Abstract

Polycystic ovary syndrome (PCOS), characterized by polycystic ovaries, anovulation, and hyperandrogenism, is believed to be an evolutionary mismatch disease. Past research has examined PCOS as a uniform disease, despite variation in phenotypes across diagnostic categories, but establishing an evolutionary mismatch requires a focus on individual traits. We suggest PCOS hyperandrogenism may have been beneficial in ancestral environments because it reduced fracture risk and associated morbidity and mortality due to increased bone mineral density (BMD). We test this hypothesis by assessing fracture frequency, a proxy for BMD, in highly active females with and without PCOS hyperandrogenism. Sixty-seven reproductive-aged women were surveyed and grouped as: high intensity interval training (HIIT; a proxy for metabolic and physical stress) athletes with hyperandrogenic PCOS (31.24%), HIIT athletes without PCOS (29.85%), and nonathletes with hyperandrogenic PCOS (38.81%). Fracture occurrence was compared between the groups using independent samples Kruskal-Wallis tests for non-normally distributed data, and multiple regression analysis was used to examine anthropometrics, lifestyle and reproductive factors, PCOS status, and exercise frequency on fracture occurrence. Fracture occurrence was higher in non-PCOS athletes (3.8 ± 4.3) than PCOS-athletes (1.2 ± 1.4, p = .11) and PCOS-non-athletes (1.0 ± 1.4, p < .01). PCOS-athletes and nonathletes did not differ significantly in fracture occurrence (p = .33). These results were independent of factors associated with bone health. These preliminary findings suggest females with PCOS-related hyperandrogenism may be less likely to experience bone fractures and provide an initial step to explaining why PCOS has persisted despite marked negative reproductive consequences in modern populations.

Full Text
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