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Departments of Internal Medicine, Clinical Nutrition, and Biochemistry, the Center for Human Nutrition, the Center for Mineral Metabolism and Clinical Research, and the Center for Diabetes Research, University of Texas Southwestern Medical Center, and the Veterans Administration Medical Center Dallas, Texas 75235
Address all correspondence and requests for reprints to: Scott M. Grundy, M.D., Ph.D., Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75235-9052.
Transient hypercalciuria has been noted after high carbohydrate meals which is independent of dietary calcium and is probably due to impaired renal calcium reabsorption mediated by an increase in plasma insulin levels. Based on these observations, some investigators believe that long term intake of high carbohydrate diets may increase the risk of nephrolithi-asis and possibly osteoporosis. Using a randomized cross-over design, we compared high carbohydrate diets (60% carbohydrate and 25% fat) with high fat diets (50% fat and 35% carbohydrate) for effects on metabolism of calcium and other minerals in eight normal subjects and eight euglycemic patients with noninsulin-dependent diabetes mellitus. All other dietary constituents, such as protein, fiber, fluid, minerals (including Ca, Mg, Na, K, and P), and caffeine intake, were kept constant.
Despite higher daylong levels of plasma insulin on the high carbohydrate diets compared to the high fat diet in both normal and noninsulin-dependent diabetic subjects, no changes in daily urinary excretion of calcium or other constituents, associated with renal stone risk, were observed. Furthermore, there was no change in fractional intestinal 47Ca absorption. Although hyper-calciuria may ensue transiently after high carbohydrate meals, we conclude that substitution of simple or complex carbohydrates for fats in an isocaloric manner for a longer duration does not result in significant urinary calcium loss, and therefore, high intakes of digestible carbohydrates may not increase the risk of nephrolithiasis or osteoporosis via this mechanism.
* This work was supported in part by Grants HL-29252, DK-2700, PO1-DK20543, POl-AM-205431, RO1-AR16061, and MO1-RR00633 from the NIH, V.A. Grants 549-8000 and 549-8676, the Southwestern Medical Foundation, the European Economic Community, and the Moss Heart Foundation of Dallas, TX.
Received July 6, 1989.
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