The Rise and Fall of the Third Chimpanzee

by Jared Diamond

  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 750 IL, 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 in 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 not 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 of Jutland. H. M.S. Hood blew 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 expend
iture 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.