Risk factors for vitamin D deficiency are premature and dysmature birth, pigmented skin, low sunshine exposure, obesity, malabsorption and advanced age as the aged skin produces much less vitamin D than the skin in younger people. Rickets was highly prevalent around 1900 in large cities. Nowadays in the Netherlands it is observed among immigrant children due to low sunshine exposure, skin pigmentation and diet. The prevalence of vitamin D deficiency is also high in elderly people compared with adults and especially in residents of homes for the elderly, nursing homes and patients with hip fracture (Lips, 2001). The prevalence of vitamin D deficiency is much higher in Europe than in Asia, Australia or the USA. Within Europe, serum 25(OH)D is positively related to latitude, contrary to what should be expected (Lips et al., 2001). The highest serum 25(OH)D levels were observed in Scandinavian countries and the lowest levels were found in Southern Europe. This may be due to high sun exposure, a light skin and multivitamin use in northern countries while shadow-seeking behaviour and a darker skin are more common in mediterranean countries. Vitamin D deficiency is very common in elderly people, especially in the institutionalized, with a prevalence up to more than 75% in nursing home residents (Holick, 1994). The prevalence of vitamin D insufficiency is also high in Afro-Americans, in which the highly pigmented skin makes the ultraviolet light much less efficacious (Holick, 1994). A high prevalence of vitamin D deficiency has been reported in non-western immigrants in the Netherlands (Grootjans-Geerts, 2001) and similar data have been obtained in the Middle East (Gannage-Yared et al., 2000), where life-style factors probably play a role.<br />Consequences of vitamin D deficiency<br />Severe vitamin D deficiency causes rickets or osteomalacia. In osteomalacia, most surfaces of trabecular and cortical bone are covered with thick osteoid seams. It is very different from osteoporosis where usually only small amounts of osteoid are visible. Vitamin D deficiency also causes higher secretion of PTH due to the low serum 1,25(OH)2D and low serum calcium, and this results in high bone turnover and increased bone resorption. This causes bone loss, mainly from cortical bone and this may contribute to the pathogenesis of osteoporosis. So, on one side severe vitamin D deficiency causes a mineralization problem and osteomalacia and on the other side the high PTH levels cause high bone turnover, bone resorption and osteoporosis and both mechanisms may lead to fractures, especially hip fractures (Lips, 2001). So, there is an inverse relationship between serum 25(OH)D and parathyroid hormone. This was investigated in the Longitudinal Aging Study Amsterdam in 1320 older men and women. Serum PTH decreases when serum 25(OH)D increases and serum PTH stabilizes when there is sufficient 25(OH)D. This plateau was reached around 75 nmol/l, a much higher level than was previously assumed (Lips et al., 2005). Similar data also have been reported from the USA and France. Vitamin D supplementation to vitamin D-deficient elderly results in an increase of serum 25(OH)D levels and decrease of serum PTH and an increase of bone mineral density. This increase may depend on variations in the vitamin D receptor DNA structure, so called polymorphisms. In the vitamin D study performed in Amsterdam, the increase of bone mineral density in the femoral neck with vitamin D supplementation depended on the vitamin D receptor genotype (Lips, 2001).<br />Al-Mustaqbal University the first university in Iraq