These findings suggest that PCOS and endometriosis represent maladaptive extremes of both female life‐history variation and expression of sexually dimorphic female reproductive traits. Furthermore, the contrasts between endometriosis and PCOS in humans parallel differences among nonhuman animals in effects of low versus high prenatal testosterone on female reproductive traits. The hypothesis of diametric phenotypes between endometriosis and PCOS is strongly supported across these diverse fields of research. To evaluate these predictions, we review and synthesize existing evidence from developmental biology, endocrinology, physiology, life history, and epidemiology. This diametric disorder hypothesis predicts that, for characteristics shaped by the HPG axis, including hormonal profiles, reproductive physiology, life‐history traits, and body morphology, women with PCOS and women with endometriosis will manifest opposite phenotypes. Here, we propose and evaluate the novel hypothesis that endometriosis and PCOS represent extreme and diametric (opposite) outcomes of variation in HPG axis development and activity, with endometriosis mediated in notable part by low prenatal and postnatal testosterone, while PCOS is mediated by high prenatal testosterone. PCOS and endometriosis have yet to be considered as related to one another, although both conditions involve alterations to prenatal testosterone levels and atypical functioning of the hypothalamic–pituitary–gonadal (HPG) axis. Endometriosis and polycystic ovary syndrome (PCOS) each affect up to 10% of women and significantly reduce the health, fertility, and quality of life of those affected. Evolutionary and comparative approaches can yield novel insights into human adaptation and disease. , in good faith we will correspond therefore, please.
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