Physiological mechanisms underlying lactational amenorrhea.

Breastfeeding delays the resumption of normal ovarian cycles by disrupting the pattern of pulsatile release of GnRH from the hypothalamus and hence LH from the pituitary. The plasma concentrations of FSH during lactation are sufficient to induce follicle growth, but the inadequate pulsatile LH signal results in a reduced estradiol production by these follicles. When follicle growth and estradiol secretion does increase to normal, the suckling stimulus prevents the generation of a normal preovulatory LH surge and follicles either fail to rupture, or become atretic or cystic. Only when the suckling stimulus declines sufficiently to allow generation of a normal preovulatory LH surge to occur will ovulation take place with the formation of a corpus luteum of variable normality. Thus suckling delays the resumption of normal ovarian cyclicity by disrupting but not totally inhibiting, the normal pattern of release of GnRH by the hypothalamus. The mechanism of suckling-induced disruption of GnRH release remains unknown. It does not appear to involve prolactin, dopamine or opiates although a combination of these factors might be involved. Prolactin is the major hormone responsible for milk production and is present in sufficient quantities in almost all women to allow the establishment of normal lactation. Oxytocin is essential for milk let down and is susceptible to inhibition of release by stress. The successful initiation of lactation which would lead to the potential of utilizing breastfeeding as contraceptive may require more attention to be paid to the establishment of non-stress release of oxytocin.