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[T]he rather definite age of menopause seems conspicuously ignored by the as yet gently rising curve of the force of mortality. It is, moreover, a matter of common knowledge that the post menopausal woman normally remains a useful and healthy member of the community for some time… . [This] can be attributed to the beneficial effects of continued survival on the survival and reproduction of descendants…. In fact … the comparatively healthy life of the postreproductive woman … inevitably suggests a special value of the old woman as a mother or grandmother during a long ancestral period….

Such a grandmother hypothesis, subsequently elaborated with comparative and phylogenetic evidence not available when the classic papers appeared, can explain not only the evolution of human longevity but other similarities and differences in life history between humans and the other great apes. We live longer; we take longer to mature but have shorter birth intervals; and we share common ages of terminal female fertility with the other great apes (Hawkes et al., 1998; Robson et al., 2006). The hypothesis focuses on females because as noted by both Williams and Hamilton our mid-life menopause is a central clue to human life history evolution and because the hypothesis employs E. L. Charnov’s (1991, 1993) model of tradeoffs faced by females to explain mammalian life history variation. The forces of selection explored by Williams (1957, 1966), Hamilton (1966), Charnov (1993), and many other students of life history evolution (Stearns, 1992; Charlesworth, 1994) attend to fitness effects and not to proximate mechanisms, but T. B. L. Kirkwood’s disposable soma model (Kirkwood and Rose, 1991) based on the same evolutionary tradeoffs between current and future reproduction has directed attention to processes of cellular maintenance and repair that affect somatic aging rates (Kirkwood and Holliday, 1979; Finch, 2007). Such processes likely have similar effects in both sexes, because longer-lived mothers pass on their cellular maintenance mechanisms to both sons and daughters.

I briefly summarize this elaborated grandmother hypothesis, then turn to patterns that initially seem inconsistent with the tradeoffs between current and future reproduction identified in evolutionary explanations for senescence. I focus on two apparent inconsistencies between theoretical expectations and empirical observations. First, theory predicts that current reproductive output should subtract from effort invested in maintenance for survival and reproduction in the future, yet individuals with higher fertility rates tend to continue bearing offspring to older ages; and in humans, women with later last births then survive longer afterward (Perls et al., 1997; Jacobsen et al., 2003; Emery Thompson et al., 2007; Gagnon et al., 2009). Second, theory predicts that lower adult mortality should slow rates of senescence, yet when populations of the same species are compared, the groups with lower mortality have steeper increases in death risk

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