Abstract

Evolutionarily plausible scenarios of how senescence, although detrimental to the individual soma, could evolve via natural selection on individuals were first developed more than 50 years ago (Medawar 1952). The premise behind what we will call classical evolutionary senescence theory is that, due to the inescapability of death from extrinsic hazards such as predators, environmental degradation, and infectious disease, the cumulative probability of surviving to older and older ages grows ever smaller even in the absence of senescence. Medawar (1952) pointed out that following from this self-evident premise, if traits affecting evolutionary fitness—reproduction and survival—were expressed in an age-specific manner, the power of natural selection to affect the evolutionary fate of these traits would gradually wane with age. Put slightly differently, a lethal genetic allele expressed only in centenarians has no evolutionary fitness disadvantage, both because it is so unlikely to be expressed at all (only about one person in 10,000 survives to 100 years in modern populations) and because reproduction has long since ceased by age 100. By the same logic, an allele improving survival in centenarians confers no evolutionary advantage either. In contrast, similar alleles expressed at age 20 would have an enormous impact on fitness. From the preceding scenario, senescence could evolve by one or both of the following hypothetical genetic mechanisms: (1) Deleterious alleles that affect survival or reproduction only very late in life, when selection is weak, could accumulate in the genome over evolutionary time by mutation pressure checked only weakly by mutation-selection...

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