45 Facts About Vitamin D

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

Dietary recommendations typically assume that all of a person's vitamin D is taken by mouth, because sun exposure in the population is variable and recommendations about the amount of sun exposure that is safe are uncertain in view of the skin cancer risk.

Vitamin D has a significant role in calcium homeostasis and metabolism.

Vitamin D supplements are given to treat or to prevent osteomalacia and rickets.

Chemically, the various forms of vitamin D are secosteroids, that is, steroids in which one of the bonds in the steroid rings is broken.

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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 affects the immune system, and VDRs are expressed in several white blood cells, including monocytes and activated T and B cells.

Severe vitamin D deficiency in children causes rickets, a softening and weakening of bones, which is a rare disease in the developed world.

Vitamin D deficiency is found worldwide in the elderly and remains common in children and adults.

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.

An increase in the proportion of animal protein in the 20th century American diet coupled with increased consumption of milk fortified with relatively small quantities of vitamin D coincided with a dramatic decline in the number of rickets cases.

Vitamin D deficiency is common in Hispanic and African-Americans in the United States, with levels dropping significantly in the winter.

Supplementation with vitamin D is a reliable method for preventing or treating rickets.

Vitamin D supplements do not alter the outcomes for myocardial infarction, stroke or cerebrovascular disease, cancer, bone fractures or knee osteoarthritis.

Research on vitamin D supplements, including large-scale clinical trials, is continuing.

Harm from vitamin D appears to occur at a lower vitamin D level in the black population than in the white population.

Low serum vitamin D levels have been associated with falls, and low bone mineral density.

Vitamin D supplementation is not associated with a reduced risk of stroke, cerebrovascular disease, myocardial infarction, or ischemic heart disease.

Low levels of vitamin D appear to be a risk factor for tuberculosis, and historically it was used as a treatment.

In general practice, supplementation with vitamin D is not recommended for treatment or prevention of asthma.

Low levels of vitamin D are associated with two major forms of human inflammatory bowel disease : Crohn's disease and ulcerative colitis.

In prospective studies, high versus low level of vitamin D was respectively associated with significant decrease in risk of type 2 diabetes mellitus, combined type 2 diabetes mellitus and pre-diabetes, and pre-diabetes.

ADHD - A meta-analysis of observational studies showed that children with ADHD have lower vitamin D levels, and that there was a small association between low vitamin D levels at the time of birth and later development of ADHD.

Several small randomized controlled trials of vitamin D supplementation indicated improved ADHD symptoms such as impulsivity and hyperactivity.

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

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Schizophrenia - Trials have demonstrated lower vitamin D levels are highly prevalent in patients with schizophrenia, particularly those with acute episodes.

Vitamin D supplementation is likely to reduce the risk of gestational diabetes, undersized babies and of their poor rate of growth.

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 Conversion: 1µg = 40IU .

Dietary reference intake for vitamin D issued in 2010 by the Institute of Medicine, superseded previous recommendations which were expressed in terms of Adequate Intake.

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

Vitamin D2 is found in fungi and is produced by ultraviolet irradiation of ergosterol.

The dietary reference intakes for vitamin D are chosen with a margin of safety and 'overshoot' the targeted serum value to ensure the specified levels of intake achieve the desired serum 25D levels in almost all persons.

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.

Main symptoms of vitamin D overdose are hypercalcemia including anorexia, nausea, and vomiting.

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

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

Vitamin D3 is produced photochemically from 7-dehydrocholesterol in the skin of most vertebrate animals, including humans.

Vitamin D is produced in the keratinocytes of two innermost strata of the epidermis, the stratum basale and stratum spinosum, which are able to produce calcitriol and express the VDR.

Vitamin D can be synthesized only by a photochemical process.

Vitamin D3 is produced industrially by exposing 7-dehydrocholesterol to UVB and UVC light, followed by purification.

Vitamin D2 is produced in a similar way using ergosterol from yeast or mushrooms as a starting material.

Vitamin D is carried via the blood to the liver, where it is converted into the prohormone calcifediol.

Whether synthesized in the skin or ingested, vitamin D is hydroxylated in the liver at position 25 to form 25-hydroxycholecalciferol .

Vitamin D was discovered in 1922 following on from previous research.

In 1969, 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.

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