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.

mineral

Iron

Canonical supplement identity

ODS source attached

Canonical ID: entity:supplement:iron
Identity layer: Supplement concept
Evidence status: source backed demonstration not medically reviewed
Medical review: not medically reviewed

Modeled ingredients

No ingredient relationship is modeled in this pilot.

Modeled forms

No form relationship is modeled in this pilot.

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

Iron

Iron — Fact Sheet for Health Professionals

Source ID: source:nih-ods:iron-health-professional
Source revision ID: source-revision:nih-ods:iron-health-professional:2026-08-10.fa6273f9305d
ODS revision date: September 4, 2025
Medical review: not medically reviewed
Source fingerprint: fa6273f9305dfba9ea81d7c31ede31b36a0be1e035ebefbee0715ec605840e21
Retrieved: 2026-08-10T22:07:05.577Z

Inspect the official NIH ODS source

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

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: September 4, 2025 for Iron and June 27, 2025 for Vitamin D.
Iron and Vitamin D have different modeled ingredient relationships. This is an identity distinction, not a clinical ranking.
Iron 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 6 references for Iron 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 19 references for Iron 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 11 references for Iron 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 9 references for Iron 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 Iron and 6 references for Vitamin D.
The evidence profiles identify different reference types for “Evidence-backed dosage information”.
The selected source blocks for “Populations needing caution” link 21 references for Iron and 16 references for Vitamin D.
The evidence profiles identify different reference types for “Populations needing caution”.
The selected source blocks contain different source-described limitation tags for “Populations needing caution”.
Source-backed evidence for “Pregnancy and lactation considerations” is unavailable for both selected supplements.
The selected source blocks for “Laboratory and test considerations” link 14 references for Iron and 13 references 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

Iron

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: 6 identified
Human evidence: Human evidence not identified in the frozen metadata
Randomized trials: Randomized trials not identified in the frozen metadata
Reviews and meta-analyses: Systematic reviews or meta-analyses not identified in the frozen metadata
Evidence recency: 2001–2014
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 determined5
Government reference1

Source-described limitations

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

Classified references

Wessling-Resnick M. Iron. In: Ross AC, Caballero B, Cousins RJ, Tucker KL, Ziegler RG, eds. Modern Nutrition in Health and Disease. 11th ed. Baltimore, MD: Lippincott Williams & Wilkins; 2014:176-88.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Aggett PJ. Iron. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012:506-20.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Murray-Kolbe LE, Beard J. Iron. In: Coates PM, Betz JM, Blackman MR, et al., eds. Encyclopedia of Dietary Supplements. 2nd ed. London and New York: Informa Healthcare; 2010:432-8.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Hurrell R, Egli I. Iron bioavailability and dietary reference values. Am J Clin Nutr 2010;91:1461S-7S. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc : a Report of the Panel on Micronutrients. Washington, DC: National Academy Press; 2001.
Government reference · Population basis: unknown · Directness: not assessed
Drakesmith H, Prentice AM. Hepcidin and the Iron-Infection Axis. Science 2012;338:768-72. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed

Read imported source wording for Iron

Iron is a mineral that is naturally present in many foods, added to some food products, and available as a dietary supplement. Iron is an essential component of hemoglobin, an erythrocyte (red blood cell) protein that transfers oxygen from the lungs to the tissues [1]. As a component of myoglobin, another protein that provides oxygen, iron supports muscle metabolism and healthy connective tissue [2]. Iron is also necessary for physical growth, neurological development, cellular functioning, and the synthesis of some hormones [2,3].

Dietary iron has two main forms: heme and nonheme [1]. Plants and iron-fortified foods contain nonheme iron only, whereas meat, seafood, and poultry contain both heme and nonheme iron [2]. Heme iron, which forms when iron combines with protoporphyrin IX, contributes about 10% to 15% of total iron intakes in western populations [3-5].

Most of the 3 to 4 grams (g) of elemental iron that is present in adults is found in hemoglobin [2]. Much of the remaining iron is stored in the form of ferritin or hemosiderin (a degradation product of ferritin) in the liver, spleen, and bone marrow, or it is located in the myoglobin of muscle tissue [1,5]. Transferrin is the main protein in blood that binds to iron and transports it throughout the body. Humans typically lose only small amounts of iron in urine, feces, sweat, and shed skin cells. Losses are greater in menstruating women because of blood loss. Hepcidin, a circulating peptide hormone, is the key regulator of both iron absorption and the distribution of iron throughout the body, including in plasma [1,2,6].

Where did MEDucated get this?

Iron — 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: September 4, 2025
Retrieved: 2026-08-10T22:07:05.577Z
Source fingerprint: fa6273f9305dfba9ea81d7c31ede31b36a0be1e035ebefbee0715ec605840e21
Cited reference numbers: 1, 2, 3, 4, 5, 6

Inspect the official NIH ODS source

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

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

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

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

Evidence topic

Common reasons people use it

Unavailable for both

Iron

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

Iron

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

Iron

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

Iron

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: 19 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trials not identified in the frozen metadata
Reviews and meta-analyses: Systematic review or meta-analysis identified
Evidence recency: 1973–2020
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

Study type could not be determined14
Government reference1
Clinical guideline2
Case report1
Systematic review1

Source-described limitations

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

Classified references

Aggett PJ. Iron. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012:506-20.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Murray-Kolbe LE, Beard J. Iron. In: Coates PM, Betz JM, Blackman MR, et al., eds. Encyclopedia of Dietary Supplements. 2nd ed. London and New York: Informa Healthcare; 2010:432-8.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc : a Report of the Panel on Micronutrients. Washington, DC: National Academy Press; 2001.
Government reference · Population basis: unknown · Directness: not assessed
Manoguerra AS, Erdman AR, Booze LL, Christianson G, Wax PM, Scharman EJ, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila) 2005;43:553-70. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessed
Bacon BR, Adams PC, Kowdley KV, Powell LW, Tavill AS. Diagnosis and management of hemochromatosis: 2011 practice guideline by the American Association for the Study of Liver Diseases. Hepatology 2011;54:328-43. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessed
Solomons NW. Competitive interaction of iron and zinc in the diet: consequences for human nutrition. J Nutr 1986;116:927-35. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Whittaker P. Iron and zinc interactions in humans. Am J Clin Nutr 1998;68:442S-6S. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Aggett PJ. Iron. In: Marriott BP, Birt DF, Stallings VA, Yates AA, eds. Present Knowledge in Nutrition. 11th ed. Cambridge, MA: Elsevier; 2020:375-92.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Bryce K, Hawthorne M, Ewing I. Unusual gastric lesion in an iron-deficient patient. Gut. 2019;68:2141-78. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Hashash JG, Proksell S, Kuan SF, Behari J. Iron pill-induced gastritis. ACG Case Rep J. 2013;1:13-5. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Meliţ LE, Mărginean CO, Mocanu S, Mărginean MO. A rare case of iron-pill induced gastritis in a female teenager: A case report and a review of the literature. Medicine (Baltimore). 2017;96:e7550. [PubMed abstract]
Case report · Population basis: unknown · Directness: not assessed
Motwani K, Rubin J, Yfantis H, Willard M. Iron pill induced gastritis causing severe anemia. Clin J Gastroenterol. 2020;13:732-5. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Chang TP, Rangan C. Iron poisoning: a literature-based review of epidemiology, diagnosis, and management. Pediatr Emerg Care 2011;27:978-85. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Food and Drug Administration. Iron-Containing Supplements and Drugs; Label Warning Statements and Unit-Dose Packaging Requirements; Removal of Regulations for Unit-Dose Packaging Requirements for Dietary Supplements and Drugs. 2003.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Code of Federal Regulations. Title 21 (Food and Drugs), Section 101.17 (Food labeling warning, notice, and safe handling statements).
Study type could not be determined · Population basis: unknown · Directness: not assessed
Consumer Product Safety Commission. Poison Prevention Packaging: A Guide For Healthcare Professionals. 2005.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Substances Requiring Special Packaging. 16 CFR 1700.4. 1973.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Fleming RE, Ponka P. Iron Overload in human disease. N Engl J Med 2012;366:348-59. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Whitlock EP, Garlitz BA, Harris EL, Beil TL, Smith PR. Screening for hereditary hemochromatosis: a systematic review for the U.S. Preventive Services Task Force. Ann Intern Med 2006;145:209-23. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessed

Source safety wording remains visible

The risk of iron overload from dietary sources of iron is low among adults who have normal intestinal function, but high doses of iron supplements can cause a range of gastrointestinal effects. With extremely high doses, these effects can be severe, including corrosive necrosis of the intestine, multisystem organ failure, and even death. The Tolerable Upper Intake Level for iron is 45 mg for adults, and it ranges from 40 mg to 45 mg for infants, children, and adolescents, depending on age.

UL reference intakeSource-described amount

Adults with normal intestinal function have very little risk of iron overload from dietary sources of iron [2]. However, supplements containing 25 mg iron or more can reduce zinc absorption and plasma zinc concentrations [3,87,88]. High-dose iron supplements can also cause gastrointestinal effects, including gastric upset, constipation, nausea, abdominal pain, vomiting, and diarrhea [5,89]. Taking iron supplements with food can help minimize these adverse effects. Case reports, some of which involved doses of 130 mg iron, suggest that some people develop even more serious gastrointestinal effects, including gastritis and gastric lesions (along with iron deposits in the gastric mucosa in some cases) [90-93].

Source-described amount

Acute intakes of more than 20 mg/kg iron (about 1,365 mg iron for a person weighing 150 pounds [lb]) from supplements or medicines can lead to corrosive necrosis of the intestine, which might lead to fluid and blood loss, shock, tissue damage, and organ failure, especially if food is not taken at the same time as the iron [89]. In severe cases (e.g., one-time ingestions of 60 mg/kg, or about 4,090 mg iron for a 150-lb person), overdoses of iron can lead to multisystem organ failure, coma, convulsions, and even death [27,94].

Source-described amount

Between 1983 and 2000, at least 43 U.S. children died from ingesting supplements containing high doses of iron (36–443 mg iron/kg body weight) [27]. Accidental ingestion of iron supplements caused about a third of poisoning deaths among children reported in the United States between 1983 and 1991.

Source intake rangeSource-described amount

In 1997, FDA began requiring oral supplements containing more than 30 mg elemental iron per dose to be sold in single-dose packaging with strong warning labels. At the same time, many manufacturers voluntarily replaced the sugar coating on iron tablets with film coatings. Between 1998 and 2002, only one child death due to ingesting an iron-containing tablet was reported [27]. As a result of a court decision, FDA removed its single-dose packaging requirement for iron supplements in 2003 [95]. FDA currently requires that iron-containing dietary supplements sold in solid form (e.g., tablets or capsules but not powders) carry the following label statement: “WARNING: Accidental overdose of iron-containing products is a leading cause of fatal poisoning in children under 6. Keep this product out of reach of children. In case of accidental overdose, call a doctor or poison control center immediately” [96]. In addition, since 1978, the Consumer Product Safety Commission has required manufacturers to package dietary supplements that contain 250 mg or more elemental iron per container in child-resistant bottles or packaging to prevent accidental poisoning [97,98].

Source-described amount

Hemochromatosis, a disease caused by a mutation in the hemochromatosis (HFE) gene, is associated with an excessive buildup of iron in the body [3,39,99]. About 1 in 10 Whites carry the most common HFE mutation (C282Y), but only 4.4 Whites per 1,000 are homozygous for the mutation and have hemochromatosis [100]. The condition is much less common in other ethnic groups. Without treatment by periodic chelation or phlebotomy, people with hereditary hemochromatosis typically develop signs of iron toxicity by their 30s [3]. These effects can include liver cirrhosis, hepatocellular carcinoma, heart disease, and impaired pancreatic function. The American Association for the Study of Liver Diseases recommends that treatment of hemochromatosis include the avoidance of iron and vitamin C supplements [39].

The FNB has established ULs for iron from food and supplements based on the amounts of iron that are associated with gastrointestinal effects following supplemental intakes of iron salts (see Table 3). The ULs apply to healthy infants, children, and adults. Physicians sometimes prescribe intakes higher than the UL, such as when people with IDA need higher doses to replenish their iron stores [5].

UL reference intake

Table 3: Tolerable Upper Intake Levels (ULs) for Iron [5]
Age	Male	Female	Pregnancy	Lactation
0–6 months	40 mg	40 mg
7–12 months	40 mg	40 mg
1–3 years	40 mg	40 mg
4–8 years	40 mg	40 mg
9–13 years	40 mg	40 mg
14–18 years	45 mg	45 mg	45 mg	45 mg
19–50 years	45 mg	45 mg	45 mg	45 mg
51+ years	45 mg	45 mg

UL reference intakeSource-described amount

Where did MEDucated get this?

Iron — 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 Iron
ODS revision: September 4, 2025
Retrieved: 2026-08-10T22:07:05.577Z
Source fingerprint: fa6273f9305dfba9ea81d7c31ede31b36a0be1e035ebefbee0715ec605840e21
Cited reference numbers: 2, 3, 5, 87, 88, 89, 90, 91, 92, 93, 27, 94, 95, 96, 97, 98, 39, 99, 100

Inspect the official NIH ODS source

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

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

Inspect technical evidence details

Evidence types identified

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

Source-described limitations

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

Classified references

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

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]
Age	Male	Female	Pregnancy	Lactation
0–6 months	25 mcg (1,000 IU)	25 mcg (1,000 IU)
7–12 months	38 mcg (1,500 IU)	38 mcg (1,500 IU)
1–3 years	63 mcg (2,500 IU)	63 mcg (2,500 IU)
4–8 years	75 mcg (3,000 IU)	75 mcg (3,000 IU)
9–13 years	100 mcg (4,000 IU)	100 mcg (4,000 IU)
14–18 years	100 mcg (4,000 IU)	100 mcg (4,000 IU)	100 mcg (4,000 IU)	100 mcg (4,000 IU)
19–50 years	100 mcg (4,000 IU)	100 mcg (4,000 IU)	100 mcg (4,000 IU)	100 mcg (4,000 IU)
51–70 years	100 mcg (4,000 IU)	100 mcg (4,000 IU)
>70 years	100 mcg (4,000 IU)	100 mcg (4,000 IU)

UL reference intakeSource-described amount

Where did MEDucated get this?

Vitamin D — Fact Sheet for Health Professionals

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

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

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Iron

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Iron

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Evidence source: NIH ODS evidence synthesis
Linked references: 11 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trials not identified in the frozen metadata
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Study type could not be determined11

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Classified references

Murray-Kolbe LE, Beard J. Iron. In: Coates PM, Betz JM, Blackman MR, et al., eds. Encyclopedia of Dietary Supplements. 2nd ed. London and New York: Informa Healthcare; 2010:432-8.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Campbell NR, Hasinoff B. Ferrous sulfate reduces levodopa bioavailability: chelation as a possible mechanism. Clin Pharmacol Ther 1989;45:220-5. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Campbell RR, Hasinoff B, Chernenko G, Barrowman J, Campbell NR. The effect of ferrous sulfate and pH on L-dopa absorption. Can J Physiol Pharmacol 1990;68:603-7. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Greene RJ, Hall AD, Hider RC. The interaction of orally administered iron with levodopa and methyldopa therapy. J Pharm Pharmacol 1990;42:502-4. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Novartis. Stalevo Package Insert. 2010.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Merck & Co. I. Sinemet Package Insert. 2011.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Campbell NR, Hasinoff BB, Stalts H, Rao B, Wong NC. Ferrous sulfate reduces thyroxine efficacy in patients with hypothyroidism. Ann Intern Med 1992;117:1010-3. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Forest Laboratories I. Levothroid Package Insert. 2011.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Abbvie Inc. Synthroid Package Insert. 2012.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Stewart CA, Termanini B, Sutliff VE, Serrano J, Yu F, Gibril F, et al. Iron absorption in patients with Zollinger-Ellison syndrome treated with long-term gastric acid antisecretory therapy. Aliment Pharmacol Ther 1998;12:83-98. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Ajmera AV, Shastri GS, Gajera MJ, Judge TA. Suboptimal response to ferrous sulfate in iron-deficient patients taking omeprazole. Am J Ther 2012;19:185-9. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed

Source safety wording remains visible

Iron supplements may interact with medications, including levodopa and levothyroxine. In addition, proton pump inhibitors can potentially reduce iron absorption.

Iron can interact with certain medications, and some medications can have an adverse effect on iron levels. A few examples are provided below. Individuals taking these and other medications on a regular basis should discuss their iron status with their health care providers.

Some evidence indicates that in healthy people, iron supplements reduce the absorption of levodopa (found in Sinemet and Stalevo), used to treat Parkinson’s disease and restless leg syndrome, possibly through chelation [101-103]. In the United States, the labels for levodopa warn that iron-containing dietary supplements might reduce the amount of levodopa available to the body and, thus, diminish its clinical effectiveness [104,105].

Levothyroxine (Levothroid, Levoxyl, Synthroid, Tirosint, and Unithroid) is used to treat hypothyroidism, goiter, and thyroid cancer. The simultaneous ingestion of iron and levothyroxine can result in clinically significant reductions in levothyroxine efficacy in some patients [106]. The labels for some of these products [107,108] warn that iron supplements can reduce the absorption of levothyroxine tablets and advise against administering levothyroxine within 4 hours of iron supplements.

Gastric acid plays an important role in the absorption of nonheme iron from the diet. Because proton pump inhibitors, such as lansoprazole (Prevacid) and omeprazole (Prilosec), reduce the acidity of stomach contents, they can reduce iron absorption [3]. Treatment with proton pump inhibitors for up to 10 years is not associated with iron depletion or anemia in people with normal iron stores [109] but patients with iron deficiency taking proton pump inhibitors can have suboptimal responses to iron supplementation [110].

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Iron — 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: September 4, 2025
Retrieved: 2026-08-10T22:07:05.577Z
Source fingerprint: fa6273f9305dfba9ea81d7c31ede31b36a0be1e035ebefbee0715ec605840e21
Cited reference numbers: 101, 102, 103, 104, 105, 106, 107, 108, 3, 109, 110

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Vitamin D

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Linked references: 13 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trial identified
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MEDucated evidence rating: Not assigned

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

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Study type could not be determined10
Systematic review1
Randomized controlled trial2

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

Classified references

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

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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Iron

Evidence unavailable

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Vitamin D

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Food and nutrient interactions

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Iron

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Typical forms

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Iron

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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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Linked references: 9 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: 2000–2010
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MEDucated evidence rating: Not assigned

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

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Study type could not be determined7
Government reference1
Clinical guideline1

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Classified references

Murray-Kolbe LE, Beard J. Iron. In: Coates PM, Betz JM, Blackman MR, et al., eds. Encyclopedia of Dietary Supplements. 2nd ed. London and New York: Informa Healthcare; 2010:432-8.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Hurrell R, Egli I. Iron bioavailability and dietary reference values. Am J Clin Nutr 2010;91:1461S-7S. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc : a Report of the Panel on Micronutrients. Washington, DC: National Academy Press; 2001.
Government reference · Population basis: unknown · Directness: not assessed
Manoguerra AS, Erdman AR, Booze LL, Christianson G, Wax PM, Scharman EJ, et al. Iron ingestion: an evidence-based consensus guideline for out-of-hospital management. Clin Toxicol (Phila) 2005;43:553-70. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessed
U.S. Department of Agriculture, Agricultural Research Service. What We Eat in America, 2009-2010. 2012.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Bailey RL, Gahche JJ, Lentino CV, Dwyer JT, Engel JS, Thomas PR, et al. Dietary supplement use in the United States, 2003-2006. J Nutr 2011;141:261-6. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Cogswell ME, Kettel-Khan L, Ramakrishnan U. Iron supplement use among women in the United States: science, policy and practice. J Nutr 2003;133:1974S-7S. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Lonnerdal B. Calcium and iron absorption--mechanisms and public health relevance. Int J Vitam Nutr Res 2010;80:293-9. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Lynch SR. The effect of calcium on iron absorption. Nutr Res Rev 2000;13:141-58. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed

Read imported source wording for Iron

Ferrous and ferric iron salts are the most common forms of iron found in dietary supplements, although other forms are also used. The various forms of iron contain different amounts of elemental iron, and certain forms may be more likely to cause gastrointestinal side effects at high doses. In addition, experts recommend taking calcium and iron supplements at different times to avoid potential interference with the absorption of iron.

Iron is available in many dietary supplements. Multivitamin/mineral supplements with iron, especially those designed for women, typically provide 18 mg iron, which is 100% of the Daily Value (DV). Multivitamin/mineral supplements for men or seniors frequently contain less or no iron. Iron-only supplements usually deliver more than the DV, with many providing 65 mg iron (360% of the DV).

Source-described amount

Frequently used forms of iron in supplements include ferrous and ferric iron salts, such as ferrous sulfate, ferrous gluconate, ferric citrate, and ferric sulfate [3,27]. Because of its higher solubility, ferrous iron in dietary supplements is more bioavailable than ferric iron [3]. High doses of supplemental iron (45 mg/day or more) may cause gastrointestinal side effects, such as nausea and constipation [5]. Other forms of supplemental iron, such as heme iron polypeptides, carbonyl iron, iron amino-acid chelates, and polysaccharide-iron complexes, might have fewer gastrointestinal side effects than ferrous or ferric salts [27].

Source-described amount

The different forms of iron in supplements contain varying amounts of elemental iron. For example, ferrous fumarate is 33% elemental iron by weight, whereas ferrous sulfate is 20% and ferrous gluconate is 12% elemental iron [27]. Fortunately, elemental iron is listed in the Supplement Facts panel, so consumers do not need to calculate the amount of iron supplied by various forms of iron supplements.

Approximately 14% to 18% of Americans use a supplement that contains iron [28,29]. The proportion of people who use supplements that contain iron varies by age and gender, ranging from 6% of children age 12 to 19 years to 60% of women who are lactating and 72% of pregnant women [28,30].

Calcium might interfere with the absorption of iron, although this effect has not been definitively established [4,31]. For this reason, experts suggest that people take individual calcium and iron supplements at different times of the day [32].

Where did MEDucated get this?

Iron — 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: September 4, 2025
Retrieved: 2026-08-10T22:07:05.577Z
Source fingerprint: fa6273f9305dfba9ea81d7c31ede31b36a0be1e035ebefbee0715ec605840e21
Cited reference numbers: 3, 5, 27, 28, 29, 30, 4, 31, 32

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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 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
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MEDucated evidence rating: Not assigned

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

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Classified references

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

Read imported source wording 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.

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

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Iron

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Linked references: 1 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 reviews or meta-analyses not identified in the frozen metadata
Evidence recency: 2001–2001
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MEDucated evidence rating: Not assigned

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Classified references

Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc : a Report of the Panel on Micronutrients. Washington, DC: National Academy Press; 2001.
Government reference · Population basis: unknown · Directness: not assessed

Read imported source wording for Iron

The Food and Nutrition Board at the National Academies of Sciences, Engineering, and Medicine has established Recommended Dietary Allowances and Adequate Intakes for iron. These values range from 8 to 27 mg for adults and from 0.27 to 27 mg for infants, children, and adolescents, depending on age, sex, and life stage. People who follow vegetarian diets need more iron than those who include animal products in their diet due to the decreased bioavailability of nonheme iron from plant-based foods.

RDA reference intakeAI reference intakeSource intake rangeSource-described amount

Intake recommendations for iron and other nutrients are provided in the Dietary Reference Intakes (DRIs) developed by the Food and Nutrition Board (FNB) at the National Academies of Sciences, Engineering, and 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 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

Table 1 lists the current iron RDAs. The requirement for iron is 1.8 times higher for people who follow vegetarian diets than those for people who include animal products in their diet, such as meat. This is because heme iron from meat is more bioavailable than nonheme iron from plant-based foods. In addition, animal products such as meat, poultry, and seafood increase the absorption of nonheme iron [5].

For infants from birth to 6 months, the FNB established an AI for iron that is equivalent to the mean intake of iron in healthy, breastfed infants.

AI reference intake

Table 1: Recommended Dietary Allowances (RDAs) for Iron in Milligrams (mg) [5]
Age	Male	Female	Pregnancy	Lactation
0–6 months	0.27 mg*	0.27 mg*
7–12 months	11 mg	11 mg
1–3 years	7 mg	7 mg
4–8 years	10 mg	10 mg
9–13 years	8 mg	8 mg
14–18 years	11 mg	15 mg	27 mg	10 mg
19–50 years	8 mg	18 mg	27 mg	9 mg
51+ years	8 mg	8 mg

RDA reference intakeSource-described amount

* Adequate Intake (AI)

AI reference intake

Where did MEDucated get this?

Iron — Fact Sheet for Health Professionals

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

Source section: Recommended Intakes
ODS revision: September 4, 2025
Retrieved: 2026-08-10T22:07:05.577Z
Source fingerprint: fa6273f9305dfba9ea81d7c31ede31b36a0be1e035ebefbee0715ec605840e21
Cited reference numbers: 5

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

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Classified references

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

Read imported source wording 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]
Age	Male	Female	Pregnancy	Lactation
0–6 months*	10 mcg (400 IU)*	10 mcg (400 IU)*
7–12 months*	10 mcg (400 IU)*	10 mcg (400 IU)*
1–3 years	15 mcg (600 IU)	15 mcg (600 IU)
4–8 years	15 mcg (600 IU)	15 mcg (600 IU)
9–13 years	15 mcg (600 IU)	15 mcg (600 IU)
14–18 years	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)
19–50 years	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)	15 mcg (600 IU)
51–70 years	15 mcg (600 IU)	15 mcg (600 IU)
>70 years	20 mcg (800 IU)	20 mcg (800 IU)
*Adequate Intake (AI)

RDA reference intakeAI reference intakeSource-described amount

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

RDA reference intakeSource-described amount

Where did MEDucated get this?

Vitamin D — Fact Sheet for Health Professionals

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

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

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Iron

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

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Evidence source: NIH ODS evidence synthesis
Linked references: 21 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trial identified
Reviews and meta-analyses: Systematic review or meta-analysis identified
Evidence recency: 2001–2015
Source-described consistency: Not characterized in these source blocks
MEDucated evidence rating: Not assigned

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Study type could not be determined15
Government reference1
Narrative review1
Randomized controlled trial1
Clinical guideline1
Systematic review1
Meta-analysis1

Source-described limitations

ODS describes limited evidence
Women of reproductive age who have menorrhagia, or abnormally heavy bleeding during menstruation, have an increased risk of iron deficiency. At least 10% of menstruating women are believed to have menorrhagia, but the percentage varies widely depending on the diagnostic criteria used [46-48]. Women with menorrhagia lose significantly more iron per menstrual cycle on average than women with normal menstrual bleeding [49]. Limited evidence suggests that menorrhagia might be responsible for about 33% to 41% of cases of IDA in women of reproductive age [50,51].

Classified references

Aggett PJ. Iron. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012:506-20.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc : a Report of the Panel on Micronutrients. Washington, DC: National Academy Press; 2001.
Government reference · Population basis: unknown · Directness: not assessed
Black MM, Quigg AM, Hurley KM, Pepper MR. Iron deficiency and iron-deficiency anemia in the first two years of life: strategies to prevent loss of developmental potential. Nutr Rev 2011;69 Suppl 1:S64-70. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
World Health Organization. Iron Deficiency Anaemia: Assessment, Prevention, and Control. World Health Organization, 2001.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Domellöf M. Iron requirements in infancy. Ann Nutr Metab 2011;59:59-63. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Matthews ML. Abnormal uterine bleeding in reproductive-aged women. Obstet Gynecol Clin North Am 2015;42:103-15. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Bitzer J, Heikinheimo O, Nelson AL, Calaf-Alsina J, Fraser IS. Medical management of heavy menstrual bleeding: a comprehensive review of the literature. Obstet Gynecol Surv 2015;70:115-30. [PubMed abstract]
Narrative review · Population basis: unknown · Directness: not assessed
El-Hemaidi I, Gharaibeh A, Shehata H. Menorrhagia and bleeding disorders. Curr Opin Obstet Gynecol 2007;19:513-20. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Napolitano M, Dolce A, Celenza G, Grandone E, Perilli MG, Siragusa S, et al. Iron-dependent erythropoiesis in women with excessive menstrual blood losses and women with normal menses. Ann Hematol 2014;93:557-63. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Vannella L, Aloe Spiriti MA, Cozza G, Tardella L, Monarca B, Cuteri A, et al. Benefit of concomitant gastrointestinal and gynaecological evaluation in premenopausal women with iron deficiency anaemia. Aliment Pharmacol Ther 2008;28:422-30. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Philipp CS, Faiz A, Dowling N, Dilley A, Michaels LA, Ayers C, et al. Age and the prevalence of bleeding disorders in women with menorrhagia. Obstet Gynecol 2005;105:61-6. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Kiss JE, Brambilla D, Glynn SA, Mast AE, Spencer BR, Stone M, et al. Oral iron supplementation after blood donation: a randomized clinical trial. JAMA 2015;313:575-83. [PubMed abstract]
Randomized controlled trial · Population basis: unknown · Directness: not assessed
Cable RG, Glynn SA, Kiss JE, Mast AE, Steele WR, Murphy EL, et al. Iron deficiency in blood donors: analysis of enrollment data from the REDS-II Donor Iron Status Evaluation (RISE) study. Transfusion 2011;51:511-22. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Aapro M, Osterborg A, Gascon P, Ludwig H, Beguin Y. Prevalence and management of cancer-related anaemia, iron deficiency and the specific role of i.v. iron. Ann Oncol 2012;23:1954-62. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Bayraktar UD, Bayraktar S. Treatment of iron deficiency anemia associated with gastrointestinal tract diseases. World J Gastroenterol 2010;16:2720-5. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Gasche C, Berstad A, Befrits R, Beglinger C, Dignass A, Erichsen K, et al. Guidelines on the diagnosis and management of iron deficiency and anemia in inflammatory bowel diseases. Inflamm Bowel Dis 2007;13:1545-53. [PubMed abstract]
Clinical guideline · Population basis: unknown · Directness: not assessed
Bermejo F, Garcia-Lopez S. A guide to diagnosis of iron deficiency and iron deficiency anemia in digestive diseases. World J Gastroenterol 2009;15:4638-43. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Kulnigg S, Gasche C. Systematic review: managing anaemia in Crohn's disease. Aliment Pharmacol Ther 2006;24:1507-23. [PubMed abstract]
Systematic review · Population basis: unknown · Directness: not assessed
Groenveld HF, Januzzi JL, Damman K, van Wijngaarden J, Hillege HL, van Veldhuisen DJ, et al. Anemia and mortality in heart failure patients a systematic review and meta-analysis. J Am Coll Cardiol 2008;52:818-27. [PubMed abstract]
Meta-analysis · Population basis: human · Directness: not assessed
Parikh A, Natarajan S, Lipsitz SR, Katz SD. Iron deficiency in community-dwelling US adults with self-reported heart failure in the National Health and Nutrition Examination Survey III: prevalence and associations with anemia and inflammation. Circ Heart Fail 2011;4:599-606. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Lipsic E, van der Meer P. Erythropoietin, iron, or both in heart failure: FAIR-HF in perspective. Eur J Heart Fail 2010;12:104-5. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed

Read imported source wording for Iron

Certain groups of people are more likely than others to have inadequate iron intakes, including pregnant women, infants and young children, women with heavy menstrual bleeding, and frequent blood donors. People with certain conditions, such as cancer, gastrointestinal disorders, and heart failure, may also have inadequate iron intakes.

The following groups are among those most likely to have inadequate intakes of iron.

AI reference intake

During pregnancy, plasma volume and red cell mass expand as maternal red blood cell production increases to meet the needs of the fetus and placenta [2]. As a result of this expansion, the amount of iron that women need increases during pregnancy. Iron deficiency during pregnancy increases the risk of maternal and infant mortality, premature birth, and low birthweight [44].

Infants—especially those born preterm or with low birthweight or whose mothers have iron deficiency—are at risk of iron deficiency because of their high iron requirements due to their rapid growth [34,45]. Full-term infants usually have sufficient iron stores and need little if any iron from external sources until they are 4 to 6 months old [2]. However, full-term infants have a risk of becoming iron deficient at 6 to 9 months unless they obtain adequate amounts of solid foods that are rich in bioavailable iron or iron-fortified formula.

Women of reproductive age who have menorrhagia, or abnormally heavy bleeding during menstruation, have an increased risk of iron deficiency. At least 10% of menstruating women are believed to have menorrhagia, but the percentage varies widely depending on the diagnostic criteria used [46-48]. Women with menorrhagia lose significantly more iron per menstrual cycle on average than women with normal menstrual bleeding [49]. Limited evidence suggests that menorrhagia might be responsible for about 33% to 41% of cases of IDA in women of reproductive age [50,51].

Frequent blood donors have an increased risk of iron deficiency [5]. In the United States, adults may donate blood as often as every 8 weeks, which can deplete iron stores. About 25% to 35% of regular blood donors develop iron deficiency [52]. In a study of 2,425 blood donors, men who had given at least three whole-blood donations and women who had given at least two whole-blood donations in the previous year were more than five times as likely to have depleted iron stores as first-time donors [53]. A clinical trial of iron supplementation found that of 215 adults who had donated a unit of blood within the past 3 to 8 days, those randomized to take an iron supplement (37.5 mg/day elemental iron from ferrous gluconate) for 24 weeks recovered their lost hemoglobin and iron in less than half the time of those not given the supplement [52]. At 24 weeks, two-thirds of the donors who did not receive iron supplementation had not recovered the iron had they lost.

Source-described amount

Up to 60% of patients with colon cancer have iron deficiency at diagnosis, probably due to chronic blood loss [54]. The prevalence of iron deficiency in patients with other types of cancer ranges from 29% to 46%. The main causes of iron deficiency in people with cancer are anemia of chronic disease (discussed in the Iron and Health section below) and chemotherapy-induced anemia. However, chronic blood loss and deficiencies of other nutrients (due, for example, to cancer-induced anorexia) can exacerbate iron deficiency in this population.

People with certain gastrointestinal disorders (e.g., celiac disease, ulcerative colitis, Crohn’s disease) or who have undergone certain gastrointestinal surgical procedures (e.g., gastrectomy, intestinal resection) have an increased risk of iron deficiency because their disorder or surgery requires dietary restrictions or results in iron malabsorption or blood loss in the gastrointestinal tract [55-57]. The combination of low iron intake and high iron loss can lead to a negative iron balance; reduced production of hemoglobin; or microcytic, hypochromic anemia [58].

Approximately 60% of patients with chronic heart failure have iron deficiency and 17% have IDA, which might be associated with a higher risk of death in this population [59,60]. Potential causes of iron deficiency in people with heart failure include poor nutrition; malabsorption; defective mobilization of iron stores; cardiac cachexia; and the use of aspirin and oral anticoagulants, which might result in the loss of some blood in the gastrointestinal tract [61].

Where did MEDucated get this?

Iron — Fact Sheet for Health Professionals

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

Source section: Groups at Risk of Iron Inadequacy
ODS revision: September 4, 2025
Retrieved: 2026-08-10T22:07:05.577Z
Source fingerprint: fa6273f9305dfba9ea81d7c31ede31b36a0be1e035ebefbee0715ec605840e21
Cited reference numbers: 2, 44, 34, 45, 46, 47, 48, 49, 50, 51, 5, 52, 53, 54, 55, 56, 57, 58, 59, 60, 61

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Vitamin D

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Evidence source: NIH ODS evidence synthesis
Linked references: 16 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trials not identified in the frozen metadata
Reviews and meta-analyses: Systematic review or meta-analysis identified
Evidence recency: 2001–2020
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
Systematic review2
Study type could not be determined10
Clinical guideline2
Narrative review1

Source-described limitations

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

Classified references

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

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.

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

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Iron

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Classified references

Aggett PJ. Iron. In: Erdman JW, Macdonald IA, Zeisel SH, eds. Present Knowledge in Nutrition. 10th ed. Washington, DC: Wiley-Blackwell; 2012:506-20.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Institute of Medicine. Food and Nutrition Board. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc : a Report of the Panel on Micronutrients. Washington, DC: National Academy Press; 2001.
Government reference · Population basis: unknown · Directness: not assessed
Taylor CL, Brannon PM. Introduction to workshop on iron screening and supplementation in iron-replete pregnant women and young children. Am J Clin Nutr. 2017 Dec;106(Suppl 6):1547S-54S. [PubMed abstract]
Study type could not be determined · Population basis: human · Directness: not assessed
Powers JM, Buchanan GR. Disorders of iron metabolism: New diagnostic and treatment approaches to iron deficiency. Hematol Oncol Clin North Am. 2019 Jun;33(3):393-408. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Lynch S, Pfeiffer CM, Georgieff MK, Brittenham G, Fairweather-Tait S, Hurrell RF, et al. Biomarkers of Nutrition for Development (BOND)-Iron Review. J Nutr. 2018 Jun 1;148(suppl 1):1001S-67S. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
World Health Organization. Report: Priorities in the Assessment of Vitamin A and Iron Status in Populations, Panama City, Panama, 15-17 September 2010. Geneva; 2012.
Study type could not be determined · Population basis: unknown · Directness: not assessed
DeLoughery TG. Microcytic anemia. N Engl J Med. 2014 Oct 2;371(14):1324-31. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
DeLoughery TG. Iron deficiency anemia. Med Clin North Am. 2017 Mar;101(2):319-32. doi: 10.1016/j.mcna.2016.09.004. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Short MW, Domagalski JE. Iron deficiency anemia: evaluation and management. Am Fam Physician. 2013 Jan 15;87(2):98-104. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Gibson RS. Assessment of Iron Status. In: Principles of Nutritional Assessment. 2nd ed. New York: Oxford University Press; 2005:443-76.
Study type could not be determined · Population basis: unknown · Directness: not assessed
Camaschella C. Iron-deficiency anemia. N Engl J Med. 2015 May 7;372(19):1832-43. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Suchdev PS, Williams AM, Mei Z, Flores-Ayala R, Pasricha SR, Rogers LM, Namaste SM. Assessment of iron status in settings of inflammation: challenges and potential approaches. Am J Clin Nutr. 2017 Dec;106(Suppl 6):1626S-33S. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
Centers for Disease Control and Prevention (CDC). Recommendations to prevent and control iron deficiency in the United States. MMWR Recomm Rep 1998;47:1-29. [PubMed abstract]
Study type could not be determined · Population basis: unknown · Directness: not assessed
MedlinePlus [Internet]. Bethesda (MD): National Library of Medicine (US). Hematocrit.
Study type could not be determined · Population basis: unknown · Directness: not assessed

Read imported source wording for Iron

Hemoglobin and hematocrit are the most commonly used measures to screen patients for iron deficiency, although they are neither sensitive nor specific. Serum ferritin concentration, which is a measure of the body’s iron stores, is also used, but it can be affected by inflammation. Often, health care providers will use multiple measurements to diagnose iron deficiency. They may also consider a patient’s dietary and supplemental iron intakes and how those compare to intake recommendations.

The assessment of iron status depends almost entirely on hematological indicators [7]. However, these indicators are not sensitive or specific enough to adequately describe the full spectrum of iron status, and this can complicate the diagnosis of iron deficiency. A complementary approach is to consider how iron intakes from the diet and dietary supplements compare with recommended intakes.

Iron deficiency progresses from the depletion of iron stores (mild iron deficiency), to iron-deficiency erythropoiesis (erythrocyte production), and finally to iron deficiency anemia (IDA) [8,9]. With iron-deficiency erythropoiesis (also known as marginal iron deficiency), iron stores are depleted and transferrin saturation declines, but hemoglobin levels are usually within the normal range. IDA is characterized by low hemoglobin concentrations and decreases in hematocrit (the proportion of red blood cells in blood by volume) and mean corpuscular volume (a measure of erythrocyte size) [2,10].

Serum ferritin concentration, a measure of the body's iron stores, is currently the most efficient and cost-effective test for diagnosing iron deficiency [11-13]. Because serum ferritin concentration decreases during the first stage of iron depletion, it can be used to identify low iron status before the onset of IDA [7,9,14]. A serum ferritin concentration that is lower than 30 micrograms/liter (mcg/L) suggests iron deficiency, and a value lower than 10 mcg/L suggests IDA [15]. However, it should be noted that inflammation (e.g., in those with infectious diseases) can elevate serum ferritin concentrations [16].

Source-described amount

Hemoglobin and hematocrit tests are the most commonly used measures to screen patients for iron deficiency, even though they are neither sensitive nor specific [5,7,17]. Often, hemoglobin concentrations are combined with serum ferritin measurements to identify IDA [7]. Hemoglobin concentrations lower than 11 g/deciliter (dL) in children under 10 years of age, or lower than 12 g/dL in individuals age 10 years or older, suggest IDA [8]. Normal hematocrit values are approximately 41% to 50% in males and 36% to 44% in females [18].

Source-described amount

Where did MEDucated get this?

Iron — Fact Sheet for Health Professionals

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

Source section: Assessing iron status
ODS revision: September 4, 2025
Retrieved: 2026-08-10T22:07:05.577Z
Source fingerprint: fa6273f9305dfba9ea81d7c31ede31b36a0be1e035ebefbee0715ec605840e21
Cited reference numbers: 7, 2, 8, 9, 10, 11, 12, 13, 14, 15, 16, 5, 17, 18

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Vitamin D

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Linked references: 13 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trials not identified in the frozen metadata
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Government reference1
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Classified references

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

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

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

Where did MEDucated get this?

Vitamin D — Fact Sheet for Health Professionals

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

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

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