Polycystic Ovarian Syndrome (PCOS) is the most common cause for menstrual disturbance and impaired ovulation, effecting one in twenty women of reproductive age. As the majority of women with PCOS are either overweight or obese, a dietary or adipose tissue related trigger for the development of the syndrome is quite possible. It has now well established that PCOS is characterised by a chronic state of inflammation and insulin resistance, but the precise underlying triggers for these two key biochemical disturbances is presently unknown. In this paper we present support for a microbiological hypothesis for the development of PCOS. This novel paradigm in PCOS aetiology suggests that disturbances in bowel bacterial flora ("Dysbiosis of Gut Microbiota") brought about by a poor diet creates an increase in gut mucosal permeability, with a resultant increase in the passage of lipopolysaccaride (LPS) from Gram negative colonic bacteria into the systemic circulation. The resultant activation of the immune system interferes with insulin receptor function, driving up serum insulin levels, which in turn increases the ovaries production of androgens and interferes with normal follicle development. Thus, the Dysbiosis of Gut Microbiota (DOGMA) theory of PCOS can account for all three components of the syndrome-anovulation/menstrual irregularity, hyper-androgenism (acne, hirsutism) and the development of multiple small ovarian cysts.
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