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Endocrine Control of Lactational Infertility. I Maternal Nutrition and Lactational Infertility, edited by I. Dobbing. Nestld Nutrition, Vevey/ Raven Press, New York © 1985. Endocrine Control of Lactational Infertility. I *Alan S. McNeilly, *Anna Glasier, and fPeter W. Howie *MRC Reproductive Biology Unit, Edinburgh EH3 9EW, and 1'Department of Obstetrics and Gynaecology, University of Dundee Medical School, Ninewells Hospital, Dundee DD1 951, Scotland Although there is no doubt that breastfeeding suppresses ovarian activity, the reasons for the immense variability in the duration of this suppression and the mechanisms by which the suckling stimulus causes it remain unclear. The interbirth interval in women who breastfeed can be divided into three main components: (a) the period of lactational amenorrhoea, (b) a period when menstruation returns either during or after lactation, and (c) pregnancy. The length of periods a and b will vary considerably depending on the pattern of breastfeeding, and in a few cases pregnancy will occur during the period of lactational amenorrhoea without an intervening period of menstrual cycles. In an attempt to clarify the mechanisms controlling each of periods a and b above, the changes in endocrine and ovarian activities will be explored. GONADOTROPHIC CONTROL OF THE MENSTRUAL CYCLE Before discussing in detail the influences of suckling on ovarian activity, it is first necessary to outline the basic mechanisms controlling the growth and devel- opment of follicles and subsequent formation of the corpus luteum in the normal menstrual cycle. The basic changes in the four principal hormones involved are shown in Fig. 1. At the time of menses following the demise of the corpus luteum of the previous cycle, follicle development starts, and usually a single follicle begins to grow. This growth is initiated by the pituitary gonadotrophin follicle-stimulating hormone (FSH). The continuation of growth, although requiring the continued presence of FSH, is dependent on oestradiol secreted from the growing follicle in response to luteinizing hormone (LH). LH is released in a pulsatile manner from the pituitary, the frequency of these pulses increasing through the follicular phase of the cycle. This increase in LH-stimulated oestradiol secretion, together with the continued stimulation of FSH, stimulates follicle growth and increased oestrogen secretion. Around midcycle, when the single dominant follicle is approximately 18 to 22 mm in diameter, the increase in oestradiol secretion is sufficient to trigger the release 1 ENDOCRINE CONTROL. I OVULATION CORPUS LUTEUM ® PREOVULATORY 4h LH SURGE 0 14 28 DAYS FIG. 1. Schematic diagram of the endocrine changes during the menstrual cycle. Note that the initial growth of the follicle is due to an increase in FSH around menstruation, whereas continued follicle growth occurs in response to oestradiol. This is secreted by the follicle in response to pulses of LH, the frequency of which increase towards midcycle. The increase in oestradiol trig- gers the preovulatory surge of LH, which induces ovulation, and transformation of the follicle into the corpus luteum, which secretes progesterone. of the preovulatory surge of LH and FSH. This temporarily inhibits ovarian steroid secretion, alters the steroidogenic machinery of the follicle to make it secrete predominantly progesterone (luteinization); and some 36 hr after the start of the LH surge, ovulation occurs, with the oocyte being ejected from the follicle. The follicle then collapses and forms the corpus luteum, which, under the influence of LH, secretes progesterone and oestradiol (Fig. 2). Of critical importance to this sequence of events is the maintenance of LH secretion in the follicular phase of the cycle. As mentioned above, LH is released in a pulsatile manner from the pituitary. This occurs as a result of pulsatile release of gonadotrophin-releasing hormone (GnRH) from the hypothalamus, reaching the pituitary gland via the hypophysial portal blood system. While the overall controller of GnRH release remains to be determined, it is sufficient to think in terms of a hypothalamic GnRH pulse generator, the frequency of which is modulated by the ovarian steroids. Thus, oestradiol appears to increase the GnRH pulse secretion, whereas progesterone and oestradiol decrease pulse release. In many amenorrhoeic states pulsatile secretion of LH, which can be measured, is abnormal, either slow or absent. Many of these states can be treated by pulsatile infusion of GnRH delivered subcutaneously or intravenously by a minipump worn by the patient. ENDOCRINE CONTROL. I Brain Hypothalamus p Portal blood — SUCKLING Pituitary Blood Ovary HYPOTHALAMUS -RELEASE PREOVULATORY LH SURGE FIG. 2. Schematic diagram of the hypothaiamic control of gonadotrophin secretion. Note that GnRH is released in pulses from the hypothaiamic pulse generator and induces pulsatile LH release from the pituitary. The subsequent sequence of events in terms of follicle development is outlined in Fig. 1. It is envisaged that suckling either via a direct neural input and/or by increasing prolactin secretion alters the frequency of LH pulse secretion by affecting the hypothaiamic GnRH pulse generator. In lactation a similar alteration in the pulsatile secretion of GnRH has also been identified, suggesting that the principal site where suckling affects ovarian activity is at the hypothaiamic GnRH pulse generator. LACTATIONAL AMENORRHOEA Recovery from Pregnancy During pregnancy, the high circulating plasma levels of placental steroids suppress pituitary levels of both LH and FSH to approximately 1% of normal (1), whereas the increase in oestrogen secretion substantially increases the number of lacto- trophes in the pituitary and plasma levels of prolactin (2). Following parturition and the clearance of these steroids, pituitary and plasma prolactin levels decline, and plasma levels of FSH and LH increase within 30 days in a non-breastfeeding woman (3-5). This resumption of the pulsatile secretion of LH (6) leads to an early return of follicle growth and menstruation, although first menstruation is usually preceded by an inadequate (80%) or absent (20%) luteal phase in terms of preg- nanediol secretion (7). Luteal function subsequently improves, so that by the third 4 ENDOCRINE CONTROL. I postpartum cycle, normally between 70 and 120 days postpartum (8), the majority of cycles (88%) have normal luteal function (7). Thus, the delay in the resumption of normal ovulatory cycles in non-breastfeeding women depends mainly, if not exclusively, on the time taken for the recovery of the hypothalamo-pituitary-ovarian axis from the suppressive effects of pregnancy. Suppression of Ovarian Activity The results in non-breastfeeding women suggest that even limited corpus luteum function will result in the recurrence of menstruation. Thus, it can be assumed that during lactational amenorrhoea ovarian activity is sufficiently suppressed that ovulation normally does not occur. Assessment of follicular development either in terms of plasma levels of oestradiol (3-5) or total urinary oestrogen (8-10) confirm that follicular development rarely occurs during lactational amenorrhoea (Fig. 3). More recently we have confirmed by ultrasound the absence of medium- or large- sized follicles within the ovary in breastfeeding women (11). However, although urinary oestrogen levels are below those which would indicate follicular develop- ment equivalent to that seen around day 5 to 7 of the normal menstrual cycle, we have recently observed, by estimation of urinary oestrogens in daily early morning urine specimens, that there may be periods during which follicle growth is initiated, indicated by a rise in oestrogen, but not sustained. Solid food 100 Die "? C O CD 50 il3 l 3-= C/3 T3 C iff 3000 2000 1000 8 10 12 14 16 18 20 22 24 26 28 30 32 34 36 38 40 42 44 46 48 50 52 54 Weeks after delivery FIG. 3. Changes in urinary total oestrogens and pregnanediol in relation to the suckling fre- quency and duration and plasma levels of prolactin in a breastfeeding woman. Note that even at four feeds each day with a suckling duration of 50 min/day, follicular development in terms of oestrogen is below the lower limit of normal (10 (ig/24 hr), whereas prolactin remains at or above the upper limit of normal (500 mU/liter). First menstruation is not preceded by ovulation, and the four subsequent cycles have inadequate corpus luteum function. (From ref. 12.) ENDOCRINE CONTROL. I 5 It is clear that the period of lactational amenorrhoea is dependent on the suckling input (2,12). While this is maintained, ovarian activity is suppressed. However, the amount of suckling input is very difficult to define, since suckling patterns vary considerably among different societies. In our own study group of over 70 women in Edinburgh, a suckling frequency of more than five times and more than 65 min (minimum, 10 min per feed) each day is sufficient to maintain complete suppression of ovarian activity (7,13). Any decrease below these limits in either suckling frequency or duration results in the resumption of follicular development. A lon- gitudinal study in Denmark also suggests that suckling five times each day is the minimum required to protect against pregnancy in developed countries (14). While further studies of women in Edinburgh have confirmed our findings, similar lon- gitudinal studies in other societies must be undertaken to determine the parameters necessary for maintenance of lactational amenorrhoea. It is probable, with a fre- quency which is considerably greater than the Edinburgh norm, that duration of each individual suckling episode may lose importance in maintaining amenorrhoea. It is well known that suckling causes the release of prolactin, that the amount of prolactin released appears to decline with time postpartum (1,2), and that there is a close correlation between basal plasma levels of prolactin and both suckling frequency (2-4) and duration (8,9). Although during the period of lactational amenorrhoea both suckling frequency and duration are maintained (9,10), there is a gradual decline in basal levels of prolactin. However, basal levels remain above the upper limit of those in the menstrual cycle (Fig.
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