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Salem Health: Nutrition

Iron

by Cherie Marcel, BS, Suzanne Dixon, MPH, MS, RD

What We Know

Iron (Fe) is an essential trace mineral that was first recognized as an essential nutrient in the 1860s. The average adult human body contains 3–4 g of iron, nearly 70% of which is found in RBCs as part of the heme portion of the hemoglobin molecule that carries oxygen to body cells. In the body, iron is stored as ferritin and hemosiderin; these stored forms of iron account for about 25% of total body iron. The remainder exists in myoglobin (i.e., the oxygen-carrying molecular found in cardiac and skeletal muscles); as a key component of numerous enzymatic pathways; as transferrin, a blood plasma protein that is the transport form of iron; and as the labile iron pool, a rapidly recycling form of iron that is directly involved in cell iron prodiction.

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  • About 90% of iron is recycled and reused by the body. Iron is essential for oxygen and carbon dioxide transport. It is necessary for aerobic energy production due to its role as a component of enzymes, and as an electron transporter in the metabolic pathway (called the Krebs cycle) that converts carbohydrate, protein, and fat into usable energy. Iron-deficiency anemia is common among women and children. Up to 58% of healthy young women have some level of iron-deficiency anemia, and more than 9% of children under 3 years are iron deficient. Paradoxically, iron is highly toxic in large amounts, and iron poisoning is the most common cause of fatal poisoning in children under the age of 5 years.

Action of Iron

  • Key functions of iron arise from its role in oxidation and reduction (called redox) reactions, which is the ability to donate and accept electrons. This electron transport activity is critical to how hemoglobin and myoglobin transport oxygen and carbon dioxide.

  • Iron is present in enzymes that drive the conversion of energy from food, in the form of calories, into cellular energy, which is supplied by adenosine triphosphate (ATP).

  • The cytochrome P-450 system, which breaks down compounds that are foreign to the body (called xenobiotics) requires iron to convert water-insoluble medications into water-soluble compounds for excretion.

  • Iron is chemically reactive and must be protein-bound in the body to prevent damage to cell membranes and DNA. The tissue damage associated with iron overload syndromes (e.g., hemochromatosis) is due to iron’s highly reactive nature.

  • The many important roles of iron in the body are evident in the wide range of signs and symptoms present in persons with iron deficiency, including lethargy, breathlessness, headaches, irritability, dizziness, weight loss, deficits in learning and concentration, difficulty maintaining body temperature, and reduced immunity.

Sources of Iron

  • Dietary iron is present in heme and nonheme forms. Heme iron is bound in the hemoglobin molecule. Because hemoglobin is present only in organisms with blood, heme iron comes exclusively from foods of animal origin, including meat, fish, and poultry. Plants and iron-fortified foods provide non-heme iron, which is not part of the hemoglobin molecule, to the diet. Heme iron is more absorbable than non-heme iron (15–45% compared with 1–15%), but non-heme iron accounts for more total iron in the diet. Good sources of iron include the following:

    • Heme iron

      • Organ meats, such as liver and kidney

      • Beef, chicken, and fish

      • Oysters, crab, shrimp, and other shellfish

    • Non-heme iron

      • Fortified cereals, bread, pasta, and rice

      • Beans, lentils, and chickpeas

      • Green leafy vegetables, especially spinach

      • Tofu and other soy products

      • Canned tomato products

      • Molasses

      • Raisins

    • Dietary supplements can be used to increase iron intake and correct deficient serum levels of iron-containing compounds, such as hemoglobin, hematocrit, ferritin, and transferrin in individuals with inadequate dietary intake or impaired iron absorption.

    • The preferred route of iron administration is oral.

    • 325 mg of ferrous sulfate 3 times daily is recommended for individuals with iron deficiency.

    • Iron supplementation can cause gastrointestinal (GI) effects, including nausea, constipation, and diarrhea. Reduction of the dose of iron supplementation, followed by a gradual increase in dose over several days, may improve tolerance.

      • Increasing fiber intake may help alleviate constipation associated with iron supplementation.

    • Patients prescribed oral iron supplements should be advised that iron will darken stools. In liquid iron preparations, a straw or spoon should be used to place the liquid iron at the back of the mouth to avoid staining the teeth.

    • Ferrous sulfate is best absorbed on an empty stomach.

    • Vitamin C–rich foods, such as citrus fruit, can increase non-heme iron absorption.

    • Other iron formulations, such as ferrous gluconate and ferrous fumarate, typically cause fewer GI adverse effects; these forms of iron are less readily absorbed and should be prescribed only for patients who do not tolerate ferrous sulfate.

    • Iron supplementation should continue for several months after resolution of iron-deficiency anemia to allow for rebuilding of iron stores.

Recommended Intake of Iron

  • Recommended dietary intake of iron (mg/day) has been established for various age groups:

    • Birth to 6 months: 0.27 mg

    • 7–12 months: 11 mg

    • 1–3 years: 7 mg

    • 4–8 years: 10 mg

    • 9–13 years: 8 mg

    • Adolescents, 14–18 years

      • Females: 15 mg

      • Males: 11 mg

    • Adults, 19–50 years

      • Females: 18 mg

      • Males: 8 mg

    • Adults, 51+ years: 8 mg

    • Pregnant women: 27 mg

    • Lactating women: 9 mg

Iron Deficiency

  • The World Health Organization (WHO) cites iron deficiency as the number one nutritional disorder in the world. It is reported that up to 80% of people worldwide are iron deficient, and 30% exhibit clinically evident iron-deficiency anemia. Iron-deficiency anemia is the most common form of anemia worldwide, and can arise from low dietary intake of iron, inadequate absorption of iron, or excessive blood loss. Iron deficiency anemia affects 47% of preschool children, 30% of women of childbearing age, and 42% of pregnant women worldwide.

  • Populations at risk for iron deficiency include:

    • preterm and low birth weight infants

    • breastfed infants who do not receive iron supplementation

    • infants and young children who consume large quantities of milk and too few iron-containing foods; milk contains minimal iron and calcium inhibits iron absorption from the diet as well

    • pregnant women, especially those with a history of 2 or more previous pregnancies or who have had several pregnancies in a short period of time

    • women of childbearing age and women with heavy menstrual blood loss

    • women on low-calorie diets (e.g., < 1,500 calories/day); for smaller individuals, a low calorie intake may be adequate to maintain weight but lacks sufficient dietary iron

    • persons with protein-energy malnutrition (e.g., persons failing to consume adequate calories and protein to sustain health and/or promote growth in children)

    • persons with kidney failure, especially those treated with dialysis

    • patients who have had a partial or complete gastrectomy (i.e., removal of parts of the stomach)

    • persons with achlorhydria (i.e., low or absent gastric acid production)

    • patients receiving medical treatments that decrease the number of red blood cells and/or platelets (e.g., chemotherapy)

    • patients who have experienced significant blood loss due to injury or surgery

    • persons with vitamin A deficiency

    • persons with conditions involving inflammation of the small intestine (e.g., Crohn’s disease)

  • Body stores of iron vary from person to person; women and children often have little ferritin and hemosiderin (e.g., stored forms of iron) compared to men.

  • Persons with mild iron-deficiency may have no signs and symptoms due to physiologic compensation; iron is shifted from storage (e.g., ferritin) to hemoglobin, which prevents overt symptoms such as fatigue and lethargy. Serum hemoglobin levels may indicate a person has a normal iron status, but tests of other forms of iron will indicate the early stages of iron deficiency.

  • If men or postmenopausal women are iron-deficient, evaluation for the source of iron loss is needed; gastrointestinal blood loss is the most common cause of iron deficiency in these populations.

  • Signs, symptoms and health consequences of more pronounced iron deficiency include fatigue; lethargy; weakness; breathlessness; headaches; irritability; dizziness; weight loss; deficits in learning and concentration; difficulty maintaining body temperature; impaired immunity, exercise intolerance; constipation, menstrual irregularity; muscle twitching; tingling and numbness in the extremities; tinnitus; heart palpitations; growth retardation, reduced school achievement, and impaired motor and cognitive development in children, pallor, fingernail “spooning;” blue-tinged sclera (i.e., whites of the eyes have blue tint); pica (i.e., craving for nonnutritional items such as ice, chalk, or clay); esophageal stricture (e.g., as occurs in Plummer-Vinson syndrome); glossitis; and angular stomatitis (i.e., irritation and cracking at the corners of the mouth).

Iron Toxicity and Medication Interaction

  • Other than through blood loss, the body does not readily secrete iron. This means that chronic iron toxicity, which may result from long-term, excessive iron intake (e.g., high dose supplementation when a person is not iron deficient), or from medical conditions leading to excessive iron absorption (e.g., hemochromatosis), is a serious concern.

  • Iron poisoning, which refers to acute iron overload typically resulting from a one-time iron overdose, is the most common cause of fatal poisoning in children under the age of 5 years.

    • The one-time dose of iron that leads to signs and symptoms of acute iron poisoning in children is dependent upon the size and weight of the child. Iron toxicity signs and symptoms in children begin to appear at doses of 10 mg of iron per kg of body weight of the child (for details, see the bulleted statement on iron overdose signs and symptoms, below).

    • Signs and symptoms of acute iron poisoning in adults begin to appear after a one-time ingestion of > 20 mg of iron per kg of body weight.

    • More severe acute iron poisoning, in which some of the toxic effects may not be reversible, occurs in adults when one-time iron intake exceeds 40 mg of iron per kg of body weight.

    • A one-time iron dose exceeding 60 mg of iron per kg of body weight can result in severe toxicity, and can be lethal in persons of all ages.

  • Signs and symptoms of acute iron poisoning occur in 5 somewhat overlapping stages, and are defined as gastrointestinal (stage 1), latent (stage 2), metabolic/cardiovascular (stage 3), hepatic (stage 4), and delayed (stage 5)

    • Stage 1: initial signs and symptoms typically develop within 6 hours of overdose and include vomiting, vomiting of blood, diarrhea, abdominal pain, irritability, drowsiness, unconsciousness, and seizures; rapid breathing, rapid heart rate, low blood pressure, and coma may develop.

    • Stage 2: within 6–48 hours after overdose, the condition appears to improve, with lessening of signs and symptoms; improvement is not an indication that the poisoning is resolving, but rather indicates a lull before onset of stage 3 signs and symptoms.

    • Stage 3: signs and symptoms 12–48 hours after overdose include very low blood pressure, which can lead to shock; fever; bleeding; jaundice (i.e., yellowing of skin and eyes) with or without complete liver failure; seizures; and hypoglycemia (i.e., low blood sugar).

    • Stage 4: manifestations 2–5 days after acute iron overdose include confusion, lethargy, and in some cases, coma; liver failure and death may occur due to liver failure, shock, bleeding, and/or blood-clotting abnormalities.

    • Stage 5: signs and symptoms in survivors 2–5 weeks after overdose include GI blockage and/or crampy abdominal pain and vomiting due to constricting scars and severe liver scarring (i.e., cirrhosis).

  • Acute iron poisoning is a medical emergency; treatment includes stomach and whole bowel irrigation to remove unabsorbed iron from the GI tract and administration of iron binders (e.g., deferoxamine) by injection or intravenously; serum iron levels roughly correlate with clinical severity of acute iron poisoning as follows:

    • Normal serum iron: 65–165 µg/dL

    • Mild acute iron poisoning: 165–300 µg/dL

    • Moderate acute iron poisoning: 300–500 µg/dL

    • Severe acute iron poisoning: > 500 µg/dL

  • Iron overload is caused most often by excessive iron absorption in the GI tract from hemochromatosis, ineffective erythropoiesis (i.e., decreased RBC production), or repeated transfusions; chronic high-dose iron supplementation in the absence of iron deficiency may also lead to iron overload.

    • Untreated iron overload leads to iron deposition in soft tissues, resulting in liver dysfunction, diabetes mellitus and other endocrine abnormalities, and/or cardiovascular complications.

    • Iron overload is treated with regular phlebotomy (i.e., intentional blood removal, including for donation). In cases of iron overload in the presence of severe anemia, a medical condition in which hemoglobin values are low but levels of stored iron are excessively high, chelation therapy (e.g., administration of iron binders) may be initiated.

  • Normal serum hemoglobin ranges from 14–17 g/dL for males and 12–15g/dL for females. Low serum hemoglobin is commonly considered an indicator of iron-deficiency anemia. However, normal values for hemoglobin vary slightly from laboratory to laboratory, a serum hemoglobin < 14 mg/dL in adult males and < 12 mg/dL in adult females is considered indicative of iron-deficiency anemia.

  • Depletion of ferritin and hemosiderin, the stored forms of iron, occurs prior to a drop in hemoglobin concentration, so low hemoglobin concentrations indicate long-standing anemia.

  • Indicators of iron deficiency that are more sensitive than serum hemoglobin are serum ferritin and transferrin, and total iron-binding capacity (TIBC); normal values are as follows:

    • Ferritin: 12–300 ng/mL for males, 12–150 ng/mL for females

    • Transferrin: 200–360 mg/dL

    • TIBC: 240–450 µg/dL

  • Other laboratory tests relevant to evaluation of iron levels include hematocrit, red blood cell distribution width (RDW), mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC); normal values are as follows:

    • HCT: 40–50% for males; 36–44% for females

    • RDW: 11–15%

    • MCV: 80–95 femtoliters

    • MCH: 27–31 pg/cell

    • MCHC: 32–36 gm/dL

  • Low values for ferritin, hemoglobin, MCV, MCH, and MCHC indicate iron-deficiency anemia; values for TIBC, transferrin, and RDW increase with iron deficiency

  • If a patient is experiencing an acute phase response (e.g., during infection or acute inflammation), some measures of iron status may be inaccurate representation of true iron status due to alterations in production of blood proteins.

  • Supplemental iron can bind tightly with certain compounds to form iron-drug complexes, if iron is taken concurrently with certain medications. This greatly decreases medication effectiveness; medications with which iron can form iron-drug complexes include tetracycline (i.e., an antibiotic) and its derivatives (e.g., demeclocycline, doxycycline, methacycline, minocycline, oxytetracycline), penicillamine (i.e., a copper binder), methyldopa, levodopa, carbidopa (i.e., medications for Parkinson’s disease), ciprofloxacin (i.e., and antibiotic), thyroxine (i.e., hypothyroidism medication), captopril (i.e., blood pressure lowering medication), and folic acid.

  • Iron supplements can also decrease the efficacy of other medications, including chloramphenicol (i.e., an antibiotic), cimetidine (i.e., heartburn and ulcer medication), nalidixic acid (i.e., an antibiotic), and ofloxacin (i.e., an antiobiotic) and its derivatives (e.g., cinoxacin, enoxacin, levofloxacin, lomefloxacin, norfloxacin, sparfloxacin).

  • To reduce the likelihood that iron will form iron-drug complexes with medications or decrease medication efficacy in any way, it is typically recommended that iron supplements be taken 2 hours before or 2 hours after taking medication.

Research Findings

  • Researchers examined the Childhood Autism Risks from Genetics and the Environment (CHARGE) study to determine if a relationship exists between maternal iron intake and autism spectrum disorder (ASD) risk in offspring. Resulting data indicates that low iron intake, in combination with advanced maternal age (i.e., > 35 years) and metabolic conditions (e.g., DM2 and obesity), is associated with a 5-fold increase in risk of ASD in offspring.

  • The authors of a systematic review of 33 trials involving 13,314 children under the age of 12, concluded that intermittent iron supplementation (i.e., 1–3 times per week rather than daily) is as effective as daily supplementation for improving hemoglobin and ferritin concentrations; but is less effective for preventing anemia.

  • Researchers who conducted a systematic review of 14 studies, found that iron supplementation for at least 2 months has modest positive effects on cognition and psychomotor outcomes in infants and children with anemia.

  • There is some evidence that supplementation with iron and/or zinc can improve ADHD symptoms in children who are deficient in these nutrients. Supplementation is not recommended for children who are not deficient.

  • Correction of anemia with I.V. iron in patients with heart failure (HF) may improve HF outcomes, but randomized trials are necessary to confirm that this approach is universally beneficial to persons with HF.

  • Observational studies suggest that higher iron intake may be associated with increased risk of Parkinson’s disease, particularly in persons with low serum cholesterol levels and low intake of vitamin C.

  • The hypothesis that high iron intake and high levels of the storage forms of iron contribute to cardiovascular disease through promotion of oxidation is not supported by current literature.

  • Obesity is associated with iron deficiency. Results of a study conducted on rats showed that the larger rats required more iron than the lean rats, independent of hepcidin, inflammation, or intestinal iron absorption. Increasing food consumption did not meet the higher iron needs of the larger rats. Researchers suggest that obesity increases the susceptibility to iron deficiency due to higher iron needs that are not easily met through diet.

  • Results of a prospective, observational study conducted on 316 newborns with risk factors of infantile iron deficiency anemia (IDA) indicate that maternal obesity and excessive weight gain during pregnancy are independent risk factors for iron deficiency in offspring.

Summary

Consumers should become knowledgeable about the role and importance of iron. Iron is necessary for the production of red blood cells, DNA, and energy. A well-balanced diet includes good sources of iron such as beef, chicken, fish, green vegetables, and beans. Vitamin C rich foods are known to increase the body’s absorption if iron. Iron-deficiency anemia is the most common form of anemia worldwide. Signs and symptoms of iron deficiency include fatigue, weakness, and dizziness. The body does not readily excrete iron so certain individuals should be aware of the potential for iron poisoning from excessive intake or supplementation. Individuals should be aware of the potential interactions between iron and certain medications. Research studies on the physiological impact of iron intake and supplementation suggest the following; maternal iron intake may decrease the risk of autism in children, iron supplementation may improve cognition and reduce ADHD symptoms in children, higher iron intake may reduce the risk of developing Parkinson’s disease, I.V. iron correction of anemia in heart failure patients may improve outcome, and obesity may be linked to iron deficiency.

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Reviewer(s)

Darlene Strayer, RN, MBA, Cinahl Information Systems, Glendale, CA

Jennifer Kornusky, RN, MS, Cinahl Information Systems, Glendale, CA

Nursing Executive Practice Council, Glendale Adventist Medical Center, Glendale, CA

Citation Types

Type
Format
MLA 9th
Marcel, Cherie, and Suzanne Dixon. "Iron." Salem Health: Nutrition, edited by Sharon Richman, Salem Press, 2016. Salem Online, online.salempress.com/articleDetails.do?articleName=Nutr_0292.
APA 7th
Marcel, C., & Dixon, S. (2016). Iron. In S. Richman (Ed.), Salem Health: Nutrition. Salem Press. online.salempress.com.
CMOS 17th
Marcel, Cherie and Dixon, Suzanne. "Iron." Edited by Sharon Richman. Salem Health: Nutrition. Hackensack: Salem Press, 2016. Accessed December 14, 2025. online.salempress.com.