Vitamin D is a hormone critically important for the maintenance of a healthy skeleton and for maintaining calcium and phosphorus homeostasis (Holick, 2003). Vitamin D from dietary sources and from endogenous synthesis is stored in adipose tissue and circulates in the blood bound to alpha2-globulin D-binding protein. Vitamin D occurs primarily in two forms. One form is ergocalciferol (vitamin D2), which is found in irradiated milk, yeast and some plants. The second form is cholecalciferol (vitamin D3), which is formed in human skin by the action of ultraviolet radiation from sunlight. Vitamin D3 is rich in fish liver oils and egg yolks but is generally very low in most other foods.
The major source of vitamin D is normally from skin synthesis but it is only the UV-B component of sunlight light that produces vitamin D, i.e. the component blocked by sunscreen with a sun protection factor of 8 or greater. Vitamin D, either as D3 or D2, does not have significant biological activity and must be metabolized in a two-step process. In the first step, cholecalciferol is hydroxylated to 25-hydroxycholecalciferol within the liver. In the second step, the 25-hydroxycholecalciferol is further hydroxylated within the kidney to 1,25-dihydroxycholecalciferol, which is the biologically active form of vitamin D.
Vitamin D deficiency can occur due to low dietary intake, by limited exposure to sunlight, by inability of the kidney to convert vitamin D to its active form, or by poor absorption from the gastrointestinal tract. Unfortunately, the only means to test for vitamin D deficiency is by a blood assay. Vitamin D deficiency or insufficiency can be quite common during winter months, particularly for people living at latitudes distant from the equator. 'Even in sunny southern California vitamin D deficiency or insufficiency is prevalent in part due to avoidance of midday sunlight and the use of sunscreens' ( http:// sunlightandvitamind.com/main.html ).
Excessive intake of vitamin D in fortified food, over-the-counter supplements or excessive ingestion of anti-rickets pharmaceuticals can result in vitamin D poisoning. An acute toxic dose has not been established but the chronic toxic dose is more than 5O OOO IU/day in adults for 1-4 months and, in children, 4OO IU/day is potentially toxic. Acute toxicity effects may include muscle weakness, apathy, headache, anorexia, nausea, vomiting, and bone pain. Chronic toxicity effects include the above symptoms and constipation, anorexia, polydipsia, polyuria, backache, hyperlipidemia, and hypercalcemia. Hypercalcemia may cause permanent damage to the kidney (see http://www.emedicine.com/emerg/ topic638.htm). Arterial hypertension and aortic valvular stenosis can also result from hypervitaminosis D.
Recent research has revealed that vitamin D has an importance beyond mineralization of bone tissue since vitamin D receptors have been found in a wide variety of cells. The active form of vitamin D is now known to bind to intracellular receptors that, in turn, function as transcription factors to modulate gene expression.
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