The Telomere Effect

A Revolutionary Approach to Living Younger, Healthier, Longer


By Dr. Elizabeth Blackburn

By Dr. Elissa Epel

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The New York Times bestselling book coauthored by the Nobel Prize winner who discovered telomerase and telomeres’ role in the aging process and the health psychologist who has done original research into how specific lifestyle and psychological habits can protect telomeres, slowing disease and improving life.

Have you wondered why some sixty-year-olds look and feel like forty-year-olds and why some forty-year-olds look and feel like sixty-year-olds? While many factors contribute to aging and illness, Dr. Elizabeth Blackburn discovered a biological indicator called telomerase, the enzyme that replenishes telomeres, which protect our genetic heritage. Dr. Blackburn and Dr. Elissa Epel’s research shows that the length and health of one’s telomeres are a biological underpinning of the long-hypothesized mind-body connection. They and other scientists have found that changes we can make to our daily habits can protect our telomeres and increase our health spans (the number of years we remain healthy, active, and disease-free).

The Telemere Effect reveals how Blackburn and Epel’s findings, together with research from colleagues around the world, cumulatively show that sleep quality, exercise, aspects of diet, and even certain chemicals profoundly affect our telomeres, and that chronic stress, negative thoughts, strained relationships, and even the wrong neighborhoods can eat away at them.

Drawing from this scientific body of knowledge, they share lists of foods and suggest amounts and types of exercise that are healthy for our telomeres, mind tricks you can use to protect yourself from stress, and information about how to protect your children against developing shorter telomeres, from pregnancy through adolescence. And they describe how we can improve our health spans at the community level, with neighborhoods characterized by trust, green spaces, and safe streets.

The Telemere Effect will make you reassess how you live your life on a day-to-day basis. It is the first book to explain how we age at a cellular level and how we can make simple changes to keep our chromosomes and cells healthy, allowing us to stay disease-free longer and live more vital and meaningful lives.


Authors' Note: Why We Wrote This Book

With a life span of 122 years, Jeanne Calment was one of the longest-living women on record. When she was eighty-five, she took up the sport of fencing. She was still riding a bike into her triple digits.1 When she turned one hundred, she walked around her hometown of Arles, France, thanking the people who'd wished her a happy birthday.2 Calment's relish for life captures what we all want: a life that is healthy right up to the very end. Aging and death are immutable facts of life, but how we live until our last day is not. This is up to us. We can live better and more fully now and in our later years.

The relatively new field of telomere science has profound implications that can help us reach this goal. Its application can help reduce chronic disease and improve wellbeing, all the way down to our cells and all the way through our lives. We've written this book to put this important information into your hands.

Here you will find a new way of thinking about human aging. One current, predominant, scientific view of human aging is that the DNA of our cells becomes progressively damaged, causing cells to become irreversibly aged and dysfunctional. But which DNA is damaged? Why did it become damaged? The full answers aren't known yet, but the clues are now pointing strongly toward telomeres as a major culprit. Diseases can seem distinct because they involve very different organs and parts of the body. But new scientific and clinical findings have crystallized into a new concept. Telomeres throughout the body shorten as we age, and this underlying mechanism contributes to most diseases of aging. Telomeres explain how we run out of the abilty to replenish tissue (called replicative senescence). There are other ways cells become dysfunctional or die early, and there are other factors that contribute to human aging. But telomere attrition is a clear and an early contributor to the aging process, and—more exciting—it is possible to slow or even reverse that attrition.

We've put the lessons from telomere research into the full story, as it is unfolding today, in language for the general reader. Previously this knowledge has been available only in scientific journal articles, scattered in bits and pieces. Simplifying this body of science for the public has been a great challenge and responsibility. We could not describe every theory or pathway of aging or lay out each topic in fine scientific detail. Nor could we state every qualification and disclaimer. Those issues are detailed in the scientific journals where the original studies were published, and we encourage interested readers to explore this fascinating body of work, much of it cited in this book. We have also written a review article covering the latest research on telomere biology, published in the peer-reviewed scientific journal Science, which will give you several good directions into the molecular-level mechanisms.3

Science is a team sport. We have been truly privileged to participate in research with a broad range of scientific collaborators from different disciplines. We have also learned from research teams from all over the world. Human aging is a puzzle made up of many pieces. Over several decades, new pieces of information have each added a critical part to the whole. The understanding of telomeres has helped us see how the pieces fit together—how aged cells can cause the vast array of diseases of aging. Finally a picture has emerged that is so compelling and helpful that we felt it was important to share it broadly. We now have a comprehensive understanding of human telomere maintenance, from cell to society, and what it can mean in human lives and communities. We are sharing with you the basic biology of telomeres, how they relate to disease, to health, to how we think, and even to our families and communities. Putting together the pieces, illuminated by knowledge of what affects telomeres, has led us to a more interconnected view of the world, as we share with you in the last section of the book.

Another reason we've written this book is to help you avoid potential risks. The interest in telomeres and aging is growing exponentially, and while there is some good information in the public domain, some of it is misleading. For example, there are claims that certain creams and supplements may elongate your telomeres and increase your longevity. These treatments, if they actually work in the body, could potentially increase your risk of cancer or have other dangerous effects. We simply need larger and longer studies to assess these potential serious risks. There are other known ways to improve your cell longevity, without risk, and we have tried to include the best of them here. You won't find any instant cures on these pages, but you will find the specific, research-supported ideas that could make the rest of your life healthy, long, and fulfilling. While some ideas may not be totally new to you, gaining a deep understanding of the behind-the-scenes reasons for them may change how you view and live your days.

Finally, we want you to know that neither of us has any financial interest in companies that sell telomere-related products or that offer telomere testing. Our wish is to synthesize the best of our understanding—as it stands today—and make it available to anyone who may find it useful. These studies represent a true breakthrough in our understanding of aging and living younger, and we want to thank all who have contributed to the research that we are able to present here.

With the exception of the "teaching story" that appears on the first page of the introduction, the stories in this book are drawn from real-life people and experiences. We are deeply grateful to the people who shared their stories with us. To protect their privacy, we have changed some names and identifying details.

We hope this book is helpful to you, your families, and all who can benefit from these fascinating discoveries.


A Tale of Two Telomeres

It is a chilly Saturday morning in San Francisco. Two women sit at an outdoor café, sipping hot coffee. For these two friends, this is their time away from home, family, work, and to-do lists that never seem to get any shorter.

Kara is talking about how tired she is. How tired she always is. It doesn't help that she catches every cold that goes around the office, or that those colds inevitably turn into miserable sinus infections. Or that her ex-husband keeps "forgetting" when it's his turn to pick up the children. Or that her bad-tempered boss at the investment firm scolds her—right in front of her staff. And sometimes, as she lies down in bed at night, Kara's heart gallops out of control. The sensation lasts for just a few seconds, but Kara stays awake long after it passes, worrying. Maybe it's just the stress, she tells herself. I'm too young to have a heart problem. Aren't I?

"It's not fair," she sighs to Lisa. "We're the same age, but I look older."

She's right. In the morning light, Kara looks haggard. When she reaches for her coffee cup, she moves gingerly, as if her neck and shoulders hurt.

But Lisa looks vibrant. Her eyes and skin are bright; this is a woman with more than enough energy for the day's activities. She feels good, too. Actually, Lisa doesn't think very much about her age, except to be thankful that she's wiser about life than she used to be.

Looking at Kara and Lisa side by side, you would think that Lisa really is younger than her friend. If you could peer under their skin, you'd see that in some ways, this gap is even wider than it seems. Chronologically, the two women are the same age. Biologically, Kara is decades older.

Does Lisa have a secret—expensive facial creams? Laser treatments at the dermatologist's office? Good genes? A life that has been free of the difficulties her friend seems to face year after year?

Not even close. Lisa has more than enough stresses of her own. She lost her husband two years ago in a car accident; now, like Kara, she is a single mother. Money is tight, and the tech start-up company she works for always seems to be one quarterly report away from running out of capital.

What's going on? Why are these two women aging in such different ways?

The answer is simple, and it has to do with the activity inside each woman's cells. Kara's cells are prematurely aging. She looks older than she is, and she is on a headlong path toward age-related diseases and disorders. Lisa's cells are renewing themselves. She is living younger.


Why do people age at different rates? Why are some people whip smart and energetic into old age, while other people, much younger, are sick, exhausted, and foggy? You can think of the difference visually:

Figure 1: Healthspan versus Diseasespan. Our healthspan is the number of years of our healthy life. Our diseasespan is the years we live with noticeable disease that interferes with our quality of living. Lisa and Kara may both live to one hundred, but each has a dramatically different quality of life in the second half of her life.

Look at the first white bar in figure 1. It shows Kara's healthspan, the time of her life when she's healthy and free of disease. But in her early fifties, the white goes gray, and at seventy, black. She enters a different phase: the diseasespan.

These are years marked by the diseases of aging: cardiovascular disease, arthritis, a weakened immune system, diabetes, cancer, lung disease, and more. Skin and hair become older looking, too. Worse, it's not as if you get just one disease of aging and then stop there. In a phenomenon with the gloomy name multi-morbidity, these diseases tend to come in clusters. So Kara doesn't just have a run-down immune system; she also has joint pain and early signs of heart disease. For some people, the diseases of aging hasten the end of life. For others, life goes on, but it's a life with less spark, less zip. The years are increasingly marred by sickness, fatigue, and discomfort.

At fifty, Kara should be brimming with good health. But the graph shows that at this young age, she is creeping into the diseasespan. Kara might put it more bluntly: she is getting old.

Lisa is another story.

At age fifty, Lisa is still enjoying excellent health. She gets older as the years pass, but she luxuriates in the healthspan for a nice, long time. It isn't until she's well into her eighties—roughly the age that gerontologists call "old old"—that it gets significantly harder for her to keep up with life as she's always known it. Lisa has a diseasespan, but it's compressed into just a few years toward the end of a long, productive life. Lisa and Kara aren't real people—we've made them up to demonstrate a point—but their stories highlight questions that are genuine.

How can one person bask in the sunshine of good health, while the other suffers in the shadow of the diseasespan? Can you choose which experience happens to you?

The terms healthspan and diseasespan are new, but the basic question is not. Why do people age differently? People have been asking this question for millennia, probably since we were first able to count the years and compare ourselves to our neighbors.

At one extreme, some people feel that the aging process is determined by nature. It's out of our hands. The ancient Greeks expressed this idea through the myth of the Fates, three old women who hovered around babies in the days after birth. The first Fate spun a thread; the second Fate measured out a length of that thread; and the third Fate snipped it. Your life would be as long as the thread. As the Fates did their work, your fate was sealed.

It's an idea that lives on today, although with more scientific authority. In the latest version of the "nature" argument, your health is mostly controlled by your genes. There may not be Fates hovering around the cradle, but the genetic code determines your risk for heart disease, cancer, and general longevity before you're even born.

Perhaps without even realizing it, some people have come to believe that nature is all that determines aging. If they were pressed to explain why Kara is aging so much faster than her friend, here are some things they might say:

"Her parents probably have heart problems and bad joints, too."

"It's all in her DNA."

"She has unlucky genes."

The "genes are our destiny" belief is, of course, not the only position. Many have noticed that the quality of our health is shaped by the way we live. We think of this as a modern view, but it's been around for a long, long time. An ancient Chinese legend tells of a raven-haired warlord who had to make a dangerous trip over the border of his homeland. Terrified that he would be captured at the border and killed, the warlord was so anxious that he woke up one morning to discover that his beautiful dark hair had turned white. He'd aged early, and he'd aged overnight. As many as 2,500 years ago, this culture recognized that early aging can be triggered by influences like stress. (The story ends happily: No one recognized the warlord with his newly whitened hair, and he traveled across the border undetected. Getting older has its advantages.)

Today there are plenty of people who feel that nurture is more important than nature—that it's not what you're born with, it's your health habits that really count. Here's what these folks might say about Kara's early aging:

"She's eating too many carbs."

"As we age, each of us gets the face we deserve."

"She needs to exercise more."

"She probably has some deep, unresolved psychological issues."

Take a look again at the ways the two sides explain Kara's accelerated aging. The nature proponents sound fatalistic. For good or for bad, we're born with our futures already encoded into our chromosomes. The nurture side is more hopeful in its belief that premature aging can be avoided. But advocates of the nurture theory can also sound judgmental. If Kara is aging rapidly, they suggest, it's all her fault.

Which is right? Nature or nurture? Genes or environment? Actually, both are critical, and it's the interaction between the two that matters most. The real differences between Lisa's and Kara's rates of aging lie in the complex interactions between genes, social relationships and environments, lifestyles, those twists of fate, and especially how one responds to the twists of fate. You're born with a particular set of genes, but the way you live can influence how your genes express themselves. In some cases, lifestyle factors can turn genes on or shut them off. As the obesity researcher George Bray has said, "Genes load the gun, and environment pulls the trigger."1 His words apply not just to weight gain but to most aspects of health.

We're going to show you a completely different way of thinking about your health. We are going to take your health down to the cellular level, to show you what premature cellular aging looks like and what kind of havoc it wreaks on your body—and we'll also show you not only how to avoid it but also how to reverse it. We'll dive deep into the genetic heart of the cell, into the chromosomes. This is where you'll find telomeres (tee-lo-meres), repeating segments of noncoding DNA that live at the ends of your chromosomes. Telomeres, which shorten with each cell division, help determine how fast your cells age and when they die, depending on how quickly they wear down. The extraordinary discovery from our research labs and other research labs around the world is that the ends of our chromosomes can actually lengthen—and as a result, aging is a dynamic process that can be accelerated or slowed, and in some aspects even reversed. Aging need not be, as thought for so long, a one-way slippery slope toward infirmity and decay. We all will get older, but how we age is very much dependent on our cellular health.

We are a molecular biologist (Liz) and a health psychologist (Elissa). Liz has devoted her entire professional life to investigating telomeres, and her fundamental research has given birth to an entirely new field of scientific understanding. Elissa's lifelong work has been on psychological stress. She has studied its harmful effects on behavior, physiology, and health, and she has also studied how to reverse these effects. We joined forces in research fifteen years ago, and the studies that we performed together have set in motion a whole new way of examining the relationship between the human mind and body. To an extent that has surprised us and the rest of the scientific community, telomeres do not simply carry out the commands issued by your genetic code. Your telomeres, it turns out, are listening to you. They absorb the instructions you give them. The way you live can, in effect, tell your telomeres to speed up the process of cellular aging. But it can also do the opposite. The foods you eat, your response to emotional challenges, the amount of exercise you get, whether you were exposed to childhood stress, and even the level of trust and safety in your neighborhood—all of these factors and more appear to influence your telomeres and can prevent premature aging at the cellular level. In short, one of the keys to a long healthspan is simply doing your part to foster healthy cell renewal.

Figure 2: Telomeres at the Tips of Chromosomes. The DNA of every chromosome has end regions consisting of DNA strands coated by a dedicated protective sheath of proteins. These are shown here as the lighter regions at the end of the chromosome—the telomeres. In this picture the telomeres are not drawn to scale, because they make up less than one-ten-thousandth of the total DNA of our cells. They are a small but vitally important part of the chromosome.


In 1961 the biologist Leonard Hayflick discovered that normal human cells can divide a finite number of times before they die. Cells reproduce by making copies of themselves (called mitosis), and as the human cells sat in a thin, transparent layer in the flasks that filled Hayflick's lab, they would, at first, copy themselves rapidly. As they multiplied, Hayflick needed more and more flasks to contain the growing cell cultures. The cells in this early stage multiplied so quickly that it was impossible to save all the cultures; otherwise, as Hayflick remembers, he and his assistant would have been "driven out of the laboratory and the research building by culture bottles." Hayflick called this youthful phase of cell division "luxuriant growth." After a while, though, the reproducing cells in Hayflick's lab stopped in their tracks, as if they were getting tired. The longest-lasting cells managed about fifty cell divisions, although most divided far fewer times. Eventually these tired cells reached a stage he called senescence: They were still alive but they had all stopped dividing, permanently. This is called the Hayflick limit, the natural limit that human cells have for dividing, and the stop switch happens to be telomeres that have become critically short.

Are all cells subject to this Hayflick limit? No. Throughout our bodies we find cells that renew—including immune cells; bone cells; gut, lung, and liver cells; skin and hair cells; pancreatic cells; and the cells that line our cardiovascular systems. They need to divide over and over and over to keep our bodies healthy. Renewing cells include some types of normal cells that can divide, like immune cells; progenitor cells, which can keep dividing even longer; and those critical cells in our bodies called stem cells, which can divide indefinitely as long as they are healthy. And, unlike those cells in Hayflick's lab dishes, cells don't always have a Hayflick limit, because—as you will read in chapter 1—they have telomerase. Stem cells, if kept healthy, have enough telomerase to enable them to keep dividing throughout our life spans. That cell replenishment, that luxuriant growth, is one reason Lisa's skin looks so fresh. It's why her joints move easily. It's one reason she can take in deep lungfuls of the cool air blowing in off the bay. The new cells are constantly renewing essential body tissues and organs. Cell renewal helps keep her feeling young.

From a linguistic perspective, the word senescent has a shared history with the word senile. In a way, that's what these cells are—they're senile. In one way it is definitely good that cells stop dividing. If they just keep on multiplying, cancer can ensue. But these senile cells are not harmless—they are bewildered and weary. They get their signals confused, and they don't send the right messages to other cells. They can't do their jobs as well as they used to. They sicken. The time of luxuriant growth is over, at least for them. And this has profound health consequences for you. When too many of your cells are senescent, your body's tissues start to age. For example, when you have too many senescent cells in the walls of your blood vessels, your arteries stiffen and you are more likely to have a heart attack. When the infection-fighting immune cells in your bloodstream can't tell when a virus is nearby because they are senescent, you are more susceptible to catching the flu or pneumonia. Senescent cells can leak proinflammatory substances that make you vulnerable to more pain, more chronic illness. Eventually, many senescent cells will undergo a preprogrammed death.

The diseasespan begins.

Many healthy human cells can divide repeatedly, so long as their telomeres (and other crucial building blocks of cells like proteins) remain functional. After that, the cells become senescent. Eventually, senescence can even happen to our amazing stem cells. This limit on cells dividing is one reason that there seems to be a natural winding down of the human healthspan as we age into our seventies and eighties, although of course many people live healthy lives much longer. A good healthspan and life span, reaching eighty to one hundred years for some of us and many of our children, is within our reach.2 There are around three hundred thousand centenarians worldwide, and their numbers are rapidly increasing. Even more so are the numbers of people living into their nineties. Based on trends, it is thought that over one-third of children born in the United Kingdom now will live to one hundred years.3 How many of those years will be darkened by diseasespan? If we better understand the levers on good cell renewal, we can have joints that move fluidly, lungs that breathe easily, immune cells that fiercely fight infections, a heart that keeps pumping blood through its four chambers, and a brain that is sharp throughout the elderly years.

But sometimes cells don't make it through all their divisions in the way they should. Sometimes they stop dividing earlier, falling into an old, senescent stage before their time. When this happens, you don't get those eight or nine great decades. Instead, you get premature cellular aging. Premature cellular aging is what happens to people like Kara, whose healthspan graph turns dark at an early age. Chronological age is the major determinant of when we get diseases, and this reflects our biological aging inside.

Figure 3: Aging and Disease. Age is by far the largest determinant of chronic diseases. This graph shows the frequency of death by age, up to age sixty-five and older, for the top four causes of death by disease (heart disease, cancer, respiratory disease, and stroke and other cerebrovascular diseases). The death rate due to chronic diseases starts to increase after age forty and goes up dramatically after age sixty. Adapted from U.S. Department of Health and Human Services, Centers for Disease Control and Prevention, "Ten Leading Causes of Death and Injury,"

At the beginning of the chapter, we asked, Why do people age differently? One reason is cellular aging. Now the question becomes, What causes cells to get old before their time?

For an answer to this question, think of shoelaces.


Do you know the protective plastic tips at the ends of shoelaces? These are called aglets. The aglets are there to keep shoelaces from fraying. Now imagine that your shoelaces are your chromosomes, the structures inside your cells that carry your genetic information. Telomeres, which can be measured in units of DNA known as base pairs, are like the aglets; they form little caps at the ends of the chromosomes and keep the genetic material from unraveling. They are the aglets of aging. But telomeres tend to shorten over time.

Here's a typical trajectory for the life of a human's telomere:

Age: Newborn baby

Telomere Length (in base pairs): 10,000 base pairs

Age: 35 years old

Telomere Length (in base pairs): 7,500 base pairs

Age: 65 years old

Telomere Length (in base pairs): 4,800 base pairs

When your shoelace tips wear down too far, the shoelaces become unusable. You may as well throw them away. Something similar happens to cells. When telomeres become too short, the cell stops dividing altogether. Telomeres aren't the only reason a cell can become senescent. There are other stresses on normal cells that we don't yet understand very well. But short telomeres are one of the primary reasons human cells grow old, and they are one mechanism that controls the Hayflick limit.

Your genes affect your telomeres, both their length when you're born and how quickly they dwindle down. But the wonderful news is that our research, along with research from around the globe, has shown you can step in and take some control of how short or long—how robust—they are.

For instance:

Some of us respond to difficult situations by feeling highly threatened—and this response is linked to shorter telomeres. We can reframe our view of situations in a more positive way.

Several mind-body techniques, including meditation and Qigong, have been shown to reduce stress and to increase telomerase, the enzyme that replenishes telomeres.

Exercise that promotes cardiovascular fitness is great for telomeres. We describe two simple workout programs that have been shown to improve telomere maintenance, and these programs can accommodate all fitness levels.

Telomeres hate processed meats like hot dogs, but fresh, whole foods are good for them.

Neighborhoods that are low in social cohesion—meaning that people don't know and trust one another—are bad for telomeres. This is true no matter what the income level.

Children who are exposed to several adverse life events have shorter telomeres. Moving children away from neglectful circumstances (such as the notorious Romanian orphanages) can reverse some of the damage.

Telomeres on the parents' chromosomes in the egg and sperm are directly transmitted to the developing baby. Remarkably, this means that if your parents had hard lives that shortened their telomeres, they could have passed those shortened telomeres on to you! If you think that might be the case, don't panic. Telomeres can build up as well as shorten. You can still take action to keep your telomeres stable. And this news also means that our own life choices can result in a positive cellular legacy for the next generation.



  • "Blackburn and Epel demonstrate that how we live each day has a profound effect not just on our health and well-being, but how we age, as well. It's a manual for how to live younger and longer."—Arianna Huffington

  • "A classic. One of the most exciting health books to emerge in the last decade. It explains how we can slow the way we age at a fundamental level."—Eric Kandel, Nobel laureate and author of In Search of Memory

  • "THE TELOMERE EFFECT explains the often-invisible things that affect all of our lives, helping us make better choices individually and socially for greater health and longevity. It will change the way we think of aging and disease."—David Kessler, MD, JD, former FDA commissioner and New York Times bestselling author of The End of Overeating

  • "A revolutionary set of findings-with a wealth of science-based suggestions-that can transform the way we live our lives, shaping the very health of our cells by how we use our minds."—Daniel J. Siegel, MD, New York Times bestselling author of Brainstorm

  • "This book is revolutionary, transforming the way our world thinks about health and living well, disease, and death. It reveals a stunning picture of healthy aging-it's not simply about individuals, it's about how we are connected to each other, today and through future generations. It is hard to overstate this book's importance."—Dean Ornish, MD, founder and president, Preventive Medicine Research Institute, and New York Times bestselling author of The Spectrum

  • "Grounded in cutting-edge science, this is the best book on how to have long-term health that I have read in a very long time. Written with clarity, verve, and heart, it is chock-full of practical suggestions based on fascinating research on our own DNA. Tremendous."
    Rick Hanson, PhD, author of Buddha's Brain: The Practical Neuroscience of Happiness, Love, and Wisdom

  • "An extraordinary, illuminating synthesis of biological and psychosocial factors that enhance healthful longevity by their effects on telomeres. These new advances in knowledge enable people to attain longer, healthier lives."—Albert Bandura, professor emeritus, Stanford University, United States National Medal of Science awardee

  • "THE TELOMERE EFFECT gives us, in high relief and with exactly the practical level of detail we need, the long and the short of a new science revealing that how we live our lives, both inwardly and outwardly, individually and collectively, impinges significantly on our health, our well-being, and even our longevity. Mindfulness is a key ingredient, and importantly, issues of poverty and social justice are shown to clearly come into play as well. This book is an invaluable, rigorously authentic, and at its core, exceedingly compassionate and wise contribution to our understanding of health and well-being."—Jon Kabat-Zinn, author of Full Catastrophe Living

  • "From basic science to practical life style advice, THE TELOMERE EFFECT is an extraordinary compendium of wisdom from a remarkable collaboration between a molecular biologist and a health psychologist. It is the supreme user-friendly guide to scientific research on telomeres and why knowing about them is important for your everyday life. This book is a must read for anyone who wishes to live with optimal health."—Richard J. Davidson, New York Times bestselling author of The Emotional Life of Your Brain and co-author of Altered Traits

On Sale
Jan 3, 2017
Page Count
302 pages

Dr. Elizabeth Blackburn

About the Author

Elizabeth Blackburn, PhD, received the Nobel Prize in Physiology or Medicine in 2009 alongside two colleagues for their discovery of telomerase and telomeres’ role in the aging process. She is currently president of the Salk Institute. Blackburn was elected president of the American Association for Cancer Research and is a recipient of the Albert Lasker Basic Medical Research Award, among many other awards. In 2007, she was named one of TIME magazine’s 100 most influential people.

Elissa Epel, PhD, is a leading health psychologist who studies stress, aging, and obesity. She is the director of UCSF’s Aging, Metabolism, and Emotion Center and is associate director of the Center for Health and Community. She is a member of the National Academy of Medicine and serves on scientific advisory committees for the National Institutes of Health, and the Mind and Life Institute. She has received awards from Stanford University, the Society of Behavioral Medicine, and the American Psychological Association.

Learn more about this author