This is the standard antagonistic pleiotropy hypothesis. While there are some examples of specific proteins and pathways that work this way (beneficial in early

This is the standard antagonistic pleiotropy hypothesis. While there are some examples of specific proteins and pathways that work this way (beneficial in early life, detrimental in late life), it is far from certain that this is the key driver of aging in evolution (for animals in general, as well as for humans specifically). For one thing, even in primitive human societies, the life expectancy is well into the 30s or higher (after you discount infant and early-life mortality). Yet aging starts rapidly deteriorating physical capabilities in the mid 20s. Secondly, one of the key definitions of aging is decreasing resilience with increasing age: so in reality, you cannot treat average lifespan as if it is a constant and the rate of aging is evolutionarily determined from that. Even in primitive man, which died of predation and infectious disease primarily, aging makes older humans much more susceptible to these things (physically weaker and weaker immune system). Finally, antagonistic pleiotropy does not explain why different organisms have very different maximum lifespans (in protected conditions), and some do not seem to appreciably age at all. Some more detailed criticisms: http://www.programmed-aging.org/theories/antagonistic_pleiotropy.html http://www.programmed-aging.org/theories/antagonistic_pleiot... Antagonstic pleiotropy probably plays some role, but it is a needlessly complex explanation when a simpler one exists: the body is a system, and over time, systems degrade and components are damaged. Its ability to repair this damage is considerable, but finite, since the repair mechanisms themselves can become damaged.