Supplements

Iron

Updated · 24 sources · Editorial policy

Iron is an essential mineral. Most of the body’s iron sits in hemoglobin, the protein in red blood cells that carries oxygen, and the rest is stored or built into muscle myoglobin and energy-producing enzymes. As a supplement it is sold mainly as iron salts such as ferrous sulfate, and as chelated forms such as ferrous bisglycinate.

Iron is a two-sided nutrient for athletes and for people using performance drugs. Iron deficiency is common in endurance athletes, especially women, and iron supplements can correct it. Yet the body controls its iron mainly through absorption rather than excretion, so too much can build up, and accidental overdose of iron products was once a leading cause of fatal poisoning in young children. That is why US law requires a warning on every iron-containing supplement in tablet or capsule form.

This page summarizes what the National Academies’ Dietary Reference Intakes, clinical trials, meta-analyses and US regulations report. It is for education only and is not medical advice.

Property Detail
Class Essential trace mineral; dietary supplement and over-the-counter iron salts
Common oral forms Ferrous sulfate, ferrous fumarate, ferrous bisglycinate
Typical tablet 325 mg ferrous sulfate supplies 65 mg of elemental iron
Adult RDA 8 mg/day for men and for women over 50; 18 mg/day for women 19–50; 27 mg/day in pregnancy
Adult upper limit (UL) 45 mg/day, set to avoid stomach and gut side effects
Body iron turnover Biologic half-life of body iron ≈1,200–1,300 days in non-exercisers and ≈1,000 days in trained distance runners
Key regulator Hepcidin, a liver hormone that blocks iron entry into the blood
US label rule Mandatory accidental-overdose warning on solid oral iron supplements (21 CFR 101.17(e))
WADA status Iron is not named on the list; IV infusions over 100 mL per 12 hours are a prohibited method

What it is

A 75 kg adult man carries about 4 g of iron, roughly 50 mg/kg; a menstruating woman has about 40 mg/kg (Institute of Medicine DRI report, 2001). The report describes where it sits:

Location Share of body iron Role
Hemoglobin in red blood cells Almost two-thirds Carries oxygen from lungs to tissues
Readily mobilized stores (ferritin, hemosiderin) About 25% Reserve for new red cells
Myoglobin and enzymes Most of the remaining ≈15% Oxygen diffusion inside muscle; energy metabolism

Iron works by switching between its ferrous (+2) and ferric (+3) forms, which lets it carry electrons and bind oxygen. In muscle, myoglobin speeds the movement of oxygen from capillaries to mitochondria, and its concentration falls sharply in tissue iron deficiency (IOM 2001).

Food contains two kinds of iron:

  • Heme iron, from hemoglobin and myoglobin in meat and fish, is highly bioavailable and little affected by the rest of the meal.
  • Nonheme iron, from plant foods, dairy and iron salts, makes up most dietary iron. Its absorption depends heavily on the meal and on the body’s iron status.

How it works in the body

Absorption is the only control point

Outside of bleeding, menstruation and pregnancy, the body loses only a small amount of iron each day. Adult men need to absorb only about 1 mg/day to stay in balance, and menstruating women about 1.5 mg/day on average (IOM 2001). Balance is kept by adjusting absorption in the upper small intestine. As iron stores rise, the percentage absorbed falls.

The hormone that sets this is hepcidin. It is made in the liver in response to iron loading and inflammation. In cell-culture work, hepcidin bound ferroportin, the iron exporter on gut cells, macrophages and liver cells, which caused ferroportin to be pulled inside the cell and degraded, cutting off iron export (Nemeth et al., Science 2004). High hepcidin therefore means less iron absorbed and less iron released from stores. The drug rusfertide is a synthetic hepcidin mimetic built on this mechanism.

What raises or lowers absorption

The DRI report lists these meal factors for nonheme iron (IOM 2001):

Factor Effect reported
Ascorbic acid (vitamin C) About 2-fold higher absorption with 25 mg added to a meal, 3- to 6-fold with 50 mg
Meat, fish, poultry Supply heme iron and enhance nonheme iron absorption
Phytate (legumes, rice, grains) Inhibits absorption in proportion to phytate content
Polyphenols (tea, coffee, red wine) Markedly inhibit absorption
Calcium 300–600 mg added to wheat rolls cut iron absorption by 50–60%

Overall, the report estimated that about 18% of iron is absorbed from a mixed Western diet but only about 10% from a vegetarian diet. On that basis it concluded that the iron requirement is 1.8 times higher for vegetarians.

Ferritin as a measure of stores

Serum ferritin tracks the size of iron stores in healthy people. In adults, each 1 mcg/L of serum ferritin corresponds to about 8 mg of stored iron, and below 12 mcg/L the stores are totally depleted (IOM 2001). The RDA was set to maintain normal function with only a minimal store, marked by a ferritin of about 15 mcg/L. Ferritin can also be raised by fatty liver disease and alcohol-related liver disease, so a high value does not always mean iron overload (Kowdley et al., ACG guideline 2019).

The NIH Office of Dietary Supplements fact sheet could not be retrieved for this page, so the values below come directly from the National Academies (then Institute of Medicine) DRI report (IOM 2001). All values are total iron from food and supplements.

Group RDA (mg/day) UL (mg/day)
Boys and girls 9–13 years 8 40
Boys 14–18 years 11 45
Girls 14–18 years 15 45
Men 19 and older 8 45
Women 19–50 years 18 45
Women 51 and older 8 45
Pregnancy 27 45
Lactation, 19–50 years 9 45

The adult UL is based on gut side effects, not on organ damage. In a double-blind Swedish study, 60 mg/day of supplemental iron as fumarate caused significantly more constipation and total side effects than placebo. The panel added 11 mg/day of food iron to get a lowest-effect level of about 70 mg/day, then divided by an uncertainty factor of 1.5 to reach 45 mg/day (IOM 2001).

The report notes that the UL may not protect people with hemochromatosis, chronic alcoholism or other liver disease, thalassemias and other iron-loading disorders. It also notes that the UL is set for daily intake, and that medically supervised intermittent dosing can exceed it.

A typical ferrous sulfate tablet contains 65 mg of elemental iron, listed as 361% of the Daily Value (ferrous sulfate supplement label, DailyMed). A single tablet therefore supplies more than the adult UL.

Iron in athletes

Why athletes run low

The DRI report summarizes several routes by which hard training drains iron (IOM 2001):

  • Higher daily losses. One estimate put losses at 1.75 mg/day in male athletes and 2.3 mg/day in female athletes during prolonged training, against about 1.08 mg/day in adult men and 1.45 mg/day in menstruating women generally.
  • Faster turnover. Highly trained distance runners had a biologic half-life of body iron of about 1,000 days, compared with 1,300 and 1,200 days in male and female non-exercisers.
  • Blood loss and red cell breakdown. Gut bleeding after running, blood in the urine, and rupture of red cells in the foot during running have all been proposed.

For these reasons, the report estimated that the average requirement is at least 30% higher in people who do regular intense exercise, and possibly up to 70% higher in athletes.

Exercise also raises hepcidin. An individual-participant meta-analysis found that exercise is associated with a 1.5- to 2.5-fold rise in hepcidin, which peaks 3–6 hours after the session. Longer sessions produced larger rises (Fensham et al., Sports Med 2023). This temporarily reduces how much iron can be absorbed from food or supplements in that window.

A 2019 narrative review reported iron deficiency in roughly 15–35% of female athlete cohorts and 5–11% of male athlete cohorts (Sim et al., Eur J Appl Physiol 2019). A 2025 systematic review gave a figure of up to 60% in female athletes (Pengelly et al., J Sport Health Sci 2025).

Blood donation is a further loss. One 0.5 L donation removes 200–250 mg of iron, and donors have lower ferritin than non-donors (IOM 2001).

What the research shows

Iron-deficient athletes without anemia

The open question is whether iron helps athletes who have low stores (low ferritin) but normal hemoglobin, a state called iron deficiency without anemia (IDNA). Four reviews reach different conclusions:

Review Studies, participants Main finding
Burden et al., BJSM 2015 (meta-analysis, IDNA endurance athletes) 17 studies Large effect on ferritin (Hedges’ g 1.09, 95% CI 0.91–1.26); moderate effect on hemoglobin (g 0.70) and VO2max (g 0.61, 95% CI 0.40–0.82)
Rubeor et al., Sports Health 2018 (systematic review, IDNA athletes) 12 studies, 283 participants Performance improved in 6 studies and not in 6; evidence “equivocal.” All positive studies used oral iron and treated athletes with ferritin ≤20 mcg/L
Houston et al., BMJ Open 2018 (meta-analysis of RCTs, IDNA adults, not only athletes) 18 trials, 1,170 participants Less self-reported fatigue (SMD −0.38, 95% CI −0.52 to −0.23); no difference in VO2max (SMD 0.11, 95% CI −0.15 to 0.37) or timed exercise tests
Pengelly et al., J Sport Health Sci 2025 (systematic review, iron-deficient female athletes, ferritin under 40 mcg/L) 23 studies, 669 athletes Endurance performance improved 2–20% with about 100 mg/day oral elemental iron for up to 56 days; most studies had 20 or fewer athletes per group

Taken together:

  • Iron reliably raises ferritin and iron markers in deficient athletes.
  • Whether it improves performance is less certain. The Burden meta-analysis found a moderate VO2max gain, but the Houston meta-analysis of randomized trials did not.
  • Benefits appear more likely when ferritin is very low (around 20 mcg/L or less) at the start.
  • The trials are small, and none supports iron in athletes whose stores are already normal.

Daily vs alternate-day dosing

A series of stable-isotope trials from ETH Zurich changed how oral iron dosing is studied. The key finding: a dose of 60 mg or more raises hepcidin for about 24 hours, which blunts absorption of the next day’s dose.

Trial Participants Design Main result
Moretti et al., Blood 2015 54 non-anemic women, ferritin ≤20 mcg/L 40–240 mg labeled ferrous sulfate, single or consecutive days 24 h after doses ≥60 mg, hepcidin rose and fractional absorption fell 35–45%. A sixfold higher dose (40 to 240 mg) gave only a threefold rise in iron absorbed (6.7 to 18.1 mg)
Stoffel et al., Lancet Haematol 2017, study 1 40 iron-depleted women (ferritin ≤25 mcg/L) 60 mg daily for 14 days vs alternate days for 28 days Cumulative fractional absorption 21.8% vs 16.3% (p = 0.0013); total absorbed 175 mg vs 131 mg, favoring alternate days
Stoffel 2017, study 2 20 women 120 mg once vs 60 mg twice daily No difference in absorption; split dosing raised hepcidin more
Stoffel et al., Haematologica 2020 19 women with iron-deficiency anemia 100 or 200 mg ferrous sulfate, consecutive vs alternate days (crossover) Fractional absorption 40–50% higher on day 2 and day 5 than on day 3, the second consecutive day
von Siebenthal et al., EClinicalMedicine 2023 150 women, ferritin ≤30 mcg/L 100 mg daily for 90 days vs alternate days for 180 days, double-blind Same ferritin at equal total dose (43.8 vs 44.8 mcg/L); GI side effects 1.56 times as frequent with daily dosing; iron deficiency at 6 months 11.4% vs 3.0%

These trials were done in young women, mostly with ferrous sulfate, and measured absorption and ferritin rather than athletic performance. The 2017 authors noted that their results needed confirmation in women with anemia, which the 2020 trial then provided.

Ferrous sulfate vs ferrous bisglycinate

Ferrous sulfate is the standard, inexpensive iron salt. Ferrous bisglycinate is an iron–amino acid chelate that is thought to be better absorbed and to cause fewer GI side effects (Fischer et al., Nutr Rev 2023).

A meta-analysis of 17 randomized trials compared bisglycinate with other iron supplements for at least 4 weeks (Fischer et al., Nutr Rev 2023):

  • Pregnant women (9 trials): bisglycinate for 4–20 weeks gave higher hemoglobin (SMD 0.54, 95% CI 0.15–0.94) and fewer GI adverse events (incidence rate ratio 0.36, 95% CI 0.17–0.76). Ferritin showed only a non-significant trend.
  • Children (4 trials): no significant difference in hemoglobin or ferritin.
  • Men and non-pregnant women (4 trials): too few to pool; the authors called for more trials.

No trial in athletes was included, so the advantage of bisglycinate in this group is untested.

Side effects and risks

Gut side effects

Constipation, nausea, vomiting and diarrhea are the most common effects of iron supplements. The DRI report notes that the effects depend on how much elemental iron is released in the stomach, and are reduced when iron is taken with food (IOM 2001). In one 8-week study, 50% of people taking 50 mg/day of iron as ferrous sulfate reported moderate-to-severe GI effects.

A meta-analysis of 43 randomized trials with 6,831 adults found that ferrous sulfate raised the odds of GI side effects compared with placebo (OR 2.32, 95% CI 1.74–3.08) and compared with intravenous iron (OR 3.05, 95% CI 2.07–4.48). It found no clear relationship with dose (Tolkien et al., PLoS One 2015).

Accidental overdose in children

FDA regulations require every dietary supplement in tablet or capsule form that contains iron as an iron source to carry this boxed warning (21 CFR 101.17(e)):

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.

The DRI report describes acute iron poisoning as starting with vomiting and diarrhea, then involving the heart, nervous system, kidneys, liver and blood. Symptoms occur at 20–60 mg/kg of elemental iron, with gut irritation at the low end and systemic toxicity at the high end (IOM 2001).

FDA also issued a regulation requiring unit-dose packaging of iron supplements in 1997. Comparing the 10 years before with the 5 years after, iron ingestion calls per 1,000 poison-center calls for children under 6 fell from 2.99 to 1.91, and deaths fell from 29 to 1 (Tenenbein, Arch Pediatr Adolesc Med 2005). The packaging requirement was removed in 2003, but a later analysis of US poison data from 2000–2017 found that severe pediatric iron exposures continued to decline (Leonard et al., Clin Pediatr 2020).

Hemochromatosis and iron overload

Hereditary hemochromatosis is a genetic disorder in which the body absorbs too much iron. It affects between 1 in 200 and 1 in 400 people of northern European descent. In people of Celtic ancestry, a single mutation of the HFE gene (C282Y) is found in over 90% of affected individuals (IOM 2001). Iron builds up in the liver, and liver iron accumulation is a clear risk factor for liver cancer in hemochromatosis.

The American College of Gastroenterology guideline states that (Kowdley et al., Am J Gastroenterol 2019):

  • a serum ferritin under 1,000 ng/mL at diagnosis identifies patients at low risk of advanced liver fibrosis;
  • ferritin can also be raised by fatty liver disease and alcohol-related liver disease, which are more common causes of high ferritin than hemochromatosis in people who are not C282Y homozygotes;
  • phlebotomy (removing blood) remains the mainstay of treatment.

The DRI report lists hemochromatosis among the conditions in which people may not be protected by the UL, and states that a safe upper intake for this group cannot yet be set (IOM 2001). The report also called for effective and widespread screening for early detection of hemochromatosis.

Interactions

  • Antibiotics. The ferrous sulfate supplement label states that oral iron interferes with absorption of certain antibiotics and that the two should not be taken within two hours of each other (DailyMed).
  • Zinc. Large iron doses inhibit zinc absorption when both are taken fasting, but not when taken with food (IOM 2001).
  • Calcium, tea and coffee. These reduce nonheme iron absorption (see the table above).

Testosterone, high hematocrit and iron

Testosterone raises hemoglobin and hematocrit (the share of blood made up of red cells), and part of this effect runs through iron regulation. This section summarizes what studies report; it is not guidance on iron use for anyone on testosterone.

  • Testosterone suppresses hepcidin. In 109 healthy men given weekly testosterone enanthate (25–600 mg) for 20 weeks with their own testosterone suppressed, high testosterone levels markedly suppressed serum hepcidin within one week. The suppression was dose-dependent in older men, and hepcidin at weeks 4 and 8 predicted the later rise in hematocrit (Bachman et al., JCEM 2010).
  • Ferritin falls as red cell production rises. In older men randomized to testosterone gel or placebo for 6 months, hemoglobin and hematocrit rose 7–10%. This came with higher erythropoietin and lower ferritin and hepcidin at 1 and 3 months, consistent with stored iron being drawn into new red cells (Bachman et al., J Gerontol A 2014).
  • Phlebotomy depletes iron. A 2024 review of testosterone-induced erythrocytosis found that evidence for the efficacy and safety of therapeutic phlebotomy is lacking. It noted that phlebotomy eventually depletes iron stores, which might itself trigger pathways that raise thrombotic risk (Bond et al., Endocr Connect 2024).

None of these studies tested iron supplementation in men using testosterone. Low ferritin in this setting can reflect increased iron use for red cells or iron removed by phlebotomy and blood donation, rather than a simple dietary shortfall. For how the testosterone itself drives hematocrit, see testosterone cypionate. For a hepcidin-mimetic drug that lowers hematocrit by restricting iron supply to the marrow, see rusfertide.

Erythropoietin also ties red cell production to iron supply. The EPO (epoetin alfa) label instructs prescribers to evaluate iron status before and during treatment, and to give supplemental iron when ferritin is under 100 mcg/L or transferrin saturation is under 20%. It adds that most patients with chronic kidney disease will need supplemental iron during treatment (Epogen label, DailyMed).

In the US, iron is sold as a dietary supplement and as over-the-counter iron salts. Solid oral iron supplements must carry the accidental-overdose warning described above (21 CFR 101.17(e)).

Iron is not named on the WADA Prohibited List. However, intravenous infusions or injections totaling more than 100 mL per 12 hours are a prohibited method (M2.2), except when legitimately received in hospital treatment, surgery or clinical investigations (WADA 2026 Prohibited List).

Key takeaways

  • Requirements differ widely. The adult RDA is 8 mg/day for men and 18 mg/day for women aged 19–50, and about 1.8 times higher for vegetarians. The National Academies estimate needs are 30–70% higher in athletes who train intensely.
  • The adult UL is 45 mg/day. It is based on gut side effects; one standard 325 mg ferrous sulfate tablet supplies 65 mg of iron.
  • Iron helps deficient athletes’ iron status, less clearly their performance. Meta-analyses agree that iron raises ferritin; results on VO2max conflict, and benefits look most likely when ferritin is around 20 mcg/L or lower.
  • Alternate-day dosing absorbs better. In ETH Zurich trials in iron-depleted women, single doses on alternate days gave higher fractional absorption and fewer GI side effects than daily or split dosing.
  • Overload and poisoning are real risks. Hemochromatosis affects about 1 in 200–400 people of northern European descent, and iron overdose was a leading cause of fatal childhood poisoning, which is why labels carry a mandatory warning.
  • Testosterone changes iron handling. It suppresses hepcidin and draws down ferritin as red cell production rises, but no trial has tested iron supplements in this setting.

Sources

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