Polycystic Ovarian Syndrome (PCOS)
Polycystic Ovarian Syndrome (PCOS) is a major cause of infertility, menstrual irregularity, and reduced quality of life in reproductive age women. PCOS is one of the most common endocrine disorders of reproductive aged women affecting 6-10% of the population with this going as high as 18%. The condition results from a cluster of hormonal abnormalities, namely elevated insulin, elevated androgens, reduced progesterone, which contribute to the signs and symptoms which may include:
- Weight gain
- Mood swings
- Pelvic pain
- Anovulatory menstrual cycles
- Hair loss on the head
Despite the name of the syndrome, many women who receive this diagnosis do not have cysts on their ovaries, so the condition is somewhat of a misnomer. A closer look at the hormones involved reveals that true PCOS is not merely the absence of ovulation or menstrual periods; it is fundamentally a metabolic disorder.
PCOS is associated with – if not outright caused by – blood sugar and insulin dysregulation. As with metabolic syndrome, PCOS is classified as a syndrome and not a disease, as there is not one individual test or biomarker that is diagnostic of the condition, but rather, several indicators that point to a unifying underlying cause. However, chronic hyperinsulinaemia and insulin resistance are cardinal features of PCOS. Whilst obesity is a common feature, about half of those diagnosed with PCOS have a normal weight.
Insulin resistance is implicated in the ovulatory dysfunction of PCOS by disrupting the hypothalamic-pituitary-ovarian axis. The actions of insulin lead to other hormonal alterations that have profound ramifications for the menstrual cycle, fertility, and overall quality of life for women. Chronically elevated insulin stimulates ovarian and adrenal androgen production and decreases levels of sex hormone binding globulin (SHBG). Hyperinsulinaemia augments luteinizing hormone-stimulated androgen production by the ovaries and stimulates adrenal androgen production, while inhibiting hepatic synthesis of sex hormone binding globulin (SHBG) resulting in increased free testosterone levels. Various feeback loops are modulated such that production of luteinizing hormone (LH) is increased, follicle-stimulating hormone (FSH) is reduced, resulting in increased androgen synthesis and interference with normal follicular development and ovulation. All women normally produce ovarian testosterone from LH stimulating pre-dominant follicles. In PCOS, abnormally elevated LH influences excessive ovarian testosterone production. A dominant follicle does not develop properly (which in a normal cycle would culminate in ovulation), but instead becomes cystic. Insulin may drive abnormal LH hypersecretion, which then drives ovarian testosterone hyperproduction. Interventions that reduce insulin levels may help normalize these other hormones and allows the cycle to operate normally.
A recent systematic review of low-carbohydrate diets on fertility hormones and outcomes in overweight and obese women concluded that restricting dietary carbohydrate load can reduce insulin levels, improve hormonal balance, and facilitate ovulation to improve pregnancy rates.
In a small study of overweight women with PCOS who were instructed to limit their carbohydrate intake to <20 g/day for 24 weeks, there were decreases in body weight (12%), free testosterone (22%), LH/FSH ratio (36%), and fasting insulin (54%). Two of the subjects became pregnant despite previous fertility problems. Other studies have shown similar decreases in body weight and insulin with a very low-carbohydrate diet without specifically counting calories. In a crossover study of obese women with PCOS comparing 3 weeks of a conventional diet (60% CHO; 25% fat) to an isocaloric higher fat diet (40% CHO; 45% fat), both with 15% of total energy from protein, the higher fat diet resulted in a 30% decrease in daylong insulin levels along with improvements in the lipid profile.
This means that a ketogenic diet or, at the very least, a low carbohydrate diet, may prove extremely beneficial in women with PCOS.