Abstract
Vitamin D plays a major role in calcium and phosphorus homeostasis. The natural forms of vitamin D are ‘ergocalciferol’ from vegetable food, and ‘cholecalciferol’ from the synthesis beneath our skin when exposed to ultraviolet light. These two forms of vitamin D have to change into 25-hydroxyvitamin D (25(OH)D), the main reservoir of vitamin D in our body, by hydroxylation in the liver. Then 25(OH)D undergoes further hydroxylation in the kidney to 1α,25(OH)2D, the active functioning hormone in our body. 1α,25(OH)2D will interact with vitamin D receptor (VDR) at the cellular level and result in the transcription and translation of many vitamin D dependent proteins. Nowadays we can detect VDR in various tissues which confirms the many biological effects that 1α,25(OH)2D might have, apart from calcium and phosphorus homeostasis. Those unexpected tissues include pancreas, placenta, pituitary, ovary, testis, mammary gland, muscle and heart. Our understanding of vitamin D deficiency syndrome has changed over the past 10 years. Hypovitaminosis D or vitamin D insufficiency refers to the low level of serum 25(OH)D which induces the depletion of tissue levels and the elevation of parathyroid hormone levels. Hypovitaminosis D can be defined as the serum level of 25(OH)D below 30 ng/ml (75 nmol/l). Hypovitaminosis D is more prevalent among postmenopausal women, ranging from 40 to 70 % of this population and increasing with age. This high prevalence of hypovitaminosis D causes depletion of muscle function as well as an increased risk of falls in this elderly group. Many studies show that replacement of vitamin D can improve muscle function and reduce the risk of falls in subjects that have hypovitaminosis D.
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