The cause of polycystic ovarian syndrome is unknown.
There may be some women who are genetically predisposed to the development of the syndrome (1).
Among women with the syndrome, raised testosterone levels are found in 30% and raised luteinising hormone (LH) levels are found in 40% (2)
It has been proposed that the primary defects in the polycystic ovarian syndrome are:
- insulin resistance in adipose tissue and skeletal muscle
- insulin sensitivity in the ovary
Compensatory hyperinsulinaemia results in androgen secretion by the ovaries. For example, hyperinsulinaemia can stimulate the production of androgens in the ovaries and inhibit the production of sex hormone binding globulin in the liver - these changes can lead to increased serum concentrations of free (active) testosterone.
In women with PCOS, ovarian theca cells seem to be more efficient at converting androgenic precursors to testosterone than are theca cells in unaffected women (3).
Androgens result in the main clinical and endocrine abnormalities.
Women with polycystic ovarian syndrome also are more likely than other women of the same age to have cardiovascular risk factors (central body fat distribution, obesity, hypertension, hypertriglyceridaemia, reduced HDL-cholesterol concentrations). Women with polycystic ovary syndrome are twice as likely to develop diabetes and almost three times as likely to have a transient ischaemic attack or stroke (4). Women with this disorder are also more likely to develop endometrial cancer (4) although they do not appear to be at an increased risk of developing coronary heart disease (4).
(1) Balen A (1999). Pathogenesis of polycystic ovary syndrome - the enigma unravels? Lancet, 354, 966-7.
(2) Balen AH et al (1995). Polycystic ovary syndrome: the spectrum of the disorder in 1741 patients. Hum Reprod, 10, 2107-11.
(4) Wild S et al (2000). Cardiovascular disease in women with polycystic ovary syndrome at long-term follow-up: a retrospective cohort study. Clin Endocrinol, 52, 595-600.
Last reviewed 02/2021