The underlying cause of the menopausal transition is a dwindling supply of FSH-responsive follicles available for ovulation. Additional factors may include dysregulation of existing follicles and concurrent follicle and oocyte deficits that may be strictly anatomic or consequences of the hormonal milieu. In the early transition, menstrual irregularity is infrequent but cycle length shortens by 1-4 days. Oestrogen production may be overall elevated, even in ovulatory cycles. As anovulatory cycles become more common, and amenorrhoea of greater duration, evidence of impaired hypothalamic-pituitary function is present. Oestradiol has been implicated as an agent responsible for the impaired positive feedback response. A model of the early menopausal transition suggests that the loss of FSH restraint by the inhibins, due to a critically diminished follicle pool, is the early event that precedes overt follicle failure and may initiate intervals of hyperoestrogenaemia. The hormonal fluctuations in the early and late menopausal transition may account for some of the signs and symptoms seen during these phases.