Developmental Origin of Polycystic Ovary Syndrome: A Hypothesis

The document from 2002 presents a hypothesis that polycystic ovary syndrome (PCOS) may have its origins in genetic and environmental factors that affect the body before adolescence, possibly even in utero. It suggests that early hypersecretion of androgens could program the hypothalamic-pituitary unit to overproduce luteinizing hormone (LH) and predispose individuals to abdominal obesity and insulin resistance, which are key features of PCOS. The severity of these conditions is thought to be influenced by genetic variations, such as those in the insulin gene regulatory region, and environmental factors like obesity. This hypothesis is backed by studies on prenatally androgenized sheep and rhesus monkeys, as well as human data. The authors propose that PCOS is a linear developmental disorder that can be modified by later genetic and environmental interactions, affecting the expression of PCOS traits, especially the risk of anovulation. They conclude that understanding the developmental origins of PCOS could lead to better-targeted treatments for the reproductive and metabolic issues associated with the syndrome.