Bone Turnover during Lactation—Can Calcium Supplementation Make a Difference?1

Steven A. Abrams, M.D.

U.S. Department of Agriculture/ Agricultural Research Service Children’s Nutrition Research Center Department of Pediatrics Baylor College of Medicine and Texas Children’s Hospital Houston, Texas 77030

Address all correspondence and requests for reprints to: Steven A. Abrams, M.D., U.S. Department of Agriculture/Agricultural Research Service, Children’s Nutrition Research Center, 1100 Bates Street, Houston, Texas 77030.


    Introduction
 Top
 Introduction
 References
 
Sometimes, what seems like an obvious idea does not stand the test of research. In this case, there is clear evidence of maternal bone loss during lactation due to calcium secretion into breast milk (1, 2, 3). This has led to many years of dietary recommendations to increase calcium intake during lactation (4). Unfortunately for this "obvious" recommendation, an increasing body of evidence suggests that, for most women, there is little apparent benefit to taking calcium supplements while lactating. Several recent studies have failed to find any effect of supplementation either on the calcium content of breast milk or on maternal bone mineralization (1, 2, 5).

These findings are surprising, in that the decreased urinary calcium excretion during lactation is not sufficient to prevent a significant negative calcium balance (4, 6). Therefore, it is rational to assume that getting more calcium into the body, by increasing intake, would prevent bone loss. This, however, does not appear to be the case. No benefit to calcium supplementation has been shown.

These findings require consideration of the mechanism of bone loss during lactation and the potential effects of calcium supplementation on this bone loss. In this issue of The Journal of Clinical Endocrinology and Metabolism, Prentice and colleagues report on longitudinal changes in hormonal and biochemical markers of bone turnover in lactating women from the Gambia, whose usual very low calcium intake was supplemented with calcium to achieve intakes comparable to those recommended in Western countries (7). They found that lactation was not associated with significant hyperparathyroidism or increases in the 1,25-dihydroxyvitamin D concentration, but was associated with greater alkaline phosphatase activity and deoxypyridinoline excretion. Calcium supplementation did not affect the lactation-related changes in any of these values. Taken together, these findings suggest that bone loss is related to increased bone resorption in early lactation, which cannot readily be altered by supplemental calcium.

Of key importance in interpreting this and similar studies is to consider the effects of habitual diet and ethnicity on the data. Most previous studies have primarily or exclusively evaluated Caucasians. The current study by Prentice focuses on black African women consuming their native diet. This population might be different from those previously studied in terms of both genetics and diet and exercise patterns. For example, the Gambian women may have a unique long term adaptation to low calcium. Differences in PTH and other hormones between Gambian women and British women are described in this report.

Such ethnic differences, however, do not seem to affect the primary findings of this study: that bone turnover markers are not altered by calcium supplementation, and that there was no apparent benefit to calcium supplementation of these women despite the fact that their calcium intake was very low. This conclusion is virtually identical to that reported in a study of Caucasian women in the United States, whose habitual calcium intake was much greater than that of the Gambian women (1, 2).

One question that may be asked is whether the biochemical bone turnover markers accurately reflect the changes in bone that occur during lactation. Although definitive answers to this cannot be provided, it is noteworthy that lactation-associated increases in bone formation and resorption during low and normal calcium diets have been found in stable isotope studies of calcium kinetics as well as in studies using biochemical markers of bone turnover (6, 8). Although the stable isotope studies involved few subjects, they support the basic pattern of increased bone resorption relative to bone formation during lactation that has been suggested by studies using biochemical markers (7, 9, 10).

Of note in the current Prentice study (7) (see JCEM page 1059) is that a marker associated with bone resorption (urinary deoxypyridinoline excretion) was elevated earlier in lactation than osteocalcin, which is usually associated with bone formation. This difference in the timing of the changes in the markers was not apparent in a previous study primarily involving Caucasian American women (9). Prentice et al. suggest that these findings may relate to a bone-remodeling cycle explaining the pattern of bone loss and reformation that occurs in lactation (6). It is not possible from the available data to further evaluate these issues, and it may be that they cannot be resolved using biochemical markers. As it is not feasible to perform sequential bone labeling and biopsy studies in healthy lactating women, longitudinal studies of calcium kinetics using stable isotopes may be a useful way to further investigate the relative timing of changes in bone formation and resorption during lactation and weaning.

The Prentice study (6) and other longitudinal studies of hormonal and biochemical changes during lactation and weaning have not fully identified the mechanisms of bone loss during lactation and its recovery postweaning (1, 3, 7, 8, 9, 10). It is likely that changing estrogen levels during these time periods are one important mechanism. This relationship with estrogen status is suggested by the close relationship between the resumption of menses during late lactation or weaning and bone recovery (9, 11). A positive correlation between serum estradiol and bone mineral density has been reported in one study (12). Furthermore, an early study demonstrated that use of some forms of oral contraceptives postweaning was associated with a greater bone mass than nonuse of oral contraceptives (13). However, these studies have not been performed in a controlled trial, and any benefit to estrogen supplementation during lactation or postweaning on bone mass remains speculative. Potentially negative effects of estrogen supplementation on milk volume may limit the ability to evaluate these issues before weaning (14).

Recovery of bone loss related to lactation is likely to be multifactorial. The current study by Prentice and co-workers (7) did not demonstrate increased PTH levels during early lactation, as have other studies, but found a slight increase in PTH levels during late lactation. Various patterns of PTH response during lactation have been reported in other studies (1, 3, 9, 10, 15). In general, however, a slight increase in PTH during weaning has been found (1, 3, 6, 11). Kalkwarf et al. recently reported an increase in fractional absorption of calcium correlated with changes in the 1,25-dihydroxyvitamin D concentration postweaning (16), indicating that improved calcium absorption may be important in recovery of bone mass postweaning.

One likely reason for differences among studies in the timing and nature of hormonal and biochemical changes during lactation is ethnic differences in mineral metabolism. Differences in vitamin D metabolism and PTH between African-American and Caucasian women regulation have been well described (17). Mild hyperparathyroidism and bone resistance to PTH have been identified in African-American women. Lower rates of bone formation have also been reported in African-Americans compared to Caucasians (18). At the present time, the etiology of these ethnic differences in bone mineral metabolism is unclear.

If studies cannot identify benefits from calcium supplementation during lactation, the question is: where do we go from here? First, it is necessary to carefully identify the problem being addressed. Current data indicate that a cycle of bone resorption and bone mass loss followed by recovery of bone mass is a usual consequence of lactation and weaning. For most women, this cycle does not appear to have a long term deleterious effect on their bone mineral status. Epidemiological studies do not generally support an increased risk of maternal postmenopausal osteoporosis related to lactation. Some studies, in fact, suggest the opposite, that lactation may decrease the risk of postmenopausal osteoporosis (19).

This is a key message to get across to the general public. In a society which is, appropriately, very concerned about osteoporosis, the message should clearly be conveyed that lactation is not a problem for most women in this regard. The bone loss-reformation cycle associated with lactation is an important topic for research, but should not be emphasized in a way that would discourage lactation.

As with all dietary recommendations, the suggestion that calcium supplementation is not useful during lactation needs to be tempered with the possibility that there are high risk groups for whom this recommendation is not appropriate. Therefore, it is crucial to identify populations who are at risk for not adequately recovering postweaning and to assess whether increased calcium or other forms of intervention (i.e. exercise, hormonal therapy, or a combination of calcium supplementation with other therapies) might be appropriate.

There are several groups of women who may be at increased risk for bone loss during lactation compared to "most" women. Women who are nursing more than one child, women with closely spaced pregnancies, and lactating adolescents may be at increased risk (20). With regard to women nursing multiple infants, it is noteworthy that some lactating women can have very high levels of milk output that completely support the milk needs of twins or triplets. Daily human milk volumes of 1–2 L or more are possible. It is likely that the secretion into milk, for example, of 400–600 mg/day calcium, would lead to greater loss of maternal bone mass than the 200–250 mg/day associated with nursing one child. However, few data are available regarding this issue, and there are no controlled trials of calcium supplementation in women who are providing milk for more than one infant.

One study suggested that bone loss might be substantial in lactating adolescents (21). However, the magnitude of bone loss in that study was unlikely to be representative of most lactating adolescents (22). In view of recent data indicating that rates of bone formation greatly diminish within 2–3 yr of menarche, it seems less likely that excessive or unrecoverable bone loss occurs in lactating adolescents (15, 19, 23). Nonetheless, this is an important group to evaluate regarding the effects of lactation on maternal bone mass and in whom to identify optimal calcium intake.

Finally, it is important to caution that negative studies regarding calcium supplementation and bone loss do not indicate that calcium intake is unimportant during the reproductive cycle. Clearly, women in the Gambia are able to adapt to extremely low intakes of calcium. Less clear is whether other groups of women can adapt to low intakes, or whether African-American women have the same adaptive capacity as women from the Gambia. Markedly different intakes of protein, salt, and other dietary constituents as well as lifestyle differences (such as exercise) may affect this relationship. Furthermore, usual calcium intakes in most women in the United States are well below the current dietary guidelines (1000 mg/day for adults and 1300 mg/day for ages 9–18 yr) (19). Small calcium supplements, such as the 200–250 mg/day frequently found in multivitamin supplements given to pregnant and lactating women, may be needed by many women to meet these dietary guidelines. Although much lower calcium intakes are tolerated by women in the Gambia, this does not indicate that levels below the dietary guidelines are appropriate for women of any ethnic group in North America.

In summary, Prentice and co-workers have carefully studied a group of women whose very low calcium intakes and prolonged lactation initially seemed to indicate that supplementation would be of benefit. In this case, however, the obvious did not withstand careful research, and dietary supplementation did not cause any identifiable benefit.


    Footnotes
 
1 This work is a publication of the USDA/Agricultural Research Service, Children’s Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine and Texas Children’s Hospital (Houston, TX). This project has been funded in part with federal funds from the USDA/Agricultural Research Service under Cooperative Agreement 58–6250-6–001. The contents of this publication do not necessarily reflect the views or policies of the USDA, nor does mention of trade names, commercial products, or organizations imply endorsement by the U.S. government. Back

Received January 5, 1998.

Accepted January 7, 1998.


    References
 Top
 Introduction
 References
 

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