Vitamin D

[박대선]

Vitamin D

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From Wikipedia, the free encyclopedia

For other uses, see Vitamin D (disambiguation).

This article is about the family of D-"vitamins". For individual forms, see ergocalciferol, cholecalciferol, vitamin D4, vitamin D5, and calcitriol.

Vitamin DClass identifiersSynonymsUseATC codeBiological targetClinical dataDrugs.comExternal linksMeSHLegal status

Drug class

Cholecalciferol (D3)

Calciferols

Rickets, osteoporosis, osteomalacia, vitamin D deficiency

A11CC

vitamin D receptor

MedFacts Natural Products

D014807

In Wikidata

Vitamin D is a group of structurally related, fat-soluble compounds responsible for increasing intestinal absorption of calcium, magnesium, and phosphate, along with numerous other biological functions.[1][2] In humans, the most important compounds within this group are vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol).[2][3]

Unlike the other twelve vitamins, vitamin D is only conditionally essential, as with adequate skin exposure to the ultraviolet B (UVB) radiation component of sunlight there is synthesis of cholecalciferol in the lower layers of the skin's epidermis. For most people, skin synthesis contributes more than diet sources.[4] Vitamin D can also be obtained through diet, food fortification and dietary supplements.[2] In the U.S., cow's milk and plant-based milk substitutes are fortified with vitamin D3, as are many breakfast cereals. Government dietary recommendations typically assume that all of a person's vitamin D is taken by mouth, given the potential for insufficient sunlight exposure due to urban living, cultural choices for the amount of clothing worn when outdoors, and use of sunscreen because of concerns about safe levels of sunlight exposure, including the risk of skin cancer.[2][5]: 362–394 

Cholecalciferol is converted in the liver to calcifediol (also known as calcidiol or 25-hydroxycholecalciferol), while ergocalciferol is converted to ercalcidiol (25-hydroxyergocalciferol). These two vitamin D metabolites, collectively referred to as 25-hydroxyvitamin D or 25(OH)D, are measured in serum to assess a person's vitamin D status. Calcifediol is further hydroxylated by the kidneys and certain immune cells to form calcitriol (1,25-dihydroxycholecalciferol; 1,25(OH)2D), the biologically active form of vitamin D.[3] Calcitriol attaches to vitamin D receptors, which are nuclear receptors found in various tissues throughout the body.

Vitamin D is essential for increasing bone density, therefore causing healthy growth spurts.[6]

The discovery of the vitamin in 1922 was due to an effort to identify the dietary deficiency in children with rickets.[7][8] Adolf Windaus received the Nobel Prize in Chemistry in 1928 for his work on the constitution of sterols and their connection with vitamins.[9] Present day, government food fortification programs in some countries and recommendations to consume vitamin D supplements are intended to prevent or treat vitamin D deficiency rickets and osteomalacia. There are many other health conditions linked to vitamin D deficiency. However, the evidence for the health benefits of vitamin D supplementation in individuals who are already vitamin D sufficient is unproven.[2][10][11][12]

Types[edit]

NameChemical compositionStructureVitamin D1Vitamin D2Vitamin D3Vitamin D4Vitamin D5

Mixture of molecular compounds of ergocalciferol with lumisterol, 1:1
ergocalciferol (made from ergosterol)
cholecalciferol(made from 7-dehydrocholesterol in the skin).
22-dihydroergocalciferol
sitocalciferol(made from 7-dehydrositosterol)

Several forms (vitamers) of vitamin D exist, with the two major forms being vitamin D2 or ergocalciferol, and vitamin D3 or cholecalciferol.[1] The common-use term "vitamin D" refers to both D2 and D3, which were chemically characterized, respectively, in 1931 and 1935. Vitamin D3 was shown to result from the ultraviolet irradiation of 7-dehydrocholesterol. Although a chemical nomenclature for vitamin D forms was recommended in 1981,[13] alternative names remain commonly used.[3]

Chemically, the various forms of vitamin D are secosteroids, meaning that one of the bonds in the steroid rings is broken.[14] The structural difference between vitamin D2 and vitamin D3 lies in the side chain: vitamin D2 has a double bond between carbons 22 and 23, and a methyl group on carbon 24. Vitamin D analogues have also been synthesized.[3]

Biology[edit]

The active vitamin D metabolite, calcitriol, exerts its biological effects by binding to the vitamin D receptor (VDR), which is primarily located in the nuclei of target cells.[1][14] When calcitriol binds to the VDR, it enables the receptor to act as a transcription factor, modulating the gene expression‎ of transport proteins involved in calcium absorption in the intestine, such as TRPV6 and calbindin.[15] The VDR is part of the nuclear receptor superfamily of steroid hormone receptors, which are hormone-dependent regulators of gene expression‎. These receptors are expressed in cells across most organs. VDR expression‎ decreases as age increases.[1][4]

Activation of VDR in the intestine, bone, kidney, and parathyroid gland cells plays a crucial role in maintaining calcium and phosphorus levels in the blood, a process that is assisted by parathyroid hormone and calcitonin, thereby supporting bone health.[1][16][4] VDR also regulates cell proliferation and differentiation. Additionally, vitamin D influences the immune system, with VDRs being expressed in several types of white blood cells, including monocytes and activated T and B cells.[17]

Deficiency[edit]

Main article: Vitamin D deficiency

Worldwide, more than one billion people[18] - infants, children, adults and elderly[19] - can be considered vitamin D deficient, with reported percentages dependent on what measurement is used to define "deficient".[20] Deficiency is common in the Middle-East,[19] Asia,[21] Africa[22] and South America,[23] but also exists in North America and Europe.[24][19][25][26] Dark-skinned populations in North America, Europe and Australia have a higher percentage of deficiency compared to light-skinned populations that had their origins in Europe.[27][28][29]

Serum 25(OH)D concentration is used as a biomarker for vitamin D deficiency. Units of measurement are either ng/mL or nmol/L, with one ng/mL equal to 2.5 nmol/L. There is no consensus on defining vitamin D deficiency, insufficiency, sufficiency, or optimal for all aspects of health.[20] According to the US Institute of Medicine Dietary Reference Intake Committee, below 30 nmol/L significantly increases the risk of vitamin D deficiency caused rickets in infants and young children and reduces absorption of dietary calcium from the normal range of 60–80% to as low as 15%, whereas above 40 nmol/L is needed to prevent osteomalacia bone loss in the elderly, and above 50 nmol/L to be sufficient for all health needs.[5]: 75–111  Other sources have defined deficiency as less than 25 nmol/L, insufficiency as 30–50 nmol/L[30] and optimal as greater than 75 nmol/L.[31][32] Part of the controversy is because studies have reported differences in serum levels of 25(OH)D between ethnic groups, with studies pointing to genetic as well as environmental reasons behind these variations. African-American populations have lower serum 25(OH)D than their age-matched white population, but at all ages have superior calcium absorption efficiency, a higher bone mineral density, and as elderly, a lower risk of osteoporosis and fractures.[5]: 439–440  Supplementation in this population to achieve proposed 'standard' concentrations could, in theory, cause harmful vascular calcification.[33]

Using the 25(OH)D assay as a screening tool of the generally healthy population to identify and treat individuals is considered not as cost-effective as a government-mandated fortification program. Instead, there is a recommendation that testing should be limited to those showing symptoms of vitamin D deficiency or who have health conditions known to cause vitamin deficiency.[4][26]

Causes[edit]

Causes of insufficient vitamin D synthesis in the skin include insufficient exposure to UVB light from sunlight due to living in high latitudes (farther distance from the equator with resultant shorter daylight hours in winter). Serum concentration by the end of winter can be lower by one-third to half that at the end of summer.[5]: 100–101, 371–379 [4][34] The preval‎ence of vitamin D deficiency increases with age due to a decrease in 7-dehydrocholesterol synthesis in the skin and a decline in kidney capacity to convert calcidiol to calcitriol,[35] the latter seen to a greater degree in people with chronic kidney disease.[36] Despite these age effects, elderly people can still synthesize sufficient calcitriol if enough skin is exposed to UVB light. Absent that, a dietary supplement is recommended.[35] Other causes of insufficient synthesis are sunlight being blocked by air pollution,[37] urban/indoor living, long-term hospitalizations and stays in extended care facilities, cultural or religious lifestyle choices that favor sun-blocking clothing, recommendations to use sun-blocking clothing or sunscreen to reduce risk of skin cancer, and lastly, the UV-B blocking nature of dark skin.[25]

Consumption of foods that naturally contain vitamin D is rarely sufficient to maintain a recommended serum concentration of 25(OH)D in the absence of the contribution of skin synthesis. Fractional contributions are roughly 20% diet and 80% sunlight.[4] Vegans had a lower dietary intake of vitamin D and lower serum 25(OH)D when compared to omnivores, with lacto-ovo-vegetarians falling in between due to the vitamin content of egg yolks and fortified dairy products.[38] Governments have mandated or voluntary food fortification programs to bridge the difference in, respectively, 15 and 10 countries.[39] The United States is one of the few mandated countries. The original fortification practices, circa the early 1930s, were limited to cow's milk, which had a large effect on reducing infant and child rickets. In July 2016 the US Food and Drug Administration approved the addition of vitamin D to plant milk beverages intended as milk alternatives, such as beverages made from soy, almond, coconut, and oats.[40] At an individual level, people may choose to consume a multivitamin/mineral product or else a vitamin-D-only product.[41]

There are many disease states, medical treatments, and medications that put people at risk for vitamin D deficiency. Chronic diseases that increase risk include kidney[36] and liver failure, Crohn's disease, inflammatory bowel disease, and malabsorption syndromes such as cystic fibrosis, and hyper- or hypo-parathyroidism.[25] Obesity sequesters vitamin D in fat tissues, thereby lowering serum levels,[42] but bariatric surgery to treat obesity interferes with dietary vitamin D absorption, also causing deficiency.[43] Medications interacting with vitamin D metabolism include antiretrovirals, anti-seizure drugs, glucocorticoids, systemic antifungals such as ketoconazole, cholestyramine, and rifampicin.[4][25] Organ transplant recipients receive immunosuppressive therapy that is associated with an increased risk to develop skin cancer, so they are advised to avoid sunlight exposure, and to take a vitamin D supplement.[44]

Treatment[edit]

Daily dose regimens are preferred to admission of large doses at weekly or monthly schedules, and D3 may be preferred over D2, but there is a lack of consensus as to optimal type, dose, duration or what to measure to deem success. Daily regimens on the order of 4,000 IU/day (for other than infants) have a greater effect on 25(OH)D recovery from deficiency and a lower risk of side effects compared to weekly or monthly bolus doses, with the latter as high as 100,000 IU. The only advantage of bolus dosing could be better compliance, as bolus dosing is usually administered by a healthcare professional rather than self-administered.[4] While some studies have found that vitamin D3 raises 25(OH)D blood levels faster and remains active in the body longer,[45][46] others contend that vitamin D2 sources are equally bioavailable and effective for raising and sustaining 25(OH)D.[47][48] If digestive disorders compromise absorption, then intramuscular injection of up to 100,000 IU of vitamin D3 is therapeutic.[4]

Dark skin as deficiency risk[edit]

Melanin, specifically the sub-type eumelanin, is a biomolecule consisting of linked molecules of oxidized amino acid tyrosine. It is produced by cells called melanocytes in a process called melanogenesis. In the skin, melanin is located in the bottom layer (the stratum basale) of the skin's epidermis. Melanin can be permanently incorporated into the skin, resulting in dark skin, or else have its synthesis initiated by exposure to UV radiation, causing the skin to darken as a temporary sun tan. Eumelanin is an effective absorbent of light; the pigment can dissipate over 99.9% of absorbed UV radiation.[49] Because of this property, eumelanin is thought to protect skin cells from sunlight's ultraviolet A (UVA) and ultraviolet B (UVB) radiation damage, reducing the risk of skin tissue folate depletion, preventing premature skin aging and reducing the risks of sunburn and skin cancer.[50] Melanin inhibits UVB-powered vitamin D synthesis in the skin. In areas of the world not distant from the equator, abundant, year-round exposure to sunlight means that even dark-skinned populations have adequate skin synthesis.[51] However, when dark-skinned people cover much of their bodies with clothing for cultural or climate reasons, or are living a primarily indoor life in urban conditions, or live at higher latitudes which provide less sunlight in winter, they are at risk for vitamin D deficiency.[25][52] The last cause has been described as a "latitude-skin color mismatch".[51]

In the United States, vitamin D deficiency is particularly common among non-white Hispanic and African-American populations.[30][51][53] However, despite having on-average 25(OH)D serum concentrations below the 50 nmol/L amount considered sufficient, African Americans have higher bone mineral density and lower fracture risk when compared to European-origin people. Possible mechanisms may include higher calcium retention, lower calcium excretion, and greater bone resistance to parathyroid hormone,[51][53][54] also genetically lower serum vitamin D-binding protein which would result in adequate bioavailable 25(OH)D despite total serum 25(OH)D being lower.[55] The bone density and fracture risk paradox does not necessarily carry over to non-skeletal health conditions such as arterial calcification, cancer, diabetes or all-cause mortality. There is conflicting evidence that in the African American population, 'deficiency' as currently defined increases the risk of non-skeletal health conditions, and some evidence that supplementation increases risk,[51][53] including for harmful vascular calcification.[33] African Americans, and by extension other dark-skinned populations, may need different definitions for vitamin D deficiency, insufficiency, and adequate.[33]

Infant deficiency[edit]

Comparative studies carried out in lactating mothers indicate a mean value of vitamin D content in the breast milk of 45 IU/liter.[56] This vitamin D content is too low to meet the vitamin D requirement of 400 IU/day recommended by several government organizations ("...as breast milk is not a meaningful source of vitamin D."[5]: 385 ). The same government organizations recommend that lactating women consume 600 IU/day,[2][57][58][59] but this is insufficient to raise breast milk content to deliver recommended intake.[56] There is evidence that breast milk content can be increased, but because the transfer of the vitamin from the lactating mother's serum to milk is inefficient, this requires that she consume a dietary supplement above the government-set safe upper limit of 4,000 IU/day.[56] Given the shortfall, there are recommendations that breast-fed infants be fed a vitamin D dietary supplement of 400 IU/day during the first year of life.[56] If not breastfeeding, infant formulas are designed to deliver 400 IU/day for an infant consuming a liter of formula per day[60] - a normal volume for a full-term infant after the first month.[61]

Excess[edit]

Further information: Vitamin D toxicity

Vitamin D toxicity, or hypervitaminosis D, is the toxic state of an excess of vitamin D. It is rare, having occurred historically during a time of unregulated fortification of foods, especially those provided to infants,[5]: 431–432  or in more recently, with consumption of high-dose vitamin D dietary supplements following inappropriate prescribing, non-prescribed consumption of high-dose, over-the-counter preparations, or manufacturing errors resulting in content far in excess of what is on the label.[41][62][63] Ultraviolet light alone - sunlight or tanning beds - can raise serum 25(OH)D concentration to a bit higher than 100 nmol/L, but not to a level that causes hypervitaminosis D, the reasons being that there is a limiting amount of the precursor 7-dehydrocholesterol synthesized in the skin and a negative feedback in the kidney wherein the presence of calcitriol induces diversion to metabolically inactive 24,25-hydroxyvitamin D rather than metabolically active calcitriol (1,25-hydroxyvitamin D).[64] Further metabolism yields calcitroic acid, an inactive water-soluble compound that is excreted in bile.[65]

There is no general agreement about the intake levels at which vitamin D may cause harm. According to the IOM review, "Doses below 10,000 IU/day are not usually associated with toxicity, whereas doses equal to or above 50,000 IU/day for several weeks or months are frequently associated with toxic side effects including documented hypercalcemia."[5]: 427  The normal range for blood concentration of 25-hydroxyvitamin D in adults is 20 to 50 nanograms per milliliter (ng/mL; equivalent to 50 to 125 nmol/L). Blood levels necessary to cause adverse effects in adults are thought to be greater than about 150 ng/mL.[5]: 424–446 

An excess of vitamin D causes abnormally hypercalcaemia (high blood concentrations of calcium), which can cause overcalcification of the bones and soft tissues including arteries, heart, and kidneys. Untreated, this can lead to irreversible kidney failure. Symptoms of vitamin D toxicity may include the following: increased thirst, increased urination, nausea, vomiting, diarrhea, decreased appetite, irritability, constipation, fatigue, muscle weakness, and insomnia.[66][67][68]

In 2011, the U.S. National Academy of Medicine revised tolerable upper intake levels (UL) to protect against vitamin D toxicity. Before the revision the UL for ages 9+ years was 50 μg/d (2000 IU/d).[5]: 424–445  Per the revision: "UL is defined as "the highest average daily intake of a nutrient that is likely to pose no risk of adverse health effects for nearly all persons in the general population".[69] The U.S. ULs in microgram (mcg or μg) and International Units (IU) for both males and females, by age, are:

• 0–6 months: 25 μg/d (1000 IU/d)
• 7–12 months: 38 μg/d (1500 IU/d)
• 1–3 years: 63 μg/d (2500 IU/d)
• 4–8 years: 75 μg/d (3000 IU/d)
• 9+ years: 100 μg/d (4000 IU/d)
• Pregnant and lactating: 100 μg/d (4000 IU/d)

Although in the U.S. the adult UL is set at 4,000 IU/day, over-the-counter products are available at 5,000, 10,000 and even 50,000 IU (the last with directions to take once a week). The percentage of the U.S. population taking over 4,000 IU/day has increased since 1999.[41]

Treatment[edit]

In almost every case, stopping the vitamin D supplementation combined with a low-calcium diet and corticosteroid drugs will allow for a full recovery within a month.[66][67][68]

Special cases[edit]

Idiopathic infantile hypercalcemia is caused by a mutation of the CYP24A1 gene, leading to a reduction in the degradation of vitamin D. Infants who have such a mutation have an increased sensitivity to vitamin D and in case of additional intake a risk of hypercalcaemia.[70] The disorder can continue into adulthood.[71]

Health effects[edit]

Supplementation with vitamin D is a reliable method for preventing or treating rickets. On the other hand, the effects of vitamin D supplementation on non-skeletal health are uncertain.[72][73] A review did not find any effect from supplementation on the rates of non-skeletal disease, other than a tentative decrease in mortality in the elderly.[74] Vitamin D supplements do not alter the outcomes for myocardial infarction, stroke or cerebrovascular disease, cancer, bone fractures or knee osteoarthritis.[11][75]

A US Institute of Medicine (IOM) report states: "Outcomes related to cancer, cardiovascular disease and hypertension, and diabetes and metabolic syndrome, falls and physical performance, immune functioning and autoimmune disorders, infections, neuropsychological functioning, and preeclampsia could not be linked reliably with intake of either calcium or vitamin D, and were often conflicting."[5]: 5  Evidence for and against each disease state is provided in detail.[5]: 124–299  Some researchers claim the IOM was too definitive in its recommendations and made a mathematical mistake when calculating the blood level of vitamin D associated with bone health.[76] Members of the IOM panel maintain that they used a "standard procedure for dietary recommendations" and that the report is solidly based on the data.[76]

Mortality, all-causes[edit]

Vitamin D3 supplementation has been tentatively found to lead to a reduced risk of death in the elderly,[77][74] but the effect has not been deemed pronounced, or certain enough, to make taking supplements recommendable.[11] Other forms (vitamin D2, alfacalcidol, and calcitriol) do not appear to have any beneficial effects concerning the risk of death.[77] High blood levels appear to be associated with a lower risk of death, but it is unclear if supplementation can result in this benefit.[78] Both an excess and a deficiency in vitamin D appear to cause abnormal functioning and premature aging.[79][80] The relationship between serum calcifediol concentrations and all-cause mortality is "U-shaped": mortality is elevated at high and low calcifediol levels, relative to moderate levels. Harm from elevated calcifediol appears to occur at a lower level in dark-skinned Canadian and United States populations than in light-skinned populations.[5]: 424–435 

Bone health[edit]

Rickets[edit]

Main article: Rickets

X-ray of the legs in a two year old child with rickets showing bowing of the femur and low bone density.

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. Maternal vitamin D deficiency can cause fetal bone defects from before birth and impairment of bone quality after birth.[81][82] Rickets typically appear between 3 and 18 months of age.[83] This condition can be caused by vitamin D, calcium or phosphorus deficiency.[84] Vitamin D deficiency remains the main cause of rickets among young infants in most countries because breast milk is low in vitamin D, and darker skin, social customs, and climatic conditions can contribute to inadequate sun exposure.[citation needed] A post-weaning Western omnivore diet characterized by high intakes of meat, fish, eggs and vitamin D fortified milk is protective, whereas low intakes of those foods and high cereal/grain intake contribute to risk.[85][86][87] For young children with rickets, supplementation with vitamin D plus calcium was superior to the vitamin alone for bone healing.[88][89]

Osteomalacia and osteoporosis[edit]

Main articles: Osteomalacia and Osteoporosis

Calcium and Vitamin D3 are often combined, with claims for adult bone health (This label predates current U.S. Food and Drug Administration regulations on health claims.[90])

Characteristics of osteomalacia are softening of the bones, leading to bending of the spine, bone fragility, and increased risk for fractures.[1] Osteomalacia is usually present when 25-hydroxyvitamin D levels are less than about 10 ng/mL.[91] Osteomalacia progress to osteoporosis, a condition of reduced bone mineral density with increased bone fragility and risk of bone fractures. Osteoporosis can be a long-term effect of calcium and/or vitamin D insufficiency, the latter contributing by reducing calcium absorption.[2] In the absence of confirmed vitamin D deficiency there is no evidence that vitamin D supplementation without concomitant calcium slows or stops the progression of osteomalacia to osteoporosis.[10] For older people with osteoporosis, taking vitamin D with calcium may help prevent hip fractures, but it also slightly increases the risk of stomach and kidney problems.[92][93] The reduced risk for fractures is not seen in healthier, community-dwelling elderly.[11][94][95] Low serum vitamin D levels have been associated with falls,[96] but taking extra vitamin D does not appear to reduce that risk.[97]

Athletes who are vitamin D deficient are at an increased risk of stress fractures and/or major breaks, particularly those engaging in contact sports. Incremental decreases in risk are observed with rising serum 25(OH)D concentrations plateauing at 50 ng/mL with no additional benefits seen in levels beyond this point.[98]

Cancer[edit]

While serum low 25-hydroxyvitamin D status has been associated with a higher risk of cancer in observational studies,[99][100][101] the general conclusion is that there is insufficient evidence for an effect of vitamin D supplementation on the risk of cancer,[2][102][103] although there is some evidence for reduction in cancer mortality.[99][104]

Cardiovascular disease[edit]

Vitamin D supplementation is not associated with a reduced risk of stroke, cerebrovascular disease, myocardial infarction, or ischemic heart disease.[11][105][106] Supplementation does not lower blood pressure in the general population.[107][108][109] One meta-analysis found a small increase in risk of stroke when calcium and vitamin D supplements were taken together.[110]

Immune system[edit]

Vitamin D receptors are found in cell types involved in immunity. Functions are not understood. Some autoimmune and infectious diseases are associated with vitamin D deficiency, but either there is no evidence that supplementation has a benefit or not, or for some, evidence indicating there are no benefits.[111][112][113][114]

Autoimmune diseases[edit]

Low plasma vitamin D concentrations have been reported for autoimmune thyroid diseases,[115] lupus,[116] myasthenia gravis,[117] rheumatoid arthritis,[118] and multiple sclerosis.[119] For multiple sclerosis and rheumatoid arthritis, intervention trials using vitamin D supplementation did not demonstrate therapeutic effects.[112][120]

Infectious diseases[edit]

Vitamin D supplementation does not reduce the risk of acute respiratory disease.[121] In general, vitamin D functions to activate the innate and dampen the adaptive immune systems with antibacterial, antiviral and anti-inflammatory effects.[122][123] Low serum levels of vitamin D appear to be a risk factor for tuberculosis.[124] However, supplementation trials showed no benefit.[113][114]

Inflammatory bowel disease[edit]

Vitamin D deficiency has been linked to the severity of inflammatory bowel disease (IBD).[125] However, whether vitamin D deficiency causes IBD or is a consequence of the disease is not clear.[126] Supplementation leads to improvements in scores for clinical inflammatory bowel disease activity and biochemical markers,[126][127] and less frequent relapse of symptoms in IBD.[126]

Asthma[edit]

Vitamin D supplementation does not help prevent asthma attacks or alleviate symptoms.[128]

COVID-19[edit]

See also: COVID-19 drug repurposing research § Vitamin D, and COVID-19 misinformation § Vitamin D

In July 2020, the US National Institutes of Health stated "There is insufficient evidence to recommend for or against using vitamin D supplementation for the prevention or treatment of COVID-19."[129] Same year, the UK National Institute for Health and Care Excellence (NICE) position was to not recommend to offer a vitamin D supplement to people solely to prevent or treat COVID-19.[130] NICE updated its position in 2022 to "Do not use vitamin D to treat COVID-19 except as part of a clinical trial."[131] Both organizations included recommendations to continue the previously established recommendations on vitamin D supplementation for other reasons, such as bone and muscle health, as applicable. Both organizations noted that more people may require supplementation due to lower amounts of sun exposure during the pandemic.[129][130]

Vitamin D deficiency and insufficiency have been associated with adverse outcomes in COVID-19.[132][133][134][135][136] Supplementation trials, mostly large, single, oral dose upon hospital admission, reported lower subsequent transfers to intensive care and to all-cause mortality.[137][138][139]

Other diseases and conditions

[박대선]

https://en.wikipedia.org/wiki/Vitamin_D