In the body, vitamin D acts mainly on bone metabolism, on calcium absorption in the gut, on the kidneys and the parathyroid. However, vitamin D metabolism and its action are often disturbed, especially in the elderly. Primary vitamin D deficiency (hypovitaminosis) is a combination deficit of reduced uptake or absorption in the gut or reduced synthesis in the skin as a result of low exposure to sunlight. A clear distinction must be made between these and primary 1.25(OH)2 vitamin D3 deficiency and vitamin D resistance, which is characterized by a vitamin D receptor deficiency in the gut and in bone. The active metabolite of vitamin D, 1.25(OH)2D3, is produced in the kidney and is subject to strict control by the body. Reduced 1.25(OH)2D3 levels result in reduced calcium absorption in the gut and increase parathyroid hormone secretion, which in turn promotes bone loss. Treatment with the active vitamin D metabolites (Calcitriol or the pro-drug Alfacalcidol) can prevent loss of bone mass. What is very important is that it can do so fully independently of the pathogenetic cause of the increased parathyroid hormone level. It is also known to have a positive influence on the myasthenia due to the deficiency of active vitamin D metabolites, and it is possible that this specific therapy reduces the tendency to fall. Alfacalcidol might be preferable to calcitriol, since it harbours a lower risk of hypercalcaemia and is more effective in lowering the serum parathyroid hormone titre.