However, this view ignores the fact that the human male reproductive tract, and every other biological function of both women and men, continue to function in most people for many decades after age forty. One would therefore have to assume that every other biological function was able to adjust quickly to our new long life span, leaving unexplained why female reproduction was uniquely incapable of doing so. The claim that formerly few women survived until the age of menopause is based on paleodemography, that is, on attempts to estimate age at time of death in ancient skeletons. Those estimates rest on unproven, implausible assumptions, such as that the recovered skeletons represent an unbiased sample of an entire ancient population, or that ancient adult skeletons really can be aged accurately. While paleodemographers’ ability to distinguish the ancient skeleton of a ten-year-old from that of a twenty-five-year-old is not in question, the ability they claim to distinguish an ancient forty-year-old from a fifty-five-year-old has never been demonstrated. One can hardly reason by comparison with skeletons of modern people, whose different lifestyles, diets, and diseases surely make their bones age at different rates from the bones of ancients.
A second objection acknowledges human female menopause as a possibly ancient phenomenon but denies that it is unique to humans. Many or most wild animals exhibit a decrease in fertility with age. Some elderly individuals of a wide variety of wild mammal and bird species are found to be infertile. Many elderly female individuals of rhesus macaques and certain strains of laboratory mice, living in laboratory cages or zoos where their lives are considerably extended over expected spans in the wild by gourmet diets, superb medical care, and complete protection from enemies, do become infertile. Hence some biologists object that human female menopause is merely part of a widespread phenomenon of animal menopause. Whatever that phenomenon’s explanation, its existence in many species would mean that there is not necessarily anything peculiar about menopause in the human species requiring explanation.
However, one swallow does not make a summer, nor does one sterile female constitute menopause. That is, detection of an occasional sterile elderly individual in the wild, or of regular sterility in caged animals with artificially extended life spans, does nothing to establish the existence of menopause as a biologically significant phenomenon in the wild. That would require demonstrating that a substantial fraction of adult females in a wild animal population become sterile and spend a significant portion of their life spans after the end of their fertility.
The human species does fulfill that definition, but only one or possibly two wild animal species are definitely known to do so. One is an Australian marsupial mouse in which males (not females) exhibit something like menopause: all males in the population become sterile within a short time in August and die over the next couple of weeks, leaving a population that consists solely of pregnant females. In that case, however, the postmenopausal phase is a negligible fraction of the total male life span. Marsupial mice do not exemplify true menopause but are more appropriately considered an example of big-bang reproduction, alias semelparity—a single lifetime reproductive effort rapidly followed by sterility and death, as in salmon and century plants. The better example of animal menopause is provided by pilot whales, among which one-quarter of all adult females killed by whalers proved to be postmenopausal, as judged by the condition of their ovaries. Female pilot whales enter menopause at the age of thirty or forty years, have a mean survival of at least fourteen years after menopause, and may live for over sixty years.
Menopause as a biologically significant phenomenon is thus not unique to humans, being shared at least with one species of whale. It would be worth looking for evidence of menopause in killer whales and a few other species as possible candidates. But still-fertile elderly females are often encountered among well-studied wild populations of other long-lived mammals, including chimpanzees, gorillas, baboons, and elephants. Hence those species and most others are unlikely to be characterized by regular menopause. For example, a fifty-five-year-old elephant is considered elderly, since 95 percent of elephants die before that age. But the fertility of fifty-five-year-old female elephants is still half that of younger females in their prime.
Thus, female menopause is sufficiently unusual in the animal world that its evolution in humans requires explanation. We certainly did not inherit it from pilot whales, from whose ancestors our own ancestors parted company over fifty million years ago. In fact, we must have evolved it since our ancestors separated from those of chimps and gorillas seven million years ago, because we undergo menopause and chimps and gorillas appear not to (or at least not regularly).
The third and last objection acknowledges human menopause as an ancient phenomenon that is unusual among animals. Instead, these critics say that we need not seek an explanation for menopause, because the puzzle has already been solved. The solution (they say) lies in the physiological mechanism of menopause: a woman’s egg supply is fixed at her birth and not added to later in her life. One or more eggs are lost by ovulation at each menstrual cycle, and far more eggs simply die (termed atresia). By the time a woman is fifty years old, most of her original egg supply has been depleted. Those eggs that remain are half a century old, increasingly unresponsive to pituitary hormones, and too few in number to produce enough estradiol to trigger the release of pituitary hormones.
But there is a fatal counterobjection to this objection. While the objection is not wrong, it is incomplete. Yes, depletion and aging of the egg supply are the immediate causes of human menopause, but why did natural selection program women such that their eggs become depleted or unresponsive in their forties? There is no compelling reason why we could not have evolved twice as large a starting quota of eggs, or eggs that remain responsive after half a century. The eggs of elephants, baleen whales, and possibly albatrosses remain viable for at least sixty years, and the eggs of tortoises are viable for much longer, so human eggs could presumably have evolved the same capability.
The basic reason why the third objection is incomplete is because it confuses proximate mechanisms with ultimate causal explanations. (A proximate mechanism is an immediate direct cause, while an ultimate explanation is the last in the long chain of factors leading up to that immediate cause. For example, the proximate cause of a marriage breakup may be a husband’s discovery of his wife’s extramarital affairs, but the ultimate explanation may be the husband’s chronic insensitivity and the couple’s basic incompatibility that drove the wife to affairs.) Physiologists and molecular biologists regularly fall into the trap of overlooking this distinction, which is fundamental to biology, history, and human behavior. Physiology and molecular biology can do no more than identify proximate mechanisms; only evolutionary biology can provide ultimate causal explanations. As one simple example, the proximate reason why so-called poison-dart frogs are poisonous is that they secrete a lethal chemical named batrachotoxin. But that molecular biological mechanism for the frogs’ poisonousness could be considered an unimportant detail because many other poisonous chemicals would have worked equally well. The ultimate causal explanation is that poison-dart frogs evolved poisonous chemicals because they are small, otherwise defenseless animals that would be easy prey for predators if they were not protected by poison.
We have already seen repeatedly in this book that the big questions about human sexuality are the evolutionary questions about ultimate causal explanation, not the search for proximate physiological mechanisms. Yes, sex is fun for us because women have concealed ovulations and are constantly receptive, but why did they evolve that unusual reproductive physiology? Yes, men have the physiological capacity to produce milk, but why did they not evolve to exploit that capacity? For menopause as well, the easy part of the puzzle is the mundane fact that a woman’s egg supply gets depleted or impaired by around the time she is fifty years old. The challenge is to understand why we evolved that seemingly self-defeating detail of reproductive physiology.
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The ag
ing (or senescence, as biologists call it) of the female reproductive tract cannot be profitably considered in isolation from other aging processes. Our eyes, kidneys, heart, and all other organs and tissues also senesce. But that aging of our organs is not physiologically inevitable—or at least it’s not inevitable that they senesce as rapidly as they do in the human species, because the organs of some turtles, clams, and other species remain in good condition much longer than ours do.
Physiologists and many other researchers on aging tend to search for a single all-encompassing explanation of aging. Popular explanations hypothesized in recent decades have invoked the immune system, free radicals, hormones, and cell division. In reality, though, all of us over forty know that everything about our bodies gradually deteriorates, and not just our immune systems and our defenses against free radicals. Although I have had a less stressful life and better medical care than most of the world’s nearly six billion people, I can still tick off the aging processes that have already taken their toll on me by age fifty-nine: impaired hearing at high pitch, failure of my eyes to focus at short distances, less acute senses of smell and taste, loss of one kidney, tooth wear, less flexible fingers, and so on. My recovery from injuries is already slower than it used to be: I had to give up running because of recurrent calf injuries, I recently completed a slow recovery from a left elbow injury, and now I have just injured the tendon of a finger. Ahead of me, if the experience of other men is any guide, lies the familiar litany of complaints, including heart disorders, clogged arteries, bladder trouble, joint problems, prostate enlargement, memory loss, colon cancer, and so on. All that deterioration is what we mean by aging.
The basic reasons behind this grim litany are easily understood by analogy to human-built structures. Animal bodies, like machines, tend to deteriorate gradually or become acutely damaged with age and use. To combat those tendencies, we consciously maintain and repair our machines. Natural selection ensures that our body unconsciously maintains and repairs itself.
Both bodies and machines are maintained in two ways. First, we repair a part of a machine when it is acutely damaged. For example, we fix a car’s punctured tire or bashed-in fender, and we replace its brakes or tires if they become damaged beyond repair. Our body similarly repairs acute damage. The most visible example is wound repair when we cut our skin, but molecular repair of damaged DNA and many other repair processes go on invisibly inside us. Just as a ruined tire can be replaced, our body has some capacity to regenerate parts of damaged organs such as by making new kidney, liver, and intestinal tissue. That capacity for regeneration is much better developed in many other animals. If only we were like starfish, crabs, sea cucumbers, and lizards, which can regenerate their arms, legs, intestines, and tail, respectively!
The other type of upkeep of machines and bodies is regular or automatic maintenance to reverse gradual wear, regardless of whether there has been any acute damage. For example, at times of scheduled maintenance we change our car’s motor oil, spark plugs, fan belt, and ball bearings. Similarly, our body constantly grows new hair, replaces the lining of the small intestine every few days, replaces our red blood cells every few months, and replaces each tooth once in our lifetime. Invisible replacement goes on for the individual protein molecules that make up our bodies.
How well you maintain your car, and how much money or resources you put into its maintenance, strongly influence how long it lasts. The same can be said of our bodies, not only with respect to our exercise programs, visits to the doctor, and other conscious maintenance, but also with respect to the unconscious repair and maintenance that our bodies do on themselves. Synthesizing new skin, kidney tissue, and proteins uses up a lot of biosynthetic energy. Animal species vary greatly in their investment in self-maintenance, hence in the rate at which they senesce. Some turtles live for over a century. Laboratory mice, living in cages with abundant food and no predators or risks, and receiving better medical care than any wild turtle or the vast majority of the world’s people, inevitably become decrepit and die of old age before their third birthday. There are aging differences even among us humans and our closest relatives, the great apes. Well-nourished apes living in the safety of zoo cages and attended by veterinarians rarely (if ever) live past age sixty, while white Americans exposed to much greater danger and receiving less medical attention now live to an average of seventy-eight years for men, eighty-three years for women. Why do our bodies unconsciously take better care of themselves than do apes’ bodies? Why do turtles senesce so much more slowly than mice?
We could avoid aging entirely and (barring accidents) live forever if we went all out for repair and changed all the parts of our bodies frequently. We could avoid arthritis by growing new limbs, as crabs do, avoid heart attacks by periodically growing a new heart, and minimize tooth decay by regrowing new teeth five times (as elephants do, instead of just once, as we do). Some animals thus make a big investment in certain aspects of body repair, but no animal makes a big investment in all aspects, and no animal avoids aging entirely.
Analogy to our cars again makes the reason obvious: the expense of repair and maintenance. Most of us have only limited amounts of money, which we are obliged to budget. We put just enough money into car repair to keep our car running as long as it makes economic sense to do so. When the repair bills get too high, we find it cheaper to let the old car die and buy a new one. Our genes face a similar tradeoff between repairing the old body that contains the genes and making new containers for the genes (that is, babies). Resources spent on repair, whether of cars or of bodies, eat away at the resources available for buying new cars or making babies. Animals with cheap self-repair and short life spans, like mice, can churn out babies much more rapidly than can expensive-to-maintain, long-lived animals like us. A female mouse that will die at the age of two, long before we humans achieve fertility, has been producing five babies every two months since she was a few months old.
That is, natural selection adjusts the relative investments in repair and reproduction so as to maximize the transmission of genes to offspring. The balance between repair and reproduction differs between species. Some species stint on repair and churn out babies quickly but die early, like mice. Other species, like us, invest heavily in repair, live for nearly a century, and can produce a dozen babies in that time (if you are a Hutterite woman), or over a thousand babies (if you are Emperor Moulay the Bloodthirsty). Your annual rate of baby production is lower than the mouse’s (even if you are Moulay) but you have more years in which to do it.
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It turns out that an important evolutionary determinant of biological investment in repair—hence of life span under the best possible conditions—is the risk of death from accidents and bad conditions. You don’t waste money maintaining your taxi if you are a taxi driver in Teheran, where even the most careful taxi driver is bound to suffer a major fender-bender every few weeks. Instead, you save your money to buy the inevitable next taxi. Similarly, animals whose lifestyles carry a high risk of accidental death are evolutionarily programmed to stint on repair and to age rapidly, even when living in the well-nourished safety of a laboratory cage. Mice, subject to high rates of predation in the wild, are evolutionarily programmed to invest less in repair and to age more rapidly than similar-sized caged birds that in the wild can escape predators by flying. Turtles, protected in the wild by a shell, are programmed to age more slowly than other reptiles, while porcupines, protected by quills, age more slowly than mammals comparable in size.
That generalization also fits us and our ape relatives. Ancient humans, who usually remained on the ground and defended themselves with spears and fire, were at lower risk of death from predators or from falling out of a tree than were arboreal apes. The legacy of the resultant evolutionary programming carries on today in that we live for several decades longer than do zoo apes living under comparable conditions of safety, health, and affluence. We must have evolved better repair mechanisms and decreased rates of
senescence in the last seven million years, since we parted company from our ape relatives, came down out of the trees, and armed ourselves with spears and stones and fire.
Similar reasoning is relevant to our painful experience that everything in our bodies begins to fall apart as we grow older. Alas, that sad truth of evolutionary design is cost-efficient. You would be wasting biosynthetic energy, which otherwise could go into making babies, if you kept one part of your body in such great repair that it outlasted all your other parts and your resultant expected life span. The most efficiently constructed body is the one in which all organs wear out at approximately the same time.
The same principle, of course, applies to human-built machines, as illustrated in a story about that genius of cost-efficient automobile manufacture, Henry Ford. One day, Ford sent some of his employees to car junkyards, with instructions to examine the condition of the remaining parts in Model T Fords that had been junked. The employees brought back the apparently disappointing news that almost all components showed signs of wear. The sole exceptions were the kingpins, which remained virtually unworn. To the employees’ surprise, Ford, instead of expressing pride in his well-made kingpins, declared that the kingpins were overbuilt, and that in the future they should be made more cheaply. Ford’s conclusion may violate our ideal of pride in workmanship, but it made economic sense: he had indeed been wasting money on long-lasting kingpins that outlasted the cars in which they were installed.
The design of our bodies, which evolved through natural selection, fits Henry Ford’s kingpin principle, with only one exception. Virtually every part of the human body wears out around the same time. The kingpin principle even fits men’s reproductive tract, which undergoes no abrupt shutdown but does gradually accumulate a variety of problems, such as prostate hypertrophy and decreasing sperm count, to different degrees in different men. The kingpin principle also fits the bodies of animals. Animals caught in the wild show few signs of age-related deterioration because a wild animal is likely to die from a predator or accident when its body becomes significantly impaired. In zoos and laboratory cages, however, animals exhibit gradual age-related deterioration in every body part just as we do.
Why Is Sex Fun?: The Evolution of Human Sexuality Page 11
