Long for This World: The Strange Science of Immortality - Jonathan Weiner (2010)
Part II. THE HYDRA
They are ill discoverers that think there is no
land, when they can see nothing but sea.
THE ADVANCEMENT OF LEARNING
Chapter 5. THE EVOLUTION OF AGING
Not long ago I was talking about the problem of mortality with a physicist and he told me, with a smile, that it’s in the nature of everything to fall apart. That is what the law of entropy tells us about inanimate objects like planes, trains, and automobiles. That’s also what common sense tells us about animate objects like our own warm, breathing bodies. But we don’t fall apart between the years of, say, six and twelve. We grow bigger and stronger in those years. If we can do that much when we are growing, then why can’t we at least hold steady, hold our ground, from the ages of twenty to a hundred and twenty? We don’t, but that doesn’t mean our failure to do so is mandated by the laws of physics. If that’s breaking the laws of physics and common sense, then we’ve already broken them. Every human body breaks those laws in the womb from the moment sperm meets egg. Those two microscopic cells meet in the dark and nine months later, after a miraculous construction project, a baby is born with a body made of trillions upon trillions of cells, from the brain cells inside the still-soft skull to the skin cells in the ten fingers and ten toes. And the history of the development of life on Earth is at least as spectacular as the development of each life in the womb. Life on Earth, from small beginnings, has attained extraordinary profusion. Three billion years ago, life was all microscopic single cells. And now there are millions of species of living things, from shrimp to whales, from mites to elephants. The development of life on Earth is like the development of a life in the womb: it defies common sense, and the intuitions of physicists, like a ball that rolls uphill.
If life can do so much in the first half, why does it fail in the second? Why can’t it keep the ball rolling? Bacon makes this point in the first pages of his History of Life and Death. He chastises the physicians and philosophers of his time for missing it. Conventional wisdom in Bacon’s day held that there is something in the body that can’t be repaired, some “radical moisture” that can never be replenished. Our bodies lose that moisture and dry out and that’s why we get old. But that idea is “both ignorant and vain,” Bacon writes; “for all things in living creatures are in their youth repaired entirely; nay, they are for a time increased in quantity, bettered in quality.” So much so that “the matter of reparation might be eternal, if the manner of reparation did not fail.”
We grow up, and then we seem to hold steady for years. A woman between the end of puberty and the onset of menopause balances the building up and the tearing down of her bones so perfectly that they grow neither too heavy nor too light. Her whole body—flesh, blood, bone, and sinew—is a kind of fountain in which the new continually replaces the old and the form stands as if it would stand forever. Then, after menopause, the balance fails, and bone mass declines, and osteoporosis sets in. But why does the balance have to fail? Why did this failure evolve? Which is to ask the most fundamental question of the science of mortality: How did old age and death come into the world?
The answer that has now emerged in the science of mortality gives hope to the field’s optimists.
Darwin himself does not seem to have thought about this question. Apparently, like most of us, he took aging for granted. But one of Darwin’s first great supporters, the German biologist August Weismann, did think about it. His own conclusion was dark—so dark that it may have contributed to the doldrums that gripped the field for much of the twentieth century.
Weismann laid out his argument about the evolution of aging in one of his first lectures as prorector of the University of Freiburg in the spring of 1883. He published the lecture that summer as an essay, “Upon the Eternal Duration of Life.” “In my opinion,” Weismann said, “life became limited in its duration, not because it was contrary to its very nature to be unlimited, but because an unlimited persistence of the individual would be a luxury without a purpose.” In other words, he believed that life on Earth had been immortal, once upon a time. Immortality was just as natural a state for living creatures as mortality. “Among unicellular organisms natural death was impossible,” Weismann wrote. An amoeba and the paramecium never die only because they can’t—because they are too simple to die. But as soon as multicellular life evolved on this earth, aging did become possible for them, and they began to grow old and die.
In the beginning, in Weismann’s view, death did not exist; and then life invented it. In fact, if human beings ever did find a way to make ourselves immortal, said Weismann, then our descendants would just evolve mortality all over again. “Let us imagine that one of the higher animals became immortal,” Weismann writes; “it then becomes perfectly obvious that it would cease to be of value to the species to which it belonged.” Think of it this way, he says. Even if a tree or an elephant or a mouse never got killed by some accident, even if it lived for eternity—which is, of course, impossible—it would be bound to get damaged and then crippled by this and that affliction, somewhere along the line; “and thus the longer the individual lived, the more defective and crippled it would become, and the less perfectly would it fulfill the purpose of its species.” The species would have to keep producing new and healthy specimens to take the place of its sick, hobbled, and infirm; “and this necessity would remain even if the individuals possessed the power of living eternally.”
So death is a sacrifice that each generation has to make for the sake of the next. We reproduce, and then we have to die. “Worn-out individuals are not only valueless to the species, but they are even harmful,” he says, “for they take the place of those which are sound. Hence by the operation of natural selection, the life of our hypothetically immortal individual would be shorted by the amount which was useless to the species.” Life’s invention of death proved to be so successful and necessary, death made species that possessed it so vital, that once death arose it became universal; so that “the higher organisms, as they are now constructed, contain within themselves the germs of death.”
In Weismann’s view, then, aging and death are accomplishments that we complicated creatures should be proud of. Amoebae and other single-celled organisms are forced to remain immortal because they do nothing but divide and divide. But the immortality of protozoa is primitive compared with the mortality of metazoa like ourselves.
There’s a certain fascination in this idea, dark as it is. In Weismann’s view of life, aging is an adaptation. Death itself is an adaptation. Death is more important to us than eyes, ears, teeth, and hands; or flukes, gills, and flippers; or roots, branches, and green leaves. Just as a beetle never grows as large as a horse, because there are natural limits to its growth, so a beetle never lives as long as a horse, and a horse never lives as long as a man, because there are natural limits to their longevity.
Besides the protozoa, Weismann did recognize one other form of biological immortality on this earth. Our bodies are divided into two kinds of seeds, two kinds of cells, the mortal and the immortal. The seeds in our eggs and sperm have been passed down to us from generation to generation. Weismann called these seeds the germ cells, and the rest of our bodies the soma. The soma is doomed, but our germ cells are potentially immortal.
That part of his argument is still regarded as well established. But his basic premise is not, even though most of us still assume that it is true, because it makes intuitive sense. If asked why we grow old and die, most people today would answer, just as Weismann did, that we have to wear out and die to make room for the next generation.
And most biologists in Weismann’s generation and for several generations afterward did think his point made sense. Weismann’s argument helped inspire Sigmund Freud’s famous theory of the death instinct. “What lives,” Freud wrote in Beyond the Pleasure Principle, “wants to die again. Originating in dust, it wants to be dust again.”
The biologist who spotted the flaw in Weismann’s argument was Peter Medawar, who won a Nobel Prize for work in immunology during World War Two, when he developed new methods for skin grafts. A few years after the war, Medawar published two celebrated essays on the problem of aging, “Old Age and Natural Death” and “An Unsolved Problem of Biology.” There he both posed and solved the problem of aging, in the view of most gerontologists today; he explained why evolution brought old age and natural death into the world. At the time I visited Maria Rudzinska, back in 1984, Medawar was by far the greatest living scientist in their still-small field, even though the problem of aging was only one of a vast number of his interests. That year, he gave a public lecture in New York—at the Explorers Club, I think—and I went to hear him. He was a handsome, elegant, and sophisticated old man, crippled by a stroke. He lectured from a wheelchair, with his equally elegant wife standing at his side.
Medawar had studied Weismann’s argument about old age and decided that Weismann was completely wrong. In his essay “Old Age and Natural Death,” Medawar quotes those wise-sounding lines of Weismann’s about worn-out bodies, which are useless to the species, and even harmful, because they get in the way—so harmful that even if their ancestors had once been immortal, natural selection would have shortened their life spans and made them mortal.
“In this short passage,” says Medawar, “Weismann canters twice around the perimeter of a vicious circle. By assuming that the elders of his race are decrepit and worn out, he assumes all but a fraction of what he has set himself to prove.” Why are they worn out? That’s the whole question, says Medawar. That’s Weismann’s first canter around the vicious circle. And if bodies are worn out, then natural selection will weed them out. Bodies don’t have to invent or evolve an elaborate adaptation like Death by Old Age to take themselves off the stage. Give mortal bodies enough time on this earth, and sooner or later a cold winter or a hot summer, a drought or a flood, a famine, a pestilence, the wolf at the door, a chicken in the snow, or any one of nature’s myriad dangers will come and find them. Plain bad luck will take them out.
Mother Nature is infinitely inventive when it comes to fatal accidents. Because we have managed so successfully at insulating ourselves from most of them, we forget how tough it is out there, even for creatures that are young and healthy. Darwin makes this point in the most famous chapter in the Origin of Species, “Struggle for Existence,” which begins, “Nothing is easier than to admit in words the truth of the universal struggle for life, or more difficult—at least I have found it so—than constantly to bear this conclusion in mind.”
As Darwin goes on to say in “Struggle for Existence,” most animals die young. Take wild mice. Nine out of ten wild mice die before they have lived a year. Some of them get pounced on by a cat or an owl. More of them die of the cold, at night, hungry and shivering. They die because they don’t have enough fuel in their bodies to keep warm. If you think of the life span of a mouse as having Seven Ages, like a man, then most wild mice don’t survive beyond the young lover in As You Like It, composing a sonnet to his mistress’s eyebrow. They don’t die of old age; they die huddling together for warmth in the long hours of the night. Virtually no wild mouse is ever so lucky as to survive to extreme old age, or about three years, which is the age when a well-fed mouse in a safe warm cage finally totters to its end, “sans teeth, sans everything.”
It’s the same with gray squirrels. They can climb trees to get away from cats and dogs and kids with slingshots. But even so, only about thirty in a hundred survive longer than one year. Only six or seven in a hundred survive more than four years. And yet when gray squirrels are kept in zoos they can sometimes live twenty years.
From the fact of the struggle for existence, Darwin drew a conclusion that seems simple in retrospect. Darwin’s process works by selecting slight variations—those that make a difference in the survival of an individual. There are times when the slightest variation will determine who lives and who dies; who gets to reproduce and who dies without passing on the genes.
And from this same hard fact of life, Medawar drew a second conclusion. In the wild, life is so hard that variations are weighed in the balance, with the best selected and the rest rejected, when the individual is young. It is only among the young that variations will be weeded out. Those that appear later in the creature’s life span won’t be culled, because the creature will almost never live that long anyhow. Again, as a general rule, life in the wild is so dangerous that no matter how fit they are, most creatures don’t live long enough to grow up, let alone grow old. Most don’t live long enough to pass on their genes. “We behold the fact of nature bright with gladness, we often see superabundance of food,” Darwin writes in “Struggle for Existence” “we do not see, or we forget, that the birds which are idly singing round us mostly live on insects or seeds, and are thus constantly destroying life.” They are cutting short the lives of many of those bugs and plants before they make more bugs or plants. And if the birds themselves run out of bugs and seeds, they die young, too.
You can convince yourself that most wild things die young by doing a simple thought experiment. Suppose, says Darwin, an oak produced only two seeds a year—“and there is no plant so unproductive as this.” If each of those two seedlings grew up the next year and produced just two more, and each of those produced two, and so on, and if each of the seeds germinated, then in twenty years that first oak would have produced a forest of one million oaks. Or take elephants, which are the slowest-breeding animals on the planet. Elephants start breeding at the age of thirty. If one pair began breeding when they were thirty and produced only six baby elephants by the time they were ninety, and if all of those babies grew up and bred, then, well before a thousand years had passed, that matriarch and patriarch would have produced a herd of almost nineteen million elephants. If oaks and elephants went on like that the whole planet would soon be oaks and elephants. What this arithmetic suggests is the brevity of life throughout all its kingdoms. Most animals don’t live long enough to become parents. Most seeds don’t live long enough to set seed themselves. One spring, Darwin tested that point with an experiment in his garden. He marked out a plot of ground three feet long and two feet wide. He dug and cleared it and counted all the weeds as they came up. Out of 357 weed seedlings, he says, 295 were destroyed, most of them chewed and swallowed by slugs and bugs. Those seedlings never passed on their genes. Even weeds die young—which is why they don’t completely take over the planet either.
Since oaks and elephants and dandelions never take over and engulf the earth, Darwin concludes, we may be sure “that this geometrical tendency to increase must be checked by destruction at some period of life.” And that period, Medawar adds, is youth. Death hovers everywhere and prevents the conquest of the planet by oaks or elephants or anything else alive. Everywhere in the living world a lucky few survive while the rest die young.
So that, Medawar argues, is why animals and plants are mortal: that’s why they get frail when they get old. It’s not that elephants and dandelions have evolved progressive frailty as an adaptation, to get themselves off the stage of life and make way for new elephants and dandelions. It’s not that death is an adaptation. It’s just that genes that cause progressive frailty do not matter in the wild. Genes that cause late-onset diseases are invisible in nature. They don’t matter because animals and plants almost never live long enough for those problems to develop. Way before they reach the age of late-onset diseases, they are long dead anyway. Think of those mice in the fields and woods. Nine out of ten of them will die before they are one year old. If they put their energy into building bodies that will last longer than a year, only one in ten will profit from the investment, and nine out of ten will be the poorer for it. They’ll be less competitive because they wasted resources they could have used when they were young. Why put your precious energy into building with the best materials if your time is so short? The wolf at your door will blow down a house of bricks just as fast as a house of wood or a house of straw. Why plan for a retirement that only one out of ten will live to see? Better use every drop of energy for hustling and making babies. And it is literally energy we’re talking about. Our mortal bodies do a huge amount of work maintaining our libraries of DNA, and scraping away the rust to keep ourselves from browning inside like sliced apples, and just keeping warm. All that manufacturing, importing, and exporting of ATP. Most of us have no idea the Herculean effort required by the body to find all that energy and pay for it, to keep up with the heating bills and the repair bills.
This was Medawar’s great insight. It’s a striking conclusion, almost as broad as the conclusion that Darwin drew when he contemplated the struggle for existence. Like Darwin’s argument, it applies everywhere in the tree of life. What’s true for elephants and dandelions would have been true for our own ancestors, too, until we invented civilization and saved ourselves from life spans that were nasty, brutish, and short. As Darwin says in the Origin of Species, the slightest variations will sometimes determine who shall live and who shall die. Those of our ancestors who could see the lion first and outrun it fastest survived to make it back to the comforts of the cave or the tent, and the arms of their mates that night. That is why they had the chance to become our ancestors. Those who did not live long enough to be parents are not among our ancestors.
And our ancestors’ genes are now our genes.
Think of Shakespeare’s Seven Ages of Man: the infant, the schoolboy, the young lover, the soldier, the judge, the retiree, and then the senile old man, withering back toward nothingness. Among our ancestors in the wild it was only in our First, Second, or Third Age that crippling variations would be weeded out. Variations mattered only up until the age of the young lover. And that’s still true today, on average, even though we no longer live in the wilderness. Suppose, for instance, that you are born with a mutation that will cause trouble only when you reach the Fourth Age of Man. You carry a defective gene that won’t do you any harm at first, but later on will make you very sick. You are just fine as a mewling and puking baby, you are healthy as a schoolboy, and as a lover writing sonnets to your mistress’s eyebrow. You are still fit and strong at the fourth age when you play the part of the soldier charging the cannon’s mouth. But just as you reach middle age, the fifth age, the age of the judge sitting on the bench, you begin to have fits. You thrash your arms around in the air. You attack the plaintiff when he approaches the bench. You go home and attack your children. You start speaking in tongues. You are suffering from Huntington’s disease, which is caused by a mutation in a single gene on Chromosome Four. It is a horrible, progressive, fatal disease, and there is no cure. You will not live to your Sixth Age, the age of the retiree with the spectacles on the nose, the age of the shrunk shanks and slippered pantaloons (as Shakespeare pitilessly puts it). But you have already passed on your genes, just as your father or mother passed them on to you. If you have two children, the odds are that one of them has Huntington’s disease. Natural selection cannot prevent that Huntington’s gene from passing this way through the generations, century after century. Darwin’s process could stop the spread of Huntington’s disease only if the mutation made people sick in the first half of life, when they are most likely to become the fathers or mothers of children. After that, whatever the mutation does, it goes unpunished.
Fortunately, Huntington’s is a rare disease. But the same argument applies to each and every gene that causes human bodies harm when they are beyond the Third Age, the age of the young lover. Suppose you carry genes that maintain your muscles when you are young and then allow them to weaken and shrivel away in your forties, fifties, sixties, and seventies. Genes that allow old muscles to shrink are very common in the human species, and so is the condition. Geriatricians call it sarcopenia. It is one of the most common problems of old age. Or suppose you have genes that allow the lenses of your eyes to stiffen as you reach the age of forty. Genes that fail to prevent that condition are extremely common, and so are reading glasses. Almost all of us carry genes like those and pass them on to our children. We’re horrified by a rare disease like Huntington’s, but we all carry innumerable genes that let us develop problems around middle age, and in the end they’re fatal, too.
In our comfortable civilization, we can put up for a long time with weaker arms and legs and back and weaker eyesight. We can survive with them even into our eighties or beyond with the help of walkers and glasses and cataract operations. Back when we lived in the wild, as our ancestors did for millions of years with bodies very much like those we have now, those conditions would have been just as fatal in middle age as Huntington’s is today. Back then you had to run away from a lion. But once again, Darwin’s process would have been powerless to weed out those genes, for the same reason that it could not weed out Huntington’s. Those are all problems that start to bother us long after our bodies have reached puberty. By the time our muscles and our eyes are weakening badly, by the time our necks and backs begin to bother us, most of us have passed on our genes to our children. Darwin’s process, evolution by natural selection, the process that gave us all of this miraculously intricate living machinery, cannot prevent most of that machinery from beginning to slow down and fall apart in the Fifth, Sixth, and Seventh Age of Man.
And of course what is happening at the level we can feel and see and notice, the level that bothers us—the stiff neck, the stiff knees, the dry skin, the brittle fingernails—is happening inside the body, too, where the machinery is far more intricate than the stuff we can see and feel. Darwin’s process gave the cell the machinery of the Phoenix, the machinery of repair and self-renewal. It gave us the mitochondria that produce our energy and the autophagosomes that clean up the mess. But Darwin’s process cannot prevent that beautifully intricate machinery from slowing down in our forties and breaking down in our eighties. Some of the slow failure of our muscles begins there, in the failure of their mitochondria. But again, by the time sarcopenia starts to bother us, we have long since passed on our genes.
Our bodies are capable of producing a state of extraordinary health and stability. If we could stay at that stage of health, the stage of the Second Age of Man, when we are about twelve, then, according to some actuarial estimates, we would live, on average, for about 1,200 years. One in a thousand of us would live 10,000 years. But in the wild, our distant ancestors could not expect to survive past the age of one or two, and only the very lucky reached the age of twelve or twenty. So our bodies put everything they have into making it to twenty, and the rest be damned.
That is why the Phoenix burns so brightly in our youth and then begins to burn down, like a small flame aglow on its own ashes.
Medawar thought he was burying Weismann with this argument, but in fact the two biologists’ ideas bear a strong family resemblance. Medawar’s is a story of sacrifice, too. In Medawar’s vision, as in Weismann’s, each generation dies for the next. According to Medawar’s argument, the only mortal bodies that pass on their genes are those that are quick to reproduce—to get into the game while they are still among the living. In other words, our bodies are built to grow up fast. They aren’t built to last.
In some ways the sacrifice in Medawar’s story is even more painful. As Medawar pointed out, his argument has an awful wrinkle. Any gene that helps you grow up fast in your teens will be favored by natural selection even if that same gene turns on you and kills you later on. If it helps the body with quick-and-dirty construction in the womb, or during its first twenty years of life, then that gene will be likely to be passed on, even if it makes the shoddy body fall apart in forty years. As long as Jack and Jill can get up the hill, it doesn’t make any difference if their genes make them tumble down.
It’s bad enough that evolution allows you to pass on a time bomb like Huntington’s. Evolution may actually encourage you to pass on such time bombs. Natural selection may favor time bombs. If they help you in some way to reach puberty fast, then they will be favored because you will be more likely to survive long enough to pass them on. By the time you’ve reached your fifties and those bombs begin to explode, you’ve long since passed them on to your babies. And again, in the wild, the odds were against reaching your fifties anyhow.
This is a chilling vision when you take it in. It gives new meaning to the expression “over the hill.” On tall steep tropical islands that lie in trade winds, the winds almost always blow from one side. The windward side of the island is often wet with rain because that’s where the clouds form, while the leeward side is usually dry and barren because the rains have already fallen by the time the wind reaches that side. Rain falls only on the windward side. The leeward side of the island is stuck in what is known as a rain shadow. So half the island stays wet and green and young, and the other half stays dry, bare, and old. That is how it is with us, if Medawar’s argument is correct. As soon as we are just one step past our peak, we begin to descend into the shadow of Darwin’s mountain. We descend from the green crest, and we walk down toward the valley of the shadow of death.
Medawar’s argument has gotten more and more support since the middle of the twentieth century. In the late 1950s, the American evolutionary biologist George Williams reviewed Medawar’s logic and agreed with him that aging is a surprising feature of life, a feature that can’t be explained as Weismann did by calling it an adaptation. If an embryo can grow into an adult and an adult can keep itself up for decades, then why can’t the adult keep itself up indefinitely? “It is remarkable,” Williams wrote, “that after a seemingly miraculous feat of morphogenesis a complex metazoan should be unable to perform the much simpler task of merely maintaining what is already formed.” Williams agreed with Medawar that each line of life must carry genes that help it to grow up, and then turn around and betray it and bring it down.
In the late 1970s a British biologist, Tom Kirkwood, put this evolutionary theory of aging in contemporary terms in a fresh series of papers. Kirkwood gave this argument a memorable name: the theory of the disposable soma. Once we are past the age of reproduction, once we are no longer making babies and raising families, our bodies become disposable. Once we’ve passed on our genes, we’re trash.
Gerontologists have recognized this nightmarish possibility in the theory for decades, and they have proposed a few examples, most of which have yet to be proved conclusively. An interesting example has been proposed by Caleb Finch, of the Andrus Gerontology Center at the University of Southern California, Los Angeles. Finch is one of the greatest scholars among gerontologists today. He argues that inflammation may be a crucial problem in aging. Since the year 1800 or so, we have increased the average human life span on this earth by 100 percent. We have reduced childhood mortality by 90 percent. Since 1850, we have also reduced mortality in old age, with most of the gains in the last few decades. Most gerontologists attribute these epic, century-by-century victories to the broad progress of medicine, to the growth of economies, to near-global improvements in nutrition. But Finch and his colleagues argue that what may matter most in this story is quite specific: we catch fewer infections when we are children. Infections can cause chronic inflammation, and Finch believes that inflammation may be the single most important factor in the decline of old age. Chronic inflammation is now thought to increase one’s risk of heart attacks, strokes, cancer, and even, possibly, Alzheimer’s disease.
As Finch notes, some infections cause long-term damage directly. For instance, childhood strep infections, if untreated, can lead to rheumatic heart disease, and the damage to the heart valves can be fatal decades after the strep. But in millions of cases the links of cause and effect may be more subtle and may show up only in statistics. Cohorts of babies with high levels of infant diarrhea and enteritis, for instance, have been found to have more heart problems and more respiratory problems when they grow up. If you are an American in your fifties, and you had a major illness as a child, you are 15 percent more likely to have a heart condition, and you are twice as likely to have a chronic lung condition. You are also twice as likely to have cancer, although no one knows precisely why. Finch thinks all this damage may be done by elevated serum levels of certain inflammatory proteins, such as C-reactive protein (CRP). People who live in places where they are likely to be exposed to chronic tuberculosis, diarrheas, and malaria are likely to have elevated levels of CRP throughout their lives. This is why your dental hygienist is always reminding you to floss. The inflamed gums of periodontal disease can cause chronic high levels of CRP, and, it’s now thought, raise your risk of heart disease, stroke, and cancer.
It may be that the body’s response to short-term infections when we are children works to help us recover quickly when we are young, but then the inflammation lingers in ways that make us sick when we are old. If so, that would be an example of the kind of juggling act that the evolutionary biology of aging predicts. If what heals us as babies makes us sick as old bodies, then evolution will favor the healing of the young and ignore the damage to the old.
That may be why the elderly in developed countries started living longer in the last decades of the twentieth century. They may have lived more years in old age because they’d contracted fewer infections when they were very young, in the early decades of the century. They were cleaner, better-fed, and better-doctored as children, and their bodies had lower levels of inflammation for the rest of their lives.
(On the other hand, many people think our health is suffering because we are kept too clean while we’re young. The rise of asthma in developing countries may be caused by our lack of exposure to pathogens early in life. That’s the very opposite of Finch’s idea of early exposure and inflammation.)
In any case, if you’re a body and you’ve got to survive long enough to reproduce and you’ve got limited resources, then you’re going to put those resources into the task of reaching reproductive age, finding a mate, and passing on those genes. If you divert too many of your limited resources into building a body that will last into old age, then you may not live long enough to pass on your genes. Bodies that follow that losing strategy will get weeded out by natural selection. In this way, evolution selects for decrepitude. Yeats said that each of us is forced to choose between perfection of the life or perfection of the work. In a sense, our genes choose perfection of the work—the work of reproduction, that is—rather than perfection of the life—the long life well lived. Our genes made this choice in the time of our distant ancestors, long, long ago and far away. Now our bodies make the sacrifice whether we like it or not.
Medawar himself was not the kind of man who found it comfortable or easy to step aside as one stage of life advanced to the next. One of his adages was, “Humility is not a state of mind conducive to the advancement of learning.” In a memoir that he wrote in his old age, he confessed that he had put his scientific life far ahead of his family life. “I had thought, when I was a boy, that I should be a good father, one who wisely and kindly guided my children, shaping their minds and morals by imperceptible degrees. My performance fell so far short of these ambitions that I was an outstandingly rotten father and neglected my children disgracefully.”
Medawar had also fought retirement. He’d gone back to the lab after a first stroke in 1970. “No working scientist ever thinks of himself as old,” Medawar said. He kept working in spite of not one but two grand retirement parties. In an after-dinner speech at the second retirement, Medawar told a long table of colleagues that it was his ambition to stay on until he’d become a notorious pest. “I hope to continue working until as I career down the corridors in my electric wheelchair, newcomers flattening themselves against the wall will say to each other, ‘That’s Medawar, you know: they simply can’t get rid of him.’”
“We’re saying that already, Peter!” cried a voice from the other end of the table.
He died a few years later.
Bleak as it is, Medawar’s view of life does have some hopeful features for us, because our species may be a special case. Those of our ancestors who survived and stayed fit as grandparents, for instance, might have been able to help their grandchildren enough to make a difference for their survival. If they were wonderful grandparents, then their longevity genes would have been more likely to be passed down. Families fortunate enough to be blessed with those grandparents and longevity genes would have been more likely to grow and thrive, generation after generation. And this process might have been self-reinforcing: not a vicious circle, but a virtuous circle. Because of our big brains and our gift for culture, our Old Ones would have retained a value to their kith and kin that old chimps or apes would not. The value of the older and wiser heads among us would have grown the more human culture grew—that is, the more there was to know. Consequently those of our ancestors with genes to make them last a long time would have tended to pass on those genes through their grandchildren. Consequently we evolved to last longer and longer. This virtuous circle might help to explain the longevity of grandmothers and grandfathers. They are able to help their sons and daughters raise children of their own. This is known as the Grandmother Hypothesis.
To study the evolution of human life spans, some physical anthropologists have made a specialty of Paleolithic dentistry. By inspecting the wear on our ancestors’ teeth, they can estimate how long the owners of those teeth used them. They count baby teeth, adult teeth, and examine through microscopes the wear and tear on the molars, because the life of hunters and gatherers puts a lot of stress on chewing. Recently two anthropologists, Rachel Caspari, at the University of Michigan, Ann Arbor, and Sang-Hee Lee, at the University of California, Riverside, examined the whole Paleolithic dental database and made a provocative discovery about the evolution of human life expectancy.
In the past, anthropologists have been hampered in such studies because the number of people who lived to a ripe old age in the Stone Age was very small, and because by the time they reached old age, our ancestors’ teeth were in such bad shape that they no longer provided much of a fossil record. There are huge gaps, so to speak, in their fossil dental records. So anthropologists had assumed that they would never be able to use fossil teeth to trace fine-scale trends in the evolution of human life expectancy. They could not do so because the evidence for assessing the maximum life spans of our ancestors was gone. If any of our ancestors survived to the Seventh Age, “sans teeth…sans everything,” they had no teeth left to bequeath to science. Nothing left for Caspari and Lee to study.
But Caspari and Lee reasoned that to reconstruct life expectancy you don’t have to count the Seventh Age, the age of the oldest old. By definition, the oldest old are a tiny minority. They don’t matter much to the overall pattern. All you need to know is how many people in the Stone Age lived to be old. So Caspari and Lee reexamined the Paleolithic dental records, focusing on the third molars—commonly called the wisdom teeth—which erupt at about the time that we reach puberty. They studied all of the fossil teeth they could find in the biggest sample ever analyzed of Stone Age skeletons, and they sorted them into three groups: children, who died before their third molars had erupted; young adults, who had those molars but showed very little wear on them; and older adults, defined as people whose molars were worn enough that they had lived at least fifteen years with wisdom teeth. Thirty is a significant year in a life cycle where fertility begins at fifteen. If a girl became enough of a woman to have a baby at fifteen, she would be old enough to become a grandmother at the age of thirty. Boys who fathered children at the age of fifteen or so could be grandfathers at thirty.
Caspari and Lee found that in the Upper Paleolithic, which began roughly thirty thousand years ago, more and more of our ancestors lived to be old. In the course of the Upper Paleolithic, the number of adults who lived long enough to be grandparents rose fourfold.
The very ability to live to older ages may have been fostered by the culture that grew and deepened as increasing numbers of elders helped to raise the children of the tribe and pass on what they had learned. And so the two may have advanced together, the survival of the young and the survival of the old, literally hand in hand.
This advance in human life expectancy may explain why populations in the Upper Paleolithic suddenly grew in numbers and went trekking farther and farther into the landscapes around them. Generation after generation carved new trails, built new settlements. It may be that the elders’ investments in the children gave these tribes and villages an advantage that helped them grow and prosper and wander. The change began about 30,000 years ago, and by about 15,000 years ago we had colonized almost all of the planet. Anthropologists have argued for decades about what caused this extraordinary expansion of culture and geography, which they sometimes call the creative explosion. Was our ancestors’ increase in longevity, our growing length of days, at the heart of the change? Did our longevity help lead to what we think of as modern human life? We may never know which came first, the length of days or the improvements in human culture and society that led to the length of days. They too may have advanced hand in hand. “We suggest,” Caspari and Lee write, “that this increase in longevity addresses the meaning of modernity itself.”
If this argument about our evolution is correct, and longevity has played a part in the human success story from the beginning, then we are partial exceptions to the rule of the disposable soma. We are worth something in our old age, after all. Our longevity is of adaptive value. If so, then some of the changes in our aging bodies may be adaptive—including the big one we call The Change. Why is it that women approach the end of their fertility at the age of forty-five or fifty, when they are still relatively healthy and fit? It is true that they are running out of eggs, but why do they have to run out so young? Men still have sperm. The human reproductive system ages faster in women than the body as a whole, and by age forty-five, according to one authority, it “can be said to be in the state that a woman’s other organs have reached by eighty.”
Menopause may be a by-product of the evolution of our particular niche as a species. The Change may have helped us succeed in our niche as knowledge-gatherers. The argument runs like this. Those among our ancestors who were better knowledge-gatherers survived longer and had more offspring, who survived longer yet. So we evolved bigger brains. Birds and bats have wings, tortoises have shells, we have big brains. We evolved on the African savannah among dozens of sibling species of primates. Our unusually big and agile brains gave us the ability to cope with predators and prey, and to share ridiculous quantities of useful and useless information. And our life spans evolved until they were much longer than any other primates on the planet. But the development of our big brains presented evolution by natural selection with a difficult engineering problem. Babies with bigger brains have more trouble passing through the birth canal, whether headfirst or breech. And because we walk on our hind legs rather than on all fours, there were constraints on how large the birth canal could be. One solution was for human infants to be born early and for their heads and skulls to continue to grow after birth. That meant that they were dependent for a long time after they were born. They could learn a great deal from their mothers in that time, but they needed their mothers if they were to survive. Every modern parent copes with this human trait day and night, the long dependency of kids in their own knowledge-gathering phases. E. B. White was driving his young stepson to school one day; they were talking about the boy’s arithmetic homework when they saw a mother cat and her kittens in the tall grass of a field. The mother was catching a mouse while the kittens looked on. White describes the scene in one of his essays. He says he could not help reflecting how many lessons his son would need to learn before he could go out and catch his first mouse.
Because birth is so hard, and child-rearing goes on for so long, a woman of forty-five or fifty, still fit in many ways, might find it difficult to start all over again as the mother of a new baby. Primitive conditions were so often nasty and brutish. Life was so often cut short. It might have been to her advantage, in the great task of passing on genes, if a woman stopped making babies and began helping her children’s children, giving them the fruits and harvests of her lifetime as a knowledge-gatherer. She could do more for her genes as a grandmother.
If you complain to your friends about the aches and pains of getting older, they tell you: Consider the alternative. Aging is hard, but the only other option is worse. The view of the evolution of aging that opened up after Medawar, the view of the disposable soma, is pretty bad, but from some points of view it does suggest a new alternative.
To Medawar and those who followed him it was at least encouraging to think that aging and death are accidents. Aging did not evolve because there was something good about it for the individual or the tribe or the species. Death was not designed. This is the same hopeful message that is written in the Wisdom of Solomon: “For God made not death: Neither hath he pleasure in the destruction of the living.” You can look at Medawar’s theory as more optimistic than Weismann’s. Weismann contemplates the aged, with all their weaknesses and infirmities, and finds it obvious that evolution would have to get rid of them. Evolution has to get rid of them because they are unfit. But why are they unfit? Why do we grow weak as we grow old? After all, as we grow older we grow in experience. In terms of experience, we should be fitter at forty or fifty than we were at twenty. We have wisdom as mushroom-gatherers, say, or mastodon-hunters. We also have immunological “wisdom,” which is why parents don’t catch as many bugs as their babies. As Medawar puts it, “It must be obvious that, senescence apart, old animals have the advantage of young. For one thing, they are wiser. The Eldest Oyster, we must remember, lived where his juniors perished.”
Death is not a punishment for our sins, and aging and death are not designed by Darwin’s process either. Aging and dying are not adaptations in the way that our hands, eyes, and brains are adaptations. Aging and dying are misfortunes that visit us because Darwin’s process is looking elsewhere, so to speak, busy doing other things. Weismann’s argument assumes that we have to decline and fall. That assumption has a lot of evidence behind it; it has the weight of all of human experience behind it; but it is still an assumption. With the problem of mortality, we often do assume what we seek to explain. Aristotle admired nature’s wisdom in making our teeth fall out when we get old, because we won’t need them when we are dead. The Reverend Thomas Malthus, when he tried to refute the optimistic Marquis de Condorcet on the likelihood of making ourselves immortal, explained death this way: we are mortal “because the invariable experience of all ages has proved the mortality of those materials of which his visible body is made.” In the same way, Weismann admired evolution’s wisdom in inventing aging as a way of getting rid of the aged. These arguments don’t get us very far. Compare the bitter epigram of Jules Renard: “Death is sweet; it delivers us from the fear of death.”
If we want to understand why we are mortal we have to learn not to assume that we just have to be mortal. Aging is not an adaptation; aging is just an accident. Death is not made by Darwin’s process; it arises because there are places where Darwin’s process is powerless to go. Richard Dawkins has called the process of evolution by natural selection the blind watchmaker, because the process creates such intricate machinery without ever looking ahead at what it is making. The forms are made simply by the success of some in each generation and the failure of others—a simple but profound story that we are still in the process of absorbing and digesting a century and a half after the Origin. But not only is the watchmaker blind; there is a place the watchmaker cannot reach, a place the watchmaker’s fingers cannot touch. That is the desolate place we call old age.
This opens an interesting possibility, a door that we had thought was closed forever. On the old view of aging and death as punishments for our sins, or sacrifices for our children, we could not dream of opening the door without a feeling of enormous guilt and preposterous futility. But on this new view the project of eternal youth and perpetual health becomes as plausible as any other human dream that evolution itself has not granted us but that we might have some hope, with industry and luck, to arrange for ourselves, like flying through the air, or curing the whooping cough, or making life so comfortable that most of us can expect to reach the age of eighty. This view of life suggests the possibility that we might be able to do what the blind watchmaker could not do, and fix and improve, or at least maintain, the clock.
As Medawar observes in “An Unsolved Problem of Biology,” we have trouble even imagining that we might get older without declining. “It is,” he says, “a curious thing that there is no word in the English language that stands for the mere increase of years; that is, for aging silenced of its overtones of increasing deterioration and decay.” Think of test tubes in a laboratory closet, Medawar suggests, or tumblers on a high shelf in the back of a pub. They never get scratched or microscopically chipped along the rims like their siblings out front. Most of them last until they’re taken out and put to work, or dropped. Until that fatal day they’re practically ageless. In other words, they get older without aging. And so did we when we were children, in a sense—to repeat the point that Francis Bacon makes in the first pages of the History of Life and Death. As children we got bigger and stronger every day. Then something happened. And now that we are grown up and falling apart, we are almost as confused about aging as we were when we were children.
Another eminent British medical man of the twentieth century, Robert Platt, a president of the Royal College of Surgeons (later Baron Platt of Grindleford), illustrated this point with an anecdote in his retirement speech in 1963, “Reflections on Aging and Death.” Platt said, “The story is told in my family how my brother and I, as small boys, were admitted to an Edwardian tea-party in our house in Hampstead, and my brother in the shrill clear voice of a little boy said, ‘Daddy, is Miss So-and-So a young lady?’ My father, ever tactful, said: ‘Yes, Maurice, of course she’s a young lady.’ Maurice thought for a few moments and then said, ‘She looks as if she’s been young for a very long time.’”
In essence, we get old because our ancestors died young. We get old because old age had so little weight in the scales of evolution; because there were never enough Old Ones around to count for much in the scales. But now if we like we can do more to help our bodies in the first half of life so that we will not progress so quickly to the decline of the second—or, in the dream of the greatest optimists, so that they never grow old at all.
And we can begin to do this most efficiently, in the view of those who campaign for the conquest of aging, if we accept the implications of evolutionary theory and come to view aging not as an inevitable and natural process but as a disease. Aging is a disease, like Huntington’s. It is just a kind of accident or series of accidents, failures to maintain the body. Aging evolved back when the struggle for existence was more intense than it is for us now, back when we had to race to survive and multiply; when we were much too busy surviving and multiplying to build bodies that would have a chance to last. “Back when” being most of human prehistory and all of living history before that, back to the origin of life almost four billion years ago.
The disposable soma theory helps to explain many confusing things about the problem of mortality. Most important, the theory explains the sheer diversity of the aging process: why so many things go wrong with us as we grow older. That’s just what you would expect if evolution cares only about getting you to a certain age; if it doesn’t give a damn what happens afterward. In other words, life has a meticulously careful plan for your rise, but no plan at all for your decline and fall. That’s why the phenomenon of aging is so hard to explain if you look for a single cause. Aging really has many causes, because none of our myriad working parts was built to last forever. That’s why aging is so unlike the orderly development of the embryo. Our development and birth are tightly programmed, but not our deaths. In this sense, the end is not written. It is not written in our stars, and it is not written in our genes.
Once you see the hopeful side of the disposable soma theory, you can begin to put together a grand plan, an escape plan. Maybe—just maybe—we can do for ourselves what evolution has neglected to do. Maybe—just maybe—we can intervene and extend our life spans even more dramatically than they lengthened on the African savannah when we evolved our big brains. Maybe it is now possible to help ourselves to more time—much more time.