Endocrine control of lactational infertility. I.

Breastfeeding suppresses ovarian activity but the reasons for the immense variability in the suppression and the mechanisms by which the suckling stimulus causes it remain unclear. The interbirth interval in women who breastfeed can be divided into 3 main components: (1) the period of lactational amenorrhea; (2) a period when menstruation returns either during or after lactation; and (3) pregnancy. To clarify the mechanisms controlling each of periods (1) and (2) this discussion explores the changes in endocrine activity. Before covering the influences of suckling on ovarian activity the discussion outlines the basic mechanisms controlling the growth and development of follicles and subsequent formation of the corpus luteum in the normal menstrual cycle. The studies reported confirm conclusively that breastfeeding even in an industrial and well-nourished population will suppress fertility for a considerable period of time (up to 75 weeks). Resumption of ovarian follicular development and ovulation occurs only when suckling frequency decreases below 5 feeds each day with a total daily suckling duration of less than 65 minutes/day. Ovulation resumes if total suckling activity is below this level. This is the case even if no supplementary food is being given and the baby receives breast milk as its sole source of nutrition. The resumption of follicular development and ovulation occurs when there is a significant decrease in suckling input. This can be precipitated by the introduction of supplementary food presumably by reducing the babys dependence on breast milk but resumption of ovarian activity is not dependent on age of baby or maternal body weight. 1st menstrual cycles normally are associated with inadequate luteal function which tends to continue if suckling is maintained. A rapid reduction in suckling or weaning especially if occuring after prolonged lactation can result in ovulation with normal luteal function with the potential to carry a pregnancy if conception occurs. This appears to explain the occurrence of pregnancies during lactational amenorrhea in the cases where adequate data are available. Reduction in the pulsatile secretion of luteinizing hormone (LH) seems to be responsible primarily for the absence of follicular development during lactational amenorrhea. Whereas pulsatile LH secretion may occur between 20-30% of the time and stimulate limited follicular development suckling appears to reduce the ability of the hypothalamus to maintain pulsatile gonadotropin-releasing hormone (GnRH) and hence LH secretion and follicular development decreases. The mmechanisms whereby the suckling stimulus decreases GnRH output from the hypothalamus remain unknown. The maintenance of infertility during breastfeeding is directly dependent on the strength of the suckling stimulus. Anything that undermines or reduces this stimulus results in a resumption of ovarian activity with a variable return in fertility.