Bullet with Your Name on It: What You'll Probably Die From and What You Can Do About It

“An enormously valuable program for living long and well.” Health family history plays in your health. You’ve also hea...

Author: Avery Hurt

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“An enormously valuable program for living long and well.”

Health

family history plays in your health. You’ve also heard all the advice about what good habits you need to develop. The problem is there’s so much contradictory information and hype out there, you don’t know what to believe. One thing is for certain: something’s going to kill you eventually. Soldiers in battle use the phrase “a bullet with your name on it.” Here’s the good news—if you know your personal risk factors, you can increase your chances of living a long and healthy life. With no pharmaceutical nor institutional agenda to support, veteran medical reporter Avery Hurt wades through the most current medical information to give you practical, straightforward guidance on your key health issues.

What You Will Probably Die From and What You Can Do About It

You’ve heard all the warnings about what is bad for you and the role

BULLET WITH YOUR NAME ON IT

YOU CAN TAKE CONTROL OF YOUR HEALTH

—Richard Stein, Spokesperson for the AHA and Director of Preventive Cardiology at Beth Israel Hospital in New York

BULLET WITH YOUR NAME ON IT

What You Will Probably Die From and What You Can Do About It

Avery Hurt, a medical writer for Newsweek, Better Homes and Gardens, and many other publications, cuts through the clutter and confusion to present a holistic picture of what you need to do to ﬁgure out the odds—and beat them. Bullet with Your Name on Itt is like an informed friend by your side, giving you the skinny on the most common diseases and conditions.

Hurt

$14.95 ISBN 10: 1-57860-303-X ISBN 13: 978-1-57860-303-9

Avery Hurt 9 781578 603039

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Bullet with Your Name on It What You'll Probably Die From and What You Can Do About It

Avery Hurt

Cincinnati

Bullet with Your Name on It: What You'll Probably Die From and What You Can Do About It by Avery Hurt Copyright © 2007 by Avery Hurt. All rights reserved. No portion of this book may be reproduced in any fashion, print, facsimile, or electronic, or by any method yet to be developed, without express permission of the copyright holder.

Library of Congress Cataloging-in-Publication Data Hurt, Avery. Bullet with your name on it : what you'll probably die from and what you can do about it / by Avery Hurt. p. cm. Includes index. ISBN-13: 978-1-57860-303-9 ISBN-10: 1-57860-303-X 1. Health risk assessment. 2. Diseases—Risk factors. I. Title. RA427.3.H873 2007 616—dc22

2007031130

Printed in the USA 1 2 3 4 5 6 7 8 9 10 For further information, contact the publisher at

Distributed by Publishers Group West Edited by Saleha Ghani Cover designed by Travis Bryant Interior designed by Angela Wilcox

For Bobby

A C K N O W L E D G M E N T S

As you can imagine, a book that covers this many areas requires the help of dozens of experts in dozens of fields. I do not have room to thank everyone who helped, from providing sources of info to answering questions to reading and commenting on chapters. But I do want to mention a few researchers and physicians whom I have consulted over the years, and a few whom I’ve imposed on perhaps more than was strictly fair. All helped me with generosity and kindness. Any remaining mistakes are of course solely my own. Marie Savard, MD, Tanya Paull, PhD (who graciously treated me to a mini-course in cancer genetics 101), John C. Bailar III, MD, epidemiologist and Professor Emeritus in the Department of Health Studies at the University of Chicago, Kenneth Setchell, PhD, William Helferich, PhD, Mark Messina, PhD, Marion Nestle, PhD, Professor of Nutrition, Food Studies, and Public Health at NYU, Thomas Weber, MD, associate professor of endocrinology at Duke University Medical Center, David S. Ludwig, MD, PhD, Director Obesity Program of Boston Children’s Hospital Associate Director, General Clinical Research Center, Philip Barnett, MD, PhD, Director of the Diabetes Program at the Pituitary Center at Cedars-Sinai Medical Center, Eva Obarzanek, PhD, at the National Institutes of Health, Richard Jackson, MD at the Joslin Diabetes Center, Molly Wagster, PhD, Chief of the Neuropsychology of Aging Branch at the National Institute of Aging, Paul M. Coates, PhD, director of the Office of Dietary Supplements at the National Institutes of Health, Kenneth J.

Mukamal, MD, PhD, of Beth Israel/Deaconess Medical Center, Alice Lichtenstein, MD, chair of the American Heart Association’s Nutrition Committee, John Zaia, MD, City of Hope Cancer Center in Los Angeles, William Dietz, MD, Director of Nutrition and Physical Activity at the CDC, Susan Yanovski, MD, of the National Institute of Diabetes, Digestive, and Kidney Diseases (NIDDK), Kelly Brownell, PhD, Director of the Yale Center for Eating and Weight Disorders, David Allison, PhD, Director of the Clinical Nutrition Research Center at the University of Alabama at Birmingham School of Medicine, Jeffrey Conklin, MD, Medical Director of the Esophageal Center at Cedars Sinai Hospital in Los Angeles, Stuart Spechler, MD, Professor of Gastroenterology at University of Texas Southwestern Medical Center, Emily Chew, MD, deputy director of the Division of Epidemiology and Clinical Research at the NEI, Richard Stein, MD, Director of Preventive Cardiology at Beth Israel Hospital in New York Not all the experts who assisted in this effort were medical experts. I’d like to thank my team of computer gurus, Joe Stafford, Lenise Crow, and Steve Bushery. These heroes saved the day on more occasions than I like to remember. And they were fun to work with, too. Thanks to Bob Sehlinger and Jack Heffron for great editorial (and all too often emotional) support, Katie Carroll for copyediting (an exacting and exhausting task), Saleha Ghani for her efforts in locating and selecting illustrations, and Howard Cohen for getting the word out. And of course, a crowd of friends and family hover at the back of any long-term project. Thanks to my parents, Avery L. and Kathryn

Hurt, and my sister, Phyllis Hammond. Thanks also to: Connie and Don Harbor, Carolyn and Dick Smith, Dee Turner, Rick and Jackie McConatha, Elinor Nauen, Christian Millman, Dale Turnbough (who taught me how to be a reporter), Martha Frase, Kristin Erb, Craig Beard, Hank Black, Susan Hart, Beth and Joe O’Donnell, Michele Nailen, Donna Florio, Carol Padgett, Kenny Pate, Steven Chappell, and Georgia Steen. There are no words sufficient to thank my family, Bobby Jones, Garth Jones, and Wil Jones. They are both my motivation and my reward for staying healthy. May you all live long and well.

C O N T E N T S

Introduction

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1

1 What the Numbers Tell Us and What They Don’t

. . . . . . . . . . . . . . . . . . . . . . . . . . . 5

2 Cardiovascular Disease A Disheartening Problem

. . . . . . . . . . . . . . . . . . . . . . . 51

3 Cancer The Many-Headed Monster

. . . . . . . . . . . . . . . . . . . . 93

4 Diabetes A Big Fat Sweet Epidemic

. . . . . . . . . . . . . . . . . . . . . . 127

5 Alzheimer’sand Other Dementias The Forgetting

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 165

6 Osteoporosis and Arthritis Bad Bones

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 177

7 Gastrointestinal Diseases Stop Bellyaching

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195

8 Odds and Ends

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203

Index

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214

Introduction I have a rendezvous with Death At some disputed barricade, When Spring comes back with rustling shade And apple-blossoms fill the air— I have a rendezvous with Death When Spring brings back blue days and fair. —ALAN SEEGER

We all die. The sun may shine today, but we know with certainty that we, too, have a rendezvous with death. Will it be a disease, an accident, or something totally unimaginable that ends our life? Whatever it is, we know it’s coming, this final event that soldiers fatalistically refer to as “the bullet with your name on it.” The truth is that there are probably a number of bullets with your name on them, and that if you know where to look and what action to take, you may be able to duck most of them. And though you will not be able to dodge all of the bullets forever, evading any of them will extend your life. Certain life-ending events, like some accidents, are random and almost impossible to foresee. But even with accidents there are clues that suggest from which direction the bullet with your name on it is coming. Dialing a cell phone or eating a Big Mac while weaving through rush-hour traffic would be recognizable to most observers

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Bullet with Your Name on It

as a habit that you might likely regret someday. Bullets arising from natural causes are frequently easy to detect if you know where to look. Good places to start are your family history, your personal health history, and your lifestyle. A careful examination of these can help you assess what most likely will kill you, and by extension, what actions you can take to improve your odds. There is information everywhere on what to do to avoid the bullets with your name on them—what to eat, what not to eat, what to do, what not to do. Books on cancer, books on heart disease, Web sites on everything from major diseases to obscure syndromes. We are drowning in information. And that is the problem. If you want to know what to do to stay healthy you can wear out a library card and surf the net until your vision is so weak you can’t read the Web page. And then when you’re finished, you don’t really know if you’ve been getting good solid information, well-intentioned but not-ready-forprime-time reporting of the latest research, or information designed to sell someone’s latest snake oil. With this book you have an authoritative guide through this jungle. Here you will find sensible, straightforward advice about your risk of getting the diseases most likely to make you ill or kill you, and what to do and what not to do to prevent them. And you’ll find it all in once place. In my many years as a health reporter, I have discovered that there are many, many excellent experts out there. I take advantage of their expertise on a daily basis, both by reading their published research and by phoning them with questions of all kinds. But one of the best things about experts is also one of the worst. Each expert

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Introduction

knows a tremendous amount about his or her area of expertise, but not so much about everything else. I once interviewed a breast surgeon who was absolutely up to date on every aspect of breast surgery. I was completely astonished to discover, however, that he knew almost nothing about the body of research into the side effects of chemotherapy. I shouldn’t have been surprised. Chemotherapy is an oncologist’s department, not a surgeon’s. The surgeon knew what he was supposed to know and knew it well. He did not have time to be an expert on everything. Many health books are written by MDs. When a book is about a specific health issue, that can be a very good thing. A person with a degree in medicine who specializes in the topic at hand is likely to be a very good source of information. One of the best books I’ve ever read that explains heart surgery to the general population was written by a famous heart surgeon. However, the book you’re reading, Bullet with Your Name on It, is not about the technical aspects of any branch of medicine. It is about understanding, interpreting, and most importantly, applying health information, based on the wide body of medical information currently available. Unfortunately, medical doctors have very little time to follow the research in any area other than their chosen specialty. (And sadly, they rarely have time to follow the literature even in their own fields. That is why they are so dependent on pharmaceutical representatives to explain medications and suggest which ones to use.) Finding and interpreting health information, and sharing that information with the general public is a very different skill from practicing medicine. Among other things, it requires an ability to confront the experts and

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question the standard explanations, to dig for the truth that underlies the obvious answers. To ignore the requirements of standard practice and carefully note what seems to be working, what doesn’t seem to be working, and what the people who are on the cutting edge of the research are finding out. That is a job for a journalist. I am not a medical expert. I am an expert on getting medical information. I spend my days reading studies, following the medical news, and scrutinizing the research that backs it up. Over the years it has occurred to me that it is incredibly easy to lose sight of the forest when being bombarded by details about the trees. That is what so often happens to the medical consumer. We read about a study that shows a decrease in breast cancer risk among women who take a lot of aspirin. Then we see an article telling us that lots of fruits and veggies can reduce our risk of eye disease. Turn the page and there is an article saying that the research on aspirin and breast cancer was oversold. What we never seem to get is the big picture: What does all this mean for me? Now. Should I take aspirin or not? Do I need to wait for more research on fruits and veggies or do they already know something about food and risk of eye disease? Looking at all the data and then stepping back for the big picture is my job. I’ve been distressed to see how little of the big picture is easily accessible to the consumer, the average reader who wants just solid information. That’s why I wrote this book. With it, you can quickly find out which health problems present the greatest risk to you and what you can do to reduce that risk—based not on the latest reports, but on the body of research so far. I hope it saves you time and effort and is helpful as you try to live a long, healthy, and happy life.

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C H A P T E R

O N E

What the Numbers Tell Us and What They Don’t “A man with a watch always knows what time it is. A man with two watches is never sure.” —OLD

PROVERB

“If you live to the age of a hundred you have it made, because very few people die past the age of a hundred.” —GEORGE BURNS

Our lives are encompassed by numbers. As soon as we are born, our parents tell our relatives our sex and name, then they start with the numbers: weight and length, and of course everyone makes a note of the birth date. All too soon the numbers multiply. These days, before we’re out of preschool, we have social security numbers. Soon there are other numbers to memorize: library card number, student ID, driver’s license, home phone, work phone, cell phone . . . The most important numbers, of course, have to do with our health. Blood pressure, cholesterol levels, and the one that started it all off, weight. Numbers can provide a huge amount of information about who we

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are, where we live, what we do, and, if we inspect them closely and interpret them carefully, what is likely to make us ill and what we can do about it.

It’s a Process Sometimes it seems as if science can’t make up its mind. One day you read about a study indicating that moderate coffee drinking is harmless, and may even offer some benefits. As you pour one more cup of joe and flip over to the editorial section, you think that is very good news. The next day you pick up the paper only to discover a warning: careful with the java; it may contribute to osteoporosis. It’s enough to make you forget the whole thing, brew up some nice, strong espresso and have a donut to go with it. The problem is not with the science—not exactly anyway. The problem is with the reporting of it, and, frankly, with our expectations of it. Science is a long, slow, often arduous process. Yes, there are those wonderful “eureka” moments, but they tend to come after and as a result of years of careful and painstaking work. It can’t be stressed too strongly that no single study or research project (no matter if it is published in the Journal of the American Medical Association and written up in the health section of the New York Times) is the definitive answer to anything. Science proceeds by deliberate and careful steps, checking and verifying and repeating itself all along the way. And because nutritional questions are so nuanced, the process in nutritional science is

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What the Numbers Tell Us

even more complex. Imagine, for example, that you are trying to determine if eating a newly discovered root plant (let’s call it yamaloo) prevents colds. First you might look at a group of people who regularly eat yamaloo (in this case, members of the EasyEarth commune where the plant is plentiful) and see how many colds they’ve had over the past few years. You discover that the average EasyEarther had one cold during the past five years, whereas the general, non-yamaloo eating population averaged ten colds during that same five-year period. You write up your findings and publish them in the prestigious Journal of Emerging Root Crops. These results are, no doubt, utterly fascinating and they justify the time and expense involved in further research. But in and of themselves, they don’t confirm anything. It could be that some factor other than yamaloo consumption is responsible for fewer colds among the EasyEarthers. Perhaps their mostly vegetarian diet boosts their immune systems. Maybe the lack of stress in this laid-back community is responsible. The relative isolation of the group might be a factor as well—they simply aren’t exposed to as many cold viruses. But something does seem to be going on, and yamaloo could well be involved. So you design more experiments. The first will involve feeding yamaloo to lab animals, most likely mice, and seeing if it prevents colds in them. You’ll do several animal studies. Then, if things are still looking promising (and funding is available), you’ll try a randomized, doubleblind, placebo controlled study. For this study, you select a

7


group of people from the general population (people who don’t usually eat yamaloo). These people are randomly divided into two groups. For one year, one group is fed a daily serving of yamaloo. The other group is fed a mushy paste that looks and tastes like yamaloo, but is in fact an inert substance. The participants in the study do not know if they are getting the yamaloo or the fake paste (a placebo). You don’t know either. This is to keep your interpretation of the study’s results from being influenced by what you know about who ate what. (This is the double-blind, part). A year later, you see how many colds the participants got during the study. If the yamaloo-eating group got fewer colds, you are really onto something. But you still don’t know anything for certain. Other scientists who have seen your results will conduct similar experiments and see if their results are similar to yours. And you, or other scientists, will go into the lab, take apart some yamaloo and see if you can find a possible mechanism by which yamaloo prevents colds. After many years, and plenty of experiments, you’ll have a rather large body of evidence about the relationship between yamaloo and colds. If the evidence is reasonably consistent, most of the studies are without serious flaws (such as being very small, or using as participants people who take huge amounts of vitamin C) then you’ll be able to make a much stronger claim for the cold-preventing properties of yamaloo. You still haven’t proven beyond doubt that yamaloo prevents colds. Very little is ever proven beyond doubt in any form of science, especially not in nutritional science. The best you can

8


do is get a good feel for the probabilities involved. During all this time that you and your scientific colleagues have been testing and retesting yamaloo roots, the news has gotten out. Right after you completed the first study, the one that measured the EasyEarther’s colds, the public relations department of your university sent out a press release about your research to thousands of journalists (people like me). Intrigued, some of us read your published results and wrote articles for magazines and newspapers across the country. Of course, we called you and asked questions about your research (questions like “what were the weaknesses of the study? Is anyone else doing similar research? What else do these EasyEarthers eat?”), and we called other scientists (ones who are knowledgeable about nutrition and colds, but who aren’t working on the yamaloo project) and asked what they think of all this. And in our articles, we (well, most of us anyway) were careful to say things like “while the research is only preliminary” and “much, much more research is needed before we can know if yamaloo is a worthwhile addition to our diets.” But the sheer volume of stories about yamaloo carries a certain weight of its own and the message came through that yamaloo is the secret key to preventing colds. Food manufacturers, always looking for new products to sell, started marketing yamaloobased foods and snacks. The supplements industry got into the act, too, and yamaloo tablets began popping up on grocery store shelves everywhere. Of course, the Food and Drug Administration won’t let anyone make claims about the nutritional proper-

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ties of yamaloo until still more solid evidence is in. But they don’t need to. Everyone knows that yamaloo prevents colds, right? They read it in the newspaper. Of course, occasionally a study indicates that yamaloo might not be the miracle food we suspect it to be. Perhaps a few groups of test subjects do not respond to yamaloo in the way others have. And perhaps some researchers have found some flaws in the previous studies that were not noticed before, such as the fact that many of the people who participated tended to have stronger immune systems than average to begin with. Because journalists want to be fair and to give the public all the information available, they report these studies, too. Many readers simply ignore these articles and continue to pop their yamaloo pills each morning. Others notice and get the feeling that the scientific community is totally confused. The fact is that at this time, there is strong evidence that yamaloo can help prevent colds, as more research is done, the evidence may shift in another direction. But at some point, it is likely that the evidence will be so compelling that scientists and the government can make stronger claims, claims such as: Yamaloo is a good food choice for healthy adults who want to reduce their chances of contracting colds. But all good, honest scientists are open, always open, to evidence that will cause them to question their assumptions. Keeping an open mind and looking carefully at all the evidence is what makes science a worthwhile endeavor. For the average citizen, this means that if you want to get solid information about the state of science on a particular nutrition-

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al issue, you have to work a little harder, dig a litter deeper, and evaluate a lot of evidence. But that is much better than having someone give you a definitive answer to something for which there are no totally definitive answers, don’t you think? I hope that after reading this book, you will have a better feel for the general scope of the evidence on most of the chronic diseases that worry us. At least the evidence as it stands now! And trust me, things do change, but rarely suddenly.

If you are an adult American in reasonably good health when you are reading this, there is a good chance that you will die of cardiovascular disease (CVD)—eventually. I’m not trying to tell your fortune here; it’s just that more us will die of CVD than of any other disease. It’s a matter of odds. Cardiovascular disease is the leading killer of Americans. Almost a million people die of it each year, amounting to about 40 percent of all deaths. Of course, you don’t have to be a math wizard to figure out that if 40 percent of the people who die each year die of cardiovascular disease, then 60 percent are dying of something else. And if every third person in your family has died of cancer, you might be a bit more concerned about cancer than heart disease. In other words, your personal odds may well be different. But no matter what your personal situation, with a little savvy, you can adjust those odds in your favor. And just as the odds can predict your chances of dying of a particular disease, they can also suggest ways to change those odds. No matter what disease poses your greatest risk (because of family history, previous lifestyle choic-

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es, environmental exposures), there are steps you can take to reduce the chances that you’ll eventually succumb to the disease that killed Grandpa or the disease likely to be caused by your adolescent fondness for carbonated beverages. Knowing the probabilities and what they mean can help you identify your real risk of various diseases and help you make choices that will reduce those risks.

The Bugs Are Still Out There Today’s big killers (at least in the developed world) are for the most part chronic diseases of ageing (heart disease, cancer, diabetes), not infectious diseases (diphtheria, smallpox). It is interesting, however, that in the list of “multiple factors” that contribute to the onset of diseases such as heart disease, Alzheimer’s, some cancers, and many other illnesses, infections seem to play an important role. For example, it is known that the bacterium known as Helicobacter pylori contributes to some types of heart disease as well as liver cancer and peptic ulcers. And there is mounting evidence that many other diseases that we think of as degenerative have some kind of infection (bacterial or viral) as a contributing factor. Of course untangling the web of causes for these diseases is challenging enough and the work on the role of infections in these diseases is relatively new and in most cases preliminary so researchers have not yet drawn any firm conclusions. Often the suspicion is based on circumstantial evidence. Multiple Sclerosis is a good example. For some reason, MS is more common in women who spent all or part of their childhoods before the age of fifteen in tropical or semi-tropical

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climates. This may or may not mean anything, but it is intriguing enough to get researchers looking into the possibility that some infection acquired during childhood in these regions contributed to the later development of MS. Some scientists, notably Paul Ewald at Amherst College, think that we will discover that infections play a significant role in most if not all the chronic diseases that plague us today. If we find that infections are a causative factor, they will have to join hands with genetics, diet, and other lifestyle factors as we try to untangle the fascinating but frustrating web of cause and effect that leads to the onset of so many common diseases. Because it is still too early to sort out the role of infections in most of the diseases we’ll be talking about in this book, I won’t consider that factor when taking about chances of getting a disease and the things you can do to reduce those chances. But it is something worth keeping an eye on. I’m sure that you’ll be hearing more about this in the years to come.

Of course few of us are terribly interested in the numbers themselves. When the experts start talking about risks factors and odds ratios, it is the rare person who can keep up with the conversation for long without a stiff jolt of a caffeinated beverage (a beverage that may or may not increase by some factor or other your chances of contracting one of a variety of alarming diseases). On the other hand, even those of us who tend to think of numbers as the useful little bits on the spines of library books, very much do want to know

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what diseases pose the most serious risks to us, how serious is that risk, and what we can do to reduce that risk. In this book, I will try to give you that information without spending too much time over specific numbers (most of which are rather meaningless anyway). And when we do talk numbers, I’ll explain what they really mean and how you can easily understand what people are talking about when they promise that some strategy or other reduces your risk of a given disease by this or that percentage.

Change the Things You Can Change Members of Alcoholics Anonymous are fond of what is sometimes called the Serenity Prayer: “God grant me the serenity to accept the things I cannot change, courage to change the things I can, and wisdom to know the difference.” (The quote is generally attributed to theologian Reinhold Niebuhr.) Not bad advice for those concerned about their health. There’s absolutely nothing you can do about some risk factors. You can’t change your parents or your gender or your race. So it is especially important to pay close attention to the things you can change, the modifiable risk factors. These factors pretty much fall into one of two obvious categories: Things you should do less of and things you should do more of. As you will see in the coming chapters, with the exception of smoking, doing more of the good things is more likely to make a difference in your health than doing less of the bad things. Exposure to air pollution, for example, is a risk factor for several diseases. But avoiding polluted air seems to make a much smaller difference in

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your overall risk of disease than the difference made by increasing your intake of fruits and vegetables. (Of course, it can’t be said too often: If you smoke, the single best thing you can do to reduce your risk of ill health is to stop smoking.)

Prevention/Risk Reduction Although we will use the terms somewhat interchangeably throughout this book, it is important to note the distinction between something that prevents a disease and something that reduces your risk of that disease. Even if you eliminate all the risk factors and do everything possible to reduce your risk of a given disease, you may still not be able to prevent it. Your risk will be lower, maybe even much lower but will not be totally eliminated. For example, you can reduce your risk of dying in an auto accident by wearing seat belts, driving defensively, avoiding rush hour traffic, and high-risk highways. But even if you take all these precautions there will still remain some chance that a drunk driver or a self-involved idiot on a cell phone will swerve into your lane at high speed and take you out. You can, however, prevent dying in an auto accident by never traveling in a car. Along the same lines, you can totally prevent being eaten by a shark by spending your entire life in Kansas. Unfortunately, in this sense of “prevent,” there is no real way to prevent most of the diseases we will talk about in this book. We do, however, use the term “prevent” somewhat loosely, I’m afraid. Just to be clear, I want to point out that when in the coming chapters I say that something is “preventive of ” a

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disease, what I mean is that it can help reduce the risk of contracting that disease. I know, I know, if I really wanted to be clear, I would say that. But if I said it every time you’d be more tired of reading the phrase than I would be of typing it. Even in our quest for precision and honesty, we have to make these little compromises.

For most people and most diseases, doing more of the good things amounts primarily to getting more exercise and making certain dietary changes. There is a great deal of research out there on how diet affects health, and more is being done every day. Specific studies on particular nutrients tell us a lot. For example, vitamin D is clearly a major player in prevention of osteoporosis, and probably several cancers as well. And epidemiological studies, such as studies that compare the disease rates from one culture to another or between groups within cultures are also very useful in giving us a good idea of what works and what doesn’t. It is important to remember, however, that the science of nutrition is still very young. One hundred years ago, we didn’t know that food contained vitamins; fifty years ago we had never heard of beta carotene; ten years ago the idea of a glycemic rating for foods would have seemed odd to most people; and researchers are still trying to figure out how the various types of cholesterol work together in the development or prevention of heart disease and whether the phytoestrogens in soy are good for us or bad for us. There is still much to be discovered, and much to be sorted through. Many of the recom-

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mendations made by governments and health agencies, as well as the recommendations in this book, are based on current knowledge, which is somewhat limited, and also based on a very general view of what works and what doesn’t. Of course it is highly unlikely that scientists will someday learn that broccoli causes cataracts or that combining brown rice with red wine increases one’s risk of lupus. Nonetheless, it is important to realize that much about which nutrients are contained in the foods we commonly eat, and how these nutrients work together to maintain health, is still not fully understood. As the well-known breast cancer surgeon Susan Love wrote, “Medicine is a work in progress.” This is especially true of nutrition. It would be foolhardy, however, to discount the plethora of information being made available by current nutritional studies. The field is absolutely booming and is overflowing with information that we can use to help make lifestyle choices that will protect our health. And that is what this book is all about—using the currently available data to determine what you are most at risk for, and what you can do to reduce that risk. Getting a grasp on that risk can be tricky, though, for many reasons.

The Risks of Risk-Factor Estimates When it comes to estimating risk we run into two big problems. The first is that risks are determined for large populations, such as “all women over sixty years old” or “men who have smoked for more than ten years.” These estimates may or may not apply to any one individual. And, let’s be honest, what we’re interested in is the risk of

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disease for one individual—ourselves or a particular loved one. Getting a realistic grasp on our risk for any particular disease takes a bit of creative thinking. And that brings us to the other problems with risk estimates. Some scholars believe that the human mind is naturally programmed, if you will, to think mathematically. The theory makes a certain kind of sense when you think about it. If, as you graze along the savanna, you are being closely watched by two lions from a safe distance away and you glance up and notice that suddenly only one lion is visible, the ability to subtract one from two might just save your life. You would look around to see where the other lion went (with hope, not right behind you!).

Not in Our Stars, but in Our Genes As the calendar pages flipped over into the twenty-first century, humanity celebrated what it collectively considered one of its greatest achievements: the sequencing of the human genome. Many people viewed this as a medical miracle that would lead, sooner rather than later, to treatments and cures for diseases from the devastating to the merely annoying. Hyperbole was spewing forth from politicians, journalists, even scientists who should know better than to expect sudden miracles—men and women who understand better than most that when miracles do come, they come slowly and painstakingly, not with a flourish of the miracle worker’s hands but with a cramp in the back from long hours bent over the lab bench, a squint in the eye from continuous peering into the microscope. Long before Craig Venter and the consortium of scientists

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involved in the Human Genome Project announced that they had sequenced the human genome (variously described as having decoded the book of life, found biology’s holy grail, or located the treasure map that must eventually chart the way to long life and good health for all), long before we even knew that DNA existed (much less how it was shaped), we knew that many diseases have genetic causes. We also knew that the mysterious relationship between genes and environment is an exceedingly complex dance. Any attempt to understand risk and prevent disease cannot ignore the important role of genes. That role, however, is both incredibly complex and, at this point, still not well understood—perhaps more confusing than before the genome was sequenced. For many years biologists proceeded on the basis of what James Watson called “the central dogma” of biology: DNA codes for proteins, RNA carries the messages. The system was simplicity itself: one gene codes for one protein. When the genome turned out to contain not the expected 100,000 or so genes, but closer to 35,000, the central dogma was called into serious question. Unless there are quite a few genes that were not caught by the sequencing machines (an actual a possibility—although not the most likely scenario), the central dogma turns out, like most dogmas, to need some rethinking. And indeed, it seems that much more is involved in the process of using the genetic blueprints to make proteins and cells, and well, human beings, than we had realized. For example, we are discovering a far greater and more complex role for RNA than simply as DNA’s copy boy.

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Obviously there is much work to be done. All of this is fascinating in the extreme, and has deep implications for our understanding of the process of disease. But for our purposes here, the take-home message is that when it comes to genetics, saying that medicine is a work in progress is the understatement of the year. That is not to say, however, that we can discount the role of genes in our discussion of risk factors. We just need to be very clear about what we know and what we don’t—and what we really need to consider and what we can put on hold for now. When it comes to risk factors, one of the most important things to understand is the distinction between “genetic” diseases and “inherited diseases.” A disease that has a genetic cause is one that is either caused by inherited mutations in the genes (making it likely to run in families) or one that develops when changes occur to the genes during life. These changes can result from environmental assaults, such as exposure to gene-damaging chemicals, or from the aging process itself. During the course of life, as cells reproduce, they make copies of themselves. Just like a medieval monk copying a manuscript, mistakes are occasionally inserted. These mistakes are repeated in subsequent copies. After many years of life and many, many copies of genes, the mistakes can multiply. This is why cancer in particular, a genetic disease, is much more common in older people than in young ones. There has simply been more time for genetic changes to accumulate. A disease that runs in families it is also likely to be a genetic

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disease, but the specific mutation that causes the disease is present in the genome of the parents and passed on to the children at birth. Depending on the disease, inheriting a mutation does not always mean that you will have the disease. Some diseases, such as muscular dystrophy and cystic fibrosis, can be traced to mutations on one specific gene. But for many diseases, it takes more than one mutated gene to result in development of the disease. For example, having a defective in the BRCA1 gene certainly increases a woman’s risk of breast cancer, but does not mean that she will necessarily contract the disease. The development of cancer depends on several genetic dice all rolling the wrong way at the same time. Being born with a defective gene, just puts you ahead of the game at the start, meaning that fewer other things have to go wrong to induce cancer. Because even the experts aren’t sure exactly how to parse the numbers on genetics and disease risk, for now it is best to just keep in mind that having a strong family history of certain diseases probably means that your chances of getting that disease are higher than they would be if fewer of your family members had it. In fact, when genetics counselors meet with patients to advise them about their chances of getting breast cancer, long before any blood is taken, they sit down with the patients and take a detailed family history and create what is called a medical family tree. The information on this chart tells much more about the patient’s chances of getting breast cancer than do DNA tests. When considering your own chances of getting diseases that

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are known to have a genetic component, the best strategy is to take a careful look at your family history—who died of what, and how old they were when they died of it. If a particular disease seems to show up more often in your family than it does in the general population, and if those family members died fairly young of the disease, add it to your list of risk factors for that disease. In my own family, diabetes and stroke are unusually common (and the two are almost certainly related) and cancer is relatively rare. Therefore I am especially careful about behaviors that are thought to contribute to diabetes and cardiovascular disease. When it comes to something that increases my risk of cancer but may reduce my risk of CVD and/or diabetes, I will lean slightly toward the choices that prevent CVD (alcohol is a good example—see chapters two and three for a more in-depth discussion of the risks and benefits of alcohol consumption). Simply being aware of what killed your ancestors and what is making your relatives ill won’t give you hard numbers to crunch when determining risk factors, but will most definitely tell point out areas where you need to be most cautious.

An intuitive understanding of statistics is probably helpful as well and is also likely a survival skill that we all use from time to time. A keen observer with an intuitive statistical sense will notice that he sees more auto accidents on rainy days and will drive more cautiously in wet weather. Most of us, however, aren’t good at using our statistical intuition. The classic example is the intuitive belief that if

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you’ve flipped a coin five times and come up with heads all five times, the chances that you’ll get another heads on the next flip can’t be too good. (They are, in fact, exactly the same as they were on all the previous flips.) This faulty reasoning makes casino owners rich. Our natural intuitions also cause us problems when making sense of risk estimates. Once again, a classic example: Breast cancer advocates frequently state that a woman’s chances of getting breast cancer are one in eight, which is a fairly accurate estimate. But it can be very misleading. Reading that you have a one in eight chance of developing breast cancer can be alarming. But the real risk is not quite so disturbing. A woman has a one in eight chance of getting breast cancer sometime during her life. But by far most cases of breast cancer occur in women over sixty, so for a forty-year-old woman, the chances that she will get breast cancer within the next twenty years are much, much lower. She might want to take steps to protect herself, but unless she has a strong family history of breast cancer, she doesn’t need to be too worried right now. And as counterintuitive as it may sound, by the time you are seventy or eighty, if you have not gotten breast cancer already, while your chances of getting it now are much greater than they were when you were forty, you’ve already passed most of the lifetime that the one-in-eight figure referred to. So the fact is that there is never one given point in your life when your odds of getting breast cancer are exactly one in eight. Personal emotions can also cause us to misinterpret our risks for certain diseases. A person who has watched a friend suffer and die from colon cancer may be much more concerned about getting the disease than someone who has never had any personal experience with it, even

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though his or her risk for this cancer may be roughly the same. Sometimes, however our intuitions are correct. When the paleontologist Stephen J. Gould was diagnosed with abdominal mesothelioma, a rare cancer of the abdominal lining, he discovered an alarming number: This disease carried a median mortality of eight months after diagnosis. This means that half the people who are diagnosed with this disease die sooner than eight months after diagnosis and half live longer. Gould, ever the optimist, reasoned that if some people were dying sooner and some were living longer than eight months, and since there wasn’t much time between now and eight months, some of the people who weren’t falling in the median area were probably living much longer. Because of his age and otherwise good health, Gould had a good chance of falling into the later category. How much of this was a perceptive grasp of statistics and how much was an extremely clever, if desperate, manipulation of the data in order to muster some much-needed hope, we will never know. But the fact is, Gould lived another twenty years after his diagnosis—and died of a totally unrelated cancer. The point of this story is that statistics can be misleading. As Gould puts it in his book Full House, we must be “wary of averages—which are, after all, abstract measures applicable to no single person, and often largely irrelevant to single cases.” Just because someone tells you that you have a certain chance of developing a particular disease, don’t start investing in extra health policies just yet. There are far too many factors to be considered for any one number to mean much. Yet a broad understanding of where you stand in the big picture can be extremely useful. That is why in

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this book, I am not going to bore you with too many numbers and will not be giving you charts and formulas for calculating your risk for particular diseases. Figuring out, based on an insurance company formula, that you have a point-something-or-other risk of having a heart attack in the next ten years won’t help you. You can find these guides on the internet (including the American Heart Association Web site), and many doctors use this kind of rough guide to advise their patients. The problem with these handy formulas is that they must necessarily choose certain information to include in the calculations. Typically they will factor in your age, a few basic risk factors (Do you smoke? Are you overweight? Do you have a family history of this disease?). However, because they are designed to apply to anyone who happens to visit the Web site or the doctor using this chart, they will miss many of your personal nuances. You may have a certain situation that changes your odds dramatically, but the algorithm for calculating your risk doesn’t take this into account. Say you are a seventy-year-old woman with high cholesterol. Those details are factored in. But the fact that you also exercise regularly, eat well, and have almost no heart disease in your family is not. The numbers will even out across the larger population, which is why they are so useful to researchers and insurance companies, but they may not be at all accurate for you. And so these formulas are rarely as simple as they seem to be and can be deceiving. On the other hand, the numbers are not without a general validity, and understanding them can be very helpful indeed. Knowing what factors contribute to your risk and what you can do to lower that risk can be the key to better health. So that is what we are

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going to do here. In each section of the book I will discuss the disease or diseases in questions, then tell you what the primary risk factors are for that disease. Then we’ll talk about specific, concrete steps you can take to reduce those risks. If you notice that you have one or more of the risk factors, then you can make a special effort to work on that risk. An obvious (extremely obvious) example: Smoking is a major risk factor for heart disease. If you are interested in reducing the odds that you’ll get heart disease, don’t smoke. Simple enough. And no math.

The Usual Suspects As I said in the introduction, what I am trying to do in this book is to draw on the body of health research to give you good advice about what you can do to adjust in your favor the odds for a long, healthy life. In doing this, I have read and listened to and cited all the usual suspects, The Known Experts: researchers at universities, the National Institutes of Health, and places like the American Cancer Society and the American Heart Association to mention just a few. I have also listened closely to the voices at the fringe—often experts as well, but those with views that are off the mainstream. And when looking at the research, I have looked very carefully. The reason you have to be so careful is that there are a lot of experts out there and they are all looking at whatever issue we are talking about from wherever they happen to be standing. And for that reason sometimes even the most honest, most well-intentioned people will tell you something that is simply not true—or even more

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problematic, something that is true, but you need to know much more to make any use of this particular truth. Sometimes this is in fact because the person giving you the “facts” stands to gain by your seeing them in a certain way (or even believing something that is not true). The obvious example here is the pharmaceutical industry. They certainly weren’t eager to announce that there was some evidence that common newer medications for arthritis are no better than aspirin or Tylenol, yet may cause serious heart problems. And they don’t want to publicize any potential risks of antidepressant medications or impotence drugs. They’re making buckets of money on this stuff. Other times, the hedging and fudging and occasional outright lying is done for less mercenary, but no less compelling reasons. Careers are made and broken at medical conferences and in the pages of prestigious journals. However, despite the occasional highly publicized incident of a researcher faking data or a pharmaceutical company hiding it (or buying it), a consciously dishonest scientist is a rare bird. Unconscious bias, however, is impossible to avoid. Medicine and research is a culture—and a very “in” sort of culture at that. It can be hard to live and work there without absorbing much of the cultural viewpoint, whatever that happens to be at the moment. Newton said that if he saw further it was because he stood on the shoulders of giants. That is of course how good science is done—you learn what was done before and build on that. However, Einstein would never have developed relativity theory

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if he had not been able to twist around a bit and look at things from all sorts of perspectives as he stood on Newton’s shoulders. That was easier to do at the patent office than it might be now at a large university dependent on grants and publicity to keep running. Large institutions, even the best of them, the National Institutes of Health, the American Heart Association, the Mayo Clinic, are still institutions and they tend to get a bit set in their ways. The dictionary on my computer defines the term “institutionalized” as “having become an established custom or an accepted part of the structure of a large organization or society because it has existed for so long.” Ideas often become institutionalized. The notion that the best way to fight cancer is to catch it early and then zap it with the entire arsenal of anticancer weapons and hope for the best is an idea that has become institutionalized. It may be the best we can do now; it may do more harm than good. But challenges to this thinking are risky and rare and the progress of opposing ideas is slow. That taking cholesterol-reducing drugs is the best way to prevent heart disease is another idea so institutionalized that any challenges to it face a steep uphill battle. It can be very hard for someone who lives and works within an institution to challenge ideas that institution created and is committed to. One of the best examples of this phenomenon and the damage it can do is the recent development in hormone replacement therapy. For a generation, hormone replacement therapy (HRT) was standard treatment for preventing heart disease and osteoporosis in post-menopausal women, despite the fact that there

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was almost no solid evidence to support the practice. (Heart disease and osteoporosis increase dramatically after menopause, so it seemed logical to assume that replacing the hormones that diminish at menopause would help. Assuming is not science, however.) When evidence from the Women’s Health Initiative strongly indicated that the practice very likely increased the risk of heart disease (and breast cancer, too), millions of women felt betrayed (or at least confused). HRT as a preventive was an idea so institutionalized that few people even thought to question it. Honest, well-intentioned people made this mistake. Science is a wonderful thing. The basic idea is to look carefully at what you see, take it apart, see how it works, make a guess, test it, test the guess, guess again, test some more, change your assumptions based on the results of your testing and observation and experience and gradually learn something— always being open to learning more as you go. Unfortunately, the demand for better health care (easier menopause, less heart disease, smoother skin) often rushes the process. And the very nature of the big institutions that make expensive, timeconsuming science possible, often leads to mistakes like the HRT mistake. The answer is not to disregard the science or to assume that any big institution is necessarily hidebound and behind that data curve. The answer is to look very carefully at what they are saying and to listen to all the voices—holding the mainstream institutions to the same standards of support and logic that you hold everyone else to. Don’t believe something just because the

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American Cancer Society or the Head of Neurology at Johns Hopkins said it. That kind of thinking is why you’ll find that not everything in this book reflects the current mainstream thinking. I am personally highly suspicious of the role of statins in preventing heart disease. There is evidence out there to suggest that while they work, they are not nearly the low-risk miracle drugs they are being promoted as. My personal jury is still out on this one. I also have serious doubts about much of what is being done to treat cancer. But know this: When I challenge the mainstream, I will tell you that I am challenging it and why I am challenging it (for example see the chapter on osteoporosis). I’ll cite the usual suspects often and criticize them occasionally as well. But I’ll give you my reasons for doing so. That, I suppose, is the main reason a journalist and not a scientist had to write this book: I can’t ask you to trust me because I’m a medical expert. I’m not one. I’m just an expert and finding out what’s going on (and in the process, I’ve gotten pretty good at noticing when things aren’t adding up). The important thing is to simply pay attention. And that is why in this book I’ll be going a bit beyond simply throwing the latest numbers at you.

But How Much Is That, Really? Numbers don’t mean much out of context. You have a 1 in 4 (some estimates say 1 in 5) chance of dying of a heart attack. But just how high is that risk? Getting a feel for these estimates can be easier when you can compare the risk of many different activities. So here are a few things that could kill you and what

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the lifetime odds are of them doing so. Keep in mind of course, that these numbers are calculated by finding out how many people in the United States die each year of these various calamities and dividing by how many people there are in the U.S. This means that the figures aren’t very exact for any single person. Many factors can change your personal risk. Obviously if you live in the Midwest, your personal odds of dying in a hurricane will be lower than that of someone who lives near the Gulf of Mexico. In addition, the risk estimates themselves may change from year to year. The number of deaths in a plane crashes was higher than normal in 2001, and of dying in a hurricane, it was higher in 2005. And, of course, these are lifetime odds. As I mentioned earlier, the chances of dying of a particular disease (or of coming down with a disease) sometime during the course of your life are very different from your chances at any given point that your will succumb to the disaster in question. Think of it this way: the odds that you will die are 1 in 1. Everyone eventually dies. Not good odds at all. But the chances that you’ll die this weekend are probably pretty low. The idea here is to give you a basis for comparison so that when we talk about your lifetime odds of getting this or that, you’ll have some rough (and some of these numbers are pretty rough—see next page) idea of how those estimates fit into the bigger scheme of things. By the way, keep in mind that the more rare the event, the more difficult it is to come up with accurate estimates. Experts pretty much agree on the chances you’ll die of heart disease

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(allowing for some messing around with the numbers, as mentioned above), but when it comes to rare events such as shark bites the estimates are less solid. For some of these (such as snakebite) the estimates are all over the place, so don’t hold me to any of these numbers (and please ask your survivors not to either), although I am pretty confident about my prediction for your weekend. (While writing this I got an eerie feeling. It occurred to me that if a lot of people read this book—and I do hope a lot of people read it—it is not unlikely that at least one or two of them will die this weekend. The odds that it will happen to any given reader are very low, however. I tend to think of readers as individuals rather than demographic groups, so I can’t really imagine that happening to any one of you. Nonetheless, this is the kind of weird thinking you get into when you spend too much time thinking about the odds of dying. So do me a personal favor and be sure to buckle up and watch out for sharks this weekend, okay?)

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Cause of Death:

Lifetime Odds:

Airplane crash

1 in 40,000

Car crash

1 in 88

Shark attack

1 in 3,700,000

Hurricane

1 in 220,000

Lightning strike

1 in 39,000

Murder

1 in 240

Flu

1 in 1,700

Venomous snake or lizard

1 in 1,240,000


If Only I Had Known We in the developed world are enjoying longer and healthier lives than people ever have before. Life spans have reached unprecedented lengths as many diseases that were once the scourge of humanity have been eliminated altogether, and the diseases we do get are better managed every day. At the beginning of the twentieth century, the average lifespan was around thirty years. In 2000, Americans averaged a lifespan of seventy-seven years (seventy-four for men, eighty for women). Ironically, however, in the midst of all this robust good health we are almost obsessively concerned with disease. This obsession is due, in part, to the fact that recent progress in medical science has given us so much health information to consider. We know more about our bodies and what can go wrong with them than ever before. When life spans were short and illness and suffering the usual lot for most people, no one expected to be healthy. Yet it is important to understand that both the reason for and the result of the increased lifespan is that the diseases that do kill us (or make us ill) have changed. One hundred years ago, when life spans were around thirty years, most people died fairly young of infectious diseases. The fact that so many people died before their twentieth birthday means that some people lived well beyond the average. Old age wasn’t unheard of; the average was just much lower. Now that most of the infectious diseases that killed our ancestors have been banished, more of us are living long enough to suffer from the chronic diseases of aging. It reminds one of that old joke, “If I had known I was going to live this long, I’d have taken better care of myself.” We are living longer, but if we don’t take good care of ourselves, those extra years will be spent

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struggling with heart disease, diabetes, cancer, or some other disease that was uncommon not that long ago. So, in part, our obsession with health, at a time when we lead longer, healthier lives than ever before, is because our lives are longer. We want to know what we can do (and can avoid doing) to make sure those extra years aren’t made miserable by chronic disease. Our expectations are different as well. Our experience with infectious diseases—such as smallpox, tuberculosis, diphtheria, polio, and cholera—has led us to expect relatively quick and thorough responses from science. Once the basics of microbiology were figured out, antibiotics and vaccines made quick work of most of the major infectious diseases. And so thorough was the job that in 1969, then–Surgeon General William H. Stewart said that it was time to close the book on infectious disease. The diseases that afflict us now, however, are not so amenable to the quick fix. Whereas antibiotics pretty much banished diseases such as diphtheria, and vaccines have made many once common childhood diseases rare, diseases such as heart disease and cancer pose unique problems. A medical researcher I interviewed once joked that when a scientist says the causes of a disease are “multifactorial” what he or she really means is “I don’t have a clue what causes this disease.” In fact, the reason it can be so hard to nail down the causes of some diseases is because so many factors influence their incidence and progression. If only cancer were as straightforward as measles. Chronic diseases pose an entirely new set of challenges. Genetics plays an important (and complex) role, as do environmental exposures, diet, and other lifestyle choices. And even when the causes are

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well understood (which they are not for most chronic diseases) curing them can pose an even greater obstacle. That cigarette smoking causes lung cancer is beyond any serious debate. Yet that awareness doesn’t help much in formulating a cure. Most cancers, and for that matter most chronic diseases, resist cures like two-yearolds resist naptime. Because the causes are so complex and the mechanisms of these diseases not fully understood, cures are exceedingly difficult to isolate. In fact, looking for cures may be the wrong approach altogether. As anyone who has recovered from bacterial pneumonia, or as parents who no longer expect to lose most of their children to childhood diseases such as whooping cough and measles, will tell you, antibiotics and vaccines are medical miracles for many diseases. I’m certainly not disputing that fact. It has been argued, however, that the reduction in deaths from infectious causes is due as much to preventive efforts as to technological fixes. A close reading of the history of medicine indicates that the death rates from TB, scarlet fever, measles, diphtheria, and whooping cough began declining before the advent of modern medicine. Public health measures were mostly responsible. Long before scientists had developed the germ theory of disease, John Snow, the father of modern epidemiology, figured out that a contaminated water supply was responsible for frequent outbreaks of cholera in London. Removing the pump handles on the offending wells took care of the problem. The why was worked out later. Of course, it is still very important to be able to relieve the suffering of those who do get diseases, and modern scientific and technological advances have saved many, many lives. But the real progress

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in health has been, and I believe will continue to be, in prevention. This is encouraging news at a time when the diseases we are at most risk of acquiring are diseases for which there are no definitive cures (and for which the treatments we do have are often as unpleasant as the disease itself, as with most cancers). If you don’t want to die of cancer or heart disease or complications of diabetes, your best bet is not to get these diseases in the first place. And while frequent news reports of medical breakthroughs often blind us to the less flashy progress of prevention, there is much encouraging news in the area of preventing these diseases. In order to work out cures for diseases, it is helpful (though not always necessary) to understand the mechanisms of the disease. But to prevent them, you can simply notice certain patterns, and tendencies. Frequent outbreaks of cholera were stopped when Snow had the pump handles removed from the offending wells. It was not necessary to understand the mechanism of the contamination to avoid its devastating results. Of course, the more you understand about a disease, the greater the chances that you can both prevent and cure it. That is why pure bench science is so important. But fortunately, you don’t have to wait until the answers are all in to start making changes that can help prevent a great deal of disease and suffering.

Risk Factors to the Rescue Now that we know that when it comes to preventing disease, there are few definitive answers, we find that there is handy tool for getting a grasp on how likely we are to get this or that disease—a tool called the risk factor.

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Sources of Numbers: The Good, the Bad and the Alarmed When citing lifetime risk estimates, I tried to use data from the Centers for Disease Control, the National Institutes of Health, the American Academy of Family Physicians, the American Medical Association, or other respectable independent sources. In some cases where the data was thin or contradictory, I checked several sources and quoted numbers that landed somewhere in the middle. You have to be very careful when looking at lifetime risk estimates. Organizations that exist to create awareness and generate research funds for a particular disease will understandably tend to quote the highest possible numbers, and present the numbers in a way that makes them as alarming as possible (see the chapter on osteoporosis). And of course the press will want to use these attention getting numbers as well (how are you going to persuade an editor to run an article on a disease that affects on only 2 percent of her readers?). Of course not all journalists list in this direction. A colleague of mine has pitched a story on exaggerated risk estimates called “You May Already Be Dead,” warning readers of the tendency to exaggerate risk. So please know that I have done my best to find good, reasonable risk numbers. You may see different estimates in other places. Keep in mind when looking at any of them (the ones I cite as well as the ones you see other places) that they are all only estimates and there are many approaches to getting estimates.

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The concept of risk factors for disease is fairly new. Of course, people have always known that certain behaviors could contribute to illness and that other behaviors could prevent illness—or at least reduce the chances of getting ill. But until recently, advice about what behaviors were to be avoided and what behaviors might be helpful was vague in the extreme. Your grandmother probably told you to eat your vegetables and get plenty of rest, and adages such as “early to bed and early to rise” or “moderation in all things” were common enough. But hard data on precisely how to go about implementing this advice and exactly what good would come of it if you were to eat lots of veggies and turn in early has been, until recently, sorely lacking. In the days when the most serious threats to health were from infectious diseases, prevention was largely out of the individual’s control. Public health changes, improvements in sanitation and in food and water supplies made a huge difference, but even when measures could be taken by individuals to prevent disease, few people were in a position to make these changes. If disease was being spread because of overcrowding, only the wealthy few could afford to repair to their country homes to avoid the problem. If the water was contaminated, where was one to get cleaner water? And even if it had been known that it made a difference, eating a wide variety of vegetables was not much of an option for most of the world before the advent of refrigerated transportation (and is still, due in large part to economic constraints, difficult advice for many to follow, even in the developed world). As social conditions improved and the pattern of disease shifted from the infectious to the chronic, lifestyle changes began to make more of a difference in the chances that one would get ill. Still, how-

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ever, any quantitative understanding of how lifestyle changes affected health was minimal. Oddly enough, it was the insurance industry that started changing the situation by introducing the concept of the risk factor. A risk factor is a behavior or characteristic of a group that increases the probability of occurrence of a specific illness or disease within that group. It is important to note that risk factors are estimated and evaluated for groups not individuals. In the late nineteenth century, life insurance companies were using mortality statistics to determine how much money they needed to keep in reserve to pay out for claims each year. They soon discovered that certain characteristics increased the chances that they would have to pay many claims. For example, men with high blood pressure are more likely to die of cardiovascular disease. So if a large percentage of an insurance company’s customers have high blood pressure, the company can expect to pay more claims than if most of their customers have normal blood pressure. Life insurance companies found this kind of information so useful that they began requiring the doctors who examined prospective customers to do routine screening tests (blood pressure readings for example) as a part of the medical examination. As it turned out, however, the concept was extremely useful for getting a handle on chronic disease—a group of diseases that did not have one, easily identifiable cause and that, by definition, developed over many years. When a disease is not attributable to a single, easily identified factor but is instead influenced by many factors, and these factors do their damage over the course of many years, all the while being modified in various ways by still other factors, the situation gets very

39


complex very quickly. The HIV virus causes AIDS. Avoiding exposure to HIV prevents AIDS. In real life, putting this into practice may be somewhat less than straightforward, but the concept is simple enough. Heart disease, on the other hand, is a different matter altogether. Many, many factors contribute to the development of heart disease, factors such as cholesterol and blood pressure levels, weight, family history, diet and exercise patterns, and so on. Keeping up with these many interconnected factors can be quite complex and advising the public about prevention measures can be almost as risky as offering life insurance. The risk factor came to the rescue as a useful tool for predicting and preventing chronic disease. And once analyzing risk factors was a routine part of medicine, researchers began earnestly studying all kinds of behaviors and characteristics to see which ones increased and which ones reduced risk and how much effect they had. By using the mathematical tools of probability and statistics (the same tools the insurance companies used to calculate their chances of having to pay claims), researchers can get a pretty good idea of how many of a group of people sharing certain characteristics will succumb to a given disease. In this way they can tell you that if you have X, Y, or Z characteristic, what is your probability of getting A, B, or C disease. X, Y, and Z are risk factors for the disease in question. Of course, it is just a probability. Not a certainty—and therein lies the rub. Think of these probability statements as something like weather forecasts. If the National Weather Service tells you that there is a 90 percent chance of rain in your area today, what they are really saying is that in the past one hundred occasions that the weather conditions

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have been like they are today, it has rained on ninety of those occasions. This doesn’t mean today will follow that pattern, but you’d be unwise to plan an outdoor picnic. Take your umbrella.

Scary Monster or Misunderstood Giant? You won’t notice genetically modified food on the list of risk factors for any of the diseases in this book—and frankly, as far as we know now, the risk of harm to your health is very low. Nonetheless a discussion of measures to take to protect health would be remiss not to mention this. So here goes—but do keep in mind that my practice of looking at the body of evidence to make an evaluation fails me here. This issue is just too new to say much of anything stronger than “well we just don’t know yet.” Genetically modified food is nothing new. The Better Boy tomatoes I grow in my garden each summer have been drastically genetically modified from the original ancestor of the tomato—and they have been modified from the tomatoes I grew in my garden 30 years ago. Open most garden seed catalogs and on the first few pages you will see an array of “new” varieties. Plant breeders are continually tinkering with plants to produce snap beans without strings, super sugary sweet corn, tomatoes that resist certain viruses common to tomatoes, and so forth. In fact most of the food you and I have eaten our entire lives has been genetically modified along the way. Humans have been influencing the genetic profile of plants since the development of agriculture (and of animals since the domestication of

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animals). But this was done by the long, slow, old-fashioned method, the one Mendel used with his peas. That is to say by selective breeding, crossing plants with other plants (or farm animals with other farm animals) choosing the ones that have the characteristics you like best and going on from there. This is also what Darwin called “artificial selection,” as opposed to natural selection. What’s going on now, what we are typically referring to when we say “genetically modified food,” is of a very different order. Rather than simply crossing plants and breeding for desired traits, scientists are now able to take the actual genes responsible for certain traits in one plant (or in some cases, animals) and splice them into the DNA of another plant or animal. The most often mentioned example of this (but by no means the most common in practice) is the splicing into tomatoes a cold-resistant gene from flounder. This supposedly keeps the tomatoes tasty even when they are kept in cold storage for transport, suggesting an answer to the long debated question of whether a tomato is a fruit or a vegetable: It’s a fish! While the fish in tomatoes example is undoubtedly the most fun, it is probably not the most frightening. Many crops, particularly soybeans, corn, and potatoes, have been genetically altered to make them resistant to certain insect predators; or able to withstand spraying by herbicides so that farmers can spray for weeds they don’t want without harming the crop they do want (I am thinking here of “Round-Up ready” crops made by Monsanto, who also makes Round-Up, a herbicide); or sim-

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ply to make seed that can be patented by the seed maker and therefore cannot be saved to plant again next year, a windfall for seed companies. Opponents of genetically modified foods like to refer to them as “Frankenfoods.” This is an interesting appellation, for like Dr. Frankenstein’s monster, these foods may actually be more misunderstood than harmful. There is not yet much evidence that genetically modified foods are dangerous to physical health. On the other hand, there is not much evidence that they are safe. This is an area we know so little about, it is certainly not yet clear whether they are safe or not—and I don’t think it will be clear for a very long time. Any health problems that result from eating modern genetically engineered foods are unlikely to show up immediately. The genetic damage done by smoking can take decades to manifest as lung cancer. If these foods are damaging our DNA, we may not know it for years. I certainly can’t tell you to avoid these foods based on any strong evidence that they are harmful to your health (the harm to the environment and to the independence of farmers is another matter, but not within the scope of this book). I can, however, suggest that you use caution, common sense, listen to your instincts, and keep a close eye on the research in this area.

In the same way, medical researchers are telling you that among hundreds of thousands of people who share certain characteristics with you (roughly your same age, weight, socio-economic status,

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smoking, eating and activity patterns, for example) this number of them came down with this disease during their lifetimes (or within ten years of being studied or however the number is being calculated). This kind of estimate does not tell you that you will get a certain disease or that you need not worry about getting it. It does, however, give you an idea of what the probabilities are—whether or not you should keep your umbrella handy. Eliminating risk factors (such as stopping smoking) can vastly improve the probabilities. Adding preventive behaviors, such as increasing exercise, can change those probabilities as well. So risk factors are a handy tool for estimating your risk of various diseases and making lifestyle choices that will reduce these chances. Sometimes the numbers can seem very precise. A doctor or an interactive quiz on a Web site might tell you that you have a two percent probability of developing heart disease within the next ten years (meaning that of 100 people with the characteristics you have provided to the doctor or the interactive quiz, two of them will die of heart disease within the next ten years). A study that you read about in the Sunday paper might tell you that by walking for an hour a day five days a week, you can reduce that risk by 50 percent. Another similar study might find that daily walking reduces your risk by only 45 percent. Specific as they seem, these numbers are only guidelines. Factors other than the ones considered in the calculation might have an influence and the relative importance of various factors (weight and blood pressure, for example) might vary from individual to individual. When considering large groups of people, the way insurance

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companies and public health officials do, these numbers are amazingly accurate. For individuals like you and me, they are not precise. In fact, the exact numbers themselves don’t mean much at all. They do, however, give a very good guideline for making decisions about health. An individual can usually dispense with the serious math and just get down to the basics. Most chronic diseases have a list of risk factors that make it more likely that an individual will eventually face that disease. If you find that you have more than one or two risk factors (or that you have one of the big risk factors—smoking for heart disease or obesity for diabetes, for example), then you want to look at the data on behaviors that reduce your risk, and swing the balance back into your favor. The rest of the chapters in this book will help you decide what diseases you need to be concerned about and what you can do to reduce the chances that you’ll ever come down with that disease. And you won’t have to do any math—I promise. We’ll leave that to the insurance company.

The Bad Guys We are always hearing about things that are bad for us. But what really is all that bad for us, and why are these things bad? Here is a partial of list of some of the bad guys out there (and a few that aren’t as bad as we tend to think) and why they pose harm.

Soft Drinks For sodas the problem is primarily the sugar. Most of these guys are just flavored sugar water. As your mom used to say, sodas are “nothing but empty calories,” filling us up in place of the

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nutrients we need. With obesity running rampant, we need more good food, but we sure don’t need more calories. However, there is more to the harm in soda than just the calories themselves. Insulin resistance (see chapter four) is a serious health problem and a precursor of type 2 diabetes, in which the insulin that is supposed to clear the blood of glucose is less effective than it should be. Jolts of sugar solution spike the blood with glucose and stress what is in many of us an already stressed system. There has also been some evidence that soft drinks, particularly colas, contribute to the formation of kidney stones.

Cell Phones There have many questions about the effects of cell phones on the brain. Some studies have suggested that frequent and extended use of cell phones can contribute to brain cancer, but guess what? The evidence on this is extremely thin for the moment. I wouldn’t worry about getting brain cancer from my cell phone. Your cell phone can kill you, though. Talking on the phone while driving is dangerous; studies are pretty clear on this.

Saturated Fats We’ve been hearing about the dangers of saturated fat for so long, most of us have forgotten by now exactly what the problem was. The terms saturated, monounsaturated and polyunsaturated refer to the chemical composition of the fatty acids that make up the fat in the food, a description of how many hydrogen atoms

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they contain. A saturated fat is one in which all the possible sites for hydrogen atoms are filled—thus the fat is “saturated” with hydrogen atoms. This type of fat is found primarily in animal products (there are a few exceptions, coconut oil and palm oil contain saturated fats). The problem with saturated fats is that they tend to increase the bad kind of cholesterol in the blood causing several problems, the most well-understood being to clog up the arteries and make the heart have to work harder to get blood through.

Trans Fats Trans fats are a particularly nasty addition to our modern menu. Trans fats are created when hydrogen molecules are added to liquid oils “hydrogenating” them and making them into a more solid type of fat (most margarines and vegetable shortenings are hydrogenated). Fats that have been hydrogenated have better keeping properties, which is one reason you tend to see them in processed foods. They also have carcinogenic properties and increase cholesterol and the risk of heart disease.

Grilled Meat When meat is cooked at very high temperatures, such as over hot coals (or deep fried) several chemicals are produced that are known or suspected carcinogens. At this point, the risk seems to be minimal, however. The saturated fat in the steak is probably more harmful (and certainly the harm is more thoroughly documented) than the chemicals in those delicious black crispy bits

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around the edges. Eating less meat overall is probably a pretty good strategy. The occasional barbeque, however, shouldn’t pose any undue hazards.

Salt Salt in the diet is known to increase blood pressure. Some people are more sensitive to this than others, presumably there is a genetic component. There are probably several mechanisms involved, but the most obvious is that salt causes you to retain water and retaining water increases blood pressure. In addition, too much salt in the diet can throw off the body’s sodium-potassium ratio and that seems to increase blood pressure as well. Some evidence even suggests that it is not so much too much sodium as too little potassium that causes the problem. In any case, dietary sodium doesn’t increase blood pressure in everyone.

Smoking How do I kill thee? Let me count the ways. Everyone by now knows that smoking is dangerous. But exactly how smoking kills and maims is less well known. That’s probably because the list of nasty things smoking does to the body is so long people give up and just say: Don’t. The fact is, even though we sometimes think of cigarettes as somehow “natural” because tobacco is a plant, a typical cigarette contains over four thousand toxic chemicals, including such charmers as formaldehyde, cyanide, and carbon monoxide. These toxins damage DNA, which is one of the necessary steps to cancer. They also interfere with the

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lungs’ ability to repair themselves from even the normal damage of living (much less the damage being done by smoking). Cigarette smoke destroys the alveoli, the air sacs in the lungs where the exchange of oxygen and carbon dioxide takes place. They make it difficult to breathe and contribute to the many other health problems that ensue when the body is forced to operate on too little oxygen, such as heart failure. Smoking increases the “bad” kind of cholesterol and decreases the “good” kind; it increases blood pressure; it decreases tolerance to exercise and increases the tendency for the blood to clot—all risk factors for cardiovascular disease. And as if that weren’t enough, smoking also wreaks havoc with the body’s ability to maintain normal blood-sugar levels, increasing the risk of diabetes. Oddly, after listing all the seriously horrible things smoking does, that it also contributes to impotence (by restricting blood flow) and premature ageing of the skin is often the news many people need to motivate them to give up smoking.

Alcohol As we see in chapter two, alcohol is two-faced. For most people, moderate amounts seem to be very healthful, better in fact than not drinking at all. However, alcohol definitely increases the risk of some cancers. It is not totally understood how alcohol does its damage, but at least part of the mechanism involves damage to DNA (see chapter three for a description of the “multiple hits” theory of cancer).

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Footnote During the oil embargo in the 1980s, gas prices were skyrocketing and Americans were doing everything they could think of to improve the mileage in their cars. I heard a joke that went something like this: “I’ve done everything they recommend to improved my gas mileage: increased the air pressure in my tires, avoided jack-rabbit starts and stops, slowed down to fifty-five mph. I’ve improved my mileage so much that now I have to stop at gas stations just to let off some gas.” If you follow all the health advice telling you what to do to reduce your chances of dying by this or that percentage, you may think that pretty soon you’ll have so reduced your chances of dying that you’ll soon be wondering how to spend your eternal life. Of course it doesn’t work that way. These things overlap and percentage decreases never reach zero (just ask Achilles and the tortoise). Once again, as important as the numbers are, don’t get hung up on the math. Just take the precautions that suit you and you’ll improve your health.

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C H A P T E R

T W O

Cardiovascular Disease A Disheartening Problem T H E

N U M B E R S

A T

A

G L A N C E

Cardiovascular disease claims over 900,000 lives each year, amounting to 37.3 percent of all deaths, or 1 of every 2.7 deaths. Approximately 70 million Americans have some form of cardiovascular disease.

The phrase “cardiovascular disease” brings to mind many different images. An apparently healthy man struck down in the prime of life by a sudden heart attack; an elderly woman, breathless and weak from congestive heart failure; a middle-aged man undergoing coronary by-pass surgery to relieve angina; the drawn face and halting speech of a stroke victim. All of these—and more—are manifestations of cardiovascular disease. Many different diseases and condi-

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tions result when the delicate arrangement of heart, vessels and valves is not operating as it should. The fact that these images of CVD are so familiar is testimony to the fact that, with alarming frequency, the cardiovascular system doesn’t operate as it should. Heart disease is the number one killer in the west. And it doesn’t come in by a nose, either. If you include all forms of cardiovascular disease, including stroke, nearly one million Americans die each year of CVD of one type or another. When you count CVD as a contributing factor of death, the number jumps to almost one million and a half. Approximately seventy million Americans struggle with from some form of CVD. If you do not know someone who suffers from or who has died from CVD, you must be living the life of a virtual hermit (and if not, the National Institutes of Health badly wants to know more about your friends and relatives!). The United States has committed huge resources of time and money to wage a metaphorical war on cancer, while every thirty-four seconds someone dies of heart disease. While we should take these numbers very seriously, it is also good to keep in mind that the incidence of heart disease can seem a bit overblown. The fact is, if you don’t die of something else first (cancer, AIDS, getting run over by a bus), you’ll almost certainly die of heart disease. One of the reasons that heart disease is the number one killer of Americans is that we aren’t dying of other causes. And many of those who die of heart disease are in their seventies, eighties, and nineties. This is not to say that cardiovascular disease is not a serious threat or that we should be cavalier about it. In fact, cardiovascular disease is one the diseases most amenable to lifestyle

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Cardiovascular Disease

changes. And the fact that there is a lot you can do to reduce your risk is a good reason to take that risk seriously. The term cardiovascular disease covers several distinct diseases and conditions of the heart and vascular system: coronary heart disease, hypertensive heart disease, heart failure, and others. When it comes to prevention, the situation is both very complex and ultimately rather simple. It is complex because the diseases of the cardiovascular system interact and overlap in a variety of ways. (And they interact and overlap with other conditions as well—particularly certain types of dementia and diabetes and insulin resistance. See chapter four for more info on the relationship between cardiovascular disease and diabetes and chapter five for the cardiovascular system’s role in dementia.) On the other hand, the situation is refreshingly simple, at least in terms of prevention, because the steps to take to prevent CVD are for the most part the same no matter what the form of the disease. Building a stronger cardiovascular system, keeping the heart and vessels in top-notch shape, protects you from most kinds of CVD.

Risk Factors Cardiovascular disease is one of the diseases in which lifestyle choices make a huge difference—and generally we know what works and what doesn’t when it comes to prevention. It’s not at all certain, but many experts estimate that as much as 80 percent of CVD is due to lifestyle choices. Most of the primary risk factors for heart disease are things you can control. A few, however, are not. One of the most important risk factors for cardiovascular disease is family history. If

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you have a lot of heart disease in your family, and your father or brothers became ill before age 55 or your mother or sisters before sixty-five, you are at higher risk than someone whose family members and ancestors lived to ripe old age without heart problems. Being male also increases your risk (although women tend to catch up after menopause) as does being black. And so does being old. The older you get, the more likely you are to die of heart disease. There’s nothing you can do about your family, your race, or your gender, and alas, you can’t do anything to make yourself younger, but if you do have any of these unmodifiable risk factors (especially family history), you need to be even more careful to reduce the risk factors you can control. And fortunately, when it comes to heart disease, most of the risk factors are at least in part under your control. Smoking is probably the biggest risk factor for CVD. If you smoke, your risk of heart attack is more than twice that of someone who doesn’t smoke—some experts say even 3-4 times higher. Smoking damages the blood vessels, causing plaque to build up there. In addition, smoking can reduce HDL cholesterol (the good kind), and low HDL is itself a risk factor for heart disease. If you are concerned about your health (and if you are reading this book, you probably are) the single biggest step you can take to improve it is to stop smoking. It’s not easy, but the benefits are huge—and they kick in as soon as you stop smoking. You’ve heard this lecture before, but it really can’t be said enough. High blood pressure (hypertension) is a problem in and of itself, but it also one of the key risk factors for heart disease. When your blood pressure is high, the heart has to work harder to pump blood and

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that extra effort can eventually weaken the heart. Hypertension is often called the “silent killer” because it rarely has warning signs or symptoms you can detect. Being stressed or upset may make you feel as if your blood pressure is going up, and when you are feeling relaxed and happy, you may expect that your blood pressure is low. But the fact is the only way to really tell is to measure it. For most people, getting your blood pressure taken at routine doctor’s visits is enough to keep an eye on things. If your blood pressure is high at one visit, your doctor will probably ask you to come back for another check or two to see if there is a pattern of high blood pressure. If you do have a pattern of high blood pressure and are working to get it down with diet and exercise, you might want to get a home blood pressure monitor to help you keep an eye on it. Good ones aren’t cheap, but they aren’t all that expensive, either. Good models can be had for around fifty dollars. And if you follow the instructions carefully, they are as accurate as the measurements your doctor takes. In fact they might even be more accurate. Many people suffer from “white coat hypertension.” The stress of being at the doctor’s office causes their blood pressure to be a bit higher than normal when they are there. But if you are getting high readings at your doctor’s office, don’t assume it is just white coat hypertension. Because hypertension is more than just a risk factor for cardiovascular disease, I will talk about it in greater detail below. See the page 71 for risk factors for hypertension and advice on how to lower your blood pressure. High cholesterol. The situation with cholesterol is not as straightforward as you may sometimes think (see page 65), but it is one of the main risk factors for heart disease—at least in people under 60 or so.

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Like high blood pressure, high cholesterol presents no symptoms. If it’s high, the only way you’ll ever know it is to get a blood test. These days, your doctor will test for both your HDL (good) cholesterol and your LDL (bad) cholesterol. A total cholesterol level of more than 200 (that’s milligrams of cholesterol per deciliter of blood) is considered to raise your risk. Between 200 and 239 is borderline, over 240 is cause for alarm. When you break it down to good and bad, you want to shoot for less than 100 mg/dL LDL and higher than 60 mg/dL HDL. However, you won’t want to consider cholesterol medications until you hit 160 if you have no other risk factors, or 130 if you have one or two risk factors. If you have diabetes, have had a stroke or already have heart disease, then you may need to start medication at a lower cholesterol level. Triglycerides are another kind of fat that circulate in the blood. Since people who have heart disease often also have high triglycerides, high levels of this kind of fat are considered a risk factor as well. Less than 150 mg/dL is considered normal, between 150 and 199 is borderline and above 200, high. A diet designed to reduce cholesterol is also good for reducing triglycerides. Diabetes. Both type 1 and type 2 diabetes are risk factors for heart disease. Type 2 diabetes has been increasing rapidly in the past few years. Obesity and lack of exercise contribute to Type 2. One reason it is so dangerous is that although people often do not know they have it for many years, it is doing its damage all the while. Even if you know you have diabetes and are keeping your blood sugar under control, it is still a risk factor for heart disease. In fact, 80 percent of diabetics die from heart disease. If you have diabetes, it is especially

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crucial that you stay on top of other risk factors. (See chapter four for more detail on diabetes, risk factors and prevention.) Obesity and overweight. Having too much body fat, especially if it is concentrated around the waist is an independent risk factor for heart disease. In fact, having that extra weight around the middle is beginning to look like a major indicator of heart disease. A recent study (INTERHEART) found that waist to hip ratio is three times more powerful a risk factor for cardiovascular disease than just being overweight (see box on page 128). In any case, being overweight contributes to many other risk factors, such as high blood pressure, high cholesterol, diabetes, etc. But even if you don’t have any other risk factors, being overweight in and of itself puts you at higher risk for heart disease. These days optimal weight is determined by something called Body Mass Index (BMI). BMI is just a fancy formula for determining weight in relation to height. The BMI chart on page 142 will help you find your BMI. If you are an adult and your BMI is between 18.5 and 24.9, you are in good shape. Between 25 and 29.9 is considered “overweight” and 30 or above is considered obese. Body mass index is a pretty good tool for getting an easy handle on weight relative to height, but it is not perfect. If you have a lot of muscle and very little body fat, you may have a BMI in the overweight range, even if you are extremely fit. If you are one of these types, you don’t have much to worry about and you probably know it. As anyone who has tried to do it knows—losing weight is a complex issue, so I’ve devoted a section just to that in chapter four, the chapter on diabetes. But when thinking about reducing your risk factors, keep in mind that even a small amount of weight loss can make

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a big difference. You may want to look like a supermodel, but that is not necessary to substantially reduce your chances of heart disease. Losing just 5 to 10 percent of your body weight can reduce cholesterol levels and may help control blood pressure. Inactivity. Don’t think you are off the hook, skinny people. Even if you aren’t at all overweight, you could still be packing a lot of visceral fat (that dangerous belly bulge). And lack of exercise is a risk factor for heart disease in and of itself. Exercise is good for reducing other risk factors, such as hypertension and high cholesterol, but lack of exercise is a risk factor in and of itself. As one researcher told me, “the body likes to exercise.” One of the best things you can do to lower your risk of heart disease (and of many other diseases as well as we will see) is to get up and move around (see page 82 for prevention tips). This is such an important issue that I talk about in some detail as well in chapter four.

Coronary Artery Disease: The Crown Jewel of Heart Disease If heart disease is the most common disease, coronary heart disease (CHD, also known as coronary artery disease, CAD) is the most common form of heart disease. Fifty-four percent of all deaths from heart disease are of the type of known as coronary heart disease. And almost all heart attacks are the result of CAD. We usually think of the heart as pumping blood to take oxygen and nutrients to the various parts of the body. This is certainly an accurate image, but sometimes we forget that the heart needs to take care of itself, too. Just like the other organs, the heart needs oxygen. The arteries that take blood directly to the heart muscle are called

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the coronary arteries. They are called “coronary” because they surround and cap the heart in a way that somewhat resembles a crown. (It doesn’t look anything like a crown to me, but apparently it did to the guys who coined the term “coronary arteries.”) Atherosclerosis is the primary culprit in most cases of heart disease. Atherosclerosis is the build up of deposits on the large and mediumsized arteries. Fatty deposits made up mostly of cholesterol accumulate along the inner lining of these arteries. These fatty deposits, called plaques, can block the flow of blood in the arteries that supply the heart, causing chest pain (called angina pectoris). The real problem, however, occurs when the plaque ruptures—and this can happen, in fact often does happen, even to small ones. What happens is this: Plaques form on the endothelial layer, a layer of cells along the inside of the arteries. Excess LDL cholesterol gets into these endothelial cells. Then free radicals come along and oxidize it, making it active. Free radicals are the by-products of metabolism and are a natural and inevitable waste product of the break down of fats and sugars. When things are working well, the body sops up free radicals and neutralizes them before they can do any damage. However, when you have more free radicals than your body can take care of they can oxidize LDL, causing a cascade of problems, often leading to heart attack. When the LDL is oxidized, it attracts a kind of white blood cells called macrophages. The macrophages eat up the oxidized LDL—or as much as they can manage. This is your immune system trying to deal with the problem of the oxidized LDL. When the macrophages get full, they look foamy, so they are known as foam cells. The foam is at the edges and the center is filled with gooey

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cholesterol. (Sounds kind of like a confection, doesn’t it? Foamy on the outside with a gooey center. But unfortunately it is not sweet at all.) The foam cells produce cytokines and several other chemicals that produce inflammation—basically the same red, puffy swelling you get at the site of an injury on the outside of the body. Inflammation is another marker for heart disease. The foam cells also secrete an enzyme that dissolves the collagen in the arterial plaque, making it weaker (the collagen provides the strength to the outer surface of the plaque) and more likely to rupture. At the place where the clot ruptures, a clot or thrombus forms, and that can block the artery completely, stopping the blood from reaching heart muscle, causing the heart muscles to start to die—this is a heart attack, technically known as a myocardial infarction—a very silly sounding name for a very serious problem. As the condition worsens, deposits of this fatty material (called plaque) form patches or clumps that protrude into the open part of the artery. Eventually the artery walls become stiff and inflexible, unable to expand and contract as necessary to keep the blood flowing smoothly and adequately. Blood flow is thus restricted or even completely blocked. If a fractured or eroded plaque occurs in the main artery taking blood to the tissues of the brain, a stroke can result (or if the blood flow is not totally blocked, but seriously diminished, dementia can result—see chapter five). In this case, the clot does not block the artery, as it does in the heart, but a piece of the clot breaks off and travels with the blood to the brain where it becomes wedged in a smaller artery to the brain, blocking the blood supply to the brain.

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Take a Quarter of an Aspirin and Call Me in the Morning Aspirin may seem terribly old-fashioned and low-tech now that Tylenol, Ibuprofen, and Celebrex are muscling in on the action. But aspirin is still a very valuable member of the pharmaceutical team—and with its competition looking more reckless every day, it is making a comeback. But if it is good for pain, fever, and inflammation, it may be even better for your heart. Aspirin has been proven to reduce the risk of a second heart attack in people who have already had one heart attack and to reduce the risk of stroke in people who have already had a stroke. Its role in preventing first heart attacks or strokes is less clear. The problem is the risk/benefit ratio. Aspirin is probably the oldest and safest pharmaceutical you’ll ever take, but that doesn’t mean it is totally safe. In some people, aspirin can cause dangerous intestinal bleeding and even more dangerous (but more rarely as well) bleeding in the brain. So the benefit of preventing a heart attack or stroke that you aren’t even at very high risk to have, might not be worth the risk. On the other hand, the risks are pretty low and the benefit can be high. So most doctors prescribe a daily dose of aspirin only to people who have several risk factors for heart disease, but not for the general population. This is why aspirin therapy is generally not recommended for women under 65 unless they have significant risk factors. The risk-benefit ratio of aspirin is nudged just a bit in the benefit direction because in order to get the preventive effect,

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you need take only 75 milligrams a day (a regular-strength aspirin is 325 milligrams; the little orange ones they used to call baby aspirin typically contain 81 milligrams). This is another example of using drugs as preventives, but if you have more than one risk factor for heart disease, you might want to discuss aspirin therapy with your doctor.

A massive industry has developed to provide high-tech means of coping with the problems of CHD. Angioplasty and stenting involve placing a catheter across the portion of the artery that has a large plaque or a thrombus on the surface of the plaque. The catheter has an inflatable balloon on its outside. The blood is inflated pushing the plaque into the wall of the artery and opening the inside of the artery. Most commonly a thin wire mesh on the outside of the balloon stays in the artery after the inflating procedure in order to keep the artery open. And of course, there is the ubiquitous coronary bypass surgery. When the blockages are too numerous or too close to a fork or a bend the in arteries, bypass surgery is often the only option for surgical intervention. According to some experts, between 15 and 30 percent of all CHD patients eventually require bypass surgery. The premise is simple. Arteries to the heart are blocked, so surgeons use a vein or artery taken from another part of the body to bypass the blocked section. The process itself, as you might expect, is a bit more complex. The first bypass surgery was done in 1964 and surgeons have been perfecting it since. Today it is a routine procedure for the many specialists who do these day in and day out. (As you can imagine, it is

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not so routine for the patients.) Don’t let the word routine fool you, though. As elective surgeries go, bypass surgery is surprisingly high risk. The average mortality rate from bypass surgery is 2-3 percent and can get as high as 5 percent for patients with serious complications such as diabetes and other heart conditions—and many of the patients who get this surgery have these sorts of complications. What many people do not realize is that neither bypass surgery nor any of the other, less invasive procedures such as stents and angioplasty, actually cure CHD. At best they buy time for the patient to make the necessary lifestyle changes to prevent the need for more surgeries or other costly and risky interventions. (Bypass patients often have to have additional procedures or even have another bypass eventually.) When the process has gone so far that medications, procedures and surgeries are required to buy this time, these high-tech measures for dealing with heart disease have been very successful in saving lives. The rate of death from heart disease has lowered over the past few years. It is not clear, however, how much of this improvement is due to high-tech interventions and how much is due to people making lifestyle changes (even when they make them late in the game, after that first heart attack or angioplasty). A great deal of evidence indicates that in many cases all these risky and expensive procedures are neither necessary nor really helpful. In any case, the rate of heart disease itself has increased. As more people are being saved from sudden death from heart attack, more people are living with heart disease as a chronic disease. Even if this is a major accomplishment of modern medicine, it is a bit like sticking your finger in the dyke. We now have to figure out how to keep people

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from getting heart disease in the first place. Fortunately, preventive measures seem to be very helpful when it comes to heart disease. Even for those already suffering from CHD, preventive measures can make a huge difference. And for those who are not that far along, prevention is crucial. According to data from the Nurses Health Study and others, if everyone made the necessary lifestyle changes, we could reduce the incidence of CHD by 80 percent. That may or may not be a totally accurate estimate, but it is enough to make you take your diet and workout program a bit more seriously.

Heart Failure The good news is that more and more people are surviving heart attacks and other acute cardiac problems. The bad news is that the people who survive heart attacks or manage to avoid them do not necessarily go on to a long life of robust good health. Instead they often suffer from long-term chronic heart problems. One of the commonest of these is heart failure. The term heart failure sounds like a synonym for heart attack, but it actually refers to a chronic disease. Unfortunate victims of heart failure can live with and suffer from their condition for years. Heart failure kills slowly and makes its victims miserable on their way out. Heart failure occurs when the damage to the heart muscle (usually due to the same factors that cause heart attacks and angina—atherosclerosis and hypertension) becomes so severe that the heart is not up to its job of supplying oxygen to the rest of the body. The heart has to work harder to pump blood and in the process the muscles in the wall of the heart weaken, the heart becomes enlarged, and the

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rest of the body suffers from lack of nutrients.

Cholesterol: Sticky Yellow Ichor From all the bad press it gets, you’d think we’d be better off if the world were totally rid of cholesterol once and for all. But the fact is, like most things, cholesterol has a good side and a bad side. It is actually essential to healthy functioning and most of it is made in our very own livers. Cholesterol is a type of fat that circulates in the blood. It is an important building block of many hormones, including estrogen, testosterone, and vitamin D. Trust me, you need it. But your body makes ample amounts. You don’t need to eat any. Because cholesterol is plentiful in meat and dairy products, most Americans have far too much of this sticky, waxy stuff circulating in their blood. And that, of course, is the problem we hear so much about. The Framingham Heart Study, and many studies since, established a clear connection between elevated levels of cholesterol in the blood and cardiovascular disease. Since the early days of Framingham, we have learned a lot more about cholesterol. For example we now know that there are at least two kinds: “good” cholesterol (HDL) and “bad” cholesterol (LDL). Simply put, the bad cholesterol junks up your arteries and the good cholesterol comes along and scoops out some of the junk and takes it to the liver for disposal. Scientists now think that the total cholesterol number is not as important and the ratio of good to bad (especially in women). An important point to catch here is that not too many years ago, we didn’t even know there were two kinds of

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cholesterol. There is still very much to be learned. It might be well to approach the cholesterol issue with caution. Do you know your numbers? Your cholesterol levels, that is. I’ll bet you do. I’ll bet you’ve had your cholesterol checked within the past couple of years—and if your cholesterol was high, there is a good chance that you are taking medication to lower it. And there is also a very good chance that your medication has had the desired effect—of lowering your cholesterol. Whether or not it is also reducing your chances of dying (from heart disease or anything else) is another matter altogether. In the late 80s, the pharmaceutical industry made one of those “breakthrough” discoveries you hear so much about. A new class of drugs, called statins, was approved for use in reduction of cholesterol levels, and by extension, it was believed, these drugs would lower the incidence of heart disease and deaths from heart disease. Now, less than twenty years after the first statin hit the market, statins are among the most widely prescribed drugs (you may know some of these drugs as Lovastatin, Pravachol, Zocor, or Crestor). They are considered standard care for people with high cholesterol that can’t be controlled by diet. Despite the enormous popularity of these drugs, the research supporting their benefits is not as strong as you might expect. Despite the general perception that statins are miracle drugs that will save us all from heart disease, the actual research is much more timid. These drugs can certainly lower cholesterol, but they do not necessarily reduce the chances of dying.

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In fact, in the studies used to support their widespread use, deaths from all causes actually increased very slightly. The marginal benefit of statins on the risk of heart disease was wiped out by the increased risk of death from other causes. There is no doubt that statins do save some lives, but the risk-benefit analysis is not so good as the manufacturers of these lucrative drugs would have us believe. If you have high cholesterol (and especially if you have other risk factors for heart disease), you would do well to make a serious effort to lower your cholesterol through exercise and dietary changes before jumping on the pharmaceutical bandwagon and filling that prescription for statins. While there is good data that patients who have already had a heart attack have fewer second heart attacks when they bring their LDL cholesterol down with statins, the evidence is less compelling for primary prevention. In men, there is a definite reduction in cardiac events in men treated with statins, but less evidence that there is any change in longevity. On the other hand, many good, well-designed studies have shown that dietary changes and exercise can be just as, if not more, effective as medication in reducing cholesterol levels. For example, a widely cited study published in the Journal of the American Medical Association (JAMA) in 1999 looked at 25,000 men and found that being out of shape and overweight was a greater risk factor for heart disease than having high cholesterol readings. There are similar findings for women. Recent data from the WISE (Women’s Ischemia Syndrome Evaluation) study has also shown that exercise is crucial for good heart health—

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even when other risk factors are present. (In fact, data from the WISE study indicates that fitness is more important than weight in predicting the likelihood of heart attacks and heart failure.) In addition, several studies, including the Lyons Heart Study, provide strong evidence that dietary changes can be as effective as medication in reducing the chances of death from heart disease. In fact, in the Lyons study, the reduction of heart disease was independent of lowered cholesterol levels. The reason so many people end up on drugs, despite clear evidence that there is a better way to protect your health, is that making these lifestyle changes is not easy. The people who make serious money selling drugs to lower cholesterol and reduce the risk of heart disease feel pretty safe recommending that you try lifestyle changes first. They don’t expect you to stick with it. They’ll get your business soon enough. If you are serious about lowering your cholesterol levels without drugs, you are going to have to get serious about exercise and a good diet. If you are not already active, you should start small—very small if you have been sedentary for most of your adult life. Some experts recommend that people who’ve spent the past twenty to thirty years sitting at a desk or in front of the TV start with something as small as ten minutes a day of mild to moderate activity. But in order to see real benefits (and get those cholesterol readings down), you want to aim for the same magic numbers that keep coming up everywhere else: sixty or more minutes a day of moderate intensity exercise and seven to nine servings of vegetables and fruits.

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It is easier (though not necessarily more fun) to just pop a pill. But the risks of exercise are small and the benefits go well beyond just lowering cholesterol. It’s an effort worth making. And as far as I know, no one has any financial incentive to cook the data and try to convince you and your doctor that exercise and good food are good for you. I can’t say that for cholesterol lowering drugs.

In its early stages, symptoms of heart failure are subtle or nonexistent. But once the damage to the heart muscle is really underway the most common effects are fatigue, shortness of breath, swelling in the legs and feet, reduced ability for exercise (eventually this comes to mean exercise such as walking from the bedroom to the kitchen) and irregular heartbeats. From the perspective of the patient, heart failure makes you feel just lousy. It is a very disabling and eventually deadly disease. While the causes and mechanisms of heart failure are somewhat different from Coronary Artery Disease, the preventive measures are the same. If you don’t have heart failure already, the best way to prevent it is to take good care of your cardiovascular system in general. And—you guessed it—that means eating well and getting plenty of exercise.

Stroke A stroke is technically known as a cerebrovascular accident. That is a truly weird name for something so awesomely awful. Another com-

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mon name for a stroke seems more evocative of both its suddenness and its horrific results: Brain attack. Most medical books place stroke in the category of neurological diseases because the blockage that results in a stroke happens in the vessels that supply blood to the brain and results in damage to brain tissue, a definite neurological problem. But the cause of strokes originate in blood vessels (that’s why it is also considered a cardiovascular disease). Because our concern is prevention, rather than treatment, we will focus on it here in the cardiovascular chapter. The seeds of a stroke are most definitely sown in the same field as heart disease, even if the results blossom in the brain. A brain attack, like a heart attack, occurs when circulation is suddenly interrupted, either because of a blockage in the blood vessels (ischemic stroke) or a rupture in the blood vessels (hemorrhagic stroke). In the case of a stroke, however, the damage is in one of the blood vessels that carry blood to parts of the brain. This causes damage to brain tissue. In addition, one in seven strokes is caused by atrial fibrillation. This occurs when a piece of a blood clot that has formed in the top chamber of the heart breaks off and travels with the blood to the brain to block an artery. A stroke is very often immediately fatal. Of those who do survive, about half will suffer permanent disability and eventually (within weeks, months, or sometime years) suffer another stroke. When listed separately from heart disease (not in the larger category of cardiovascular disease), a stroke is the third leading cause of death. Because of its sudden onset and devastating results, a stroke is one of the most frightening diseases. The risk factors for having a

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stroke are very similar to (but not exactly the same as) those for other cardiovascular diseases: family history, increasing age, hypertension (BP of 140/90 or higher), high cholesterol, smoking, artery disease or other heart disease (including a previous heart attack or stroke), diabetes. Taking care of overall cardiovascular health is paramount in preventing stroke. This includes the basics: maintain a healthy weight, eat well, get plenty of exercise, and don’t smoke. For most of the diseases we discuss in this book, reducing risk of disease primarily means making these and other lifestyle changes; drugs are used to treat disease once it has occurred. In the case of preventing a stroke, however, drugs may be necessary to reduce the risk of having a stroke in the first place. If you are at high risk for a stroke, the benefits far outweigh the risks of the medications required to lower that risk. Unless you have already had a stroke, or have some other medical condition that vastly increases your risk of a stroke, that medication is likely to be a blood-pressure lowering drug. The effects of blood-pressure medication on overall heart disease are questionable. But one thing is not at all in question: Getting blood pressure into the safe range one way or another is absolutely essential for reducing stroke risk. That can often be done through diet and exercise, but when it can’t, medications are required. Don’t take chances with blood pressure.

Hypertension Hypertension, also known as high blood pressure, is both a disease and a risk factor for other diseases. It is both a cause and an effect of heart disease, though most often a cause. When cholesterol or other

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fatty deposits accumulate in the arteries, stiffening and narrowing them, the heart has to work harder to pump blood, and blood pressure increases. In turn the extra stress on the heart and the arteries caused by high blood pressure (for example when blood pressure is high for other reasons, such as increased blood volume due to increased fluid) is the cause of cardiovascular problems. High blood pressure can cause stroke, loss of eyesight, and kidney failure as well as heart disease.

How High Is High? Like so many things in medicine these days, the experts keep moving the bar when it comes to blood pressure. 140/90 is considered hypertension. But now you are considered to have prehypertension, and urged to make a vigorous effort to reduce blood pressure, when your blood pressure gets beyond 130/85 or so. The goal to strive for is 120/80 or less.

As you can imagine from the nature of the problem, risk factors for hypertension partially overlap those for heart disease. But hypertension has some risk factors of its own. Heredity, of course, is a big factor. If you have close relatives who have hypertension or who have suffered strokes, you are at higher risk. Age is also an important risk factor. Blood pressure increases with age (or at least it does in Western industrialized nations). Blacks also have a higher incidence of hypertension than whites. Other risk factors, however, aren’t so out of our control. Obesity is a major contributor to hypertension,

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and many people can get their blood pressure into the safe range by losing just a few pounds. A sedentary lifestyle is another big risk factor. Getting regular, moderate exercise can have a profound impact on blood pressure. Alcohol has been shown to increase blood pressure, but it is not clear how much you have to drink to cause problems. A little bit of alcohol may actually help. A high sodium intake can be a problem, too, but only, it seems, in individuals who are salt sensitive (but as there is no test to see if you are salt sensitive, it is best to keep salt intake on the low side if you are concerned about hypertension). Oral contraceptives can increase blood pressure, especially in older women. Hypertension is the bane of over 50 million Americans, many of whom do not even know that their blood pressure is high. Hypertension is often called the “silent killer” because it typically does not cause any noticeable symptoms. It is easy and inexpensive to keep a check on your blood pressure and it can be a good guideline to your overall cardiac health. Of course, having normal blood pressure doesn’t mean that everything else is A-okay. But if your readings are consistently high, that is definitely an indication that something is wrong or soon will be and you need to take action. Lifestyle changes are the first-line approach to reducing hypertension (unless it is already so dangerously high that taking the time to bring it down naturally would be foolhardy). And for many, if not most people with high blood pressure, these approaches can be very successful. The problem is that the lifestyle changes required to lower blood pressure and keep it down aren’t easy. Taking a pill everyday is no big deal. Maintaining a lifestyle that is blood-pressure friendly

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takes time and commitment (and when it comes to eating right, it can take a bit of money as well). First and foremost is weight reduction. For many people, simply losing weight is all that is necessary to see a significant reduction in blood pressure. As everyone knows, however, losing weight and keeping it off can be difficult. Diet is important in more ways than just keeping off the extra pounds, though, and a diet that is good for blood pressure will also be good for weight maintenance. It is all a matter of getting into the right eating habits and staying there.

Lose It Of all the numbers of life we are talking about in this book, probably the single most important number is your weight. Excess weight correlates to several chronic diseases, heart disease foremost among these. Besides smoking, losing even just a few pounds is for most people the single most important step they can take to reduce their chances of heart disease. Important? Yes. Easy? Well, probably not. As the plethora of books, articles, and Web sites on the topic attest, there are many methods of dieting and many philosophies about why some things work and others don’t. The basic principle of weight loss is the same, though, regardless of the approach you take. Burning more calories than you take in will cause you to lose weight—and conversely, taking in more calories than you burn in activity will cause you to gain weight. For most people, the key to healthy, sustainable weight loss is consistency and patience. Simply eat less and exercise more. And be patient. The

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pounds might not melt off before your very eyes, but in time you will see a difference. A loss of ten pounds over the course of a year is very doable with only moderate changes in the ratio of calories in and calories out. There are some tricks to make weight loss easier, though. Certain foods are processed quickly so you get hungry again soon after eating. Eat a bag of potato chips and you might be prowling the kitchen for another snack in just a little while. An apple, however, will stick with you longer. An apple and a handful of grapes will probably get you through until the next meal—and you’ve still not eaten more calories than you would have taken in from the bag of chips (and you’ve gotten two servings of fruit). There is also some evidence that liquid calories can slip under the body’s calorie regulation sensors, making sodas and fruit juices, too, poor choices if you are trying to lose weight. A diet high in fruits and vegetables and whole grains is not only good for overall health but can keep you satisfied on fewer calories, making losing weight much easier. When choosing a weight loss program, keep in mind that you are not looking for a “diet” in the sense of something you “go on” for a while to lose a bit of weight in time for the holidays your class reunion. You are looking for a “diet” in the sense of an eating plan that will keep you healthy and at a healthy weight for the rest of your life. Not only can fad diets be dangerous, they rarely provide lasting weight loss. After all “going on a diet” means eventually going off of it. Permanent lifestyle changes are the only way to achieve permanent weight loss. Get

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in the habit of eating reasonable amounts of healthful food and getting enough exercise and you’ll be both healthier and thinner—and won’t have to worry about this diet business again.

Most studies on diet are a combination of epidemiological studies, cohort studies, and metabolic studies. But in 2000, the National Institutes of Health (NIH) published results of a clinical trial called DASH (for Dietary Approaches to Stopping Hypertension). The DASH study was remarkable in that it was actually a clinical trial, designed like the kinds of trials they do to test new drugs. Some of the participants in the DASH study had high blood pressure, others did not. The participants were randomly assigned to one of three different diets: 1) a diet called the control diet that was similar to the typical American diet—roughly three servings of fruits and vegetables, 40 percent of calories from fat and one dairy product per day; 2) a diet called the fruit and vegetable diet that was essentially the same as the first group except that it contained eight servings of fruits and vegetables a day and C) A diet called the combination diet that derived less than 30 percent of its calories from fat and included 9 servings of fruits and vegetables and three servings of low-fat dairy foods. The results were impressive—and very encouraging to those with hypertension. After eight weeks on the diet, researchers found that the volunteers who were on the combination diet had much lower blood pressure readings than when they started the diet. The volunteers who were on the fruit and vegetable diet saw improvements,

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too, though their improvements were not as great. No changes were made other than the dietary ones—no additional exercise or restrictions on particular foods such as salt. Even the people who did not already have hypertension found that the DASH diet lowered their blood pressure, indicating that it is good for prevention as well as treatment of hypertension.

Here’s to Your Heart If you want to make a family physician nervous, just ask him or her if drinking is good for your heart. In recent years evidence has been mounting that moderate drinking is indeed very good for your heart (and other things as well). But alcohol can still be dangerous when not used responsibly and may raise blood pressure as well as the risk of certain cancers. Most doctors and major health organizations deal with the issue this way: They point out that moderate drinking may be useful in preventing heart disease, but advise patients not to start drinking if they do not already drink. That’s probably not bad advice. But you are reading this book because you want to make your own decisions, specific to your own situation. The fact is the evidence is very strong that moderate drinking is healthful. The overall benefit probably outweighs any slight increase in cancer risk. The catch is we don’t yet know why. It may be a substance in the alcohol itself (this is looking more likely every day) or it may be that people who drink moderately tend to have other healthy habits as well. This is especially true with wine. Wine is a food and goes well with good food. Most regular, moderate wine

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drinkers also eat well. And alcohol of any kind isn’t cheap. People who can afford a couple of drinks a day are probably taking care of their health in other ways as well. Those who can’t afford it, but drink anyway, are not likely to be moderate drinkers. And the money spent on alcohol is not being spent on broccoli and whole grain bread. Having said that, there has been some evidence that some components of wine (particularly reservatrol, a polyphenol), do have a health benefit independent of other factors, but this research is not robust and has been questioned. In addition, drinking other spirits seems to reduce heart risk somewhat as well, so even if the reservatrol is helping, that is probably not all there is to it. Other substances in alcohol are being studied. Until we know more, it is certainly safe and almost as certainly beneficial to drink moderately if you enjoy wine or spirits. If you have a family history of substance abuse or depression, however, you should be extra cautious.

The evidence from the DASH study indicates that merely increasing the amount of fruits and vegetables in the diet can go a long way to reducing hypertension. But it does take some effort. Nine servings of fruits and vegetables may seem like a lot. (It may help to think of it as three servings per meal.) And as I said earlier, keeping blood pressure down requires continual attention. You can’t simply “go on” a diet such as the DASH diet and expect to lower your blood pressure and then get back to your normal lifestyle. This has to become a

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part of your regular lifestyle, something you make a regular habit for the rest of your life.

New Kids on the Block The familiar risk factors for heart disease are all too familiar indeed. But there are a few newcomers to the risk factor club that are getting a lot of attention. In most cases your doctor won’t even test you for these, but if you have a family history of heart disease and few other risk factors or if you are getting a particularly thorough heart-risk work-up you may be tested for one of the following. As more research comes in validating the connection between these factors and heart disease (if subsequent research does support the connection), screening for these risk factors may one day become routine. The primary emerging risk factors are homocysteine, C-reactive protein, and fibrinogen. Homocysteine is an amino acid that occurs naturally in the blood. There is some evidence that when you have too much of it circulating in the blood, your risk for heart disease is increased. Folic acid and B vitamins break down homocysteine and lower homocysteine levels in the blood, but it is not yet clear whether lowering them reduces heart disease. This is an area where the research is still relatively new. A recent trial, called NORVIT (for Norwegian Vitamin Trial—I get such a kick out of the names of these trials) showed no survival benefit when people with recent heart attacks were treated with folic acid, B6 and B12 to lower homocysteine. If it pans out like so

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many other supplement studies, my guess is that we’ll eventually be advised to get our B vitamins from food rather than supplements. Keep an eye on this research. Levels of C-reactive protein increase when there is inflammation in the blood vessels. The inflammation may be due to an infection or injury, such as an injury to the blood vessels caused by arteriosclerosis. Some experts think that C-reactive protein is a better indicator of heart disease than cholesterol levels. But more research needs to be done before it is fully understood. Meanwhile, it appears that cholesterol-lowering drugs also lower C-reactive protein, so you can expect that the pharmaceutical companies that make these drugs will be sure you hear about any research that supports the connection between C-reactive protein and heart disease. Fibrinogen is a protein made in the liver. It is necessary for clot formation. Because heart attacks and strokes are often caused by clots that break off from the plaque lining the vessels, high levels of fibrinogen seem to be a marker for heart disease. Again, research is underway to determine how seriously to take this marker.

Another approach to lowering hypertension that has been proven successful in many studies is plain old exercise. If you are sedentary, just getting up and moving about more can make a big difference. But like the large quantity of fruits and veggies in the DASH diet, if you really want to see some differences, you’ll do best to get serious

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about exercise. An hour a day of moderate exercise, such as brisk walking, is more helpful than less vigorous or less frequent exercise. In my experience, nine servings of fruits and vegetables a day sounds like a lot, but getting them into your diet isn’t really that hard to manage (although it can be expensive). Add a grapefruit and a small glass of orange juice to the half-cup of blueberries on your cereal and you’ve knocked out four servings and it’s not even lunch yet. Working in an hour a day of exercise, on the other hand, can be a challenge. Work, family, and preparing all those healthful meals take a lot of time. Getting up an hour earlier for a jog around the neighborhood might do the trick. Or putting an exercise bike in your office and taking a couple of thirty-minute exercise breaks during the day is another strategy that might work. (It’s not very mindful as the Buddhist say, but you can attach a rack to the exercise bike so that you can read while you cycle. That way your exercise break isn’t really a break from work at all.) However you have to do it, it is worth the effort. Watching those blood pressure numbers tumble down is almost as much fun as loping around the park watching the leaves change color or the spring flowers bloom. Keep in mind that, just as with your diet, this has to be a permanent lifestyle change. Most people find that as soon as they stop exercising (or even miss several regular sessions) their blood pressure begins to go back up. The good news is that once something is a regular part of your lifestyle you don’t even have to think about it any more; as the ad slogan says, you “just do it”. The change may be difficult to make, but once made, it is simply how you live your life. You find that you are no longer on a “program” or a “diet” you are just

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someone who eats well and exercises regularly—and who, by the way, no longer has high blood pressure.

Prevention When it comes to prevention of heart disease, diet and exercise are the heavy hitters. Heart disease is one of the few chronic diseases in which researchers are almost certain (science is never totally certain) that changes in lifestyle can make a dramatic difference in your chances of getting the disease. Experts pretty much agree that between 50 and 80 percent of heart disease can be prevented by a good diet and exercise—and not smoking. (It’s when you factor in not smoking that the epidemiological numbers begin to approach 80 percent.) That’s why you hear so much of what to eat and what not to eat for heart health. But even after years and years of being told that eating well can save your life, you’re probably still wondering what specifically you should and should not eat. More to the point, you are probably wondering how the heck you are supposed to know what to eat when you are getting so many mixed messages from the media. For years you were told to cut fat on pain of death. Then all of a sudden guys with flashy books and MDs after their names were telling you not to worry at all about fat—in fact to just dig into that steak and put as much butter as you like on that potato. The real culprits are carbohydrates, they warned. Watch that carrot! It might kill you! If the experts can’t agree, how are you supposed to know what to do? Well, the fact is, the experts do pretty much agree. When it comes to weight loss, there is still some disagreement (though when

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it comes down to actually analyzing what people are really saying, there is not so much disagreement as it at first seems). So what is the real connection between heart disease and diet? What do the experts know and what are they just speculating about? Well, they know more than you might think from reading the popular press and looking over the diet section at the bookstore. There is enough reliable research to actually make specific dietary recommendations—at least when it comes to preventing heart disease. But first a little background.

Seven Countries and Framingham, Massachusetts The important thing to remember, as I’ve said before, is that nutritional science is a work in progress. Scientists have been carefully studying the connection between diet and health for less than sixty years. When our parents and grandparents picked up the morning paper, they may have read about the progress on the polio vaccine or an advertisement for a new health tonic, but they didn’t likely see anything on how good blueberries are for your heart or speculations on whether drinking two cups of coffee a day is more prudent than drinking three. Life was so much easier then, eh? But this blissful ignorance was not to last. In 1948, researchers began the still-ongoing Framingham Heart Study, a long-term study designed to find out what risk factors contribute most to cardiovascular disease. Researchers chose to follow the medical records and lifestyle habits of the good people of Framingham, Massachusetts. Framingham was chosen because it represented a typical small American city. It also had a fairly stable population and a city gov-

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ernment that kept good records on population. Framingham, and subsequently many other studies, showed that high cholesterol levels were strongly associated with heart disease. Cholesterol (see box on page 65) is made naturally in the body, but only a small percentage of people with high cholesterol suffer from a genetic condition that keeps cholesterol levels high. Dietary cholesterol seemed to be the culprit. So researchers began to zero in on the role of diet in heart disease. One of the first and still one of the most influential nutritional studies ever done (and one that is still considered a tight, well-designed study—though not totally without flaws) was what came to be known as the Seven Countries Study. Ancel Keys, a public health scientist at the University of Minnesota (and as it happens the man responsible for the military K-ration) compared the traditional diets and heart disease rates among seven different countries: The United States, Italy, Greece, Yugoslavia, Japan, the Netherlands, and Finland. The results were astonishing. The highest rates of heart disease were found in Finland, the lowest in Greece, followed by Italy and Japan. After the data had been carefully analyzed the evidence seemed to strongly suggest that the best diet for heart disease was one low in meat, eggs, and dairy, but generous with pasta, bread, olive oil, fish and containing copious amounts of fruits and vegetables. Of course the Seven Countries Study was the first large-scale study to investigate the relationship between diet and heart disease, and we know that one study does not science make. In the pattern of research described in the yamaloo section of the introduction, much work has been done since to crunch the data, verify or challenge the

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results of the crunching, and to identify the biochemical factors underpinning these observations. Meanwhile, several other large, ongoing studies have expanded on the original missions of Framingham and Seven Countries, studies such as the Nurses Health Study, the Physician’s Health Study, the Epic Study, and many, many more). Much of the useful data about risk factors for diseases comes from these studies and others like them. But so far the evidence is pretty consistent that some variation of the basic diet eaten by those healthy Greeks, Italians and their neighbors is an excellent choice if you’re trying to eat for heart health. You’ve heard it before described as the Mediterranean diet. Of course the Mediterranean is pretty big region and there are many variations in the diets of the people who live there. But the general outlines are easy enough to manage: very little saturated fat (meaning small amounts of meat and dairy), olive oil, plenty of vegetables and fruit, fish, pasta and whole grain breads, along with moderate amounts of wine. Much later another study, called the Lyons Heart Study, actually compared the traditional Mediterranean diet to the diet that was then considered a prudent, heart healthy diet (as recommended by the American Heart Association). The Lyons study was investigating whether a Mediterranean diet could reduce the risk of a subsequent heart attack or death from cardiovascular problems in people who had already had one heart attack. The Lyons study so clearly showed the advantages of the Mediterranean diet that it was stopped ahead of schedule. Interestingly, even after the Lyons study was stopped, most of the people in the group eating the Mediterranean diet con-

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tinued to eat that way. Maybe it is the one diet that is delicious enough to stay on! As more research is done and more data comes in from ongoing studies, we can fine-tune our approach to nutrition. The basic four food groups (remember them from grade school?) have given way to more complex dietary recommendations, which are updated every five years—the last time being January 2005. The advice has changed as the research has come in. When nutritionists recommend grain servings, they now specify whole grains; when they say milk or dairy, they generally mean low fat milk or dairy. But the basics, a wide variety of natural whole foods, plenty of fruits and vegetables, is not too controversial and come to think of it, is advice our grandmothers would be comfortable with. If I seem to be making an outrageously complex issue seem simple, that because it really is—sort of. The weight of fifty-plus years of nutritional research seems to say—actually it seems to shout—one overriding message: eat whole grains, low fat dairy, lots of fruits and vegetables, limit refined grains (or better yet, avoid them altogether); limit sweets and alcohol (yes, small amounts are good for you, but alcohol is still not a good idea in large doses—see page 49), and eat freshly prepared, home cooked food as much as possible. Avoid processed food—especially those containing trans fats, high fructose corn syrup, and large amounts of sodium). That advice may be hard to put into practice (especially the part about avoiding processed food), but it’s not hard to understand. Don’t be deceived by the apparent bickering over details; the basic message is simple enough and there is a wealth of research to back it up.

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The evidence from Seven Countries and Lyon (and many subsequent studies that verified and expanded on these findings) shows very clearly the advantages of a Mediterranean-type diet. The intriguing thing about this diet is that it is not exactly the kind of diet that the American Heart Association and the FDA have been advocating over the past twenty years or so (not incidentally, I think, a period in which both obesity and heart disease have increased). For one thing, the Mediterranean diet can be considerably higher in fat than the AHA recommends. This is because in the Mediterranean diet, the type of fat is more important than the amount. The people of Greece, who had the lowest rate of heart disease, also had the highest amount of fat in their diets—around 40 percent of their calories. The fat they ate, however, was mostly olive oil—not the type of fat that is in cheeseburgers and French fries. One of the most compelling messages of these important studies (and many studies since have corroborated this) is that saturated fat is bad for you; unsaturated fat is good for you. In fact, your chances of heart disease are reduced more if you replace the saturated fat in your diet with mono- and polyunsaturated fats (olive oil, canola oil) than if you replace them with carbohydrates. These unsaturated fats are actually good for you. You don’t want to start soaking your pasta in olive oil or drowning your salad in an oily vinaigrette, but a moderate amount of these fats is not only harmless, it is also quite beneficial. Up to 40 percent of calories from fat is probably not a problem for most people—as long as they are the right kinds of fats. Do keep in mind, though, that if you simply add fat to your diet, you’ll also be adding calories. Instead you want to replace the saturated fat you already eat

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with these healthful unsaturated fats.

One for the Ladies Close your eyes and imagine a typical heart-attack patient. He’s middle-aged, balding, and slightly paunchy, right? It’s a common image and not too far off the mark—for slightly less than half of heart attack victims, that is. But though it might surprise many, he is more likely to be “she.” Yep, that’s right. More women than men die of heart disease each year. The stereotype of men and heart disease is not without foundation, however. Men do get heart disease earlier than women, making them far more likely than women to be the victims of heart attacks in their 40s and 50s. But women begin to catch up once they pass menopause. (They never catch up totally, but because women live longer than men, the older the population becomes, the more women outrank men in heart disease deaths.) The relatively low rate of heart disease in premenopausal women has been thought to be because estrogen has a heart protective effect. When estrogen levels drop after menopause, the lead women had before menopause is quickly tightened, and in the end, more women means more women with heart disease. It might seem, then, that replacing estrogen after menopause would remedy the problem. And so it was thought for several years. Many women went on Hormone Replacement Therapy (HRT) in part because of the supposed cardio-protective effect. However, in late 2003, as results from the huge Women’s Health Initiative study (WHI) were analyzed, the data were very com-

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pelling that not only did HRT not provide protection, it actually seemed to increase the risk of heart attacks and stroke (and breast cancer too, it appears). The results were so convincing (and alarming) that the HRT portion of the research was stopped in mid-study. The risk to the volunteers was too great to justify continuation. The number crunching and bench work from the WHI study is still ongoing, and it is not clear why HRT had this unexpected effect. And it will no doubt take some time to sort this all out. But the important point for our discussion here is that with or without HRT, and whether falling estrogen levels have anything to do with it or not, half a million women die each year from cardiovascular disease of one form or another. Nevertheless, the perception that heart disease is a man’s problem runs deep. In a recent survey, 61 percent of women named cancer as the disease they most feared, while only 9 percent named heart disease—despite the fact that twice as many women die each year from heart disease as die from cancer of all types. Women spend many hours fretting over breast cancer while heart disease sneaks up from behind. And what’s worse, the idea that women need not worry about heart disease is not limited to the non-medical community. Doctors are far more likely to send women than men home with a prescription for indigestion medicine when they present with heart attack symptoms. This is partly understandable, because women’s symptoms of heart disease tend to be somewhat different than men’s. Oddly enough, a study published in

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Circulation (the peer-reviewed journal of the American Heart Association) found that a month before a heart attack, the symptoms women were most aware of were not chest pain and aching in the arm, as one might expect, but fatigue and trouble sleeping. We have to give doctors and patients alike a break for missing this. Those are symptoms almost all women have from time to time. Fatigue and trouble sleeping are also symptoms of a wide range of diseases and disorders. Despite these unusual precursors of heart disease, the same risk factors apply for women as for men. Blood pressure, cholesterol, weight, diabetes, and family history are still the indicators to watch. And if these readings are out of whack, these are the problems that need to be addressed—whether you are male or female, pre- or post menopausal, paunchy and balding or thin with a great mane.

The other area where the nutritional advice of the FDA and the AHA was a bit too simplistic and therefore misleading was when it came to carbohydrates. We’ve been told for years that complex carbohydrates are good for us and we should eat more of them and that simple carbohydrates are bad and we should avoid them. Following this advice turned us into a nation gorging on white bread and pasta, while at least giving a nod to avoiding cane sugar. It also may have turned us into an obese nation with rampant heart disease and type 2 diabetes. An increasing body of evidence, however, seems to indicate that the real difference we should pay attention to is how refined are

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the carbohydrates. Whole grains, such as whole grain bread, brown rice rather than white, oatmeal and other whole grains are not only better for you because they contain more essential nutrients and fiber, but because they break down more slowly in the digestive system, helping with weight control and blood sugar control. We’ll talk about this in more detail in chapter four, but since cardiovascular disease and diabetes are so intertwined, it is important to pay attention to this. If the evidence is so consistent and so clear, why am I always hearing so much blather about it all, you may well ask. The hard part comes at the micro-level. If you are counting calories, fat grams, and servings of carbohydrate—or if you are counting servings of broccoli or milligrams of folic acid to make sure you meet the daily minimum you read somewhere would ward off some disease or other, then you run into problems. What’s an obsessive-compulsive to do? As you’ll see in the rest of this book, though there are some variations, a sensible diet is just that, sensible. And it will protect you from a great deal more than just heart disease.

Move It When it comes to heart disease prevention, diet gets most of the attention, but exercise is just as important, if not more so. Evidence is mounting that being fit is even more important than being thin. But if trotting out to the gym every evening or taking up jogging or ultimate frisbee doesn’t appeal to you, you’ll be happy to know that regular, moderate exercise most likely does as much to reverse the indicators

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for heart disease as more vigorous exercise. This is at least in part because moderate exercise is easier to stick with and in part because of the risk/benefit ratio (you don’t lose two weeks for recuperation for every week you spend exercising!). You’ve heard it before, but the best exercise you can do for your heart is walking. Getting more movement into your life one way or the other is the trick. Simple things like parking further from the office and walking the last couple of blocks or playing in the yard with the kids instead of plopping on the sofa to watch a football game really do make a difference. Because exercise is a key component to diabetes prevention, I’ve gone into more detail about it in chapter four. All the recommendations there apply to heart disease as well.

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C H A P T E R

T H R E E

Cancer The Many-Headed Monster T H E

N U M B E R S

A T

A

G L A N C E

For every 5 people in the population, 2 will eventually develop some form of cancer. 1 in 5 will die from it.

Cancer is probably the most feared of all diseases. So threatening is cancer that the United States government declared war on it in 1971, enacting the National Cancer Act in an ambitious attempt to cure cancer before the end of the twentieth century and giving the effort the metaphorical moniker “The War on Cancer.” The war has not gone well. Since 1971 the rates of cancer incidence and cancer deaths have remained largely unchanged. A few gains here, a few losses there—but overall nothing to celebrate. The American Cancer Society estimates that 1,444,920 new cases of cancer will be diagnosed in 2007 and 559,650 Americans will die of some form of cancer—not much improvement, statistically, over the 1971 data. And these figures do not include skin cancers—one of the most common, though not very lethal, cancers. However, these numbers do show a small decline in deaths (but not in incidence rates), and the decline

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seems to indicate a tiny, tiny trend. During the three decades we’ve been waging war on cancer, death rates from all cancers have decreased by roughly 3 percent. To get an idea of why this is so unexciting, note that during this same period, the death rate of stroke has decreased by 63 percent, heart disease 52 percent, and accidents 41 percent.

On the Road Even when cells containing mutated DNA have become cancerous and bypassed the body’s elaborate repair or destroy system, growing out of control, the situation is not necessarily dire. Localized cancers can often be surgically removed with a promising prognosis. When cancer metastasizes, however, it becomes deadly and efforts to stop its progress are much less often successful. Normal cells stay where they belong. A healthy breast cell doesn’t suddenly decide to pack up and take up residence in the liver. An ambitious bladder cell doesn’t get a sudden urge to try out life in the brain. But one of the many amazing attributes of cancer cells is that they tend to get wanderlust and head for other sites. They often defeat the immune system’s attempt to wipe them out when they cross the border from home into foreign tissue. And once they are ensconced in their new location, the trouble begins in earnest. This is called metastasis, and is often the difference between a cancer that can be cured and one that can’t.

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Each year, the National Cancer Institute releases its annual report to the nation, detailing progress in the war on cancer (as of the last year for which data was available, usually two or three years back). The latest statistics were presented with cheerful proclamations about declining death rates and promising new therapies. The numbers, however, did not match the cheery tone. While death rates have declined a little, much of this is due to a decrease in smoking, which contributes to several cancers, not just lung cancer. Women, who have not kicked the habit as successfully as have men, have seen only a 0.8 percent decline in death from cancer. And incidence has held steady, actually increasing in several cancers. In just the past few years, there has been an indication that deaths from breast cancer are decreasing (ever so slightly) and incidence may be leveling off as well. This is indeed very good news, though it is not at all clear how robust this shift is, or to what it can be attributed. What is clear is that there is not much to shout about when it comes to the cancer data. Though progress has been made on some fronts, the fact is that however you crunch the numbers, cancer is still a major health threat and efforts to change that have been largely unsuccessful. The massive research effort over the past 30-odd years has provided an enormous amount of extremely useful knowledge about cancer and molecular biology generally. And in some cases, this knowledge has translated into victories in the war. Several childhood cancers that were once hopeless are now curable. A great deal of progress has been made in treating testicular cancer and certain lymphomas as well. Stomach cancer and cervical cancer can be counted huge successes (though not because of better treatments but because of social

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changes, such as refrigeration and improved hygiene). Death rates for breast cancer and colon cancer seem to have declined very, very slightly. But for most cancers, increased survival in cancer patients is measured in months rather than years. We’ve won a few battles, but we’re not winning the war. Steady, if small, declines in death rates might not be as encouraging as they at first seem. Death rates are calculated based on five-year survival rates, and that can be misleading because of earlier detection. For example, thanks to intense efforts to be sure women get regular mammograms, many breast cancers are being detected earlier than they were previously. In some cases this can mean removing a cancer before it spreads, and sometimes curing cancers that if caught later might have been incurable. However, it can also mean detecting and removing many cancers that would never have become deadly. And when those that are deadly are detected earlier, the time from diagnosis to death is longer. The patient may die at the same time she would have died had the cancer not been detected early, but because she was diagnosed earlier and lived with the knowledge of the cancer longer, the survival rate looks better. Prostate cancer is another example. More and more prostate cancer is being found, but much of the cancer that is being detected would never have caused symptoms and would not have been deadly. Doctors have a joke about prostate cancer: More men die with prostate cancer than from it. I am not pointing this out just to throw cold water on the precious little optimism to be found in this frustrating “war,” but to point out that even when the numbers look promising, the reality is still pretty dismal. In the past thirty years, we have

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made an amazing amount of progress in understanding cancer, and a great deal of progress in detecting it. But precious little in curing it. The good news for those who do not already have cancer, however, is that while progress toward a cure has been frustratingly slow, we are learning more and more about prevention. In fact, there is good reason to believe that if we had put as much effort into preventing cancer as we have into trying to cure it, deaths from cancer would have dropped tremendously—enough to claim some serious gains in the “war.” At least 30 percent of all cancers are related to environmental, that is potentially modifiable, behaviors: smoking, obesity, low fruits and vegetable consumption and alcohol use being the primary culprits. Preventing cancer is not nearly as straightforward as preventing heart disease, however. Cancer is a vastly more complex disease and the way it goes about doing its nasty work is an intricate puzzle that provides endless hours of satisfying work for the world’s molecular biologists.

Sunshine on My Shoulders Makes Me—Healthy? I’ll bet you were wondering why I just skimmed right over sun exposure when I was talking about risk factors for cancer. If you’re like most Americans, you’ve been told so many times about the evils of sun exposure, that you hardly question the advice. You stay out of the sun when possible, and if you have to be in the sun, you cover up with hats and sleeves and slather on sunscreen. I must be an irresponsible wacko for not putting sun exposure in bold, italicized, red print at the top of the list of cancer risk factors, right?

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Well, the situation is not so simple. There are several factors that complicate the equation “sun=cancer.” Often when you look at incidence or mortality data for cancers, skin cancer is excluded. This is because including it tends to give a skewed impression of the data. Skin cancer is far and away the most common of all cancers. It is also one of the least deadly. There are three basic types of skin cancer: basal cell carcinoma, squamous cell carcinoma, and melanoma. Ninety-five percent of all skin cancers are either basal cell or squamous cell carcinomas, but almost 80 percent of the deaths from cancer are caused by melanomas, a type of cancer that accounts for only 4 percent of cases. (The numbers don’t add up to 100 because of those rare cases of other kinds of skin cancer.) Melanoma is a serious disease and unfortunately its incidence is rising. But it is important to keep things in perspective. If you do get skin cancer it is far more likely to be the relatively harmless, easy-to-cure kind. There has also been a great deal of confusion about the role of the sun as a cause of skin cancer. Sunburn is certainly a risk factor for skin cancer. But regular, moderate sun exposure can be very healthful, possibly actually preventing skin cancer as well as several other diseases. I’m not kidding. And this is not a new idea—researchers have been working on this one for years. People who live in sunnier climes have lower rates of several major cancers (including breast, ovarian, and colon) than people who live in places where they get less sun. Rates of osteoporosis also seem to be lower in sunny lands. Rates of skin cancer are of course higher in the sunbelt, but as we noticed the

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death rates from these cancers are lower (because 95 percent of these cancers aren’t deadly and the one that is deadly, melanoma, is still relatively rare). Researchers are not yet sure why the sun seems to have this protective effect, but the popular theory at the moment is that it has something to do with vitamin D. They are even working on a possible cancer drug based on vitamin D. In fact, even as this book is being readied for publication, a spate of studies on vitamin D and a whole array of diseases indicates that it is likely more important to overall health than we currently know. Again, stay tuned. In any case, the point is that moderate, responsible sun exposure is very good for you—and we already know that. Whatever you do, don’t let yourself burn. Sunburn is bad. It damages the skin and damages DNA. I am not by any means recommending oiling one’s body and lying on the beach (or even in the backyard) for hours at a time. But exposing a good chunk of skin (the forearms, for example) to fifteen minutes or so of sun each day is an excellent idea. The use of sunscreens has also been confusing. Several recent studies have indicated that some sunscreens might actually cause changes in the DNA of skin cells—changes that often lead to cancer. Interestingly, the increasing rate of melanoma parallels the rise in the use of sunscreens. This may have something to do with the ingredients in sunscreen or the fact that you aren’t getting the benefits of the sun when you block it with sunscreen. Or it may be due to some other unrelated factor. But the fact remains that, like so many things, the sun is good for us

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in moderate doses and only dangerous when abused. Until more research is in, it is probably prudent to use sunscreen when you have to be out in the midday sun for more than a few minutes. The safest approach is to get regular, moderate sun exposure, avoid harsh sun for long periods and use sunscreen only when necessary to prevent burning. When it comes to sun exposure, keep in mind the old maxim, “moderation in all things.” Be moderate in your exposure to the sun and in your avoidance of it as well.

The Cell that Wouldn’t Die When in Greek mythology Sisyphus dared to outwit Thanatos, the god of death, the gods fashioned for Sisyphus a particularly elaborate and cruel punishment—endlessly rolling a boulder up a hill only to have it roll back down again. The gods understood that death is necessary to life (actually, the gods were just control freaks who didn’t want any mortals muscling in on their immortality, but the humans who made up the myth certainly understood this). Gardeners understand this, too, as they lovingly work their compost piles. But some of the cells within the body do not seem to get the point. When we think of our bodies, all the metabolic action going on inside us, we hardly imagine death. But in fact, the death of cells is just as important to our lives as the production and growth of those cells. When cells break out of the pattern of birth, growth, and eventual death, and strive for immortality, refusing, like Sisyphus, to die, that is cancer. Just like the rest of us, normal cells die after a while. Cancer cells,

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on the other hand, appear to be well-nigh immortal. As we mentioned earlier, cancer is a collection of many different diseases, but what they all have in common, what makes them all cancer, is this runaway cell growth. When normal cells turn cancerous, they proliferate uncontrollably, crowding out healthy cells and organs and disrupting the body’s normal functions. The factors that cause a perfectly normal cell to turn rebellious and refuse to heed the call of Thanatos are many and varied. Cancer is fundamentally a disease of the DNA. Something goes wrong in the genes, either causing cells to get the message to reproduce uncontrollably, or to ignore the message to die when their time comes. These mistaken messages are caused by mutations, or changes, to the DNA. It takes several mutations in several different genes—some researchers estimate as many as ten to twenty genes may need to be involved—to lead to cancer. This much damage does not happen overnight. That is one reason that cancer is primarily a disease of ageing. Most cancers occur predominately in people between fifty and eighty years old. During the course of life, a little damage here and a little damage there can eventually lead to cancer. In one way of thinking about it, simply living is carcinogenic. One researcher once said to me that the truly intriguing question about cancer is not why some people get it, but why less than half of us ever get it at all. While all cancer is genetic, very little of it is inherited. Only about 10 percent of cancer is caused by inheriting faulty genes. Genetic mutations can be inherited, putting an individual one step ahead on the road to cancer. But most of the changes to the DNA that eventually lead to cancer are acquired after conception. As noted above,

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much of it comes from simply being alive. Just like monks in a medieval monastery making copies of ancient manuscripts, cells occasionally make mistakes when they make copies of themselves. Cells have a complex and elaborate system for catching and repairing these mistakes. Some get through, but most of the time, if the mistake is a serious one, it will either be repaired or the cells that have the mutation will be eliminated so that they cannot reproduce and make more mutated cells. When cells with defective DNA are not repaired or destroyed, they continue to reproduce, repeating the mistake in each subsequent generation (just like the mistakes in the monk’s manuscripts).

More on Mutations Not all transcription errors result in mutations that increase the risk of cancer, of course—only when those errors involve the genes that tell the cell when the die or when to reproduce. Other types of mutations can cause other problems, different diseases or in the case of inherited mutations slightly different traits in the offspring. More often slight occasional mutations have no apparent or immediate effect. In the big picture, these occasional mutations are one of the driving forces of evolution. It is what gives natural selection something to select from. This is the reason sexual reproduction (when two organisms combine and shuffle their genes, rather than one organisms just splitting into two) is such a dandy idea. By tossing out millions of combinations, and getting some of them scrambled, nature creates a huge pool of diversity from which the organisms that work best in whatever situation they find themselves manage to sur-

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vive with the new mutations in tact, passed on next time not as mutations, but as clever innovations. In short, that is why we have over 350,000 species of beetles (and that’s just the ones we’ve name so far!). Problems with the detection or repair process are themselves the result of genetic mutations. Some genes (more are being discovered) work sort of like a molecular “hit man,” responsible for forcing mutated cells to die. When these genes are damaged, other cells with damaged DNA are more likely to survive and reproduce, and the risk of cancer rises substantially. A defect in one of these genes has been implicated in many types of cancer. Of course, cancer is caused by many things other than the body simply wearing out and accumulating transcription errors. If that were the only cause of cancer, few people would ever die of it. Remember, it takes many mutations to cause cancer. Causes of mutations include some viruses (such as the human papilloma virus), the chemicals in tobacco smoke, certain types of radiation, and the ultraviolet rays of the sun. In addition, we often worry about the carcinogenic properties of things such as food additives, pesticides, and other nasty stuff that modern life puts into our paths. While many of these substances have been shown to be carcinogenic to lab animals and to human cells in test tubes, so far there is little evidence to link very many of them with actual cancer in humans. Most experts agree that the contribution to cancer made by pesticides, food additives and the like are miniscule compared to other factors such as obesity and cigarette smoke. However, as more research comes in, we’ll know more about the risks posed by such things. Evidence is mounting rather quickly

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that the chemicals of our daily life, from those used to make plastics to those in our cosmetics, make a significant contribution to cancer development. Just as I was writing this chapter, research was published suggesting that air pollution caused DNA damage in unborn fetuses. Remember the humble yamaloo. This research must be replicated and more work done before we start putting gas masks on pregnant women. But it would be prudent to keep an eye on this and similar research as it develops.

A Breath of Fresh Air We don’t, however, need more research to know that air pollution contributes to asthma and heart attacks. Lobbying for stronger clean air regulation is an excellent move toward a healthier populace. As more and more research comes in, we may eventually have enough evidence to determine which of these risks are serious enough to worry about and which are not. For the time being, however, we have plenty of things to worry about that we know increase cancer risk.

Seek and Ye Shall Find Mammograms, PSA tests, colonoscopies, full body scans—there are all kinds of diagnostic tests and screening tests for cancer. Many of these are done routinely and you may think you are endangering your health if you take a pass on them. Such screening tests are not strictly preventive, of course, even though you will often see them listed in articles on how to prevent cancer. But a diagnostic or screening test is checking to see

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if you already have cancer. If you already have cancer it’s a bit too late to prevent it. People are trying not to prevent contracting cancer with all these tests, but dying from it. Whether or not these tests reduce deaths from cancer is not entirely clear. What is clear is that they tend to find many more and smaller cancers than would ever be found without these tests. What is not clear is how many of these small, barely detectable cancers would ever cause any trouble if they were not found. Many cancers develop in the body during the course of a life. And many of them just sit there and do nothing. Many of them are zapped by a healthy immune system without our ever knowing of the drama going on inside our bodies. But once these tiny, young cancers are found, we face a dilemma. We can’t tell which ones will eventually kill and which ones won’t. The temptation to treat is huge. And treatment itself is not without risk. Chemotherapy drugs are rough on the immune system and are themselves carcinogenic. Radiation therapy can cause cancer. So by hitting these small cancers with the full force of our anti-cancer arsenal, we may be increasing the chance that they will become deadly and hinder our immune system in its attempts to take care of the problem (and other potential cancers that might be lurking in there somewhere). If the data indicated that catching cancers early prolonged life, I might think it worthwhile to embark on these search and destroy missions. But the data doesn’t show that at all. Five-year survival rates might increase, but as we saw earlier, that is probably because we are finding killer cancers earlier and thus living

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with them longer, not because the treatments are any more effective for cancers found early. The cure rate might even seem better. But if a substantial majority of these cancers would never have become deadly, we are “curing” a lot of cancer that doesn’t need to be cured. And that is not the only, or even the most serious problem. Researchers are increasingly beginning to fear that the amounts of radiation absorbed by these scans, particularly CT scans, are high enough to pose a cancer risk in themselves. That’s a nice irony, isn’t it? You get cancer from trying to find out if you have cancer. It is not known how much radiation poses how serious a risk. It is, however, known that exposure to radiation increases your risk of cancer. And diagnostic radiation machines are not regulated by the FDA, so no one is watching to make sure the machines are properly calibrated. In any case CT scans expose you to a great deal of radiation all at once. A recent government report found that Americans are getting up to 600 percent more radiation per year than we were twenty years ago, and much of the increase is attributed to a parallel increase in the number of CT scans. Radiation is everywhere, but it pays to avoid it when you can. CT scans are useful, often indispensable diagnostic tests. But it is foolhardy to use them willy-nilly. If you are thinking of having any kind of diagnostic test that exposes you to radiation, find out how much radiation you’ll be exposed to and make sure the test is necessary. Of course whether or not to have regular diagnostic tests is a very personal matter and should be discussed with your health

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care provider. But since they do not actually fall in the category of prevention, they really don’t fit in our discussion. We are talking about how to reduce your risk of getting disease in the first place, not about catching it early. However, if you are tempted to go looking around in your nooks and crannies for stray cancer cells, you might want to do some research on this topic first. It’s not as straightforward an enterprise as you might think. To paraphrase an old bit of wisdom: Be careful what you look for, you might find it.

Living Well Risk factors for cancer vary from cancer to cancer (see page 117 for risk factors for some specific cancers). Rates of most cancers are much higher in developed countries than in undeveloped ones. Epidemiologists have noted that when people move from a country with a low rate of a certain cancer to a country with a high rate of that cancer and adopt the lifestyle and diet of their new countries, their cancer risk soon rises to match that of the native population. This strongly suggests that lifestyle factors are very important in the development of cancer. Of course the number-one risk factor for cancer is smoking. Cigarette smoke is responsible for around 30 percent of all cancer (and not just lung—smoking contributes to several other cancers as well including mouth, esophagus, kidney and bladder cancer). It is also likely that another 30 percent of cancers (some experts even say as much as 40 percent) are related to diet and exercise (more precise-

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ly, poor diet and lack of exercise). This is a truly amazing statistic. It means that if everyone were to stop smoking, eat well and get enough exercise, the incidence of cancer would drop enormously (but not necessarily by 60 percent because the population of smokers and poor eaters overlaps)! And for each of us individually, it means that not smoking, eating well and getting enough exercise can make a major dent in our risk of getting cancer. No new drug or other therapy can even approach this kind of response. Yet this sort of risk reduction is within our grasp. (Do keep in mind that I’m not saying that eating well and exercise will necessarily reduce your personal risk of cancer by anything like 60 percent, or even 30 percent. The factors that lead to cancer vary tremendously from individual to individual and are far too complex to make that kind of claim based on current evidence. However, if smoking and diet/exercise contribute to the majority of cancers in the general population, modifying these factors is an excellent way to reduce your own risk by a substantial margin. After all, our conclusion that reducing cholesterol reduces individual risk for heart disease is based primarily on population-wide epidemiological data. And, of course, eating well and getting exercise is an approach with no known side-effects and one that also reduces the risk of several other chronic diseases, including heart disease and diabetes.) Okay, so let’s talk specifically about diet and exercise and how they can be helpful in reducing cancer risk.

You Are What You Eat—and Aren’t What You Don’t Eat Experts agree that eating well can reduce your overall cancer risk significantly. That’s the good news—and excellent news it is. When we

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get down to specifics, however, the situation gets a bit complex. If you read the chapter on heart disease, you saw that plenty of data from many, many studies—some of them quite large and some of them clinical trials—have given us a good picture of what to eat and what not to eat to reduce our chances of heart disease. Unfortunately, the situation with cancer and diet is not quite so clear. We can’t (yet) point specifically to a particular dietary pattern and say eat this way and you’ll reduce your chances of cancer of any sort by X percent. However, hundreds of studies have looked at the link between diet and cancer—studies on many different foods and many different cancers. And that’s the rub. Once again, keep in mind that cancer is not one disease, but over a hundred different diseases. A diet high in citrus fruit may be helpful in preventing lung cancer, a diet high in whole grains reduces risk of colon cancer, and so on, but a large, consistent body of evidence on specific foods or a specific type of diet and general cancer risk just isn’t yet available. But as far as overall risk of cancer, there is a consensus that a good diet is one of your best defenses. The American Institute of Cancer Research (AICR) performed a huge analysis of some 4,500 studies on diet and cancer and concluded that the evidence that high fruit and vegetable consumption was associated with lower cancer risk was convincing. Researchers crunching the numbers from the Nurses Health Study (a large cohort study tracking the health and habits of 120,000 nurses over a long period of time), however, did not find a strong association. Some experts questions the methodology of the nutritional data collection and analysis in the nurses health study—particularly in light of the

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fact that a similar cohort study in Europe (the EPIC study) used different methods and found results more in keeping with the 4,500 other studies that the AICR examined. Once again, remember the yamaloo. Just as one study doesn’t prove anything, one study doesn’t disprove anything either (well, at least one of this kind of study doesn’t disprove anything). The reasons the research analyzing the Nurses Health Study data has raised so many questions is because that data has proven very useful in other areas and because while there is abundant research on the benefits of a good diet on preventing cancer, that research, as I’ve already mentioned is difficult to analyze. A study on broccoli and prostate cancer here, a study on blueberries and colon cancer there can be hard to assimilate into the big picture—and much (though not all) of the research on cancer and diet takes this form. There are several reasons, however, to place your bets on fruits and vegetables as preventive of cancer. First, while specifics vary, there is still a great deal of evidence that a diet rich in fruits and vegetables and other whole foods is protective for cancer. Second, research is coming in almost every day indicating that a diet high in fruits and vegetables (and real, whole foods generally) boosts the immune system and reduces the risk of a variety of diseases. It is hard to imagine that such a diet does not reduce the risk of cancer as well. And last, it is a no-lose proposition. As far as I know, there has been no evidence that eating plenty of fruits and vegetables can make you sick. But if the data on diet and cancer is short on specifics, in general terms it does offer some helpful, useful information that enables us to draw some scientifically responsible conclusions. The bottom line

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will seem very familiar if you have already read the chapter on heart disease. A diet rich in fruits and vegetables has been shown in several studies to reduce the risk of cancer generally. Though there is not evidence linking all cancers to diet, overall it does seem to be an important factor. Because different foods seem to be preventive of different cancers, eating a wide variety of fruits and vegetables seems to be a good strategy. Eating plenty of fruits and vegetables has been shown in numerous studies to reduce the risk of several specific cancers as well (lung, esophageal, oral, stomach, and colon). There has been some evidence (though not as much) that such a diet can help prevent prostate and breast cancer.

Immediate Payoff If you have been smoking for many years you might be tempted to think, “well, the damage is done. It wouldn’t do me any good to stop now.” That is dangerous thinking. The fact is the body has an amazing ability to recuperate from astonishing amounts of abuse. Within an hour of taking that last drag, the body begins repairing the damage. In as few as five years after quitting a former smoker’s risk of dying of any cause (cancer, heart attack, stroke) is approximately that of a nonsmoker. Smokers who have already had a heart attack can half their risk of having another heart attack simply by giving up cigarettes. This is true no matter what your age or how long you’ve been smoking.

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Many studies have indicated that a diet high in fiber reduces the overall risk for cancer. However, it is not clear if it is the fiber itself or the fact that the most healthful foods, the ones that contain the most nutrients and micronutrients (whole grains, beans and fruits and vegetables) happen to be high in fiber. Once again, the take-home message is to eat the good stuff. Whole grains have also been shown to reduce cancer risk; once again, this is probably because of many components of the grains (some we know about, some we probably have yet to discover) rather than just the fiber. Eating red meat or processed meats has been shown to increase the risk of some cancers—particularly cancer of the colon. High fat diets may also increase cancer risk, although as with heart disease, if you look closely at the data, it seems that they type of fat is more important than the amount. Saturated fats (the kind found in meat and diary products) and trans fats (found in many processed foods and fast foods, and usually identified on the label as “partially hydrogenated oil”) seem to increase cancer risk whereas monounsaturated fats (olive oil, canola oil, avocados) and polyunsaturated fats (corn, soybean, sesame oils) don’t seem to pose a cancer risk. There is much research currently being done on different kinds of fats and their role in health, so this is another area to keep an eye on. So far what has been good for the heart has been good for the DNA (do you notice a pattern here?). But when it comes to alcohol, the situation is a bit different. While alcohol in moderation has been shown pretty convincingly to reduce the risk of heart disease in both men and women (see chapter two for more detail), alcohol has also been shown to increase cancer risk. It does seem, however, that the

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benefits to the heart of moderate drinking outweigh the risk of cancer posed by the same amount of drinking. In any case, however, anything more than three drinks a day for men and two drinks a day for women is probably risky. Even less if you are at high risk for cancer for other reasons. The data is not as strong yet, but is accumulating quickly, that processed foods may increase risk of cancer. Trans fats, which are known to increase cancer risk, are found in many processed foods (although now that they are required to disclose the ingredient on their labels, food manufacturers seem to be dropping trans fats like hot bricks. By the time this books sees print, they may no longer be a common ingredient in processed foods). Other ingredients in processed foods and some of the methods used to manufacture them in all likelihood pose serious health risks, and cancer is almost certainly among them. Work is still being done in this area, but it is certainly true that cultures that eat a lot of processed food (and less fresh, locally grown, and homemade food) have higher rates of cancer. It is a safe bet to try to steer your diet toward real food and away from foods that come in boxes and pouches and bags. My children’s pediatrician one suggested as a rule of thumb not to eat any food that wasn’t available a hundred years ago. “If it comes wrapped in plastic,” she advised, “don’t eat it.” As a rule of thumb that’s pretty good advice—although keep in mind that Coca-Cola was introduced in 1886. And cheese, wine, and tofu, though ancient, are all highly processed foods—and all are delicious, real foods, which, in moderation, can be very good for you. Rules of thumb are, of course, approximations.

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We Are Family—But Just What Degree of Family? When your doctor asks if you have a family history of a disease, she usually asks about your “first-degree” relatives. She doesn’t want to know who was the first person in your family to graduate. First-degree relatives are those with whom you share half your genes—your parents, children, and siblings. Second-degree relatives are those with whom you share a quarter of your genes: grandparents, grandchildren, uncles, aunts, nephews, nieces, half-siblings. Obviously, the closer the genetic connection, the greater the chance that you’ll suffer from the same diseases, hence the fixation on first-degree relatives when assessing your risk for disease.

Despite these cautions, the harm done by eating the wrong things seems to be less severe than the benefit derived from eating the right things. That’s good news, because the right things to eat—fresh fruits and vegetables, whole grains, fish, and real food (as opposed to processed food or fast food)—also happen to be the basis of a delicious diet. This is starting to look a lot like our old friend from chapter two: the Mediterranean diet. While it is certainly not the only healthful approach to eating, the Mediterranean diet (with variations to suit your personal taste) does step to the plate for cancer as well as heart disease, making taking care of your health a delicious experience.

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Get Moving The right foods are extremely important. But exercise may be even more important. While the specifics about how a good diet prevents cancer are sketchy in places and the evidence is sometimes weaker than we’d like (at least for now), the evidence that exercise prevents cancer is much more robust. This is not because there is lots more research on cancer and exercise (there is not), but because the research is much more straightforward. For three of the four leading cancers, colon, breast, and prostate, exercise has been shown to make a decided contribution to prevention. And it seems a safe bet that exercise is a great way to reduce the risk of cancer generally. The exercise doesn’t have to be killer workouts, either. Thirty minutes of moderate activity at least five days a week seems to do the trick. More is better, of course. Sorting out the research on cancer and exercise can be a bit tricky, however, because people who get plenty of regular exercise tend to also have other good health habits such as not smoking and eating well. (Of course this may not always be the case. I remember playing tennis one day while a fifty-something man on the court next to me played a fairly decent game while simultaneously smoking a cigarette.) It is also difficult to sort out the role of exercise per se from the role of obesity. It could be that the apparent benefits of exercise are simply due to the fact that exercise reduces weight, and excess weight in a known risk factor for cancer. On the other hand, when it comes to cancer, it may be that there are benefits to exercise that go beyond simply keeping us trim. This certainly seems to be the case when it

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comes to heart disease. If you are trying to prevent heart disease, it is best to be slim and fit. But if you can’t be slim and fit, being fit seems to be the more important of the two. Skinny people who get no exercise are probably at higher risk for heart disease than heavy people who are fit (of course, you don’t see all that many people who are both heavy and fit). This could be the same with cancer, but so far there is not enough research to say for sure. There is enough research, plenty of it in fact, to say for sure that being overweight increases the risk of cancer generally and several specific cancers as well.

Stay Slim Being overweight is thought to contribute to cancer in a variety of ways. For example, excess weight can lead to acid reflux which can lead to esophageal cancer. Being overweight results in higher circulating levels of hormones such as estrogen and insulin, which stimulate the growth of certain cancers. But however it happens, it is clear that maintaining a healthy weight is one of the most important things you can do to reduce your risk of cancer. Of course, the same diet (whole grains, fresh fruits and vegetables, moderate amounts of low-fat dairy products, fish, little or no meat) that is best for preventing cancer is also best for maintaining an ideal weight. It’s sort of a two-for-one deal (and when you consider that the same diet also helps prevent diabetes and heart disease and maybe even Alzheimer’s, it becomes a several-for-one deal). For a more complete discussion of how to achieve and maintain a healthy weight, see chapter four.

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SEER Data SEER (Surveillance Epidemiology and End Results) data with current deaths and incidence rates on major cancers broken down by gender: http://seer.cancer.gov

Risk Factors We think of and often speak of cancer as if it were one disease. In fact, it is a collection of over a hundred different diseases, all with their own specific characteristics, challenges, and risk factors. As I said earlier, the take-home message for preventing cancer generally is not that different from preventing heart disease: Don’t smoke. Get plenty of exercise. Eat a healthy diet of whole grains and plenty of fruits and vegetables, not much saturated fat. Drink moderately if you drink at all. However, the relative importance of these risks does vary from cancer to cancer (at least as far as we can tell from current research). So below is a list of several common cancers and what we know about the risk factors for each. Keep in mind, though, that particularly when it comes to exercise and diet, much research is underway and in the cases where diet and exercise don’t seem to be a strong factor, you might want to keep watching. That is likely to change as evidence accumulates.

Breast Breast cancer probably takes top honors in the contest for the most publicized cancer. Pink ribbons, 5K runs, survivor banquets, all attest

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the efforts of the breast cancer support groups and lobbyist to bring popular attention to the disease and get more money for research. This is probably because breast cancer is the most common cancer in women and the second leading cause of cancer deaths in women (second only to lung cancer), and in part because breast cancer tends to strike middle-aged women more often than other cancers. But all the attention has somewhat distorted the facts. Breast cancer is common among cancers and it is a tragic killer. But it is probably not as common as you think. We often hear the statistic that one in eight (or sometimes one in nine) women will get breast cancer. This is true. But it means that one in eight women will get breast cancer sometime during their lives. The one in eight number is only realistic for women in their eighties and even then not quite that bad. An average woman in her forties has something more like a 1-in-67 risk of getting breast cancer. And keep in mind that we are talking here about getting breast cancer, not dying from it. Your chances of dying from breast cancer are much lower. Having said that, no one wants to be the one in anything to get breast cancer, so let’s look at the risk factors: • Being over fifty (see what I mean?) • Having a family history of breast cancer • Never having given birth or having given birth for the first time after age thirty • Having started menstruating early or having a late menopause (the pattern here is that researchers believe that the longer you are exposed to estrogen, the greater your changes of getting breast cancer) • Being overweight

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Most of these risk factors increase risk only slightly and most women who get breast cancer don’t have any of the above risk factors other than being over fifty (and perhaps being overweight).

Prostate While the ladies worry about breast cancer, the men worry about prostate cancer. Prostate cancer is incredibly common. Next to skin cancer, it is the most common form of cancer in men. It is not, however, one of the most deadly cancers. In fact, many, many prostate cancers don’t cause much trouble at all. Autopsies show that many men who die of other causes actually had prostate cancer. They didn’t know they had it because the cancer wasn’t causing them any problems—and probably never would have. So the biggest risk factor for prostate cancer is probably simply being male. Others are: • Family history. You are at higher risk if your father or brother had prostate cancer • Age. Most prostate cancers (75 percent) are found in men over sixty-five years old • Being African-American. Prostate cancer occurs 60 percent more often in African-American men than in men of other races • Being sedentary and having a diet high in red meats, processed meats and high fat dairy products • Being obese

Colon/Rectal Colorectal cancer is the second leading cancer killer in the United

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States, and the third most common cancer overall. Interestingly, more women over the age of 75 die of colon cancer than breast cancer: • Family history • Age. Again, as with most cancers, this is primarily a disease of the older set. More than 90 percent of people with colorectal cancer are over 50 • A history of inflammatory bowel disease, such as colitis or Crohn’s disease • A diet high in animal fat, processed meat, full fat dairy products, and low in fiber. Studies on colon and cancer and fiber seem to indicate that it is not so much the fiber itself as the whole state of the food that makes a difference • A sedentary lifestyle • Obesity • Diabetes. People with diabetes have as much as a 30-40 percent increase in the risk of colon cancer • Smokers also have a higher rate of colon cancer • Heavy alcohol use

Lung Lung cancer is still the leading cancer killer. It seems to be declining somewhat in males (both white and African American), but is still on the rise in women: • Smoking. Almost 90 percent of lung cancers are believed to be caused by smoking, or by exposure to tobacco smoke • Exposure to asbestos, a fibrous material that was once widely used in insulation, fireproofing, electrical insulation and other

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building and industrial materials. Exposure to a few other chemicals such as diesel exhaust, radon, arsenic and radioactive ores such as uranium may increase lung-cancer risk as well • Air pollution may pose a slight increase in lung cancer risk, but nothing to match that of smoking • Tuberculosis and recurring pneumonia. The inflammation in the lungs from these diseases can cause scarring of the lung tissue and that can increase the risk of lung cancer • Radiation therapy to the chest area (such as for breast cancer treatment)

Esophageal This is a blessedly rare cancer, but has been increasing dramatically in recent years: • Age (this is going to be the case with almost all cancers). By far most esophageal cancer occurs in people over fifty-five • Being male. Men are three to four times as likely to get this cancer than are women • Being a black man. This cancer is 50 percent more common in African-American men than in men of other races • Obesity • Tobacco use • Too few fruits and veggies—and overeating of any kind of food • Heavy drinking • Gastroesophageal reflux disease (GERD) can lead to Barrett’s esophagus which can lead to cancer • Exposure to certain dry cleaning chemicals

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Ovarian Ovarian cancer is not common. The lifetime risk is only 2 percent. Both incidence and mortality are increasing, however: • Age again. Most ovarian cancer occurs after menopause and half in women over sixty-three • Family history of ovarian cancer, breast cancer, or colon cancer • Personal history of breast cancer • Obesity is a risk factor for getting the disease and also increases the risk of dying from it • Starting menstruation before age twelve and going through menopause after age fifty • Not having given birth or having given birth after age thirty • Estrogen replacement therapy appears to slightly increase the risk of ovarian cancer

Cervical This is one of the cancers known to be caused by a virus: human papilloma virus: • Infection with human papilloma virus (HPV). There are many forms of this virus, not all of which cause cancer. It is believed that infection with one of the dangerous types is necessary to develop cervical cancer • Family history of cervical cancer • Having had sex at an early age or having many sexual partners • Smoking • Having a diet low in fruits and vegetables • Being overweight

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• Use of oral contraceptives (slight risk) • Having had multiple pregnancies (slight risk)

Stomach Stomach cancer is widely believed to be caused in part by infection with the Helicobacter pylori bacterium: • Age. Most common in people in their sixties, seventies, and eighties • Family history of stomach cancer • Infection by Helicobacter pylori bacteria • Being male. This one is also more common in men than women • A diet high in smoked and/or salted food • Smoking • Previous stomach surgery • Having type A blood. Weird but true. No one knows why

Brain There aren’t very many identifiable risk factors for brain cancer. Most brain cancers appear for no reason at all. Despite all the press, the evidence is weak that cell phones or electromagnetic fields contribute to brain cancer: • Radiation. This usually occurs when people are given radiation in the head and neck area to treat another cancer • An impaired immune system—sometimes as a side-effect of treating another cancer

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Bladder Another cancer caused primarily by smoking. Interestingly, incidence of bladder cancer has remained fairly stable over the years despite a slight reduction in the number of people who smoke: • The nasty chemicals in cigarette smoke are filtered by the lungs into the blood where they are filtered by the kidneys into the urine for disposal. This accumulation in the urine can and often does lead to bladder cancer • Being white. Whites are twice as likely as blacks to get bladder cancer • Being male. Men are four times as likely to get bladder cancer • Certain chemicals used in the textile, printing, and paint industries • Arsenic. Some areas have higher rates of arsenic in drinking water than others. Recent changes to environmental regulations may result in more cases of bladder cancer • History of chronic inflammation of the bladder • Chemotherapy and radiation treatments. (Are you noticing a pattern here? Cancer treatment causes cancer.)

Kidney This is another cancer that seems to be increasing alarmingly. That is probably due to better detection rather than some more sinister reason. However, rising obesity rates and sedentary lifestyles may be partly to blame: • Family history • Age. Mostly occurs in people over fifty

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• Being male. Kidney cancer is twice as common in men as in women • Smoking (see the entry above on bladder cancer for an idea of how smoking causes kidney cancer) • Obesity • Sedentary lifestyle • Exposure to asbestos, benzene, and perhaps some herbicides • High blood pressure. People with high blood pressure have higher rates of kidney cancer, but it is not clear if the cause is the blood pressure itself or the diuretics used to treat it (another reason to try to get that BP under control with diet and exercise. If you can’t do it that way, though, the risks associated with high blood pressure outweigh the risk of kidney cancer)

Testicular Testicular cancer is rare, but is the most common cancer in teen and young adult men (who rarely get other kinds of cancer). It is also one of the most curable cancers. Around 70 percent of testicular cancer can be cured: • Age. This one is not more common in older men. Most testicular cancer is found in men between fifteen and forty • Family history of testicular cancer • Having an undescended testicle. Only about 3 percent of boys are born with at least one undescended testicle, but 14 percent of testicular cancer occurs in men who have had this problem • Being white. Testicular cancer is four times as common in white men than in black men

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Melanoma Melanoma is not nearly as common as the other main types of skin cancer, but it is the one that can be deadly. And the incidence of melanoma is increasing. It is not clear if the increase is due to more cancer or more awareness of it. Primary care physicians and dermatologists are far more vigilant than they used to be in examining and biopsying suspicious moles: • Family history • Having certain types of moles • Fair skin/tendency to sunburn easily. Dark pigmentation protects the skin from solar radiation. The rate of melanoma is twenty times higher for whites than blacks • Exposure to extreme sunlight, previous sunburn (see page 97 for more detail on this) • Suppressed immune system (caused by certain drugs or health conditions)

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C H A P T E R

F O U R

Diabetes A Big Fat Sweet Epidemic T H E

N U M B E R S

A T

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1 in 3 Americans will develop diabetes. Males have a lifetime risk of 1 in 3, females 2 in 5.

When people talk about diseases they often stress alarming trends and frightening possibilities (“one in eight women will get breast cancer,” “someone dies every thirty-four seconds of heart disease”—I said that myself in chapter two!) Sometimes these claims are exaggerated, or if accurate, misleading. As I’ve explained before, the breast cancer figure is lifetime risk. During most of a woman’s life, she does not have anything like a one-in-eight risk. Diseases such as cancer and heart disease are the leading killers in our world, and if we want to live long, healthy lives, we do well to try to avoid them. Other diseases can kill us or make us miserable, so we do our best to try to stay healthy—that’s why we read and write books like this one. But the fact is that we in the industrialized world are living longer and healthier than ever before. Most of the alarming headlines are not

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quite as alarming as they seem at first pass. Except when it comes to type 2 diabetes. This is one truly frightening disease and it is no hyperbole to call the recent and rapid increase in its incidence a serious epidemic. In fact, diabetes (Unless I specifically say “type 1”, from now on when I say “diabetes” I will be referring to type 2 diabetes. For our purposes here it is the only type worth discussing. Type 1 is much less common, but unfortunately cannot be prevented, so a discussion of risk factors and how to reduce risk is not possible.) could be the factor that reverses the trend toward longer and healthier lives. If the increasing flow of diabetes is not staunched, the next generation of Americans may be the first to have shorter life expectancies than their parents. And those shorter lives may well be nasty and brutish.

The Fruit Basket Are you an apple or a pear? The popular diet-book distinction between body shapes—“apples” carry fat around the waist, “pears” around the hips—sounds a bit silly and way too cute to be of use for anything more than selling diet books. But it turns out that there is something to it. Belly fat tends to be a strong predictor of heart disease risk. Certain hormonal states (having too much circulating insulin and cortisol) can cause your body to store fat around the mid-section. This has been associated with a higher risk of diabetes as well as heart disease. So if you are an “apple,” even if you are otherwise slim, you might want to take a close look at your other indicators such as blood glucose and blood pressure.

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Some of the increase in diabetes incidence may be due to an increased awareness of the problem, and therefore more diagnoses. But even if that accounts for some of the increase, the rise is still alarming and the concurrent (and in part causative) rise in obesity rates (see page 134 for more on the connection between obesity and diabetes) indicates that this problem is just getting rolling. If we don’t reverse this trend, the worst is yet to come. Here are the alarming numbers: In the two decades between 1980 and 2002 the number of Americans with diabetes more than doubled. And this is reflects only those who have been diagnosed with the disease. Many people have diabetes and don’t yet know it (the symptoms are subtle for a long time). According to some high-end estimates, 41 million adults (between forty and seventy-four) already have prediabetes, a condition that puts them well on their way to full-blown diabetes. Diabetes is the sixth leading cause of death in the U.S. But it is likely that deaths from diabetes are vastly underreported. Eighty percent of diabetics die of heart disease that results from diabetes, and many of the rest die of kidney disease or other complications of diabetes. Therefore many deaths that are reported as deaths from heart disease or some other cause are actually a result of diabetes. More than eighteen million Americans have diabetes now and the number is expected to more than double by 2050. The numbers look bad. But what is even worse is the nature of the disease. The complications of diabetes include, but (as they say in the fine print) are not limited to, heart disease, stroke, hypertension, kidney failure, impotence, nerve damage, amputations, and blindness. Diabetes sounds like such a sweet little disease (too much sugar

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in the blood, oh my), but in fact it is a killer that does its work slowly, gradually eating you from the inside out. Watching someone live with and die from this disease is motivation enough to make the lifestyle changes necessary to prevent it. And that’s the good news (and I’ll bet you were ready for some). In most cases, type 2 diabetes can be prevented and, if addressed soon enough, even reversed.

The Cancer Connection As if the list of complications from diabetes weren’t frightening enough, there is some evidence that having diabetes also increases your risk for cancer. Several studies have suggested a connection between diabetes and cancer. It is known that obesity is a risk factor for both cancer and diabetes, so it is possible that the diabetes/cancer connection is actually a connection between obesity and both diseases. However, it is beginning to look like that is not all there is to the story. A well-designed 2005 study on over one million South Korean men and women indicated that having diabetes increased the risk of several types of cancer, including cancer of the liver, esophagus, colon and pancreas. The participants in the study who had diabetes were 30 percent more likely to get cancer than participants without diabetes. In addition, the increased risk of cancer began at blood glucose levels well below what is considered diabetes, indicating that increased risk, although slight at first, begins as soon as the blood sugar trouble starts and gets worse as the blood sugar problem gets worse. The significance of this study (in addition to its size) is that most of the people in the study

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were not overweight, removing the possibility that obesity was the underlying connection. If diabetes does increase the risk of cancer, independently of obesity, we don’t know why. Researchers speculate that it may be that the hormone insulin may influence cell growth.

The Nature of the Beast So what is this monster that is killing and maiming so many people? The short definition of diabetes is that it is the disease that occurs when glucose, or blood sugar, is too high. Glucose provides energy to all the cells in the body. A hormone called insulin is used to get glucose out of the blood and into cells so that they can use the glucose for energy. Insulin is made in the pancreas by special cells called beta cells. When not enough insulin is produced or when the insulin is available but can’t seem to get the cells to take up the glucose, excess glucose stays in the blood for way too long and that causes a plethora of problems (those mentioned above, and unfortunately, more). In people with type 1 diabetes, the problem is that their bodies don’t make any insulin. We don’t yet know for sure what causes this, but it is thought that the body’s own immune system goes haywire and attacks and kills the beta cells (the ones that make insulin). There is also some evidence to suggest that a viral infection may be involved in the destruction of the beta cells. However it happens, people with type 1 diabetes usually are depleted of beta cells during childhood and have to take insulin injections for the rest of their lives. Type 2 is somewhat different. In most (but not all) cases, the body makes plen-

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ty of insulin, but for some reason the insulin can’t coax the glucose into the cells. This is called insulin resistance and happens before full diabetes has developed (the blood levels of glucose aren’t high enough yet to qualify as diabetes). When the levels of glucose in the blood stay too high (because the insulin isn’t doing its job), the beta cells keep helpfully cranking out more and more insulin. After a while, the poor beta cells, sweating and puffing and trying to make more and more insulin, get exhausted and die. Over time the supply of beta cells becomes lower and lower, making an already poorly functioning system less and less efficient. Eventually the supply of beta cells peters out completely. At this point, people with type 2 diabetes have to take insulin every day, just like people with type 1. But I’m getting ahead of myself. The process is actually a very gradual one (and that’s a good thing—it gives us time to reverse it). Insulin resistance—when the insulin doesn’t do a very good job of getting glucose into the cells—is the first step in the long march toward diabetes. For people who have insulin resistance, the more glucose there is in the blood, the more insulin they’ll need to get it all processed into the cells. It is also likely that some people produce too few beta cells (due to a genetic disorder). In this case, even if the insulin is doing its job just fine there may not be enough beta cells to crank out the insulin necessary to process the glucose. In both of these cases (and it may be that many people have both problems), the more glucose there is in the blood, the worse the problem is and the sooner it will become critical. The more food you eat, the more glucose in the blood. The more glucose in the blood, the more insulin you need. If your insulin isn’t working at top capaci-

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ty, it will face even more of a challenge. If beta cells are in short supply, the supply is soon likely to get even shorter. As you can see, one factor driving this process is the amount of glucose in the blood. The more you eat, and the type of food you eat, can make a big difference in how serious the problem is. Fortunately it also means that eating less food and the right kind of however much food you do eat can often keep the problem from developing in the first place—and can certainly slow the process down considerably.

Play Period Some people are simply turned off by the very concept of exercise. Too many years of being intimidated, humiliated, and generally abused by gym teachers, perhaps. Or maybe you’ve been scarred by the jocks at the gym or by all those twenty-somethings who look so good in their tights and leotards. Or perhaps it was a bad experience years ago with Jane Fonda. Whatever the problem, if you can’t bear even the thought of exercise, it might be useful for you not to think of movement as exercise at all. Think of it as play period. And come up with some really creative ways to get movement (not exercise, mind you) into your life. Forget the jumping jacks and the jogging shoes and come up with something fun. The weirder the better—just to show Jane and that sadistic gym teacher that you are not impressed. Here are a few ideas to get you started: • Put on your favorite music and dance around. This does not have to be any kind of regular dance steps. Think “creative movement.” Jump from one foot to the other, swing your

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arms, sway and pivot—let the music guide your body. This can be really fun and as good for the mood as it is for the waistline. • In the fall, on a breezy day, go outside and try to catch falling leaves before they hit the ground. • Take a beach ball outside and try to keep it in the air for as long as possible. • Walk around the house while kicking a small plastic or fabric ball between your feet. • Ask a friend to play catch—and it doesn’t have to be a baseball. Tossing a couple of stuffed animals back and forth at the same time can be great fun. You have to toss your toy while simultaneously getting ready to catch the one coming at you. I know it sounds weird, but it really is fun. • Table tennis is listed on the American Heart Association’s Web site as moderate activity, right up there with walking. Who would have thought it? • Remember Frisbee?

Dangerous Duo Obesity and diabetes are intimately related, but exactly what the connection is not yet fully understood. Several theories and explanations based on ongoing research have emerged recently. But the fact is, even the experts don’t yet understand exactly how the connection works. So don’t let me give you the impression that the connection is straightforward and perfectly well understood. But as you can see

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from the above description (simplified though it is), the more you eat and the more what you eat elevates the glucose levels in your blood, the more likely you are to develop diabetes, if you have a genetic tendency to do so (a tendency toward insulin resistance or a paucity of beta cells). I keep talking about the genetic tendency toward diabetes, so perhaps I’d better clarify that a bit. As we saw earlier, the body has a very elegant system for keeping the levels of blood glucose under control. The beta cells make insulin and the insulin stores the glucose in the cells. (It really is a bit more complicated that than. There are many types of cells and the way glucose is stored and used it very complex. But this is the gist of it.) In healthy people, this system works pretty well. In fact the range of safe levels of blood glucose is very narrow and most of the time things stay just right—no matter what or how much people eat. Some people, however, have certain genetic flaws that make them more likely to develop insulin resistance or to produce too few beta cells. For these people, the chances of developing diabetes are greatly increased when they eat too many calories, a habit that seems to be very hard to avoid in what the National Institutes of Health has called our obesogenic environment. It might be reassuring to know that you aren’t among those with a genetic tendency toward diabetes. The problem is, other than looking at family history, we can’t know who has this genetic tendency and who doesn’t. And having a family free of the disease is no guarantee. Your family may have just not pushed their systems quite far enough to tip over into full diabetes. This is especially likely because our parents and grandparents typically had more active lifestyles and less highly

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caloric diets. (They didn’t make Zingers in the old days, and there wasn’t a fast food joint on every corner and two cars in every garage.) Or your ancestors may have in fact had diabetes and not known it, and died of heart disease or kidney failure or some other complication never knowing the true cause.

Syndrome X Syndrome X. The name has a certain science fiction ring to it, and even sounds a bit shady—not something you want to tell your mother you’ve been diagnosed with. I prefer its less catchy but also somewhat less mysterious-sounding name “metabolic syndrome.” Whatever you call it, it is simply a way of identifying a collection of indicators that often cluster together and suggest a heightened risk for both heart disease and diabetes. For many years doctors noticed that a particular group of health factors tended to cluster together: high blood pressure, high triglycerides (a type of fat in the blood), low HDL (the good kind of cholesterol), poor blood sugar control, and, oddly enough, excess fat around the midsection (see the box on apples and pears). You don’t have to be overweight to meet this criterion. People with metabolic syndrome often have acceptable body mass indices. These factors, when all are present in one patient, are believed to be a strong risk factor for diseases such as cardiovascular disease and diabetes. All of the conditions that make-up metabolic syndrome are known to play a role in heart disease, diabetes or both. But the tendency for them to run in a pack intrigues researchers. It may

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be that by treating each of the components of metabolic syndrome separately (medications for high blood pressure, other meds for high cholesterol, etc.), we are treating the symptoms and missing the underlying cause. If, as some experts suspect, the underlying cause is related to insulin resistance (too much circulating insulin because the beta cells keep cranking out more and more insulin when it is not performing adequately), taking care of the insulin resistance could correct a batch of problems at one time without having to resort to dangerous drugs. It also might explain why bringing blood pressure down with medication has not been convincingly shown to reduce incidence of or death from heart disease (although it does reduce the risk of stroke). It may be that in this case, the hypertension is a symptom of a far more serious and complex problem.

Risk Factors One of the main risk factors for diabetes, of course, is a family history of type 2 diabetes. A family history of the disease indicates that you do have a genetic predisposition to it, but as we just saw, lack of a family history is no assurance of safety. Other risk factors include being overweight, not getting much exercise, being over 40 years old (As you can see from the previous discussion, it takes a long time to develop diabetes. So typically it occurs in older people. That is why type 2 used to be called “adult onset diabetes” to distinguish it from type 1, which usually manifests before age 20. In recent years, however, the age of onset of type 2 diabetes has been steadily decreasing.

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Children as young as 8 and 10 are developing it. This is thought to be because poor diet and lack of exercise is becoming more and more common. With far too much rich food and a sedentary lifestyle, it doesn’t take nearly as long to develop the disease.) Having prediabetes (more on that in a paragraph or two), and being of almost any ethnic persuasion other than white of European descent (whites get it too, but not quite as commonly as others) are the other primamry risk factors. The best defense against diabetes is getting plenty of exercise and eating well. If you don’t already have prediabetes, you are not overweight, and you are taking steps to protect yourself from heart disease and cancer (as outlined in the previous two chapters), you are probably doing what you need to do to protect yourself from diabetes. If however, you have prediabetes, sometimes called borderline diabetes or impaired blood glucose control, you have to take a more rigorous approach. Interestingly, the approach is not dramatically different from the approach you take to reduce your risk of other chronic diseases. You just have to be much more vigilant about it. The problem is that many, many people have prediabetes and don’t even know it. And not all of them are overweight.

Prediabetes This is a fairly new term. In the past, people who did not have diabetes, but who had insulin resistance or simply showed signs of having less than optimal blood sugar control were told that they had “borderline diabetes” or that their blood sugar “was a touch high,” and that they should cut back on sweets. Little more was said, and in

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most cases very little was done until diabetes arrived in full force. That was very unfortunate, because this period of prediabetes is the window of opportunity for reversing the process and preventing the disease from developing. Having been diagnosed with prediabetes is, of course, the single biggest risk factor for developing diabetes. If you have been told that you have prediabetes or if you suspect that you may have it, take it very seriously. This is a disease that, in the majority of cases, can be prevented or at the very least postponed for many years. And because so many of the complications of diabetes result from years of uncontrolled blood sugar swings, postponing the onset of the disease for as long as possible can prevent some of the worst problems. If you develop diabetes at thirty-five and live to be eighty-five, the disease has fifty years to destroy your body. If you postpone the disease until you are seventy-five, then it has only ten years to work its horrors and you aren’t likely to suffer as many of the devastating consequences. Of course, you don’t want to get diabetes at any age. Total prevention is the goal. But if that can’t be achieved (because your body simply doesn’t make enough beta cells to get you through a lifetime, for example), prudent living can put it off for many years. A major clinical trial called the Diabetes Prevention Program (DPP) found that people with prediabetes can substantially lower their risk of the disease by making relatively simple lifestyle changes. Participants in the study who reduced their weight by a mere 7 percent, (I know what some of you are thinking! If you are trying to lose weight and keep it off 7 percent doesn’t seem all that “mere.” More on this in a moment.) and exercised for 150 minutes a week (that’s thirty minutes a day, five days a week) reduced their risk

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of diabetes by 58 percent. If 58 percent doesn’t seem good enough to you, keep in mind that these people were all overweight and already suffering from prediabetes. They were at very high risk.

The Diet Bazaar (and Diets Bizarre) There are probably as many weight loss plans out there as there are recipes for chocolate cookies. Basically, however, the current batch of popular weight-loss approaches tend to work variations on one of four themes: low fat, low carb, simple calorie restriction, and the gimmicks. Except for the truly weird ones (putting crystals in your pantry), even the gimmicks tend to be built around at least a kernel of scientific truth, and when stripped down to their basics (and adjusted for personal needs and to get rid of any potentially hazardous aspects) probably work well for some people.

Losing It, Redux Other than already having prediabetes, being overweight is the biggest risk factor for diabetes. So if you are overweight, even slightly overweight, your first step in preventing diabetes is to lose weight. I discussed weight loss briefly in the chapter on heart disease. But since obesity is intimately connected with diabetes, I think this is the place for a fuller discussion of weight loss. Many, many books (far too many, you may be thinking) have been written on weight loss, so it is unlikely that in one small section I can do justice to this huge topic. There are, however, a few points that distill nicely from the

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messy topic of how to lose weight. But first let’s be clear about what is overweight and what isn’t. I’m sure you’ve heard the old joke, “I’m not overweight, I’m underheight.” Because the taller you are, the more you can weigh and still be within a healthy range, the experts have developed an easy way to measure weight in relation to height (well, it looks a bit difficult at first, but it really is easy once you get the hang of it). It’s called body-mass index, BMI for short. To calculate your BMI take your weight in pounds and divide by your height in inches, then divide by your height in inches again, then multiply the result by 703. For those of you who are more comfortable with formulas it’s this: (wt/ht/ht)703. For those who think even that much math is too much, there is a handy chart on the next page. It is not quite as precise as doing it yourself, but close enough. A body-mass index of 25 or greater is considered overweight. Thirty and over is considered obese. But before you relax and congratulate yourself on your nice, safe BMI, I do need to point out a couple of things. Disappointing as it sounds, a BMI of 25 may still be a bit on the high side. Research has shown that ill health effects begin around a BMI of 22 and accelerate from there. There is no magic cut-off number and the health risks are certainly lower at 23 than at 25, but it is good to know that if you can get your BMI closer to 20 than to 25, you’ll be doing yourself an even greater favor. Second, research has also shown that people who gain more than a few pounds (10 or so is generally considered the max) after they reach their adult weight are at higher risk of ill health than those who maintain a more or less steady weight during adulthood. For example, say you are a 45-

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Body Mass Index (BMI) Table BMI 19 20 21 22 23 24 25 26 27

28

29

30

31 32

33

34

35

HEIGHT WEIGHT (IN POUNDS)

58" 91

96

100 105 110 115 119 124 129 134 138 143 148 153 158 162 167

59" 94 9 9 1 04 109 114 119 124 128 133 138 143 148 153 158 163 168 173 60" 97

102 107 112 118 123 128 133 138 143 148 153 158 163 168 174 179

61" 100 106 111 116 122 127 132 137 143 148 153 158 164 169 174 180 185 62" 104 109 115 120 126 131 136 142 147 153 158 164 169 175 180 186 191 63" 107 113 118 124 130 135 141 146 152 158 163 169 175 180 186 191 197 64" 110 116 122 128 134 140 145 151 157 163 169 174 180 186 192 197 204 65" 114 120 126 132 138 144 150 156 162 168 174 180 186 192 198 204 210 66" 118 124 130 136 142 148 155 161 167 173 179 186 192 198 204 210 216 67" 121 127 134 140 146 153 159 166 172 178 185 191 198 204 211 217 223 68" 125 131 138 144 151 158 164 171 177 184 190 197 203 210 216 223 230 69" 128 135 142 149 155 162 169 176 182 189 196 203 209 216 223 230 236 70" 132 139 146 153 160 167 174 181 188 195 202 209 216 222 229 236 243 71" 136 143 150 157 165 172 179 186 193 200 208 215 222 229 236 243 250 72" 140 147 154 162 169 177 184 191 199 206 213 221 228 235 242 250 258 73" 144 151 159 166 174 182 189 197 204 212 219 227 235 242 250 257 265 74" 148 155 163 171 179 186 194 202 210 218 225 233 241 249 256 264 272 75" 152 160 168 176 184 192 200 208 216 224 232 240 248 256 264 272 279

year-old, 5'4" female who weighed 115 pounds when you were 25 and now weigh 130. You have a body-mass index of 22.3—excellent. However, the fact that you have gained 15 pounds since you were 25 might indicate that you are still a bit overweight for you. And lastly, even otherwise thin people can be at risk if they have too much belly fat. Some experts say that women who measure more than 35 inches and men more than 40 inches around the part of the belly close to the navel, are technically overweight, even if everything else looks good (and, as you probably suspected, these measurements put you

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at very high risk. But health risks begin to increase at even lower measurements, 37 inches for men, 31 inches for women). This is because belly fat is particularly dangerous when it comes to diabetes and heart disease. Bodies that tend to store fat around the middle (rather than around the hips and thighs) have been shown to be at much higher risk of cardiovascular disease as well as diabetes. And unfortunately, in my experience at least, this can be the hardest weight to lose. I don’t say all this to put pressure on people to lose more weight than is realistic. In fact, as I mentioned earlier, losing even as little as 5 to 10 percent of your body weight can result in major differences in health indicators such as blood pressure and cholesterol and in disease risk overall. And putting pressure on yourself to be very skinny is probably a health risk in itself (as are many of the kinds of diets people go on to try to achieve these very low weights). I just want to point out that risk for disease does seem to increase at weight levels that are lower than we often think.

Calories In/Calories Out When it comes to losing weight everybody wants some trick, some scheme that will make it all easier. Eat cabbage soup every day; eat a grapefruit before each meal (the grapefruit diet, weird as it seems, may actually be based on sound physiology. Recent studies indicate that certain enzymes in grapefruit influence insulin levels and discourage the body from storing fat.) don’t eat anything after dark. But the truth is much simpler and we all know it—really we do. If your body takes in more calories than it burns, you’ll gain weight; if your

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body burns more calories than it takes in, you’ll lose weight. If you want to lose weight, eat less food and get more exercise and be patient. The trick is to do this without getting so hungry that you toss the diet and polish off an entire chocolate cake just to make yourself feel better. Or, what is more likely to happen, just gradually start eating more and wondering why you aren’t losing weight. I’ve seen a lot of methods for getting around this problem, and two of them seem to be based on sound biology and don’t use any weird techniques that might compromise your health. Earlier, I talked about foods with a low-glycemic rating. These foods keep blood sugar from soaring too much and too quickly after a meal. The same kinds of foods also tend to fill you up faster and keep you from getting hungry again soon after eating. Foods with lots of fiber and/or a high water content work this way. Whole grains are much more filling than processed grains (and have far more nutrients). I can eat an entire can of Pringles potato chips in one mad dash and still have room to wash them down with a Coca-Cola (we all have our weaknesses), but I fill up on just a few whole grain Triscuits. A turkey sandwich on white bread definitely needs chips on the side. And even with the chips, you’ll likely be hungry again in no time. A turkey sandwich on whole wheat bread with tomatoes and sprouts and an apple on the side can keep you going for hours— until the next meal. And frankly, once you get used to whole grains and fresh vegetables, that white mushy stuff quickly loses its appeal. Simply replacing refined grains with whole grains (whole wheat bread, brown rice, oatmeal) and adding lots of fruits and vegetables

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to your diet can help you to feel full and satisfied on fewer calories. Eating a salad with a small amount of dressing before the entrée works for some. Having an apple or some cucumbers along with a sandwich rather than chips or fries is another strategy. The important thing is to find something that works for you—something that you enjoy eating and that makes you feel full and satisfied on fewer calories.

Programmed Eating I recently saw in a national women’s magazine an article on how to “get rid of your belly.” The article began with some very straightforward and commonsensical advice. If you want to get rid of belly fat, you’ll need to take a combination approach— lose weight and build muscle. Muscle building won’t get rid of the fat, but just getting rid of the fat won’t strengthen weak muscles. So the article suggested exercises that targeted the abdominal muscles and a walking program to lose weight. So far so good. Very good indeed, I thought. Then I flipped past the intro to the meat of the “program.” It was so complex you needed a separate daily planner just to coordinate your belly fat reduction plan. You did one kind of exercise for so many minutes on day one and another kind for so long on day two and so forth; the walking program (how fast, how far) shifted and varied from day to day. There was a handy multicolored chart to help you keep track of when you were supposed to be doing what (and for how long, and at what intensity). By the time I finished reading the article I was too exhausted to take a walk, much less

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exercise my abdominals. Yet the basic idea was quite sound: walk and work those abs. I’ve never quite understood the need to quantify and systematize everything. I suspect it may be a peculiarly American trait. In any case, we don’t seem to be satisfied with common sense advice unless it is dressed up as a program and hedged about with rules and guidelines and some vaguely mathematical talk. Maybe there is some subtle psychology to this. Perhaps people are more likely to get on and stay on a complicated program. Or maybe it just makes it easier to sell diet books. In any case, you’ll often find, buried underneath the gimmicks, sound basic ideas. My favorite example is a program called the sevenminute miracle. The plan promises that you can lose weight and tone specific areas of your body by working at it for only seven minutes at a time. What a miracle! Too good to be true? Well, maybe not, exactly. It turns out, like the belly fat program, that when you strip the program of its gimmick, it’s pretty sound stuff—the same sound stuff you are told by health experts without plans or charts or programs. During the seven-minute workouts (which are done three times a day) you do an intense aerobic and muscle-strengthening workout. You choose particular exercises depending on what part of your body you want to tone (abs, thighs, upper arms, whatever). Then you combine this effort with a sensible diet that is lower in calories and high in good nutritious food (the diet part of the plan is, of course, dressed with specific timing and a special name, “the spot meal”). The plan bets on two things: First, that many of the

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people who try the program aren’t getting much of any exercise to start with. Even twenty-one minutes a day is an improvement (after all, that’s almost up to the suggested thirty minutes per day, and trust me, these are pretty intense minutes). And second, that exercising before eating (you are told to exercise on an empty stomach and not to eat for forty minutes after exercising) will reduce the appetite (studies have shown this to often be the case) and forestall the tendency to grab a bag of chips and a soda right after a workout. It probably does work for a lot of people. But not because of the gimmick, the magic seven-minutes (or any of the vaguely scientific mumbo-jumbo the author puts in supporting the program) but because buried underneath all the specific rules and directions is the same, sound healthful advice you get from people who aren’t pushing a diet: Get some aerobic exercise every day, do some muscle-building exercises, eat good food and a little less of it. Sound familiar?

A Caveat Let me be perfectly clear here: I am not endorsing this diet or exercise plan. I am simply using it as a example of a complicated plan that uses all kinds of rules and gimmicks to cover some variation of the same theme: exercise more, eat less, lose weight. When you get beyond the overly structured, gimmicky, dietof-the-week plans, most weight-loss approaches tend to take a position in the great protein/carbohydrate debate, although most of the best ones are just good old calorie reduction programs. Depending on what you read and how you interpret it,

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there is scientific evidence (and plenty of anecdotal evidence) to support both the idea that eating fewer carbs and more protein can help lose weight and that eating a high-carb diet is the way to go for a lean, healthy body. As I discussed elsewhere, the details that devil us here tend to be more with what kind of carbohydrates and what kind proteins we are talking about. As long as the high-carb diets are focusing on whole, unrefined carbohydrates (fruits, vegetables, whole grains, beans) this plan can indeed help reduce weight and is undoubtedly extremely healthful in a variety of ways. On the other hand, if a high-protein diet focuses on proteins that are low in saturated fats (beans, fish, low-fat dairy), it can also be quite healthful (as long as it doesn’t deny you good fruits and vegetables) and many people find these diets to be very effective when it comes to losing weight. What works for one person won’t work for another. In order to be successful losing weight, you have to find something that works for you and does not skimp on the basic principles of good health. In order to find your own prince of a diet, you may have to kiss a lot of frogs (and buy or check out a lot of diet books). But eventually you’ll find something that works for you. Just be careful to look beneath the “program” to make sure the plan is nutritionally sound. And keep in mind that even though programs and plans and structure might be just what you need to interest you in a diet and help you stick with it, the only thing that’s really necessary for eating healthfully and losing weight is to get regular exercise, eat healthful food, and eat slightly less.

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The second technique that holds up to scientific scrutiny is the idea of boosting your metabolism. While this is not a magic trick to weight loss, being aware of the general principle may be helpful. You’ve probably heard people who seem to stay skinny no matter what they eat explain this enviable phenomenon by saying that they just have a naturally high metabolism. There is something to this idea. The amount of energy your body uses to just maintain its normal functions (while it is on idle, so to speak) varies from person to person. A recent study discovered that fidgeters—those annoying people who just can’t seem to sit still, always swinging their legs or hopping up to do this or that—have a higher resting metabolic rate than people who can sit like the Buddha for hours at a time without moving very much. If you’re not blessed with a high metabolic rate, it may be possible to goose it just a bit. Some studies have shown that eating slowly and eating in a calm, relaxed mood can boost metabolic activity. Exercise also raises the metabolism and keeps it up for several hours after exercising. And it doesn’t take a lot of exercise to do it. If you take fifteen minutes or so, spaced out evenly throughout the day, and do a little bit of vigorous exercise (jumping rope, climbing up and down the stairs, riding an exercise bike, or just taking a brisk walk) you can boost your metabolism and coax your body into using more calories even after you are back in your chair.

The Big Guys We all throw around food terms: carbs, proteins, fats—but what are we really talking about here? When you look at what we are actually eating, what is in food, you find that the greatest por-

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tion of dinner can be classified as belonging to one of three groups, called the macronutrients. They are fats (also known as lipids), proteins, and carbohydrates. We know them as food, but here is how they break down: Carbohydrates: These are sugars and starches and are the body’s favorite way to get energy to power our obvious activities (running, walking, eating, as well as the bodies more subtle work, cell metabolism and so forth). Carbohydrates are found primarily in grains, vegetables, fruits, legumes, milk, honey, sugar. Proteins: Proteins are necessary for growth and maintenance of muscles, blood, skin and internal organs, hair, nails. They also play an important role in producing the hormones and enzymes and antibodies that keep the human machine chugging on along. Protein is found in meat and dairy, of course, but is also plentiful in beans, eggs and grains. Fats (lipids): Since most of us get far more dietary fat than we need, we tend to think of fat as a bad guy. But don’t be fooled. Fat is as essential to healthy functioning as any other nutrient. Many vitamins, minerals, and hormones are produced and processed by fat. Dietary fat is found primarily in meat, oils, milk, cheese, and butter. Nuts and avocados also contain a lot of fat.

And that brings us to the exercise part of the weight loss equation. Eating less (even if only a bit less) is essential to weight loss, but

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may not do much good by itself. In part for the reason described above. If you start taking in fewer calories, your body is likely to slow down a bit to make sure that it can get the most out of its newly limited resources. When most people diet, their resting metabolic rates slow down, too. If they cut back food even more, the body may shift into starvation mode and really start cutting back, storing what food it does get as fat for the crisis it senses is coming and generally mucking up your plans to get back your youthful slim figure. (This is generally only a problem when calories are cut fairly significantly, though. If you just cut a hundred or so calories a day from a 2,000calorie per day diet, you may not run into this effect.) However, if you add exercise to the program, you get two benefits. First, and most obviously, you are burning more calories. Even if you don’t eat less food, you will be changing part of the equation, and in time should lose weight (as long as you don’t start eating more food). Second, and a bit more mysteriously, your metabolism will be ratcheted up a bit so you use more calories even when not exercising, and what you do eat is used more efficiently. Many people report (and I find this to be true myself) that when they exercise regularly they tend to have less appetite (although some studies have shown that some people, especially women, tend to eat more after vigorous exercise, so be careful. If you exercise too much or too vigorously, you might end up eating more calories than you lose by exercise).

How Much Is “Plenty”? Everyone is telling you to eat “plenty” or “lots” of fresh fruits and vegetables and whole grains. But how much is plenty?

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The government issues guidelines about how much to eat of what and tells what a serving of this or that amounts to, and I mention a few recommendations myself. But keep in mind that getting too focused on quantities (weighing your strawberries before dumping them on your cereal is a bit excessive, don’t you think?) can not only divert your attention from the big picture of living well, it can also make something that should be extremely joyful into a chore. Besides, you don’t have time to spend counting calories and weighing food. You’ve got exercises to do! Nonetheless, when someone tells you to eat so many servings a day of this or that, you need to know what a serving is. So here are some helpful guidelines for that, too, courtesy of the U.S. government. (By the way, you might notice that the amounts that are considered a serving are quite small—a bonus if you’re trying to squeeze in more fruits and veggies, possibly a shock if you’re trying to cut down on total food intake.)

Dairy One serving equals 1 cup milk or yogurt, one and a half to 2 ounces of cheese.

Protein Foods One serving equals: 2-3 ounces of cooked lean meat or fish 1-11⁄2 ounces cooked beans 2 eggs 4 tablespoons peanut butter

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Grains One serving = 1 slice of bread, 1

⁄2 cup of cooked pasta, rice, or cereal,

1 ounce of cold cereal.

Fruits One serving equals 1 piece of fruit, 3⁄4 cup of juice, ⁄2 cup canned fruit, 1⁄4 cup dried fruit.

1

(You’ll have to use some common sense in the fruit and vegetable category. A piece of fruit can be a tangelo or a grapefruit, a banana or a fig.)

Vegetables One serving equals 1⁄2 cup raw or cooked vegetables or 1 cup raw greens.

Keep in mind that you are shooting for (according to these latest government guidelines) two cups of fruits and 2 and a half cups of vegetables a day, 3 or more ounces of whole grains per day, and three cups of fat-free or low fat milk per day. These amounts are based on an average calorie intake of 2,000 calories a day. If you eat less or more, you can adjust the recommendations accordingly.

You may want to try one of the many weight-loss schemes on the market these days. But do keep in mind that simpler is often better. If

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you cut back on food and add some exercise, you’ll lose weight. This method won’t happen fast, but it will be safe and most important, it is an approach that will last. The cabbage soup diet might work for a month or two, but pretty soon you are going to get sick of cabbage soup and head straight for the golden arches. The key to sustainable weight loss is not to diet, but to make lifestyle changes.

Which Is Which? The Skinny on the Popular Diets Low Fat Pritikin Ornish

Low Carb Atkins South Beach (at least in first two stages) Sugar Busters

Calorie Reduction (These vary quite a bit in philosophy and approach, but the common denominator is a calories in/calories out philosophy coupled with an emphasis on eating good, healthful food and getting exercise.) Weight Watchers Jenny Craig Andrew Weil Volumetrics

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Having said all this, I do want to make one thing clear: Losing weight is very difficult for some people. Because of the recent dramatic increase in obesity, much research is being done of food and metabolism, what makes us fat and what keeps us slim. The precise workings of the hormones that regulate appetite and store and process fats and carbohydrates are still not fully understood. And each body is unique. What works for you might not work at all for your best friend. You have to find something that works for you and something you can fit comfortably into your life. In my experience, most popular diet and/or weight-loss programs have a lot of marketing hype wrapped around a grain of scientific truth (or at least a scientific study or two to make them look good). One of these might work for you. A custom-designed plan that fits your lifestyle and your appetite will probably work better. But whatever you choose, remember that if your goal is optimal health and not just getting into that blue dress in time for the high-school reunion, you’ll need to come up with a diet and exercise plan that you can make a part of your life for the rest of your life. Here are a few other tips that might help make losing and maintaining weight easier:

• Plan your meals. If you have something good to look forward to for lunch or dinner, you are less likely to grab a snack when the first small hunger pains hit. You also aren’t likely to eat something you know is not good for you just because it is handy and you are hungry.

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• Don’t let yourself get too hungry. Better to have a small healthful snack in the afternoon such as fruit, plain yogurt, or a few nuts (and use up a couple hundred calories) than to rush into the kitchen at six o’clock so hungry that you eat twice as much as you need before you realize you’ve had enough. Getting really hungry also tempts you to eat junk food and other high calorie, rich foods.

• Eat foods you really like and think of food as something special. Sometimes good food can be expensive, but it is not nearly so expensive as glucose monitors and insulin injections. Become a health food gourmet. If you decide to have a salad before dinner, splurge on exotic greens and a scattering of goat cheese or almonds on top. If you are a chocolate lover, have a small piece of really good imported chocolate rather than an entire Snickers bar. Regularly eating something wonderful and delicious will make your new eating plan seem less like a “diet” and more like a lifetime pass to a four-star restaurant. You may also be surprised at how quickly and easily you can prepare real food at home.

Cookbook Tips A few cookbook books I’ve found to have recipes that are healthful and quick and easy to prepare are The Complete Italian Vegetarian Cookbook by Jack Bishop, any of the several excellent cookbooks by Jeanne Lemlin, Vegetarian Suppers by Deborah Madison, and Moosewood Cooks at Home by the Moosewood collective (all the Moosewood cookbooks are excellent, but this one focuses more on quick and easy dishes).

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• Small amounts of low-fat dairy have been shown to aid in weight loss (though the evidence is still coming in on this, and not all of the research has been funded by the dairy industry). If, like most people who aren’t of northern European descent, you can’t tolerate milk, try yogurt. It’s exceptionally good for you as well as being easier to digest.

• Pay attention to what you are eating. Slow down and savor each bite. It takes a few minutes for the stomach to tell the mind that it is full. You can stuff in a lot of extra calories during this delay if you go too fast. It is also likely that if you really take the time to notice and enjoy your food, it will take less to make you feel satisfied.

• And keep in mind that this is a lifetime strategy. Depriving yourself will only work for so long. Rewarding yourself with small amounts of good food, well-prepared and well-appreciated, is a habit that you can live with for the rest of your life. Food is a wonderful thing and shouldn’t be associated with deprivation and punishment. Eat well and live well.

What about Those Pills? Hidden in food are all kinds of tiny little goodies that are supposed to be extremely good for us: Vitamins and minerals and things we’ve just recently begun to hear about, substances with very unappetizing names like antioxidants, flavenols, polyphenols and caretenoids. In fact, just about every day we hear of some micronutrient that can prevent all kinds of disease, maybe

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even save our lives, if only we get the right amount of whatever it is. “Oh my gosh,” we think, “how many servings a day of delicious pomegranate seeds do I have to eat to ensure a long healthy life free of tumors and arthritis? Now where did I put my triple-beam balance scale?” Seriously though, there are all kinds of micronutrients in foods and those micronutrients do have a lot to do with keeping us healthy. The problem is, we don’t know much about them yet. Nutrition experts have only just started finding out what’s there; there’s no telling what’s yet to be found. I don’t have to tell you that it is very silly to rush about calculating servings of blueberries based on their antioxidant content. Blueberries are good for you; eat them on your cereal and get on with your life. But what about supplements? Mightn’t it be a good idea to take a pill or two (or four or five or six or eight) containing all these goodies that are supposed to be so healthful—just in case I don’t get enough in my food, sort of as insurance? Well, actually the theory that supplements might not help, but can’t do any harm is open to question. When it comes to how micronutrients work in food, what we know is far less than what we don’t yet know. A good example comes from experience researching beta-carotene. Beta-carotene is a substance contained in food and used by the body to make vitamin A. It is one of the antioxidants you hear so much about. Antioxidants neutralize “free radicals,” which are cell-damaging by-products of everyday cell metabolism. A solid body of research has shown that foods that are high in beta-carotene might reduce

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the risk of lung cancer (and other cancers as well, and maybe heart disease, too). People who eat a lot of fruits and vegetables high in beta-carotene seem to have a lower risk of cancer, lung cancer especially. However, when the substance was tested as a supplement it didn’t work out at all as expected. A large study by the National Institutes of Health was even stopped early because when given to people at high risk for lung disease (smokers, former smokers, and people who had been exposed to asbestos), beta-carotene supplements actually seemed to increase the risk of disease. No one knows exactly why it worked out this way, but the leading theory is that (surprise!) beta-carotene works in synergy with other substances in food to do its magic. Antioxidants, it seems, can be very dangerous if they get out of balance. You don’t want a bunch of extra beta-carotene running around in you if you don’t have enough vitamin C for example (and smokers tend to be woefully short on vitamin C). Too much of an antioxidant, such as beta-carotene, can have the same detrimental effect as too little, acting as pro-oxidants rather than antioxidants and causing damage of their own. The proper balance of these micronutrients is essential, it seems. Food is intricately and delicately balanced and probably has all sorts of fail-safe mechanisms built in as well. You can’t just hack out one tiny substance (or manufacture something chemically identical in a lab) and get the same result. When I was a kid we used to fret about the possibility of a future in which no one would eat food; we’d all just take pills. That’s not likely to happen any time soon. We still have a long way to go in understanding precisely how food does

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what it does to keep us healthy. The lesson from the beta-carotene experience is that when we say of a supplement “it can’t hurt” we really don’t know that for sure. Before the two big studies on beta-carotene, no would have thought beta-carotene could possibly be dangerous (it tended to turn your skin orange in large does and that was pretty much it for side-effects). The fact that these supplements appear to cause harm in smokers (and maybe not in others—at least in the short term) is not really reassuring. It just points out that there are many factors to be considered and we don’t even know what they are. Smoking seemed to make a serious difference with beta-carotene. Other factors might have made a difference as well; they just weren’t a part of the study. Does stress make a difference? What about hormonal fluctuations? Perhaps drinking alcohol changes the equation. With other supplements other factors may be at issue. No one knows yet. Eating real food is a pretty safe bet. I’d stick with that. So the bottom line is that popping a pill version of the latest thing you’ve heard is good for you is almost certainly a waste of money and may very well be dangerous. On the other hand, taking a multivitamin supplement every day (just some namebrand multi-vitamin/mineral supplement you can buy at the supermarket or drugstore) has not been shown to do any harm and they have been pretty well studied and have been taken by lots of people for a long time. When I interview biomedical researchers on the topic of supplements, I always ask them if they take one. Most say yes—even the folks who have just spent

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30 minutes telling me why they aren’t necessary and maybe aren’t a good idea. But when they say they take vitamins, they are always talking about a plain old garden variety multi-vitamin, such as a Centrum or a Flintstone. Basic model multi-vitamins are probably safe and they seem to make a lot of us feel better. But don’t get carried away and start popping this and that. And I would avoid the ones that have added all kinds of extra goodies, such as beta-carotene for example. Stick to the basic vitamins and minerals that we have been supplementing for years.

Exercise: One More Rep Exercise is, of course, an essential ingredient in weight management and weight management is an essential ingredient in preventing diabetes. But as we have seen in connection with heart disease and cancer, exercise is so much more than just a way to keep slim. Exercise in and of itself reduces the risk of diabetes. Exercise makes the body’s cells more sensitive to insulin. And, of course, the more you exercise, the more glucose you burn as immediate fuel, cutting down on how much is circulating in the blood. Muscle is also much better at processing glucose than is fat, so exercise that builds muscle can be doubly helpful. You may have noticed that recommendations for how much exercise you need vary quite a bit. Some say thirty minutes of moderate exercise three times a week. Others say an hour a day most days. Are the people who recommend an hour a day a bunch of sadists? Or are

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the folks who think we can get by on a half hour here and there simply being nice? Well, it really comes down to what your aims are. Thirty minutes three times a week is more exercise than most Americans get—far more. And even that small an amount of exercise will make a noticeable difference in people who are currently sedentary. (Even ten minutes a day will make a difference for these folks.) But if you really want to optimize your health, reduce your risk of diabetes (and heart disease and cancer . . . ) you’ll do well to put in a bit more effort. An hour of moderate intensity exercise on most days is great—and not really that onerous if you can find the time for it. A good example of moderate intensity exercise is walking at a pace of around a mile in fifteen minutes. This is brisk enough to get you breathing a little harder, but not really all that strenuous.

Don’t Be a Yo-Yo Like everyone else who is interested in keeping you healthy, I strongly suggested to keep your weight at a healthy level. For many people this will mean losing weight—dieting. As you can tell, I don’t hold much with dieting as it is generally done these days. Adopting a sustainable lifestyle that incorporates more exercise and focuses on moderate amounts of real, nutritious food is the way to go. A diet that is intended to banish a few or a lot of pounds fast, might work in the short run, but you can’t live on apple juice and cabbage forever (or whatever the plan is this time), so once you’re off the diet, you’ll gain the weight back, so after a while, you’ll have to go on another diet. This is not only silly, it’s bad for your health. Research has shown that

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this kind of yo-yo dieting, as it’s called, is worse for you than being a bit overweight. The body just doesn’t respond well to these intermittent bouts of weird eating and zipping up and down the scale. By far the safest approach is to find a diet in the sense of an eating plan (or better yet, don’t use the word diet at all) that you can stay on for the rest of your life. This is a lifestyle change, not a diet you “go on.” If you’re eating healthy food and getting plenty of exercise, you’ll almost certainly reach and achieve a healthy weight for you. The process may not be fast, but it will be safe.

A common rule of thumb for beginners is that if you can’t talk while exercising, you are probably working too hard. But if you can sing, you’re not doing enough. Walking (brisk walking—not sauntering or moseying or strolling) is one of the most widely recommended exercises because it has been proven to be just about as effective as jogging in terms of health outcomes, and is much less likely to cause injury. (The main advantage of running over walking is that you can get more exercise in less time if you run rather than walk.) Walking is something almost everyone can do and it costs nothing more than a good pair of shoes. If your neighborhood is not suitable for walking, or the weather is not, you can usually find an indoor track or even a shopping mall that will do. But if you don’t enjoy walking there are many other possibilities: Swimming, riding a bike (outside or a stationary bike), stair climbing, gardening, playing with the kids or the dog, even just putting some good music on the hi-fi

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and dancing around the living room. Remember, you are aiming for regular episodes of brisk movement—not a place on the Olympic team. It doesn’t have to be graceful or pretty; it doesn’t even have to have a name. It just has to get you up and moving around. The emphasis on “regular” is important, too. There are several reasons that regular low-key exercise is better than intermittent bouts of intense exercise. The biggest danger of intermittent exercise is the risk of injury, or even minor aches and pains that can sideline you for days and make doing it again sound like torture. And there is the simple fact that it is easier to make small amounts of regular exercise a part of your life. And beyond that, serious intensity is not really needed for good health, just something modest—as long as it’s regular. Of course, if you absolutely can’t find time to exercise except on weekends, that’s better than not doing it at all. Just be careful not to strain your muscles (especially the big one!). As with dieting, the important thing is to find something that works for you—something you enjoy and that you can make a regular part of your life. Whatever it is, getting more movement into your life is one of the best steps you can take to prevent diabetes.

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Alzheimer’sand Other Dementias The Forgetting T H E

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Your lifetime risk of developing dementia is between 10 and 15 percent.

The most exciting scientific frontier today is the study of the mind. Even if we don’t know nearly enough about how to heal it when things go wrong, we do know rather a lot about how the rest of the body works. We know much less about the workings of the mind, however. How memories are formed, stored and retrieved, what it means to have a sense of oneself, how identity is maintained over time—questions both philosophical and neurological—are at this point all still unanswered. Alzheimer’s, a disease that affects an estimated 4.5 million Americans, eats at the very foundations of the mind. Victims of this tragic disease lose not only memory, and all that goes along with

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memory—personal history, relationships with family, an ability to function in society—they eventually lose even their identities, their sense of themselves. It is both heartbreaking and terrifying to watch a loved one slip into the uncertainty and confusion of dementia, to gradually cease to be the person you’ve known and loved. We do not know what causes this disease and we do not know how to cure it. For many aspects of it, we do not even understand exactly what it is that the disease robs us of—such are the mysteries of mind. Yet there is nothing mysterious about the suffering caused by Alzheimer’s and related dementias. Alzheimer’s is the most common and most well-known of several dementias that affect older people. The second most common dementia is vascular dementia and together they account for the vast majority of dementia cases. While these two diseases are very similar, and in later stages it can be hard to identify which one a given patient has, the origins and biological characteristics of the diseases are really quite different. Alzheimer’s is characterized by dense protein deposits known as amyloid plaques and tangles of fibers inside the brain cells. Vascular dementia, on the other hand, is associated with a series of small strokes deep inside the brain. The brain depends on a constant and reliable blood flow to do its work. Vascular diseases, such as high blood pressure and atherosclerosis can interfere with the brain getting the blood it needs. Because these small strokes are so deep inside the brain, they are very often undetectable, making it difficult to determine whether the dementia is caused by Alzheimer’s or vascular dementia. Early in the progress of disease, vascular dementia can sometimes be distinguished by its

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A Look at an Aged Brain

The appearance of amyloid plaques, sticky build-up outside nerve cells, in the brain can precede the behavioral symptoms of Alzheimer’sby years.

intermittent nature. Strokes will cause memory problems and then as the brain recovers, things seems to get better. Then another episode occurs. As time goes on recovery is less complete and the disease progression begins to look just like Alzheimer’s. The confusion is made worse by the fact that many people with Alzheimer’s also have some degree of vascular dementia. In any case, the risk factors and preventive measure are very similar. What we don’t know about the mind is a fascinating challenge and is providing interesting work for a new generation of scientists and scholars. What we do know, though, is very useful in determining how best to prevent and treat these diseases. For like so many of the diseases we will discuss in this book, there is no cure for dementia,

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but there is excellent reason to believe that a healthy lifestyle can reduce the risk of vascular dementia and increasing evidence that the same habits can also reduce the risk of Alzheimer’s.

More Elastic Than We Thought For many years it was thought that lost brain cells are not replaced. You have what comes with the standard package and when those are gone (due to ageing or accident or abuse), you have to make do with what you have left. We now know that this is not true. The brain does indeed generate new cells throughout life. We do not necessarily lose mental function as we age. Many people live even to advanced old age without any serious loss of mental capacity. (It is normal, though, to lose a bit of short-term memory. If you lose your keys now and then or find yourself having to work a bit harder to come up with the name of an acquaintance, don’t worry. This is not a sign of Alzheimer’s or any other kind of dementia—just sign that you are over forty, or perhaps that you have too much on your plate, or that you have teenaged children. . . ). Nurturing your brain through a variety of lifestyle measures can greatly reduce the risk of dementia. But first let’s talk about the risk factors.

Risk Factors It won’t come as a surprise that the biggest risk factor for dementia is age—hence the joke “old-timer’s disease”—though the risk of vascular dementia increases earlier, at around 50. The risk of Alzheimer’s doubles every five years after age sixty-five. Only about 10 percent of people between sixty-five and seventy-four get Alzheimer’s; by

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eighty-five almost 50 percent of people have some kind of dementia. These numbers are a bit frightening, but keep in mind that this also means that half of the very old never get Alzheimer’s at all and very few people get it before they become very old. Family history is important, but probably not as important as you think. A kind of early onset Alzheimer’s (usually diagnosed before the age of 60, sometimes as early as the mid-twenties) is caused by mutations in several chromosomes and has a strong hereditary connection. This type of Alzheimer’s is very rare, however. Only about 5 percent of the people who have Alzheimer’s have this kind. Otherwise the family connection is pretty weak. Even if you have a first degree relative (a parent or a sibling) with dementia, your risk is increased only slightly. So if someone in your family has dementia, don’t panic—at least not about your own risk. No one has figured out why yet, but being female seems to put you at slightly greater risk of Alzheimer’s after the age of around 75, even when adjusting for the fact that at that age there are more women alive than men. The data is conflicting on this, but there has been some evidence that women who have had hysterectomies without estrogen replacement have a higher rate of Alzheimer’s. Preliminary data from the Women’s Health Initiative study indicates that estrogen replacement might decrease the risk of dementia. It could be that estrogen deficiency contributes to the problem, but this is still being studied. A history of alcohol and/or drug abuse puts you at greater risk for dementia. That drug abuse endangers the brain is not surprising, but alcohol has been shown in moderate amounts to actually prevent

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Alzheimer’s. As best we can tell, it is quite simply that, as with so many things, a little bit of alcohol is exceptionally good for you while a lot is exceedingly dangerous (for more on the risks/benefits of alcohol use, see chapter 2 on cardiovascular disease). Cardiovascular disease, including high blood pressure, atherosclerosis, and high cholesterol, increases your risk of dementia. The connection with vascular dementia is obvious, but cardiovascular disease also seems to pose an increased risk of Alzheimer’s. This is probably because the same mechanisms that cause the arterial blockage that leads to heart attacks and strokes also deny the brain the blood and vital nutrients it needs to function properly. Inflammation seems to play a role as well. As we saw in the previous chapter, diabetes works its horrors in almost every area of the body. The brain is no exception. Diabetes contributes to hypertension and heart disease, so that is part of the problem. But it is also likely that uncontrolled blood sugar interferes with memory and other cognitive functions. A personal history of depression can also increase the risk of dementia. The biochemical causes and effects of depression are not yet well understood (but are currently being studied), yet it is clear that depression does cause significant changes in the brain. Some of these changes may directly or indirectly contribute to dementia. However, it is important to keep in mind that in the elderly, depression itself can cause the memory loss and confusion that is the hallmark of dementia. If you or a loved one is showing symptoms of dementia, the problem may in fact be depression. Lack of exercise is also a familiar but undeniable troublemaker

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here. For many of the same reasons that a sedentary lifestyle contributes to heart disease and diabetes, it also contributes to dementia. But lack of exercise probably assists in the development of Alzheimer’s all on its own. Exercise increases blood flow. Even if your sedentary lifestyle doesn’t lead to heart disease or diabetes, the reduced blood flow to the brain alone can push you toward dementia. Another contributor to Alzheimer’s is previous head trauma. Those knocks on the head that cause concussions in so many young athletes are often forgotten once the initial trauma is over. But they can come back to haunt them long after their days on the playing field have passed. Even one good concussion can increase your risk a bit. Repeated head injury is even more of a problem. And last on our list, but probably near the top in terms of importance, is smoking. Of course smoking contributes to cardiovascular disease and so indirectly contributes to dementia. But there may be a more direct connection as well. There has been some confusion about the role of nicotine in Alzheimer’s. Several years ago, some research indicated that nicotine (only one of the many dangerous compounds in cigarettes) might actually prevent Alzheimer’s. This set off a flurry of research, most of which contradicted the previous results and indicated that not only was nicotine not a preventive, it actually contributes to the brain damage that causes Alzheimer’s. Even if research did bear out some beneficial effect of nicotine, taking up smoking to prevent Alzheimer’s would not be a good strategy. You would be increasing your risk of a host of health problems (including vascular dementia) far more than you would be reducing your risk of this one illness. If nicotine itself has any value, and that

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still has to be worked out in the lab, it will most likely find its way into a pharmaceutical application.

Reducing Those Risks Because there is so much still to be learned about dementia, and we don’t know exactly what causes it, people tend to think that there’s not much that can be done to prevent it. But as you could tell from looking at the risk factors, there are several good strategies that promise to make a dent in your chances of ending up very confused. The obvious connection between cardiovascular disease and dementia suggest that the same strategies you take to protect your heart should also help protect your brain. And indeed research is bearing this out. Eating well (see chapters two, three and four), getting plenty of exercise, and not smoking are the all-around health promoters. While the same diet that is good for preventing heart disease is probably prudent for preventing dementia, a slew of studies on particular foods has produced some interesting results. People with Alzheimer’s have been shown to have low levels of a particular type of Omega 3 fatty acid. This is consistent with other risk factors (Omega 3’s seem to be preventive of heart disease as well) and indicates that adding fish, particularly tuna and salmon would be a good idea. Antioxidants, such as vitamins C, E, and A, selenium, and the various caretenoids, also show promise in maintaining brain health. Vitamins C and E particularly have been associated with better memory and less loss of cognitive abilities. The best way to get plenty of antioxidants in your diet is to put some color on your plate. Colorful foods such as blueberries, cantaloupe, broccoli, leafy greens

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and tomatoes are all good sources of antioxidants. Tea, especially but not only green tea, is also a good source of antioxidants as well as several other compounds that may help reduce the risk of dementia. When it comes to exercise, the steps you want to take are simple. Just take more steps. Regular exercise has long been considered an important part of any dementia reduction plan. But recent research suggests that simply walking regularly can make a huge difference. While the amount of exercise recommended for weight control or diabetes prevention is somewhat more demanding, easy walking for as little as three hours a week can greatly reduce the risk of Alzheimer’s. A recent study (just one so far) has also indicated that a variety of types of activity is better than doing the same thing every day. Perhaps boredom contributes to dementia? As you can see, the same type of lifestyle that protects against heart disease and diabetes is what you want to aim for if you are trying to prevent dementia. But when it comes to protecting your brain, there is more to the equation. The old phrase “use it or lose it” seems to apply to the brain as well as to the muscles. Staying active mentally as well as physically is likely to reduce the risk of dementia. Studies have shown, however, that it is not good enough to just do mentally demanding tasks. You have to learn new things. Say you are an economist and spend your days crunching data and analyzing complex and ever-changing economic relationships. You use your brain on a daily basis. But you are doing something that you are good at, have been good at for your entire career. You don’t have to learn anything new to do it. In order to prevent Alzheimer’s, you need to take on mental challenges.

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Famous People with Alzheimer’s Joe Adcock, baseball player

Rita Hayworth, actress

Dana Andrews, actor

Raul Silva Henriquez, Roman Catholic cardinal, human rights advocate

George Balanchine, dancer, choreographer James Brooks, artist

Charlton Heston, actor and political activist

Charles Bronson, actor, film director

Jack Lord, actor

Abe Burrows, author Joyce Chen, chef Perry Como, singer, entertainer Aaron Copeland, composer Willem DeKooning, artist James Doohan, actor Thomas Dorsey, singer Arlene Francis, actor Mike Frankovich, film producer John Douglas French, physician Barry Goldwater, Senator of Arizona

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Ross MacDonald, author Burgess Meredith, actor Iris Murdoch, author Otto Preminger, director Ronald Reagan, fortieth president Sugar Ray Robinson, boxer Norman Rockwell, artist Betty Schwartz, Olympic gold medal winner in track events Alfred Van Vogt, science fiction writer E.B. White, author Harold Wilson, British prime minister


Working crossword puzzles and playing Scrabble may help, but an even better choice is learning a new language, taking up a musical instrument, or learning some other complex new skill. Reading is good, too, but once again, zipping through spy thrillers or mystery novels won’t do the trick. Seek out reading material that challenges you, something you have to think hard about. Relationships are important, too. People who have good social networks seem to have a lower risk of dementia. This does not mean you have to become a social butterfly. Good solid relationships with one’s spouse, children, and a few close friends or family members can be very helpful. The jury is still out on hormone replacement therapy (HRT). There has been some indication that HRT can help prevent dementia, but more evidence that it is risky for the cardiovascular system (and increases the risk of breast cancer as well). At this point, it doesn’t seem prudent to take HRT to try to prevent dementia. It seems almost too easy, but if you stay active, both physically and mentally, take good care of your health in general, and stay in touch with those you love, you are probably doing more than you realize to reduce your chances of any kind of dementia.

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Osteoporosis and Arthritis Bad Bones T H E

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If you are a non-Hispanic white woman, your lifetime risk of hip fracture (the most serious result of osteoporosis) is 1 in 6. Men and black women are at a slightly lower risk. Approximately 20 million Americans suffer from osteoarthritis. Dry Bones—and Not So Dry Bones When we see bones, usually in biology class or from a dead animal we come across on a hike, the bones are dry and crusty—dead. Living bone, however, is a different matter. While we are alive, bone is living tissue and is continually being torn down and rebuilt.

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During the first thirty or so years of life, the emphasis is on building bone. At about age thirty-five or so you reach what experts call “peak bone mass.” After this point, loss exceeds gains. This is normal. Some bone building does still go on after age thirty-five, though, and this is important. You don’t want to lose any more than you have to and even a little bit of building helps. We’ll talk about how to nudge this balance in your favor a bit later. When you lose too much bone mass, however, the bones become thin and weak, a condition called osteoporosis, which means “porous bones.” Having low bone mass or porous bones is not in and of itself painful, nor is it a problem, really, as long as low bone mass is all that happens. Asian women tend to have very low bone mass, but relatively few fractures. However in most people, low bone mass is an indication that a problem may be one on the way. Low bone mass is itself actually a risk factor for fracture (and the loss of height and stooped posture that accompanies spinal fractures) and fracture is what you want to avoid.

Sins of the Past A common nightmare is finding out that some act will kill you—perhaps being told that if you open a certain door or look in a certain box that you will die—and then realizing that you’ve already done it. You’re doomed. Osteoporosis can seem something like that dream. Part of what determines how much bone you have when you are old is how much bone you have at peak bone mass, and that is determined by lifestyle factors that occurred long before you even gave the matter any thought. A good diet and regular exercise during

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childhood, and especially adolescence, is the best way to prevent osteoporosis in old age. For those of us who spent the wastrel years of youth lying around listening to Rolling Stones albums and chugging sodas, it seems that the damage is done. We long ago doomed ourselves to a stooped and aching old age of crumbling bones. Fortunately, however, that is not quite the whole story. There is much that can be done to prevent or reduce the ravages of osteoporosis, even if you do get a late start. And the story itself is really not quite such a nightmare as you might think from reading about this disease.

Disease of the Month Osteoporosis has gotten a lot of attention in recent years. It’s hard to imagine it now, when you can open the pages of almost any women’s magazine and see cautionary photos of stooped old women and happy young ones cheerfully measuring their height and suggesting we all take medications to prevent this scourge from getting us. But before about 1980 few people had never heard of osteoporosis. This is not because the condition was unknown, but because nothing could be done about it and most medical professionals thought of it less as a disease to be treated than as a not uncommon feature of old age—especially in women. All that changed when researchers noticed a connection between the hormone estrogen and bone loss. Men get osteoporosis less often and later in life than do women, and the rate of bone loss in women accelerates at menopause. Suddenly there seemed to be something we could do, treat it with hormones, a prescription that may have proved more profitable for the manufacturers of hormones than helpful for women with thinning bones. In

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addition, research began to look into the connection between thinning bones and calcium and vitamin D intake, a development that was not lost on the dairy industry. Much was being learned about this condition and many people stood to make a lot of money if it was considered a disease, and a very frightening one at that. Next thing you know, the amount of bone mass considered problematic is getting higher and higher and healthy middle-aged women are worried sick that they are going to fall apart just any minute. Despite the hype, osteoporosis is frightening. For younger women, fractures of the spine that lead to loss of height and stooped posture may be the most feared consequence of osteoporosis. Nonetheless hip fractures are the most devastating consequence, although fractures of the wrist, upper arm, and spine are also common. Hip fractures are the beginning of the end for many otherwise healthy people. Twenty-four percent of people who fracture their hips die within the first year and many more are permanently disabled, often spending the rest of their lives in nursing homes. The pain and suffering caused by these fractures is very real and a very serious problem for those who experience the nasty results of this disease. However, many women are being frightened out of proportion to the risk. Only about 25 percent of women ever become seriously inconvenienced by thinning bones, and most who do suffer trouble only very late in life. And frankly, the emphasis on preventing this disease with medications (hormones and other, newer types of drugs) and exaggerated descriptions of the risk may have distracted us from the simple measures that have been proven to prevent the

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disease. I am certainly not making light of this condition. The results of porous bones can be tragic indeed. The pain and suffering caused by osteoporosis and the fractures it often leads to are very real. I just want to keep the issue in perspective. Many studies have shown that you don’t have to increase your risk of other diseases (by taking hormones or other potentially risky medications) to significantly reduce your risk of osteoporosis. But before we talk about how to do that, let’s get an idea of just what puts you at risk.

Risk Factors It is very important to keep in mind that osteoporosis (a condition of less than optimal bone mass) is not the same thing as fractures. One can and very often does lead to the other, but the risk factors are not the same. Osteoporosis is not the only risk factor for fracture. General frailty, lack of muscle, poor balance, poor vision, and smoking all contribute to fracture risk. If you have risk factors for osteoporosis (but don’t yet have osteoporosis), this does not mean that you are at high risk for fractures. It does, however, mean that you are more likely than others to have low bone mass and would be very wise to take steps to increase it in order to prevent fractures and a collapsing spine on down the road. It is sort of like saying that if you are at risk for alcoholism, you must be careful because if you succumb to that risk, then you’ll be at greater risk for liver disease. However, just being at risk for alcoholism doesn’t put you at risk for liver disease. I stress this point because the steps to prevent fracture are not the same as the steps to prevent osteoporosis in the first place. Having said that, let’s look at the risk factors for osteoporosis.

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The number one risk factor for osteoporosis is advanced age. We all lose bone mass as we age. Keep in mind that some bone loss as you age is normal. Graying hair and wrinkled skin are not considered diseases (at least not yet!) and a certain amount of bone loss shouldn’t be either. The problem is when we lose too much bone. The older we get, the more we lose. That is why osteoporosis becomes more common as people age. Keep in mind that we are talking about the risk of osteoporosis, thinning bones, not fracture. You can have less than optimal bone mass for many years before you experience any obvious problems, such as fractures. For women the increased risk begins around 50 and continues to increase as they age. However, even in women, most fractures occur after the age of 80. Age is a problem not just because of declining estrogen (the primary reason risk jumps at around age 50 in women), but because older people are less efficient in absorbing calcium and other nutrients that keep bones strong. In addition the elderly are less likely to eat well and often get less exercise than younger people. We think of osteoporosis as a disease of little old ladies, and this is at least partly true. But men do get it. Age is even more of a risk factor for men, actually. From age 50 or so, around the time of menopause, women are at greater risk than men. At about 75, though, the risk evens out and men are just as much at risk as women. Being small-boned and thin also puts you at greater risk. The simple fact is that smaller bones tend to be less dense. Not weighing very much seems to increase risk as well. This may be one of the few chronic diseases of ageing in which a few extra pounds can help more than they hurt. Being thin is a preventive for most chronic dis-

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eases, but for osteoporosis, it is certainly possible to be too thin. Estrogen is produced in fat, so that may be part of the reason. Don’t take this an excuse to gorge on donuts, though. The health risks of being overweight are enormous and the reduction in risk of osteoporosis you’ll get by gaining a few pounds is probably not worth it, unless you are already underweight. If your BMI is under 18.5, however, it might be a good idea to try to gain a little weight (by eating more healthful foods of course. Put down those donuts!).

An A for Vitamin D As I was putting the finishing touches on this book, lots of new research was coming out on vitamin D. The evidence is getting pretty strong, compelling even, that vitamin D plays a huge role in many health conditions.

For some reason Caucasians, particularly light-skinned, northern European types have higher rates of osteoporosis. This may or may not have something to do with sunlight and vitamin D (more on this later). It could be genetic. No one is exactly sure. A family history of osteoporosis, and especially family history of hip fracture, is another risk factor. If your mother or father had a broken bone after forty or a broken hip at any age, you should be extra cautious and take the prevention steps below very seriously. Lack of exercise. As more and research is being done on this disease it is becoming increasingly evident that lack of exercise is a major contributor. Exercise builds bone. But it also builds muscle.

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And muscle helps in several ways. Muscle processes certain nutrients more efficiently than does fat. In addition, when it comes to the risk of fracture, where falling is the greatest risk, good muscle development not only helps you keep your balance, it also provides a good cushion if you do fall. Is there an illness we’ve talked about so far that isn’t made worse by smoking? You guessed it; smoking is incredibly bad for the bones. Smoking inactivates estrogen, so that is at least part of the problem. But it also interferes with the absorption of many other nutrients. And of course if you have no stamina or are chronically short of breath because you are a smoker, you aren’t likely to get enough exercise. Once again, alcohol is the Janus-faced food. Some pretty good evidence indicates that a little bit can actually help. Too much alcohol, on the other hand, can be a problem. Alcohol interferes with calcium balance and hormonal balance as well as absorption of many nutrients—all things that can help speed the process of thinning bones. Caffeine is still somewhat questionable. Small amounts, even moderate amounts, are probably fine. But if you drink more than 4 or so cups of coffee or lots of soft drinks (a problem for so many other diseases) daily, you may be increasing your risk of osteoporosis somewhat. And of course the most talked about risk factor is too little calcium and vitamin D. Not getting enough of these essential nutrients (and other ones as well, see below) is most definitely a contributor to osteoporosis. How important this is relative to other factors (such as exercise) is a vexed question. Because this is such an important, com-

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plex, and most important, modifiable risk factor, we’ll give it a great deal of attention in the prevention section. In addition to the above risk factors, ones that affect almost every one (at least almost all women), some medications can also cause thinning bones. Steroids, thyroid medications, some antacids and some anticonvulsants can cause bone problems. Quite a few drugs used for mental illness are hard on the bones as well, including, according to some recent research, antidepressants. Most of these are not drugs that you have much option about taking—if you need them, you really need them—but if you are taking something that might interfere with your bone health, you’ll want to make sure you are doing everything else you can to take care of those bones.

Boning Up For many women the short answer to osteoporosis prevention is HRT. And indeed, reducing the risk of osteoporosis is one of the few benefits of hormone replacement therapy (aside from treating menopausal symptoms). The risks of HRT, however, seem to far outweigh the benefits. Few women are willing to increase their risk of breast cancer, heart attack, blood clots, and stroke in order to reduce the risk of osteoporosis—especially when the same amount of risk reduction can be achieved with much less risky methods. The single best step you can take to reduce your risk of thin bones is to exercise more. I really can’t emphasize enough how important it is to exercise if you want to keep your bones strong. Several studies have shown the tremendous value of exercise in preventing both osteoporosis and fractures. One large NIH study found

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that women who exercised regularly had 36 percent fewer hip fractures than those who did not exercise. If you are already doing aerobic exercise for your heart, you are already helping your bones. Adding weight bearing exercise will help even more. This does not necessarily mean lifting weights, although lifting small hand weights can be a good idea. What you want to do is provide some resistance for your bones. This can be done in a number of ways. As in most things, walking is an excellent choice. It is a low-risk, high-benefit means of keeping bones strong. One study indicated that women who garden have a lower than average risk of osteoporosis. Researchers can only speculate about why, but it seems to me that the combination of movement, lifting, and being out in the sunshine makes gardening an excellent choice. In addition, if you are a vegetable gardener, you’re probably eating well, too.

Not Just Calcium When it comes to diet, we are back in that nightmare we talked about earlier. Most of the damage done by a poor diet was done when we were young and not thinking too much about nutrition. Although for many of us who grew up before the ubiquity of fast food and sodas, we might have gotten off to a better start than we realize. In any case, while calcium is crucial to good bone health, it may have been somewhat overrated in recent years. It may come as a surprise to many, but the nations that have the highest intake of dairy foods also have the highest rates of osteoporosis. This may be (in fact probably is) because dairy products are high in protein. Cultures with a high dairy intake typically have a high intake of meat

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as well. High protein diets have been shown repeatedly to increase the risk of osteoporosis. This is because when you eat a lot of protein, you excrete more calcium. So even if you are taking in a lot of calcium if you are excreting more of it than you keep, you are still at a net loss for calcium. That’s why it is a good idea to keep dairy and meat intake moderate and try to get at least some of your calcium from vegetable sources. Almonds, broccoli, greens (kale, turnip greens, collards), okra, and tofu are all good choices if you are trying to get more calcium in your diet. But calcium, as important as it is, is not the whole story. Like a car without a driver, calcium is not much good without vitamin D. And vitamin D is far more important than most people realize. Although we call it “vitamin” D, it is actually a hormone, or at least it fits the definition of one (a substance made by an organ or tissue in one part of the body that has a regulatory effect on other parts of the body). In addition to other amazing things vitamin D does, it regulates calcium absorption. Without D, all that calcium wouldn’t do any good. The primary way we get vitamin D is from the sun. When the skin is exposed to sunlight, it manufactures vitamin D. Most people these days don’t get enough D. Older people, especially, are at risk of vitamin D deficiency, in part because, as we noticed earlier, as you get older, it can be more difficult to metabolize vitamins. But also, older folks are less likely to get out in the sun each day. And quite frankly, they aren’t the only ones. Many of us spend our days in offices far from windows. And when we do get out, we are so worried about skin cancer that we slather ourselves with sunscreen, drape ourselves with clothing and cancel out the benefits of the sun.

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It is important to prevent sunburn, of course. But 15 minutes a day of sun on skin (exposed forearms are fine) can do a world of good. Of course, for those who live at higher latitudes, this is really not much of an option during almost half the year. Supplements are the next best choice. Be careful, though, too much vitamin D (not likely to happen from moderate, responsible sun exposure, but a distinct possibility with supplements) can be toxic. Don’t go overboard. While this is very much still a work in progress, the research is pretty clear that if your aim is to prevent osteoporosis (and thereby reduce your changes of suffering a debilitating fracture later in life), you best strategy is to stay active and eat well (including a wide variety of calcium containing foods) and make sure you get enough vitamin D one way or another.

Arthritis Like diabetes, arthritis comes in two main forms (Even within these divisions, there are many types of arthritis. Plain old osteoarthritis is by far the most common form. We will limit the discussion here to that type.)—very different in causes, but similar in effects. Rheumatoid arthritis (RA) is a systemic disease, and is believed to be, like type 1 diabetes, an autoimmune disease. More and more is being understood about rheumatoid arthritis, but at this point, nothing is known about how to prevent it. A more common form of arthritis is osteoarthritis (OA). It is often called a “wear and tear” disease. Most people over the age of 40 have some degree of OA. How bad and how early it hits is something that can be modified, however.

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OA is a degenerative disease of the joints. The part of the joint that degenerates is the cartilage. Cartilage is a sponge-like material that covers and cushions the ends of the joint where bone meets bone. Cartilage works something like a shock absorber in the joint. It also reduces friction as the bones move against one another. When the cartilage begins to wear out, the bones rub against one another without enough protective cartilage in between. This causes the pain, stiffness, and limited range of motion that is characteristic of arthritis. This process can occur in any joint, but is most common in the knees, hips, back, neck and hands.

Risk Factors Osteoarthritis is very common. Even animals get it. While most people eventually develop some arthritis in their joints, most do not feel any pain as a result. Nonetheless, age is the biggest risk factor. The older you are, the greater chance that you’ll have some arthritis in one joint or another. It’s interesting, though, that after around age seventy-five, the increase seems to taper off. If you make it to seventy-five without any arthritis, you may escape it altogether. As you may have noticed in your own family, family history is a risk factor for some kinds of OA. Arthritis of the hands is especially likely to occur in people whose parents had the disease. Here’s another familiar risk factor. Being overweight increases your risk. Overweight women are about nine times as likely to get osteoarthritis, while in men the risk is increased by about four times (more on the gender gap in a minute). This makes sense because the more weight you carry the more stress you are putting on your joints

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(and those important shock absorbers), especially the hips and knees. It’s kind of like carrying too much cargo in your car. Even if the engine can pull it, it can be rough on the suspension. Being female puts you at greater risk as well, whether or not you are overweight. Women are about twice as likely as men to develop OA. Part of the reason for this is that women tend to live longer than men. But that cannot account for all of the increased risk. As always, when women have either a higher or a lower rate of some disease, estrogen is the prime suspect. However, there is not much evidence that estrogen plays a major role here. Having had a previous injury to a joint (particularly a weightbearing joint such as the knee) increases risk. Both the injury and surgery to repair knee injuries can increase the chances of getting OA later in life. That said, exercise itself, even fairly strenuous exercise such as jogging or running does not seem to increase the risk of OA. Ironically, even though it is often called the “wear and tear” disease using those joints regularly does not accelerate the process of degeneration. This is probably for two main reasons. First, good muscle development (more on this below) is very protective. And second, exercise helps keep fluid around the joint reducing the negative effects of use. There has been some evidence that our old friend vitamin D may play a big role in preventing OA. Vitamin D interferes with the activation of certain enzymes that accelerate the breakdown of cartilage. Other vitamins and minerals probably play a role as well, but there is not much clear evidence on this as yet. And surprisingly, people who smoke seem to have a lower risk of

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OA than non-smokers. (It finally happened. We came across a disease for which smoking is not a risk factor.) The reason is not known. This is good news to smokers, I suppose, but the risks of smoking so far outweigh any reduced risk of OA that it is hardly worth mentioning. I include it here only because I’ve spent so much time trashing smoking that it wouldn’t seem fair if I didn’t mention this small benefit. Don’t worry, though, I’ll be back on my antismoking tear soon enough.

Joint Protection Keeping joints healthy and reducing risk of OA is pretty much a matter of common sense. We won’t be spending much time comparing competing theories in this section. As I mentioned above, though it may seem intuitively that resting joints is the best way to protect them, using them is actually your best approach. Of course, this is one of those cases where the adage “moderation in all things” applies. Exercise helps by strengthening the muscles around the joints. Strong muscles provide protection and cushioning and shock absorption of their own. It also increases flexibility, which is a big help in keeping joints from getting stiff. And of course, exercise can keep you lean and reduce another risk factor, overweight. It is important, especially for the older crowd, not to overdo it. Regular brisk walking is a great help for the hips and knees and is relatively low risk. Probably the most important thing to keep in mind when exercising to reduce OA risk, is to completely lose the idea of “no pain, no gain.” If it hurts, don’t do it, is great advice (in

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most things, really). Simple adjustments, such as walking a bit slower or running on a dirt path instead of concrete or asphalt can make a big difference. Also be sure to wear good-fitting, good-quality shoes. The right kind of shoes—not just when you are on the track, but all of the time—can greatly reduce discomfort from sore bones. Some other things that may be helpful don’t seem as obvious, but can make a big difference: Keeping well-hydrated is very important. The fluid around your joints (synovial fluid) lubricates the joints during movement. But if, like many in the modern world, you are in a state of chronic dehydration, your body won’t have enough total fluid to keep your joints adequately lubricated. Be sure to get your fluids from water, high-water content fruits and veggies, or fruit juices (if you aren’t watching calories and don’t have blood sugar control issues). Caffeine and alcohol are dehydrating and don’t offer much overall benefit when it comes to hydration. Even more surprisingly, getting enough sleep is very helpful as well. Much of the body’s repair work is done during sleep. Small damage that is done during the day is repaired during sleep. Not getting enough sleep shortchanges the repair process and leaves joints less able to cope with normal stress. These days it is common for people to get by on too little sleep. This is not a good idea. So far most of the prevention we’ve talked about has been most helpful for preventing OA in the knees and hips. When it comes to the rest of the body, one of your best bets is to watch your posture. Slumping over a desk or keyboard, curving your spine around to the side when you write, slouching in chairs while reading or watching television, holding a telephone between the ear and shoulder—all of

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these are murder on the back and shoulders. When your mother used to nag you to “stand up straight,” she really did have your best interest at heart. Making sure that you maintain good posture when sitting as well as standing can mean the difference between peace and pain. If you spend a large portion of your day sitting at a desk or computer, make sure you have a well-designed chair and that your computer workstation is arranged in a way that encourages you to maintain good posture. Proper lifting techniques are also very important. It’s not just acute injuries that are caused by poor lifting technique. Years of bad habits can result in cumulative damage to joints.

Food, Again Eating habits are crucial to reducing risks of most major diseases. With OA, diet has not been proven to be a major factor, but it does play a role. As with osteoporosis, calcium and vitamin D are important. Even though with OA, it is break down of cartilage, not bone, that causes the problem, having strong bones can be a big help. (When the cartilage is weak or thin, the bones take more stress. The stronger they are, the better they withstand it.) In addition, some studies (though there is not a tremendous body of research supporting this), suggest that vitamins A, C, and E might be protective of cartilage. Fish oils have also shown some promise in keep joints mobile and well-lubricated. Once again, the same basic dietary principles we’ve talked about in other chapters apply here. Eat well and be sure to include plenty of fruits and vegetables.

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Gastrointestinal Diseases Stop Bellyaching T H E

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Between 60-70 million Americans suffer from some form of digestive disorder, most of which are not life-threatening. GERD Gastrointestinal reflux disease, commonly known by the much shorter and cuter acronym, GERD, is an increasingly common problem in the United States. A bit of indigestion or even acid reflux (when you get that miserable feeling of stomach acid creeping back into your throat) is nothing to worry about, unpleasant as it is. Most people have it from time to time. But if it happens often, it could indicate a potentially serious problem. In fact, the main difference between, run-of-the-mill, don’t-worry-about-it indigestion and GERD is frequency. If you find yourself reaching for the Pepcid more than a couple of times a month, it is probably a good idea to have a talk

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with your doctor—even if you are getting adequate relief from the medications. GERD is typically managed with either over-the-counter or prescription medications and is rarely a huge problem, but it is one of the leading risk factors for esophageal cancer. GERD sometimes leads to a condition called Barrett’s esophagus and people with Barrett’s are at much higher risk for esophageal cancer. I don’t want to raise too many alarms here. Esophageal cancer is a rare cancer. The problem is that it is on the rise—in a big way. In fact, at the moment it is the most rapidly increasing cancer is the United States. In the past 30 years the incidence of esophageal cancer has increased some 600 percent. On top of that, the survival rate once the cancer is established is only around 10 percent (some estimates are even lower). Keep in mind that even with the recent increase, this cancer is still rare, and by far most people who have GERD do not end up with cancer. Nonetheless, it is something you don’t want to take lightly.

Risk Factors for GERD The risk factors for GERD pretty much explain the reason for the recent increase. Being overweight is a big risk factor, as is eating large, high fat meals. (See how our current society is just sitting duck for this problem?) Again, smoking increases risk as well. Alcohol use (more than a few drinks a day) and stress are also considered prime risk factors. Diets high in spicy foods and/or caffeinated beverages have also been suggested as risk factors, but the evidence on this is not too strong. Some people have problems when they eat too soon before going to bed or when they exercise shortly after eating. But again, studies on how these things affect people are scarce. In any

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case, this is one disease, unlike hypertension and diabetes, that is not silent. When you have digestive problems, you usually know it. Pay close attention to what gives you problems and avoid those foods and behaviors.

GERD Prevention Beyond paying close attention to your body and avoiding what ails you, good preventive measures include keeping a healthy weight, eating small meals, avoiding high calorie, high fat, highly processed foods, and not drinking too much. And, of course, don’t smoke. Told you I’d be back on that smoking thing soon enough.

Irritable Bowel Syndrome The bowel may be irritated, but people who have this problem are more than just irritated. They are seriously inconvenienced and often plain miserable. IBS, as it is called, differs from most of the diseases we’ve been talking about in this book in that it often begins in early adulthood. It is also quite common. Some estimates suggest that one in five Americans suffer from IBS. IBS is characterized by bouts of cramping, bloating, diarrhea and sometimes constipation. The good news is that though IBS is inconvenient and uncomfortable, it causes no lasting harm. As far as we know, it doesn’t lead to bleeding, ulcers or cancer.

Risk Factors for IBS Being female is a big risk factor. In fact, 80 percent of IBS patients are women. This may have something to do with hormones (always

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the first suspect when women get a disease more often than men), or perhaps it reflects the way women deal with stress (more on stress in a moment). IBS also tends to plague teens and young adults more than it does older people. It is most common in people who are between twenty and forty. Stress can contribute to IBS as well. Certain foods seem to trigger episodes in people who are prone to IBS, but do not seem to be risk factors for getting the problem in the first place.

IBS Prevention The only real preventive measures for IBS are eating small meals, and avoiding stress and foods or activities that seem to trigger it. Because stress is such a big risk factor and trigger of IBS, reducing stress and learning how to deal with it are good means of prevention. Relaxation techniques, such as meditation, have proven useful for many. It can be important, however, to locate and deal with any psychological problems that may be contributing to the problem.

Gastritis Gastritis is actually a group of disorders, but all are characterized by an inflammation of the lining of the stomach. The chemicals in the stomach that digest food are very caustic. You may have heard that one of the stomach acids, hydrochloric acid, is strong enough to dissolve iron nails, and this is true. Fortunately, the tissues of the stomach are protected by several layers of protective material. It is when these protective materials are compromised in some way, that gastritis develops. Gastritis usually exhibits itself as stomach pain, bloating, nausea and vomiting.

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Risk Factors for Gastritis Probably the biggest risk factor for gastritis is infection with the Helicobacter pylori bacteria. Infection with this little corkscrewshaped rascal can also cause peptic ulcers and stomach cancer. Don’t panic, though. Infection with this bacteria is extremely common. Most people in the world are infected, although less so in the West. And most people who have the infection get neither cancer, nor ulcers, nor gastritis. It is likely that Helicobacter pylori works along with other factors to initiate these diseases. Researchers are also looking into the possibility that a reduction in the number of people with H. pylori is part of the cause of the rise in esophageal cancer. Our little microbial companions can do us good as well as harm and it can be difficult to sort through all the relationships. In any case, there are other risk factors that are more amenable to change. Frequent use of NSAIDs (non-steroidal anti-inflammatory drugs, such as Aspirin, Ibuprofen, Naproxen, and Cox-2 inhibitors) can increase your risk. Excessive alcohol use and cocaine use can contribute as well. Both alcohol and cocaine can irritate the stomach lining. Being black, Native American, or Hispanic also puts you at higher risk. Because the stomach lining thins with age (everything wears out, doesn’t it?) people over sixty are at increased risk as well.

Gastritis Prevention The only practical prevention is to be cautious in your use of pain medications and alcohol. NSAIDs are often necessary, especially for people with severe arthritis, and aspirin has many benefits, the most well-studied being its potential for reducing the risk of heart disease

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(see chapter two). However, these drugs should be used with extreme caution. If you take a daily aspirin for heart disease prevention, a small dosage should be ample. If you take NSAIDs for relief of pain and inflammation, you’ll want to use the lowest does possible and keep in touch with your doctor about any gastrointestinal problems you may develop.

Diverticular Disease Diverticula are small pouches that protrude from the wall of the colon. Having these pouches is called diverticulosis. When they become infected or inflamed it is called diverticulitis. Diverticulosis (just having pouches) becomes more common as we age. About 10 percent of people over forty have these pouches; by age sixty the rate is about 50 percent. Between 10 and 25 percent of people with the pouches get diverticulitis. Diverticulosis usually doesn’t cause any symptoms, although some people experience cramps, bloating, and constipation as a result. Diverticulitis is another matter, however. It can cause all the above symptoms and pain as well, usually in the left side of the lower abdomen. If the pouches are infected, fever, chills, nausea and vomiting can also occur. Untreated it can lead to bleeding, blockages, and tears in the wall of the colon, although these extreme cases are rare.

Risk Factors for Diverticular Disease Obviously the risk factor for diverticulitis is diverticulosis. When it comes to getting the pouches in the first place, the two main risk factors are old age and eating a low-fiber diet. Incidence increases after

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the age of forty, and by age sixty almost half of the population has diverticulosis. Only a small percentage of those with diverticulosis ever experience symptoms or develop diverticulitis, however.

Diverticular Disease Prevention The key to avoiding the unpleasantness of diverticular disease is eating a diet high in fiber. Whole grains, fruits and vegetables are, once again, your best strategy.

Peptic Ulcer Peptic ulcer is fortunately becoming less common in the U.S. than it once was. This is probably because of the reduced incidence of Helicobacter pylori infection. Peptic ulcer is basically a sore or hole in the lining of the stomach (see gastritis above). For many years people thought that ulcers were caused by stress or spicy foods. It has been discovered, however, that most ulcers are caused by infection with the Helicobacter pylori bacteria (once again, see gastritis, above). Luckily it can usually be cured with a round of antibiotics.

Risk Factors for Peptic Ulcers Like gastritis, risk factors for peptic ulcers are infection with Helicobacter pylori and excessive use of NSAIDs. Alcohol abuse is also a risk factor.

Peptic Ulcer Prevention Once again, if you use NSAIDS, use them with care, and avoid drinking too much.

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Odds and Ends Most of the worrisome diseases we’ve discussed have fallen into handy categories—heart disease, cancer, bone diseases and so forth. But by working in this fashion, I’ve left out a couple of things that I think are worth a mention. So here in this last chapter, I’ll include just a few odds and ends along with some closing comments.

Age-Related Macular Degeneration Age-Related Macular Degeneration (AMD) is leading cause of vision loss in Americans over 60. AMD causes you to lose sight in the central part of your vision, making it difficult to recognize faces and making driving, reading, and other close tasks all but impossible. The causes of AMD are not fully understood, but risk factors are well-established, the primary one being advanced age. A family history of AMD also increases risk somewhat, as does smoking, hypertension, and excessive exposure to ultraviolet light. Preventive measures center on controlling hypertension, wearing good quality sunglasses when out in bright sunlight, and stopping smoking if you smoke. In addition, there is strong evidence that a diet high in fruits and vegetables is protective. Researchers are currently investigating the possibility that Omega-3 fatty acids, such as are found in fish might be protective as well. So far it is looking very likely.

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Allergies and Asthma Allergies occur when the immune system overreacts to substances that would normally be harmless. Pollens, molds and other common triggers of seasonal allergies pose no serious health threat. But the bodies of people with allergies react as if they do, creating no small amount of misery. Certain antibodies in the human immune system evolved to defend against parasites and other foreign substances entering the body. We rarely encounter these threats anymore, but our defense mechanisms are still on the job—and eager to see some action. It’s rather like having a huge, well-trained, fully-equipped army during peacetime. Small incidents can cause big trouble. And if it weren’t bad enough, allergies are on the rise. According to the National Institute of Allergy and Infectious Diseases, the incidence of hay fever (as well as many other types of allergies) has increased substantially in the past few decades. There has been much speculation as to why this is so. Some experts think increasing average temperatures may be creating ideal conditions for the growth of more pollens and molds, common allergy triggers. Increased pollution may also be a factor. My favorite theory, however, is what is known as the hygiene hypothesis. This intriguing and increasingly popular theory holds that because in the modern, developed world, we keep our environments cleaner and spend less time around farm animals, people are exposed to fewer allergens, such as dust mites and animal dander, when they are children. Young immune systems do not get a chance to learn to respond appropriately to these substances. When they do encounter allergens, their bodies overreact and the result is an overzealous, allergic response. At this point, this

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is still mostly speculation, although evidence is mounting in support of it. If it turns out to be true, the slovenly among us will have the last laugh. Allergies are no joke, though. Besides making millions of people miserable during the loveliest times of year, they often lead to asthma (a condition that can be life-threatening) in what allergists call “the allergic march” from allergies to asthma, so it is a good idea to keep allergies under control if you have them. The main risk factors for allergies are a family history of them— not too much you can do about that. However, you can do a lot to prevent allergic attacks. The first step is to find out what your particular triggers are (are you bothered by pollen? Dust mites? Animal dander? Mold?) and avoid those triggers. Avoiding them can take some doing sometimes (especially if you aren’t fond of vacuuming), but is certainly worth it if you have allergies. And if you aren’t sure what is triggering your attacks, a simple allergy skin test can settle the matter for you. Allergy shots are helpful to many people as well. These work a bit like vaccines by giving the body small doses of the offending substances to reduce the chances of an overreaction.

Kidney Stones Kidney stones are one of the most common disorders of the urinary tract and are also one of the most painful. Usually they are passed without any medical intervention, but the process is no fun whatsoever. Kidney stones are formed when chemicals in the urine crystallize and build up on the inner surface of the kidney. Like so many of the conditions we’ve discussed in this book, kidney stones seem to be

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on the rise—no one is sure why. Men are more likely to suffer from them than women, and whites more likely than African Americans. The incidence seems to increase with age, starting around forty. Having had one bout with kidney stones increases your risk for subsequent trouble. Certain inherited diseases and conditions can predispose you to kidney stones, but these are very rare. The very first and best step to preventing kidney stones is to drink lots of water. There are many types of kidney stones but one of the most common is formed from calcium. The data is a bit contradictory on whether dietary calcium contributes to or actually prevents stones. In any case, it is certainly not prudent to avoid calcium in order to prevent kidney stones, but it might be wise to avoid supplements. If you’ve had one bout with stones, you might want to discuss this with your doctor. It also may be helpful to avoid excessive amounts of meat, poultry and fish, because these foods can increase the acidity in your urine and contribute to the problem. Once again, though, it would probably not be prudent to make serious dietary changes just to prevent kidney stones if you haven’t already had trouble with them. Drinking more water, however, is an excellent idea.

Gallstones Gallstones are very different from kidney stones, but almost as painful, so they say. Gallstones form when the bile in the gallbladder hardens into little (or sometimes not so little—they can get as big as golf balls) hard rocks. Gallstones come in two types. Cholesterol stones account for about 80 percent of gallstones. As you can guess, they are made of hardened cholesterol. The other type of stone, pig-

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ment stones, are made of bilirubin. Risk factors for gallstones are being female, over sixty, and overweight. Native Americans, Mexican Americans, and people who have diabetes are at higher risk, as are people who have recently lost a lot of weight or have been fasting. In addition, pregnant women, women on hormone replacement therapy or birth control pills are at increased risk. There is also some evidence that cholesterol lowering medications increase risk, because although they lower the amount of cholesterol in the blood, they increase the amount secreted in bile. Maintaining a healthy weight is the best prevention, especially for women. Eating a diet low in animal fat has also been shown to reduce risk. There are several other diseases that you might have been wondering about, even concerned about, but did not find mentioned in this book. I have tried to cover most of the illnesses that you are likely to encounter for which you can make lifestyle changes to reduce your risk. Some diseases, unfortunately, just aren’t so amenable to lifestyle changes. I’ll just mention a few of these and their probable causes so that you’ll know why I didn’t cover them in earlier sections.

Multiple Sclerosis Multiple Sclerosis (MS) is an autoimmune disease. It affects the brain and spinal cord resulting in a wide array of symptoms, including weakness or paralysis in the extremities, vision disturbances, muscle atrophy, dizziness, difficulty urinating, slurred speech and fatigue. Women are at greater risk than men and most commonly experience their first attack between 20 and 40. Because MS is more common in

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northern latitudes, people who live up north are at higher risk. Family history also plays a role.

Parkinson’s Disease Parkinson’s is a neurological disease that causes tremors, stiffening in the limbs and trunk, and difficulty with movement. Parkinson’s is both chronic and progressive. There is no cure, but there are medications that slow the progression and make it easier to live with. The cause is not known, but there may be a connection with some industrial chemicals. Previous repeated head injuries, such as are experienced in boxing, may increase risk. There is probably some genetic component as well.

Herpes Simplex Herpes simplex is a viral infection that affects the mouth area (Type 1, HSV-1) and the genitals (mostly Type 2, HSV-2). Type 1 is very common. Ninety percent of adults have antibodies to Herpes Simplex Type 1 (HSV-1). It causes cold sores and fever blisters. These usually heal on their own in a week or so, but as anyone who has them can tell you, it’s not a pleasant experience. Outbreaks usually occur when the immune system is low (during or right after a cold or other infection) or when you are overly tired or under some type of emotional stress. HSV-1 is transmitted through infected saliva even when symptoms aren’t present. Prevention is all but impossible. You can prevent (or at least lessen) outbreaks by staying healthy generally and getting enough rest. Fortunately, genital herpes is not nearly so common—affecting

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perhaps 20 percent of adolescents and adults in the U.S. HSV-2 is transmitted sexually and manifests as genital sores, and can, in rare circumstances, lead to complications such as infection in the brain or the cornea. However, in many infected people outbreaks are rare and so mild that they don’t even know they have the infection. There is also some evidence that genital herpes makes one more susceptible to infection with HIV. The best way to prevent HSV-2 is to avoid sex with someone who has active lesions, and use condoms with anyone you are not sure is free of the virus.

Amyotrophic Lateral Sclerosis (ALS) ALS is often called Lou Gehrig’s Disease, after the New York Yankees first baseman who died of it. It is characterized by a gradual deterioration of the nerve cells that control the muscles, resulting in loss of control and eventual paralysis. The muscles that control breathing and swallowing are affected as well. It is always fatal and there is no known cure. It is more common in men than women and usually strikes after the age of forty. The cause is unknown. There has been speculation that it is an autoimmune disorder and/or that it is caused by an underlying virus. At this point there seems to be a genetic component in only a small percentage of cases.

Endometriosis Endometriosis occurs when endometrial tissue, the tissue that lines the uterus begins to grow in other places, such as in the ovaries or elsewhere in the pelvic cavity. Symptoms include abnormal uterine bleeding (including not having periods when you should), in some

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instances pain, and infertility. The cause is unknown, although there is some genetic predisposition. A depressed immune system seems to be a factor, suggesting an infectious cause, but little is known for certain at this point. There is no known way to prevent endometriosis.

Hepatitis A and B The hepatitis alphabet is actually up to E at the moment, but A and B are the most common. All the letters refer to diseases that affect the liver. Hepatitis A is usually contracted when stool from in infected person is transmitted to the mouth of another. (Sounds gross, I know, but it happens. In areas where sanitary conditions are poor, or when water is contaminated after a flood or other disaster it is especially common). Sometimes, especially in children, the infection causes no symptoms at all. When it does cause symptoms, they are typically things such as fever, tiredness, loss of appetite, nausea and/or abdominal pain, and jaundice. You are unlikely to suspect hepatitis from these symptoms (well, the jaundice might be a hint). A blood test can determine if you’ve ever had it, though. You can avoid getting or spreading hepatitis A by always washing up after using the bathroom or changing a diaper, and before eating or preparing food. Like hepatitis A, hepatitis B can cause no symptoms at all. When symptoms do occur, they are typically the same as hepatitis A—not obvious for what they are. Hepatitis B is spread primarily by blood and sexual contact. Health care workers, IV drug users, and people who have multiple sex partners are at high risk. You can avoid hepatitis B by practicing safe sex, not doing IV drugs, and not getting other people’s blood on

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Odds and Ends

you. Vaccines are available for both hepatitis A and B.

Age-Related Hearing Loss This one also goes by the name presbycusis. The hearing loss is progressive and starts with high frequency sounds. This is a common fact of ageing—about 25 percent of people between the ages of sixtyfive and seventy-five suffer from it, and the risk increases as we age. By seventy-five years, between 70 and 80 percent people have some degree of hearing loss. Exposure to loud noise, such as working with high-pitched factory machines or standing too close to the speakers at a Metallica concert can speed the process, but some degree of hearing loss is likely by the seventies or eighties even if you are a professional librarian who enjoys bird watching on the weekends. Presbycusis runs in families as well. If it’s in your genes you probably can’t prevent it altogether, but you should still wear hearing protection whenever you are around loud noises. One caveat: If you are starting to notice a decline in your hearing, don’t simply write it off to age. It could be earwax. Wax that gets trapped deep in the ear canal (too deep to get at with the washcloth) can stop up your ears and seriously interfere with hearing. Your doctor can easily unplug the channel.

Ulcers There are several kinds of ulcers, but generally they are lesions in the mucous membrane lining the digestive tract. It was once thought that stress and spicy food caused ulcers. These things probably do play a role, and may be the major factor in some ulcers, but it has

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recently been discovered that infection with the bacteria Helicobacter pylori is responsible for a large number of ulcers. Frequent use of NSAIDs (non-steroidal anti-inflammatory drugs, such as acetaminophen) can also cause ulcers. Thinning of the mucosa due to aging is probably also a factor.

Epilepsy Epilepsy is a condition in which the brain is subject to recurring seizures—abnormal electrical discharges of the neurons in the brain. In at least half of the cases, no one knows what caused the problem. In other cases it is caused by brain damage from birth trauma, a head injury, infection, or ingestion of certain toxins including mercury, lead or carbon monoxide.

Rules of Thumb After all these lists of risk factors and preventive measures, it seems as if when it comes down to preventing the diseases most likely to make us ill, mom was right all along. Eating well and getting outside to play are the best things you can do to stay healthy. Of course, that is much easier said than done and the devil is most certainly in the details. But I hope that after reading this book, you’ll have a much more comprehensive—and less confusing—idea of what it takes to stay healthy. Much of it is just luck, of course. But you can dramatically reduce your odds of having bad luck by taking just a few simple precautions. Thomas Jefferson said that he was a big believer in luck and that the harder he worked, the more of it he had. The same principle applies to health. It is very much a matter of luck, but by paying

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Odds and Ends

close attention to your lifestyle, you may find that you have much better luck. As you probably noticed as you read the previous chapters, a healthy lifestyle reduces the risk of most of the health problems we are at risk for. Getting enough sleep, enough exercise and eating real, whole foods is the basic ticket. After years of swimming in the health data, if I were asked the three most important things you can do to improve your health and reduce your risk of serious disease it would be this:

1. Move more. Get up and do something—not necessarily exercise, but something that gets you up and around.

2. Eat well. Eat good food: Fresh fruits and vegetables, good quality oils, whole grains, moderate amounts of wine or other alcohol, fish and low fat dairy (if you are not a vegetarian).

2. Enjoy your life. What good is good health if you are so obsessed with protecting it that you do not enjoy it? Perhaps the best tonic available is to spend time enjoying good food and fun with people you love. It is sure to improve your health and the quality of your life however long that life is.

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I N D E X

acid reflux, 195 alcohol, 49, 73, 77–78, 112–113 and joint health, 192 American Academy of Family Physicians, 37 American Cancer Society, 93 American Heart Association, 87, 90 American Institute of Cancer Research (AICR), 109 American Medical Association, 37 angioplasty, 62, 63 antioxidants, 158, 159 aspirin, 61–62, 199 beta-carotene, 16, 159, 160 beta cells, 131, 133 bile, 206 blood pressure, high. See high blood pressure blood sugar, 130–132, 133, 135, 136 BMI. See Body Mass Index Body Mass Index (BMI), 57, 141–143, 183 body shape, 128, 136 bone density, 177–178, 180–181 bypass surgery, 62–63 C-reactive protein, 79, 80 caffeine and GERD, 196 and joint health, 192 See also coffee, soft drinks calcium, 186–188, 193. See also dairy carbohydrates, 90–91, 148, 149–150 cartilage, 189, 193 cell phones, 46 Centers for Disease

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Control, 37 chemotherapy, 105, 124 cholesterol drugs to control, 66–70, 80 HDL, 56, 65 high, 55–56, 65 LDL, 56, 59, 65, 136 need for, 65 stones, 206 Circulation, 90 coffee, 184 colonoscopies, 104 CT scans, 106 dairy, 152, 157, 186–187. See also nutrition diabetes, as risk factor, 56 Diabetes Prevention Program (DPP), 139 diet. See nutrition diets, weight loss calorie reduction, 154 fiber in. See fiber low fat, 154 low carb, 154 See also obesity; inactivity under risk factors Dietary Approaches to Stopping Hypertension (DASH), 76–77, 78–79, 80 earwax, 211 Epic study, 85 estrogen, 65, 116, 183 exercise, 81, 115–116, 133–134, 138, 147, 161–162, 163–164, 213 effect on bone density, 185–186, 190 and cancer risk, 107–111, 115 effect on cholesterol, 68 effect on heart disease, 91–21 planning, 145–147

walking as, 186, 191 family history. See under risk factors fatigue, 90 fats dietary, 150. See also nutrition monounsaturated, 87, 112 polyunsaturated, 87 saturated, 46–47, 112 trans fats, 47, 86, 112 fiber, 112 fibrinogen, 79, 80 fish oils, 193. See also Omega-3 fatty acids folic acid, 79–80, 91 Food and Drug Administration, 9, 87 Framingham Heart Study, 65, 83–84, 85 “Frankenfoods.” See genetically modified foods fruits, 68–69, 153, 203. See also nutrition genetically modified foods, 41–43 genetics, as risk factor. See family history under risk factors glucose. See blood sugar glycemic index, 16 144 Helicobacter pylori bacteria, 12, 123 high blood pressure, 54–55, 64, 71–74 age as factor in, 72 alcohol and, 73 diet and, 78–79 drugs to control, 73–74 exercise and, 81 inactivity and, 73 obesity and, 73 oral contraceptives and, 73 race and, 72

salt and, 73 homocysteine, 79 hormone replacement therapy, 28–29, 88–90, 122, 180, 185 Human Genome Project, 19 hydration and kidney stones, 206 and joint health, 192 hygiene effect on allergies, 204–205 hypertension. See high blood pressure ibuprofen, 199 inactivity, as risk factor, 58. See also under risk factors indigestion, 195–195 insulin, 116, 131 insulin resistance, 132 Journal of the American Medical Association, 6, 67 life expectancy, 33–34 Lyons Heart Study, 68, 85 mammograms, 96, 104 meal planning, 155 meat grilled, 47–48 processed, 112 red, 112 Mediterranean diet, 85–87, 114 micronutrients, 158 mutation, 102–103 National Cancer Act, 93 National Cancer Institute, 95 National Institute of Allergy and Infectious Diseases, 204

National Institutes of Health, 37, 76, 135, 158, 185 Norwegian Vitamin Trial (NORVIT), 79–80 NSAIDs, 199–200 Nurses Health Study, 64, 85, 109, 110 nutrition, 16, 68–69, 74–77, 81, 85–88, 108–111, 213 obesity, 57–58, 74–76, 116. See also under risk factors Omega-3 fatty acids, 203 partially hydrogenated oil. See trans fats Physician’s Health Study, 85 phytoestrogens, 16 placebos, 8 posture, and osteoarthritis, 192–193 processed foods, 113 protein, 148, 149–150, 152. See also nutrition PSA tests, 104 radiation, 130, 106, 121 reservatrol, 78 risk factors age, 71, 118, 119, 120, 121, 122, 123, 125, 168, 197 for age-related macular degeneration (AMD), 203 air pollution, 121 alcohol, 112–113, 117, 120, 121, 169–170, 184 for Alzheimer’s disease, 168–175 arsenic exposure, 124 asbestos exposure, 121, 125 bladder inflammation, chronic, 124 blood type, 123 bowel disease, inflammatory, 120 caffeine, 184

for cancer, 107–126 for cardiovascular disease, 53–58, 67 chemical exposure, 122, 124, 125 chemotherapy, 124 childbirth, 122 combinations of, 39–40 diabetes as, 56, 71, 120, 197, 207 diet, 82, 120, 123 for diverticular disease, 200–201 drug abuse, 169–170 exercise, lack of. See inactivity family history, 53–54, 71, 101, 114, 118, 119, 120, 122, 123, 125, 126, 135, 137, 168, 183 for gallstones, 207 for gastritis, 199 gastroesophageal reflux disease (GERD) as, 122 for gastroesophageal reflux disease (GERD), 196–197 geography, 15, 208 Helicobacter pylori bacteria, 123, 199, 201 high blood pressure, 71–74, 125, 197. See also high blood pressure high cholesterol, 55–56, 71 hormone replacement therapy, 122, 180, 207 human papilloma virus (HPV), 122 immune system disorder, 124, 126 inactivity, 58, 71, 82, 119, 120, 125, 183–184 for irritable bowl syndrome (IBS), 197–198 lifestyle changes and, 38–39, 63, 73, 79, 81 menstrual history, 118, 122

moles, 126 NSAIDs, use of, 201–202 obesity, 57–58, 119, 121, 123, 125, 134–136 oral contraceptives, 123 for osteoarthritis, 189–191 for peptic ulcers, 201 personal history, 122 pneumonia, recurring, 121 prediabetes, 138–140 pregnancy, 123 race, 72, 119, 121, 124, 177, 183, 207 radiation, 121, 123–124 sex, 121, 123, 124, 125, 177, 190, 197, 207 sexual history, 123, 208–209 skin tone, 126 smoking, 44, 71, 83, 107–108, 117, 120, 121, 123, 124, 184, 197 sources of, 37 for stroke, 70 sun exposure, 97–100, 126 surgery, 123 tuberculosis, 121 undescended testicle, 125–126 risk reduction, 15–16, 25. See also risk factors salt, 48, 73, 86 saturated fats, 46–47, 112 Seven Countries Study, 84–85 sleeping, difficulty in, 90 smoking, risks of, 35, 48–49, 54, 107–108, 159 benefits of quitting, 111 See also under risk factors sodium. See salt soft drinks, 45–46, 113, 144, 184 statistics, understanding, 22–24, 30–31, 40 steroids, 185

Surveillance Epidemiology and End Results (SEER), 117 testosterone, 65 tests, diagnostic, 104–107. See also individual tests thyroid medications, 185 trans fats, 47, 86, 112 triglycerides, 56, 136 ultraviolet radiation. See radiation vegetables, 68–69, 153, 203. See also nutrition vitamin A, 193 vitamin B12, 80 vitamin B6, 80 vitamin C, 8, 159, 193 vitamin D, 16, 65, 99, 183, 184 calcium and, 187 prevention of osteoarthritis and, 16, 190, 193 sun exposure and, 99, 187–188 supplements, 188 vitamin E, 193 vitamin supplements, 157–161, 188 weight reduction, 140–149, 162–163. See also obesity whole grains, 91, 144, 153. See also nutrition Women’sHealth Initiative (WHI), 88–89, 169 Women’sIschemia Syndrome Evaluation, 67

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T H E

A U T H O R

Photo by Wil Jones

A B O U T

AVERY HURT is a freelance health and science writer. Her work appears regularly in many national publications, including Better Homes and Gardens, Newsweek, and The New Physician. She lives in Birmingham, Alabama.

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