A blog about biology, self-improvement, and the future

Peter Godfrey-Smith’s Other Minds, which is mostly a combination of a discussion on the evolution of intelligence/consciousness and a collection of fun cephalopod anecdotes, surprised me by having a very nice presentation of the core ideas of non-adaptive theories of ageing.

On mutation accumulation:

If we are thinking in evolutionary terms, it’s natural to wonder if there is some hidden benefit from aging itself. Because the onset of aging in our lives can seem so “programmed,” this is a tempting idea. Perhaps old individuals die off because this benefits the species as a whole, by saving resources for the young and vigorous? But this idea is question-begging as an explanation of aging; it assumes that the young are more vigorous. So far in the story, there’s no reason why they should be.

In addition, a situation of this kind is not likely to be stable. Suppose we had a population in which the old do graciously “pass the baton” at some appropriate time, but an individual appeared who did not sacrifice himself in this way, and just kept going. This one seems likely to have the chance to have a few extra offspring. If his refusal to sacrifice was also passed on in reproduction, it would spread, and the practice of sacrifice would be undermined. So even if aging did benefit the species as a whole, that would not be enough to keep it around. This argument is not the end of the line for a “hidden benefit” view, but the modern evolutionary theory of aging takes a different approach. […]

Start with an imaginary case. Assume there is a species of animal with no natural decay over time. These animals show no “senescence,” to use the word preferred by biologists. The animals start reproducing early in their life, and reproduction continues until the animal dies from some external cause—being eaten, famine, lightning strike. The risk of death from these events is assumed to be constant. In any given year, there is a (say) 5 percent chance of dying. This rate does not increase or decrease as you get older, but there is some number of years by which time some accident or other has almost certainly caught you. A newborn has less than a 1 percent chance of still being around at ninety years in this scenario, for example. But if that individual does make it to ninety, it will very probably make it to age ninety-one.

Next we need to look at biological mutations. […] Mutations often tend to affect particular stages in life. Some act earlier, others act later. Suppose a harmful mutation arises in our imaginary population which affects its carriers only when they have been around for many years. The individuals carrying this mutation do fine, for a while. They reproduce and pass it on. Most of the individuals carrying the mutation are never affected by it, because some other cause of death gets them before the mutation has any effect. Only someone who lives for an unusually long time will encounter its bad effects.

Because we are assuming that individuals can reproduce through all their long lives, there is some tendency for natural selection to act against this late-acting mutation. Among individuals who live for a very long time, those without the mutation are likely to have more offspring than those who have it. But hardly anyone lives long enough for this fact to make a difference. So the “selection pressure” against a late-acting harmful mutation is very slight. When molecular accidents put mutations into the population, as described above, the late-acting mutations will be cleaned out less efficiently than early-acting ones.

As a result, the gene pool of the population will come to contain a lot of mutations that have harmful effects on long-lived individuals. These mutations will each become more common, or be lost, mostly through sheer chance, and that makes it likely that some will become common. Everyone will carry some of these mutations. Then if some lucky individual evades its predators and other natural dangers and lives for an unusually long time, it will eventually find things starting to go wrong in its body, as the effects of these mutations kick in. It will appear to have been “programmed to decline,” because the effects of those lurking mutations will appear on a schedule. The population has begun to evolve aging.

On antagonistic pleiotropy:

Is it worth saving enough money so that you will live in luxury when you are 120? Perhaps it is, if you have unlimited money coming in. Maybe you will live that long. But if you don’t have unlimited money coming in, then all the money you save for a long retirement is money you can’t do something else with now. Rather than saving the extra amount needed, it might make more sense to spend it, given that you are not likely to make it to 120 anyway.

The same principle applies to mutations. A lot of mutations have more than one effect, and in some cases, a mutation might have one effect that is visible early in life and another effect that is visible later. If both effects are bad, it is easy to see what will happen—the mutation should be weeded out because of the bad effect it has early in life. It is also easy to see what will happen if both effects are good. But what if a mutation has a good effect now and a bad effect later? If “later” is far enough away that you will probably not make it to that stage anyway, due to ordinary day-to-day risks, then the bad effect is unimportant. What matters is the good effect now. So mutations with good effects early in life and bad effects late in life will accumulate; natural selection will favor them. Once many of these have arisen in the population, and all or nearly all individuals carry some of them, a decay late in life will come to seem preprogrammed. Decay will appear in each individual as if on a schedule, though each individual will show the effects a bit differently. This happens not because of some hidden evolutionary benefit of the breakdown itself, but because the breakdown is the cost paid for earlier gains.

[Mutation accumulation and antagonistic pleiotropy] work together. Once each process gets started, it reinforces itself and also magnifies the other. There is “positive feedback,” leading to more and more senescence. Once some mutations get established that lead to age-related decay, they make it even less likely that individuals will live past the age at which those mutations act. This means there is even less selection against mutations which have bad effects only at that advanced age. Once the wheel starts turning, it turns more and more quickly.

The book discusses various wrinkles in the theory as it applies to different kinds of organisms, then goes on to discuss the question of why most cephalopods are so short-lived. Recommended.