LAUSR

Common human reproductive inefficiencies have multiple etiologies. Going against chance, many effects, such as polycystic ovaries, endometriosis, and folate metabolic issues, have genetic components, while aneuploid losses arise from diverse mitotic and meiotic errors at different stages, some transitory. This can be advantageous, since greater overall survival with fewer offspring can increase reproductive success. Benefits primarily accrue to mothers, who bear most child related costs, and for whom early losses are less costly than late. Different adaptations to different situations reflect human evolutionary history. For early speciation, periodic climate extremes repeatedly reduced resources, favoring limitations while contracted populations helped fix relevant genes. Later, under better conditions, evolving social cooperation could increase fecundity faster than it added resources, further supporting reproductive suppression through mitotic aneuploidy, with very early losses minimizing maternal costs. The grandmother hypothesis suggests benefits in limiting reproduction as maternal age increased pregnancy risks in order to support grandchildren as they arrived, selecting for maternal age-related meiotic aneuploidy. Finally, with variable short-term agricultural shortages, acute reproductive responses arose through chromatin “nutrient sensor”-regulated epigenetic effects that also shifted some lethal effects earlier, reducing both maternal and mutation load costs. Overall, despite suggestions to the contrary, it is likely that human selective pressures have not decreased with civilization, but that many of the costs have been shifted to early reproduction.