SEVEN
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.