A successful evolutionary theory of aging must explain how a mix of species with shorter and longer life spans can emerge from a common ancestor with a longer life span. Putting theories of programmed aging to one side for a moment, as in that case one only has to argue that a shorter life span is more optimal for the ecological niche in question, antagonistic pleiotropy is the most readily available explanation for shorter lifespans to arise from natural selection. The theory here is that evolution selects for mechanisms and systems that both (a) ensure reproductive success in early life and (b) damage health in later life. There are all too many examples of biological systems that work well in childhood and youth, but inevitably fail because they are not capable of comprehensive repair and therefore accumulate damage, or because they are otherwise limited in some important capacity, and that limit will eventually be reached.
Can the evolution of shorter life spans appear in models without employing the assumption of antagonistic pleiotropy, and without invoking programmed aging, however? The authors of this paper argue that it can, and arises as an inevitable consequence of