Abstract
It has long been recognized that women who develop endometrial cancer are often overweight1 and obesity is now clearly established as a major risk factor for the disease.2 In pre-menopausal women, obesity is associated with an increased frequency of anovulatory cycles and, as a result, the endometrium is exposed to oestrogen in the absence of progesterone. Among post-menopausal women, obesity is again associated with exposure to higher levels of endogenous oestrogen as a result of increased conversion of androstenedione to oestrone in adipose tissue and lower levels of sex-hormone binding globulin (SHBG). In the absence of progesterone, unopposed oestrogen stimulates cellular proliferation in the endometrium leading to hyperplasia and, potentially, cancer.3