments we can do to test and improve our understanding of the detectors.\n\nUnfortunately, not all systematic uncertainties are independent. Of those that are not, the most important is the uncertainty in the theoretical calculations. The theory tells us what a Higgs boson of a given mass should look like, and also what the background \u2013 non-Higgs production events \u2013 should look like. CMS and ATLAS both rely on this. When we say 'we have an excess of events' we mean we have more events than one would expect if there were no Higgs boson. And we are both using the same theory to do this. So if it is wrong, we could both see a false signal.\n\nThe theory we have is actually very good. However, it is only a theory. To reduce the systematic uncertainty here, the method is similar to the way we reduce detector systematic uncertainties, but also involves theorists. We have to do more control experiments, measuring the production of different kinds of particles at LHC energies, and see how well the theory describes them. And if it doesn't, we have to find out why and fix it. In this case especially we needed to measure the production of W bosons, since most of the excess we were seeing at that time was in events where two W bosons were produced.\n\nOn to the next round, and the next conference. It was August 2011 and every big conference was getting updates on progress in the big Higgs hunt. I had missed Grenoble, but was heading to Mumbai.\n\n#### 5.8 Mumbai\n\nThe tea on the plane was excellent.\n\nI never thought I'd write that sentence, but I suppose if you are ever going to get excellent tea at 30,000 feet it will be on a BA flight to India. India were losing to England at cricket, but the taxi driver still talked about little else all the way through the suburbs. This was a proper car: the little three-wheeled autorickshaws teem through the outskirts but are banned from central Mumbai, and I suspect from the airport too.\n\nI travel a lot as a particle physicist, but I'm not really very widely travelled. Most trips are back and forth to Geneva, but even before the Large Hadron Collider induced that semi-regular commute I mostly stayed in Europe, with the occasional trip to North America or Japan. Basically, the richer and more industrialised bits of the world, I guess. Perhaps that isn't so surprising. Even I would not put major particle-physics facilities at the top of the wish list in the first stages of developing an economy.\n\nThat said, particle physics would feature quite early on. The activity has lots of economic benefits and is an essential part of any national research infrastructure that attempts to address big questions about the nature of the physical world we inhabit. Plus, the subject is by necessity very collaborative. Rolf Heuer, Director General of CERN, said in his final address at the European Physical Society meeting that the 'E' in CERN now stands for 'everyone', not just for 'European'. If you want to do physics at the energy frontier, then at the moment you have to go to CERN, wherever you are from. And to carry on doing science at this frontier in the future will require global collaboration.\n\nIndia has been part of this for a long time. The famous Indian physicist Satyendra Nath Bose gave his name to the generic class of particles with integer angular momentum \u2013 bosons \u2013 of which the Higgs was at this point a still-hypothetical example, but the W and Z bosons (and the photon) were well established. The Tata Institute in Mumbai has a long history of involvement in fundamental science. In 2011 it was hosting the Lepton Photon conference. Cue visa hassles, immunisations, tea and taxis, and the realisation that I had been jetting about inside a bit of a cocoon.\n\nAt Lepton Photon conferences there are no parallel sessions. The talks are all plenary 'rapporteur' talks \u2013 a great place to get an overview of the field. At Lepton Photon 1999 at Stanford, USA, I gave a talk on photon structure.95 The thing I remember most from that meeting, though, is hearing Saul Perlmutter describe the results on supernova brightness that were part of the new and mounting evidence for dark energy in the cosmological standard model. Those results won the Nobel Prize for Perlmutter, Brian Schmidt and Adam Riess in 2011.\n\n95. It doesn't really have a structure, but in an interesting way.\n\nTo be honest, I also remember the Napa Valley tour and the excellent wine selections we had for the lunches and dinners on the Stanford campus, for which I think Jo-Anne Hewitt96 and the other organisers still deserve credit.\n\n96. See 3.5 Super Symmetry.\n\nThe other Lepton Photon meeting I attended was in Uppsala, Sweden, in 2005. I gave the talk on experimental studies of QCD. Gavin Salam (as seen in _Colliding Particles_ ) was giving the theory talk on the same subject. I remember being asked many times whether I was related to Ian Butterworth, a former research director at CERN, and thought it odd that no one asked Gavin if he was related to Abdus Salam (Nobel Prize-winning theorist). As far as we know, neither of us is related to either of them, anyway.97 I also remember very long queues in bars for the toilets because apparently (some) Swedes don't believe in gender-specific toilets, thus making men suffer along with women in an admirably egalitarian fashion, but without actually providing additional capacity. They should have put up notices: _Dear Men, Please \u2013 like women must do normally \u2013 plan your toilet visits 30 minutes in advance to avoid discomfort_. Also the fish was brilliant, especially for breakfast. A herring breakfast beats even English bacon and eggs, in my opinion.\n\n97. Although it turns out that Ian Butterworth was my PhD supervisor's supervisor's supervisor. My great-grand-supervisor, I suppose.\n\nGiven the depth of my analysis of cultural differences \u2013 wine, toilets and herring \u2013 I suppose tea and cricket in India were to be expected.\n\nThere was a slight tone of disappointment at Lepton Photon in the reports of the Higgs updates, which was understandable. A month before at EPS, ATLAS and CMS both had hints in the data that, while not statistically very significant, could have risen in significance at this meeting. However, even though we added more data, the significance did not rise \u2013 in fact it dropped a bit. But again, not significantly. All consistent with statistical noise in either direction, up or down.\n\nAt EPS, it became a little more likely that the Higgs was around in the mass region 130 to 150 GeV. At Lepton Photon it became a little less likely. The 95 per cent exclusion went down to 145 GeV. At higher masses, huge swathes of possibilities had been excluded. But still we had said nothing about the region between 115 GeV and 125 GeV.\n\nWe would do so soon, however.\n\n#### 5.9 Which Leads, Theory or Experiment?\n\nOne recurring theme when you talk about science in public is a perception that fundamental physics is too theory-led; that we are obsessed with proving beautiful, reductionist theories when it would be better if we just explored. And that we spend too much time arguing about untestable things. This is not a criticism to be dismissed lightly, and some of the time, for some physicists, it is almost certainly a fair one. However, even though 'hunting the Higgs' was explicitly a major part of the reason for building the LHC, I'd make three arguments against the idea that there is too much theory.\n\n##### 1) Thought experiments\n\nTheoretical discussions about currently untestable things can flush out conflicts and inconsistencies in our understanding. Black holes, for example, in one sense amount to an 'extreme thought experiment', highlighting a conflict between three amazingly successful theories, or 'laws of physics', if you prefer. Quantum mechanics, gravitation and thermodynamics have their laws, and their underlying picture of the universe. They have credibility by virtue of each being able to describe a vast range of phenomena, from steam engines through planets to the central processing unit in your computer. In a black hole, these laws come into apparent conflict. The territories of three giants overlap. By thinking through the contradictions that arise, we can find gaps in the theories, develop new understanding, and in the end hopefully derive observable predictions that could be used to test such understanding. It is a hugely worthwhile exercise, unless you are utterly uninterested in understanding how things work or in benefiting from such understanding.\n\n##### 2) Electroweak symmetry-breaking\n\nTo some it appears that the Large Hadron Collider is a disproportionate investment of time, money and expertise in chasing some theorists' dreams. I disagree, of course. While the Higgs is the headline, the LHC is genuinely exploring new territory for whatever might be there. The energy frontier (or, if you like, the short-distance frontier \u2013 we study nature at smaller-distance scales than anywhere else) remains a frontier of knowledge, whether Peter Higgs says it is or not. Plus, we have very good reason, from experiment alone, to think that this part of the frontier is special. Look at this plot:\n\nData from the ZEUS and H1 experiments at DESY, Hamburg.\n\nWhat this shows is essentially the probability of an electron bouncing off a proton, with the energy of the bounce increasing as you go from left to right. The clear points show the times when it bounces because of its electric charge \u2013 the electromagnetic force. The solid points are the times when it bounces by swapping a W boson \u2013 the weak force. You can see that at low energies (towards the left) the electromagnetic bounce is much more likely. But at high energies (on the right) the weak force is just as likely to be responsible as the electromagnetic. There is a symmetry between the two forces that is restored at this energy. These are data from the HERA experiments. Measured. No theory. (Actually the curves are theory, but you can ignore them if you wish.)\n\nThe LHC, for the first time in the history of science, was allowing us to explore properly above that energy, into the region where the symmetry holds. Our theory says the Higgs breaks the symmetry. But even without that theory, you might think exploring physics above this fundamentally important energy scale is an exciting thing to do and might tell us how these forces work and why they are sometimes the same and sometimes different.\n\n##### 3) Gloating\n\nFinally, the LHC data had even by this stage, after just of a year of running, led to a bonfire of theories. While big ideas like supersymmetry or extra dimensions had not been completely disproved, many options for them have been closed off.\n\nOn the last day of the Lepton Photon conference, the Mumbai monsoon let rip in a big way. The noise of rain was so loud at lunch that you could hardly hear the SUSY theorists weeping into their curries after the results reported by LHCb that morning. LHCb is the one of the four big experiments on the LHC but has featured least in this story so far, largely because it is designed to measure rare particle decays (especially of hadrons containing b quarks, hence its name) and as such does not participate in the hunt for the Higgs. However, it does have very good sensitivity to physics beyond the Standard Model. The SUSY theorists were not really quite in tears, but the LHCb talk by Gerhard Raven had dealt their favourite theory a blow. He reported a beautiful measurement of a specific decay of the Bs meson (a hadron containing a beauty quark and a strange quark). This agreed very well with the Standard Model, which, despite the confidence of some theorists, does not include SUSY. Previous, less precise measurements had been a bit away from the standard model and the difference could have been due to SUSY. It wasn't. More hopes dashed. SUSY is even more slippery than the Higgs, though, and rumours of her demise are exaggerated.\n\nAlso at the meeting, a friend of mine, Jenny Thomas, reported on recent and future long-baseline neutrino experiments such as T2K. One thing she had to say was that yet another 'hint of new physics' \u2013 this time from her experiment, MINOS \u2013 had gone away. This was an apparent unexpected difference between the behaviour of neutrinos and antineutrinos, which had first been reported at ICHEP in Paris the previous year. The measurement was interesting but not very precise and, as with LHCb, more precision had again vindicated the Standard Model, to the disappointment of many.\n\nJenny made the point that we often start taking such anomalies too seriously too soon. People talk about 90 per cent exclusions, or 10 per cent probabilities that some piece of data is consistent with the Standard Model. But 10 per cent is not a small number. You will have many 10 per cent chances coming up if you do a lot of science. And as we saw in Mumbai, results are flooding in all the time, from the LHC but also from elsewhere. It's fine to be interested, excited even, but we have to keep a realistic attitude. For the Higgs search at least we talk about 95 per cent exclusions. But '3 sigma', which is the conventional standard for real evidence, is 99.7 per cent probability.98 And 5 sigma, conventionally a discovery, is 99.99994 per cent. And there are good reasons for these conventions. Even with such high levels of certainty, odd things happen and mistakes still get made.\n\n98. See Glossary: Sigmas, Probabilities and Confidence.\n\nIt is true that many of us have our favourite theories, but in the end the data decide, and as an experimentalist I seriously enjoy making myriad bright ideas face the music. We had waited a long time, theorising and guessing. Now, at last, we were able to look at some more of the answers.\nSIX\n\n## First Higgs Hints and Some Crazy Neutrinos\n\n### September\u2013December 2011\n\n#### 6.1 Faster-than-Light Neutrinos: A Case Study\n\nWe were now building up to the CERN Council meeting in December. We would be required to give an end-of-year report on the LHC results, especially (of course) the Higgs boson search.\n\nThe CERN Council is the governing body of CERN. CERN was set up by 12 European states99 in 1954 to help rebuild European physics after the Second World War, when many of the world's best physicists had fled Europe, often initially for the UK, where they were in general immediately encouraged to head for the USA, which they did.100 And many of them then helped build the bombs that were dropped on Hiroshima and Nagasaki.\n\n99. Belgium, Denmark, France, the Federal Republic of Germany, Greece, Italy, the Netherlands, Norway, Sweden, Switzerland, the United Kingdom and Yugoslavia. 100. Thankfully, of course, the UK would never be so stupid and unwelcoming to asylum seekers and talented would-be immigrants these days. Would it?\n\nCERN was set up to be explicitly non-military. Several countries not aligned in the cold war (including, for example, Switzerland) were founder members, and even at the height of international tensions cooperation with the Soviet Union and other Warsaw Pact countries continued. The summer school I attended in 1991 was organised jointly by CERN and its nearest Soviet equivalent, the Joint Institute for Nuclear Research ( JINR). I got to visit Dubna, the big Russian lab near Moscow, and we spent two weeks in Alushta on the Black Sea, in the Crimea. A few weeks later, Gorbachev was staying in a hotel quite near ours when the coup took place that triggered the break-up of the Soviet Union.\n\nThe Council is made up of two representatives from each CERN member state, as well as the Director General and his immediate team. It is also often attended by representatives from observer states and states applying for admission. The UK delegates are a senior civil servant from the ministry responsible (Business, Innovation and Skills, at this time) and the chief executive of the relevant research council (currently the STFC). When one of these can't make it, I often attend instead. As well as overseeing the running of the laboratory in Geneva, the CERN Council is also mandated with the 'organisation and sponsoring of international cooperation in the field'.\n\nI find it easy to imagine Director General Rolf Heuer's face when, just as we were building up to the December reports that might be decisive in terms of the Higgs, another CERN-related experiment knocked on his door and asked to give a seminar claiming to have measured a particle travelling faster than the speed of light.\n\nThe particles were neutrinos, and the experiment was OPERA.101 At the same time as the seminar, they submitted a paper to the arXiv102 and a journal, so we could read and review the evidence behind this extraordinary claim.\n\n101. Oscillation Project with Emulsion-tRacking Apparatus. Dodgy acronym, dodgy experiment? 102. arxiv.org\/abs:1109.4897.\n\nOPERA measures neutrinos produced from the SPS. The SPS (Super Proton Synchrotron) is one of the accelerators in the CERN accelerator complex. In a previous incarnation as the Super Proton\u2013Antiproton Synchrotron, it was responsible for the collisions in which the UA1 and UA2 experiments discovered the W and Z bosons in 1983. Carlo Rubbia and Simon van der Meer received a Nobel Prize for this a year later, and in retrospect, though CERN had made important breakthroughs before, this looks like the moment it became a really world-leading laboratory. The SPS is now also an injector for the LHC. So, a very useful piece of kit.\n\nThe neutrinos are regularly fired 732km under the Alps and beyond to the Gran Sasso National Laboratory in Italy, where some of them are detected by the OPERA experiment. This experiment is designed to measure how the neutrinos change their properties as they go. They are trying to measure the appearance of tau-neutrinos, in fact. But they also have some very precise Global Positioning System (GPS) position and timing measurements. So they know the distance the neutrinos travel, they know how long it takes them and they can therefore measure the speed. Since neutrinos have a tiny mass, the speed should be very close to the speed of light. But they measured neutrinos arriving early \u2013 thus travelling faster than the speed of light.\n\nIf this result were valid, it would be an amazing breakthrough. The speed of light, _c_ , as a maximum speed limit is built very deeply into the maths of how we understand the universe.103 It is one of the foundations of the theory of relativity, which precisely describes all kinds of physics, including the physics behind the GPS systems used to make the measurements and the accelerators used to make the beam. So it can't just be thrown out. Some better theory would have to be found that contained and extended Einstein's edifice.\n\n103. See 2.2 Minimum Bias.\n\nIt might be hard to imagine what such a theory might be, but pretty quickly the fans of 'extra dimensions' theories came up with some thoughts whereby the neutrinos take a short cut across another dimension. Sort of the equivalent of a two-dimensional Londoner living on the surface of the globe taking a short cut to Sydney via the Earth's core.\n\nFun to think about, but all a bit premature. It was just a single result, and the OPERA people themselves could hardly believe it. The paper looked like quite a careful publication, and the collaboration had reviewed it at some level, though some members did say publically that this had not been as thorough as they would have liked. Dario Autiero, the OPERA physics coordinator, gave a scientific seminar at CERN on 23 September, when they received and answered a lot of questions. This is the way science is done, and I didn't blame them for speaking to the press too, and being excited about the potential implications of their data. What should they have done, kept it secret? Imagine the conspiracy theories if they had done that. 'CERN suppresses evidence that Einstein was wrong!!' I already get plenty of green-ink letters and emails shouting about that. Preventing OPERA from showing the data they wanted to show would have justified some of those.\n\nI also did not and would not blame the media for getting excited by this. What should they have done, ignored it? Gratifyingly, people are interested in physics and this was a proper story. It may have been overexposed and in some cases overhyped, but this was a genuine scientific debate, going on in real time about an intriguing result. It was not a manufactured controversy. As long as people appreciated that, maybe seeing science done in public could become a new, educational, spectator sport. Ideally even a participation sport. That would be a good thing, surely?\n\nThe big question of course was, 'Is it correct?' What might have gone wrong? It looked like a careful study, the result of years of work by a pretty big team, so to fire off 'It must be wrong' comments without due care seemed unfair, even though I must admit that was my immediate reaction. Jim Al-Khalili had no such qualms, promising to eat his boxer shorts if it was right. But in the spirit of doing science in public, I tried to explain my main concerns with the results.\n\nThis was to do with the time distribution of the protons at the source in CERN. The protons hit a target and ended up producing neutrinos. OPERA also measured the time distribution of neutrinos arriving at Gran Sasso. They fitted one distribution to the other, and when they lined up, that gave them the time of flight, and thus the speed. Most of the power of the measurement came from the leading and trailing edges of the pulse \u2013 that is, the arrival times of the first and late neutrinos in the pulse.\n\nThe claim was that fitting to the distribution gave an accuracy of about 10 nanoseconds (6.9ns statistical and 7.4ns systematic uncertainty). This seemed bold to me. But the main worry I had was they seemed to assume that the shape of the time distribution should match exactly. There was no allowance in their estimate of their systematic uncertainties for the possibility that they might not, and it wasn't hard to imagine reasons that the shape, as a function of time, of the neutrino pulse at Gran Sasso might not be a true reflection of the shape of the neutrino 'turn on' and 'turn off' at CERN. To me that looked like an odd, possibly serious, omission. For example, at CERN, where the neutrinos were produced and measured initially, all the protons were included in the time profile. By the time it got to Gran Sasso the beam fanned out to cover an area much bigger than the OPERA detector, so OPERA would only see neutrinos from part of the beam. So any correlation between the production time of the neutrinos and the angle they were produced at (which would determine whether they actually got to OPERA or not) could distort the shape, leading to an uncertainty in the fit and hence an uncertainty in the speed.\n\nI ended up sketching this on a napkin for a BBC documentary presented by Marcus du Sautoy that was made impressively quickly after the first results came out. I thought it was an interesting discussion to have, though I didn't claim it to be a debunking of the result.\n\nI'm glad I didn't. A few weeks later, the OPERA collaboration submitted an updated version of their paper. The most important change since their first version was that a new test had been done. Now, instead of firing long blobs of neutrinos, CERN had been firing short pulses, just three billionths of a second long. So now to measure the time, the OPERA physicists did not need to know the shape of the pulse, they just needed to know which pulse the neutrino came from. They redid the study, and after seeing just 20 neutrinos they came up with the same answer: the neutrinos still appeared to be travelling a bit faster than the speed of light.\n\nThat was one test survived, but there were other tests that needed doing. To be honest, this was such a remarkable result, with such profound implications if correct, that we needed at least one completely independent experiment to check it. The other long-baseline experiments \u2013 MINOS in the USA and T2K in Japan \u2013 started gearing up to do this.\n\nThe scientific discussion continued in public. According to their inclinations, scientists were assuming it must be wrong, thinking about what could be wrong, thinking about how to test it, or wondering what might be the implications (for physics and Jim's shorts) if it were right.\n\nNow, unsurprisingly, it was wrong. More surprisingly, and embarrassingly, it was wrong in a way that no one outside the collaboration could have worked out from the paper. There was a cable connector, converting between electrical and optical transmission, that had not been plugged in properly. Once that was fixed, the answer came out to be consistent with the speed of light. This was a disappointing end to a fun story. It should have been possible for the OPERA physicists to work out that there was a possible single point of failure like that. It should have been checked before they went public. The leaders of the experiment who made those decisions stepped down.\n\nThere are three reasons why I think it is still worthwhile going through all this here, even if it is a bit of shaggy-dog story.\n\nOne is that it is worth thinking about the opposite situation. If the measurement had agreed with expectations, and showed neutrinos travelling at or below light speed, how carefully would we have examined the uncertainties? Would that connector have been checked? How much time would I have spent reading the paper? And if the result had been expected but wrong, would we ever have found out? This would be an example of confirmation bias in science \u2013 where if something aligns with expectation, you count it and credit it and stop looking for mistakes. I have measured many things that 'agree' with the Standard Model. I have also made measurements that didn't agree with the Standard Model, but this always made me suspicious, and I went looking for errors. I have always found them \u2013 either in my own measurement, or in the way we were using the theory in the comparison. We check all our measurements carefully, but I cannot honestly say that we check them equally carefully whether they agree or not with the Standard Model. If enough people repeat honest experiments, this will still be corrected in the end, but it takes time and is a subtle biasing effect.\n\nA second reason is just to point out, again if necessary, that scientific progress is not as neat and tidy as it might appear with hindsight. I am writing an account of some scientific history here. Without giving away the ending, I must say there is a chance it might end up looking like an inevitable progression towards a triumphant conclusion. This is not how it appeared at the time. Science has many blind alleys and mistakes. In the end they are irrelevant and so are forgotten, if and when the data are eventually unambiguous. But we kid ourselves, and do little credit to the process or the history, if we only remember the correct experiments.\n\nThere is a third reason.\n\nThere are quite a few people out there who are obsessed with 'turning physics on its head' (often professional physicists and journalists), or at least with proving Einstein wrong (amateurs, usually with green pens), or who are just generally outraged at science's claims to some kind of objective truth and special status (the more mediocre philosophers or sociologists, mostly, but sometimes people with a political or religious agenda at odds with the reality emerging from data). The idea that new data can disrupt science is a wonderful thing, and the fact that it can still happen even with all the confirmation biases I've already discussed is precious. In fact, there are huge incentives for scientists to produce disruptive, paradigm-shifting data. You will be famous \u2013 briefly, like OPERA, if you are wrong, but for a long time if you are right. But this does not mean that when we find something new, we throw out what we already know.\n\nThere were plenty of overviews in the media of what we hoped to learn from the LHC, many giving lists of theories we might find evidence for, or disprove. The sort of theories listed \u2013 supersymmetry, extra dimensions, whatever \u2013 typically addressed some of the problems or omissions in the Standard Model. They generally postulated new phenomena \u2013 particles or forces, on the whole \u2013 that might be visible at the LHC. A list of new theories provides short cuts for experimentalists like me. If you know what you are looking for because some theory tells you, you can do a focused and efficient search. But if you don't find whatever it was, the usefulness of the search depends on how seriously the theory was taken in the first place. This is a somewhat subjective criterion. Producing results that exclude some forms of supersymmetry, for example, has been of great interest, since many people take supersymmetry very seriously as a candidate for an extension of the Standard Model. As some kind of measure of this, if you write such a paper, it will get cited lots of times.\n\nThis approach on its own is somewhat dissatisfying to me as an experimentalist, and is not the whole story. I don't see my career as consisting of chasing evidence for particular new theories, or trying to confirm the Standard Model, for that matter. The most important thing is to make measurements of what actually does happen in the new energy regime to which the LHC gives us access, and to use these measurements to challenge and improve our understanding of nature. This involves comparisons to theoretical predictions, of course, but the approach is different. The measurements are usually quite independent of the theory, in that they stand whether or not a particular theory turns out to be the right one.\n\nMany LHC papers, perhaps too many, consist of unsuccessful searches for evidence for specific theories of physics beyond the Standard Model. Many others, however, consist of measurements more independent of the theory. The two approaches are complementary, and there is also a grey area where searches are made for rather generic, and so less theory-dependent, new phenomena.\n\nIf evidence for one of these new theories turns up, or we find something that doesn't fit the predictions of the Standard Model, one could say the Standard Model is wrong. It surprises people sometimes to know that such an occurrence would be greeted with pretty much universal joy by particle physicists.\n\nThe scientist and author Isaac Asimov wrote a nice little essay (a letter, really) describing how the framework within which we understand nature is refined by science. Theories are thrown out, new ones replace them, but the process is not circular. Theories are not just intellectual fashions. In science, each successful new theory corresponds to a more complete set of natural phenomena, thus giving greater understanding, being more useful, and in this sense being more true. Asimov gives a fascinating discussion of the merits of different theories about the shape of the Earth: flat? spherical? oblate spheroid? pear-shaped? At one point he says:\n\nWhen people thought the earth was flat, they were wrong. When people thought the earth was spherical, they were wrong. But if you think that thinking the earth is spherical is just as wrong as thinking the earth is flat, then your view is wronger than both of them put together.\n\nOn the scale of a few miles, the Earth is quite flat, if you average over mountains and valleys. That's quite a sophisticated observation. But it is slightly wrong \u2013 there is a small curvature, which is of course crucial. Similarly, if the Higgs boson didn't show up soon, that would mean the Standard Model was wrong. Even if the Higgs boson showed up, the theory could be (and probably would be) 'wrong' somewhere else eventually. But over the distances and energies we'd studied so far, it could only be slightly wrong, because it described the existing data so well.\n\nJust as with the small curvature of the Earth, any small deviations from the Standard Model we see could be critical for our understanding. They would lead to the replacement of the Standard Model by some bigger, better theory.\n\nThat would not mean the Standard Model was a waste of time. It is much more right than what we had before. And the new theory would be even more right. As Asimov also said, it probably makes more sense to describe previously successful but now discarded theories as 'incomplete' rather than 'wrong'. The new theory would have to do everything the Standard Model did in terms of describing existing observations, and also describe the new observations. It would be more complete, and in this specialised sense, more true. Hence the joy.\n\nIn just the same way, anyone 'proving Einstein wrong' really has to incorporate the results of Einstein's theories where they agree with data, show where they are incomplete, and make them more complete. This is not a matter of fashion. I am old enough to remember Manchester, my home town, when purple flares were ubiquitous, then despised, then everywhere again, and then once more not. This is not science. Science advances, and is different from fashion, or philosophy. It amazes me how many academics study the sciences as a phenomenon without being able to acknowledge or understand this, the most fascinating and distinguishing aspect of this human activity.\n\nI had been booked to discuss the neutrino controversy at the Cheltenham Science Festival as part of a panel discussion chaired by Jim Al-Khalili, secure now in his boxer shorts. By the time the festival came along, the controversy was over and the results unambiguously wrong. Yet the discussion went ahead in front of a packed hall and covered a lot of this ground. Physics can be interesting even when it's wrong, I guess.\n\n#### 6.2 Perturbation Theory: Are We Covering Up New Physics?\n\nThe big question we are addressing at the LHC could be summed up as: Does the Standard Model of particle physics work at LHC energies or not? And 'LHC energies' are a significant step forward, since they are above this energy of electroweak symmetry-breaking, where two forces unify and where the mass of the W and Z bosons, and possibly all the other fundamental particles, originates.\n\nIf the Standard Model works in the new regime, there would be a Higgs boson but not much else new. If it doesn't, there might not be a Higgs but there must be something weird and new going on. There is a key question lurking behind this, which is: How well do we really understand the predictions of the Standard Model at these energies? This isn't an easy one. In general we can't solve the Standard Model exactly. We use approximations. Most of these rely on the fact that the 'coupling', that is the strength of the fundamental forces,104 is not very large.\n\n104. The number associated with each vertex in the relevant Feynman diagram \u2013 see Glossary: Feynman Diagrams.\n\nThe strength of a force can be expressed as a number. If it was 0.1, say, then the chances of two particles interacting would be proportional to 0.1 x 0.1 = 0.01. But if a third particle were involved it would be 0.1 x 0.1 x 0.1 = 0.001, a fourth would be 0.0001 and so on. This means when the coupling is small, you can ignore the contributions that involve more than say four particles \u2013 they are just a small perturbation on the main result, because they are multiplied by 0.1 x 0.1 x 0.1 x 0.1 x 0.1 = 0.00001. They don't change the result much. This is an example of 'perturbation theory', widely used in solving many problems in physics and chemistry. It is accurate if the coupling is small \u2013 that is, if the force is weak.\n\nThis approximation is not always valid. The bits when it does not work mostly involve the strong force, QCD. That's why it's called the strong force. (We don't intentionally obfuscate, it's tough enough as it is.)\n\nFor example, some aspects of how quarks and gluons are distributed inside the protons we collide can't be calculated from first principles.105\n\n105. See 4.5 Inside a Proton.\n\nNeither can the way the quarks and gluons turn into new hadrons in the end. We have some constraints from our theory, we have basic stuff like the conservation of energy and momentum, and we have a lot of data from other places. But we can't use perturbation theory. The coupling number gets near to one, and 1 x 1 x 1 x . . . = 1. This means no matter how many particles you include in your calculation, you don't converge on a reliable answer. In the end we have to make educated guesses, or models. And these are always adjustable.\n\nA serious worry, then, is that we might adjust these models in such a way that we actually cover up exciting new physics. To avoid this happening, you need to have calculations of what you know, made with perturbation theory, linked up to models of what you don't know very well, which you have some freedom to adjust. I think of this rather gruesomely as a skeleton of hard predictions inside a squidgy body of best guesses. The body can change shape. You can push in its stomach or squeeze its cheeks relatively painlessly, but it has two of each kind of limb, and you really know about it if you break a bone.\n\nAnyway, marrying the squidgy models to the rigid perturbation theory is mostly done using computer programs known as Monte Carlo event generators. These not only encode much of what we know about what happens when particles collide, but they are also an invaluable tool in designing new experiments and working out how your existing experiment is responding to data. 'Monte Carlo' is an allusion to the fact that, like roulette, they use a lot of random numbers.\n\nThere's an interesting bit of sociology of science around all this. As a theorist you can sometimes lose out from being involved in one of these generators. You can have a paper with thousands of citations and people will say 'It's only software' or 'It's just a Monte Carlo thing,' whereas with a similar number of citations in string theory you might stride the world like a colossus, despite the fact that the generator will describe data, whereas string theory struggles to predict anything remotely measurable.\n\nMonte Carlos are not the only way, but in general they are part of an effort to understand the implications of the Standard Model and to try and get it to make as many precise predictions as possible. Given the relative size of the communities, this is an effort on a scale comparable to the effort of building the LHC itself. As some recognition of this, in 2011 the American Physical Society's J.J. Sakurai Prize was awarded to three theorists, Bryan Webber, Guido Altarelli and Torbj\u00f6rn Sj\u00f6strand, who work in this area. The citation read:\n\nFor key ideas leading to the detailed confirmation of the Standard Model of particle physics, enabling high energy experiments to extract precise information about Quantum Chromodynamics, electroweak interactions and possible new physics.\n\nThis made me very happy because, for one thing, two of them are close colleagues, and for another, calculations and code written by all three of them are essential to understanding pretty much everything we are doing at the LHC, including making sure we don't cover up any new physics by mistake. As we continued trying to quantify and reduce our uncertainties in the Higgs search, looking for the crucial 3 sigma evidence or 5 sigma discovery, comparisons between Monte Carlo generators and the incoming data were carrying on around the clock.\n\n#### 6.3 Counting Sigmas\n\nAnd so, on 13 December 2011, we made our end-of-year report to the CERN Council. And, it turned out, to a sizeable fraction of the world's media. By the time I thought to get in the queue, the main auditorium at CERN was completely full. People had been eating their breakfast in there in advance of the afternoon talks. So I went into the overspill room, the 'Filtration Plant', which was also set up for the media. All the buildings at CERN have numbers, but some lucky ones have names, too. The Filtration Plant is actually (now) quite a nice meeting room, whereas the Pump Room is a large, cold garage with a few fold-up chairs and a projector in the corner. You have to know these things when you run a working group at CERN. The meeting-room booking system defaults to Pump Room.\n\nThe Filtration Plant was full too, with about half-and-half journalists and physicists like me who had not got up early enough to find a space in the main auditorium. The talks, from our glorious leader, Fabiola Gianotti, and Guido Tonelli, the head of CMS, were to be webcast, and there was a feed into our room. The atmosphere was intense. Not only were journalists prowling for comments and sound bites, but there was a real anticipation amongst the scientists about the results.\n\nI knew what Fabiola was going to show, of course. We had a hint of a signal, mostly in the two-photon mass spectrum,106 but it was less than 3 sigma (the conventional point at which one declares 'evidence for . . .') and a long way from the conventional 5 sigma threshold for a declaring a discovery. This in itself was exciting, of course, and I was beginning to think there might actually be a Higgs boson after all. But what I was really keen to see was what CMS had. Rumours had inevitably been spreading, and we expected that they had some hints too, similarly suggestive but inconclusive. There was a chance, though, when one saw the details, that the hints would either be contradictory (which would be disappointing, even a bit worrying) or would line up so well that they might at least push the combined result close to or over the 3 sigma level. So today might conceivably see the first official declaration of 'evidence for a Higgs boson'.\n\n106. See 5.1 Why Would a Bump Be a Boson?\n\nWhat no one was prepared for was the great font controversy. There were gasps when Fabiola began her talk \u2013 she was using the much loathed Comic Sans. Somehow people could grasp this more easily than the content of the slides, and Twitter went into some kind of paroxysm. Much more importantly, the CMS hint neither entirely strengthened nor contradicted the ATLAS result. This was a bit frustrating, both for the physicists and for the journalists trying to work out whether there was a story there and if so, what it was.\n\nWell, there was a story, anyway. Long after the rest of the room had cleared, I was standing in the Filtration Plant being interviewed over a link by Jon Snow on Channel 4 News while Mike Paterson meta-filmed the interview for the _Colliding Particles_ films. Jon Snow seemed very interested in the lack of linearity in our progress. I'm not sure we were being non-linear here, just experiencing an erratic pace of progress along a line. But of course there was no guarantee it was the right line, and hopefully the previous rumours, CDF bumps and neutrino mistakes have given you some idea of why we remained cautious. Cagey, even.\n\nChannel 4 News was not even the end of the day. With a few friends I went back to the UCL flat in Meyrin to celebrate, but also to have a teleconference with Brian Cox, who was on stage at the Hammersmith Apollo with Robin Ince doing their _Uncaged Monkeys_ show. The audio was not good, and I think mostly people just got the impression of happy physicists and drinks, but the audience reacted enthusiastically despite the hiccups (technical and beverage-induced). The evening after it went a bit better, and John Womersley, the CEO of STFC, joined us and was a little more coherent. After all the technical troubles and battles with funding that Brian, John and I had been very much involved with, it was rather hard to believe that Brian was standing on the stage talking about gauge theory to about 4000 people and video conferencing to CERN to talk to miscellaneous scientists, including the head of our research council, and everyone was cheering. And we hadn't even discovered anything yet. Some kind of dream, but a lovely one.\n\nThat day we also had the ATLAS Christmas dinner. It was in the Pump Hall, which is OK for events like that. I was too exhausted to write anything sensible for the _Guardian_ on this at the time, so I wrote a limerick that summed up the main conclusion:\n\nA physicist saw an enigma  \nAnd called to his mum 'Flying pig, ma!'  \nShe said 'Flying pigs?  \nNext thing you'll see the Higgs!'  \nHe said, 'Nah, not until it's five sigma!'\n\nSeriously, I had been a confirmed Higgs sceptic until now. This was the point at which I started to think it was probably there. Of course, that's when you have to be most careful and watch your judgement.\n\n#### 6.4 Higgs Boson in Coupling Shocks, Bumps and Stupidity\n\nIt might sound as though the situation was not too different from that of the previous summer. What made this result \u2013 inconclusive though it was \u2013 more compelling was the fact that it was in the two-photon distribution, where a bump is expected, whereas in the summer the 'hint' had been in the WW decay mode of the Higgs. As I have already described,107 this mode is not very good for telling us the mass of any candidate Higgs boson there might be. The neutrinos, from the decaying W bosons, carry away too much information and we don't see them. The WW decay mode still featured in both ATLAS and CMS, contributing to the hints. But the main interest was now focused on two other ways the Higgs can decay and therefore show up in our detectors.\n\n107. See 4.3 Prospecting and Surveying.\n\nBoth of these decay modes can tell us the mass of the Higgs, if it is there. Both should show bumps and so are less susceptible to theoretical and systematic uncertainties. This is why I was now taking the statistical evidence (which said it was likely but not certain a Higgs existed) seriously. Statistical uncertainties are much easier to assess than systematic ones.\n\nBoth the decay modes we were focused on were a bit weird, though, for different reasons.\n\nThe first decay mode is the Higgs decay to two photons, which I have already talked about.108 The weirdness here is that the Higgs boson is famous for \u2013 or was deduced from, or invented to explain, according to taste \u2013 mass. Fundamental particles get mass by interacting with the BEH field, of which the Higgs boson is an excitation. By the same token, then, the Higgs will generally decay to heavy things. The more massive they are, the more likely it is that the Higgs boson will decay to them, because it interacts most strongly with them. Conversely, things with no mass don't interact with the Higgs.\n\n108. See 5.1 Why Would a Bump Be a Boson?\n\nSo why photons? Photons are quanta of light. They have no mass. They should not interact with the Higgs boson!\n\nIndeed, the Higgs decays to photons very rarely. If the Higgs boson mass is about 125 GeV, and you make 1000 of them, fewer than ten will decay to two photons. Most will decay to bottom quarks, in hadronic jets (jets containing a bottom quark are called b-jets). But these are very hard to distinguish from other collision debris that doesn't involve a Higgs. Jets, even b-jets, are cheap at the LHC. Picking out the Higgs decays to bottom quarks is the subject of the paper I had written with Gavin, Adam and Mathieu just before the LHC started,109 and as I write, we still haven't done it successfully. It will have to wait for the higher-energy data.\n\n109. See 1.7 Boost One.\n\nIn contrast to b-jets, pairs of high-energy photons, not surrounded by other stuff, are much rarer and can be measured more accurately. But since the photon's mass is zero, the Higgs really ought not to decay to photons at all. And it does not, directly. It has to go through a loop of some other particle, as in this cartoon:\n\nFeynman diagram of Higgs decay to two photons\n\nThis is why the decay rate is low. Referring back to the perturbation theory idea, every vertex where three particles meet carries with it a number less than one \u2013 the coupling \u2013 and the loop has more of these (three) than direct decay would (one). So probability of a decay to photons is small, but it can still happen. This is fine. In quantum mechanics, anything that can happen has to be included in your calculation. There might even be other new particles we've never seen going round that triangle, though in the Standard Model it's usually a W boson or a top quark.\n\nThe other important decay mode at this stage is the decay to pairs of Z bosons. If the Z bosons each decay to pairs of charged leptons, specifically an electron and an antielectron or a muon and an antimuon, then this is also a striking signature of an unusual event, and we can measure the four leptons precisely and reconstruct the candidate 'Higgs' mass.\n\nThat's all well and good, except . . . The hint we were seeing corresponded to a Higgs mass of 125 GeV. Remember, mass is just the energy at rest. And the mass of a Z boson is 91.1876 \u00b1 0.0021 GeV. So to make two real Z bosons we need 182.38 GeV of energy, and the Higgs just doesn't have enough. It is short by 57 GeV or so.\n\nThe key to this conundrum is the word 'real' in the previous sentence. A 'real' particle is one that lives for a long time on the timescale of our experiment. The Z bosons are not, in this sense, real. They decay after about 10-23 seconds (0.01 trillionths of a nanosecond), and only betray their presence via the bump in the mass distribution of pairs of leptons. It is the leptons that are real.110\n\n110. See Glossary: Feynman Diagrams.\n\nHere's the main diagram for this process involving a Higgs boson:\n\nFeynman diagram of Higgs decay to two Z bosons, which then decay to four leptons\n\nIn a Feynman diagram, only the incoming and outgoing particles are 'real'. All the internal lines, including the Z bosons in this case, and the Higgs, and anything going round the loop in the previous diagram, are 'virtual' particles. They have an effect, their contribution can be inferred by measuring the real particles, but it can't be pinned down uniquely. And importantly in this context, they are therefore less restricted. Specifically, they do not have to have exactly the right mass.\n\nConsider this plot, which summarises a lot of what we know about the Z boson:\n\nData from CESR, DORIS, PEP, PETRA, TRISTAN and LEP machines (in Cornell, USA), DESY (Germany), KEK (Japan), SLAC (USA) and CERN (Switzerland)\n\nA bump can be a boson, remember.111 This bump is the Z boson, made in various electron\u2013positron colliders up to and including the LEP2 machine running until the year 2000 in the tunnel at CERN now occupied by the LHC. Along the horizontal axis is the total energy of the colliding electron pairs; this is equivalent to the mass of the virtual particle they produce when they annihilate each other, labelled Z\/\u03b3 in this diagram:\n\n111. See 5.1 Why Would a Bump Be a Boson?\n\nUp the left-hand side of the plot is the cross section, which is just a measure of the number of times such a collision happens for a given luminosity of incoming electrons and positrons. There is a bump at an energy of about 91 GeV, meaning 91 GeV\/cs of mass.112 This is due to the Z boson. In a sense it is the Z boson.\n\n112. . . . if you aren't happy with natural units where _c_ = 1.\n\nYou can see a lot of physics in this plot. The dominant ways in which electrons and positrons interact are summarised in that cartoon \u2013 they either annihilate to a photon (\u03b3) or a Z. A real photon has a mass of zero. If a virtual particle in a Feynman diagram can have the correct mass, the chances of that process happening are hugely enhanced. Thus at the left of the plot, near a centre-of-mass energy of zero, the chance of a collision (the total cross section) is very high. To the right, as the energy goes up, the photon is forced further and further away from its correct mass and the cross section falls rapidly. Until, at about 60 GeV, the cross section stops falling, and starts to rise again. This is because the Z boson can now be produced close to its correct mass. This enhances the probabiltity of the collision, and causes the big bump at 91 GeV. Then, as the energy goes still higher, the virtual particle in the middle of the diagram has to have a mass even higher than the Z boson mass, and so the cross section falls again.\n\nHiggs boson decays into two Z bosons are still important, even though the Higgs mass is less than twice the Z mass. The reason is in that plot. Imagine one Z boson is produced at the peak, at the correct mass of 91 GeV. The other one then has to be at about 34 GeV to make the energy sum add up. But the probability of a lepton pair being produced with this mass is far from zero in that plot, and it is similarly not zero in the LHC either. In this plot, at 34 GeV it looks like it would mostly be photons in fact, but of course we know the Higgs does not decay directly to photons. However, it will to the Z, because it is heavy, and there are some 'virtual' Z bosons being produced even at 34 GeV. The key point is that the Z peak is not just a spike at 91 GeV. It has a width, and this allows a 125 GeV Higgs to decay to two Zs. It's just that one of them will not be at its preferred mass. So even for a Higgs that does not have enough mass to create two real Z bosons, the decay to two Z bosons remains important.\n\nGiven this kind of craziness, it is important to be aware of what we really measure. That is, the leptons. It is actually impossible to say whether a given electron\u2013positron pair came from a photon or from a Z. In fact, as I mentioned in the glossary about them, it is easy to get carried away with these cartoons, these Feynman diagrams. They are super intuitive and elegant representations of what goes on, but they are not like a time-lapse of a snooker shot. They do not represent a unique history of what happened in a given collision.\n\nThis is one of the deeply strange things about quantum mechanics, about quantum field theory, the bedrock on which the Standard Model is built. Particle physics is wrongly named. Or at least, particles aren't what we usually think they are.\n\nFeynman diagrams represent amplitudes, not probabilities. If you understand that, you've understood something very deep about the way the world works. And interestingly, though in principle all particle physicists (despite the misnomer) know it, many of them forget it in their everyday work, and this can be dangerous, scientifically at least.\n\nTo break down that statement about amplitudes and probabilities, it's best to start where Richard Feynman started when illustrating the weirdness of quantum mechanics \u2013 the two-slit experiment. If you send waves (water, sound, light, whatever) towards a barrier that has two slits in it, and if the width of the slits and the distance between them is not too far from the wavelength of the wave, you'll see a pattern in the waves after they have passed through the slits in your screen. If they are water waves, for instance, some areas of the water will be very still, others will have quite large waves.\n\nThis is a phenomenon called 'interference', and it is to do with what an amplitude is. A wave is something oscillating about an average \u2013 the maximum distance from the average value of the something that a wave reaches. So if the peak of a wave is 10m above sea level, the average is zero (sea level), and the amplitude is 10m. The same goes for the minimum. The trough will be 10m below sea level, or at -10m.\n\nThe interference effect comes when waves get out of step with each other. If there are two sets of waves, one passing through each slit in the screen, it is possible that for some bits of sea the waves from both slits arrive at the same time. One will be peaking at 10m at the same as the other, and you get a wave with a 10 + 10 = 20m peak \u2013 they add up. When the troughs arrive they will also add up, so you get -10 + -10 = -20. This is a region of constructive interference.113 Conversely, in some areas the trough of one wave arrives at the same time as the peak of another. In this case, they cancel each other out: 10 \u2013 10 = 0. Everything just sits still at sea level \u2013 this is destructive interference. The amplitudes of the waves are 10m everywhere, but the disturbance in the sea is the sum of all the amplitudes, and varies from 20m to zero depending upon how they combine.\n\n113. Though if you are in a boat, I guess it might be quite destructive.\n\nAs with waves, so with quantum fields. The very odd thing about the two-slit experiment is it doesn't just work with water or sound waves, or light waves (which we already know are actually photons, which behave like particles sometimes). It works with electrons. If you fire electrons at a screen, you can detect them, one at a time, bing, bing, arriving at a detector, just like respectable particles (which I have to think of as very small snooker balls). But they will build up a pattern just like the waves \u2013 areas with no electrons, and areas with lots of electrons. Interference is happening.\n\nThe probability that an electron will appear somewhere is not proportional to the amplitude of the individual waves, it is proportional to the sum of them. Actually, it is proportional to the sum of them squared, so it is always positive (-20 squared is -20 x -20 = 400, the same as 20 squared). This is how Feynman diagrams work. You have to calculate all the possible diagrams that could produce a particular set of particles (say the four leptons in one of our collisions). You have to add them all up and square the result to get the cross section.114 Sometimes adding another possibility can reduce the cross section, because it destructively interferes. Sometimes it increases it. And for any given measured set of particles you cannot say which exact Feynman diagram it was produced by, because all the possibilities contribute. Sometimes positively, sometimes negatively.\n\n114. See Glossary: Feynman Diagrams.\n\nThis is not to say that we can't learn anything from the measurements \u2013 the bumps in the distributions are equivalent to the patterns in the waves in the two-slit experiment \u2013 we can work out where the slits were. (In fact, such patterns in X-ray crystallography are used to work out the structure of molecules. Rosalind Franklin's patterns were used to work out the structure of DNA.) And we can work out whether there was a Higgs boson, or a Z, in some of the diagrams involved. But we can't work out exactly which diagram matches which event. All we can really measure are the final particles, the ones that live long enough to travel away from the collision and make the patterns in our detector. It is actually astonishing how many professional particle physicists forget this and take the cartoons far too seriously.\n\nSo don't be like them. Remember that we look for sets of four leptons in three possible combinations,115 we plot the total mass reconstructed from them, and we look for a bump. Just like we do with the pairs of photons.\n\n115. Electron\u2013positron\u2013muon\u2013antimuon, electron\u2013positron\u2013electron\u2013positron, and muon\u2013antimuon\u2013muon\u2013antimuon\n\n#### 6.5 Muons: The Last Onion Layer\n\nMuons aren't very common in everyday life. At least, they are a lot less common than photons, electrons and hadrons. Therefore if you spot one passing through your detector, the chances that something interesting just happened are relatively high. In fact, muons are crucial in the Higgs-to-ZZ search \u2013 the best sensitivity in this channel comes from the four-muon final state, when both Z bosons decay to muon\u2013antimuon pairs. They are also vital in measuring Z and W bosons in general, and useful in searching for lots of beyond-the-Standard-Model physics.\n\nYou might think muons would be easy. Travelling from the collision point at the heart of a detector, by the time a particle has got to the muon tracking systems, the final layer of technology surrounding the collisions, it has passed through the inner tracking detectors and the calorimeter. All charged particles, including muons, should have been measured in the inner tracker, and all particles except for muons (and neutrinos, which bother no one) should have stopped in the calorimeters. Life should be quiet and simple.\n\nIn some ways that is true. But there are other challenges, and as muons are very important, the muon detectors are a high priority for any experiment. It cannot be a coincidence that the 'M' in CMS stands for 'muon', and the 'T' in ATLAS stands for 'toroidal', after the toroidal magnets of the ATLAS muon system. OK, it is true that being on the outside of both detectors the muon system is the biggest component, and the first thing you see, but that just goes to show, doesn't it?\n\nOne challenge is the fact that even though the detectors are deep underground, there are still particles from cosmic rays and from background radiation that can hit the outside of ATLAS, where the muon detectors are. Possibly the major challenge, though, is the sheer surface area you have to cover to surround the inner trackers and the calorimeter. While it would be technically possible to do this with semiconductors, as is done with the inner layers of particle trackers, it would be prohibitively expensive and largely pointless, since most of the silicon would see nothing most of the time.\n\nWhat is needed is a precise, fairly fast technology that can cover a very large volume cost-effectively. In ATLAS most of the muon system uses 'Monitored Drift Tubes', which are essentially long, electrically-grounded, metal tubes, about 3cm in diameter, with a positively charged wire running along the middle. There is gas in the tubes and when a muon passes by it can knock electrons off the gas molecules, ionising them. The electrons and ions drift towards the anode and cathode respectively, and a pulse is read out, from which the position of the muon can be determined. In some parts of the muon system a different layout (Cathode Strip Chambers) is used, but the principle \u2013 gas that gets ionised and a voltage to accelerate the electrons and ions \u2013 underlies it. The CMS muon system likewise uses a mix of technologies that exploit the same principle. And both ATLAS and CMS have large magnets, bending the charged muons (remember the solenoid surrounding the inner tracker was left behind long ago) so that their momentum can be independently measured.\n\nA high-momentum muon track, measured in the inner trackers, penetrating the calorimeter, and matched to a track in the muon system, is one of the clearest and most precisely measured signs that an interesting collision occurred in the LHC. And as I said, in the crucial Higgs-to-four-lepton search, muons were a determining factor.\n\n#### 6.6 What Is It?\n\nGiven the trickiness of quantum field theory, where one has to state carefully what has actually been seen and then discuss possible interpretations, it was clear that if we did see something new, there would be much repeating of the questions, 'What is it?' and in particular, 'Is it the Standard Model Higgs boson?' And there would be a lot of cagey answers.\n\nIn the end, proving something exactly with experiment is impossible. 'Exactly' is a statement that requires infinite precision and if you want that, you'd better be a mathematician, not a scientist. You can never know exactly how long a piece of string is. The scientific question is really, 'Are its properties consistent with it being a Higgs boson or not?' and you have to decide how many different things need to be consistent, and to what precision, before you start calling it a Higgs. This is a matter of judgement.\n\nThe Standard Model is remarkably predictive when it comes to the Higgs boson. It predicts that it exists, for a start. And it must have zero electrical charge, and zero 'spin' (that is, it carries no intrinsic angular momentum \u2013 it is a scalar boson). The Standard Model does not predict its mass very well, but once the mass is fixed, everything else follows, including a precise prediction of what particles it will produce when it decays. The whole point of the exercise is to give particles mass, and this means that generally, the heavier a particle is, the more likely it is to be produced in a Higgs decay, assuming it is possible to do this and conserve energy.\n\nIn 2011, of course, we had no significant signal. However, we did have sensitivity, such that the data _could_ have been inconsistent with the existence of a Higgs boson, down to about 130 GeV in Higgs masses. But the data remained consistent. This statement relied mainly on comparisons to predicted event rates. We also knew something about the distribution of the events, with a possible but not solid mass peak.\n\nTo start calling this a 'Higgs boson' rather than an 'excess' or a 'candidate', we would not only need to have much more confidence that it was real, we would have to measure more of its properties. The main thing would be to see the whatever-it-was (assuming it was something) decay in at least two, and preferably more, different ways. If the relative decay rates were to look as expected for a Higgs boson, it would become pretty compelling, progressively more so as more decay modes were accumulated. The more we measured, the more the discussion would move from 'possible excess' to 'Higgs-boson candidate' to 'Higgs boson' to 'Standard Model Higgs boson'.\n\nAnd even if we did find something, we would never be able to show a picture of an event and say, 'This event definitely involved a Higgs boson.' This is a bit of a shame, but the reason behind it provides a resolution to a severe parental dilemma, and explains why I am in fact sometimes the tooth fairy. Bear with me.\n\nOne of the developing pieces of evidence for a Higgs was the tiny bump in the two-photon mass distribution. I can certainly show a collision event containing a pair of photons that exactly gives the 'Higgs mass', i.e. at the top of the bump. But it would still not be possible to be sure that a particular pair of photons came from a Higgs boson. Very roughly, if at the peak there were about 70 events, probably only about ten of these would be due to the new boson. With our detector we can't tell the difference between these and the 60 or so background events. In fact, even with a perfect detector, some of that background would remain and be quantum-mechanically mixed with the signal. All that is definite is what goes in and what goes out. These you can measure.116\n\n116. The actual numbers of Higgs candidate events are much higher than this, but the principle is the same.\n\nThere may be several possible ways of producing a set of new particles from the incoming ones, but if the resulting set is identical, it is not physically meaningful to say which possibility occurred. To calculate the probability of that result occurring, you have to add up all the possibilities in a particular fashion.\n\nNow to the parental dilemma. It is especially acute around Christmas, but if you have children who are losing their milk teeth, it is ever present. Is Father Christmas real? What about the tooth fairy?\n\nDo you spoil the fun or do you lie? Something in me hates the idea of lying to my kids and undermining trust. On the other hand, I don't want to be a miserable bastard. Here's my way out.\n\nAnything that has the same initial state (tooth) and final state (money) might in fact be an event in which a tooth fairy was present. To put it another way, anything that removes the tooth and delivers money shares such an essential property with a tooth fairy that it can be said in a sense to be one.117\n\n117. Anything removing both teeth and money is probably a dentist. Or possibly a mugger.\n\nThese days, my son doesn't believe a word of it, of course. But in the early days it was _the truth_. We managed this transition without lies, betrayal or tears because actually, when tiptoeing into the bedroom with a shiny pound coin, I really am the tooth fairy. I am, of course, at the same time Dad. This seemed to work, and now he's older, it's still fun.\n\nIt's not much of a stretch to extend this to Father Christmas, and it also explains why sometimes Father Christmas uses the same wrapping paper as your parents \u2013 he and they are, in a sense, indistinguishable quantum possibilities for the delivery process.\n\nMaybe. Either way, in physics the answer to 'What is it?' is always, 'It's a thing that behaves like this.' And we were feeling increasingly confident that we were closing in on something that behaved very much like the Higgs.\nSEVEN\n\n## Closing In\n\n### January\u2013June 2012\n\n#### 7.1 Eight TeV\n\nObviously, after these tantalising hints the pressure to follow up and answer one way or the other was going to be huge. The BBC showed up, filming a _Horizon_ programme that started off being about particle physics in general, but grew increasingly focused on the Higgs hunt as it became clear things were heading for some kind of conclusion.\n\nOn 7 February 2012, the Higgs search results from December were submitted to journals and the arXiv.118 The break between this and the talks in December had involved a lot of cross-checking and a lot of work (and Christmas), but had not seen a great deal of change in the results. After peer review, the ATLAS and CMS papers were both published, essentially providing retrospective vindication of what we had shown.\n\n118. http:\/\/arxiv.org\/abs\/1202.1408; http:\/\/arxiv.org\/abs\/1201.1487.\n\nOn the same day these papers came out, I went to Google London (the offices, I don't mean I searched for it, I know where London is) for breakfast and the launch of a film about CERN. Two nice things about this. I met Phillip Greenish, one-time member of the council of STFC, and CEO of the Royal Academy of Engineering at the point that it had suggested (during a crucial part of a UK funding debate) that particle physics should bear the brunt of the cuts. His presence at what was an LHC-based launch, and some of the things he said, seemed to imply that perhaps we'd moved on a bit from those fratricidal attacks. Also, in the film I liked a snippet featuring US colleague Zach Marshall at the ATLAS barbecue. He talked about theorists inventing weird new physics scenarios that might show up at the Large Hadron Collider:\n\nYou have these people trying to just predict, and predict as many different things as they can. Because if one of them is right, they'll be famous. And if all of them are wrong \u2013 they'll be like everybody else!\n\nAnd he's right. So there you have it. Experimentalists get ignored if they are right (e.g. about the speed of neutrinos), and hugely cited if they are wrong. Theorists are ignored if they are wrong, but get a Nobel Prize if they are right.\n\nNot quite true, but not completely false, either.\n\nThe LHC started giving us data again on 5 April. Preparing for the new collisions required quite some work, because they were at a centre-of-mass energy of 8000 GeV (so beam energies of 4000 GeV each), an increase from the 7000 GeV of 2011. This was generally a good thing \u2013 more energy means we have more chance of creating new particles, for instance, since the heaviest particle you can possibly produce has a mass of _m_ = _E\/c_ 2 where _E_ is energy and _c_ is the speed of light (exercise for the reader \u2013 rearrange that to make a famous equation). But a change of energy did also mean we had to revisit all our simulation programs and get ready to check that they would work just as well at the new energy as they did at the old.\n\nAt a lecture I gave in February to 16\u201319-year-olds as part of the Institute of Physics' 'Physics in Perspective' series, I was asked how come, if we have proton\u2013proton centre-of-mass energies of 7000 GeV, the reach in energy for new particles (including the Higgs) is much lower than that?\n\nIn the specific case of the Higgs (where most of the action was by now down below 130 GeV), there is plenty of energy, but the difficulty is more to do with identifying a Higgs boson amongst the backgrounds. However, there's a more general point. ATLAS and CMS can make the equivalent of the plot shown in section 6.4. In this case, instead of electrons and antielectrons annihilating to a photon or Z boson, which then decays, the incoming particles are quarks and antiquarks, like this:\n\nAs you already know,119 there are plenty of antiquarks, and gluons, inside our protons, as well as the quarks. So that is where the antiquark comes from. In the ATLAS and CMS plots, there is also a bump at 91 GeV due to the Z boson, just as in the electron\u2013positron plot. But the LHC gets us to much higher energies than LEP \u2013 as far as about 1500 GeV, compared to about 100 GeV with LEP. In its later running as LEP2, the machine went up to about 210 GeV, but that was the limit. That was the highest collision energy the beams could get to. However, even though the LHC was delivering collision energies of 8000 GeV in the search for bumps, it doesn't get close to this hypothetical limit. Why is this?\n\n119. From 4.5 Inside a Proton.\n\nThe reason is, of course, that protons are not fundamental particles. The really short-distance, energy-frontier physics takes place at distances much smaller than the proton radius, so effectively, from this point of view, the LHC is a quark and gluon collider, rather than a hadron collider. And unfortunately, even though the protons have an energy of 4000 GeV each (so a total energy of 8000 GeV available), any given quark or gluon only carries a fraction of the full energy of the proton, so the available energy to make new particles is generally a factor of five or ten lower than the proton energy might indicate.\n\n#### 7.2 The Curse of Meetings\n\nThe summer conferences were clearly going to be the make-or-break moment in the Higgs search. It hardly seemed possible, but the frequency of meetings intensified.\n\nGiven the time zones involved, it would be possible to spend every hour of every European working day, and most of the night, in an ATLAS meeting. Since they are nearly all available via some form of teleconference, with enough connections you could spend most of the day in half a dozen of them at the same time. This would of course melt your brain.\n\nTo add insult to injury, a curious phenomenon has emerged. The moment a meeting begins to get interesting, one of the participants (usually the chair) will almost invariably suggest they 'take it offline'. And we move on to the next topic.\n\nThere are a few cases which provoke this.\n\n##### 1. The unexpected moron\n\nSomeone, perhaps senior (sometimes me), has totally missed the point of the presentation or discussion. They ask a question displaying such profound ignorance and confusion that the rest of the meeting can only stare at their shoes or the ceiling in embarrassment. A variation on this case is simply a question so basic ('What particles are we actually colliding?') that one can only assume the questioner walked in off the street by mistake. Either way, a good chair moves that discussion offline as soon as possible to save everybody's blushes.\n\n##### 2. The grudge match\n\nThere aren't so many particle-physics experiments in the world. If, as a PhD student, you meet an arrogant pedant suffering from acute Dunning\u2013Kruger effect,120 the chances are you will bump into them, on and off, for the rest of your career. If they ask you a stupid, tedious and hostile question in a meeting, it might provide a diverting floor show for the other participants, but the chair will most likely take it offline. You should agree to this. Perhaps take it to a darkened corridor, with a couple of menacing friends. 'Ahem. Jon wanted us to talk to you about that question you asked . . .'\n\n120. Delusions of superior ability. Pretty much the opposite of the much more common 'impostor syndrome'.\n\n##### 3. The technical tumble\n\nTo be honest, this one is where some actual progress is made. Someone in the meeting has deep technical knowledge of an issue that has just been raised. It is pertinent to the topic, and indeed quite often someone presenting a result will realise immediately that this needs checking in detail and would rather go into a huddle and do this than potentially crash and burn in front of their colleagues. Also it may take days. Take it offline.\n\n##### 4. The dodgy connection\n\nSomeone suddenly starts talking as if they have inhaled helium, turned into a Cyberman (for Doctor Who fans) or put their head into a bucket of water. This is always blamed on a poor Internet connection or bad microphones, though I suspect in at least a couple of cases Cybermen have really been involved. While it is undoubtedly true that the teleconferencing equipment is generally to blame, this is also a handy cover if you find yourself unwillingly embroiled in any of the examples above. It more or less forces it offline. Oddly, in almost all cases the 'take it offline' phrase means 'continue it online in a series of lengthy emails'. So perhaps we aren't so cool after all.\n\nThere are many good things about Switzerland. The flag is a big plus. Also \u2013 possibly in reaction to the excess of meetings at CERN, the United Nations or the World Trade Organization \u2013 a Swiss political party formed in 2011 with a policy to ban PowerPoint. Contingency plans, including holding all meetings over the French border in the Pr\u00e9vessin site of CERN or (clearly very popular) enforcing a strict LaTeX-only121 policy, were discussed extensively.\n\nIn meetings.\n\n121. No, not a kinky dress code. LaTeX is a typesetting program, written largely by scientists, which I wish I had written this book in, really.\n\n#### 7.3 Waves\n\n_Angels and Demons_ is a best-selling thriller by Dan Brown, and a film starring Tom Hanks. It features CERN quite heavily. When people ask me about it, they expect to be disabused.\n\n'Yeah, yeah, of course we don't have private jets, or parachute-training-tower whatsits,' I say.\n\n'I don't even own a white coat. It's fiction, enjoy it!' I say.\n\n'What's that? Antimatter? Oh no, that's real, obviously.'\n\nIn fact, antielectrons (i.e. positrons), antiprotons and other antiparticles are commonplace in even moderate-energy physics facilities. Even in hospitals, in positron emission tomography (PET). This is a diagnostic technique in which a radioactive isotope of an element that decays and emits positrons is introduced into the body.\n\nAn isotope is an atom in which the atomic nucleus has the same number of protons as usual, but a different number of neutrons. The radioactive decay time of an atomic nucleus is fixed by the mix of neutrons and protons it contains. However, chemical properties of an element depend only on the number of electrons, which in turn is fixed by the number of protons, so that the electric charges cancel out and the resulting atom is neutral. Thus the unstable isotope carbon-11 with six protons but only five neutrons will be chemically identical to the stable isotope carbon-12, which has six of each.\n\nThis means, for example, that molecules and compounds such as sugars or proteins can be made containing carbon-11. These sugars or proteins will behave just like the common versions, but the carbon-11 nuclei will decay after some time, emitting a positron.\n\nHanging around inside a human body, this positron will quite rapidly meet up with an electron and they will annihilate, producing two photons. Each photon will carry an energy very close to the mass of an electron multiplied by the speed of light squared (it's that equation again), which in particle-physics units is 0.51 MeV. By measuring these photons, it is possible to map out very precisely (and for a very low dosage of radiation) where the isotope went in the body and this, for a careful choice of isotopes and molecules, can tell you rather a lot about what is going on in there.\n\nAntiprotons are harder to make, simply because they are nearly 2000 times heavier and so it requires about 2000 times the energy to create one. Even so, by particle-physics standards this is very doable. The problem is, they have to be created in a collision with something, usually a proton beam hitting some material, and when they are created, most of them are moving quite quickly. The tricky bit is to catch them, slow them down, store them and \u2013 if this is your plan \u2013 let them combine with positrons to make antihydrogen.\n\nAll the while, you have to stop them from annihilating with all the normal matter hanging around. Then, if you want to really know what you have got, you have to store them long enough to study their properties.\n\nThe ALPHA experiment at CERN did all this, and published the results in March 2012. Not only did they trap atoms of antihydrogen, but they fired photons (microwaves in this case) at them. These photons make the positrons inside the antihydrogen change energy levels. They can make the spin of the positron change its alignment, so that it either lines up with, or against, the spin of the proton. When this happens, the magnetic properties of the antiatom change, which means it isn't trapped any more, it escapes and then annihilates.\n\nThe frequency to which the microwave has to be tuned in order to cause this gives a measure of the difference between the various energy levels inside the antihydrogen. To within the precision of the measurement, the difference between them is the same as it is for hydrogen.\n\nThis was the first time anyone had measured inside antiatoms. The result \u2013 'It looks the same' \u2013 was not a surprise. It would have been a huge surprise if it had been different. The symmetry between matter and antimatter in their interactions with photons is built very deeply into our theory. The existence of antimatter was predicted by combining quantum theory and special relativity in the Dirac equation, and within this theory the electric charge of the electron has to be _exactly_ opposite that of the positron, and their masses have to be identical. The point is that even if the initial measurements weren't very precise, and even if theory told us the answer to expect, this was the first actual measurement. More precise ones will come. Prediction and extrapolation from theory, even a very well-tested theory, are not the same kind of knowledge as an actual measurement.\n\nThe field of antimatter spectroscopy had just begun. Matter spectroscopy, on the other hand, has been around for a long time and is a stunning branch of science with enormous implications and applications. It is through spectroscopy that we know what stars and galaxies are made of, and the presence of different distinct emission or absorption lines in the light from particular elements was one of the main puzzles driving the development of quantum mechanics.\n\nBecause they are fermions,122 the electrons around an atom cannot all be in the same quantum state, which means they can't all be at the same energy. An even deeper property, though, is the fact that they are in 'quantum states' at all. What this means is that there are only certain values of energy that electrons are allowed to have when they are bound to an atomic nucleus. Because of this, if you want to move an electron from a low-energy state to a higher-energy state you have to put in exactly the right amount of energy. The energy would normally come in as a photon. A fixed energy for a photon means a fixed wavelength, so a fixed colour, if it is in the visible part of the spectrum. And that is the heart of spectroscopy.\n\n122. See Glossary: Bosons and Fermions.\n\nIf you have a whole bunch of atoms at a high temperature, for instance in a star, this means they are continually bumping into each other, swapping photons, and the electrons around them keep changing energy levels. Imagine two specific energy levels, for instance in sodium123 in a street lamp. The energy gap between them has a fixed value, corresponding to a fixed wavelength of yellow light in this case. If you separate the light from a sodium lamp into its different wavelengths (as Newton did for sunlight using a prism), you'll see a bright band corresponding to electrons jumping down from the higher-energy level to the lower, and emitting a photon as they do so.\n\n123. The example I used already in section 2.1.\n\nThe element helium was discovered like this, in sunlight, during an eclipse in 1868. A French astronomer, Pierre Jules C\u00e9sar Janssen, spotted the bright line at 587.49 nanometres, corresponding to an energy of 2.11 eV, and coincidentally also appearing as yellow, quite near the sodium lines. A couple of months later, Norman Lockyer also spotted the line and correctly concluded that it must come from an element not at that point known on Earth, but present in the Sun. It was named helium (from the Greek _helios_ , meaning the Sun) and first detected on Earth by the Italian Luigi Palmieri 14 years later.\n\nSpectroscopic analysis of the lines in light \u2013 sometimes 'emission lines' like these, where there are more photons because of electrons jumping down a level, and sometimes absorption lines, where there is a darker patch because electrons are absorbing photons at a certain wavelength to jump up a level \u2013 can, in laboratories on Earth, be used to spot tiny traces of elements or compounds in samples of material. They can also tell us the composition of objects in space we could never reach to study directly. Astonishingly, the fact that these patterns of lines shift lower in energy (and therefore longer in wavelength, towards the red side of the spectrum \u2013 'red shift') when something is moving away from the observer is what allowed us to see that the universe is expanding. All the distant galaxies have the characteristic patterns of spectral lines shifted to longer wavelengths, so they are moving away from us.\n\nSpectroscopy gets us a long way, but it is just one aspect of the concept of waves in physics. Waves are possibly the best bit of physics. They pop up everywhere. The fact that an electron behaves like a wave is why distinct energy levels exist around atoms in the first place. Niels Bohr put together the first model of atoms that could explain the lines in spectroscopy, by proposing that the electrons orbited the nucleus in certain allowed orbitals, with the ones in between them forbidden.\n\nIf you imagine the electron as a wave, this provides a really good way of seeing why some orbits might be allowed. They will be the orbits where a whole number of wavelengths just fit with the length of the orbit, so that when the wave goes round the orbit, it meets itself at just the right point to add up, and you get a 'standing wave'. Any wave that doesn't meet itself at the right point, so that the peaks line up with each other, will cancel itself out, and the energy corresponding to that wavelength is therefore not allowed.\n\nThe business about standing waves may sound a little esoteric, but not only is it very close to the eventual quantum mechanical picture that emerged from solving Schr\u00f6dinger's equation for electrons around atoms, it is also, on a bigger scale, how musical instruments work. The string of a harp gives out one principle note, corresponding to a vibration in the string with a wavelength that is double the length of the string. What is happening is that waves move out in both directions from the point at which the string is plucked, then reflect off each end of the string and add up (interfere) with each other. Just like Bohr's electrons, if the peaks coincide, the wave survives, and if not, they cancel each other out. Thus the string plays a particular note.\n\nAt a concert in the Barbican once I found my mind drifting to physics. This doesn't imply any criticism of the music, which was stunning, but the fact is that when stunned, my mind often wanders off. It considers the fact that the London Symphony Orchestra logo does in fact look like a conductor with a baton. It admires Susanna's cheekbones. It wonders what Szymanowski did with the rest of his vowels, and what it must have felt like to be Bart\u00f3k, creating beauty while Europe headed towards horror. And in the middle of Bart\u00f3k's Violin Concerto no. 2, it began wondering about physics and harps.\n\nThe orchestra had two harps. Beautiful, sweeping things, nearly triangular but with a distinctive curve in the top edge. Why is that curve like that? I wondered. Maybe because it looks nice, but since the curve affects the length of the strings, and the length of the strings affects the note played, it was probably not just ornamental.\n\nFour quantities characterise a wave: speed, frequency, wavelength and amplitude. You could add a fifth maybe, the shape of the wave, which is where all the tone and other subtleties come in. That's where Stradivarius made his cash. But being a physicist I want to keep things simple.\n\nAmplitude is a bit boring. It is just the height of the peaks of the wave, or the depths of the troughs. So for sound it is basically the pressure difference between the highest-pressure bit of a wave and the average pressure. It's the volume.124\n\n124. I'm not sure why we use the word volume for loudness, really, but at least amplifiers do increase amplitude, so that's nice.\n\nSpeed, frequency and wavelength are related: speed is equal to the wavelength multiplied by the frequency. And in fact the speed is a property of the medium through which the wave travels. The speed of sound in air (at room temperature and pressure) is a fixed 1,236km per hour. So for a sound wave, once you have fixed the frequency, you have also fixed the wavelength.\n\nThe frequency is what we hear as the pitch of the note. When a harp string is plucked, it vibrates with a certain frequency, vibrating the soundbox and compressing and decompressing the air inside it, thus making sound waves of the same frequency and, in the right hands, leading to music.\n\nThe frequency of the vibration in the string is set by the length of the string, the tension in the string and the material it is made of. If you want to have all your strings made of the same stuff (so they have similar tone) and at the same tension (so they take the same effort to pluck), you have to increase the length to get deeper notes. Unfortunately, you have to double the length every octave. This means an exponential growth in length.\n\nA triangular-shaped harp, without the curve in the upper frame, gives only a linear growth in string length, not an exponential one. If you wanted to cover enough octaves, this would lead to an unfeasibly big harp. The curve in the top of the frame looks to me as though it is there to allow the lengths of the strings to grow exponentially as far as this is feasible. So, for the shortest strings, they can have the same tension, be made of the same stuff and be about equally spaced along the frame. But if you extrapolate that curving shape as you go away from the harpist, you can see the harp would get too big before you got to the next octave. So the curvature in the frame changes, and the type of string has to change, too, to keep the frequency dropping exponentially and thus allowing more octaves. So the graceful curves are functional as well as ornamental.\n\nI often use harp, or double-bass, strings as an analogy to try and explain one of the reasons why high-energy collisions are an exciting place to do physics. One way of explaining it is that since _E_ = _mc_ 2, we need a lot of _E_ to make a new particle with mass, _m_. Another is to talk about how we are probing the physics of the early universe, a few moments after the big bang.125 But my favourite is to talk about waves and resolution.\n\n125. See 4.6 Heavy Ions for Christmas.\n\nWhich gets us to the question: Is light a wave or a particle? What about an electron? A gluon?\n\nThe answer I give myself to that whole wave\/particle duality question is, 'No.' Or rather, I tell myself that the concept of a wave, like the concept of a particle, is an imperfect everyday analogy for a quantum of something. So, 'particle' describes some of the ways a photon, or an electron, behaves, and 'wave' describes others. In the end the reality is an excitation in the quantum field.126\n\n126. See Glossary: Fields, Quantum and Otherwise.\n\nCertainly, quanta have energy, momentum, wavelength and frequency, and all these are related to each other. Energy and frequency are proportional to each other, and momentum is proportional to the inverse wavelength.127 So high energy means high frequency. And high momentum means short wavelength. If you are talking about a high-energy collider like the LHC, the momentum and energy are proportional to each other as well. So the bottom line is that high energy means high momentum means short wavelength.\n\n127. In the appropriate units, energy ( _E_ ) equals Planck's constant multiplied by frequency ( _n_ ), and momentum ( _p_ ) equals Planck's constant divided by wavelength ( _l_ ). Also, for a massless particle, _E_ = _pc_ and _nl_ = _c_. I put this here in case it helps. Equations seem clearer than words sometimes. But don't worry if not.\n\nThis is important because the wavelength sets the resolution, or, if you prefer, the size of the smallest thing you can see. Radar, with a wavelength of metres, is great for seeing boats and planes. But if our eyes were sensitive only to radar, we would not be able to see each other, because we are smaller than the wavelength. Optical light, with wavelengths of hundreds of nanometres, is much more practical and allows us to see rather fine detail. It is also lucky that this is the peak wavelength of the Sun's radiation, of course. Given that our eyes presumably evolved to make use of the brightest wavelength, if the Sun mainly radiated in the infrared, we'd have infrared-sensitive eyes and everything would start getting blurred just below a millimetre. Tricky for threading needles.\n\nBecause it has the highest-energy beams ever achieved in a laboratory, the LHC therefore has the shortest wavelength quanta ever (mostly gluons, in fact) and can therefore probe nature at the shortest distances we have ever been able to reach. We are looking not only into the heart of an atomic nucleus, but into the protons inside it, and at the quarks inside that. And potentially, if they have anything inside them, we might see that too. This is the way I prefer to think about the 'energy frontier'. And this is why we learn about small things like quarks from big things like the Large Hadron Collider. It is also because \u2013 even at these tiny distance scales \u2013 quarks and electrons do not appear to be made of anything else that the puzzle of mass shows up here. This is where either we find out that electrons and quarks are not fundamental and are made of some other stuff \u2013 or we find a Higgs boson to give them mass.\n\n#### 7.4 The Neutrino Matrix\n\nOne of the weirder things about QCD and the weak force is that they are non-Abelian128 theories. This means that the algebra of the symmetries at the heart of the force129 does not commute. Which means that A times B does not equal B times A.\n\n128. After the Norwegian mathematician Niels Henrik Abel, who was not, as far as I know, murdered by his brother. 129. See Glossary: Gauge Theories.\n\nNow common sense, and experimenting with counters, will tell you that for two numbers, A and B, multiplying A by B always gives the same result as multiplying B by A. Two lots of three pence make six pence, and so do three lots of two pence. This is always true for numbers, in fact. However, it is perfectly possible to define kinds of mathematics where AB is not equal to BA. Indeed, mathematicians have been studying such things for a long time.\n\nWhat might be more surprising is that physicists use it all over the place, because there are physically relevant objects for which AB does not equal BA. One way of representing such an object is by using a matrix. Matrix mechanics is included in the first-year Mathematical Methods course I was teaching at UCL around this time. Because my school did an experimental 'New Maths' syllabus, I even learned something about it when I was about 15.\n\nIn maths, a matrix is just a bunch of numbers arranged in rows and columns. When you multiply two matrices, A and B, together to get another matrix, C, you multiply rows by columns.130\n\n130. That is, multiplying the first row of A by the first column of B gives the entry in the (first row, first column) position of C; the first row of A by the second column of B gets you the (first row, second column) entry of C; and so on.\n\nThis kind of matrix may sound less enthralling than an all-controlling virtual-reality supercomputer filmed in bullet time and black leather, but it is also more useful.\n\nYou can use a matrix to describe what happens when you move something around, for example. This is a case when order (AB or BA) clearly matters. If you first turn 90 degrees, then walk 10 metres, you obviously get to a different place than if you first walk 10 metres, then turn 90 degrees. If B is a matrix representing the turn, and A represents the walk, then the combined 'walk after turning' matrix (C = AB) must be different from the combined 'turn after walking' matrix (call it D = BA). So C doesn't equal D, AB doesn't equal BA. If AB always equalled BA, matrices would be useless for representing such operations. It's because they don't commute \u2013 that is, they are non-Abelian \u2013 that they are useful.\n\nMatrices also proved to be what Paul Dirac needed when he was trying to work out the quantum mechanics for electrons moving at high speeds. In fact, the features that forced him to use matrices were the same features that allowed him to describe the spin of electrons, which is crucial to the whole behaviour of atoms and the structure of the periodic table. The same features also led him to predict the existence of antimatter.\n\nIt amazes me that mathematics and the behaviour of the real world seem to be so closely connected. Good research is as much about choosing good questions to address as it is about answering them. There are always more questions than answers, and research costs time and money, so we have to make choices. Maths is one very good way of interrogating data and using it to suggest which new experiments are the most interesting, even when the methods and results, like matrices and antimatter, can seem rather exotic.\n\nIn that spirit, before continuing with the Higgs hunt, here is a final detour into neutrinos, this time for a real and important result. On 7 March 2012, new results131 were announced by the Daya Bay Reactor Neutrino Experiment in China. These results have had a huge impact on the Standard Model, and on the future of particle physics. If you just want to follow the Higgs story, feel free to skip lightly ahead, see you in the next section. Neutrino fans, hang on.\n\n131. <http:\/\/arxiv.org\/abs\/1203.1669>.\n\nNeutrinos mix up amongst themselves,132 and this mixing is a sort of rotation between one set of neutrino labels (the flavour \u2013 electron, muon or tau) and another (the masses). This rotation can also be described by a matrix, containing three mixing angles.\n\n132. See 5.5 Meanwhile in the Neutrino Sector.\n\nA vital open question was whether the three types of neutrinos genuinely mix three ways, or whether what we were seeing was just two separate pair-wise mixings. Two of the three possible mixing angles had already been measured, but one remained that had not.133 It is called \u03b813 (theta one-three).\n\n133. Though the MINOS and T2K long-baseline experiments, as well as the Double Chooz reactor experiment in France, had some evidence that it was not zero.\n\nDaya Bay produced134 the first clear measurement of \u03b813, showing that indeed it was not zero \u2013 in fact it is about 9 degrees. This was quickly supported by a similar measurement from the Korean RENO experiment.135\n\n134. <http:\/\/arxiv.org\/abs\/arXiv:1203.1669>. 135. <http:\/\/arxiv.org\/abs\/arXiv:1204.0626>.\n\nSince \u03b813 is a fundamental parameter in the Standard Model of particle physics, this would be an important measurement anyway. But there was a bit more to it than that.\n\nIf \u03b813 were zero, we would just have had two-way neutrino mixing. The flavour states might just mix up neutrinos 1 and 2, and neutrinos 2 and 3. With \u03b813 bigger than zero, neutrino 1 also mixes with neutrino 3. In this case, and _only_ in this case, a fourth parameter is also allowed in the matrix. This fourth parameter (delta, \u03b4) is one we haven't measured yet, but now we know it is there. And the really important thing is, if it is there, and also not zero, then it introduces an asymmetry between matter and antimatter.\n\nThis is important because currently we don't know why there is more matter than antimatter around. We also don't know why there are three copies of neutrinos (and indeed of each class of fundamental particle \u2013 three charged leptons, three charge -\u2153 quarks and three charge \u2154 quarks). But we know that three copies is the minimum number that allows some difference in the way matter and antimatter experience the weak nuclear force. This is the kind of clue that sets off big klaxons in the minds of physicists: _New physics hiding somewhere here!_ It strongly suggests that these two not-understood facts are connected in some bigger, better theory than the one we have.\n\nWe've already measured a matter\u2013antimatter difference for quarks; a non-zero \u03b813 means there can be a difference for neutrinos too. More clues.\n\nSo, not only had we seen the start of antimatter spectroscopy, which will check that there really is no matter\u2013antimatter asymmetry in the electromagnetic force. We now, in the same week, saw the result showing that experiments such as T2K in Japan and NOvA in the US, which are looking for matter\u2013antimatter asymmetry in the weak force, amongst neutrinos, were not wasting their time.\n\nChinese and Korean scientists have long collaborated on major particle-physics experiments, but these are two of the biggest particle-physics results to come out of experiments actually constructed and operated there. It used to take a long time for results to cross continents, but not any more. Like most physicists (but, disappointingly, unlike the ALPHA antihydrogen experiment at CERN), the Daya Bay people put their result up on the arXiv. This has been standard practice in particle physics and astronomy for quite some years, even predating the World Wide Web. I did my doctoral research in the days before the World Wide Web (just). But we had the Internet, and when Herbi Dreiner and I had finished what was my first ever academic paper,136 he added it to a 'bulletin board' managed by Los Alamos National Laboratory in the US. It was then emailed around the world to particle physicists who subscribed to the bulletins.\n\n136. See 3.5 Supersymmetry.\n\nThis was all new to me. Theorists were ahead of the experimentalists (as usual). But pretty soon experiments joined in. And when the web came along, the whole thing moved over there and is now the wonder that is the arXiv, curated by Cornell University, funded in an international collaborative model and free at the point of submission and at the point of access. My first paper is still there. The arXiv stores the full text and figures of papers.137 Basically, all particle-physics, astrophysics and astronomy papers are there, regardless of whether they are also in a journal or not. There is also coverage in condensed matter, nuclear physics, mathematics, biology and more, though I don't know what fraction of publications in those areas are uploaded.\n\n137. Though if you look at the paper (<http:\/\/arxiv.org\/abs\/hep-ph\/9211204>) you might notice we didn't upload the figures for our paper. This was because I was still struggling with postscript inclusion with LaTeX. These days, figures are all there. And if you look on INSPIRE-HEP you can see that KEK even scanned it in with the figures. We posted it to them. Ah, those were the days . . .\n\nTo see why this is important, consider the fact that my first paper was also published in a journal called _Nuclear Physics B_. Last time I checked, you could still get it there, too, a snip at $31.50, of which Herbi and would I receive . . . well, nothing. Unfortunately the only way of getting the ALPHA results seems to be to pay Nature Publishing Group $32, despite the fact that your taxes probably already contributed to the cost of the experiment. Prohibitive fees either at publication time or when you want to read the paper restrict the results of research to an elite of well-funded institutions and individuals. They deprive scientists elsewhere of opportunities, thereby depriving science of their skills. Demand for open access to research results is growing, and we had already decided that any definitive result on the Higgs would be freely accessible, even if this ruled out some very prestigious journals.\n\n#### 7.5 Is Nature Natural?\n\nMostly I work on measuring what happens in proton\u2013proton collisions at the LHC. But just as the 2012 LHC running began I went to a meeting about what wasn't happening \u2013 and still hasn't so far. The meeting, at the University of Maryland, was 'Supersymmetry, Exotics and Reaction to Confronting the Higgs'. SEARCH \u2013 a quality acronym (type 1) if ever there was one.\n\nAs already discussed,138 at the energy the LHC can reach, special things happen in physics. Electroweak symmetry-breaking happens, the W and Z bosons have masses in this energy range, and that was why we were sure that if the Standard Model Higgs boson existed, it would eventually be visible at the LHC.\n\n138. See 5.9 Which Leads, Theory or Experiment?\n\nMore general but weaker arguments based on 'naturalness' are often used to argue that other new physics should show up at the LHC too. Naturalness, in this context, is the assumption that the parameters in a theory should be about the same size as each other. So, say the ratio of two parameters should be between 0.1 and 10, and that these ratios should not have to be fantastically fine-tuned in order to make the theory work.\n\nIn the Standard Model, unfortunately, it looks like the Higgs mass does have to be fantastically fine-tuned. This is one of the problems supersymmetry might solve. For that to be the case, we ought to see some evidence for SUSY particles, and we hadn't. Many physicists were getting puzzled by the absence of supersymmetry, and in fact the absence of any new physics that could do its job, in the LHC data. It was too soon to give up on the idea of naturalness, but things had gone far enough that at the end of the SEARCH meeting, several eminent theorists advised people to work on understanding the QCD. Partly because it is interesting but mainly because if we can understand it better we can search more effectively for new physics that might be hiding in the data at the LHC.\n\nThis is, of course, what lots of us are doing already. For example, at about this time ATLAS released the first measurements of some new jet substructure variables, useful for searching for new particles. The conclusion of this new ATLAS paper was that we do understand QCD (and our experiment) well enough to use these variables; some of the ideas had even been used already in the CMS Higgs search. All this was close to my heart because I'd worked on those studies myself (they were the topic of the regular 'Boost' meetings), but many similar precise measurements, and calculations, need to be done before we can learn all the LHC can tell us. If in the end we do not find supersymmetry, or something similar, the idea of naturalness, that the theory should be elegant and not require fine-tuning, will be in real trouble.\n\nI went through Washington (Dulles) on the way to a physics meeting and queued for ages. There were about 30 desks, only one of which was manned, and the guy at that desk spent the whole time dealing with one family. I suppose the fact that the woman was wearing a niqab and the husband had a very full beard might have slowed them down a bit. In the end, the other staff got embarrassed and let us use some of the desks allocated to US citizens. This was my second-worst experience with US Immigration. My worst so far had been on my first trip to the US in December 1995, to Penn State University. That trip was made entirely to get my visa processed. It almost failed.\n\nI'd accepted a position with Penn State University. I had only a vague idea where this was, but that hardly seemed to matter since it was a good university and wanted to pay me to live in Hamburg and do physics with the ZEUS experiment, which is what I wanted to do.\n\nTo get my visa processed (a J-1, which would allow me to work for a US institution and get paid), I actually had to go to Penn State, however briefly. I was supposed to fly out a few days after the oral examination for my doctorate. Not wishing to take anything for granted, I had not booked my plane ticket, but was otherwise ready to go. My exam would be on the Thursday and I would fly out to the US the weekend after, assuming I passed.\n\nUnfortunately, the Saturday before, my bag got stolen. In it were some brand-new M&S underpants, a very long scarf I had knitted myself and my passport, including the J-1 visa.\n\nThe pants were easy to replace, the scarf impossible (I had forgotten how to knit). The visa and passport could be replaced but it would be tricky, and it would have to be quick.\n\nThe first half of the week was spent on trains, going to Manchester (parents, birth certificate), then Liverpool (Passport Office). I then popped back to Oxford for my exam. On the plus side, I didn't have time to get nervous. I passed, although I still wince when I remember some of the things I got wrong. A fellow DPhil student, Rick Gaitskell, then drove me to London. Friends in need, with cars, are great. Rick is a professor at Brown University these days, working on dark matter searches. I hope he has a better car now.\n\nI rushed to Grosvenor Square and bounced off the US Embassy because I had my travel bag with me. No bags allowed. What to do? Eventually I remembered I was a member of the Institute of Physics, and sure enough those lovely people let me leave my bag with them. Back to Grosvenor Square. Visa, done. Travel agent. Ticket, done. Hurry, hurry.\n\nOn the tube, I looked at my tickets. They said Newark. Where the hell was that? I had asked for tickets to New York. The guy must have misheard! Newark could be on the West Coast for all I knew!\n\nEventually I stopped palpitating. I can't remember whether I asked a random tube traveller or at the airline check-in desk whether Newark was near New York, but either way I was reassured. I barely remember the flight, but I do remember being rather spaced out when my new employer, Jim Whitmore, met me out of Immigration.\n\nI was then driven through heavy snow from Newark to State College, PA, geometrically centred in Pennsylvania (i.e. essentially nowhere). The car nearly spun off the road at least once. ('Should have come in the pickup, said Jim nonchalantly), but I was delivered, dazed, to a motel. I remember marvelling at the size of the toilet bowl, worrying that I might fall in. Later that evening I woke up in bed, completely confused as to where I was.\n\nThere's a scene in the film _10_ in which Dudley Moore, having drunkenly followed Bo Derek from California, wakes up in Mexico and staggers astonished and disorientated onto the balcony to the sound of Spanish guitars. I did this, although in my case a winter wonderland of small-town America in the deep snow, rather than a row of frantic strummers, greeted me.\n\nStumbling down the snow-lined street like Jimmy Stewart in _It's a Wonderful Life_ (America is so cinematic), I ended up in the nearest thing to a pub that I could find. Sitting at the bar, sipping a beer and watching a game show on TV, I began to regain some equilibrium. Until the barman, who I had been chatting to on and off, leaned over and said: 'You're not gay, are you?'\n\n'Erm, no. Why?'\n\n'This place becomes a gay singles bar at about this time of the evening, and you might feel a bit uncomfortable.'\n\n'Oh. Oh, right. Thanks for the tip.'\n\n'Actually, I'm finishing my shift. You want to come and play some pool in a different bar?'\n\nThis confused the hell out of me all over again. But I went anyway. And either he was straight or he didn't fancy me. We met up with a bunch of students and I beat them all at pool. The affinities between particle physics and games of marbles are well documented, but less well known is the fact that we particle physicists all excel at pool and snooker.\n\nThe next day I met a giant of particle physics in the lift.139 John Collins is one of the people who proved that, in one important sense, quarks and gluons are real.\n\n139. Elevator.\n\nThe proton is made of quarks and gluons. We work out how they are distributed inside the proton mostly by scattering electrons off them \u2013 this is what the experiment I worked on at the time in Hamburg was doing. Collins (with two colleagues) had proved that this knowledge 'factorised'.\n\nThe way quarks and gluons are distributed in the proton is difficult, maybe impossible, to calculate. But the factorisation theorem tells you that if you measure it in one kind of collision, you can use the information in others. That is, you could use what you learned at our experiment to predict what would happen at different experiments involving protons. Since this is something that we assume, for instance when predicting results of proton collisions at the LHC, it was a very important proof to have.\n\nAs to how well he plays pool, I haven't yet found out. I was a bit shy. I think I said 'Hello.' Or possibly, 'What floor is the Human Resources office on?'\n\nSo spaced out was I still that it took us more than a day to realise that when I had said 'Business' in response to the official's question about my three-day visit, he had not spotted, or processed, the J-1 visa that would let me work and which was the whole point of the trip. He had instead stamped a B-1 visitor visa in my pristine passport.\n\nLuckily the HR department managed to sort out the missing J-1. Whether the LHC will sort out the missing supersymmetry remains to be seen. In fact, at this stage, the Higgs boson was still missing.\n\n#### 7.6 Fun for Some, But Dangerous\n\nThe LHC was running well, data were accumulating at quite a rate, and we were glued to the four-lepton and two-photon mass distributions, seeing whether hints of the previous year would be confirmed, or vanish like mist in the new statistics.\n\nThere was a collaboration meeting in May where the first update on the two-photon distribution using 2012 data was shown, strictly for internal consumption. I was not working directly on the analysis, and it was very hot off the press. Rumours had been flying around the collaboration, but they changed every day, so it was very hard to get a sense of what was going on. I remember sitting in the audience waiting to see the crucial plot. For some reason, I did not look ahead in the slides. It's possible they had not been uploaded to the agenda page.\n\nIn December, with our hints and the CMS hints, I had started to think the odds were better than evens that the Higgs existed. Quite a step, for a confirmed Higgs sceptic. Now, when I saw the first 2012 mass distribution, I knew in my guts that we had it. The data needed checking, and were not really significant enough to be sure, but there was a small bump in the same place as the December results. This felt real. I could not actually, scientifically, be sure. But my stomach was having none of that.\n\nThis is a very dangerous phase for a scientist.\n\nThe next update on the ongoing Higgs hunt was planned for 4 July. Data were still coming in, cross-checks were still being made. We lapsed into a strange kind of state, desperate to know the answer but desperate to avoid any spoilers, any credible rumours from CMS. The rumour mill had been running for a while, of course. There was even a hashtag higgsrumors (US spelling!) that trended briefly on Twitter. All very entertaining for the neutrals, and it was pleasing that we were not the only ones interested in and excited by our experiment.\n\nBut . . . when it came to CMS data, I really did not want to know.\n\nPart of the point of having two independent experiments is that they cross-check each other \u2013 independently. We do that most effectively when we are blind to the other experiment's data, right up to the last minute. In fact, up to a point we even try to blind ourselves to our own data. As much as possible of the analysis should be optimised and decided in advance, before looking at the key data. This prevents even the possibility of subconscious bias entering the studies. If you are biased, the truth will probably still out in the end, but in the meantime your statistical estimations of confidence and significance will all be wrong. When your guts think they have the answer, you have to be even more careful. Guts can be wrong.\n\nSo hearing gossip from CMS would be at best distracting, a babble of inaccurate noise. At worst, it would be accurate and would bias our analysis. Likewise, as well as betraying confidences and damaging trust within the collaboration, leaking our own ATLAS data could bias CMS.\n\nThere was a period back on ZEUS when we had a few more events than we expected, right at the highest energies we could reach. This was terra incognita, no one had done the physics we were doing up there before. So it could have been something really new and exciting. While we were working on this, before we had published our results, rumours flew around that the other experiment on the HERA ring, H1, had also got something weird happening at high energies. They also got rumours about our data. The rumours reinforced each other, lots of people got overexcited. But it was a false alarm, sadly. Once the data got out, it was clear that while we both had anomalies, neither was very significant; worse still, they were not the same. So rather than reinforce each other, our results cancelled each other out.\n\nNo great harm was done. Lots of speculative theory papers were written, but that happens anyway. In my first (and, for a very, very long time, only) Radio 4 experience, I was interviewed by Nick Clarke on the _World at One_ , which was tremendous. He was a brilliant interviewer. But in the research, some time was wasted, and if we had not gone on to take more data that made it completely clear nothing odd was happening, the result might still be causing confusion today. On the LHC, we didn't want this to happen with the Higgs. We wanted the real answers, as unbiased as possible, as soon as possible. I'm all in favour of scientific openness. In the end it's essential. But _in the end_ , not during the experiment. Right then, we really didn't want to know.\n\nThe CERN seminar was to be at the start of the International Conference on High Energy Physics (ICHEP). There is one of these every two years. In 2008 in Philadelphia, the LHC had been about to turn on for the first time and the Tevatron had just ruled out their first mass point for the Higgs. Two years later, in Paris 2010, first LHC data were shown and Higgsteria was intense. This time, in Melbourne, would not be the last. But we all knew it would be another big step, one way or another.\n\nWe would be surprised at how big a step it would turn out to be.\nEIGHT\n\n## Discovery\n\n### July 2012\n\n#### 8.1 The Announcement\n\nIt was 3 July 2012 and I was in Salle Curie, one of the conference rooms below Building 40 at CERN. There are four of these rooms (Andersson, Bohr, Curie, Dirac), and the weekly meetings of the Standard Model group were usually held in Salle Curie. However, this morning Fabiola Gianotti, the spokesperson (meaning boss) of ATLAS, would be rehearsing the talk she would give the following morning. The talk was entitled, with studied neutrality, 'Status of Standard Model Higgs Searches in ATLAS'. It would be given on the morning of the following day, with a webcast around the world and especially to ICHEP, which was just opening in Melbourne.\n\nIt had become increasingly clear, initially to us and gradually to the media, that this was likely to be the big one. Peter Higgs had been sighted in town (having lunch with Edinburgh colleagues involved in the search) and Fran\u00e7ois Englert would be in the audience on Wednesday too. There was a definite tension in the air as Fabiola prepared to speak. Very few of us had seen all the ATLAS results collected together. Some of them were only hours old. We all knew we had something special, but how would it stack up? And would Fabiola stick with Comic Sans?\n\nThat question was answered immediately. ATLAS and CERN are not very corporate, and no one is going to tell Fabiola how to make slides. Comic Sans it was. The content was more important, of course, though presentation makes a difference and as Patrick Kingsley pointed out in the _Guardian_ :\n\nSo, perhaps not a bad choice for communicating tricky new results in as friendly and accessible a way as possible.\n\nThe question of how the data would stack up was answered over the next hour. The 2012 run had, up until two weeks earlier, delivered 6.6 inverse femtobarns of data. The recorded data equated to something like 5km of CDs stacked on top of each other, and more than 90 per cent of it had already been analysed and would be included in these results, along with the data from previous years. Several important Standard Model processes had been measured quite precisely, showing that both the detector and the physics were pretty well understood in these collisions.\n\nThe key results would be the search for a bump in the two-photon mass distribution and in the four-lepton mass distribution, and Fabiola spent some time discussing the details of the photon identification before showing the result. From the 2011 data alone, we had a 3.5 sigma significance. From the new data alone we had 3.4. The combined data set was 4.5 sigma. Very strong evidence, but not, on its own, up to the conventional 5 sigma threshold to call it a discovery.\n\nBut there was more. Fabiola then gave a brief discussion of electron and muon reconstruction, and showed the four-lepton distribution. Another bump. In 2011 it had a significance of 2.3 sigma. In the new data alone, 2.7. Combined, 3.4 sigma. More strong evidence, still not 5 sigma. But put these together, also with the WW and other decay channels from the 2011 data (the 2012 update for those was not yet ready) and the magic number came up. Five sigma.\n\nAn arbitrary threshold, just a convention. But one we had set ourselves in advance \u2013 we couldn't move the goalposts even if we wanted to be more cautious. We didn't have to beat about the bush. We had a discovery.\n\nThis was a very powerful experience. The moment when Fabiola showed our data, and our conclusions, hit me hard. I had seen some of the slides already, and the documentation and the analyses behind them. These were the work of hundreds of colleagues, many of them more directly involved than me in this particular analysis. And years and years of work for us all lay behind the results. But even knowing what was coming, seeing Fabiola declare to all of us what we had done was surprisingly emotional.\n\nAt the end of the talk, we decided to stop calling it an 'excess of events' and call it a new boson.\n\nThe rest of the day for me was spent in a Meyrin kebab-and-pool hall with Channel 4 News, which is where we came in at the start of the book. I then went to the airport for my semi-regular 20:05 flight to London City Airport. I would not be in Geneva or Melbourne for the announcement, but in Westminster, watching the webcast with lots of UK particle physicists and journalists, the science minister David Willetts, and many other members of the UK science establishment.\n\nWe were there rather early in the morning. Jim Virdee from CMS and I were going to talk to the BBC Radio 4 _Today_ programme before the talks by Joe Incandela (the CMS spokesperson) and Fabiola. I still didn't know the final CMS result. Rolf Heuer, Director General of CERN, had seen both the ATLAS and CMS results. Did he look excited? Relaxed? Anxious? Worried? Actually, he looked completely inscrutable, as usual. Jim and I were frantically showing each other the results of our respective experiments so we would know what to expect. CMS showed their results first (we had gone first in December) and had 5 sigma if the photon and lepton channels were combined. I was glad I'd had a moment with Jim, because by the time Joe began the first talk we really didn't have much time to actually listen, as there were a lot of people looking for physicists to talk to. I really liked the fact that the seminars were clearly aimed at fellow scientists, not the media or public, but this did mean they had to be translated.\n\nA moment that everyone understood, at which I turned round mid interview and clapped, was the spontaneous round of applause when Fabiola showed our 5 sigma result. Then there was an emotional Peter Higgs meeting Fran\u00e7ois Englert for the first time, and Rolf Heuer's famous declaration that 'As a layman, I would now say \u2013 I think we have it. Do you agree?'\n\nWe agreed.\n\nAfter all the rumours and the hints, all the projections and the hows and whys, finally we had, beyond reasonable doubt, discovered something fundamentally new.\n\nPretty much anything could in principle have turned up at the LHC, since no one had done this before. But if the Higgs boson had not shown up, our understanding of fundamental physics, as encapsulated in the Standard Model, would have been shown to be incomplete. Well, let's be frank, it would have been wrong.\n\nThe chain of reasoning is amazing. We knew that the origin of mass occurs at LHC energies. We knew this because two fundamental forces, electromagnetism and the weak nuclear force, unify at these energies. The reason these forces look different to us in everyday, low-energy life is that the force-carrying particles for the weak force, the W and Z, have mass and the photon does not. We had, in the Standard Model, come to the conclusion that this mass can only happen if a certain kind of quantum field fills the universe and sort of sticks to some particles to give them mass. That is indeed quite an extreme leap to make, based on some fairly esoteric mathematics. The only way of proving whether we'd done the right thing or not, whether the field is real or not, was to make a wave, an excitation, in the field. This wave is, or would be, the Higgs boson. And it has to show up at the LHC or the field is either not there or is very different from what we expected. There was nowhere to hide.\n\nInventing a whole-universe-filling field to make your maths come out right is pretty radical. But it was looking as though it might just have worked. On 4 July 2012, we had seen something fundamentally new, which fitted the description of the particle predicted by mathematical understanding of previous data, coupled with some prejudices about aesthetics, symmetry and how a decent universe ought to hang together. I don't know about you, but this still amazes me.\n\nA nice touch at the end of the event in Westminster was that Alison Boyle from the Science Museum in London got John Womersley (Chief Executive of the Science and Technology Facilities Council, which is responsible for funding particle physics in the UK), Jim Virdee (ex CMS spokesperson) and me to sign a copy of the press release 'for posterity'. It would have been better if David Charlton from Birmingham had signed for ATLAS, since he was Fabiola's deputy (and later became head of ATLAS), but he was busy in Melbourne. And anyway, it was a team effort . . .\n\n#### 8.2 Beyond the Onion: The LHC Computing Grid\n\nI mentioned the huge amount of data we had analysed to get these results. Those data were collected by the different layers of technology surrounding the collision point (tracking detectors, calorimeters, muon systems) and pre-selected by the 'trigger', the high-speed online electronics and computing that made sure the fraction of information we could record contained the most interesting events. They were then reconstructed, as discussed in section 5.1,140 as the first step of working out what particles had been produced, and in the end leading to the result that Fabiola could show.\n\n140. 5.1 Why Would a Bump Be a Boson?\n\nThe computing power to do this did not all exist at CERN, and still doesn't. There is a worldwide grid of more than 140 computing centres, in 35 or so countries,141 connected by high-speed networks and serving the physicists on all the LHC experiments, as well as some other projects around the world too. The data transfer rates are often over 10 gigabytes (the equivalent of two DVDs) per second. When not processing data from LHC, the grid runs simulation programs; the simulated data are also vital for making sense of the real data.\n\n141. The main UK centre, our so-called 'Tier 1', is at the Rutherford Appleton Laboratory at Harwell in Oxfordshire.\n\nWatching the online monitoring of the data flow and processing on this grid gives a powerful and somewhat eerie sense of the global scale of the LHC project, as data snake from Geneva to North America, Taiwan, Scandinavia, India and elsewhere to end up somewhere on a physicist's laptop and be turned into new information about the fundamental workings of the physical universe.\n\n#### 8.3 Don't Think Twice, It's All Right\n\nThe physicists at Westminster talked to a lot of journalists on 4 July. Amid the questions, two recurrent themes emerged that still make me smile, and which are still at play in the ongoing coverage of CERN and the LHC.\n\nHaving spent the previous few years hedging, being cautious, talking of hints and probabilities, we were now ready to say we definitely had a discovery. This was the big breakthrough \u2013 for us. As I said, even in Fabiola's practice talk we were still using cautious language such as 'excess of events', and only then steeled ourselves to say 'new boson'. It felt great. But it wasn't enough for some of the media. We were prepared to say it looked like the Higgs boson, or some kind of Higgs boson anyway, but we would not say 'We have the Higgs boson!' We'll see exactly what it might take for us to say that in the next section, but it became really clear to me in these conversations that there was still a bit of a communication gap between the people working on the LHC and the people reporting on it. For me to be able to say 'We've definitely found a new boson' was the most exciting thing ever to happen to me (professionally, at least). If it turned out to be the Higgs boson, that would be great. But if it turned out to be something else, that would be in some ways even more exciting. The fact that we did not know, for sure, right then, was irrelevant. What really mattered was that it was not a statistical blip or some other artefact of the analysis. It was real, and it was something utterly new. But communicating all that to someone who wants to hear you go, 'Yay, we found the God particle!' is a bit tricky. Especially when you are overexcited and tired.\n\nAnd now I have said 'God particle', even if it was in direct quotation marks. Which brings me to the second recurrent theme.\n\nThe last of the media engagements I did that day was a BBC World Service radio programme called _World Have Your Say_. This was to be a live discussion of the implications of the discovery. Lovely. They did warn me that 'religious implications' would be part of the discussion, but since there were none, I naively assumed this would be a small part and we could spend most of the hour talking about what had really happened.\n\nThe programme began sensibly enough, and we had a good 15 minutes or so discussing what had just happened, what CERN was and the technology behind the experiments. All good. In the studio with me was an engaging and smart guy called Sonny Williamson, a composer who had apparently been doing serial interviews all day as a non-physicist, non-expert big fan of the whole thing who had visited CERN on his holidays. There was also a Welsh Hindu. On the phone were Caitlin Watson from the Institute of Physics and the science writer Marcus Chown. All fine.\n\nI worried a little when Marcus left, with 40 minutes remaining, to be replaced by an unsuspecting cosmologist, Andrew Jaffe, and the presenter said we'd move on to the religious implications.\n\nSonny said there were none. Caitlin said there were none. Andrew and I said there were none, unless you have the kind of religion that instructs you to disregard evidence, in which case you had many bigger problems than the Higgs boson. The age of the Earth, for example. But in general there was no special religious implication in this discovery.\n\nThis wasn't enough. There was a phone call to a Christian minister, who said there were no religious implications. The Hindu guy claimed his religion had sort of predicted it all already, which made the scientists splutter slightly. We got a rabbi, and she said there were no implications. There was a phone call to an imam somewhere. He also said there were no implications. In the end it was a workaday pub discussion of how religion and science talk past each other. The presenter at some point got a bit fed up with the fact that the scientists were being 'too diplomatic', and specifically not being Richard Dawkins. But the religious guys were being reasonable, too, on this occasion (with the possible exception of the quantum Hindu chap). There are some pretty odd belief systems out there, but I haven't come across a religion teaching a dogmatic denial of the existence of a scalar field with non-zero vacuum expectation value, and indeed, the Hindu, the imam, the rabbi and the minister seemed to concur.\n\nSo, I wasted the evening of the greatest discovery in my field for decades trying not to start a science-versus-religion war with a bunch of reasonable religious people who were also not trying to start a war. It wasn't so much that it was bad, it was just dull. There were so many more interesting things we could have discussed on that day than whether the mutually incompatible myths of the world's religions were or were not compatible with nature.\n\nThe whole thing reminded me of a _Channel 4 News_ discussion I was part of when Stephen Hawking and Leonard Mlodinow brought out a book containing the claim that God was no longer necessary. Again, this seemed completely specious, albeit presumably on a par with Leon Lederman's regrettable invention of the name 'God particle' when it comes to enhancing book sales.142\n\n142. Yes, I know Lederman claims he wanted to call it _The Goddamn Particle_ and blames his publisher for the change. But my publishers wanted to call this book something really silly, and I managed to stop them.\n\nMy guess is that if you can accommodate evolution, astrophysics and the rest with your religious world view, then theoretical cosmology is unlikely to bother you either. And if you are already denying those things, then your faith already has you so nicely cocooned from reality that nothing Hawking says will have any impact. At least the Channel 4 discussion took place on a day when nothing much else was on. The occasion was a new book, not a massive scientific breakthrough, so we weren't really wasting precious time.\n\nA final comment on the relationship between science and religion. Sometime later (in May 2013) I participated in a celebration of the life of Richard Feynman at the Bloomsbury Theatre, organised by Robin Ince. Feynman is by any stretch of the term an iconic figure in science, especially in physics. He won the Nobel Prize with Tomonaga and Schwinger in 1965 for the discovery and formulation of quantum electrodynamics, the first internally consistent and quantum field theory. This theory describes electromagnetism with astonishing precision. He represented this in Feynman diagrams, used throughout particle physics and in this book. He had a childlike curiosity and a way of talking and teaching without being patronising or condescending. He played bongos.\n\nTom Whyntie and Andrew Pontzen (a particle physicist and an astrophysicist) were doing a turn in the show, and like me they took their copies of the _Feynman Lectures_ onstage with them. These were essential reading for me as an undergraduate, and still should be for anyone studying physics now. However, they were written in the early 1960s (around the time Peter Higgs wrote his famous paper, in fact), so while they contain many beautiful insights that easily stand the test of time, they most certainly do not contain all of physics. The Higgs-boson discovery is just one example of the vast amounts of new knowledge acquired since they were written.\n\nFeynman remains an inspiration, but he was never a saint and he certainly didn't encode the whole of physics for us to study and interpret in some process of divine revelation. Physics has moved on, beyond where Feynman could have seen, because of the experiments done since. He is one of the giants upon whose shoulders we stand. As in the quotation from Max Gluckman at the start of this book, 'A science is any discipline in which the fool of this generation can go beyond the point reached by the genius of the last generation.' We've gone beyond Feynman, and this would of course not dismay him in the slightest. He was more aware than most that science has no holy books, that it is a work in progress \u2013 the joy of finding things out.\n\n#### 8.4 The Definite Article?\n\nThe first conference I went to after the July announcement was another in the annual 'Boost' series, this time organised by Marcel Vos in Valencia. Long Spanish lunches should feature in more conferences. Paella and red wine are excellent aids to discussion, and somewhat to my surprise I found it easier than usual to pay attention in the afternoon talks.\n\nThe discovery of the new boson made the meeting even more exciting than the previous year's. One thing our minds were quite focused on was exactly the question that many journalists had been grappling with on 4 July. We were sure we had discovered something, but we insisted on calling it a 'Higgs-like' boson. What would it take to remove the caveat? Why do we not just come out and say we've found 'the Higgs boson'?\n\nOne of the properties the new boson definitely shared with the Standard Model Higgs boson was the fact that it decayed very rapidly. Typically, a rapidly decaying particle has several decay options open to it and will 'choose' amongst the options randomly. For the Standard Model Higgs boson, the randomness of this choice is weighted by probabilities that are precisely predicted by the relevant Feynman diagrams calculated in the Standard Model.\n\nThis is a common situation in quantum physics: probabilities are predicted, but individual events are not. The decay of a radioactive nucleus shows the same situation: we can measure the 'half-life'. Take the unstable carbon-11 isotope143 as an example. The half-life is 20 minutes.\n\n143. See 7.3 Waves.\n\nThis means that if I have a number of carbon-11 atoms at some point in time, 20 minutes later half of them will have decayed, on average. For small numbers, there will be a significant statistical uncertainty in the time taken for half of them to decay, but the half-life remains the most reliable estimate. If the number of atoms is very large, the half-life is a very precise prediction. But there is nothing in physics that can tell you when an individual carbon-11 nucleus will decay. It may decay immediately, or it may last for ages. All you know is that the chances of it lasting for twice the half-life are \u00bd x \u00bd = \u00bc. Three times, \u00bd x \u00bd x \u00bd = \u215b . . . And so on. But that is just a probability, not a prediction for the exact decay time.\n\nSo as we create more and more Higgs bosons and watch them decay, we can build up a better and better measurement of the probability for each decay mode. These are call 'branching ratios'. Think of a Feynman diagram for a Higgs-boson decay. It is reminiscent of a tree, with the Higgs as the trunk branching into a number of decay products.\n\nAn example of a Higgs boson decay\n\nThe branching ratios give us a lot of information about the particle that is decaying. As I said, they are precisely predicted for a Standard Model Higgs boson, at least they are once you know the new boson's mass. This mass is known, from the position of the bumps in the two-photon and four-lepton mass distributions, and is about 125 GeV. Therefore, measuring the branching ratios is a good way of getting some evidence as to whether the new boson we are dealing with is a Standard Model Higgs boson. Do the measured branching ratios agree with the predictions?\n\nThe branching ratio measurements have a broader significance, though. In particular, knowing the separate branching ratios to bosons and to fermions is vital. The Higgs in the Standard Model is there to give mass to both bosons and fermions, but the mechanism is very different in each case. Fermion masses are allowed by the presence of this new scalar field \u2013 call it the Brout\u2013Englert\u2013Higgs (BEH) field \u2013 all over the universe. By coupling to this field, they acquire energy that appears as a mass in the equations governing their behaviour.\n\nThe relationship between the gauge bosons and the Higgs is much more intimate than this. When the Higgs field breaks the symmetry between the weak and the electromagnetic forces, by giving the W and the Z mass while leaving the photon massless, something subtle happens to do with the spin of the particles.\n\nThe W, the Z and the photon all have a single unit of angular momentum, that is, they have a spin of one. And without the Higgs, they all have mass of zero.\n\nA zero-mass, spin-1 particle has two independent spin states. The spin can point along its direction of motion, or against it. Quantum mechanics tells us there is no other possibility. A boson can be in a mixture of these two quantum states, but whenever you measure it you will find either one or the other.\n\nThis is fine for massless bosons, because massless particles always travel at the speed of light. The speed of light is an unattainable maximum speed for a body with mass, so you, as a massive body, can never overtake a massless boson, and indeed you can never even match speed with one. If you could match speeds, the 'direction of motion' of the boson would be undefined, because relative to you it would _have_ no motion. But since this can never happen, it is not a problem. The speed of a massless particle is _c_ , to all observers, and so a direction of motion is always defined.\n\nIf a formerly massless boson acquires mass, however, there is a problem. Now it is possible for the particle to be at rest, stationary, not moving. Where does its spin point then? To fully describe all the options for a particle at rest with one unit of angular momentum, a third option is needed. Choose a direction and call it 'up', and the spin can point up, down or at right angles to the direction. This happens for atoms with spin-1, for example. We measure three possible spin states. For a moving particle with mass this is the same as saying that the spin can point backwards, forwards or at right angles to the direction of motion.\n\nThis may sound a long way from everyday reality, but the fact that the spin-1, massless photon only has two options open to it is observable in the fact that light can be polarised in two (and only two) different ways. This is how Polaroid sunglasses work to reduce glare. When light is reflected from a surface, the amount that is reflected depends upon the polarisation, as well as on the wavelength and the angle at which the light hits the surface. For a range of angles and wavelengths, that polarisation of the light with the electric field oscillating parallel to the surface is reflected more efficiently than the other component.144 Polaroid material can select one of the two polarisations, cutting out that transverse polarisation and letting the other one through. This has the effect of allowing half the direct light through the glasses, but drastically reducing the glare from reflected light, for example from a wet road. If you take two pieces of a polarising material and put them at right angles to each other, all the light is stopped. There is no third polarisation available to photons.\n\n144. The quantum mechanics behind this is beautifully explained in Feynman's book on QED, which is aimed at a general audience. While hard work, it is well worth a try if you want to better understand quantum physics.\n\nFor a massive spin-1 particle, though, there have to be three possible polarisations. This is what we physicists call another 'degree of freedom'. It is an extra thing needed in order to fully describe a physical system \u2013 in this case a boson. Degrees of freedom aren't supposed to suddenly appear like that in fundamental physics. This looks like a big problem for the Standard Model. If the W and Z are to acquire mass, they have to get this extra degree of freedom, and where is that going to come from?\n\nOne of the most beautiful things about how the whole BEH mechanism works is the way this problem is solved, at the same time as evading the Goldstone theorem and removing the massless scalar bosons it would predict.145 The BEH mechanism introduced a new quantum field (the BEH field), which is non-zero everywhere. Because of the type of field it is,146 it has four possible ways of getting excited, four possible particles, if you like, or four different types of waves it can transmit \u2013 four different degrees of freedom. This was a problem for the idea, because three of these four particles would be massless, and none of them had been seen in nature.\n\n145. See 4.7 Putting the Higgs in its Place. 146. A complex scalar doublet if you must know, but you don't have to care.\n\nThe amazing thing is that when these two problems \u2013 the extra massless scalar Goldstone bosons and the stubbornly massless gauge bosons with only two degrees of freedom \u2013 are put together, they cancel out. Here are the steps:\n\n  1. We have four massless bosons \u2013 three from the SU(2) bit of the Standard Model and one from the U(1) bit.147\n  2. Of the three SU(2) bosons, one is positively charged, one negatively charged, and one is neutral. The U(1) boson is also neutral.\n  3. Three of these bosons (the charged ones from SU(2), which are the W+ and W-, and a combination of the two neutral bosons that becomes the Z) absorb, or 'eat', the three massless scalar bosons and use them to provide the missing polarisation degree of freedom needed for those bosons to become massive.\n  4. The photon disdains the food and stays massless.\n  5. There is one out of the four scalar bosons left. It has mass.\n\n147. See Glossary: Gauge Theories for the meaning of the U(1) and SU(2) notation.\n\nThat was still a problem, until 4 July, when we found it.\n\nAll of this is why we knew the Higgs has to have a mass not too far from the W and Z, and that's why we knew we would find it at the LHC, if it were there. In a sense, it's the same particle, or field, totally mixed up with the W and Z.\n\nThat's the intimate connection between gauge bosons and the Higgs. The connection to fermions, on the other hand, is less intimate. The role played by the Higgs here is that it simply allows the fermions to have mass. There's no real prediction for what the masses are, and the way it gives them mass is qualitatively different from the way it gives mass to the W and the Z.\n\nWe discovered the new boson through its decays to pairs of photons and pairs of Z bosons, with some indication that it also decays to W bosons. The fact that we saw these decays at roughly the expected rate was strong evidence that whatever we had found, it was connected to electroweak symmetry-breaking. So I was already comfortable calling it a Higgs boson. But we had not yet seen the boson decay to fermions.\n\nThe most common decay of a 125 GeV Standard Model Higgs boson is to fermions \u2013 to a b-quark\u2013antiquark pair. Unfortunately, at the LHC there are many other ways such pairs can be produced, and the experiments have trouble extracting the signal from background noise. Similar problems applied at the Tevatron, where this decay mode was the best way of looking for the Higgs. This is the problem that the paper I wrote with Adam, Mathieu and Gavin on 'boosted Higgs' searches was meant to address, and one of the reasons the 'Boost' meetings began. In that paper we made some bold claims about how our new technique148 would have a big effect on Higgs physics at the LHC. One of the things we were discussing over those long lunches in Valencia was whether those claims had been justified.\n\n148. See 1.7 Boost One.\n\nOur paper pointed out a few ways the b-decays of a Higgs can be picked out from amongst the backgrounds more easily, based around the idea that quite a few of the Higgs bosons produced at the LHC will be travelling quickly \u2013 i.e. boosted. The methods we invented work better when the LHC is running at higher energy, closer to its 14 TeV design energy that the 8 TeV we had in 2012. Higher luminosity would also be very helpful. Even so, the paper we wrote had had an effect on the searches in the 8 TeV data \u2013 the boost of the Higgs in particular is important \u2013 and was cited by both CMS and ATLAS in their Higgs-to-b-quarks search papers. The techniques also inspired a bunch of other papers, some related to the Higgs but some of them about the strong interaction, or about searches for other new physics beyond the Standard Model. Much of that was also under heated discussion in the 'Boost' meetings. I would say the claims had been partly justified so far, but the jury was still out on the full impact of jet substructure on Higgs searches.\n\nApart from b quarks, the only other fermion decay we had a chance of measuring in these data was the decay to tau leptons. That search was also still going on.\n\nIt's a matter of judgement and preference, but if and when we see the Higgs decaying in these two channels \u2013 taus and b quarks \u2013 at roughly the predicted rates, I will probably start calling this new boson _the_ Higgs rather than _a_ Higgs. It won't prove it is exactly the Standard Model Higgs boson, of course, and looking for subtle differences will be very interesting. But it will be close enough to justify the definite article.\n\n#### 8.5 What's in a Name?\n\nAstonishingly, no sooner had a Higgs boson been discovered than some people with access to the media began agitating to change its name. The idea being that naming it after a single person is unfair. This made me unreasonably annoyed.\n\nIt's true that many people contributed to the theory behind the masses of fundamental particles. It's true the symmetry-breaking mechanism that gives particles mass should not really be called the 'Higgs mechanism', and I hope I have managed to avoid doing that in this book. The mechanism was proposed independently by several people, two of them (Brout and Englert) predating Higgs slightly, and Hagen, Guralnik and Kibble giving a version that was in some ways more complete, and closer to what is now the Standard Model, but a (very) little later. So it goes.\n\nEven so, Peter Higgs has a claim on the boson itself that no one else has. While its existence was certainly implicit in the other two papers, Higgs' paper was the first to explicitly mention the fact that if the mechanism were to be realised in nature, there would be a new massive scalar boson to find.\n\nFor other reasons, an attempt at this point to dispute the name was an embarrassing sideshow, and had a whiff of theorists' arrogance about it. Remember, the theory papers in question date back to 1964. This was before much of the rest of the Standard Model was put together. As the other pieces of the knowledge fell into place \u2013 the electroweak and QCD sectors, the discovery of the W, Z and gluon and the full set of quarks and leptons \u2013 the mass mechanism became more and more central and the hunt for the missing boson became a higher and higher priority. People started calculating seriously how a Higgs might appear in a collider detector, a very influential and early example being a paper by John Ellis, Mary Gaillard and Dimitri Nanopoulos entitled, significantly, 'A Phenomenological Profile of the Higgs Boson'. Note the name of the boson. That was published in 1975 \u2013 only just after first evidence for the Z boson had been seen at CERN in the Gargamelle bubble chamber in 1973, and well before the first real W and Z bosons were observed, also at CERN, ten years later.\n\nThousands of people contributed to this huge advance in knowledge. The UA1 and UA2 collaborations that discovered the W and Z wrote papers on searching for the Higgs boson, naming it as such. Many of them, on ATLAS and CMS, on the Tevatron and LEP experiments through the nineties and noughties, worked in 'Higgs groups'. Many theorists painstakingly calculated how a Higgs boson would appear in a detector, and they called it a Higgs boson as they did so. Sandra Kortner and Eilam Gross were convening the ATLAS Higgs group when we announced our results on 4 July. All these other people and more had earned a stake in the name by now, and they called it a Higgs. To suggest changing it at this late stage because it looked as though we might actually have found it bordered on insulting.\n\nOf course, it was probably part of the positioning battle now that a Nobel Prize was on the horizon \u2013 especially given the arbitrary rule that a maximum of three individuals (not three collaborations) could be awarded the prize in physics. But it was an absurd attempt, at a time when not only were all right-thinking physicists simply celebrating a great piece of new knowledge, but the general public were more aware of a physics result than at any time we could remember, and knew it as a Higgs boson (if we were lucky and they didn't call it a God particle, of course). Not only did Tim Berners-Lee, who invented the World Wide Web at CERN, feature in the Olympics opening ceremony in London that summer, but the Paralympics ceremony included some kind of interpretive dance rendition of the Higgs boson. And called it a Higgs boson. So there.\nNINE\n\n## What Next?\n\n### August 2012 onwards\n\n#### 9.1 I Want an Interstellar Higgs Drive\n\nLife, of course, goes on.\n\nTen days after the discovery was announced, I was discussing it with Brian Cox in a session chaired by Robin Ince at the Latitude Festival, an annual music and arts festival in the south of England, having earlier recorded an episode of their science chat show _The Infinite Monkey Cage_ for BBC radio. I mention this mostly for the bragging rights, of course. Brian may have become used to a world containing rock-star scientists, but I haven't, yet. It is honestly not just for my bragging rights that I mention it, though: the thousands of colleagues who worked on the discovery, as well as the governments and taxpayers who funded it, have bragging rights. So do the thousands (really!) of people who crowded the enormous 'Literary' tent on a Saturday afternoon at a music festival. I think we should all be quite proud of this, the achievement and the public support.\n\nThis is evidence, of a sort, that this discovery has had an impact. Impact is a vexed topic amongst researchers, though, and was especially so around this time for various reasons. The 'Science is Vital' campaign149 had successfully communicated the message that the economic and societal impact of scientific research is huge and, indeed, vital. It's a rather utilitarian approach, where the benchmark is 'The greatest happiness of the greatest number' as a measure not just of whether something is worth doing, but of right and wrong. This was the philosophy of Jeremy Bentham, who was very influential in the founding of UCL (and whose dressed skeleton still sits in a glass box in our cloisters), so you might expect me as a UCL person to have some sympathy. And indeed I do.\n\n149. See 4.1 Science is Vital.\n\nBut other voices in the science community, and broader academia, are frequently raised in objection to this Benthamite approach as a way of judging research. In the UK, academia was gearing up to the 'Research Excellence Framework' (REF), a massive exercise that involved collecting and collating information about research done in all UK universities. As well as looking at academic papers and other 'outputs', this assessment was going to include a look at the 'impact' of research beyond academia. Quite apart from the arguments about the cost of the exercise, the idea of even trying to assess this impact was very controversial.\n\nIt is worthwhile unpicking this controversy a bit. We didn't go looking for the Higgs boson because it was useful, or because it would make money; we did it because it was interesting and we are curious people.150\n\n150. Yes, OK, in all senses of the word.\n\nDo we care about the wider impact or not? Are we trying to have our cake and eat it? Should the success of research be judged by its impact? And what is impact, really? Indeed, quite a few questions at the Latitude event were along the lines of 'What useful stuff can we do with the Higgs now we know it's there?'\n\nA legitimate response is to reply that the sheer wonder of the new knowledge is worth the investment. Part of what it means to be human is to be curious about our surroundings and how they behave, whether you view this as a divinely implanted imperative or a successful evolutionary trait, or both.\n\nIt would also be true to say that the technology and training, which are inevitably produced as spin-offs from this kind of research, more than pay for it. The Institute of Physics is one of the organisations in the UK that points this out most regularly, and in October 2012 MP Alok Sharma hosted a launch event of a new report from the Institute of Physics on 'The Importance of Physics to the UK Economy'.151 Meeting rooms of the Palace of Westminster can be disconcerting places in which to give speeches: as soon as Frances Saunders, president-elect of the Institute of Physics, began hers, the division bell rang deafeningly for several minutes. When she finally managed to restart, a background rumble from some elderly men in the corner, hitting on the free wine, provided a distracting backdrop. I was told they were lords, which seems too clich\u00e9d to really be true. All part of mixing in the corridors of power, I guess.\n\n151. <http:\/\/www.iop.org\/publications\/iop\/2012\/page_58712.html>.\n\nThat Institute of Physics report is full of information about the importance of physics to the UK economy. It defines 'physics-based sectors' of the economy as those where 'the use of physics \u2013 in terms of technologies or expertise \u2013 is critical to their existence', i.e., if there was no physics, these sectors would not exist. Of course, a similar report could be written about any technologically advanced nation. The use of physics \u2013 in terms of technologies and expertise \u2013 is critical to the existence of lots of economic activity. To be sure, a physicist would claim that physics is critical to the existence of everything: without it the Earth wouldn't go round the Sun, the atoms of your body would not hang together, and nothing would have mass. But it is possible to delineate a large part of the economy that would quickly be in trouble if we all stopped doing physics research and education.\n\nThere are some impressive numbers. The direct contribution to the UK's economic output is \u00a377 billion, or 8.5 per cent. This rises to more than \u00a3220 billion if you include indirect spend. Some 3.9 million jobs are supported by these industries in the wider economy, with the average worker in a physics-based industry adding a factor of two more 'gross value' than the average worker overall.152 It's not the main reason I do physics, but it is one reason that we should as a nation. And I'm glad someone writes these numbers down, because unless we know these things, physics might stop being done in the UK.\n\n152. At least two of the successful attendees at the event were ex-students of mine. Gratifying though that was, I was beginning to feel a bit too senior at that stage and was quite glad of the presence of those maybe lords to remind me that I wasn't that far gone yet.\n\nBut the question stands and is a good one. What will be the specific impact of the knowledge that this boson exists?\n\nScientists have many motivations, but one of the fundamental ones is surely a sense of progress: there are things to find out that are important, that are not currently known, and that once you have found them out are added to the body of human knowledge to the eventual benefit of us all. Paul Dirac was a theoretician working on very fundamental physics \u2013 relativistic quantum mechanics \u2013 and not at all driven by the search for direct applications. However, as recounted in Graham Farmelo's excellent biography, even he cared about impact. He said:\n\nIn my case this article of faith is that the human race will continue to live for ever and will develop and progress without limit. This is an assumption that I must make for my peace of mind. Living is worthwhile if one can contribute in some small way to this endless chain of progress.\n\nGiven that, for example, Dirac's equation predicted the existence of antimatter, he certainly contributed.\n\nFrom the point of view of the arts and humanities, such an idea of progress may appear naive, and certainly it is not obvious that it applies there. Whether human thought genuinely progresses is arguable, and our ability to regress is, sadly, pretty plain. One can even argue about what constitutes progress or regress, and many do. Nevertheless, the recorded history of the human race has a thread running through it of increasing understanding of the universe we live in (including our own bodies), and increasing ability to influence it one way or another. This progress, and the sense of progress, has a big impact on our lives. Our society is built on the fruits of past progress, and we rely on ongoing progress to meet new challenges.\n\nIn the UK, as in many other countries, assessment of the 'impact' of research is now embedded in the way funding bodies decide what to fund. This is not only in the REF, but is done by research councils too, who when considering grants for new projects require an 'impact statement', which is a guess as to the future impact of the work beyond academia. You might measure this in terms of patents, jobs created or skills imparted to people, and as I said, it is all controversial. If there is a sliver of Dirac in the heart of every scientist, why so?\n\nOne reason is that many groundbreaking applications are serendipitous. The breakthrough comes from an unexpected direction not anticipated at the start of the research and often unrelated to its initial purpose. This is true, though it works in both directions. Breakthroughs in understanding the universe are sometimes unintended consequences of research aimed at direct application. Lots of groundbreaking astronomy, for instance, came about from research directed at improving navigation for trade and the projection of imperial power. Still, it is a fair criticism that guesses as to the future impact of research are likely to miss the most radical benefits, precisely because they will be radically new, unexpected and unpredictable.\n\nA second, much less justifiable reason for controversy is that some academics view the acquisition of knowledge as somehow morally or intellectually superior to the application or dissemination of knowledge. I don't have much sympathy with this one. While a certain detachment from personal gain is morally attractive, I really don't see why striving to understand the origin of life (or mass) is morally superior to striving to cure cancer, for example. Anyway, the fact is that the two activities are very likely to aid each other.\n\nThe third reason is that 'impact' assessments are a tool for directing research, and it is not obvious who is best qualified to do this. In fact, many academic researchers resent hugely the idea that research councils or universities try to do this. Like it or not, though, I think someone has to. No single researcher is competent to compare excellence across, say organic chemistry, particle physics, pharmacology and planetary science. So even if, within these areas, peer-reviewed excellence of science were to be the sole criterion, someone has to decide how much resource goes into each area. Unless this is to be done entirely by politicians and civil servants, at least some researchers must engage, sit on committees and argue the balance. And at that level the relative benefits, i.e. impact, of excellent science in each area will inevitably, and correctly, be a factor.\n\nWe need a research culture where applications are seized upon and encouraged, not by every single scientist, but by someone in the culture in which they work. Colleagues who take time out of finding new knowledge in order to ensure their work has an impact deserve recognition via the funding system. As a head of a physics department, putting together the evidence for these things was a useful exercise for me and helped the people who do it get recognised. We need both. When she was five, my daughter did a science experiment in school, shining a torch through materials to see which would make the best curtains. Cardboard won. Great science, but poor impact, I fear. I don't think cardboard curtains will rescue our economy.\n\nI'm less convinced that writing predictions of the future impact of all research grants is sensible. In some cases, where research really is directed towards solving a problem with clear applications, perhaps yes. But then presumably you'd write the whole funding case that way anyhow. For other proposals, very often it will be at best a waste of time and at worst it will stifle unexpected breakthroughs and add a short-term bias to research activity and funding decisions. Taxpayer-funded research really ought to be free of such bias, if only to counter the bias that must be present in commercial research.\n\nHard evidence on this is difficult to collect. I guess ideally one would have to compare two canonical arrays of economies, with one group funding excellent research for its general benefit, and another funding only research with a guaranteed, foreseeable pay-off. I really would not want to be in the second group.\n\nAnyhow, back to the original question: applications of the Higgs. I would be disappointed to think there will never be any, and I think there probably will be some at some point, even though I can't imagine them credibly now. I would not be surprised if I don't live to see them. But if our descendants get an interstellar Higgs drive, or other wild things, they will hopefully thank us for accumulating the basic knowledge behind their amazing new technologies.\n\nAnd in the meantime, we just have to settle for the spin-offs, and the wonder.\n\n#### 9.2 What Next for the Higgs Boson?\n\nThe newly discovered boson can look forward to a period of intense scrutiny, where particle physicists from all over the world measure its properties as precisely as we can to see what secrets it is hiding and whether it will yield any clues that might help us solve some of the remaining puzzles in physics.\n\nSeveral questions have already been answered. Because we measured the new boson decaying to pairs of Z bosons, and to pairs of photons, we knew immediately it must be a boson itself, that is, it must have an integer angular momentum: 0, 1, 2, etc. This is due to conservation of angular momentum.153\n\n153. There is no way to make a half integer (that is a fermionic) spin by combining two integer spins (either two spin-1 Z bosons, or two spin-1 photons).\n\nIn fact, because the photon is massless, we know the new boson can't have spin-1. This comes from the Landau\u2013Yang theorem, which dates back to 1948 when QED was very fresh and people were trying to understand what mesons were. Skip over this if you like, it is quite involved, but it goes something like this:\n\nFirstly, the massless photon has only two possible orientations for its spin, corresponding to the two possible polarisations of light.154 These orientations are either along or against any direction you choose. We can choose as an axis the direction of travel of one of the photons, so the other photon will be travelling in the opposite direction (at least in the reference frame where the new boson is not moving). There are then two distinct options for how the spins of the photons can be arranged.\n\n154. See 8.4 The Definite Article?\n\nOne option is that the photon spins both point in the same direction, so their spins add up, giving a magnitude of two for the total spin of the photon pair along that axis. If the new boson only had a spin of one, there is no way to generate a spin of two from it. So we can rule out that option.\n\nWe are left with the option that the photons point in opposite directions, so their spins cancel, giving a total spin of zero. This in itself is no problem. The new boson could still be spin-1, since because it is massive, the spin can point perpendicular to the axis we chose. In that case it could decay to two photons that have no net spin along the axis. However, Landau and Yang (working independently) noticed another thing. These photons are identical. The only thing that might distinguish them from each other is the orientation of their spin relative to their own direction of travel. But in this configuration, that orientation is the same \u2013 either both photons have spin pointing along their direction of motion, or both have it pointing against. When you have a quantum system and you swap over identical bosons, you get the same system back again, with no relative minus sign.155 You could do this by rotating the whole system by 180 degrees around the origin, about an axis perpendicular to the axis the photons are travelling along. But for a spherical system such as the new boson, with angular momentum one, rotating by 180 degrees this way introduces a minus sign.156\n\n155. This is not as obvious as it sounds, and not true for fermions, as discussed in Glossary: Bosons and Fermions. 156. This is true of all odd-numbered spherical harmonics, which are the equations describing waves on a sphere. Think of a wave oscillating on the surface of a sphere, when the northern hemisphere goes up, the southern hemisphere goes down. If you turn the sphere upside down, the phase of the oscillation changes by 180 degrees, or equivalently the amplitude gets multiplied by -1.\n\nWe have finally got there then, because this -1 in the initial state (the new boson) would be incompatible with the +1 required in the final state for the exchange of identical bosons. So a spin-1 boson cannot decay to two photons in this configuration either. If we see a two-photon decay mode (and we do), the new boson cannot have spin-1.\n\nI told you it was involved. But it is something that is said in physics talks very often and not explained, so I wanted to understand it myself well enough to explain it. If you just skipped that bit, welcome back.\n\nMore information than this can be extracted from the decays we observe. The angles at which the Zs and the photons are produced contain information on the angular momentum of the new boson, and over the months after the discovery we measured these precisely enough to show that the spin was zero. This doesn't entirely rule out the possibility of a small contribution from other spins, say spin-2, but the main thing we are seeing is definitely a scalar boson.\n\nAnother property the Standard Model Higgs boson has to have is that it is 'CP-even'. CP is a combination of two symmetries. The 'C' symmetry (for 'charge') of a system depends on whether it changes when you swap all the additive quantum numbers. This basically means swapping matter for antimatter, so positive charges become negative charges. If the system doesn't change at all then it is said to be even under C symmetry. 'P' is 'parity'. This is easier to grasp: it just means swapping left for right, or inverting the system. This changes the direction of spin, for instance.157\n\n157. Back to the spherical harmonics, all those with even angular momentum (0, 2, 4 . . .) have parity +1, and all those with odd angular momentum (1, 3, 5 . . .) have odd parity, that is, they change sign under inversion.\n\nCP symmetry is almost an exact symmetry of the Standard Model, which is a way of saying that physics almost doesn't care whether we are made of matter or antimatter. And yet the observable universe clearly does care \u2013 it is overwhelmingly made of matter. To get such an asymmetric universe from such a symmetric theory is a challenge, and requires some source of CP-symmetry violation, which many new theories (such as supersymmetry) can provide. All this boils down to the fact that measuring the properties of the new boson under a CP inversion is an important thing to do, since any difference from the Standard Model might give a clue as to why we are made of matter rather than antimatter.\n\nSo CP symmetry depends on what a system looks like when you simultaneously reflect in a mirror and flip all the charges. Since the new boson has spin-0 and no charge, you might think that it is obvious that it does not change under this symmetry, and therefore is CP-even. However, there are examples in nature of scalar bosons with no electric charge that are nevertheless CP-odd. The neutral pion \u2013 \u03c00 is such a particle. It is made of a mixture of up quarks and anti-down quarks, and anti-up quarks and down quarks, combined in such a way that when you swap matter for antimatter (C) nothing changes, but when you reflect in a mirror, the quantum wave function describing the mixture picks up a minus sign. So it is C-even, P-odd, and CP-odd.\n\nThe Standard Model Higgs boson is CP-even. The angular distributions of the decay products are also sensitive to the CP of the new particle, and they also indicate quite strongly that, as expected for the Higgs, it is CP- even. Both this and the spin itself will be determined with more confidence as more measurements are made.\n\nAs I described in the previous chapter, the Higgs boson can decay in several different ways, and measuring the branching ratio \u2013 that is the relative rate \u2013 of each of these tells us something new. The decays to the W and the Z are crucial because of the role the Higgs plays in electroweak symmetry-breaking. In addition to providing mass, and giving rise to the Higgs boson, the scalar field of the BEH mechanism provides the extra longitudinal polarisation states that the W and Z need when they acquire mass. Measuring these more precisely will always be a hot topic, since this is such an important and fundamental part of the Standard Model, and there are plenty of options for subtle modifications of the theory.\n\nThe decay to photons is a weird one, since because the photon has no mass, it doesn't couple directly to the Higgs boson and is produced via a quantum loop.158 Any particle that has mass and electric charge could in principle go round this loop \u2013 mass is enough to couple it to the Higgs, and charge is enough to couple it to the photon. In the Standard Model, the main contributions are from W bosons and top quarks. But who knows, perhaps particles as yet unseen also contribute? Again, precision measurements of this will always be interesting.\n\n158. See 6.4 Higgs Boson in Crumpling Shocks, Bumps and Stupidity.\n\nThen there are the fermions: the quarks and the leptons. As already pointed out, picking these out from the backgrounds is a big challenge, but we need to do it because the way the Higgs couples to fermions and gives them mass is completely different from the case of the W and the Z, and so one does not really imply the other.\n\nWe can deduce something about the coupling to the top quark because according to the Standard Model, many of the Higgs bosons we see are produced by another quantum loop, this time involving gluons from the proton, which are again massless, coupling to a quark (usually a top quark because it is so heavy) that then couples to a Higgs boson, like this:\n\nSo the fact that we see about the same number of Higgs bosons as expected is indirect evidence that the boson couples to the top quark, and thus that the BEH mechanism gives mass to the top quark. However, the top is a bit of an outlier, the heaviest fundamental particle in the Standard Model, and so it is not hard to imagine that something else might be happening with the more 'normal' quarks. Measuring the Higgs decay to b and anti-b quarks is an important test to make, and doing this in the high-energy running will most likely make use of jet substructure in the boosted Higgs events.\n\nLeptons could be different again. The easiest one \u2013 because it is heaviest and thus the most likely to be produced \u2013 is the tau-lepton. In December 2013, after an exhaustive analysis of the data taken in 2011 and 2012, ATLAS and CMS released compelling evidence (not quite 5 sigma, but well above 3) that the Higgs-to-tau-antitau decay was occurring. Thus the first direct evidence that the BEH mechanism gives mass to leptons. Obviously, making this more significant and measuring it more precisely will be a priority.\n\nAll those fermions \u2013 tau, bottom and top \u2013 are in the 'third generation', containing (along with the tau-neutrino) the heaviest particles. It would be very good to see the Higgs coupling to other generations, to check there is nothing weird going on there. The first generation (up, down, electron, electron-neutrino) is beyond reach for the foreseeable future because their masses are so small that the Higgs decays to them very rarely indeed. But in the second generation (charm, strange, muon, muon-neutrino) we have a shot at the muons and the charm quarks.\n\nFor each measurement of a new decay, you can ask whether it really came from the same kind of particle as the other decays. So, repeating the spin and parity measurements for each is important. It is also important to measure the mass. The masses measured in the ZZ and two-photon decays so far are consistent within the experimental uncertainties of a GeV or so, but there is some 'tension', as we particle physicists like to say when we are watching something nervously. The ATLAS measurements are different from each other by about 2 sigma. When the uncertainties shrink and the measurements move around as we get more data, we will be watching very carefully in case it turns out we have two bosons with different masses, one decaying to photons and the other to Z bosons. For the decays to WW and tau-antitau it is difficult, perhaps impossible, to measure the mass with any precision, since invisible neutrinos are produced in tau decays, as well as when W bosons decay to leptons. We should be able to get some measurement of the mass if we can pick out the decay to b quarks, though it will not be as precise as the Zs or photons. If we see it, the two-muon decay channel will have a very precise mass measurement, since muons are precisely measured by both ATLAS and CMS.\n\nIf the Higgs mass had been a few GeV lower or higher, we would have had fewer decay channels to measure. Higher, and the Higgs-to-quarks and Higgs-to-lepton channels would have become practically impossible, since the decay to ZZ and WW would dominate once the Higgs mass is high enough to produce real pairs of these particles.159 A bit lower, and the W and Z decays would have become so rare they would probably be too hard to spot, or at least very much more difficult. As Fabiola said on 4 July: 'If it is the Standard Model Higgs, it's very kind of it to be at that mass.'\n\n159. Twice the W mass is 160 GeV, and twice the Z mass is 182 GeV.\n\nTwo more things I can think of that I would like to know about this boson.\n\nThe decays to the first-generation particles (up, down and electron), all the neutrinos and the strange quark may well be impossible to measure directly. However, it is possible, with the right machine, to measure the total width. This is the real width of the bump in the mass distributions. The width of the bump in mass, or energy, tells us the lifetime of the particle.160 Unfortunately, in the case of the measured distributions, the width we see is dominated by the experimental resolution of the detectors. To measure it properly, we probably need a lepton collider, of which more later.\n\n160. They are inversely proportional to each other. You can think of this as an expression of Heisenberg's uncertainty principle, if you like. The uncertainty in the energy multiplied by the uncertainty in the time is roughly equal to Planck's constant.\n\nFinally, for the whole Standard Model to hang together, the BEH field must not only give mass to the other particles, but also to the Higgs boson itself. The way it does this involves a 'self-coupling' \u2013 Feynman diagrams in which three or four Higgs bosons come together at a point. In fact, pinning this down would allow us to determine the full set of characteristics of the symmetry-breaking field in the BEH mechanism. This is equivalent to a measure of the shape of the bottom of the wine bottle, or if you prefer, the Mexican hat. It is the shape of the background field of the universe. Quite something to know.\n\nOverall, the Higgs boson should have a busy future.\n\n#### 9.3 What Next for Peter Higgs?\n\nWhen asked how he celebrated the announcement of 4 July, for which he was present at CERN in the auditorium, Peter Higgs replied that he had had a glass of London Pride ale on the aeroplane home from Geneva.\n\nHe had more celebrating to come. On 8 October 2013 a substantial fraction of the ATLAS collaboration were clustered around a video screen in Marrakesh waiting for the winners of the Nobel Prize in Physics to be announced.\n\nThe will of Alfred Nobel states his estate should fund annual prizes:\n\nTo those who, during the preceding year, shall have conferred the greatest benefit to mankind. The said interest shall be divided into five equal parts, which shall be apportioned as follows: one part to the person who shall have made the most important discovery or invention within the field of physics . . .\n\n(and then goes on to mention four other less interesting fields).161\n\n161. Joke! Really! They are Chemistry, Physiology or Medicine, Literature and Peace. Economics is funded, and awarded, by other means.\n\nFor some reason the Nobel Physics Prize committee doesn't seem to bother too much about the 'preceding year' bit \u2013 typically the prize is awarded many years after the discovery. It also stretches 'the person' to mean 'up to three persons'. But it will not award it to more than three and it will not, unlike the Peace Prize committee, treat organisations or collaborations as 'persons'. It also does not award posthumous prizes.\n\nThis meant that it seemed very unlikely that anyone who actually discovered the boson experimentally would be in with a shout. It would be impossible to pick out fairly a short enough list of individuals, even if (as some other prestigious prizes have done) the spokespeople of the experiments and the leader of the accelerator were chosen as representatives. The committee was also left with a dilemma in that Hagen, Guralnik and Kibble, the third independent group to publish the mechanism, could not all be squeezed in.\n\nThe other dilemma for the Nobel committee was, presumably, at what point could you be sure that the bump in our data, the new boson, was really anything to do with electroweak symmetry-breaking and the origin of mass, and therefore at what point did it constitute evidence that the mechanism proposed by Brout, Englert, Higgs, Hagen, Guralnik and Kibble was actually present in nature? I wasn't party to their deliberations, but for me the combination of the fact that the data said it was most likely a CP-even scalar boson and that it coupled to the Z and W boson,162 was enough. Probably more than enough. This still didn't mean we could be certain it was 'the Standard Model Higgs Boson'. In a sense we will never be certain of this, since a deviation from the expectations of the Standard Model could show up any time when we measure some property of the particle more precisely than before. In any case, the 'gang of six' did not write down 'the Standard Model Higgs Boson'. The Standard Model did not even exist then, and it would take the work of many theorists and the data from many experiments before it did. The important innovation of the six in the 1960s was to propose a mechanism by which forces based on gauge symmetries could coexist with massive fundamental particles. In the Standard Model, as it eventually emerged, this mechanism was especially relevant to electroweak symmetry-breaking, and therefore the decays to the W and Z bosons were crucial.\n\n162. The ATLAS and CMS data together constituted very significant signals in both the WW and ZZ decay channels by this stage.\n\nThe prize went, of course, to Fran\u00e7ois Englert and Peter Higgs, with the third possible slot left empty, which many saw as a fitting tribute to the sadly departed Robert Brout.163 This raised a cheer in Marrakesh, as did the fact that ATLAS, CMS and the LHC were all acknowledged in the citation.\n\n163. This is of course why I have been using the term 'Brout\u2013Englert\u2013Higgs' (BEH) mechanism throughout.\n\nPrizes, eh? I guess they serve a purpose, and Fran\u00e7ois Englert and Peter Higgs certainly deserved this one. But (and there is a 'but') prizes give a distorted view of how science is done. They encourage the idea that the typical manner of progress in science is the breakthrough of a lone genius. In reality, while lone geniuses and breakthroughs do occur, incremental progress and collaboration are more important in increasing our understanding of nature. Even the theoretical breakthrough behind this prize required a body of incrementally acquired knowledge to which many brilliant people contributed. The discovery of a real Higgs boson, showing that the theoretical ideas are manifested in nature, was thanks to the work of many thousands. There are 3000 or so people on ATLAS, a similar number on CMS, and hundreds who worked on the LHC. While the citation gives handsome credit for all this, part of me still wishes the prizes could have acknowledged it, too. Anyway, perhaps another year. This was a great moment to celebrate, for physics, for particle physics, and for Englert and Higgs.\n\nHiggs, definitely not a man to push himself into the limelight, did a fantastic job, being photographed cheerfully with everyone who asked (including many of those who worked on the experiments), shaking hands with all comers and, for example, being very visible when the Science Museum opened a big exhibit on the LHC a couple of weeks after the prize announcements. His workload there included a long public question-and-answer session with school pupils, and sharing a platform with the Chancellor of the Exchequer George Osborne, who emphasised the importance of basic research and could be seen as a representative of a long line of UK governments who have consistently backed our membership of CERN.\n\nA nice touch was the fact that Fuller's, the brewers of London Pride, produced a specially labelled edition of 'Outstanding Professor Peter Higgs' bottles of the beer. A bottle (empty) is proudly displayed in my office now.\n\nAfter a few weeks of this, including the Stockholm trip to get the prize itself, Peter Higgs said he was looking forward to re-retiring.\n\n#### 9.4 What next for the LHC?\n\nHigh-energy proton\u2013proton collisions in the LHC resumed shortly after the 4 July announcements and continued until 17 December 2012. The additional data reinforced the discovery of the new particle, and allowed us to make some of those more detailed measurements I discussed earlier.\n\nAfter some running with heavy ions and some technical runs early in the new year, the LHC was switched off for a 'long shutdown'. The message on the status screen said: _End of Run 1. No beam for a while. Access required time estimate: ~2 years_.\n\nThere was a big programme of work to complete during these two years. The accelerator would be warmed up from its working temperature of 1.9K (-271 \u00b0C) so that people could get to all the connectors of the type that failed so spectacularly in 2008 and test, replace and protect them properly so that the current could be increased to the design value. This will enable the bending magnets to run at full power, and thus allow the energy of the proton beams to be increased towards the 7 TeV per beam, 14 TeV centre-of-mass collision energy that was originally intended.\n\nThe detectors are also undergoing extensive maintenance; for example, the entire pixel tracking detector of ATLAS was removed, refurbished and reinserted. The performance improvements and, most importantly, the extra energy will allow us to explore still further beyond the electroweak symmetry-breaking scale, and may throw up surprises. More of that shortly. As I write this, the restart with higher-energy beams for physics is expected early in 2015 \u2013 1 April, in fact.\n\nLooking to the more distant future of the LHC, we will not be able to increase the energy further without completely rebuilding the bending magnets. However, we will get an effective increase in energy, as well as an increase in precision, by increasing the rate of the collisions that the accelerator can provide to the detectors. This is because what really matters is the energy of the quark and gluon collisions. From this perspective, the LHC is a quark-and-gluon collider. The maximum quark or gluon energy we can reach is determined by the energy of the protons multiplied by the fractions of the protons' energy carried by the quarks or gluons. So, if in a given 14 TeV proton\u2013proton collision each quark carried a third of the respective proton's energy, the energy of the quark\u2013 quark collisions would be 14 TeV x \u2153 = 4.7 TeV. The chances of finding a quark inside a proton carrying a third of the proton's energy are unfortunately quite small, and as the fraction of energy gets closer and closer to one, the chances drop very quickly. However, it is still true that the more proton\u2013proton collisions you have, the more high-energy quark\u2013quark collisions you will collect, and so the effective energy reach of your measurement is increased.\n\nThis is the main motivation behind the LHC luminosity upgrade, proposed to happen in two stages. Phase I is proposed to take place after a couple of years of high-energy running, so sometime in 2017\u201318 the LHC will shut down again for this. The timescales for Phase II, as well as its scope, are still under discussion. In addition to upgrades to the LHC itself, this will require major upgrades of the detectors so that they can cope with increased data rates. Between them these upgrades would allow the LHC to continue making exciting new physics measurements up to 2030 and beyond.\n\n#### 9.5 What Next for the Standard Model?\n\nOne thing we will definitely do with that upgraded LHC, and hopefully with other machines, too, is examine very closely how well the Standard Model works above the electroweak symmetry-breaking scale. This goes beyond the studies of the Higgs boson properties discussed in section 9.2. Remember, this energy regime is qualitatively different from anything we have looked at before. In this regime, the electromagnetic and weak forces are in some sense unified. Certainly their strengths are now comparable. Without the discovery of the Higgs boson, this would have been a no-go area for the Standard Model. The theory would have been unable to make predictions for these energies, and would have been relegated to a low-energy 'effective theory', stunningly accurate for energies below a couple of hundred GeV, but completely out of its depth above the electroweak symmetry-breaking scale.\n\nWith the discovery of the Higgs, the Standard Model has a new lease of life. It can make predictions for very high-energy physics \u2013 certainly covering everything even an upgraded LHC is able to reach. This is a bold claim, and putting it to the test will be intriguing. One area I find fascinating is the theoretical activity stimulated by the very fact of observing a new boson with a definite mass. A lot of this work is very technical, but one general theme is a re-examination of symmetries and quantum corrections already in the Standard Model to see if they contain more physics than we first thought. There are all kinds of (possibly misleading) clues scattered around and games that can be played. For example, consider a numerical coincidence. The sum of the masses squared of the fermions is very close to the sum of the masses squared of the bosons164 to within a percentage or so, and given that there are significant uncertainties in the top and Higgs masses, the equality could well be exact. To put it another way, if you had found a symmetry that imposed a condition that the sum of the fermion masses must equal the sum of the boson masses, you could have predicted a Higgs mass of about 123 GeV. Not too far off what we have measured!\n\n164. That is, Mtop2 \\+ Mbottom2 = MW2 \\+ Mz2 \\+ MHiggs2 (all the other particle masses are too small to make much difference). Putting the known numbers in gives: 1732 +52 \u2248 80.42 \\+ 91.22 \\+ 1252, i.e. 29954 \u2248 30406.\n\nThe catch is that there is no symmetry we know of that imposes this, so at present it is just a curiosity. There are several numerological games one can play which are at least as plausible. For example, there are three different colors of quark, so should there not be a factor of three in front of those numbers? And there are two W bosons (plus and minus), so why no factor of two? If you did that, you'd get a Higgs mass 'prediction' of 262 GeV. No prizes for that. There are other ways one could make 'predictions' or hunt for coincidences, and the more ways of looking for a coincidence, the less significant a coincidence is if you find it. Look a million different places, and you'll probably find a million-to-one chance turning up. Equally, while a bit of numerology might give a clue, it is only useful if it is a clue to a real dynamical theory. If it doesn't lead anywhere, it is worthless. The way to go is to make measurements and do real calculations, not play number games.\n\nInterestingly, though, there is in fact a similar relation, one that really was derived before the Higgs boson was discovered, and which is based on real Standard-Model calculations. This is to do with the quantum corrections to the Higgs mass that supersymmetry is supposed to help with.165 Martinus Veltman, who later (1999) won the Nobel Prize with Gerardus 't Hooft for 'elucidating the quantum structure of electroweak physics', worked out what these quantum corrections would be,166 just considering the known particles \u2013 so not including supersymmetry. In fact, since this was 1981, neither the top quark nor the Higgs boson had been discovered, so he was well ahead of his time, and even though he assumed both particles existed, he did not know their masses. Going ahead anyway, he worked out that the first set of corrections (those involving only one quantum loop) would all cancel out if a particular relationship between the particle masses167 were to hold. Playing around with possibilities, he suggested from this that if the Higgs boson were to be very light, the top mass would have to be about 69 GeV, which back then it could have been. More realistically, if the Higgs mass were to be about the same as the W mass, the top mass would be about 78 GeV.\n\n165. See 4.7 Putting the Higgs in its Place. 166. Acta Phys.Polon. B12 (1981) 437. 167. 4Mtop2 \u2248 4MW2 \\+ 4Mz2 \\+ 4MHiggs2.\n\nUnfortunately, when in 1995 the Tevatron experiment finally discovered the top, its mass was much higher, and is now known to be about 173 GeV, and thus the 'Veltman condition' would imply a Higgs mass of about 314 GeV . . . far too high. But all these particle masses pick up quantum corrections and so change with energy, and there are papers being written now suggesting that the Veltman condition or close relatives to it may well play a role in determining the high-energy behaviour of the Standard Model and perhaps avoiding the ugly 'fine-tuning' of the Higgs mass that seems otherwise to be required. Different papers have appeared that claim the Higgs mass is controlled and protected by other approximate symmetries of the Standard Model, such as chiral or 'left\u2013right' symmetry. It is an enthralling spectator sport for us experimentalists, and certainly adds motivation to the efforts to make increasingly precise measurements of key Standard-Model processes.\n\nAn important example of these is a set of processes involving the production of pairs of vector bosons \u2013 WW, WZ, ZZ especially. The most interesting process here is vector-boson scattering. I talked about this in section 1.2, because without the Higgs this process can't be predicted in the Standard Model. Then I was being a pessimist, suggesting that if the Higgs boson did not show up, vector-boson scattering might be the only place to get a clue as to the mechanism of electroweak symmetry-breaking. Now we have a Higgs, the process is predicted, and measuring it becomes a very important test of whether the BEH mechanism is really doing the job it is supposed to.\n\nThere are plenty of other rare and not-so-rare processes that we can now calculate and which we will be able to measure in the future. We are at the beginning of physics beyond the electroweak symmetry-breaking scale.\n\n#### 9.6 What Next for Supersymmetry and Beyond the Standard Model?\n\nIf you believe the headlines, supersymmetry is a particularly tenacious zombie theory that is 'killed', or at least 'maimed' or 'hospitalised', by the LHC every month or two, yet never seems to go away.\n\nThere is some truth in this. The LHC data, from the LHCb experiment as well as from ATLAS and CMS (and previous experiments at CERN, too, and HERA and the Tevatron), have ruled out huge swathes of previously possible variants of supersymmetric theories. Yet despite this, as an idea supersymmetry is never likely to go away. The beauty and elegance of the mathematics behind it, coupled with the fact that it is required by string theory, or M-theory, or most likely any other attempt to bring gravity and quantum field theory together, will ensure, I guess, that it remains an important part of the toolbox of theoretical physics, cosmology and mathematics more or less indefinitely.\n\nWhat is at stake is whether supersymmetry has anything to do with electroweak symmetry-breaking, or with dark matter, or indeed whether it has anything to do with any phenomenon ever likely to be measured in a particle-physics experiment. Does it have any role to play in rescuing the idea of 'naturalness'?168\n\n168. See 7.5 Is Nature Natural?\n\nThis is very much connected with the loop corrections and mass relations just discussed in the previous section. Supersymmetric particles also enter those quantum loops, and they guarantee the cancellations the Standard Model on its own seems unable to provide. In doing so, they avoid the fine-tuning problem with the Higgs mass. But fine-tuning is a slippery concept. As well as the LHC and other collider data, precision measurements of the neutron and electron 'electric dipole moments' (essentially a measure of whether the charge distribution of an electron, or a neutron, is spherically symmetric) have constrained the possible parameters of supersymmetry, and to avoid all of these experimental constrains already implies a certain amount of tuning. Most of all, if supersymmetry is to tame the quantum corrections to the Higgs mass, the masses of at least some of the supersymmetric particles should be somewhere close to the electroweak symmetry-breaking scale. If the next run of the LHC does not find anything, this will be become significantly less tenable and many theorists will start to give up on supersymmetry, at least as a solution to the fine-tuning problem. Either way, I doubt 'supersymmetry is just around the corner' will be used as a strong justification for any other large experiment in the future.\n\nSupersymmetry is only (currently) the most popular extension to the Standard Model, however. And cock-a-hoop though the Standard Model may be with its latest success in predicting a fundamental scalar boson and extending its region of applicability well above the electroweak energy scale, the Standard Model is clearly not the full story. There still must be something beyond it, supersymmetry or no.\n\nThe most glaring omission is gravity. We have, thanks to Einstein, a very good theory of gravity, but it is not a quantum theory. Space\u2013time is the stage on which quantum field theory plays its part, but at some high energy the idea of a classical space\u2013time comes into conflict with quantum field theory, and we don't know what happens then.\n\nOther problems and omissions include the small point of the missing 85 per cent or so of matter in the universe \u2013 the dark matter that is only visible by its gravitational effects on galaxies and other astrophysical objects. Is it a new fundamental particle? It certainly doesn't seem to be explainable by any Standard Model particle. Worse, there is dark energy, which makes up 68 per cent of the stuff (matter plus energy) in the universe. From one point of view, 'dark energy' is just a label for the fact that the rate of expansion of the universe is increasing, for reasons that are unclear. While we are at it, why are we made of matter and not antimatter? And why are there three copies, three generations, of the fundamental particles? And why does the weak force see only particles with left-handed spin, ignoring the right-handed ones? And then what about the neutrinos in all of this, and why are they so light when the top is so heavy? There are a lot of seemingly arbitrary features of nature here that, to a certain type of mind (e.g. mine), plead for a more elegant explanation than 'just because'.\n\n#### 9.7 What next for CERN?\n\nCountries are still joining CERN. In 2012 Cyprus became an associate member. In 2013 Ukraine did likewise, and in 2014 Israel became the first new full member since 1999. Several other countries are in various stages of negotiation to join or to deepen their collaboration. The governments and people of Europe currently show no sign of faltering in their belief that a world-leading particle-physics lab is a good thing to have in the middle of the continent.\n\nObviously, CERN has its hands rather full upgrading and running the LHC for the next few years. Nevertheless, activities at the laboratory are diverse, with research on new accelerators and new techniques, on antimatter and on nuclear physics, all going on around the site.\n\nThese activities include a research effort to design a linear collider, one that could beat the LEP2 record for high-energy electron\u2013positron collisions. Linear colliders have the advantage of avoiding the beam-energy loss due to synchrotron radiation,169 since the beams do not have to bend around corners. However, for the same reason, the beam cannot be stored \u2013 the whole beam is lost after one shot and you have to start again. The acceleration then has to be very rapid and the collider has to be very long. The combination of the maximum accelerating gradient you can achieve and the length of the accelerator sets the maximum energy. The only high-energy linear collider built to date was in California, at the Stanford Linear Accelerator Center (SLAC). It contributed to the precision measurements of the Z boson, running concurrently with LEP. Follow-up designs, capable of higher energy, were produced by SLAC and by the Japanese lab, KEK. However, the current favourite is a design that was led by the DESY lab in Hamburg using superconducting accelerating cavities. CERN collaborates in the worldwide effort to construct this machine, and is also conducting research on its own alternative, the Compact Linear Collider \u2013 CLIC. Depending on the energy, the superconducting design is several tens of kilometres long. CLIC could shorten this by using a low-energy, high-intensity beam to accelerate a lower-intensity beam to much higher energies.\n\n169. See 1.1 Why So Big?\n\nAnother strand is an even bigger circular collider. First surveys have been carried out indicating that it would be possible to build a tunnel for an even bigger circular collider. This would probably collide protons, like the LHC, but would be 80\u2013100km long compared to the 27km of the LHC. The tunnel would extend under Lake Geneva and would surround a couple of mountains, and the maximum energy would dwarf the LHC; the exact value would depend (as with the LHC) on how powerful the bending magnets could be made.\n\nA final example for now is a research project into a really novel method of acceleration \u2013 so-called 'plasma wakefield' acceleration. Plasma is a superheated state of matter reminiscent of conditions in the early universe, about 300,000 years after the big bang, in which the temperature is so high that the electrical attraction between electrons and nuclei is insufficient to hold atoms together under the intense rate of high-energy collisions going on. So, electrons and nuclei fly around free, smashing into each other all the time. If a short pulse of a high-intensity beam \u2013 usually a laser \u2013 is fired through such a plasma, the charged particles in the plasma oscillate in its wake, and this can lead to very high-voltage differences, as all the positive charges move one way and the negative charges move in the opposite direction. With skill and timing, such a wakefield can be used to accelerate a second beam more rapidly than any other known technique. This has been shown to be a practical way of getting relatively low-energy beams relatively cheaply. The AWAKE ('Advanced Wakefield') project at CERN is trying to do this using a proton beam instead of a laser. Simulations show that in principle if you could fire a beam from the LHC into a suitable plasma, you could get an electron beam with an energy of hundreds of GeV in a few hundred metres, instead of 35km or so for a superconducting linear collider. There are many snags, though, including the fact that the beam intensity would currently be unusably low. It is a speculative, long-term project, and CERN should certainly be doing some of those.\n\nThose are some examples in which the lab is involved. Beyond the Geneva site, though, the council of CERN is charged with 'the organisation and sponsoring of international cooperation' in what the convention calls nuclear research (as of 1953) but is stated elsewhere in the convention as meaning 'research of a pure scientific and fundamental character relating to high-energy particles'. (It also includes cosmic rays.) To address this, as well as the future of the lab, a strategy process was carried out in 2012\u201313, which fitted in alongside a similar process in the United States and was also strongly influenced by proposals from Japan. The message seems to be that the futures of particle physics and of CERN are inextricably entwined, and you can only really discuss the future of particle physics in a global, rather than a purely European, context. So, on with that, then.\n\n#### 9.8 What Next for Particle Physics?\n\nIt was a dark and stormy night. Also, very cold.\n\nHailstones ricocheted sporadically but fiercely from the ancient stone-framed windows of my large, sparsely furnished room. The walls were also stone, as was the uncarpeted floor. A determined but inadequate space heater gamely plugged away, warming a circular zone about 30cm in radius. I cowered in my big brass bed and struggled to find a WiFi signal. Icy water, the remnant of spent hailstones, ran down the inside of the window frame.\n\nThis was January 2013 in Erice, a science centre based in the monastic buildings of a village atop a mountain at the very southwestern edge of Sicily. I was incarcerated there for a week along with the other CERN member-state delegates and representatives of major laboratories and various other partners and organisations from around the world, including from the US and Japan. Our task, before we were released, was to agree on an update of the European Strategy for Particle Physics. There was a lot to update. Quite apart from the Higgs discovery the previous summer (summer seemed so, so far away), the measurement of the neutrino angle \u03b813 was an achievement with profound implications for the future of the field.\n\nThe amount of time and money needed to construct a large particle-physics project, and to eventually get science from it, is huge. People who are now too young to have started school will eventually be involved in analysing the data, and many of the people making decisions now won't even live to see the results. So it is important to make a good choice, based on a strategy, and to stick by it, otherwise nothing gets built. The decisions involve many parameters and constraints, and they involve discussions between many well-informed, self-interested parties independently trying to obtain the best outcome for themselves and their cherished sub-field of science. Some of these discussions took place around roaring fires over pasta and wine in the few small restaurants that the organisers had persuaded to open off-season for us. I think this helped. A convivial meal round a fire, with the weather battering the exterior, encourages a certain team spirit. And when the hail and fog were absent, Erice was beautiful, with stunning sunsets and views from the cliffs to encourage long-term vision. I am less sure about the guitars in the Marsala Room, though the Marsala itself definitely helped.\n\nThere are the long-term LHC upgrades, which have not yet been approved, or even designed in full. There is a serious Japanese proposal to build a superconducting linear collider, and they were keen to hear what the European attitude to this was \u2013 did we want to work on it? Would we contribute to it? There are the neutrinos, and the need for a new 'long-baseline' neutrino facility to explore how neutrinos oscillate. Now that \u03b813 is known to be quite large, there is a real chance we can observe matter \u2013 antimatter asymmetry in neutrino oscillations, and thus maybe get a better idea of why we did not all annihilate shortly after the big bang. There are other questions about neutrinos \u2013 are they their own antiparticle, for instance?\n\nReturning to higher energies, there are ideas to collide muons. These are heavy versions of electrons, so they have all the advantages of electrons but much less synchrotron radiation (1.6 billion times less, since they are 200 times heavier than electrons). One problem here is they decay in 2.2 microseconds. If you can accelerate them quickly enough, relativistic time dilation helps \u2013 time slows down at high speeds and their decay time is therefore much longer. But it's tricky. A nice side effect is that when muons decay they give off neutrinos, so an intense muon beam could be a good way to get an intense neutrino beam almost for free, as it were.\n\nIn the end, four large priority projects were identified. I spent two days at the end of the meeting in a freezing-cold room sitting behind a triangular label marked _United Kingdom_ while we argued about every single word of a three-page masterpiece.170 In honour of this and out of respect for my colleagues, I will not presume to paraphrase but will reproduce the four big priorities verbatim here:\n\n170. The full text can be found in the last four pages of this document: <http:\/\/cds.cern.ch\/record\/1551933>, which was signed off formally in Brussels in May 2013. This was in itself a fascinating event, though it's a little vague in my memory due to stopping for 'a couple of pints' of Belgian beer on the way back to the hotel with my fellow delegate.\n\n(c) The discovery of the Higgs boson is the start of a major programme of work to measure this particle's properties with the highest possible precision for testing the validity of the Standard Model and to search for further new physics at the energy frontier. The LHC is in a unique position to pursue this programme. _Europe's top priority should be the exploitation of the full potential of the LHC, including the high-luminosity upgrade of the machine and detectors with a view to collecting ten times more data than in the initial design, by around 2030. This upgrade programme will also provide further exciting opportunities for the study of flavour physics and the quark\u2013gluon plasma_.\n\n(d) To stay at the forefront of particle physics, Europe needs to be in a position to propose an ambitious post-LHC accelerator project at CERN by the time of the next Strategy update, when physics results from the LHC running at 14 TeV will be available. _CERN should undertake design studies for accelerator projects in a global context, with emphasis on proton\u2013proton and electron\u2013positron high-energy frontier machines. These design studies should be coupled to a vigorous accelerator R & D programme, including high-field magnets and high-gradient accelerating structures, in collaboration with national institutes, laboratories and universities worldwide_.\n\n(e) There is a strong scientific case for an electron\u2013positron collider, complementary to the LHC, that can study the properties of the Higgs boson and other particles with unprecedented precision and whose energy can be upgraded. The Technical Design Report of the International Linear Collider (ILC) has been completed, with large European participation. The initiative from the Japanese particle physics community to host the ILC in Japan is most welcome, and European groups are eager to participate. _Europe looks forward to a proposal from Japan to discuss a possible participation_.\n\n(f) Rapid progress in neutrino oscillation physics, with significant European involvement, has established a strong scientific case for a long-baseline neutrino programme exploring CP violation and the mass hierarchy in the neutrino sector. _CERN should develop a neutrino programme to pave the way for a substantial European role in future long-baseline experiments. Europe should explore the possibility of major participation in leading long-baseline neutrino projects in the US and Japan_.\n\nSo there you have it. And there were another dozen or so paragraphs on smaller-scale activities, organisational issues and the notorious 'impact'. Obviously particle physics has a lot on its plate.\n\n#### 9.9 What next for Science?\n\nThere was surprisingly little backlash in the UK media after the Higgs discovery. I had expected a certain amount, along the lines of 'What a waste of money on something useless that we don't understand.' However, it seems that in Britain at least a pretty large fraction of the public appreciate the significance of the project and to have enjoyed the excitement of the whole thing. It wasn't just a nine-day wonder.171 Many people had stayed with us from the construction through the initial technical failure, the rumours and hints, the excitement of July 2012 and the eventual Nobel Prize. The fact that the UK winner was the modest and generous Peter Higgs, a Geordie living and working in Scotland, was the icing on the cake. And all that for a couple of quid per person per year. Politically, the economic case for basic research seemed to have made a lot of headway, too. The devil is always in the detailed actions, but the language of many politicians in all the parties about research funding is at least positive at the moment, and I hope and believe the high profile of the LHC has contributed to this. The case has to be remade and reexamined continuously, of course.\n\n171. OK, it did blow up nine days after the first switch-on, but that wasn't the end of the matter . . .\n\nOne interesting line of criticism that did show up, though, was that physics had become too divorced from experiment, that experiment was too driven by theory, and that the search for a theory of everything was an obsession that was sustaining a generation of theoreticians who were predicting nothing that could ever be tested against data. This is not a new line of criticism, even within theoretical physics. Lee Smolin of the Perimeter Institute, Ontario, and Peter Woit, of the mathematics department of Columbia University, both published books in 2006 critiquing string theory from this point of view, and Jim Baggott published _Farewell to Reality_ hot on the heels of the Higgs discovery, arguing along some similar lines.\n\nThere is a reasonable point here, that particle theory probably became too focused on a single track \u2013 in this case string theory and its descendants. Such things have happened before. As the _Guardian_ 's Ian Sample describes in his book _Massive_ , S-matrix theory was all the rage when Brout, Englert, Higgs and the rest were coming up with their ideas, and quantum field theory was something of an unfashionable backwater. They were outside the mainstream, but gradually data drove the mainstream their way. There should always be some people branching out, but it is important they don't all take the same branch \u2013 unless the data drive them there. Personally (and it is just a personal preference), I am more interested in the branches that try to solve real observational problems, of which there are many, rather than those that strive for a theory of everything. I wouldn't ban any of them, but I'm a lot more interested in trying to understand this universe than speculating about multiverses.\n\nThe LHC is also an illustration of why theorists go wandering sometimes, and why they need to be able to. The Higgs boson was postulated nearly fifty years ago, and the LHC took more than ten years to build \u2013 more like twenty if you include the R & D needed before construction could even start. That's a long time to wait. If some people go and do some wild mathematical speculation in the meantime, that doesn't do any harm and may well do a lot of good.\n\nRaising these issues on the back of the Higgs discovery did seem a bit odd. While the existence of the boson had been assumed by some theorists for years, the experimental fact of its existence has fundamentally changed the field, and results from the LHC will continue to do so. The discussion of possible new experiments requires theoretical as well as technical and political insight. Far from losing touch, the political and technical challenges of such machines force us into daily contact with reality, and the data give us access to more of it.\n\n#### 9.10 What Next for Me?\n\nAfter two years of weekly commuting back and forth between London and Geneva, more or less living on adrenalin and airline food and running a physics group at CERN while teaching at UCL and living in London, I decided that my next managerial role would be in the same city as my family.\n\nSo I agreed to become head of the Department of Physics and Astronomy at UCL. This has so far been rather rewarding and means that (counter to the trend for specialisation that pervades much of academia) I have had to broaden my physics knowledge in order to have some clue what the condensed-matter, astro- and atomic physicists in the department are up to.\n\nMy research, however, remains centred on the LHC. As I write, In\u00eas, my PhD student, is finishing up the ATLAS Higgs-to-bottom-quark results from the 2012 data, and we have several projects going in preparation for the 2015 restart and the upgrades beyond that. I'll be back.\n\nIn the meantime, I also thought it would be worth writing a book about this remarkable period in physics. I hope you enjoyed reading it.\n\n## Acknowledgments\n\nI have some people to thank.\n\nFirstly my family, all of them. Thanks for putting up with my frequent absences (mental and physical), and for generally cheering me on or up, as appropriate.\n\nThanks also to many wonderful friends and colleagues all over the world, several of whom did much more than me to bring about these events: some of you are mentioned in the book, some not. Apologies to those who deserved a mention but didn't get in, and equal apologies to those who are mentioned and might have preferred not to be.\n\nI'd also like to thank UCL and CERN, for the freedom to do this and write about it.\n\nI want to thank Wordpress, Twitter and most especially the _Guardian_ , for giving me somewhere to write and an audience to write for.\n\nI owe an enormous debt to that audience, and to many people I have met online, who have encouraged, challenged, educated and amused me, especially through many dull waits in airline lounges. Thank you all.\n\nI'm grateful to many people, including Matthew Wing, Peter Jenni, Albert De Roeck, Bryan Webber, Nikos Konstantinidis, Herbi Dreiner and Nicholas Cizek, for pointing out slips and errors in the first edition. Any remaining problems are still my own fault though.\n\nThanks to Diane and my publishers, especially Simon (who didn't really suggest a daft title for the book).\n\nAnd finally, thanks to everyone who pays the taxes, and sustains the society, that allows us to explore the edges of knowledge. It feels quite weird writing something with an author list of less than a few hundred. This book is entirely my fault, but the story of the LHC could have an author list of billions.\n\n## Index\n\nAl-Khalili, Jim ,\n\nALPHA experiment\n\nAltarelli, Guido\n\namplitude\n\n_Angels and Demons_ (Dan Brown)\n\nAntarctic Impulsive Transient Antenna (ANITA)\n\nantielectrons (positrons)\n\nantihydrogen\n\nantimatter ,\n\nantimatter spectroscopy\n\nantiprotons\n\nantiquarks\n\nargon, liquid\n\nart\n\narXiv\n\nAsimov, Isaac ,\n\nAsquith, Lily\n\nasymptotic freedom\n\nATLAS , ,\n\ncalorimeter\n\nCopenhagen meeting\n\njet algorithm\n\njet substructure measurements\n\nmeasuring data\n\nmeetings\n\nmuon detection\n\nname ,\n\nreporting results , , ,\n\nreview process\n\nrumours of Higgs discovery\n\nStandard Model group\n\natoms ,\n\nauthor lists\n\nAutiero, Dario\n\nAWAKE (Advanced Wakefield) project\n\nb-quark decay of Higgs boson\n\nBacon, Francis\n\nBaggott, Jim\n\nBahcall, John\n\nBardeen-Cooper-Schrieffer (BCS) theory\n\nbarns\n\nbaryons\n\nBCS (Bardeen-Cooper-Schrieffer) theory\n\nBEH (Brout-Englert-Higgs) field , ,\n\nBell, Alice\n\nBernius, Catrin\n\nbig bang\n\nBohr, Niels , ,\n\nBoost meetings , ,\n\nBose, Satyendra Nath\n\nbosons\n\n_see also_ Higgs boson; W bosons; Z bosons\n\nbottom quarks\n\nBoyle, Alison\n\nbranching ratios\n\nBritish Chiropractic Association (BCA)\n\nBritton, Dave\n\nBrout, Robert\n\nBrout-Englert-Higgs (BEH) field , ,\n\nbumps , , ,\n\nas evidence for Higgs boson ,\n\nsignificance\n\nTevatron\n\nZ boson\n\nbunches of protons\n\nButterworth, Ian\n\ncalorimeters ,\n\ncarbon-11\n\nCDF experiment ,\n\nCERN ,\n\ndoubt over UK participation\n\nfuture activities ,\n\nreporting results\n\nCERN Council\n\nChadwick, James\n\nChannel 4 News\n\ncharge inversion\n\nCharlton, David\n\ncharm quarks\n\nCheltenham Science Festival\n\nchemical elements\n\nChown, Marcus\n\ncitations ,\n\nCit\u00e9 Meyrin\n\nClarke, Nick\n\nClarke, Tom\n\nCLIC (Compact Linear Collider)\n\nCMS (Compact Muon Solenoid) , ,\n\ncalorimeter\n\nreporting results , ,\n\n_Colliding Particles_ (films) , , ,\n\nCollins, John\n\ncollision events ,\n\nanalysing\n\ndetecting\n\nreconstructing\n\nin upper atmosphere\n\ncolor\n\nComic Sans font ,\n\nCompact Linear Collider (CLIC)\n\ncomputing grid\n\ncomputing model of tracking detector\n\nconfidence levels\n\nconfirmation bias\n\nconservation of momentum\n\nconstructive interference\n\ncontinuous symmetry\n\n_Copenhagen_ (Michael Frayn)\n\nCopenhagen interpretation\n\nCopenhagen meeting\n\ncopies (generations) of particles\n\ncosmic microwave background ,\n\ncosmic rays ,\n\ncoupling\n\nCox, Brian , , , , ,\n\nCP symmetry\n\ncross sections ,\n\ncuriosity-led research\n\nD0 Tevatron experiment , ,\n\ndark energy\n\ndark matter ,\n\nDartnell, Lewis\n\nDavis, Ray\n\nDavison, Adam , , , ,\n\nDaya Bay Reactor Neutrino Experiment\n\ndecay modes of Higgs boson , , ,\n\nDelta particles\n\nDenham, John ,\n\ndestructive interference\n\nDiamond Light Source, Harwell ,\n\ndiffractive collisions\n\nDirac, Paul , ,\n\nDirac equation\n\ndoomsday scenarios\n\nDrayson, Lord ,\n\nDreiner, Herbi\n\ndu Sautoy, Marcus\n\nearly universe\n\nEarth destruction scenarios\n\neconomic contribution of physics\n\nEdinburgh\n\nEinstein, Albert\n\nelectromagnetism (quantum electrodynamics) , , ,\n\nelectrons , , ,\n\ncollision\n\nkinetic energy\n\ntwo-slit experiment\n\nelectronvolts (eV)\n\nelectroweak symmetry-breaking scale , ,\n\nEllis, John\n\nenergy\n\nenergy conservation\n\n'Engineering the Large Hadron Collider' discussion\n\nEnglert, Fran\u00e7ois , ,\n\nErice\n\nEuropean Physics society (EPS) meeting\n\nEuropean Strategy for Particle Physics\n\neV (electronvolt)\n\nEvans, Lyn , ,\n\nexperiment verification ,\n\nexplosion at LHC\n\nfalse reports of Higgs discovery ,\n\nFaraday, Michael\n\n_Farewell to Reality_ (Jim Baggott)\n\nFarmelo, Graham\n\nfemtobarns\n\nFermilab, Tevatron particle collider , , ,\n\nfermions\n\n_see also_ electrons; neutrinos; quarks\n\nFeynman, Richard , , ,\n\nFeynman diagrams , ,\n\nHiggs boson decay , ,\n\n_Feynman Lectures_\n\nfields\n\nFischmarkt, Hamburg\n\nflavour\n\nForshaw, Jeff , ,\n\nFranklin, Rosalind\n\nFrayn, Michael\n\nfrequency\n\nFriedman, Jerome\n\nFuller's brewery\n\nfundamental particles\n\nfunding research ,\n\nprotest about cuts\n\nGaillard, Mary\n\nGaitskell, Rick\n\ngauge bosons ,\n\nand mass\n\ngauge theories\n\nGEANT\n\nGell-Mann, Murray ,\n\ngenerations of particles\n\nGianotti, Fabiola , , ,\n\nGillies, James\n\n'Giving New Physics a Boost' _see_ Boost meetings\n\nglobal symmetry\n\nGluckman, Max\n\ngluons , ,\n\n'God particle' ,\n\nGoldacre, Ben\n\nGoldstone theorem\n\ngravity\n\nGreenish, Phillip\n\nGross, David J.\n\nGross, Eilam\n\n_Guardian_ newspaper , , ,\n\nGuerilla Science\n\nGuru-Murthy, Krishnan ,\n\nhadronic jets\n\nhalf-life\n\nHamburg\n\nharps\n\nHarris, Evan\n\nHawking, Stephen\n\nheavy ion collisions\n\nHeisenberg, Werner\n\nhelium\n\nHERA (Hadron Electron Ring Anlage) ,\n\n_see also_ ZEUS\n\nHeuer, Rolf , , ,\n\nHewitt, JoAnne ,\n\nhidden symmetry\n\nHiggs, Peter , , , , , ,\n\nHiggs boson , , ,\n\ndecay modes , , ,\n\ndiscovery announcement\n\nevidence for ,\n\nfuture research\n\nimpact of discovery\n\nmass , ,\n\nmedia coverage of discovery\n\nname\n\nrumours of discovery ,\n\nsignificance of\n\nHomestake experiment\n\nHooft, Gerardus 't , ,\n\n_Horizon_ (BBC)\n\nHoward, Ronald\n\nHumphrys, John ,\n\nhydrogen\n\nIceCube array\n\nICHEP (International Conference on High Energy Physics) , ,\n\nILC (International Linear Collider)\n\nIMB (Irvine-Michigan-Brookhaven) experiment\n\nIncandela, Joe\n\nInce, Robin , , ,\n\n_Infinite Monkey Cage, The_ (BBC)\n\ninfinities\n\ninfrared-safe jet algorithm\n\nInstitute of Physics ,\n\ninterference\n\ninternal symmetries\n\nInternational Conference on High Energy Physics (ICHEP) , ,\n\nInternational Linear Collider (ILC)\n\ninvariant mass\n\nIrvine-Michigan-Brookhaven (IMB) experiment\n\nISIS\n\nisotopes\n\nJ.J.Sakurai Prize\n\nJ-PARC facility\n\nJaffe, Andrew\n\nJanssen, Pierre Jules C\u00e9sar\n\nJenni, Peter\n\njets ,\n\nalgorithms ,\n\ncross sections ,\n\nmeasurements\n\nJha, Alok\n\nJimmy Generator\n\nJones, Tegid\n\njournal review process\n\nkaons\n\nKendall, Henry\n\nKilminster, Ben\n\nkinetic energy\n\nKing, David ,\n\nKingsley, Patrick\n\nKonstantinidis, Nikos\n\nKortner, Sandra\n\nLagrangian equations\n\nLandau-Yang theorem\n\nLarge Electron-Positron Collider (LEP) ,\n\nLarge Hadron Collider ,\n\nbreakdown\n\nbreaking luminosity record\n\ncollisions at 7 TeV\n\ncomputing grid\n\nearly collisions\n\nfuture plans\n\nheavy ion collisions\n\ninauguration\n\nincreasing energy ,\n\nname\n\nproton energy\n\npublic interest\n\nswitch-on\n\nLatitude Festival\n\nlead ions collisions\n\nlead tungstate crystals\n\nLederman, Leon\n\nLEP (Large Electron-Positron Collider) ,\n\nLepton Photon conferences\n\nleptons ,\n\nleptoquarks\n\nLHC _see_ Large Hadron Collider LHCb experiment\n\nlibel reform campaign\n\nliquid argon\n\nLlewellyn Smith, Chris\n\nLockyer, Norman\n\nlow-energy collisions\n\nluminosity\n\nLHC ,\n\nM-theory\n\nmagnets ,\n\nconnector fault\n\nMain Injector Neutrino Oscillation Search (MINOS)\n\nmaintenance programme, LHC\n\nmarble in wine bottle analogy ,\n\nMarshall, Zach\n\nmass of particles\n\nHiggs boson , ,\n\n_Massive_ (Ian Sample) ,\n\nmatrices\n\nMaxwell, James Clarke\n\nmedia engagement\n\nat LHC switch-on\n\nat 7 TeV collision\n\nmeetings\n\nMeyrin\n\nmicromorts\n\nminimum bias collisions\n\nMINOS (Main Injector Neutrino Oscillation Search)\n\nMlodinow, Leonard\n\nmolecules\n\nmomentum ,\n\nMonitored Drift Tubes\n\nMonte Carlo event generators\n\nMumbai Lepton Photon conference\n\nmuons ,\n\nNambu, Yoichiro\n\nnaming\n\nof Higgs boson\n\nof projects ,\n\nNanopoulos, Dimitri\n\nnaturalness\n\nneutral kaons\n\nneutrinos , , ,\n\nfaster than speed of light\n\nfuture research\n\nneutrons , ,\n\nneutron beam applications\n\n_Newsnight_ (BBC)\n\nNewton's first law\n\nNichol, Ryan ,\n\nno-lose theorem\n\nNobel Prize for Physics\n\n1965 ,\n\n1984 ,\n\n1990\n\n1999 , ,\n\n2004\n\n2011\n\n2013\n\nNoether, Emmy\n\nNoether's theorem ,\n\nnon-Abelian theories\n\nnon-diffractive events\n\nnucleus\n\nNutt, David\n\nOPERA\n\noscillation, neutrinos\n\nOzcan, Erkcan\n\nparticle physics\n\nfuture developments\n\nimpacts of research\n\ntheories\n\nparticle spin _see_ spin\n\nparticle-tracking detectors\n\nparticles\n\nmovement\n\nPaterson, Mike , , ,\n\nPearson, Ian\n\nPenn State University\n\npentaquarks\n\nPenzias, Arno\n\nPerlmutter, Saul\n\nperturbation theory\n\nPET (positron emission tomography)\n\n'A Phenomenological Profile of the Higgs Boson'\n\nphoton decay of Higgs boson , ,\n\nphotons , ,\n\nenergy\n\nphysics\n\neconomic importance of\n\nfuture of\n\n'Physics in Perspective' lecture\n\npile-up\n\nplasma wakefield acceleration\n\npolarisation\n\nPolitzer, David\n\nPontzen, Andrew\n\npositron emission tomography (PET)\n\nprecision-lens manufacturing\n\nprobabilities\n\nproject names ,\n\n'prospecting' publications\n\nproton bunches\n\nprotons , ,\n\nspeed in LHC\n\npublic interest in LHC\n\npublications\n\nauthor lists\n\ncitations ,\n\nQCD (quantum chromodynamics) ,\n\nQED (quantum electrodynamics) ,\n\nquantum field theory ,\n\nquantum numbers\n\nquark-gluon plasma ,\n\nquarks , , , , ,\n\ndistribution, ,\n\nand Higgs decay\n\nquench\n\nRaven, Gerhard\n\nreal particles\n\nreconstruction\n\nReeperbahn, Hamburg\n\nREF (Research Excellence Framework) ,\n\nRelativistic Heavy Ion Collider (RHIC)\n\nreligion and Higgs boson discovery\n\nRENO experiment\n\nrenormalisability\n\nresearch\n\naccess to results\n\nvalue of ,\n\nResearch Excellence Framework ,\n\nreviewing results ,\n\nRHIC (Relativistic Heavy Ion Collider)\n\nRiess, Adam\n\nrisk\n\nRohn, Jenny\n\nRubbia, Carlo ,\n\nRubin, Mathieu , ,\n\nSainsbury, Lord\n\nSakurai Prize\n\nSalam, Abdus\n\nSalam, Gavin , , , ,\n\nSample, Ian ,\n\nSarkozy, Nicolas\n\nSaunders, Frances\n\nscalar fields\n\nscaling\n\nSchmidt, Brian\n\nSchwinger, Julian\n\nscience\n\nfunding , ,\n\nfuture of\n\nScience Blogging Talkfest\n\nScience and Technology Facilities Council (STFC)\n\nScience is Vital campaign , ,\n\nSEARCH (Supersymmetry, Exotics and Reaction to Confronting the Higgs)\n\nSecret Garden Party\n\nsemiconductor detectors\n\nsemiconductors ,\n\nSeymour, Mike ,\n\nSharma, Alok\n\nsigmas\n\nsilicon technology in tracking detectors\n\nSingh, Simon\n\nSj\u00f6strand, Torbj\u00f6rn\n\nSkeptics in the Pub\n\nSLAC National Accelerator Laboratory ,\n\nSmith, Beck\n\nSmolin, Lee\n\nSnow, Jon\n\nsocial media\n\nsolar neutrino problem\n\nspecial relativity\n\nspectroscopy\n\nspeed\n\nprotons in LHC\n\nwaves\n\nSpiegelhalter, David\n\nspin , ,\n\nSPS (Super Proton Synchrotron)\n\nStandard Model ,\n\nand Higgs boson , , ,\n\nat LHC energies\n\nand neutrino mass\n\nand supersymmetry\n\nStandard Model group, ATLAS\n\nstanding waves\n\nStanford Linear Accelerator Center (SLAC) ,\n\nstatistical uncertainties ,\n\n'Status of Standard Model Higgs Searches in ATLAS'\n\nSTFC (Science and Technology Facilities Council)\n\nstrange quarks\n\nstrength of fundamental forces\n\nstring theory\n\nstringed instruments\n\nstrong force (quantum chromodynamics) , , , , ,\n\nSudbury Neutrino Observatory\n\nSuper-Kamiokande experiment ,\n\nSuper Proton Synchrotron (SPS)\n\nsuperconductivity\n\nsupersymmetry , , ,\n\nSupersymmetry, Exotics and Reaction to Confronting the Higgs (SEARCH)\n\n'surveying' publications\n\nSUSY (supersymmetry) , , ,\n\nsymmetry ,\n\ngauge symmetry\n\nglobal symmetry\n\nhidden symmetry\n\n_see also_ supersymmetry\n\nsynchrotron radiation\n\nsystematic uncertainties ,\n\n't Hooft, Gerardus , ,\n\nT2K long-baseline neutrino experiment ,\n\ntau-lepton decay\n\nTaylor, Richard\n\ntemperature field\n\nTeV (teraelectronvolt)\n\nTevatron particle collider , , , , ,\n\ntheoretical particle physics\n\ntheory development\n\ntheory-led research, defence of\n\nThomas, Jenny\n\nthought experiments\n\n_Today_ programme (BBC) , ,\n\nTomonaga, Sin-Itiro\n\nTonelli, Guido\n\ntooth fairy\n\ntop quarks ,\n\ntracking detectors\n\nLHC\n\nZEUS\n\ntravel\n\nTwitter\n\ntwo-photon decay of Higgs boson ,\n\ntwo-slit experiment\n\ntwo-Z boson decay, Higgs boson\n\n_Uncaged Monkeys_ show\n\nUS immigration\n\nvan der Meer, Simon ,\n\nvector-boson scattering ,\n\nvector fields\n\nvelocity\n\nVeltman, Martinus , , ,\n\nverification of results ,\n\nVerlinde, Erik\n\nVillaplana, Miguel\n\nVirdee, Jim ,\n\nW bosons , , ,\n\nHiggs boson decay\n\nWalker, David\n\nWatson, Caitlin\n\nwave function collapse\n\nwave-particle duality ,\n\nwavelength\n\nwaves\n\ntwo-slit experiment\n\nweak force ,\n\nWebber, Bryan\n\nWhitmore, Jim\n\nWhyntie, Tom\n\nWilczek, Frank\n\nWilliamson, Sonny\n\nWilmshurst, Dr Peter\n\nWilson, Robert\n\nwine bottle and marble analogy ,\n\nWoit, Peter\n\nWomersley, John ,\n\nwork\n\n_World at One_ (BBC)\n\nworld destruction risks\n\n_World Have Your Say_ (BBC World Service)\n\nWW scattering\n\nZ bosons ,\n\nHiggs boson decay ,\n\nZEUS , , ,\n\nZimmerman, Eric \n\n## About the Author\n\n**JON BUTTERWORTH** is one of the leading physicists at the Large Hadron Collider and is Head of Physics and Astronomy at University College London. He writes the popular Life & Physics blog for the _Guardian_ and has written articles for a range of publications including the _Guardian_ and _New Scientist_. He was awarded the Chadwick Medal of the Institute of Physics in 2013 for his pioneering work in high energy particle physics, especially in the understanding of hadronic jets. For the last 13 years, he has divided his time between London and Geneva, Switzerland.\n  1. Cover \n  2. Praise \n  3. Title Page \n  4. Copyright \n  5. Dedication \n  6. Contents \n  7. Epigraph \n  8. Foreword \n  9. Introduction \n  10. 1. Before the Data \n  11. 2. Restart \n  12. 3. High Energy \n  13. 4. Standard Model \n  14. 5. Rumours and Limits \n  15. 6. First Higgs Hints and Some Crazy Neutrinos \n  16. 7. Closing In \n  17. 8. Discovery \n  18. 9. What Next? \n  19. Acknowledgments \n  20. Index \n  21. About the Author\n\n","meta":{"redpajama_set_name":"RedPajamaBook"}}
+{"text":" \nCopyright\n\n**Available in the same series:**\n\n_Monday Night is Chicken Night_\n\n_Tuesday Night is Pasta Night_\n\n_Wednesday Night is Vegetarian_\n\n_Thursday Night is Hearty Meat_\n\nCopyright \u00a9 2010 Filipacchi Publishing, a division of Hachette Filipacchi Media U.S., Inc.\n\nFirst published in 2010 in the United States of America by Filipacchi Publishing\n\n1633 Broadway\n\nNew York, NY 10019\n\n_Woman's Day_ is a registered trademark of Hachette Filipacchi Media U.S., Inc.\n\nAll rights reserved. No part of this book may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without permission in writing from the publisher.\n\nFirst eBook Edition: April 2010\n\nISBN: 978-1-933231-89-1\nContents\n\nCopyright\n\nFISH\n\nMoroccan Fish\n\nTuscan Bass with Squash & Beans\n\nCrunchy Fish Sticks & Smashed Potatoes\n\nEnglish Oven-Fried Fish 'n' Chips\n\nBaja Fish Tacos\n\nWasabi Baked Halibut\n\nWalnut-Crusted Halibut with Orange Salsa\n\nThai Fish Cakes\n\nDilled Lemon Salmon with Couscous\n\nSalmon-Potato Skillet\n\nSalmon with Lentils\n\nMustard-Glazed Salmon Steaks\n\nGlazed Salmon on Greens & Orange Salad\n\nMustard Salmon\n\nRoasted Salmon & Grape Tomatoes\n\nTuscan Salmon Hero\n\nGinger-Soy Salmon & Bok Choy\n\nCorn & Tomato Chowder with Salmon\n\nMediterranean Fish Stew\n\nTilapia Veracruz\n\nCrispy Tilapia with Avocado Pico de Gallo\n\nCod Veracruz-Style\n\nBow-Tie Salad with Tuna\n\nPasta Puttanesca & Tuna\n\nTuna Stuffed Shells\n\nMediterranean Tuna\n\nTuna Ni\u00e7oise\n\nPan Bagna\n\nGreek Lemon & Oregano Mahi-Mahi\n\nAsian Black Cod\n\nQuick French Fish & Potato Stew\n\nNew England Seafood Chowder\n\nSushi Salad\n\nSHELLFISH\n\nShrimp & Linguine Alfredo\n\nShrimp Arrabbiata with Linguine\n\nGarlic Shrimp with Angel Hair\n\nShrimp Marinara\n\nIsland Shrimp & Fruit Salad\n\nNew Orleans Shrimp 'n' Grits\n\nSmoky Marinated Shrimp\n\nShrimp with Chesapeake Dipping Sauce\n\nShrimp Stir-Fry\n\nCrispy Asian-Spiced Shrimp\n\nSweet & Sour Shrimp\n\nThai Shrimp & Rice\n\nMojo Seafood Skewers\n\nCrispy Scallops with Chipotle-Tartar Sauce\n\nScallops with Lemon & Capers\n\nCioppino\n\nHearty Clam Chowder\n\nMussels Fra Diavolo\n\nLemon & Mint Seafood Skewers with Tabbouleh\n\nPhoto Credits\nFISH\n\n# Moroccan Fish\n\n**FILLETS \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 8 MINUTES \u2022 TOTAL: 20 MINUTES**\n\n1 lb frozen fish fillets or steaks\n\n4 tsp olive oil\n\n\u00bc tsp pepper\n\n1 cup chopped onion\n\n2 tsp minced garlic\n\n\u00bd tsp ground cumin\n\n\u00bc tsp cinnamon\n\n1 can (14 to 15 oz) diced tomatoes\n\n\u00bc cup pitted Kalamata or other olives, halved\n\n**1.** Heat broiler. Line a rimmed baking sheet with nonstick foil.\n\n**2.** Place fish on pan and drizzle with 2 tsp of the olive oil. Sprinkle with the pepper. Broil as package directs until fillets are just cooked through.\n\n**3.** Meanwhile, heat remaining 2 tsp oil in a large saucepan. Add onion; cover and cook 5 minutes, stirring occasionally, until tender. Add garlic, cumin and cinnamon, and cook, stirring, 1 minute or until fragrant.\n\n**4.** Stir in tomatoes and olives, and bring to a simmer. Simmer 3 minutes for flavors to blend.\n\n**5.** Spoon about \u00bc cup sauce over each serving of fish.\n\n**PER SERVING : 184 cal, 19 g pro, 10 g car, 3 g fiber, 7 g fat (1 g sat fat), 43 mg chol, 354 mg sod**\n\n# Tuscan Bass with Squash & Beans\n\n**BASS \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 10 MINUTES \u2022 TOTAL: 22 MINUTES**\n\n1 Tbsp olive oil\n\n1 cup sliced onion\n\n12 oz zucchini and\/or yellow squash\n\n2 cloves garlic, sliced\n\n1 can (19 oz) cannellini beans, rinsed and drained\n\n1 can (8 oz) tomato sauce\n\n\u00bd cup water\n\n1\u00bd tsp chopped fresh rosemary\n\n\u00bc tsp pepper\n\nFour 6-oz striped bass, black cod or mahi-mahi fillets (about \u00be in. thick)\n\n**1.** Heat 1\u00bd tsp of the oil in a large nonstick skillet. Add onion; saut\u00e9 3 minutes. Add squash; saut\u00e9 2 minutes. Add garlic; saut\u00e9 1 minute or until fragrant.\n\n**2.** Add beans, tomato sauce, water, rosemary and pepper; stir and bring to a boil. Reduce heat; place fish on top. Cover and simmer 7 to 8 minutes until fish is just cooked through.\n\n**3.** On plates, top bean mixture with fish; drizzle with remaining 1\u00bd tsp olive oil.\n\n**PER SERVING : 340 cal, 37 g pro, 28 g car, 8 g fiber, 8 g fat (1 g sat fat), 136 mg chol, 632 mg sod**\n\n# Crunchy Fish Sticks & Smashed Potatoes\n\n**FLOUNDER \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 35 MINUTES**\n\n1\u00bd lb red potatoes, scrubbed and cut in 1-in. chunks\n\n1 cup (4 oz) shredded Cheddar cheese\n\n\u00bd cup milk\n\n\u00bc cup thinly sliced scallions\n\n\u00bc tsp each salt and pepper\n\n1 large egg\n\n1 lb flounder or sole fillets, cut in 1-in.-wide strips\n\n1\u00bc cups crushed baked potato chips\n\n\u00be tsp each paprika and salt\n\n\u00bd cup tartar sauce\n\n\u00be cup grape or cherry tomatoes, cut up\n\n**1.** Heat oven to 450\u00b0F. Set a wire rack on a foil-lined (for easy cleanup) rimmed baking sheet; coat rack with nonstick spray.\n\n**2.** Cook potatoes in lightly salted boiling water 10 to 15 minutes until tender. Drain; return to pot and mash with a potato masher. Add cheese; stir until melted. Add milk, scallions, salt and pepper; stir to blend. Cover to keep hot.\n\n**3.** While potatoes cook, beat egg in a bowl until foamy. Add fish strips; toss to coat. In another bowl, mix crushed chips, paprika and salt. Put a few fish strips at a time into chip mixture. Using a fork, toss strips to coat. Place on prepared rack.\n\n**4.** Bake 10 minutes, or until coating is crisp and fish is cooked through. With a broad spatula, transfer fish to a platter.\n\n**5.** Mix tartar sauce and tomatoes. Serve with the fish.\n\n**PER SERVING : 706 cal, 34 g pro, 62 g car, 6 g fiber, 36 g fat (11 g sat fat), 149 mg chol, 1,421 mg sod**\n\n# English Oven-Fried Fish 'n' Chips\n\n**FLOUNDER \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 45 MINUTES**\n\n**LIME TARTAR SAUCE**\n\n\u00bd cup light mayonnaise\n\n1 tsp grated lime zest\n\n2 Tbsp lime juice\n\n1 Tbsp capers, chopped\n\n**FISH 'N' CHIPS**\n\n2 large russet potatoes, cut in \u00bd-in. spears\n\nNonstick cooking spray\n\n\u00bc tsp each salt and pepper\n\n1 large egg\n\n1 tsp low-sodium Old Bay Seasoning (McCormick)\n\n1\u00bd cups panko bread crumbs\n\n1\u00bc lb flounder, tilapia or catfish fillets, halved lengthwise\n\n**1.** Heat oven to 450\u00baF. You'll need two rimmed baking sheets lined with foil; coat with nonstick spray.\n\n**2. S AUCE:** Stir ingredients in small bowl, cover and refrigerate.\n\n**3. F ISH 'N' CHIPS:** Place potatoes on a baking sheet, coat with nonstick spray, sprinkle with salt and pepper and toss. Bake 30 minutes, turning after 15 minutes.\n\n**4.** Meanwhile, beat egg and Old Bay Seasoning in pie plate or shallow bowl with fork until foamy. Place panko crumbs on a sheet of wax paper.\n\n**5.** Dip fish in egg mixture, roll in crumbs to cover and place on second baking sheet. Coat fish with nonstick spray and bake 12 minutes or until fish is cooked through and browned. Serve with Lime Tartar Sauce and potatoes.\n\n**PER SERVING : 492 cal, 31 g pro, 55 g car, 4 g fiber, 16 g fat (3 g sat fat), 63 mg chol, 625 mg sod**\n\n# Baja Fish Tacos\n\n**HALIBUT \u2022 GRILL \u2022 SERVES 4 \u2022 ACTIVE: 10 MINUTES \u2022 TOTAL: 25 MINUTES**\n\n2 cups shredded cabbage\n\n3 Tbsp lime juice\n\n  cup chopped cilantro\n\n2 tsp olive oil\n\n1 tsp chili powder\n\n1\u00bc lb halibut or mahi-mahi fillets (about \u00be in. thick)\n\n8 corn tortillas, warmed as package directs\n\n1 avocado, diced\n\n\u00bc cup sliced radishes\n\nACCOMPANIMENTS: light sour cream, salsa\n\n**1.** Toss cabbage and 1 Tbsp of lime juice in a bowl. Mix remaining lime juice, 1 Tbsp of cilantro, the oil and chili powder in a pie plate. Add fish, turn; marinate 10 minutes.\n\n**2.** Coat outdoor grill or stovetop grill pan with nonstick spray; heat. Add fish; cook 5 to 7 minutes, turning once, until just cooked through. Remove to plate and break into chunks.\n\n**3.** Fill tortillas with cabbage, fish, avocado, radishes and remaining cilantro. Top with accompaniments as desired.\n\n**PER SERVING : 382 cal, 34 g pro, 31 g car, 6 g fiber, 14 g fat (2 g sat fat), 45 mg chol, 183 mg sod**\n\n# Wasabi Baked Halibut\n\n**HALIBUT \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 20 MINUTES**\n\n1\u00bd lb halibut, hake or cod fillet, cut in 4 equal pieces\n\n  cup wasabi mayonnaise\n\n  cup cornflake crumbs\n\n**1.** Heat oven to 425\u00b0F. Line a rimmed baking sheet with nonstick foil.\n\n**2.** Arrange fillet pieces on foil. Spread top of fish with mayonnaise, then sprinkle with cornflake crumbs.\n\n**3.** Bake 15 minutes or until fish is opaque at centers and crumbs just begin to brown.\n\n**PER SERVING : 290 cal, 36 g pro, 11 g car, 0 g fiber, 10 g fat (2 g sat fat), 68 mg chol, 360 mg sod**\n\n**DIFFERENT TAKES**\n\n\u2022 Top fish with crushed potato chips instead of cornflake crumbs.\n\n\u2022 Add   cup chopped cilantro to the wasabi mayonnaise.\n\n\u2022 Serve with lime wedges.\n\n# Walnut-Crusted Halibut with Orange Salsa\n\n**HALIBUT \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 25 MINUTES**\n\n2 Tbsp flour\n\n  tsp each salt and ground red pepper (cayenne)\n\n1 large egg white\n\n1 cup walnuts, toasted and finely chopped\n\nFour \u00bd- to 1-in.-thick pieces (6 oz each) skinless halibut fillet\n\n**SALSA**\n\n3 red or regular navel oranges, peel and white membrane removed, cut in chunks\n\n3 Tbsp red onion slivers\n\n2 Tbsp chopped fresh mint or cilantro\n\n1 jalape\u00f1o pepper, seeded and minced\n\n1 tsp cider vinegar\n\n**1.** Heat oven to 450\u00b0F. Line a rimmed baking sheet with nonstick foil.\n\n**2.** Mix flour, salt and pepper on a sheet of wax paper. Beat egg white and 2 tsp water in a shallow bowl. Spread walnuts on another sheet of wax paper.\n\n**3.** Coat fish in flour mixture, dip in egg-white mixture, then press into walnuts to coat. Arrange on pan.\n\n**4.** Bake 5 to 10 minutes until fish is barely opaque at center when tested with tip of knife.\n\n**5.** Meanwhile stir Salsa ingredients in a medium bowl to combine. Serve with the fish.\n\n**PER SERVING : 453 cal, 42 g pro, 22 g car, 4 g fiber, 22 g fat (2 g sat fat), 54 mg chol, 185 mg sod**\n\n**NOTE:** Serve with quick, healthy sides such as steamed or saut\u00e9ed bagged mixed greens (like turnip and kale) and couscous. \n\n# Thai Fish Cakes\n\n**FILLETS \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 20 MINUTES \u2022 TOTAL: 25 MINUTES**\n\n**SWEET & SOUR SAUCE**\n\n4 Tbsp lime juice\n\n1 Tbsp each low-sodium soy sauce and sugar\n\n\u00bc tsp red pepper flakes\n\n**FISH CAKES**\n\n\u00bd medium red bell pepper\n\n  cup packed fresh cilantro\n\n1 clove garlic\n\n1 slice (\u00bd in. thick) fresh ginger\n\n2 tsp red curry paste\n\n1 tsp each grated lime zest and sugar\n\n1\u00bd lb skinned salmon, halibut, tilapia or flounder fillets, cut in chunks\n\n1 Tbsp vegetable oil\n\n**1. S AUCE:** Stir all ingredients in a small bowl until well blended.\n\n**2. F ISH CAKES:** Pulse all ingredients except fish and oil in food processor until just blended. Add fish; pulse until fish is just blended.\n\n**3.** Shape level \u00bc-cupfuls fish mixture into twelve 3-in. patties. (At this point, fish cakes may be refrigerated, loosely covered, up to 4 hours.)\n\n**4.** Heat oil in large nonstick skillet over medium-high heat. Cook fish cakes in two batches, 1 minute on each side, or until just cooked through. Drain on paper towels. Drizzle fish cakes with Sweet & Sour Sauce.\n\n**PER SERVING : 304 cal, 35 g pro, 8 g car, 1 g fiber, 14 g fat (2 g sat fat), 93 mg chol, 260 mg sod**\n\n# Dilled Lemon Salmon with Couscous\n\n**SALMON \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 30 MINUTES**\n\n4 salmon fillets (5 oz each), 1-in.-thick\n\n1 Tbsp grated lemon zest\n\n3 Tbsp chopped fresh dill\n\n\u00bc tsp each salt and pepper\n\n1 box herbed couscous mix\n\n1 cup frozen peas\n\n\u00bd cup light mayonnaise\n\n1 scallion\n\n1 Tbsp each lemon juice and water\n\n**1.** Remove broiler pan and rack from oven. Heat to 425\u00baF. Coat broiler rack with nonstick spray. Place salmon fillets, skin side down, on rack.\n\n**2.** Mix lemon zest and 1 Tbsp dill with salt and pepper. Rub over salmon. Bake 10 minutes, or until cooked through.\n\n**3.** Meanwhile, prepare herbed couscous mix as package directs, adding frozen peas. Also, in a food processor, pulse light mayonnaise, remaining 2 Tbsp dill, scallion, lemon juice and water to blend. Serve with the salmon.\n\n**PER SERVING : 503 cal, 40 g pro, 38 g car, 4 g fiber, 21 g fat (3 g sat fat), 100 mg chol, 843 mg sod**\n\n# Salmon-Potato Skillet\n\n**SALMON \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 10 MINUTES \u2022 TOTAL: 25 MINUTES**\n\n1 can (14.5 oz) chicken broth\n\n\u00bd cup water\n\n1 lb red potatoes, thinly sliced\n\n1 red bell pepper\n\n  cup each thinly sliced white and green part of scallions (keep separate)\n\n4 center-cut pieces salmon fillet (5 to 6 oz each)\n\n2 Tbsp creamy mustard spread (such as Dijonnaise)\n\n**1.** Bring broth and water to a boil in a large, deep nonstick skillet with a lid.\n\n**2.** Meanwhile, scrub and thinly slice potatoes. Add to broth; return to a gentle boil and cook 10 minutes.\n\n**3.** While potatoes cook, halve, core and thinly slice red pepper and prepare scallions. Place salmon on potatoes; top with pepper strips and white part of scallion. Bring to a simmer; cover and cook 10 minutes, or until salmon is cooked through and potatoes are tender. Remove skillet from heat.\n\n**4.** Using a slotted spoon, transfer salmon, vegetables and potatoes to dinner plates. Add mustard and green part of scallion to liquid in skillet; stir until blended. Spoon over salmon.\n\n**PER SERVING : 407 cal, 34 g pro, 25 g car, 3 g fiber, 19 g fat (3 g sat fat), 92 mg chol, 584 mg sod**\n\n**PER SERVING : 407 cal, 34 g pro, 25 g car, 3 g fiber, 19 g fat (3 g sat fat), 92 mg chol, 584 mg sod**\n\n# Salmon with Lentils\n\n**SALMON \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 40 MINUTES**\n\n1 cup dried lentils\n\n1 small onion, chopped\n\n1 each carrot and celery rib, chopped\n\n2 Tbsp red wine vinegar\n\n1 Tbsp olive oil\n\n1 Tbsp Dijon mustard\n\n1 garlic clove, minced\n\n1 lb salmon fillet\n\n\u00bc tsp each salt and pepper\n\n**1.** Heat broiler. In a medium saucepan, combine lentils and 3 cups water. Bring to a boil over high heat. Reduce heat to low, cover and simmer 5 minutes. Add onion, carrot and celery; cover and continue cooking until lentils are tender, about 20 to 25 minutes. Drain, reserving cooking liquid.\n\n**2.** In a small bowl, whisk cooking liquid with vinegar, oil, mustard and garlic. Toss lentils with half of dressing.\n\n**3.** Season salmon with salt and pepper. Coat a baking pan with nonstick spray. Place salmon, skin side down, on prepared pan; broil until salmon is cooked through, about 8 to 10 minutes. Divide lentil mixture among 4 plates. Flake salmon on top of lentils and drizzle with remaining dressing.\n\n**PER SERVING : 397 cal, 39 g pro, 33 g car, 12 g fiber, 12 g fat (2 g sat fat), 72 mg chol, 315 mg sod**\n\n# Mustard-Glazed Salmon Steaks\n\n**SALMON \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 3 MINUTES \u2022 TOTAL: 17 MINUTES**\n\n4 salmon steaks (about 7 oz each), 1-in.-thick\n\n\u00bc cup each light brown sugar and Dijon mustard\n\n**1.** Heat oven to 425\u00baF. Line a rimmed baking sheet with nonstick foil. Place salmon steaks on top.\n\n**2.** Whisk brown sugar and mustard in small bowl until blended. Evenly divide on top of each salmon steak, spreading to cover.\n\n**3.** Bake 15 minutes or until cooked through. Broil, 4 in. from top, 2 minutes or until top is golden.\n\nServe with boiled broccoli, mixed nuts and red onion slices.\n\n**PER SERVING : 352 cal, 40 g pro, 15 g car, 0 g fiber, 14 g fat (2 g sat fat), 109 mg chol, 178 mg sod**\n\n# Glazed Salmon on Greens & Orange Salad\n\n**SALMON \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 10 MINUTES \u2022 TOTAL: 30 MINUTES**\n\n4 salmon fillets (5 oz each)\n\n  cup Asian ginger salad dressing\n\n2 Tbsp clementine or orange juice\n\n\u00bd cup thinly sliced red onion\n\n8 cups salad greens (we used arugula, mizuna and fris\u00e9e)\n\n4 clementines, peeled and sliced\n\n  cup chopped unsalted toasted almonds\n\n**1.** Place salmon skin side down on foil-lined rimmed baking sheet. Spoon on or brush salmon with 2 Tbsp of the dressing. Let stand 15 minutes.\n\n**2.** Put remaining dressing and the juice in a large bowl; add onion and toss to coat. Heat broiler.\n\n**3.** Broil salmon 8 to 10 minutes or until just cooked through.\n\n**4.** Add salad greens and clementines to bowl with onion; toss to mix and coat. Arrange salad on serving plates. Lift salmon off foil, leaving the skin behind. Place salmon on salad and sprinkle with almonds.\n\n**PER SERVING : 406 cal, 37 g pro, 18 g car, 4 g fiber, 21 g fat (2 g sat fat), 90 mg chol, 245 mg sod**\n\n# Mustard Salmon\n\n**SALMON \u2022 OVEN \u2022 SERVES 5 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 15 MINUTES**\n\n1 salmon fillet (1\u00bd-lb), cut into 5 equal pieces\n\n\u00bc cup coarse-grain mustard\n\n2 Tbsp pure maple syrup or maple-flavored pancake syrup\n\n**1.** Heat oven to 450\u00baF and line a rimmed baking sheet with foil. Place salmon pieces 1 in. apart, skin side down, on baking sheet.\n\n**2.** Stir mustard and maple syrup in small bowl until blended; spoon evenly on salmon.\n\n**3.** Bake 10 minutes or until salmon is opaque in centers.\n\n**PER SERVING : 194 cal, 27 g pro, 8 g car, 0 g fiber, 5 g fat (1 g sat fat), 64 mg chol, 356 mg sod**\n\n**DIFFERENT TAKES**\n\n\u2022 Evenly pat about \u00bc cup panko crumbs on top of each mustard-coated salmon fillet before baking.\n\n\u2022 Add 1 Tbsp chopped fresh dill to mustard mixture.\n\n\u2022 Omit maple syrup and add \u00bc cup packed brown sugar and 1 Tbsp low-sodium soy sauce to mustard.\n\n# Roasted Salmon & Grape Tomatoes\n\n**SALMON \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 27 MINUTES**\n\n1 pint grape tomatoes\n\n1\u00bd Tbsp chopped fresh thyme\n\n2 tsp olive oil\n\n\u00bc tsp each salt and pepper\n\nFour 6- to 8-oz salmon steaks or fillets\n\n**1.** Heat oven to 425\u00baF. Line a rimmed baking pan with nonstick foil.\n\n**2.** Toss tomatoes, 1 Tbsp of the thyme, the olive oil, and   tsp each salt and pepper on baking pan. Roast 10 minutes.\n\n**3.** Remove from oven. Push tomato mixture to one side of pan. Add salmon to other side. Sprinkle salmon with the remaining   tsp each salt and pepper and the remaining \u00bd Tbsp thyme. Roast 10 minutes or until salmon is just cooked through and tomatoes are tender.\n\n**4.** To serve, spoon tomatoes and juices over salmon.\n\n**PER SERVING : 316 cal, 41 g pro, 3 g car, 1 g fiber, 15 g fat (2 g sat fat), 109 mg chol, 237 mg sod**\n\n# Tuscan Salmon Hero\n\n**CANNED SALMON \u2022 SANDWICH \u2022 SERVES 4 \u2022 ACTIVE: 11 MINUTES \u2022 TOTAL: 11 MINUTES**\n\n  cup bottled Italian dressing\n\n1 Tbsp Dijon mustard\n\n14.75-oz can red or pink salmon\n\n15.5-oz can rinsed cannellini beans\n\n\u00bd cup diced celery\n\n\u00bc cup each chopped red onion and black olives\n\n2 Tbsp chopped parsley\n\n4 hero rolls\n\nGARNISH: baby arugula\n\n**1.** Mix Italian dressing with Dijon mustard.\n\n**2.** Flake salmon in large bowl; toss with cannellini beans, celery, red onion, black olives, parsley and 3 Tbsp dressing mixture.\n\n**3.** Split hero rolls lengthwise in half. Remove some of the bread from the top half; brush insides with remaining dressing. Evenly divide salmon mixture onto rolls; top with some baby arugula and bread tops.\n\n**PER SERVING : 497 cal, 35 g pro, 53 g car, 7 g fiber, 17 g fat (3 g sat fat), 59 mg chol, 1,309 mg sod**\n\n# Ginger-Soy Salmon & Bok Choy\n\n**SALMON \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 10 MINUTES \u2022 TOTAL: 25 MINUTES**\n\n2 tsp canola oil\n\n2 Tbsp minced fresh ginger\n\n2 tsp minced garlic\n\n1\u00bd lb bok choy, halved lengthwise, then sliced crosswise in 1-in. strips\n\n4 oz shiitake mushrooms, stems discarded, caps sliced\n\n1 cup shredded carrots\n\n4 salmon fillets (5 to 6 oz each)\n\n3 Tbsp low-sodium soy sauce\n\n3 Tbsp orange marmalade\n\nGARNISH: toasted sesame seeds\n\nSERVE WITH: 90-second microwavable brown rice\n\n**1.** Heat broiler. Heat oil in a large, deep ovenproof nonstick skillet. Add 1 Tbsp ginger and the garlic; cook over low heat a few seconds until fragrant.\n\n**2.** Add bok choy, mushrooms and carrots. Stir-fry 4 to 6 minutes, until bok choy and carrots are crisp-tender. Remove to a serving bowl; cover to keep warm.\n\n**3.** Place salmon skin side down in skillet. In a small cup, mix remaining 1 Tbsp ginger, the soy sauce and marmalade. Spoon about half of soy sauce mixture over salmon.\n\n**4.** Broil 4 to 6 minutes until salmon is just cooked through. Drizzle with remaining soy sauce mixture and serve with the vegetables. Top with sesame seeds, if desired.\n\n**PER SERVING : 363 cal, 38 g pro, 20 g car, 3 g fiber, 14 g fat (2 g sat fat), 99 mg chol, 879 mg sod**\n\n**NOTE:** If salmon isn't a family favorite, you can use any firm white fish such as grouper, sea bass or mahi-mahi. \n\n# Corn & Tomato Chowder with Salmon\n\n**SALMON \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 15 MINUTES**\n\n1 can (10\u00be oz) condensed cream of potato soup\n\n1 soup can milk\n\n1 can (15\u00bc oz) whole-kernel corn, drained\n\n1 can (14 oz) diced tomatoes with roasted garlic and onion\n\n1 Tbsp oil\n\n4 pieces 1-in.-thick skinless salmon fillet (about 6 oz each)\n\n1 tsp salt\n\n\u00bc tsp pepper\n\nGARNISH: Snipped chives\n\n**1.** Combine soup, milk, corn and tomatoes in a medium saucepan. Cook over high heat just until simmering.\n\n**2.** Meanwhile heat oil in a 12-in. nonstick skillet over medium-high heat. Season both sides of salmon with salt and pepper. Add to skillet and cook 2 minutes or until bottom is browned. Turn salmon over; add soup mixture and cook uncovered 10 minutes or until salmon is cooked through.\n\n**3.** Using a broad spatula, transfer salmon to soup plates; add chowder and sprinkle with chives.\n\n**PER SERVING : 529 cal, 40 g pro, 32 g car, 2 g fiber, 26 g fat (6 g sat fat), 115 mg chol, 1,899 mg sod**\n\nA green salad pairs well with this hearty soup.\n\n# Mediterranean Fish Stew\n\n**TILAPIA \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 10 MINUTES \u2022 TOTAL: 25 MINUTES**\n\n2 tsp olive oil\n\n4 small red potatoes (1 lb), sliced \u00bc in. thick\n\n1 bag (1 lb) frozen pepper stir-fry mix\n\n2 cloves garlic, chopped\n\n  cup water\n\n1 jar (26 oz) marinara sauce\n\n1 lb tilapia or catfish fillets, cut into 3-in. pieces\n\n\u00bc cup sliced pimiento-stuffed green olives\n\n2 Tbsp chopped cilantro\n\n**1.** Heat oil in a large nonstick skillet over medium-high heat. Spread potatoes in an even layer. Top with frozen peppers; sprinkle with garlic. Cover; cook 5 minutes.\n\n**2.** Add water, cover and reduce heat. Simmer 5 minutes or until potatoes are tender, stirring a few times. Add marinara sauce and bring to a boil. Reduce heat; place fish on top. Cover and simmer 4 to 5 minutes until fish is just cooked through. Sprinkle with olives and cilantro.\n\n**PER SERVING : 359 cal, 29 g pro, 42 g car, 6 g fiber, 8 g fat (2 g sat fat), 58 mg chol, 980 mg sod**\n\n# Tilapia Veracruz\n\n**TILAPIA \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 10 MINUTES**\n\n4 tilapia fillets (5 to 6 oz each)\n\n1 tsp olive oil\n\n\u00bc tsp each salt and pepper\n\n1 cup mango and peach salsa\n\n1 ripe avocado, diced\n\n**1.** Brush stovetop grill pan or broiler pan with oil and heat.\n\n**2.** Brush tilapia with 1 tsp oil; sprinkle with salt and pepper.\n\n**3.** Place on hot pan. Grill or broil 5 minutes or until cooked through, turning once.\n\n**4.** Mix salsa and avocado. Top each fillet with about \u00bd cup. Sprinkle with chopped cilantro if desired.\n\n**PER SERVING : 269 cal, 36 g pro, 11 g car, 3 g fiber, 10 g fat (2 g sat fat), 70 mg chol, 273 mg sod**\n\n**DIFFERENT TAKES**\n\n\u2022 Sprinkle fish with a little ground cumin or chili powder before cooking.\n\n\u2022 Make recipe with mahi-mahi or sea bass instead of tilapia.\n\n\u2022 Try using a chipotle-flavored salsa; add a squeeze of fresh orange juice.\n\n# Crispy Tilapia with Avocado Pico de Gallo\n\n**TILAPIA \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 12 MINUTES \u2022 TOTAL: 12 MINUTES**\n\n1 firm-ripe avocado\n\n1 cup pico de gallo\n\n\u00bc cup chopped cilantro\n\n\u00bd cup yellow cornmeal\n\n\u00bd tsp each chili powder, ground cumin and salt\n\n\u00bc cup milk\n\n1\u00bd lb tilapia fillets\n\n3 Tbsp oil\n\n**1.** Coarsely chop avocado. Stir into pico de gallo with chopped cilantro; set aside.\n\n**2.** Mix cornmeal, chili powder, ground cumin and salt on sheet of wax paper. Place milk in shallow bowl or pie plate. Dip tilapia fillets into milk, then cornmeal mixture to coat.\n\n**3.** Heat oil in large nonstick skillet over medium heat. Cook tilapia 2 to 3 minutes per side. Top with avocado mixture; serve with corn on the cob.\n\n**PER SERVING : 370 cal, 37 g pro, 26 g car, 3 g fiber, 14 g fat (2 g sat fat), 87 mg chol, 694 mg sod**\n\n# Cod Veracruz-Style\n\n**COD \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 10 MINUTES \u2022 TOTAL: 24 MINUTES**\n\n2 Tbsp flour\n\n\u00bc tsp each salt and pepper\n\nFour \u00be-in.-thick pieces cod fillet (about 6 oz each)\n\n1\u00bd Tbsp olive oil (preferably extra-virgin)\n\n1 medium onion, thinly sliced\n\n1 tsp minced garlic\n\n1 can (14.5 oz) diced tomatoes (preferably fire-roasted) with green chiles\n\n\u00bd cup water\n\n  cup pimiento-stuffed green olives, halved\n\n1 Tbsp capers, rinsed\n\n\u00bd tsp dried oregano\n\nGARNISH: chopped parsley\n\n**1.** Mix flour, salt and pepper on sheet of wax paper; add fish and turn to coat.\n\n**2.** Heat 1 Tbsp oil in a large nonstick skillet. Add cod and cook over medium-high heat, turning once, 5 to 7 minutes until golden and just cooked through. Remove to a platter; cover to keep warm.\n\n**3.** Heat remaining \u00bd Tbsp oil in skillet. Add onion and saut\u00e9 over medium-high heat 3 minutes or until golden. Add garlic; cook 1 minute or until fragrant. Stir in remaining ingredients, bring to a boil, reduce heat and simmer 2 minutes to develop flavors. Spoon over fish.\n\n**PER SERVING : 247 cal, 32 g pro, 11 g car, 3 g fiber, 8 g fat (1 g sat fat), 73 mg chol, 1,000 mg sod**\n\nGood with boiled or steamed new potatoes.\n\n# Bow-Tie Salad with Tuna\n\n**CANNED TUNA \u2022 ONE POT \u2022 SERVES 8 \u2022 ACTIVE: 30 MINUTES \u2022 TOTAL: 30 MINUTES**\n\n1 lb bow-tie (farfalle) pasta\n\n**DRESSING**\n\n1 can (6 oz) oil-packed solid light tuna\n\n\u00bc cup each red-wine vinegar and olive oil\n\n2 Tbsp honey-Dijon mustard\n\n\u00be tsp salt\n\n1 can (15 to 16 oz) chickpeas, rinsed\n\n3 large ripe tomatoes, cut in chunks\n\n1 large cucumber, cut in chunks\n\n8 oz feta cheese, cut in cubes\n\n1 cup quartered thin slices red onion\n\n1 cup slivered basil leaves\n\n**1.** Cook pasta as package directs. Drain; rinse under running cold water.\n\n**2. D RESSING:** Drain oil from tuna into a large serving bowl; reserve tuna. Whisk remaining Dressing ingredients into the oil.\n\n**3.** Add pasta to bowl, then remaining ingredients. Add tuna and gently break up. Toss well to mix and coat. Serve salad at room temperature.\n\n**PER SERVING : 467 cal, 20 g pro, 58 g car, 5 g fiber, 17 g fat (6 g sat fat), 29 mg chol, 736 mg sod**\n\n# Pasta Puttanesca & Tuna\n\n**CANNED TUNA \u2022 ONE POT \u2022 SERVES 6 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 25 MINUTES**\n\n1 lb cellentani or other pasta\n\n1 jar (25 oz) puttanesca pasta sauce\n\n1 can (6 oz) light tuna in oil, drained\n\n**1.** Cook pasta in a large pot of lightly salted water as package directs.\n\n**2.** Drain pasta in colander. Add pasta sauce and tuna to pasta pot. Bring to a simmer, breaking up tuna with a wooden spoon. Remove from heat.\n\n**3.** Add pasta to pot; toss to mix and coat. Transfer to a serving bowl and garnish with chopped parsley if desired.\n\n**PER SERVING : 369 cal, 17 g pro, 61 g car, 3 g fiber, 6 g fat (1 g sat fat), 15 mg chol, 786 mg sod**\n\n**DIFFERENT TAKES**\n\n\u2022 Add some crushed red pepper flakes.\n\n\u2022 Use canned clams instead of tuna.\n\n\u2022 Stir in some chopped fresh basil just before serving.\n\n# Tuna Stuffed Shells\n\n**CANNED TUNA \u2022 OVEN \u2022 SERVES 6 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 50 MINUTES**\n\n18 jumbo pasta shells\n\n1 can (6 oz) light tuna in oil, well drained\n\n1 cup fresh white bread crumbs\n\n\u00bc cup finely chopped onion\n\n1 large egg\n\n\u00bc cup minced fresh parsley\n\n1 tsp fresh lemon juice\n\n1 can (10\u00be oz) condensed cream of celery soup\n\n\u00bd cup milk\n\n2 Tbsp grated Parmesan cheese\n\nPaprika (optional)\n\n**1.** Heat oven to 350\u00b0F. You'll need an 11 \u00d7 7-in. baking dish lightly coated with nonstick spray.\n\n**2.** Boil pasta as package directs until just firm-tender.\n\n**3.** Meanwhile mix tuna, bread crumbs, onion, egg, half the parsley and the lemon juice to blend.\n\n**4.** Drain pasta shells. Rinse gently to cool; drain. Fill each shell with 1 Tbsp tuna mixture. Place in prepared dish.\n\n**5.** Whisk soup and milk in a small saucepan over medium heat until hot. Remove from heat; stir in remaining parsley. Pour evenly over shells. Sprinkle with cheese and paprika. Bake and serve or cover with foil and refrigerate up to 1 day.\n\n**6. T O SERVE:** Bake 25 minutes or until hot and bubbly.\n\n**PER SERVING : 270 cal, 16 g pro, 34 g car, 1 g fiber, 8 g fat (2 g sat fat), 50 mg chol, 573 mg sod**\n\n# Mediterranean Tuna\n\n**CANNED TUNA \u2022 SALAD \u2022 SERVES 4 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 13 MINUTES**\n\n8 oz green beans, ends trimmed\n\n2 bags (8 oz each) Mediterranean salad greens, or other lettuce greens\n\n2 cucumbers, peeled, halved, seeded and sliced\n\n1 pt grape tomatoes\n\n1 can (12 oz) chunk light tuna in oil, drained\n\n12 country-style mixed Kalamata olives\n\n\u00bd cup each Greek salad dressing and crumbled basil-and-tomato feta cheese\n\n**1.** Cook green beans in water to cover, or steam 7 to 8 minutes just until crisp-tender. Drain well.\n\n**2.** Empty the salad greens into a large bowl. Toss together with vegetables, tuna, olives, dressing and cheese.\n\n**PER SERVING : 385 cal, 25 g pro, 40 g car, 6 g fiber, 25 g fat (5 g sat fat), 50 mg chol, 1,016 mg sod**\n\n# Tuna Ni\u00e7oise\n\n**CANNED TUNA \u2022 SALAD \u2022 SERVES 4 \u2022 ACTIVE: 30 MINUTES \u2022 TOTAL: 30 MINUTES**\n\n1 lb red potatoes, quartered\n\n2 large eggs\n\n\u00bc lb trimmed green beans\n\n2 cans (6 oz each) solid light tuna in olive oil\n\n2 Tbsp red wine vinegar\n\n1 Tbsp Dijon mustard\n\n\u00bd can (6 oz) large pitted olives, sliced\n\n2 plum tomatoes, quartered\n\nSalt and pepper (optional)\n\n**1.** Combine potatoes and eggs in the shell with enough water to cover (salt is optional) in a saucepan. Heat to a gentle boil over medium-high heat. Cook 8 minutes. Remove eggs and rinse under cold water to stop cooking. Set aside; once cooled, peel off shells and quarter.\n\n**2.** Add green beans to saucepan with potatoes and continue cooking until vegetables are fork-tender, about 8 minutes more. Drain and cool 5 minutes.\n\n**3.** Drain oil from tuna, reserving 3 Tbsp. Whisk vinegar and mustard into oil until well blended. Arrange all salad ingredients on a platter and drizzle with dressing.\n\n**PER SERVING : 403 cal, 25 g pro, 25 g car, 4 g fiber, 23 g fat (4 g sat fat), 149 mg chol, 725 mg sod**\n\n# Pan Bagna\n\n**CANNED TUNA \u2022 SANDWICH \u2022 SERVES 6 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 65 MINUTES**\n\nOne 8-in. round loaf Italian bread (about 1 lb)\n\n2 cans (6 oz each) solid light tuna, packed in olive oil\n\n2 Tbsp balsamic vinegar\n\n2 cups arugula\n\n1 Tbsp nonpareil capers\n\n3 cups ratatouille (from Slow-Cooker Ratatouille)\n\n**1.** Cut bread in half horizontally. Scoop out bread from top and bottom so that you're left with about a 1-in.-thick shell.\n\n**2.** Drain \u00bc cup oil from tuna into a small bowl; whisk in vinegar. Brush dressing over cut sides of bread.\n\n**3.** Arrange arugula on bread bottom; spoon on tuna. Stir capers into ratatouille; spoon on top. Cover with bread top and wrap in plastic wrap. Refrigerate at least 1 hour or overnight. Cut into wedges.\n\n**Slow-Cooker Ratatouille**\n\n1 medium onion, chopped\n\n3 tsp chopped garlic (3 cloves)\n\n1 medium eggplant (1\u00bd lb)\n\n3 medium zucchini (1\u00bd lb)\n\n2 bell peppers\n\n6 plum tomatoes\n\n1 can (8 oz) tomato sauce\n\n1 Tbsp each chopped fresh oregano and thyme (or 1 tsp each dried)\n\n\u00bd tsp salt and pepper\n\n2 Tbsp each red wine vinegar and extra-virgin olive oil\n\n**1.** Place onion and garlic in a 6-qt slow-cooker.\n\n**2.** Cut eggplant, zucchini, peppers and tomatoes into 1-in. chunks; toss in large bowl with tomato sauce, herbs, salt and pepper. Add to slow-cooker.\n\n**3.** Cook on low 5 to 8 hours until vegetables are tender. Stir in vinegar and oil.\n\n**4.** Remove 3 cups ratatouille; save for Pan Bagna recipe. (Ratatouille can be refrigerated for up to 1 week.)\n\n**PER SERVING : 390 cal, 20 g pro, 39 g car, 5 g fiber, 18 g fat (4 g sat fat), 30 mg chol, 732 mg sod**\n\n# Greek Lemon & Oregano Mahi-Mahi\n\n**MAHI-MAHI \u2022 GRILL \u2022 SERVES 4 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 23 MINUTES**\n\n\u00bc cup lemon juice\n\n1\u00bd Tbsp olive oil\n\n\u00bd tsp dried oregano\n\n\u00bc tsp each salt and pepper\n\nFour 6-oz mahi-mahi or halibut fillets (about 1 in. thick)\n\nFour \u00bc-in.-thick slices red onion\n\nNonstick cooking spray\n\nGARNISH: grilled lemon wedges or slices, Kalamata olives, fresh oregano\n\n**1.** Mix lemon juice, oil, oregano, salt and pepper in a pie plate or shallow bowl. Remove and reserve 1 Tbsp. Add fish to pie plate and turn to coat. Marinate 10 minutes.\n\n**2.** Meanwhile, heat outdoor grill or stovetop grill pan. Coat onions with cooking spray. Grill 5 minutes, or until lightly charred and tender, turning once. Remove.\n\n**3.** Grill fish 8 to 10 minutes, turning once, until just cooked through. Remove to serving platter and drizzle with reserved lemon juice mixture. Scatter onions on top.\n\n**PER SERVING : 205 cal, 32 g pro, 4 g car, 1 g fiber, 6 g fat (1 g sat fat), 124 mg chol, 296 mg sod**\n\n# Asian Black Cod\n\n**COD \u2022 OVEN \u2022 SERVES 4 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 30 MINUTES**\n\n1 cup chicken broth\n\n2 Tbsp hoisin sauce\n\n1 Tbsp rice vinegar\n\n2 tsp vegetable oil\n\n4 black cod or halibut fillets (5 oz each), about 1 in. thick\n\n8 oz shiitake mushrooms, stems removed, caps cut in \u00bd-in. strips\n\n1 medium red pepper, cut in \u00bd-in. strips\n\n1 Tbsp minced fresh ginger\n\n\u00bd tsp minced jalape\u00f1o or serrano chile\n\n\u00bd cup sliced scallions\n\n**1.** Heat oven to 400\u00baF. You'll need a rimmed baking sheet lined with foil.\n\n**2.** Mix broth, hoisin sauce and vinegar in bowl. Heat oil in a large nonstick skillet over medium-high heat. Cook fillets in skillet, skin side up, 3 minutes or until just browned. Place fillets skin side down on prepared baking sheet. Bake fillets 10 to 12 minutes until fish is cooked through.\n\n**3.** Meanwhile, saut\u00e9 in same skillet the mushrooms, red pepper strips, ginger and chile 5 minutes. Stir in scallions and the broth mixture; cook 30 seconds.\n\n**4.** With slotted spoon, evenly spoon vegetables onto each serving plate and top each with a fillet. Spoon broth over fillets.\n\n**PER SERVING : 360 cal, 21 g pro, 14 g car, 2 g fiber, 24 g fat (5 g sat fat), 70 mg chol, 326 mg sod**\n\n# Quick French Fish & Potato Stew\n\n**COD \u2022 ONE POT \u2022 SERVES 6 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 50 MINUTES**\n\n2 large cloves garlic, peeled\n\n2 tsp fennel seeds\n\n\u00bd tsp each dried thyme and salt\n\n2 tsp olive oil\n\n1\u00bd cups each chopped onions and thinly sliced carrots\n\n4 cups chicken broth\n\n2 lb (about 4 medium) baking potatoes, peeled and cut in 1-in. chunks\n\n1 can (14 oz) diced tomatoes\n\n1\u00bd lb cod or scrod fillets, cut in 1-in. chunks\n\n\u00bd to 1 tsp freshly ground pepper\n\n**1.** Put garlic, fennel seeds, thyme and salt on a cutting board. Chop, then mash to a paste with the side of a large, heavy knife.\n\n**2.** Heat oil in a 4- to 5-qt pot over medium heat. Add garlic mixture and cook, stirring, 1 minute, or until fragrant. Stir in onions and carrots. Cook, stirring often, 5 minutes or until onions are translucent.\n\n**3.** Stir in chicken broth and potatoes. Bring to a boil, reduce heat, cover and simmer 15 to 20 minutes until potatoes are tender. Stir in tomatoes, increase heat to medium and gently boil 2 to 3 minutes.\n\n**4.** Stir in fish. Cover and simmer 5 minutes or until fish is opaque at center. Stir in pepper. Ladle into a serving bowl.\n\n**PER SERVING : 265 cal, 26 g pro, 32 g car, 4 g fiber, 4 g fat (1 g sat fat), 49 mg chol, 1,050 mg sod**\n\nServe with French bread to sop up the juices.\n\n# New England Seafood Chowder\n\n**COD \u2022 SLOW-COOKER \u2022 SERVES 6 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 6 TO 8 HR ON LOW**\n\n2 leeks, halved lengthwise and thinly sliced (white & light green only)\n\n8 oz red new potatoes, cut in eighths\n\n1\u00bd cups fresh corn or 1 can (11 oz) corn niblets, drained\n\n1 can (10 oz) condensed cream of celery soup\n\n1\u00bd cups water\n\n1 bay leaf\n\n\u00bc tsp dried thyme\n\n  tsp ground red pepper (cayenne)\n\n8 oz cod fillets, cut into 1-in. chunks\n\n8 oz raw large shrimp, peeled\n\n1 cup milk\n\n4 slices precooked bacon (from a 2.1-oz box)\n\n**1.** Place leeks, potatoes and corn in a 3\u00bd-qt or larger slow-cooker. Add soup, water, bay leaf, thyme and cayenne; mix gently.\n\n**2.** Cover and cook on low 6 to 8 hours until potatoes are tender. Add seafood about 15 minutes before serving; heat until fish is just cooked through. Stir in milk; remove bay leaf. Turn off heat.\n\n**3.** Heat bacon as package directs; crumble over bowls of chowder.\n\n**PER SERVING : 250 cal, 20 g pro, 28 g car, 3 g fiber, 7 g fat (2 g sat fat), 88 mg chol, 628 mg sod**\n\n# Sushi Salad\n\n**IMITATION CRABMEAT \u2022 SALAD\u2022 SERVES 4 \u2022 ACTIVE: 10 MINUTES \u2022 TOTAL: 10 MINUTES**\n\nOne 10-oz bag frozen steam-fresh rice\n\n\u00bd seedless cucumber\n\n4 scallions\n\n6 radishes\n\n6 oz bite-size pieces imitation crabmeat\n\n1 cup thawed, shelled edamame\n\n1 cup shredded carrot\n\n  cup bottled Asian salad dressing\n\n**1.** Microwave frozen steam-fresh rice as package directs. Put rice in a large bowl, cover and freeze 5 minutes to quick-chill.\n\n**2.** Meanwhile, slice cucumber, scallions and radishes.\n\n**3.** Toss with rice mixture, imitation crabmeat, edamame, carrot and Asian salad dressing.\n\n**PER SERVING : 243 cal, 9 g pro, 39 g car, 4 g fiber, 6 g fat (1 g sat fat), 8 mg chol, 623 mg sod**\nSHELLFISH\n\n# Shrimp & Linguine Alfredo\n\n**SHRIMP \u2022 SKILLET \u2022 SERVES 6 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 25 MINUTES**\n\n**ALFREDO SAUCE**\n\n3 Tbsp olive oil spread\n\n3 Tbsp flour\n\n2 cups fat-free half-and-half\n\n\u00bd tsp each salt and freshly ground pepper\n\n\u00bc tsp ground nutmeg\n\n\u00be cup grated Parmesan cheese\n\n1 lb linguine pasta\n\n1 bag (9 to 10 oz) baby spinach\n\n1 bag (12 oz) frozen peeled and deveined raw extra-large shrimp, thawed\n\n1 Tbsp minced garlic\n\n1 pt (12 oz) grape tomatoes\n\n**1.** Bring a large pot of lightly salted water to a boil.\n\n**2.** Meanwhile, make Alfredo sauce: Melt olive oil spread in a 2-qt saucepan over medium heat. Whisk in flour to blend. Add half-and-half, salt, pepper and nutmeg. Cook, whisking constantly, 5 minutes or until simmering and slightly thickened. Remove from heat; whisk in cheese until well blended. Cover to keep warm.\n\n**3.** Stir pasta into the boiling water. Cook as package directs, adding spinach 1 minute before pasta is done.\n\n**4.** While pasta cooks, put 2 Tbsp water, the shrimp and garlic in a large nonstick skillet. Saut\u00e9 over medium-high heat 2 to 3 minutes. Add tomatoes; saut\u00e9 2 minutes or until tomatoes just begin to split and shrimp are opaque at centers. Remove from heat.\n\n**5.** Drain pasta and spinach and return to pot. Add sauce, shrimp and tomatoes. Toss to mix and coat.\n\n**PER SERVING : 521 cal, 27 g pro, 76 g car, 5 g fiber, 9 g fat (3 g sat fat), 94 mg chol, 942 mg sod**\n\n# Shrimp Arrabbiata with Linguine\n\n**SHRIMP \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 21 MINUTES**\n\n12 oz linguine\n\n1\u00bd tsp olive oil\n\n1 lb peeled raw large shrimp (26 to 30), thawed if frozen\n\n\u00bc cup dry white wine (optional)\n\n1 tub (15 oz) refrigerated arrabbiata sauce (we used Buitoni)\n\n  cup chopped parsley\n\n**1.** Cook pasta in a large pot of lightly salted boiling water as package directs.\n\n**2.** Meanwhile heat oil in a large nonstick skillet. Add shrimp; saut\u00e9 over high heat 1 minute or just until shrimp turn pink.\n\n**3.** Add wine, if using; cook a few seconds until most evaporates. Add sauce; heat just until simmering and shrimp are cooked through.\n\n**4.** Drain pasta; return to pot. Add sauce and parsley; toss to mix.\n\n**PER SERVING : 503 cal, 35 g pro, 72 g car, 4 g fiber, 10 g fat (2 g sat fat), 173 mg chol, 985 mg sod**\n\nDelicious with warm garlic bread and bagged green salad.\n\n# Garlic Shrimp with Angel Hair\n\n**SHRIMP \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 15 MINUTES**\n\n12 oz angel hair pasta\n\n2\u00bd Tbsp butter\n\n2 Tbsp olive oil\n\n2 Tbsp minced garlic\n\n1 lb peeled, deveined large shrimp, thawed if frozen\n\n1 Tbsp grated lemon zest\n\n\u00bc tsp each salt and crushed red pepper\n\n\u00bc cup lemon juice\n\n  cup chopped parsley\n\n**1.** Bring a large pot of lightly salted water to a boil. Add pasta and cook as package directs, reserving about 1 cup of cooking water before draining.\n\n**2.** Meanwhile, heat 2 Tbsp of the butter and the oil in a large nonstick skillet over medium-high heat. Add garlic and cook over medium-low heat 30 seconds or until fragrant.\n\n**3.** Add shrimp, lemon zest, salt and crushed red pepper; saut\u00e9 over medium heat 3 to 5 minutes until shrimp is just cooked through.\n\n**4.** Stir in lemon juice; remove from heat. Pour over drained pasta; add remaining \u00bd Tbsp butter, the parsley and about \u00bd cup of the cooking water (more if desired). Toss to mix and coat.\n\n**PER SERVING : 586 cal, 34 g pro, 66 g car, 2 g fiber, 18 g fat (6 g sat fat), 191 mg chol, 455 mg sod**\n\n# Shrimp Marinara\n\n**SHRIMP \u2022 ONE POT \u2022 SERVES 4 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 15 MINUTES**\n\n2 tsp olive oil\n\n1 medium onion, finely chopped\n\n1 large carrot, shredded\n\n2 cloves garlic, minced\n\n1 can (28 oz) crushed tomatoes in pur\u00e9e\n\n1 can (14.5 oz) diced tomatoes with Italian herbs\n\n\u00bc tsp each salt, sugar and freshly ground pepper\n\n1 lb peeled large shrimp\n\n\u00bd cup pitted Kalamata olives\n\n**1.** Heat oil in a 3-qt saucepan over medium-high heat. Add onion, carrot and garlic; saut\u00e9 4 minutes.\n\n**2.** Stir in tomatoes, salt, sugar and pepper. Simmer, covered, 6 minutes. Add shrimp to simmering marinara; cover and cook about 5 minutes until cooked through. Stir in Kalamata olives; serve over brown rice.\n\n**PER SERVING : 307 cal, 28 g pro, 25 g car, 2 g fiber, 8 g fat (1 g sat fat), 172 mg chol, 1,152 mg sod**\n\n# Island Shrimp & Fruit Salad\n\n**SHRIMP \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 18 MINUTES**\n\n1 pouch (8.8 oz) ready rice (about 1\u00be cup cooked; you can use leftover cooked rice)\n\n1 jar (24 oz) tropical mixed fruit in light syrup; reserve \u00bd cup syrup\n\n1 Tbsp plus 1 tsp oil\n\n1 Tbsp rice-wine vinegar or cider vinegar\n\n1 tsp salt\n\n  tsp ground red pepper (cayenne), optional\n\n1 head napa cabbage (about 1 lb), halved lengthwise, thinly sliced crosswise\n\n\u00bd cup thinly sliced red onion\n\n\u00bd cup chopped cilantro\n\n1 lb raw large shrimp, peeled\n\n1 tsp dry Caribbean jerk seasoning\n\nGARNISH: chopped macadamia nuts and\/or cashews\n\n**1.** Heat rice as package directs. Cool slightly.\n\n**2.** Meanwhile, in a large bowl, whisk reserved fruit syrup, 1 Tbsp oil, the vinegar, salt and pepper until blended. Add mixed fruit, cabbage, onion and cilantro; toss to mix and coat. Set aside.\n\n**3.** Heat remaining 1 tsp oil in a large nonstick skillet. Sprinkle shrimp with jerk seasoning. Add to skillet and saut\u00e9 2 to 3 minutes, or until pink and cooked through.\n\n**4.** Add shrimp and rice to fruit mixture; toss to mix. Sprinkle servings with nuts.\n\n**PER SERVING : 392 cal, 26 g pro, 55 g car, 4 g fiber, 7 g fat (1 g sat fat), 173 mg chol, 792 mg sod**\n\n# New Orleans Shrimp 'n' Grits\n\n**SHRIMP \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 40 MINUTES**\n\n**CREAMY GRITS**\n\n2 cups milk\n\n1\u00bd cups water\n\n2 cloves garlic, crushed\n\n\u00bc tsp salt\n\n\u00be cup grits\n\n**SHRIMP**\n\n1 Tbsp oil\n\n1 red pepper, chopped\n\n1 cubanelle or green frying pepper, chopped\n\n1 small onion, chopped\n\n1 tsp minced garlic\n\n1 lb peeled large shrimp\n\n\u00be tsp each low-sodium Old Bay Seasoning (McCormick) and Cajun seasoning\n\n4 plum tomatoes, coarsely chopped\n\n\u00bd cup shredded reduced-fat Cheddar\n\n**1. G RITS:** Bring milk, water, garlic and salt to a boil in a medium saucepan. Whisk in grits, cover, reduce heat to simmer and cook, stirring occasionally, 20 minutes or until smooth and thickened.\n\n**2. S HRIMP:** Meanwhile, heat oil in large nonstick skillet over medium-high heat. Saut\u00e9 red and green peppers, the onion and garlic 5 minutes. Add shrimp and Old Bay and Cajun seasonings; cook 2 minutes. Add tomatoes; cook until shrimp are just cooked through, about 1 minute.\n\n**3.** Remove grits from heat; stir in cheese. Serve shrimp and vegetables over grits.\n\n**PER SERVING : 424 cal, 35 g pro, 41 g car, 3 g fiber, 13 g fat (5 g sat fat), 199 mg chol, 632 mg sod**\n\n# Smoky Marinated Shrimp\n\n**SHRIMP \u2022 ONE POT \u2022 SERVES 12 \u2022 ACTIVE: 15 MINUTES TOTAL: 18 MINUTES (PLUS CHILLING OVERNIGHT)**\n\n**MARINADE**\n\n1 cup cider vinegar\n\n1 bottle (5 oz) chipotle hot pepper sauce (  cup)\n\n\u00bd cup ketchup\n\n1 Tbsp minced garlic\n\n1 tsp salt\n\n1 cup oil\n\n2\u00bd lb large shrimp, peeled and deveined, tails left on\n\n1 each red and yellow pepper, cut in 1-in. pieces\n\n1 medium red onion, thinly sliced\n\n**1. M ARINADE:** Mix vinegar, hot pepper sauce, ketchup, garlic and salt in a large glass bowl. Whisk in oil until blended.\n\n**2.** Add shrimp to a large saucepan of boiling water and cook 1 to 2 minutes until pink and just cooked through. Drain; chill under running cold water.\n\n**3.** Add to Marinade along with the peppers and onion. Cover and refrigerate overnight.\n\n**4. T O SERVE:** Remove shrimp, peppers and onion with a slotted spoon to a serving bowl.\n\n**PER SERVING : 121 cal, 15 g pro, 4 g car, 1 g fiber, 4 g fat (1 g sat fat), 140 mg chol, 233 mg sod**\n\n**PLANNING TIP:** Best if prepared through Step 3 one day ahead. \n\n# Shrimp with Chesapeake Dipping Sauce\n\n**SHRIMP \u2022 ONE POT \u2022 SERVES 4 \u2022 ACTIVE: 13 MINUTES \u2022 TOTAL: 13 MINUTES**\n\n12 oz beer or 1\u00bd cups water\n\n2 Tbsp crab and shrimp boil (sometimes called fish boil) or pickling spice\n\n**DIPPING SAUCE**\n\n  cup light mayonnaise\n\n3 Tbsp each ketchup, minced dill pickle and onion\n\n2 Tbsp white horseradish\n\n1\u00bd lb raw medium shrimp, in the shell\n\n**1.** Bring beer and spices to a boil in a 3-qt saucepan over medium heat. Cover and boil gently 5 minutes.\n\n**2.** Meanwhile, mix Dipping Sauce ingredients and leave at room temperature while cooking shrimp.\n\n**3.** Add shrimp to saucepan, return to a boil, cover, reduce heat and simmer, stirring once, 4 to 5 minutes until shrimp turn pink and are barely opaque at center. Drain and serve immediately with the sauce.\n\n**PER SERVING (with \u00bc cup sauce): 234 cal, 29 g pro, 8 g car, 0 g fiber, 9 g fat (2 g sat fat), 217 mg chol, 757 mg sod**\n\n**FYI:** Cooking shrimp in their shells conserves flavor\u2014and it's easier on the cook when diners peel the shrimp. \n\n# Shrimp Stir-Fry\n\n**SHRIMP \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 10 MINUTES \u2022 TOTAL: 10 MINUTES**\n\n1 tsp oil\n\n1 lb shelled and deveined large shrimp\n\n1 container (3.5 oz) sliced shiitake mushrooms, 2 cups\n\n1 bag (16 oz) frozen stir-fry bell pepper blend\n\n1 cup frozen shelled edamame\n\n\u00bd cup bottled sesame-ginger stir-fry sauce\n\n1 pkg (9 oz) fresh linguine\n\nGARNISH: sliced scallions\n\n**1.** Bring 4 cups water to boil in a medium-size covered saucepan.\n\n**2.** Heat oil in a large nonstick skillet until hot but not smoking. Add shrimp; stir-fry 3 to 4 minutes until cooked through; remove.\n\n**3.** Add mushrooms to skillet; stir-fry 2 minutes. Add peppers, edamame, shrimp and stir-fry sauce; heat until simmering.\n\n**4.** Meanwhile, add linguine to water and cook 2 to 3 minutes, stirring frequently, until tender; drain. Serve shrimp and vegetables on top.\n\n**PER SERVING : 477 cal, 41 g pro, 58 g car, 6 g fiber, 9 g fat (1 g sat fat), 219 mg chol, 364 mg sod**\n\n# Crispy Asian-Spiced Shrimp\n\n**SHRIMP \u2022 SKILLET \u2022 SERVES 8 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 10 MINUTES**\n\n  cup white or brown rice flour (we used Bob's Red Mill)\n\n2 lb extra-large shrimp, peeled, tails on (16 to 20 ct)\n\n2 cups vegetable oil (see Note)\n\nSERVE WITH: Asian-style Spiced Sea Salt (McCormick)\n\n**1.** Place rice flour in large plastic food bag. Add shrimp; shake bag until shrimp are evenly coated.\n\n**2.** Meanwhile, heat oil over high heat in a 10- to 12-in. deep-sided skillet (not nonstick) or large wok (you may need less oil if you use a wok). When a bread cube dropped in the oil sizzles and browns in 60 seconds, the oil is hot enough. Shake excess flour from shrimp; add in small batches to oil. Fry about 2 minutes until golden, crispy and just cooked through.\n\n**3.** Remove with slotted spoon to paper towel. Serve immediately with a small bowl of spiced sea salt for sprinkling. Fry remaining shrimp in batches, checking temperature of oil often.\n\n**PER SERVING : 133 cal, 18 g pro, 4 g car, 0 g fiber, 5 g fat (1 g sat fat), 168 mg chol, 193 mg sod**\n\n**NOTE:** If you saut\u00e9 the coated shrimp in a little oil, they will not be as crisp as when skillet-fried and may absorb slightly more oil. \n\n# Sweet & Sour Shrimp\n\n**SHRIMP \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 20 MINUTES**\n\n1 Tbsp plus 2 tsp oil\n\n2 Tbsp cornstarch\n\n1 lb shrimp, shelled\n\n4 cups mix of the following vegetables: small broccoli florets, small cauliflower florets, sliced shiitake mushrooms, sliced white button mushrooms, shelled edamame, \u00bd-in. red or yellow pepper strips, \u00bd-in. cubanelle pepper strips, thinly sliced carrots, 1\u00bd-in.-long slices asparagus, snow peas, \u00bd-in.-thick red onion wedges\n\n**SAUCE**\n\n\u00bd cup apricot preserves\n\n  cup ketchup\n\n2 Tbsp cider vinegar\n\n1 tsp minced garlic\n\n**1.** Heat 1 Tbsp oil in large nonstick skillet. Put cornstarch and shrimp into a large ziptop bag, seal bag and shake to coat.\n\n**2.** Add shrimp to skillet; stir-fry over medium-high heat 3 to 5 minutes until cooked through. Remove to plate.\n\n**3.** Add remaining 2 tsp oil to skillet; heat. Add 4 cups of any one or combination of vegetables; stir-fry 3 to 5 minutes until crisp-tender.\n\n**4.** Stir all sauce ingredients in a small bowl until blended. Add sauce to skillet; bring to simmer. Add shrimp; simmer 1 to 2 minutes until sauce thickens and coats mixture.\n\n**5.** Serve with brown rice, and top with bits of almonds.\n\n**PER SERVING : 264 cal, 23 g pro, 40 g car, 3 g fiber, 3 g fat (0 g sat fat), 168 mg chol, 438 mg sod**\n\n# Thai Shrimp & Rice\n\n**SHRIMP \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 25 MINUTES \u2022 TOTAL: 25 MINUTES**\n\n1 tsp vegetable oil\n\n\u00bd cup sliced scallions\n\n1 Tbsp chopped garlic\n\n1 can (14 oz) lite coconut milk\n\n1\u00bd cups jasmine rice or converted white rice\n\n1 cup shredded carrots\n\n1 tsp salt\n\n12 oz raw medium shrimp, peeled and deveined\n\n8 oz fresh snow peas\n\n2 tsp freshly grated lime zest\n\nGARNISH: lime wedges and chopped cilantro\n\n**1.** Heat oil in a large nonstick skillet over medium heat. Add scallions and garlic; saut\u00e9 1 to 2 minutes until aromatic.\n\n**2.** Pour coconut milk into a 1-qt liquid measure and add enough water to make 3\u00bc cups. Add to skillet and bring to a boil. Add rice, carrots and salt. Cover, reduce heat and simmer 12 minutes or until rice is nearly tender.\n\n**3.** Stir in shrimp, snow peas, lime zest and, if rice looks dry, another \u00bc cup water. Bring to a simmer, cover and cook 3 to 4 minutes until shrimp are cooked through and the snow peas are crisp-tender. Garnish with lime wedges and chopped cilantro.\n\n**PER SERVING : 442 cal, 22 g pro, 72 g car, 3 g fiber, 8 g fat (4 g sat fat), 107 mg chol, 742 mg sod**\n\n# Mojo Seafood Skewers\n\n**SHRIMP & SCALLOPS \u2022 GRILL \u2022 SERVES 4 \u2022 ACTIVE: 15 MINUTES \u2022 TOTAL: 30 MINUTES**\n\n  cup each Mojo Criollo marinade (we used Goya), orange juice and chopped cilantro\n\n16 peeled and deveined extra-large shrimp (about 1 lb)\n\n8 large sea scallops (about 8 oz), halved crosswise\n\n1 small cubanelle pepper, cut into 16 pieces\n\n**1.** In a bowl, mix marinade, orange juice and cilantro; reserve 2 Tbsp. Add shrimp, scallops and peppers to bowl; toss to coat. Let stand 10 minutes.\n\n**2.** Coat outdoor grill rack with nonstick spray; heat grill. You'll need 8 metal skewers. If using wooden, soak in water for 10 minutes to prevent burning.\n\n**3.** Thread shrimp, scallops and peppers alternately on skewers. Discard marinade in bowl. Grill 3 to 4 minutes, turning once, until seafood is just barely opaque at centers.\n\n**4.** Remove to serving plates and drizzle with reserved 2 Tbsp marinade mixture. Serve with black beans heated with a little sliced garlic and olive oil.\n\n**PER SERVING : 144 cal, 28 g pro, 3 g car, 0 g fiber, 1 g fat (0 g sat fat), 187 mg chol, 421 mg sod**\n\n# Crispy Scallops with Chipotle-Tartar Sauce\n\n**RAW OR FROZEN SCALLOPS \u2022 SKILLET \u2022 SERVES 4 ACTIVE: 7 MINUTES \u2022 TOTAL: 10 MINUTES**\n\n**CHIPOTLE-TARTAR SAUCE**\n\n\u00bd cup tartar sauce\n\n2 Tbsp thinly sliced scallions\n\n1 Tbsp orange juice\n\n1\u00bd tsp chipotle hot-pepper sauce\n\n1 lb fresh or thawed frozen sea scallops (see Buying & Storing Scallops)\n\n3 Tbsp yellow cornmeal\n\n\u00bd tsp salt\n\n\u00bd tsp paprika\n\n1 Tbsp oil\n\n**1. C HIPOTLE-TARTAR SAUCE:** Mix sauce ingredients in a small bowl. Let stand while cooking scallops.\n\n**2.** Gently blot scallops dry between layers of paper towel (see Tip). Mix cornmeal, salt and paprika in a medium bowl (or in a plastic food bag); add scallops and toss to coat.\n\n**3.** Heat oil in a large nonstick skillet over medium-high heat. Add scallops in one layer and cook 3 minutes, carefully turning once with tongs, until golden on the outside and just opaque at centers. Serve with the sauce.\n\n**PER SERVING : 303 cal, 20 g pro, 13 g car, 1 g fiber, 19 g fat (3 g sat fat), 48 mg chol, 674 mg sod**\n\n**TIP:** Patting scallops dry helps the coating to adhere.\n\nNo tartar sauce in the house? Try a chipotle-barbecue sauce or wasabi mayonnaise instead.\n\n**BUYING & STORING SCALLOPS**\n\nLook for firm, moist scallops with a creamy white color and fresh scent. Those that are not fresh have an unmistakable sulfurous odor. The best scallops are also \"dry,\" that is, not oozing liquid into the package, and have a pearly look. Cook scallops within a day of buying them, or freeze them. To freeze large scallops, cut them into thinner disks. Spread them out between plastic wrap on a baking sheet and freeze. When hard, pack them, still in plastic, into a container or ziptop bag. The thin pieces of scallop will thaw quickly. Cook them as soon as possible to maintain flavor and texture. \n\n# Scallops with Lemon & Capers\n\n**SEA SCALLOPS \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 4 MINUTES \u2022 TOTAL: 10 MINUTES**\n\n1 cup chicken broth\n\n1 Tbsp capers\n\n1\u00bd tsp cornstarch\n\n1 tsp minced garlic\n\n1 tsp grated lemon zest\n\n2 Tbsp lemon juice\n\n\u00bc tsp each salt and pepper\n\n3 tsp stick butter\n\n1\u00bd lb sea scallops, patted dry\n\n1 Tbsp chopped parsley\n\n**1.** In a 2-cup liquid measure, stir broth, capers, cornstarch, garlic, zest, juice, salt and pepper until cornstarch dissolves.\n\n**2.** Melt 2 tsp butter in large nonstick skillet over medium-high heat. When butter just starts to brown, add scallops and cook, turning once, 4 to 5 minutes until golden and cooked through. Remove to a plate.\n\n**3.** Add broth mixture to skillet. Bring to a boil; boil 1 minute until slightly thickened. Remove from heat; stir in remaining butter and parsley. Spoon over scallops.\n\n**PER SERVING : 192 cal, 29 g pro, 6 g car, 0 g fiber, 5 g fat (2 g sat fat), 64 mg chol, 765 mg sod**\n\n# Cioppino\n\n**MUSSELS, SCALLOPS & HALIBUT \u2022 SLOW-COOKER \u2022 SERVES 6 ACTIVE: 10 MINUTES \u2022 TOTAL: 7 TO 9 HR ON LOW, PLUS 20 TO 40 MIN ON HIGH**\n\n2 cups thinly sliced fennel\n\n2 leeks (white and pale green parts only), rinsed and thinly sliced (1 cup)\n\n12 oz small red potatoes, quartered\n\n1 jar (26 oz) marinara sauce\n\n1 can (14\u00bd oz) chicken broth\n\n1 cup water\n\n  cup dry red wine (optional)\n\n1 tsp fennel seeds (optional)\n\n\u00bc tsp hot pepper flakes\n\n24 cleaned mussels\n\n12 sea scallops, halved if very large\n\n1 lb skinless halibut fillet, cut into 1\u00bd-in. chunks\n\nSERVE WITH: sourdough bread and olive oil for drizzling\n\n**1.** Mix all ingredients except seafood in a 5-qt or larger slow-cooker.\n\n**2.** Cover and cook on low 7 to 9 hours until vegetables are tender.\n\n**3.** Raise heat to high; stir in seafood. Cover and cook 20 to 40 minutes until mussels open and seafood is cooked. (Discard any mussels that don't open.)\n\n**PER SERVING : 297 cal, 33 g pro, 28 g car, 4 g fiber, 6 g fat (1 g sat fat), 54 mg chol, 943 mg sod**\n\n# Hearty Clam Chowder\n\n**CANNED CLAMS \u2022 ONE POT \u2022 SERVES 4 \u2022 ACTIVE: 12 MINUTES \u2022 TOTAL: 22 MINUTES**\n\n\u00bd lb red potatoes, diced\n\n3 slices bacon, chopped\n\n1 small onion, chopped\n\n1 garlic clove, minced\n\n\u00bd tsp thyme\n\n2 cans (6.5 oz each) chopped clams\n\n1 can (10.75 oz) cream of celery soup\n\n1 cup milk\n\nSERVE WITH: hot sauce\n\n**1.** Place potatoes with enough water to cover in a glass bowl and microwave for 10 minutes or until softened.\n\n**2.** In a large saucepan, cook bacon and onion over medium-high heat until bacon is cooked through. Add garlic and thyme; cook, stirring, for 1 minute.\n\n**3.** Add clam juice to bacon mixture, reserving clams. Stir in potatoes with \u00be cup of cooking liquid, the soup and milk. Whisk to combine and heat to boil.\n\n**4.** Reduce heat to low and simmer 5 minutes. Add clams and cook 2 minutes. Serve with hot sauce.\n\n**PER 1\u00bd CUP SERVING : 273 cal, 14 g pro, 25 g car, 2 g fiber, 13 g fat (5 g sat fat), 43 mg chol, 1,352 mg sod**\n\n# Mussels Fra Diavolo\n\n**MUSSELS \u2022 SKILLET \u2022 SERVES 4 \u2022 ACTIVE: 5 MINUTES \u2022 TOTAL: 15 MINUTES**\n\n12 oz linguine\n\n1 jar (25 oz) fra diavolo sauce or other spicy marinara\n\n2 lb scrubbed mussels, beards removed\n\nGARNISH: chopped chives or parsley\n\n**1.** Cook linguine as package directs in large pot of salted boiling water.\n\n**2.** Meanwhile, heat sauce over medium-high heat in large straight-sided skillet until simmering. Add mussels; cook, covered, 8 minutes or until mussels are opened. Discard any mussels that don't open.\n\n**3.** Drain linguine, spoon mussels with sauce on top and sprinkle with chives.\n\n**PER SERVING : 452 cal, 18 g pro, 79 g car, 7 g fiber, 7 g fat (1 g sat fat), 14 mg chol, 957 mg sod**\n\n**DIFFERENT TAKES**\n\n\u2022 Substitute 1 lb peeled large shrimp for the mussels.\n\n\u2022 Add   cup white wine when heating the sauce.\n\n\u2022 Serve mussels over soft polenta instead of pasta.\n\n# Lemon & Mint Seafood Skewers with Tabbouleh\n\n**SHRIMP & SEA SCALLOPS \u2022 GRILL \u2022 SERVES 4 ACTIVE: 15 MINUTES \u2022 TOTAL: 35 MINUTES**\n\n1 cup uncooked bulgur\n\n\u00bc cup lemon juice\n\n1 Tbsp plus 1 tsp olive oil\n\n1\u00bd tsp minced garlic\n\n\u00bc tsp plus   tsp each salt and pepper\n\n12 oz peeled extra-jumbo shrimp\n\n12 oz large sea scallops\n\n1 cup chopped tomatoes\n\n1 kirby cucumber, chopped\n\n\u00bc cup each chopped parsley and mint and sliced scallions\n\n**1.** Soak bulgur in a large bowl according to package directions.\n\n**2.** About 15 minutes before bulgur will be done, combine 2 Tbsp lemon juice, 1 tsp oil, the garlic and   tsp each salt and pepper in a ziptop bag. Add shrimp and scallops to bag and marinate 10 minutes. Meanwhile, coat outdoor grill rack with nonstick spray; heat grill. You'll need 8 large metal or wooden skewers.\n\n**3.** Thread shrimp and scallops alternately on skewers. Grill 3 to 4 minutes, turning once, until just barely opaque at centers. Remove to serving plate.\n\n**4.** Add remaining 2 Tbsp lemon juice, 1 Tbsp oil and \u00bc tsp each salt and pepper to bulgur. Add remaining ingredients and toss to mix. Serve with skewers.\n\n**PER SERVING : 357 cal, 37 g pro, 37 g car, 8 g fiber, 7 g fat (1 g sat fat), 157 mg chol, 498 mg sod**\n\n**VARIATION:** Omit scallops and double the amount of shrimp used. \n\n# Photo Credits\n\nPage : Iain Bagwell; page : Mark Thomas; page : Sang An; pages , : Mark Thomas; page : Mary Ellen Bartley; page : Tom McWilliam; page : Mark Thomas; page : Antonis Achilleos; page : Anastasios Mentis; page : Iain Bagwell; page : Kate Sears; page : Iain Bagwell; page : Kate Sears; page : Mary Ellen Bartley; page : Laura Moss; page : Anastasios Mentis; page : Mary Ellen Bartley; page : Iain Bagwell; page : Ellen Silverman; page : John Uher; page : Stephanie Foley; page : Mark Thomas; page : Tom McWilliam; page : Jim Franco; page : Mary Ellen Bartley; pages , : Mark Thomas; page : Sang An; page : Mary Ellen Bartley; page : Kate Sears; page : Ann Stratton; page : Dasha Wright; page : Iain Bagwell; page : Alison Miksch; page : Ann Stratton; page : Mark Thomas; page : John Uher; page : Jacqueline Hopkins; page : Caren Alpert; page : Mary Ellen Bartley; page : Kate Sears; page : John Uher; page : Charles Schiller; page : James Baigrie; page : Dasha Wright; page : Stephanie Foley; page : Charles Schiller; page : Caren Alpert. \n","meta":{"redpajama_set_name":"RedPajamaBook"}}
+{"text":"\n\n\" _And His disciples answered Him: from  \nwhence can anyone fill them here  \nwith bread in the wilderness?\"_\n\nMARK, 8:4\n\n_To Jean Danielou, S.J_.\n\n# CONTENTS\n\nLE DEVOT CHRIST\n\nPROLOGUE\n\nI PSALMS AND CONTEMPLATION\n\n1. _Contemplation in the Liturgy_\n\n2. _The Testimony of Tradition_\n\n3. _Meanings in Scripture_\n\n4. _Songs of the City of God_\n\n5. _Errors to Avoid_\n\nII POETRY, SYMBOLISM AND TYPOLOGY\n\n1. _Poetry, Symbolism and Typology_\n\nIII SACRAMENTA SCRIPTURARUM\n\n1. _Words as Signs and \"Sacraments\"_\n\n2. _Transformation in Discovery_\n\n3. \" _Visible Mysteries_ \"\n\n4. \" _When Israel came out of Egypt_ \"\n\nIV THE PERFECT LAW OF LIBERTY\n\n1. \" _Thou hast opened my ears_ \"\n\n2. _From Praise to Ecstasy_\n\nV THE SHADOW OF THY WINGS\n\n1. _Dark Lighting_\n\n2. _The Silence of the Psalms_\n\nEPILOGUE\n\nNOTES\n\n_The pictures in this book are of a famous Crucifix, venerated for centuries in a chapel adjoining the Cathedral of Perpignan, in Southern France. Nobody knows who carved this terrible masterpiece. No one is quite sure where it came from. Was it brought to Perpignan from Germany or Spain? Or was it, as most people believe, the work of an anonymous Catalan, living in Perpignan or in the nearby Pyrenees? Whatever may be the origin of the_ Devot Christ, _there has probably never been a work of Christian art that so powerfully expressed the suffering of Christ on the Cross. This is indeed the Christ Whom the prophet Isaias described as a twisted root laid bare to the sun on the parched rocks of the desert. This is truly the Christ of whom Isaias cried: \"There is no beauty in Him nor comeliness: and we have seen Him and there was no sightliness that we should be desirous if Him, despised and the most abject of men, a man of sorrows and acquainted with infirmity:... Surely He hath borne our infirmities and carried our sorrows, and we have thought Him as it were a leper, and one struck by God and afflicted.\" This too is the Christ of the twenty-first Psalm and of the other Psalms we discuss in this book. It is the Christ of the Dark Night of St John of the Cross. It is the Christ Who shares His agony with the mystics. And finally it is the Christ of our own time\u2014the Christ of the bombed city and of the concentration camp. We have seen Him and we know Him well. This_ Devot Christ _is the image of what the men of our time are doing to one another for they are murdering Him in one another. But because there are many in whom He dies again, there are also many in whom He lives again, for Christ dies only in order to rise again from the dead. This picture, therefore is the picture of our Redeemer, the Saviour of the World. Of Him Isaias said, in the same fifty-third chapter of his prophecy: \"He was wounded for our iniquities, He was bruised for our sins; the chastisement of our peace was upon Him, and by His bruises we are healed. All we like sheep have gone astray, every one hath turned aside into his own way: and the Lord hath laid upon Him the iniquity of us all_.\"\n\n_Small wonder that this_ Devot Christ _is sought out day by day by penitents and pilgrims in the French Catalan country. This Crucifix is held to be miraculous, to grant many favors to those possessed of pure devotion_ \u2014ab los que tenan pura devocio. _And there is a legend about Him. The bowed head is said to fall, each year, a fraction of an inch toward the chest. The Catalans say that when the chin finally comes to rest upon the chest, it will be the end of our world_.\n\n# PROLOGUE:\n\n_What is this book about? For whom is it written?_\n\n_It is a book about the Psalms. The Psalms are perhaps the most significant and influential collection of religious poems ever written. They sum up the whole theology of the Old Testament. They have been used for centuries as the foundation for Jewish and Christian liturgical prayer. They still play a more important part than any other body of religious texts, in the public prayer of the Church. Benedictine and Cistercian monks chant their way through the entire Psalter, once a week. Those whose vocation in the Church is prayer find that they live on the Psalms\u2014for the Psalms enter into every department of their life. Monks get up to chant Psalms in the middle of the night. They find phrases from the Psalter on their lips at Mass. They interrupt their work in the fields or the workshops of the monastery to sing the Psalms of the day hours. They recite Psalms after their meals and practically the last words on their lips at night are verses written hundreds of years ago by one of the Psalmists_.\n\n_For the monk who really enters into the full meaning of his vocation, the Psalms are the nourishment of his interior life and form the material of his meditations and of his own personal prayer, so that at last he comes to live them and experience them as if they were his own songs, his own prayers_.\n\n_This would not be possible if the Psalms were nothing more than literature to those who have to pray them every day. \"Art\" and \"literature\" as such no doubt have a part to play in the monastic life. But when a man lives in the naked depths of an impoverished spirit, face to face with nothing but spiritual realities for year after year, art and literature can come to seem peculiarly shabby and unsubstantial\u2014or else they become a lure and a temptation. In either case, they are a potential source of unrest and of dissatisfaction_.\n\n_Yet the liturgical prayer of the monk is one of the great pacifying influences in a life that is all devoted to serenity and interior peace. There is only one explanation for this. The Psalms acquire, for those who know how to enter into them, a surprising depth, a marvelous and inexhaustible actuality. They are bread, miraculously provided by Christ, to feed those who have followed Him into the wilderness. I use this symbol advisedly. The miracle of the multiplication of the loaves usually suggests the Sacrament of the Eucharist, which it foreshadowed: but the reality which nourishes us in the Psalms is the same reality which nourishes us in the Eucharist, thoughin a far different form. In either case, we are fed by the Word of God. In the Blessed Sacrament, \"His flesh is food indeed.\" In the Scriptures, the Word is incarnate not in flesh but in human words. But man lives by every word that proceeds from the mouth of God_.\n\n_This book is not a systematic treatise, but only a collection of personal notes on the Psalter. They are the notes of a monk, written in the monastic tradition, and one supposes that they might appeal above all to monks. But in this mysterious age, there is no telling whom the book may reach\u2014although no one expects it to reach everybody. Perhaps, by its very nature, the book should pretend to address itself to those who do not quite understand why they are obliged, by reason of their vocation, to make the Psalms the substance of their prayer. In any case these pages attempt to put forth a few reasons why the Psalms in spite of their antiquity ought to be considered one of the most valid forms of prayer for men of all time. As for those readers who can only regard the Psalms as \"literature\"\u2014this book will at least offer them some of the reasons why the Psalter seems to be more than literature to those of us who have made it our bread in the wilderness_.\n\n# 1:\n\n# _The Problem: Contemplation in the Liturgy_\n\nST BENEDICT OF NURSIA, WRITING HIS RULE FOR monks, was writing for men who have no other purpose in life but God. After all, is there any other purpose for anyone? All men seek God, whether they know it or not. As St Paul told the citizens of Athens: \"God, who made the world and all things therein... hath made all mankind to dwell upon the whole face of the earth, determining appointed times and the limits of their habitation. That they should seek God if haply they may feel after Him or find Him, although He be not far from every one of us: For in Him we live and move and have our being.\" [1] Even those who say they do not believe in God, seek Him by the very fact that they deny Him: for they would not deny Him unless they thought their denial were true: and God is the source of all truth.\n\nAmong those who do believe in Him some seek Him more explicitly and more intently than others. Monks have no other occupation in life than the search for God. That is what makes the monastic life essentially simple. What could be simpler than the search for one whom we have already found? That, indeed, is the nature of the search: a realization that we have found Him. This realization begins in an act of faith and culminates in an experience of His presence and of His inscrutable and infinite identity, made known to us in the descent of His mercy upon our souls which already exist only in Him and by Him and for Him alone.\n\nWith this conception of the monastic life as a search for God in which nothing is to be preferred to the love of Christ, St Benedict never speaks in any but the simplest and most concrete terms. The concrete realities of simple everyday human existence are nowhere better appreciated than in a monastery where the monks, by their \"flight from the world,\" have actually found not only God but the world also in Him. No one better than a monk realizes the dignity and meaning of manual labor\u2014not because labor is a penance, an ascetical exercise, a means of livelihood or something else like that; but because labor is itself worship, in a world which is sacramentalized by the presence of a creating and redeeming God.\n\nTherefore, St Benedict does not deal in notions like \"the Liturgical life,\" the \"contemplative life,\" \"infused contemplation.\" Nor is he in any way concerned with a supposed theoretical opposition between \"public official prayer\" and \"private prayer,\" between \"vocal\" and \"mental prayer.\" He does not worry very much about the precise point at which contemplation ceases to be \"acquired\" and becomes \"infused\" \u2014or whether two such categories actually exist. Such abstract matters have their place in modern theological dispute, but they were not very important to men who spent their lives not in arguing about \"spirituality\" but in loving God. This love led them to the knowledge which is true life, eternal life. \"For this is eternal life, that they should know Thee the one true God and Jesus Christ whom Thou hast sent.\"[2]\n\nThese are the very reasons why the monks were true contemplatives, why they entered so deeply into that experience of the mysteries of God which is called \"infused contemplation\" and why, at the same time, they reached the end for which \"liturgy\" and the \"liturgical life\" have always been intended.\n\nWe, who are the descendants of St Benedict and who are often disturbed by some of the abstract questions I have mentioned, would do well to understand clearly, once and for all, that the neglect of theoretical dispute does not necessarily imply a neglect of the values which are being disputed. On the contrary the only way in which we can at last enter into the possession of these realities, which lie at the very roots of our monastic existence, is to stop talking about them and lay hands on them by living them out in the work of our contemplative vocation.\n\nIn saying that the Divine Office, the \"work of God,\" held a central and dominant position in the monk's daily life, St Benedict was only reaffirming the truth that the monk came to the monastery to seek God. The term \" _opus Dei_ \" (work of God), signifies the chanting of the canonical hours\u2014the prayer of the monastic community. This choral office is made up above all of Psalms. But if we were to say that the chief purpose of the monk's life was the chanting of psalms we would certainly end up with a completely false notion of monasticism. It is not hard to see why. For if we define the monastic life merely in terms of the material obligation which the monk has to fulfil, we soon lose sight of the end which the legislator has in view. The monk does not exist for the sake of an obligation: the obligation exists for the sake of the monk. Duties and obligations are merely the signposts which point out the road to some ultimate end in which our whole nature and its capacities are fulfilled. The fulfilment of an obligation does not, in itself, satisfy the aspirations of our being; but it brings us into contact with the One we seek. It unites us to God in a union of wills. And where the obligation is one of prayer, the union is more than a conformity of wills. Prayer demands intelligence. The Psalms bring our hearts and minds into the presence of the living God. They fill our minds with His Truth in order to unite us with His Love. Now there is a difference between praying and \"saying prayers.\" I can, perhaps, exteriorly fulfil an obligation by \"saying prayers\"; but the reason for my being a monk is to _pray_ , because in praying I find God.\n\nThe value of the work of God, the _opus Dei_ , lies not so much in the fact that it is a work or a service ( _opus_ ), but in the fact that it is service _of God_. Everything the monk does is done in the service of God. But the _opus Dei_ is more perfectly and exclusively directed to God and penetrates more deeply into the deepest recesses of the monk's soul than any other thing he does. Of course, I am now taking liberties with St Benedict's term and extending it to include the Mass which is, in the strictest sense, our \"Liturgy,\" and for which the office only forms a liturgical setting.\n\nThat is why the _opus Dei_ opens to us the deep springs of interior contemplation.\n\nBut we must not imagine that the chanting of psalms involves a \"technique\" of contemplation. The Psalms are not to be regarded as spiritual instruments, which, when they are properly manipulated, will lead us into some special psychological state. It is quite true that the tradition of the Fathers has always regarded \"psalmody\" as a step to \"contemplation\" and the Fathers always understood contemplation to be an _experience_ of God. Since it is an experience, it clearly involves us in a psychological state, or at least in a psychological act. One of the Fathers of the Church who has the most to say about this contemplative experience is St Gregory the Great. And Gregory looms rather large in \"liturgical spirituality\" since it is from him that the Gregorian Sacramentory and Gregorian chant take their names. I mention this in order to show that the mythical opposition between \"liturgical prayer\" and \"contemplative experience\" which gets some people so excited at the present day was unknown to the Fathers. For them \"liturgy\" and \"contemplation\" blended in a spontaneous harmony since both were expressions of the basic need for God and both contributed to the fulfilment of that need. For after all, \"liturgy\" turns into \"contemplation\" as soon as our prayer ceases to be a search for God and turns into a celebration, by interior experience, of the fact that we have found Him.\n\nNevertheless, I repeat, the psalms are not designed to \"produce\" contemplation. They are not, of themselves, supposed to induce any particular psychological effect. They lead to contemplation precisely because their impact on us is _theological_ rather than _psychological_. There is no end of frustration in some monasteries where this truth has not been clearly understood. Neophytes in the contemplative life conceive that the \"office\" is an \"obstacle to contemplative prayer\" because it tends to prevent them from bringing upon themselves a certain degree of interior abstraction which is psychological in its origin and in its term. Their frustration is only increased, of course, when they are told by ascetics that the office is to be accepted merely as a form of penance. This amounts to a declaration that the Psalms have no meaning, that understanding has no place in prayer, that monastic choirs were invented only as a test of humility, abnegation and dogged endurance.\n\nBut the problem is not solved, either, by throwing the crumbs of David and Gregory to the monk's starved sense of art. The desire for contemplation has nothing essential to do with art or with the aesthetic sense. It cannot be satisfied by poetry, any more than it can by philosophy, or music, or ceremonies, or biblical speculation. After all, we will never come to contemplation unless we desire something infinitely more than contemplation. The Psalms, then, are not to be exploited for their psychological effects. These exist, but they are secondary. The psalms are theology. That means that they place us in direct contact with God, through the assent of faith to His Revelation. It is because of this theological and dynamic effect that the psalms are steps to contemplation. This theological effect depends ultimately on a free gift of God. It is useless, then, to seek some secret esoteric \"method\" of reciting the Psalter in order to \"get contemplation.\" If we chant the psalms with faith, God will manifest Himself to us; and that is contemplation.\n\n# 2:\n\n# _The Testimony of Tradition_\n\nTHE MOVEMENT AWAY FROM SOCIAL AND LITURGICAL forms of prayer, which gained momentum in the high Middle Ages, made many Christians imagine that \"interior\" prayer \"in spirit and in truth\" was incompatible with exterior forms of worship. The Illuminists in sixteenth-century Spain taught their disciples that the chanting or recitation of the Divine Office was an obstacle to progress in interior prayer. Even some spiritual writers of a more orthodox stamp, who realized that the objective dignity and worth of the Divine Office as the public prayer of the Church, had to be defended and maintained, nevertheless treated it is a \"duty\" which the contemplative had to \"accept\" in all humility and submission, rather than as a manifestation of loving union with God.\n\nUnderlying this error was, first of all, a false psychology of contemplation. This false psychology was an oversimplification of the true doctrine. The false view went something like this. All contemplative prayer is purely passive prayer and is incompatible with any interior or exterior activity. The Divine Office involves exterior and interior activity. Therefore the Divine Office and contemplative prayer are incompatible.\n\nThe Quietist, Michael de Molinos, held that \"interior (that is, contemplative) souls should never give thanks to God with words or with their tongue, but should remain in silence, placing no obstacle to His action in them.\" This sweeping statement was condemned. Molinos added (and this was also condemned) that the more perfectly these \"interior\" souls resigned themselves passively into the hands of God the more they would find it impossible to recite vocal prayers at all.\n\nThe reason heresies have to be condemned is that they contain elements that resemble the truth and therefore lead well-meaning Christians into error. It is quite true that in mystical or infused contemplation, the soul becomes increasingly passive under the guidance of the Holy Spirit, and it is also quite true that sometimes (but not _all the time_ ) the soul that is thus passively led by God finds it difficult or even impossible to elicit the various acts that enter into ordinary forms of prayer. But these passive states of prayer, which are a pure gift of God, are normally only granted by Him to souls who have faithfully exercised themselves in the practice of virtue and in the familiar types of meditative and vocal prayer. The road to this passivity is an active way, although that does not mean that passive prayer can be \"acquired.\" That, in fact, was at the root of Molinos's errors. He believed that true contemplation could be acquired, in the strict sense of the word, by a mere cessation of activity. All you had to do was to renounce all prayer of petition, renounce all desire for virtue, for progress and for a supernatural reward, renounce all solicitude for your own body and soul, abandon all reflection on yourself and remain empty and passive in the hands of God and you automatically became a contemplative. This spiritual vacuum was itself contemplation because as soon as we ceased to act, God acted in us. It is easy to see why Molinos did not think vocal prayer was an aid to contemplation.\n\nSt Theresa, one of the best exponents of true mystical doctrine, seems to have been thinking of the Quietists when she wrote her _Way of Perfection_. She told the nuns of her first foundation, St Joseph's at Avila, that vocal prayer, well made, was necessarily also mental prayer, because if you did not apply your mind to what you were saying you were not \u2014as far as she could see \u2014praying at all. St Theresa was not here concerned with establishing the absolute minimum for satisfying an obligation in prayer. She had no hesitation in saying that vocal prayer, far from being an obstacle to contemplation, was one of the ordinary means by which we could dispose ourselves to receive this great gift of God. She said that \"anyone ignorant of the subject\" might imagine that vocal prayer and the (infused) prayer of quiet had nothing to do with each other, but that this was \"certainly not true.\" [3] She went on to give examples of mystics who, in her own experience, had arrived at mystical union by the mere practice of vocal prayer. St Theresa herself believed and wrote that in the Pater Noster \"Our Lord has taught us the whole method of prayer and high contemplation from the very beginnings of mental prayer, to quiet and union.\"[4]\n\nWhen she said that the vocal prayers of the Church could lead us to the highest contemplation, St Theresa had centuries of tradition behind her. How else had the Fathers of the Desert found their way into the regions of mystical prayer, save by the meditative recital of the Psalter? How else was the mysticism of a Gregory of Nyssa and a Cyril of Alexandria nourished but by the Liturgy, and above all by the Psalms? What prayer did more than the Divine Office to make mystics of the monks who once lived in great monastic communities like Jumieges, St Gall or Cluny, Calmaldoli or Clairvaux?\n\nWherever Catholics have lived as solitaries the claims of their solitude have always yielded at certain times to the demands of the _synaxis_ \u2014the assembly of the hermits in communal, liturgical prayer. The lives of the Desert Fathers show that the liturgical and sacramental life of the Church played an essential part in their contemplation. The _Historia Lausiaca_ [5] gives us plenty of evidence that the test of false mysticism, among the hermits, was their attitude toward the Liturgy. Visionaries who came to believe that some private experience of the Absolute elevated them above the common sacramental life of the Church eventually proved\u2014in ways as spectacular as they were disturbing\u2014that their interior life did not flow from springs divine. The reason for this is, of course, that there is no true mysticism without charity and there is no charity without incorporation in the Mystical Body of Christ, for charity is the life of that Mystical Body. But the life of the Mystical Body is nourished by the Sacraments and by the prayer of the Mystical Body, which is the Liturgy. The Desert Fathers who ran spiritually amok in the third and fourth centuries did not fail in asceticism. Their fasts and their penances were almost incredible. They were not without interior experiences: on the contrary, they often had the most spectacular visions. Where, then, did they fail? In humility and in charity. This failure was expressed in a contempt for mankind in general, for the other hermits, a contempt for the common prayer life of the Church and a conviction that they could do without Mass and the Sacraments. One of them even had a vision in which he believed that Christ appeared and told him he was now so perfect that he could do without the Holy Eucharist. He was too perfect to go to communion!\n\nCassian describes the Night Office of the Egyptian monks. They have come together by starlight and fill the shadows of the hut which is their chapel. How many are there? Cassian cannot tell. It takes him a long time to realize that the building is full of men, so great is the silence in which they stand, immobile, deep in recollection, while the solitary singer chants the Psalms in Coptic... The Office consists of twelve Psalms, chanted slowly. We can imagine the strange pathos of the Oriental melody, long since forgotten. Every one is intent upon the meaning of the Psalms, for the Desert Fathers, like the patriarchs and prophets of Israel, are haunted by the living reality of the Redeemer revealed to the world in the Psalter. He is the Word of God, hidden in these \"words of God.\" Contemplation will come to them when the revelation that is given, in these inspired words, to the whole Church, suddenly opens out and becomes a personal experience, a deep, transforming, mystical light that penetrates and absorbs their whole being. That light, which is the fire of the Holy Spirit, will reach them through the Psalms. It is something far greater and more mysterious than the mere light of faith, and yet faith remains the key to it, for the way to contemplation is the way of faith. There is no other.\n\nWe must remember why the Desert Fathers lived the life they did. Their vocation\u2014and this is the foundation stone of all monastic spirituality\u2014had a twofold end. _Finis nostrae professionis regnum Dei...destinatio vero nostra, id est scopos, puritas est cordis_. \"The ultimate end of our profession is the Kingdom of God... the proximate end, to which we direct our immediate strivings, is purity of heart.\" [6]\n\nEverything the monk does then is ordered ultimately not only to his own fruition of God in heaven, but also to the transformation and glorification of all things in Christ, the \"summing up of all things in Christ\" which is the Kingdom of God. In order to achieve this last end, the monk directs his whole life to the acquisition of sanctity, purity of heart. _Puritas cordis_ means much more to the Fathers than moral or even ascetic perfection. It is the end of a long process of spiritual transformation in which the soul, perfect in charity, detached from all created things, free from the movements of inordinate passion, is able to live absorbed in God, and is penetrated from time to time with vivid intuitions of His action, intuitions which plumb the depths of the divine mysteries, which \"grasp\" God in a secret and intimate experience not only of Who He is, but of what He is doing in the world. The man who is pure in heart not only knows God, the Absolute Being, pure Act, but knows Him as the Father of Lights, the Father of Mercies, Who has so loved the world as to give His only begotten Son for its redemption. Such a man knows Him not merely by faith, not by theological speculation, but by intimate and incommunicable experience.\n\nThis purity of heart, which is the reason for the monk's existence since it perfects his union with God in experience and brings him to the gate of heaven, becomes the rule and measure of all his activities. Everything that brings him closer to this end is good. Everything that draws him away from the end is either useless or obnoxious. Things that are good in themselves may become harmful when the manner in which they are used turns them into obstacles to purity of heart. \"It is necessary,\" said Abbot Isaac to Cassian in the desert, \"that we carry out our exercises, fasts, vigils, prayers... for the sake of this end, purity of heart. But it is not fitting that we should disturb the order of this supreme virtue for the sake of our exercises. Indeed, if purity of heart is kept integral and untouched in our souls, nothing will be lost if, by necessity, we should have to pass over something that is secondary.\" [7]\n\nThe struggle for purity of heart goes through two phases: first the control of our actions and the acquisition of virtues and extinction of the passions. Then comes the more difficult part of the ascent: constant recollection of the mind in God. Cassian is often preoccupied with one of the great problems of monks: the problem of distractions. It is here that the meditation of Scripture and particularly the use of Scripture in liturgical and private prayer assumes a place of great importance.\n\nThe Egyptian monks memorized whole Books of the Bible. St Anthony, who is supposed not to have been able to read, meditated for years on the Scriptures in his solitude. He had learned them by heart from hearing them read and recited in the liturgical texts used in the churches. The words of Scripture are given to the monk first of all to drive out distracting and evil thoughts and replace them by good ones. We go to the Scriptures to find those \"ascending\" thoughts which raise us up to God against the gravitation of passion, in which \"descending\" thoughts constantly drag us earthward and tighten the chains which keep the spirit enslaved to the flesh. More than that, the meditation of the Scriptures leads to contemplation. Here Cassian strikes deep into the traditional doctrine which associates purity of heart with the restoration of the divine likeness to the soul, created in God's image but defaced by selfishness and sin.\n\n_you should show yourself diligent, indeed constant, in the reading of Scripture, until continual meditation fills your heart and forms you as it were after its likeness: while you make out of it in some way an ark of the covenant, having within you two tables of stone, which are the two testaments eternal and sure; and a golden pot that signifies a pure and sincere memory preserving with continual carefulness the manna hidden within it, the manna of everlasting and heavenly sweetness of the spiritual meaning and the bread of angels: the rod of Aaron, too, which represents the saving standard of our supreme and true High Priest, Jesus Christ, which for ever buds with the freshness of immortal memory... All these are guarded by two Cherubim, the fulness of historical and spiritual knowledge_.[8]\n\nCassian goes on to elaborate this symbolism\u2014which he does in perfect accord with a tradition dating back to the Apostles\u2014by explaining that the \"spiritual knowledge\" of Scripture, like the Cherubs which overshadowed the Ark in the Holy of Holies, protects and overshadows the inner sanctuary of the soul. This knowledge of Scripture is not contemplation. It leads to contemplation. It preserves the atmosphere necessary for contemplation. It is the bulwark of purity of heart. It protects the soul against movements of passion, against the temptations of the evil spirits. Overshadowed by the spiritual understanding of Scripture, the soul, gathered in silent recollection in its own depths, adores the Living God Who is present there. \"Thus\" says Cassian, \"the soul advances not only into the ark of the Covenant but into the priestly kingdom, and there, with a love unchanging in its purity, absorbed incontemplative prayer ( _spiritualibus disciplinis_ ), it fulfils the office of the High Priest who is commanded in the Law not to come out of the holy of holies... which is his own heart, where God promises to dwell at all times, saying 'I will dwell in them and walk among them.'\"[9]\n\nOver and over again in the Fourteenth Conference, on the spiritual understanding of Scripture, Cassian keeps telling us that this understanding goes hand in hand with purity of heart and with true contemplation. The Spiritual Master who attempts to teach this understanding of the Scriptures without having experienced it himself only multiplies vain words, learned though they may be. It is true that worldly, impure and proud men seem to possess this knowledge of the Scriptures, but it is a false science, a combination of rhetorical skill and academic subtleties. The Psalms, says Cassian, teach us the true path to the spiritual understanding of Scripture: the path of active purification and of meditation on the Law. When the Psalmist says that only those who are \"undefiled in the way\" can arrive at a spiritual understanding of the Law of God, he is saying that no one can reach this end \"unless he travel without fault in the way of Christ.\" We shall see later what the Fathers meant by the spiritual understanding of the Law.\n\nThis spiritual understanding of Scripture is acquired after meditation of the Scriptures in the silence of the night, and in solitude. But the fruit of the monk's private meditations is tasted in the recitation of the Psalms in choir. In order to preserve the contemplative character of the office, the number of Psalms was restricted to twelve and in between Psalms the monks prostrated themselves on the ground for brief periods of silent interior prayer. The \"office\" was deliberately kept simple, without ornament, without useless accretions, and the monks resisted the temptation to pile litanies upon litanies and prayers upon prayers, substituting quantity for quality. _Non enim multitudine versuum sed mentis intelligentia delectantur_. [10] \"They do not delight in the number of verses they recite but in the spiritual understanding with which they recite them.\" And he goes on, \"They hold it to be of greater importance to recite ten verses in an intelligent and orderly fashion than to rush through a whole Psalm in confusion of mind.\"\n\nIn the Ninth Conference, on prayer, Cassian goes into details about pure prayer and the need for detachment and interior recollection. He discusses the ordinary degrees of prayer. He gives a short commentary on the Our Father, the model of all prayer, and then turns to contemplative prayer, to which we are drawn if we make good use of vocal prayers and especially of the Our Father. This contemplative prayer has various degrees. Prayer is pure and perfect, according to the authority of St Anthony, when the contemplative no longer realizes that he is praying or indeed that he exists at all.[11]\n\nA lower degree of contemplation is one in which the effects of grace are more positively felt. Cassian has a picturesque name for it. He calls it the \"Prayer of Fire.\" It is the sort of prayer that characterises the flamelike movements of spiritual understanding stirred by the finger of God in the heart of the monk chanting the Psalms in recollection, with deep compunction, and with a sudden poignant realization of the concrete, intimate reality of the mercy of God, of the presence of Christ, of union with God, through Christ, in the Holy Spirit!\n\nCassian believed that this kind of spiritual understanding was supposed to be the ordinary fruit of vocal prayer, choral prayer, and of the Our Father. He interprets the Gospel references to Christ praying alone on the mountain, or in the Garden of the Agony, as implicit counsels of the Savior urging His followers to aspire to this perfect prayer. Yet the \"Prayer of Fire,\" he says, \"is known to few.\"\n\n_Soaring above every human sense, it is uttered not by the sound of the voice nor by the movement of the tongue nor by any formation of words. Filled and illumined with light from heaven, the mind does not utter this prayer in limited and human expressions, but with all its powers gathered together in unity it pours forth this prayer abundantly as from a most copious fountain and offers it up to God in a way beyond expression, telling Him so much in that brief moment of time that when we return to ourselves afterwards we are not able easily to state or even to go over in our minds all that took place_.[12]\n\n# 3:\n\n# _Meanings in Scripture_\n\nMANY OF THE PSALMS SEEM TO HAVE LITTLE OR nothing to do with contemplation. What do Og the King of Basan and Sehon the King of the Amhorrites have to offer the contemplative soul, the _anima sitiens Deum?_ [13] In many of the Psalms we seem to be incited to thirst not for God but for the blood of our enemies. We sometimes are invited to relax, not so much in the obscure experience of a merciful and loving Presence, as in the neolithic satisfaction with which \"the just man shall wash his hands in the blood of a sinner.\" When we are not joining in the war-cry of a race of savages, perhaps we are considering the history of that race's barbarity, its superstitions, lusts, its treacheries without number, all the prevarications that called down upon it the vengeance of a jealous God. Are we supposed to enter into the prayer of fire as we travel through a \"land polluted with blood\" in which the Children of Israel are engaged in sacrificing their sons and daughters to devils? [14]\n\nThe case against the Psalter would be devastating if we assumed that the Psalms were supposed to contain a system of precepts and techniques for the interior life like for instance the _Baghavad Gita_. Taking the Psalter as a whole, and in its relation to the rest of the Old Testament, we find that the spiritual wisdom contained in it is something quite different from anything to be found in the writings of pagan philosophers and mystics. Only a few of the Psalms are didactic in the ordinary sense of that word. And even when the Psalms do give us ethical precepts, these appear to be rather prosaic and down to earth in their practicality. \"Blessed the man who follows not the counsel of the ungodly, And enters not into the way of sinners, and sits not in the company of the insolent; But his delight is in the law of the Lord, and on his law he ponders day and night. And he is like a tree planted by running waters, That yields its fruit in due season, and whose leaves wither not, and whatsoever he does, prospers.\" [15] The Psalms themselves later on have to face the unpleasant question presented by the fact that the just man does not, in fact, always prosper. His leaf does fall off and he does not bear fruit, while the storehouses of the wicked are full, their sheep fruitful, their oxen fat and their daughters go about in jewels, as the Vulgate has it, \"sculptured like pillars of the temple.\" [16]\n\nYet although the literal meaning of the Psalter is sometimes glorious, sometimes bloody and sometimes simply sensible and prosaic the Psalms have, in fact, always formed contemplatives since the first days of the Church, and they have provided the constant basic spiritual nourishment of Catholic mysticism, along with the rest of Scripture. The Fathers of the Church and the contemplative saints, aware that their deepest experience of God was always somehow associated with the Liturgy and intimately dependent on the Psalms, have sometimes proceeded to argue, _a posteriori_ , that the true meaning of the Psalms was a hidden and allegorical meaning. This is what has sometimes been called the \"mystical\" sense of Scripture. The literal sense, with its battles, its triumphs, its agonies and its moralizing, is only an outer shell. The \"real\" meaning of the Psalms is held to be a spiritual kernel which must be arrived at by penetration of the \"letter.\" To cling to the literal meaning alone is, according to this line of thought, to miss the whole significance of the Psalms, for \"the letter killeth.\"\n\nA Catholic contemplative instinctively seeks something more than the testimony of individual mystics and saints about their experience of God. Catholic contemplation is essentially founded on dogmatic truth. It is more than a quest for the Absolute which can be satisfied by appropriate techniques of recollection. The Catholic mystic seeks, above all, the mind and truth of God. And he seeks it in the word of God. If he withdraws from the world and stands at the frontiers of eternity, it is because he somehow hopes to see God, or at least to hear His voice. If he calls out to God in prayer, it is because he desires an answer. And the answer he desires is not merely the voice of his own fancy, or the echo of another human experience like his own. It must be God's answer.\n\nThe Church urges us to seek above all the _theology_ that is revealed to us in Scripture. The true function of scriptural interpretation is to make clear the Truths that God has revealed to us about Himself and about His action in time and in human history. It is this above all that the contemplative will seek. It cannot be found without a healthy respect for the literal sense of the Bible. But all the other senses will have a certain importance.\n\nI do not intend to enter into a technical discussion of the various senses of Scripture here. The terminology itself would be infinitely confusing. It is enough to say that there are two senses in Scripture that are really vitally important for the contemplative. These are the _literal_ sense of Scripture, which is the meaning of the words of the text, and the _typical_ sense of Scripture which is the meaning of events narrated in the text. All the other senses of Scripture that have any theological value can be reduced to these two.\n\nThe miracle of the brazen serpent is recorded in the _Book of Numbers_. The literal sense of the passage simply records the miracle. It tells us what took place. The Children of Israel were complaining of the hardships they suffered in the Arabian desert. As a punishment for their complaints, they became the victims of \"fiery serpents\" which bit them and killed many. This brought about a prompt change of heart, and the people begged Moses to intercede for them and get rid of these snakes. At the command of God, Moses made a brazen serpent, and set it up for a sign and everyone who looked upon the sign was cured of his snake-bite. So much for the letter. But the event itself has a symbolic significance. It contains within itself a hidden truth, it points to another event. It is intended by God to signify this other reality. The miracle of Moses is called a \"type\" and the reality it signifies is called its \"antitype\". The full theological import of the miracle of the brazen serpent does not become clear to us until we see the type fulfilled in its antitype.\n\nBut who is to tell us the typical sense of any given passage of Scripture? God alone. Why? Because the typical sense of Scripture is a hidden sense, known only to the author of Scripture, who is God. Therefore if we are to find out the typical sense of any part of Scripture we must consult the Author of Scripture. How? In His revelation. That is to say that if the types in the Old Testament are to be made clear to us in their antitypes, this clarification must come from God Himself, either in some other passage of Scripture or in some other fount of revelation.\n\nIn the case of the brazen serpent there is no difficulty, because Jesus himself explained to Nicodemus that \"as Moses lifted up the brazen serpent in the desert, so must the Son of Man be lifted up: that whosoever believeth in Him may not perish, but may have life everlasting.\" [17] The Mystery hidden in the miracle of the brazen serpent is the Mystery of the Cross.\n\nThe Christian contemplative therefore can use this passage of the _Book of Numbers_ just as well as any passage in the New Testament as a fruitful subject of meditation. Indeed, this mysterious \"typology\" which everywhere compenetrates the Old Testament and New, accounts in large part for the contemplation the Fathers and Saints of the Church were able to draw from the Divine Office.\n\nNow we must never confuse \"typology\" and \"allegory.\" The typical sense of Scripture is not allegorical. In allegory there is only one reality, signified in improper terms. In typology there are two realities, one signifying the other. The abuse of Scriptural allegory in the Middle Ages has left a certain mark of opprobrium on the spiritual interpretation of the Bible. Some theologians, failing to make the proper distinctions, still believe that the \"typical\" sense of Scripture is to be distrusted. One of the characteristics of Counter-Reformation Catholic theology was a reaction against allegory and against a too independent interpretation of the Scriptures, in favor of the liturgical and critical study of the sacred texts. At the same time, the trend of modern thought away from symbolism has frustrated the basic human need for symbol and metaphor to the point of perversion: we have become instinctively suspicious of that for which we are starved. A world without imagination, which is no longer able to cope with the immaterial and which is incapable of the simplest efforts to link two terms of an analogy, condemns all symbolism as mystification. A superficial glance at the Scriptural allegories of some of the Fathers, or, for that matter, of the Talmud and the _midrashim_ , is enough to confirm these suspicions beyond hope of appeal. The \"spiritual sense\" of Scripture has, in fact, been stretched at times to excessive lengths. Often it has had no serious foundation in the despised \"letter.\" Obviously, a mystery that is drawn forth from what the letter does not say cannot be regarded as divine revelation. It comes not from God but from the exegete's own imagination. Very often, too, the extension of the spiritual sense has been over-estimated. Only a few texts in the Bible are clearly capable of a mystical interpretation.\n\nThe Jews had already developed an allegorical interpretation of the Old Testament before the Fathers of the Church began to produce systematic \"mystical\" commentaries along the lines of the Jewish _Midrashim_. The Jewish contemplative, Philo of Alexandria, paved the way for Origen, St Gregory of Nyssa, and for a long line of Christian exegetes. At the same time, the Gnostics had been interpreting the Old Testament in a figurative sense and their ideas were later taken up by the Manichaeans. Christian spiritual exegesis began to appear first of all in fragmentary fashion, in controversy against the Jews, Gnostics and other sects. It was the task of the Christian apologists of the second and third centuries to prove, against the Gnostics, that the two Testaments formed an organic unity and, against the Jews, that the Old Testament was incomplete and indeed incomprehensible without its fulfilment in the New. Proofs of this were found in the fulfilment of literal messianic prophecies and confirmed else where by mystical \"figures\" or \"types.\"\n\nThe discovery of these types in the Old Testament had characterized the exegesis of the Apostles and of Christ Himself, and we find the typical sense of the Old Testament affirmed everywhere in the New. Indeed, the first words uttered by St Peter on Pentecost when the Church, visibly filled with the fire of the Holy Ghost, first began to speak for herself, were an assertion of the fulfilment of the whole Old Testament in the death and resurrection of Jesus and the formation of the Church. St Peter told the Jews, who had gathered in Jerusalem from all parts of the world and who wondered at the fact that the Galilean disciples of Christ were speaking all the languages of the earth, that this very fact was a fulfilment of a messianic utterance of the prophet Joel. \"It shall come to pass in the last days, (saith the Lord) I will pour out my Spirit upon all flesh....\" The expression, \"the last days\" refers of course to the definitive establishment of the messianic kingdom, everywhere foretold in the Old Testament.\n\nSt Peter had no need to appeal to any hidden \"figure\" in the text he quoted from Joel. The charisms Joel had referred to were evidently verified. The Spirit had been poured out. The literal sense of the prophecy was plainly fulfilled before their eyes. But then St Peter went on from this to argue that if the Kingdom had come, if the \"last days,\" \"the fulness of time\" had now arrived, it must be because Jesus was the Messias. And in fact, Jesus Whom they had crucified had risen from the dead. He was the Son of God. It was His to pour out the Spirit of God upon the earth. All this, Peter reasoned, had been foretold of Christ in the Psalms. And here we come to the truly spiritual sense of Scripture. In the Psalms David speaks as if he were not to die, as if God were not to \"leave him in hell\" or allow him to \"see corruption.\" God was to raise up David, and make him sit at His right hand. And yet David was dead. David had not risen, nor had he ascended into heaven and his Kingdom had vanished from the earth. What was all this about victory over death, and about an everlasting Kingdom?\n\n\"Yemen, brethren,\" said St Peter, \"let me freely speak to you of the Patriarch David; that he died and was buried: and his sepulchre is with us to the present day. Whereas therefore he was a prophet and knew that God hath sworn to him with an oath that of the fruit of his loins one should sit upon his throne. Fore seeing this, he spoke of the resurrection of Christ. For neither was he left in hell, neither did his flesh see corruption.\" [18]\n\nThe Psalms were seen by the Apostles to be the utterances not only of David but of the future Christ. God Himself, Who spoke in David and Who was to become incarnate as the \"Son of David,\" was speaking of His own coming as the Christ. The \"mystical\" sense of Scripture shows us everywhere God gradually manifesting Himself in the world, manifesting not only His Divine Nature and attributes but also His plan for the salvation of men. The plan is finally made known in its fulfilment. It is only fully understood by those _in whom it is fulfilled_.\n\nOrigen and the exegetical School of Alexandria developed the spiritual interpretation of Scripture to a high degree of perfection and the influence of Origen was to extend down through the Christian Middle Ages in spite of the reaction of the School of Antioch. This school was somewhat suspicious of the freedom with which the \"mystical\" interpretation handled the Scriptures, and it returned to a more cautious emphasis on the \"letter.\"\n\nOne of the interesting implications of Origen's distinction between the \"letter\" and the \"spirit\" was the fact that the \"spiritual sense\" laid open its secrets only to those who were advanced, perfect in the spiritual life. It was therefore closely associated with sanctity and with _gnosis_ \u2014contemplation. The lavish use of Old Testament texts in a typological sense by the Church in her liturgy tended to confirm the Origenist tendency, without sanctioning all its exaggerations. At the same time, the Antiochian suspicion of the \"spiritual sense\" finally brought upon itself an open condemnation of extreme literalism in the interpretation of Scripture. The odore of Mopsuestia, who had commented on the Psalms and reduced the number of messianic \"types\" in the Psalter to an absolute minimum, was condemned by the second Council of Constantinople. Mopsuestus had maintained that only seven of the Psalms were messianic. Four were messianic in the literal sense and three in the typical sense. The real reason for his condemnation was his Nestorianism, of which this exegetical error was only a result and an expression.\n\nIt is interesting to notice that the merits of the spiritual and literal senses of Scripture are being debated today with almost as much heat as they were in the third and fourth centuries\u2014although perhaps the debate does not affect quite so many people, since it can be carried on without political repercussions!\n\nPaul Claudel, for instance, has come out as an ardent champion of the \"spiritual\" sense of the Scriptures and has himself commented on some of the books of the Old Testament\u2014Ruth, the Canticle of Canticles, and so on\u2014making a rather free and individual use of the old \"allegorical\" tradition. Claudel's commentaries have a value that is literary rather than exegetical. They make good reading, and they do us the service of recognizing the _poetic_ character of poetic books. But that does not mean that Claudel's beautiful intuitions into the poetic value of the text necessarily always penetrate to the real meaning of the inspired writer. Paul Claudel has simply rebelled against the stupidity and bad taste of a passing generation of commentators who have had a peculiar talent for burying essentials under useless details. What is the good of an erudition so short-sighted that it cannot even recognize the literary character of the book which it pretends to be studying? Can a poem be understood when it is treated merely as an archeological document? Yet when the poem is, in fact, ancient, we need more than the connatural affinity of poetic taste to get at its real meaning.\n\nOther interpreters of Scripture have gone too far in their reaction against rationalism and higher criticism. They have come out with an assertion that certain exegetical problems can only be solved by an appeal to a hidden, spiritual meaning, without any need for scientific scrutiny of the letter. The Holy See, which is driving ahead with full force toward a new critical edition of the Bible and which encourages every form of scientific study of the Scriptures has condemned this futile expedient.\n\nAt the same time, Pius XII, in his Encyclical _Divino Afflante Spiritu_ , has called our attention to the right use of the spiritual sense of Scripture and has once more urged interpreters of the Bible to return to the Fathers and make use of their labors in this matter. The most important task of the Scripture scholar, Pius XII says, is to discover and to expound the real meaning of the books which the Church believes to have God for their Author. The study of ancient languages, of biblical archeology and history, the use of all the modern critical apparatus which explores the texts and versions of the Bible, has only one end: to lead us to a deeper and more accurate understanding of what God has revealed, for our salvation. The chief task of the exegete is, of course, to discover the literal sense of the Scriptures. Without that, \"typology\" would be a pure illusion. Nevertheless, the Holy Father regrets the fact that so many commentaries have applied themselves almost exclusively to matters belonging to \"the historical, philological and other auxiliary sciences.\" The Church desires above all that the full content of revelation be made known, and this in such a way that it may be accessible to everyone. Now the full theological meaning of the Bible, as Pius XII clearly indicates in the encyclical we are discussing, is not arrived at without an understanding of the spiritual sense. Even though the letter of Scripture contains in itself enough to nourish a deep interior life, we must also understand the spiritual sense, and here Pius XII gives a simple description of what the \"mystical\" sense of Scripture really is:\n\n_What was done and said in the Old Testament was ordained and disposed by God with such consummate wisdom that things past prefigured in a spiritual way those that were to come under the new dispensation of grace. Wherefore the exegete, just as he must search out and expound the literal meaning of the words intended and expressed by the sacred writer, so also must he do likewise for the spiritual sense, provided it is clearly intended by God. For God alone could have known this spiritual meaning and could have revealed it to us. Now our Divine Saviour Himself points out to us and teaches this same sense in the Holy Gospel; the Apostles also, following the example of the Master, profess it in their spoken and written words; the unchanging tradition of the Church approves it; finally the most ancient usage of the liturgy proclaims it, wherever may be rightly applied the well-known principle_ , The rule of prayer is the rule of faith. _Let Catholic exegetes then disclose and expound this spiritual significance, intended and ordained by God, with that care which the dignity of the divine word demands; but let them scrupulously refrain from proposing as the genuine meaning of Sacred Scripture other figurative senses_.[19]\n\nAn important aspect of the mystical sense of Scriptures was developed by the Fathers of the Alexandrian school. This was the application ofthe figures of the Old Testament to the interior life of the soul in whom the Kingdom of God has come through the charity, poured out by the Spirit sent by Christ. According to this moral sense already indicated in the Epistles of St. Paul, the realities externally fulfilled in the Mystery of Christ are also fulfilled at the same time, in their own appropriate way, in the souls of those who have entered into that mystery and whose life is Christ.\n\nThe writers of the New Testament everywhere assert that the _pascha Christi_ , the descent of the Word of God into the world, His death on the Cross, His resurrection and ascent into heaven, opening heaven to the sons of men, is the fulfilment of the \"type\" which was the exodus of the Jews out of Egypt. Already the prophets of the Old Testament had seen in this exodus a prophecy of the return of the Jews from that other captivity, in Babylon. The Christians themselves saw the return from Babylon to Jerusalem as a type of the messianic kingdom, the establishment of the Church. After all, was not Jerusalem destroyed, and were not the Jews scattered to the ends of the earth? One might well argue, in the same way, that the Church herself has always been subject to attack and is never too secure in this world. But the Church herself looks ahead to a final and definitive fulfilment of the \"Exodus\" when all the redeemed shall ascend in glory to heaven and time shall be no more.\n\nMeanwhile, we are passing through the desert on our way to the promised land.\n\nNow what is already fulfilled in Christ, in the Church and in her sacraments, finds its realization in each individual soul who, by the sacraments, enters upon and lives the \"mystery of Christ,\" the _pascha Christi_. Hence the spiritual interpretation of Scripture discovers an evident continuity between the first born of the Jews spared by the exterminating angel because of the blood of the paschal lamb, Jesus the first born of a new humanity, conquering death by His own blood, and finally the Christian, marked by the Blood of this true Lamb of God in the sacrament of baptism which \"buries him in the death of Christ.\" [20] The univocal character of grace in the old law and the new\u2014since all grace and all sanctification come from Christ\u2014guarantees an essential likeness between the experience of the chosen people in the desert, the experience of the prophets who not only foretold Christ but prefigured Him, the experience of Christ Himself, and finally the experience of the saints mystically united to Christ. All these are the work of one Spirit who reveals to us in Scripture His pattern, His mode of action and the fulfilment of His plan. In those who accept the \"word of the Cross\" that is preached to them, the same Holy Spirit begins at once to work the mystery of the Cross. The initial act of faith which admits us, by grace, into the divine mysteries foreshadowed and worked out in the Scriptures, reproduces in us the death of Christ and His resurrection from the dead. Even from the psychological view point the act of faith is like a passage through the Red Sea and a journey, nourished by miraculous food, through the blighted heart of a land without vegetation. As we grow in faith, the mystery of Exodus, and the _pascha Christi_ tend to become more and more a matter of experience in our lives. Nevertheless the experience itself is not the important thing: it is only the accidental effect of a deeper theological reality, and this reality is infinitely beyond experience, _it is God Himself in us_.\n\nUltimately, the spiritual understanding of Scripture leads to a mystical awareness of the Spirit of God Himself living and working in our own souls, carrying out, by His mysterious power, in our own lives, the same salvific actions which we can see prefigured and then realized in the Old and New Testaments. This was the profound truth on which St John of the Cross could base his whole mystical theology, which, as we have shown elsewhere, is entirely centered in and dependent upon the mystery of Christ. [21]\n\nBut it must be remembered that this experience itself is only accessory and accidental. The substantial reality of our spiritual life is nourished and maintained by faith, hope and love through the instrumentality of the Seven Sacraments. These Sacraments are the prolongation, in the New Law, of the \"mighty works of God\" in the Old. The whole sacramental and liturgical life of the Church not only contemplates the wonders of God in the Old Testament, not only comments on them, explains them, re-enacts them but actually lives them and fulfils them.\n\nThe Church is made up of living individual men. It is a kind of \"mystical person\" composed of many persons who are one in Christ and who share His own divine life. The mystical sense of Scripture is then not merely something which the Church _studies_ but something which the Church _lives_ and _is_. But this cannot be so unless we, who are the Church, experience in our lives the mystery of Christ. That is why the Liturgy would have us constantly go back to the beginning and work our way down to what we are through the types and figures which foreshadowed the whole Christ, the Head and the Members, the Jesus Who died on Calvary and Who lives in us, Who dies in us that others may live in Him.\n\nThe fruitful use of the Liturgy then can be summed up in this experience of the Mystery of Christ. Liturgical prayer does not endeavor to raise us up to something we are not: it reminds us that we have already been to some extent transformed: it assures us that the beginnings of transformation are a pledge and foreshadowing of its completion. The spiritual understanding of the Psalter will therefore not introduce us to some esoteric technique of prayer, nor will it tempt us to induce within our minds some peculiar psychological state. It will, above all, tell us not merely what we ought to be but the unbelievable thing that we already _are_. It will tell us over and over again that we are Christ in this world, and that He lives in us, and that what was said of Him has been and is being fulfilled in us: and that the last, most perfect fulfilment of all is now, at this moment, by the theological virtue of hope, placed in our hands. Thus the liturgy of earth is necessarily one with the liturgy of heaven. We are at the same time in the desert and in the Promised Land. The Psalms are our Bread of Heaven in the wilderness of our Exodus.\n\n# 4:\n\n# _Songs of the City of God_\n\nWE HAVE ONLY ONE MASTER OF THE SPIRITUAL life, one Master in the ways of prayer: Christ. _Unus est Magister Vester, Christus_. The Church, the Mystical Body of Christ, continues His teaching and sanctifying office among us. She has the aim, obligation and function of bringing all men to the knowledge, love and contemplation of God and of \"restoring all things in Christ\" Who is the light of the world. The Church is therefore entrusted with the greatest of all functions: that of fulfilling the whole purpose of God in creating the universe and in creating man. The whole meaning of human existence is in the hands of the Church, man's fate depends on her Sacraments, her Liturgy and her priesthood. But the teaching and sanctifying power of the Church are inseparable from her jurisdiction. She teaches and administers the Sacraments by virtue of an authority divinely committed to her, and she has the power to support her teaching and her ritual with doctrinal pronouncements and disciplinary decrees.\n\nIf we are ever to become contemplatives, we must be formed, remotely or more directly, by all these. The Church and no other can rightly direct and dispose us to mystical prayer. She it is who must guide us in our understanding of Scripture as well as in our use of the inspired text for our liturgical prayer. But at the same time it is she who protects us in our interior liberty, defends us against the tyranny of restricted human systems and \"schools of spirituality\" that might tend to narrow us down to a particular esoteric outlook and leave us something less than Catholics.\n\nHer Liturgy is at once a safe and universal school of contemplation. Why? Because the Church is guided by the Spirit of God Who embraces all in His infinite simplicity. The Holy Ghost is her life and He is also the source and mover of her prayer. The Holy Ghost prays in the Liturgy and when we pray with the Liturgy the Holy Ghost, the Spirit of Christ, prays in us. He teaches us how to pray by praying in us. He not only gives us words to say and sing, He also sings them in our hearts. And when, as must inevitably happen, we fall far short of understanding or appreciating what the prayers mean, the Spirit of God \"helps our weakness,\" asking on our behalf, with a fervor of infinite love we shall never be able to comprehend.\n\n\"The things that are of God no man knoweth, but the Spirit of God,\" says St Paul. \"Now we have received not the spirit of this world but the Spirit that is of God that we may know the things that are given us from God.\" [22] This text tells us quite evidently not only that all our contemplation is a work produced in us by the Holy Spirit, but also that the Holy Ghost teaches us contemplation in the Scriptures which He Himself inspired, because the revealed word of God is one of the most important of \"the things that are given us from God.\" It is the Holy Ghost, then, who will lead us to contemplation by opening to us the depths of meaning hidden in the Psalms. We have received this Holy Spirit in Baptism. Our progress in the supernatural life, which is also the life of interior prayer, normally means a progressive _revelation_ of God, to us, in our souls and in all His gifts to us.\n\nThe Mass, which is the central Mystery of the whole Christian economy, since it is the Sacrifice in which Christ offers Himself to the Father for the sins of the world, is the center of the Liturgy. But by means of the Sacraments, Sacramentals and above all of the Divine Office, the Church seeks to vivify every moment of the Christian's day and every department of his life with the streams of grace and truth which flow into our souls from Christ's Cross. Pope Pius XII, in his Encyclical on the Liturgy [23] speaks of this great work of sanctification in terms which suggest, to anyone familiar with Christian mystical tradition, that contemplation is the normal fulfilment of the liturgical life, for he says: \"The ideal of the Christian life is that each one be united to God in the closest and most intimate manner.\" The Holy Father continues:\n\n_For this reason the worship that the Church renders to God and which is based especially on the Eucharistic Sacrifice and the use of the Sacraments, is directed and arranged in such a way that it embraces, by means of the Divine Office, the hours of the day, the weeks and the whole cycle of the year, and reaches all the aspects and phases of human life_.[24]\n\nIn the same encyclical, Pope Pius XII describes the interior activity of a soul engaged in liturgical prayer, showing how an active participation in the Liturgy brings about union with God. He says:\n\n_It is not merely a question of recitation or of singing which, howeverperfect according to the norms of music and the sacred rites only reaches the ear, but it is especially a question of the ascent of the mind and the heart to God so that, united with Christ, we may completely dedicate ourselves and all our actions to Him_.\n\nFor the Psalms to fulfil the function Christian tradition has always demanded of them, which is to dispose the souls of men for union with God, they must not only \"raise the minds and hearts of men to God\" but they must inspire us to give ourselves entirely to God. Finally, most important of all, this gift of ourselves must be made in Christ and with Christ. Our sacrifices have no supernatural value except in so far as they are united with the One Sacrifice which alone is acceptable to God and infinitely pleasing in His sight.\n\nThere is a contemplation proper to the metaphysician, in which the mind of man can rest in a pure but abstractive intuition of an \"Infinite Being.\" This is not what Christianity means by \"raising the mind and heart to God.\" Christianity is not content with finding God in His immanence\u2014as He is present in the metaphysical depths of everything that is\u2014it also seeks Him in His infinite transcendence. He is so far above all being that He cannot be said to \"be\" in the same sense as contingent beings. No system of asceticism, no mystical cult, however esoteric, however pure, can suffice to bridge the abyss between us and this Transcendent Creator of all being. And yet He is our Creator and our Father, and we can speak to Him and hear Him answer us. How? Because He has revealed Himself to us in our own language and has given us human words in which to praise and pray to Him. More than that, He descends into our sphere and takes part in our own life. He has manifested Himself not only in creation, not only in revelation, but in the divine and mysterious acts by which He has entered into human history and appropriated it to Himself, so that Christ's Cross has become the key to a history whose purpose is to separate the City of God from the city of this world, which has Babylon for its symbolic name.\n\nThe Psalms are the songs of this City of God. They are therefore the voice of the Mystical Body of Christ. They are the songs of Christ. They are the songs of God in this world. Singing them, we become more fully incorporated into the mystery of God's action in human history.\n\nPope Pius XII emphasizes this traditional Catholic doctrine in his _Mediator Dei_ :\n\n_By assuming human nature, the Divine Word introduced into this exile a hymn which is sung in heaven for all eternity. He unites to Himself the whole human race and with it sings this hymn of praise to God_.\n\nIn this same passage, the Holy Father illustrates his statement with a quotation from St Augustine's commentary on the Psalms. No theologian has ever set forth the doctrine of the Mystical Body of Christ with such clarity and in such detail as St Augustine who is, in every respect, the most Catholic of the Fathers, for his theological horizons are never narrowed down to anything less comprehensive than the \"Whole Christ.\" Not only in his _City of God_ , but precisely in his exegesis of the Psalms, St Augustine lays open to us the Mystery of our union with God in Christ. There above all he shows us that the Liturgy is the voice of Christ.\n\nWhat could be more evident than the words of Pius X in his _Motu Proprio_ of 1903? In contemplation, as in everything else that is Christian, \"the Liturgy is the primary and indispensable source of the genuine Christian spirit.\"\n\n# 5:\n\n# _Errors to Avoid_\n\nIF A CONTEMPLATIVE WERE TO REGARD THE Mass and Office as secondary in his interior life, he would run a serious risk of coming to a standstill in his prayer, and even of falling into illusion. But here a distinction must be made. It must be admitted that the individual vocation to contemplative prayer is conditioned by individual temperament, and that there will always be souls who will usually find a deeper conscious peace and absorption in the presence of God when they are silent and alone than when they are praying in choir. Generally speaking\u2014and here we follow the authority of St John of the Cross\u2014the soul called by God to infused contemplation is by that very fact called to a state of \"restful tranquillity in which it is abundantly infused with the spirit of Divine wisdom, which is the loving, tranquil, lonely, peaceful, sweet, inebriator of the spirit. Hereby the soul feels itself to be gently and tenderly wounded and ravished, knowing not by whom, nor whence, nor how.\"[25]\n\nIt is important for such souls to realize that the graces of the Office actually nourish and stimulate this solitary contemplation. After chanting the Psalms in choir they will be more surely and sweetly drawn than ever, to this intimate absorption in God and the more fervent they have been in the chanting of God's praises in choir, the greater fruit will they draw, as a result, from the silent communion in which the Holy Spirit inspires them to prolong their prayer after the Office has ended. St Benedict did not expect all his monks to receive such graces but he explicitly legislated to protect those who did, and to keep them from being distracted by their more active brethren.[26]\n\nThe heart of contemplative prayer is a selflessness that assimilates the soul to God and enables it to receive those supernatural \"touches\" of grace by which it becomes aware of God, as He is in Himself, not through the medium of ideas and species, which cannot perfectly represent Him as He is in Himself, but in the immediate contact of obscure love. The secret of contemplation is the gift of ourselves to God. This, too, is the secret of the Psalter. God will give Himself to us through the Psalter if we give ourselves to Him without reserve, in our recitation of the Psalms. This implies three things: a pure faith and an intense desire of love and above all a firm hope of finding God hidden in His revealed word. To say this is only to say that the worthy chanting of the Divine Office involves a constant and perfect exercise of the theological virtues which are the only path to contemplative prayer.\n\n# 1:\n\n# _Poetry, Symbolism & Typology_\n\nTHE PSALMS ARE POEMS, AND POEMS HAVE A meaning\u2014although the poet has no obligation to make his meaning immediately clear to anyone who does not want to make an effort to discover it. But to say that poems have meaning is not to say that they must necessarily convey practical information or an explicit message. In poetry, words are charged with meaning in a far different way than are the words in a piece of scientific prose. The words of a poem are not merely the signs of concepts: they are also rich in affective and spiritual associations. The poet uses words not merely to make declarations, statements of fact. That is usually the last thing that concerns him. He seeks above all to put words together in such a way that they exercise a mysterious and vital reactivity among themselves, and so release their secret content of associations to produce in the reader an experience that enriches the depths of his spirit in a manner quite unique. A good poem induces an experience that could not be produced by any other combination of words. It is therefore an entity that stands by itself, graced with an individuality that marks it off from every other work of art. Like all great works of art, true poems seem to live by a life entirely their own. What we must seek in a poem is therefore not an accidental reference to something outside itself: we must seek this inner principle of individuality and of life which is its soul, or \"form.\" What the poem actually \"means\" can only be summed up in the whole content of poetic experience which it is capable of producing in the reader. This total poetic experience is what the poet is trying to communicate to the rest of the world.\n\nIt is supremely important for those who read the Psalms and chant them in the public prayer of the Church to grasp, if they can, the poetic content of these great songs. The poetic gift is not one that has been bestowed on all men with equal lavishness and that gift is unfortunately necessary not only for the writers of poems but also, to some extent, for those who read them. This does not mean that the recitation of the Divine Office is an aesthetic recreation whose full possibilities can only be realized by initiates endowed with refined taste and embellished by a certain artistic cultivation. But it does mean that the type of reader whose poetic appetites are fully satisfied by the Burma Shave rhymes along our American highways may find it rather hard to get anything out of the Psalms. I believe, however, that the reason why so many fail to understand the Psalms\u2014beyond the fact that they are never quite at home even with Church Latin\u2014is that latent poetic faculties have never been awakened in their spirits by someone capable of pointing out to them that the Psalms really are poems.\n\nSince, then, they are poems, the function of the Psalms is to make us share in the poetic experience of the men who wrote them. No matter how carefully and how scientifically we may interpret the words of the Psalms, and study their historical background, if these investigations do not help us to enter into the poetic experience which the Psalms convey, they are of limited value in showing us what God has revealed in the Psalms, for the revealed content of the Psalter is _poetic_. Let it therefore be clear, that since the inspired writer is an instrument of the Holy Spirit, who, according to the Catholic Faith, is the true Author of the Psalms, what is revealed in the Psalter is revealed in the _poetry_ of the Psalter and is only fully apprehended in a poetic experience that is analogous to the experience of the inspired writer. However, when I speak of the poetry of the Psalter and the content conveyed by its poetic form, I do not mean to imply that it is necessary for everyone to read or recite the Psalms in their original Hebrew, in which alone they possess their authentic and integral artistic form. I imagine that every contemplative would, at some time or other, wish that he could chant the Psalms in the same language in which they were chanted by Jesus on this earth, and in which He quoted them when He was dying on the Cross! This is a longing that very few of us will ever be able to satisfy. But it is accidental.\n\nActually, the simplicity and universality of the Psalms as poetry makes them accessible to every mind, in every age and in any tongue and I believe that one's poetic sense must be unusually deadened if one has never at any time understood the Psalms without being in some way moved by their deep and universal religious quality.\n\nThe Psalms are more than poems: they are _religious_ poems. This means that the experience which they convey, and which the reader must try to share, is not only a poetic but a religious experience. Religious poetry\u2014as distinct from merely devotional verse\u2014is poetry that springs from a true religious experience. I do not necessarily mean a mystical experience. Devotional poetry is verse which manipulates religious themes and which does so, perhaps, even on a truly poetic level. But the experiential content of the poem is at best poetic only. Sometimes it is not even that. Much of what passes for \"religious\" verse is simply the rearrangement of well known devotional formulas, without any personal poetic assimilation at all. It is a game, in which souls, no doubt sincere in their piety, play poetic checkers with a certain number of familiar devotional clich\u00e9s. This activity is prompted by a fundamentally religious intention, if the poem be written for the glory of God or for the salvation of souls. But such poems rarely \"save\" any souls. They flatter those who are comfortably \"saved\" but irritate the ones who really need salvation. A truly religious poem is not born merely of a religious purpose. Neither poetry nor contemplation is built out of good intentions. Indeed, a poem that springs from no deeper spiritual need than a devout intention will necessarily appear to be at the same time forced and tame. Art that is simply \"willed\" is not art, and it tends to have the same disquieting effect upon the reader as forced piety and religious strain in those who are trying hard to be contemplatives, as if infused contemplation were the result of human effort rather than a gift of God. It seems to me that such poetry were better not written. It tends to confirm unbelievers in their suspicion that religion deadens instead of nurtures all that is vital in the spirit of man. The Psalms, on the other hand, are at the same time the simplest and the greatest of all religious poems.\n\nNo one will question the truly religious content of the Psalms. They are the songs of men\u2014and David was the greatest of them\u2014for whom God was more than an abstract idea, more than a frozen watchmaker sitting in his tower while his universe goes ticking away into space without him. Nor is the God of the Psalms simply an absolute, immanent Being spinning forth from some deep metaphysical womb an endless pageantry of phenomena. The Psalms are not incantations to lull us to sleep in such a one.\n\nThe human symbolism of the Psalter, primitive and simple as it is, should not deceive us into thinking that David had an \"anthropomorphic\" God. Such a mistake could only be made by materialists who had lost all sense of poetic form and who, moreover, had forgotten the violent insistence of the great Jewish prophets on the transcendence, the infinite spirituality of Jaweh, Who was so far above all things imaginable that He did not even have an utterable name. The God of the Psalter is \"above all gods,\" that is to say, above anything that could possibly be represented and adored in an image. To one who can penetrate the poetic content of the Psalter, it is clear that David's concept of God was utterly pure. And yet this God, Who is \"above all the heavens\" is \"near to those who call upon Him.\" He Who is above all things is also in all things, and He is capable of manifesting Himself through them all.[27]\n\nThe men who wrote the Psalms were carried away in an ecstasy of joy when they saw God in the cosmic symbolism of His created universe.\n\n_The heavens declare the glory of God, and the firmament proclaims the work of his hands_.\n\n_Day unto day heralds the message, and night unto night makes it known_.\n\n_There is no speech nor words, whose voice is not heard_ :\n\n_Their sound goes forth unto all the earth, and their strains unto the farthest bounds of the world_.\n\n_There he has set his tabernacle for the sun, which like to the bridegroom coming out from the bridal chamber, he exults like a giant to run his course_.\n\n_His going forth is from one end of the heavens, and his circuit ends at the other_ . . . [28]\n\n_Praise ye the Lord from the heavens, praise ye him in the high places_.\n\n_Praise ye him, all his angels, praise ye him, all his hosts_.\n\n_Praise ye him, O sun and moon, praise him, all ye shining stars_.\n\n_Praise him, ye heavens of heavens, and ye waters that are above the heavens_ :\n\n_Let them praise the name of the Lord, for he commanded and they were created_ ,\n\n_And he established them for ever and ever: he gave a decree, which shallnot pass away_.\n\n_Praise the Lord from the earth, ye sea-monsters and all ye depths of the sea_.\n\n_Fire and hail, snow and mist, stormy wind, that fulfil his word_ ,\n\n_Mountains and all hills, fruitful trees and all cedars_ ,\n\n_Beasts and all cattle, serpents and feathered fowls_ ,\n\n_Kings of the earth and all people, princes and all judges of the earth_ ,\n\n_Young men and even maidens, old men together with children_ :\n\n_Let them praise the name of the Lord, for his name alone is exalted_ ;[29]\n\nAlthough we tend to look upon the Old Testament as a chronicle of fear in which men were far from their God, we forget how many of the patriarchs and prophets seem to have walked with God with some of the intimate simplicity of Adam in Eden. This is especially evident in the first days of the Patriarchs, of which the Welsh metaphysical poet Henry Vaughan, speaks when he says:\n\n_My God, when I walke in those groves,  \nAnd leaves thy spirit doth still fan,  \nI see in each shade that there growes  \nAn Angell talking with a man  \nUnder a juniper some house,  \nOr the coole mirtles canopie,  \nOthers beneath an oakes greene boughs,  \nOr at some fountaines bubling Eye;  \nHere Jacob dreames, and wrestles; there  \nElias by a Raven is fed,  \nAnother time by th' Angell, where  \nHe brings him water with his bread;  \nIn Abr'hams Tent the winged guests  \n(O how familiar then was heaven!)  \nEate, drinke, discourse, sit downe, and rest  \nUntill the Coole, and shady even;\"_\n\nAs age succeeded age the memory of this primitive revelation of God seems to have withered away, but its leaf is still green in the Psalter. David is drunk with the love of God and filled with the primitive sense that man is the _Leitourgos_ or the high priest of all creation, born with the function of uttering in \"Liturgy\" the whole testimony of praise which mute creation cannot of itself offer to its God.\n\nThe function of cosmic symbols in the Psalter is an important one. The revelation of God to man through nature is not the exclusive property of any one religion. It is shared by the whole human race and forms the foundation for all natural religions.[30] At the same time the vision of God in nature is a natural preamble to supernatural faith, which depends upon distinct and supernatural revelation. Hence even those modern readers who may be repelled by the \"historical\" Psalms, will nevertheless be attracted by those in which the keynote is struck by cosmic symbolism, and by the vision of God in nature.\n\nHowever, the cosmic symbolism in the Old Testament is something much more than an element which Judaeo-Christian revelation shares with the cults of the Gentiles. The Old Testament writers, and particularly the author of the creation narrative that opens the _Book of Genesis_ , were not only dealing with symbolic themes which had made their appearance in other religions of the Near East: they were consciously attempting to purify and elevate the cosmic symbols which were the common heritage of all mankind and restore to them a dignity of which they had been robbed by being degraded from the level of theistic symbols to that of polytheistic myths.\n\nThis question is so important that I hope I may be permitted a brief digression in order to touch upon it.[31]\n\nEveryone knows with what enthusiasm the rationalists of the late nineteenth century berated the Judaeo-Christian revelation for being fabricated out of borrowed materials, because the religious themes and symbols of the Old Testament were similar to those of many other Eastern religions, and because the New Testament made use of language and concepts which bore a great resemblance to the formulas of Platonic philosophy, the ritual language of the mystery cults and the mythological structure of other Oriental beliefs. Even today the world is full of honest persons who suppose that this parallelism somehow weakens the Christian claim to an exclusive divine revelation. The writers of the Old and New Testament were simple men, but St John the Evangelist was certainly not so simple as to imagine that the Greek word _logos_ , which he may well have borrowed from the Platonists, was a personal discovery of his own. The fact that the Biblical writers were inspired did not deliver them from the common necessity which compels writers to clothe their ideas in words taken from the current vocabulary of their culture and of their time. When God inspired the author of _Genesis_ with the true account of the creation of the world, the writer might, by some miracle, have set the whole thing down in the vocabulary of a twentieth century textbook of paleontology. But that would have made _Genesis_ quite inaccessible to anyone except a twentieth century student of paleontology. So instead, the Creation narrative was set down in the form of a poem which made free use of the cosmic symbolism which was common to all primitive mankind.\n\nLight and darkness, sun and moon, stars and planets, trees, beasts, whales, fishes and birds of the air, all these things in the world around us and the whole natural economy in which they have their place have impressed themselves upon the spirit of man in such a way that they naturally tend to mean to him much more than they mean in themselves. That is why, for example, they enter so mysteriously into the substance of our poetry, of our visions and of our dreams. That too is why an age, like the one we live in, in which cosmic symbolism has been almost forgotten and submerged under a tidal wave of trademarks, political party buttons, advertising and propaganda slogans and all the rest\u2014is necessarily an age of mass psychosis. A world in which the poet can find practically no material in the common substance of every day life, and in which he is driven crazy in his search for the vital symbols that have been buried alive under a mountain of cultural garbage, can only end up, like ours, in self-destruction. And that is why some of the best poets of our time are running wild among the tombs in the moonlit cemeteries of surrealism. Faithful to the instincts of the true poet, they are unable to seek their symbols anywhere save in the depths of the spirit where these symbols are found. These depths have become a ruin and a slum. But poetry must, and does, make good use of whatever it finds there: starvation, madness, frustration and death.\n\nNow the writers of the Bible were aware that they shared with other religions, the cosmic symbols in which God has revealed Himself to all men. But they were also aware that pagan and idolatrous religions had corrupted this symbolism and perverted its original purity [32]. The Gentiles had \"detained the truth of God in injustice\" [33] and \"changed the truth of God into a lie.\"[34]\n\nCreation had been given to man as a clean window through which the light of God could shine into men's souls. Sun and moon, night and day, rain, the sea, the crops, the flowering tree, all these things were transparent. They spoke to man not of themselves only but of Him who made them. Nature was symbolic. But the progressive degradation of man after the fall led the Gentiles further and further from this truth. Nature became opaque. The nations were no longer able to penetrate the meaning of the world they lived in. Instead of seeing the sun a witness to the power of God, they thought the sun was god. The whole universe became an enclosed system of myths. The meaning and the worth of creatures invested them with an illusory divinity.\n\nMen still sensed that there was something to be venerated in the reality, in the peculiarity of living and growing things but they no longer knew what that reality was. They became incapable of seeing that the goodness of the creature is only a vestige of God. Darkness settled upon the translucent universe. Men became afraid. Beings had a meaning which men could no longer understand. They became afraid of trees, of the sun, of the sea. These things had to be approached with superstitious rites. It began to seem that the mystery of their meaning, which had become hidden, was now a power that had to be placated and, if possible, controlled by magic incantations.\n\nThus the beautiful living things which were all about us on this earth and which were the windows of heaven to every man, became infected with original sin. The world fell with man, and longs, with man, for regeneration. The symbolic universe, which had now become a labyrinth of myths and magic rites, the dwelling place of a million hostile spirits, ceased altogether to speak to most men of God and told them only of themselves. The _symbols_ which would have raised man above himself to God now became _myths_ and as such they were simply projections of man's own biological drives. His deepest appetites, now full of shame, became his darkest fears.\n\nThe corruption of cosmic symbolism can be understood by a simple comparison. It was like what happens to a window when a room ceases to receive light from the outside. As long as it is daylight, we see through our windowpane. When night comes, we can still see through it, if there is no light inside our room. When our lights go on, then we only see ourselves and our own room reflected in the pane. Adam in Eden could see through creation as through a window. God shone through the windowpane as bright as the light of the sun. Abraham and the patriarchs and David and the holy men of Israel\u2014the chosen race that preserved intact the testimony of God\u2014could still see through the window as one looks out by night from a darkened room and sees the moon and stars. But the Gentiles had begun to forget the sky, and to light lamps of their own, and presently it seemed to them that the reflection of their own room in the window was the \"world beyond.\" They began to worship what they themselves were doing. And what they were doing was too often an abomination. Nevertheless, something of the original purity of natural revelation remained in the great religions of the East. It is found in the _Upanishads_ in the _Baghavad Gita_. But the pessimism of Buddha was a reaction against the degeneration of nature by polytheism. Henceforth for the mysticisms of the East, nature would no longer be symbol but illusion. Buddha knew too well that the reflections in the window were only projections of our own existence and our own desires, but did not know that this was a window, and that there could be sunlight outside the glass.\n\nSo much, then, for cosmic symbols. In the Psalms we find them clean and bright again, where David sings:\n\n_O Lord, our Lord, how glorious is thy name in all the earth, thou who hast exalted thy majesty above the heavens_...\n\n_When I gaze at the heavens, the work of thy fingers, the moon and stars, which thou hast made_ :\n\n_What is man, that thou are mindful of him? or the son of man, that thou hast care of him?_\n\n_And thou hast made him a little lower than the angels, thou hast crowned him with glory and honor;_\n\n_Thou hast given him dominion over the works of thy hands; thou hast put all things under his feet_ :\n\n_Sheep and oxen, all of them, and the beasts of the field, too_ ,\n\n_The birds of the heaven and the fishes of the sea: and whatever traverses the paths of the seas_.\n\n_O Lord, our Lord, how wonderful is thy name in all the earth!_ [35]\n\nBut it is not the cosmic symbolism that is the most important symbolism in the Bible. There is another. This is the symbolism we have already referred to as _typology_. The typological symbolism of the Bible is not common to other religions: its content is peculiar to the Judaeo-Christian revelation. It is the vehicle of the special message, the \"Gospel\" which is the very essence of Christian revelation. And it is typology above all that makes the Psalms a body of religious poems which are, by their own right, altogether unique.\n\nI have already brought up the subject of the typical sense of the Psalter. I have discussed the significance of type and antitype, and suggested briefly that the important antitypes in Scripture all have something to do with the Incarnation of the Word of God, and with man's Redemption by the Sacrifice of Christ on Calvary, for this is the central Mystery of the Christian faith. It is now time to add a few remarks on the importance of typology in the Psalms.\n\nPope Pius XII said, we remember, that \"By assuming human nature, the Divine Word introduced into this exile a hymn which is sung in heaven for all eternity.\" The context of this important declaration suggested to us that if the Psalter and the Liturgy can become for us means to contemplation, it is simply because they are capable of uniting us with Christ in this \"hymn which is sung in heaven.\" That is as much as to say that if the Psalter is to lead us to contemplation we must know how to find Christ in the Psalms. Apart from a few clear messianic prophecies it is typology that reveals Christ to us, even in some of the most unexpected lines of the Psalms.\n\nScriptural typology is a special kind of symbolism. It is something far purer and more efficacious than allegory. I would even add that in the Psalms allegory is altogether negligible. There is almost nothing in the Psalter that reminds us of the tissue of allegorical complexities which goes to make up a poem like Spenser's _Faerie Queene_. It seems to me that the personification of moral abstractions is foreign to the spirit of true contemplation.\n\nThe relation of types and antitypes in Scripture is a special manifestation of God: it is the testimony of His continuous providential intervention in human history. Unlike the universal cosmic symbols, which repeat themselves over and over with the seasons, historical and typical symbols are altogether singular. Cosmic symbols reflect the action of God like the light of the sun on the vast sea of creation. Typological symbols are meteors which divide the dark sky of history with a sudden, searing light, appearing and vanishing with a liberty that knows no law of man. Cosmic symbolism is like clouds and rain: but typology is like a storm of lightning wounding the earth unpredictably with fire from heaven.\n\nConsider for a moment the typology of the Deluge. In the Deluge, God purifies the world, destroying sin. The Deluge is simply a type of the one great redemptive act in which God destroyed sin: Christ's passion and death. But the symbolism of the Deluge goes further: it also manifests to us the activity of God destroying sin in the souls of individuals by the sacraments, for instance Baptism and Penance, in which the merits of Christ's Passion are applied to our souls. This also corresponds to another Old Testament type: the crossing of the Red Sea by the people of Israel. Finally, all these symbols are tied together in one, final, climax of significance. All Scriptural types point to the last end, the crowning of Christ's work, the establishment of His Kingdom, His final and manifest triumph in His mystical body: the Last Judgment. There again, the same creative action by which God manifested Himself in the Deluge will once more strike the world of sin. But this time it will have the nature of a final \"accounting\" in the sense that then all men will come forth to give testimony to their personal response to God's action in the world. Those who have believed, and who have freely accepted the light and the salvation offered to them from heaven, will pass, like the Israelites, through the Red Sea; they will be rescued in Christ as Noah's sons were saved in the Ark; they will have lived out the meaning of their Baptism because they will have died and risen with Christ. Those who were not with Christ\u2014and all who are not with him are against Him\u2014will manifest what they too have chosen. It will be by their own choice that they will drown in the Deluge, and perish with the chariots of Egypt in the closing waters of that last sea.\n\nNot only do many of the Psalms literally foretell the suffering and glory of Christ, but David is a \"type\" of Christ. The Psalter as a whole is \"typical\" of the New Testament as a whole and often the particular sentiments of the Psalmist are, at least in a broad sense, \"typical\" of the sentiments in the Heart of the Divine Redeemer. Even the sins of David belong to Christ, in the sense that \"God hath laid upon Him the iniquity of us all.\"[36]\n\n# 1:\n\n# _Words as Signs and \"Sacraments\"_\n\nST AUGUSTINE DOES NOT HESITATE TO APPLY to the Scriptures the analogical term \"sacraments.\" Nor should we be surprised at his use of the expression _sacramenta scripturarum_ when we remember, for instance, the external reverence with which the Church emphasizes the dignity of the Gospel in a Solemn Mass. It is well known that the Church's reverence for the Scriptures resembles to some extent the honor she pays to the Blessed Sacrament Itself.\n\nThe Scriptures are one of the Church's greatest sacramentals, for the \"Word of God is living and effectual and more piercing than any two-edged sword and reaching unto the division of the soul and the spirit, of the joints also and the marrow, and is a discerner also of the thoughts and intents of the heart.\" [37]\n\nAll the revealed words of God are partial manifestations of the Word, Who is the splendor of God's Truth. All the revealed words of God are, as it were, species under which is hidden the one Word, Who is the way, the truth and the life. That is why Jesus, the word made flesh, could calmly say: \"Search the Scriptures... the same are they that give testimony of me.\" He was speaking to the Doctors of the Law, who were right in hoping to find in the Scriptures \"life everlasting\": but they were wrong in expecting that the life, promised by the Scriptures and contained in them, would be anything or anyone but Jesus. Therefore our Lord added \"and you will not come to me that you may have life.\"[38] St Paul showed clearly that Christ was the \"end of the Law,\" that is the fulfilment of the whole Old Testament. He is the life contained in the revealed word and communicated by it. \"The word is nigh thee, even in thy mouth and in thy heart. This is the word of faith, which we preach, for if thou confess with thy mouth the Lord Jesus and believe in thy heart that God hath raised Him from the dead, thou shalt be saved.\"[39]\n\nOf whom can it more truly be said that the \"word is nigh them, even their mouth and in their heart,\" than those who daily recite or chant the Divine Office? If that word is to become for them living and effectual, if it is to penetrate the depths of their interior life and make them contemplatives, they must discover in it the Christ Who is the light of the world. He who is the center of the Old Testament and of the New is, above all, the life of the Psalter. When we recite the Psalms we must learn to recognize in them the suffering and triumphant Messias, confessing Him with our mouth and believing in our heart that God has raised Him from the dead, Then we reap the abundant fruits of His Redemption. The salvific life that flows from His Cross will swell in our heart until it bursts our veins and we will cry out with Philip: \"We have found Him of whom Moses and the prophets did write, Jesus the son of Joseph of Nazareth.\" [40]\n\n# 2:\n\n# _Transformation in Discovery_\n\nJUST AS IN THE PATRISTIC AGE THE FAITHFUL used to bring their gifts to the altar at Mass, and matter for the Sacrifice was set apart from among the offerings of bread and wine, so we who recite the Psalms for the whole Church bring to this \"action\" our own matter for sacrifice. I use the word action advisedly, because all liturgical prayer is an action, and it is all a more or less close participation in the one central Redemptive Act of Sacrifice which is the heart of our Liturgy as it is of our religion and of all human history: the death and resurrection of Jesus Christ. We ought to consider the Psalms of the Office as an extension of the Mass, and find in them the movement of the same action which is the Sacrifice of the Mass. And so, here too, there is an \"offertory\" and we bring matter for sacrifice. We bring our sorrows, our problems, our difficulties, and immerse them in Psalms. We bring our personal struggles and interior conflicts and offer them up to God the Father, not in our own words but in those of the Psalms. We identify ourselves with the one who suffers, who struggles, who labors\u2014and who triumphs\u2014in the Psalter.\n\nAt first, this may not be very illuminating. It may not give us much comfort. Nevertheless we must persevere in faith and in desire. We must go on plunging our leprosy, like Naaman, in this Jordan, this stream of Psalmody. Like Naaman we may be strangers, and our hearts may hark back to all the rivers of Damascus, and we may feel very little kinship with this man in the Psalms whose joys and sorrows are dressed in language so unlike our own. And yet the very unfamiliarity of Scriptural language, says St Augustine, has its purpose.[41] The language of revelation is mysterious not in order that its meaning may be concealed from us, but in order that we may be moved to seek it with a more fervent love. For God only reveals His secrets to those who love Him, and who seek to know Him in order to love Him better.\n\nWhen we bring our sorrows to the Psalter we find all our spiritual problems mirrored in the inspired words of the Psalmist. But we do not necessarily find these problems analyzed and solved. Few of the Psalms offer us abstract principles capable of serving as a ready and sensible palliative for interior suffering. On the contrary, what we generally find is a suffering just as concrete as our own, and more profound. We encounter this suffering at one of its most intense and articulate moments. How many of the Psalms are simply cries of desperate anguish: \"Save me, O God, for the waters have come up to my neck. I am plunged into the mire of the deep and there is nowhere to set my foot; I am come into deep waters and the waves overwhelm me. I am wearied with crying; my throat has become hoarse; my eyes have failed, while I await my God.\"[42]\n\nWhat were the dispositions of the saints and the Fathers, in chanting such a Psalm? They did not simply \"consider\" the Psalm as they passed over it, drawing from it some pious reflection, or twirling one of its verses between their fingers as a spiritual nosegay. They entered into the \"action\" of the Psalm. They allowed themselves to be absorbed in the spiritual agony of the Psalmist and of the One he represented. They allowed their sorrows to be swallowed up in the sorrows of this mysterious Personage and then they found themselves swept away, on the strong tide of his hope, into the very depths of God. \"But unto thee, O Lord, is my prayer, in the time of mercy, O God; Hear me, O God, in thy great goodness, according to thy faithful help.\" [43] So, in the end, all sorrow turns to triumph and to praise: \"I will praise the name of God with song, and I will glorify Him with thanksgiving... For God will save Sion and build up the cities of Juda and they shall dwell therein and possess it. And the seed of his servants shall inherit it and they that love His name shall abide therein.\"[44]\n\nWe too, when we chant these verses as the old saints must have chanted them, experience the truth which the Fathers reveal to us in their writings. We find out that when we bring our own sorrows and desires and hopes and fears to God and plunge them all into the sorrows and hopes of the mysterious One who sings this Psalm, a kind of transubstantiation is effected. We have put all that we have\u2014or rather all our poverty, all that we have not\u2014into the hands of Christ. He who is Everything and has everything pronounces over our gift words of His own. Consecrated by contact with the poverty He assumed to deliver us, we find that in His poverty our poverty becomes infinite riches: in His sufferings our defeats are transubstantiated into victory, and His death becomes our everlasting life.\n\nWhat has happened? We have been transformed. The process is more than a tragic _catharsis_. This is more than the psychological impact of a work of art, in which our emotions, clenched in a dramatic crisis, have been sprung, have been released, and have achieved a vital fulfilment by a successful poetic solution of the problem in which we have allowed ourselves to become emotionally involved. There is something much deeper. It is a spiritual solution. It is a kind of death and a sea-change, operated as it were at the bottom of a spiritual ocean, because it can just as well happen to us when the Psalm, having become insipid to us by continual repetition, has ceased to have any immediate artistic appeal. And I may add that it might even happen to someone who has never quite been attuned to the full poetic quality of the Psalms.\n\nThis transformation is operated in us by the power of the Holy Spirit Who lives and acts in the word He has inspired. He, if you like, is the poet. But He also is the poetry. Or rather Christ, Whose Spirit He is, is the poetry of the Psalms. But the Holy Spirit, besides being the artist, is also the spectator. He is at the same time the poet, the poetry and the reader of the poetry; the music and the musician, the singer and the hearer. The peculiar mystical impact with which certain verses of Psalms suddenly produce this silent depth-charge in the heart of the contemplative is only to be accounted for by the fact that we, in the Spirit, recognize the Spirit singing in ourselves.\n\nWe are transformed in the midst of a discovery. What discovery? God's discovery of Himself in His own Psalm. Only God is really capable of appreciating the things contained in the verses God has written. The word of God is full of the Word of God. Christ is conceived in human language through the Holy Ghost, as He was conceived in human flesh, of the Holy Ghost. The Christ Who is born to us of Scripture is just as hard to recognize as the Christ Who is born to us of Mary. In fact, He cannot be recognized unless His Spirit recognize Him in us, illuminating our minds with his secret presence. \"A man cannot receive anything unless it be given him from heaven.\"[45] Such was the testimony of John the Precursor who told all Israel that he himself would never have recognized the Messias unless he had seen the Spirit descending upon Him from heaven.[46] Only the Spirit of God can point out Christ to us. But the instant in which he does so opens to us something of the depths of that infinite and eternal flash of recognition in which God sees and loves Himself. God's discovery of Himself has been going on for ever. So great a thing is this discovery of God by God that its moments are the processions of Divine Persons. The Father, the Beholder, is a Person. His Vision is the generation of a Person. Love springs from this Vision, proceeds and is another Person, and these Three are one Discovery of their own one infinite Actuality. Jahweh, _Ego sum, I am_.\n\n\"To as many as received Him,\" writes St John the Evangelist of the Word made flesh, \"He gave the power to become the sons of God.\"[47]\n\nThe acceptance of this grace of recognition, in which the Spirit signifies to us, by the touch of a secret experience, that Christ speaks, sings, suffers, triumphs in a Psalm, is a new awakening to our own divine sonship. We lift up our heads in the valley of the shadow and we draw breath, and light momentarily trembles in our eyes that have been too long filled with the waters of death. Then our spirit cracks the walls of its tomb with something of the power Christ shed into our souls on the morning of His Resurrection.\n\nFear has been turned into fortitude. Anguish has become joy without somehow ceasing to be anguish and we triumph over suffering not by escaping it but by completely accepting it. This is the only triumph, because there is no victory in evasion.\n\nMore than that, we ourselves have become Someone else. We remain ourselves, fully ourselves. Yet we are aware of a new principle of activity. We are fulfilled by an Identity that does not annihilate our own, which is ours, and yet is \"received.\" It is a Person eternally other than ourselves who identifies Himself perfectly with ourselves. This Identity is Christ, God. We discover something of the theological reality that human nature has been, by Him, not absorbed, but _assumed_. He took to Himself a concrete individual nature: but that nature was our nature, and by virtue of this assumption, it was I who died with Him on the Cross, I who rose with Him to sit at the right hand of the Father in Heaven because it is He who now still suffers and dies in me on this earth of bitter battle and sin. _Convivificavit nos in Christo_ \"He has given us all life together in Christ\" _Consedere nos fecit in caelestibus in Christo: Jesu_ : \"He has enthroned us together in heaven with Christ Jesus,\" says St Paul. [48] And the Church asks in her prayer for Ascension Day that we may always live thus with Christ, Who is our Life, in Heaven.[49]\n\n# 3:\n\n# \" _Visible Mysteries_ \"\n\nSINCE WE HAVE JUST SPOKEN OF THE MASS OF Ascension Day, let us take up another idea that is emphasized in that Mass. The Postcommunion prayer is one of the many dogmatic statements of the spiritual power that is exercised upon souls, by the Holy Ghost, through the Mysteries and Sacraments of the Faith, to transform men into Christ. The prayer runs: \"Grant us, we beseech Thee, O almighty and merciful Lord, that what we have received as our nourishment in visible Mysteries we may enjoy in its invisible effect.\"[50]\n\nWhat is meant by the term \"visible Mysteries\"? It is evident from this particular context that it is an expression which the liturgical language of the Church uses when it speaks of Holy Communion. And of course it refers not to Communion in the abstract, but to Communion as the vital act of participation in the Sacrifice of the Mass by receiving the Body of Christ. The word \"Mysteries,\" in the liturgical language of the Church, means the Mass, in all its essentials and all its integral parts and all its accidents. The \"Sacred Mysteries\" are the Mass and all that surrounds the Mass. The ceremonies and functions of the Divine Office are not usually referred to as \"Mysteries.\" However, they bear a close relation to the Mass which is the center of the whole Liturgy. What is more, there is a whole gamut of meanings in which the word \"Mysteries\" transcends its merely liturgical reference. And the Mystery of Faith in these higher and broader senses is also contained in Scripture and is accessible above all in the Gospels and the Psalms.\n\nIn the first place, God Himself, the Holy Trinity, is the infinite Mystery and of Him all other \"Mysteries\" are a revelation. He manifests Himself to us in the \"Mysteries\" with which the Scriptures are filled. But above all He has spoken to us directly in His Son, _locutus est nobis in Filio_.[51]\n\nIt is also customary to speak of the \"Mysteries of Christ.\" These \"Mysteries\" are groups of significant actions in the Life of Jesus\u2014the Mystery of the Nativity, of the Hidden Life, the Baptism, the Passion, and so on\u2014considered as God's revelations of Himself to us in Christ. For Christ, the Man, is the Word of God and all His actions and virtues as man give the most perfect possible human expression to the Life He leads as Word _in sinu Patris_ , in the depths of the God head. His Sacrifice of Himself on the Cross for us, an unfathomable Mystery of disinterested Love, is a most perfect concrete expression of that Charity which is the very Nature of God: for God is Love.\n\nThese \"Mysteries\" of Christ are not merely called \"Mysteries\" because they are too deep for us to understand and are therefore proposed to us to be contemplated with silent and adoring faith. They are not just something you think about and look at. The term _mysterium_ in St Paul has a dynamic sense. It is the fulfilment of a divine plan, springing forth from the eternal wisdom of God, producing its effect in time and, by virtue of this effect, elevating men from the level of time to that of eternity, from the human level to the divine.\n\nNow it is by the redemptive sufferings and death of Christ that men are elevated above a natural order which Adam's sin and all the sins that grew from it had turned into an endless cycle of frustrations. Therefore the true Mystery of Christ, the one central Mystery of Faith to which everything else points, is not the Incarnation alone, or the Public Life of Christ, but His Passion, Death, and Resurrection from the dead.\n\nNor do we enter into that Mystery most fully by thinking about it or by producing in our hearts the affections which such a meditation might inspire. It is necessary that the full power of this theandric action of Christ which is the summit of all Mysteries, should enter into our lives and be prolonged in them. How is this to be done? Christ has bequeathed this theandric action of His to His Church. He has given her the Mass, which perpetuates and daily renews, not in symbol only but in literal fact, the Sacrifice of Calvary. Hence this Mystery of Mysteries is not merely something that once happened, the memory of which is preserved for our study and admiration. The central Mystery of the Faith is living and efficacious and is in the possession of Christ's Mystical Body, the Church. But does the Church merely possess this Sacrifice as a rite which she exercises, as it were, exteriorly, without entering into it herself? Then the Blessed Eucharist would merely be a drama, not a Sacrament.\n\nThe Mystery of Faith would then be no more of a mystery than a medieval mystery play.\n\nIn order to receive the effects of the Sacrifice of Christ, the Church has to offer herself completely to God, with Christ. The Body must be united in all things with its Head, or it is not a living body and does not live the life of the Head. The Church, say some of the Fathers, was born when blood and water (signifying the Sacraments) flowed from the pierced side of Christ on Calvary. If this be so, then the very nature and identity of the Church are inseparable from the notion of Christ's Sacrifice. She exists by virtue of that Sacrifice, she goes on existing in order to continue that Sacrifice and her final exaltation will be the consummation of that Sacrifice. The Church is nothing else but the Mystical Body of those who have been baptized in Christ's death, [52] and who, by that fact, have risen to a new life in God with Him Who is both God and Man. This participation in the theandric action by which Christ redeemed the world is nothing merely passive. The Church must take a living and active part in the Mystery of Christ. The Sacrifice of the Mass is, therefore, just as much hers as it is His. The Church is a Body of living members and what we say, abstractly, of her, must be verified concretely in them. We, who live in Christ, possess and offer the Sacrifice which is one great Mystery. In this Mystery God supernaturally manifests Himself in the world, enters temporally into the stream of human history in order to sanctify part of that stream for Himself and bring it into the ocean of eternity.\n\nThe priest at the altar more than represents Christ. When the Sacred Species are consecrated, it is Christ Who speaks through the priest in His own Name and in the first Person: \"This is MY body.\" That same priest turns from the altar to the people and says: \"Pray brethren that my sacrifice and yours may be acceptable to God the Father almighty.\" The Sacrifice, the Mystery, belongs to all of us who love God because in it we are all offered to the Father in and with Christ, all enter into His Passion and rise with Him from the dead. The union of each one of us with Christ is not merely moral and symbolic, it is physical and real because Jesus and His Church are physically united in the Sacrifice offered by the priest.\n\nHowever, this union has a double aspect. It is true that the Sacraments produce grace _ex opere operato_. This physical union is effected by the mere fact that the Sacraments are conferred upon a subject that is properly disposed. But as soon as we speak of the dispositions of the one receiving the Sacrament we are in the moral or, if you prefer, the ascetic order. In actual practice, we must enter into the mysteries of Christ not only sacramentally but also ascetically because the sacramental order is meant to be fulfilled by our application of the graces of the Sacraments to our own lives. This means that we share in Christ's Passion and Resurrection not merely in a hidden and mystical sense, but also by active imitation of His virtues. To enter into His Mysteries means to die, as He died, to the desires of the flesh and to rise to a new life in the Spirit. This cannot be done without suffering and self-sacrifice. Jesus Himself made it clear that the asceticism He demanded of His disciples was an essential condition of that union with Him in the Mysteries in which He overcame death. \"He who does not take up his cross and follow me, is not worthy of me. He that would save his life will lose it, and he that would lose his life for my sake shall find it.\"[53]\n\nJust as Jesus patiently suffered injustice, calumny, abuse and physical torture, so too we must make an effort to accept the hardships and pains and trials and misfortunes of life, and even to embrace voluntary privations and sacrifices, with something of His gentleness, humility and love. The Mass is our Sacrifice only if we offer ourselves in it, with Christ, to God. But our offering is meaningless if it does not represent some willingness to verify our offering in self-sacrifice.\n\nTherefore, in actual fact, it is by this _ascetic prolongation_ of the sacramental life of the Church that Christ wills to manifest and realize in each one of us the Mystery of Faith, which is the greatest revelation of the love of God. The whole Christian ascesis is built up like a pyramid. It is an ascending scale of the reconciliation of opposites. Strength must combine with gentleness, humility with courage, the prudence of the serpent with the simplicity of the dove. But at the top of the pyramid is that charity which is the summary of all the virtues and the life and form of them all because in it is perfected our union with the God Who is Love. By this love for God and for one another we give evidence that we have entered into the Mystery of Christ's Sacrifice. Charity is not only the fulfilment of the Law but the fulfilment of the \"Mysteries.\" Charity must be the fruit of all devotion, all asceticism, and above all of the Liturgy, because without charity the Liturgy is only a tinkling cymbal.\n\nThat is why the Mass is called the Sacrament of Love. The Eucharist is the _sacramentum unitatis_. Christ, in His high priestly prayer at the Last Supper (a prayer which forms the model and the basis of the Canon of the Mass) prayed to the Father to make all souls one in His Mystery. \"I in them and Thou in me, that they may be consummated in one and that the world may know that Thou hast sent me, and hast loved them as thou hast loved me.\"[54]\n\nClearly, this unity of the faithful in charity is the full expression of the Mystery of Christ on earth. In this charity the light of the Mass is poured out upon the world, for Jesus makes it evident that it is above all by our union with one another in Him that the Father's love for us is made known to men. It is therefore insufficient to consider the Mass merely as legal Sacrifice for the expiation of sin: we must see it also, as the early Christians did, as a feast of love, an _agape_. We must look at it through the eyes of the great theologian of the Blessed Eucharist, St Thomas Aquinas, who wrote: \"the full spiritual reality ( _res sacramenti_ ) of this Sacrament of the Eucharist is _the unity of the Body of_ Christ.\"[55]\n\nSt Leo the Great teaches, in the strongest terms, the reality of this physical union of the Christian with Christ through the worthy reception of the Sacraments, prolonged and expressed by the ascetic life of charity that culminates in contemplation. \"The body of the man who is reborn in Christ _becomes the very flesh of Christ_.\" ( _Corpus regenerati fit caro Christi_.)[56] In all those who prove the vitality of their union with Christ by works of charity, it is Christ Himself who does their good works in them, says the Saint ( _ipsum piorum operum intelligamus auctorem_.) [57]\n\nChrist, he continues, pours out His graces upon the whole Church in such a way that the actions of Christians shine like rays of light emanating from the one sun, who is Christ. That is why the merits of the Saints all give glory to Christ. They are expressions of the power of Christ and bear witness to the sanctity of Christ\u2014the sanctity which He has received from His Father from all eternity, and which He has communicated to them.\n\n_The effect of our communion in the Body and Blood of Christ is that we are transformed into what we consume, and that He in Whom we have died and in Whom we have risen from the dead, lives and is manifested in every movement of our body and of our spirit_.[58]\n\n# 4:\n\n# \" _When Israel came out of Egypt_... \"\n\nTHE PSALTER CANNOT BE APPRECIATED UNTIL it is seen in the light of the great Mystery of Faith which is centered in the Mass. There is an extraordinarily intimate connection between the Psalter and the Mass. Not only are the sufferings and death of the Redeemer literally and typically foretold in the Psalms; not only are the Psalms often chanted in the celebration of the Mass itself, as part of the Proper of the saints or of the time, but also the very Canon of the Mass, the most ancient and most sacred of liturgical prayers, is an echo of the group of Psalms called the _Hallel_ , which were chanted in the Passover rites of the Jews. This is easy to understand, since the Mass, the Sacrifice of the New Law, is the fulfilment of the sacrifice of the Paschal Lamb which had been instituted, at God's command, as a type foreshadowing the Sacrifice of Christ, _Agnus Dei_ , the Lamb of God. The Psalms of the _Hallel_ are concerned with the \"Passover,\" that is the deliverance of the children of Israel from Egypt, their passage through the Red Sea, their miraculous preservation in the wilderness of the Arabian Desert and their entrance into the Promised Land.\n\nSt Paul saw that the Passover contained, in figure and symbol, the Mystery of Christ.[59] His _Epistle to the Hebrews_ is an argument, based in great measure upon the Psalter, as well as on the Pentateuch, that the Sacrifice of Christ is the real Passover by which the true Israel, the Church, is delivered from bondage to Pharaoh (the world, the devil, sin), is protected in her journey to the Promised Land and is finally admitted to the peace of perfect union with God in heaven.\n\nThe Psalms, then, are not merely ancient poems which the Church fancifully adapts to her own liturgical uses. Everything in them is charged with vital urgency by virtue of the fact that they are full of Christ. Either they speak to us directly of the Redeemer Himself in His sufferings, His kingship, His priesthood: or else they narrate the trials and progress of the Mystical Christ, the Church, His people. When Israel went out of Egypt and wandered in the desert, God became a pilgrim with them in the dark years of their tribulation. He came down to them on the mountain in cloud and fire, speaking to them through Moses who was a type of Christ. He fed them in the desert with manna, foreshadowing the Holy Eucharist. Water sprang from a rock in the desert at the command of Moses, and never ceased to supply them until they settled in the Land of Promise. \"The rock,\" says St Paul, \"was Christ.\" [60] The Kings of strange desert tribes have survived in the Psalms; they were the enemies of Israel. Their mysterious names do not mean anything definite to us. These kings emerge from the verses of the Psalms like the weird symbolic enemies that menace us in dreams and fade away. They are the powers of evil that are still fighting the Church today. We know that Sisara is dead with the tent peg in his temple, and Jabin's bones long ago whitened in the ravine of Cisson. Yet Jabin and Sisara still rise up from Hell to plague us, though they cannot prevail. But we know, on the nights when their names pass before us, in the small hours, at the chanting of Matins, that the old battles we are celebrating are more than ever actual. Actual too are the same miracles by which Israel overcame her enemies and entered glorious, through divided Jordan, to occupy the Promised Land.\n\nThese battles and these victories go on without ceasing, generation after generation and century by century, because the whole Church is still passing out of Egypt, company by company. The shining tribes of Israel are still crossing the desert in the slow, interminable march that Balaam saw from his mountain when his curse against them choked in his gullet and turned into a song of praise:\n\n_Then Balaam, turning his face to the desert, saw Israel dwelling in tents, tribe by tribe, and the Spirit of God rushed down upon him and he prophesied and said_ :\n\n_Thus said Balaam, the son of Beor,  \nThus said the man whose eyes were stopped up.  \nThus said he who heard the speech of God,  \nWho saw the vision of the Almighty,  \nWho fell down and his eyes were opened:  \nHow beautiful are thy tents, O Jacob,  \nAnd thy camps, O Israel,  \nLike the wooded valleys  \nAnd like gardens all along the streams of water,   \nLike tents which the Lord has planted  \nNext to the rivers, like cedars...  \nGod has brought Israel out of Egypt  \nStrong as a rhinoceros.  \nThe nations shall devour Israel's enemies  \nAnd crush their bones and riddle them with arrows.  \nIsrael lay down and slept like a lion  \nAnd like a lioness, that no man dares to waken_.[61]\n\nWe are the children of Abraham, but only if we do the works of Abraham. His faith does not justify us unless it live and act in us and be our faith. Our ancestors overcame Amalec, leaving us an example, showing us how to fight when we, too, cross the desert in our turn. \"Christ suffered for us leaving you an example, that you might follow in His steps.\"[62]\n\nIt is in chanting the Psalms that we too are leaving Egypt. The Liturgy is the Church's greatest weapon against her enemies because it is filled with the might of the Mystery which is its center. The Mystery of Christ is the heart of all history and extends backwards and forwards to embrace all time. It was in Christ that Israel crossed the desert and it is in Christ that we, the tribes of Israel, are going up to Jerusalem. [63] The Mystery of Christ is timeless: but we enter into it by consecrating to Him the little part that is ours of history and of time. It is by the Liturgy and its ascetic fulfilment that we do so.\n\nThis is the secret of the Psalms: they contain in themselves all that matters to a Christian of the history of the world, because in a mysterious and quasi-sacramental manner, by virtue of their intimate connection with the Sacrifice of the Mass, the salvation of the world is all worked out in them. Breviary, Psalter and Missal, charged with the grandeur of the Word of God, contain the mighty secret of Christ's spiritual victory. The secret is placed in the hands of each Christian. It only needs to be discovered and fulfilled in our own lives.\n\nThe history of Israel\u2014that is of the people of God, the Church\u2014is also in some measure the history of each individual soul in the Church. As in the natural order each individual man is a microcosm, so in the supernatural order each individual soul is a little church, a miniature heaven and a temple of God. Just as the whole people of God is still crossing the desert to the Promised Land, still passing through the Jordan, still building Jerusalem and raising God's temple on Sion, so each individual soul must normally know something of the same journey, the same hunger and thirst, the same battles and prayers, light and darkness, the same sacrifices and the same struggle to build Jerusalem within itself.\n\nJust as Jesus is entirely present in every consecrated Host and also singly present in them all at once, and just as the soul of a man is entirely present in every cell of his body and is also present in its unity over all his whole body, so Christ lives entirely in each individual Christian and singly in them all. By virtue of His Mysteries, His life becomes the life of each Christian as He is also the life of the whole Church. In each one and in all, He is all. _Omnia in omnibus Christus_.\n\nOur growth in Christ is growth in charity. Charity is created and strengthened within us by the action of the Holy Spirit\u2014most of all in times of trial and sacrifice, because it is then that we are pressed and compelled, by circumstances, to make heroic choices that confirm our union with Christ, and teach us to know Him as He is. For Christ without the Cross is not our Christ. True, He is now the risen Christ. He knows no suffering. He \"dieth now no more.\" But He has wounds. Even though they be glorious, they are wounds. His Cross is not absent from heaven, but it is there the sign of victory. And it will blaze in the heavens when Christ returns in judgment. The Cross is our only glory, says St Paul.[64] He has sketched out the asceticism of tribulation in a verse of _Romans_. We glory, says he, not only in the hope of the glory of the sons of God (as if we were to enter Heaven without suffering) but we especially glory in tribulation, because tribulation makes us patient; our patience under suffering proves us true Christians; and by this proof we have hope; and this hope cannot be shaken because when we have it, the fulness of love is poured out into our hearts by the Holy Ghost. The Holy Ghost, living and acting in our souls, intimately present to us, is Himself God's gift to us. _Caritas Dei diffusa est in cordibus nostris per Spiritum Sanctum qui datus est nobis_.[65]\n\nThe more the Spirit of God pours out into our hearts the love of God, the better we are able to know God. The Mystery of Christ is a dark cloud into which we enter that the Spirit may teach us with His lightning. Says St Paul: \"We utter the wisdom of God in Mystery, a Mystery which is hidden, which no one of the princes of his world has known... which the eye of man hath not seen, nor hath his ear heard, nor hath the thought of it risen up in his heart, but God has prepared it _for those who love Him_. And God has revealed this wisdom to us in His Spirit, for the Spirit looks into all things, even the depths of God.\"[66]\n\nThe deepest abyss of the love of God, and therefore the perfect knowledge of God, can only be entered through the pierced Heart of the Redeemer. This is the narrow gate that leads us to salvation and to glory. The Holy Spirit opens this gate to us, and we have learned that His key is tribulation.\n\nYet God is not to be found in suffering as such. Sanctity and love are not born in us by the love of pain for pain's own sake. Suffering is not the cause of holiness but only its occasion. Love, expressed in sacrifice, is what makes us saints. We are made saints not by undergoing pain but by overcoming it. That is why the Cross means joy and not despair, life and not death, fulfilment and not annihilation. All this is the work of the Spirit in our souls, uniting us to God in the Mystery of Christ. It is Christ Who is our Heaven, not the Cross. The Cross without Christ would be Hell\u2014just as suffering, for those who do not know Christ, is always Hell.\n\nChrist in the Psalter is our rock in the desert of Sinai. The Psalms, written and quickened by His Spirit, feed us with bread in the wilderness. They slake us (as Isaias says) at the Saviour's fountains!\n\nWe find Him by recognizing both Him and ourselves in the sufferings of David, of Israel. This recognition, like a spark, kindles a flame. The spark is faith, and the flame love. This true love is charity. Charity is the fire of the Holy Spirit and the Spirit is the Spirit of Christ, the Spirit of God. In this one flame we are united to God in Christ. The experience of this flame is an experience of union, first with Christ suffering, then with Christ in glory. For, as St John of the Cross says, it is the same flame that first attacks our selfishness as its implacable enemy, then when selfishness is gone, rewards our love by flooding it with glory.[67]\n\nBut at the same time, our growth in Christ is measured not only by intensity of love but also by the deepening of our vision, for we begin to see Christ now not only in our own deep souls, not only in the Psalms, not only in the Mass, but everywhere, shining to the Father in the features of men's faces. The more we are united to Him in love the more we are united in love to one another, because there is only one charity embracing both God and our brother.\n\nIn this union we discover, and the conviction gains more and more power as we are emptied of selfishness by suffering, that there is so to speak \"One mystical Person,\" after all, chanting the Psalms. It is now no longer we alone who pronounce the words of David or of some long dead Jew. It is the eternal Christ. He is \"chanting the Psalms in heaven,\" because His glorified Humanity is the center of their Mysteries and the life of all who enter into these mysteries. All we who are members of His Body are one in Him and one with Him. His Church and bride is one with Him, according to the Apostle, \"two in one flesh.\" And St Augustine comments: \"Thus of these two (the Church and Christ) there is made as it were _one Person_... If they are two in one flesh, why not also _two in one voice?_ Let Christ then speak, for in Christ the Church speaks and in the Church speaks Christ. The Head speaks in the Body and the Body in the Head.\" [68]\n\nIt is not merely the solution of one man's problem that is achieved in the Psalms or in the Mystery of Christ. If in my chanting of the Psalms I arrive only at a sense of individual and personal fulfilment in Christ, a sense that does not reach out and embrace all the other members of the Body who find their fulfilment in Him, then I fall far short of the contemplation that the Psalter holds in store for those who give themselves entirely to its Mysteries. The One Man who suffers in the Psalms, who cries out to God in them and by God is heard, this One Man is the Whole Christ. The consolations and help that are sent from heaven through the Psalms are poured out not simply on Jesus and myself but upon the Whole Christ, and I will find their strength far less potent in my own regard if I do not realize that they are shared among us all. It is a relatively small thing to awaken, in the recitation of a Psalm, to my own personal sonship of God. Far more marvelous is the greater consolation of the Mystery of my oneness with all the other sons of God in the One Son of God, the Mystical Christ. \"The sons of God,\" says St Augustine, \"are the body of the only Son of God; and since He is the Head and we the members, there is but One Son of God. Therefore he who loves the sons of God, loves the Son of God and he who loves the Son of God loves the Father. Nor can anyone love the Father unless he loves the Son; and whoever loves the Son must also love the sons of God... And by loving he himself becomes a member in the union of the Body of Christ and there shall be One Christ loving Himself.\"[69]\n\nThe secret of our fulfilment, then, is charity. We bring to the Psalms the raw material of our own poor, isolated persons, with our own individual conflicts and sufferings and trials. We throw them all into the fire of Christ's Love\u2014or, if you prefer it, into the furnace of the Holy Spirit. In those flames we are purified of everything that isolates us, everything that is merely private, merely our own, and we are melted down to become a \"new creature\" with a new identity, a higher \"personality.\" The discovery of our true selves, our own inviolable and individual beings united without confusion in this One Mystical Person, united to one another in the flame of Christ's infinite and selfless ecstasy of Love for His Father and for us, will constitute one of the purest perfections of our joy in heaven. Meanwhile, our recital of the Psalms should be a constant and progressive discovery of this Person who we all are. _Debemus intelligere Personam nostram, Personam Ecclesiae nostrae, Personam Corporis Christi_. \"We must understand our Person, the Person of our Church, the Person of the Body of Christ.\" These are the words of St Augustine.[70]\n\nThis will help us to understand the importance of the Choral recitation of the Divine Office. The mere fact of standing in choir and of hearing twenty or thirty or fifty or a hundred voices all blending into one voice, crying out to God in the first person singular, is a great help toward realizing the truth we have just tried to set down.\n\nWe all differ, we all have our own problems and troubles, and yet we all sing together: \"O God, hear _my_ cry, hearken to _my_ prayer...\" The very syntax makes us one. And when we add: \"From the ends of the earth _I cry_ to thee,\"[71] our vision goes out to embrace the whole Mystical Body, in all its scattered members in every part of the world. And wherever they may be, those men and \"women are also here, and we are there with them, because we are all \"one Man.\" Wherever two or three are gathered together in His Name, Christ, in the midst of them, imparts to them His identity. He becomes the \"I\" who sings and prays and praises in us all.\n\n# 1:\n\n# \" _Thou hast opened my ears_...\"\n\nTHE \"GRADUAL PSALMS\" ARE THOSE WHICH some suppose to have been sung by Jewish pilgrims on their way to celebrate the great feasts of the old Law in the City of David.[72] They are the shortest of the Psalms but not the least moving. St Augustine finds in them an expression of the joy of the Pilgrim Church on earth ascending to the Celestial Jerusalem. But, in a sense, all the Psalms are \"gradual Psalms.\" They are the chants that lighten the fatigue of our journey homeward from the long exile of sin. Even when they are sorrowful, their very sorrow holds a hidden promise of beatitude, for \"blessed are they that mourn.\" [73] This peculiar sorrow of the third beatitude, the sorrow of the soul that realizes its exile and can no longer find any consolation save in longing for home, is the beginning of our liberation. It teaches us the way to freedom by teaching us the truth that St Augustine expressed in six words: _Nisi beatus non vivit ut vult_. \"Only the blessed live as they please.\" And he adds four more words that distinguish liberty from licence: _Nemo beatus nisi justus_. \"No one is blessed unless he first be just.\" This sentence from The _City of God_ [74] should be taken as a corollary of his famous aphorism, \"Love God and do what you will,\" which is as much as to say that if everything we do is an act of love for God, we will be free, because we will be unable to sin. Sin is captivity and love is liberty.\n\nThe Psalms teach us the way back to Paradise. Christ died that we might recover all that Adam lost in Eden, and more besides. What had Adam in Eden? This is not the place to study all his gifts and prerogatives. Let us think only, for the moment, of his blessedness, which was his liberty. But his blessedness and liberty were rooted in the possession of God. That possession was the work of love, uniting His will with the will of God, and of vision, filling His intellect with God. \"Man lived just as he pleased in Paradise,\" says St Augustine, \"as long as he willed what God commanded. His whole life was fruition of God, and by the possession of this infinite Good, Adam himself was made good.\" _Vivebat fruens Deo, ex quo bono erat bonus_.[75]\n\nIndeed the Psalms not only show us the way back to Paradise, they are themselves a Paradise. In them the truth and love of God are not only shown to us but communicated to us in the Mystery of Christ, if we can only receive them. The Mystery of the Psalter is above all the Mystery of God's will: the history of Israel is a history of trial and suffering not so much because of the enemies of God's people, still less because Israel was forsaken by God, but because, of all things, Israel kept forsaking God by disobeying His will and mistrusting His Providence. The prevarication of the Chosen people is answered and \"the problems it causes are solved by the obedience of the Redeemer who comes to do God's will. \"... But thou hast opened my ears. Burnt-offering and sin-offering thou didst not require. Then I said; 'Behold I come, in the volume of the book it is written of me: I delight to do thy will, O my God, and thy law is in the depths of my heart.' \" [76]\n\n\"Thou hast opened my ears,\" says Christ in the Psalm. That is to say, \"Thou hast made me perfectly obedient to the inspirations of Thy Spirit.\" \"Thy Law is in the depths of my heart.\" St Bernard of Clairvaux knew what this Law was, because he was a contemplative and a saint. And to be a saint means to live by that Law, to be formed by it, and to be transformed by it and perfectly united to God.\n\nLet us meditate a little on this mysterious \"Law\" since it is the secret of sanctity and of contemplation and since it is also the secret of the Psalter, hidden in the very center of the Mystery of Christ.\n\nIn the first place, this Law must not be understood as the Law of Moses, the \"law of fear.\" The \"Law\" that is in the \"depths of the heart\" of the saint is not a law that paralyzes love. It is not and can never be a narrow, exterior religiosity, concentrated on the literal fulfilment of external precepts, a law that merely weighs and measures sins in the balance of a pitiless scrupulosity. St Paul travelled all over the Roman Empire to tell people that they had been delivered forever from such a law. \"If you are led by the Spirit,\" he said, \"you are not under the Law... For you have been called unto liberty.\" [77] But he immediately added that if they were unable to tell the difference between liberty and lawlessness, they would fall under the dominion of a far more terrible law, the law of the flesh. \"Make not liberty an occasion for the flesh... for the flesh lusteth against the Spirit and the spirit against the flesh, and these two are contrary to one another _so that you do not the things that you would_.\" [78]\n\nThere are, then, three laws in the New Testament: first, the law of the flesh, the tyranny of passion, binding the soul of man to the treadmill of lust and hatred and greed and cruelty like blind Samson in Gaza; for the liberty of the flesh makes slaves. But the Law of Moses although it set itself up against the tyranny of the flesh, was not able to liberate any man from the flesh. Under the Old Law, man fell under a double tyranny. He was bound by one law of sin and by another law that accused him of sin and punished him for sin and imposed a weary burden of practices to expiate sin: and yet there was not one of these ablutions or sacrifices that could cleanse him of sin or deliver him from passion. Still the Old Law was not evil, for it had its function: it was the \"type\" of another Law, and its sacrifices foreshadowed the Mystery in which men would at last recover liberty. The Old Law was a gradual \"education\" and preparation for the liberty of the New. The Law of Moses was good not in itself but in its fulfilment, \"For the end of the Law is Christ,\" [79] and \"love is the fulfilling of the Law.\" [80]\n\nIt is of this third Law that St James speaks when he says: \"He that hath looked into the perfect Law of liberty and hath continued therein, not becoming a forgetful hearer but a doer of the work, this man shall be blessed in his deed.\" [81] The Law of Christ is the Law of liberty because it is the Law of love\u2014which is to say that it is above all law, since love, being free, knows no compulsion.\n\nThat is why St Bernard says that the saint is neither bound by law nor without law: _non sub lege nec sine lege_. What is the solution of this paradox? It is this. The Law of love is a law in the sense that it is a standard, but it is not a law in the sense of a limitation. It is an ideal but it is not a restriction: for love has no limits. We are called to love God without measure and for no other reason than that He is God. [82]\n\nTo love Him thus is to love Him as He loves Himself. To do so perfectly is to be transformed into Him, because it is to live by the same \"Law\" that rules the interior life of God. But that Law is not a law: it is a Person. It is Charity, the Holy Spirit. By virtue of this \"Law\" the Three Divine Persons cannot be anything but One, and they cannot be anything but infinitely happy. For God, infinite love, freedom and peace are compulsory. He is all these things and cannot wish to be otherwise. The saints, too, when they live by the same Law, as God, possess everything that He is. This, says St Bernard, is the \"immaculate law of God\" that we read of in the Psalms and which transforms souls. [83]\n\nCharity is the only power, the only \"Law\" that can effect this mystical transformation. No other force can elevate us above our own nature. Charity is our only deliverance from human limitations. Note that I say charity and not love, for there is an immense distinction between them.\n\nLove is a movement of the will toward what the intellect sees to be good. I speak only of spiritual love here. Sensual love is a movement of the will, guided by the senses, seeking their own satisfaction. There is a desire of God that is called charity although it remains a love for God as the highest good I can desire for myself. The desire for my own fulfilment in God, can be charity: but it must be educated and formed. For charity is the love of God, not precisely as my own highest good, but because He is good in Himself.\n\nThe highest and most perfect fruition of God is found in a love that rests in Him purely for His own sake alone. This love follows from the vision of Him as He is in Himself. I can and should desire this vision and love as my own highest good. Every Christian must, in fact, have something of the theological virtue of hope, which is explicitly directed towards this end: the fruition of God in heaven.\n\nThis is the great paradox of charity: that unless we are selfish enough to desire to become perfectly unselfish, we have not charity. And unless we love ourselves enough to seek perfect happiness in the total forgetfulness of ourselves, we will never find happiness. Charity is a self-interest which seeks fulfilment in the renunciation of all its interests. If I have charity I will seek my highest good in God, but I will find it in Him, not by taking Him to myself but by sacrificing myself for love of Him. And when my charity is thus perfect, I shall find and possess myself in Him.\n\nAs long as I am on earth, this paradox can serve as matter for discussion. In heaven, the vision of God disposes of the problem. St Thomas and Duns Scotus no longer need to argue, there, about the nature of charity and of blessedness. When we see Him, there will be no question of our loving anyone but Him. When we see Him, we will see that the only way to love any creature is to love God: for all creatures are meant to be loved in their Creator, and only in Him. We will see that it is only in Him that we can really love them: and that in thus loving them we are also loving Him. That is why St Bernard can say that we reach the highest degree of pure love when we finally love even ourselves in God and for His sake.\n\nThere too, love has ended in liberation. It has delivered us from complication, problem and paradox. There at last we arrive at the simplicity that God created us to have: for, after all, if He loves us, we cannot say we are not good, or that we are not to be loved. The perfection of love is a peak of unselfishness so lofty that it is above the stained atmosphere of this earth in which even humility and unselfishness have, in spite of all our good will, to suffer certain distortions. On that mountain top we are at last selfless enough to love God in ourselves without any need for comment or for excuse. For what we thus love is only His will in us. We love ourselves in the perfection to which He has brought us, not because we are perfect, not because we are happy, but because His will is done. And we are at last perfect, at last perfectly happy, because we no longer care whether or not we are perfect or happy. We simply find our peace in this: that in our souls, as in all else, His will is done. [84]\n\nIt is clear that this love is the fulfilment of the law because it is the perfect fulfilment of the will of God. Such love as this, when it is found on earth, fulfils every smallest detail of the most minute rubric of the Liturgy, every jot and tittle of its religious rule and its other obligations, not in a spirit of hair-splitting Pharisaism but with the freedom of a child of God to whom these things are no longer a matter of compulsion but a source of joy: and that is why the just man needs no law. This too is the explanation of Christ's words that He came not to destroy the Law of Moses, but to fulfil it. [85] Only this love can satisfy Christ's injunction that our justice must abound beyond that of the Scribes and Pharisees. [86]\n\nSt Bernard knew that such perfection of love was a kind of ecstasy. And he found it everywhere in the Psalms. This pure and ecstatic love, this love which is the mystical marriage of the soul with God, is what is meant by the word \"justice\" in the line, \"Thy justice is as the mountains of God.\" [87] This love is the _mons coagulatus, mons pinguis_ of the Vulgate version of Psalm 67 (the new translation calls it a \"high-ridged and wooded mountain.\") This pure and mystical love, continues St Bernard, is the mountain of God in Psalm 23\u2014where the Psalmist asks: \"Who can go up to the mountain of the \"Lord?\" It is therefore the term of the ascetic life that is outlined in the middle of the Psalm:\n\n_Who can go up to the mountain of the Lord or who shall stand in his holy place?_\n\n_He that has clean hands and a pure heart, who does not set his mind on vain things, and has not sworn deceitfully to his neighbor_.\n\n_He shall receive a blessing from the Lord and mercy from God his Saviour_.\n\n_This is the generation of them that seek him, of them that seek the face of the God of Jacob_. [88]\n\nThis same Psalm is one of the cornerstones of monastic spirituality, since it has an important place in the Prologue to St Benedict's Rule. It is therefore interesting to see how much a monastic saint like Bernard of Clairvaux could find in it. A detailed commentary of the apparently prosaic little virtues mentioned in these two or three lines would reveal that the Fathers believed \"purity of heart\" to be a function of that gift of understanding which is one of the keys to mystical contemplation.[89]\n\n# 2:\n\n# _From Praise to Ecstasy_\n\nIF, AS THE FATHERS TELL US, THIS PURE AND ECSTATIC love for God, which flows from a knowledge of God as He is in Himself, is the secret of contemplation, and if the Psalms are everywhere full of this love, then it is clear that the Psalter is a school of contemplation which has no equal except the Gospels and St Paul. Yet, in a certain sense, the Psalms have an accidental advantage over the New Testament. We _pray_ them. We chant them together. They form part of an action into which the whole Church enters, and in that action, that prayer, the Spirit of Love Who wrote the Psalms and Who communicates Himself to us in them, works on us all and raises us up to God. To make the Psalms a preparation for contemplative prayer we must do all that we can to pray them with pure minds and pure hearts, living out their meaning with a charity that praises God as they praise Him. There is no purer praise of God than we find in the Psalms. If we make that purity our own, we lay ourselves open as targets, which fire from heaven can strike and consume: and this is all our desire, and God's desire for us.\n\nThe spirit of praise which is that of the Psalms is nothing else but the ecstatic love for God because He is God. Over and over again their inspired verses echo with the refrain: _confitemini Domino quoniam bonus_. \"Give praise to the Lord because He is good, and because His mercy endureth for ever.\" To praise God thus, says St Bernard, simply because He is good in Himself, is to live by the \"law of charity which is the law of His sons.\"[90]\n\nWhen King Solomon dedicated the Temple of Jerusalem to God it is written that the Levites and the people lifted up their voices to praise God, singing the Psalms and chanting, \"Give praise to the Lord for He is good\" and immediately the \"house of God was filled with a cloud.\" [91] This cloud was the sign of the presence of God, as we read in many places in _Exodus_ , and it has become the traditional symbol of mystical contemplation. So too when we, in the temple of our souls, chant pure praise to God in the words of His Psalms, we can hope that He will fill us with this gift of His obscure and pacifying presence which is the first sign of infused contemplation. He will do so when our love for Him is sufficiently pure to exclude every other affection.\n\nTh e echo of this refrain, _confitemini Domino quoniam bonus_ resounds in all the pages of the Old Testament where are recorded the triumphs of Israel over the enemies of God's people. They are the song of a people united to their God as He intended them to be, putting all their trust in Him not only because He is good, but because He alone is good. This ecstasy of praise sums up the mysticism of the Old Testament and of David above all. And its echo is the living flame of those Psalms which, grouped together in the _Hallel_ , first kindled the new fire which was to be the Liturgy of our Mass. Therefore, this praise of God \"because He is good and because His mercy endureth forever\" has passed over, with all the transfigured symbols and types of the Old Testament, into the New. The song that resounded on the shores of the Red Sea and shone on the dark desert in Israel's tents, burst from the Sepulchre with Christ, clad in a new and invisible splendor, and ascended with Him from Olivet into heaven where it is at once the vision, the love, the praise of all the blessed.\n\nThis mystical love is not only a song of victory in the sense that it follows and celebrates all our victories, but also in the sense that by itself alone it has power to overthrow our spiritual enemies and to put victory in our hands. It is because the Church is always singing it, that the gates of hell cannot prevail against her. But if they sometimes seem to prevail, it is perhaps because those members of the Church's fighting army whose task it is to sing these Psalms on earth, do not have the light or the purity to enter into their spirit. They cannot hurl down her enemies at once because they form the words on their lips without realizing and without living the pure love which is their meaning.\n\nIt was not soon the day when King Josaphat prayed to God, and, guided by the voice of a prophet, led the army of Juda out against Moab and Ammon and Seir with singers at their head and Levites chanting and blowing trumpets in the desert:\n\n_And they rose early in the morning, and went out through the desert of Thecua: and as they were marching, Josaphat, standing in the midst of them, said: \"Hear me, ye men of Juda and all the inhabitants of Jerusalem:  \nbelieve in the Lord your God and you shall be secure: believe His prophets and all things shall succeed well.\" And he gave counsel to the people and appointed the singing men of the Lord to praise Him by their companies and to go before the army and with one voice to say: \"Give glory to the Lord, for His mercy endureth for ever_.\" [92] The Scriptures go on to tell us what happened. While Juda sang in the desert, the armies of Moaband Ammon rose up against their allies from Mount Seir and slaughtered them. Then they turned upon one another in their camp. \"And when Juda came to the watch tower that looketh toward the desert, they saw afar off all the country for a great space full of dead bodies, and that no one was left that could escape death.\"[93]\n\nSo too will it be one day with the Church, when her Levites have entered into the simplicity of the Psalms and have found in them their strength, who is their Christ, and have lost themselves in contemplation and in the pure love of God against which there is no prevailing: for those who taste the fruits of the Spirit come under no law. [94]\n\nTo chant the Psalms in such a spirit is to join in the Liturgy of heaven. It is to praise God with something of the same love with which He is praised by the blessed spirits. Tradition, in fact, everywhere points out that the monastic life brings the monk into close participation with the angels and saints of heaven. They are all one in the heavenly city by virtue of the pure love that unites them in God. It is therefore this charity most of all that is demanded of us when we go to choir to chant the Psalms.\n\nSt Augustine's commentary on Psalm 53 contains a passage that can fittingly serve as a summary to all that we have been saying about the liberty of the sons of God which is the reward of pure love and which opens paradise to us even while we remain in exile here below.\n\nWhat is the Mystery of the fifty-third Psalm? It is sung by David after his deliverance by God from the hands of Saul. David\u2014the type of Christ and therefore a personification of the Mystical Christ and of each member of that Christ\u2014has fled with six hundred men from Ceila, and now \"he abode in the deserts in strongholds and remained in a mountain in the desert of Ziph, in a woody hill.\" [95] David hiding in the forests of Ziph, says St Augustine, is Christ hidden in the desert of this world. The Ziphites represent those who do not recognize the chosen one of God in one who has no temporal power and who has to flee before the face of Saul, the prince of this world. In their contempt for the Holy One they seek to betray Him to Saul, and they send messengers to the king in Gabaa, saying \"Lo, doth not David lie hid with us in the strongholds of the wood in Mount Hacila, which is on the right hand of the desert?\" Saul sends them back to follow David's movements while he prepares a force of men to encircle David and trap him in the forest. David hears of this, and moves with his guerillas to the wilderness of Maon. There Saul catches up with him and surrounds him. David's situation is so desperate that he sees no human hope of salvation, but just then a messenger comes and informs Saul that the Philistines have invaded his kingdom, so that he retires, with his army, and David is saved. Psalm 53 gives both David's prayer for help and his thanksgiving to God when the prayer is answered. The whole story is telescoped in the short Psalm in which the prayer and its answer are immediately joined together without transition because when the Church prays she is already answered.\n\n\"Behold,\" sings David, \"God helps me; the Lord is the support of my life... I will freely sacrifice to thee; I will praise thy name, O Lord, for it is good.\" [96]\n\nThe line that concerns us most is this one: _Voluntarie sacrificabo tibi_. \"I will freely sacrifice to thee.\" What is the meaning of this word \"freely\"? We have by this time seen something of the theology of Christian freedom, which is the spiritual freedom of pure and ecstatic love, perfected in the union of the soul with God in contemplation and mystical union. St Augustine asks, \"Who can understand this spiritual gift ( _hoc bonum cordis_ ) when another speaks of it, if he has not first himself tasted it in himself?\" And he goes on to explain it, saying that those who know it by experience will understand his words, and that those who have not experienced this pure love should pray to do so in order that they too might know what it is.\n\nThe perfection of sacrifice, says St Augustine, is found in the freedom that makes sacrifice gratuitous and pure. This purity although it does not reflect upon itself, does not consider its own interests, is not, nevertheless, without its reward. It is its own reward. This pure praise, this \"free sacrifice,\" consists then in praising God not merely because we are delighted with the favors He has granted or will grant us, but because we are delighted with Him, the giver of all gifts. And this delight is situated in the praise itself. We rejoice in praising Him because praise itself is our joy. _Gratis amo quod laudo. Laudo Deum et in ipsa laude gaudeo_. [97]\n\nIf we praised God merely for the sake of obtaining something from Him, then our praise would be contingent upon a gift of His. It would therefore be dependent upon an uncertainty, for although God will never fail to answer all our prayers, He will not necessarily give us precisely the thing we ask of Him. If our praise depends, then, on an uncertainty, it is bound by a restriction. And if it is restricted, the heart with which we pray to God will also be narrowed and limited by the restriction imposed upon us by our own desire, which is centered upon something less than the infinite God. Therefore our praise will not be perfectly \"free.\" It will be fettered, it will be imprisoned by the limitations of our own heart But we cannot give God perfect praise and sacrifice if we remain the captives of our own insignificance. \"How shall we sing the song of the Lord in a strange land?\" [98]\n\nThat is why we so often find ourselves chanting our Psalter by the waters of Babylon instead of on the towers of Sion. No wonder our Office is not contemplation. We have hung up our harps \"on the willows of that land,\" that is to say, we have suspended our prayer upon the stunted branches of human desires. Our contemplation is something grey and dusty. It hangs inert upon a pale green thing with shallow roots in the mud of a jaundiced river. It shines in a heart that is not the wide-open mirror of heaven but a sandy prison of human hopes, centered on transient things.\n\n\"If you praise God in order that He may give you something that is not Himself,\" says St Augustine, \"you do not love Him freely. You would blush if your wife loved you for your money. If perchance, you were to become poor, she might look about for some other partner! Well, if you want your wife to love you freely, for what you are, why do you love God for something other than Himself?\"[99]\n\nThis lesson has a subtler application than the reader may think. I am passing over those whose main intention, in praying to God, has to do with health, pleasure, or money. There is nothing the matter with such an intention. It is quite true that we are meant to ask God for everything we need, for God has ordered us to do so. But there is a perfect way of so praying, which rests in God and not in our temporal intention.\n\n# 1:\n\n# _Dark Lightning_\n\nCONTEMPLATION, IS A GIFT OF GOD, IN WHICH THE soul, purified by His infused love, suddenly and inexplicably experiences the presence of God within itself. This experiential recognition of God springs from the fact that pure charity has reformed the likeness to God which makes our soul like a mirror created only to reflect Him. Because contemplation is produced through the grace of an intimate union with Christ, Who is the Son of God by nature, it is essentially a full and mature participation of His divine Sonship. In contemplation, we know God formally as our \"Father,\" that is to say not only as our Creator in the natural order, but as the living and intimately active source of our supernatural life as well. Contemplation is our personal response to His mystical presence and activity within us. We suddenly realize that we are confronted with the infinitely rich source of all Being and all Love, and although we do not literally \"see\" Him, for our meeting takes place in the dark night of faith, yet there is something in the deepest center of our being, something at the very spiritual apex of our life, that leaps with elation at this contact with the Being of Him who is almighty. The spark that is struck within us by this touch of the finger of God kindles a sheet of flame that goes forth to proclaim His presence in every fibre of our being and to praise Him from the marrow of our bones.\n\nGenerally speaking, this \"experiential recognition\" of God by the contemplative takes place on two different levels. When Jesus met the two Disciples on the road to Emmaus, on the afternoon of the first Easter Sunday, \"their eyes were held and they did not know Him,\" but nevertheless \"their heart was burning within them whilst He spoke to them in the way and opened to them the Scriptures.\" But when they reached the village of their destination and Jesus, pressed by their ardent love, sat down to break bread with them, \"their eyes were opened and they knew Him and He vanished out of their sight.\" [100] The first of these recognitions suggests to us the common experience of what is called \"living faith.\" The second offers a good analogy for mystical contemplation properly so-called. [101]\n\nAlthough faith is formally in the intellect, it is nevertheless a perception of God that is impregnated with affectivity. On the one hand the God we attain by faith is at the same time infinite Truth and infinite Love, and on the other, the faith that attains to Him is an act of the intellect moved by the loving will. In actual fact,\" then, \"living faith\" is a faith that obscurely responds to the reality of God by a movement of love. Faith is penetrated with love. It \"only establishes a living contact between the soul and God in so far as it is vitalized by charity. But the more intense is the love that moves us to seek God beneath the analogical formulas of revealed truth, the more vital will be the grasp of our faith upon the hidden reality of God. So, in the experience of living faith our \"eyes are held\" in so far as the intellect is in darkness and assents without intrinsic evidence to the truths proposed to us. We do not realize how close God is to us, and yet our \"hearts burn within us\" because of the ardor of our love.\n\nThis ardor of love constitutes a kind of indirect experience of God. The interior soul, without yet realizing how much this experience can mean, becomes aware, by a kind of ingenuous reflection upon this burning of love, that this must be a sign or an effect of the presence of God. And thus it seeks Him with a more or less conscious and enlightened ardor in the pages of Scripture and especially in the prayers of the Liturgy and the verses of the Psalms. Such a person soon finds that there is hardly a line in the Office, hardly a word in the Mass, that is not capable at one time or another of awakening this interior burning of love that mutely betrays the fact that God is close at hand. This \"living faith\" then becomes habitual. It transforms the Office from a routine into a constant joy. Living faith prepares us for contemplation. The experience I have just described is not contemplation in the strict sense. It is only a \"masked\" or \"veiled\" contemplation\u2014one that is not fully developed or consciously aware of its own potentialities. Nevertheless, it is quite sufficient to make the recital of the Office contemplative in a broad sense. It enlivens our choral prayer with frequent \"recognitions\" of God in His inspired words, it trains us to sense His comings and goings in our own heart, it gives us eyes that penetrate into the deepest meanings of the Psalms and brings us under the intimate guidance of the Holy Spirit, who is ever anxious to lead us on to a deeper and deeper penetration of the mysteries of our Redemption. Finally, these movements of obscure and loving faith soon gain a hold over our minds and wills. If we are quick to respond to them, we find that they lovingly retain us and hold us, for long, thoughtless moments, under their spell. Thus we quite easily and spontaneously come to spend much of the time of our Office in these smooth flights of simple repose, gliding through the verses of the Psalms with our hearts absorbed in a simple gaze upon the God Who is invisible but near, and Whose love now holds us captive by its unworldly charm.\n\nBut it also happens\u2014and this is rarer\u2014that under the pressure of a very great love, or in the darkness of a conflict that exacts a heroic renunciation of our whole self, or in the ecstasy of a sudden splendid joy that does not belong to this earth, the soul will be raised out of itself. It will come face to face with the Christ of the Psalms. In an experience that might be likened to a flash of dark lightning, a thunderclap on the surface of the abyss, \"its eyes will be opened and it will know Him and He will vanish from its sight.\" [102] This momentary blaze of recognition is not produced by a created species or image in the soul. It is the flash of a flame that is touched off by an immediate contact of the substance of the soul with God Himself. In one terrific second that belongs not to time but to eternity the whole soul is transfixed and illumined by the tremendous darkness which is the light of God. And from the heart of that darkness speaks the voice of the eternal Christ, and now, although we still cannot be said to \"see,\" we experience in all truth what before we only believed, and we \"know\" that He is the Son of God, the King of Glory, and that \"He is in the Father and we are in Him and He is in us.\" [103]\n\nIt is sometimes given to a soul, in an experience of love that is absolutely terrible, to enter deeply into the mystery of Christ's Passion as it is presented to us by the Holy Spirit, in the Psalms. At such a moment, one can experience something of what St Paul spoke of. The text of his which I have in mind is the keynote of the Holy Week Liturgy, since it opens the Epistle for Palm Sunday, is repeated at the Gradual of Holy Thursday, and recurs over and over again in the antiphon of all the canonical hours from Holy Thursday to the Holy Saturday: \" _Let this mind be in you which was also in Christ Jesus, who, being in the form of God, thought it not robbery to be equal with God; but emptied Himself taking the form of a servant... He humbled Himself becoming obedient unto death, even the death of the Cross. For which cause God hath exalted Him and hath given Him a name that is above all names_...\" [104]\n\n_Hoc enim sentite in vobis_. Perhaps the old expression, \"let this mind be in you,\" does not quite convey to us all that St Paul means. We are to experience what Christ experienced. The same thing has to happen to us. We have to live through it. Or rather, Christ has to live through it again _in us_. And what does He have to live through? This _emptying_ , this total outpouring of ourselves, until we too have to cry _Consummatum est!_ \"Round about me are many bulls, the strong bulls of Basan hem me in. They open their mouth against me like a lion ravening and roaring. 1 am poured out like water, and all my bones are disjointed: my heart has become like wax, it melts in my bowels. My throat is dried up like a potsherd and my tongue cleaves to my jaws; thou hast brought me down to the dust of death.... [105]\n\nIt can sometimes happen that we too are brought down by Christ's love, into the dust of death. Then we know, somewhat as He knew, what it is to be \"poured out like water.\" It is the terrible experience of seeing oneself slowly turned inside out. It is the frightful taste of a humility that is not merely a virtue but the very agony of truth. This ghastly emptying, this inexorable gutting of our own appalling nonentity, takes place under the piercing light of the revealed word, the light of infinite Truth. But it is something far more terrible still: we find ourselves eviscerated by our own ingratitude, under the eyes of Mercy.\n\nThis is the experience that will come to one who once thought he had virtue, who once thought he had a \"degree of prayer,\" who once thought, perhaps, that he loved God indeed, and was God's good friend and who then, one day, is brought up for judgment, to be purified of all that is too human in his dream. For he has been cornered and accused, pierced and emptied by the shame of remembering who he really is. God seems to turn away His face. God seems to withdraw His protecting hand, and all the things he treasured, that were not God, have wasted away like shadows with the loss of His presence. This emptiness, this sense of spiritual annihilation which is due to us all as men born in sin and grown old in sin, Christ took upon Himself when it was not due to Him at all and He emptied Himself of all His power and glory in order to descend into the freezing depths of darkness where we had crawled to hide ourselves, cowering in blind despair.\n\nBut because Christ came down into this no-man's land of sin, to find us and bring us back to His Kingdom, we are able to discover the living God in the very darkness of what seems to be His utter absence. And what is more, it may be that we find Him there more truly than when we thought we saw Him in the light of our own dim day.\n\nSo it can happen that a soul enters upon the recital of a Psalm applicable to Christ's Passion\u2014let us say Psalm 87. It is a day on which we seem to be buried alive under an inhuman burden of temptation. Perhaps we may also suffer sickness, physical as well as moral desolation. But the worst thing of all remains the inescapable vision of our own almost infinite capacity for pettiness and degradation. \"O Lord my God, I cry by day, in the night I weep before thee. Let my prayer come before thee, incline thy ear to my cry. For my soul is full of evils and my life is on the verge of the grave... Thou hast laid me in a deep pit, in darkness, in the abyss. Thine indignation weighs upon me and with all thy waves thou dost overwhelm me. Thou hast taken away my friends from me; thou hast made me abominable to them; I am shut up, I can no longer go forth.\" [106] This is practically the only Psalm that ends on a note of complete dejection. There is a faint flame of hopeful prayer, but it is beaten down by the cold darkness of apparent refusal, and here is how the Psalm ends: \"Thy wrath has swept over me and thy terrors have destroyed me. They surround me like water all the time: they assail me all together. Thou hast taken from me friend and companion; The darkness is my intimate.\" And that is all.\n\nYet at such a moment, and in such a Psalm, the soul, catching and comprehending in its own black mirror the fearful darkness of revelation, is confronted in its own depths with the countenance of the murdered Christ. This is more than a meeting. It is an identification. We have entered into a Baptism of darkness in which we are one with His death. But to die with Christ is to rise with Him, we cannot be dead with Him without our life being hidden with Him in God. [107] Although there remains a formal difference between the grace of the Passion of Christ by which we are delivered from sin, and the grace of His Resurrection in which supernatural life is communicated to us, nevertheless in fact both are poured out in the wonderful night of which the Liturgy sings in the _Exultet_. [108] This night of Mystery in which we rise from death with the hidden Christ is the spiritual Red Sea of which the Psalms have sung to us all along. Now we have entered into it in truth and have passed through it to be nourished by God with His Body in the wilderness.\n\nThis is a death in which we have found Him Who is the way, the truth and the life. We now know that this darkness, which seems to annihilate us, is not the darkness of death but, if such an expression can be understood, the darkness of life. The tides of light that pour down upon the whole Church from the mountain top which is the soul of the Risen Saviour, blind us by their intense purity and drown us in darkness although they are essential Light, and so the Night of the Spirit is already a sharing of the Resurrection. If the paradox may be allowed, this frightful death is our first taste of glory.\n\nThen we begin to discover that the night in which we seem to be lost is the protection of the shadow of God's wings.[109] If God has brought us into this darkness it is because He wishes to guard us with extreme care and tenderness, or, in the words of the Psalm, \"like the apple of His eye.\"[110] The new life of the soul united Christ in His Mystery is something too delicate and tender to be let loose in a crowd that may contain hidden enemies, and therefore God has isolated the soul in a soundless and vast interior solitude, the solitude of His own Heart where there is no human spectator and where the soul can no longer even see itself. True, the depths of that solitude open and close in a flash: but the soul remains enveloped and penetrated with divine emptiness, saturated with the vastness of God, charged with the living voice of silence in which His Word is eternally uttered.\n\nThe protection of darkness and silence is extremely necessary for the soul that begins to burn with these touches of the Spirit of God. If it should come close to Him Who is Life without being enclosed and hidden in His life, it will find itself charged with more power than it can stand and it will burn itself out with an ardor that it cannot control. For when the soul has thus known God divinely, the memory of the encounter is sometimes stirred up by the lines of Psalms, to a blaze that unnerves it beyond its capacity to bear. In this degree of prayer there may arise high seas of inspiration that destroy the mind with the weight of a superhuman demand. But we have no help from God to tackle this demand. It is not the wave of His present power, but an undertow that follows after His passing. Caught in the clenched fist of this bullying sea of love that is neither human nor divine and which seems to be something elemental in its brutality, we are drawn under and seem to drown until God catches us again and holds us under, not under the sea but under the Mystery of His eternity, where alone there is breathing.\n\nThis undertow, too, flows through the Psalms. It tends to attack us most where there are appeals made to our mind and will by the word of God, by ceremony and liturgy and chant. These aids to prayer which were a help to us at the very beginning and which went unnoticed as we advanced in living faith and in the prayer of quiet, which were sources of light and brought us into intimate union with Christ in His Mysteries, now turn against us like Goliath and we have no stones and sling with which to fight back. This is the time when every line of the Psalms bursts forth with lights that we no longer need, spurious and tremendous inspirations that exhaust the soul and contribute nothing to its peace. And the soul seems to find no refuge where it may flee them. They come upon it like an army from every side and there is no resistance. The only safety is in darkness, the protection that can only be extended over us by the outstretched hand of God. We need that protection, and more and more we sense our need. For the devils too, understand our position. They stand to profit if they can destroy and exhaust us with false lights and raptures of their own devising. This is the stage when the soul that is too tough for its own good, too well able to stand the overpowering sweetness of halfnatural ecstasies, will be in danger of entering the ways of false mysticism. Prayer will become debauchery, the Liturgy a riot of prophecy and carnal exaltation. The mark of all this falsity is violence. It is sealed with the seal of contention and brutality and strain. These are the spiritual footprints of the devil who, if he cannot deceive the soul with false raptures, soon tears off his mask and lets loose against us a jungle full of terrors and we live in nightmare on the threshold of the deepest darkness that alone can save us.\n\nIn this tribulation the Lord God is ever with us, no matter how much we fear. _Cum ipso sum in tribulatione_. These are words from Psalm 90 which are chanted every night in the monastic Compline when the shadows fall upon the cloister and the monks are ending their day of prayer. \"I will be with him in trouble, I will rescue him and honor him.\"[111] The angels are at our side, holding us up lest we should dash our foot against a stone. We could not travel through the forest that the spiritual life has now become, unless His power carried us onward, where we tread upon the asp and basilisk and never feel their sting, and never suffer harm! _Altissimum posuisti refugium tuum_. We have made the Most High God our refuge. The scourge will never touch us.\n\nWhat are the horizons that lie ahead, in the ascent to the City of God in heaven? There are high peaks before us now, serene with snow and light, above the level of tempest. They are far away. We almost never see them they are so high. But we lift up our eyes toward them, for there the saints dwell: and these are the mountains of holiness whence cometh our help. _Levari oculos meos in montes unde veniet auxilium mihi_. [112]\n\n# 2:\n\n# _The Silence of the Psalms_\n\nONE THING REMAINS TO BE EXPLAINED. WE HAVE emphasized, in this book, the truth that the Psalms most often become contemplation when, through them, we manage to unite our sufferings with the sufferings of Christ, so that He in turn lifts us up in His own triumph and raises us to a foretaste of His glory. Why this emphasis on suffering? Suffering is not the only theme in the Psalter.\n\nWe bring the substance of our own lives to the Psalter and offer it to Christ to be transformed by Him. It is all matter for sacrifice. But since life on earth is what it is, we all have plenty of trouble, plenty of suffering, plenty of misery. We have our joys too. And we should not omit to offer them to Christ and unite them with His joys. But I insist on the importance of bringing Him our sufferings because it is precisely these that He wishes to transfigure into His purest joys. After all, the real joys of life do not come when we supernaturalize our trifling little human successes with an act of pure intention. We enter into true joy through the center of our own nothingness. We find true happiness by dying, because our truest happiness belongs to heaven and we can only enter heaven by dying to the things of earth. It is quite normal, then, that the theme of suffering in the Psalms should lend itself very readily to contemplative union because \"through many tribulations we must enter into the Kingdom of God.\" [113]\n\nBut, finally, here is the deepest reason of all for the intimate connection between the Cross and contemplation. It is a theme that comes before us more than once in the Liturgy of Passiontide. Christ said \"Unless the grain of wheat, falling into the ground, die, _itself remaineth alone_.\" [114] It is by His Passion and death that Jesus gathers to His Heart the sons of God, those whom His Father has given Him, of whom not one shall be lost. It is \"when He is lifted up that he draws all things to Himself.\" It is in His passion that He wins them all for His own, and earns the right to offer them all to His Father and raises them all into the life of grace and glory. It is by dying for us that Jesus has drawn us all into the triumph of His Resurrection. All this is set before us with a clarity that is as beautiful as it is terrifying, in the unwitting prophecy of the High Priest Caiphas: \"It is expedient that one man should die for the people and that the whole nation perish not. And this he spoke not of himself, but being the high priest of that year he prophesied that Jesus should die for the nation, and not only for the nation, _but to gather together in one the children of God that were dispersed_.\" [115]\n\nThat is why the Cross of Christ is the key to the Psalms. The Mystery of the Mystical Body, as St Augustine so often insisted, is central to the Psalter and essential for its proper use as prayer, and the texts we have just quoted show us the connection between the Cross and the Mystical Body. Hence it is from the tree of the Cross that all the other mysteries in the Psalter bud forth and spread out before the gaze of the contemplative, and once we have entered into the Mystery of Christ's Death, the Resurrection and Ascension into heaven are assured us. Indeed, since the Mystery of Christ's death is the Mystery of Unity of His Mystical Body, by entering into His death we are helping Him to \"draw all things to Himself.\" When we are most intimately united with Him by love and hidden in the \"secret of His Face\" we are in the truest sense Apostles. [116] Those who exercise the greatest power, in the Communion of Saints, are those whom the Lord has \"hidden in His tent from the wrangling of tongues.\" [117] I am not here talking of exterior silence or of a vocation to an enclosed Order, but of the interior silence of the mystic, in no matter what walk of life he may happen to find himself, for it may happen, and it should happen, that even one who has to preach and teach should remain protected from the inanity of vain speech, should keep His heart a sacred sanctuary for the word of God, hidden in the urn of contemplation like manna in the Ark. There is more than meets the eye in this Mystery which the Psalmist speaks of as the \"wrangling of tongues.\"\n\nThe \"wrangling of tongues\" symbolizes the confusion that was sent down by God upon the builders of Babel, who, seeking to scale heaven with a structure of their own devising, were darkened and scattered in a division of tongues. [118] Babylon, the city of division, the city of those who \"love themselves unto the hatred of God,\" [119] was born in a curse of tongues and the Church, the City of union, the City of those who love God unto hatred of themselves was born of the gift of tongues. The Holy Ghost was poured out at Pentecost in tongues of flame, and made the Apostles speak in all languages in order that men might be drawn back into union and that the division, laid open at Babel, might be closed again and healed in Christ and in His peace. For there is only one language spoken in the City of God. That language is charity. Those who speak it best, speak it in silence. For the eternal Word of Truth is uttered in silence. If He is uttered in silence, He must be heard in deepest silence. And His Spirit, the Spirit of Love, is also poured out into our hearts, proceeding from the Father and the Son, in an everlasting silence.\n\nThe Psalms are more than language. They contain within themselves the silence of high mountains and the silence of heaven. It is only when we stand at the bottom of the mountain that it is hard for us to distinguish the language of the Psalter from the tongues of this earth: for Christ must still perforce travel among us as a pilgrim disguised in our own tattered garments. The Psalter only truly begins to speak and sing within us when we have been led by God and lifted up by Him, and have ascended into its silences. When this is done, the Psalms themselves become the Tabernacle of God in which we are protected forever from the rage of the city of business, from the racket of human opinions, from the wild carnival we carry in our hearts and which the ancient saints called \"Babylon.\"\n\nThe Liturgy of Heaven is a most perfect harmony which, like the music of the spheres, sees song transfigured into silence. The Psalter is the prelude to that Liturgy. A prelude is a real beginning. We who chant the Psalms are standing in the courts of Heaven. That, indeed, is our chosen testimony. It is the Christian vocation: to begin on earth the life and Liturgy of Heaven. St John in his Apocalypse describes the songs of the four-and-twenty elders and of the blessed spirits. Their Liturgy is full of echoes of the Psalter. Theirs are the same themes for theirs is the perfect liberty which the Psalms foreshadow. They sing of the great mercy of God their liberator, and in doing so they burn with glory because they see and love Him as He really is. We have already entered with them but obscurely, into this Mystery. We have tasted the wine of their wedding feast paid out to us in droplets in moments of our own earthly Liturgy.\n\nThe wine of the Psalter and the wine of Heaven are the same, and they are ours, because whether in Heaven or on earth there is only one chalice, and that chalice itself is Heaven. It is the cup Jesus gave to His Disciples on the night when He said to them: \"With desire have I desired to eat this Pasch with you.\" [120] There is one Mystery\" in the Kingdom of heaven, which is the light of that Kingdom, replacing the sun, moon and stars. It is the light also of the Psalter and of the Church on earth, though it shine in darkness. Its light is wine. It was of this wine that Jesus said: \"I shall not drink the fruit of this vine again until I drink it with you now in the Kingdom of my Father.\" [121] He had just chanted the Psalms of the _Hallel_ with His Apostles. He knew His Blood would flow like silence through our Psalter.\n\n# EPILOGUE\n\n\"I WILL PRAY WITH THE SPIRIT\" WROTE ST PAUL to the Corinthians, \"I will pray also with the understanding; I will sing with the spirit, I will sing also with the understanding.\"[122]\n\nSo, too, when we sing the Psalms, the words that are placed before us by the Church are supposed to awaken all the deepest powers of our being and raise us up to God\u2014or rather to show us that, because of the death and Resurrection of Christ, we find ourselves at this very moment _in_ God, Whose Kingdom has come and is waiting to be revealed in us His sons. How will it be revealed to the world unless it first be realised in us, in whom the Scriptures are to be fulfilled?\n\nThe Spirit of God, pouring out the charity of God in our hearts, makes us love the sanctity of God. He makes us reach out to receive the gift of holiness which is offered to us in Christ by The Father's infinite mercy. The deep fire of prayer which burns in the heart of the Psalter is therefore a fire of sacrifice, the same fire which consumed the Heart of Jesus Himself and brought Him to the Cross for us, and brings us gladly and triumphantly down into the gates of death for love of Him. This love, this chaste and selfless passion that drives us out into the desert, seeking holiness in the renunciation of all things, this is the key to the understanding of the Psalter because it is itself the fulfilment of the Psalter.\n\nSt Paul says that love is the fulfilment of the Law. Now the Old Law as a whole is a type or figure of the New. The \"spiritual meaning\" of the Old Law is therefore to be sought in the charity which is the very substance of the New Testament. St Thomas points out that the New Law is something more than a written document. It is grace itself living and acting in the hearts of the faithful. It is the Holy Spirit, present in the souls of those who have died together with Christ and have risen with Him from the dead. The Angelic Doctor quotes St Augustine, who says:\" The Laws of God, written in our hearts, are nothing else but the presence of the Holy Spirit in us.\"[123]\n\nHence we may dare to say that charity, not as a pale abstraction but as the flame breathed through our being by the presence and action of the Holy Spirit, alone enables us to plumb the depths of the \"spiritual sense\" of Scripture. What is hidden beneath the literal meaning is not merely another and more hidden _meaning_ , it is also a new and totally different _reality_ : it is the divine life itself. This \"meaning\" of Scripture is never grasped if it is merely \"known.\" It must be possessed and lived. God is not fully known when He is only \"known\" by the understanding. He is best known by us when He takes possession of our whole being and unites us to Himself. Then we know Him not in an idea but beyond ideas, in a contact of love, in an experience of Who He is, in a realization that He and He alone is our life and that without Him we are nothing. It is our joy to be nothing, and to know that He is all.\n\nSt Augustine long ago brought out this aspect of the distinction between \"letter and spirit.\" He knew that Paul's phrase: \"the letter killeth but the spirit giveth life,\" was intended to tell us more than the obvious truth that some passages of Scripture had a figurative or typical sense. The \"letter\" kills us not only by tempting us to miss a meaning. Even when the meaning (whether literal or spiritual) is abundantly clear, even when we fully grasp its implications, it \"kills\" us if we get no further than _knowledge_ of what it means.\n\nThe Law tells us: \"thou shalt not covet.\" No hidden sense here. The literal meaning is plain enough. Selfish desires are the root of all evil. But, says St Augustine: to know this truth without conforming our lives to the commandments not to covet, is to be _killed_ , by that commandment. If we had never known our responsibility we could not have been held guilty for not living up to it. In order to fulfil the law, we must be dead to the kind of life which the law intends to kill, and live by the new life which the law sets before us. This is a matter not of knowledge but of love. Everyone knows the ten commandments. Few keep them, because few love them. Men do not love the law of God because they cherish a contrary love, a contrary law, in their flesh, which defeats and denies the law of God. Knowing His law, they still fall short of knowing it, because they only possess the wisdom of the flesh, which cannot be subject to the law of God. It is foredoomed to rebel against Him because it has refused, in advance, to love Him.\n\nThe law was given by God to manifest the living death of sin, not to cure it. St Augustine's tract \" _De Spiritu et Littera_ \" is therefore not a treatise on the senses of the Scripture but on the law and on Grace. Yet it has most interesting implications for the meaning of Scripture, because charity is the fulfilment of the Law. The Law can only be undertood when it is kept. It cannot be kept unless God drives out the contrary law, the law of selfishness, of cupidity, and infuses into our hearts His selfless charity. Without grace, the \"letter\" of the Law, the truth of the Law, serves only to condemn us, because even though we understand it we do not keep it. But the \"spirit,\" grace, fills us with charity, gives us the power to love what the Law tells us. Loving the truth, we are able to live by the truth. When we live by the truth our lives themselves become true. We become what we ought to be. We not only exist, we _live_. We not only hear the word, we keep it, and therefore we _fulfil_ it. We live in God. God lives in us. His will is done in us. He is manifested in us. He is glorified in us. This was not possible until He sent His Son to be a propitiation for our sins. St. Augustine says:\n\n_Where the Holy Spirit does not help us, inspiring us with good desires to replace evil desires, that is to say pouring out Charity in our hearts, it is evident that the Law, good as it may be, by its very prohibition only intensifies our evil desires_. [124]\n\nWithout the Holy Spirit we can admire the goodness of God and His truth. We can even attempt to see Him. But a love that is not inspired and directed by His Spirit misses its aim, even though it be aimed at Him: for only God can reach God. That is why He sent us His Son, to be the \"way.\" We must then receive His Holy Spirit, the Spirit of Jesus, Who will lead us to God by the power of a secret and spiritual delight in the things of God, by a taste for the hidden truth of God, by love that finds Him in the mystery of a presence that is only secret because it is too blinding in its obviousness to be seen by us. _Accipiat homo Spiritum sanctum quo fiat in animo ejus delectatio dilectioque summi atque incommutabilis boni quod Deus est_.[125]\n\nThe outpouring of the Spirit is the fulfilment of the Law the Psalms and the Prophets. When Jesus appeared to His disciples in the cenacle after His resurrection, He told them that it was \"necessary for all things to be fulfilled which are written in the Law of Moses and in the Prophets and in the Psalms concerning me.\"[126] Then he \"opened their understanding\" and showed them the \"spiritual meaning\" of the Scriptures\u2014as well as the letter. What was this fulfilment? Not only the death and Resurrection of Jesus\u2014these were ordered to something else, to His life in us. It was therefore written not only that Christ should \"suffer and rise again from the dead the third day\" but also that great effects should follow from these things: \"that penance and remission of sins should be preached in His name unto all nations beginning at Jerusalem.\" The charity of the Saints is the fulfilment of the Scriptures. The outpouring of the Holy Spirit makes this a fact, and enables those in whom He acts to understand what has happened. \"And you are witnesses of these things. And I send the promise of my Father (the Holy Spirit) upon you: stay you in the city until you be endued with power from on high.\"[127]\n\nWe who chant the Psalms, hope to praise God. We praise Him best if we understand the things we sing. We understand them if we, too, are \"endued with power from on high.\" When the Spirit of Divine Love sets our souls on fire with charity we realize, at last, that it is not necessary for us to scale heaven to bring down Christ to us by some mysterious technique of contemplation. The Liturgy does not have to bring Christ from heaven. It is the manifestation of His presence and His power on earth. It does not have to prepare our hearts for a future Kingdom. It tells us that His Kingdom has already come. _Regnum Dei intra vos est_. It is established in full power in the midst of a godless humanity. Heaven is within us and all around us, even though we seem to be living in hell.\n\nThe Psalms are the language of His Kingdom. They were spoken by prophets to those who were able to understand them centuries before the Kingdom was established. They were sung as they were fulfilled by the Saviour as He hung on the Cross, so that the voice of the Psalms is the voice of Christ Himself. He lives in us, being both the Kingdom and its King. And we, when we take His words upon our lips, speak not our thoughts but His, provided that the Spirit of His Promise lives in our own spirit and is the inspiration of our own song.\n\nTherefore, when a Christian chants the Office, if he is fully a Christian, that is to say if He is one who has attained to the knowledge of Christ, who has experienced what it means to live in the great mystery of Christ, who longs to see all things restored in Christ, then he not only understands the Psalms, but _he fulfils_ them. The deep contemplative penetration of the Psalms, is only achieved by their fulfilment. It is the realization of their fulfilment in us. It shows us our own place in the Mystery of Christ, and our own vocation, to make up what is wanting to His sufferings in our own moment of history. But the Psalms are the songs of eternity since His Kingdom is the Kingdom that will never end. In the simultaneous totality of possession, which is what eternity means, the Psalms reach out to possess the reward together with the suffering, the victory in the midst of the battle. We have only begun to fight and yet if we believe in Him Who overcomes the world, we have already won. \"For whatsoever is born of God overcomes the world: and this is the victory which overcomes the world, our faith.\"[128]\n\nLaws, rules and methods are for those who seek to get something for themselves. They therefore savor of this earth and of its slavery, although they are necessary even for those who would begin to be children of the kingdom. But after all, it is not by seeking to \"get something out of the Psalms\" that we will finally arrive at an understanding of the Psalter or of our Canonical Office. Although the Psalms are given us for our benefit it is not enough to think only of our own benefit: they are first of all for the glory of God. God is glorified most in those who have given up everything for Him and have found everything in Him. The Psalms profit us most when they give God most Glory. This they do when we realize that the Liturgy is not a search for something we have not, but the celebration of what we already have.\n\nThe Psalms are the new song, the _canticum novum_ , the song of those who have been reborn in a new creation, the song of those for whom there is no law, because in them Christ has fulfilled the Law. How, then, should the Psalms offer them a method, a technique, that is to say a \"law\" of contemplation? The true meaning of the Psalms is most fully apprehended by those who have been swept, by an experience of God's mercy, beyond the reach of any rule or any method. The new song of the Psalms is the song of God's children who live by no other rule than God their Father, Who is His own Rule. He is also therefore theirs. His love is their Law. They always do what is pleasing Him. Thus for them there is no law, not because the law has been abrogated but because it has been perfectly fulfilled.\n\n## _Author's Note_ :\n\nIn dealing with the spiritual sense of Scripture in this book, it has been my intention to follow as closely as possible the norms laid down in recent Papal documents, especially the Encyclical _Divino Afflante Spiritu_. If my ignorance and stupidity have led me to misinterpret the teaching of the Church, I wish it to be known that I renounce any error that I may have made. In places where I have presumed to hold that any particular Scriptural text had a spiritual sense, and where I have expressed some opinion regarding that sense, I invite those who strongly disagree with my interpretation to disregard my opinion and to act as if I were merely making a pious application of the text. They will then, I hope, be more inclined to see and appreciate the practical consequences of my opinions in the life of prayer.\n\n## _Notes_ :\n\n1 _Acts of the Apostles_ , 17: 24\u201328.\n\n2 _John_ , 17: 3.\n\n3 _The Way of Perfection_ , Chapter 30.\n\n4 _Ibid_., Chapter 37.\n\n5 _Ibid_. See especially Chapters 25, 26, 27.\n\n6 Cassian, _Collatio_ , I, iv. _Patrologia Latina_ , Volume 49, Column 486.\n\n7 _Patrologia Latina_ , Volume 6, Column 489.\n\n8 _Collatio_ xiv, 10; Translation from Owen Chadwick, _John Cassian_. Cambridge, 1950.\n\n9 _Ibid_. xiv, 10. cf. _Leviticus_ , 26: 12 and _II Corinthians_ , 6: 16.\n\n10 _De Coenobiorum Institutis_ , II, 11. _Patrologia Latina_ , Volume 49, Column 100.\n\n11 _Collatio_ , IX, 31. _Patrologia Latina_ , Volume 49, Column 808. \" _Non est perfecta oratio in qua se monachus vel hoc ipsum quod orat intelligit_.\"\n\n12 _Collatio_ , IX, 25. _Patrologia Latina_ , Volume 49, Column 801.\n\n13 \"The soul that is athirst for God.\"\u2014St Bernard.\n\n14 _Psalm_ 105.\n\n15 _Psalm_ 1, 1\u20133.\n\n16 _Psalm_ 143, 12\u201315.\n\n17 _John_ , 3:14.\n\n18 _Acts of the Apostles_ , 2: 29\u201331.\n\n19 _Divino Afflante Spiritu_ , nn. 26\u201327. N.C.W.C. edition of English translation emanating from the Vatican.\n\n20 See Jean Dani\u00e9lou _Bible et Liturgie_ , Paris, 1951, and _Sacramentum Futuri_ , Paris, 1950.\n\n21 _The Ascent to Truth_ , New York, 1951, p. 302, cf. also an important article \"Scripture in the Spiritual Theology of St John of the Cross,\" by Fr. Barnabas Mary Ahearn in _Catholic Biblical Quarterly_ , Volume 14, n.1, p. 6.\n\n22 _1 Corinthians_ 2: 11\u201312.\n\n23 _Mediator Dei_ (November 4, 1947).\n\n24 _Ibid_., Part III.\n\n25 _The Living Flame of Love_ , III, 38; translated by Peers, Volume III, 181.\n\n26 \"Expleto Opere Dei omnes cum summo silentio excant, et agatur reverentia Deo, ut Frater, qui forte sibi peculiariter vult orare, non impediatur alterius improbitate.\"\u2014 _Rule of St Benedict_ , Chapter 52. Cf. Chapter 20: \"Brevis debet esse et pura oratio: nisi forte ex affectu inspirationis divinae grati\u00e6 protendatur.\"\n\n27 Cf. _The Roman Missal_ : Collect for the Mass of the Dedication of a Church.\n\n28 _Psalm_ 18, 2\u20137.\n\n29 _Psalm_ 148, 1\u201313.\n\n30 Cf. _Romans_ , 1: 18 and _Acts_ , 14: 15.\n\n31 I am especially indebted to the article of P\u00e8re Jean Dani\u00e9lou, S. J.: \"The Problem of Symbolism\" in _Thought_ , September, 1950. See also his book _Sacramentum Futuri_ , Paris, 1950.\n\n32 The classical passage in this connection is the first chapter of St Paul's _Epistle to the Romans_.\n\n33 _Romans_ , 1: 18.\n\n34 _Romans_ , 1: 25.\n\n35 _Psalm_ 8, 2, 4\u201310. Every line of this Psalm has anti-polytheistic repercussions. Man, who can see God _through_ His creation is in possession of the truth which makes him free. ( _John_ , 8 : 32). Thus he leads a spiritualized existence \"a little less than the angels\" and stands in his rightful place in the order of creation, above the irrational animals. The Gentiles, on the other hand, have descended lower than the animals since they have lost the knowledge of God though God remains evident in His creation. For by their ignorance of God, they have doomed themselves to the worship of beasts. ( _Romans_ , 1: 23). Compare also: St Bernard; _De Diligendo Deo_. Chapter II, n. 4; _Patrologia Latina_ , Volume 182, Column 970.\n\n36 _Isaias_ , 53: 6.\n\n37 _Hebrews_ , 4: 12.\n\n38 _John_ , 5: 39\u201340.\n\n39 _Romans_ , 10: 4, 8\u20139.\n\n40 _John_ , 1: 45.\n\n41 _Enarratio in Psalmum_ , 93, Paragraph I. _Patrologia Latina_ , Volume 37, Column 1189.\n\n42 _Psalm_ 68, 1\u20134.\n\n43 _Psalm_ 68, 14\u201315.\n\n44 _Psalm_ 31, 36\u201367.\n\n45 _John_ , 3: 27.\n\n46 _John_ , 1: 33.\n\n47 _John_ , 1: 12.\n\n48 _Ephesians_ , 2: 5\u20136.\n\n49 \"Grant, we beseech Thee, almighty God, that we who believe Thine only begotten Son to have ascended this day into heaven, may also ourselves dwell in spirit in heavenly places.\"\u2014 _The Roman Missal_ : Collect for Ascension Day.\n\n50 \"... ut quae visibilus mysteriis sumenda percepimus, invisibili consequamur effectu.\"\u2014 _The Roman Missal_ : Postcommunion for Ascension Day.\n\n51 \"God who of old in many ways spoke to the Father in the Prophets has lastly in these days spoken to us in His Son...\"\u2014 _Hebrews_ , 1: 1.\n\n52 \"Do you not know that as many of us as have been baptized in Christ Jesus, are baptized in his death? We are buried together with Him by Baptism in death in order that, just as Christ rose from the dead by the glory of the Father, we also might walk in newness of life. For if we are sown in the likeness of His death, we shall share in the likeness of His Resurrection... But if we are dead with Christ, we believe that we shall also live with Christ, knowing that Christ, rising from the dead, dieth now no more, and death shall no longer have dominion over Him, because He died to sin, He died once; but because He lives, He lives unto God. So you also, consider yourselves as dead to sin but living unto God in Christ Jesus our Lord.\"\u2014 _Romans_ , 6:3\u201411.\n\n53 _Matthew_ , 10: 38\u201339.\n\n54 _John_ , 17: 23.\n\n55 The term _res sacramenti_ is a technical one, used to distinguish the mere external conferring of a Sacrament ( _sacramentum tantum_ ) from the notion of the Sacrament considered as fully and concretely realizing the purpose of its institution by a fruitful production of its signified effect.\n\n56 St Leo: _Sermon IXIII. Patrologia Latina_ , Volume 84, Column 357. He is speaking of Baptism, but the same is true _a fortiori_ of the Holy Eucharist.\n\n57 _Ibid_.\n\n58 _Ibid_.\n\n59 See _Hebrews_ , 3. Compare also: _1 Corinthians_ , 10:6, 11.\n\n60 _1 Corinthians_ , 10: 4.\n\n61 _Numbers_ , 24: 2\u20139.\n\n62 _I Peter_ , 2: 21.\n\n63 \"Jerusalem quae aedificatur ut civitas, cujus participatio ejus in idipsum: illi enim ascenderunt tribus, tribus Domini, testimonium Israel ad confitendum nomini Domini.\"\u2014 _Psalm_ 121: 3\u20134.\n\n64 _Galatians_ , 6: 14.\n\n65 \"The charity of God is poured forth in our hearts by the Holy Spirit Who is given to us.\"\u2014 _Romans_ , 5:5.\n\n66 _1 Corinthians_ , 2: 6\u201310.\n\n67 St John of the Cross: _The Living Flame of Love_ , Stanza I, n. 15.\n\n68 _Enarratio in Psalmum_ , 30, Paragraph 4.\n\n69 _In Epistolam, Joannis ad Parthos_ , Tractatus V, Chapter 5, Paragraph 3. _Patrologia Latina_ , Volume 35, Column 2055.\n\n70 _Enarratio in Psalmum_ , 61. _Patrologia Latina_ , Volume 36, Column 730. It is the teaching of the Fathers that we are all originally created mystically as \"one man\" and that this \"Person\", divided by the sin of Adam, is reconstituted in one mystical Body in Christ, the new Adam. Compare St Cyril of Alexandria, in _Evangelium Joannis, i_ , \"Sumus omnes in Christo, et communis humanitatis persona in ipsum revivisciti.\"\n\n71 \"A finibus terrae ad te clamavi.\"\u2014 _Psalm_ , 60: 3.\n\n72 The \"Gradual Psalms\" are the group from Psalm 119 to 133 inclusive. Each one is entitled \"Canticum graduum\" in the Vulgate.\n\n73 _Matthew_ , 5: 5.\n\n74 _De Civitate Dei_ , XIV, 25.\n\n75 _De Civitate Dei_ , XIV, 26. The terms \"blessedness\" and \"fruition\" are of course only relative here.\n\n76 _Psalm_ 39: 7\u20139.\n\n77 _Galatians_ , 5: 13 and 17.\n\n78 _Galatians_ , 5: 13 and 17.\n\n79 _Romans_ , 10: 4.\n\n80 _Romans_ , 13: 10.\n\n81 _James_ , 1: 25.\n\n82 \"Causa diligendi, Deum Deus est, modus sine modo diligere,\"\u2014St Bernard: _De Diligendo Deo_ , I: 1.\n\n83 \"Lex Domini immaculata convertens animas\"\u2014 _Psalm_ 18: 8. It is not for us to enter into a technical discussion of the fact that perhaps for the author of the Psalms the word \"law\" may have meant the Law of Moses. Since the establishment of the New Testament the Fathers of the Church have taken it in St Paul's higher sense: with the consequence that St Ambrose's commentary on Psalm 118 (the longest Psalm, and all in praise of the \"Law\") becomes a treatise on the mystical Love of God in which Psalm 118 is considered as if it were the equivalent of the Canticle of Canticles.\n\n84 \"Delectabit sane non tam nostra vel sopita necessitas vel sortita felicitas, quam quod ejus in nobis et de nobis voluntas adimpleta videbitur, quod et quotidie postulamus in oratione cum dicimus fiat voluntas tua sicut in coelo et in terra.\"\u2014St Bernard: _De Diligendo Deo_ , X, 28.\n\n85 See _Matthew_ , 5: 17\u201320.\n\n86 _Matthew_ , 5: 20.\n\n87 _Psalm_ , 35: 7. St John of the Cross gives much the same interpretation of \"judicia Domini vera\" ( _Psalm_ 18: 10\u201311). _The Ascent to the Cross_ II, 26.\n\n88 _Psalm_ , 23: 3\u20136.\n\n89 See St Augustine: _De Sermone Domini in Monte_. St Thomas Aquinas, II, IIae, Q. 8, a.7.\n\n90 _De Diligendo Deo_ , XII, 34.\n\n91 _II Paralipomenon_ , 5: 13.\n\n92 _II Paralipomenon_ , 20: 20\u201321.\n\n93 _II Paralipomenon_ , 20: 24.\n\n94 _Galatians_ , 5: 23.\n\n95 _I Kings_ , 23: 14.\n\n96 _Psalm_ 53: 6\u20138.\n\n97 _Enarratio in Psalmum_ 53, Paragraph 10.\n\n98 _Psalm_ 136: 4.\n\n99 _Loc cit_. Note that it is no sin _not_ to love God gratuitously. But this \"freedom\" is the perfection of love.\n\n100 _Luke_ , 24: 16, 32, 31.\n\n101 I only wish here to make a legitimate application of this Gospel text. Although the first example taken is probably a literal expression of the experience of \"living faith\", the second is not precisely what I mean by mystical contemplation since it was, probably, a grace of the order of \"gratiae gratis datae\" and, in any case, it was a vision. The mystical contemplation which concerns us here is an experience of God in obscurity, a recognition that is not achieved by the senses or through the medium of any species, intelligible or otherwise. The second Gospel example, then, is used here only as an analogy.\n\n102 _Luke_ , 24: 31.\n\n103 This is another of the key texts in the Mystical Theology of Christ's discourse at the Last Supper. \"In that day you shall know that I am in my Father and you in me and I in you.\"\u2014 _John_ , 14: 20. We are not here speaking of a formal illumination of the intellect such as is enjoyed by the blessed in Heaven. This is not an immediate intuition of God as He is in Himself, face to face, but an immediate experience of God by contact of love, in darkness.\n\n104 _Philippians_ , 2: 5\u201310.\n\n105 _Psalm_ 21: 13\u201316.\n\n106 _Psalm_ 87, 1\u20134, 7\u20139.\n\n107 _Colossians_ , 3:3.\n\n108 _The Roman Missal_. Blessing of The Paschal Candle, Holy Saturday.\n\n109 _Psalm_ 16: 8.\n\n110 _Psalm_ 16: 8. Compare also: _The Cistercian Breviary_ : Versicle for Compline.\n\n111 _Psalm_ 90: 15.\n\n112 _Psalm_ 120: 1.\n\n113 _Acts_ , 14: 21.\n\n114 _John_ , 12: 24.\n\n115 _John_ , 11: 50\u201352. Gospel for Friday in Passion Week.\n\n116 _Psalm_ 30: 21 \"Abscondisti eos in abscondito facie tuae.\"\n\n117 _Psalm_ 30: 21.\n\n118 _Genesis_ , 11: 7.\n\n119 St Augustine: _De Civitate Dei_ , XIV, 28.\n\n120 _Luke_ , 22: 15.\n\n121 _Matthew_ , 26: 29.\n\n122 _1 Corinthians_ , 14: 15\n\n123 I IIae. Q.106. A.1. and St Augustine, _De Spiritu et Littera_ , 26.\n\n124 _De Spiritu et Littera_ , Chapter iv.\n\n125 _Ibid_., Chapter iii.\n\n126 _Luke_ , 24: 44.\n\n127 _Luke_ , 24: 48\u201349.\n\n128 _I John_ , 5: 4.\nEX PARTE ORDINIS\n\n_Nihil Obstat_  \nFrater M. Maurice Malloy, O. C. S. O.  \nFrater M. Paul Bourne, O. C. S. O.  \n _Imprimi Potest_  \nFrater M. Gabriel Sortais, O. C. S. O.  \n _Abbas Generalis_\n\nNIHIL OBSTAT\n\nJohn M. A. Fearns, S.T. D.  \n _Censor Librorum_\n\nIMPRIMATUR\n\n  Francis Cardinal Spellman  \n _Archbishop of New York_\n\nCopyright 1953 by Our Lady of Gethsemani Monastery\n\nAcknowledgment: The photographs of \"Le Devot Christ\" at Perpignan, France, are by J. Comet and are reproduced in this volume and on the cover by his kind permission.\n\nAll rights reserved. Except for brief passages quoted in a newspaper, magazine, radio, television, or website review, no part of this book may be reproduced in any form or by any means, electronic or mechanical, including photocopying and recording, or by any information storage and retrieval system, without permission in writing from the Publisher.\n\nPublished simultaneously in Canada by Penguin Books Canada Limited.  \nFirst published clothbound by New Directions in 1953. First published as New  \nDirections Paperbook 91 in 1960 and as a New Directions Classic in 1997.\n\nThe Library of Congress has cataloged the printed edition as follows:  \nMerton, Thomas, 1915-1968.\n\nBread in the wilderness \/ Thomas Merton.\n\np. cm. \u2014(A New Directions classic)\n\nOriginally published: 1953.  \nISBN 978-0-8112-2416-1 (e-book)  \n1. Bible. O.T. Psalms\u2014Criticism, interpretation, etc. 2. Spritual  \nlife\u2014Catholic Church. 3. Catholic Church\u2014Doctrines.  \nI. Title. II. Series: New Directions Classics.  \nBS1430.2.M445 1997  \n248.3\u2014dc21 97-509\n\nCIP\n\nISBN 978-0-8112-1348-6\n\nNew Direction Books are published for James Laughlin  \nby New Directions Publishing Corporation  \n80 Eighth Avenue, New York 10011\n\n","meta":{"redpajama_set_name":"RedPajamaBook"}}
+{"text":"\n\nJ. Chris Hansen is a wildlife and nature photographer who lives and works in the redwoods of Northern California. His images have been published in numerous outdoor magazines, including _Mule Deer_ and _California Hunter._ He has a passion for bird photography and can often be found photographing in his backyard.\n\n<http:\/\/christhephotog.blogspot.com\/>\n**Secrets of Backyard Bird Photography**\n\nJ. Chris Hansen\n\nJ. Chris Hansen (christhephotog.blogspot.com)\n\nProject Editor: Maggie Yates\n\nCopyeditor: Maggie Yates\n\nLayout: Hespenheide Design\n\nCover Design: Helmut Kraus, www.exclam.de\n\nPrinter: Friesens Corporation, Altona, Canada\n\nPrinted in Canada\n\nISBN 978-1-937538-55-2\n\n1st Edition 2014\n\n\u00a9 2014 by J. Chris Hansen\n\nRocky Nook Inc.\n\n802 East Cota St., 3rd Floor\n\nSanta Barbara, CA 93103\n\nwww.rockynook.com\n\nLibrary of Congress Cataloging-in-Publication Data\n\nHansen, J. Chris, author.\n\nSecrets of backyard bird photography \/ by J. Chris Hansen. -- 1st edition.\n\npages cm\n\nISBN 978-1-937538-55-2 (hardbound : alk. paper)\n\n1. Photography of birds. 2. Photography--Digital techniques. 3. Single-lens reflex cameras. I. Title.\n\nTR729.B5H36 2014\n\n778.9'328--dc23\n\n2014008573\n\nDistributed by O'Reilly Media\n\n1005 Gravenstein Highway North\n\nSebastopol, CA 95472\n\nAll rights reserved. No part of the material protected by this copyright notice may be reproduced or utilized in any form, electronic or mechanical, including photocopying, recording, or by any information storage and retrieval system, without written permission of the publisher.\n\nMany of the designations in this book used by manufacturers and sellers to distinguish their products are claimed as trademarks of their respective companies. Where those designations appear in this book, and Rocky Nook was aware of a trademark claim, the designations have been printed in caps or initial caps. All product names and services identified throughout this book are used in editorial fashion only and for the benefit of such companies with no intention of infringement of the trademark. They are not intended to convey endorsement or other affiliation with this book.\n\nWhile reasonable care has been exercised in the preparation of this book, the publisher and author assume no responsibility for errors or omissions, or for damages resulting from the use of the information contained herein or from the use of the discs or programs that may accompany it.\n\nThis book is printed on acid-free paper.\n_This book is dedicated to God, who makes all things possible,  \nand to my family, Lenore, Jay, and Annika, for their loving support of the writing of this book._\n\n**Acknowledgements**\n\n_To Steve Hellman, for helping bring this book to life with his editing expertise and encouragement._  \n _To my parents, John and Betty Hansen, for raising me with a love for the outdoors and all of God's creation.  \nFor the team at Rocky Nook, Joan Dixon, Maggie Yates, Alison Smith, and Matthias Rossmanith, for their professionalism and invaluable help in making this book a reality._\n\n## **Table of Contents**\n\n**Introduction**\n\nChapter 1 **The Best Camera and Equipment**\n\nChapter 2 **The Basics of Attracting Birds**\n\nChapter 3 **A Few Tricks of the Trade**\n\nChapter 4 **The Use of Blinds**\n\nChapter 5 **How to Capture the Best Bird Images**\n\nChapter 6 **Photographing Hummingbirds**\n\nChapter 7 **Beyond the Backyard**\n\nChapter 8 **Showing Your Bird Photography**\n\nChapter 9 **DIY Projects**\n\nPeter Pan Feeder\n\nA Changeable Perch Feeder\n\nSmall Water Feature: Bird Baths\n\nThe Knothole Feeder\n\nBuilding a Window Blind\n\nGround Pod for Shooting from a Windowsill\n\nBuilding a Large Water Feature\n\nBuilding a Chair Blind\n\nA Permanent Blind\n\nA Shooting Shelf for a Permanent Blind\n\n**Resources and Suppliers**\n\n**Recipes for Suet**\n\n**Conclusion**\n\n_Varied thrush on rocks set in a backyard pond_\n\n## **Introduction**\n\nThis comprehensive guide offers a variety of techniques and projects for backyard bird photography. You will learn how to use feeders, perches, backgrounds, blinds, and the proper camera equipment to create professional-quality images. In its simplest form, photographing birds in your backyard is convenient, economical, and very rewarding; ultimately, it can become an addictive adventure.\n\nAny type of backyard, from the wide-open space of a western ranch to a city apartment with a patio or deck, can yield excellent images of local birds. By providing perches, feeders, and water sources, and by utilizing blinds, the photographer can create an inviting environment for birds. With the help of the information in this book and some practice, you will have the tools to begin creating fantastic bird images.\n\nThe advantages of backyard bird photography are many. The primary advantage is the fact that travel is unnecessary. No flights, car rentals, or hotel rooms; no big expenses paying for meals or gas; no fighting traffic to go anywhere. When your primary location for shooting is your backyard, you don't even have to shave or put on your makeup. The birds won't care if you've shaved or not.\n\nThe second advantage of shooting in your yard is that your bird subjects are often easier to find and capture than wild birds. Because neighborhood birds are accustomed to sharing their space with people, they don't typically see us as a threat\u2014unless you get too close. While you have to travel to the habitats of wild birds to photograph them, backyard birds are easy to find because they come to you. Your backyard _is_ their habitat! This book offers ideas for ways to draw the birds into your camera range.\n\nShooting bird images in your own backyard is also a huge time saver. The time you would have spent traveling can now be spent in the comfort of your own location shooting images at your convenience. You won't risk spending hundreds or thousands of dollars on travel to a place where you could get rained out.\n\nThere are disadvantages to backyard bird photography, as well. The biggest problem is that you are limited to the species of birds that you can attract to your backyard. If you are shooting from your apartment in the Bronx, it is unlikely that you'll have the opportunity to photograph penguins. Another consideration is the limits of migration: you'll only be able to photograph some species of birds during certain times of year.\n\nAnother disadvantage to shooting only in your backyard is that it can be easy to fall into a rut. It's up to you to provide the spark to keep your bird photography fresh. One of the most creative aspects of backyard birding is setting up the backyard habitat. You have the opportunity to design and produce beautiful set-ups and backgrounds for your images.\n\n_Goldfinch on blossom next to a tube feeder_\n\n## CHAPTER 1 **The Best Camera and Equipment**\n\nI have found that the best camera to use is a Digital Single Lens Reflex (DSLR), with a pixel count of six megapixels or larger. These cameras have interchangeable lenses that can be purchased in varying powers of up to 800 mm. Any of the major manufactured cameras, such as Canon, Nikon, Pentax, Sigma, Olympus, Panasonic, Sony, and Fuji, will work quite well for this purpose.\n\nAs far as lenses are concerned, it is best to use a telephoto lens with a focal length of at least 200 mm or longer. The longer the zoom of your lenses, the better they are for bird photography, but the more expensive they will be. My personal favorite is a 100-400 mm telephoto zoom lens. A zoom lens allows you to move in closer or pull further away from your subject, so you don't have to change positions the way you would with a prime lens. This is advantageous when a variety of birds of different sizes visit your bird feeder set-ups, and you need a tighter (or wider) shot.\n\n_DSLR with a 300mm lens_\n\nIf you do not own a DSLR, a Point-and-Shoot (P&S) camera can work as long as it has a few critical features. The most important feature is that it should have little to no shutter lag. This means that when you push the shutter button to take the picture, there shouldn't be any delay until the picture is taken. If you do decide upon using a camera with shutter delay, be prepared for the frustration of a lot of missed pictures, since birds can move rather quickly.\n\n_Point-and-shoot camera_\n\nYour camera should also have a 10x optical (not digital) zoom or longer, and have a place for a tripod mount on the bottom. In terms of megapixels, the best is a camera with a minimum of six megapixels or higher.\n\nA tripod or camera support of some kind is a must. You will spend a lot of time waiting, and when the action does occur, you are going to want your camera to be in a stable, secure position ready for you to click the shutter.\n\nIn choosing a tripod, you usually get what you pay for. I'm not saying that cheap tripods don't work\u2014they typically just don't have a tough enough build to last very long without something stripping, breaking, or some part coming loose. Do you want to trust your camera on something that may fail? Choose a tripod that is sturdy and well made. Tripods manufactured by Bogen\/Manfrotto, Gitzo, Cullman, and Benbo are all considered to be reliable.\n\n_Beanbag with DSLR camera and a 400mm lens_\n\n_Sturdy mid-range tripod with ballhead_\n\nIf you feel that a tripod is beyond your budget, consider using a beanbag or other similar camera support. In a pinch, a folded up jacket, sweater, or towel can be used to support and stabilize your camera.\n\n_Wireless remote and a wired shutter release_\n\nA special warning is needed here. Never leave your tripod and camera standing up unattended. Children, pets, or a clueless person can easily knock over your equipment. I know this from personal experience.\n\nA must-have when using any kind of zoom or telephoto lens is a cable shutter release. It minimizes the camera shake caused by pressing the shutter so you don't end up with a blurry image. DSLRs can be equipped with an electronic cable release, and some even use a remote release. P&S cameras are very limited in this department, although some do come equipped for a wireless remote.\n\n_Oak titmouse on an apple blossom branch placed above a platform feeder_\n\n## CHAPTER 2 **The Basics of Attracting Birds**\n\nThe basic premise of backyard bird photography is to provide what the birds need to survive. Like humans, birds need food, water, and shelter. If you can provide a relatively safe perch in your backyard, along with feed and water nearby, you will most likely get a variety of birds coming to have their portraits taken. If you already feed the birds in your yard, you are already one step ahead.\n\nOverall, you will find bird feeders to be the most successful tool for your photography. They draw the birds to your yard and concentrate them in one specific location, making them easier to photograph. There are many commercially available feeders and seeds for sale, everywhere from your local hardware store to the grocery store. The types of seeds you put out will affect what kinds of birds you will lure.\n\nThe key starting point is to provide a feeder with food on or in it. Near that feeder, place a perch for the birds to land on when they come to eat, drink, or bathe. While they are pausing to decide what to eat, you can create an image of them.\n\n### **Types of Food**\n\nYou can plant your yard with native seed and fruit bearing plants or you can provide a feeder stocked with goodies in a safe location in your yard. Two of the best basic birdseeds are black sunflower seed and niger seed, because they bring in a wide variety of birds. Black sunflower seed is known to attract the most species of birds. Niger seed is attractive to all types of finches and many other small birds.\n\nSunflower seed can be served up to your local bird population from a wide variety of feeders.\n\nNiger seed is best served to birds from a finch or niger feeder, which is a type of tubular feeder with small holes made for such tiny seed. Niger seed has a distinct advantage\u2014most squirrels don't like it.\n\n_Black sunflower seed_\n\n_Niger Seed_\n\n_Finch Seed_\n\n_Hen scratch_\n\n_Dried Mealworms_\n\nOther types of foods available for birds are finch feed, hen scratch, and mealworms. Finch feed is typically served to birds in a tube feeder. Hen scratch is usually placed in a platform feeder, and mealworms can be offered in a mealworm feeder.\n\n_Recycled plastic containers screwed to the backside of a branch_\n\n### **Types of Feeders**\n\nPlatform, hopper, and tube feeders are probably the most common types of feeders available. Feeders can be fancy commercial feeders or something as simple as a two-liter plastic soda bottle with holes cut into it for the birds to feed out of, or a flat board with seed poured onto it. In addition to the commercially made models, I have used nearly everything and the kitchen sink for feeders. Almost anything can be pressed into service. This is important to consider, because many commercial feeders are much too large to be of practical use for creating some bird images. The best feeders are bottle caps and the bottoms of soda bottles, which can be hidden on the backsides of small branches or rocks to lure birds into photogenic locations.\n\n_Steller's jay coming to the feeders_\n\n_Cordless drill being used to attach feeder cups to the backside of a branch_\n\nMy favorite two tools for creating and installing feeders are a cordless drill and a pair of scissors. I use the scissors to cut down plastic containers to hide them on the backsides of branches and logs. I use the cordless drill and wood screws to hold them there in place.\n\n_Platform feeder_\n\nPlatform feeders are mounted on a pole or hung from something such as a tree limb or the edge of a roof. They are flat surfaces onto which seed is poured so birds can feed upon it. The advantage of platform feeders is that they draw in a wide variety of birds. Doves, jays, sparrows, finches, and many other birds like platform feeders.\n\nA platform feeder can be made out of a small flat board: nail or screw it to the top of a post, and then pouring some seed on it. It is easy to attach perches to platform feeders, if necessary. These feeders allow the birds plenty of visibility to see predators coming. The disadvantage, though, is that they don't work as well in inclement weather because the seed gets wet.\n\n_Hopper feeder_\n\nHopper feeders have bins or containers fitted on a narrow platform. The bins contain the seed, and have a slot at the bottom that allows the seed to fall onto the platform as the birds feed from it. Of all the types of feeders, hopper feeders attract the widest variety of species. Their advantage is that they can often hold a good supply of seed and don't need to be refilled as often as platform feeders.\n\n_Tube feeder with a squirrel screen around it_\n\nTube feeders are usually made of a cylinder of clear plastic, with openings placed up and down the tube for the birds to feed from. Usually there is a short perch below each opening for the birds to land on. These feeders attract a lot of the smaller perching birds, such as finches, nuthatches and chickadees. Larger birds such as grackles, blackbirds, and jays have a more difficult time with this feeder if it has very short perches or no perches at all. Tube feeders are great because they can be hung almost anywhere. They are easy to attach perches to, and very transportable if you decide to move them to a new location. The biggest drawback of most tubular feeders is that they can sometimes be very difficult to clean if the seed gets wet or moldy.\n\n_Suet feeder_\n\nAnother type of feeder is the suet feeder. Suet feeders are typically open wire cages with a suet block placed inside. The feeder is then hung from a tree. Suet is fat mixed with a variety of things, including seeds. It is best served in winter or cooler regions where it won't go rancid, although many commercial types of suet are said to be heat resistant. Suet can be homemade (see Recipe section) or purchased relatively cheaply in small blocks. It is a great source of feed for bringing in woodpeckers, tufted titmouses, nuthatches, and chickadees.\n\nA very successful feeder, especially in late spring and early summer, is the mealworm feeder. This type of feeder works well because baby birds need a lot of proteinous food\u2014for example, insects. Mealworms can be purchased live or dried from commercial suppliers or pet stores. Dried mealworms can be rehydrated by placing them in warm water for about fifteen minutes. Bluebirds find them to be quite tasty. A mealworm feeder consists of a clear enclosure that holds the mealworms. They only have openings big enough for smaller birds, to keep out larger birds such as blackbirds and jays. In a pinch, any tray can be used as a mealworm feeder.\n\n_Fruit feeder set up on a board_\n\nAdding fruit and nectar feeders to your backyard can attract many fruit-eating birds that might not come to other types of feeders. Nectar feeders are available commercially and are similar to hummingbird feeders. Fruit feeders are also available, although a fruit feeder can be as simple as half an orange impaled on a nail stuck through a board, with a bowl of cut fruit beside it.\n\n_Wooden mealworm feeder_\n\nIf you have a lot of squirrels and don't wish to feed them or photograph them, there are a variety of solutions to the squirrel problem. The first one\u2014if you have a yard that is big enough\u2014is to set up a diversionary feeder before you put out your primary bird feeder. Stock it with sunflower seeds, peanuts, and corn, and place it out of sight of your bird feeder. The squirrels will get used to feeding at their feeder, and will ignore your other feeder, especially if you have chased them off a few times.\n\n_Western gray squirrel visiting feeder cups on the back side of the branch_\n\nA second solution is to buy squirrel-proof feeders. These come in a variety of ingenious sizes and styles designed to outsmart the squirrels. Some have cages built around them that are only big enough for small birds, thus keeping out both the jays and the squirrels. Another system uses a perch bar that will only support the weight of a bird. It will spin if too much weight is applied, throwing off the offending squirrel. Other feeders use pole baffles to prevent the squirrels from climbing them. Check the back resource section of this book for sources.\n\n### **Feeder Care**\n\nAll bird feeders need to be maintained on a regular basis. They should be periodically cleaned to remove old seed and shells. The type and style of the feeder will determine how often. Always remove any wet or moldy seed, since it can make birds sick or even kill them. I would suggest at least a weekly inspection at the very least.\n\n### **Types of Water Sources**\n\nProviding water doesn't need to be very complicated. Just a shallow platter or bowl of water will do. One of the simplest things to use is a plant potholder that is roughly twelve inches in diameter. Just pour water in until it is a quarter to a half an inch deep and it will keep most birds happy, especially if you place it in a safe location where the birds can feel secure from predators.\n\nOther types of water sources you can make available to the birds can be as elaborate as a backyard pond or a bird drip, which is a set-up in which water drips into a pool of water below. This can be simply done by using a water container and hanging it by its handle above a platter, and poking a small hole in the bottom of it with a small finish nail or a large pin. The flow rate can be set to a drip by tightening or loosening the cap.\n\n_Water drip hung above a platter of water_\n\nIn winter, open, unfrozen water is a big draw for many birds. This can be accomplished by purchasing a pet water-bowl heater to keep the water from freezing over. Obviously this won't be of much use in the Virgin Islands.\n\n_Dark eyed junco visiting the pond for a bath_\n\n_Garden pond in a backyard_\n\n### **Refuge and Cover**\n\nBirds need a safe cover. You don't need to provide them with housing so much as a safe place of refuge. Birds need this in the form of bushes and trees to protect them from predators.\n\nJust as we have our own individual comfort zones, different species of birds have theirs. Some feel vulnerable if they have to go too far out into the open to get food and water. You can cater to these species by placing your feeders and birdbaths close to sources of cover, such as the bushes and the trees in your yard. If you have a yard that is sparse in plant growth, or you live in apartment with only a balcony or small patio, you may need to buy some potted bushes or small trees in order to provide the needed cover for your birds to feel safe.\n\nHow far is too far between feeder and refuge? It varies based on the type of bird and the conditions of the environment. A general rule of thumb is to place your feeders within six feet of some type of cover. If the birds in your area are extremely habituated to people and there are few predators, you may be able to place your feeder out in the middle of the lawn, patio, or deck.\n\n### **Location of Feeders**\n\nJust as realtors always espouse living in a good location, the placement of your feeders is critical to your success. We have already discussed placing your feeders close to cover, but there are a few more variables to be considered. The first and most important is light and its direction. Bird photography is best within the first three hours after sunrise and in the late afternoon.\n\nPlace your feeders with the quality and direction of light in mind. The birds should be lit up by the sun coming from behind or slightly to the side of the location you will be photographing from, so think about where you plan to locate your camera, and set the feeders based on that. Wander around in your backyard in the early morning to pick out a good location.\n\nUsually the east is the best direction to photograph birds from in the morning, followed by the south, and then the west as a last resort\u2014unless you are trying to create a silhouette. I prefer photographing from the south side, since it places the sun at my back and allows me to photograph from sunrise until about ten o'clock in the morning. I like the soft-colored light given by the early morning sunrise (or sunset) when photographing from the east and the west. The east is often better, since most backyard birds are more active in the morning than in the afternoon.\n\nAnother key point in feeder placement is the background behind the feeder you intend to photograph. Keep this in mind! The background can make or break a bird image. The best backgrounds are clean and fairly even in color. These can be grass, shrubbery, or hedges. Manmade backgrounds, including walls, fences, or backdrops made of canvas or other materials, can be used if they are placed far enough behind the feeder. These can be homemade or commercially purchased.\n\nThe background, whether it is a backdrop or bushes or a fence, should be a minimum of six feet behind the feeder. This helps to leave them out of focus at wider open F-stops.\n\nOther key factors to consider are your pets, family, neighbors, and traffic. Consider where the feeders can be placed so the birds will have the least amount of disruptions from outside elements.\n\nThe height at which you place your feeders is crucial for how your bird pictures will appear. If you place the feeders too high or too low, the birds will usually look less intimate to your viewers. The best height to place feeders at is at the eye level of your camera. For example, if you are taking bird images from your bedroom windowsill, you should place your feeders at the same height as the windowsill.\n\nThe goal is to take your pictures from the same level at which the birds are feeding. This creates a more intimate feel for the viewers. You don't need a bunch of images of birds' behinds that look like they were taken from the ground looking up into a tree. It's probably not very flattering for the birds or for you.\n\nIn addition to height, you want to consider how far away the feeder should be placed from the spot you are planning to photograph from. Keep in mind that the feeder still needs to be placed close to cover so that birds feel comfortable approaching it. A typical distance from your camera to the feeder is six to ten feet, although if you are using a P&S or a 200 mm lens you may need to make that distance much shorter and be very, very quiet and still when you photograph.\n\nA good test for distance is to go to a dollar store and buy a fake little bird about four inches tall. Set up your feeder, put the fake bird on it, and take a test picture from where you plan on photographing. If the bird doesn't cover more than a third of the frame, you will need to move the perch and your shooting location closer together. By the way, a ruler will work just as well as a fake bird if you mark it with tape at the height of the type of birds you plan on photographing.\n\n_Fake stand-in bird_\n\n### **Providing a Perch**\n\nNow that you've got the feeder and food prepared, the next step is to look at the choice of perches you can use for the birds to land on when they come to visit your gourmet shooting spot.\n\nPerches can vary in size from a small twig to a whole branch. The most important thing to consider here is the aesthetics. You will want to use a perch that is appropriate to the size of the bird. Generally speaking, the smaller the bird, the smaller the perch size can be. Picture if you will a sparrow on a tree trunk. In the image, the tree trunk would overwhelm the sparrow\u2014unless, of course, the log is covered in delicate moss or lichen. However, if you were to create an image of a sparrow on a tiny branch, the perch would appear to be more balanced with the size of the sparrow.\n\nWhere do you get perches? The best and easiest place is your own backyard. Take a pair of rose clippers and snip off a small cutting from the backside of one of your plants. Ask neighbors for clippings when they are trimming their roses or bushes. After storms, look for branches on the side of the street that were blown off by the wind. Don't overlook buying what you need. For that special look, go to the local nursery and buy a beautiful flower to stick next to your feeder.\n\nChoose a perch that is pleasing to the eye. Interesting weeds or cuttings from bushes and trees of your yard that are budding, in bloom, or yielding berries will look fantastic. Look for small branches that are covered in moss or have an interesting wood grain pattern to them. Be sure to choose a perch that can be easily attached to the feeder, or that can be placed close enough to the bird feeder that the birds will land on it.\n\nIn addition to using plants and cuttings from your yard as perches, consider the use of interesting sections of small logs, old mossy stumps, or volcanic rocks placed on a platform feeder. Quail and other ground perching birds can look fantastic on perches like these.\n\n_Some methods of attaching perches to feeders: Top l-r: wired, clamped, and screwed on. Bottom l-r: drilled, placed in feeder hole, and bread wire tied._\n\nWhatever perches you use, be sure to change them often so that your images don't become repetitious to your viewers. I like to change my perches after every session to something new so my images don't look like they were taken in the same location each time.\n\nHow do you attach perches to your feeders? A lot depends upon which style of feeder you decide to use. The goal here is to get the bird to land upon the perch before feeding. This means that it needs to be placed in a position that is just slightly above or off to the side of the feeder. Perches can be attached to feeders in a wide variety of ways. They can be tied onto the feeder with string, wire, bailing wire, or ties for bread bags. My favorite tools for attaching perches are a cordless drill and wood screws. Other possibilities are to use duct tape, wood clamps, spring clamps, or even strips of Velcro. A hammer and nails will work as well, although I recommend the use of duplex nails so they can be pulled out more easily when you decide you want to change or reposition perches.\n\n### **Placement of Perches**\n\nPlacement of perches is critical in terms of light and other factors. It is very important that you place the perch in a location that is evenly front-lit with no shadows being cast upon it. The perch should be placed within six feet or less of cover so that birds will feel comfortable using it. Height-wise, the perch should be placed above the feeder so that birds will alight on it before they drop down to the feeder. Usually a distance of six inches to a foot will work. Larger birds and smaller birds will use different distances depending upon their comfort level. A lot of experimentation will be needed to find out what height will work best. Don't forget you want the feeder to be at the eye level of your camera, so raising or lowering the feeder may be required.\n\nHow many perches should you use? It's best to start with one, and typically try not to use more than three. The primary reason for this is that you want to prevent the birds from landing on perches out of your frame. If you provide too many perches, birds will land where you aren't focused. Start out by limiting yourself and the birds to one perch at your feeder. This will help you practice focusing and composing images in one location without the added complexity of having to move your camera.\n\nIf you decide to use more than one perch, I would limit it to three. Beware of \"Perch Envy.\" You know the old adage, \"the grass is greener on the other side of the fence\"? This can apply to situations in which you are using more than one perch. When you are focused and composed on one perch, stick with it. Avoid chasing the birds from perch to perch with your lens. Stick with your original vision. Perch envy may get you to start looking from perch to perch with your camera and lens, trying to capture all the birds as they land. This can be distracting to both you and the birds; the movement may make them nervous, and they might fly away.\n\nAfter I have created at least one great image on a perch, I will focus my attention on another perch, or reset the perch if it isn't working and try to figure out why birds aren't using it.\n\nWhen using more than one perch, it's important to try and set each perch at roughly the same distance from the location you are photographing from. This will limit the time you spend refocusing and recomposing when you change your focus to a different perch. If you decide to switch to a different view, very, very carefully and slowly move your lens to focus on another perch.\n\nWith a little bit of creativity, you can nudge the birds into using the perches you want them to use. Some commercial feeders give you the option to block off one or more of the various feeding ports. If you are using a feeder like this, you can direct the birds to your perch by temporarily blocking off all feeder ports other than the one closest to your perch. Use electrical tape or masking tape that can be easily removed later. If you are using more than one feeder, you can take down or cover up the feeders you do not plan to photograph in order to push more birds to the feeder you are using. When using platform feeders, you can cover part of the platform with cardboard to limit the birds to the side of the feeder where your perch is attached.\n\nAt what direction do perches need to be placed in relation to your camera? Perches should usually be placed so that they are parallel to the front of the lens element and ninety degrees to the feeder opening. In other words, they should be placed like a crossing gate at a railroad crossing. The purpose of this is that the whole perch will be in focus and you can photograph the front or back of the bird when they land. This makes for a very pleasing image.\n\n_Quail on a mossy rock placed next to a bowl of food on a TV tray_\n\n## CHAPTER 3 **A Few Tricks of the Trade**\n\nI often use temporary mini-feeders on the back side of medium and large perches. I fill a plastic salsa container or the cut-off bottom of a soda bottle, and use some wood screws to drill it onto the back side of a branch where it can't be seen in the image of the bird. It's important to check your set-ups through your camera before attempting any photography. From experience, there has been too many times where I have looked through the lens to spy the corner of a feeder cup sticking up into the image.\n\n_Mossy branch with feeder cups_\n\n_Steller's jay on mossy branch_\n\n_Peanut butter with sunflower seed smeared on the back of a log_\n\n_View of set-up from the photo blind_\n\nIf you don't feel like using any tools, you can prop up a branch and smear the backside of it with a mixture of birdseed and peanut butter. This mixture can also be smeared onto the back side of rocks. You can't be too fussy or neat when doing this. Just be sure to keep it out of your camera's view.\n\n_Final image of a Steller's jay_\n\nWhen using tube feeders, it is quite easy to just insert a small branch into one of the feeder holes and let the weight of the seed hold the perch in place. This works with really small perches like twigs or very small branches. It is the perfect set-up for very small birds like nuthatches and finches, since they prefer these types of feeders.\n\n_Daffodil set-up_\n\n_Resulting image of a junco on daffodils_\n\nBy using flowers, such as daffodils or zinnias, as perches, you can add a beautiful splash of color to your bird photos. Just stick them into a block of floral foam or lean them out of a vase weighted to keep it from toppling over. One of the really neat tricks I use is to insert a stiff wire into the stalk of the flower to give it more rigidity when a bird lands on it.\n\nThere is an incredible variety of perch set-ups that can be used to attract birds, including rocks, sections of logs, branches and twigs, and flowers. One great idea for a perch-and-feeder set-up is to use a Christmas tree stand to hold up feeders on posts. The stands make it quite easy to move feeders around your yard in response to changing light conditions or in relation to your background.\n\n_Platform feeder on a Christmas tree stand_\n\n_Chestnut backed chickadee on a Sorghum stem drilled into the feeder_\n\nFlowering branches are an incredible and beautiful source for perches. Early springtime, when trees are just coming into bloom, can be the perfect time to cut some branches to use for perches. Tape or wire one perch to a pole, just barely in reach of a tube feeder. One or two inches away is just about right for smaller birds. Cut several more branches to be placed six to eight feet behind the feeder to provide color and an out-of-focus background at a wide open F-stop of F-5.6 or larger. Check the set-up with your camera to make sure no poles (or the feeder) are in the image. Some adjustment of the branch by the feeder may be needed once birds start using it.\n\n_Flowering branch next to tube feeder_\n\n_Resulting image of a pine siskin coming to feed_\n\nPlastic feeder cups work great as a short-term feeder. They do, however, have a couple of problems. One is that they are easily dislodged or broken by bigger birds and squirrels. The other is that they can't be placed on the sides of vertical perches because they will be visible to the camera and appear in the image. For larger perches, the solution to this problem is to use a spade bit on your drill to drill a hole into the side or back of the perch. Then fill the hole full of seed.\n\n_Hole (drilled with a spade bit) with seed, in the side of a section of branch_\n\n_Red-breasted nuthatch coming for some seed_\n\n_Perch set above an orange half on a pole with bouquets of fake flowers behind._\n\nSometimes a simple perch can be enhanced with the placement of bunches of brightly colored fake flowers. Yes, fake flowers! Silk flowers, when placed out of focus behind the perch, can really set an image apart\u2014especially if you use flowers with the same or complementary colors to the plumage of your subject.\n\n_Bullock's oriole coming for some orange_\n\nHere is a set-up composed entirely of artificial flowers. Keep in mind that if you are using artificial materials for your perches, you may be able to tell\u2014especially when the photos are zoomed in, or when the print in enlarged. To avoid this, replace your artificial perches with natural ones for those really tight shots.\n\n_Dark eyed junco coming for seed at an artificial set-up_\n\n_Branch used for ramping up to the rock next to the feeder_\n\n### **Ramping Up and Laddering Down**\n\nCertain ground birds, such as quail, pigeons, and doves, prefer to use ground-level feeders. They will sometimes use platform feeders, but it is not their favorite. So how do you get them onto a perch? One really effective technique for luring hard-to-photograph birds onto a perch is called ramping up. This process involves creating a ramp of rocks, boards, and branches to entice the birds to walk up to a platform feeder. Place attractive perches along the way for birds to stop on as they make their way toward the feeder.\n\n_Mountain quail coming for some seed_\n\n_Warbler on perch coming for water_\n\n### **Laddering Down**\n\nMany birds, such as warblers, don't often come to bird feeders. They will, however, come in for water. Laddering down is the technique used here. Provide plenty of perches starting about six feet up, and place them alternating, going back and forth about a foot apart, down to a water source. When birds are laddering down they will often pause on the last perch just above the water. The last perch should be placed about three inches above the level of the water.\n\n_Laddering perches coming down to water_\n\n### **Backgrounds**\n\nAnother concern of note is backgrounds. I can't emphasize the importance of backgrounds enough. Make sure the area behind the feeder is evenly colored and free from bright spots. The perch should be six feet or farther from the background. This will help you create a nice backdrop for your bird images.\n\n_Backdrops l-r: posterboard, commercial pop-up, painted plywood, and painted hardboard_\n\n### **The Use of Artificial Backgrounds**\n\nWhat if you don't have a nice even backdrop or you want to create an image with a colored background different from what is already there? The answer is as close as your nearest office supply or art store. There is a bountiful supply of tag board and presentation boards in a wide range of colors. Just be sure to choose ones that have a matte surface so they won't be too reflective and create bright spots in your images.\n\nIt is also better to stick to a color palette that is earth toned unless you are trying to create some special image that is bright and unnatural.\n\nOne other handy choice for artificial backgrounds is to use pop-up studio backgrounds. These have become a favorite choice of mine because they are easy to store and come in a range of earthy colors. They fold down into an easy-to-store flat case and they can be assembled with a pop just by taking them out of their case. A cautionary note here is to unfold these backgrounds carefully; the pop can come with some force that can be quite painful. They are typically available in two sizes: 5 \u00d7 6 feet or 6 \u00d7 7 feet. These are the best artificial backgrounds I have ever used for bird photography. The only disadvantage that I have experienced with them is that they can be difficult to use in the wind.\n\nThe other possibility is to paint your own backdrop on watercolor paper. You can create a washed look and add blotches of color to resemble out-of-focus flowers.\n\nYet another possibility is to use photographic posters or prints, including your own images. Just print your own interesting 16\u2033 \u00d7 20\u2033 print with a matte finish. A background like this is placed 2\u20133 feet back from your perch. Other possibilities include putting up fabric screens or other material on frames. Regardless of what you use, just make sure the material is large enough to cover the background behind your perch. Usually 16\u2033 \u00d7 20\u2033 is large enough.\n\nWhen using artificial backgrounds, be aware of shadows and bright spots being cast upon your backdrop. I sometimes solve these problems by attaching a piece of cardboard above or to the side of the backdrop to keep it in permanent shade while I am photographing. Also remember that it is usually best to use the widest F-stop your lens has in order to keep the background out of focus\u2014unless it is your intent to have the background in focus. I tend to prefer the softer, out-of-focus backgrounds that place the viewer's attention on the main subject: the bird.\n\n### **The Use of Reflectors**\n\nOften times you will want to photograph in an area that is lacking in light. Whether it is too dark to photograph or it just needs a little bit more light to makes things pop or stand out, using reflectors can help. Sometimes I place a reflector under the perch to bounce more light onto the breast of the bird so it doesn't fall into shadow when I'm photographing it. There are commercially available reflectors in gold, silver, and white. The larger and closer a reflector is, the more even the light it will cast. You can also make your own reflector by using a piece of white cardboard or covering a piece of cardboard with crumpled aluminum foil. I find mirrors to be too direct for my taste. Another possibility is to use a sunshade for a car's windshield, like in the case shown above.\n\n_Car windshield shade used as a reflector to bounce light onto the perch_\n\n### **Using Interesting Items to Enhance the Scene**\n\nDon't overlook the possibility of using interesting items from your home or backyard. Many manmade objects, such as shovel handles, garden utensils, and old antiques can be used for perches as well. Natural materials also work very well. Fungi, for example, can be impaled upon a needle or a sharpened finish nail that has been driven into the wood.\n\n_Steller's jay looking for seed by a mushroom impaled on a sewing needle_\n\n### **Inclement Weather**\n\nRain, snow, and cloudy weather can be used to produce some beautiful images. When other feed sources start being covered with snow, birds are drawn to backyard bird feeders like a magnet. Foggy or cloudy weather helps produce a very even, soft light that can be quite appealing on the plumage of birds. Rain is a bit harder to photograph in, but with the proper precautions, such as wrapping up your camera with a camera raincoat and using a permanent blind, you can produce some very appealing bird images. Keeping your camera warm and dry is the key to success. Either photograph from inside your home or, if you are in an outside photo blind, be sure to dress for the conditions.\n\n_Dark eyed junco on a perch in the snow_\n\n_White-breasted nuthatch coming to a rock placed on a platform feeder_\n\n## CHAPTER 4 **The Use of Blinds**\n\nA \"blind\" (as it pertains to photography) is a concealment device used to camouflage the photographer from the subject of the photograph. When photographing birds, you can either sit in plain view of the birds, or use a blind to remain hidden from them. Personally I prefer to use a blind whenever possible. It typically allows for a closeness that is difficult to get with many species of birds that are wary of humans. Working from a blind can be comfortable; it allows you to move, have a drink or a snack, or reposition yourself as needed without startling the birds you are trying to photograph.\n\nA blind is anything that can be used to block the birds' view of you, but still have some sort of opening for the camera\u2014the purpose is to have a clear view of the birds without the birds having a clear view of you. Simple blinds can be made by using objects at hand, such as the latticework of a deck or a wooden fence. Cut a small viewing hole to look and photograph through. Other good examples of simple blinds are a sheet hung over a piece of rope, or a large cardboard box from a new appliance like a washer or dryer.\n\nOne of the best blinds of all is often equipped with heating and air conditioning, a phone, TV, computer, and a bathroom. You guessed it\u2014the inside of your house. Just set a comfortable chair near an open window from which to photograph. Cover the window with an old sheet or some leftover wrapping paper. Set up your camera and cut a small opening in your blind for a viewing port at the height of your camera. Now you're in business!\n\nThe advantage of using your home as a blind is that you can take short breaks to accomplish other tasks around the house. Just be sure to use earphones or shut the window so as to not scare the birds. The main disadvantage is that you may miss the crucial moment to photograph that special bird you've been waiting for.\n\n_Cardboard dryer box photo blind_\n\nMore permanent or semi-permanent window blinds can be made from thin plywood or heavy cardboard. The edges can be wrapped and taped to prevent scratches to the windowsill. They can be stored easily behind the couch or other furniture, or against the wall, ready for when you want to use them. Measure the inside dimensions of your window, and then transfer those measurements onto a piece of cardboard or plywood and cut out your blind. Then cut an opening for the camera. If the opening is rather large, you might consider covering it with a dark piece of fabric to help conceal your movements while still allowing the hole to be accessed by your camera lens.\n\n_Wrapping paper covering a window for a photo blind_\n\n_Wooden window blind in a bedroom_\n\nThe disadvantage of using a room in your house is the potential for interruptions and distractions within your home that will ruin prime moments of photographic opportunity. Make it clear to other household members that you wish to be left undisturbed while you are photographing.\n\nOther blinds that can be used out in your yard are hunting blinds. These can be purchased commercially from sporting goods stores and other suppliers. Many of them are quite simple to use and can be set up or taken down in a matter of minutes. The other possibility is to go the DIY route and make a blind by either sewing one yourself or building one out of wood or plywood, or making frames and covering them with material. There is an incredible amount of options. If you live in the far north you can make a blind out of an ice fishing shack. The main advantage these types of blinds have is that they are not limited to use in your yard. They are usually small and portable enough that you can take them with you on photo excursions in other places in the world!\n\n_Plywood rolling photo blind_\n\n_Outhouse photo blind_\n\n_Doghouse photo blind_\n\nShould you decide to build a more permanent blind in your yard, be very sure of its location, since it will be difficult to move. Make careful note of the backgrounds and direction of the sun.\n\n_Nuttall's woodpecker on an old wooden fence post with seed cups on the back side_\n\n## CHAPTER 5 **How to Capture the Best Bird Images**\n\nWhen photographing birds, you will learn that patience is a virtue. This means keeping your activities in the blind to a minimum. No loud noises or waving your lens around through the lens opening. Birds aren't always predictable and it may take some time for them to come and start using the feeders that you have set up. It is important to let them get used to visiting your feeders so they will consider your yard a safe location. Your job is to quietly observe them to learn where they land when they come to feed. Watch for patterns in bird behavior. You will notice that birds each have their own particular way of approaching the feeder.\n\nThe vast majority of birds do one thing that is really critical to your success as a bird photographer. They almost always pause for a second or two after they have landed on the perch to look around for predators. This spot on the perch is where you want to focus your camera to capture these moments\u2014they make for some great bird images. Make note of the background behind this spot in the frame because it is very important to have a clean, uncluttered background. Be sure it is clear of bright spots and has a nice even color to it.\n\nOnce you have learned the birds' behavior and patterns and are satisfied with your set-up, you can start taking some images. I would suggest checking your images after every sequence to see if there are any changes that need to be made. Take the time to carefully review your images. Check for exposure, composition, and lighting. There should be no harsh or distracting shadows on the bird. If you are not familiar with composition, see \"Composition: The Rule of Thirds.\"\n\n_Sample head angles: the one on the far right is the most pleasing_\n\n### **Head Angle**\n\nHead angle refers to the angle of the bird's head in your image. A bird that is looking away versus one that is looking ever so slightly towards you can mean the difference between a mediocre image and a fantastic one.\n\n### **Catch Light**\n\nThe \"catch light\" is a bright spot of specular light in the eye of the bird. Images with a catch light in the eye make a huge difference to the quality of your bird photograph. In photographs without the catch light, the birds' eyes appear lifeless and flat. Always look for it when you are photographing your birds and when you are editing your images. Birds with a catch light look much more alive in images than birds without one.\n\n_Band-tailed pigeon without and with a catch light in the eye_\n\n_California valley quail illustrating the rule of thirds_\n\n### **Composition: The Rule of Thirds**\n\nWhen composing an image in bird photography, it is a good idea to apply the rule of thirds. The rule of thirds is a **guideline** of where to place the focal point or the main center of interest in the image. In bird photography, usually the center of interest is the center of the body of the bird.\n\n_Blank white image showing the rule of thirds with power points shown by black squares_\n\nSo what is the rule of thirds? First divide the frame or image into equal, vertical thirds. Next divide the image horizontally into thirds. What you end up with is a pattern that looks like a tic-tac-toe diagram placed over the top of your image. The locations where the lines intersect on the four corners of the central rectangle are sometimes called power points. These power points are the locations where you should try to place your bird within the frame of the picture. Try to compose the image with the bird facing into the frame. Provide space for the bird to look into. A bird facing the edge of the frame looks like it's trying to leave or escape, which creates a feeling of unease.\n\n_Vertical blank white image showing the rule of thirds with power points shown by black squares_\n\n_White-breasted nuthatch\u2014illustrating the rule of thirds_\n\nWhen photographing birds, I simplify things by setting up and prefocusing my camera, and precomposing the image. I visualize where the bird will be on the perch using the rule of thirds. This way, when a bird does come and land I'm prepared to press the shutter release and not cause a lot of motion that may scare it off.\n\n### **Where to Focus**\n\nWhen focusing on a bird, the most important focus point is the center of the eye. If your camera has adjustable focus points you should set them so they will be at the approximate point of where the bird's eye will be (assuming the bird's body will be centered on a power point). If your camera does not have adjustable focus points, you should prefocus on that area instead, and lock in the focus.\n\n### **The Preferable F-Stop**\n\nBecause birds are almost always moving, you'll want to use the largest lens opening possible. To do this you should set your camera to Aperture Priority and set the F-stop to the largest available lens opening. The camera will automatically choose the highest shutter speed to match it, which is desirable because high shutter speeds help prevent camera shake and minimize any movement by your subject. Wide-open F-stops are also preferable because they allow the background behind your subject to appear out of focus, which makes the bird stand out.\n\n### **The Best ISO Setting**\n\nIt is preferable to set your ISO to 400 at the very least. Birds move quickly and you are going to need all the speed you can get. On dark or cloudy days, moving up to ISO 800 is a good idea.\n\n_The focus point is on the eye of this wild turkey at a ground feeder_\n\n_Anna's hummingbird resting after eating_\n\n## CHAPTER 6 **Photographing Hummingbirds**\n\nAre you up for a challenge? Photographing hummingbirds is incredibly challenging, but also quite addictive and a lot of fun. It takes more of an investment in equipment than other types of backyard bird photography, but the results are well worth the effort when you capture a sharp image of one of these dazzling birds in flight.\n\nSo you need a really, really fast shutter camera or shutter speed for photographing hummingbirds in flight, right? No! What you actually need is a hummingbird feeder and a really, really fast flash, or better yet, several flashes. The vast majority of the incredible hummingbird images you've seen in magazines were done with a hummingbird feeder and a flash set-up.\n\nA basic flash set-up for photographing hummingbirds consists of four flashes. More complicated set-ups can use six or more, but for now we will just stick to the basics. The best flashes for hummingbird photography are hot shoe flashes that have a manual setting for power reduction (1\/16 power or less is ideal). Some hot shoe flashes have the unique ability to shorten their flash duration as the power is manually lowered. Most hot shoe flashes working at 1\/16 power have a flash duration of less than 1\/5000 of a second or faster, depending upon the model. This incredibly fast flash duration is what freezes the action of hummingbird wings in flight\u2014not a fast shutter speed on the camera. Typically studio flashes won't work as well for images of hummingbirds in flight, because the flash duration is too long to effectively freeze motion. One exception to this is the Einstein E640 studio flash, which is designed for stopping action. However, these are a bit pricey.\n\n_Control panel of a Canon 540EZ flash set on manual at 1\/16 power_\n\n_Typical hummingbird flash set-up_\n\nFlashes that work well for hummers include the Canon 430EZ, 430EX, 550EX, and 580EX. Also, Nikon Speedlites SB-26, SB-600, SB-700, and SB-800 work well, as does the Metz 48 and the Vivitar 283 with a VP-1 module. Again, the key feature required is the ability of the flash to be manually dialed down to 1\/16 power to achieve that short flash duration. There is a trade off, however. In reducing the power of the flash you also reduce its effective range. At such a low power, the flashes need to be placed two feet or less from the hummingbird.\n\nThere are many older flashes that can be manually used off-camera, but should never be used on-camera or with a pc\/sync cord because the high trigger voltage can damage modern DSLR cameras. However, when they are used with a wireless flash triggering system, this isn't a problem because they aren't connected directly to the camera.\n\nSo what do I mount these flashes on? One of the best supports for flashes are light stands with an umbrella\/flash holder. These can be raised and lowered to a variety of heights, and the flash holder allows the flash to be tilted or angled in almost any direction. I highly recommend anchoring down your flash stands with sand bags, cinder blocks, or water bags to prevent them from being knocked over. You could also use old tripods to hold your flashes. My personal set-up is a mix of tripods and light stands.\n\nThe camera best suited for photographing hummers is a DSLR that can be set to manual mode and has a hot shoe. Point-and-Shoot cameras, for the most part, are unsuited for this type of photography unless they are equipped with a hot shoe. Cameras with a PC connection port may be used, but this involves the connection of wires to each flash and is a bit of a hassle.\n\nSo if I don't use a PC or sync cord, how do I trigger my flashes? The vast majority of hummingbird photographers now use wireless flash triggers. They are quite reliable and don't require a direct line of sight like optical slaves (I used to use optical slaves; they were a pain to set up and not always reliable). There is a wide variety of triggering systems out there. I use Ishoot Snipers and they work well.\n\nWireless flash triggers use a transmitter that slides into the hot shoe on top of the camera. Each flash unit has a receiver mounted to the underside of the flash foot. The flash foot then fits onto a \u00bc-inch stud on the top of each flash holder on a light stand. When the shutter button or release is pushed on the camera, the transmitter in the hot shoe sends a radio signal simultaneously to the flashes to fire them at the same time. Flash triggers are available from many major camera manufacturers or they can be purchased at many auction sites on the web.\n\n_Wireless radio flash trigger. On the left is the sending unit for the camera, and the receiving unit for the flash is on the right._\n\nIn a basic hummingbird set-up, two flashes are placed roughly two feet from the feeder spout of a hummingbird feeder at a 45-degree angle. They are aimed at a point about 7 inches away from the feeder to catch the hummingbird when it backs up to take a break from feeding. The other two flashes are used to light up the backdrop. They are placed at the same height as the feeder at 45-degree angles facing the background. The key here is to use the light of the flashes to expose your subject, and to use as little ambient light as possible.\n\nIn order to minimize ambient light, it's best to photograph hummingbirds in the shade. One simple solution is to photograph under an awning or porch, or to use an instant shade pop-up that is 8 feet \u00d7 8 feet or larger. That way most of the light is coming from the flashes. A shady spot is also a pleasant place to photograph on a hot, sunny day. When photographing using a pop-up, be aware that flashes will pick up a slight color cast of the fabric that will be apparent in the image. White pop-ups are the best because they have no color cast and act as a giant reflector. However, they have the disadvantage of being able to cut less ambient light. This issue can be solved by throwing a dark tarp over the top of the pop-up before beginning to photograph. Take down your pop-up before it rains or snows, and be sure to have it properly anchored to keep it from blowing over in the wind. I speak from experience when I say that they have a tendency to self-destruct under these conditions.\n\n_Diagram showing the top view of a basic hummingbird set-up_\n\n_Image of a basic set-up_\n\nOnce you have all of your equipment organized, it is time to work on the set-up. The premise of hummingbird photography is quite simple: hide the feeder with flowers or use the flowers themselves for hummingbirds to feed from. A typical setup uses flowers placed close to or in front of the hummingbird feeder spout in order to cover it from view. It's good to include flowers just behind the feeder as well. Many photographers will include the feeder spout in the initial creation of the image and then remove it later in Photoshop.\n\nThe other option is to feed the hummingbirds at one location using a single-spout hummingbird feeder. Replace the feeder spout with a tubular flower, like a honeysuckle or a trumpet vine. Then use an eyedropper to load up the flower with sugar water, and the hummingbirds will use the flower instead of the feeder spout. It really works well! If an eyedropper is unavailable, sugar water can be placed in a flower blossom by using a drinking straw. Just dip the straw in sugar water, and then press your finger over the top of the straw to seal off the opening. Still holding your finger tightly over the hole, place the bottom of the straw inside the flower blossom and lift your finger to release the liquid. Now you've got your flowers. What's next?\n\nBackgrounds of a wide variety of colors and designs can be used for photographing hummers, and are extremely important. If a backdrop isn't used, the hummingbirds will look like they were photographed at night with a black background. The backdrops used for other backyard birds work perfectly well. They should be placed about 4\u20138 feet behind the feeder.\n\nA few shots of green, black, or colored spray paint on a piece of tag board can create an amazing backdrop. Some photographers use a blow-up of an image of out-of-focus flowers as a backdrop. Whatever backdrop is used, make sure it is large enough to cover the image area behind the feeder. Set it up and check it out by looking through the camera before attempting to use it.\n\nExposure is dependent upon the flashes and the camera's sync speed. It's typical to use a shutter speed of 1\/200 of a second at F-stops ranging from of F-13 to F-18. Stopping down helps to keep the hummingbird's eye in focus. The camera's white balance should be set to flash. Check the lighting set-up before starting to photograph hummingbirds. Take a test shot, and then check the camera's histogram for proper exposure. You will save yourself a ton of time by doing this before starting to photograph.\n\nFor focusing manually, prefocus on the tip of the hummingbird feeder with the camera on a tripod. Then turn the camera so that it is pointed to an area with the feeder spout just out of the frame before changing the camera back to autofocus. A typical camera position is about six feet away from the feeder.\n\nThe best lenses for photographing hummingbirds are in the telephoto range of 200 to 500 millimeters. My personal choices are 100-300mm zooms and 100-400mm zooms with an extension tube added for close focusing. Zoom lenses have the added advantage over fixed lenses because you can design your image without having to change your position to alter the composition of the shot.\n\n_Hummingbird with a sunset gradient tagboard purchased at an office supply store_\n\n_Anna's hummingbird sipping sugar water from a petunia_\n\n_Small inverted-style hummingbird feeder_\n\n_Saucer-style hummingbird feeder_\n\nA hummingbird feeder is a critical item to have when photographing hummingbirds. Unless you live in a climate where you have hummingbirds year-round, it's best to put up feeders in early spring. Fill your feeders with a mixture of plain white sugar mixed at a ratio of one part sugar to four parts tap water. Hang out multiple feeders to attract the hummers, and then reduce to one when it comes time to take some pictures. A single-spout feeder is the best for photography. A multi-spout feeder can be used by blocking off all but one feeder spout with tape.\n\nThere is a wide variety of hummingbird feeders out there. For the most part they fall into a couple of basic styles: the inverted and the saucer. Inverted feeders store the sugar water above the feeding port and the birds feed from the side or bottom. Saucer feeders have feeding ports above a simple dish filled with sugar water.\n\nHummingbirds typically approach inverted feeders from below and saucer feeders from above. Because of this, you can get different looks depending upon the type of feeder being used. Inverted feeders work really well when using hanging tubular flowers like honeysuckle, fuchsia, and salvia. Saucer feeders work best with flower blossoms that point upward, like zinnias and petunias. Matching the flower blossom and the style of feeder can make your hummingbird photography much easier and more visually pleasing. Regardless of which style of feeder you choose, the best ones are those that don't use a perch\u2014otherwise you'll only get photographs of hummingbirds on plastic perches instead of hovering in mid-air!\n\n_Hummingbird coming up to an inverted feeder_\n\n_Hummingbird turning away from an inverted feeder_\n\nWith hummingbirds it is a bit of a waiting game. If you don't use a blind you must sit as motionless as possible with your finger on the shutter release. Wait for the hummingbird to begin feeding before blasting away with the flashes. Start off slowly, and eventually they will get used to the flash. Usually the best time to click the shutter is when they back off from the feeder to take a break from feeding. They will move forward to feed, then back off 4\u20138 inches or so and hover for several seconds before moving forward to feed again.\n\nI have photographed hummers both with and without a photo blind. I have discovered that I get a lot more hummingbirds coming to the feeders when I use a blind, and as result, I have more successful images. Keep in mind that your home can be used as a comfortable photo blind. It's quite easy to tack up some fabric or cardboard over an open window, and then cut a small opening in it to photograph from.\n\nDon't neglect photographing perching hummingbirds. If you carefully observe hummingbirds you will find that many are very territorial. After feeding, they will invariably go back to the same perch to rest and guard the feeder until they feed again. You can capture some beautiful hummingbird images by setting up a portable blind or using a very slow approach to their perching spot.\n\nRegardless of whether you photograph them flying or perched, you will find that hummingbirds are exciting and beautiful birds. They are like flying jewels. So put some gear together and go photograph some hummingbirds!\n\n_Male Anna's hummingbird guarding the feeder_\n\n_Bullock's oriole on a perch above a fruit feeder_\n\n## CHAPTER 7 **Beyond the Backyard**\n\nWhat can you do when you have exhausted all the bird species in your backyard? Branch out! Think of all the people you know that have birds in their yards. The home of friends, relatives, and coworkers are all possible places where you may be able to photograph, if you ask politely and explain what you would like to do. Show them samples of your work and possibly even show them your set-up in your backyard.\n\nIf you do get permission, just be sure to keep things simple and neat. Try to have the least amount of impact that you can on their lives and property. It always helps to give them prints or cards of your work in appreciation for being able to use their property to photograph birds.\n\nOther than the homes of friends and relatives, think about open space areas. National forests are a really good example, as are parks and other natural areas nearby your home or work. Some of these areas may work well for photography. Please check local laws and ordinances about setting up a blind or feeders. Sometimes talking to the local ranger or manager can open the door into places where you can photograph. It can help to carry around a three-ring binder or a small portfolio of some of your best bird images. Often times you can work out a trade of donating prints to their organization in exchange for a permit to photograph there.\n\nIn the past I have used a cardboard appliance or refrigerator box as a blind when photographing in public places where I want to leave my blind set up overnight. One time I returned to find my box blind vandalized\u2014I'm glad it was only a cardboard box instead of one of my portable commercial photo blinds!\n\nMany of the techniques discussed in the previous chapter can be used when you are traveling. But how do I carry all those feeders and seed? I've found that it's easier to buy cheap plastic feeders and small bags of seed at the arrival point. When I am done photographing I can give away my feeder and seed, or donate it to a nearby nature center.\n\n_My binder with sample images_\n\n_Dollar store bird feeder_\n\nWhat about perches and supports to hold up the feeders? Some good equipment is easy to acquire in the garden supply center of the nearest major box store. Buy some duct or electrical tape, some electrical ties, and most important of all\u2014some plant stakes. Plant stakes are made of either plastic or bamboo and come in lengths of 18 inches to eight feet. They are perfect for holding up your feeders and perches when used in combination with electrical ties and tape. For perches, walk down the garden aisle and pick out some good plants to use.\n\n_Feeder set-up with plant stakes from a garden center and a discarded plastic container_\n\n_Photo blind on a National Wildlife Refuge_\n\nYou can always give the plants away when you are done with them.\n\nWhat if you want to avoid the hassle of setting up feeders or blinds? There are many places around the world that cater to bird photographers by providing blinds and set-ups. The majority of them can be rented for a daily fee, although some of them require that you also pay for a guide. A few of these places are included in the resource section at the back of this book.\n\nThink out of the box. Don't forget that many of the techniques that work for small birds also work for larger birds, including birds of prey. They will all use a perch if it is properly positioned near a food source. This image of a vulture was created by wiring a wooden perch to a metal fence post. The Turkey Vultures were feeding on a dead deer beside the road. Cars make a great photo blind\u2014most birds are comfortable around cars, as long as they don't move.\n\n_Snow geese lifting off next to the photo blind_\n\n_Turkey vulture on a wooden perch_\n\n_American goldfinch on a perch above a platform feeder_\n\n## CHAPTER 8 **Showing Your Bird Photography**\n\nWith a little practice you may end up creating some images that you are really proud of and want to share with others. There are so many ways to show off your photographs. The most common way to show your work is to have a print made, and then mount and frame it. You can also have it enlarged and printed onto a canvas. Alternatively, you can have a canvas wrap made.\n\nYou can also make or have made blank note cards or greeting cards from your images. Send your friends a note card or give them a boxed set of cards.\n\n_Steller's jay on an anniversary card_\n\nFor personal use, a simple thing to do is to create stationary with your image. You can use this in all your correspondence to help spread the word of your great bird photography skills.\n\n_Framed poster of an oak titmouse above a living room couch_\n\nPosters are a wonderful option. There is an incredible amount of online services that are available to make them for you. Frame the photograph yourself or have it professionally framed and provide some wall space for it in your home or give it as a gift to a bird lover that you know.\n\nPostcards are a wonderful and simple option. They can be created on your own ink jet printer or by an online service. They too are another great way to spread the word of your photography. Another possibility is to make yourself a coffee mug that you can use to sip your coffee while you're sorting your bird images. You could have a set of mugs made with six of your images.\n\nWhen you have a dozen great images, you can have a calendar created. You can gift these calendars to your family and friends, or donate calendars to sell at a fundraiser for a local conservation group.\n\n_A series of backyard bird images made into a book_\n\nYou can use an online service to create a book. Blurb.com is one of many.\n\nDon't forget entering your images in photography contests, like the Veolia Environment wildlife photography competition. You can also consider showcasing your work in local art galleries and exhibits. Check to see what their framing and exhibition requirements are. Online photo-sharing sites like Flickr, Smug Mug, and Photo Bucket are other options for ways to share your work with others.\n\n_Lesser goldfinch image on a coffee mug_\n\nFor photo-critiques and ways to improve your bird photography, there is no better site than _Birdphotographers.net._ This site has a large number of bird photographers participating on it. It is primarily for images of birds out in nature, but many of the techniques and tutorials you'll find here can be applied to backyard bird photography as well.\n\n_Red-breasted nuthatch coming down the side of perch to a platform feeder_\n\n## CHAPTER 9 **DIY Projects**\n\n### **PETER PAN FEEDER**\n\n#### **Level: Easy**\n\n_Materials list:_\n\n\u2022 Empty plastic jar (I use Peter Pan peanut butter jars) with lid\n\n\u2022 Wood screws\n\n\u2022 Power drill\n\nOne of the simplest ways to get small birds such as nuthatches and chickadees to go upside down or into unusual spots is to put out a \"Peter Pan Feeder.\" I gave it this name because the first one I created used a recycled Peter Pan peanut butter jar. The concept is very simple. Use a drill and bore a small hole in the bottom of a plastic container that has a lid. Make the hole just big enough that seed won't flow out of the container unless a bird picks it out. Then use wood screws to attach it to the back side of a perch. Fill it full of birdseed and put the lid on. Larger jars can be used for large perches and small prescription bottles can be used on smaller perches. Metal containers need to be used where squirrels are a problem because they will chew through the plastic ones.\n\n_Step 1: Drill a hole in the bottom of a plastic container. Get it as close to the edge as you can._\n\n_Yep, it's a hole_\n\n_Step 2: Attach to the back of a likely perch_\n\n_Step 3: Fill with seed and put the lid on_\n\n_White-breasted nuthatch hanging upside down from a mossy board to get seed from a Peter Pan Feeder_\n\n### **A CHANGEABLE PERCH FEEDER**\n\n#### **Level: Easy**\n\n_Materials list:_\n\n\u2022 Cookie tin\n\n\u2022 Floral foam block\n\n\u2022 Two wood screws\n\n\u2022 Power drill\n\n\u2022 1\u00bc\u2033 or 1\u00bd\u2033 spade bit\n\n\u2022 Spray paint (optional)\n\nRecently I was creating some images of chickadees using small branches with bright red berries on them next to the feeder. I was having a problem with the angle of the branch and the fact that the birds were landing too close to the platform feeder I was using. I knew I needed to try a new type of feeder. First I tried a tube feeder\u2014that solved the issue of the birds landing too close to the feeder. They moved out just far enough onto the branch to make it workable.\n\n_Basic supplies and tools needed_\n\nThere was still the problem of changing the angle of the branch. While perusing goods in the local dollar store, I stumbled upon some floral foam. You can stick a stem into that stuff and it will hold it at any angle. I thought it would be too difficult to put it into a tube feeder, but what else could I use to hold the foam block?\n\nWhen I got home I discovered two cookie tins that I had purchased from the same store around Christmas time. One of those worked great. I drilled a couple of holes into the tin, and then added the foam block with some black sunflower seed. I screwed it to a scrap of lumber and then added the berry branch to it. It works perfectly for perching birds.\n\n_Step 1: Drill two holes in the lid_\n\n_Step 2: Screw the bottom of the tin to a 1_ \u2033 _\u00d7 2_ \u2033 _or similar piece of wood_\n\n_Step 3: Spray paint the lid (optional)_\n\n_Step 4: Place the foam block at the bottom and pour seed around it_\n\n_Step 5: Put the lid on and stick a light perch into the foam block_\n\n_Chestnut-backed chickadee tries out the feeder as soon as it is put up!_\n\n### **SMALL WATER FEATURE: BIRD BATHS**\n\n#### **Level: Easy**\n\n_Materials list:_\n\n\u2022 A piece of plywood\u2014any shape or size greater than your platter\n\n\u2022 Jigsaw\n\n\u2022 Plate, shallow bowl, or platter\n\n\u2022 Spray paint (black usually works best)\n\n\u2022 Natural decorations of your choice\n\nI love to do bird photography during the arrival of spring. That's not to say I don't like doing it at other times of the year, but in the spring, birds are in their breeding colors. Also, because I live in Northern California, all the water sources start drying up as soon as the rainy season ends in March. You know the song, \"It Never Rains in California\"? With few available water sources, birds start searching for new places to drink and bathe.\n\n_Step 1: Trace the base of the platter or plate on the plywood_\n\n_Step 2: Cut a hole about_ \u215b\u2033 _larger than the base of the platter_\n\n_Step 3: Set the plate or platter into the hole in the plywood and spray paint black_\n\n_Platter set within the plywood_\n\n_Step 4: Decorate your birdbath to make it look more natural_\n\nThis is where the dollar store comes in handy. They have wonderful flat platters and shallow bowls that work perfectly for birdbaths. Add some rock, sand, and gravel around them, and even some plants, and you have a perfect water set-up to photograph birds drinking and bathing.\n\nStart with scrap plywood and cut a hole about \u215b\u2033 bigger than the base of the platter with a jigsaw. Set the platter in the hole and spray paint it with flat black spray paint. Then find something level on which to support the plywood. Sawhorses or cinder blocks and bricks on a picnic table work very well.\n\nThe last and most creative step is to decorate around the outside of the platter to make it look natural. You can use mossy rocks, branches, plants, and leaves. Add some water dripping into it overhead from a hose and wait for the birds. Most of the time I also place a few seed feeders close by. This seems to attract more birds. The last thing you will need to do is set up some sort of blind. Mornings are usually best for lighting, and birds seem to be more abundant at this time of day. On hot days, mid-afternoon seems to work best because the birds are looking for a place to cool down.\n\n### **THE KNOTHOLE FEEDER**\n\n#### **Level: Medium**\n\n_Materials list:_\n\n\u2022 An empty can (size dependent on your knothole)\n\n\u2022 Piece of thick bark from a chunk of 24\u2033-long firewood with a knothole\n\n\u2022 Wood screws\n\n\u2022 Plaster of Paris\n\n\u2022 Hole saw\n\n\u2022 Spray paint (I recommend black)\n\n\u2022 1\u2033 \u00d7 3\u2033 \u00d7 3' piece of wood for a post\n\n\u2022 Drill\n\n\u2022 Natural decorations of your choice\n\n_Materials for a knothole feeder_\n\nHave you ever seen those cool pictures of birds and squirrels poking their heads out of knotholes in trees? The photographer must have spent days following birds around trying to find their nests. When I have actually done that I've gotten some neat shots of birds bringing food to their young. But what do you do when it's not nesting season? One day when I was getting some wood from the woodpile, I came up with a great idea. I picked up a piece of firewood that had a knothole in it, and the bark came right off of the wood! I got to thinking, \"why not add a feeder to the back side of the bark?\" After a number of attempts using wood, wire, and string, I finally settled upon using wood screws, a coffee can, and some Plaster of Paris.\n\nBasically, it's a simple, messy process. You'll need wood screws, the can, and a 1\u2033\u00d73\u2033\u00d73\u2032 (or similar) piece of wood for the post.\n\nOne of the best ways of imitating a nest hole in the side of a tree is to actually use what would have eventually become a nest hole in the first place. Find a piece of firewood or a section of a downed tree where a branch has broken off and a cavity is starting to form where the dead material is rotting out. Most pieces of wood are too small for a knothole feeder, or the cavity isn't big enough. The solution is to enlarge what's already there by drilling out the hole from the back.\n\n_The hardest part is finding a suitable piece of wood_\n\n_Step 1: Drilling out the back with a hole saw_\n\nStep 1: Drill out the back side of the bark or wood with a hole saw.\n\nStep 2: Spray paint the inside of the can black.\n\nStep 3: Use wood screws to add the 1\u2033 \u00d7 3\u2033 post to the back of the can so that you have something with which to mount the feeder once you're ready to secure it.\n\nStep 4: Put the can opening on the back of the piece of bark, centered over the knothole. Drill a circle of wood screws into the back of the thick bark to fit around the can. Be careful not to go through the bark with the wood screws.\n\nStep 5: Mix up a batch of Plaster of Paris and build up a wedge or ramp around the can onto the bark, making sure to cover the wood screws to hold it all together. Let it set for a couple of hours and you're done.\n\nStep 5 (alternate): If you don't want or need to use plaster, you can simply screw the can to the back of the wood with wood screws. The size of the tin cans will vary depending upon the size of the wood. Using tin snips, make vertical cuts all the way around the top of the can, roughly \u00bd to \u00be of an inch apart to create tabs. Bend these tabs down with a pair of pliers, and screw them into the back of the piece of wood with wood screws.\n\n_Step 3: Adding a post to the can_\n\n_Step 4a: Drill a circle of wood screws to create a \"basket\" structure for the can_\n\n_Step 4b: Place the can within the structure created by the circle of wood screws_\n\n_Step 5: Use Plaster of Paris to anchor the can into the structure of wood screws_\n\n_Step 5a (alternate): Cutting tabs in the can and folding them down_\n\n_Step 5b (alternate): Wood screws are used to fasten the can tabs to the backside of the piece of wood_\n\nStep 6: Once the feeder is completed, add seed to the can. Now find a convenient fence or pole on which to mount the feeder. It is best to place it near other feeders to help critters discover the feed that you put inside of it. Be sure to take into consideration what kind of light you want to fall on it. It also helps with birds to place feeders near bushes for cover. They are a lot more comfortable feeding in places where they know they can dive off into safety if a predator comes near. The nice thing about these feeders is they make for an extremely natural looking nest hole.\n\n_1_ \u2033 _\u00d7 3_ \u2033 _post screwed to the knothole wood in preparation for placement_\n\n_Completed knothole feeder screwed in place_\n\n_You may find that other critters enjoy knothole feeders, too!_\n\n_Red-breasted nuthatch gathering black sunflower seed from the knothole feeder_\n\n### **BUILDING A WINDOW BLIND**\n\n#### **Level: Medium**\n\n_Materials list:_\n\n\u2022 \u215b\u2033 Masonite (cut to the size of your window)\n\n\u2022 Strips of a towel, enough to surround the edges of the Masonite\n\n\u2022 Circular saw\n\n\u2022 Tape\n\n\u2022 Netting or batting material, cut into 2\u2033 strips\n\n\u2022 1\u2033 \u00d7 4\u2033 boards (optional)\n\nYes, it's true. I have a custom, luxury blind that has a TV, fridge, and a computer with Internet. It's also heated. On top of that it has the most comfortable chair I have ever used in a blind. So before you think I'm nuts, let me say that this blind is the office inside my house. I do a good percentage of my bird photography right out the back window of my house. I place my rolling feeder in appropriate lighting with a good background right next to my office window. There are holes drilled in the rolling feeder so I can place branches of different types as perches for the birds to land on.\n\nCreating a blind out of one of your windows can be as simple as tacking up a piece of fabric with a hole in it for your camera over the window. I like something a little more secure, so I use a piece of \u215b\u2033 Masonite that is cut to the window size.\n\nStep 1: To create the blind, first measure the window and then cut the board to size. Keep in mind when cutting your board that you'll need to subtract \u00bd\u2033 from all sides to accommodate for the frame of towels.\n\nStep 2: Tape strips of towel around the outside perimeter of the pressed hardboard to keep the windowsill from getting scratched up.\n\n_Step 1a: Measure the inside of the window_\n\n_Step 1b: Transfer the measurements to a piece of plywood or hardboard (I use Masonite). Subtract \u00bd_ \u2033 _from each side to allow for wrapping the edges in the towel._\n\n_Step 1c: Cutting the sides with a circular saw_\n\n_Step 2a: Taping the towel material to the back of the hardboard_\n\n_Step 2b: Taping the front side of the hardboard_\n\n_Step 3a: Checking for the correct window height to cut the opening_\n\nStep 3: Next I sit down (in the chair I intend to use for shooting) in front of the board with my tripod set-up. This gives me a really good idea of where the opening in the hardboard or Masonite should be cut. I mark the place I want to cut, create the opening, and then place the board back in the window to see if it works. Sometimes I may need to modify the opening with further cutting.\n\nStep 4: Tape a piece of netting or batting material to hang over the hole. I like to cut it in strips about 2\u2033 wide.\n\nStep 5: After having used the window blind for a while I reinforced the hardboard by screwing on some 1\u2033 \u00d7 4\u2033 boards to the outside edges to stiffen it.\n\nThe flat board will fit easily behind a door, or it can be stored in the garage or basement, ready for use. You can cut boards to fit all the windows in your home to allow yourself a variety of shooting locations.\n\n_Step 3b: Cut an opening and spray paint the outside_\n\n_Completed window blind in place_\n\n### **GROUND POD FOR SHOOTING FROM A WINDOWSILL**\n\n#### **Level: Medium**\n\n_Materials list:_\n\n\u2022 Clamp\n\n\u2022 Bogen ballhead (or equivalent)\n\n\u2022 Scrap board (1\u2033 \u00d7 12\u2033)\n\n\u2022 \u215c\u2033 carriage bolt\n\n\u2022 Epoxy\n\n\u2022 Netting or batting material, cut into 2\u2033 strips\n\n\u2022 1\u2033 \u00d7 4\u2033 boards (optional)\n\nOver the years I have struggled with ways to photograph from my office window. The main problem is that I can't get up next to the wall because the legs of the tripod are in the way. I've tried using rolled up towels and beanbags to stabilize the camera instead of a tripod, but towels aren't very stable and beanbags aren't very adjustable. The commercial beanbags come with a \u00bc\u2033 mounting screw on top, and you have to spin the bag to attach it to your camera. These don't allow you to maintain the camera in a locked and focused position.\n\nI finally settled on a solution that works really well\u2014clamping a DIY ground pod to the windowsill ledge.\n\nStep 1: Use an old Bogen ballhead (or equivalent) from a long dead tripod.\n\nStep 2: Drill and mount it to a piece of scrap board (1\u2033 \u00d7 12\u2033) with a \u215c\u2033 carriage bolt, and then epoxy the bolt in place. Be sure to check and see what size bolt your tripod head uses before epoxying one into place.\n\nVoil\u00e0! A new ground pod is born. It is light and easy to carry with a camera mounted on it. I can easily switch from horizontals to verticals. (Try that with a commercial beanbag pod!) I clamp it to the windowsill of my office (behind the blind) using a large spring clamp, and I'm ready for some bird photography.\n\n_Ground pod made with a 1_ \u2033 _\u00d7 12_ \u2033 _board and a_ \u215c\u2033 _carriage bolt_\n\n_Ground pod clamped to a windowsill, ready for use_\n\nThe following projects are more elaborate and extensive, and require more construction or sewing experience, and materials.\n\n### **BUILDING A LARGE WATER FEATURE**\n\n#### **Level: Complex**\n\n_Materials list:_\n\n\u2022 Table (picnic table or similar)\n\n\u2022 Qt of sealer or waterproof paint\n\n\u2022 1\u2033 \u00d7 4\u2033 \u00d7 8\u2032 pieces of wood (2)\n\n\u2022 1\u2033 \u00d7 4\u2033 \u00d7 4\u2032 piece of wood\n\n\u2022 Sheet of 4\u2032 \u00d7 8\u2032 plywood, \u215c\u2033 or thicker\n\n\u2022 1\u00bc\u2033 wood screws (20)\n\n\u2022 Circular saw\n\n\u2022 Black plastic sheeting (Visqueen), 10\u2032 \u00d7 6\u2032\n\n\u2022 Rocks and gravel to line the edge of the pond\n\n_Step 1: Here are the needed supplies. First, apply a sealant to the plywood._\n\nThis water feature is a project for someone with a yard with plenty of room, as it is 4 feet \u00d7 8 feet in size. The birds absolutely love it. You will have birds visiting it throughout the day. The pond is a 4\u2032 \u00d7 8\u2032 sheet of plywood set on top of an old table (an old picnic table or a table picked up cheap from a garage sale will do).\n\nStep 1: Seal the sheet of plywood with enamel paint, varathane, polyurethane, or some other type of wood sealer.\n\n_Step 2: Cut the 1_ \u2033 _\u00d7 4_ \u2033 _\u00d7 8' in half, diagonally_\n\n_Step 3: Screw the 1_ \u2033 _\u00d7 4_ \u2033 _diagonals and the 1_ \u2033 _\u00d7 4_ \u2033 _\u00d7 4_ \u2032 _deep-end piece to the top of the plywood_\n\nStep 2: Cut both 1\u2033 \u00d7 4\u2033 \u00d7 8\u2032 pieces of wood diagonally lengthwise. One set will be used to make the sides for the pond. The other set will be placed on edge lengthwise on the table, and the plywood will set on top of it. The angle of these planks will provide some slope for the pond to have a deep end.\n\nStep 3: Use some 1\u2033 wood screws to fasten the sides (one set of the 1\u2033 \u00d7 4\u2033 \u00d7 8\u2032 diagonal pieces for either long side of the pond) and the deep-end frame piece of 1\u2033 \u00d7 4\u2033 \u00d7 4\u2032 to the plywood. This is a little tricky because you have to screw them from the underside of the plywood. Be careful when you get to the shallow end that you don't go all the way through the thin edge of the board with the wood screws.\n\n_Step 4: One set of 1-inch \u00d7 4-inch boards placed on edge on the top of the table. The edge closest to the viewer will be the shallow end of the pond._\n\n_Step 5: Place plywood at an angle on the table. Cover the pond area in plastic Visqueen sheeting._\n\nStep 4: Place the other set of diagonal 1-inch \u00d7 4-inch boards on edge lengthwise on the table. The thick end will be the shallow end. These do not need to be screwed down because the weight of the water feature holds them in place. It also helps to leave them unscrewed so that they can be moved to help adjust the level of the water in the pond.\n\nStep 5: Set the plywood on top of the 1\u2033 \u00d7 4\u2033 \u00d7 8\u2032 wood pieces so that the thick ends of the 1\u2033 \u00d7 4\u2033 \u00d7 8\u2032 pieces on top of the plywood match up with the thin ends of the 1\u2033 \u00d7 4\u2033 \u00d7 8\u2032 pieces between the plywood and the table. Carefully cover the pond area with black Visqueen plastic.\n\n_Step 6: Fill with water and begin placing river rock_\n\n_Step 7: Complete covering the water feature with gravel and sand_\n\nStep 6: Place rocks all around the edges of the pond. Place two of your biggest rocks at the front corners to hide the sides of the pond. Place the rest of the bigger rocks across the back to provide a backdrop. Fill the pond with water so the water level is right at the brim of the deep end of the pond. You can get better reflections this way.\n\nStep 7: The final step is to fill in the pond with rocks and gravel. Place a thin layer of very fine gravel and sand across the middle to cover up the bottom of the pond.\n\nFrom here you can add plants, sticks, moss, and any other natural-looking items you can think of. I attached a platform feeder to the side of my pond and filled it with black sunflower seed. On the other side, I put a bowl of hen-scratch. I keep this away from the water because otherwise the birds tend to kick it around and knock corn into the pond.\n\nI set up my blind about six feet away from the deep end of the pond and I set my tripod height to about two inches above water level. You can go lower, but the water will sometimes look milky from a lower angle.\n\nWhat's nice about this project is that you can move it if you have to. First pick of all the big rocks. Then get a flat shovel and shovel the gravel and smaller rocks into five gallon buckets. With someone's help you can easily move the plywood and the table to a new location and set it up again.\n\nOne final tidbit: Keep a hose with a small valve and a clear plastic line going from the blind to the pond. If the pond's water level goes down too much when you are shooting, you can add water without disturbing the birds.\n\n_Steller's jay bathing in large water feature_\n\n### **BUILDING A CHAIR BLIND**\n\n#### **Level: Complex**\n\n_Materials list:_\n\n\u2022 Camping chair with canopy\n\n\u2022 4\u00bd yds. of camouflage fabric (or more, if you have a very large chair)\n\n\u2022 Black or green thread\n\n\u2022 Sewing machine\n\n\u2022 \u00be\u2033 PVC slip couplings (2)\n\n\u2022 \u00be\u2033 90 degree PVC elbows (2)\n\n\u2022 Ten feet of \u00be\u2033 PVC pipe\n\n\u2022 Hacksaw or PVC pipe cutter\n\n\u2022 Duct tape\n\nI have been really busy shooting images of birds, turtles, millipedes, and a number of portraits among other things. Through all of this, my burning desire has been to create a new chair blind. I have been using an Ameristep chair blind for a lot of my nature photography; it works really well, but after much use I have found that it lacks a few essentials for photographers, since it was designed as a hunting blind. The biggest problem with it is that the front of the blind is too far away from the seat (it was designed with a rifle barrel in mind). Another problem is limited side-visibility. Finally, these types of blinds are fairly heavy. With those thoughts in mind, I set out on a quest to build a reasonably cheap chair blind.\n\n_Step 1: Underside of canopy showing PVC frame taped to canopy frame_\n\nA good chair is the most important aspect of this project. The best thing I found was a folding camping chair with a canopy sunshade at a local store for 23 bucks.\n\nStep 1: Tape a piece of \u00be\u2033 PVC pipe and a slip coupling to the canopy frame with duct tape. The length of PVC will vary depending upon canopy chair used.\n\n_Step 2: Layout of PVC to be duct taped to chair blind canopy_\n\nStep 2: Make a U-shaped extension with 3 pieces of PVC pipe and a couple of 90-degree elbows. This will fit right into the slip couplings on the piping already attached to the canopy. I don't glue mine so the blind is easy to break down and transport.\n\n_PVC frame duct taped to the sides of the chair blind canopy with white duct tape_\n\nStep 3: Set the chair up. You'll need to measure your chair so that you know how much fabric to buy. Measure from the front of the chair to the back, so you know how deep the chair is. Then measure from the bottom of the left side of the chair up over the top, and down the right side of the chair to the ground. These will be the dimensions of the piece of fabric that will drape from the bottom of the left side of the chair over the canopy and down to the bottom of the right side of the chair.\n\n_Step 3: Measuring the left side of the chair blind for fabric._\n\nStep 4: The pieces of fabric that will cover the front and back of the chair should be about the same size. Measure the chairs height and width, so you'll know how much fabric you'll need for these panels.\n\n_Inside the chair blind_\n\nStep 5: Add \u00bd\u2033 to the measurements of the fabric on all sides to make room for the seams. Purchase fabric and cut three panels: two panels for the front and back of the chair, and one long panel to cover the left, right and top of the blind. See the chair blind pattern.\n\n_Sewing pattern for chair blind_\n\nStep 6: Drape the long piece of fabric over the chair so it falls from the top of the chair to the ground on both sides. Pin or baste the top of the front and back panels to the roof section of the blind. When you are satisfied with the way the blind fits over your chair, sew the pieces together, attaching the top edges of the front and back panels to the appropriate places on the long piece of fabric.\n\nStep 7: Sit in the blind with your camera, lens, and tripod, and mark where the openings for the lens port and viewing ports should be on the fabric.\n\nStep 8: Cut the lens port and sew a flap to cover it. Cut the viewing ports and cover them by sewing mesh over the openings.\n\nStep 9: Sew the edges of the blind together so the right front corner and both back corners are completely stitched together from top to bottom. The fabric should create an enclosed box except for the front left edge, which will be left open.\n\n_Chair blind set up in the backyard_\n\nStep 10: Use a snap tool and add black metal snaps to the front left corner of the blind to create an access point to get in and out of the blind.\n\nThere you have it! A chair blind that is lighter and far more camera-friendly than a commercial blind, at half the cost.\n\n### **A PERMANENT BLIND**\n\n#### **Level: Complex**\n\n_Materials list:_\n\n\u2022 \u215c\u2033 plywood, 48\u2033 \u00d7 48\u2033 (4) (these are the three sides and the floor)\n\n\u2022 \u215c\u2033 plywood 40\u215d\u2033 \u00d7 48\u2033 (this is the back door)\n\n\u2022 \u215c\u2033 plywood 48\u2033 \u00d7 60\u2033 (this is the roof)\n\n\u2022 \u215c\u2033 plywood 13\u00bd\u2033 and 5\u2033 \u00d7 48\u2033 (2) (these are the upper left and right sides)\n\n\u2022 \u215c\u2033 plywood 16\u00be\u2033 \u00d7 48\u2033 (this is the upper front piece)\n\n\u2022 \u215c\u2033 plywood 12\u2033 \u00d7 12\u2033 (this is the back door slider)\n\n\u2022 2\u2033 \u00d7 4\u2033 \u00d7 48\u2033 studs (10) (for framing)\n\n\u2022 2\u2033 \u00d7 4\u2033 \u00d7 41\u2033 studs (2) (for framing)\n\n\u2022 2\u2033 \u00d7 4\u2033 \u00d7 45\u2033 stud (for framing)\n\n\u2022 2\u2033 \u00d7 4\u2033 \u00d7 10\u2033 studs (2) (for framing)\n\n\u2022 1\u2033 \u00d7 2\u2033 \u00d7 45\u2033 furring strips (4) (frames for sliders, right and left sides)\n\n\u2022 1\u2033 \u00d7 2\u2033 \u00d7 38\u2033 furring strips (4) (frames for sliders, right and left sides)\n\n\u2022 1\u2033 \u00d7 2\u2033 \u00d7 41\u2033 furring strips (2) (frames for front sliders)\n\n\u2022 1\u2033 \u00d7 2\u2033 \u00d7 34\u2033 furring strips (2) (frames for front sliders)\n\n\u2022 1\u2033 \u00d7 2\u2033 \u00d7 13\u2033 furring strips (4) (frames for back door sliders)\n\n\u2022 1\u2033 \u00d7 2\u2033 \u00d7 40\u215d\u2033 furring strips (2) (for door frame)\n\n\u2022 1\u2033 \u00d7 2\u2033 \u00d7 46\u00bd\u2033 furring strips (2) (for door frame)\n\n\u2022 1\u2033 \u00d7 6\u2033 \u00d7 11\u00bd\u2033 planks (tongue and groove) (24) (sliders)\n\n\u2022 Hinges (3)\n\n\u2022 Wood pallet roughly 48\u2033 \u00d7 48\u2033\n\n\u2022 Roll of landscape cloth\n\n_Step 1: Cover the pallet with plywood_\n\nWinter can be a difficult time to photograph birds. Depending upon your geographical location, it can be windy, rainy, or snowy, which has the potential to make photography quite miserable. However, if you are prepared for heavy downpours and snowstorms, these conditions give you the potential to create some incredible bird images. Most canvas or cloth blinds are fairly waterproof, but they will only put up with so much water and wind, which is why building winter or permanent blinds can be such a good decision. Permanent blinds are snug, dry, and exceptionally useful for photography.\n\nTo create my permanent blind, I started off by going to the lumber yard. I picked up a 4\u2032 \u00d7 4\u2032 pallet. I just asked nicely, and they gave it to me for free (they get tons of them daily). Other possible places to get these are discount and warehouse stores, or anywhere that gets supplies delivered by truck. Please note that not all pallets are exactly 4\u2032 \u00d7 4\u2032 so some of the dimensions given may vary depending upon the pallet you choose.\n\nFor this project you need to have some basic carpentry skills. I'm not a skilled woodworker, but I do know how to use basic tools. If you aren't very confident with this sort of thing, just get someone who knows what they're doing to help you.\n\nStep 1: Cut plywood to fit your pallet, and screw it down to the top of pallet.\n\n_Step 2a: Cut and frame up one side and screw it down to the base_\n\n_Step 2b: Cut and frame the other side and screw it down to the base_\n\nStep 2: Frame up the right and left sides of the blind using four 2\u2033 \u00d7 4\u2033 \u00d7 48\u2033 studs and four 2\u2033 \u00d7 4\u2033 \u00d7 35\u2033 upright studs. Add the framed side panels by screwing them down to the pallet. Frame in the back of the blind by toeing in two 2\u2033 \u00d7 4\u2033 \u00d7 41\u2033 studs between the two sides on the top and the bottom. Screw on the plywood to the back frame. The final step to the lower framing is to screw one 2\u2033 \u00d7 4\u2033 \u00d7 48\u2033 stud across the top of the front, between the two sides.\n\n_Step 2c: Cut and frame the back and screw it to the base_\n\n_Step 3: Frame up the roof_\n\n_Step 4: Cut the sides and top of the roof section and screw them to the framing_\n\nStep 3: The next and most complicated step is to frame the roof. Start by making a 13\u2033 \u00d7 48\u2033 rectangle out of 2\u2033 \u00d7 4\u2033 pieces of wood (indicated by the green box). Nail or screw this down to the top of the back wall of the blind. Use the two 2\u2033 \u00d7 4\u2033 \u00d7 10\u2033 and two 2\u2033 \u00d7 4\u2033 \u00d7 48\u2033 studs to accomplish this.\n\nNext, use a 2\u2033 \u00d7 4\u2033 \u00d7 48\u2033 stud, and nail or screw it in (on edge) to the 2\u2033 \u00d7 4\u2033 \u00d7 48\u2033 stud above the front door opening. Be sure to screw or nail it in from the underside. Following that is the most difficult part. Measure and cut two pieces (size 2\u2033 \u00d7 4\u2033 \u00d7 48\u2033) to create a triangular frame (in yellow) between the rectangular frame above the back wall and the 2\u2033 \u00d7 4\u2033 above the door. The easiest way to do this is to hold a 2\u2033 \u00d7 4\u2033 up in between these two points and mark the length and angles for the cut with a pencil. Make the cuts and toe in the last of the framing with screws or nails.\n\nStep 4: To keep it all nice and dry, cut out a piece of plywood, 48\u2033 wide by 60\u2033 long, for the roof (in green). Screw the roof down to the top section of the roof frame. Cut a 16\u00be\u2033 \u00d7 48\u2033 piece of plywood to cover the rectangle of 2\u2033 \u00d7 4\u2033s that is above the front wall of the blind. This piece should overlap the plywood below to keep the blind dry inside.\n\n_Step 5: Frame the door with 1_ \u2033 _\u00d7 2_ \u2033 _lumber. Install hinges and hang the door._\n\nMeasure and cut out plywood to cover the two triangular spaces below the roof (in yellow). Screw those on before you move on to the door. These pieces are 48\u2033 long and 13\u2033 tall on one end, and 5\u2033 tall on the other.\n\nStep 5: You'll need to be able to get in and out of the blind, so frame the door with 1\u2033 \u00d7 2\u2033 lumber. Use the two 46\u00bd\u2033 and 48\u2033 pieces, and add hinges to one side. Hang the door.\n\n_Step 6: Set up the tripod, and cut a hole for your camera_\n\nStep 6: Set up a tripod and camera to figure out a comfortable camera height. Mark and cut out the window openings on the wood.\n\n_Step 7: Cut rectangular openings for the sides and back_\n\nStep 7: Cut the window openings in the sides and the back of the blind. Please note that the opening is cut 6\u00bd inches from one edge to allow for room to take the sliders (see next step) in and out. Cut a 10\u2033-diameter circular opening in the back door for the camera. The left and right openings are 38\u00bd\u2033 long and 9\u00bd\u2033 high. The front opening is 35\u00bd\u2033 \u00d7 9\u00bd\u2033.\n\nStep 8: Install the slider guides for the windows. The slider guides are made of 1\u2033 \u00d7 2\u2033 furring strips. Two 1\u2033 \u00d7 2\u2033 pieces are screwed together to make an \"L\" shape. This is the guide at the bottom of the window. Two pieces are screwed together to make an upside down \"L\" shape above the window. Screw these pieces to the blind from the outside. The longer pieces of the pair go at the top and bottom for the guides. It is best to have someone help you at this stage by putting the sliders between the guides and holding them in place while the guides are being screwed on from the outside. The sliders should have plenty of free room to be able to slide from side to side. Check the materials list to see which pieces go with which window opening.\n\n_Step 8: Mock-up of a slider to show construction details_\n\n_Slider assembly_\n\n_Slider assembly in detail_\n\n_Slider over the door opening_\n\n_Interior of photo blind with shooting shelves and window coverings\u2014interior is painted black to mask movement_\n\n_Complete unpainted photo blind_\n\nStep 9: Create and install a shooting shelf (see \"A Shooting Shelf for a Permanent Blind\").\n\nStep 10: It's a good idea to paint the inside of the blind black.\n\nStep 11: Next, install the window coverings. I used landscape fabric, which is both waterproof and mildew proof. It has the advantage of being transparent enough to see through, but still opaque enough to hide your movements from outside the blind.\n\nStep 12: The last step is to paint the outside with colors that will blend in with your yard.\n\nThe primary disadvantage of a permanent blind is that it is designed to stay in one place, and can be difficult to move. I put a set of wheels under one end and attached some two by fours to the side (like a wheelbarrow) for when I needed to move mine. It was a difficult job, so remember that proper placement of your blind is critical. Some people choose to scout a location first, and build the blind in place.\n\n### **A SHOOTING SHELF FOR A PERMANENT BLIND**\n\n#### **Level: Complex**\n\n_Materials list:_\n\n\u2022 2\u2033 \u00d7 2\u2033 \u00d7 8\u2032 stud\n\n\u2022 12\u2033 \u00d7 16\u2033 piece of \u215c\u2033 plywood cut into two triangles\n\n\u2022 12\u2033 \u00d7 41\u2033 piece of \u215d\u2033 plywood\n\n\u2022 1\u2033 \u00d7 2\u2033 \u00d7 2' furring strip\n\n\u2022 \u215c\u2033 dia \u00d7 \u00be\u2033 bolt\n\n\u2022 \u00bd\u2033 dia \u00d7 2\u2033 bolt\n\n\u2022 \u00bd\u2033 dia \u00d7 5\u2033 carriage bolts (2)\n\n\u2022 \u00bd\u2033 wing nut (2)\n\n\u2022 \u00bd\u2033 flat washer (2)\n\n\u2022 12\u2033 \u00d7 2\u2033 \u00d7 \u00bc\u2033 channel iron\n\nI believe that one of the best features that a permanent or semi-permanent blind can have is a shooting shelf. A shooting shelf is an adjustable platform to support your tripod head so you don't have to use a tripod in your blind. The shelf also frees you from having to fight with tripod legs, while still giving you a stable platform to shoot from. It also allows you to place your camera closer to the lens opening of the blind.\n\nThe shelf can easily be adjusted to the desired camera height by loosening two wing nuts, then raising or lowering the shelf and tightening the wing nuts again. A swing arm ballhead support on the shelf allows the photographer to move the camera position closer or farther from the window sliders as well as to the right or left. Additionally, the swing arm can be moved to the far end of the shelf to enable shooting from the side window sliders. To make full use of the side sliders, the shelf can be repositioned to those windows by undoing the wing nuts and moving the shelf.\n\nThe combination of the shooting shelf, swing arm ballhead, and the window sliders make a blind very comfortable and easy to shoot from. If you are planning on building a blind or want to make a nice addition to one you already have, consider this key, additional feature.\n\n_Step 1: Finished piece of plywood_\n\nStep 1: Start with a 12\u2033 \u00d7 41\u2033 \u00d7 \u215d\u2033 piece of plywood. Cut two horizontal \u215d\u2033 wide by 14\u215c\u2033 long slots, 3\u2033 in from the outside 12\u2033 edge. The slots should be 7\u2033 from the back edge and 3\u2033 from the right and left sides. Please see the top view of the shooting shelf.\n\nStep 2: Cut two 2\u2033 \u00d7 4\u2033 pieces of wood, 18\u2033 long. Cut a \u215d\u2033 slot down the center of both of them, 1\u00bd\u2033 from each end.\n\n_Step 2: 2_ \u2033 \u00d7 _4_ \u2033 _pieces of wood with cuts down the center_\n\nStep 3: Screw the end of the 2-inch \u00d7 4-inch pieces to the underside of the plywood and frame them in with 2-inch \u00d7 2-inch pieces. The outside edges of the 2-inch \u00d7 4-inch pieces should be 8\u00bc\u2033 from the outside edge of the plywood.\n\n_Step 4: View of the underside framing of the shooting shelf_\n\nStep 4: Brace the 2-inch \u00d7 4-inch pieces with 12\u2033 \u00d7 16\u2033 plywood triangles, with the 16\u2033 edge of one triangle screwed (at a perpendicular) to the 18\u2033 \u00d7 2\u2033 side of the 2\u2033 \u00d7 4\u2033. Add a 1\u2033 \u00d7 2\u2033 \u00d7 24\u00bc\u2033 piece of bracing wood in between the two triangle corners on the bottom edge of the shelf.\n\nStep 5: In the photo blind, choose the wall you are most likely to photograph from. Add two vertical 2\u2033 \u00d7 4\u2033 supports centered the same distance apart as the slots in the 2-inch \u00d7 4-inch pieces on the shelf. Drill a \u00bd\u2033 hole 6 inches down from the top end of each 2\u2033 \u00d7 4\u2033. Put a \u00bd\u2033-diameter carriage bolt (5\u2033 long) through the hole from the outside of the blind to secure the 2-inch \u00d7 4-inch pieces to the plywood. You may need help with this step by having a person thread the bolt through from the outside while you place the slot in the 2\u2033 \u00d7 4\u2033 over the bolt. While holding the 2\u2033 \u00d7 4\u2033 in place, have the person outside the blind place several screws through the blind wall and into the 2-inch \u00d7 4-inch pieces to hold them in place.\n\n_Step 5: Thread the bolts through the outside of the wall_\n\n_Step 6: The secured shooting shelf_\n\nStep 6: Secure the shelf to the bolts with two \u00bd\u2033 wingnuts. Adjust the shelf to a comfortable photographing height and tighten the wing nuts at that level. You can always reposition the shelf height once you have placed your camera on it.\n\nStep 7: Drill a \u215c\u2033 hole 1\u00bd\u2033 from the end of a 12\u2033 \u00d7 2\u2033 piece of channel iron, and drill a \u00bd\u2033 hole \u00be\u2033 from the other end.\n\nStep 8: Tack weld a \u215c\u2033 \u00d7 \u00be\u2033 bolt into the \u215c\u2033 hole. Then tack weld a \u00bd\u2033 \u00d7 2\u2033 bolt into the \u00bd\u2033 hole in the channel iron as shown, with the threaded sides opposite one another. Any welding or machine shop should be able to do this for you quite cheaply.\n\n_Step 9: Swing arm secured in place by a wing nut with a camera and ballhead mounted on it_\n\nStep 9: To attach the swing arm to the shooting shelf, put the \u00bd\u2033 bolt side of the channel iron into the slot in the plywood and tighten it up to the underside of the plywood with a flat washer and a \u00bd\u2033 wing nut. To attach a tripod head, screw the tripod head onto the \u215c\u2033 stud sticking up from the channel iron. Please make sure the tripod head is tight and secure!\n\n_Camera mounted to photograph out the side of the photo blind_\n\n_Goldfinch on tulips waiting for the feeder. There is a tube feeder just out of the frame to the right._\n\n## **Resources and Suppliers**\n\n**Photo Blinds:**\n\nAmeristep  \nameristep.com\/blinds\/doghouse.html\n\nCabelas Outfitters  \ncabelas.com\n\nBass Pro Shops  \nbasspro.com\n\nDicks Sporting Goods  \ndickssportinggoods.com\n\n**Bird Feeders \u2013 Brands:**\n\nOpus\n\nPerky Pet\n\nDroll Yankee\n\nHeritage Farms  \nheritagefarms.biz\n\nStokes  \nstokesbirdsathome.com\n\n**Camera Equipment Suppliers**\n\nB+H Photo and Video  \n420 9th Avenue  \nNew York, NY 10001  \nBhphotovideo.com\n\nAdorama  \n42 West 18th Street  \nNew York, NY 10011  \nAdorama.com\n\nHunts  \nHuntsphotoandvideo.com  \n(Multiple locations on the US East Coast)\n\nKEH, Inc  \n4900 Highlands Parkway SE  \nSmyrna, GA 30082  \nkeh.com  \nWorld's largest supplier of used camera equipment\n\nBristol Cameras Ltd  \n47 High Street, Bristol, BS1 2AZ  \nBristolcameras.co.uk\/contact_us.php\n\n## **Recipes for Suet**\n\nBasic Suet Mix\n\n1 cup peanut butter\n\n1 cup shortening\n\n1 cup flour\n\n3 cups cornmeal\n\n1 cup cracked corn or hen scratch\n\nSlowly melt shortening and peanut butter in a large saucepan on low heat. Stir in other ingredients slowly. Pour into aluminum pie tins and let cool.\n\nYou can add one small handful of black oil sunflower seeds and\/or mixed seed (optional).\n\nBirdy Suet Mix\n\n1 cup chunky peanut butter\n\n2 cups ground oatmeal\n\n2 cups oatmeal\n\n1 cup shortening or rendered suet\n\n\u2153 cup sugar\n\n1 cup white flour\n\nMelt the shortening or suet and peanut butter on low heat until melted in a large saucepan. Stir in the other ingredients one at a time. Pour into aluminum pie tins and set aside to cool.\n\nFor variations on these recipes add peanuts, berries, or dried cut fruit pieces to the mix in small quantities.\n\n_Mountain quail on a piece of burned redwood burl with moss. There is a feeder cup filled with black sunflower seed on the backside of the burl._\n\n## **Conclusion**\n\nIt has been over three years since I began writing _Secrets of Backyard Bird Photography_. To complete this book, I drew on my years of experience, but it was still a learning process. Along the way I was able to create and compose some beautiful bird images using the techniques covered in this book. I feel privileged to be able to pass along these projects to you!\n\nYou now have a wide variety of techniques and projects available to you for the creation of some quality backyard bird images, including the secrets to using blinds, feeders, perches, and set-ups. We have covered information on types of bird feeders and seed, and how to effectively hide birdseed so it does not appear in the image. We have looked at many different kinds of photo blinds, be it a room in your house, a purchased blind, or a permanent photo blind for your backyard that you created from raw materials.\n\nRemember the importance and fun of creating a beautiful set-up in your yard. Be creative! You can use any combination of interesting items, including flowers, gnarly branches, twigs, mossy rocks, and other natural materials to create attractive perches in your pursuit of images of backyard birds. You can choose from a wide variety of backgrounds, both man-made and natural, to position behind your perches for an awesome image. You also have the knowledge to capture the best bird images with great composition. Remember that a good head angle and a catch light in the eye will make for an aesthetically pleasing image of the birds in your yard.\n\nI hope these tips and tricks will help you to find satisfaction and joy in photographing the wildlife in your backyard. I wish you the very best in your pursuit of bird photography. Now gather up some gear and go out and create some beautiful bird images!\n\nJ. Chris Hansen\n\n**Contact Information**\n\nYou can follow my photographic exploits on my  \nphotoblog: _Chris the Photog_\n\n<http:\/\/christhephotog.blogspot.com>\n\nI am very open to hearing from you if you have questions about backyard bird photography. You can leave a note in the comment section of my photoblog on the most current blog entry, or you can email me with your questions directly at: chrishansen@instawave.net\n","meta":{"redpajama_set_name":"RedPajamaBook"}}