The mystery of life beyond menopause

The quantitative genetics of reproduction and lifespan in a Utah population from the 1800s reveal no support for any of the three most prominent hypotheses invoked for why women live so long past menopause.

Since George Williams’ landmark 1957 paper on the evolution of aging1, the evolutionary paradox of menopause (or, more precisely, human female post-reproductive lifespan) has stimulated extensive reflection and research by evolutionary biologists and anthropologists. How could fitness ever be improved by ceasing reproduction? Williams proposed that maternal care of existing offspring might explain it; this idea was later expanded to include grandmaternal care and became known as the grandmother hypothesis2. Two major alternative hypotheses include covariation in lifespan between the sexes3 and trajectories of decline that are optimized for early life health rather than precise timing of death4. However, until now, all discussion has been theoretical.

Writing in Nature Ecology & Evolution, Moorad and Walling5 provide the first empirical test of whether any of these processes actually shaped post-reproductive lifespan in a historical human population. Their study population comprises residents of the Utah Territory in the late 1800s, as recorded in the Utah Population Database6. This is a particularly rich and precise dataset that capitalizes on the importance of careful genealogical records to the Mormon faith. The authors apply sophisticated quantitative genetic methods to these data to show that, in fact, there is no evidence in this population for any of the three major hypotheses posited to explain human post-reproductive lifespan, a rather striking finding.

The particular innovation of the approach lies in a careful conceptual model that outlines all the potential paths by which selection, direct and indirect, might influence lifespan. For example, to support the grandmother hypothesis, the authors required hypothetical alleles prolonging lifespan post-menopause to be genetically correlated with alleles that cause grandmothers to improve the fitness of their grandchildren. This conceptual model is thoroughly diagrammed (see Fig. 1) and should serve future studies attempting to replicate this finding in other populations.

Fig. 1: A simplified version of the conceptual model developed by Moorad and Walling5 to examine the evolution of human post-reproductive lifespan.

Arrows between phenotypes and fitness are selection gradients. Arrows between genes and phenotypes are genetic variances. Arrows between different genes are genetic correlations. As female post-reproductive lifespan cannot directly affect fitness, selection for it must arise indirectly through other pathways. These pathways are shown via the colours; only arrows in the pathways for the three key hypotheses tested are shown (red, grandmother; green, inter-age; dark yellow, inter-sex). Using genealogical data from the Utah Population Database, it was possible to estimate the coefficients for each arrow. Support for a hypothesis is assessed by multiplying the coefficients along the relevant pathway. The full model also includes terms for survival to age 50 years and male lifespan after 50, which permit tests of additional hypotheses related to life-history theory. The map shows the boundary of the Utah Territory from 1851.

The absence of support for the three main hypotheses to explain post-reproductive lifespan was not the only important finding generated by this analysis. For example, male lifespan after 50 years of age was found to increase by 0.14 years per generation, an effect apparently attributable to genetic correlations between late male lifespan and early life fitness in both sexes. Likewise, no negative correlations between early and late fitness/survival were observed, contradicting Williams’ proposed antagonistic pleiotropy theory1. Each of these findings deserves substantial follow-up and has important implications.

What could explain the failure to support any of the three existing hypotheses for female post-reproductive lifespan? The authors suggest that one or more of the hypotheses must have been operating in the past, but was perturbed by changing ecological conditions — notably the major demographic upheaval created by mass migration to the American West, loss of kinship support from relatives who remained in the east, and particularly high birth rates. I concur, and this represents perhaps the greatest limitation of the research, but one that forces us to think critically about how such questions are approached. We know that there is substantial variation among populations of most/all species in terms of ecology, demographics, selection pressure and so on. Therefore, it is not realistic to think that a brief snapshot of any given population is likely to give a satisfying answer for how selection has produced stable traits of the species. Put differently, had the authors found clear support for any one hypothesis, there would have been a strong possibility that this result, although correct in the short-term, did not represent an accurate long-term portrait of how selection shaped menopause as we know it. Yet we would probably have believed it and over-extrapolated.

The caution then is much broader: the kinds of quantitative genetic approach applied here have clear limits when applied to historical human populations. Few, if any, of the populations available for study are in conditions remotely similar to those of our ancestors during the bulk of our history when key human life-history traits evolved. I hope this study will be replicated in other suitable datasets (for example, church registers from pre-industrial Finland7 and Québec8), but those results will need to be interpreted with substantial prudence.

Our understanding of life beyond menopause may thus have to continue to rely at least partially on studies based more on the plausible than the documentable. Indeed, such studies have done an excellent job, with some cost–benefit analyses questioning the sufficiency of the grandmother hypothesis9 and others proposing complementary forces such as intergenerational reproductive conflict10. There is now substantial support for the idea that the physiology of female mammalian reproductive senescence creates a predisposition to a short, but not necessarily ecologically significant, post-reproductive period4,11; under appropriate social conditions, this can be substantially prolonged, as observed in humans and several species of toothed whale12. The exact list of those social conditions is a field of active research, with candidates including maternal and grandmaternal care, male philopatry, intergenerational conflict, small group size and the importance of retaining ecological knowledge.


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Cohen, A.A. The mystery of life beyond menopause. Nat Ecol Evol 1, 1604–1605 (2017).

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