Superhuman

8 LONGEVITY

For age is opportunity no less

Than youth itself, though in another dress,

And as the evening twilight fades away

The sky is filled with stars, invisible by day.

—Henry Wadsworth Longfellow

At 70, you are still a child. At 80, a young man or woman.

If at 90, someone from Heaven invites you over, tell him:

“Just go away, and come back when I am 100.”

—Saying carved into a rock facing the sea near the village of Kijioka, in Okinawa, Japan

As I write this, I am 16,931 days old. My life expectancy comes in at 30,736 days. So, to a good approximation, I have 13,805 days left.

In more conventional notation, that means I’m forty-six, can expect to live until I’m eighty-four, and have thirty-eight years left. But reckoning your life in days is a quickening thing to do. Try it. Calculate how many days you’ve already lived. If you’re like me you get a feeling like sand slipping through your fingers. You’ll probably think, oh my God I should do more with my days. Don’t worry, this feeling will pass, and you’ll carry on living your life as usual. There aren’t many people who can live a breathless, carpe diem life. It’s just too much effort, constantly seizing the day. What we’d like, what we’ve wanted for thousands of years, is the promise of limitless days, so we can waste them as we like, but use them as we like, too. I don’t want much, I won’t even ask for immortality, just more than my predicted 30,736 days. And I’d like them to be healthy days.¹

Elizabeth Love has already lived for 37,164 days. She’s 101 and is the oldest person I’ve ever met. But centenarians are becoming more common. In 2000, there were an estimated 180,000 centenarians worldwide and the United Nations says there will be 3.2 million of them by 2050.² Life expectancy has been increasing for decades now. It’s why my daughter has a longer life expectancy than me, coming in at just over ninety-five years. As I write, she’s only lived 1,546 days, and has a projected 33,180 left. In Japan, life expectancy is even higher: a child born in Japan today has more than a 50 percent chance of living to be 107.

That’s all very well and good for them, isn’t it? But we want that longevity here and now. We want to have youth and vigor now and into our old age. Many scientists and research institutes are working toward this. One, the Methuselah Foundation, based in Springfield, Virginia, aims explicitly to slow the clock. By 2030, it says, technology will have us looking and feeling fifty when our chronological age is ninety. Aging, to a growing number of scientists, is a disease—a genetic one we all suffer from. It is the number one cause of death, because all the diseases we die from—cancer, cardiovascular disease, dementia, diabetes—are those sprung from a common cause: old age. Old age is a disease we can cure.

You might not care about bravery, you might not care about singing ability. You might not even care much about intelligence. But you surely care about how long you will live. In this chapter we’ll look at how lifespan has been increasing, and what we’re learning about the factors behind it. We’ll meet some very old people, and see what we can learn from them. I’m far from the only one doing this—centenarians around the world are being studied in the hope that we can glean their secrets, and have some long life for ourselves. But as I meet them I’m going to bear in mind a fact that no one seems to mention in the hundreds of books and articles claiming to reveal the secrets of living to a hundred, or how to eat your way to that age. It’s this: few of the centenarians, if any, tried to live to a hundred. They just did it. They weren’t pill-popping or calorie-restricting or whatever—they just blundered through. Let’s see if we can find out how.

• • •

Elizabeth Love was born in 1915, so she has lived through two world wars, but, as Gandalf once said of Bilbo, she seems extraordinarily well preserved for someone 101 years and 269 days old.

Her age, she says right away, must be something to do with having good genes. Longevity runs through the family. Her own grandmother was ninety-three when she died. “My mother was the youngest of three sisters,” she tells me. “She was eighty-four when she died, the second sister was ninety-three, and the eldest sister was 101. My cousin, the son of the middle sister, he only recently died, at ninety-six. All the same genes, there must be something in that.”

There must indeed. We feel, just from knowing our family histories, that longevity is to a certain extent inherited. Turning that feeling into an understanding, however, has been tricky. Much of our understanding of the heritability of lifespan comes from an influential and long-running Danish twin study. As we’ve seen in earlier chapters, twin studies are invaluable to biologists trying to tease out what is genetic and what is not. Since identical twins share all their genes and fraternal twins half their genes—and because all have almost the same environment—it’s possible to examine a trait such as lifespan and determine how much is influenced by genetics and how much by other things. The first big paper on this, which came out in 1996, looked at 2,872 pairs of twins born between 1870 and 1900 and followed them until the mid-1990s, when almost all of them had died. The analysis showed that genetics accounted for 26 percent of the variation in lifespan for men, and 23 percent for women. In other words, not a huge amount.³

For a while that seemed to shut the door on any search for longevity genes. Genetics didn’t seem to have much to do with it, and it seemed that lifestyle and environment were far more important. That feeling still persists among some gerontology researchers I’ve spoken to, and indeed no one will dispute that these nongenetic things are important. But ten years after that study, Kaare Christensen’s team, at the Institute of Public Health, University of Southern Denmark, took a closer look at what was going on with the very old, and noticed something interesting.

The Danish twin data set was now a bit bigger, and extended to people born up to 1910. This gave the researchers 20,502 individuals to look at. Christensen’s team now found evidence that genetics is much more important than previously thought in determining whether you live into your nineties and beyond. “These findings,” the authors wrote in the journal Human Genetics, “provide support for the search for genes affecting longevity in humans, especially at advanced ages.”⁴

So the search is on again. To call it a gold rush might be going a bit far—but not much. For thousands of years people have yearned for a longer life. In Hindu mythology it was amrita, the nectar of immortality; in ancient China the elixir was thought to contain (disastrously for the emperors who drank it) mercury; in medieval Europe the philosopher’s stone was a substance supposedly able to grant eternal life. Now the objects of fascination and study have names such as ApoE, rapamycin, FOXO3a and others, as we shall see. The search for the factors linked to lifespan is the modern equivalent of the historical search for the fabled elixir of life.

• • •

When I arrive at Mrs. Love’s spacious and warm flat in Beaconsfield, about twenty-five miles northwest of London, it’s 2 p.m. Her daughter has told me that her mother fell and broke her hip earlier in the year, so I’m prepared for someone quite frail, but Elizabeth Love is standing up to greet me, and looks, remarkably, at least twenty years younger than her chronological age.

She asked that I arrive after lunch. This is after, I now find out, her daily glass of sherry. “I have a glass of sherry before lunch every day. And I have a gin martini every night before my supper. And have done for years.” There’s just a hint of defiance. (I should’ve arrived before lunch, I think.) She had other vices, too.

“I smoked all my life, not heavily, but I did. I gave it up about ten years ago.”

This wasn’t on doctor’s advice; she just gave it up, just like that.

“I smoked about ten a day, so I wasn’t a terribly heavy smoker, but I did smoke and I still drink.”

Ten cigarettes a day for the best part of seventy years seems like quite a lot to me, and any doctor will tell you that for most people, the vast majority, smoking like this will see you off well before you reach old age. And yet. You hear of people who can get away with it. Mrs. Love appears to be one of those herself. Jeanne Calment, the most famous person in aging research and the oldest human to have ever lived, was another. She apparently smoked for ninety-six years.⁵ She is not, however, thought to have smoked more than one or two cigarettes a day, nor is it known if she even inhaled.⁶ Still, even very light smoking is harmful, so she must’ve been protected, somehow. She got away with it.

Calment lived her whole life in Arles in the south of France, dying in 1997, aged 122. She ate a diet rich in olive oil and chocolate: she reportedly put away a kilogram of chocolate a week. We feast upon factoids like this, grasping for justification for our own bad habits. When I casually mentioned that Mrs. Love had a glass of sherry before lunch every day, my partner immediately said no, I couldn’t use Mrs. Love as justification for drinking.

Inevitably, Mrs. Love and I start off talking about the Second World War. She lived on Kensington Church Street in London until her flat was bombed in the Blitz. “The blast blew the windows out,” she says. “I wasn’t able to go back then, much to my disgust.” Her husband was a South African who enlisted in the navy then worked for the Admiralty. He was three years younger than her and died in 2004.

“We got married in 1941 when he was home on leave,” she says. Their plan had been to marry in September, but in July her fiancé was told he was going to be posted abroad. They had no option but to arrange a snap wedding for the next Saturday. The day after they married, he was posted away with the navy for eighteen months. “Our communication, my husband and I, was through air letters. I was lucky if I got one every three weeks. And that was the only communication we had for eighteen months.”

Mrs. Love joined the Women’s Voluntary Service. She had learned to drive before the war, so she was tasked with delivering supplies to those homeless after bombing raids. “I was driving an army lorry, we went to Coventry, when Coventry was virtually flattened. We were at the Blitz in Liverpool. I was driving a water carrier, and we delivered food to the people.”

By the end of the war she was living back in London with her husband. “We were in the crowd outside Buckingham Palace, on VE Day,” she says. “We saw the Royal Family come out.”

She doesn’t really have friends now. “When we first came here I used to play bridge with people in the flats, but one by one they gave up.” She corrects herself. “They died, let’s face it. And so it all died a death, so I don’t play bridge anymore.”

Her daughter interjects. “You’ve never done any exercise, have you, Mum?” Mrs. Love happily agrees she’s never bothered with anything like that. It’s a counterintuitive point that we’ll come back to: on average, centenarians don’t do any more or less exercise than the rest of the population. Not all have engaged in a healthier lifestyle, nor have they all set out to be long-lived. Swapnil Rajpathak and colleagues at the Albert Einstein College of Medicine in New York, surveyed 477 exceptionally long-lived people (their average age was ninety-seven) and compared them with a selection of younger people from the general population. All the participants were asked about their lifestyles. Rajpathak found that the super-old group were just as likely as younger members of the population to be overweight or obese, had similar patterns of alcohol consumption and physical activity (or lack of it), and were just as likely (or not) to have a low-calorie diet.⁷ The environment, what they do, or what they eat are not factors for centenarians reaching old age.

I ask Mrs. Love if she’s lonely, and she says no, although her daughter is with us and the denial is not wholly convincing. She’s not worried about loneliness, she says. Every day she does the Telegraph crossword, goes for a walk with her carer, and chats with someone. They all know her in the shops. One of her daughters visits almost every day. “I’ve got eight grandchildren and ten-and-one-on-the-way great-grandchildren, so it’s a big family. They’ve kept me young. It keeps me going, keeps my interest in life, I listen to all the tales of the family in various age groups and generations, and it definitely keeps me ticking over, it gives me a huge interest in life.”

She’s had to broaden her views. “I’ve had to accept things I don’t approve of,” she says, and I brace myself for some awful and anachronistic view. “This boy and girlfriend living together thing, I don’t approve of that out of marriage.” That’s as bad as it gets. “There’s no doubt about it,” she says. “Having a big family has kept my brain ticking over.”

• • •

No one has yet beaten Jeanne Calment’s longevity record. The closest is an American, Sarah Knauss, who died in 1999 aged 119. Knauss and Calment mark the current crest of a remarkable surge in life expectancy over the last two hundred years, a surge that has encouraged wild optimism about how far it might go.

In the nineteenth century, you could expect to live to somewhere between thirty and forty. People did live longer than that, of course, but because it was common for children to die young, the average life expectancy was dragged down. But in rich countries, for every year over the last two centuries, three months has been added to life expectancy. At the same time, people are having fewer babies—fertility has crashed throughout most of the world. The proportion of older people to younger is shifting.

The shape and composition of human society is changing more rapidly than at any point in history. The gigantic shift in demographics will have profound implications that governments are only just waking up to. It raises the question of whether the increase in longevity will just carry on.

Jan Vijg, of the department of genetics at the Albert Einstein College of Medicine in New York, thinks not. In 2016 he and his colleagues published a paper in Nature suggesting that we’d reached the natural limit of the human lifespan.⁸ Sure, our life expectancy has been rocketing, they said. But now it’s plateaued. It’s one thing to show how the lifespan of nematode worms or lab mice can be extended, but quite another to extrapolate to humans. The steepness of the life expectancy curve has beguiled us. By analyzing births and deaths in these databases of lifespan from around the world, Vijg’s team found that the age at which the oldest person died each year increased gradually throughout the twentieth century, but juddered to a halt in the nineties. No one, they found, seems to make it much beyond 115. The plateau in the rise in lifespan is evidence that humans, like all other animals we know of, have an upper limit to their age. There is a biological ceiling, and we’ve reached it.

But the conclusion was immediately attacked. James Vaupel, director of the Max Planck Institute for Demographic Research, in Rostock, Germany, pointed out that lifespan records have often been broken, and he robustly criticized the quality of the Vijg analysis, saying, “They just shoveled the data into their computer like you’d shovel food into a cow.” A rebuttal paper by Stuart Ritchie (who we met in Chapter 1) and other scientists, published in Nature in 2017, attacked the statistical methods used in Vijg’s paper and dismissed the conclusion.⁹

So whether or not Jeanne Calment reached the natural limit of our species’ lifespan remains to be seen. In a way, many researchers don’t care: they are an optimistic bunch and are forging ahead to find ways to lengthen our healthy lifespan, regardless of any potential “natural” limit. “Attempts to intervene in aging in general are going to be frustrated by complexity, but this is not a reason to not try,” says Jay Olshansky, a leading researcher on human aging, based at the School of Public Health at the University of Illinois at Chicago.

Lifespan is an incredibly complicated trait, and to push it to remarkable levels will take some extraordinary interference. We know that some exceptional individuals, such as Elizabeth Love, reach extreme old age without suffering debilitating disease: they are protected, somehow. We know we won’t be able to keep pushing the top end of life upward just by eating well. We’ll need to find out more about what centenarians have in common. Fortunately, if you look at demographic data from around the world, you find that centenarians tend to cluster in certain areas. These are the longevity hotspots otherwise known as Blue Zones.

• • •

Drive up Highway 58, the seaside road on the western side of the main island of Okinawa, in the far southwest of the Japanese archipelago, and head north toward the jungle zone. On your left are subtropical waters of corals and bright reef fish and even a few dugongs, curious marine mammals also known as sea cows. The north of the island, Yanbaru, is a heavily forested jungle, rich in biodiversity. At dusk you see giant fruit bats and, if you’re lucky, the Okinawa rail, a rare flightless bird (once when I was there I think I caught a glimpse of one). The habu, a much-talked-about venomous snake, lives in the jungle, and I definitely saw some of these when I was working there as an insect biologist, although you’re more likely to see one coiled in a bottle of the local awamori sake than on the path in front of you. Pickling the snakes in alcohol is supposed to imbue the drink with stimulating properties.

What you will also see, especially in the village of Kijioka, are super-sprightly octogenarians. That’s remarkable enough, but these old people are considered youngsters by the centenarians here. I met some of them, but it was hard to communicate as they spoke the Okinawan dialect and I spoke only standard Japanese. Still, there’s something amazing about a place where an eighty-something is called, in perfect seriousness, a youngster. One elder, a 105-year-old woman from Kijioka called Nabi Kinjo, became famous when she encountered a habu on her porch. She clubbed it to death with a fly swat.

Japan has consistently topped the world longevity charts for years. It helps that every town and village in Japan maintains a koseki, a register of births, deaths, and marriages dating back to the 1870s. The data in these koseki support the claim that long life in Japan isn’t a recent phenomenon. Sure, the average lifespan has been increasing in Japan as it has elsewhere, but there’s something that puts the Japanese at an advantage.

Of course not everyone in Japan lives to a great age. There is variation, and there are hotspots where individuals enjoy an especially long life. But within the country, it is the people on the island of Okinawa who live the longest, and within Okinawa it’s the people of the village of Kijioka. The people on Okinawa’s western edge are the longest lived in the world.

The people here have been well studied for clues to their remarkable lifespan. Diet (high in tofu, fresh vegetables, and fresh fish), social structure (tight-knit, supportive), lifestyle (activities such as bashofu—a traditional form of fabric weaving that keeps people occupied into old age and supposedly maintains cognitive health) are all considered factors. As is the habit of hara hachi bu, a Confucian practice of eating only until you are 80 percent full.

Several genetic studies have been conducted too, as they have among various other groups of centenarians. Unsurprisingly, Okinawa has been declared a Blue Zone.

As well as Okinawa, I’m lucky enough to have been to some other Blue Zones—Sardinia, in the Italian Mediterranean, and the Nicoya peninsula of Costa Rica—and I can appreciate why their environment could be so conducive to a long life. They are warm and comfortable, food is healthy and abundant. Another, as we saw in Chapter 7, is the Greek island of Ikaria, home of ultrarunner Dean Karnazes’s mother. Surprisingly, there’s a Blue Zone in the continental United States, the homeland of fast food and the epicenter of the obesity epidemic: it’s the city of Loma Linda, in California.

Loma Linda was classed as the only Blue Zone in the US by Dan Buettner, an explorer and writer who came up with the concept after researching longevity hotspots around the world. Men in Loma Linda have a life expectancy of eighty-eight, and women a year more. It’s a lifespan some eight to ten years longer than that of the average American, and the reason is fairly straightforward: the town has been extensively settled by members of the Seventh Day Adventist Church. Seventh Dayers don’t drink or smoke (smoking is banned in the town) and most don’t eat meat. The religion strongly encourages exercise and healthy living, and members of the church also regularly attend services and activities. The people of the town represent, according to the scientists at the New England Centenarian Study, the baseline lifespan for the rest of us, if only we ate well and took better care of ourselves—and, crucially, maintained social connections.

Surprisingly, there’s a mini Blue Zone in central London. It’s been there since 1682, and the people who work there say living there can add ten years to your life. It’s a retirement home for soldiers from the British Army: the Royal Hospital Chelsea, home to the Chelsea Pensioners.

• • •

The hospital and grounds, designed by Christopher Wren, are grand and imperial; the place exudes wealth, like an Oxford college, its Hogwarts-style communal dining hall standing alongside modern hospital facilities. I have a coffee at the café when I arrive, and sit among veterans, some in the famous scarlet uniform with shiny brass buttons and medals, some in more casual fleece jackets, but still bearing the Royal Hospital Chelsea coat of arms. Despite the impressive Grade I– and II–listed architecture and its location in one of the most expensive parts of an insanely priced city, the hospital was designed for rank-and-file soldiers. You don’t have to be rich to live here, you just need to have been a soldier. If you apply and are accepted, you sign over your military pension to the hospital, which is subsidized by the Ministry of Defence. And that’s it. You then have all your needs taken care of. It’s the security, but perhaps more than that, the community, that seems to be behind the longer lifespans here. I doubt it’s the diet—you don’t get Okinawan seaweed and miso-rich superfoods here. When I visited in 2017, the menu included black pudding and fried pig’s liver, deviled lamb kidneys on toast, and creamed semolina pudding. It was like seeing a menu from the war.

But then being here is like stepping back in time. I meet John Humphreys, ninety-eight, who shakes my hand with the grip of a man seventy years younger. It’s no exaggeration to say he’s lived the life of a Hollywood action hero. I wasn’t sure he’d want to rake over old memories of the war, but he didn’t mind telling the stories. They certainly reflect on his character. Gerontology researchers are finding that personality does seem to have an impact on lifespan, and with Mrs. Love I was struck by her no-nonsense attitude. We sit in John’s room, overlooking the beautiful gardens that run down toward the river, and he tells me about the time in 1942 when he was captured by the Germans in North Africa. He was twenty. Wounded and knocked out, he came round to see two large enemy soldiers standing over him. “For you, Tommy, the war is over,” one said.

He was held in a POW camp in Italy. “I didn’t like being incarcerated in a blimmin’ prisoner of war camp, so I decided to escape.” It took nine months before he had his opportunity. He spent the time learning Italian and used it to bluff his way past the guards dressed in a scrounged Greek army uniform that looked similar to the Italian uniform. Shepherding a couple of his mates in front of him, he told the guard in Italian that he was transferring them as prisoners to another location. The guard waved him through, and once clear of the camp, John and his friends hiked south for days, living off the land. He recounts a heart-stopping moment when a German convoy passed by them—now dressed like Italian farm laborers—on the road. The final car of the convoy stopped and an SS officer got out. This is it, thought John: it was one thing bluffing his way past a bored Italian prison guard, but quite another to do it to a member of the fearsome SS. The Nazi officer called him over, and asked him, in broken Italian, where the nearest river was. John managed to explain, and the Germans drove on. John and his friends made it to a village held by British soldiers and got six weeks’ home leave.

By 1944 he had joined the Parachute Squadron Royal Engineers and jumped into Arnhem, for one of the major battles of the late stages of the war. Captured again, it didn’t take him long to bust out. Some POWs he asked didn’t want to try to escape as their morale was low, but he found three mates who were up for it. Again in the classic war-movie manner, he scraped the cement from around the bars of a window, replacing it with ash from the cooking stove so that the guards couldn’t tell what he’d been doing. Eventually he’d done enough to remove the window bars and escape. The four men stole a boat and escaped down the Rhine to Nijmegen. On the wall in his room there’s a photo of him and his fellow escapees in their boat. Humphreys looks every inch the invincible war hero. There’s also a colorized wartime-era photo of his now-dead wife.

“I’ve always had a positive outlook on life,” he says; he thinks some people are just born that way. But he can’t say whether his parents had the same attitude.

“I didn’t know my parents very well,” he says, and I’m reminded of the generational gulf that separates us. “My mother gave all her love and affection to my older brother. I was the gopher.”

The gopher?

“John, go for this; John, go for that.”

So much for nurture. Still, he seems to have been mentally and physically in good shape his whole life. “I was in the parachute squadron, so you’ve got to be fit. My left patella was smashed.”

John describes how he got hold of a bike after he injured his knee, and carried out his own physiotherapy. Six months later, he won the 100 meters and the 200 meters in the platoon athletics. “You’re not going to live a quiet life if you’re a paratrooper. I’ve broken both collarbones, scapula, both wrists, right leg. But they healed fairly quickly. They don’t give me any bother.”

He’s clearly a determined and goal-driven man.

“My advice for a long life,” he says, “is to be positive. Do what you can, the best way you can. If you have a setback, you’ve got to put up with that. You can’t have a garden of roses without a few thorns.”

• • •

Nimmi Hutnik is a psychologist at London’s South Bank University, where she specializes in mental health issues such as depression, anxiety, low self-esteem, and PTSD. I came across her through a remarkable survey she and colleagues had made of centenarians living in the UK. Hutnik researches mental resilience (which we will explore more fully in the next chapter), and became interested in how it might be expressed in centenarians. Her team traveled around the country and interviewed sixteen centenarians: five men and eleven women. The researchers’ approach was simple but effective. They started by asking the interviewees to tell their story, following up and prompting with questions such as: Can you tell us something that has shaped your life? What is it like to live to a hundred and beyond? What’s the secret of positive aging?

The centenarians were self-selected. They had replied to recruitment notices for the interviews, so there may be an element of bias here, but nevertheless the general theme is fascinating. The centenarians don’t seem to have achieved an extraordinary lifespan because they’ve had an easy life, Hutnik says, but because they’ve dealt with stress efficiently when it struck. They used phrases such as “accept whatever life brings,” “don’t worry about the past,” “take each day as it comes,” and “do what you can to make things better and then forget it.” They described accepting things they could not change.¹⁰

Take Phyllis, who was 102 when interviewed. Quite a lot had happened in her life, she recounted: “Different things, what with my father being killed and then my husband going to the war and my brother being killed and things like that. But then again, you’re left and you’ve got to get on and that’s it. You just have to cope with it, don’t you? I’m afraid I’m one of those resilient people.”

And then there’s Albert, also 102 at the time. “If you can’t change it and alter it, don’t worry about it,” he said. Albert had been a miner since he was fourteen and the coal dust had damaged his lungs, but he still went dancing as often as he could. Nita, also 102, said: “If you can manage and you’ve not got pain, you’ve got to try and push worry away and not be miserable.”

We’ve all probably heard from elderly relatives about how they just got on with things back in the day. The implication—sometimes it’s more of an accusation—is that the current generation is too hesitant and coddled. That may be true, but then more of us are living to a great age, so we can’t be that coddled. Perhaps it’s just one of those things old people say and we’ll say it when we’re old, too.

When Mrs. Love and I first started talking, she mentioned that during the war she had a baby who died. At first I don’t pursue the subject, reluctant to press her on such a tragic event, even if it was something that happened seventy-five years ago. But later I ask her what her recipe is for positive living. Every life has its ups and downs, and even more so very long lives, so what’s her advice on getting through it? “You have to get on with it,” she says. “I learned that when our baby died at one year old. It was devastating.” This last word is spoken with an exhalation, a sigh. “But I thought: ‘You just get on with it.’ ” You just had to pick yourself up and have another baby. “There was no counseling in those days. You have to be positive to get on with things. No good everybody doing everything for you.”

For a while during the war this attitude was widespread, she says, but she thinks that not everyone has it naturally. This attitude, this positivity, is reminiscent of Ellen MacArthur and of Petra Kasperova, of Dave Henson and Barbara Hannigan. In fact, it reminds me of almost everyone I’ve met while writing this book. “You’ve got to have it in yourself to do it,” says Mrs. Love. And she still has it. After she broke her hip in the summer, her daughter tells me, the physiotherapists were impressed with her mother’s determination to get better. “I still get out every day,” Mrs. Love says. “I was determined to get over that. Not my scene to flop around, really.”

• • •

Mrs Love’s comments—which I find humbling and inspiring at the same time—remind me of something I’ve read about Jeanne Calment. According to a biographer, she was biologically immune to stress. She had a saying, “If you can’t do anything about it, don’t worry about it.” She also ascribed her longevity to her calm approach to stress, telling the zoologist and writer Desmond Morris, “that’s why they call me Calment.”¹¹

When I first read this about Calment, I was immediately reminded of a common Japanese expression, sho ga nai. It means “nothing can be done about it.” A variant, shikata ga nai, means something similar, or “it cannot be helped.” After meeting Mrs. Love, and reading what the centenarians in Hutnik’s survey said to her, I am reminded of it again.

I noticed in Japan that Japanese people got less riled about things than I did. Sometimes it riled me that people didn’t get riled. There are surely some things worth getting passionate about, I felt. The passivity and acceptance of fate encapsulated in sho ga nai got my goat at times. But eventually I found it admirable. The attitude certainly helps make a very pleasant and harmonious society to live in, and probably helps keep your blood pressure down. Whether it accounts for the long life of the Japanese is another matter. You can’t will yourself to a longer life. We know stress has a range of important ill-effects on the body, but it’s not enough to live calmly, or positively, or even to be determined not to flop around: we want to know what are the concrete links to longevity, and for that we need to explore the genome.

• • •

Neither John Humphreys nor Elizabeth Love have had their genome sequenced, but it’s a fair bet that they carry a particular variant of a gene that has been the subject of huge amounts of research over the last twenty-five years. The gene is called ApoE, it lives on chromosome 19, and it makes a protein called apolipoprotein E. If you look at a picture of apolipoprotein in the protein database you’ll see a hefty, curly beast of a protein made of 299 amino acids. Its job is to transport cholesterol, and it comes in several forms.

Since 1994, when the gene was first linked with extreme lifespans,¹² it has spawned hundreds of research papers. From the number of people studying it and the amount of money going into it, you might think ApoE is the most exciting gene in the genome. But as with everything, it’s complicated. One version of the gene, E4, has been linked to Alzheimer’s and cardiovascular disease, and thus an early death, but an analysis of 2,776 centenarians and a control group of younger people showed that if you carry either of two other versions, E2 and E3, you are more likely to reach extreme old age.¹³ There is a longevity benefit to having E2, especially, and a cost to having E4.¹⁴

Kaare Christensen’s influential Danish study of the role of genetics in aging tracks cohorts of people born in 1895, 1905, 1910, and 1915. Christensen has found that the “bad” ApoE4 variant decreases in frequency with each successively older cohort, being found in about 20 percent of the cohort at fifty years old and 10 percent at a hundred:¹⁵ “If you look at centenarians there will be fewer with ApoE4. For sure, it’s not a good gene to have but it’s not like you’re definitely weeded out if you have this gene.”

Christensen, a physician who works in public health, says one of the criticisms he’s heard of his longevity findings is that modern society is failing because it helps weak people to scrape through to old age. This is called the “failure of success”: the success is that we’re living longer but the failure is that we’re in bad shape when we get there.

He set out to test this idea in a 2017 study.¹⁶ “We followed the 1905 cohort until they turned a hundred to see if they got more disabled, and they didn’t.” He then looked at the 1915 cohort. Not only did more of them survive to ninety and a hundred, but they were in better physical and mental health than previous cohorts had been at that age. “This is very encouraging,” Christensen says. “It gives us reason to believe that in the next thirty, forty, fifty years we’ll arrive at high ages with better cognition.” IQ has been steadily increasing throughout the twentieth century, in a phenomenon known as the Flynn effect, after its discoverer, James Flynn. “This effect seems to hang in there when we arrive at high ages,” Christensen says. I’m reminded that Mrs. Love does the crossword every day.

Most of the variation in survival up to about the age of eighty is due to environmental influences: the diet you’ve eaten throughout your life, the support you’ve had from family and friends, the medical care you’ve received. Environmental components include behavioral factors such as whether you smoke, how much alcohol you drink, what exercise you do. But for the very old, genetics plays a much more important role. “One reason is there’s been longer time for your genes to make their marks on you in either a good or a bad way,” says Christensen.

However, despite the robust findings that ApoE contributes to longevity, the effects are seen only when you analyze large numbers of genomes. On an individual level, even a gene such as ApoE has only a small effect. “Oh, it’s trivial,” says Christensen. Its actual influence on our individual lifespan is tiny, just as any of the gene variants related to intelligence have only a tiny effect on their own. “There’s little doubt that there are thousands of genetic factors each with very small effects.”

To some this means there’s no point chasing genetics to try and “solve” aging. To others, it just means the problem is harder, but it’s no reason to quit.

• • •

Thomas Perls, based at Boston University School of Medicine, runs the New England Centenarian Study (NECS). The study was launched in 1995 to track centenarians living in the Boston area, primarily to investigate dementia. It has enrolled around more than 1,600 centenarians and now has on its database around 150 supercentenarians, people aged 110 or older. It is the largest such sample in the world, and it has included the second oldest person ever to have lived, Sarah Knauss, who reached the age of 119. Knauss, incidentally, was another who seemed to handle stress well. She never let anything faze her, her daughter said. When Knauss was informed in 1998 that she was the oldest person in the world, she replied with two words: “So what?”

So what? The “so what” is that she lived so long without major illness or cognitive decline. “Supercentenarians,” says Perls, “are the crème de la crème when it comes to compressing the time they are sick toward the end of their very long lives.”

Compression is a term you hear a lot from longevity researchers. “Compressed morbidity” refers to the fact that the very old often stay healthy in body and mind right to the end, like the two elderly people we’ve met in this chapter.¹⁷ This period of physical and cognitive function is called the healthspan, and it is this that Christensen has found is growing longer in his Danish cohorts. It is here where we are most likely to see extension in the coming years, rather than lifespan itself.

The NECS team divides the subjects in their database into three groups: escapers, delayers, and survivors. The first group accounts for about 15 percent of the study members, and as their name suggests, they have, remarkably, escaped any kind of serious disease. Elizabeth Love and John Humphreys are classic escapers (in John’s case, literally). Around 43 percent of the NECS members are delayers, and have avoided contracting any serious age-related disease until the age of at least eighty. Then there are the survivors, accounting for around 42 percent of the members, who have had a serious disease before they were eighty, but have fought it off.

“Probably seventy-five percent of their ability to get to their age is genetic,” says Perls. “Thus they may be the key to our ability to discover longevity-associated genes and biological mechanisms that slow aging and protect against age-related diseases.”

There are a few ways to measure this genetic component, a common one being, as we’ve seen, the genome-wide association study (GWAS). This is a way of scanning the genomes of many different people, looking for genetic variants that are associated with a disease or a particular condition—in this case, longevity. The method looks at the variants in the genome called single nucleotide polymorphisms, or SNPs. We each have many thousands of these tiny variations, and a GWAS attempts to identify those that are linked to the trait in question.

Perls’s team have applied this to 801 centenarians, with 914 control people. Now, one of the criticisms of GWAS as a useful tool is that there may be thousands of SNPs relating to any given condition. That’s certainly the case, as we saw, with complex traits such as intelligence. You need huge sample sizes to be confident about what you find, and 801 centenarians is not a lot. This means you can’t seize upon a particular SNP and say, “You need this to be a centenarian!” Still, it’s a start, and a GWAS search represents an unbiased sift through a giant pond. Perls’s team has found 281 SNPs that they call signatures of exceptional longevity.¹⁸ Follow-up GWAS studies on a further 2,070 people who were among the longest-lived 1 percent of Americans born in 1900 identified yet more new variants associated with long life.¹⁹

It confirms, the team writes, that exceptional longevity is influenced by the combined effects of a large number of SNPs. A 2014 study by Kaare Christensen and colleagues failed to find evidence for the same effect on longevity among those SNPs,²⁰ but according to Perls that’s because the Danish study didn’t look at extreme old age, only nonagenarians. Christensen is among those who say that to perform a decent GWAS scan you need far larger samples than is possible—there just aren’t enough centenarians around.

All this has a crucial take-home message. It means you can do all you like in terms of diet (or dietary restriction) and pill-popping, but unless you’ve got the genes, you just ain’t gonna be a centenarian. Or as Nir Barzilai, director of the Institute for Aging Research at New York’s Albert Einstein College of Medicine, put it to me: “Environment may take you beyond eighty but not close to a hundred.”

It seems to kill the idea of Blue Zones, too. At least, it kills the idea that you can move there, or emulate the diet of the place, and reap the benefits. We saw from the work of Christensen that the environment doesn’t seem to influence whether you reach a hundred or not, and Barzilai and colleagues have used a clever method to show how the environment, Blue Zone or not, is less important than we might think. The Albert Einstein College of Medicine runs the LonGenity project, a long-term study of the factors contributing to long life. The subjects are Ashkenazi Jewish, recruited from the northeastern United States, which means they are from a similar genetic background, making it easier to spot any influential genetic factors.

The participants in the project, aged sixty-four to ninety-five, are divided into two groups. They are defined either as the offspring of parents with exceptional longevity (OPEL), meaning that they have at least one parent who lived to age ninety-five or older; or as the offspring of parents with usual survival (OPUS), where neither parent survived to the age of ninety-five. Barzilai’s team test the participants on a range of physical parameters, such as balance, grip strength, and mobility. They have found that people in the OPEL group perform better on average than those in the OPUS group: if your parent is exceptionally long-lived, you can look forward to a slower physical decline.²¹

Barzilai’s team has gone further, and looked at the medical and lifestyle histories of the participants, including their diets. They have found no difference in calorific intake between OPEL and OPUS members, nor any differences in the types of food they ate—the proportion of fruit and vegetables, or grains, or meat. So the “nutritional environment” for all members is the same. However, OPEL members have a 29 percent lower chance of having hypertension, 65 percent lower odds of having a stroke, and the risk of cardiovascular disease was 35 percent lower, compared with OPUS members.²²

“I think Blue Zones are mainly genetic islands and not environmental islands,” says Barzilai. “I don’t think we have capacity to survive over the age of a hundred with environment only.”

The sifting for genetic markers continues. In another study by Thomas Perls and colleagues, two supercentenarians, a man and a woman, had complete genome sequences. The pair were selected from the NECS database because they had attained the age of more than 114, still without any disabling illness. In other words, as we’ve seen, the lifespan of these supercentenarian escapers closely matched their healthspan. When Perls’s team examined the complete genome sequence of the two, they found they did not carry most of the known longevity variants. The two did, however, carry a number of variants associated with disease. They had a similar number of these disease variants to those found in regular, noncentenarian samples.²³

So what does this mean? First, that the known longevity variants are not the whole set. There are many more remaining to be discovered. This idea is supported by the finding that the supercentenarian pair had many novel genetic variants at locations in the genome close to the longevity SNPs found in the previous study.

Second, it shows that you can live with “disease genes.” Perls was surprised at first when the genome sequence showed disease-associated gene variants. Scientists had assumed that centenarians would have clean and tidy genomes, but they don’t. Again, however, this points to the protective effect they get from elsewhere in the genome. This protective effect extends to ameliorating the damage done by smoking or drinking or having a poor diet. Remember, Jeanne Calment smoked for ninety-six years and Elizabeth Love had a seventy-year habit. The upshot is that there are hundreds of genes and thousands of variants of genes influencing longevity. It means we can’t hope to tinker with them to make improvements, there are just too many. It’s the same issue we saw with intelligence. Perhaps a better bet is to mimic their effects by using drugs.

• • •

It would be useful now to look briefly at attempts to live forever.

“Geriatric medicine can be defined as the attempt to eliminate the diseases of old age directly,” says Aubrey de Grey. “It has been an abject failure.” A prodigiously bearded real-ale enthusiast, De Grey is one of the central figures in the lifespan-extension movement. A longevity researcher, he is a cofounder of the SENS Research Foundation, a gerontology research institute based in California. SENS stands for Strategies for Engineered Negligible Senescence. The reason geriatric medicine doesn’t work, he says, is because the diseases of aging are nothing like infections. “They shouldn’t really even be called diseases, because they are inseparable from aging other than semantically. Being side effects of being alive, they can’t be cured.”

This is becoming a mainstream view among longevity researchers and public health officials. Aging is the common factor in the diseases that hamper and kill us. Even a cure for cancer would increase the population of older people by only 0.8 percent over fifty years, because other diseases—cardiovascular, diabetes, stroke—would take its place. Delaying aging itself would increase the population by 7 percent—and provide significant economic returns. Dana Goldman, professor of public policy and pharmaceutical economics at the University of Southern California in Los Angeles, estimates that such a delay of aging would generate $7.1 trillion over fifty years.²⁴ Jay Olshansky, at the University of Illinois, calls this the longevity dividend. We enjoy health care, which means we have a relatively long life, but most of us suffer ill health at the end. This is very expensive, not to mention a poor way to end life. If we tackle aging as a disease, we can increase health span and save money, and increase the vigor of the elderly.

Where de Grey differs from this kind of thinking is in statements claiming that the first person to reach 1,000 has already been born.

People will go to almost any lengths for a longer life. More than a hundred years ago, a French-American physiologist named Charles-Édouard Brown-Séquard reported that an injection prepared from the crushed testicles of guinea pigs and dogs could rejuvenate and prolong life. He was seventy-two. He also claimed that his own sexual prowess had been boosted after he ate extracts of monkey testes.²⁵ Even back then (it was 1890), and even in Paris, where they are more open to outré suggestions, his ideas were treated by fellow scientists with disdain—though, one suspects, with a twinge of envy in case it was true.

He was eccentric, for sure, but Brown-Séquard was not entirely wrong. He was among the first to show that substances in the blood have effects on organs in the body—substances we now call hormones. His elixir didn’t do much for him, and he died at the age of seventy-six, but he has a whole range of spiritual descendants: people willing to try anything. Even, for example, having infusions of a child’s blood.

In 2011 at Stanford University, Saul Villeda’s team showed that old mice given the blood of young mice received a boost to the growth of their brain cells.²⁶ Then Amy Wagers at Harvard University and colleagues performed an experiment whereby an old mouse was physically joined to a young one, such that their blood circulation was shared. The old mouse was a twenty-three-month-old with cardiac hypertrophy. That’s when the heart muscle becomes thickened and the size of the chamber is decreased. It was joined to a healthy young pup, a two-month-old mouse with no heart problems. Four weeks later, the researchers found that the heart of the older mouse had returned almost to the size of that of the younger animal.²⁷

Villeda is careful to state that his goal is to extend healthspan. It would be a bit much to publicly declare that he wants immortality through the blood of the young. He wants to compress morbidity and delay the onset of dementia. Wagers’s lab and others are trying to isolate the factors in young blood that are responsible for the rejuvenation. One is a protein called GDF11, which young mice have much more of than old mice. When Wagers injected just the GDF11 protein into older, hypertrophic mice, she found that after a thirty-day treatment their hearts were similarly reduced in size. In 2015 Villeda, now at the University of California at San Francisco, found an “anti-elixir” of life in the brains of old mice. The compound, a protein called beta2-microglobulin, operates in the immune system to help differentiate between the body’s cells and invading cells, and is also active during the development of the brain.²⁸

You can imagine the nightmarish scenarios that some people have dreamt up after hearing about this work. Or if you can’t, here’s Debora Price, professor of social gerontology at the University of Manchester, and president of the British Society for Gerontology: “In the extreme scenario you could get baby farms. Clandestine clinics where babies are sewn to old people.”

Gene therapy is another option. In 2016 an American businesswoman named Elizabeth Parrish made headlines when she announced that she had traveled to Colombia the year before to receive two gene therapy treatments aimed at prolonging life. Parrish, the boss of BioViva, a Seattle-based biotech company working to develop treatments to slow the aging process, was forty-four at the time of the treatment.²⁹ The target is the caps on the ends of our chromosomes, called telomeres. These caps are made of around 1,500 repeats of six genetic letters, TTAGGG. Each time the chromosome divides, the cap shortens by one, until eventually it is unable to divide anymore. At this point the cell has reached the end of its life. Centenarians have longer telomeres, and this is associated with protection from both diseases of aging and cognitive decline.³⁰ The tantalizing idea is that if you can extend the length of the telomere, you can stave off the aging process. This has been demonstrated in mice by a team of Spanish researchers in 2012,³¹ although its effectiveness in humans is unknown.

Because BioViva had not done the preclinical safety work necessary to progress to studies on people, the US Food and Drug Administration did not authorize Parrish’s experiment—hence her trip to an unnamed clinic in Colombia. She claimed that the therapy had reversed her cellular age by twenty years, but other scientists were skeptical both of the claim and of the effectiveness even if it turned out to be true. You can see similarities to Paris 120 years ago.

Other people starve themselves. Michael Rae is one. He works with Aubrey de Grey at the SENS Foundation. The recommended calorific intake for an adult male is 2,500 calories; Rae, forty-six, has restricted himself to only 1,900 calories for more than fifteen years. There are many more like him. For example, Dave Fisher, from Bracknell in the UK, is fifty-nine and has been on a punishing 1,600-calorie diet for more than twenty-five years.³²

Drastic diets extend lifespan in a range of lab animals, from nematodes to flies and mice, by up to 50 percent. This works because on a restricted diet, stress-resisting genes are switched on, and it is through the action of these genes that protection from aging is achieved. Mice on restricted diets are resistant to the usual age-related diseases such as cancer and heart disease. One concern for people trying this method of longevity enhancement is that calorie restriction does not seem to work in primates. In a twenty-five-year study, scientists from the US National Institute of Aging found that rhesus monkeys fed a third less than normal did not live any longer,³³ although the healthspan of calorie-restricted monkeys may be better.³⁴

Is it worth it? To the half-starved men (and it does seem to be overwhelmingly men) who do this, clearly the answer is yes. They profess to love life so much they want to extend it beyond the usual allotted years; it’s a shame they can’t enjoy the intervening period a bit more, too. De Grey said calorie restriction had looked mighty hopeful for a while, but no longer, although “lots and lots of experts in aging who should be ashamed of themselves are still doing it, of course.” De Grey’s preferred solution is to repair the molecular and cellular damage of aging so it doesn’t become a problem.

When de Grey came up with the concept of comprehensive damage repair as a mechanism to extend lifespan, he coined the term “longevity escape velocity.” This is the moment when life expectancy starts to increase by more than a year, per year. This situation would mean we rejuvenate at a quicker rate than we age; we would outpace death. In some longevity circles it is the fabled moment they are aiming for; in others it is seen as irritating science fiction. Here is De Grey’s current thinking as to when we might reach this point: “I think we have a 50 percent chance of getting there within about twenty years from now, so long as funding for the early-stage work that’s going on right now improves soon. Otherwise it could be an extra ten years.”

Alex Zhavoronkov, CEO of Insilico Medicine, a biotech firm in Baltimore, Maryland, is more optimistic: “I have no doubt that the escape velocity has already been achieved. The recent advances in deep learning and reinforcement learning, digital medicine, cancer immunology, gene therapy, and regenerative medicine, made over the past five years give me confidence.” Zhavoronkov points to the sheer number of scientists working in this area, and the progress he says is being made, especially in South Korea and China. We saw earlier that an increase in healthy lifespan could generate significant income for the world economy. I mention Zhavoronkov to show how despite calls for caution and moderation from many longevity researchers in academic institutions, the prize is such that dozens of other researchers are charging ahead. Zhavoronkov is an optimist, a futurist, and a businessman. His main fear is that research isn’t happening fast enough: “We are likely to see a global economic collapse before the major developed nations embrace productive longevity as the new source of economic growth.”

• • •

I’m also keen to talk to Zhavoronkov because he has experimented with antiaging drugs in the past. In particular he’s tested rapamycin, a drug that mimics the effects of the genes turned on during dieting, and which seems to offer the benefits of starvation without the pain.

Alan Green lives in Little Neck, Queens, off Interstate 495, which happens to be just a few miles past Flushing Meadows, the scene of Petra Kasperova’s Sri Chinmoy triumph.

“When I was seventy-two years old, I had a thirty-eight-inch waistline and could not walk my dogs in the park without angina and shortness of breath going up small hills,” Green tells me. A physician, he trained at SUNY Downstate Medical Center in New York, qualifying as an MD in 1967. The angina forced him to confront the fact that he was growing old and deteriorating. He started reading up on what was known about aging, and came across the work of Mikhail Blagosklonny, at the time a professor of oncology at the Roswell Park Cancer Institute in New York.

Blagosklonny’s major interest is in rapamycin, which is used to suppress the immune system during kidney transplants, but which also extends lifespan in mice. The drug operates on a pathway called mTOR, the “mammalian Target Of Rapamycin,” which seems to be key to several important diseases of old age, such as dementia and cancer. Blagosklonny has admitted to using it experimentally in the past,³⁵ and Green decided to try it, using, he says, common sense to work out the dose.

“I am now seventy-four years old. This spring I just took up cycling. I cycled 1,000K in May and then 1,000 miles in June and plan to cycle 1,000 miles in July and August. The reason for the cycling is just the incredible joy of feeling fit after suffering from aging.”

He now has a thirty-one-inch waist. “My heart is good to go,” he says.

It’s tantalizing, and Green is a passionate, practically evangelical believer in the power of rapamycin, but the antiaging benefits of the drug are completely unverified in people. “Rapamycin is not safe for humans yet,” says Barzilai. It’s why he is trying to get the US Food and Drug Administration to approve clinical trials. He has one project ready to go, designed to test the diabetes drug metformin specifically for its antiaging properties (the trial is called TAME: Targeting Aging with Metformin). The drug has already been used for years for people with type II diabetes, so we know it is safe, but Barzilai wants to give it to people with cancer, heart disease, and cognitive decline, to see if the drug alleviates their symptoms and prolongs their life. “We need field trials,” he says.

• • •

But is aging itself wrong?

To me, the moral issue around trying to cure a natural process is beside the point. It’s not Gradgrindish to ask that we look at this scientifically. We try to cure cancer and heart disease and all the other diseases associated with old age and there’s no dilemma there. But a better way to solve these problems—scientifically, technically, socially, and economically—seems to be to slow aging itself. The worry, of course, is that solutions will be available only to the rich.

I started this chapter by asserting that I wanted my days to be unlimited. But I can’t know what I’ll want when or if I reach old age. When our oldest daughter was born, we named her after her great-grandmother Molly, who was then ninety-three. In recent years, the older Molly had lost her mobility and was pretty much confined to her house, where she still lived independently. I remember her saying that she had come to terms with her own mortality. It seems an extraordinary thing, to be prepared to stop existing. But at the same time it’s understandable: many, if not all, your friends are dead, the lives led by your family, if you have any, are very different from yours. Add to that the ill-health that many elderly people face, and you can see why some people don’t mind dying. It shouldn’t feel taboo to say so. But then nor should it be taboo to try and escape death for as long as possible.