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© 2005 The American Society for Nutritional Sciences J. Nutr. 135:1678-1682, July 2005


Human Nutrition and Metabolism

Cholesterol Metabolism Is Affected by Calcium Phosphate Supplementation in Humans

Bianka Ditscheid, Sylvia Keller and Gerhard Jahreis1

Friedrich Schiller University, Institute of Nutrition, Department of Nutritional Physiology, D-07743 Jena, Germany

1To whom correspondence should be addressed. E-mail: Gerhard.Jahreis{at}uni-jena.de.

Dietary calcium and phosphate precipitate in the small intestine to form insoluble amorphous calcium phosphate (ACP). The ability of ACP to bind and inactivate luminal bile acids might have an effect on cholesterol metabolism. To test this hypothesis, a placebo-controlled, double-blind, crossover study with pentacalcium hydroxy-triphosphate supplementation (CaP; 1.0 g elemental calcium) was conducted in 31 young healthy volunteers. The CaP was incorporated into bread. Serum cholesterol concentrations were lower after 4 wk of supplementation than after 4 wk of placebo (4.36 vs. 4.60 mmol/L; P = 0.008). Serum LDL cholesterol and the ratio of LDL:HDL cholesterol also tended to be lower after CaP supplementation than after placebo (–5.6%, P = 0.083 and –5.4%, P < 0.062, respectively). The participants’ fat and cholesterol intakes and fecal fat excretion did not differ in the 2 periods. Although the analysis of fecal samples showed no difference in the excretion of total neutral sterols (sum of cholesterol and its transformation products), the excretion of cholesterol itself increased (9.64 vs. 5.80 µmol/g dry matter; P = 0.025; n = 25), whereas the excretion of the metabolite coprostanol decreased (18.5 vs. 21.0 µmol/g dry matter; P = 0.025; n = 25) in the CaP period. Bile acid excretion increased during the CaP period compared with the placebo period (25.4 vs. 22.9 µmol/g dry matter; P = 0.003). The observed beneficial effects on cholesterol metabolism are not the result of an increased excretion of cholesterol, but might be explained by an increased bile acid excretion and a subsequent regeneration of bile acids from endogenous cholesterol in the liver.


KEY WORDS: • cholesterol • calcium phosphate • fecal sterols • bile acids • human




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