Vitamin D is a fat-soluble vitamin. Very few foods naturally contain vitamin D (fatty fish livers are the exception), so dermal synthesis is the major natural source of the vitamin. Vitamin D from the diet or dermal synthesis is biologically inactive and requires enzymatic conversion to active metabolites (figure 1). Vitamin D is converted enzymatically in the liver to 25-hydroxyvitamin D (25[OH]D), the major circulating form of vitamin D, and then in the kidney to 1,25-dihydroxyvitamin D, the active form of vitamin D.
Vitamin D and its metabolites have a significant clinical role because of their interrelationship with calcium homeostasis and bone metabolism. Rickets (children) and osteomalacia (children and adults) due to severe vitamin D deficiency are now uncommon except in populations with unusually low sun exposure, lack of vitamin D in fortified foods, and malabsorptive syndromes. Subclinical vitamin D deficiency, as measured by low serum 25(OH)D, is very common. In the National Health and Nutrition Examination Survey (NHANES) 2005 to 2006, 41.6 percent of adult participants (≥20 years) had 25(OH)D levels below 20 ng/mL (50 nmol/L) . This degree of vitamin D deficiency may contribute to the development of osteoporosis and an increased risk of fractures and falls in the elderly. Vitamin D may also regulate many other cellular functions.
This topic review provides an overview of vitamin D. Other reviews discuss specific issues related to vitamin D:
●(See "Causes of vitamin D deficiency and resistance".)
●(See "Overview of rickets in children" and "Etiology and treatment of calcipenic rickets in children".)