Abstract
The source of polycystic ovarian syndrome (PCOS) is much debated and is likely to be multifactorial. There is an apparent familial inheritance with first-degree relatives of sufferers more likely to be affected. Twin studies have suggested a genetic cause but candidate genes are yet to be verified. Genes affecting insulin resistance, steroid hormone production, and inflammatory cytokine responses have all been implicated. Current thinking supports the theory that exposure to environmental factors in utero predisposes a female foetus to hyperandrogenism, insulin resistance, and polycystic ovaries in adult life. Which environmental factors have an impact on the foetus and the mechanisms of exposure are still to be confirmed. Animal studies have shown a clear correlation between hyperexposure of the foetus to androgens in utero and future development of a PCOS pattern of symptoms. Placental aromatases should neutralise androgens from the maternal circulation and prevent them reaching the foetal circulation. Our hypothesis is that the high maternal anti-Mullerian hormone (AMH) levels in PCOS block the placental aromatase and allow passage of testosterone through the placenta. This maternal testosterone acts on the foetal ovaries and 'programmes' them to recruit more preantral follicles and so produce higher AMH levels when they become functional at around 36 weeks of gestation. The high AMH concentrations in PCOS also seem to increase luteinizing hormone release and inhibit follicle stimulating hormone action on aromatase, so adding to the hyperandrogenic environment of adult PCOS.