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LETTER TO THE EDITOR |
USDA/ARS Children's Nutrition Research Center
Department of Pediatrics
Baylor College of Medicine and Texas Children's Hospital
Houston, TX 77030
Department of Family Medicine
Jos University Teaching Hospital
PMB 2076
Jos Nigeria
Department of Pediatric and Adolescent Medicine
Mayo Clinic
299 First Street, SW
Rochester, MN 55905
E-mail: fischer.phil{at}mayo.edu
Division of Foods and Nutrition
Emory University
771-2 Houston Mill Road
Atlanta, GA 30329
Division of Endocrinology, Diabetes, and Clinical Nutrition
Department of Medicine
Oregon Health Sciences University School of Medicine
Portland, OR 97201
Department of Paediatrics
University of Jos
PMB 2084
Jos Nigeria
MRC Mineral Metabolism Research Unit
Department of Paediatrics
University of the Witwatersrand and Chris Hani Baragwanath Hospital
PO Bertsham 2013
South Africa
Dear Sir:
The letter from Heaney raises one of the major issues concerning the methodology for measuring intestinal calcium absorption. We recognize that there are no perfect methods for evaluating usual dietary absorption of calcium or any isolated nutrient within the context of whole diets as typically consumed. Balance methods often involve the use of nonrepresentative diets and do not isolate nutrient sources. Furthermore, tracer methods can only trace, as Heaney notes, certain aspects of the diet. Therefore, such studies must evaluate either the bioavailability of calcium from a particular food, which requires either intrinsic labeling or assurance of full distribution of the extrinsic label, or a component of absorptive capacity by providing the label as part of a meal, which may not completely mix with all of the components. The former method does not necessarily assess whole dietary absorption and is most suitable for supplement and fortification studies, such as those referenced by Heaney. The second method, although it may overestimate food-based absorption, provides substantial information regarding absorptive capacity.
In our study, a large amount of phytates in the diet, which are known inhibitors of calcium absorption, might have been expected to inhibit the absorption of calcium from the test meal. In fact, this did not occur in children with or without rickets, undoubtedly because of the very low calcium content of the test meals. At low calcium intakes, vitamin D-dependent active transport is most critical for calcium absorption (1). It is reasonable to conclude from our data that there is no evidence that Nigerian children with rickets have a fundamental inability to absorb calcium; thus, vitamin D deficiency is excluded as a factor in the causation of the disease. Our results are also consistent with those of early calcium balance studies conducted in South African children with dietary calcium-deficiency rickets (2). After nutritional rehabilitation, calcium absorption increased to a very high level in children who previously had rickets. This finding is inconsistent with Heaney's hypothesis that the tracer was absorbed independent of nutritional status and suggests that children with rickets may appropriately respond to overall nutritional rehabilitation with bone growth and remineralization.
It should be noted that we recently found fractional calcium absorption to be similar in rachitic children and in pubertal children with low calcium intakes (3), in whom calcium was traced from milk (in which there has been shown to be appropriate interchange between the tracer and natural calcium). Although the children in that study and in another study involving pregnancy (4) and very high absorption levels were in physiologic states of high absorption, these data indicate that a direct comparison of our values with those of adults may be erroneous and that the absorption values we found are probably not spuriously elevated.
ACKNOWLEDGMENTS
None of the authors had a conflict of interest.
REFERENCES
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