The endocrinology of dizygotic twinning in the human

Abstract

Heredity, higher maternal age and increased parity are well defined conditions associated with dizygotic twinning. An endocrine model of excessive secretion of pituitary gonadotrophic hormones explains multiple ovulation as a result of multiple follicle growth. In hereditary conditions FSH levels are indeed clearly elevated because of increase in stimulating mechanisms that regulate pituitary gonadotropin secretion while in most non-hereditary conditions, overshoot FSH secretions occurs as a result of diminished ovarian feedback. Puberty is a condition in which the hypothalamic LHRH pulse generator is reinitiated and this is typically characterized by temporary overshoot LH and FSH secretion, probably due to not yet fully operational ovarian feedback. In adult females situations can be found that mimic this peripubertal event such as while recovering from hypothalamic amenorrhea. Under these circumstances more DZ twinning can be observed. Elevated FSH levels along with ageing in premenopausal women probably underlie the age related increased risk of dizygotic twinning. The apparent paradox in the combination of age related decline in fecundity and rise in twinning risk can be explained by incidental presence in the cohort of more than one follicle, containing vital oocytes under deficient feedback mechanisms that lead to high FSH.