Maternal Health Effects of Breastfeeding
Most studies of human lactation have focused on the quality and quantity of milk produced or on the effects of human milk on infants. Far fewer studies have targeted the effects of lactation on short- or long-term maternal health, and the subcommittee found no studies that evaluated the effects of maternal nutrition on long-term outcomes related to lactation. Reasons for this imbalance are unclear. The perception that the infant's level of risk during breastfeeding may be much higher than that of the mother is a potential factor responsible for a lack of interest in maternal outcomes. From a nutritional standpoint, however, the stress on the mother is substantial relative to the nutritional needs imposed by pregnancy (a condition that has attracted much more attention). The breastfed infant doubles its weight in the first 4 to 6 months after birth and has additional energy demands beyond the gains in energy stores associated with growth. The metabolic adjustments that redirect nutrient use from maternal needs to milk synthesis and secretion involve nearly every maternal organ system.
The decline in breastfeeding from the mid-1940s to the early 1970s (see Chapter 3) also may have been partially responsible for the lack of interest in long-term maternal health outcomes. Socioeconomic and demographic differences between groups that choose to breastfeed and those that choose to feed their infants formula and historical changes in the characteristics of populations who have chosen to breastfeed or formula feed may have discouraged population-based studies of the relationship between long-term maternal outcomes and lactation history.
This chapter focuses on limited examples of maternal health consequences
of lactation. Because the focus of this report is on healthy women, the discussion omits the influence of lactation on underlying chronic disease states, such as diabetes mellitus, cardiovascular disease, and cystic fibrosis. The discussion is subdivided into two sections: short-term effects (return of ovulation and maternal sexuality) and long-term effects (obesity, osteoporosis, and breast cancer). The effects of breastfeeding on maternal nutritional status are considered in Chapter 9.
SHORT-TERM HEALTH EFFECTS
Return of Ovulation
Lactation has long been known to increase the length of time between the delivery of a baby and return of regular ovulation. Despite considerable research on this subject, the mechanisms by which lactation exerts this effect on ovarian activity remain incompletely understood (see review by McNeilly et al. ). There is general agreement that suckling suppresses the pulsatile release of gonadotropin-releasing hormone from the hypothalamus and also stimulates the release of prolactin. Gonadotropin-releasing hormone is necessary for the pulsatile release of luteinizing hormone from the pituitary. Luteinizing hormone, in turn, is essential for maturation of the ovarian follicle and, thus, for ovulation. Any direct role prolactin might have in modifying ovarian function remains unresolved.
The characteristics of suckling by the infant appear to be the principal factors that affect the duration of postpartum anovulation (the period of functional importance) or amenorrhea (the length of time that is usually measured) in well-nourished lactating women (McNeilly et al., 1985). Frequency, intensity, and timing of suckling sessions all appear to influence the endocrinologic responses that modulate ovulatory status. These nursing characteristics change as lactation progresses, especially at the time solid foods are added to the infant's diet (Howie et al., 1981).
Maternal nutritional status during lactation may also be an important factor in regulating the duration of postpartum amenorrhea. Observational data show a clear association between poor maternal nutritional status and prolonged postpartum amenorrhea accompanied by persistently elevated prolactin values (see, for example, Hennart et al. ). However, interpretation of this association is not straightforward because there also are differences in suckling characteristics between the infants of well and poorly nourished women.
Several mechanisms have been proposed for the effect of maternal nutritional status on the duration of postpartum amenorrhea. Frisch (1978) hypothesized that a critical proportion of body fat is necessary for the return of normal ovarian function after delivery. Another idea is that the hormonal status that is characteristic of women with chronically inadequate food intake
prolongs postpartum amenorrhea (Lunn et al., 1984). Finally, the duration of postpartum amenorrhea might also be a function of (1) characteristics of the milk related to maternal nutritional status (such as volume, composition, and the rate of milk flow) that would lead to changes in the infant's breastfeeding behavior (such as the strength or duration of suckling) or (2) characteristics of the mother's interaction with her infant (number, timing, and duration of breastfeeding sessions) that may vary with her nutritional status (such as would be expected with seasonal agricultural labor and food shortages).
Interventions designed to improve nutritional status among poorly nourished women have consistently produced reductions in the length of postpartum amenorrhea (Bongaarts and Delgado, 1979; Chavez and Martinez, 1973; Lunn et al., 1981). These observations are in accord with the hypothesis proposed by Frisch (1978). However, from this hypothesis one would expect there to be an association between the attainment of a particular body composition and ovulation; this has not been supported by published data (Huffman et al., 1978) and remains controversial (Quandt, 1984).
Plasma concentrations of prolactin, cortisol, insulin, and triiodothyronine decreased in subjects in The Gambia in response to food supplementation during lactation (Prentice et al., 1983b). The authors' interpretation of these results was that supplementation had altered the subjects' state of metabolic adaptation to chronic malnutrition. These women also experienced the most dramatic decrease in the length of postpartum amenorrhea (from 66 to 42 weeks) that has been reported.
However, it is not clear if the consistent decrease in the duration of postpartum amenorrhea results directly from improved maternal nutritional status or from factors that vary with maternal nutritional status, such as the infant's breastfeeding behavior (which may be changed by alterations in milk composition or in the characteristics of the breastfeeding sessions). For example, in the Gambian study, a reduction in the number of daytime breastfeeding sessions (Prentice et al., 1983a) accompanied maternal supplementation, and there was anecdotal evidence of an increase in the women's work activities (Coward et al., 1984). Either of these changes could, in turn, influence maternal endocrinologic status and thereby the duration of postpartum amenorrhea.
Finally, another mechanism by which maternal nutritional status could influence the duration of postpartum amenorrhea is possible but has never been evaluated. In this possibility, enhanced maternal nutritional status would result in improved infant growth that, in turn, would increase the infant's suckling vigor and demand for milk. These differences could result in a lengthening of the duration of postpartum amenorrhea. Testing of this hypothesis requires a demonstrated change in milk volume, composition, or both in response to food supplementation and an appropriate assessment of the amenorrhea outcome.
It is of considerable importance to public health to understand the mechanism by which maternal nutritional status modifies the duration of postpartum
anovulation. Worldwide, breastfeeding provides important contraceptive benefits. Its potential usefulness for child spacing on an individual basis has been affirmed (Kennedy et al., 1989) and supported by a clinical trial (M. Labbok, Georgetown University Medical Center, personal communication, 1990; see guidelines used in Labbok et al. ). Thus, it would be wise to examine the time it takes to return to menses and ovulation in experimental studies designed to improve maternal nutritional status during lactation.
Few of the studies examining sexuality in the postpartum period have separated the effects of breastfeeding on sexuality from the changes in sexual receptivity and function that women normally undergo at this time (see the review by Reamy and White ). Because the hormonal changes that accompany lactation are likely modulators of mood and sexuality and because these changes are likely to vary with the intensity of breastfeeding (see Chapter 5), it is reasonable to expect that lactation will affect sexuality but that the effects may vary among lactating women.
In a laboratory study of six women during and after pregnancy, Masters and Johnson (1966) found that such sexual responses to stimulation as genital vasoconstriction and vaginal lubrication were sluggish in the first 3 months post partum and that orgasmic contractions were shorter and weaker. They attributed this to the reduced ovarian function that is normal during this period, and noted that these effects were more frequent among nursing mothers. They also found that the enlarged lactating breast did not consistently increase further in size during sexual arousal. Despite this, 24 nursing mothers queried (as part of a group of 24 nursing and 77 nonnursing women) in the third month after delivery rated their level of sexual interest higher than nonnursing mothers did. In addition to reporting sexual arousal induced by their infants' suckling on some occasions, they expressed interest in returning as soon as possible to sexual relations with their husbands. Masters and Johnson (1966) provide no data on breastfeeding frequency and describe duration only as having successfully nursed for at least 2 months.
These findings are contradicted by those of Alder and Bancroft (1988), who followed women longitudinally from early pregnancy through 6 months post partum. Women who breastfed reported later resumption of sexual intercourse despite antenatal measures of sexual arousal and motivation similar to those of bottle feeders. Within this group of breastfeeding women, the longer women breastfed, the longer they delayed resumption of intercourse. Alder and Bancroft (1988) associated this delay with the more frequent reports of painful intercourse among breastfeeding women, compared with those who bottle fed their infants. The pain has been attributed to poor vaginal lubrication resulting from low estrogen levels, a loss of sexual interest related to low androgen levels, and
maternal stress and fatigue associated with the demands of lactation and child care (Alder et al., 1986; Masters and Johnson, 1966).
Similar findings of reduced sexual response were reported by Kayner and Zagar (1983) among a self-selected group of lactating women whose nursing practices were judged to be intensive, based on reports of unrestricted nursing, frequent sleeping with the infant, and delayed introduction of formula or other food supplements for an average of 6.3 ± 1.99 (standard deviation) months. The period of amenorrhea was found to correlate strongly with the duration of reduced sexual desire.
Positive attitudes toward breastfeeding have been associated with the woman's comfort with her own sexuality (Newton, 1973), whereas negative feelings have been related to a dislike of nudity and sexual feelings (Newton and Newton, 1967). Thus, the positive association of breastfeeding and sexuality found by Masters and Johnson (1966) may be due in part to the highly self-selected nature of the breastfeeding sample used in their research. In addition, some women may meet their sensual and affectional needs by substituting breastfeeding and caretaking of infants for sexual activity (Kayner and Zagar, 1983; Lawrence, 1989; Waletsky, 1979).
The relationship of breastfeeding to female sexuality is therefore complex. The most informative studies thus far have included the collection of antenatal data, a longitudinal approach, and controls for socioeconomic factors. Further research should include those elements as well as controls for nursing intensity and evaluations of both endocrinologic responses and nonhormonal factors as determinants of sexuality.
LONG-TERM HEALTH EFFECTS
No comprehensive studies have been conducted in humans to examine the long-term maternal consequences of lactation on the prevalence and severity of, or predisposition toward, obesity. Some studies have been conducted in animals to examine the effects of pregnancy not followed by lactation on maternal body composition. In humans, studies have focused on energy expenditure, adjustments in the metabolism of adipose tissue, and changes in body weight during lactation and on maternal body mass at various times after lactation has ceased. Changes in the pattern of maternal energy expenditure during lactation are reviewed in Chapter 5.
Changes in Adipose Tissue
Studies in rats (Bogart et al., 1940; Jen et al., 1988; Moore and Brasel, 1984) indicate that pregnancy without subsequent lactation results in increased adipose tissue stores and increased fat cell numbers. Conversely, lactation
between pregnancies in rats reduces both of these indices of maternal obesity. Major differences between rats and humans in the relative energy costs of lactation, however, limit the inferences that can be made from studies in rats about the long-term health consequences in humans.
Studies of adipose tissue in lactating women (Lafontan et al., 1979; Rebuffe-Scrive et al., 1985) indicate that there are site-specific changes in the metabolism of energy stores during lactation. Basal rates of fat breakdown (lipolysis) are similar in femoral and abdominal adipose tissues in nonpregnant women, but are significantly higher in the femoral depot of lactating women. The lipolytic effect of noradrenaline administration is similar in both tissue sites during lactation but is much less in the femoral region of nonpregnant women and of women during early pregnancy.
In femoral adipose tissue, lipoprotein lipase activity decreases in lactating women; in abdominal adipose tissue, it remains about the same. Levels of adenosine, a locally acting insulin-like effector, have been reported to be lower in femoral than in abdominal adipocytes in lactating women; the lower levels may promote greater lipid mobilization from the femoral site (Stoneham et al., 1988). In nonpregnant and pregnant women, lipid assimilation appears to be favored in femoral sites over abdominal depots, and during lactation, lipid mobilization is favored in femoral adipose tissue.
Changes in Anthropometric Characteristics
Several investigators have followed anthropometric characteristics of well-nourished women (Brewer et al., 1989; Butte et al., 1984; Manning-Dalton and Allen, 1983; Morse et al., 1975; Naismith and Richie, 1975) and marginally nourished women (Adair et al., 1984; Brown et al., 1986; Harrison et al., 1975) during lactation (see also Chapter 4). In a few of those studies, fat stores were estimated. In general, anthropometric changes during lactation were minor. The range of mean daily energy deficits is reported to be 110 to 343 kcal/day in presumably well-nourished women living at home and followed longitudinally during lactation for 4 to 6 months (Brewer et al., 1989; Butte et al., 1984). These deficits could be expected to result in loss of approximately 2.6 to 7.9 kg (˜6 to 17 lb) of fat over 6 months.
The wide range of reported values for postpartum weight change among lactating women may be attributable to differences in baseline weight measurements. In some studies (e.g., Butte et al., 1984), baseline weights were obtained at approximately 35 days post partum, whereas others (e.g., Brewer et al., 1989) used maternal body weight on the first postpartum day as the basis for subsequent comparisons. The marked changes in fluid compartments in the early postpartum period most likely result in an overestimation of the net energy deficit when based on early postpartum weights. If the average energy deficit during lactation is closer to 110 than to 343 kcal/day (see above), it is unlikely
that adipose tissue stores accumulated during pregnancy will be mobilized fully after 4 to 6 months of lactation, especially with the higher weight gains now recommended during pregnancy (IOM, 1990).
Longitudinal data tend to support the view that the rate of maternal weight loss is higher during the first 4 to 6 months of continued lactation than it is with longer durations of breastfeeding (see Chapter 4). It is more difficult, however, to evaluate longer-term changes in body mass following lactation. Data on 49 women reported by Rookus and coworkers (1987) through 9 months post partum suggest that women who breastfeed for more than 2 months may gain more weight than women whose lactation is purposely suppressed by bromocriptin administration and others who breastfeed for less than 2 months. The analyses were adjusted for age, socioeconomic status, parity, maternal employment status, and smoking; however, only 18 women who breastfed for more than 2 months were studied, and no information was given regarding the extent to which all groups ate until satisfied or the extent to which specific strategies were used by the different groups to achieve weight changes. Data from the late 1940s indicate that weight changes may be similar 24 months post partum among women regardless of the duration of lactation (McKeown and Record, 1957).
Newcomb (1982) estimated the modifying effect of lactation on weight gain associated with increasing parity and found that the positive impact of parity on maternal body weight was 30% greater when parity was associated with subsequent lactation. However, the design of this study was limited: the method of feeding during the index pregnancy was used as a marker for the mode of feeding in previous pregnancies, and the duration and degree of breastfeeding were not defined.
Breastfeeding and the Onset of Obesity
The subcommittee found only two studies addressing the relationship between breastfeeding and the diagnosis of obesity whose onset was associated with pregnancy (Richardson, 1952; Sheldon, 1949). Sheldon (1949) found that approximately 65% of both obese and control women reported positive breastfeeding histories. Richardson (1952) retrospectively studied 40 women who became obese either during or soon after pregnancy and 30 women who became obese several years after their last pregnancy. He found that a significantly greater proportion of women whose obesity onset was related to pregnancy breastfed their infants than did the comparison group (87 and 55%, respectively). Among those in the pregnancy-related obesity group who breastfed, 19% became obese during pregnancy and the remainder became obese following delivery. These observations are limited by the lack of key information, such as maternal socioeconomic characteristics and the duration and degree of lactation.
There is little doubt that major physiologic adjustments influence energy
stores during lactation. Animal data support the view that excess fat is more likely to accumulate in women who do not breastfeed after pregnancy and who have adequate food intakes. The consequences of lactation on long-term maternal energy balance, however, are less clear in humans than in animals and require detailed investigation.
The calcium content in humans is approximately 23 g/kg of fat-free body mass (Avioli, 1980). In a 55-kg (121-lb) woman with approximately 25% body fat, the calcium content is approximately 900 to 1,000 g. A lactating woman with a milk output of 750 ml/day for 6 months loses approximately 50 g of calcium in milk, or about 5% of total body calcium. If one assumes that there are no changes in the efficiency of calcium absorption during lactation, approximately 660 mg of dietary calcium is needed, on average, to replace the 262 mg lost through milk per day. However, there is evidence from animal studies that calcium absorption rates may increase during lactation (Halloran and DeLuca, 1980). One should also consider that approximately 30 g of calcium is transferred to the fetus during gestation. Therefore, the rebuilding of maternal calcium stores, especially over successive pregnancies and lactations, is of potential concern in populations at risk of osteoporosis.
Bone metabolism during and after lactation is understood incompletely. Several mechanisms may act during pregnancy and lactation to ameliorate the impact of lactational demands for calcium. Serum osteocalcin levels are higher in lactating women early in the postpartum period compared with those of pregnant and of nonpregnant, nonlactating control women (osteocalcin is a hormone released at rates proportional to the formation of new bone). However, serum calcium and serum immunoreactive parathyroid hormone (iPTH) levels are unchanged, and no correlations have been reported between calcium and iPTH serum concentrations and osteocalcin serum concentrations (Cole et al., 1987). The higher osteocalcin levels nonetheless suggest that lactating women have higher bone turnover than those of the other groups studied. Data from a rat model suggest that osteoclast and osteocyte responses during pregnancy result in significantly greater bone mechanical strength (Currey, 1973). These responses and the decreased lacunar volume observed during lactation suggest that osteocytes are mobilized to deposit bone during pregnancy and serve as an effective buffer during lactation (Mercer and Crenshaw, 1985).
Few studies have been conducted to measure bone mineralization at distinct
periods of the reproductive cycle of women who have breastfed. In general, published studies suggest that bone mineralization decreases acutely in lactating women but that remineralization occurs in the postlactation period. Chan et al. (1982, 1987), Hayslip et al. (1989), Wardlaw and Pike (1986), and Tylavsky et al. (1989) reported acute bone loss among lactating women. Those studies have used single-or dual-photon absorptiometry to measure bone mineralization.
Studies in which bone mineralization has been examined at intervals following the cessation of lactation have shown either no effects or positive effects of lactation on bone mineralization. No effect was found when bone mineral content was measured by single- or dual-beam absorptiometry in women aged 25 to 37 (Koetting and Wardlaw, 1988) and in older women (mean age, 49 years) (Johnell and Nilsson, 1984). A preliminary report of a longitudinal study of women followed from before conception to 4 months after the cessation of lactation found a loss of bone mineralization with pregnancy and lactation and a recovery of losses in the postlactation period (Tylavsky et al., 1989).
In other studies, no effect was attributable to lactation when assessments were made by radiography in women aged 30 to 44 subdivided into two groups that had breastfed for relatively long periods (presumably more than 6 months): those who had one or two children, and those who had seven or more children (Walker et al., 1972). Similarly, no effect was found in investigations by Alderman and coworkers (1986) of the relation between reproductive history and the occurrence of hip and forearm fractures in postmenopausal women (over age 50).
In contrast to those studies, Aloia and colleagues (1983) reported that 80 white, postmenopausal women (mean age, 52 years) who had breastfed had a higher bone mass than those who had not breastfed. Bone mass was measured by total body neutron activation analysis and photon absorptiometry of the distal radius. Breastfeeding and pregnancy were associated with higher bone mass. In a subsequent comparison of 58 women with postmenopausal osteoporosis and 58 age-matched normal women, osteoporotic women were found to have undergone an earlier menopause (age 46 years versus 49 years, respectively), smoked cigarettes more (59 versus 30%, respectively), and breastfed less (16 versus 35%, respectively), than controls (Aloia et al., 1985).
Hreshchyshyn et al. (1988) examined the relationship between parity, breastfeeding, and bone densities of the lumbar spine and femoral neck. Measurements were obtained by dual-photon absorptiometry in 588 ambulatory white women aged 21 to 95. No statistically significant differences in lumbar spine bone mineral density were detected between women who had breastfed compared with those who had not; however, parous women who breastfed longer than 2 weeks had higher bone mineral density than those who had not. Breastfeeding was reported to increase lumbar spine density by 1.5% per breastfed child. Femoral neck density was not related to lactation history.
These data suggest that acute bone loss is likely to occur during lactation;
however, the magnitude of the losses is difficult to estimate from the few published data. Assessments in older women suggest either than calcium repletion occurred more effectively among women who had lactated or that other behavioral characteristics among that group promoted enhanced bone mass over the long-term. The data are not conclusive. Future studies should focus greater attention on the definition of breastfeeding, the estimation of calcium intakes, and an improved definition of the interval between measurements of interest and timing of breastfeeding.
The association of lactation history with a variety of cancer risks has been examined sporadically (Kvåle and Heuch, 1987). Breast cancer has received the most attention, but the biologic plausibility of a relationship between a positive lactation history and reduced risk of breast cancer has not been well described (deWaard and Trichopoulos, 1988; Henderson et al., 1985; Kelsey and Berkowitz, 1988; Korenmon, 1980; Yuan et al., 1988). In general, the link to breast cancer is believed to be the modifying effect of lactation on the potential exposure of the breast to estrogen and other steroids during the reproductive period.
Factors usually related to breast cancer have been age, country of birth, socioeconomic class, place of residence, race, age at first full-term pregnancy, oophorectomy, body build, age at menarche, age at menopause, family history of premenopausal bilateral breast cancer, history of cancer in one breast, fibrocystic disease, primary cancer in an ovary or in the endometrium, radiation to the chest, or first-degree relatives with breast cancer (Kelsey and Berkowitz, 1988). Lactation history was not listed. MacMahon et al. (1970) reported that although nulliparous women had a greater risk of breast cancer than parous women did, neither parity nor lactation had an effect on risk after controlling for the age at the first full-term pregnancy.
Byers and colleagues (1985) summarized the findings of 17 epidemiologic studies of the relationship between lactation and breast cancer risk reported between 1966 and 1983. Relative risks associated with ''ever" having breastfed were calculated for women of all ages in 15 of the studies; in 10 of those studies, the relative risk was less than 1.00, denoting a protective effect. Relative risk associated with "ever" having breastfed among women younger than age 50 was less than 1.00 in 11 of the 13 studies in which this estimate was made. Among women over age 50, the relative risk was less than 1.00 in only 5 of the 12 studies that estimated risk for that population.
Byers et al. (1985) also reported the results of a case-control study of 453 white women with breast cancer and 1,365 white women without breast cancer selected randomly from the same geographical area. A negative association between lactation and breast cancer risk (which implies a protective effect of
lactation) was reported among premenopausal women and was not accounted for by other associated variables, namely, age, parity, age at menarche, age at first pregnancy, years of education, or stopping lactation because of insufficient milk.
Several other investigators (Layde et al., 1989; McTiernan and Thomas, 1986; Tao et al., 1988; Yuan et al., 1988) also reported a protective effect of breastfeeding against cancer. In some studies, protection was found in both premenopausal and postmenopausal women. In all, the protection appeared to increase with increasing duration of lactation. The degree of protection afforded by various durations of breastfeeding, however, was highly variable among studies, even though analyses were adjusted for parity, age at first full-term pregnancy, age at interview, and other potentially confounding or modifying variables. The wide range of protection (odds ratios varied from 0.4 to 0.8) is probably due to nonreproductive risk factors related to breast cancer.
Other reports present less consistent findings or conclude that breastfeeding is not protective. Kvåle and Heuch (1987) evaluated relationships between previous lactation experience and risk of breast cancer in 50,274 parous Norwegian women (approximate age range, 20 to 69 years) studied prospectively between 1961 and 1980. A nonlinear relationship was reported between duration of lactation per birth and risk of breast cancer: that is, for the first, second, and third births the highest risk was observed for those with an intermediate duration of breastfeeding (4 to 10 months), and the lowest risk was observed for those with short (less than 4 months) or long (greater than 12 months) durations. The total duration of breastfeeding for all children showed significant inverse associations with breast cancer, but no consistent relationship was detected when results were adjusted for parity.
London and colleagues (1990) examined the relationship between breast cancer and lactation in a cohort of 89,413 parous women (age range, 30 to 55 years) who were free from cancer in 1976 and provided retrospective information on the total duration of lactation through 1986. No relationship between the risk of breast cancer and the duration of lactation (≤23 months) was observed in this study after adjustments for age and parity.
The reasons for the discrepancies among studies are not clear. Disagreement among studies may be due to different methods and designs (e.g., variations among methods used to ascertain lactation duration, selection and characterization of controls, and retrospective compared with prospective approaches), diverse lactation practices among distinct cohorts, differences in diets or other nonreproductive factors among various populations, or any combination of these.
A better understanding of breastfeeding's effects could be expected from increased knowledge of mammary gland functions that modulate the risk of breast cancer and from more detailed consideration of nursing histories, duration of breastfeeding for each child, extent of breastfeeding, intervals between
pregnancies, maternal diet and body composition, and other factors appropriate to individual environments (Byers et al., 1985).
Lactation normally delays the return to regular ovulation. The effect of maternal nutritional status on this delay is not understood. Although lactation provides important contraceptive benefits on a worldwide basis, it is not a dependable method of contraception for individuals.
Lactation appears to have a negative impact on sexuality; however, the relationship between both functions is complex and requires further study to understand the factors that modulate this relationship.
There are insufficient data to determine whether lactation influences maternal risk of adult-onset obesity.
There are insufficient data to determine whether lactation influences maternal risk of osteoporosis.
Most recent epidemiologic evaluations suggest that breastfeeding may be protective against breast cancer, but there is conflicting evidence.
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