The endocrinology of dizygotic twinning in the human

Heredity, higher maternal age and increased parity are well defined conditi ons associated with dizygotic twinning. An endocrine model of excessive sec retion of pituitary gonadotrophic hormones explains multiple ovulation as a result of multiple follicle growth. In hereditary conditions FSH levels ar e indeed clearly elevated because of increase in stimulating mechanisms tha t regulate pituitary gonadotropin secretion while in most non-hereditary co nditions, overshoot FSH secretions occurs as a result of diminished ovarian feedback. Puberty is a condition in which the hypothalamic LHRH pulse gene rator is reinitiated and this is typically characterized by temporary overs hoot LH and FSH secretion, probably due to not yet fully operational ovaria n feedback. In adult females situations can be found that mimic this peripu bertal event such as while recovering from hypothalamic amenorrhea. Under t hese circumstances more DZ twinning can be observed. Elevated FSH levels al ong with ageing in premenopausal women probably underlie the age related in creased risk of dizygotic twinning. The apparent paradox in the combination of age related decline in fecundity and rise in twinning risk can be expla ined by incidental presence in the cohort of more than one follicle, contai ning vital oocytes under deficient feedback mechanisms that lead to high FS H. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.