Vitamin D

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 D
Drug class
Cholecalciferol (D3)
Class identifiers
SynonymsCalciferols
UseRickets, osteoporosis, osteomalacia, vitamin D deficiency
ATC codeA11CC
Biological targetvitamin D receptor
Clinical data
Drugs.comMedFacts Natural Products
External links
MeSHD014807
Legal status
In Wikidata

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

The primary natural source of vitamin D is the synthesis of cholecalciferol in the lower layers of the skin’s epidermis, triggered by a photochemical reaction with ultraviolet B (UV-B) radiation from sunlight or UV-B lamps.[1] Cholecalciferol and ergocalciferol can also be obtained through diet and supplements.[1][2] Foods such as the flesh of fatty fish are good sources of vitamin D, though there are few other foods where it naturally appears in significant amounts.[2][4] In the U.S. and other countries, cow's milk and plant-based milk substitutes are fortified with vitamin D, as are many breakfast cereals.[1] Mushrooms exposed to ultraviolet light also provide useful amounts of vitamin D2.[2][5] Dietary recommendations typically assume that all of a person's vitamin D is taken by mouth, given the variability in sunlight exposure among the population and uncertainties regarding safe levels of sunlight exposure, particularly due to the associated risk of skin cancer.[2]

Vitamin D obtained from the diet or synthesised in the skin is biologically inactive. It becomes active by two enzymatic hydroxylation steps, the first occurring in the liver and the second in the kidneys.[1][3] Since most mammals can synthesise sufficient vitamin D with adequate sunlight exposure, it is technically not essential in the diet and thus not a true vitamin. Instead it functions as a hormone; the activation of the vitamin D pro-hormone produces calcitriol, the active form. Calcitriol then exerts its effects via the vitamin D receptor, a nuclear receptor found in various tissues throughout the body.[6]

Cholecalciferol is converted in the liver to calcifediol (also known as calcidiol or 25-hydroxycholecalciferol), while ergocalciferol is converted to ercalcidiol (25-hydroxyergocalciferol).[1] 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.[7][8] Calcifediol is further hydroxylated by the kidneys and certain immune cells to form calcitriol (1,25-dihydroxycholecalciferol), the biologically active form of vitamin D.[9][10] Calcitriol circulates in the blood as a hormone, playing a major role in regulating calcium and phosphate concentrations, as well as promoting bone health and bone remodeling.[1] Additionally, calcitriol has other effects, including influencing cell differentiation, neuromuscular and immune functions, and reducing inflammation.[2]

Vitamin D has a significant role in calcium homeostasis and metabolism.[1] Its discovery was due to effort to identify the dietary deficiency in children with rickets, the childhood form of osteomalacia.[11] Vitamin D supplements are commonly used to treat or to prevent osteomalacia and rickets.[1] The evidence for other health benefits of vitamin D supplementation in individuals who are already vitamin D sufficient is inconsistent.[2] The effect of vitamin D supplementation on morbidity and mortality is also unclear, with one meta-analysis finding a small decrease in mortality in elderly people.[12] Except for the prevention of rickets and osteomalacia in high-risk groups, any benefit of vitamin D supplements to musculoskeletal or general health may be small and in some cases, may have adverse effects on health.[13][14][15]

  1. ^ a b c d e f g h i "Vitamin D". Micronutrient Information Center, Linus Pauling Institute, Oregon State University, Corvallis. 11 February 2021. Archived from the original on 8 April 2015. Retrieved 14 March 2022.
  2. ^ a b c d e f g h "Vitamin D". Office of Dietary Supplements, US National Institutes of Health. 12 August 2022. Archived from the original on 9 April 2021. Retrieved 22 February 2022.
  3. ^ a b Bikle DD (March 2014). "Vitamin D metabolism, mechanism of action, and clinical applications". Chemistry & Biology. 21 (3): 319–29. doi:10.1016/j.chembiol.2013.12.016. PMC 3968073. PMID 24529992.
  4. ^ Lehmann U, Gjessing HR, Hirche F, Mueller-Belecke A, Gudbrandsen OA, Ueland PM, et al. (October 2015). "Efficacy of fish intake on vitamin D status: a meta-analysis of randomized controlled trials". The American Journal of Clinical Nutrition. 102 (4): 837–47. doi:10.3945/ajcn.114.105395. PMID 26354531.
  5. ^ Cardwell, Glenn et al. “A Review of Mushrooms as a Potential Source of Dietary Vitamin D.” Nutrients vol. 10,10 1498. 13 Oct. 2018, doi:10.3390/nu10101498
  6. ^ Norman AW (August 2008). "From vitamin D to hormone D: fundamentals of the vitamin D endocrine system essential for good health". The American Journal of Clinical Nutrition. 88 (2): 491S–9S. doi:10.1093/ajcn/88.2.491S. PMID 18689389.
  7. ^ "Vitamin D Tests". Lab Tests Online (USA). American Association for Clinical Chemistry. Archived from the original on 7 November 2017. Retrieved 23 June 2013.
  8. ^ Hollis BW (January 1996). "Assessment of vitamin D nutritional and hormonal status: what to measure and how to do it". Calcified Tissue International. 58 (1): 4–5. doi:10.1007/BF02509538. PMID 8825231. S2CID 35887181.
  9. ^ Cite error: The named reference pmid4323790 was invoked but never defined (see the help page).
  10. ^ Cite error: The named reference pmid4325863 was invoked but never defined (see the help page).
  11. ^ Wolf G (June 2004). "The discovery of vitamin D: the contribution of Adolf Windaus". The Journal of Nutrition. 134 (6): 1299–302. doi:10.1093/jn/134.6.1299. PMID 15173387.
  12. ^ Cite error: The named reference Bj2014 was invoked but never defined (see the help page).
  13. ^ Cite error: The named reference reid was invoked but never defined (see the help page).
  14. ^ Cite error: The named reference Futil2014 was invoked but never defined (see the help page).
  15. ^ "The Lancet Diabetes & Endocrinology: Vitamin D supplementation in adults does not prevent fractures, falls or improve bone mineral density". EurekAlert!. Archived from the original on 24 March 2022. Retrieved 23 February 2022. The authors conclude that there is therefore little reason to use vitamin D supplements to maintain or improve musculoskeletal health, except for the prevention of rare conditions such as rickets and osteomalacia in high risk groups, which can be caused by vitamin D deficiency after long lack of exposure to sunshine.