An article in the April, 2009 issue of Evolution, offers provocative support for George Williams’s 1957 prediction that decreased extrinsic mortality rates will select for slower rates of aging. The article compares data from subsistence and European societies in the past 200 years, and concludes that selection may have slowed aging rates in just 10 generations, and it may account for differences in aging rates in different populations.  The multiple measures of aging rates are a strength of the article, but they also add complexity that makes interpretation of the results challenging, as the authors note.

Has Actuarial Aging “Slowed” Over the Past 250 Years?
A Comparison of Small-Scale Subsistence Populations and European Cohorts

Michael Gurven and Andrew Fenelon

Evolution 63(4):1017-1035. 2009
doi: 10.1111/j.1558-5646.2008.00592.x

Williams’s 1957 hypothesis famously argues that higher age-independent, or ‘extrinsic,’ mortality should select for faster rates of senescence. Long-lived species should therefore show relatively few deaths from extrinsic causes such as predation and starvation. Theoretical explorations and empirical tests of Williams’s hypothesis have flourished in the past decade but it has not yet been tested empirically among humans. We test Williams’s hypothesis using mortality data from subsistence populations and from historical cohorts from Sweden and England/Wales, and examine whether rates of actuarial aging declined over the past two centuries. We employ three aging measures: mortality rate doubling time (MRDT), Ricklefs’s ω, and the slope of mortality hazard from ages 60–70, m′50–70, and model mortality using both Weibull and Gompertz-Makeham hazard models. We find that (1) actuarial aging in subsistence societies is similar to that of early Europe, (2) actuarial senescence has slowed in later European cohorts, (3) reductions in extrinsic mortality associate with slower actuarial aging in longitudinal samples, and (4) men senesce more rapidly than women, especially in later cohorts. To interpret these results, we attempt to bridge population-based evolutionary analysis with individual-level proximate mechanisms.