Both obesity and polycystic ovary syndrome (PCOS) are the raising epidemics in the world today. Polycystic ovarian syndrome (PCOS) is one of the most leading causes of female infertility, affecting 5-10% of women of reproductive age. The syndrome is characterized by anovulation, hyperandrogenism and polycystic ovaries.
Obesity (defined as a BMI ≥30 kg/m2) occurs in approximately 30% to 60% of women with PCOS. Central or abdominal obesity is a typical pattern. Central obesity is a risk factor for development of diabetes, heart disease and when present in a woman with PCOS worsens the clinical features of the syndrome. Obesity may play a pathogenic role in the development of the syndrome in susceptible individuals. Therefore lifestyle modifications with appropriate diet and exercise is a corner stone of therapy for many women with PCOS.
Weight gain is an important contributor (both genetic and environmental) in women with polycystic ovarian syndrome. Obesity in women does not always results in the development of PCOS. So it is incorrect to state that obesity causes pcos. Obese women with PCOS experience greater menstrual irregularity when compared to non-obese patients. Therefore exercise and diet modifications are the front line therapy for the management of PCOS.
PCOS is the most common hormonal abnormality in reproductive-age women affecting ~7% of this population. The reproductive features of PCOS include increased androgen production and disordered gonadotropin secretion leading to menstrual irregularity, hirsutism, and infertility. In addition to these important reproductive manifestations, PCOS has metabolic characteristics that include prominent defects in insulin action and β-cell function, defects that confer a substantially increased risk for glucose intolerance and type 2 diabetes. Obesity is a common finding in women with PCOS and between 40–80% of women with this condition are reported to be overweight or obese. Familial aggregation of PCOS strongly supports a genetic susceptibility to this disorder.
Furthermore, the metabolic abnormalities associated with PCOS, such as β-cell dysfunction and type 2 diabetes, have heritable components in families of women with PCOS. To date, the genes responsible for PCOS have not been clearly identified. Considering the close association between PCOS and obesity, it is likely that similar or interrelated genes may also predispose to obesity in affected women. No doubt environmental factors (high-caloric diets and reduced exercise) also play a major role in the high prevalence of obesity in women with PCOS.
Insulin resistance is a common finding in PCOS that is independent of obesity. Insulin-mediated glucose disposal, reflecting mainly insulin action on skeletal muscle is decreased by 35–40% in women with PCOS compared to weight comparable reproductively normal women.
Reproductive disturbances are more common in obese women regardless of the diagnosis of PCOS. Obese women are more likely to have menstrual irregularity and anvolatory infertility than normal-weight women. In reproductive-age women, the relative risk of anovulatory infertility increases at a BMI of 24 kg/m2 and continues to rise with increasing BMI. Consistent with a pathophysiologic role for obesity, weight reduction can restore regular menstrual cycles in these women.
There appears to be an epidemic of both obesity and polycystic ovary syndrome (PCOS) in the world today. However, obesity per se is not a part of the phenotype in many parts of the world. Obesity is likely not a cause of PCOS, as the high prevalence of PCOS among relatively thin populations demonstrates. However, obesity does exacerbate many aspects of the phenotype, especially cardiovascular risk factors such as glucose i