Lactational amenorrhea.

Abstract

There is no doubt that suckling can cause a substantial delay in the resumption of fertility postpartum in all societies regardless of nutritional status. The variability in duration of infertility is directly related to the different patterns of suckling, an uncontrollable variable specific to the mother and child. Resumption of fertility proceeds in two parts, an initial phase of amenorrhea in which ovarian follicle growth is suppressed or attenuated followed by a resumption of menstrual cycles often associated with inadequate luteal function contributing to the reduced fertility of lactating menstruating women. Suckling appears to suppress the normal pattern of pulsatile release of GnRH and hence LH and prevents the normal growth of follicles. The normal positive feedback effect of estrogen on LH release is abolished, and estradiol exerts an enhanced negative feedback effect on both LH and FSH. Thus, while suckling continues, any follicle that starts to develop and secrete estradiol will inhibit further LH release and therefore stop growing. When suckling declines, the pulsatile pattern of LH returns to normal, sensitivity to estrogen negative feedback declines, and follicle growth can continue and ovulation will occur. Opiates do not appear to be mediators of the suckling-induced suppression of GnRH or the release of prolactin in women. There is no clear role for prolactin per se or nutritional status in the suppression of ovarian activity postpartum. Thus, while the suppression of fertility in breast-feeding women plays an extremely important role in limiting populations, the mechanism whereby the suckling stimulus from the nipple causes the disruption in GnRH release from the hypothalamus remains to be elucidated.