HOW TO PREVENT AND TREAT VITAMIN D DEFICIENCY Many patients and physicians think that adequate vitamin D intake can be obtained via diet alone. This assumption is erroneous. With the exception of fatty fish, the vitamin D content of most foods, including fortified dairy products, is relatively low to nonexistent. Even some dairy products in the United States are not fortified, making it important to read food labels to ensure the vitamin D content of foods. Vitamin D supplementation is safe17 and inexpensive, but vitamin D deficiency often remains undiagnosed or is undertreated. Possible explanations for this disparity include (1) the recommended age-dependent adequate intake (AI) of vitamin D was established before publication of studies suggesting that 25(OH)D levels of greater than 30 ng/mL are needed to ensure PTH suppression into the normal range; (2) the current AI for vitamin D can easily be met by diet and/or a daily multivitamin,18 but this intake level may still be inadequate to reach optimal levels in many people, especially those at risk; and (3) physicians may be uncomfortable recommending larger doses of vitamin D. That fear is generally unmerited given the dearth of reports of vitamin D toxicity compared with the expansive literature on vitamin D deficiency. The rarity of reports of vitamin D toxicity can be explained in part by the kidneys ability to limit production of active calcitriol. Increased calcitriol levels inhibit PTH both directly (through the vitamin D response element on the PTH gene) and indirectly (by increasing intestinal calcium absorption), causing calcitriol production in the kidney to decrease. Renal 24-hydroxylase activity further limits the availability of calcitriol by creating inert metabolites of both calcitriol (1,24,25-trihydroxyvitamin D) and calcidiol (24,25-dihydroxyvitamin D). The 24-hydroxylase gene is under the transcriptional control of calcitriol, thereby providing tight negative feedback.
Posted on: Fri, 07 Mar 2014 05:15:57 +0000
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