Understanding vitamin D deficiency
Abstract
Vitamin D deficiency is a global health problem caused mainly by insufficient exposure to sunlight. It is estimated that 1 billion people have vitamin D deficiency or insufficiency worldwide [1], particularly prevalent among elderly people [2]. Vitamin D exists in two forms—D2 (ergocalciferol), which is obtained from yeast and plants and D3 (cholecalciferol), obtained from the diet through the ingestion of vitamin D containing products (fatty fish and eggs), vitamin D fortified milk or margarine and /or the use of multivitamins. However, the primary source of vitamin D3 (80–90% of the body stores) is via ultraviolet irradiation of the precursor molecule 7-dehydrocholesterol in the skin. Vitamin D (D2 and D3) are then subsequently hydroxylated in the liver by 25-hydroxylase to produce 25-hydroxyvitamin D (25OHD). 25OHD is then further hydroxylated in the kidney by the 1-alpha hydroxylase to form 1,25-di25OHD (1,25(OH)2D) or calcitriol), which is the biologically active form of vitamin D. The 1-alpha hydroxylation can also occur in a multitude of other tissues, generating locally active vitamin D, which leads to auto and /or paracrine effects. The principal index of vitamin D status is the serum 25OHD concentration, with a half-life of ∼3 weeks, when compared with the biologically active form 1,25(OH)2D which has a half-life of only 4–6 h [3]. 25OHD levels are measured in ng/ml or nmol/l (1 ng/ml is equivalent to 2.5 nmol/l). However, several technical problems should be…
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