Obesity is commonly associated with polycystic ovarian syndrome (PCOS), featuring both elements of insulin resistance and metabolic syndrome. Understanding the causes of obesity, its impact on health and its comorbidities, as well as its regulation, are important factors in relation to the treatment of obesity and more particularly the effect of weight loss in PCOS. The various modalities of treatment include the conservative approach, utilizing lifestyle and dietary techniques, pharmacotherapy and the more invasive surgical approach, which has been shown to have better weight-loss results and less recidivism.

Polycystic ovarian syndrome (PCOS) affects up to 18% of women internationally, with widespread effects on their reproductive, metabolic and cardiovascular health. To date, the etiology of this syndrome remains unclear. Patterns of expression within family groups suggest a genetic inheritance but neither a clear inheritance pattern nor candidate gene(s) has been discovered to date. Animal studies have proven that in utero exposure to high levels of androgen can elicit PCOS-like traits in various mammals, including rhesus monkeys who share a similar reproductive biology with humans. An alternate mechanism for etiology is the epigenetic alteration in programming of the fetal ovaries in response to androgen exposure. This chapter summarizes the evidence available and hypothesizes possible mechanisms of action via which PCOS could be transmitted from an affected mother to her offspring. The origins of androgens in the fetal circulation as well as the role of AMH and luteinizing hormone (LH) are discussed as are the actions of the placenta and the difference in placental function and hormone secretion patterns in PCOS females compared to “normal” physiology.