How grandmother effects plus individual variation in frailty shape fertility and mortality: Guidance from human–chimpanzee comparisons

Abstract

In the first paper to present formal theory explaining that senescence is a consequence of natural selection, W. D. Hamilton concluded that human postmenopausal longevity results from the contributions of ancestral grandmothers to the reproduction of their relatives. A grandmother hypothesis, subsequently elaborated with additional lines of evidence, helps explain both exceptional longevity and additional features of life history that distinguish humans from the other great apes. However, some of the variation observed in aging rates seems inconsistent with the tradeoffs between current and future reproduction identified by theory. In humans and chimpanzees, our nearest living relatives, individuals who bear offspring at faster rates do not cease bearing sooner. They continue to be fertile longer instead. Furthermore, within both species, groups with lower overall mortality rates have faster rates of increase in death risk with advancing age. These apparent contradictions to the expected life history tradeoffs likely result from heterogeneity in frailty among individuals. Whereas robust and frail alike must allocate investments between current and future reproduction, the more robust can afford more of both. This heterogeneity, combined with evolutionary tradeoffs and the key role of ancestral grandmothers they identify, helps explain aspects of human aging that increasingly concern us all.evolution of senescence | heterogeneity of frailty | human life history | menopause | human aging L ong postmenopausal survival is a characteristic of our species.

The multiple facets of Peto's paradox: a life-history model for the evolution of cancer suppression

“…Thus, many extant human phenotypic traits evolved in response to selection forces that have, over the past 100 years, greatly changed. To examine the evolutionary dynamics of humans prior to the industrial revolution, we examine the life table for primitive humans [28]. When these data are used to parametrize our model, we predict that early humans would, relative to elephants and naked mole rats, have lower cancer suppression and less likelihood of dying from cancer relative to other sources of mortality.…”

Was skin cancer a selective force for black pigmentation in early hominin evolution?

“…That argument relates to a longstanding view, expressed by JBS Haldane, Peter Medawar and others, that phenotypes associated with ageing lie outside the reach of natural selection. Notwithstanding the 'grandmother' effect that could operate postreproductively via kin selection [6,86], the observation that BCC and SCC are mostly benign or post-reproductive in character is misleading. The observation is essentially correct in the context of contemporary white-skinned Caucasians inhabiting temperate United States [44] or subtropical zones (for example Queensland, Australia, at 10-208 latitude) [22].…”

On the apparent rarity of epithelial cancers in captive chimpanzees

“…Given the important role of telomere caps at chromosomal ends in modulating cell survival, ageing and cancer [55,56], it was reasonable to look for a difference in humans. Paradoxical to the finding of extended lifespan in humans [32,57], telomere lengths were found to be greater in nonhuman primates than in humans, and telomere shortening rates were not apparently different between humans and chimpanzees [58,59]. Given the importance of genome damage and DNA repair in cancer, it is also interesting that one study indicated that humans and chimpanzees differ in their cellular response to DNA damage and noncoding sequence elements of DNA repair-associated genes, with evidence for accelerated evolution in some promoter regions and introns [60].…”