Polycystic Ovarian Syndrome and Fertility

Introduction: Polycystic ovary syndrome (PCOS) encompasses a group of clinical presentations, the clinical and biochemical features are apparently centrally driven by insulin resistance, leading to incidence, disease progression, complications, or suboptimal clinical outcomes. In this review presentation, the pathobiology of PCOS has been evaluated from the standpoint of insulin resistance as the central driver.

 

Description: Insulin resistance and metabolic dysfunctions are hallmark and key pathological features in PCOS which lead to several associated abnormalities like irregular cycles, anovulation, infertility, hyperandrogenemia and hirsutism which adversely affects the quality of life in women. Further, it also has a psychological impact on daily life including poor self-esteem. Hyperinsulinaemia and metabolic dysfunctions are known to stimulate ovarian androgen production and decrease hepatic sex hormone-binding globulin, resulting in hyperandrogenism and the associated clinical features of PCOS. An extensive review of literatures establishes this concept, and hence management should also consider these elements more specifically. Conventional treatment for PCOS includes diet and lifestyle changes, specific medications, targeted to address different facets of the pathological events. To that end, we explored the possible role of magnesium as a therapeutic agent in the totalitarian management of PCOS. Several randomized trials and retrospective cohort studies found subclinical magnesium deficiency (SMD) in this set of populations. SMD in turn leads to lack of vitamin D absorption, transportation and pharmacological actions. Both magnesium and vitamin D have a potential role in insulin action and metabolic control. It has been well-established that

in PCOS women, magnesium deficiency was found to be in the range of 14.5% to 81% in the affected individuals and vitamin D deficiency in the range of 67%-85%. Deficiency of both these nutritional factors exacerbates metabolic abnormalities in PCOS which further adversely affects mainstream therapy outcomes.

 

Conclusion: Critical review of literatures shows that magnesium increases vitamin D level, and both have beneficial effects in controlling metabolic dysfunctions. Of note, magnesium itself has a crucial role in insulin signalling and thus improves insulin sensitivity and metabolic improvements along with a reduction in cardiovascular risk factors. So, supplementing magnesium in PCOS should be a novel and routine therapeutic approach in managing metabolic syndrome thus improving primary therapy outcomes.