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Evidence-grounded comparison · non-production preview

Compare supplement evidence clearly.

Review two canonical supplement records topic by topic, with evidence availability, source boundaries, and limitations kept explicit—without rankings or recommendations.

What this comparison can establish

This comparison organizes two separately sourced supplement records. It describes evidence structure and availability without ranking supplements or recommending use.

Reference counts are descriptive. More references do not necessarily mean better or stronger evidence.

Identity boundaries

Selected supplement concepts

Supplement concepts, ingredients, and forms remain separate. Relationship differences do not establish clinical meaning.

fatty acid

Omega-3

Also known as Fish oil, Omega 3 fatty acids
ODS source attached
Canonical ID
entity:supplement:omega-3
Identity layer
Supplement concept
Evidence status
source backed demonstration not medically reviewed
Medical review
not medically reviewed

Modeled ingredients

  • Eicosapentaenoic acidingredient
  • Docosahexaenoic acidingredient

Modeled forms

  • EPAfatty acid
  • DHAfatty acid

vitamin

Vitamin D

Also known as Calciferol
ODS source attached
Canonical ID
entity:supplement:vitamin-d
Identity layer
Supplement concept
Evidence status
source backed demonstration not medically reviewed
Medical review
not medically reviewed

Modeled ingredients

  • Ergocalciferolingredient
  • Cholecalciferolingredient

Modeled forms

  • Vitamin D2vitamin form
  • Vitamin D3vitamin form

Source boundaries

Selected ODS revisions

Each supplement retains its own immutable source revision, fingerprint, official URL, and medical-review state.
Selected NIH ODS revision

Omega-3

Omega-3 Fatty Acids — Fact Sheet for Health Professionals

Source ID
source:nih-ods:omega-3-fatty-acids-health-professional
Source revision ID
source-revision:nih-ods:omega-3-fatty-acids-health-professional:2026-08-10.80b4434afaf7
ODS revision date
August 22, 2025
Medical review
not medically reviewed
Source fingerprint
80b4434afaf71303420a09ab193258a2d656c3bdec58a108fe3d14961d1bb750
Retrieved
2026-08-10T22:07:06.488Z
Inspect the official NIH ODS source (opens in a new tab)

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

Selected NIH ODS revision

Vitamin D

Vitamin D — Fact Sheet for Health Professionals

Source ID
source:nih-ods:vitamin-d-health-professional
Source revision ID
source-revision:nih-ods:vitamin-d-health-professional:2026-08-10.825b1a553a4a
ODS revision date
June 27, 2025
Medical review
not medically reviewed
Source fingerprint
825b1a553a4a177e2d87fc412b0b4b21daa72ca92f4334a0096bc0dfa7f70a3c
Retrieved
2026-08-10T22:07:04.753Z
Inspect the official NIH ODS source (opens in a new tab)

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

Structural orientation

What differs in these records

These statements describe record structure only and do not assign medical importance.

27 structural observations are available. Topic states remain visible in the aligned comparison below.

Inspect all structural observations
  • The selected ODS revision dates differ: August 22, 2025 for Omega-3 and June 27, 2025 for Vitamin D.
  • Omega-3 and Vitamin D have different modeled ingredient relationships. This is an identity distinction, not a clinical ranking.
  • Omega-3 and Vitamin D have different modeled form relationships. No clinical interpretation is assigned to that difference.
  • The selected source blocks for “What it is” link 23 references for Omega-3 and 4 references for Vitamin D.
  • The evidence profiles identify different reference types for “What it is”.
  • Source-backed evidence for “Common reasons people use it” is unavailable for both selected supplements.
  • Source-backed evidence for “What evidence has studied” is unavailable for both selected supplements.
  • Source-backed evidence for “Potential benefits studied” is unavailable for both selected supplements.
  • The selected source blocks for “Known risks and safety considerations” link 7 references for Omega-3 and 10 references for Vitamin D.
  • The evidence profiles identify different reference types for “Known risks and safety considerations”.
  • Source-backed evidence for “Side effects” is unavailable for both selected supplements.
  • The selected source blocks for “Medication interaction evidence” link 6 references for Omega-3 and 13 references for Vitamin D.
  • The evidence profiles identify different reference types for “Medication interaction evidence”.
  • Source-backed evidence for “Supplement interaction evidence” is unavailable for both selected supplements.
  • Source-backed evidence for “Food and nutrient interactions” is unavailable for both selected supplements.
  • The selected source blocks for “Typical forms” link 14 references for Omega-3 and 10 references for Vitamin D.
  • The evidence profiles identify different reference types for “Typical forms”.
  • The selected source blocks for “Evidence-backed dosage information” link 1 reference for Omega-3 and 6 references for Vitamin D.
  • The evidence profiles identify different reference types for “Evidence-backed dosage information”.
  • The selected source blocks contain different source-described limitation tags for “Evidence-backed dosage information”.
  • The selected source blocks for “Populations needing caution” link 1 reference for Omega-3 and 16 references for Vitamin D.
  • The evidence profiles identify different reference types for “Populations needing caution”.
  • Source-backed evidence for “Pregnancy and lactation considerations” is unavailable for both selected supplements.
  • Source-backed evidence for “Laboratory and test considerations” is unavailable for Omega-3 and available for Vitamin D.
  • The evidence profiles identify different reference types for “Laboratory and test considerations”.
  • Source-backed evidence for “Regulatory information” is unavailable for both selected supplements.
  • Source-backed evidence for “Evidence limitations” is unavailable for both selected supplements.

Topic-by-topic evidence

Compare evidence availability and provenance

Each source block, reference, evidence profile, and inspector remains attached to its own supplement and ODS revision.

Evidence topic

What it is

Available for both

Omega-3

Source-backed preview

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

Structural characterization

Evidence profile

No overall rating assigned
Evidence source
NIH ODS evidence synthesis
Linked references
23 identified
Human evidence
Human evidence identified
Randomized trials
Randomized trials not identified in the frozen metadata
Reviews and meta-analyses
Systematic reviews or meta-analyses not identified in the frozen metadata
Evidence recency
2004–2015
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 determined22
  • Government reference1
Source-described limitations

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

Classified references

  1. Jones PJH, Rideout T. Lipids, sterols, and their metabolites. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler TR, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014.

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  2. Jones PJH, Papamandjaris AA. Lipids: cellular metabolism. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012:132-48.

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  3. Harris WS. Omega-3 fatty acids. In: Coates PM, Betz JM, Blackman MR, et al., eds. Encyclopedia of Dietary Supplements. 2nd ed. London and New York: Informa Healthcare; 2010:577-86.

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  4. Lichtenstein AH, Jones PJH. Lipids: absorption and transport. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012:118-31.

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  5. Institute of Medicine, Food and Nutrition Board. Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids (macronutrients). Washington, DC: National Academy Press; 2005.

    Government reference · Population basis: unknown · Directness: not assessed

  6. SanGiovanni JP, Chew EY. The role of omega-3 long-chain polyunsaturated fatty acids in health and disease of the retina. Prog Retin Eye Res 2005;24:87-138. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  7. Gabbs M, Leng S, Devassy JG, Monirujjaman M, Aukema HM. Advances in our understanding of oxylipins derived from dietary PUFAs. Adv Nutr 2015;6:513-40. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  8. Simopoulos AP. The importance of the omega-6/omega-3 fatty acid ratio in cardiovascular disease and other chronic diseases. Exp Biol Med 2008;233:674-88. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  9. James M, Proudman S, Cleland L. Fish oil and rheumatoid arthritis: past, present and future. Proc Nutr Soc 2010;69:316-23. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  10. Wang C, Chung M, Lichtenstein A, Balk E, Kupelnick B, DeVine D, et al. Effects of omega-3 fatty acids on cardiovascular disease. Summary, evidence report/technology assessment no. 94. (Prepared by the Tufts New England Medical Center Evidence-based Practice Center, Boston, MA.) AHRQ Publication No. 04-E009-1. Agency for Healthcare Research and Quality, 2004.

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  11. Stanley JC, Elsom RL, Calder PC, Griffin BA, Harris WS, Jebb SA, et al. UK Food Standards Agency workshop report: the effects of the dietary n-6:n-3 fatty acid ratio on cardiovascular health. Br J Nutr 2007;98:1305-10. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  12. Harris WS, Davidson MH. RE: Plasma phospholipid fatty acids and prostate cancer risk in the SELECT trial. J Natl Cancer Inst 2014;106:dju019. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  13. Fritsche KL. Too much linoleic acid promotes inflammation-doesn't it? Prostaglandins Leukot Essent Fatty Acids 2008;79:173-5. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  14. Brasky TM, Till C, White E, Neuhouser ML, Song X, Goodman P, et al. Serum phospholipid fatty acids and prostate cancer risk: results from the prostate cancer prevention trial. Am J Epidemiol 2011;173:1429-39. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  15. Brasky TM, Darke AK, Song X, Tangen CM, Goodman PJ, Thompson IM, et al. Plasma phospholipid fatty acids and prostate cancer risk in the SELECT trial. J Natl Cancer Inst 2013;105:1132-41. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  16. Harris WS, Sands SA, Windsor SL, Ali HA, Stevens TL, Magalski A, et al. Omega-3 fatty acids in cardiac biopsies from heart transplantation patients: correlation with erythrocytes and response to supplementation. Circulation 2004;110:1645-9. [PubMed abstract]

    Study type could not be determined · Population basis: human · Directness: not assessed

  17. Harris WS. Are n-3 fatty acids still cardioprotective? Curr Opin Clin Nutr Metab Care 2013;16:141-9. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  18. Sun Q, Ma J, Campos H, Hankinson SE, Hu FB. Comparison between plasma and erythrocyte fatty acid content as biomarkers of fatty acid intake in US women. Am J Clin Nutr 2007;86:74-81. [PubMed abstract]

    Study type could not be determined · Population basis: human · Directness: not assessed

  19. Agency for Healthcare Research and Quality. Omega-3 fatty acids and cardiovascular disease - update. 2015.

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  20. Harris WS, Von Schacky C. The Omega-3 Index: a new risk factor for death from coronary heart disease? Prev Med 2004;39:212-20. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  21. Harris WS. The omega-3 index as a risk factor for coronary heart disease. Am J Clin Nutr 2008;87:1997S-2002S. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  22. Metcalf RG, Cleland LG, Gibson RA, Roberts-Thomson KC, Edwards JR, Sanders P, et al. Relation between blood and atrial fatty acids in patients undergoing cardiac bypass surgery. Am J Clin Nutr 2010;91:528-34. [PubMed abstract]

    Study type could not be determined · Population basis: human · Directness: not assessed

  23. von Schacky C. Use of red blood cell fatty-acid profiles as biomarkers in cardiac disease. Biomark Med 2009;3:25-32. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed
Read imported source wording for Omega-3

The two major classes of polyunsaturated fatty acids (PUFAs) are the omega-3 and omega-6 fatty acids. Like all fatty acids, PUFAs consist of long chains of carbon atoms with a carboxyl group at one end of the chain and a methyl group at the other. PUFAs are distinguished from saturated and monounsaturated fatty acids by the presence of two or more double bonds between carbons within the fatty acid chain.

Omega-3 fatty acids (omega-3s) have a carbon–carbon double bond located three carbons from the methyl end of the chain. Omega-3s, sometimes referred to as n-3s, are present in certain foods such as flaxseed and fish as well as dietary supplements such as fish oil. Several different omega-3s exist, but the majority of scientific research focuses on three: alpha-linolenic acid (ALA), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA). ALA contains 18 carbon atoms, whereas EPA and DHA are considered long-chain (LC) omega-3s because EPA contains 20 carbons and DHA contains 22.

PUFAs are frequently designated by their number of carbon atoms and double bonds. ALA, for example, is known as C18:3n-3 because it has 18 carbons and 3 double bonds and is an n-3, or omega-3, fatty acid. Similarly, EPA is known as C20:5n-3 and DHA as C22:6n-3. Omega-6 fatty acids (omega-6s) have a carbon–carbon double bond that is six carbons away from the methyl end of the fatty acid chain. Linoleic acid (C18:2n-6) and arachidonic acid (C20:4n-6) are two of the major omega-6s.

The human body can only form carbon–carbon double bonds after the ninth carbon from the methyl end of a fatty acid [1]. Therefore, ALA and linoleic acid are considered essential fatty acids, meaning that they must be obtained from the diet [2]. ALA can be converted into EPA and then to DHA, but the conversion (which occurs primarily in the liver) is very limited, with reported rates of less than 15% [3]. Therefore, consuming EPA and DHA directly from foods and/or dietary supplements is the only practical way to increase levels of these fatty acids in the body.

ALA is present in plant oils, such as flaxseed, soybean, and canola oils [3]. DHA and EPA are present in fish, fish oils, and krill oils, but they are originally synthesized by microalgae at the base of the marine food chain, not by the fish. As microalgae move up the food chain, fish acquire the omega-3s and accumulate them in their tissues [3].

After ingestion, dietary lipids are hydrolyzed in the intestinal lumen [1]. The hydrolysis products—monoglycerides and free fatty acids—are then incorporated into bile-salt– containing micelles and absorbed into enterocytes, largely by passive diffusion. The process is efficient, with an absorption rate of about 95%, which is similar to that of other ingested fats [1]. Within intestinal cells, free fatty acids are primarily incorporated into chylomicrons and enter the circulation via the lymphatic system [1,4]. Once in the bloodstream, lipoprotein particles circulate within the body, delivering lipids to various organs for subsequent oxidation, metabolism, or storage in adipose tissue [4,5].

Omega-3s play important roles in the body as components of the phospholipids that form the structures of cell membranes [5]. DHA, in particular, is especially high in the retina, brain, and sperm [3,5,6]. In addition to their structural role in cell membranes, omega-3s (along with omega-6s) provide energy for the body and are used to form eicosanoids. Eicosanoids are signaling molecules that have similar chemical structures to the fatty acids from which they are derived; they have wide-ranging functions in the body's cardiovascular, pulmonary, immune, and endocrine systems [1,2].

The eicosanoids made from omega-6s are generally more potent mediators of inflammation, vasoconstriction, and platelet aggregation than those made from omega-3s, although there are some exceptions [3,7]. Because both classes of fatty acids compete for the same desaturation enzymes, ALA is a competitive inhibitor of linoleic acid metabolism and vice versa [8]. Similarly, EPA and DHA can compete with arachidonic acid for the synthesis of eicosanoids. Thus, higher concentrations of EPA and DHA than arachidonic acid tip the eicosanoid balance toward less inflammatory activity [9].

Some researchers propose that the relative intakes of omega-6s and omega-3s—the omega-6/omega-3 ratio—may have important implications for the pathogenesis of many chronic diseases, such as cardiovascular disease (CVD) and cancer [8], but the optimal ratio—if any—has not been defined [10]. Others have concluded that such ratios are too nonspecific and are insensitive to individual fatty acid levels [11-13]. Most agree that raising EPA and DHA blood levels is far more important than lowering linoleic acid or arachidonic acid levels.

Currently, most clinicians do not assess omega-3 status, but it can be done by measuring individual omega-3s in plasma or serum phospholipids and expressing them as the percentage of total phospholipid fatty acids by weight [14-16]. Experts have not established normal ranges, but mean values for serum or plasma phospholipid EPA plus DHA among U.S. adults not taking omega-3 supplements are about 3%–4% [14-16]. Plasma and serum fatty acid values, however, can vary substantially based on an individual's most recent meal, so they do not reflect long-term dietary consumption [3,17].

It is also possible to assess omega-3 status via analysis of erythrocyte fatty acids, a measurement that reflects longer term intakes over approximately the previous 120 days [18,19]. The omega-3 index proposed by Harris and von Schacky reflects the content of EPA plus DHA in erythrocyte membranes expressed as a percentage of total erythrocyte fatty acids [20,21]. This index can be used as a surrogate for assessing tissue levels of EPA plus DHA [16,22,23]. EPA and DHA typically comprise about 3%–5% of erythrocyte fatty acids in Western populations with low fish intakes. In Japan, where fish consumption is high, erythrocyte EPA and DHA levels are about twice those of Western populations [3].

Where did MEDucated get this?

Omega-3 Fatty Acids — 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
August 22, 2025
Retrieved
2026-08-10T22:07:06.488Z
Source fingerprint
80b4434afaf71303420a09ab193258a2d656c3bdec58a108fe3d14961d1bb750
Cited reference numbers
1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23
Inspect the official NIH ODS source (opens in a new tab)

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

Vitamin D

Source-backed preview

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

Structural characterization

Evidence profile

No overall rating assigned
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.

Inspect technical evidence details
Evidence types identified
  • Government reference1
  • Study type could not be determined2
  • Systematic review1
Source-described limitations

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

Classified references

  1. 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

  2. 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

  3. 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

  4. 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
Read imported source wording for Vitamin D

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
Inspect the official NIH ODS source (opens in a new tab)

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

Evidence topic

Common reasons people use it

Unavailable for both

Omega-3

Evidence unavailable

No source-backed evidence is currently available for this topic in MEDucated.

The attached ODS revision does not provide an imported source section for this topic.

Vitamin D

Evidence unavailable

No source-backed evidence is currently available for this topic in MEDucated.

The attached ODS revision does not provide an imported source section for this topic.

Evidence topic

What evidence has studied

Unavailable for both

Omega-3

Evidence unavailable

No source-backed evidence is currently available for this topic in MEDucated.

The attached ODS revision does not provide an imported source section for this topic.

Vitamin D

Evidence unavailable

No source-backed evidence is currently available for this topic in MEDucated.

The attached ODS revision does not provide an imported source section for this topic.

Evidence topic

Potential benefits studied

Unavailable for both

Omega-3

Evidence unavailable

No source-backed evidence is currently available for this topic in MEDucated.

The attached ODS revision does not provide an imported source section for this topic.

Vitamin D

Evidence unavailable

No source-backed evidence is currently available for this topic in MEDucated.

The attached ODS revision does not provide an imported source section for this topic.

Evidence topic

Known risks and safety considerations

Available for both

Omega-3

Source-backed preview

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

Structural characterization

Evidence profile

No overall rating assigned
Evidence source
NIH ODS evidence synthesis
Linked references
7 identified
Human evidence
Human evidence identified
Randomized trials
Randomized trial identified
Reviews and meta-analyses
Systematic review or meta-analysis identified
Evidence recency
2005–2020
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.

Inspect technical evidence details
Evidence types identified
  • Government reference1
  • Study type could not be determined3
  • Randomized controlled trial1
  • Meta-analysis1
  • Regulatory source1
Source-described limitations

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

Classified references

  1. Institute of Medicine, Food and Nutrition Board. Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids (macronutrients). Washington, DC: National Academy Press; 2005.

    Government reference · Population basis: unknown · Directness: not assessed

  2. Bhatt DL, Steg PG, Miller M, Brinton EA, Jacobson TA, et al; REDUCE-IT Investigators. Cardiovascular risk reduction with icosapent ethyl for hypertriglyceridemia. N Engl J Med 2019;380:11-22. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  3. Nicholls SJ, Lincoff M, Garcia M, Dash D, Ballantyne CM, Barter PJ, et al. Effect of high-dose omega-3 fatty acids vs corn oil on major adverse cardiovascular events in patients at high cardiovascular risk. The STRENGTH randomized clinical trial. JAMA 2020;324:2268-80. [PubMed abstract]

    Randomized controlled trial · Population basis: human · Directness: not assessed

  4. Mazereeuw G, Lanctot KL, Chau SA, Swardfager W, Herrmann N. Effects of omega-3 fatty acids on cognitive performance: a meta-analysis. Neurobiol Aging 2012;33:1482 e17-29. [PubMed abstract]

    Meta-analysis · Population basis: unknown · Directness: not assessed

  5. Lev-Tzion R, Griffiths AM, Leder O, Turner D. Omega 3 fatty acids (fish oil) for maintenance of remission in Crohn's disease. Cochrane Database Syst Rev 2014;2:CD006320. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  6. EFSA Panel on Dietetic Products NaA. Scientific opinion on the tolerable upper intake level of eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA) and docosapentaenoic acid (DPA). EFSA Journal 2012;10:2815.

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  7. U.S. Food and Drug Administration. Qualified health claims: letters of enforcement discretion. 2019.

    Regulatory source · Population basis: unknown · Directness: not assessed
Source safety wording remains visible

For most macronutrients, the IOM has established an acceptable macronutrient distribution range (AMDR) that suggests an acceptable range of intake. The AMDR for total fat intake, for example, is based on adverse effects from either very low fat or very high fat diets. The IOM established an AMDR for omega-3s (as ALA) of 0.6% to 1.2% of energy for children and adults age 1 year and older [5]. The IOM also noted that about 10% of the AMDR can be consumed as EPA and/or DHA.

The IOM did not establish a UL for any omega-3s, although it noted that high doses of DHA and/or EPA (900 mg/day of EPA plus 600 mg/day DHA or more for several weeks) might reduce immune function due to suppression of inflammatory responses. Doses of 2–15 g/day EPA and/or DHA might also increase bleeding time by reducing platelet aggregation [5]. However, according to the European Food Safety Authority, long-term consumption of EPA and DHA supplements at combined doses of up to about 5 g/day appears to be safe [195]. It noted that these doses have not been shown to cause bleeding problems or affect immune function, glucose homeostasis, or lipid peroxidation. Similarly, FDA has concluded that dietary supplements providing no more than 5 g/day EPA and DHA are safe when used as recommended [196]. Two large clinical trials completed after these assessments found that taking 4 g/day of omega-3 supplements for several years slightly increased the risk of atrial fibrillation in people with CVD or at high risk of CVD [63,64].

UL reference intakeSource intake rangeSource-described amount

Commonly reported side effects of omega-3 supplements are usually mild. These include unpleasant taste, bad breath, heartburn, nausea, gastrointestinal discomfort, diarrhea, headache, and odoriferous sweat [161,190].

Where did MEDucated get this?

Omega-3 Fatty Acids — Fact Sheet for Health Professionals

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

Source section
Safety of Omega-3s
ODS revision
August 22, 2025
Retrieved
2026-08-10T22:07:06.488Z
Source fingerprint
80b4434afaf71303420a09ab193258a2d656c3bdec58a108fe3d14961d1bb750
Cited reference numbers
5, 63, 64, 195, 196, 161, 190
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Vitamin D

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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 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
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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

  1. 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

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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

  7. 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

  8. 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

  9. 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

  10. 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
Source safety wording remains visible

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]
AgeMaleFemalePregnancyLactation
0–6 months25 mcg (1,000 IU)25 mcg (1,000 IU)
7–12 months38 mcg (1,500 IU)38 mcg (1,500 IU)
1–3 years63 mcg (2,500 IU)63 mcg (2,500 IU)
4–8 years75 mcg (3,000 IU)75 mcg (3,000 IU)
9–13 years100 mcg (4,000 IU)100 mcg (4,000 IU)
14–18 years100 mcg (4,000 IU)100 mcg (4,000 IU)100 mcg (4,000 IU)100 mcg (4,000 IU)
19–50 years100 mcg (4,000 IU)100 mcg (4,000 IU)100 mcg (4,000 IU)100 mcg (4,000 IU)
51–70 years100 mcg (4,000 IU)100 mcg (4,000 IU)
>70 years100 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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Evidence topic

Side effects

Unavailable for both

Omega-3

Evidence unavailable

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The attached ODS revision does not provide an imported source section for this topic.

Vitamin D

Evidence unavailable

No source-backed evidence is currently available for this topic in MEDucated.

The attached ODS revision does not provide an imported source section for this topic.

Evidence topic

Medication interaction evidence

Available for both

Omega-3

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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.

Structural characterization

Evidence profile

No overall rating assigned
Evidence source
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Linked references
6 identified
Human evidence
Human evidence identified
Randomized trials
Randomized trials not identified in the frozen metadata
Reviews and meta-analyses
Systematic reviews or meta-analyses not identified in the frozen metadata
Evidence recency
1998–2015
Source-described consistency
Not characterized in these source blocks
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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 determined6
Source-described limitations

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

Classified references

  1. Natural Medicines Comprehensive Database. Fish Oil. 2015.

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  2. Svaneborg N, Kristensen SD, Hansen LM, Bullow I, Husted SE, Schmidt EB. The acute and short-time effect of supplementation with the combination of n-3 fatty acids and acetylsalicylic acid on platelet function and plasma lipids. Thromb Res 2002;105:311-6. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  3. Buckley MS, Goff AD, Knapp WE. Fish oil interaction with warfarin. Ann Pharmacother 2004;38:50-2 [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  4. Bender NK, Kraynak MA, Chiquette E, Linn WD, Clark GM, Bussey HI. Effects of marine fsh oils on the anticoagulation status of patients receiving chronic warfarin therapy. J Thromb Thrombolysis 1998;5:257-61. [PubMed abstract]

    Study type could not be determined · Population basis: human · Directness: not assessed

  5. Wachira JK, Larson MK, Harris WS. n-3 fatty acids affect haemostasis but do not increase the risk of bleeding: clinical observations and mechanistic insights. Br J Nutr 2014;111:1652-62. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  6. GlaxoSmithKline. LOVAZA® (omega-3 acid ethyl esters) capsules, prescribing information. 2008.

    Study type could not be determined · Population basis: unknown · Directness: not assessed
Source safety wording remains visible

Omega-3 dietary supplements, such as fish oil, have the potential to interact with medications. One example is provided below. People taking these and other medications on a regular basis should discuss possible interactions with their health care providers.

Fish oil can have antiplatelet effects at high doses, although it appears to be less potent than aspirin [197,198]. Fish oil might prolong clotting times, as indicated by an elevated international normalized ratio (INR), when it is taken with warfarin [199], but most research indicates that doses of 3–6 g/day fish oil do not significantly affect the anticoagulant status of patients taking warfarin [200]. The authors of a 2014 review concluded that omega-3s do not affect the risk of clinically significant bleeding [201], and the FDA-approved package inserts for omega-3 pharmaceuticals state that studies with omega-3s have not produced "clinically significant bleeding episodes" [202]. However, these package inserts also state that patients taking these products with anticoagulants should be monitored periodically for changes in INR.

Source intake rangeSource-described amount
Where did MEDucated get this?

Omega-3 Fatty Acids — 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
August 22, 2025
Retrieved
2026-08-10T22:07:06.488Z
Source fingerprint
80b4434afaf71303420a09ab193258a2d656c3bdec58a108fe3d14961d1bb750
Cited reference numbers
197, 198, 199, 200, 201, 202
Inspect the official NIH ODS source (opens in a new tab)

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Vitamin D

Source-backed preview

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

Structural characterization

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

  1. 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

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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

  7. 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

  8. 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

  9. 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

  10. 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

  11. 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

  12. 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

  13. 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
Source safety wording remains visible

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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Evidence topic

Supplement interaction evidence

Unavailable for both

Omega-3

Evidence unavailable

No source-backed evidence is currently available for this topic in MEDucated.

The attached ODS revision does not provide an imported source section for this topic.

Vitamin D

Evidence unavailable

No source-backed evidence is currently available for this topic in MEDucated.

The attached ODS revision does not provide an imported source section for this topic.

Evidence topic

Food and nutrient interactions

Unavailable for both

Omega-3

Evidence unavailable

No source-backed evidence is currently available for this topic in MEDucated.

The attached ODS revision does not provide an imported source section for this topic.

Vitamin D

Evidence unavailable

No source-backed evidence is currently available for this topic in MEDucated.

The attached ODS revision does not provide an imported source section for this topic.

Evidence topic

Typical forms

Available for both

Omega-3

Source-backed preview

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

Structural characterization

Evidence profile

No overall rating assigned
Evidence source
NIH ODS evidence synthesis
Linked references
14 identified
Human evidence
Human evidence identified
Randomized trials
Randomized trial identified
Reviews and meta-analyses
Systematic reviews or meta-analyses not identified in the frozen metadata
Evidence recency
2008–2016
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 determined11
  • Regulatory source1
  • Randomized controlled trial2
Source-described limitations

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

Classified references

  1. National Institutes of Health. Dietary Supplement Label Database. 2015.

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  2. U.S. Food and Drug Administration. Fish: what pregnant women and parents should know. 2014.

    Regulatory source · Population basis: human · Directness: not assessed

  3. ConsumerLab.com. Product review: fish oil and omega-3 fatty acid supplements review (including krill, algae, calamari, green-lipped mussel oil). 2016.

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  4. Dyerberg J, Madsen P, Moller JM, Aardestrup I, Schmidt EB. Bioavailability of marine n-3 fatty acid formulations. Prostaglandins Leukot Essent Fatty Acids 2010;83:137-41. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  5. Cunningham E. Are krill oil supplements a better source of n-3 fatty acids than fish oil supplements? J Acad Nutr Diet 2012;112:344. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  6. Davidson MH, Kling D, Maki KC. Novel developments in omega-3 fatty acid-based strategies. Curr Opin Lipidol 2011;22:437-44. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  7. Schuchardt JP, Schneider I, Meyer H, Neubronner J, von Schacky C, Hahn A. Incorporation of EPA and DHA into plasma phospholipids in response to different omega-3 fatty acid formulations--a comparative bioavailability study of fish oil vs. krill oil. Lipids Health Dis 2011;10:145. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  8. Ulven SM, Holven KB. Comparison of bioavailability of krill oil versus fish oil and health effect. Vasc Health Risk Manag 2015;11:511-24. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  9. Ramprasath VR, Eyal I, Zchut S, Jones PJ. Enhanced increase of omega-3 index in healthy individuals with response to 4-week n-3 fatty acid supplementation from krill oil versus fish oil. Lipids Health Dis 2013;12:178. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  10. Ulven SM, Kirkhus B, Lamglait A, Basu S, Elind E, et al. Metabolic effects of krill oil are essentially similar to those of fish oil but at lower dose of EPA and DHA, in healthy volunteers. Lipids 2011;46(1):37-46. [PubMed abstract]

    Study type could not be determined · Population basis: human · Directness: not assessed

  11. Salem N Jr, Kuratko CN. A reexamination of krill oil bioavailability studies. Lipids Health Dis 2014;13:137. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  12. Yurko-Mauro K, Kralovec J, Bailey-Hall E, Smeberg V, Stark JG, et al. Similar eicosapentaenoic acid and docosahexaenoic acid plasma levels achieved with fish oil or krill oil in a randomized double-blind four-week bioavailability study. Lipids Health Dis 2015;14:99. [PubMed abstract]

    Randomized controlled trial · Population basis: unknown · Directness: not assessed

  13. Köhler A, Sarkkinen E, Tapola N, Niskanen T, Bruheim I. Bioavailability of fatty acids from krill oil, krill meal and fish oil in healthy subjects--a randomized, single-dose, cross-over trial. Lipids Health Dis 2015;14:19. [PubMed abstract]

    Randomized controlled trial · Population basis: unknown · Directness: not assessed

  14. Arterburn LM, Oken HA, Bailey Hall E, Hamersley J, Kuratko CN, Hoffman JP. Algal-oil capsules and cooked salmon: nutritionally equivalent sources of docosahexaenoic acid. J Am Diet Assoc 2008;108:1204-9. [PubMed abstract]

    Study type could not be determined · Population basis: unknown · Directness: not assessed
Read imported source wording for Omega-3

LC omega-3s are present in several dietary supplement formulations, including fish oil, krill oil, cod liver oil, and vegetarian products that contain algal oil. A typical fish oil supplement provides about 1,000 mg fish oil, containing 180 mg EPA and 120 mg DHA, but doses vary widely [30]. Cod liver oil supplements provide vitamin A and vitamin D in addition to LC omega-3s. Although seafood contains varying levels of methyl mercury (a toxic heavy metal) [31], omega-3 supplements have not been found to contain this contaminant because it is removed during processing and purification [32].

Source-described amount

Dietary supplements can contain several different forms of omega-3s, including natural triglycerides, free fatty acids, ethyl esters, re-esterified triglycerides, and phospholipids [32-34]. Natural triglycerides are the form that occur naturally in fish oil, whereas ethyl esters are synthesized from natural triglycerides by replacement of the glycerol molecule of the triglyceride with ethanol. Re-esterified triglycerides are formed by the conversion of ethyl esters back to triglycerides. Omega-3s as re-esterified triglycerides, natural triglycerides, and free fatty acids have somewhat higher bioavailability than ethyl esters, but consumption of all forms significantly increases plasma EPA and DHA levels [33,35].

Krill oil contains omega-3s primarily as phospholipids. Some studies suggest that these phospholipids have somewhat higher bioavailability than the omega-3s in fish oil, whereas other studies do not [34,36,37,38,39,40,41,42].

Plant-based sources of omega-3s from algal oil usually provide around 100–300 mg DHA; some contain EPA as well. These supplements typically contain omega-3s in the triglyceride form [32]. According to a small study, the bioavailability of DHA from algal oil is equivalent to that from cooked salmon [43].

Source intake rangeSource-described amount

Formulations of omega-3 dietary supplements vary widely, so it is important to check product labels to determine the types and amounts of omega-3s in these products. The Dietary Supplement Label Database from the National Institutes of Health contains label information from many dietary supplements on the market that contain omega-3s.

Where did MEDucated get this?

Omega-3 Fatty Acids — 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
August 22, 2025
Retrieved
2026-08-10T22:07:06.488Z
Source fingerprint
80b4434afaf71303420a09ab193258a2d656c3bdec58a108fe3d14961d1bb750
Cited reference numbers
30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43
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Vitamin D

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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 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
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.

Inspect technical evidence details
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

  1. 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

  2. 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

  3. 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

  4. National Institutes of Health. Dietary Supplement Label Database. 2020.

    Study type could not be determined · Population basis: unknown · Directness: not assessed

  5. 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

  6. 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

  7. 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

  8. 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

  9. 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

  10. 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 for Vitamin D

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.

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Dietary supplements
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Cited reference numbers
13, 31, 32, 4, 33, 34, 35, 36, 37, 38
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Omega-3

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    When the IOM last reviewed omega-3s, insufficient data were available to establish an EAR, so the IOM established AIs for all ages based on omega-3 intakes in healthy populations [5].

Classified references

  1. Institute of Medicine, Food and Nutrition Board. Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids (macronutrients). Washington, DC: National Academy Press; 2005.

    Government reference · Population basis: unknown · Directness: not assessed
Read imported source wording for Omega-3

Intake recommendations for fatty acids and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board of the Institute of Medicine (IOM) (now called the National Academy of Medicine) [5]. DRI is the general term for a set of reference values used for planning and assessing nutrient intakes of healthy people. These values, which vary by age and sex, 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

When the IOM last reviewed omega-3s, insufficient data were available to establish an EAR, so the IOM established AIs for all ages based on omega-3 intakes in healthy populations [5].

Table 1 lists the current AIs for omega-3s in grams per day. Human milk contains omega-3s as ALA, EPA, and DHA, so the IOM established an AI for infants from birth to 12 months that is equivalent to the mean intake of omega-3s in healthy, breastfed infants.

AI reference intake

For infants, the AIs apply to total omega-3s. For age 1 and older, the AIs apply only to ALA because ALA is the only omega-3 that is essential. The IOM did not establish specific intake recommendations for EPA, DHA, or other LC omega-3s.

Table 1: Adequate Intakes (AIs) for Omega-3s [5]
AgeMaleFemalePregnancyLactation
Birth to 6 months*0.5 g0.5 g
7–12 months*0.5 g0.5 g
1–3 years**0.7 g0.7 g
4–8 years**0.9 g0.9 g
9–13 years**1.2 g1.0 g
14–18 years**1.6 g1.1 g1.4 g1.3 g
19–50 years**1.6 g1.1 g1.4 g1.3 g
51+ years**1.6 g1.1 g
AI reference intakeSource-described amount

*As total omega-3s **As ALA

Where did MEDucated get this?

Omega-3 Fatty Acids — Fact Sheet for Health Professionals

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

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Recommended Intakes
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5
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Vitamin D

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  • Study type could not be determined1
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Classified references

  1. 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

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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 for Vitamin D

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]
AgeMaleFemalePregnancyLactation
0–6 months*10 mcg (400 IU)*10 mcg (400 IU)*
7–12 months*10 mcg (400 IU)*10 mcg (400 IU)*
1–3 years15 mcg (600 IU)15 mcg (600 IU)
4–8 years15 mcg (600 IU)15 mcg (600 IU)
9–13 years15 mcg (600 IU)15 mcg (600 IU)
14–18 years15 mcg (600 IU)15 mcg (600 IU)15 mcg (600 IU)15 mcg (600 IU)
19–50 years15 mcg (600 IU)15 mcg (600 IU)15 mcg (600 IU)15 mcg (600 IU)
51–70 years15 mcg (600 IU)15 mcg (600 IU)
>70 years20 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.

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Recommended Intakes
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825b1a553a4a177e2d87fc412b0b4b21daa72ca92f4334a0096bc0dfa7f70a3c
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1, 9, 11, 12, 15, 16
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Omega-3

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Classified references

  1. Institute of Medicine, Food and Nutrition Board. Dietary reference intakes for energy, carbohydrate, fiber, fat, fatty acids, cholesterol, protein, and amino acids (macronutrients). Washington, DC: National Academy Press; 2005.

    Government reference · Population basis: unknown · Directness: not assessed
Read imported source wording for Omega-3

Evidence that higher LC omega-3 levels are associated with a reduced risk of several chronic diseases, including coronary heart disease, suggests that many Americans could benefit from slightly higher intakes. However, classical essential fatty acid deficiency in healthy individuals in the United States is virtually nonexistent [5]. During periods of dietary-fat restriction or malabsorption accompanied by an energy deficit, the body releases essential fatty acids from adipose-tissue reserves. For this reason, clinical signs of essential fatty-acid deficiency are usually only found in patients receiving parenteral nutrition that lacks PUFAs. This was documented in case reports during the 1970s and 1980s [5], but all current enteral and parenteral feeding solutions contain adequate levels of PUFAs.

Where did MEDucated get this?

Omega-3 Fatty Acids — Fact Sheet for Health Professionals

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

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Groups at Risk of Omega-3 Inadequacy
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Classified references

  1. 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

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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

  7. 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

  8. 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

  9. 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

  10. 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

  11. 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

  12. 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

  13. 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

  14. 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

  15. 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

  16. 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
Read imported source wording for Vitamin D

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.

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Groups at Risk of Vitamin D Inadequacy
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2026-08-10T22:07:04.753Z
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1, 56, 57, 58, 59, 60, 61, 62, 14, 4, 63, 64, 65, 66, 67, 68
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Vitamin D

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Omega-3

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Vitamin D

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2007–2024
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  • Systematic review1
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Classified references

  1. 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

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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

  7. 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

  8. 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

  9. 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

  10. 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

  11. 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

  12. 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

  13. 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 for Vitamin D

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<12Associated with vitamin D deficiency, which can lead to rickets in infants and children and osteomalacia in adults
30 to <5012 to <20Generally considered inadequate for bone and overall health in healthy individuals
≥50≥20Generally considered adequate for bone and overall health in healthy individuals
>125>50Linked 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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