The etiology of polycystic ovary syndrome (PCO)

Consideration of existing data leads to the hypothesis that polycystic ovary syndrome results from a primary abnormality in the growth hormone (GH)-insulin-like growth factor 1 (IGF-1) axis characterized by increased IGF-1 activity at multiple sites. The effect of elevated IGF-1 activity upon the ovary, the adrenal, and on peripheral tissues may lead to the clinical and biochemical features of PCO, including hyperandrogenemic chronic anovulation, insulin resistance, and elevated adrenal androgen secretion. The fundamental defect may be a consequence of feeding behavior early in life.