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Vitamin D deficiency exists when the concentration of 25-hydroxy-vitamin D (25-OH-D) in the blood serum occurs at 12 ng/ml (nanograms/milliliter), or less. The normal concentration of 25-hydroxy-vitamin D in the blood serum is 25-50 ng/ml. When vitamin D deficiency continues for many months in growing children, the disease commonly referred to as rickets will occur. A prolonged deficiency of the vitamin in adults results in osteomalacia. Both diseases involve defects in bones.
Vitamin D is a fat-soluble vitamin, meaning it is able to be dissolved in fat. While some vitamin D is supplied by the diet, most of it is made in the body. To make vitamin D, cholesterol, a sterol that is widely distributed in animal tissues and occurs in the yolk of eggs, as well as in various oils and fats, is necessary. Once cholesterol is available in the body, a slight alteration in the cholesterol molecule occurs, with one change taking place in the skin. This alteration requires the energy of sunlight (or ultraviolet light). Vitamin D deficiency, as well as rickets and osteomalacia, tends to occur in persons who do not get enough sunlight and who fail to eat foods that are rich in vitamin D.
Once consumed, or made in the body, vitamin D is further altered to produce a hormone called 1,25-dihy-droxy-vitamin D (1,25-diOH-D). The conversion of vitamin D to 1,25-diOH-D does not occur in the skin, but in the liver and kidney. First, vitamin D is converted to 25-OH-D in the liver; it then enters the bloodstream, where it is taken-up by the kidneys. At this point, it is converted to 1,25-diOH-D. Therefore, the manufacture of 1,25-diOH-D requires the participation of various organs of the body—the liver, kidney, and skin.
The purpose of 1,25-diOH-D in the body is to keep the concentration of calcium at a constant level in the bloodstream. The maintenance of calcium at a constant level is absolutely required for human life to exist, since dissolved calcium is required for nerves and muscles to work. One of the ways in which 1,25-diOH-D accomplishes this mission is by stimulating the absorption of dietary calcium by the intestines.
The sequence of events that can lead to vitamin D deficiency, then to bone disease, is as follows: a lack of vitamin D in the body creates an inability to manufacture 1,25-diOH-D, which results in decreased absorption of dietary calcium and increased loss of calcium in the feces. When this happens, the bones are affected. Vitamin D deficiency results in a lack of bone mineralization (calcification) in growing persons, or in an increased demineralization (decalcification) of bone in adults.
Author Info: Tom Brody PhD, The Gale Group Inc., Gale, Detroit, Gale Encyclopedia of Medicine, 2002
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