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LETTER TO THE EDITOR |
Centre for Conservation Science University of St Andrews The Observatory Buchanan Gardens St Andrews Scotland
To the Editor:
Recently, "52 researchers in the field of aging" have written that "aging is a product of evolutionary neglect, not evolutionary intent" (1), with some of them going on to add: "the way evolution works makes it impossible for us to possess genes that are specifically designed to cause physiological decline with age or to control how long we live" (2). These statements seem uncontentious. However, there are to be three simple, and relatively undemanding, conditions for them to be untrue. The first is that individuals' "fitness" or efficiency of resource utilization eventually declines with age due to the accumulation of physical and genetic damage. The second requirement is that individuals possess heritable resources. Thirdly, relatives must be aggregated. Provided these requirements are met, a "suicide gene" may be able to spread through a population.
Under these conditions programmed death may be considered an extreme form of altruism, and understood as a special case of Hamilton's rule of inclusive fitness (3). Provided that the gene, rather than the individual, is considered as the unit of selection, the evolution of suicide therefore presents no difficulties.
This can be simply stated mathematically. If R is the expected relatedness between the inheritors and original owner of resources, 
is the age difference between them, and f(t) is the extra fitness, in terms of reproductive potential, gained by an individual of age t from a unit of resources. Then, given general stability in the situation, you should kill yourself once:
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So, if the kids will get the house, you should leave around halfway through your reproductive decline. And they really should try and push you out sooner.
It would, therefore, seem that a certain amount of middle-aged "suicide" should be the norm in stable communities with heritable resources. During rapid evolution, this strategy has the additional advantage of reducing generation time and allowing its adopters the potential to get ahead. For plants, the freeing-up of space generally requires actual death, but mobile species may have the alternative of emigration, so long as individuals move far enough to reduce competition with their offspring. In effect, your no longer being in the way may give enough benefit to your relatives to make suicide an individually altruistic but genetically advantageous act.
The optimal reduction in life expectancy caused by programmed death will depend on the pattern of physical decline. Such deaths can only be evolutionarily beneficial if they occur after individuals' aging, in the sense of decline in reproductive potential, is well established. This means that such a mechanism cannot explain all age-related changes, though it could promote resource allocation strategies that accelerate the later stages of physical decline. Together, these may also limit the benefits directly available from just switching off such a "death gene," and imply that its existence may be masked by further adaptations that have evolved to exploit the opportunities it offers.
The size and detectability of this effect in particular species must depend on the heritability of the resources they depend upon. There are a few instances, such as the spiders consumed by their own young (4), in which its effects are obvious. However, for it to be significant for gerontology, humanity would have had to evolve under conditions where important resources could be inherited. Given the apparent low population densities of early hominids (5), and the likely relative importance of knowledge, experience, and cooperation, as opposed to physical possessions, to hunter-gatherer communities, it could be considered that the midlife crisis is actually an adaptation to, rather than a disease of, modern society.
Acknowledgments
Address correspondence to Mike Lonergan, Centre for Conservation Science, University of St Andrews, The Observatory, Buchanan Gardens, St Andrews, Fife KY16 9LZ, Scotland. E-mail: mel{at}mcs.st-and.ac.uk
References
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