The Journal of Nutrition Vol. 128 No. 2 February 1998,
pp. 381S-385S
Body Composition Changes during Lactation Are Highly Variable among Women1,2
Nancy F. Butte3 and
Judy M. Hopkinson
USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX 77030
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ABSTRACT |
Changes in body weight and composition in response to the metabolic load imposed by lactation are highly variable among and within diverse populations. In most reports, rates of weight loss did not differ between lactating and nonlactating women. Despite differences in the hormonal milieu between lactating and nonlactating women, only subtle short-term differences were observed in postpartum changes in body composition. Regional patterns of fat deposition and mobilization did not differ between lactating and nonlactating women in most studies. Changes in body composition during lactation are responses to a sequence of complex neuroendocrine and biochemical stimuli that may be significantly modified by environmental factors. Gestational weight gain was the strongest determinant of postpartum weight and fat mass change, which supports the premise that biological mechanisms are aimed at restoring prepregnancy body weight and composition.
KEY WORDS:
lactation ·
body composition ·
anthropometry ·
fat-free mass ·
fat mass
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INTRODUCTION |
Robinson (1986) succinctly put forth the following basic tenets describing changes in body composition during reproduction and lactation. "Changes in the maternal body during reproduction are characterized by their diversity and this holds true for comparisons within as well as between species. An anticipatory role for the maternal body during reproduction occurs in a number of species, including humans, that tend to deposit fat in their bodies during pregnancy and lose it during lactation. Changes in body composition during reproduction are responses to a sequence of complex neuroendocrine and biochemical stimuli that follow on from conception and which are modified in their expression by the constraints imposed by the environment. The nutritional aim must be to produce balance in the composition of the body over the breeding cycle as a whole."
In this review we will examine evidence that supports or refutes the application of these basic tenets in humans. It is generally recognized that the metabolic demand imposed by lactation in humans is relatively low, compared with other species (Prentice and Prentice 1988). In primates, the requirements for lactation are 4- to 15-fold lower than in laboratory and domesticated animals, relative to weight0.75. To meet the metabolic costs of lactation, different species use adaptive strategies to varying degrees. An animal can increase food intake, mobilize tissue stores, increase metabolic efficiency or reduce energy expenditure.
Lactation requires both an increased supply of nutrients and development of mechanisms that ensure the preferential use of nutrients by the mammary gland. Lactation is characterized by enhanced episodic secretion of prolactin and oxytocin, suppression of the hypothalamic-pituitary-gonadal axis and hypoinsulinemia (Vernon 1989). Withdrawal of estrogen and progesterone is a prerequisite for lactogenesis, because these sex steroids inhibit the lactogenic effects of prolactin. Prolactin acts locally at the mammary gland to stimulate synthesis and secretion of milk components, but it also depresses lipogenesis in the liver and adipose tissue and increases delivery of glucose and lactate, lipogenic precursors, to the mammary gland. Insulin sensitivity is enhanced in the mammary gland and diminished in muscle and adipose tissue, reducing lipogenesis in the periphery. Adipocytes appear to have increased sensitivity to lipolytic stimulation during lactation (McNamara 1995). Lipolysis was increased in response to norepinephrine stimulation in adipocytes taken from the femoral region of lactating women (Rebuffé-Scrive et al. 1985). In the postabsorptive state, plasma insulin, cortisol and thyroxine concentrations tended to be lower in lactating than in nulliparous women (Motil et al. 1994). Response of the hypothalamic-pituitary-adrenal axis to exercise-induced stress was altered during lactation (Altemus et al. 1995). Basal plasma norepinephrine was reduced, and the rise in plasma adrenocorticotrophin, cortisol and glucose during exercise was attenuated in lactating women compared with nonlactating controls. In theory, these neuroendocrine changes could conserve energy and spare substrate for milk synthesis, and facilitate nutrient delivery to the mammary gland. Lactation alters the hormonal milieu and responsiveness in favor of lipolysis.
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POSTPARTUM CHANGES IN BODY WEIGHT |
In theory, lactation is supported partially by mobilization of tissue stores. However, it is evident from the literature that postpartum weight changes in lactating women are highly variable within and across populations.
Most lactating women experience a mild, gradual weight loss in the first 6 mo postpartum. Mean rates of weight change reported for affluent and underprivileged lactating women are summarized in Table 1. Mean rates of weight loss in the first 6 mo postpartum are generally greater in affluent populations (
0.8 kg/mo) than in underprivileged populations (
0.1 kg/mo). Differences in mean weight changes likely are due to differences in gestational weight gains, cultural practices, physical activity level and seasonal food availability. However, in all studies, the mean value does not convey the high variability observed among individuals. Weight loss is not inevitable; postpartum weight gain was observed among some subjects in several studies (Adair et al. 1983, Allen et al. 1994, Barbosa et al. 1997, Butte et al. 1984, Dewey et al. 1993, Manning-Dalton and Allen 1983, Prentice et al. 1981).
Studies comparing postpartum weight changes in lactating and nonlactating women are equivocal and often inconclusive, because of the lack of information provided on the intensity and duration of breast-feeding and dieting practices. Several investigators have failed to detect an effect of breast-feeding on postpartum weight change (Boardley et al. 1995, Brewer et al. 1989, Dugdale and Eaton-Evans 1989, Öhlin and Rössner 1990, Parker and Abrams 1993, Schauberger et al. 1992). In other reports, formula-feeding women lost more weight than lactating women (Newcombe 1982, Potter et al. 1991, Richardson 1952, Rookus et al. 1987). A few studies have found greater weight loss among breast-feeding women (Dennis and Bytheway 1965, Dewey et al. 1993, Kramer et al. 1993, McKeown and Record 1957). Of the factors associated with postpartum weight change, gestational weight gain is by far the most consistent and strongest predictor across all studies. Other factors sometimes identified include prepregnancy weight, age, parity, race, smoking, exercise, return to work outside the home and lactation. In those studies in which lactation was statistically significant, it appeared to be a minor contributor to the overall variability in postpartum weight change. The biological drive to restore prepregnancy body mass, which is also evident in animal studies (McNamara 1995), apparently overwhelms the effects of other maternal characteristics.
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POSTPARTUM CHANGES IN ADIPOSITY |
Fat deposition and mobilization vary topographically throughout the reproductive cycle and lactation period. Although the mechanisms underlying this site specificity are poorly understood, there is evidence of regional differences in lipoprotein lipase (LPL)4 activity and lipolytic responsiveness to norepinephrine during reproduction (Rebuffé-Scrive et al. 1985). During pregnancy, fat is deposited preferentially at the thigh, and to a lesser extent (in descending order) at the suprailiac, subscapular, costal, biceps and triceps sites (Taggart et al. 1967). High estrogen levels during pregnancy promote a gynoid type of fat distribution (gluteofemoral). Increases in body fat, absolute as well as proportional, are greatest at central sites and least at peripheral sites. During lactation, the pattern is reversed: fat is mobilized from the trunk and thighs (Butte et al. 1984, Sohlström and Forsum 1995). Low levels of estrogen may favor partitioning of body fat to the upper body.
Lactation-associated changes in body fat have been predicted from measurements of skinfold thicknesses. In general, most skinfold thicknesses decrease along with weight loss, with the exception of the triceps skinfold, which has been shown to increase in the postpartum period (Adair et al. 1983, Brewer et al. 1989, Dugdale and Eaton-Evans 1989, Forsum et al. 1989, Manning-Dalton and Allen 1983).
In our experience with well-nourished lactating women (n = 45) studied longitudinally for the first 4 mo postpartum, triceps and biceps skinfold thicknesses did not change significantly, whereas the suprailiac and subscapular skinfolds decreased significantly (Butte et al. 1984). Body fat predicted from skinfold thickness did not differ from values measured by underwater weighing; body fat declined from 28 to 26-27% over the 4 mo. Decreases in skinfold thicknesses at the suprailiac, subscapular, thigh and costal sites in lactating women also have been reported by others (Brewer et al. 1989, Forsum et al. 1989, Manning-Dalton and Allen 1983, Prize 1983). We have recently monitored anthropometric changes for 12 mo postpartum in a group of women from Houston, Texas (unpublished). The rate of weight change over the 12 mo postpartum (lactating:
0.41 ± 0.36 kg/mo; nonlactating:
0.30 ± 0.56 kg/mo) did not differ significantly between lactating (n = 40) and nonlactating women (n = 36). An initial increase at the triceps site was seen in both groups; subcutaneous fat at the suprailiac, subscapular and thigh sites decreased similarly in lactating and nonlactating women (Fig. 1).

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| Fig 1.
Skinfold thicknesses measured in lactating (n = 40) and nonlactating women (n = 36) for 12 mo postpartum. Data are displayed as means ± SEM.
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Anthropometric measurements also have been used to assess nutritional status and changes in energy reserves of underprivileged women during lactation. Changes in skinfold measurements paralleled observed weight losses (Adair et al. 1983, Prentice et al. 1981, Schutz et al. 1980) or weight gains (Adair et al. 1983, Brown et al. 1986).
In a recent review, Dorea (1997) compiled studies relating changes in body weight and skinfold thicknesses in lactating women from affluent and underprivileged populations. Inconsistencies were seen in the direction and magnitude of the changes, which were method dependent. There was poor correspondence between the change in weight and change in skinfold thickness across studies, particularly if the change in adiposity relied solely on the triceps measurement. Certain skinfold thicknesses may be indicative of fat deposition or redistribution patterns, but are unreliable for the prediction of changes in total body fat.
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POSTPARTUM CHANGES IN BODY COMPOSITION |
Body composition changes during lactation are a function of the species, stage of lactation and nutritional state (Robinson 1986). With the high metabolic demands of lactation, the liver, gastrointestinal tract and walls of the stomach enlarge in species as diverse as sheep and rats. Mammary gland proliferation continues in some species. Blood volume expansion noted in pregnancy may be sustained or even slightly increased in early lactation. Increased tissue hydration during pregnancy, due primarily to an increase in extracellular fluid, can persist into lactation in sheep, pigs and humans. We observed a higher hydration of fat-free mass (FFM) in lactating women compared with nonlactating women at 15 d postpartum (Hopkinson et al. 1997).
Mobilization of body fat is a general feature of lactation, but the magnitude varies within and among species (Robinson 1986). The energy content of the weight change can vary depending on the diet and nutritional state of the animal. Interestingly, the high metabolic demand that lactation places on smaller mammals is not reflected by a greater dependence on maternal lipid reserves, but on a tremendous increase in appetite and dietary intake. Anthropometric data suggest that women depend on mobilization of body fat to a limited extent, and therefore must increase dietary intake to meet the increased needs of lactation.
Longitudinal studies on changes in body composition of lactating women are extremely limited. Sadurskis et al. (1988) monitored body fat changes in 23 Swedish women for 6 mo postpartum; fat mass decreased from 30.4 to 29.6% by 18O dilution and from 32.9 to 31.9% by total body potassium counting. Consistent with a minor weight loss and sedentary lifestyle, a small sample of British women (n = 10) displayed a nonsignificant increase (from 30.3 to 31.4% between 1 and 3 mo postpartum) in fat mass estimated by 2H and 18O dilution (Goldberg et al. 1991). We measured body fat changes in well-nourished American women (n = 45) for 4 mo postpartum using underwater weighing (Butte et al. 1984). Body fat decreased from 28.0% at 1 mo to 26.3% at 4 mo, providing 137 kcal/d.
More recently, we measured body composition changes in lactating (n = 40) and nonlactating women (n = 36) for 1 y postpartum using total body potassium counting and a four-component model based on total body water by 2H dilution, body volume by underwater weighing and bone density by dual-energy X-ray absorptiometry (Hopkinson et al. 1997). Lactating women lost significantly more potassium and water between 0.5 and 3 mo postpartum than nonlactating women, which resulted in a greater loss of FFM (unpublished). Fat mass declined linearly over the 12 mo postpartum in both groups; the change in fat mass between 3 and 6 mo was greater in lactating women (Fig. 2). Interestingly, weight losses of lactating women were greatest between 3 and 6 mo in other reports of American and Swedish women (Brewer et al. 1989, Dewey et al. 1993, Öhlin and Rössner 1990).

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| Fig 2.
Total body and regional fat mass (FM) measured by dual-energy X-ray absorptiometry in lactating (n = 40) and nonlactating women (n = 36) for 12 mo postpartum. Data are displayed as means ± SEM.
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Changes in adipose tissue volume (ATV) in 15 Swedish women were measured by magnetic resonance imaging through pregnancy and lactation (Sohlström and Forsum 1995). The women breast-fed for 2-10 mo. In pregnancy, the majority of the fat deposition was localized subcutaneously. Of the total fat deposited, 46% was localized in the lower trunk, 32% in the upper trunk, 16% in the thighs, 1% in the calves, 4% in the upper arms and 1% in the forearms. In the first 6 mo postpartum, the subcutaneous region accounted for the entire reduction in ATV, which decreased from 30.6 to 27.4 L; nonsubcutaneous ATV actually increased. ATV decreased in the lower and upper trunk, as well as the thighs. Fat mobilization from the thighs was the most consistent and complete in all women. Hormonally induced changes in LPL may explain the preferential use of fat at the thigh (Rebuffé-Scrive et al. 1985), but the thigh was a minor contributor overall. At 12 mo postpartum, the women had 2.1 kg more body fat than before pregnancy, localized primarily on the trunk.
Few studies have examined the effect of lactation on body fat distribution. In vitro evidence of lactation-induced changes in LPL activity suggest preferential mobilization of body fat from the femoral region (Rebuffé-Scrive et al. 1985). Björkelund and co-workers (1996) studied the effect of reproductive history on body fat distribution in 1462 Swedish women. Lactation duration did not have an independent effect on long-term waist-to-hip ratio (WHR) or body mass index. Troisi (Troisi et al. 1995) reported a weak inverse association between lactation duration and WHR. We compared regional changes in fat mass in postpartum women for 1 y postpartum using dual-energy X-ray absorptiometry (unpublished). We did not detect any significant differences in fat mobilized from the trunk, arms or legs in lactating and nonlactating women (Fig. 2).
In conclusion, Robinson's tenets describing changes in body composition during reproduction and lactation are applicable to lactating women (Robinson 1986). Changes in weight and fat mass in response to the metabolic load imposed by lactation are highly variable among and within diverse human populations. In most reports, rates of weight loss did not differ between lactating and nonlactating women. Despite differences in the hormonal milieu between lactating and nonlactating women, only subtle short-term differences were observed in postpartum changes in body composition. Regional patterns of fat deposition and mobilization did not differ between lactating and nonlactating women in most studies. Gestational weight gain was the strongest determinant of postpartum weight and fat mass change, which supports the premise that biological mechanisms are aimed at restoring prepregnancy body weight and composition. However, changes in body composition during reproduction and lactation are responses to a sequence of complex neuroendocrine and biochemical stimuli that may be significantly modified by environment factors. For the health and well-being of women, the nutritional aim should be to produce balance in the composition of the body over the pregnancy-lactation cycle as a whole.
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FOOTNOTES |
1
Presented as part of the symposium "Maternal Body Composition, Caloric Restriction and Exercise during Lactation" given at the Experimental Biology 97 meeting, April 8, 1997, New Orleans, LA. This symposium was sponsored by the International Society for Research on Human Milk and Lactation and the American Society for Nutritional Sciences and was supported in part by educational grants from the Carnation Nutrition Products Division, the Gerber Foundation, Ross Products Division, Abbot Laboratories and Wyeth-Ayerst International. Guest editors for the symposium publication were Kathryn G. Dewey, University of California, Davis, CA and Cheryl A. Lovelady, University of North Carolina, Greensboro, NC.
2
Supported by the U.S. Department of Agriculture, Agricultural Research Service, under Cooperative Agreement Number 58-6250-1-003. This work is a publication of the USDA/ARS Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX. The contents of this publication do not necessarily reflect the views or policies of the U.S. Department of Agriculture, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. government.
3
To whom correspondence and reprint requests should be addressed: Children's Nutrition Research Center, 1110 Bates, Houston, TX 77030.
4
Abbreviations used: ATV, adipose tissue volume; FFM, fat-free mass; LPL, lipoprotein lipase; WHR, waist-to-hip ratio.
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