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Iron

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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 reviews or meta-analyses not identified in the frozen metadata
Evidence recency: 2001–2014
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Study type could not be determined5
Government reference1

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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

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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

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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.

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

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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

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

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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
Reviews and meta-analyses: Systematic reviews or meta-analyses not identified in the frozen metadata
Evidence recency: 1989–2012
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

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Study type could not be determined11

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

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

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].

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: 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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Evidence source: NIH ODS evidence synthesis
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
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

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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

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

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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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No overall rating assigned

Evidence source: NIH ODS evidence synthesis
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
Source-described consistency: Not characterized in these source blocks
MEDucated evidence rating: Not assigned

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

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Evidence types identified

Government reference1

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

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

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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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
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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

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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Evidence source: NIH ODS evidence synthesis
Linked references: 14 identified
Human evidence: Human evidence identified
Randomized trials: Randomized trials not identified in the frozen metadata
Reviews and meta-analyses: Systematic reviews or meta-analyses not identified in the frozen metadata
Evidence recency: 1998–2019
Source-described consistency: Not characterized in these source blocks
MEDucated evidence rating: Not assigned

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

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Study type could not be determined13
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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

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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Iron — Fact Sheet for Health Professionals

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