Evolution Theory and the Mechanisms of Aging

Programmed, or “Adaptive,” Aging

It is sometimes suggested that despite its disadvantages to the individual, aging is beneficial and even necessary at the species level, for example, to prevent overcrowding. In this case, genes that actively cause aging might have evolved specifically to program the end of life in the same way as genes program development.

The difficulty with this view is that there is little evidence that intrinsic aging serves as a significant contributor to mortality in natural populations, which means that it apparently does not play the adaptive role suggested for it. The theory also embodies the questionable supposition that selection for advantage at the species level will be more effective than selection among individuals for the advantages of a longer life. Aging is clearly a disadvantage to the individual, so any mutation that inactivates the hypothetical adaptive aging genes would confer a fitness advantage and, therefore, the nonaging mutation should spread through the population unless countered by selection at the species or group level. Conditions under which this so-called group selection can work successfully are highly restrictive, especially when there is selection in the opposite direction acting at the level of the individual. Briefly, it is necessary that the population be divided among fairly isolated groups and that the introduction of a nonaging genotype into a group should rapidly lead to the group's extinction. The latter condition is necessary to provide the selection between groups that might, in principle, counter the tendency for selection at the level of individuals to favor the spread of nonaging mutants. Although theoretical special cases have been constructed that might permit the selection of genes to cause aging, it appears unlikely that the necessary conditions will be met with sufficient generality to explain the evolution of aging.

Selection Weakens With Age

An observation of central importance to the evolution of aging is that the force of natural selection—that is, its ability to discriminate between alternative genotypes—weakens with age. Because natural selection operates through the differential effects of genes on fitness, its discriminatory power must decline with age in proportion to the decline in the remaining fraction of the organism's lifetime expectation of reproduction. This is true whether or not the species exhibits aging.

The attenuation in the force of natural selection with age means inevitably that there is only loose genetic control over the later portions of the life span. For this reason, it has been suggested that aging might be due to an accumulation of mutations in the germline, which potentially are deleterious but are not expressed, or that produce no phenotypic effect until late in life.

The idea is that if deleterious mutations are expressed so late that most individuals will already have died from some other cause, such as predation, even though the genes involved have the potential to cause harm, they will be subject to very little selection against them. Over the generations, a large number of such genes might accumulate. These would cause aging and death only when an individual is removed to a protected environment, away from the hazards of the wild, and so would live long enough to experience their negative effects.

A stronger version of this theory was proposed by Williams, who suggested that because of the declining force of natural selection with age, any gene that conferred an advantage early in life would be favored by selection, even if the same gene had deleterious effects at older ages. Such “pleiotropic” genes could explain aging. The decline in the force of natural selection with age would ensure that even quite modest early benefits would outweigh severe harmful side effects, provided the latter occurred late enough.