Part 3 (2/2)

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 a.s.sumed 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 a.s.sessing 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 p.u.b.erty. They studied all of the fossil teeth they could find in the biggest sample ever a.n.a.lyzed 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 pa.s.s 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 sh.e.l.ls, 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 quant.i.ties 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 pa.s.sing through the birth ca.n.a.l, 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 ca.n.a.l 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 gra.s.s 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 pa.s.sing 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 G.o.d 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 a.s.sumes that we have to decline and fall. That a.s.sumption has a lot of evidence behind it; it has the weight of all of human experience behind it; but it is still an a.s.sumption. With the problem of mortality, we often do a.s.sume 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 a.s.sume 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 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 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), ill.u.s.trated 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 d.a.m.n 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.

Chapter 6.

THE GARBAGE CATASTROPHE.

”Some scientific discoveries are accepted almost immediately,” writes the gerontologist Robin Holliday. The most famous example is the double helix of Watson and Crick. Most biologists agreed within a few years that the two young men really had found the secret of life. Their sprint into the Eagle is now as famous, in scientific circles, as Darwin's voyage of the Beagle Beagle, or Newton's voyage on strange seas of thought, alone, under an apple tree.

Other great discoveries take decades to be recognized. Alfred Wegener argued in 1910 that continents drift. The idea wasn't generally accepted for more than fifty years. Gregor Mendel published the laws of inheritance in 1866. His discovery was rediscovered after thirty-four years.

Unfortunately, the solution to the problem of aging seems to be falling into this second category, Holliday complains in ”Aging Is No Longer an Unsolved Problem in Biology,” one of many dozens of triumphant articles, essays, and books that gerontologists have published in recent years. We don't know how to stop it, but we do know why it evolved. In that sense, aging is no longer an unsolved problem. And yet most people and even most scientists haven't heard the answer to one of the deepest and most profound problems that mortals can ask. They haven't heard, or else they haven't understood. ”A lot that is written about aging now is biological nonsense,” says Holliday, ”and that will undoubtedly be true in the future as well.”

In the view of the disposable soma theory, aging is simply the slow failure of maintenance. All your life, your body has to keep fixing broken DNA. Clearing away the damage done by free radicals. Repairing proteins. Repelling germs. Detoxifying poisons. Healing wounds. Clotting blood. Mending cracked bones. Adjusting the thermostat to maintain temperature. Adjusting the balance between the destruction and creation of cells to maintain all your working parts, and to prevent a rogue cell from multiplying out of control. Your body does all this internal maintenance work for you as long as you keep up the external maintenance work of eating, excreting, was.h.i.+ng, and running a comb through your hair. It takes a lot of work for the body to maintain what it has built, as Holliday notes: about 150 genes just for DNA repair, according to current estimates, and at least a thousand genes for the immune system.

And of course the body has other kinds of work to do besides maintenance. The body invests enormous time and energy into building gonads and attracting a mate to pa.s.s on those gametes. And then we put much of our life's energy into feeding and raising the young and helping them grow until they are big enough to go off on their own and maintain themselves.

According to present thinking, it behooves the body to strike the right balance between investing in its own maintenance and in the creation of new young bodies to go out into the world and multiply when it is gone. Because mice rarely live more than a year in the wild but human beings could live for twenty years or more in the wild it made evolutionary sense for the tissues of the two mammals to invest differently. Lymphocytes in the lymph nodes slowly acc.u.mulate mutations, for instance, because DNA repair isn't perfect not in mice or men. In the course of the life spans of both mice and men, these mutations acc.u.mulate about tenfold. But they do so in the s.p.a.ce of about three years in a mouse, and eighty years in a man. Apparently the mouse doesn't put as much energy into keeping itself up. The mouse lets itself go, as we say, because it is bound to go soon anyway. It makes babies and disappears.

So exactly what would it take to make the human body do even better than eighty years? What would it take to make the human animal immortal? We'd have to be able to regenerate every single one of our working parts, like the hydra, says Holliday. We'd need to be able to rebuild the heart and the blood vessels-without ever shutting it down for repairs. We'd have to repair, regenerate, and rebuild the brain-without losing the memories that make us what we are. We haven't done that because at no stage in human evolution was it ever better and more profitable for a human body to invest its resources that way than to build quickly and pa.s.s on its genes.

What we have done instead is to adjust-and fine-tune, generation after generation-the life span of each of our working parts so that they all tend to age at about the same rate. That's why we can look around us and guess the ages of the people around us, according to the disposable soma theory. Our bodies have invested just enough to maintain most of our working parts for the same period, so that they decline and fall at about the same time.

Holliday is one of many gerontologists who believe this theory solves the problem that Medawar first posed more than half a century ago. To Holliday it means that we are never going to be able to live much longer than we do now, because there are too many different kinds of things that go wrong with us that we will never be able to fix them all. So aging is irreversible. Antiaging medicine is a crock. At the end of his review, Holliday quotes Ronald Klatz, who writes in his book Advances in Anti-Aging Medicine Advances in Anti-Aging Medicine, ”Within the next fifty years or so, a.s.suming an individual can avoid becoming the victim of major trauma or homicide, it is entirely possible that he or she will be able to live virtually forever.”

Holliday concludes, with the gloomy air of QED, ”This is biological nonsense.”

In essence, in the view of the disposable soma, you could say that we come up against a modern form of the legend of the Hydra. Killing the Hydra was one of the twelve labors of Hercules. The monster had nine heads, and she helped guard the way to the Underworld. Hercules couldn't kill her by cutting off her heads with his sword, or his scythe, because each time he lopped off one head, two grew back. He had to lop off every one and cauterize each stump with a torch. Even then he wasn't done, because one of her heads was immortal. He had to bury that hideous head under a rock. And even then, long after he had slain the Hydra, venom from the monster's blood poisoned Hercules, and took the great hero down, wrapped in an intolerable cloak of pain. It was the Hydra that killed him in the end.

Aging is many-headed, like the Hydra. If you are a pessimist, or perhaps a realist, you conclude that you can never kill it. If you are other-minded, you begin to plan your attack.

The disposable soma theory makes some specific predictions. It predicts, first of all, that aging is caused by the acc.u.mulated damage of mistakes in building and repairing the body. The mistakes begin even as the construction begins. We are declining in a sense from the moment we are born. Even from before we are born. From the first moments of the union of the sperm and the egg, we are making mistakes in the hurry to get the building up and get around to the union of more eggs and sperm. As Aristotle said, the smallest error in the laying of foundations can someday bring down a house.

Not long ago I went to visit Janet Sparrow, a medical researcher at Columbia University. She is the Anthony Donn Professor of Ophthalmic Science in the Department of Ophthalmology, with a joint appointment in the Department of Pathology and Cell Biology. In her laboratory, Sparrow is trying to find ways to prevent one of the common vision problems of old age, macular degeneration. It is a simple case of the simplest aging problem, the problem of clearing away debris as we get older.

Macular degeneration is a medical condition that usually begins to develop around the age of fifty. It's a disease of the retina, which is one of those minutely engineered places in the body where you do not want debris to build up. The retina sends the messages to the brain that translate into vision. Our eyesight depends on the health of our retinas, which are extremely thin films of nerve cells at the back of each eyeball.

When a ray of light falls on the rod cells and cone cells in the retina, a certain chemical inside those cells, a chemical derived from vitamin A, has to switch very quickly from one chemical shape to another. The chemical has one shape in the dark and one shape in the light. This switching from the dark form to the light form triggers events that tickle the optical nerve, which sends a message to the brain that a ray of light has arrived. Your whole life, whenever your eyes are open, innumerable molecules of this compound are switching from the dark form (which is known as 11-cis-retinal) to the light form (all-trans-retinal), and back again.

Unfortunately, as it flashes back and forth between its two forms, which is a complicated procedure, one of these molecules sometimes brushes up against one of the molecules around it, and every once in a while the two of them get stuck together. No man is an island, no organ is an island, and no molecule is an island. All of our working parts are working next to hundreds of other working parts. If the wrong molecules happen to brush against each other and stick together, they can begin to clump. In the retina, this molecular accident often ends up as a clump of useless trash, a clunker of a molecule called A2E. The rod and cone cells try to clear away this trash by sweeping it into the lysosomes of cells nearby. But the lysosomes can't break it down. So the A2E sits there inside the lysosomes. After seventy or eighty years of this kind of slow failure, the cells in vital parts of some human retinas are often as much as 20 percent junk: that is, 20 percent A2E by volume. They are almost as bad as cameras that are one-fifth full of dust. This is one of the common problems of old age.

A2E is an ugly and pervasive kind of biological trash called lipofuscin. It's an age pigment. You really don't want lipofuscin in your retinas. When light strikes lipofuscin, it glows, and it goes on glowing for a while even in the dark.

On my visit to Sparrow's lab, I asked her if I could see some lipofuscin. ”I'll get a vial and I'll come right back,” she said.

The little gla.s.s vial she handed me was full of brown muck. She explained that since I was over fifty, my own retinas already contained quite a lot of it. The stuff looked like the kind of crud you get on steel wool when you scour a frying pan.

Meanwhile, of course, all kinds of other material changes are taking place in our eyes as we get older, Sparrow told me. ”Have you begun to notice trouble differentiating navy blue and black socks?” she asked.

<script>