Vitamin D2, if given in high enough doses, prevents infantile rickets and is capable of healing adult osteomalacia. However, the inefficiency of vitamin D2 compared with vitamin D3, on a per mole basis, at increasing 25(OH)D is now well documented, and no successful clinical trials to date have shown that vitamin D2 prevents fractures (19-21, 47). Given the assumption that the intake of any nutrient will deliver defined effects [ie, supplementation with vitamin D will lead to an increase in 25(OH)D or fracture prevention], it is clear that vitamin D2 does not fit this current nutritional notion. This is not to suggest that vitamin D2 is not efficacious, but, because the units of the 2 forms is clearly not equivalent, likely due to its distinct metabolic features and diminished binding of vitamin D2 metabolites to DBP in plasma, continual application of vitamin D2 in clinical use, including in research trials, only serves to confound our understanding of optimal vitamin D dosing recommendations. Furthermore, the public expects to derive the equivalent effect per unit dose of vitamin D, whether it is vitamin D2 or vitamin D3. The scientific community is aware that these molecules are not equivalent. Therefore, vitamin D2 should no longer be regarded as a nutrient appropriate for supplementation or fortification of foods.
Thursday, February 14, 2008
Posted by S F X at 2:30 PM