By Elizabeth Blackburn and Elissa Epel

An excerpt from The Telomere Effect, by Elizabeth Blackburn and Elissa Epel

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, nor 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, 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.”4 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

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.

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 pre- mature 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.


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 pro- found 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 lifespan, reaching eighty to one hundred years for some of us and many of our children, is within our reach.5 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.6 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 your 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.

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,”

Chronological age is the major determinant of when we get diseases, and this reflects our biological aging inside.

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 remember 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:

When your shoelace tips wear down too far, the shoelaces becomes 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.


When you think about living in a healthier way, you may think, with a groan, about a long list of things you ought to be doing. For some people, though, when they have seen and understood the connection between their actions and their telomeres, they are able to make changes that last. When I (Liz) walk to the office, people sometimes stop me to say, “Look, I’m biking to work now — I’m keeping my telomeres long!” Or “I stopped drinking sugary soda. I hated to think of what it was doing to my telomeres.”


Does our research show that by maintaining your telomeres you will live into your hundreds, or run marathons when you’re ninety-four, or stay wrinkle free? No. Everyone’s cells become old and eventually we die. But imagine that you’re driving on a highway. There are fast lanes, there are slow lanes, and there are lanes in between. You can drive in the fast lane, barreling toward the diseasespan at an accelerated pace. Or you can drive in a slower lane, taking more time to enjoy the weather, the music, and the company in the passenger seat. And, of course, you’ll enjoy your good health.

Even if you are currently on a fast track to premature cellular aging, you can switch lanes. In the pages ahead, you’ll see how to make this happen. In the first part of the book, we’ll explain more about the dangers of premature cellular aging — and how healthy telomeres are a secret weapon against this enemy. We’ll also tell you about the discovery of telomerase, an enzyme in our cells that helps keep the protective sheaths around our chromosome ends in good shape.

The rest of the book shows you how to use telomere science to support your cells. Begin with changes that you can make to your mental habits and then to your body — to the kinds of exercise, food, and sleep routines that are best for telomeres. Then expand outward to determine whether your social and physical environments support your telomere health. Throughout the book, sections called “Renewal Labs” offer suggestions that can help you prevent premature cellular aging, along with an explanation of the science behind those suggestions.

By cultivating your telomeres, you can optimize your chances of living a life that is not just longer but better. That is, in fact, why we’ve written this book. In the course of our work on telomeres we’ve seen too many Karas — too many men and women whose telomeres are wearing down too fast, who enter the diseasespan when they should still feel vibrant. There is abundant high-quality research, published in prestigious scientific journals and backed by the best labs and universities, that can guide you toward avoiding this fate. We could wait for those studies to trickle down through the media and make their way into magazines and onto health websites, but that process can take many years, is piecemeal and, sadly, information often gets distorted along the way. We want to share what we know now — and we don’t want more people or their families to suffer the consequences of unnecessary premature cellular aging.


Telomeres are an integrative index of many lifetime influences, both the good, restorative ones like good fitness and sleep, and also malign ones like toxic stress or poor nutrition or adversities. Birds, fish, and mice also show the stress-telomere relationship. Thus it’s been suggested that telomere length may be the “Holy Grail for cumulative welfare”,7 to be used as a summative measure of the animals’ lifetime experiences. In humans, as in animals, while there will be no one biological indicator of cumulative lifetime experience, telomeres are among one of the most helpful indicators that we know of right now.

When we lose people to poor health, we lose a precious resource. Poor health often saps your mental and physical ability to live as you wish. When people in their thirties, forties, fifties, sixties, and beyond are healthier, they will enjoy themselves more and will share their gifts. They can more easily use their time in meaningful ways — to nurture and educate the next generation, to support other people, solve social problems, develop as artists, make scientific or technological discoveries, travel and share their experiences, grow businesses, or serve as wise leaders. As you read this book, you are going to learn a lot more about how to keep your cells healthy. We hope you’re going to enjoy hearing how easy it is to extend your healthspan. And we hope you’re going to enjoy asking yourself the question: How am I going to use all those wonderful years of good health? Follow a bit of the advice in this book, and chances are that you’ll have plenty of time, energy, and vitality to come up with an answer.


You can start to renew your telomeres, and your cells, right now. One study has found that people who tend to focus their minds more on what they are currently doing have longer telomeres than people whose minds tend to wander more.8 Other studies find that taking a class that offers training in mindfulness or meditation is linked to improved telomere maintenance.9

Mental focus is a skill that you can cultivate. All it takes is practice. You’ll see a shoelace icon, pictured here, throughout the book. Whenever you see it — or whenever you see your own shoes with or without laces — you might use it as a cue to pause and ask yourself what you’re thinking. Where are your thoughts right now?

If you’re worrying or rehashing old problems, gently remind yourself to focus on whatever it is you’re doing. And if you are not “doing” anything at all, then you can enjoy focusing on “being.”

Simply focus on your breath, bringing all of your awareness to this simple action of breathing in and out. It is restorative to focus your mind inside — noticing sensations, your rhythmic breathing, or outside — noticing the sights and sounds around you. This ability to focus on your breath, or your present experience, turns out to be very good for the cells of your body.

Figure 4: Think of Your Shoelaces. Shoelace tips are a metaphor for telomeres. The longer the protective aglets at the ends of the laces, the less likely the shoelace will fray. In terms of chromosomes, the longer the telomeres, the less likely there will be any alarms going off in cells or fusions of chromosomes. Fusions trigger chromosome instability and DNA breakage, which are catastrophic events for the cell.

Throughout the book, you will see a shoelace icon with long aglets. You can use that as an opportunity to refocus your mind on the present, take a deep breath, and think of your telomeres being restored with the vitality of your breath.

Excerpted from the book THE TELOMERE EFFECT: A Revolutionary Approach to Living Younger, Healthier, Longer by Elizabeth Blackburn, PhD and Elissa Epel, PhD. Copyright © 2017 by Elizabeth Blackburn and Elissa Epel. Reprinted with permission of Grand Central Publishing. All rights reserved.

Find out more about Elizabeth Blackburn’s daily routine in her Thrive Questionnaire here.

Originally published at