Bone turnover during lactation--can calcium supplementation make a difference?

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 (1–3). 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, Received January 5, 1998. Accepted January 7, 1998. 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. * 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. 0021-972X/98/$03.00/0 Vol. 83, No. 4 Journal of Clinical Endocrinology and Metabolism Printed in U.S.A. Copyright © 1998 by The Endocrine Society