Vitamin D Deficienc

Once foods were fortified with vitamin d and rickets appeared to have been conquered, many health care professionals thought the major  health problems resulting from vitamin D deficiency had been resolved. However, rickets can be considered the tip of the vitamin D–deficiency iceberg. In fact, vitamin D deficiency remains common in children and adults. In utero and during childhood, vitamin D deficiency can cause growth retardation and skeletal deformities and may increase the risk of hip fracture later in life. Vitamin D deficiency in adults can precipitate or exacerbate osteopenia and osteoporosis, cause osteomalacia and muscle weakness, and increase the risk of fracture.

The discovery that most tissues and cells in the body have a vitamin D receptor and that several possess the enzymatic machinery to convert the primary circulating form of vitamin D, 25-hydroxyvitamin D, to the active form, 1,25-dihydroxyvitamin D, has provided new insights into the function of this vitamin. Of great interest is the role it can play in decreasing the risk of many chronic illnesses, including common cancers, autoimmune diseases, infectious diseases, and cardiovascular disease. In this review I consider the nature of vitamin D deficiency, discuss its role in skeletal and nonskeletal health, and suggest strategies for its prevention and treatment.

Humans get vitamin D from exposure to sunlight, from their diet, and from dietary supplements.

A diet high in oily fish prevents vitamin D deficiency.Solar ultraviolet B radiation (wavelength, 290 to 315 nm) penetrates the skin and converts 7-dehydrocholesterol to previtamin D3 which is rapidly converted to vitamin D3 Because any excess previtamin D, or vitamin D3 is destroyed by sunlight, excessive exposure to sunlight does not cause vitamin D3 intoxication.

Few foods naturally contain or are fortified with vitamin D. The “D” represents D2 or D3 Vitamin D2 is manufactured through the ultraviolet irradiation of ergosterol from yeast, and vitamin D3 through the ultraviolet irradiation of 7-dehydrocholesterol from lanolin. Both are used in over-the-counter vitamin D supplements, but the form available by prescription in the United States is vitamin D2 Vitamin D from the skin and diet is metabolized in the liver to 25-hydroxyvitamin D, which is used to determine a patient’s vitamin D status; 25-hydroxyvitamin D is metabolized in the kidneys by the enzyme 25-hydroxyvitamin D-1α-hydroxylase (CYP27B1) to its active form, 1,25-dihydroxyvitamin D. The renal production of 1,25-dihydroxyvitamin D is tightly regulated by plasma parathyroid  hormone levels and serum calcium and phosphorus levels. Fibroblast growth factor 23, secreted from the bone, causes the sodium–phosphate cotransporter to be internalized by the cells of the kidney and small intestine and also suppresses 1,25-dihydroxyvitamin D synthesis. The efficiency of the absorption of renal calcium and of intestinal calcium and phosphorus is increased in the presence of 1,25-dihy- droxyvitamin D. It also induces the expression of the enzyme 25-hydroxyvitamin D-24-hydroxylase (CYP24), which catabolizes both 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D into biologically inactive, water-soluble calcitroic acid.