That is because the explanation given in FA is erroneous and misleading. Pathophysiology of PCOS is explained in detail within various gynecology texts (such as Chapter 17 of
Williams Gynecology, 2nd Ed.). I'm going to quote the explanation found in
Blueprints Obstetrics and Gynecology, 6th Ed., Chapter 21, p. 284 (available
here): "In the case of PCOS, chronic anovulation leads to elevated levels of estrogen and androgen. The increased androgen released from the ovaries and the adrenal cortex is converted peripherally in the adipose tissue into estrone.
Further, the elevated androgens lead to a decrease in the production of SHBG, resulting in even higher levels of free estrogens and androgens.
This hyperestrogenic state leads to an increased LH:FSH ratio, atypical follicular development, and increased androgen production. Once again, the androgens are peripherally converted to estrogens, leading to a cyclical propagation of the disease. Many patients with PCOS who are hyperandrogenic and obese also develop insulin resistance and hyperinsulinemia. Not surprisingly, the incidence of type 2 DM is increased in these patients."
