Iron

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).

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.

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.

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.

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.

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.

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.

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.

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.

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.