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Nitschke, M. C.

Publications and source records attributed to Nitschke, M. C..

3 recordsLinked to original sources

Half as high for twice as long: male bias in the fertile-age sex ratio

Humans are distinguished from our closest living relatives, other great apes, by our extended postmenopausal longevity, later first births, and shorter birth intervals. Those features likely evolved as ancestral grandmothers foraging subsidized dependants in habitats lacking foods that youngsters could manage for themselves. If so, as female post-fertile years increased, older years increased in males too. Those still-fertile old males in the paternity competition pushed the average male fertility rate below the female average. As R. A. Fisher explained, Mendelian inheritance requires equal contributions from both sexes to descendant gene pools. Higher fertility in one sex makes tendencies to overproduce it pass to more grandchildren, equalising averages in descendant generations. Yet lower average number of offspring per year in men persists, their fertility lasting decades longer than womens. Here, we present a simple mathematical model to investigate this phenomenon. We show that a male-biased sex ratio in the fertile ages is consistent with an offspring sex ratio of 1:1. We show that if male fertile careers are twice as long as those of females, the extended male fertility soon balances the higher female average, maintaining Fishers equilibrium offspring sex ratio under human life history conditions. Significance StatementWhy are offspring sex ratios usually near even in humans when the fertile careers of women and men differ so much? Fishers principle explains why parents are usually expected to produce equal offspring sex ratios. Since every sexually produced grandchild has both a mother and father, the average number of grandchildren expected through offspring of either sex depends on the sex ratio of the fertile pool. If that sex ratio is biased, the average must be higher for the rarer sex. Then any tendency to overproduce the sex with higher average fertility will spread, reducing its rarity until expected averages through sons and daughters are equal. Human life history complicates this simple logic. Female fertility ends in mid-life whereas male fertility does not, creating a male-biased fertile-age population in which average number of offspring per year is lower in males than in females. We show that sex differences in fertility duration can maintain Fishers equilibrium offspring sex ratio by altering Reproductive Value in overlapping generations, providing a foundation for persistent patriarchy.

evolutionary biology↗

Evolution of human pair bonds as a consequence of male-biased mating sex ratios?

Compared to our closest primate relatives, human life history involves greater longevity, which includes a distinctive postmenopausal life stage. The extension of the human lifes-pan (and continued fertility in old males) without lengthening female fertility directly changes the ratio of fertile males to fertile females, called the adult sex ratio (ASR). Additionally, this affects a more fine-grained ratio, the operational sex ratio (OSR), defined as the ratio of males to females currently able to conceive. Here, we construct an ODE model with minimal age structure, in which males compete for paternities using either a multiple-mating or mate-guarding strategy. Our focus is on investigating the differences of strategy choice between populations with chimpanzee-like and human-like life histories. By simulating the system, we determine the dominant strategy and its dependence on various parameter combinations. We introduce a new measure we call the lifetime paternity opportunities (LPO) of a given male strategy. The LPO directly calculates the payoffs of different male strategies and hence enables us to predict when strategies may shift. Our results show that an increase in OSR and ASR correlates well with a change in the dominant strategy from multiple mating to guarding.

evolutionary biology↗

The Effect of Bottleneck Size on Evolution in Nested Darwinian Populations

Previous work has shown how a minimal ecological structure consisting of patchily distributed resources and recurrent dispersal between patches can scaffold Darwinian properties onto collections of cells. When the timescale of dispersal is long compared with the time to consume resources, patches evolve such that their size increases, but at the expense of cells whose growth rate decreases within patches. This creates the conditions that initiate evolutionary transitions in individuality. A key assumption of this scaffolding is that a bottleneck is created during dispersal, so patches are founded by single cells. The bottleneck decreases competition within patches and hence creates a strong hereditary link at the level of patches. Here we construct a fully stochastic model of nested Darwinian populations and investigate how larger bottlenecks affect the evolutionary dynamics at both cell and collective levels. It is shown that, up to a point, larger bottlenecks simply slow the dynamics, but at some point, which depends on the parameters of the within-patch model, the direction of evolution toward the equilibrium is reversed. Introducing random bottleneck sizes with some positive probability of smaller sizes can counteract this, even if the probability of smaller bottlenecks is small.

evolutionary biology↗