Ovulation and the polycystic ovary syndrome

In the 1930s, Stein and Leventhal added amenorrhoea to anovulatory dysfunctional uterine bleeding among the known clinical manifestations of the polycystic ovary syndrome (PCOS). Whatever the menstrual pattern, infrequent or absent ovulation with symmetrical enlargement of the ovaries is now a familiar abnormality in women of reproductive age. Diagnosis of PCOS has developed from just the clinically obvious to an appreciation, through ultrasound imaging of the ovaries and endocrine testing, of its subtler forms. Today's clinicians will identify PCOS on the ultrasound image of many small follicles apparent in the periphery of both ovaries, on raised serum unbound testosterone assays, on exaggeration of serum LH levels with the start of pulsatile GnRH therapy, and on follicular overresponsiveness to injections of FSH. Once among the most treatable causes of infertility, ovulation-induction for PCOS remained unsophisticated while microsurgery and assisted conception dissolved frontiers for other causes of infertility. Whereas we now have the benefit of high technology embryo cryostorage to cope with embarrassingly high yields of PCOS oocytes, we still need to explain why, the bigger the ovaries, the more likely (we have long known it to be) that PCOS can be cured simply by reducing ovarian mass. Some cases of PCOS are hereditary and most seem constitutionally determined. PCOS is so common that the questions must be asked, Are we appreciating an extreme of normal? Could the milder forms of PCOS have--or could PCOS have had--evolutionary usefulness?