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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.