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Vitamin D

Also known as Calciferol

Not medically reviewed

vitaminentity:supplement:vitamin-d

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Identity structure

Ingredients and forms

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Ingredient identities

Ergocalciferolentity:ingredient:ergocalciferol
Cholecalciferolentity:ingredient:cholecalciferol

Specific forms

Vitamin D2vitamin form
Vitamin D3vitamin form

Ingredient intelligence

Vitamin D2 (ergocalciferol)vitamin form
Vitamin D3 (cholecalciferol)vitamin form

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Evidence source: NIH ODS evidence synthesis
Linked references: 4 identified
Human evidence: Human evidence not identified in the frozen metadata
Randomized trials: Randomized trials not identified in the frozen metadata
Reviews and meta-analyses: Systematic review or meta-analysis identified
Evidence recency: 2010–2018
Source-described consistency: Not characterized in these source blocks
MEDucated evidence rating: Not assigned

Reference counts describe frozen source associations; a larger count does not establish stronger evidence.

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Government reference1
Study type could not be determined2
Systematic review1

Source-described limitations

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Classified references

Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessed
Norman AW, Henry HH. Vitamin D. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition, 10th ed. Washington DC: Wiley-Blackwell, 2012.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Jones G. Vitamin D. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease, 11th ed. Philadelphia: Lippincott Williams & Wilkins, 2014.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Silva MC, Furlanetto TW. Intestinal absorption of vitamin D: A systematic review. Nutr Rev 2018;76:60-76. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessed

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Vitamin D (also referred to as calciferol) is a fat-soluble vitamin that is naturally present in a few foods, added to others, and available as a dietary supplement. It is also produced endogenously when ultraviolet (UV) rays from sunlight strike the skin and trigger vitamin D synthesis.

Vitamin D obtained from sun exposure, foods, and supplements is biologically inert and must undergo two hydroxylations in the body for activation. The first hydroxylation, which occurs in the liver, converts vitamin D to 25-hydroxyvitamin D [25(OH)D], also known as calcidiol. The second hydroxylation occurs primarily in the kidney and forms the physiologically active 1,25-dihydroxyvitamin D [1,25(OH)2D], also known as calcitriol [1].

Vitamin D promotes calcium absorption in the gut and maintains adequate serum calcium and phosphate concentrations to enable normal bone mineralization and to prevent hypocalcemic tetany (involuntary contraction of muscles, leading to cramps and spasms). It is also needed for bone growth and bone remodeling by osteoblasts and osteoclasts [1-3]. Without sufficient vitamin D, bones can become thin, brittle, or misshapen. Vitamin D sufficiency prevents rickets in children and osteomalacia in adults. Together with calcium, vitamin D also helps protect older adults from osteoporosis.

Vitamin D has other roles in the body, including reduction of inflammation as well as modulation of such processes as cell growth, neuromuscular and immune function, and glucose metabolism [1-3]. Many genes encoding proteins that regulate cell proliferation, differentiation, and apoptosis are modulated in part by vitamin D. Many tissues have vitamin D receptors, and some convert 25(OH)D to 1,25(OH)2D.

In foods and dietary supplements, vitamin D has two main forms, D2 (ergocalciferol) and D3 (cholecalciferol), that differ chemically only in their side-chain structures. Both forms are well absorbed in the small intestine. Absorption occurs by simple passive diffusion and by a mechanism that involves intestinal membrane carrier proteins [4]. The concurrent presence of fat in the gut enhances vitamin D absorption, but some vitamin D is absorbed even without dietary fat. Neither aging nor obesity alters vitamin D absorption from the gut [4].

Where did MEDucated get this?

Vitamin D — Fact Sheet for Health Professionals

NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.

Source section: Introduction
ODS revision: June 27, 2025
Retrieved: 2026-08-10T22:07:04.753Z
Source fingerprint: 825b1a553a4a177e2d87fc412b0b4b21daa72ca92f4334a0096bc0dfa7f70a3c
Cited reference numbers: 1, 2, 3, 4

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Evidence profile

No overall rating assigned

Evidence source: NIH ODS evidence synthesis
Linked references: 10 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trial identified
Reviews and meta-analyses: Systematic review or meta-analysis identified
Evidence recency: 2006–2019
Source-described consistency: Not characterized in these source blocks
MEDucated evidence rating: Not assigned

Reference counts describe frozen source associations; a larger count does not establish stronger evidence.

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Evidence types identified

Government reference1
Study type could not be determined5
Case report2
Randomized controlled trial1
Meta-analysis1

Source-described limitations

No explicit limitation phrase was identified in these imported source blocks.

Classified references

Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessed
Galior K, Grebe S, Singh R. Development of vitamin D toxicity from overcorrection of vitamin D deficiency: A review of case reports. Nutrients 2018, 10, 953. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Auguste BL, Avila-Casado C, Bargman JM. Use of vitamin D drops leading to kidney failure in a 54-year-old man. CMAJ 2019;191:E390-4. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Vogiatzi MG, Jacobson-Dickman E, DeBoer MD. Vitamin D supplementation and risk of toxicity in pediatrics: A review of current literature. J Clin Endocrinol Metab 2014;99:1132-41. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Singh P, Trivedi N. Tanning beds and hypervitaminosis D: A case report. Ann Intern Med 2014;160:810-1. [PubMed abstract]
Case report · Population basis: unknown · Directness: not assessed
Laurent MR, Gielen E, Pauwels S, Vanderschueren D, Bouillon R. Hypervitaminosis D associated with tanning bed use: A case report. Ann Intern Med 2017;166:155-6. [PubMed abstract]
Case report · Population basis: unknown · Directness: not assessed
Perez-Castrillon JL, Vega G, Abad L, Sanz A, Chaves J, Hernandez G, Duenas A. Effects of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Am J Cardiol 2007;99:903-5. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Jackson RD, LaCroix AZ, Gass M, Wallace RB, Robbins J, Lewis CE, et al. Calcium plus vitamin D supplementation and the risk of fractures. N Engl J Med 2006;354:669-82. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Malihi Z, Lawes CMM, Wu Z, Huang Y, Waayer D, Toop L, et al. Monthly high-dose vitamin D supplementation does not increase kidney stone risk or serum calcium: Results from a randomized controlled trial. Am J Clin Nutr 2019;109:1578-87. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessed
Malihi Z, Wu Z, Stewart AW, Lawes CMM, Scragg R. Hypercalcemia, hypercalciuria, and kidney stones in long-term studies of vitamin D supplementation: A systematic review and meta-analysis. Am J Clin Nutr 2016;104:1039-51. [PubMed abstract]
Meta-analysis · Population basis: unknown · Directness: not assessed

Vitamin D toxicity can cause hypercalcemia, hypercalciuria, and high serum 25(OH)D concentrations; in extreme cases, it may lead to renal failure, calcification of soft tissues, cardiac arrhythmias, and death. Vitamin D toxicity is almost always a result of excessive intakes of vitamin D through supplements. Taking calcium supplements in combination with vitamin D supplements may increase the risk of certain adverse effects. The Tolerable Upper Intake Level for vitamin D ranges from 25 to 100 mcg (1,000–4,000 IU), depending on age.

UL reference intakeSource intake rangeSource-described amount

Excess amounts of vitamin D are toxic. Because vitamin D increases calcium absorption in the gastrointestinal tract, vitamin D toxicity results in marked hypercalcemia (total calcium greater than 11.1 mg/dL, beyond the normal range of 8.4–10.2 mg/dL), hypercalciuria, and high serum 25(OH)D levels (typically >375 nmol/l [150 ng/mL]) [158]. Hypercalcemia, in turn, can lead to nausea, vomiting, muscle weakness, neuropsychiatric disturbances, pain, loss of appetite, dehydration, polyuria, excessive thirst, and kidney stones.

Source intake rangeSource-described amount

In extreme cases, vitamin D toxicity causes renal failure, calcification of soft tissues throughout the body (including in coronary vessels and heart valves), cardiac arrhythmias, and even death. Vitamin D toxicity has been caused by consumption of dietary supplements that contained excessive vitamin D amounts because of manufacturing errors, that were taken inappropriately or in excessive amounts, or that were incorrectly prescribed by physicians, [158-160].

Experts do not believe that excessive sun exposure results in vitamin D toxicity because thermal activation of previtamin D3 in the skin gives rise to various non-vitamin D forms that limit formation of vitamin D3. Some vitamin D3 is also converted to nonactive forms [1]. However, frequent use of tanning beds, which provide artificial UV radiation, can lead to 25(OH)D levels well above 375 to 500 nmol/L (150–200 ng/mL) [161-163].

The combination of high intakes of calcium (about 2,100 mg/day from food and supplements) with moderate amounts of vitamin D (about 19 mcg [765 IU]/day from food and supplements) increased the risk of kidney stones by 17% over 7 years among 36,282 postmenopausal women who were randomly assigned to take 1,000 mg/day calcium and 10 mcg (400 IU)/day vitamin D or a placebo [164]. However, other, shorter (from 24 weeks to 5 years) clinical trials of vitamin D supplementation alone or with calcium in adults found greater risks of hypercalcemia and hypercalciuria, but not of kidney stones [165,166].

Source-described amount

The FNB established ULs for vitamin D in 2010 (Table 4) [1]. While acknowledging that signs and symptoms of toxicity are unlikely at daily intakes below 250 mcg (10,000 IU), the FNB noted that even vitamin D intakes lower than the ULs might have adverse health effects over time. The FNB recommended avoiding serum 25(OH)D levels above approximately 125 to 150 nmol/L (50–60 ng/mL), and it found that even lower serum levels (approximately 75–120 nmol/L [30–48 ng/mL]) are associated with increases in rates of all-cause mortality, risk of cancer at some sites (e.g., pancreas), risk of cardiovascular events, and number of falls and fractures among older adults.

Source-described amount

Table 4: Tolerable Upper Intake Levels (ULs) for Vitamin D in Micrograms (mcg) and International Units (IU) [1]
Age	Male	Female	Pregnancy	Lactation
0–6 months	25 mcg (1,000 IU)	25 mcg (1,000 IU)
7–12 months	38 mcg (1,500 IU)	38 mcg (1,500 IU)
1–3 years	63 mcg (2,500 IU)	63 mcg (2,500 IU)
4–8 years	75 mcg (3,000 IU)	75 mcg (3,000 IU)
9–13 years	100 mcg (4,000 IU)	100 mcg (4,000 IU)
14–18 years	100 mcg (4,000 IU)	100 mcg (4,000 IU)	100 mcg (4,000 IU)	100 mcg (4,000 IU)
19–50 years	100 mcg (4,000 IU)	100 mcg (4,000 IU)	100 mcg (4,000 IU)	100 mcg (4,000 IU)
51–70 years	100 mcg (4,000 IU)	100 mcg (4,000 IU)
>70 years	100 mcg (4,000 IU)	100 mcg (4,000 IU)

UL reference intakeSource-described amount

Where did MEDucated get this?

Vitamin D — Fact Sheet for Health Professionals

NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.

Source section: Health Risks from Excessive Vitamin D
ODS revision: June 27, 2025
Retrieved: 2026-08-10T22:07:04.753Z
Source fingerprint: 825b1a553a4a177e2d87fc412b0b4b21daa72ca92f4334a0096bc0dfa7f70a3c
Cited reference numbers: 158, 159, 160, 1, 161, 162, 163, 164, 165, 166

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Source attribution does not imply NIH or ODS endorsement of MEDucated.

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Medication interaction evidence

Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.

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Evidence profile

No overall rating assigned

Evidence source: NIH ODS evidence synthesis
Linked references: 13 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trial identified
Reviews and meta-analyses: Systematic review or meta-analysis identified
Evidence recency: 1984–2013
Source-described consistency: Not characterized in these source blocks
MEDucated evidence rating: Not assigned

Reference counts describe frozen source associations; a larger count does not establish stronger evidence.

Inspect technical evidence details

Evidence types identified

Study type could not be determined10
Systematic review1
Randomized controlled trial2

Source-described limitations

No explicit limitation phrase was identified in these imported source blocks.

Classified references

Gotfredsen A, Westergren Hendel H, Andersen T. Influence of orlistat on bone turnover and body composition. Int J Obes Relat Metab Disord 2001;25:1154-60. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
James WP, Avenell A, Broom J, Whitehead J. A one-year trial to assess the value of orlistat in the management of obesity. Int J Obes Relat Metab Disord 1997;21:S24-30. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
McDuffie JR, Calis KA, Booth SL, Uwaifo GI, Yanovski JA. Effects of orlistat on fat-soluble vitamins in obese adolescents. Pharmacotherapy 2002;22:814-22. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Robien K, Oppeneer SJ, Kelly JA, Hamilton-Reeves JM. Drug-vitamin D interactions: A systematic review of the literature. Nutr Clin Pract 2013;28:194-208. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessed
Schwartz JB. Effects of vitamin D supplementation in atorvastatin-treated patients: A new drug interaction with an unexpected consequence. Clin Pharmacol Ther 2009;85:198-203. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Perez-Castrillon JL, Vega G, Abad L, Sanz A, Chaves J, Hernandez G, Duenas A. Effects of atorvastatin on vitamin D levels in patients with acute ischemic heart disease. Am J Cardiol 2007;99:903-5. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Aloia JF, Li-Ng M, Pollack S. Statins and vitamin D. Am J Cardiol 2007;100:1329. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Buckley LM, Leib ES, Cartularo KS, Vacek PM, Cooper SM. Calcium and vitamin D3 supplementation prevents bone loss in the spine secondary to low-dose corticosteroids in patients with rheumatoid arthritis. A randomized, double-blind, placebo-controlled trial. Ann Intern Med 1996;125:961-8. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessed
de Sevaux RGL, Hoitsma AJ, Corstens FHM, Wetzels JFM. Treatment with vitamin D and calcium reduces bone loss after renal transplantation: a randomized study. J Am Soc Nephrol 2002;13:1608-14. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessed
Lukert BP, Raisz LG. Glucocorticoid-induced osteoporosis: pathogenesis and management. Ann Intern Med 1990;112:352-64. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Skversky AL, Kumar J, Abramowitz MK, Kaskel FJ, Melamed ML. Association of glucocorticoid use and low 25-hydroxyvitamin D levels: Results from the National Health and Nutrition Examination Survey (NHANES): 2001-2006. J Clin Endocrinol Metab 2011;96:3838-45. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Drinka PJ, Nolten WE. Hazards of treating osteoporosis and hypertension concurrently with calcium, vitamin D, and distal diuretics. J Am Geriatr Soc 1984;32:405-7. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Crowe M, Wollner L, Griffiths RA. Hypercalcaemia following vitamin D and thiazide therapy in the elderly. Practitioner 1984;228:312-3. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed

Vitamin D supplements may interact with medications, and some medications may affect vitamin D levels. These medications include orlistat, statins, steroids, and thiazide diuretics.

Vitamin D supplements may interact with several types of medications. A few examples are provided below. Individuals taking these and other medications on a regular basis should discuss their vitamin D intakes and status with their health care providers.

The weight-loss drug orlistat (Xenical and alli), together with a reduced-fat diet, can reduce the absorption of vitamin D from food and supplements, leading to lower 25(OH)D levels [167-170].

Statin medications reduce cholesterol synthesis. Because endogenous vitamin D is derived from cholesterol, statins may also reduce vitamin D synthesis [170]. In addition, high intakes of vitamin D, especially from supplements, might reduce the potency of atorvastatin (Lipitor), lovastatin (Altoprev and Mevacor), and simvastatin (FloLipid and Zocor), because these statins and vitamin D appear to compete for the same metabolizing enzyme [170-173].

Corticosteroid medications, such as prednisone (Deltasone, Rayos, and Sterapred), are often prescribed to reduce inflammation. These medications can reduce calcium absorption and impair vitamin D metabolism [174-176]. In the NHANES 2001–2006 survey, 25(OH)D deficiency (less than 25 nmol/L [10 ng/mL]) was more than twice as common among children and adults who reported oral steroid use (11%) than in nonusers (5%) [177].

Thiazide diuretics (e.g., Hygroton, Lozol, and Microzide) decrease urinary calcium excretion. The combination of these diuretics with vitamin D supplements (which increase intestinal calcium absorption) might lead to hypercalcemia, especially among older adults and individuals with compromised renal function or hyperparathyroidism [170,178,179].

Where did MEDucated get this?

Vitamin D — Fact Sheet for Health Professionals

NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.

Source section: Interactions with Medications
ODS revision: June 27, 2025
Retrieved: 2026-08-10T22:07:04.753Z
Source fingerprint: 825b1a553a4a177e2d87fc412b0b4b21daa72ca92f4334a0096bc0dfa7f70a3c
Cited reference numbers: 167, 168, 169, 170, 171, 172, 173, 174, 175, 176, 177, 178, 179

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Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.

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Evidence source: NIH ODS evidence synthesis
Linked references: 10 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trial identified
Reviews and meta-analyses: Systematic review or meta-analysis identified
Evidence recency: 2007–2020
Source-described consistency: Not characterized in these source blocks
MEDucated evidence rating: Not assigned

Reference counts describe frozen source associations; a larger count does not establish stronger evidence.

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Evidence types identified

Systematic review1
Study type could not be determined6
Meta-analysis1
Randomized controlled trial2

Source-described limitations

No explicit limitation phrase was identified in these imported source blocks.

Classified references

Silva MC, Furlanetto TW. Intestinal absorption of vitamin D: A systematic review. Nutr Rev 2018;76:60-76. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessed
Holick MF. Vitamin D deficiency. N Engl J Med 2007;357:266-81. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Hirsch AL. Industrial Aspects of Vitamin D. In: Feldman D, Pike JW, Adams JS, eds. Vitamin D. 3rd ed. Academic Press; 2011:73-93.
Study type could not be determined · Population basis: unknown · Directness: not assessed
National Institutes of Health. Dietary Supplement Label Database. 2020.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Tripkovic L, Lambert H, Hart K, Smith CP, Bucca G, Penson S, et al. Comparison of vitamin D2 and vitamin D3 supplementation in raising serum 25-hydroxyvitamin D status: A systematic review and meta-analysis. Am J Clin Nutr 2012;95:1357-64. [PubMed abstract]
Meta-analysis · Population basis: unknown · Directness: not assessed
Lehmann U, Hirche F, Stangl GI, Hinz K, Westphal S, Dierkes J. Bioavailability of vitamin D2 and D3 in healthy volunteers, a randomised placebo-controlled trial. J Clin Endocrin Metab 2013;98:4339-45. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessed
Logan VF, Gray AR, Peddie MC, Harper MJ, Houghton LA. Long-term vitamin D3 supplementation is more effective than vitamin D2 in maintaining serum 25-hydroxyvitamin D status over the winter months. Br J Nutr 2013;109:1082-8. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Tripkovic L, Wilson LR, Hart K, Johnsen S, de Lusignan S, Smith CP, et al. Daily supplementation with 15 µg vitamin D2 compared with vitamin D3 to increase wintertime 25-hydroxyvitamin D status in healthy South Asian and white European women: A 12-wk randomized, placebo-controlled food-fortification trial. Am J Clin Nutr 2017;106:481-90. [PubMed abstract]
Randomized controlled trial · Population basis: human · Directness: not assessed
Graeff-Armas LA, Bendik I, Kunz I, Schoop R, Hull S, Beck M. Supplemental 25-hydroxycholecalciferol is more effective than cholecalciferol in raising serum 25-hydroxyvitamin D concentrations in older adults. J Nutr 2020;150:73-81. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Quesada-Gomez JM, Bouillon R. Is calcifediol better than cholecalciferol for vitamin D supplementation? Osteoporos Int 2018;29:1697-1711. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed

Read imported source wording

Vitamin D is present in dietary supplements as either vitamin D2 or vitamin D3. Both can raise the serum level of 25(OH)D. However, research shows that vitamin D3 increases serum 25(OH)D levels to a greater extent than vitamin D2 and can maintain those higher levels for longer periods of time.

Dietary supplements can contain vitamins D2 or D3. Vitamin D2 is manufactured using UV irradiation of ergosterol in yeast, and vitamin D3 is typically produced with irradiation of 7-dehydrocholesterol from lanolin obtained from the wool of sheep [13,31]. An animal-free version of vitamin D3 sourced from lichen is also available [32]. People who avoid all animal-sourced products can contact dietary supplement manufacturers to ask about their sourcing and processing techniques.

Both vitamins D2 and D3 raise serum 25(OH)D levels, and they seem to have equivalent ability to cure rickets [4]. In addition, most steps in the metabolism and actions of vitamins D2 and D3 are identical. However, most evidence indicates that vitamin D3 increases serum 25(OH)D levels to a greater extent and maintains these higher levels longer than vitamin D2, even though both forms are well absorbed in the gut [33-36].

Some studies have used dietary supplements containing the 25(OH)D3 form of vitamin D. Per equivalent microgram dose, 25(OH)D3 is three to five times as potent as vitamin D3 [37,38]. However, no 25(OH)D3 dietary supplements appear to be available to consumers on the U.S. market at this time [32].

Where did MEDucated get this?

Vitamin D — Fact Sheet for Health Professionals

NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.

Source section: Dietary supplements
ODS revision: June 27, 2025
Retrieved: 2026-08-10T22:07:04.753Z
Source fingerprint: 825b1a553a4a177e2d87fc412b0b4b21daa72ca92f4334a0096bc0dfa7f70a3c
Cited reference numbers: 13, 31, 32, 4, 33, 34, 35, 36, 37, 38

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Evidence-backed dosage information

Imported NIH ODS source content is available for this topic. MEDucated has preserved the source wording and has not converted it into personalized guidance.

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Structural characterization

Evidence profile

No overall rating assigned

Evidence source: NIH ODS evidence synthesis
Linked references: 6 identified
Human evidence: Human evidence not identified in the frozen metadata
Randomized trials: Randomized trials not identified in the frozen metadata
Reviews and meta-analyses: Systematic review or meta-analysis identified
Evidence recency: 2010–2024
Source-described consistency: Not characterized in these source blocks
MEDucated evidence rating: Not assigned

Reference counts describe frozen source associations; a larger count does not establish stronger evidence.

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Evidence types identified

Government reference1
Clinical guideline3
Systematic review1
Study type could not be determined1

Source-described limitations

No explicit limitation phrase was identified in these imported source blocks.

Classified references

Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessed
Sempos CT, Binkley N. 25-hydroxyvitamin D assay standardisation and vitamin D guidelines paralysis. Public Health Nutrition 2020;23:1153-64. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessed
Demay MB, Pittas AG, Bikle DD, Diab DL, Kiely ME, et al. Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1907-1947. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessed
Shah VP, Nayfeh T, Alsawaf Y, Saadi S, Farah M, et al. A Systematic Review Supporting the Endocrine Society Clinical Practice Guidelines on Vitamin D. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1961-1974. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessed
Bouillon R. Comparative analysis of nutritional guidelines for vitamin D. Nat Rev Endocrinol 2017;13:466-79. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessed
Scientific Advisory Committee on Nutrition. Vitamin D and Health. 2016.
Study type could not be determined · Population basis: unknown · Directness: not assessed

Read imported source wording

The Food and Nutrition Board at the National Academies of Sciences, Engineering, and Medicine has established Recommended Dietary Allowances and Adequate Intakes for vitamin D. These values range from 15 to 20 mcg (600–800 IU) for adults and from 10 to 15 mcg (400–600 IU) for infants, children, and adolescents, depending on age.

RDA reference intakeAI reference intakeSource intake rangeSource-described amount

Intake recommendations for vitamin D and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by expert committees of NASEM [1]. DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values include the following:

Recommended Dietary Allowance (RDA): Average daily level of intake sufficient to meet the nutrient requirements of nearly all (97%–98%) healthy individuals; often used to plan nutritionally adequate diets for individuals
Adequate Intake (AI): Intake at this level is assumed to ensure nutritional adequacy; established when evidence is insufficient to develop an RDA
Estimated Average Requirement (EAR): Average daily level of intake estimated to meet the requirements of 50% of healthy individuals; usually used to assess the nutrient intakes of groups of people and to plan nutritionally adequate diets for them; can also be used to assess the nutrient intakes of individuals
Tolerable Upper Intake Level (UL): Maximum daily intake unlikely to cause adverse health effects

RDA reference intakeAI reference intakeUL reference intake

The FNB established RDAs for vitamin D to indicate daily intakes sufficient to maintain bone health and normal calcium metabolism in healthy people. RDAs for vitamin D are listed in both micrograms (mcg) and International Units (IU); 1 mcg vitamin D is equal to 40 IU (Table 2). Even though sunlight is a major source of vitamin D for some people, the FNB based the vitamin D RDAs on the assumption that people receive minimal sun exposure [1]. For infants from birth to 12 months, the FNB developed AIs based on the amount of vitamin D that maintains serum 25(OH)D levels above 20 ng/mL (50 nmol/L) and supports bone development.

Source-described amount

Table 2: Recommended Dietary Allowances (RDAs) for Vitamin D in Micrograms (mcg) and International Units (IU) [1]
Age	Male	Female	Pregnancy	Lactation
0–6 months*	10 mcg (400 IU)*	10 mcg (400 IU)*
7–12 months*	10 mcg (400 IU)*	10 mcg (400 IU)*
1–3 years	15 mcg (600 IU)	15 mcg (600 IU)
4–8 years	15 mcg (600 IU)	15 mcg (600 IU)
9–13 years	15 mcg (600 IU)	15 mcg (600 IU)
14–18 years	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)
19–50 years	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)
51–70 years	15 mcg (600 IU)	15 mcg (600 IU)
>70 years	20 mcg (800 IU)	20 mcg (800 IU)
*Adequate Intake (AI)

RDA reference intakeAI reference intakeSource-described amount

Many other countries around the world and some professional societies have somewhat different guidelines for vitamin D intakes [15]. These differences are a result of an incomplete understanding of the biology and clinical implications of vitamin D, different purposes for the guidelines (e.g., for public health in a healthy population or for clinical practice), and/or the use in some guidelines of observational studies in addition to randomized clinical trials to establish recommendations [9,15]. For example, the United Kingdom Scientific Advisory Committee on Nutrition recommends intakes of 10 mcg (400 IU)/day for individuals age 4 years and older [16]. The Endocrine Society recommends routine vitamin D supplementation for children and teens age 1 to 18 years, pregnant women, adults with pre-diabetes, and adults age 75 years and older, but not for healthy adults age 19 to 74 [11,12]. The Endocrine Society does not recommend specific doses but notes that all individuals should adhere to the RDA.

RDA reference intakeSource-described amount

Where did MEDucated get this?

Vitamin D — Fact Sheet for Health Professionals

NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.

Source section: Recommended Intakes
ODS revision: June 27, 2025
Retrieved: 2026-08-10T22:07:04.753Z
Source fingerprint: 825b1a553a4a177e2d87fc412b0b4b21daa72ca92f4334a0096bc0dfa7f70a3c
Cited reference numbers: 1, 9, 11, 12, 15, 16

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Evidence source: NIH ODS evidence synthesis
Linked references: 16 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trials not identified in the frozen metadata
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Evidence recency: 2001–2020
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Government reference1
Systematic review2
Study type could not be determined10
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Narrative review1

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Classified references

Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessed
Silva MC, Furlanetto TW. Intestinal absorption of vitamin D: A systematic review. Nutr Rev 2018;76:60-76. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessed
Brown LL, Cohen B, Tabor D, Zappala G, Maruvada P, Coates PM. The vitamin D paradox in Black Americans: A systems-based approach to investigating clinical practice, research, and public health—expert panel meeting report. BMC Proceedings, 2018;12(Suppl 6):6. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Picciano MF. Nutrient composition of human milk. Pediatr Clin North Am 2001;48:53-67. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Wagner CL, Greer FR, American Academy of Pediatrics Section on Breastfeeding, American Academy of Pediatrics Committee on Nutrition. Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Pediatrics 2008;122:1142-52. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Dawodu A, Tsang RC. Maternal vitamin D status: Effect on milk vitamin D content and vitamin D status of breastfeeding infants. Adv Nutr 2012;3:353-61. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Davis CD, Dwyer JT. The 'sunshine vitamin': benefits beyond bone? J Natl Cancer Inst 2007;99:1563-5. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Simon AE, Ahrens KA. Adherence to vitamin D intake guidelines in the United States. Pediatrics 2020;145:e20193574. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessed
Chalcraft JR, Cardinal LM, Wechsler PJ, Hollis BW, Gerow KG, Alexander BM, et al. Vitamin D synthesis following a single bout of sun exposure in older and younger men and women. Nutrients 2020; 12, 2237; doi:10.3390/nu12082237. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Sowah D, Fan X, Dennett L, Hagtvedt R, Straube S. Vitamin D levels and deficiency with different occupations: A systematic review. BMC Public Health 2017;17:519. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessed
Pappa HM, Bern E, Kamin D, Grand RJ. Vitamin D status in gastrointestinal and liver disease. Curr Opin Gastroenterol 2008;24:176-83. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Drincic A, Fuller E, Heaney RP, Armas LAG. 25-hydroxyvitamin D response to graded vitamin D3 supplementation among obese adults. J Clin Endocrinol Metab 2013;98:4845-51. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Ekwaru JP, Zwicker JD, Holick MF, Giovannucci E, Veugelers PJ. The importance of body weight for the dose response relationship of oral vitamin D supplementation and serum 25-hydroxyvitamin D in healthy volunteers. PLOS ONE 2014;9:e111265. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Chakhtoura M, Rahme M, Fuleihan E-H. Vitamin D metabolism in bariatric surgery. Endocrinol Metab Clin North Am 2017;46:947-82. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Peterson L, Zeng X, Caufield-Noll CP, Schweitzer MA, Magnuson TH, Steele KE. Vitamin D status and supplementation before and after bariatric surgery: A comprehensive literature review. Surg Obes Relat Dis 2016;12:693-702. [PubMed abstract]
Narrative review · Population basis: unknown · Directness: not assessed
Chakhtoura MT, Nakhoul N, Akl EA, Mantzoros CS, El Hajj Guleihan GA. Guidelines on vitamin D replacement in bariatric surgery? Identification and systematic appraisal. Metabolism 2016;65:586-97. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessed

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Certain groups of people are more likely than others to have inadequate vitamin D status. These include breastfed infants, older adults, people with limited sun exposure, people with dark skin, people with conditions that limit fat absorption, and people with obesity or those who have undergone gastric bypass surgery.

Obtaining sufficient vitamin D from natural (nonfortified) food sources alone is difficult. For many people, consuming vitamin D-fortified foods and exposing themselves to some sunlight are essential for maintaining a healthy vitamin D status. However, some groups might need dietary supplements to meet their vitamin D requirements. The following groups are among those most likely to have inadequate vitamin D status.

Consumption of human milk alone does not ordinarily enable infants to meet vitamin D requirements, because it provides less than 0.6 to 2.0 mcg/L (25 to 78 IU/L) [1,56,57]. The vitamin D content of human milk is related to the mother’s vitamin D status; studies suggest that the breastmilk of mothers who take daily supplements containing at least 50 mcg (2,000 IU) vitamin D3 have higher levels of the nutrient [57,58].

Source intake rangeSource-described amount

Although UVB exposure can produce vitamin D in infants, the American Academy of Pediatrics (AAP) advises parents to keep infants younger than 6 months out of direct sunlight, dress them in protective clothing and hats, and apply sunscreen on small areas of exposed skin when sun exposure is unavoidable [59]. The AAP recommends 10 mcg (400 IU)/day vitamin D supplements for exclusively and partially breastfed infants starting shortly after birth and lasting until they are weaned and consume at least 1,000 mL/day vitamin D-fortified formula or whole milk [57]. The AAP also recommends 10 mcg (400 IU)/day supplemental vitamin D for all infants who are not breastfed and ingest less than 1,000 mL/day vitamin D-fortified formula or milk. An analysis of NHANES 2009–2016 data found that only 20.5% of breastfed infants and 31.1% of infants who were not breastfed ingested these recommended amounts of supplements [60].

Source-described amount

Older adults are at increased risk of developing vitamin D insufficiency, partly because the skin's ability to synthesize vitamin D declines with age [1,61]. In addition, older adults are likely to spend more time than younger people indoors, and they might have inadequate dietary intakes of the vitamin [1].

Homebound individuals; people who wear long robes, dresses, or head coverings for religious reasons; and people with occupations that limit sun exposure are among the groups that are unlikely to obtain adequate amounts of vitamin D from sunlight [62]. The use of sunscreen also limits vitamin D synthesis from sunlight. However, because the extent and frequency of sunscreen use are unknown, the role that sunscreen may play in reducing vitamin D synthesis is unclear [1].

Greater amounts of the pigment melanin in the epidermal layer of the skin result in darker skin and reduce the skin’s ability to produce vitamin D from sunlight [1]. Black Americans, for example, typically have lower serum 25(OH)D levels than White Americans. However, whether these lower levels in persons with dark skin have significant health consequences is not clear [14]. Those of African American ancestry, for example, have lower rates of bone fracture and osteoporosis than do Whites (see the section below on bone health and osteoporosis).

Because vitamin D is fat soluble, its absorption depends on the gut’s ability to absorb dietary fat [4]. Fat malabsorption is associated with medical conditions that include some forms of liver disease, cystic fibrosis, celiac disease, Crohn’s disease, and ulcerative colitis [1,63]. In addition to having an increased risk of vitamin D deficiency, people with these conditions might not eat certain foods, such as dairy products (many of which are fortified with vitamin D), or eat only small amounts of these foods. Individuals who have difficulty absorbing dietary fat might therefore require vitamin D supplementation [63].

Individuals with a body mass index (BMI) of 30 or more have lower serum 25(OH)D levels than individuals without obesity. Obesity does not affect the skin’s capacity to synthesize vitamin D. However, greater amounts of subcutaneous fat sequester more of the vitamin [1]. People with obesity might need greater intakes of vitamin D to achieve 25(OH)D levels similar to those of people with normal weight [1,64,65].

Individuals with obesity who have undergone gastric bypass surgery can also become vitamin D deficient. In this procedure, part of the upper small intestine, where vitamin D is absorbed, is bypassed, and vitamin D that is mobilized into the bloodstream from fat stores might not raise 25(OH)D to adequate levels over time [66,67]. Various expert groups—including the American Association of Metabolic and Bariatric Surgery, The Obesity Society, and the British Obesity and Metabolic Surgery Society—have developed guidelines on vitamin D screening, monitoring, and replacement before and after bariatric surgery [66,68]

Where did MEDucated get this?

Vitamin D — Fact Sheet for Health Professionals

NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.

Source section: Groups at Risk of Vitamin D Inadequacy
ODS revision: June 27, 2025
Retrieved: 2026-08-10T22:07:04.753Z
Source fingerprint: 825b1a553a4a177e2d87fc412b0b4b21daa72ca92f4334a0096bc0dfa7f70a3c
Cited reference numbers: 1, 56, 57, 58, 59, 60, 61, 62, 14, 4, 63, 64, 65, 66, 67, 68

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Evidence source: NIH ODS evidence synthesis
Linked references: 13 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trials not identified in the frozen metadata
Reviews and meta-analyses: Systematic review or meta-analysis identified
Evidence recency: 2007–2024
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Classified references

Institute of Medicine, Food and Nutrition Board. Dietary Reference Intakes for Calcium and Vitamin D. Washington, DC: National Academy Press, 2010.
Government reference · Population basis: unknown · Directness: not assessed
Norman AW, Henry HH. Vitamin D. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition, 10th ed. Washington DC: Wiley-Blackwell, 2012.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Jones G. Vitamin D. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease, 11th ed. Philadelphia: Lippincott Williams & Wilkins, 2014.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Sempos CT, Heijboer AC, Bikle DD, Bollerslev J, Bouillon R, Brannon PM, et al. Vitamin D assays and the definition of hypovitaminosis D. Results from the First International Conference on Controversies in Vitamin D. Br J Clin Pharmacol 2018;84:2194-207. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
LeFevre ML. Screening for vitamin deficiency in adults: U.S. Preventive Services Task Force recommendation statement. Ann Intern Med 2015;162:133-40. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Brooks SPJ, Sempos CT. The importance of 25-hydroxyvitamin D assay standardization and the Vitamin D Standardization Program. Journal of AOAC International 2017;100:1223-4.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Taylor CL, Sempos CT, Davis CD, Brannon PM. Vitamin D: moving forward to address emerging science. Nutrients 2017, 9, 1308; doi:10.3390/mu9121308. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Sempos CT, Binkley N. 25-hydroxyvitamin D assay standardisation and vitamin D guidelines paralysis. Public Health Nutrition 2020;23:1153-64. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessed
Office of Dietary Supplements, National Institutes of Health. Vitamin D Standardization Program (VDSP).
Study type could not be determined · Population basis: unknown · Directness: not assessed
Demay MB, Pittas AG, Bikle DD, Diab DL, Kiely ME, et al. Vitamin D for the Prevention of Disease: An Endocrine Society Clinical Practice Guideline. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1907-1947. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessed
Shah VP, Nayfeh T, Alsawaf Y, Saadi S, Farah M, et al. A Systematic Review Supporting the Endocrine Society Clinical Practice Guidelines on Vitamin D. J Clin Endocrinol Metab. 2024 Jul 12;109(8):1961-1974. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessed
Holick MF. Vitamin D deficiency. N Engl J Med 2007;357:266-81. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Brown LL, Cohen B, Tabor D, Zappala G, Maruvada P, Coates PM. The vitamin D paradox in Black Americans: A systems-based approach to investigating clinical practice, research, and public health—expert panel meeting report. BMC Proceedings, 2018;12(Suppl 6):6. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed

Read imported source wording

Serum concentration of 25(OH)D is the main indicator of vitamin D status. However, the serum concentrations of 25(OH)D that are associated with vitamin D deficiency have not been definitively identified. The Food and Nutrition Board at the National Academies of Sciences, Engineering, and Medicine states that levels of 50 nmol/L (20 ng/mL) or more are sufficient for most people, and that the risk of deficiency increases at serum concentrations of less than 30 nmol/L (12 ng/mL).

Serum concentration of 25(OH)D is currently the main indicator of vitamin D status. It reflects vitamin D produced endogenously and that obtained from foods and supplements [1]. In serum, 25(OH)D has a fairly long circulating half-life of 15 days [1]. Serum concentrations of 25(OH)D are reported in both nanomoles per liter (nmol/L) and nanograms per milliliter (ng/mL). One nmol/L is equal to 0.4 ng/mL, and 1 ng/mL is equal to 2.5 nmol/L.

Assessing vitamin D status by measuring serum 25(OH)D concentrations is complicated by the considerable variability of the available assays (the two most common ones involve antibodies or chromatography) used by laboratories that conduct the analyses [5,6]. As a result, a finding can be falsely low or falsely high, depending on the assay used and the laboratory. The international Vitamin D Standardization Program has developed procedures for standardizing the laboratory measurement of 25(OH)D to improve clinical and public health practice [5,7-10].

In contrast to 25(OH)D, circulating 1,25(OH)2D is generally not a good indicator of vitamin D status because it has a short half-life measured in hours, and serum levels are tightly regulated by parathyroid hormone, calcium, and phosphate [1]. Levels of 1,25(OH)2D do not typically decrease until vitamin D deficiency is severe [2].

Although 25(OH)D functions as a biomarker of exposure, the extent to which 25(OH)D levels also serve as a biomarker of effect on the body (i.e., relating to health status or outcomes) is not clear [1,3].

Researchers have not definitively identified serum concentrations of 25(OH)D associated with deficiency (e.g., rickets), adequacy for bone health, and overall health. After reviewing data on vitamin D needs, an expert committee of the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and Medicine (NASEM) concluded that people are at risk of vitamin D deficiency at serum 25(OH)D concentrations less than 30 nmol/L (12 ng/mL; see Table 1 for definitions of deficiency and inadequacy) [1]. Some people are potentially at risk of inadequacy at 30 to 50 nmol/L (12–20 ng/mL). Levels of 50 nmol/L (20 ng/mL) or more are sufficient for most people. The FNB also noted that serum concentrations greater than 125 nmol/L (50 ng/mL) can be associated with adverse effects [1] (Table 1). The Endocrine Society has not identified 25(OH)D concentrations associated with vitamin D sufficiency, insufficiency, and deficiency and does not recommend routine testing of 25(OH)D concentrations in healthy individuals [11,12].

Table 1: Serum 25-Hydroxyvitamin D [25(OH)D] Concentrations and Health [1]
nmol/L*	ng/mL*	Health status
<30	<12	Associated with vitamin D deficiency, which can lead to rickets in infants and children and osteomalacia in adults
30 to <50	12 to <20	Generally considered inadequate for bone and overall health in healthy individuals
≥50	≥20	Generally considered adequate for bone and overall health in healthy individuals
>125	>50	Linked to potential adverse effects, particularly at >150 nmol/L (>60 ng/mL)
*Serum concentrations of 25(OH)D are reported in both nanomoles per liter (nmol/L) and nanograms per milliliter (ng/mL). One nmol/L = 0.4 ng/mL, and 1 ng/mL = 2.5 nmol/L.

Optimal serum concentrations of 25(OH)D for bone and general health have not been established because they are likely to vary by stage of life, by race and ethnicity, and with each physiological measure used [1,13,14]. In addition, although 25(OH)D levels rise in response to increased vitamin D intake, the relationship is nonlinear [1]. The amount of increase varies, for example, by baseline serum levels and duration of supplementation.

Where did MEDucated get this?

Vitamin D — Fact Sheet for Health Professionals

NIH Office of Dietary Supplements. Government health-professional reference material imported without MEDucated medical review.

Source section: Assessing vitamin D status
ODS revision: June 27, 2025
Retrieved: 2026-08-10T22:07:04.753Z
Source fingerprint: 825b1a553a4a177e2d87fc412b0b4b21daa72ca92f4334a0096bc0dfa7f70a3c
Cited reference numbers: 1, 5, 6, 7, 8, 9, 10, 2, 3, 11, 12, 13, 14

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Vitamin D — Fact Sheet for Health Professionals

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