Vitamin D

It takes vitamin D to maintain healthy bones. A severe deficit in youngsters causes rickets, a deformity of the bones. Less severe insufficiencies are thought to result in less effective dietary calcium utilisation. Muscle weakness results from a vitamin D shortage; in the elderly, this impact has been linked to an increased risk of falls. One common cause of secondary hyperparathyroidism is a vitamin D deficiency. PTH elevations can cause osteomalacia, accelerated bone turnover, decreased bone mass, and an increased risk of bone fractures, particularly in older vitamin D deficient persons. Reduced bone mineral density is also correlated with low amounts of vitamin D (25.OH). The findings could be helpful in evaluating bone metabolism when combined with further clinical information. Sunlight exposure is the primary source of vitamin D, a fat-soluble steroid hormone precursor that is generated in the skin. To produce the physiologically active 1,25-dihydroxyvitamin D, vitamin D must go through two consecutive hydroxylations in the liver and kidney. Vitamin D is biologically inactive. Since vitamin D (25-OH) is the primary form of vitamin D stored in the human body, it is widely accepted that this metabolite should be used to assess the overall status of vitamin D.