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The adult sex ratio (ASR) is defined as the number of fertile males divided by the number of fertile females in a population. We build an ODE model with minimal age structure, in which males compete for paternities using either a multiple-mating or searching-then-guarding strategy, to investigate the value of ASR as an index for predicting which strategy males will adopt, with a focus in our investigation on the differences of strategy choice between chimpanzees (Pan troglodytes) and human hunter-gatherers (Homo sapiens). Parameters in the model characterise aspects of life history and behaviour, and determine both dominant strategy and the ASR when the population is at or near equilibrium. Sensitivity analysis on the model parameters informs us that ASR is strongly influenced by parameters characterising life history, while dominant strategy is affected most strongly by the effectiveness of guarding (average length of time a guarded pair persists, and resistance to paternity theft) and moderately by some life history traits. For fixed effectiveness of guarding and other parameters, dominant strategy tends to change from multiple mating to guarding along a curve that aligns well with a contour of constant ASR, under variation of parameters such as longevity and age female fertility ends. This confirms the hypothesis that ASR may be a useful index for predicting the optimal male mating strategy, provided we have some limited information about ecology and behaviour., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Great apes, the other living members of our hominid family, become decrepit before the age of forty and rarely outlive their fertile years. In contrast, women - even in high mortality hunter-gatherer populations - usually remain healthy and productive well beyond menopause. The grandmother hypothesis aims to account for the evolution of this distinctive feature of human life history. Our previous mathematical simulations of that hypothesis fixed the end of female fertility at the age of 45, based on the similarities among living hominids, and then modeled the evolution of human-like longevity from an ancestral state, like that of the great apes, due only to grandmother effects. A major modification here allows the age female fertility ends to vary as well, directly addressing a version of the question, influentially posed by GC Williams six decades ago: Why isn't menopause later in humans? Our model is an agent-based model (ABM) that accounts for the coevolution of both expected adult lifespan and end of female fertility as selection maximizes reproductive value. We find that grandmother effects not only drive the population from an equilibrium representing a great ape-like longevity to a new human-like longevity, they also maintain the observed termination of women's fertility before the age of 50., (Copyright © 2018 Elsevier Ltd. All rights reserved.)

Two kinds of evidence suggest that female fertility may end at an earlier age in modern people than in ancestral populations or in our closest living relatives, chimpanzees. We investigate both to see whether fertility schedules or ovarian follicle counts falsify the alternative hypothesis that the age of terminal fertility changed little in the human lineage while greater longevity evolved due to grandmother effects. We use 19th century Utah women to represent non-contracepting humans, and compare their fertility by age with published records for wild chimpanzees. Then we revisit published counts of ovarian follicular stocks in both species. Results show wide individual variation in age at last birth and oocyte stocks in both humans and chimpanzees. This heterogeneity, combined with interspecific differences in adult mortality, has large and opposing effects on fertility schedules. Neither realized fertility nor rates of follicular atresia stand as evidence against the hypothesis that ages at last birth changed little while greater longevity evolved in our lineage.

A grandmother hypothesis may explain why humans evolved greater longevity while continuing to end female fertility at about the same age as do the other great apes. With that grandmother hypothesis in mind, we sought to compare age-specific mortality and fertility rates between humans and chimpanzees, our closest living relatives, and found two puzzles. First, we expected that lower adult mortality in humans would be associated with slower senescence, but the rate of chimpanzee demographic aging falls within the human range. Second, we expected declines in age-specific fertility to be similar in the two species but instead of falling in the thirties as it does in women, fertility remains high into the forties in some chimpanzee populations. We report these puzzles using data from nine human populations and both wild and captive chimpanzees, and suggest that systematic differences in the heterogeneity of surviving adults may explain them., (2009 Wiley-Liss, Inc.)

BACKGROUND: Mammalian oocyte stocks reach maximum size in early development and begin depletion immediately thereafter. This depletion ends women's fertility by midlife. Here we compare five models proposed to characterize human follicular depletion, highlight underlying variation in atresia, and use oocyte counts from laboratory mice to illustrate possible effects of known covariates. METHODS: We compared statistical models, of human data, from five well-known sources and also compared the models' fit to data from four genetically distinct strains of mice. RESULTS: A model first published by Hansen et al. (2008) fit the human data better than any of the alternatives. Best-fit models of oocyte loss in the four strains of mice differed substantially from the best-fit model of the aggregated mouse data. CONCLUSIONS: Although the power model published by Hansen et al. (2008) fit the human data best, Faddy and Gosden's (1996) differential equation model may be a more useful characterization of human follicular atresia. However, these models leave a great deal of variation unexplained. Mouse strain comparisons show that follicle loss in genetically distinct subpopulations can differ substantially from the pattern in the aggregate population. This indicates that differences in follicular stock size between and within populations depend upon more than a single predictor (i.e. age or follicle stocks at previous time points). Our reliance upon data from Western populations represents this study's most important limitation. Expanding data collection to include likely covariates and a wider range of human populations would improve the basis for predicting individual trajectories of follicle loss as more women worldwide opt to delay childbearing and risk aging beyond their own windows of fertility. [ABSTRACT FROM AUTHOR]