WHY DO WE GROW OLD AND DIE?
We constantly invest resources in the repair of our bodies, just as we do with our cars. Unfortunately for us and for all other animals, there is a limit to the resources that natural selection found it worthwhile to programme into our self-repair. As a result, we eventually grow old and die, but at least we age more slowly than our ape relatives. 'Mother, why did Grandpa have to die? Will you die some day? Will I die too? Why?
Death and aging constitute a mystery that we often ask about as children, deny in youth, and reluctantly come to accept as adults. I scarcely reflected on aging when I was a college student. Now that I am fifty-three years old, I find it decidedly more interesting. Life expectancy among US white adults is, presently about seventy-eight years for men, eighty-three for women. But few of us will survive to 100. Why is it so easy to live to eighty, so hard to live to 100, and almost impossible to live to 120? Why do humans with access to the best medical care, and animals kept in a cage with plenty of food and no predators, inevitably grow infirm and die? It is the most obvious fact of life, but there is nothing obvious about what causes it.
In the bare fact of our aging and dying, we resemble all other animals. In the detarh, however, we have improved considerably over the course of our evolutionary history. Not a single individual of any ape species has been recorded as achieving the current life expectancy of US whites, and only exceptional apes reach their fifties. Hence we age more slowly than do our closest relatives. Some of that slowdown may have developed recently, around the time of the Great Leap Forward, since quite a few Cro-Magnons lived into their sixties while few Neanderthals passed forty.
Slow aging is crucial to the human lifestyle because the latter depends on transmitted information. As language evolved, far more information became available to us to pass on than previously. Until the invention of writing, old people acted as the repositories of that transmitted information and experience, just as they continue to do in tribal societies today. Under hunter-gatherer conditions, the knowledge possessed by even one person over the age of seventy could spell the difference between survival and starvation or defeat for a whole clan. Thus, our long lifespan was important for our rise from animal to human status.
Obviously, our ability to survive to a ripe old age depended ultimately upon advances in culture and technology. It is easier to defend yourself against a lion if you are carrying a spear than just a hand-held stone, and easier yet with a high-powered rifle. However, advances in culture and technology alone would not have been enough, unless our bodies had also become redesigned to last longer. No caged ape in a zoo, enjoying all the benefits of modern human technology and veterinary care, reaches eighty. We shall see in this chapter that our biology became remoulded to the increased life expectancy that our cultural advances made possible. In particular, I would guess that Cro-Magnon tools were not the sole reason why Cro-Magnons lived on the average longer than Neanderthals. Instead, around the time of the Great Leap Forward our biology must have changed so that we aged more slowly. That may even have been the time when menopause, the concomitant of aging that paradoxically functions to let women live longer, evolved.
In short, cultural and biological change had to develop hand-in-hand to permit our long lives.
Along with the changes in our sexual anatomy, physiology, behaviour, and preferences discussed in Chapters Three to Six, retarded aging is the last of the life-cycle changes that made possible the third chimpanzee's rise.
The way in which scientists think about aging depends on whether they are interested in so-called proximate explanations or ultimate explanations. To appreciate this difference, consider the question, 'Why do skunks smell bad? A chemist or molecular biologist would answer,
'It's because skunks secrete chemical compounds with certain particular molecular structures. Due to the principles of quantum mechanics, those structures result in bad smells. Those particular chemicals would smell bad no matter what the biological function of their bad smell was.
But an evolutionary biologist would instead reason,
'It's because skunks would be easy victims for predators if they didn't defend themselves with bad smells. Natural selection made skunks evolve to secrete bad-smelling chemicals; those skunks with the worst smells survived to produce the most baby skunks. The molecular structure of those chemicals is a mere incidental detail; any other bad-smelling chemicals would suit skunks equally well.
The chemist has offered a proximate explanation: that is, the mechanism immediately responsible for the observation that was to be explained. The evolutionary biologist has instead offered an ultimate explanation: the function or chain of events that caused that mechanism to be present. The chemist and the evolutionary biologist would each dismiss the other's answer as not being 'the real explanation'.
Similarly, studies of aging are pursued independently by two groups of scientists who scarcely communicate with each other. One group seeks a proximate explanation, the other an ultimate explanation. Evolutionary biologists try to understand how natural selection could ever permit aging to occur, and they think that they have found an answer to this question. Physiologists inquire instead into the cellular mechanisms underlying aging, and admit that they do not yet have an answer. But I shall argue that aging cannot be understood unless we seek both explanations simultaneously. In particular, I expect that the evolutionary (ultimate) explanation will help us find the physiological (proximate) explanation of aging that has so far eluded scientists. Before I can pursue this reasoning, I must anticipate objections of my physiologist friends. They tend to believe that something about our physiology somehow makes aging inevitable, and that evolutionary considerations are irrelevant. For instance, one such theory attributes aging to the progressive difficulties that our immune system is said to face in distinguishing our own cells from foreign cells. Physiologists subscribing to this view make an implicit assumption that natural selection could not lead to an immune system without that fatal defect. Is this belief warranted? -
To evaluate this objection, let's consider biological repair mechanisms, because aging may be thought of simply as unrepaired damage or deterioration. Our first association with the word 'repair' is likely to be to those repairs that cause us the most frustration, car repairs. Our cars tend to grow old and die, but we spend money to postpone their inevitable fate. Similarly, we are unconsciously but constantly repairing ourselves too, at every level from that of molecules to that of tissues or whole organs. Our own self-repair mechanisms, like those we lavish on our cars, are of two sorts—damage control, and regular replacement.
An automotive example of damage control is that we replace a car's bumper only if it is bashed in; we do not routinely replace the bumper at every regular oil change. The most visible example of damage control applied to our bodies is wound healing, by which we repair damage to our skin. Many animals can achieve more spectacular results: lizards regenerate severed tails, starfish and crabs their limbs, sea cucumbers their intestines, and ribbon worms their poison stylets. At the invisible molecular level our genetic material, DNA, is repaired exclusively by damage control. We have enzymes that recognize and fix damaged sites in the DNA helix while ignoring intact DNA.
The other type of repair, regular replacement, is also familiar to every car-owner. We periodically change the oil, air filter, and ball-bearings to eliminate slight wear, without waiting for the car to break down first. In the biological world, teeth are similarly replaced on a pre-scheduled basis: humans go through two sets, elephants six sets, and sharks an indefinite number, during their lifetimes. Though we humans go through life with the same skeleton with which we were born, lobsters and other arthropods regularly replace their exoskeleton by moulting it and growing a new one. Still another highly visible example of scheduled repair is the continual growth of our hair: no matter how short we cut it, its growth will replace the cut portion.
Regular replacement also goes on at a microscopic or submicroscopic level. We constantly replace many of our cells about once every few days for the cells lining our intestine, once every two months for the cells lining the urinary bladder, and once every four months for our red blood cells. At the molecular level, our protein molecules are subject to continuous turnover at a rate characteristic of each particular protein; we thereby avoid the accumulation of damaged molecules. If you compare your beloved's appearance today with a photograph taken a month ago, he (or she) may look the same, but many of the individual molecules forming that beloved body are different. While all the king's horses and men couldn't put Humpty Dumpty together again, Nature is taking us apart and putting us back together every day. Thus, much of an animal's body can be repaired as needed, or is regularly replaced anyhow, but the details of how much is replaceable vary greatly with the part and with the species. There is nothing physiologically inevitable about the limited repair capabilities of us humans. Since starfish can regrow amputated limbs, why can't we? What prevents us from having six sequential sets of teeth like an elephant, rather than just baby teeth and adult teeth? With four more natural sets, we would not need fillings, crowns, and dentures as we got older. Why don't we protect ourselves against arthritis? — all we would need is to replace our joints periodically, as crabs do. Why don't we guard against heart disease by periodically replacing our hearts, as ribbon worms replace their poison stylets? One might suppose that natural selection would favour the man or woman who did not die of heart disease around the age of eighty but continued to live and produce babies at least until the age of 200. Why, for that matter, cannot we repair or replace everything in our bodies?
The answer surely has something to do with the expense of repair. Here again, the analogy of car repair is helpful. If the boasts of the Mercedes-Benz company are to be believed, their cars are so well built that, even should you do no maintenance whatsoever—not even lubrication or oil changes—your Mercedes will still run for years. At the end of that time, of course, it will fall apart from accumulated irreversible damage. So Mercedes-owners generally do choose to service their cars regularly. My Mercedes-owning friends tell me that Mercedes service is very expensive, hundreds of dollars every time they drive into the workshop. Nevertheless, they consider the expense worth it. A serviced Mercedes lasts much longer than an unserviced Mercedes, and it is much cheaper to service your old Mercedes regularly than to discard it and buy a new one every few years.
That is how Mercedes-owners reason in Germany and the US. But suppose you were living in Port Moresby, the capital of Papua New Guinea, automobile accident capital of the world, where any car is likely to be written off within a year no matter how you maintain it. Many car-owners in New Guinea do not go to the expense of maintaining their car; they use the saved money to help buy the inevitable next car.
By analogy, how much an animal 'should' invest in biological repair depends on the expense of the repairs, and on a comparison of the animal's expected lifespan with and without the repairs. But such 'should' questions belong to the realm of evolutionary biology, not physiology. Natural selection tends to maximize one's rate of producing offspring that survive to leave offspring of their own. Evolution can thus be regarded as a strategy game, in which the individual whose strategy leaves the most descendants wins. Hence the type of reasoning used in game theory is helpful in understanding how we came to be the way we are.
This problem of lifespan, and of investment in biological repair, is in turn one of an even broader class of evolutionary problems addressed by game theory: the mystery of what sets the maximum limit on any advantageous trait. There are lots of other biological traits, besides lifespan, that beg the question why natural selection has not made them longer or bigger or faster or made more of them. For instance, people who are big or smart or can run fast have obvious advantages over small, dumb, slow people—especially throughout most of human evolution, when we were still fending off lions and hyenas. Why did we not evolve to become on the average even bigger, smarter, and faster than we now are? The complication that makes these evolutionary design problems less simple than they might at first seem is this: natural selection acts on whole individuals, not on single parts of an individual. It is you, not your big brain or fast legs, that does or does not survive and leave offspring. Increasing one part of an animal's body may be beneficial in some obvious respect but harmful in other respects. For instance, that one larger part might not fit in well with other parts of the same animal, or it might drain off energy from other parts.
To evolutionary biologists, the magic word that expresses this complication is 'optimize'. Natural selection tends to mould each trait to the size, speed, or number that maximizes the survival and reproductive success of the whole animal, given the animal's basic design. Hence each trait in itself does not tend towards a maximal value. Instead, each trait converges on some optimal intermediate value, neither too big nor too small. The whole animal is thereby more successful than it would be if that trait were bigger or smaller.
Should this reasoning about animals seem abstract, think instead of our everyday machines. Essentially the same principles apply to engineering design, of machines by humans, as to evolutionary design, of animals by natural selection. For example, consider my pride and joy among my machines, my 1962 Volkswagen Beetle, the only car I have ever owned. (Car buffs will remember 1962 as the year that Volkswagen introduced the big rear window in the Beetle.) On a smooth, level road with an assisting tailwind, my VW can go at 65 mph. To BMW owners, that may sound distinctly submaximal. Why don't I junk my puny 4-cylinder, 40-horsepower engine, install instead the 12-cylinder, 296-horsepower engine from my neighbour's BMW 750IL, and roar off at 180 mph down the freeway?
Well, even I, dodo about cars that I am, know that that would not work. To begin with, that huge BMW engine would not fit into my VW's engine compartment, which would need enlarging. Then, the BMW engine is meant to go in front, but the VW engine compartment is m the back, so I would have to change the gearbox and transmission and other things. I would also have to change the shock absorbers and brakes, designed to smooth the ride and stop a car at 65 mph but not at 180 mph. By the time I had finished modifying my VW to take the BMW engine, there would not be much remaining from my original Beetle, and the Modifications would have cost me a big pile of money. I suspect that my puny 40-horsepower engine is optimal, in the sense that I could no increase my cruising speed without sacrificing other performance features of my car—as well as sacrificing other money-requiring features of my lifestyle.
While the marketplace eventually eliminates engineering monstrosities like a VW with a BMW engine, all of us can think of monstrosities that took quite a while to eliminate. To those of you who share my fascination with naval warfare, British battle-cruisers are a good example. Before and during the First World War, the British navy launched thirteen warships called battle-cruisers, designed to be as large and with as many big guns as battleships but much faster. By maximizing speed and firepower, the battle-cruisers immediately caught the public imagination and became a propaganda sensation. However, if you take a 28,000-ton battleship, keep the weight of the big guns nearly constant, and greatly increase the weight of the engines while still maintaining total weight around 28,000 tons, you have to skimp on the weight of some other parts. The battle-cruisers skimped especially on weight of armour, but also on weight of small guns, internal compartments, and anti-aircraft defence. The results of this suboptimal overall design were inevitable. In 1916 H.M.S. Indefatigable, Queen Mary, and Invincible all blew up almost as soon as they were hit by shells at the Battle ofjutland. H.M.S. Hoodblew up in 1941, a mere eight minutes after entering battle with the German battleship Bismarck. H.M. S. Repulse was sunk by Japanese bombers a few days after the Japanese attack on Pearl Harbor, thereby acquiring the dubious distinction of being the first large warship to be destroyed from the air while in combat at sea. Faced with this stark evidence that some spectacularly maximal parts do not make an optimal whole, the British navy let its programme of building battle-cruisers become extinct. In short, engineers cannot tinker with single parts in isolation from the rest of a machine, because each part costs money, space, and weight that might have gone into something else. Engineers instead have to ask what combination of parts will optimize a machine's effectiveness. By the same reasoning, evolution cannot tinker with single traits in isolation from the rest of an animal, because every structure, enzyme, or piece of DNA consumes energy and space that might have gone into something else. Instead, natural selection favoured that combination of traits that maximizes the animal's reproductive output. Thus, both engineers and evolutionary biologists have to evaluate the trade-offs involved in increasing anything; that is, its costs, as well as the benefits that it would bring. An obvious difficulty in applying this reasoning to our life-cycles is that they have many features seeming to reduce, not to maximize, our ability to produce offspring. Growing old and dying is just one example; other examples are human female menopause, bearing one baby at a time, producing babies only once every year or so at most, and not even starting to produce babies until the age of twelve to sixteen. Would not natural selection favour the woman who reached puberty at age five, completed gestation in three weeks, regularly bore quintuplets, never underwent menopause, put lots of biological energy into repair of her body, lived to 200, and thereby left hundreds of offspring?
But posing the question in that form pretends that evolution can change our bodies one piece at a time, and ignores the hidden costs. For example, a woman certainly could not reduce the length of pregnancy to three weeks without changing anything else about herself or her baby. Remember that we only have a finite amount of energy available to us. Even people doing hard exercise and eating rich food—lumberjacks, or marathon runners in training—cannot metabolize much more than about 5,000 calories per day. How should we allocate those calories between repairing ourselves and rearing babies, if our goal is to raise as many babies as possible? At the one extreme, if we put all our energy into babies and devoted no energy to biological repair, our bodies would age and disintegrate before we could rear our first baby. At the other extreme, if we lavished all our available energy on keeping our bodies in shape, we might live a long time but would have no energy left for the exhausting process of making and rearing babies. What natural selection must do is to adjust an animal's relative expenditures of energy on repair and on reproduction, so as to maximize its reproductive output, averaged over its lifetime. The answer to that problem varies among animal species, depending on factors such as their risk of accidental death, their reproductive biology, and the costs of various types of repair. This perspective can be employed to make testable predictions about how animals should differ in their repair mechanisms and rates of aging. In 1957 the evolutionary biologist George Williams cited some striking facts about aging that become comprehensible only from an evolutionary perspective. Let's consider several of Williams's examples and re-express them in the physiological language of biological repair, by taking slow aging as an indication of good repair mechanisms.
The first example concerns the age at which an animal first breeds and produces offspring. That age varies enormously among species: few humans are so precocious as to produce babies before the age of twelve years, while any self-respecting mouse a mere two months old can already make baby mice. Animals belonging to a species whose age of first breeding is late, like us, need to devote much energy to repair, in order to ensure that they survive to that reproductive age. Hence we expect investment in repair to increase with age at first reproduction.
For instance, correlated with our having a much later age of first reproduction than do mice, we humans age far more slowly than mice and are thus presumed to repair our bodies much more effectively. Even with plenty of food and the best medical care, a mouse is lucky to reach its second birthday, while we would be unlucky not to reach our seventy-second birthday. The evolutionary reason: a human who invested no more of his/her energy in repair than does a mouse would be dead long before reaching puberty. Hence it is more worthwhile to repair a human than a mouse.
What might that postulated extra energy expenditure of ours actually consist of? At first, our human repair capabilities seem unimpressive. We cannot regrow an amputated arm, and we do not regularly replace our skeleton, in the way that some short-lived invertebrates do. However, such spectacular but infrequent replacements of a whole structure probably are not the biggest items in an animal's repair budget. Instead, the biggest expense is all that invisible replacement of so many of your cells and molecules, day after day. Even if you spend all day every day just lying in bed, you need to eat about 1,640 calories per day if you are a man (1,430 for a woman) just to maintain your body. Much of that maintenance metabolism goes to our invisible scheduled replacement. And so I would guess that we cost more than a mouse in the respect of putting a bigger fraction of our energy into self-repair, and a smaller fraction into other purposes like keeping warm or caring for babies.
The second example I shall discuss involves the risk of irreparable injury. Some biological damage is potentially reparable, but there is also damage that is guaranteed to be fatal (for example, being eaten by a lion). If you are likely to be eaten by a lion tomorrow, there is no point paying a dentist to start expensive orthodontic work on your teeth today. You would do better to let your teeth rot and start having babies immediately. But if an animal's risk of death from irreparable accidents is low, then there is a potential payoff, in the form of increased lifespan, from putting energy into expensive repair mechanisms that retard aging. This is the reasoning by which Mercedes-owners decide to pay for lubrication of their cars in Germany and the US but not in New Guinea.
Biological analogies are that the risk of death from predators is lower for birds than for mammals (because birds can escape by flying), and lower for turtles than for most other reptiles (because turtles are protected by a shell). Thus, birds and turtles stand to gain a lot from expensive repair mechanisms, compared to flightless mammals and shell-less reptiles that will soon be eaten by predators anyway. Indeed, if one compares longevities of well-fed pets protected from predators, birds do live longer (that is, do age more slowly) than similarly sized mammals, and turtles live longer than similarly sized shell-less reptiles. The bird species best protected from predators are seabirds like petrels and albatrosses that nest on remote oceanic islands free of predators. Their leisurely life-cycles rival our own. Some albatrosses do not even breed until they are ten years old, and we still do not know how long they live: the birds themselves last longer than the metal rings that biologists began putting on their legs a few decades ago in order to age them. In the ten years that it takes an albatross to start breeding, a mouse population could have gone through sixty generations, most of which would already have succumbed to predators or old age. As our third example, let's compare males and females of the same species. We expect more potential payoff from repair mechanisms, and lower rates of aging, in that sex with the lower accidental mortality rate. For many or most species, males suffer greater accidental mortality than females, partly because males put themselves at greater risk by fighting and bold displays. This is certainly true of human males today and has probably been so throughout our history as a species—men are the sex most likely to die in wars against men of other groups, and in individual fights within a group. Also, in many species the males are bigger than the females, but studies of red deer and of New World blackbirds show that males are thereby more likely than females to die when food becomes scarce.
Correlated with this greater accidental death rate of men, men also age faster and have a higher non-accidental death rate than women. At present, women's life expectancy is about six years greater than that of men; some of this difference is because more men than women are smokers, but there is a sex-linked difference in life expectancy even among non-smokers. These differences suggest that evolution has programmed us so that women put more energy into self-repair, while men put more energy into fighting. Expressed another way, it just is not worth as much to repair a man as it is to repair a woman. I do not thereby mean to denigrate male fighting, which serves a useful evolutionary Purpose for a man: to gain wives and to secure resources for his children and his tribe, at the expense of other men and their children and tribe.
My remaining example of how some striking facts of aging become comprehensible only from an evolutionary perspective concerns the distinctively human phenomenon of survival past reproductive age, Specially past female menopause. Since transmitting one's genes to the next generation is what drives evolution, other animal species rarely survive past reproductive age. Instead, Nature programmes death to coincide with the end of fertility, because there is then no longer an evolutionary benefit to gain from keeping one's body in good repair. It is an exception in need of explanation to realize that women are programmed to live for decades after menopause, and that men are programmed to live to an age when most men are no longer busy siring babies. But the explanation becomes apparent on reflection. The intense phase of parental care is unusually protracted in the human species and lasts nearly two decades. Even those older people whose own children have reached adulthood are tremendously important to the survival of not just their children but of their whole tribe. Especially in the days before writing, they acted as the carriers of essential knowledge. Thus, Nature has programmed us with the capacity to keep the rest of our bodies in reasonable repair even at an age when the female reproductive system itself has fallen into disrepair.
Conversely, though, we have to wonder why natural selection programmed female menopause into us in the first place. It too, like aging, cannot be explained away as something physiologically inevitable. Most mammals, including human males plus chimps and gorillas of both sexes, merely experience a gradual decline and eventual cessation of fertility with age, rather than the abrupt shutdown of women's fertility. Why did that peculiar, seemingly counter-productive feature of ours evolve? Would not natural selection favour the woman who remained fertile until the bitter end?
Human female menopause probably resulted from two other distinctively human characteristics: the exceptional danger that childbirth poses to the mother, and the danger that a mother's death poses to her offspring. Recall from Chapter Three the enormous size of the human infant at birth relative to its mother: our big 7-pound babies emerging from 100-pound mothers, compared to little 4-pound gorilla babies emerging from a 200-pound gorilla mother. As a result, childbirth is dangerous to women. Especially before the advent of modern obstetrics, women often died in childbirth, whereas mother gorillas and chimps virtually never do.
Now recall also from Chapter Three the extreme dependence of human infants on their parents, especially on their mother. Because human infants develop so slowly and cannot even feed themselves after weaning (unlike young apes), the death of a hunter-gatherer mother would have been likely to be fatal to her offspring up to a later age in childhood than for any other primate. Hence a hunter-gatherer mother with several children was gambling the lives of those children at every subsequent childbirth. Since her investment in those prior children increased with their age, and since her own risk of death in childbirth also increased with her age, the odds of her gamble paying off got worse and worse as she got older. When you already have three children alive but still dependent on you, why risk those three for a fourth?
Those worsening odds probably led through natural selection to menopausal shutdown of human female fertility, in order to protect a mother's prior investment in children. Since childbirth carries no risk of death for fathers, men did not evolve menopause. Like aging, menopause illustrates how an evolutionary approach illuminates features of our life-cycle that would otherwise be counterintuitive. It is even possible that menopause evolved only within the past 40,000 years, when Cro-Magnons and other anatomically modern humans began frequently to survive to the age of sixty or more. Neanderthals and earlier humans usually died before the age of forty anyway, so that menopause would have brought their women no benefits if it were to occur at the same age as in modern Femina sapiens.
Thus, the longer lifespan of modern humans than of apes rests not only on cultural adaptations, such as tools to acquire food and deter predators. It also rests on the biological adaptations of menopause and increased investment in self-repair. Whether those biological adaptations developed especially at the time of the Great Leap Forward or earlier, they rank among the life history changes that permitted the rise of the third chimpanzee to humanity. The last conclusion that I wish to draw from an evolutionary approach to aging is that it undermines the approach which has long dominated the physiological study of aging. The gerontological literature is obsessed with a search for The Cause of Aging—preferably a single cause, certainly not more than a few major causes. Within my own lifetime as a biologist, hormonal changes, deterioration in the immune system, and neural degeneration have vied in popularity for the title of The Cause, without compelling support having been adduced to date for any of the candidates. But evolutionary reasoning suggests that this search will remain futile. There should not be just one, or even a few, dominant physiological mechanisms of aging. Instead, natural selection should act to match rates of aging in all physiological systems, with the result that aging involves innumerable simultaneous changes.
The basis of this prediction is as follows. There is no point doing expensive maintenance on one piece of the body if other pieces are deteriorating more rapidly. Conversely, natural selection should not permit a few systems to deteriorate long before all the others, as the cost of extra repairs on just those few systems would then buy a big increase in life expectancy and would be worth it. By analogy, Mercedes-owners should not install cheap ball-bearings when they are lavishing expense on all other parts of the car. Had they been so foolish, they could have doubled the lifetime of their costly car just by spending a few more dollars for better ball-bearings. But it would not pay either to go to the expense of installing diamond ball-bearings, when all the rest of the car would have rusted away before those ball-bearings wore out. Thus, the optimal strategy for Mercedes-owners, and for us, is to repair all parts of our cars or bodies at such rates that everything finally collapses all at once. It seems to me that this depressing prediction is borne out, and that we come closer to this evolutionary ideal than to the physiologists' long-sought Cause of Aging. Signs of aging can be found wherever one looks for them. Already I am conscious in myself of tooth wear, considerable decreases in muscle performance, and significant losses in hearing, vision, smell, and taste. For all these senses, the acuity of women is greater than that of men of equal age, whatever the age group compared. Ahead of me lies the familiar litany: weakening of the heart, hardening of the arteries, increasing brittleness of bones, decreases in kidney filtration rates, lower resistance of the immune system, and loss of memory. The list could be extended almost indefinitely. Evolution seems indeed to have arranged things so that all our systems deteriorate, and that we invest in repair only as much as we are worth.
From a practical standpoint, this conclusion is disappointing. If there had been one dominant cause of aging, curing that cause would have provided us with a fountain of youth. This thought, operating at a time when aging was thought to be largely a hormonal phenomenon, inspired some attempts at miraculous rejuvenation of old people by hormonal injections or implantation of young gonads. Such an attempt was the subject of Sir Arthur Conan Doyle's story, The Adventure of the Creeping Man, in which the aged Professor Presbury becomes infatuated with a young woman, desperately wants to rejuvenate himself, and instead is found creeping around like a monkey after midnight. The great Sherlock Holmes discovers the reason: the Professor has been seeking youth by injecting himself with the serum of langur monkeys.
I could have warned Professor Presbury that his myopic obsession with proximate causation would lead him astray. Had he thought of ultimate evolutionary causation, he would have realized that natural selection would never permit us to deteriorate through a single mechanism with one simple cure. Perhaps it is just as well. Sherlock Holmes worried greatly about what would happen if such an elixir of life were found: There is danger there—a very real danger to humanity. Consider Watson, that the material, the sensual, the worldly would all prolong their worthless lives… It would be the survival of the least fit. What sort of cesspool may not our poor world become? Holmes would be relieved to know that his worries now appear unlikely to materialize.