---
title: "Iron: Dosing & Vendor Prices — BodyHackGuide"
description: "Iron: dosing protocols, mechanism & side effects. Compare verified vendor prices."
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      "description": "Iron is a trace mineral with a biochemistry dominated by a single chemical property — the reversible one-electron redox between Fe²⁺ (ferrous) and Fe³⁺ (ferric) — that makes it indispensable for oxygen transport, electron transfer, and hundreds of enzymatic reactions, and simultaneously dangerous when unchaperoned in cells. The adult RDA is 8 mg/day for men and postmenopausal women, 18 mg/day for premenopausal women, 27 mg/day for pregnancy, and 9 mg/day for lactation; the tolerable upper limit is 45 mg/day from all sources combined. Iron deficiency is the most common nutritional deficiency worldwide, affecting over two billion people, and iron-deficiency anemia remains a leading global cause of disability-adjusted life years lost, disproportionately affecting menstruating women, pregnant women, infants, and populations with high parasitic burden or plant-based diets with low bioavailable iron. The clinical presentation ranges from subtle — fatigue, reduced exercise capacity, cognitive fog, restless legs — at early stages of iron-deficient erythropoiesis, to frank microcytic hypochromic anemia with pallor, tachycardia, and exertional dyspnea at advanced stages. Iron deficiency without anemia (low ferritin, normal hemoglobin) is increasingly recognized as clinically meaningful, especially in women with heavy menstrual bleeding and in endurance athletes with elevated losses; trials of iron repletion in non-anemic iron-deficient women have shown improvements in fatigue, physical capacity, and quality of life even in the absence of overt anemia. At the opposite end, iron overload is equally problematic. Hereditary hemochromatosis (most commonly HFE C282Y homozygosity, affecting roughly 1 in 200 people of Northern European ancestry) causes progressive tissue iron loading with eventual cirrhosis, diabetes, cardiomyopathy, hypogonadism, and arthritis if untreated — classically in middle-aged men with a characteristic bronze skin discoloration. Transfusion-dependent iron overload (thalassemia major, sickle cell, myelodysplastic syndromes) produces similar tissue injury through a different route. The body has no regulated excretory mechanism for iron — roughly 1 mg/day is lost through desquamation of intestinal and skin cells, and additional losses through menstruation or bleeding — so iron balance is almost entirely regulated at the absorption level via the hormone hepcidin. When iron stores are high, hepcidin rises and blocks iron absorption by degrading ferroportin on enterocytes; when iron stores are low or erythropoiesis is driven up (via the hormone erythroferrone released from maturing erythroblasts), hepcidin falls and absorption increases. This elegant single-hormone axis, worked out largely by Nemeth and Ganz in the 2000s, revolutionized our understanding of iron disorders — hereditary hemochromatosis is fundamentally a hepcidin-deficiency disease, and anemia of chronic inflammation is a hepcidin-excess disease. Dietary iron exists in two fundamental forms: heme iron from animal sources (hemoglobin and myoglobin of meat, fish, poultry) which is absorbed at 15–35% regardless of dietary context, and non-heme iron from plant sources (grains, legumes, leafy greens, fortified foods) which is absorbed at 2–20% and is highly sensitive to enhancers (vitamin C, meat, acidity) and inhibitors (phytates, tannins, calcium, tea polyphenols). This bioavailability gap is why vegetarians and vegans have higher iron deficiency rates despite similar or higher iron intake compared to omnivores — a point of practical importance for dietary planning. See also Copper for the ceruloplasmin ferroxidase dependency that makes iron utilization copper-sensitive, Vitamin C for the non-heme iron absorption enhancement, Vitamin B12 for the shared anemia differential, and Vitamin D for the hepcidin regulation link. This overview is educational only and is not medical advice — iron supplementation in men and postmenopausal women without confirmed deficiency is not appropriate given the absence of regulated excretion and the real risk of organ iron loading in undiagnosed hemochromatosis carriers.",
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        "name": "Iron",
        "alternateName": [
          "Fe",
          "Fe2+",
          "Fe3+",
          "Ferrous",
          "Ferric",
          "Ferrous sulfate",
          "Ferrous fumarate",
          "Ferrous gluconate",
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        "description": "Iron is a trace mineral with a biochemistry dominated by a single chemical property — the reversible one-electron redox between Fe²⁺ (ferrous) and Fe³⁺ (ferric) — that makes it indispensable for oxygen transport, electron transfer, and hundreds of enzymatic reactions, and simultaneously dangerous when unchaperoned in cells. The adult RDA is 8 mg/day for men and postmenopausal women, 18 mg/day for premenopausal women, 27 mg/day for pregnancy, and 9 mg/day for lactation; the tolerable upper limit is 45 mg/day from all sources combined. Iron deficiency is the most common nutritional deficiency worldwide, affecting over two billion people, and iron-deficiency anemia remains a leading global cause of disability-adjusted life years lost, disproportionately affecting menstruating women, pregnant women, infants, and populations with high parasitic burden or plant-based diets with low bioavailable iron. The clinical presentation ranges from subtle — fatigue, reduced exercise capacity, cognitive fog, restless legs — at early stages of iron-deficient erythropoiesis, to frank microcytic hypochromic anemia with pallor, tachycardia, and exertional dyspnea at advanced stages. Iron deficiency without anemia (low ferritin, normal hemoglobin) is increasingly recognized as clinically meaningful, especially in women with heavy menstrual bleeding and in endurance athletes with elevated losses; trials of iron repletion in non-anemic iron-deficient women have shown improvements in fatigue, physical capacity, and quality of life even in the absence of overt anemia. At the opposite end, iron overload is equally problematic. Hereditary hemochromatosis (most commonly HFE C282Y homozygosity, affecting roughly 1 in 200 people of Northern European ancestry) causes progressive tissue iron loading with eventual cirrhosis, diabetes, cardiomyopathy, hypogonadism, and arthritis if untreated — classically in middle-aged men with a characteristic bronze skin discoloration. Transfusion-dependent iron overload (thalassemia major, sickle cell, myelodysplastic syndromes) produces similar tissue injury through a different route. The body has no regulated excretory mechanism for iron — roughly 1 mg/day is lost through desquamation of intestinal and skin cells, and additional losses through menstruation or bleeding — so iron balance is almost entirely regulated at the absorption level via the hormone hepcidin. When iron stores are high, hepcidin rises and blocks iron absorption by degrading ferroportin on enterocytes; when iron stores are low or erythropoiesis is driven up (via the hormone erythroferrone released from maturing erythroblasts), hepcidin falls and absorption increases. This elegant single-hormone axis, worked out largely by Nemeth and Ganz in the 2000s, revolutionized our understanding of iron disorders — hereditary hemochromatosis is fundamentally a hepcidin-deficiency disease, and anemia of chronic inflammation is a hepcidin-excess disease. Dietary iron exists in two fundamental forms: heme iron from animal sources (hemoglobin and myoglobin of meat, fish, poultry) which is absorbed at 15–35% regardless of dietary context, and non-heme iron from plant sources (grains, legumes, leafy greens, fortified foods) which is absorbed at 2–20% and is highly sensitive to enhancers (vitamin C, meat, acidity) and inhibitors (phytates, tannins, calcium, tea polyphenols). This bioavailability gap is why vegetarians and vegans have higher iron deficiency rates despite similar or higher iron intake compared to omnivores — a point of practical importance for dietary planning. See also Copper for the ceruloplasmin ferroxidase dependency that makes iron utilization copper-sensitive, Vitamin C for the non-heme iron absorption enhancement, Vitamin B12 for the shared anemia differential, and Vitamin D for the hepcidin regulation link. This overview is educational only and is not medical advice — iron supplementation in men and postmenopausal women without confirmed deficiency is not appropriate given the absence of regulated excretion and the real risk of organ iron loading in undiagnosed hemochromatosis carriers.",
        "activeIngredient": "Iron",
        "mechanismOfAction": "Iron's mechanism of action can be divided into three domains: the biochemical roles of iron-containing proteins, the absorption-and-distribution axis regulated by hepcidin, and the cellular handling that prevents iron's pro-oxidant chemistry from causing damage. Iron is incorporated into three major classes of functional proteins. Heme proteins (hemoglobin in red blood cells, myoglobin in muscle, cytochromes in the electron transport chain and cytochrome P450 enzymes, catalase, myeloperoxidase in neutrophils, nitric oxide synthase, tryptophan pyrrolase) use a porphyrin-bound iron atom to bind oxygen, transfer electrons, or catalyze oxidation reactions — hemoglobin alone accounts for 65–70% of body iron. Iron-sulfur cluster proteins (aconitase in the TCA cycle, complexes I, II, III of the electron transport chain, succinate dehydrogenase, ferredoxin, DNA repair enzymes, ribonucleotide reductase) use Fe-S clusters assembled through the ISC/CIA machinery for electron transfer and catalysis. Non-heme iron enzymes include ribonucleotide reductase (DNA synthesis), tyrosine hydroxylase (dopamine synthesis — iron deficiency produces dopamine synthesis impairments potentially relevant to restless legs syndrome and cognitive symptoms), proline hydroxylase (collagen synthesis), lysyl hydroxylase, and the prolyl hydroxylases that oxygen-sense HIF-α stability (the oxygen-sensing machinery Kaelin/Ratcliffe/Semenza won the 2019 Nobel for). Absorption occurs almost entirely in the duodenum and upper jejunum. Heme iron enters enterocytes via HCP1/PCFT (heme carrier protein 1) and is released intracellularly by heme oxygenase. Non-heme iron requires reduction from Fe³⁺ to Fe²⁺ by duodenal cytochrome b (DCYTB) at the apical brush border, then uptake via DMT1 (divalent metal transporter 1, SLC11A2). Intracellular iron is either incorporated into ferritin for storage (the 24-subunit cage protein that sequesters up to 4,500 iron atoms as a ferrihydrite core, oxidized to the Fe³⁺ state by ferritin's H-subunit ferroxidase), or exported across the basolateral membrane by ferroportin (FPN1, SLC40A1) — the only known iron exporter — and oxidized by ceruloplasmin or its intestinal paralog hephaestin back to Fe³⁺ for transferrin loading. Circulating transferrin delivers iron to cells expressing the transferrin receptor (TfR1 ubiquitously, TfR2 in hepatocytes and erythroid cells), which internalizes the transferrin-iron complex via clathrin-mediated endocytosis, releases iron in acidified endosomes, and recycles transferrin back to the surface — this is the canonical Ashwell pathway of iron delivery. The regulatory master is hepcidin, a 25-amino-acid peptide hormone produced by hepatocytes. Hepcidin binds ferroportin on enterocytes, macrophages, and hepatocytes, triggering its internalization and degradation — blocking both dietary iron absorption and iron release from macrophage recycling of senescent erythrocytes. Hepcidin is induced by high iron stores (via the BMP6/SMAD pathway), inflammation (via IL-6/STAT3), and oral iron (producing the transient \"mucosal block\" after a large iron dose that limits further absorption for ~24 hours), and suppressed by low iron (via matriptase-2/TMPRSS6 cleavage of hemojuvelin, the BMP co-receptor) and active erythropoiesis (via erythroferrone from maturing erythroblasts). Understanding this axis explains two major clinical phenomena: hereditary hemochromatosis is a collection of conditions with insufficient hepcidin (HFE, TfR2, HJV, HAMP, TMPRSS6 mutations all converge on loss of hepcidin signaling), producing unrestrained iron absorption and progressive tissue loading; anemia of chronic disease is a state of hepcidin excess driven by IL-6, functionally trapping iron in macrophages so it cannot reach the bone marrow — this is why CRP should be checked when evaluating an anemia that looks iron-deficient but has normal or high ferritin. The pro-oxidant problem: free Fe²⁺ drives the Fenton reaction (Fe²⁺ + H₂O₂ → Fe³⁺ + •OH + OH⁻), generating hydroxyl radicals that damage lipids, proteins, and DNA. Ferritin sequestration, iron chaperones (PCBP1, PCBP2), and the rapid loading onto transferrin limit the labile iron pool that could drive this chemistry. The recently-described ferroptosis cell death program — iron-dependent lipid peroxidation — has opened a new layer of iron biology relevant to neurodegeneration, ischemia-reperfusion injury, and cancer therapy (PMID 22632970). The practical mechanistic takeaway: iron absorption is tightly regulated by hepcidin, the 24-hour mucosal block makes split dosing counterproductive and alternate-day dosing more efficient, vitamin C enhances non-heme iron absorption by reducing Fe³⁺ to Fe²⁺ at the brush border, and the absence of regulated excretion is why iron overload is a one-way street in the absence of bleeding or phlebotomy.",
        "legalStatus": "Not approved for human use — research chemical",
        "warning": "For research purposes only. Not for human consumption."
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          "name": "How much iron should I take for iron-deficiency anemia?",
          "acceptedAnswer": {
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            "text": "For most adults with confirmed iron-deficiency anemia, 100–200 mg elemental iron per day as ferrous sulfate, ferrous fumarate, or ferrous bisglycinate, split 2–3 times daily or given as alternate-day 120 mg to improve tolerance. Alternate-day dosing is supported by Stoffel et al. 2017 and 2020 studies showing equivalent fractional absorption with better GI tolerance, based on the hepcidin mucosal block lasting ~24 hours after a single oral iron dose (PMID 28895840, 32895503). Take with 250 mg vitamin C on empty stomach if tolerated; with small snack if GI-sensitive. Continue for 3–6 months after hemoglobin normalizes to fully replete ferritin. Recheck at 1 month (reticulocyte response), 3 months (hemoglobin), 6 months (ferritin)."
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          "name": "Should I take iron every day or every other day?",
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            "text": "For mild-to-moderate iron deficiency without severe symptoms, alternate-day dosing is supported by better evidence: a single 120 mg elemental iron dose every other day achieves equivalent or higher fractional iron absorption than 40–60 mg three times daily, because each oral iron dose triggers a 24-hour hepcidin mucosal block that prevents further absorption regardless of additional doses within that window (PMID 28895840). Alternate-day dosing also has better GI tolerance, which improves compliance. For severe iron-deficiency anemia where rapid hemoglobin correction is needed, daily dosing is still reasonable given slightly faster time-to-target. Alternate-day dosing is the newer evidence-based default for non-urgent mild-moderate deficiency."
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          "@type": "Question",
          "name": "What's the best form of iron?",
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            "text": "For most patients ferrous sulfate is first-line — cheap, effective, and well-studied. If GI tolerance is poor, switching to ferrous bisglycinate (Ferrochel, Albion-chelated) or ferric maltol (Accrufer, prescription) typically improves tolerance while maintaining efficacy (PMID 30916634, 29554993). Heme iron polypeptide (Proferrin) is better-tolerated still but expensive and provides less elemental iron per dose. Ferrous fumarate and gluconate are equivalent alternatives to sulfate with similar tolerance. Avoid ferric oxides and reduced iron powders with poor absorption. The 'best' form for you depends on cost, GI tolerance, and response; start with sulfate and escalate to alternatives if tolerance is problematic."
          }
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          "@type": "Question",
          "name": "Can men take iron supplements?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "Generally no, unless they have documented iron deficiency confirmed by ferritin, iron studies, and often additional workup for the source of the deficiency (GI blood loss, celiac, malabsorption). Adult men have an RDA of only 8 mg/day — easily met by diet — and the body has no regulated iron excretion pathway, so inappropriate long-term supplementation risks organ iron loading especially in undiagnosed hereditary hemochromatosis (HFE C282Y homozygosity affects roughly 1 in 200 people of Northern European ancestry). If a man has confirmed iron deficiency, investigate the cause first (GI evaluation is often warranted) and then supplement under clinical guidance. Iron-containing multivitamins are generally not appropriate for adult men unless there's a specific indication."
          }
        },
        {
          "@type": "Question",
          "name": "Why do I need vitamin C with iron?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "Vitamin C (ascorbic acid) enhances non-heme iron absorption in two ways: it reduces Fe³⁺ (the less absorbable ferric form) to Fe²⁺ (the more absorbable ferrous form) at the duodenal brush border, and it maintains iron solubility in the more alkaline small intestinal environment where iron would otherwise precipitate. Co-administration of 100–250 mg vitamin C roughly doubles non-heme iron absorption in typical study conditions. Orange juice, bell peppers, strawberries, or a vitamin C tablet all work. Heme iron (from meat) doesn't need vitamin C enhancement because heme uses a different absorption pathway. See the Vitamin C entry for the broader discussion."
          }
        },
        {
          "@type": "Question",
          "name": "Can iron deficiency cause anxiety or depression?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "Iron deficiency affects brain iron-dependent enzymes including tyrosine hydroxylase (the rate-limiting enzyme for dopamine synthesis) and tryptophan hydroxylase (serotonin synthesis), and brain iron deficiency has been associated with depressed mood, anxiety, cognitive fog, and restless legs syndrome. Non-anemic iron deficiency (low ferritin, normal hemoglobin) can cause these symptoms without the classic fatigue and pallor of frank anemia. Trials of iron repletion in iron-deficient women have shown improvements in fatigue, mood, and cognitive function even without anemia correction (PMID 22354584). If you have unexplained depressed mood, anxiety, or cognitive symptoms, checking ferritin is reasonable — target >50 ng/mL for most adults, >75 for RLS-prone patients."
          }
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          "@type": "Question",
          "name": "Should I worry about hemochromatosis?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "If you have a first-degree relative with hemochromatosis, chronically elevated ferritin (>500 ng/mL in a healthy adult, or >200 ng/mL with elevated transferrin saturation), unexplained cirrhosis, or typical features (bronze skin, diabetes, arthropathy in middle age), HFE genetic testing for C282Y and H63D mutations is appropriate. HFE C282Y homozygosity affects roughly 1 in 200 people of Northern European ancestry and is the most common autosomal recessive disorder in that population. Early diagnosis and phlebotomy (weekly until ferritin <50, then maintenance every 2–4 months) prevents organ complications and restores near-normal life expectancy (PMID 26193103). This is a major reason men and postmenopausal women should not take iron supplements without confirmed deficiency — you could accelerate undiagnosed hemochromatosis."
          }
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          "@type": "Question",
          "name": "Is IV iron better than oral iron?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "IV iron is preferred in specific settings: intolerance or failure of oral iron despite optimization, heart failure with iron deficiency (FAIR-HF, CONFIRM-HF, AFFIRM-AHF evidence, PMID 19920054, 26034145, 33245868), inflammatory bowel disease anemia, chronic kidney disease anemia on dialysis, post-bariatric surgery malabsorption, heavy uterine bleeding requiring rapid repletion, and severe pregnancy anemia. IV iron delivers a large dose in one or two sessions (ferric carboxymaltose 750–1,000 mg per infusion), eliminates GI toxicity entirely, and bypasses the hepcidin mucosal block. For uncomplicated iron deficiency without these indications, oral iron is cheaper and equally effective long-term. IV iron carries small but real risks of hypersensitivity reactions and, with ferric carboxymaltose specifically, hypophosphatemia (PMID 32189324). Discuss IV vs oral with your clinician based on severity and context."
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          "@type": "Question",
          "name": "What blocks iron absorption?",
          "acceptedAnswer": {
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            "text": "Calcium, coffee/tea (tannins), phytates (whole grains, legumes, bran), polyphenols (some berries), and high-dose zinc or copper can all reduce non-heme iron absorption when co-ingested. Practical rules: separate iron from coffee/tea by 1+ hour; from dairy/calcium by 2+ hours; from zinc/magnesium supplements by 2+ hours; from levothyroxine by 4 hours; from tetracyclines/fluoroquinolones/bisphosphonates by 2 hours. Heme iron (from meat) is much less affected by these inhibitors because it uses a different absorption pathway. Vitamin C strongly enhances non-heme iron absorption and can partially overcome some inhibitors. Soaking, sprouting, and fermentation reduce phytate inhibition in plant foods. PPIs and H2 blockers reduce gastric acid and thus iron absorption; consider acidified forms or vitamin C co-administration if you're chronically on acid suppression."
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          "name": "Can I take iron while pregnant?",
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            "text": "Yes — most pregnant women should take iron. WHO recommends 30–60 mg/day elemental iron for all pregnant women in iron-deficient regions; in the US, iron-containing prenatal vitamins covering 27 mg/day are standard, and higher doses (60–120 mg) are added for confirmed iron deficiency or anemia. Iron deficiency in pregnancy is associated with increased risks of low birthweight, preterm delivery, maternal anemia, and possibly impaired infant cognitive development. Oral iron is first-line; IV iron (ferric carboxymaltose, iron sucrose) is used in second and third trimester for severe anemia or oral iron failure with good safety records (PMID 28712751). Take with vitamin C for absorption; split doses or alternate days may improve GI tolerance in morning sickness-sensitive patients. If constipation is a problem (common in pregnancy plus iron), bisglycinate forms, adequate hydration, and fiber management help."
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        "@type": "Drug",
        "name": "Iron",
        "alternateName": [
          "Fe",
          "Fe2+",
          "Fe3+",
          "Ferrous",
          "Ferric",
          "Ferrous sulfate",
          "Ferrous fumarate",
          "Ferrous gluconate",
          "Ferrous bisglycinate",
          "Iron bisglycinate",
          "Ferrochel",
          "Ferric maltol",
          "Accrufer",
          "Heme iron polypeptide",
          "HIP",
          "Proferrin",
          "Carbonyl iron",
          "Iron-dextran",
          "Iron sucrose",
          "Ferric carboxymaltose",
          "Injectafer",
          "Ferumoxytol",
          "Feraheme",
          "Sodium ferric gluconate"
        ],
        "description": "Iron is a trace mineral with a biochemistry dominated by a single chemical property — the reversible one-electron redox between Fe²⁺ (ferrous) and Fe³⁺ (ferric) — that makes it indispensable for oxygen transport, electron transfer, and hundreds of enzymatic reactions, and simultaneously dangerous when unchaperoned in cells. The adult RDA is 8 mg/day for men and postmenopausal women, 18 mg/day for premenopausal women, 27 mg/day for pregnancy, and 9 mg/day for lactation; the tolerable upper limit is 45 mg/day from all sources combined. Iron deficiency is the most common nutritional deficiency worldwide, affecting over two billion people, and iron-deficiency anemia remains a leading global cause of disability-adjusted life years lost, disproportionately affecting menstruating women, pregnant women, infants, and populations with high parasitic burden or plant-based diets with low bioavailable iron. The clinical presentation ranges from subtle — fatigue, reduced exercise capacity, cognitive fog, restless legs — at early stages of iron-deficient erythropoiesis, to frank microcytic hypochromic anemia with pallor, tachycardia, and exertional dyspnea at advanced stages. Iron deficiency without anemia (low ferritin, normal hemoglobin) is increasingly recognized as clinically meaningful, especially in women with heavy menstrual bleeding and in endurance athletes with elevated losses; trials of iron repletion in non-anemic iron-deficient women have shown improvements in fatigue, physical capacity, and quality of life even in the absence of overt anemia. At the opposite end, iron overload is equally problematic. Hereditary hemochromatosis (most commonly HFE C282Y homozygosity, affecting roughly 1 in 200 people of Northern European ancestry) causes progressive tissue iron loading with eventual cirrhosis, diabetes, cardiomyopathy, hypogonadism, and arthritis if untreated — classically in middle-aged men with a characteristic bronze skin discoloration. Transfusion-dependent iron overload (thalassemia major, sickle cell, myelodysplastic syndromes) produces similar tissue injury through a different route. The body has no regulated excretory mechanism for iron — roughly 1 mg/day is lost through desquamation of intestinal and skin cells, and additional losses through menstruation or bleeding — so iron balance is almost entirely regulated at the absorption level via the hormone hepcidin. When iron stores are high, hepcidin rises and blocks iron absorption by degrading ferroportin on enterocytes; when iron stores are low or erythropoiesis is driven up (via the hormone erythroferrone released from maturing erythroblasts), hepcidin falls and absorption increases. This elegant single-hormone axis, worked out largely by Nemeth and Ganz in the 2000s, revolutionized our understanding of iron disorders — hereditary hemochromatosis is fundamentally a hepcidin-deficiency disease, and anemia of chronic inflammation is a hepcidin-excess disease. Dietary iron exists in two fundamental forms: heme iron from animal sources (hemoglobin and myoglobin of meat, fish, poultry) which is absorbed at 15–35% regardless of dietary context, and non-heme iron from plant sources (grains, legumes, leafy greens, fortified foods) which is absorbed at 2–20% and is highly sensitive to enhancers (vitamin C, meat, acidity) and inhibitors (phytates, tannins, calcium, tea polyphenols). This bioavailability gap is why vegetarians and vegans have higher iron deficiency rates despite similar or higher iron intake compared to omnivores — a point of practical importance for dietary planning. See also Copper for the ceruloplasmin ferroxidase dependency that makes iron utilization copper-sensitive, Vitamin C for the non-heme iron absorption enhancement, Vitamin B12 for the shared anemia differential, and Vitamin D for the hepcidin regulation link. This overview is educational only and is not medical advice — iron supplementation in men and postmenopausal women without confirmed deficiency is not appropriate given the absence of regulated excretion and the real risk of organ iron loading in undiagnosed hemochromatosis carriers.",
        "activeIngredient": "Iron",
        "mechanismOfAction": "Iron's mechanism of action can be divided into three domains: the biochemical roles of iron-containing proteins, the absorption-and-distribution axis regulated by hepcidin, and the cellular handling that prevents iron's pro-oxidant chemistry from causing damage. Iron is incorporated into three major classes of functional proteins. Heme proteins (hemoglobin in red blood cells, myoglobin in muscle, cytochromes in the electron transport chain and cytochrome P450 enzymes, catalase, myeloperoxidase in neutrophils, nitric oxide synthase, tryptophan pyrrolase) use a porphyrin-bound iron atom to bind oxygen, transfer electrons, or catalyze oxidation reactions — hemoglobin alone accounts for 65–70% of body iron. Iron-sulfur cluster proteins (aconitase in the TCA cycle, complexes I, II, III of the electron transport chain, succinate dehydrogenase, ferredoxin, DNA repair enzymes, ribonucleotide reductase) use Fe-S clusters assembled through the ISC/CIA machinery for electron transfer and catalysis. Non-heme iron enzymes include ribonucleotide reductase (DNA synthesis), tyrosine hydroxylase (dopamine synthesis — iron deficiency produces dopamine synthesis impairments potentially relevant to restless legs syndrome and cognitive symptoms), proline hydroxylase (collagen synthesis), lysyl hydroxylase, and the prolyl hydroxylases that oxygen-sense HIF-α stability (the oxygen-sensing machinery Kaelin/Ratcliffe/Semenza won the 2019 Nobel for). Absorption occurs almost entirely in the duodenum and upper jejunum. Heme iron enters enterocytes via HCP1/PCFT (heme carrier protein 1) and is released intracellularly by heme oxygenase. Non-heme iron requires reduction from Fe³⁺ to Fe²⁺ by duodenal cytochrome b (DCYTB) at the apical brush border, then uptake via DMT1 (divalent metal transporter 1, SLC11A2). Intracellular iron is either incorporated into ferritin for storage (the 24-subunit cage protein that sequesters up to 4,500 iron atoms as a ferrihydrite core, oxidized to the Fe³⁺ state by ferritin's H-subunit ferroxidase), or exported across the basolateral membrane by ferroportin (FPN1, SLC40A1) — the only known iron exporter — and oxidized by ceruloplasmin or its intestinal paralog hephaestin back to Fe³⁺ for transferrin loading. Circulating transferrin delivers iron to cells expressing the transferrin receptor (TfR1 ubiquitously, TfR2 in hepatocytes and erythroid cells), which internalizes the transferrin-iron complex via clathrin-mediated endocytosis, releases iron in acidified endosomes, and recycles transferrin back to the surface — this is the canonical Ashwell pathway of iron delivery. The regulatory master is hepcidin, a 25-amino-acid peptide hormone produced by hepatocytes. Hepcidin binds ferroportin on enterocytes, macrophages, and hepatocytes, triggering its internalization and degradation — blocking both dietary iron absorption and iron release from macrophage recycling of senescent erythrocytes. Hepcidin is induced by high iron stores (via the BMP6/SMAD pathway), inflammation (via IL-6/STAT3), and oral iron (producing the transient \"mucosal block\" after a large iron dose that limits further absorption for ~24 hours), and suppressed by low iron (via matriptase-2/TMPRSS6 cleavage of hemojuvelin, the BMP co-receptor) and active erythropoiesis (via erythroferrone from maturing erythroblasts). Understanding this axis explains two major clinical phenomena: hereditary hemochromatosis is a collection of conditions with insufficient hepcidin (HFE, TfR2, HJV, HAMP, TMPRSS6 mutations all converge on loss of hepcidin signaling), producing unrestrained iron absorption and progressive tissue loading; anemia of chronic disease is a state of hepcidin excess driven by IL-6, functionally trapping iron in macrophages so it cannot reach the bone marrow — this is why CRP should be checked when evaluating an anemia that looks iron-deficient but has normal or high ferritin. The pro-oxidant problem: free Fe²⁺ drives the Fenton reaction (Fe²⁺ + H₂O₂ → Fe³⁺ + •OH + OH⁻), generating hydroxyl radicals that damage lipids, proteins, and DNA. Ferritin sequestration, iron chaperones (PCBP1, PCBP2), and the rapid loading onto transferrin limit the labile iron pool that could drive this chemistry. The recently-described ferroptosis cell death program — iron-dependent lipid peroxidation — has opened a new layer of iron biology relevant to neurodegeneration, ischemia-reperfusion injury, and cancer therapy (PMID 22632970). The practical mechanistic takeaway: iron absorption is tightly regulated by hepcidin, the 24-hour mucosal block makes split dosing counterproductive and alternate-day dosing more efficient, vitamin C enhances non-heme iron absorption by reducing Fe³⁺ to Fe²⁺ at the brush border, and the absence of regulated excretion is why iron overload is a one-way street in the absence of bleeding or phlebotomy.",
        "legalStatus": "Not approved for human use — research chemical",
        "warning": "For research purposes only. Not for human consumption."
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          "@type": "Question",
          "name": "How much iron should I take for iron-deficiency anemia?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "For most adults with confirmed iron-deficiency anemia, 100–200 mg elemental iron per day as ferrous sulfate, ferrous fumarate, or ferrous bisglycinate, split 2–3 times daily or given as alternate-day 120 mg to improve tolerance. Alternate-day dosing is supported by Stoffel et al. 2017 and 2020 studies showing equivalent fractional absorption with better GI tolerance, based on the hepcidin mucosal block lasting ~24 hours after a single oral iron dose (PMID 28895840, 32895503). Take with 250 mg vitamin C on empty stomach if tolerated; with small snack if GI-sensitive. Continue for 3–6 months after hemoglobin normalizes to fully replete ferritin. Recheck at 1 month (reticulocyte response), 3 months (hemoglobin), 6 months (ferritin)."
          }
        },
        {
          "@type": "Question",
          "name": "Should I take iron every day or every other day?",
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            "@type": "Answer",
            "text": "For mild-to-moderate iron deficiency without severe symptoms, alternate-day dosing is supported by better evidence: a single 120 mg elemental iron dose every other day achieves equivalent or higher fractional iron absorption than 40–60 mg three times daily, because each oral iron dose triggers a 24-hour hepcidin mucosal block that prevents further absorption regardless of additional doses within that window (PMID 28895840). Alternate-day dosing also has better GI tolerance, which improves compliance. For severe iron-deficiency anemia where rapid hemoglobin correction is needed, daily dosing is still reasonable given slightly faster time-to-target. Alternate-day dosing is the newer evidence-based default for non-urgent mild-moderate deficiency."
          }
        },
        {
          "@type": "Question",
          "name": "What's the best form of iron?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "For most patients ferrous sulfate is first-line — cheap, effective, and well-studied. If GI tolerance is poor, switching to ferrous bisglycinate (Ferrochel, Albion-chelated) or ferric maltol (Accrufer, prescription) typically improves tolerance while maintaining efficacy (PMID 30916634, 29554993). Heme iron polypeptide (Proferrin) is better-tolerated still but expensive and provides less elemental iron per dose. Ferrous fumarate and gluconate are equivalent alternatives to sulfate with similar tolerance. Avoid ferric oxides and reduced iron powders with poor absorption. The 'best' form for you depends on cost, GI tolerance, and response; start with sulfate and escalate to alternatives if tolerance is problematic."
          }
        },
        {
          "@type": "Question",
          "name": "Can men take iron supplements?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "Generally no, unless they have documented iron deficiency confirmed by ferritin, iron studies, and often additional workup for the source of the deficiency (GI blood loss, celiac, malabsorption). Adult men have an RDA of only 8 mg/day — easily met by diet — and the body has no regulated iron excretion pathway, so inappropriate long-term supplementation risks organ iron loading especially in undiagnosed hereditary hemochromatosis (HFE C282Y homozygosity affects roughly 1 in 200 people of Northern European ancestry). If a man has confirmed iron deficiency, investigate the cause first (GI evaluation is often warranted) and then supplement under clinical guidance. Iron-containing multivitamins are generally not appropriate for adult men unless there's a specific indication."
          }
        },
        {
          "@type": "Question",
          "name": "Why do I need vitamin C with iron?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "Vitamin C (ascorbic acid) enhances non-heme iron absorption in two ways: it reduces Fe³⁺ (the less absorbable ferric form) to Fe²⁺ (the more absorbable ferrous form) at the duodenal brush border, and it maintains iron solubility in the more alkaline small intestinal environment where iron would otherwise precipitate. Co-administration of 100–250 mg vitamin C roughly doubles non-heme iron absorption in typical study conditions. Orange juice, bell peppers, strawberries, or a vitamin C tablet all work. Heme iron (from meat) doesn't need vitamin C enhancement because heme uses a different absorption pathway. See the Vitamin C entry for the broader discussion."
          }
        },
        {
          "@type": "Question",
          "name": "Can iron deficiency cause anxiety or depression?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "Iron deficiency affects brain iron-dependent enzymes including tyrosine hydroxylase (the rate-limiting enzyme for dopamine synthesis) and tryptophan hydroxylase (serotonin synthesis), and brain iron deficiency has been associated with depressed mood, anxiety, cognitive fog, and restless legs syndrome. Non-anemic iron deficiency (low ferritin, normal hemoglobin) can cause these symptoms without the classic fatigue and pallor of frank anemia. Trials of iron repletion in iron-deficient women have shown improvements in fatigue, mood, and cognitive function even without anemia correction (PMID 22354584). If you have unexplained depressed mood, anxiety, or cognitive symptoms, checking ferritin is reasonable — target >50 ng/mL for most adults, >75 for RLS-prone patients."
          }
        },
        {
          "@type": "Question",
          "name": "Should I worry about hemochromatosis?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "If you have a first-degree relative with hemochromatosis, chronically elevated ferritin (>500 ng/mL in a healthy adult, or >200 ng/mL with elevated transferrin saturation), unexplained cirrhosis, or typical features (bronze skin, diabetes, arthropathy in middle age), HFE genetic testing for C282Y and H63D mutations is appropriate. HFE C282Y homozygosity affects roughly 1 in 200 people of Northern European ancestry and is the most common autosomal recessive disorder in that population. Early diagnosis and phlebotomy (weekly until ferritin <50, then maintenance every 2–4 months) prevents organ complications and restores near-normal life expectancy (PMID 26193103). This is a major reason men and postmenopausal women should not take iron supplements without confirmed deficiency — you could accelerate undiagnosed hemochromatosis."
          }
        },
        {
          "@type": "Question",
          "name": "Is IV iron better than oral iron?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "IV iron is preferred in specific settings: intolerance or failure of oral iron despite optimization, heart failure with iron deficiency (FAIR-HF, CONFIRM-HF, AFFIRM-AHF evidence, PMID 19920054, 26034145, 33245868), inflammatory bowel disease anemia, chronic kidney disease anemia on dialysis, post-bariatric surgery malabsorption, heavy uterine bleeding requiring rapid repletion, and severe pregnancy anemia. IV iron delivers a large dose in one or two sessions (ferric carboxymaltose 750–1,000 mg per infusion), eliminates GI toxicity entirely, and bypasses the hepcidin mucosal block. For uncomplicated iron deficiency without these indications, oral iron is cheaper and equally effective long-term. IV iron carries small but real risks of hypersensitivity reactions and, with ferric carboxymaltose specifically, hypophosphatemia (PMID 32189324). Discuss IV vs oral with your clinician based on severity and context."
          }
        },
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          "name": "What blocks iron absorption?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "Calcium, coffee/tea (tannins), phytates (whole grains, legumes, bran), polyphenols (some berries), and high-dose zinc or copper can all reduce non-heme iron absorption when co-ingested. Practical rules: separate iron from coffee/tea by 1+ hour; from dairy/calcium by 2+ hours; from zinc/magnesium supplements by 2+ hours; from levothyroxine by 4 hours; from tetracyclines/fluoroquinolones/bisphosphonates by 2 hours. Heme iron (from meat) is much less affected by these inhibitors because it uses a different absorption pathway. Vitamin C strongly enhances non-heme iron absorption and can partially overcome some inhibitors. Soaking, sprouting, and fermentation reduce phytate inhibition in plant foods. PPIs and H2 blockers reduce gastric acid and thus iron absorption; consider acidified forms or vitamin C co-administration if you're chronically on acid suppression."
          }
        },
        {
          "@type": "Question",
          "name": "Can I take iron while pregnant?",
          "acceptedAnswer": {
            "@type": "Answer",
            "text": "Yes — most pregnant women should take iron. WHO recommends 30–60 mg/day elemental iron for all pregnant women in iron-deficient regions; in the US, iron-containing prenatal vitamins covering 27 mg/day are standard, and higher doses (60–120 mg) are added for confirmed iron deficiency or anemia. Iron deficiency in pregnancy is associated with increased risks of low birthweight, preterm delivery, maternal anemia, and possibly impaired infant cognitive development. Oral iron is first-line; IV iron (ferric carboxymaltose, iron sucrose) is used in second and third trimester for severe anemia or oral iron failure with good safety records (PMID 28712751). Take with vitamin C for absorption; split doses or alternate days may improve GI tolerance in morning sickness-sensitive patients. If constipation is a problem (common in pregnancy plus iron), bisglycinate forms, adequate hydration, and fiber management help."
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# Iron

Mineral Preclinical 

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Also known as: Fe, Fe2+, Fe3+, Ferrous, Ferric, Ferrous sulfate, Ferrous fumarate, Ferrous gluconate, Ferrous bisglycinate, Iron bisglycinate, Ferrochel, Ferric maltol, Accrufer, Heme iron polypeptide, HIP, Proferrin, Carbonyl iron, Iron-dextran, Iron sucrose, Ferric carboxymaltose, Injectafer, Ferumoxytol, Feraheme, Sodium ferric gluconate 

Iron is a trace mineral with a biochemistry dominated by a single chemical property — the reversible one-electron redox between Fe²⁺ (ferrous) and Fe³⁺ (ferric) — that makes it indispensable for oxygen transport, electron transfer, and hundreds of enzymatic reactions, and simultaneously dangerous when unchaperoned in cells. The adult RDA is 8 mg/day for men and postmenopausal women, 18 mg/day for premenopausal women, 27 mg/day for pregnancy, and 9 mg/day for lactation; the tolerable upper limit is 45 mg/day from all sources combined.

Last reviewed: Sep 2, 2026 

[

Mineral

Category



](/wiki#cat-mineral)

Preclinical

Research Stage

OverviewChemical InfoDosing & ProtocolsInteractionsResearchCompare PricesRelated

## Overview

### At A Glance

Mechanism 

Iron's mechanism of action can be divided into three domains: the biochemical roles of iron-containing proteins, the absorption-and-distribution axis regulated by hepcidin, and the cellular handling that prevents iron's pro-oxidant chemistry from causing damage. Iron is incorpora… 

### Overview

Iron is a trace mineral with a biochemistry dominated by a single chemical property — the reversible one-electron redox between Fe²⁺ (ferrous) and Fe³⁺ (ferric) — that makes it indispensable for oxygen transport, electron transfer, and hundreds of enzymatic reactions, and simultaneously dangerous when unchaperoned in cells. The adult RDA is 8 mg/day for men and postmenopausal women, 18 mg/day for premenopausal women, 27 mg/day for pregnancy, and 9 mg/day for lactation; the tolerable upper limit is 45 mg/day from all sources combined. Iron deficiency is the most common nutritional deficiency worldwide, affecting over two billion people, and iron-deficiency anemia remains a leading global cause of disability-adjusted life years lost, disproportionately affecting menstruating women, pregnant women, infants, and populations with high parasitic burden or plant-based diets with low bioavailable iron. The clinical presentation ranges from subtle — fatigue, reduced exercise capacity, cognitive fog, restless legs — at early stages of iron-deficient erythropoiesis, to frank microcytic hypochromic anemia with pallor, tachycardia, and exertional dyspnea at advanced stages. Iron deficiency without anemia (low ferritin, normal hemoglobin) is increasingly recognized as clinically meaningful, especially in women with heavy menstrual bleeding and in endurance athletes with elevated losses; trials of iron repletion in non-anemic iron-deficient women have shown improvements in fatigue, physical capacity, and quality of life even in the absence of overt anemia. At the opposite end, iron overload is equally problematic. Hereditary hemochromatosis (most commonly HFE C282Y homozygosity, affecting roughly 1 in 200 people of Northern European ancestry) causes progressive tissue iron loading with eventual cirrhosis, diabetes, cardiomyopathy, hypogonadism, and arthritis if untreated — classically in middle-aged men with a characteristic bronze skin discoloration. Transfusion-dependent iron overload (thalassemia major, sickle cell, myelodysplastic syndromes) produces similar tissue injury through a different route. The body has no regulated excretory mechanism for iron — roughly 1 mg/day is lost through desquamation of intestinal and skin cells, and additional losses through menstruation or bleeding — so iron balance is almost entirely regulated at the absorption level via the hormone hepcidin. When iron stores are high, hepcidin rises and blocks iron absorption by degrading ferroportin on enterocytes; when iron stores are low or erythropoiesis is driven up (via the hormone erythroferrone released from maturing erythroblasts), hepcidin falls and absorption increases. This elegant single-hormone axis, worked out largely by Nemeth and Ganz in the 2000s, revolutionized our understanding of iron disorders — hereditary hemochromatosis is fundamentally a hepcidin-deficiency disease, and anemia of chronic inflammation is a hepcidin-excess disease. Dietary iron exists in two fundamental forms: heme iron from animal sources (hemoglobin and myoglobin of meat, fish, poultry) which is absorbed at 15–35% regardless of dietary context, and non-heme iron from plant sources (grains, legumes, leafy greens, fortified foods) which is absorbed at 2–20% and is highly sensitive to enhancers (vitamin C, meat, acidity) and inhibitors (phytates, tannins, calcium, tea polyphenols). This bioavailability gap is why vegetarians and vegans have higher iron deficiency rates despite similar or higher iron intake compared to omnivores — a point of practical importance for dietary planning. See also [Copper](/compound/copper) for the ceruloplasmin ferroxidase dependency that makes iron utilization copper-sensitive, [Vitamin C](/compound/vitamin-c) for the non-heme iron absorption enhancement, [Vitamin B12](/compound/vitamin-b12) for the shared anemia differential, and [Vitamin D](/compound/vitamin-d) for the hepcidin regulation link. This overview is educational only and is not medical advice — iron supplementation in men and postmenopausal women without confirmed deficiency is not appropriate given the absence of regulated excretion and the real risk of organ iron loading in undiagnosed hemochromatosis carriers.

## Chemical Information

IUPAC Name

Not yet available 

CAS Number

Not yet available 

Molecular Formula

Not yet available 

Molecular Mass

Not yet available 

Chemical data is being compiled for this compound.

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## Interactions

### Contraindications

Iron supplementation is contraindicated or requires special caution in several settings. Hereditary hemochromatosis is an absolute contraindication for iron supplementation — affected patients cannot regulate iron absorption via hepcidin, and any additional iron accelerates organ iron loading with progression toward cirrhosis, diabetes, cardiomyopathy, and other complications. Family history of hemochromatosis (first-degree relative) or unexplained ferritin elevation in the 500–1,000+ ng/mL range in middle-aged patients should prompt HFE genetic testing before any iron supplementation. Thalassemia and sickle cell disease with chronic transfusions cause transfusional iron overload that requires chelation, not supplementation; iron supplements are contraindicated. Porphyria cutanea tarda (a photosensitive dermatosis with hepatic iron involvement) is worsened by iron and treated with phlebotomy. African iron overload (formerly called Bantu siderosis) from home-brewed beer fermented in iron vessels plus genetic susceptibility similarly contraindicates supplementation. Chronic infection, especially malaria and tuberculosis, requires caution — unrestricted iron supplementation in malaria-endemic regions has been associated with worsened malaria severity in some trials (the Pemba trial famously showed increased mortality in iron-supplemented young children in a malaria-endemic area, leading to WHO to restrict universal supplementation in these settings). Active bacterial infection: many bacteria are iron-dependent and iron supplementation during acute bacterial sepsis is generally avoided. Inflammatory bowel disease flare: oral iron can worsen intestinal inflammation and IV iron is preferred for documented iron deficiency in active IBD. Hemolytic anemia: iron supplements are not indicated; hemolysis recycles body iron efficiently and adding external iron risks loading. Aplastic anemia or myelodysplastic syndromes with transfusion dependence: iron overload is a major concern and iron supplements are contraindicated. G6PD deficiency: iron can catalyze oxidative hemolysis in theory; avoid high-dose iron supplements in G6PD patients without indication. Acute gastroenteritis or peptic ulcer disease: iron can worsen GI inflammation; consider delaying or switching to better-tolerated forms. Pregnancy: RDA-range iron (27 mg/day in prenatal vitamin, up to 60 mg for confirmed deficiency) is strongly recommended; higher doses should be evidence-based and lab-guided. Pediatric dosing: pediatrician-directed only; adult-strength iron in pediatric hands is a major poisoning risk. Peptic ulcer, hemochromatosis heterozygotes: use with caution and lab monitoring. Drug interactions: levothyroxine (separate 4 hours), tetracyclines and fluoroquinolones (separate 2 hours), bisphosphonates (separate 2 hours), methyldopa (chelation reduces absorption), levodopa (chelation reduces absorption, particularly relevant in Parkinson disease), penicillamine (chelates with iron), trientine (chelation), chloramphenicol (reduces response to iron), and PPIs/H2 blockers (reduce iron absorption, consider acidified forms or alternate-day dosing). Men and postmenopausal women should not take iron supplements without documented deficiency — this is the most important general cautionary principle, given the absence of a regulated excretion pathway and the substantial prevalence of undiagnosed hemochromatosis genetics in Northern European populations. If you are unsure whether iron supplementation is appropriate, get baseline ferritin and iron studies and discuss with a clinician rather than proceeding empirically. This is general educational content, not medical advice.

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### Related Compounds

[View All](/wiki)

[

### Boron

Mineral Preclinical 

Boron is an ultra-trace element whose nutritional status in humans sits in a distinctive regulatory gray zone: the Institute of Medicine (US) has not established a recommended dietary allowance (RDA) or estimated average requirement (EAR) for boron because the evidence for essentiality in humans does not meet the strict criteria applied to calcium, iron, or zinc, yet the IOM, the European Food Safety Authority (EFSA), and the World Health Organization (WHO) all set tolerable upper intake levels (ULs) — implicitly acknowledging that boron has biological activity and dose-response safety concerns.

66274 studies View Profile 

](/compound/boron)[

### Calcium

Mineral Preclinical 

Calcium is the most abundant mineral in the human body — roughly 1,000 to 1,500 grams in a 70 kg adult, with 99% sequestered in the skeleton and teeth as crystalline hydroxyapatite \[Ca10(PO4)6(OH)2\], and the remaining 1% distributed across extracellular fluid, intracellular cytoplasm, mitochondria, and the endoplasmic/sarcoplasmic reticulum.

854847 studies View Profile 

](/compound/calcium)[

### Chromium

Mineral Preclinical 

Chromium is a transition metal that occupies one of the more peculiar positions in human nutrition: long marketed as essential for carbohydrate metabolism and insulin sensitization, the evidence for chromium essentiality has progressively softened over the past two decades, and both the European Food Safety Authority (EFSA 2014) and multiple independent reviews have concluded that chromium III is not definitively essential for humans.

93196 studies View Profile 

](/compound/chromium)[

### Copper

Mineral Preclinical 

Copper is an essential trace mineral that most adults get in adequate amounts from a varied omnivorous diet — but that routinely drops into functional insufficiency when people take long-term high-dose zinc supplements, consume highly processed diets, undergo bariatric surgery, or use copper-chelating therapies.

Preclinical View Profile 

](/compound/copper)[

### Iodine

Mineral Preclinical 

Iodine is a halogen trace mineral and an obligate substrate for thyroid hormone synthesis — the single biochemical fact that dominates all clinical thinking about iodine.

Preclinical View Profile 

](/compound/iodine)[

### Manganese

Mineral Preclinical 

Manganese is an essential trace mineral and redox-active transition metal occupying a peculiar place in human nutrition: absolutely required at milligram doses for mitochondrial antioxidant defense, gluconeogenesis, urea cycle function, and connective tissue synthesis — yet potently neurotoxic at the hundredfold-higher doses encountered occupationally (welders, miners, battery workers) and in patients on long-term parenteral nutrition with inadequately controlled trace mineral content.

85480 studies View Profile 

](/compound/manganese)

[

View Full Dosage Guide →

Protocols, calculator & safety for Iron



](/guides/dosage/iron)

### Related Articles

[All Posts](/blog)

[

#### Autoimmune Gastritis: Symptoms, the Low-Acid Twist, and What Actually Helps (2026)

Autoimmune gastritis causes LOW stomach acid and hides behind unexplained low iron for years. Symptoms, the antibody and gastrin blood panel, cancer surveillance, and what actually helps.

7/7/2026 ](/blog/autoimmune-gastritis-guide)[

#### Gut Healing Supplements & Peptides: What the Research Actually Supports (2026)

Most "gut healing" supplements and peptides are sold on animal studies and mechanism, not human results. The interventions with real human trial data are unglamorous and cheap: zinc-L-carnosine for the stomach lining, L-glutamine for a measured leaky gut, strain-specific probiotics, enteric-coated peppermint oil and the low-FODMAP diet for IBS, and soluble fiber done right. The hyped peptides (BPC-157, KPV) are almost entirely rat-and-petri-dish so far. And if your "stomach problem" is unexplained low iron or B12, the real issue might be too little stomach acid, which no supplement aisle fixes.

7/7/2026 ](/blog/gut-healing-supplements-research-guide)[

#### Glutathione (GSH): What the Research Actually Supports

A grounded research reference on glutathione (GSH), the body's master endogenous antioxidant. Covers the redox biology, the strongest clinical anchor (the NAC/acetaminophen-overdose antidote), the mixed skin-whitening and Parkinson's literature, the central oral bioavailability problem, and how the research community actually discusses precursors like NAC. Research-use-only, not medical advice.

7/1/2026 ](/blog/glutathione-research-guide)

### Research Score

15 

0 PubMed studies

### Quality Indicators

Data Completeness

50% 

Description 

Mechanism of Action 

Chemical Data 

Dosing Protocols 

Safety Profile 

PubMed Studies 

Interactions 

Vendor Listings 

### Quick Facts

Trial Phase

Preclinical

[Full Dosage Guide](/guides/dosage/iron)[Calculate Your Dose](/tools/reconstitution)

Research Disclaimer

This information is for educational and research purposes only. Not intended as medical advice. Consult a healthcare professional before use.

## Frequently Asked Questions

How much iron should I take for iron-deficiency anemia?

For most adults with confirmed iron-deficiency anemia, 100–200 mg elemental iron per day as ferrous sulfate, ferrous fumarate, or ferrous bisglycinate, split 2–3 times daily or given as alternate-day 120 mg to improve tolerance. Alternate-day dosing is supported by Stoffel et al. 2017 and 2020 studies showing equivalent fractional absorption with better GI tolerance, based on the hepcidin mucosal block lasting ~24 hours after a single oral iron dose (PMID 28895840, 32895503). Take with 250 mg vitamin C on empty stomach if tolerated; with small snack if GI-sensitive. Continue for 3–6 months after hemoglobin normalizes to fully replete ferritin. Recheck at 1 month (reticulocyte response), 3 months (hemoglobin), 6 months (ferritin).

Should I take iron every day or every other day?

For mild-to-moderate iron deficiency without severe symptoms, alternate-day dosing is supported by better evidence: a single 120 mg elemental iron dose every other day achieves equivalent or higher fractional iron absorption than 40–60 mg three times daily, because each oral iron dose triggers a 24-hour hepcidin mucosal block that prevents further absorption regardless of additional doses within that window (PMID 28895840). Alternate-day dosing also has better GI tolerance, which improves compliance. For severe iron-deficiency anemia where rapid hemoglobin correction is needed, daily dosing is still reasonable given slightly faster time-to-target. Alternate-day dosing is the newer evidence-based default for non-urgent mild-moderate deficiency.

What's the best form of iron?

For most patients ferrous sulfate is first-line — cheap, effective, and well-studied. If GI tolerance is poor, switching to ferrous bisglycinate (Ferrochel, Albion-chelated) or ferric maltol (Accrufer, prescription) typically improves tolerance while maintaining efficacy (PMID 30916634, 29554993). Heme iron polypeptide (Proferrin) is better-tolerated still but expensive and provides less elemental iron per dose. Ferrous fumarate and gluconate are equivalent alternatives to sulfate with similar tolerance. Avoid ferric oxides and reduced iron powders with poor absorption. The 'best' form for you depends on cost, GI tolerance, and response; start with sulfate and escalate to alternatives if tolerance is problematic.

Can men take iron supplements?

Generally no, unless they have documented iron deficiency confirmed by ferritin, iron studies, and often additional workup for the source of the deficiency (GI blood loss, celiac, malabsorption). Adult men have an RDA of only 8 mg/day — easily met by diet — and the body has no regulated iron excretion pathway, so inappropriate long-term supplementation risks organ iron loading especially in undiagnosed hereditary hemochromatosis (HFE C282Y homozygosity affects roughly 1 in 200 people of Northern European ancestry). If a man has confirmed iron deficiency, investigate the cause first (GI evaluation is often warranted) and then supplement under clinical guidance. Iron-containing multivitamins are generally not appropriate for adult men unless there's a specific indication.

Why do I need vitamin C with iron?

Vitamin C (ascorbic acid) enhances non-heme iron absorption in two ways: it reduces Fe³⁺ (the less absorbable ferric form) to Fe²⁺ (the more absorbable ferrous form) at the duodenal brush border, and it maintains iron solubility in the more alkaline small intestinal environment where iron would otherwise precipitate. Co-administration of 100–250 mg vitamin C roughly doubles non-heme iron absorption in typical study conditions. Orange juice, bell peppers, strawberries, or a vitamin C tablet all work. Heme iron (from meat) doesn't need vitamin C enhancement because heme uses a different absorption pathway. See the [Vitamin C](/compound/vitamin-c) entry for the broader discussion.

Can iron deficiency cause anxiety or depression?

Iron deficiency affects brain iron-dependent enzymes including tyrosine hydroxylase (the rate-limiting enzyme for dopamine synthesis) and tryptophan hydroxylase (serotonin synthesis), and brain iron deficiency has been associated with depressed mood, anxiety, cognitive fog, and restless legs syndrome. Non-anemic iron deficiency (low ferritin, normal hemoglobin) can cause these symptoms without the classic fatigue and pallor of frank anemia. Trials of iron repletion in iron-deficient women have shown improvements in fatigue, mood, and cognitive function even without anemia correction (PMID 22354584). If you have unexplained depressed mood, anxiety, or cognitive symptoms, checking ferritin is reasonable — target >50 ng/mL for most adults, >75 for RLS-prone patients.

Should I worry about hemochromatosis?

If you have a first-degree relative with hemochromatosis, chronically elevated ferritin (>500 ng/mL in a healthy adult, or >200 ng/mL with elevated transferrin saturation), unexplained cirrhosis, or typical features (bronze skin, diabetes, arthropathy in middle age), HFE genetic testing for C282Y and H63D mutations is appropriate. HFE C282Y homozygosity affects roughly 1 in 200 people of Northern European ancestry and is the most common autosomal recessive disorder in that population. Early diagnosis and phlebotomy (weekly until ferritin <50, then maintenance every 2–4 months) prevents organ complications and restores near-normal life expectancy (PMID 26193103). This is a major reason men and postmenopausal women should not take iron supplements without confirmed deficiency — you could accelerate undiagnosed hemochromatosis.

Is IV iron better than oral iron?

IV iron is preferred in specific settings: intolerance or failure of oral iron despite optimization, heart failure with iron deficiency (FAIR-HF, CONFIRM-HF, AFFIRM-AHF evidence, PMID 19920054, 26034145, 33245868), inflammatory bowel disease anemia, chronic kidney disease anemia on dialysis, post-bariatric surgery malabsorption, heavy uterine bleeding requiring rapid repletion, and severe pregnancy anemia. IV iron delivers a large dose in one or two sessions (ferric carboxymaltose 750–1,000 mg per infusion), eliminates GI toxicity entirely, and bypasses the hepcidin mucosal block. For uncomplicated iron deficiency without these indications, oral iron is cheaper and equally effective long-term. IV iron carries small but real risks of hypersensitivity reactions and, with ferric carboxymaltose specifically, hypophosphatemia (PMID 32189324). Discuss IV vs oral with your clinician based on severity and context.

What blocks iron absorption?

Calcium, coffee/tea (tannins), phytates (whole grains, legumes, bran), polyphenols (some berries), and high-dose zinc or copper can all reduce non-heme iron absorption when co-ingested. Practical rules: separate iron from coffee/tea by 1+ hour; from dairy/calcium by 2+ hours; from zinc/magnesium supplements by 2+ hours; from levothyroxine by 4 hours; from tetracyclines/fluoroquinolones/bisphosphonates by 2 hours. Heme iron (from meat) is much less affected by these inhibitors because it uses a different absorption pathway. Vitamin C strongly enhances non-heme iron absorption and can partially overcome some inhibitors. Soaking, sprouting, and fermentation reduce phytate inhibition in plant foods. PPIs and H2 blockers reduce gastric acid and thus iron absorption; consider acidified forms or vitamin C co-administration if you're chronically on acid suppression.

Can I take iron while pregnant?

Yes — most pregnant women should take iron. WHO recommends 30–60 mg/day elemental iron for all pregnant women in iron-deficient regions; in the US, iron-containing prenatal vitamins covering 27 mg/day are standard, and higher doses (60–120 mg) are added for confirmed iron deficiency or anemia. Iron deficiency in pregnancy is associated with increased risks of low birthweight, preterm delivery, maternal anemia, and possibly impaired infant cognitive development. Oral iron is first-line; IV iron (ferric carboxymaltose, iron sucrose) is used in second and third trimester for severe anemia or oral iron failure with good safety records (PMID 28712751). Take with vitamin C for absorption; split doses or alternate days may improve GI tolerance in morning sickness-sensitive patients. If constipation is a problem (common in pregnancy plus iron), bisglycinate forms, adequate hydration, and fiber management help.

## Research Tools

[

### Peptide Calculator

Reconstitution & syringe units



](/tools/reconstitution)[

### Reconstitution Guide

How to mix, step by step



](/guides/how-to-reconstitute-peptides)[

### Nasal Spray Calc

mL per actuation



](/tools/intranasal)[

### Half-Life Visualizer

Decay curves



](/tools/halflife)

## Related Compounds

[View All](/wiki)

[

### Boron

Mineral Preclinical 

Boron is an ultra-trace element whose nutritional status in humans sits in a distinctive regulatory gray zone: the Institute of Medicine (US) has not established a recommended dietary allowance (RDA) or estimated average requirement (EAR) for boron because the evidence for essentiality in humans does not meet the strict criteria applied to calcium, iron, or zinc, yet the IOM, the European Food Safety Authority (EFSA), and the World Health Organization (WHO) all set tolerable upper intake levels (ULs) — implicitly acknowledging that boron has biological activity and dose-response safety concerns.

66274 studies View Profile 

](/compound/boron)[

### Calcium

Mineral Preclinical 

Calcium is the most abundant mineral in the human body — roughly 1,000 to 1,500 grams in a 70 kg adult, with 99% sequestered in the skeleton and teeth as crystalline hydroxyapatite \[Ca10(PO4)6(OH)2\], and the remaining 1% distributed across extracellular fluid, intracellular cytoplasm, mitochondria, and the endoplasmic/sarcoplasmic reticulum.

854847 studies View Profile 

](/compound/calcium)[

### Chromium

Mineral Preclinical 

Chromium is a transition metal that occupies one of the more peculiar positions in human nutrition: long marketed as essential for carbohydrate metabolism and insulin sensitization, the evidence for chromium essentiality has progressively softened over the past two decades, and both the European Food Safety Authority (EFSA 2014) and multiple independent reviews have concluded that chromium III is not definitively essential for humans.

93196 studies View Profile 

](/compound/chromium)[

### Copper

Mineral Preclinical 

Copper is an essential trace mineral that most adults get in adequate amounts from a varied omnivorous diet — but that routinely drops into functional insufficiency when people take long-term high-dose zinc supplements, consume highly processed diets, undergo bariatric surgery, or use copper-chelating therapies.

Preclinical View Profile 

](/compound/copper)[

### Iodine

Mineral Preclinical 

Iodine is a halogen trace mineral and an obligate substrate for thyroid hormone synthesis — the single biochemical fact that dominates all clinical thinking about iodine.

Preclinical View Profile 

](/compound/iodine)[

### Manganese

Mineral Preclinical 

Manganese is an essential trace mineral and redox-active transition metal occupying a peculiar place in human nutrition: absolutely required at milligram doses for mitochondrial antioxidant defense, gluconeogenesis, urea cycle function, and connective tissue synthesis — yet potently neurotoxic at the hundredfold-higher doses encountered occupationally (welders, miners, battery workers) and in patients on long-term parenteral nutrition with inadequately controlled trace mineral content.

85480 studies View Profile 

](/compound/manganese)

Free 2026 Peptide Cheat Sheet — 50 pages, PDF

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[Download Free](/guides/peptide-cheat-sheet-download?utm_source=compound-iron)

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