During recent years, a number of prospective studies have greatly contributed to our understanding of the complexity of the mechanisms involved in ERMI. Older hypotheses, such as those considering hyperprolactinaemia as the cornerstone of ERMI, have now been firmly rejected. The present hypotheses emphasise the importance of caloric deficiency and limited energy availability, although they still fail to identify the actual mechanism that causes ERMI. There is, however, evidence that ERMI is produced by a disturbance of the hypothalamic gonadotrophin-releasing hormone oscillator. This disturbance is caused by either an insufficient estrogen or progesterone feedback or by an imbalance of local opioid peptide and catecholamine activities mediated by γ-aminobutyric acid (GABA), corticotrophin-releasing hormone and insulin-like growth factor-