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Two independent lines of inquiry suggest that growing up under conditions of contextual adversity (e.g., poverty and household chaos) accelerates aging and undermines long-term health. Whereas work addressing the developmental origins of health and disease highlights accelerated-aging effects of contextual adversity on telomere erosion, that informed by an evolutionary analysis of reproductive strategies highlights such effects with regard to pubertal development (in females). That both shorter telomeres early in life and earlier age of menarche are associated with poor health later in life raises the prospect, consistent with evolutionary life-history theory, that these two bodies of theory and research are tapping into the same evolutionary-developmental process whereby longer term health costs are traded off for increased probability of reproducing before dying via a process of accelerated aging. Here we make the case for such a claim, while highlighting biological processes responsible for these effects, as well as unknowns in the epigenetic equation that might instantiate these contextually regulated developmental processes.

Contextual adversity, telomere erosion, pubertal development, and health: Two models of accelerated aging, or one?