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Although tentative data link low levels of vitamin D to asthma , evidence to support a beneficial effect on asthmatics from supplementation is inconclusive.

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

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.

Cognition and dementia -- A systematic review of clinical studies found an association between low vitamin D levels with cognitive impairment and a higher risk of developing Alzheimer's disease.

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reference intake for vitamin D issued in by the Institute of Medicine IoM renamed National Academy of Medicine in , superseded previous recommendations which were expressed in terms of Adequate Intake.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

For U. 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] [6] 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.

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 25 OH D levels in almost all persons.

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. Idiopathic infantile hypercalcemia is caused by a mutation of the CYP24A1 gene, leading to a reduction in the degradation of vitamin D.

Infants suffering from such a mutation have an increased sensitivity to vitamin D and in case of additional intake a risk of hypercalcaemia.

Pregnant or breastfeeding women should consult a doctor before taking a vitamin D supplement. 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 kidney 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 the liver and in the kidneys.

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: the inner layer called the dermis , composed largely of connective tissue , and the outer, thinner epidermis.

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.

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, respectively.

American researchers Elmer McCollum and Marguerite Davis in [12] 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 , [12] 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: "Light equals vitamin D. A meeting took place with J. Haldane , 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.

They state further: "however, most evidence for these roles comes from in vitro, animal, and epidemiological studies, not the randomized clinical trials considered to be more definitive.

Until such trials are conducted, the implications of the available evidence for public health and patient care will be debated".

Some preliminary studies link low vitamin D levels with disease later in life. Vitamin D deficiency is widespread in the European population.

Apart from VDR activation, various alternative mechanisms of action are under study, such as inhibition of signal transduction by hedgehog , a hormone involved in morphogenesis.

From Wikipedia, the free encyclopedia. Group of chemical compounds. For other uses, see Vitamin D disambiguation.

This article is about the family of vitamers. For individual forms, see ergocalciferol , cholecalciferol , vitamin D4 , and vitamin D5.

Main article: Vitamin D deficiency. Main article: Rickets. Main articles: Osteoporosis and Osteomalacia.

The examples and perspective in this article may not represent a worldwide view of the subject. You may improve this article , discuss the issue on the talk page , or create a new article , as appropriate.

February Learn how and when to remove this template message. Further information: hypervitaminosis D. The American Journal of Clinical Nutrition.

Mayo Clinic Proceedings. Retrieved July 22, October Bibcode : Sci The Journal of Nutrition. February 11, Retrieved June 6, This article incorporates text from this source, which is in the public domain.

American Association for Clinical Chemistry. Retrieved June 23, Calcified Tissue International. A metabolite of vitamin D active in intestine".

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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 kidney 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 the liver and in the kidneys.

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: the inner layer called the dermis , composed largely of connective tissue , and the outer, thinner epidermis.

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. 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, respectively.

American researchers Elmer McCollum and Marguerite Davis in [12] 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 , [12] 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: "Light equals vitamin D. A meeting took place with J. Haldane , 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. They state further: "however, most evidence for these roles comes from in vitro, animal, and epidemiological studies, not the randomized clinical trials considered to be more definitive.

Until such trials are conducted, the implications of the available evidence for public health and patient care will be debated".

Some preliminary studies link low vitamin D levels with disease later in life. Vitamin D deficiency is widespread in the European population.

Apart from VDR activation, various alternative mechanisms of action are under study, such as inhibition of signal transduction by hedgehog , a hormone involved in morphogenesis.

From Wikipedia, the free encyclopedia. Group of chemical compounds. For other uses, see Vitamin D disambiguation.

This article is about the family of vitamers. For individual forms, see ergocalciferol , cholecalciferol , vitamin D4 , and vitamin D5.

Main article: Vitamin D deficiency. Main article: Rickets. Main articles: Osteoporosis and Osteomalacia. The examples and perspective in this article may not represent a worldwide view of the subject.

You may improve this article , discuss the issue on the talk page , or create a new article , as appropriate. February Learn how and when to remove this template message.

Further information: hypervitaminosis D. The American Journal of Clinical Nutrition. Mayo Clinic Proceedings.

Retrieved July 22, October Bibcode : Sci The Journal of Nutrition. February 11, Retrieved June 6, This article incorporates text from this source, which is in the public domain.

American Association for Clinical Chemistry. Retrieved June 23, Calcified Tissue International. A metabolite of vitamin D active in intestine".

March Annals of Internal Medicine. August January The Lancet. University of California, Riverside. November Retrieved January 24, Medical Physiology E-Book.

Elsevier Health Sciences. Journal of Cellular Biochemistry. Canadian Journal of Physiology and Pharmacology.

Brain Research. Molecular Brain Research. The American Journal of Sports Medicine. National Health Service. March 8, Retrieved July 9, February The Journal of Clinical Endocrinology and Metabolism.

The New England Journal of Medicine. Nutrition Through the Life Cycle. Cengage Learning. The British Journal of Nutrition.

Lerch C ed. Postgraduate Medical Journal. Calcified Tissue International Review. Clinical Nutrition Review.

Journal of Tropical Pediatrics. The Proceedings of the Nutrition Society. Journal of Human Nutrition and Dietetics. Office of Science Education.

Archived from the original on June 8, Retrieved August 24, The Nutrition Desk Reference. NYU Press. Discovering Nutrition. A systematic review and meta-analysis".

Clinical Rheumatology. Therapeutic Advances in Musculoskeletal Disease. Progress in Cardiovascular Diseases. Nature Reviews.

September Pediatric Research. July Rheumatology International. National Academies Press.

June The Cochrane Database of Systematic Reviews. Preventive Services Task Force". Sports Health. May 27, Retrieved May 16, American Journal of Epidemiology Review.

The Oncologist. JAMA Cardiology. May Vitamins and the Immune System. Journal of Clinical Virology.

Topics in Antiviral Medicine. International Journal of Epidemiology. The American Journal of the Medical Sciences. Bibcode : PLoSO European Journal of Clinical Nutrition.

Retrieved June 29, Retrieved May 20, Discovery Medicine. Inflammatory Bowel Diseases. World Journal of Diabetes Review. April Psychosomatic Medicine.

JAMA Pediatrics. Obesity Reviews. EFSA Journal. Health Claim Regarding Calcium and Osteoporosis". May 1, June 1, Archived from the original PDF on March 6, Retrieved January 29, Australian Ministry of Health.

September 9, Archived from the original on February 27, Nutrition and Healthy Eating. Health Canada. December 5, Retrieved April 28, National Health and Medical Research Council.

Archived from the original PDF on January 21, FR page " PDF. Retrieved August 20, December 30, December 21, Australian Broadcasting Corporation.

February 18, Retrieved July 21, Public Health England. July 21, Swedish National Food Agency. Retrieved October 19, DRI, Dietary reference intakes: for calcium, phosphorus, magnesium, vitamin D, and fluoride.

Washington, D. C: National Academy Press. Journal of Nutritional Science and Vitaminology. Spec No: 79— Journal of Photochemistry and Photobiology.

B, Biology Submitted manuscript. Skip to main content. Google Tag Manager. Happy 4th of July! Quantify IFN gamma with Confidence! Assays for cell therapy and cytokine research.

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Kidney damage may be irreversible. Medicine Monsterquest. Psychosomatic Medicine. May 27, Furthermore, proteinuriaurinary castsazotemiaand metastatic calcification especially in the kidneys may develop. Enteroglucagon Taccos YY. The reference intake for vitamin D refers to total intake from food, beverages and supplements, and assumes that calcium requirements are being met. Philpot J, Webster TA October 21, The British Journal of Nutrition. Views Read Edit View history. Retrieved July 22, A metabolite of vitamin D active in intestine". Nie 9. Kommunikation der Krankenhäuser steht vor neuen digitalen Herausforderungen: Gibt https://newtheater.co/free-casino-online/spioele.php die eine Lösung? Damit bleibt der Merkzettel auch über mehrere More info hinweg bestehen. Angela Rausch Zum Blogeintrag. Führen und archivieren Sie Ihre Herstelldokumentation elektronisch. ÖWA ioam Die See more der Chargendokumentation kann in elektronischer Form erfolgen, ebenso die digitale Führung Ihres Monsterquest. Groupify :. Www D

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