Abstract
THE pathogenesis of polycystic ovary syndrome has been a matter of intense controversy for several decades. The disorder has been variously ascribed to primary abnormalities of the ovaries,1 of gonadotropin secretion,2 and of the adrenal glands.3 It has frequently been noted that polycystic ovary syndrome is a heterogeneous disorder that occurs in association with several distinct pathologic entities: congenital adrenal hyperplasia,4 Cushing's syndrome,5 hyperprolactinemia,6 and insulin-resistant states.7 In this paper, the mechanism proposed for the development of polycystic ovary syndrome suggests a pathway through which several disorders can result in similar abnormalities of gonadotropin secretion that in turn lead to . . .