Since vitamin D can be produced in our bodies by the action of sunlight on the skin, many experts consider it to be more of a hormone than a vitamin. In the skin, sunlight changes the precursor of vitamin D, 7-dehydrocholesterol, into vitamin D3 (cholecalciferol). Vitamin D3 is transported to the liver and converted by an enzyme into 25 hydroxycholecalciferol (25-OHD3), which is five times more potent than cholecalciferol. The 25-OHD3 is then converted by an enzyme in the kidneys to 1,25-dihydroxycholecalciferol (1,25-(OH)2D3), which is ten times more potent than cholecalciferol and is its most potent form.
Disorders of the liver or kidneys result in impaired conversion of cholecalciferol to more potent vitamin D compounds. In many patients with osteoporosis, the levels of 25-OHD3 are high, while those of 1,25-(OH)2D3 are quite low. This signifies an impairment of the conversion of 25-OHD3 to 1,25-(OH) 2D3 in osteoporosis. Many theories have been proposed to account for this decreased conversion, including relationships to estrogen and magnesium deficiency. Recently, the trace mineral boron has been theorized to play a role in this conversion as well.