Ageing is widely believed to be a non-adaptive process that results from a decline in the force of natural selection. However, recent studies in Saccharomyces cerevisiae are consistent with the existence of a programme of altruistic ageing and death. We suggest that the similarities between the molecular pathways that regulate ageing in yeast, worms, flies and mice, together with evidence that is consistent with programmed death in salmon and other organisms, raise the possibility that programmed ageing or death can also occur in higher eukaryotes.

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Population turnover is necessary for progressive evolution. In the context of a niche with fixed carrying capacity, aging contributes to the rate of population turnover. Theoretically, a population in which death is programmed on a fixed schedule can evolve more rapidly than one in which population turnover is left to a random death rate. Could aging evolve on this basis? Quantitative realization of this idea is problematic, since the short-term individual fitness cost is likely to eliminate any hypothetical gene for programmed death before the long-term benefit can be realized. In 2011, one of us proposed the first quantitative model based on this mechanism that robustly evolves a finite, programmed life span. That model was based on a viscous population in a rapidly changing environment. Here, we strip this model to its essence and eliminate the assumption of environmental change. We conclude that there is no obvious way in which this model is unrealistic, and that it may indeed capture an important principle of nature's workings. We suggest aging may be understood within the context of the emerging science of evolvability.