Pharmacology of Vitamin D
Vitamin D3 is formed in the skin, converted to a pre-hormone in the liver and becomes a fully active hormone in the kidney
Vitamin D3 (cholecalciferol) is formed in the skin by a photoreaction between ultraviolet (UV) rays of sunlight and a pre-cholesterol compound (7-dehydrocholesterol) in the skin. Vitamin D3 is inert, that means it is not bioactive. Vitamin D3 is also unstable, especially in the presence of air or oxygen.
As shown in the figure above, Vitamin D3 is transported in the blood stream to the liver where it is converted into the pre-hormone form, 25-hydroxy Vitamin D3 by the enzymatic addition of a single hydroxyl [OH-] group. This pre-hormone form is also largely inert and unstable in the presence of air or oxygen. This pre-hormone form is also called calcidiol.
The pre-hormone form of Vitamin D3 is then transported from the liver to the kidneys where it is converted to the active hormone form, 1, 25-dihydroxy Vitamin D3 by the enzymatic addition of a second hydroxyl [OH-] group. The hormone form of Vitamin D3 is highly bioactive and also unstable in the presence of air or oxygen. This hormone form is also called calcitriol.
- Cellular and Immune Functions
The active hormone binds into the Vitamin D receptor (VDR) that is an essential component to most cellular and immune functions.
- Vitamin D Associated Diseases
Vitamin D deficiencies can cause or contribute to diseases such as colorectal and prostate cancers, high blood pressure, and kidney and heart diseases, which affect black Americans at higher rates than whites.
- Brody J. (2102). Reasons that Vitamin D May Matter. New York Times, March 12.
- Clarke B. (2011). Medical Edge Newspaper Column. Mayo Clinic.
- Crissey S, Ange K, Jacobsen K, Slifka K, Bowen P, Stacewicz-Sapuntzakis M, Langman C, Sadler W and Kahn S. (2003). Serum concentrations of lipids, vitamin D metabolites, retinol, retinyl esters, tocopherols and selected carotenoids in twelve captive wild felid species at four zoos. The Journal of nutrition 133 (1): 160–6.
- Heaney R. (2003). Long latency deficiency disease: insights from calcium and vitamin D. American Journal of Clinical Nutrition 78:912-919.
- Institute of Medicine, Food and Nutrition Board. (2010). Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press.
- Jones G. (2008). Pharmacokinetics of vitamin D toxicity. Am J Clin Nutr. 88:582S-6S.
- NIH Office of Dietary Supplements Dietary Supplement Fact Sheet: Vitamin D. (2009).
- Vitamin D and Calcium: Updated Dietary Reference Intakes. Nutrition and Healthy Eating. Health Canada.
- Mayo Clinic. (2012). Vitamin D. Mayo Clinic website. http://www.mayoclinic.com/health/vitamin-d/NS_patient-vitamind
- Ross A, Manson J, Abrams S, Aloia J, Brannon P, Clinton S, Durazo-Arvizu R, Gallagher J, Gallo R, Jones G, Kovacs C, Mayne S, Rosen C and Shapses S. (2011). The 2011 Report on Dietary Reference Intakes for Calcium and Vitamin D from the Institute of Medicine: What Clinicians Need to Know. Journal of Clinical Endocrinology & Metabolism 96 (1): 53–8. doi:10.1210/jc.2010-2704.
- Sarubin F and Thomson C. (2007). The Health Professional's Guide to Popular Dietary Supplements. 3rd ed. Chicago, IL: American Dietetic Association.
- Vieth R. (2006). Critique of the considerations for establishing the tolerable upper intake level for vitamin D: critical need for revision upwards. J Nutr. Apr; 136 (4): 1117-22.
- Vieth R. (1999). Vitamin D supplementation, 25-hydroxyvitamin D concentrations, and safety. Am J Clin Nutr. May; 69 (5): 842-56.
- Wolf G. (2004). The discovery of vitamin D: the contribution of Adolf Windaus. J Nutr 134 (6): 1299–302.
- Wolpowitz D and Gilchrest B. (2006). The vitamin D questions: how much do you need and how should you get it? J Am Acad Dermatol. 54:301-17.