The Postpartum Period, Breastfeeding, and Contraception
Breastfeeding protects infants against infection, offers an inexpensive supply of nutrition, contributes to maternal-infant bonding, and provides contraception. The relationship between lactation and fertility is an important public health issue. A birth interval of 2 or more years improves infant survival and reduces maternal morbidity.1 In developing countries, breastfeeding provides protection from pregnancy and is important for achieving the 2-year birth interval that advances good maternal and infant health.
Giving up breastfeeding was a misguided notion of civilized times. Urbanization, education, and modernization all contributed to a decline in breastfeeding, which, fortunately, has been somewhat reversed. Even in ancient Greek and Roman societies, breastfeeding was disdained by the elite. The tradition of wet nursing (the practice of breastfeeding by someone other than the mother) was popular from the days of the ancient Greeks to the time of medieval Europe.2 A further decline in breastfeeding came with the introduction of bottle feeding.
The domestication of cattle dates back thousands of years, but the use of animal milk for infant feeding is recent. In the United States, modification of cow’s milk for infant feeding was not established until 1900. In the early 1900s, milk banks were popular, using freezing techniques to keep the milk sterile. But it was not until the 1930s that the preparation of infant “formulas” moved from the home kitchen to commercial production and promotion. Breast milk substitutes were initially developed to meet specific needs (allergies and intolerance with cow’s milk), but eventually came to be viewed as a means to free women from the responsibility of breastfeeding.
In 1922, about 90% of infants were still being breastfed at 1 year of age. A decline in breastfeeding began in the 1930s. By the 1950s, the prevalence of breastfeeding on discharge from the hospital fell to 30%, and the downward trend reached its nadir (22%) in 1972.3 This trend was followed in Europe a decade or two later.
A higher mortality rate in artificially fed infants was observed in the 1900s. By the 1940s, the mortality difference between early and late weaned infants was recognized to be due to conditions of hygiene and general care. In the developed parts of the world, where infants receive good health supervision, the mortality difference is no longer a significant problem. However,
in the developing world, excess mortality due to early weaning continues to be high.
in the developing world, excess mortality due to early weaning continues to be high.
The revival of breastfeeding can be attributed to the growth of knowledge regarding the health of infants.4 The following reasons emerged as motivations to encourage breastfeeding:
1. Breastfeeding has a child-spacing effect, which is very important in the developing world as a means of limiting family size and providing good nutrition for infants.
2. Human milk prevents infections and illnesses in infants, both by the transmission of immunoglobulins and by modifying the bacterial flora of the infant’s gastrointestinal tract. However, avoidance of breastfeeding by HIV-infected women is strongly recommended.5
3. Breastfeeding enhances the bonding process between mother and child.
Breastfeeding is a personal choice, but one influenced by custom and social and economic circumstances. Beginning in the 1960s, breastfeeding became more popular in the United States, Sweden, Canada, and the United Kingdom.3,8 Even in the developing world, there was evidence of increased breastfeeding. In general, the knowledge that breastfeeding is superior was spreading. But this upward trend in the United States peaked in 1982 (at 61% for initiation and 40% for 3 or more months).3
Unfortunately, and somewhat perplexing (did it represent more women in the workforce?), is the fact that during the 1980s, there was a steady decline in breastfeeding, reaching 52% for initiation by 1989.3 By age 6 months, only 19.6% of infants were still breastfeeding. But the good news is that since the 1980s, there has been a steady and consistent increase in breastfeeding. In the 1990s, breastfeeding began to increase slightly, 59.4% initiation in 1995.4,9 By 2001, 65.1% of children had been breastfed, with 27% still breastfeeding at 6 months of age, but only 12.3% at 1 year.10 By 2006, 74% were breastfed in the postpartum period, 43% were still breastfeeding at 6 months of age, and 23% at 1 year.11 The average duration has remained short, however, usually under 6 months, most often only 2 to 3 months, and the rate of exclusive breastfeeding is very low, only 14% through 6 months in 2006.11 This still provides a significant benefit for the infant, but as we shall see, it is not so good from a contraceptive point of view.
Breast Physiology
The basic component of the breast lobule is the hollow alveolus or milk gland lined by a single layer of milk-secreting epithelial cells, derived from an ingrowth of epidermis into the underlying mesenchyme at 10 to 12 weeks of gestation. Each alveolus is encased in a crisscrossing mantle of contractile myoepithelial strands. Also surrounding the milk gland is a rich capillary
network. The lumen of the alveolus connects to a collecting intralobular duct by means of a thin nonmuscular duct. Contractile muscle cells line the intralobular ducts that eventually reach the exterior via 15 to 20 collecting ducts in a radial arrangement, corresponding to the 15 to 20 distinct mammary lobules in the breast, each of which contains many alveoli.
network. The lumen of the alveolus connects to a collecting intralobular duct by means of a thin nonmuscular duct. Contractile muscle cells line the intralobular ducts that eventually reach the exterior via 15 to 20 collecting ducts in a radial arrangement, corresponding to the 15 to 20 distinct mammary lobules in the breast, each of which contains many alveoli.
Growth of this milk-producing system is dependent on numerous hormonal factors that occur in two sequences, first at puberty and then in pregnancy. Although there is considerable overlapping of hormonal influences, the differences in quantities of the stimuli in each circumstance and the availability of entirely unique inciting factors (human placental lactogen [hPL] and prolactin) during pregnancy permit this chronologic distinction.
The major influence on breast growth at puberty is estrogen. In most girls, the first response to the increasing levels of estrogen is an increase in size and pigmentation of the areola and the formation of a mass of breast tissue just underneath the areola. Breast tissue binds estrogen in a manner similar to the uterus and vagina. The human breast expresses both estrogen receptors, ER-α and ER-β.12 The development of estrogen receptors in the breast does not occur in the absence of prolactin. The primary effect of estrogen in subprimate mammals is to stimulate growth of the ductal portion of the gland system. Progesterone in these animals influences growth of the alveolar components of the lobule.13 However, neither hormone alone, or in combination, is capable of yielding optimal breast growth and development. Full differentiation of the gland requires insulin, cortisol, thyroxine, prolactin, and growth hormone.14 Of course, the ubiquitous growth factors are also involved, but the molecular mechanisms remain to be determined. Nevertheless, experimental evidence in mice indicates that progesterone is the key hormone required for mammary growth and differentiation; estrogen is necessary because the synthesis of progesterone receptors requires the critical presence of estrogen.13
Changes occur routinely in response to the estrogen-progesterone sequence of a normal menstrual cycle. Maximal size of the breast occurs late in the luteal phase. Fluid secretion, mitotic activity, and DNA production of nonglandular tissue and glandular epithelium peak during the luteal phase.15,16,17 This accounts for cystic and tender premenstrual changes. During the normal menstrual cycle, estrogen receptors in mammary gland epithelium decrease in number during the luteal phase, whereas progesterone receptors remain at a high level throughout the cycle.18 Studies using tissue from reduction mammoplasties or from breast tissue near a benign or malignant lesion have demonstrated a peak in mitotic activity during the luteal phase.16,19,20 Using fine-needle biopsy tissue, an immunocytochemical marker of proliferation was higher in the luteal phase than in the proliferative phase.18 And in this study there was a direct correlation with serum progesterone levels. However, important studies indicate that with increasing duration of exposure, progesterone imposes a limitation on breast cell proliferation.21,22,23 Therefore, breast and endometrium epithelial cells may be more similar than initially proposed.
Final differentiation of the alveolar epithelial cell into a mature milk cell is accomplished by the gestational increase in estrogen and progesterone, combined with the presence of prolactin, but only after prior exposure to cortisol and insulin. The complete reaction depends on the availability of minimal quantities of thyroid hormone. Thus, the endocrinologically intact individual in whom estrogen, progesterone, thyroxine, cortisol, insulin, prolactin, and growth hormone are available can have appropriate breast growth and function. During the first trimester of pregnancy, growth and proliferation are maximal, changing to differentiation and secretory activity as pregnancy progresses.
Breast tissue changes with aging. During teenage years, the breasts are dense and predominantly glandular. As the years go by, the breasts contain progressively more fat, but after menopause, this process accelerates so that soon into the postmenopausal years, the breast glandular tissue is mostly replaced by fat.
Lactation
During pregnancy, prolactin levels rise from the normal level of 10 to 25 ng/mL to high concentrations, beginning about 8 weeks and reaching a peak of 200 to 400 ng/mL at term.24,25 The increase in prolactin parallels the increase in estrogen beginning at 7 to 8 weeks’ gestation, and the mechanism for increasing prolactin secretion is believed to be estrogen suppression of the hypothalamic prolactin-inhibiting factor, dopamine, and direct stimulation of prolactin gene transcription in the pituitary.26,27 There is marked variability in maternal prolactin levels in pregnancy, with pulsatile secretion and a diurnal variation similar to that found in nonpregnant subjects. The peak level occurs 4 to 5 hours after the onset of sleep.28
Made by the placenta and actively secreted into the maternal circulation from the sixth week of pregnancy, hPL rises progressively, reaching a level of approximately 6,000 ng/mL at term. hPL, though displaying less activity than prolactin, is produced in such large amounts that it may exert a lactogenic effect.
Although prolactin stimulates significant breast growth and is available for lactation, only colostrum (composed of desquamated epithelial cells and transudate) is produced during gestation. Full lactation is inhibited by progesterone, which interferes with prolactin action at the alveolar cell prolactin receptor level. Both estrogen and progesterone are necessary for the expression of the lactogenic receptor, but progesterone antagonizes the positive action of prolactin on its own receptor while progesterone and pharmacologic amounts of androgens reduce prolactin binding.29,30,31 In the mouse, inhibition of milk protein production is due to progesterone suppression of prolactin receptor expression.32 The effective use of high doses of estrogen to suppress postpartum lactation indicates that pharmacologic amounts of estrogen also block prolactin action.
The principal hormone involved in milk biosynthesis is prolactin. Without prolactin, synthesis of the primary protein, casein, will not occur, and
true milk secretion will be impossible. The hormonal trigger for initiation of milk production within the alveolar cell and its secretion into the lumen of the gland is the rapid disappearance of estrogen and progesterone from the circulation after delivery. The clearance of prolactin is much slower, requiring 7 days to reach nonpregnant levels in a nonbreastfeeding woman. These discordant hormonal events result in removal of the estrogen and progesterone inhibition of prolactin action on the breast. Breast engorgement and milk secretion begin 3 to 4 days postpartum when steroids have been sufficiently cleared. Maintenance of steroidal inhibition or rapid reduction of prolactin secretion (with a dopamine agonist) is effective in preventing postpartum milk synthesis and secretion. Augmentation of prolactin (by thyrotropin-releasing hormone [TRH] or sulpiride, a dopamine receptor blocker) results in increased milk yield.
true milk secretion will be impossible. The hormonal trigger for initiation of milk production within the alveolar cell and its secretion into the lumen of the gland is the rapid disappearance of estrogen and progesterone from the circulation after delivery. The clearance of prolactin is much slower, requiring 7 days to reach nonpregnant levels in a nonbreastfeeding woman. These discordant hormonal events result in removal of the estrogen and progesterone inhibition of prolactin action on the breast. Breast engorgement and milk secretion begin 3 to 4 days postpartum when steroids have been sufficiently cleared. Maintenance of steroidal inhibition or rapid reduction of prolactin secretion (with a dopamine agonist) is effective in preventing postpartum milk synthesis and secretion. Augmentation of prolactin (by thyrotropin-releasing hormone [TRH] or sulpiride, a dopamine receptor blocker) results in increased milk yield.
In the first postpartum week, prolactin levels in breastfeeding women decline approximately 50% (to about 100 ng/mL). Suckling elicits increases in prolactin, which are important in initiating milk production. Until 2 to 3 months postpartum, basal levels are approximately 40 to 50 ng/mL, and there are large (about 10- to 20-fold) increases after suckling. Throughout breastfeeding, baseline prolactin levels remain elevated, and suckling produces a 2-fold increase that is essential for continuing milk production.33,34 The pattern or values of prolactin levels do not predict the postpartum duration of amenorrhea or infertility.35
Maintenance of milk production at high levels is dependent on the joint action of both anterior and posterior pituitary factors. By mechanisms to be described shortly, suckling causes the release of both prolactin and oxytocin as well as thyroid-stimulating hormone (TSH).36,37 Prolactin sustains the secretion of casein, fatty acids, lactose, and the volume of secretion, while oxytocin contracts myoepithelial cells and empties the alveolar lumen, thus enhancing further milk secretion and alveolar refilling. The increase in TSH with suckling suggests that TRH may play a role in the prolactin response to suckling. The optimal quantity and the quality of milk are dependent upon the availability of thyroid, insulin, and the insulin-like growth factors, cortisol, and the dietary intake of nutrients and fluids.
Secretion of calcium into the milk of lactating women approximately doubles the daily loss of calcium.38 In women who breastfeed for 6 months or more, this is accompanied by significant bone loss even in the presence of a high calcium intake.39 However, bone density rapidly returns to baseline levels in the 6 months after weaning.40,41 The bone loss is due to increased bone resorption, probably secondary to the relatively low estrogen levels associated with lactation. It is possible that recovery is impaired in women with inadequate calcium intake; total calcium intake during lactation should be at least 1,500 mg per day. Nevertheless, calcium supplementation has no effect on the calcium content of breast milk or on bone loss in lactating women who have normal diets.42 Furthermore, studies indicate that any loss of calcium and bone associated with lactation is rapidly restored, and, therefore, there is no impact on the risk of postmenopausal osteoporosis.43,44,45,46
Antibodies are present in breast milk and contribute to the health of an infant. Human milk prevents infections in infants both by transmission of immunoglobulins and by modifying the bacterial flora of the infant’s gastrointestinal tract. Viruses are transmitted in breast milk, and although the actual risks are unknown, women infected with cytomegalovirus, hepatitis B, or human immunodeficiency virus are advised not to breastfeed. Vitamin A, vitamin B12, and folic acid are significantly reduced in the breast milk of women with poor dietary intake. As a general rule, approximately 1% of any drug ingested by the mother appears in breast milk. In a study of Pima Indians, exclusive breastfeeding for at least 2 months was associated with a lower rate of adult-onset non-insulin-dependent diabetes mellitus, partly because overfeeding and excess weight gain are more common with bottlefeeding.47
Frequent emptying of the lumen is important for maintaining an adequate level of secretion. Indeed, after the fourth postpartum month, suckling appears to be the only stimulant required; however, environmental and emotional states also are important for continued alveolar activity. Vigorous aerobic exercise does not affect the volume or composition of breast milk, and therefore infant weight gain is normal.48 Maternal diet and hydration have little impact on lactation; the primary control of milk output is under the control of the infant’s suckling.49
Suckling studied with ultrasonography indicates that the infant’s instinctive attachment to a nipple immediately establishes a vacuum seal.50 The tongue moves up and down, increasing the vacuum and producing milk flow during the downward motion. However, the ejection of milk from the breast does not occur only as the result of a mechanically induced negative pressure produced by suckling. Tactile sensors concentrated in the areola activate, via thoracic sensory nerve roots 4, 5, and 6, an afferent sensory neural arc that stimulates the paraventricular and supraoptic nuclei of the hypothalamus to synthesize and transport oxytocin to the posterior pituitary. The efferent arc (oxytocin) is blood-borne to the breast alveolus-ductal systems to contract myoepithelial cells and empty the alveolar lumen. Milk contained in major ductal repositories is ejected from 15 to 20 openings in the nipple. This rapid release of milk is called “let-down.” This important role for oxytocin is evident in knockout mice lacking oxytocin who undergo normal parturition, but fail to nurse their offspring.51 The milk ejection reflex involving oxytocin is present in all species of mammals. Oxytocin-like peptides exist in fish, reptiles, and birds, and a role for oxytocin in maternal behavior may have existed before lactation evolved.49
In many instances, the activation of oxytocin release leading to let-down does not require initiation by tactile stimuli. The central nervous system can be conditioned to respond to the presence of the infant, or to the sound of the infant’s cry, by inducing activation of the efferent arc. These messages are the result of many stimulating and inhibiting neurotransmitters. Suckling, therefore, acts to refill the breast by activating both portions of the pituitary (anterior and posterior) causing the breast to produce new milk and to eject milk. The release of oxytocin is also important for uterine contractions that contribute to involution of the uterus.
The oxytocin effect is a release phenomenon acting on secreted and stored milk. Prolactin must be available in sufficient quantities for continued secretory replacement of ejected milk. This requires the transient increase in prolactin associated with suckling. The amount of milk produced correlates with the amount removed by suckling. The breast can store milk for a maximum of 48 hours before production diminishes.
Cessation of Lactation
Lactation can be terminated by discontinuing suckling. The primary effect of this cessation is loss of milk let-down via the neural evocation of oxytocin. With passage of a few days, the swollen alveoli depress milk formation probably via a local pressure effect (although milk itself may contain inhibitory factors). With resorption of fluid and solute, the swollen engorged breast diminishes in size in a few days. In addition to the loss of milk let-down, the absence of suckling reactivates dopamine (PIF) production so that there is less prolactin stimulation of milk secretion.
Contraceptive Effect of Lactation
In primitive human societies, the duration of the birth interval was very important for the survival of the young. Throughout human history, no preliterate society achieved a fertility rate at the maximal level possible. The hunter-gatherer, nomadic !Kung women had a high suckling frequency and gave birth about every 4 years.52 Lactational amenorrhea, lasting up to 2 years, has been nature’s most effective form of contraception.53 Indeed, lactation is the mechanism that maintains a reasonable interval between pregnancies in all non-seasonally breeding animals. In Africa and Asia, breastfeeding reduces the fertility rate by an average of about 30%.1 Birth intervals of less than 2 years are associated with a greater incidence of low birth weight, preterm birth, and neonatal death for the new infant and malnutrition, infection, and increased second year mortality for the previous child.54
The contraceptive effectiveness of lactation, that is, the length of the interval between births, depends on the level of nutrition of the mother (if low, the longer the contraceptive interval); the intensity of suckling, and the extent to which supplemental food is added to the infant diet.55 If suckling intensity and/or frequency is diminished, contraceptive effect is reduced. Only amenorrheic women who exclusively breastfeed (full breastfeeding) at regular intervals, including nighttime, during the first 6 months have the contraceptive protection equivalent to that provided by oral contraception (98% efficacy); with menstruation or after 6 months, the chance of ovulation increases.56,57 With full or nearly full breastfeeding, approximately 70% of women remain amenorrheic through 6 months and only 37% through 1 year; nevertheless with exclusive breastfeeding, the contraceptive efficacy at 1 year is high, at 92%.57 Fully breastfeeding women commonly have some vaginal bleeding or spotting in the first 8 postpartum weeks, but this bleeding is not due to ovulation.58
Mechanism of Action
Earlier experimental evidence suggested that the ovaries might be refractory to gonadotropin stimulation during lactation, and, in addition, the anterior pituitary might be less responsive to gonadotropin-releasing hormone (GnRH) stimulation. Other studies, done later in the course of lactation, indicated, however, that the ovaries as well as the pituitary were responsive to adequate tropic hormone stimulation.59 These observations suggest that high concentrations of prolactin can work at both central and ovarian sites to produce lactational amenorrhea and anovulation. Prolactin appears to affect granulosa cell function in vitro by inhibiting the synthesis of progesterone. It also may change the testosterone:dihydrotestosterone ratio, thereby reducing aromatizable substrate and increasing local antiestrogen concentrations. Nevertheless, a direct effect of prolactin on ovarian follicular development does not appear to be a major factor. The central action predominates.
Elevated levels of prolactin inhibit the pulsatile secretion of GnRH.60,61 Prolactin excess has short loop positive feedback effects on dopamine. Increased dopamine reduces GnRH by suppressing arcuate nucleus function, perhaps in a mechanism mediated by endogenous opioid activity.62,63 However, blockade of dopamine receptors with a dopamine antagonist or the administration of an opioid antagonist in breastfeeding women does not always affect gonadotropin secretion.64 The exact mechanism for the suppression of GnRH secretion remains to be unraveled. The importance of GnRH suppression by prolactin is reinforced by the demonstration that treatment of amenorrheic, lactating women with pulsatile GnRH fully restores pituitary secretion and normal ovarian cyclic activity.65
At weaning, as prolactin blood concentrations fall to normal, gonadotropin levels increase, and estradiol secretion rises. This prompt resumption of ovarian function is followed by the occurrence of ovulation within 14 to 30 days of weaning.
Prolactin concentrations are increased in response to the repeated suckling stimulus of breastfeeding. Given sufficient intensity and frequency, prolactin levels will remain elevated. Under these conditions, follicle-stimulating hormone (FSH) concentrations are in the low normal range (having risen from extremely low concentrations at delivery to follicular range in the 3 weeks postpartum) and luteinizing hormone (LH) values are also in the low normal range. These low levels of gonadotropins do not allow the ovary during lactational hyperprolactinemia to display follicular development and secrete estrogen. Therefore, vaginal dryness and dyspareunia are commonly reported by breastfeeding women. The use of vaginal estrogen preparations is discouraged because absorption of the estrogen can lead to inhibition of milk production. Vaginal lubricants should be used until ovarian function and estrogen production return.
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