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ORIGINAL RESEARCH COMMUNICATION |
1 From the Cincinnati Childrens Hospital Medical Center, Division of General and Community Pediatrics, Cincinnati
2 Supported by grants R01 AR41366 and M01 RR08084 from the General Clinical Research Centers program, National Center for Research Resources, National Institutes of Health.
3 Address reprint requests to KS Wosje, Cincinnati Childrens Hospital Medical Center, 3333 Burnet Avenue, MLC 7035, Cincinnati, OH 45229. E-mail: karen.wosje{at}cchmc.org.
| ABSTRACT |
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Objective: We addressed the following questions: 1) whether lactation enhances loss of fat mass, and 2) whether loss of fat mass during lactation and after weaning is greater in women receiving calcium supplementation than in women receiving placebo.
Design: We used data from 87 lactating and 81 nonlactating women enrolled in a randomized, double-blind, calcium supplementation trial from 2 wk to 6 mo postpartum and data from 76 previously lactating and 82 nonlactating women enrolled in a parallel trial from 6 to 12 mo postpartum. Body fat and lean masses were measured by using dual-energy X-ray absorptiometry.
Results: Nonlactating women lost whole-body, arm, and leg fat at a faster rate than did lactating women between 2 wk and 6 mo postpartum (lactation group x time effect, P
0.01). Fat mass of the trunk, arms, and legs decreased between 6 and 12 mo postpartum regardless of previous lactation status (time effect, P
0.001). Calcium supplementation did not affect postpartum fat loss.
Conclusions: Body-composition changes occur differently in nonlactating and lactating women during the first 6 mo postpartum and occur at some sites until 12 mo postpartum regardless of previous lactation status. Clinicians should use caution when advising lactating mothers about expected rates of postpartum fat loss. Calcium supplementation (1 g/d) does not promote postpartum weight loss or fat loss.
Key Words: Lactation weaning postpartum women body composition calcium fat mass obesity breastfeeding
| INTRODUCTION |
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The extent to which lactation results in fat loss is unclear. Many studies indicate that weight lost during lactation consists primarily of fat mass (3-5). Some (6, 7), but not all (8, 9), studies found no difference in postpartum anthropometric or body-composition changes according to lactation practice when other factors, such as gestational weight gain, were taken into account. Butte and Hopkinson (9) described differences in postpartum body-composition changes between lactating and nonlactating women as subtle and short term.
Because of the hypothesized fat mobilization during lactation, breastfeeding is often cited as a factor that facilitates postpartum weight loss. Dewey et al (8) showed that breastfeeding mothers lost more weight than formula-feeding mothers between 1 and 12 mo postpartum and that greater frequency of and time spent breastfeeding were associated with greater weight loss. However, another study indicated that lactation status or amount of breastfeeding did not significantly influence postpartum weight change (10). One reason for this lack of influence may be higher energy intakes in lactating women than in nonlactating women (11-13). The higher energy intake of lactating women may be a physiologic consequence of elevated concentrations of prolactin, an appetite stimulant (14). Theoretically, the reduction in prolactin concentrations after weaning may result in decreased appetite and energy intake, but little is known about the influence of weaning on postpartum changes in weight and body composition.
Parikh and Yanovski (15) recently reviewed evidence on calcium and adiposity and concluded that increasing calcium or dairy intake may inhibit gains in weight or fat mass. Zemel (16) proposed that low dietary calcium intake increases circulating 1,25-dihydroxyvitamin D [1,25(OH)D2] concentrations, which stimulates calcium influx into adipocytes and thereby results in suppression of lipolysis and increased lipogenesis. Influences of supplemental calcium on changes in weight and fat mass in postpartum women are unknown. We used data from a randomized, double-blind trial designed to determine the effects of calcium on bone mass during lactation and after weaning to address the following questions: 1) whether lactation enhances loss of fat mass during lactation and after weaning, and 2) whether loss of fat mass during lactation and after weaning is greater in women receiving calcium supplementation than in women receiving placebo.
| SUBJECTS AND METHODS |
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37 wk of gestation and had taken vitamins during pregnancy. None of the women participated in both the lactation study and the weaning study.
A total of 97 lactating and 99 nonlactating women were enrolled in the lactation study. The lactating women intended to breastfeed for
6 mo and to provide no more than one formula feeding per day. The nonlactating women fed their infants exclusively with formula. Measurements were obtained at enrollment [2.3 ± 0.2 wk postpartum (
± SD)] and at
3 and 6 mo postpartum. A total of 95 lactating and 92 nonlactating women were enrolled in the weaning study. In the weaning study, the women were enrolled at 23.3 ± 3.4 wk postpartum (baseline), and measurements were obtained at baseline and
9 and 12 mo postpartum. The lactating women in the weaning study were fully breastfeeding at enrollment and weaned their infants during the 2 mo after enrollment. The nonlactating women from the weaning cohort either had not breastfed their infants at all or had breastfed for
2 wk. Of the 383 women enrolled, 8 lost interest (6 from the lactation study), 13 became ill or required medication or iron supplementation (7 from the lactation study), 5 started using hormonal contraceptives (all from the lactation study), 6 were lost to follow-up (3 from the lactation study), 11 became pregnant (3 from the lactation study), 4 weaned their infants early (all from the lactation study), 1 could not swallow pills (from the weaning study), and 9 did not wean their infants within 3 mo after enrollment (all from the weaning study).
The original study was approved by the Institutional Review Board of Cincinnati Childrens Hospital Medical Center. All participants provided written informed consent.
Study procedures
In both the lactation study and the weaning study, participants were randomly assigned to receive either 1 g CaCO3/d (Os-Cal; Marion Merrell Dow, Kansas City, MO) or placebo. Compliance with calcium or placebo supplementation was determined by pill count. Randomization was blocked according to age, race, and lactation status (breastfeeding or formula feeding). All the women received a daily multivitamin containing 400 IU vitamin D (Dayalets; Abbott Laboratories, North Chicago, IL).
The participants kept records of the occurrence of menses and provided 3-d food-consumption records and 7-d physical activity logs during the week preceding both the second and third visits. Estimates of average daily intakes of energy and calcium were calculated by using NUTRITION DATA SYSTEM (Nutrition Coordinating Center, University of Minnesota, Minneapolis). Hours per week spent sleeping and participating in moderate (eg, house painting and lawn mowing), hard (eg, heavy gardening and walking fast), and very hard (eg, jogging and physical labor) exercise were estimated from the 7-d physical activity logs on the basis of the methods of Sallis et al (18).
Body composition (fat and lean masses) was measured by using dual-energy X-ray absorptiometry (QDR 1000W or 2000; Hologic, Waltham, MA). All measurements from a given subject were obtained with the same machine. Trunk, arm, and leg values for fat mass and lean mass were obtained from the subregion analysis of the whole-body scan. The average of the left and right limbs was used for arm and leg measures. Whole-body percentage fat values were calculated as whole-body fat (in kg) divided by whole-body mass (in kg). The CVs ranged from 1.30% to 2.03% for whole-body lean mass and from 0.88% to 1.13% for whole-body fat mass.
Statistical analyses
Students t test or Pearson chi-square was used to compare baseline and descriptive characteristics between lactation groups. Data for the studies of lactation and weaning were analyzed separately by using similar statistical methods. Repeated-measures analyses were carried out on the raw data from all 3 time points for each response variable. Whole-body, trunk, arm, and leg fat masses were considered as primary outcomes of interest. Whole-body percentage fat, lean mass, and body weight were also included as outcomes. Data were analyzed with a mixed model approach by using the MIXED procedure of SAS version 8.02 (SAS Institute Inc, Cary, NC), and the REPEATED statement was used to model within-subject (subject within lactation group by calcium group) variation with covariance structure autoregressive order one. A model containing the effects of lactation group, calcium group, and time (ie, visit), as well as all possible interactions, was first obtained. The three-way interaction term was not significant and was therefore not considered in any further model-selection procedures. In determining the statistical significance (P
0.05) of lactation group x time (ie, the lactation effect) and calcium supplementation group x time (ie, the calcium effect), the following covariates were included in all statistical models because of their potential influence on body fat and lean masses: height, dietary calcium intake (averaged from the second and third visits), and gestational weight gain. If either interaction term was significant, both interaction terms were retained in the final model. If neither interaction term was significant, a reduced model to test for the main effect of time was examined. After determining final models by using the above procedures, we simultaneously entered energy intake and hours spent in hard or very hard activity (both variables were averages from the second and third visits) into the models. We did not include energy intake or activity as covariates in the initial model-selection procedures because of the potential for "overcontrolling" for these factors, which we felt might be influenced by lactation. The inclusion of energy intake and activity in the final models did not affect our conclusions; therefore, the data presented are from models that did not include these covariates.
To illustrate the pertinent findings, data are presented as changes over time. Least-squares mean estimates were obtained from the SAS output for the repeated-measures analyses, which included in the model the lactation group x calcium group x time interaction and the covariates described above. For example, the least-squares mean for change in weight between visits 1 (2 wk postpartum) and 2 (3 mo postpartum) in nonlactating women receiving calcium was taken from the SAS output as the difference between the least-squares mean for visit 1 and the least-squares mean for visit 2 for that group of women. SAS also provided the SE for each estimate of the difference between least-squares means, and these SEs are reported here.
| RESULTS |
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80% of their pills, and 73% of the women took
90%. In both studies, the calcium and placebo groups did not differ significantly in any of the measures presented in Table 1
± SD) across all groups of women. In the lactation study, the nonlactating women were slightly taller than the lactating women and had significantly lower energy and calcium intakes and reported spending significantly more time engaged in hard and very hard exercise during the study. All the nonlactating women reported resumption of menses by 6 mo postpartum, in comparison with only 22% and 29% of the lactating women who were receiving calcium and placebo, respectively. Body weight, whole-body percentage fat, and whole-body fat and lean masses were not significantly different between the nonlactating and the lactating women in the lactation study. Regional fat and lean masses also were not significantly (P
0.1 for all) different between lactation groups at enrollment in the lactation study. In the weaning study, the nonlactating women were significantly heavier at enrollment than were the lactating women and had significantly higher whole-body percentage fat and fat and lean masses in the whole body and in all subregions (P
0.05) except for the leg (fat mass, P = 0.10; lean mass, P = 0.08). In the weaning cohort, 98% of the nonlactating women reported resumption of menses by 6 mo postpartum, in comparison with 13% and 16% of the previously lactating women who were receiving calcium and placebo, respectively.
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0.9). Trunk fat loss occurred between 2 wk and 6 mo postpartum in all the women regardless of lactation or calcium group. Changes in body weight, whole-body percentage fat, and lean mass between 2 wk and 6 mo postpartum are shown in Table 2
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| DISCUSSION |
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Pregnancy-induced body fat deposition occurs largely at central sites (ie, trunk and thighs) (9). Although data on alterations in body fat distribution during lactation and after weaning are sparse, these same fat depots also appear to be the primary energy sources mobilized to support lactation (9). We found that whereas the nonlactating women lost fat mass at all sites and achieved reductions in whole-body percentage fat, the lactating women appeared to support milk energy output by mobilizing trunk and leg fat (but gained arm fat) and did not experience significant changes in whole-body percentage fat. Our findings of higher rates of fat loss in the nonlactating women differ from those of Butte et al (19), who reported that changes in whole-body fat mass and fat-free mass, as measured by using a 4-compartment model, did not differ between nonlactating and lactating women during the first 6 mo postpartum. Furthermore, Butte and Hopkinson (9) found no indication that postpartum changes in arm and leg fat were different between nonlactating and lactating women over 1 y of follow-up. To our knowledge, there are no other reports on changes in regional fat and lean masses among postpartum women who used different infant feeding practices. Thus, further clarification as to whether postpartum changes in regional fat distribution differ by lactation status is necessary.
Estrogen and androgens are endocrine regulators of energy partitioning and body composition. Hypoestrogenemia and an increased androgen-estrogen ratio are accompanied by an increase in the ratio of trunk fat to leg fat (ie, shift to abdominal fat distribution) in women as they transition through menopause. Lactating women are hypoestrogenemic, and there is evidence that circulating concentrations of the androgen dehydroepiandrosterone sulfate increase between late pregnancy and 3 mo postpartum in lactating women but not in nonlactating women (19). However, in the present study, the hypoestrogenemic state (or increased androgen-estrogen ratio) induced by lactation did not result in a shift to abdominal fat distribution compared with the nonlactating women who had resumed menses.
Increased circulating prolactin concentrations stimulate appetite in lactating women (14). Thus, we presume that our failure to find that lactating women lose more fat and weight than do nonlactating women was due to the influence of prolactin on appetite stimulation. We found that the lactating women had higher energy intakes (ie, 327 kcal/d, or 1370 kJ/d) than did the nonlactating women in the first 6 mo postpartum. One limitation of our study, however, was that we did not know whether the women were trying to lose weight. It is possible that the nonlactating women intentionally restricted their energy intake whereas the lactating women did not because they presumed that they would lose weight by lactating. It is also possible that lactation status influences postpartum physical activity levels; the nonlactating mothers in our study reported spending significantly more time in hard and very hard activity than did the lactating mothers during the first 6 mo postpartum. Our results suggest that compensations in energy intake and physical activity occur during the first 6 mo postpartum to meet the energy needs for lactation and help spare fat mass.
On average, the women in the weaning study lost fat mass at all sites, which indicates that body-composition changes occur until
12 mo postpartum. The gain in leg lean mass between 6 and 9 mo postpartum in the previously lactating women compared with the nonlactating women supports the possibility that lean tissue energy stores from the thigh region were previously used to support lactation, with subsequent recovery of lean tissue after weaning. This speculation should be viewed with caution because our findings from the lactation study did not show that changes in leg lean mass occurred differently in the nonlactating and the lactating women during the first 6 mo postpartum. It remains possible that our crude measure of physical activity was inadequate for determining the potential effects of exercise on lean mass changes in the women in this study.
The present study had enough power (80%) to detect a 1.6-kg difference in weight loss due to calcium supplementation during the first 6 mo postpartum. This corresponds to a weight loss of 3.2 kg/y, which is a clinically relevant weight change. On the basis of the speculation by Davies et al (20) that differences in calcium intakes might be associated with changes in body weight of
0.4 kg/y, an extremely large trial would be necessary to detect a significant calcium effect. Zemel (16) suggested that high calcium intakes might suppress serum 1,25(OH)D2 concentrations and thereby result in reduced calcium influx into adipocytes. Because calcium influx into cells stimulates lipogenesis and inhibits lipolysis, suppressing 1,25(OH)D2 might have antiobesity effects. Serum 1,25(OH)D2 concentrations were previously shown to be lower in the calcium-supplemented women than in the placebo-supplemented women from the present study (21); thus, our calcium intervention was sufficient to elicit a response that has been proposed as a mechanism for weight loss, but that response had no significant weight-loss effect. We did find that in the women in the lactation study, higher rates of lean mass loss in the whole body and trunk occurred between 2 wk and 3 mo postpartum in those who received calcium than in those who received placebo. Because higher rates of lean mass loss occurred between 3 and 6 mo postpartum in the placebo group than in the calcium group, there was no significant difference between the groups in net lean mass loss (ie, the placebo group "caught up" to the calcium group). We do not have a biologically plausible explanation for these findings, and there was no significant effect of calcium supplementation on body-composition changes in the weaning study.
In summary, our findings are in agreement with those of previous reports that lean mass is spared during lactation (5, 11), because we found no difference in postpartum lean mass changes between the nonlactating and the lactating women. Postpartum weight loss consists of both fat and lean masses in both lactating and nonlactating women. Our results also differ both from those of previous studies that suggest that breastfeeding facilitates postpartum weight loss (8, 10) and from anecdotal reports about increased rates of weight loss after weaning. Calcium supplementation of 1 g/d does not appear to influence fat mass loss during the postpartum period in women with low habitual calcium intakes. The combined findings from the lactation and weaning studies presented herein indicate that postpartum body-composition changes 1) occur at different rates between lactating and nonlactating women during the first 6 mo postpartum, 2) are not beneficially influenced by calcium supplementation, and 3) occur at some sites until
12 mo postpartum. Finally, we recommend that when promoting breastfeeding, clinicians use caution in advising mothers with respect to expected rates of weight and fat loss after pregnancy.
| ACKNOWLEDGMENTS |
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| REFERENCES |
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