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Division of Nutritional Sciences, Cornell University, Ithaca, NY 14853 Ccm3{at}cornell.edu
Dear Editor,
Drs. Bronner, Sepchenko, Wood and Pansu have critically evaluated my Issues and Opinion article (1 ) and make very important points. They are clearly justified in questioning the diffusion value "extrapolated" from two points in the Ireland and Fordtran experiment (2 ). They (and I) are concerned that the interpretation depends critically on an assumed luminal calcium concentration at which calcium flux (diffusion) is zero (1.5 mmol/L). A subtle change in this value (or in either of the two values presented) drastically changes the slope and the estimate of the diffusion component at higher luminal concentrations. It is intriguing that the values in this study, as well as one conducted 15 y later (3 ) in which a completely different approach was attempted, were reasonably close when considered at intakes approaching "normal" intakes, i.e., 900 mg/d. As Bronner et al. indicate in their letter, higher diffusion values (percentages) were presented in Table 4 of that study. However, these data were derived from normal individuals consuming a meal containing 502 or 1071 mg of calcium not as indicated in the comments of Bronner et al. as an intake per day. The results shown in that table are consistent with their other data and again indicate that at higher intakes, passive diffusion may constitute a major proportion of calcium absorption; this is not disputed. However, assuming three meals per day, these values represent intakes > 1.5 g/d. I have no doubt that passive diffusion can ultimately be important, but my focus has always been on "normal" intakes for normal people; I (and perhaps others) remain to be convinced that at normal intakes, passive diffusion is the "major" route of absorption as stated by Bronner et al. in their correspondence.
It is interesting that they did not address the ineffectiveness of oral calcium in children who lack the vitamin receptor system (4
). In these children, passive diffusion is presumably the only means by which luminal calcium can be absorbed. A diet therapy in which these children consumed >2 g calcium/d (with lactose) was essentially ineffective. The authors of that study concluded that the high (calcium) lactose regimen given for 6 mo was "well tolerated but its therapeutic action was nil." I have since found a report that indicates that intakes of 
6 g/(m2 · d) are capable of "maintaining" these children after initial intravenous therapy (5
). These authors indicate that "Only after radiologic healing has been observed can oral calcium therapy be introduced." It would appear then that for passive diffusion to provide the required calcium for these children, an extraordinarily large daily intake is necessary. Perhaps this greater than sixfold apparent requirement reflects the inefficiency of passive diffusion. If so, then an estimate of the contribution of passive diffusion of nearly 20% (1
) may be too high.
A final point raised by Bronner et al. in their letter concerns the relative risk of calcium vs. vitamin D supplements and the regulation of vitamin D–mediated absorption. I would agree that higher intakes "downregulate" vitamin D–mediated calcium absorption; clearly the body adapts to changes in calcium status. Also, I would agree that supplementing calcium intake probably involves less risk than vitamin D supplements because vitamin D can be toxic at very high intakes. Perhaps the solution is a "normal" diet accompanied by moderate exposure to sunlight. This could be accomplished by 5 min of sunlight exposure to the hands and face during a short walk in the daylight hours. This would seem to be preferable to supplements.
Manuscript received 7 February 2003.
LITERATURE CITED
1. McCormick, C. C. (2002) Passive diffusion does not play a major role in the absorption of dietary calcium in normal adults. J. Nutr. 132:3428-3430.
2. Ireland, P. & Fordtran, J. S. (1973) Effect of dietary calcium and age on jejunal calcium absorption in humans studied by intestinal perfusion. J. Clin. Investig. 52:2672-2681.
3. Sheikh, M. S., Ramirez, A., Emmett, M., Santa Ana, C., Schiller, L. R. & Fordtran, J. S. (1988) Role of vitamin D-dependent and vitamin D-independent mechanisms in absorption of food calcium. J. Clin. Investig. 81:126-132.
4. Balsan, S., Garabedian, M., Larchet, M., Gorski, A. M., Cournot, G., Tau, C., Bourdeau, A., Silve, C. & Ricour, C. (1986) Long-term nocturnal calcium infusions can cure rickets and promote normal mineralization in hereditary resistance to 1, 25-dihydroxyvitamin D. J. Clin. Investig. 77:1661-1667.
5. Hochberg, Z., Tiosano, D. & Even, L. (1992) Calcium therapy for calcitriol-resistant rickets. J. Pediatr. 121:803-808.[Medline]
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