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Editor's Correspondence
February 14, 2011

Vitamin D Supplementation and Fracture Risk

Author Affiliations

Author Affiliations: Centre on Aging and Mobility and Department of Rheumatology, University of Zurich, Zurich, Switzerland (Dr Bischoff-Ferrari); USDA Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts (Dr Dawson-Hughes); and College of Pharmacy and Nutrition, University of Saskatchewan, Saskatoon, Saskatchewan, Canada (Dr Whiting).

Arch Intern Med. 2011;171(3):265. doi:10.1001/archinternmed.2010.531

In the July 12, 2010, issue of the Archives, Grey and Bolland1 incorrectly state that vitamin D does not reduce fracture risk, citing a single flawed meta-analysis2 in support and ignoring several others that reached the opposite conclusion (eg, Bischoff-Ferrari et al3,4). They dismiss as special pleading the fact that “advocates of vitamin D supplementation” point to inadequate vitamin D doses as an explanation for null effects. Serum 25-hydroxyvitamin D (25[OH]D) is defined by the Institute of Medicine as the indicator of vitamin D functional status. Trials that do not change serum 25 (OH)D level appreciably (or which are not shown to do so) do not and cannot test the hypothesis that vitamin D lowers disease risk. Most meta-analysts, seemingly unaware of the relevant biology, ignore this key point. Nor, in meta-analyses, is it appropriate to lump together studies using calcitriol or its analogs with studies using native cholecalciferol. Intracellular calcitriol concentrations needed for autocrine activity cannot be achieved by oral or intravenous calcitriol administration.

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