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Vitamin D is a group of fat-soluble secosteroids responsible for increasing intestinal absorption of calcium , magnesium , and phosphate , and multiple other biological effects.

The major natural source of the vitamin is synthesis of cholecalciferol in the skin from cholesterol through a chemical reaction that is dependent on sun exposure specifically UVB radiation.

Vitamin D from the diet or skin synthesis is biologically inactive; enzymatic conversion hydroxylation in the liver and kidney is required for activation.

As vitamin D can be synthesized in adequate amounts by most mammals exposed to sufficient sunlight, it is not an essential dietary factor, and so not technically a vitamin.

Calcitriol also has other effects, including some on cell growth, neuromuscular and immune functions, and reduction of inflammation. Vitamin D has a significant role in calcium homeostasis and metabolism.

Its discovery was due to effort to find the dietary substance lacking in children with rickets the childhood form of osteomalacia. Several forms vitamers of vitamin D exist.

The two major forms are vitamin D 2 or ergocalciferol, and vitamin D 3 or cholecalciferol; vitamin D without a subscript refers to either D 2 or D 3 or both.

These are known collectively as calciferol. In , the chemical structure of vitamin D 3 was established and proven to result from the ultraviolet irradiation of 7-dehydrocholesterol.

Chemically, the various forms of vitamin D are secosteroids , i. The active vitamin D metabolite calcitriol mediates its biological effects by binding to the vitamin D receptor VDR , which is principally located in the nuclei of target cells.

VDR activation in the intestine, bone, kidney, and parathyroid gland cells leads to the maintenance of calcium and phosphorus levels in the blood with the assistance of parathyroid hormone and calcitonin and to the maintenance of bone content.

One of the most important roles of vitamin D is to maintain skeletal calcium balance by promoting calcium absorption in the intestines, promoting bone resorption by increasing osteoclast number, maintaining calcium and phosphate levels for bone formation , and allowing proper functioning of parathyroid hormone to maintain serum calcium levels.

Vitamin D deficiency can result in lower bone mineral density and an increased risk of reduced bone density osteoporosis or bone fracture because a lack of vitamin D alters mineral metabolism in the body.

The VDR regulates cell proliferation and differentiation. Vitamin D also affects the immune system, and VDRs are expressed in several white blood cells , including monocytes and activated T and B cells.

A diet deficient in vitamin D in conjunction with inadequate sun exposure causes osteomalacia or rickets when it occurs in children , which is a softening of the bones.

In the developed world, this is a rare disease. Rickets , a childhood disease, is characterized by impeded growth and soft, weak, deformed long bones that bend and bow under their weight as children start to walk.

This condition is characterized by bow legs, [27] which can be caused by calcium or phosphorus deficiency, as well as a lack of vitamin D; today, it is largely found in low-income countries in Africa, Asia, or the Middle East [28] and in those with genetic disorders such as pseudovitamin D deficiency rickets.

Maternal vitamin D deficiency may cause overt bone disease from before birth and impairment of bone quality after birth.

Although rickets and osteomalacia are now rare in Britain, outbreaks have happened in some immigrant communities in which osteomalacia sufferers included women with seemingly adequate daylight outdoor exposure wearing Western clothing.

Vitamin D deficiency remains the main cause of rickets among young infants in most countries, because breast milk is low in vitamin D and social customs and climatic conditions can prevent adequate sun exposure.

In sunny countries such as Nigeria, South Africa, and Bangladesh, where rickets occurs among older toddlers and children, it has been attributed to low dietary calcium intakes, which are characteristic of cereal-based diets with limited access to dairy products.

Osteomalacia is a disease in adults that results from vitamin D deficiency. Characteristics of this disease are softening of the bones, leading to bending of the spine, bowing of the legs, proximal muscle weakness, bone fragility, and increased risk for fractures.

Dark-skinned people living in temperate climates have been shown to have low vitamin D levels but the significance of this is not certain.

The effects of vitamin D supplementation on health are uncertain. A United States Institute of Medicine report states: Research on vitamin D supplements, including large-scale clinical trials, is continuing.

Vitamin D 3 supplementation has been tentatively found to lead to a reduced risk of death in the elderly, [12] [53] but the effect has not been deemed pronounced or certain enough to make taking supplements recommendable.

In general, no good evidence supports the commonly held belief that vitamin D supplements can help prevent osteoporosis. Because it found mounting evidence for a benefit to bone health, though it had not found good evidence of other benefits, the US Food and Drug Administration has required manufacturers to declare the amount of vitamin D on nutrition facts labels , as "nutrients of public health significance", since May Vitamin D supplements have been widely marketed for their claimed anticancer properties.

Reviews have described the evidence as being "inconsistent, inconclusive as to causality, and insufficient to inform nutritional requirements" [56] and "not sufficiently robust to draw conclusions".

Taking vitamin D supplements does not meaningfully reduce the risk of stroke , cerebrovascular disease , cardial infarction , or ischaemic heart disease.

In general, vitamin D functions to activate the innate and dampen the adaptive immune systems. Although tentative data link low levels of vitamin D to asthma , evidence to support a beneficial effect on asthmatics from supplementation is inconclusive.

Diabetes -- A systematic review of concluded that the available studies show no evidence of vitamin D3 supplementation having an effect on glucose homeostasis or diabetes prevention.

Depression -- Clinical trials of vitamin D supplementation for depressive symptoms have generally been of low quality and show no overall effect, although subgroup analysis showed supplementation for participants with clinically significant depressive symptoms or depressive disorder had a moderate effect.

However, lower vitamin D concentrations are also associated with poor nutrition and spending less time outdoors.

Therefore, alternative explanations for the increase in cognitive impairment exist and hence a direct causal relationship between vitamin D levels and cognition could not be established.

Pregnancy -- Low levels of vitamin D in pregnancy are associated with gestational diabetes , pre-eclampsia , and small for gestational age infants.

Weight loss -- Though hypothesized that vitamin D supplementation may be an effective treatment for obesity apart from calorie restriction , one systematic review found no association of supplementation with body weight or fat mass.

Governmental regulatory agencies stipulate for the food and dietary supplement industries certain health claims as allowable as statements on packaging.

European Food Safety Authority. US Food and Drug Administration. Other possible agencies with claim guidance: Various institutions have proposed different recommendations for the amount of daily intake of vitamin D.

These vary according to precise definition, age, pregnancy or lactation, and the extent assumptions are made regarding skin synthesis of vitamin D.

The dietary reference intake for vitamin D issued in by the Institute of Medicine renamed National Academy of Medicine in , superseded previous recommendations which were expressed in terms of Adequate Intake.

The recommendations were formed assuming the individual has no skin synthesis of vitamin D because of inadequate sun exposure.

The reference intake for vitamin D refers to total intake from food, beverages and supplements, and assumes that calcium requirements are being met.

Health Canada published recommended dietary allowances RDA and tolerable upper intake levels for vitamin D in [] based on the Institute of Medicine report.

Australia and New Zealand published nutrient reference values including guidelines for dietary vitamin D intake in The European Food Safety Authority EFSA in [] reviewed the current evidence, finding the relationship between serum 25 OH D concentration and musculoskeletal health outcomes is widely variable.

The UK National Health Service recommends babies and young children aged six months to five years, pregnant or breastfeeding women, and sun-deprived elderly people should take daily vitamin supplements to ensure sufficient vitamin D intake.

Non-government organisations in Europe have made their own recommendations. Although vitamin D is not present naturally in most foods, [2] [4] it is commonly added as a fortification in manufactured foods.

In some countries, staple foods are artificially fortified with vitamin D. In general, vitamin D 2 is found in fungi and vitamin D 3 is found in animals.

The vitamin D 2 content in mushrooms and Cladina arbuscula , a lichen, increase with exposure to ultraviolet light. Manufactured foods fortified with Vitamin D include some fruit juices and fruit juice drinks, meal replacement energy bars , soy protein -based beverages, certain cheese and cheese products, flour products, infant formulas , many breakfast cereals , and milk.

While some studies have found that vitamin D 3 raises 25 OH D blood levels faster and remains active in the body longer, [] [] others contend that vitamin D 2 sources are equally bioavailable and effective as D 3 for raising and sustaining 25 OH D.

Vitamin D content in typical foods is reduced variably by cooking. Recommendations on recommended 25 OH D serum levels vary across authorities, and vary based on factors like age.

No contributions to serum 25 OH D level are assumed from sun exposure and the recommendations are fully applicable to people with dark skin or negligible exposure to sunlight.

Vitamin D toxicity is rare. Pregnant or breastfeeding women should consult a doctor before taking a vitamin D supplement. In addition, for products intended for infants, the FDA recommends the dropper hold no more than IU.

One thousand micrograms per day in infants has produced toxicity within one month. Calcitriol itself is auto-regulated in a negative feedback cycle, and is also affected by parathyroid hormone , fibroblast growth factor 23 , cytokines , calcium, and phosphate.

Vitamin D overdose causes hypercalcemia, which is a strong indication of vitamin D toxicity — this can be noted with an increase in urination and thirst.

If hypercalcemia is not treated, it results in excess deposits of calcium in soft tissues and organs such as the kidneys, liver, and heart, resulting in pain and organ damage.

The main symptoms of vitamin D overdose which are those of hypercalcemia including anorexia , nausea, and vomiting.

These may be followed by polyuria , polydipsia , weakness, insomnia, nervousness, pruritus and ultimately renal failure. Furthermore, proteinuria , urinary casts , azotemia , and metastatic calcification especially in the kidneys may develop.

Vitamin D toxicity is treated by discontinuing vitamin D supplementation and restricting calcium intake.

Kidney damage may be irreversible. Exposure to sunlight for extended periods of time does not normally cause vitamin D toxicity.

The concentrations of vitamin D precursors produced in the skin reach an equilibrium , and any further vitamin D produced is degraded.

Synthesis of vitamin D in nature is dependent on the presence of UV radiation and subsequent activation in liver and in kidney.

Many animals synthesize vitamin D 3 from 7-dehydrocholesterol , and many fungi synthesize vitamin D 2 from ergosterol.

Click on icon in lower right corner to open. Click on genes, proteins and metabolites below to link to respective articles.

The transformation that converts 7-dehydrocholesterol to vitamin D 3 occurs in two steps. The process is faster in white button mushrooms.

Vitamin D 3 is produced photochemically from 7-dehydrocholesterol in the skin of most vertebrate animals, including humans. Exposure to light through windows is insufficient because glass almost completely blocks UVB light.

The darker the skin, and the weaker the sunlight, the more minutes of exposure are needed. Vitamin D overdose is impossible from UV exposure; the skin reaches an equilibrium where the vitamin degrades as fast as it is created.

Sunscreen absorbs or reflects ultraviolet light and prevents much of it from reaching the skin. The skin consists of two primary layers: Vitamin D is produced in the keratinocytes [] of two innermost strata, the stratum basale and stratum spinosum.

Vitamin D can be synthesized only by a photochemical process. Phytoplankton in the ocean such as coccolithophore and Emiliania huxleyi have been photosynthesizing vitamin D for more than million years.

Primitive vertebrates in the ocean could absorb calcium from the ocean into their skeletons and eat plankton rich in vitamin D.

Land vertebrates required another source of vitamin D other than plants for their calcified skeletons. They had to either ingest it or be exposed to sunlight to photosynthesize it in their skin.

In birds and fur-bearing mammals, fur or feathers block UV rays from reaching the skin. Instead, vitamin D is created from oily secretions of the skin deposited onto the feathers or fur, and is obtained orally during grooming.

Vitamin D 3 cholecalciferol is produced industrially by exposing 7-dehydrocholesterol to UVB light, followed by purification.

Vitamin D 2 ergocalciferol is produced in a similar way using ergosterol from yeast or mushrooms as a starting material. Vitamin D is carried in the bloodstream to the liver, where it is converted into the prohormone calcifediol.

Circulating calcifediol may then be converted into calcitriol , the biologically active form of vitamin D, in the kidneys. Whether it is made in the skin or ingested, Vitamin D is hydroxylated in the liver at position 25 upper right of the molecule to form hydroxycholecalciferol calcifediol or 25 OH D.

The conversion of calcifediol to calcitriol is catalyzed by the enzyme hydroxyvitamin D 3 1-alpha-hydroxylase , which is the product of the CYP27B1 human gene.

The activity of CYP27B1 is increased by parathyroid hormone , and also by low calcium or phosphate. Following the final converting step in the kidney, calcitriol is released into the circulation.

By binding to vitamin D-binding protein, calcitriol is transported throughout the body, including to the classical target organs of intestine, kidney and bone.

In addition to the kidneys, calcitriol is also synthesized by certain other cells including monocyte - macrophages in the immune system.

When synthesized by monocyte-macrophages, calcitriol acts locally as a cytokine , modulating body defenses against microbial invaders by stimulating the innate immune system.

The activity of calcifediol and calcitriol can be reduced by hydroxylation at position 24 by vitamin D3 hydroxylase , forming secalciferol and calcitetrol respecively.

American researchers Elmer McCollum and Marguerite Davis in [9] discovered a substance in cod liver oil which later was called "vitamin A".

British doctor Edward Mellanby noticed dogs that were fed cod liver oil did not develop rickets and concluded vitamin A, or a closely associated factor, could prevent the disease.

In , Elmer McCollum tested modified cod liver oil in which the vitamin A had been destroyed. He called it vitamin D because it was the fourth vitamin to be named.

In , [9] it was established that when 7-dehydrocholesterol is irradiated with light, a form of a fat-soluble vitamin is produced now known as D 3.

Alfred Fabian Hess stated: A meeting took place with J. Bernal , and Dorothy Crowfoot to discuss possible structures, which contributed to bringing a team together.

X-ray crystallography demonstrated the sterol molecules were flat, not as proposed by the German team led by Windaus. In , Otto Rosenheim and Harold King published a paper putting forward structures for sterols and bile acids which found immediate acceptance.

In the s, Windaus clarified further the chemical structure of vitamin D. In , American biochemist Harry Steenbock at the University of Wisconsin demonstrated that irradiation by ultraviolet light increased the vitamin D content of foods and other organic materials.

A vitamin D deficiency is a known cause of rickets. His irradiation technique was used for foodstuffs, most memorably for milk. By the expiration of his patent in , rickets had been all but eliminated in the US.

In , after studying nuclear fragments of intestinal cells, a specific binding protein for Vitamin D called the Vitamin D Receptor was identified by Mark Haussler and Tony Norman.

In the liver, vitamin D was found to be converted to calcifediol. Calcifediol is then converted by the kidneys to calcitriol, the biologically active form of vitamin D.

The vitamin D metabolites, calcifediol and calcitriol, were identified by competing teams led by Michael F. There is considerable research activity looking at effects of vitamin D and its metabolites in animal models, cell systems, gene expression studies, epidemiology and clinical therapeutics.

These different types of studies can produce conflicting evidence as to the benefits of interventions with vitamin D. They suggest, for some people, reducing the risk of preventable disease requires a higher level of vitamin D than that recommended by the IOM.

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