PIP: A review of our current knowledge of the mechanism underlying lactation amenorrhoea suggests that there is a causal relationship between high prolactin levels and the absence of ovarian activity. During pregnancy, blood levels of prolactin continually increase. After delivery, among those women who breastfeed, the level remains; however, when breastfeeding is reduced to 3 or less episodes/day, prolactin levels quickly return to normal. The follicle stimulating hormone (FSH) is suppressed during pregnancy but increases after birth. For lactating women, FSH in the 1st year is in the high normal range and in the 2nd year it is in the normal range of the follicular phase. The luteinizing hormone (LH) remains low during lactation but at weaning, LH concentrations increase as prolactin levels decrease. Apparently this low level of LH during lactation is not due to pituitary inability to respond to the gonadotrophin-releasing hormone, but instead, is due to the increased sensitivity of the hypothalamo-pituitary axis to the negative feedback effects of estrogen. In lactating women estradiol levels remain low as long as prolactin levels remain high. Despite an adequate store of releasable FSH and LH in the pituitary, estrogen secretion does not occur and the ovaries remain inactive. In pathological hyperprolactinemia, the high levels of prolactin also appear to be related to the absence of ovarian function. Many studies have shown that in some societies prolonged breast feeding, accompanied by lactational infertility, increases the birth interval and thus serves as a form of contraception. Other studies indicate that lactation is not associated with infertility for all women and that the number of suckling episodes introduces variation in the lactational maintenance of infertility. Further studies are needed concerning the relationship between suckling frequency and prolactin level. In addition there is a need to develop a reliable method for detecting the resumption of ovulation.