NIR BARZILAI IS 57 YEARS OLD. There are wrinkles at the corners of his eyes, and his hair is turning grey. As the director of the Institute for Aging Research at the Albert Einstein College of Medicine in the Bronx, Barzilai is more interested than most of us in the process of getting older. He studies ‘super-agers’, people between the ages of 95 and 112 who have never experienced any of the four most common diseases of aging: heart disease, diabetes, cancer and cognitive decline. But after years spent tracking how and why people age, he can’t help noticing the telltale changes taking place in his own body. “You’re bothered by subtle signs of aging in yourself, like rapidly recalling colleagues’ names, or changes in your sense of coordination while biking,” he says. “Your line of work makes you extra aware of these.” He’s trying to find ways to forestall aging and death, but his work seems to just make him more anxious about the process.

David Sinclair, a close friend of Barzilai’s who also studies aging—although in mice, worms and yeast instead of people—has a more acute version of the same problem. He says he’s been haunted by death since he was four years old, when he realized that everyone around him was going to die. First his pets, then his grandparents, then his parents. “The realization that the people around me would be gone, after I assumed that we’d always be together, was a shock,” says Sinclair, 43. He’s now a tenured professor at Harvard, but it’s still an issue for him. When she was four, his daughter asked if he would always be around. He told her that, regretfully, he would not. “It’s tragic that conscious animals like ourselves get to realize our own mortality,” says Sinclair.

You’d think that as modern-day scientists, they’d be more objective, more dispassionate about their subject—possibly even a little cold-blooded—but really they are just like everyone else: they want to delay death, not just to preserve their friends and loved ones, but also themselves.

Nothing can take away the knowledge that we all are destined to grow old and die. That awareness, and the desire to delay or circumvent death, has been part of human culture since ancient times: one of the earliest surviving works of literature, The Epic of Gilgamesh, is concerned in part with the quest for eternal life. As a species, we’ve experimented widely to find the answer, bathing in the blood of virgins and injecting crushed guinea-pig testes under our skin, basking in mineral springs and preserving our brains in subzero temperatures.

More recently, reputable scientists have entered the field, trying to break away from quackery and establish aging research as a disciplined, credible pursuit. It’s been a nonstop battle against persistent waves of pseudoscience, false anti-aging ‘therapies’, and creepy press about the extreme methods of some anti-aging advocates. One of the most famous is Ray Kurzweil, a prominent inventor and technologist who ingests up to 200 vitamins a day and receives intravenous injections of a compound he believes rejuvenates his tissues. Kurzweil, like Gilgamesh, plans to live forever. If he does so, it would be an historic achievement, to say the least.

Researchers like Barzilai and Sinclair have more modest goals. They apply rigorous scientific standards to painstakingly identify the molecular and genetic underpinnings of aging. And work like theirs may, for the first time, be the path to real, legitimate drugs to ward off the diseases of ageing that cause most of our untimely ends.

I always expected to live longer than my grandparents. My paternal grandfather died at 49 after a painful battle with colon cancer. He left behind eight young children and a widow, my grandmother. She died at age 94, when her heart gave out, after two years in a nursing home. My maternal grandparents are still alive, both now in their mid-eighties. He has had melanoma several times and currently has prostate cancer; she is suffering from brain degeneration.

Still, I was taught that I would outlast them, just like they’d outlasted their own parents and grandparents. This was for good reason: life expectancy soared in the United States over the last 50 years, thanks to better health care and expanded use of vaccines. Medicine today provides my generation with a carefully curated set of healthy-living guidelines: if I don’t smoke, and if I run two miles a day, eat more vegetables and less meat, get regular health screenings and drink a glass of red wine every night, I’ll have a real shot at dancing at the weddings of my great-grandchildren.

But that assumption turns out to be wrong. In America, life-expectancy increases have been slowing, according to a recent review of mortality data. In fact, some argue that life expectancy may have already hit its upper limit. “We have always assumed that each generation will be healthier and longer lived than the prior one,” said the study’s authors. In fact, they discovered that the amount of time that we spend sick with major diseases has actually increased, and age-related diseases are more, not less, prevalent than they used to be.

The truth is, I’m likely to die around age 81, the average life expectancy for a woman in the United States. What I eat and do will help get me there, hopefully without suffering from cancer or heart disease, but not much further than that. It turns out that reaching your 100th birthday doesn’t have much to do with lifestyle. It has to do with something over which we have no control — our genes.

According to a new way of thinking that’s emerging among aging experts, exceptional longevity isn’t a reward for healthy living; it’s more like a winning lottery ticket, coded into the genes of a lucky few — only 1.73 of every 10,000 people in the U.S. have it. The remarkable longevity of centenarians, in other words, is a fluke, the consequence of rare and unique gene combinations passed from parents to children to grandchildren.

That’s the bad news. The good news is that researchers like Barzilai and other colleagues have recently identified something else, something totally unexpected, in the cells of these oldest living humans, and it could radically transform old age for the rest of us.

Besse Cooper, U.S.,

116 years old

STUDIES OF CENTENARIANS are nothing new. But attempts to investigate why some people live longer don’t always pan out. In the early 1970s, Alexander Leaf, a physician at Massachusetts General Hospital, visited remote towns in the former Soviet Union, Pakistan and Ecuador, searching for people who reportedly lived for 140 years or more. He concluded that outdoor living and healthy diet were key factors, but later had to disavow the work when it turned out that most of the ‘centenarians’ were only in their nineties. In fact, life expectancy in the communities he visited was actually lower than in the U.S

In the 1970s, Makoto Suzuki, a cardiologist and geriatrician from Tokyo, met a centenarian on the Japanese island of Okinawa. When Suzuki visited the woman, he found her outside, cutting the grass in front of her home with a sickle. She didn’t think of herself as unusual. As proof, she gestured to the home directly opposite her, where another healthy centenarian lived.

Unlike Leaf’s studies, the ages of Okinawa’s residents could be verified because town registries had records of every citizen’s birth since 1879. Suzuki learned that the prevalence of centenarians, as well as the average life expectancy of the island’s people, was higher than in any other place in Japan. He began studying the population, and today the project has collected data on more than 900 Okinawan centenarians. In one of his first experiments, Suzuki hypothesized that since the elderly appeared to be protected against illness, they might have stronger immune systems than other people. So he performed the first genetic study of centenarians and looked at a set of immune-system genes called human leukocyte antigen (HLA) genes. He found that some variants of HLA — versions of the gene with specific changes in the sequence, like different flavors of the same sweet treats — were over-represented in the Okinawa centenarian population.

Unfortunately, his results proved hard to reproduce, and Suzuki ultimately concluded that though heritable factors like HLA do exist for healthy longevity, environmental factors — including the traditional Okinawan diet of low-fat, nutrient-rich foods such as sweet potatoes and fruits — were more important.

Since then, lifestyle became the focus of aging and longevity research, primarily because a majority of scientists believed it had the most significant impact. According to numerous twin studies of aging — in which researchers compare identical and fraternal twins — most of the variability in longevity comes from environmental factors, not genetics. These studies have found that among the general population, a maximum of about one-third of the ageing process is attributable to genetic factors. In other words, only 20 to 30 percent of your chances of living to 80 are due to the genes you inherited from your parents. What you ate and drank, where you lived, how you worked: these were the crucial environmental and lifestyle factors that determined how long you lived.

Additional evidence supporting this claim can be seen in the average life span of Seventh Day Adventists, an evangelical Christian denomination that believes the body is a temple and should be cared for accordingly. Because of their beliefs, Seventh Day Adventists are taught to exercise often, get plenty of rest, and refrain from meat, alcohol, tobacco and caffeine. Studies confirm that adhering to this lifestyle can add up to eight years of life.

Australian centenarians insist that a healthy outlook on life, including maintaining social networks and mental activity, kept them young. Tokyo’s centenarians, meanwhile, eat less meat, fish and oil than ordinary people. And American centenarians in Georgia consume more whole milk, more green vegetables and less yoghurt than the average.

If that seems like a confusing combination of advice, things get even more complex when you look at wider population samples. Studies of those aged 60 or more have consistently revealed additional factors that could slow aging. Older women who eat at least one serving of blueberries or two or more of strawberries each week delay cognitive decline by up to 2.5 years. Fibre reduces the risk of death from all causes — by as much as 22 percent — in both men and women. And for those at high risk for heart disease, the fabled Mediterranean diet can reduce the chances of developing it by 30 percent.

But for every study linking healthy lifestyle to longer life, there’s another that contradicts it. When nutrition researchers in Georgia reviewed everything we know about nutrition intake in centenarians, they concluded that there was no pattern across centenarian populations and no single diet that promoted exceptional longevity. In younger populations of healthy adults, taking vitamin E, vitamin C or multivitamin supplements doesn’t significantly reduce cardiovascular disease or decrease the risk of dementia, and increasing the amount of fruit and vegetables in their diet does not help prevent chronic illnesses like cardiovascular disease or cancer.

What’s worse, the single most promising technique for extending life span in laboratory animals doesn’t seem to work in humans. Caloric restriction, which entails reducing your daily calories by 30 to 40 percent, reliably extends life span in a range of organisms, including fish, mice, and dogs. Back in 2009, the conclusions from a 20-year-long experiment on rhesus monkeys seemed to show that if they were fed a reduced-calorie diet, they lived longer and delayed the onset of age-related diseases. But in 2012, a second long-term study of rhesus monkeys found that caloric restriction did not, in fact, lengthen lifespan.

Caloric restriction has yet to be tested in a human clinical trial, so we don’t know if it will make a difference for people. However, Roy Walford, an accomplished pathologist at the University of California, Los Angeles who studied caloric restriction in mice, did take the chance to test the idea on himself. For 30 years, Walford lived on a near-starvation diet of only 1,600 calories per day. He believed that caloric restriction could extend the human life span to 150 years — but died in 2004 at 79 from complications of motor neuron disease, rendering his personal experiment moot.

BARZILAI, IN HIS EAST BRONX LAB, didn’t buy into the lifestyle theory. His own doubts began in 1998, when he initiated the Longevity Genes Project at Einstein with just three centenarians. The old people he studied seemed to undermine all the usual arguments and theories. And the more centenarians he recruited, the more he began to observe a pattern of strong family histories of longevity. In fact, compared to those with no centenarian siblings, a brother of a centenarian is at least 17 times as likely to reach age 100, while a sister of one is eight times as likely. Clearly, family is a large component of longevity, which suggested to Barzilai that those who live exceptionally long have inherited, not earned it.

Something else bothered Barzilai. If consensus opinion was true, and two-thirds of aging was attributable to lifestyle and only one-third to genetics, then centenarians should have especially healthy lifestyles, trumping even that of Seventh Day Adventists. But whenever Barzilai asked one of his centenarians what she attributed her healthy longevity to, he’d get an answer like “I have chicken fat every day” or “I eat chocolate all the time.”

Jiroemon Kimura, Japan

116 years old

His centenarians’ answers didn’t add up. At 105 years old, Sarah Sampson ascribes her healthy longevity to simple living: “I was a quiet, obedient child. I like plain, unadulterated food. And I never ran around, if you know what I mean.” Others in Barzilai’s group credit exercise. Some believe it was good luck or spirituality. Pearl Cantrell, a 105-year-old Texas woman, says her secret is to eat several pieces of bacon a day; the oldest man ever, 116-year-old Jiroemon Kimura, who passed away June 12 this year, thought his longevity was from getting out of bed early.

In 2010, Barzilai decided to prove once and for all whether lifestyle was at the root of centenarians’ longevity. From his team’s home base in an old building at the Einstein, Barzilai and his research assistants reached out to over 500 centenarians, mostly in the New York City area, and questioned them about their lifestyles when they were 70. Questions ranged from their smoking history, physical activity and habits to more measurable details like weight and height. They then compared that data to information from 3,000 non-centenarians — people from the general public who completed a national nutrition survey in the early 1970s.

The results were unmistakable: centenarians have no better habits than the rest of us: they smoke, eat as poorly and are just as lazy as the general population. The finding contradicts twin studies, which aging researchers now realize had a flaw: they studied only twins in the general population — people who normally live to 80. Exceptional longevity, it turns out, is a whole different ballgame.

Barzilai’s study discounting the effects of lifestyle came out in 2011. The next year, Tom Perls at Boston University proved it was possible to accurately predict the likelihood of someone becoming a centenarian by looking at the person’s genetics alone. With biostatistician Paola Sebastiani, Perls scanned the whole genomes of control subjects, centenarians, and supercentenarians (those who live to 110 plus). They identified 281 markers of 130 genes associated with longevity: a genetic signature, a lucky combination that wins the longevity jackpot.

Using just that set of 130 genes, Perls can tell whether someone is a centenarian or not with 61 percent accuracy. And as the bar gets higher, so his accuracy increases: He can tell who is 102 or older with 73 percent accuracy, and who is 105 or older with 85 percent accuracy.

So, after all these years of thinking about aging as a force to be fought with exercise and diet, it turns out that — for super-agers at least — something else was going on. The clustering of longevity in families; the evidence that centenarians’ lifestyles are no healthier than those of the rest of us; and the fact that genes alone can be used to predict whether a person will live to be 100 or older; these have led to a new consensus. It’s now accepted that the one-third statistic doesn’t apply to super-agers. “In centenarians, it’s probably 80-20,” says Barzilai. That is: 80 percent genetics, 20 percent lifestyle. Exceptional longevity, it turns out, is all in the genes.

Jeanne Calment (France) was the oldest person on earth at 122 years old.

LILLY PORT PERCHES on the edge of her sofa at her home in Scarsdale, New York, as straight and poised as a finishing-school student. With pink nails, she picks a piece of lint from her red sweater, a souvenir from a recent trip to the ancient Peruvian mountaintop city of Machu Picchu.

Machu Picchu is more than a mile above sea level. Lilly hiked all the way to the top. She is 100 years old.

The year before her Peru trip, she visited Cambodia and Vietnam. Next year she was thinking about Iceland, but has decided on Hawaii instead. “I’m in perfect condition,” she says.

What is it in Lilly Port’s genome, hidden inside every cell in her body, that makes her the exception to the standard rules of mortality? One possibility is what geneticist Nicholas Schork characterizes as “healthy ageing by subtraction” — the idea that centenarians are at a lower risk for disease than the general population is. “They escape disease and live to a long age because they don’t have predisposing genes,” says Schork, who is based at the Scripps Research Institute, just north of San Diego, California. “In that way, it’s the absence of a bad thing.”

Schork doesn’t necessarily subscribe to this mode of thinking, and for good reason. Although it was the commonly held belief for the last decade or so, once again, it does not appear to be true. In 2010, researchers in the Netherlands showed that individuals aged between 80 and 100 have as many disease-risk gene variants as the rest of us. And when Perls and Sebastiani scanned the genomes of centenarians for their own genetic-signature study, the results matched those of the Dutch research. “Centenarians have as many of these disease-associated genes as everybody else,” says Boston University’s Tom Perls.

Faced with that evidence, researchers like Perls and Schork are now turning to a second hypothesis: instead of the absence of a bad thing, centenarians have the presence of a good thing. Perhaps centenarians are protected from age-related diseases by certain genes that act like guards. “Even if you have genes that aren’t so good for you, the protective genes kind of trump those,” says Perls.