previtamin-d(3) and Vitamin-D-Deficiency

Vitamin D is the sunshine vitamin for good reason. During exposure to sunlight, the UV B photons enter the skin and photolyze 7-dehydrocholesterol to previtamin D3 which in turn is isomerized by the body's temperature to vitamin D3. Most humans have depended on sun for their vitamin D requirement. Skin pigment, sunscreen use, aging, time of day, season and latitude dramatically affect previtamin 13 synthesis. Vitamin D deficiency was thought to have been conquered, but it is now recognized that more than 50% of the world's population is at risk for vitamin D deficiency. This deficiency is in part due to the inadequate fortification of foods with vitamin D and the misconception that a healthy diet contains an adequate amount of vitamin D. Vitamin D deficiency causes growth retardation and rickets in children and will precipitate and exacerbate osteopenia, osteoporosis and increase risk of fracture in adults. The vitamin D deficiency has been associated pandemic with other serious consequences including increased risk of common cancers, autoimmune diseases, infectious diseases and cardiovascular disease. There needs to be a renewed appreciation of the beneficial effect of moderate sunlight for providing all humans with their vitamin D requirement for health.

Topics: Aging; Bone Diseases, Metabolic; Cholecalciferol; Dehydrocholesterols; Humans; Osteoporosis; Photolysis; Rickets; Skin; Skin Neoplasms; Skin Pigmentation; Sunlight; Sunscreening Agents; Ultraviolet Rays; Vitamin D; Vitamin D Deficiency

Vitamin D is a compound responsible for maintaining mineral homeostasis. It protects against calcium and phosphate deficiency through the effects on the intestine, kidney, parathyroid gland and bone. All mechanisms that help maintain mineral homeostasis of the body are regulated by the vitamin D hormonal form - calcitriol. Synthesis of vitamin D starts in the skin as a non-enzymatic process, which begins during exposure to sunlight, when the absorption of ultraviolet B (UVB) radiation results in convertion of 7-dehydrocholesterol, a metabolite of cholesterol that is stored in the skin, to precholecalciferol (previtamin-D₃) that is immediately converted into cholecalciferol (vitamin D₃). After the skin synthesis cholecalciferol is transported to the liver where it undergoes hydroxylation, what results in formation of calcidiol (25(OH)D₃). The second metabolic process takes place in the kidney, where calcidiol undergoes hydroxylation at the C-1 position to the hormonal, the most active metabolite - 1,25-dihydroxyvitamin D (calcitriol). Vitamin D deficiency may result in bone diseases, such as rickets in children and osteomalacia and osteoporosis in adults. Symptoms of osteomalacia affect mainly the skeletal system and are similar to that observed in rickets. It concerns thoracic kyphosis, pelvis deformities and also the varus knee. Osteoporosis is another condition that is related to abnormalities of mineral homeostasis. It is characterized by the progressive loss of bone mass, impaired bone microarchitecture, and consequently increased fragility and susceptibility to fracture. For the last several years other, non-classic actions of vitamin D₃ have been discussed. It was engendered by the discovery of vitamin D3 receptor (VDR) in the most of body tissues and cells. Hence, there are many hypotheses which suggest the inverse relationship between vitamin D status and various diseases, such as cancer, autoimmune diseases, diabetes mellitus and others.

Topics: Adult; Aged; Child; Cholecalciferol; Humans; Photosynthesis; Skin; Sunlight; Ultraviolet Rays; Vitamin D; Vitamin D Deficiency

The sun is our most important source of vitamin D. Exposure to solaria, in sub-erythemogenic doses, also gives large amounts of this vitamin. The ultraviolet radiation in these sources converts 7-dihydrocholesterol to previtamin D3 in the skin. Furthermore, heat isomerization to vitamin D3 takes place, then transport to the liver and hydroxylation to calcidiol, which is transported to the kidneys and hydroxylated to the active hormone calcitriol. The vitamin D3 status of the body is supposed to be reliably imaged by calcidiol measurements. Calcidiol levels above 12.5 nmol/l prevent rickets and osteomalacia, but optimal levels are probably higher, in the range 100-250 nmol/l. A daily food intake of 100-200 microg vitamin D3 (50-100 g cod-liver oil), or a weekly exposure to two minimal erythemal doses of ultraviolet radiation (20 to 40 minutes whole body exposure to midday midsummer sun in Oslo, Norway), will give this level. An adequate supply of vitamin D3 seems to reduce the incidence rates or improve the prognosis of several cancer forms, including prostate, breast and colon cancer, as well as of lymphomas. Several other diseases are related to a low vitamin D3 status: heart diseases, multiple sclerosis, diabetes, and arthritis. The action mechanisms of vitamin D are thought to be mainly related to its known cell-differentiating and immuno-modulating effects. Even though most of the 250 annual death cases from skin cancer in Norway are caused by sun exposure, we should, in view of the health effects of ultraviolet radiation, consider modifying our restrictive attitude towards sun exposure and use of solaria.

Topics: Calcifediol; Cholecalciferol; Female; Humans; Liver; Male; Photosynthesis; Risk Factors; Skin; Sunlight; Ultraviolet Rays; Vitamin D; Vitamin D Deficiency

Topics: Adult; Aged; Animals; Calcifediol; Calcitriol; Child; Cholecalciferol; Dehydrocholesterols; Dihydroxycholecalciferols; Ergocalciferols; Female; Humans; Hydroxycholecalciferols; Infant, Newborn; Liver; Nutritional Requirements; Pregnancy; Skin; Species Specificity; Ultraviolet Rays; Vitamin D; Vitamin D Deficiency

Severe burn injury is associated with vitamin D deficiency, low bone turnover, and abnormalities in calcium homoeostasis. Patients do not routinely receive vitamin D supplementation and sun exposure is currently not controlled. By analysis of skin biopsy samples for vitamin D3 precursors after exposure to ultraviolet B light we found that the conversion of 7-dehydrocholesterol to previtamin D3 was reduced in children a mean of 14 months after the burn. Low serum 25-hydroxyvitamin D concentrations were also found. We conclude that vitamin D supplementation is necessary after burn injury.

Topics: Adolescent; Burns; Child; Child, Preschool; Cholecalciferol; Dietary Supplements; Female; Follow-Up Studies; Humans; Male; Skin; Vitamin D; Vitamin D Deficiency

Topics: Calcitriol; Cholecalciferol; Dehydrocholesterols; Ergosterol; Humans; Isomerism; Skin; Skin Pigmentation; Stereoisomerism; Sunlight; Temperature; Ultraviolet Therapy; Vitamin D; Vitamin D Deficiency