Polycystic Ovary Syndrome as an Endogenous Alcoholic Polycystic Ovary Syndrome

Abstract

Polycystic ovary syndrome (PCOS) is a growing worldwide public health problem that affects millions of women in their reproductive age. Despite being a very common disorder among women, there are still gaps regarding knowledge of disease mechanisms. In this respect, it was recently reported that acetaldehyde (ACD) is endogenously formed during normal ovarian steroidogenesis. The researchers demonstrated that in physiological concentrations ACD caused no detrimental effect on ovarian tissue. Contrariwise, in supraphysiological levels, ACD impairs granulosa cell differentiation, reduces ovulation, and decreases oocyte quality. Gut microbiota of patients with nonalcoholic fatty liver disease (NAFLD) produces significant quantities of endogenous ethanol (EE) and ACD. Because PCOS is closely linked to NAFLD, an ethanol-producing disorder, we hypothesize that it can be an endogenous alcoholic polycystic ovary syndrome (EAPCOS). The main findings of this study were that (i) the odds ratio of having polycystic ovaries is 30-fold greater in alcohol-exposed women than among unexposed controls; (ii) NAFLD/PCOS patients produce gonadotoxic quantities of EE; (iii) NAFLD/PCOS and alcoholic hepatitis individuals share similar liver expression levels of genes regulating high-km ethanol-metabolizing enzymes; (iv) NAFLD/PCOS and alcohol-tolerant drinkers share similar high-capacity to metabolize ethanol in the gut-liver axis; and (v) low blood alcohol concentration (BAC) in NAFLD/PCOS and alcohol-tolerant individuals stem from extensive alcohol degradation in gut-liver axis and significant fecal loss of ethanol. In summary, we provide mechanistic insights supporting the hypothesis that PCOS can be indeed an EAPCOS.