Obesity is a frequent finding in PCOS and aggravates a lot of its reproductive and metabolic abilities. The connection between PCOS and obesity is more complicated, not well known, and probably involves interaction of environmental and genetic variables.
Polycystic ovary syndrome (PCOS) is a condition which affects a woman’s hormone levels.
Women with PCOS create higher-than-normal levels of male hormones.
PCOS affects a woman’s ovaries, the reproductive organs that produce estrogen and progesterone — hormones that regulate the menstrual cycle. The ovaries also produce a small amount of male hormones called androgens.
The ovaries release eggs to be fertilized by a man’s sperm. The release of an egg each month is called ovulation.
This hormone imbalance induces them to skip a menstrual cycle and makes it tougher for them to become pregnant.PCOS also causes hair growth on the body and face and hair loss. And it may promote long-term health issues such as diabetes and heart disease.
An increase in the production of androgens (male hormones) by the ovaries in PCOS may lead to excess hair growth in areas suggesting a male pattern, known as hirsutism. Thick, pigmented hair growth occurs on the upper lip, chin, around the nipples, and on the lower abdomen. Excess androgens can also lead to acne and male pattern balding.
Androgens play an important role in the determination of body composition. Men have less body fat with greater distribution of fat in the upper portion of the body (android) compared to women, who tend to accumulate fat in the lower portion of the body (gynoid). Vague first reported that the prevalence of diabetes, hypertension, and atherosclerosis was higher in women with android obesity compared to gynoid obesity. Moreover, he observed that the prevalence of android body habitus increases in women after the age of menopause and women with android obesity tend to have features of hyperandrogenism such as hirsutism. Women with upper-body obesity have also been noted to have decreased insulin sensitivity and are at higher risk for cardiovascular disease and diabetes. Independent of BMI, women with PCOS have been reported to have a high prevalence of upper-body obesity as demonstrated by increased waist circumference and waist-hip ratio compared to BMI-matched control women. Consistent with these findings, studies using dual-energy X-ray absorptiometry have revealed the increased accumulation of central fat in women with PCOS.
Chronic exposure to higher testosterone levels in women with PCOS may modify body fat distribution in these women. Support for this hypothesis is provided by studies of androgen administration in nonobese female to male transsexuals that lead to increases in visceral fat and adversely impact insulin sensitivity, post-menopausal women exposure to androgens increases visceral fat in both obese and normal-weight women. It may be that early androgen exposure adversely impacts future body fat distribution with greater accumulation of central fat.
However, few studies have examined visceral fat content in women with PCOS. Studies of isolated abdominal fat cells from women with PCOS have revealed larger-sized cells in both obese and nonobese women with PCOS compared to control women, suggesting a preferential abdominal accumulation of adipose tissue. Femoral adipocytes are smaller in obese women with PCOS than reproductively normal women consistent with a shift to android body fat distribution in PCOS women. These observations raise the hypothesis that hyperandrogenemia may contribute to the development of visceral adiposity in PCOS women necessitating further investigation in this area.