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 Weis
mann’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.
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