InteractionsGuide Index Page

Case Analysis Toolclose
Enter Each Substance:

Analysis Search Terms:


Nutrient Name: Iron.
Synonyms: Iron salts; fer; ferric sulfate; ferrous carbonate anhydrous, ferrous citrate, ferrous fumarate, ferrous gluconate, ferrous glutamate, ferrous glycinate, ferrous glycine sulphate, ferrous lactate, ferrous picolinate, ferrous pyrophosphate, ferrous succinate, ferrous sulfate; carbonyl iron; iron-polysaccharide, iron dextran, iron-ovotransferrin, iron sorbitol, iron sucrose, sodium ferric gluconate.
Elemental Symbol: Fe.

Summary Table
Drug/Class Interaction TypeMechanism and SignificanceManagement
Acetylsalicylic acid (ASA, aspirin)
Aspirin causes gastrointestinal (GI) irritation and bleeding, which may be slight but acts cumulatively with chronic use to increase risk of iron deficiency and anemia. Iron supplementation can reverse adverse hematological effects of ASA therapy.Short-term iron may be appropriate if deficiency or depletion present; separate intake, monitor. Address dietary and lifestyle factors contributing to inflammation and pain.
Angiotensin-converting enzyme (ACE) inhibitors
/ / /
Coadministration of iron can abolish cough induced by ACE inhibitors, possibly by inhibiting NO synthase activity in bronchial epithelial cells. However, iron and ACE medications may bind and reduce absorption of both agents. IV iron may be appropriate in certain anemic hemodialysis patients treated with an ACE inhibitor but this treatment is controversial, complicated, and risky.Coadminister, when indicated. Separate intake by 3 or more hours. IV iron requires active supervision by experienced provider(s), with broad antioxidant support.
Antacids and gastric acid–suppressive medications
Histamine (H2) receptor antagonists
Proton pump inhibitors (PPIs)
/ /
Inhibition of gastric acid environment can inhibit reduction of ferric iron and reduce absorption and bioavailability of dietary iron. History of GI bleeding and increased risk of iron depletion common in patient population. Some agents may bind with iron and impair absorption of either or both substances. Adverse effects on iron status may be slow to develop and difficult to assess.Short-term iron may be appropriate if deficiency or depletion present; separate intake, monitor. Address dietary and lifestyle factors contributing to dyspepsia, GERD, and ulcers.
Bile acid sequestrants
/ /
Simultaneous intake of iron and bile sequestrants may result in binding and reduced absorption due to formation of poorly absorbed chelate complexes. Drug action may be impaired with interaction. Evidence is limited and inconsistent regarding probability and significance of iron depletion.Low risk of significant interaction if oral intake separated by at least 2 hours.
Binding may occur with simultaneous intake and inhibit absorption and bioavailability of both agents. Decreased therapeutic activity probable with interaction; minimal effect with separation of intake. Limited evidence on long-term effects.If iron is indicated, separate intake by 2 or more hours to avoid interference. Monitor iron status.
Carbidopa, levodopa Antiparkinsonian medications
Simultaneous intake of carbidopa or levodopa and iron (especially ferric) may result in binding and reduced absorption due to formation of poorly absorbed chelate complexes. Medication may also cause autoxidation to ferric form.Iron may be contraindicated in this patient population. If indicated, separate intake by at least 2 hours and monitor iron status.
Cephalosporin antibiotics

Chelation between cephalosporin antibiotics and iron likely to impair absorption and bioavailability of both agents if ingested concurrently. Decreased therapeutic activity with interaction; minimal effect with separation of intake. Iron depletion plausible with extended use, but not established or probable. Caution warranted regarding supplementation during infection.Discontinue iron or separate intake during short-term therapy. Mineral supplementation may be appropriate with extended therapy but caution warranted; separate intake by several hours.
/ /
Chloramphenicol can inhibit erythropoiesis and red cell maturation, thus delaying or impeding iron therapy; it can also cause aplastic anemia. Dosage levels < 25-30 mg/kg are usually effective without adversely affecting bone marrow.Discontinuation of chloramphenicol may be necessary if treating patients with anemia. Largely replaced by alternatives as a standard treatment in recent years.

Concurrent intake of chlorhexidine and iron may stain teeth.If iron is indicated, separate intake by at least 2 hours to avoid interaction.
/ /
Chelation between clofibrate and iron likely to impair absorption and bioavailability of both agents if ingested concurrently.If iron is indicated, separate intake by 3 hours to avoid interference. Monitor iron status.
/ /
Desferoxamine is a chelating agent applied to treat overload and intoxification involving iron and other metals. It binds to iron and increases iron excretion. Intake of iron (supplemental or as iron-rich foods) is contraindicated, as contrary to the therapeutic intent.Discontinue supplemental iron and decrease dietary intake immediately. Close supervision and monitoring necessary. Supplementation with other nutrients may be appropriate; separate intake by several hours.

Dimercaprol is used as an antidote in arsenic, cadmium, lead, and mercury poisoning in inpatient settings. Iron intake during dimercaprol therapy may cause kidney damage but is often appropriate after such treatment.Avoid supplemental iron during dimercaprol therapy. Close supervision and monitoring necessary. Supplementation with iron may be appropriate 24 hours or more following conclusion of dimercaprol.
/ /
EDTA is a chelating agent applied to treat overload and intoxification involving iron and other metals. It binds to iron and increases iron excretion. Intake of iron (supplemental or as iron-rich foods) is contraindicated, as opposed to the therapeutic intent. Some iron chelates containing EDTA are used for iron fortification.Avoid supplemental iron and decrease dietary intake. Close supervision and monitoring contrary necessary. Supplementation with iron and other nutrients may be appropriate with extended therapy; separate intake by several hours.
Erythropoiesis-stimulating agents
/ / /
Synergistic interaction often used in treatment of oncology patients with functional iron deficiency or anemia but remains controversial. Coadministration may enhance epo-induced erythropoiesis, but risk of adverse effects is significant if applied prematurely, with inadequate iron stores, during anemia of chronic inflammation, or in unstable oncology patients. Further research warranted.
Iron administration in hemodialysis patients is often contraindicated, although oral heme iron may be effective.
Assess endogenous EPO level. Coadminister iron with iron deficiency if no response to initial EPO therapy, under close supervision and monitoring of iron status, especially stores. Oral forms may be safer than IV administration.
Fluoroquinolone/quinolone antibiotics
/ /
Chelation between this class of antibiotics and iron likely to impair absorption and bioavailability of both agents; similarly with other minerals. Decreased therapeutic activity with interaction; minimal effect with separation of intake.
Iron deficiency and effects of iron depletion plausible with extended use, but not established or probable. Iron-ovotransferrin combines directly with gut transferrin receptors and minimizes risk of binding to drug. Caution warranted regarding supplementation during infection.
Avoid iron or separate intake during short-term therapy. Iron-ovotransferrin may be most effective form. Mineral supplementation may be appropriate with extended therapy, but caution warranted regarding iron, even with established depletion; separate intake by several hours.
/ /
Hyoscyamine can impair iron absorption, but mechanism, occurrence, and clinical significance not fully elucidated. Potential for decreased therapeutic activity with simultaneous intake. Iron depletion and effects of iron depletion plausible with extended, use but not established or probable.Iron supplementation with iron or other appropriate minerals may be appropriate with extended therapy; separate intake by several hours.
Nonsteroidal anti-inflammatory drugs (NSAIDs)
/ / / / /
NSAIDs, especially indomethacin, can cause GI irritation and bleeding, which may be slight but acts cumulatively with chronic use to increase risk of iron deficiency and anemia. Iron supplementation can reverse adverse hematological effects of NSAID therapy.Short-term iron may be appropriate if deficiency or depletion present; separate intake, monitor. Address dietary and lifestyle factors contributing to inflammation and pain.
Interferon alpha

Iron excess can contribute to inflammatory processes, support infectious agents, and reduce response to interferon. Iron reduction can enhance positive outcomes in interferon therapy. Phlebotomy may enhance interferon therapy outcomes, as may low-iron diet.Avoid supplemental iron and recommend low-iron, vegetarian diet. Close supervision and monitoring necessary. Phlebotomy may be appropriate.
Thyroid hormones
/ / /
Thyroid therapy may be enhanced with iron coadministration. However, simultaneously ingested thyroxine and iron likely to bind to form poorly soluble chelate complex and thereby impair absorption and bioavailability of both agents. Decreased therapeutic activity with interaction; minimal effect with separate intake. Consensus regarding probability of binding, but evidence lacking for iron depletion, plausible with extended use.Comorbid conditions may require both agents. Separate intake by several hours to avoid binding and interference. Monitor TSH; may need to adjust dosage levels.
/ /
Simultaneously ingested methyldopa and iron likely to bind to form poorly soluble chelate complex and thereby impair absorption and bioavailability of both agents. Decreased antihypertensive activity probable with interaction. Decreased interference with separation of intake. However, medication may also cause autoxidation to the ferric form. Iron depletion and effects of iron depletion plausible with extended use, but not established or probable.If iron is indicated, separate intake by at least 2 hours to avoid interference.
/ / /
Neomycin known to impair absorption of iron and many other nutrients; concurrent intake may alter drug activity. Clinical significance may vary depending on individual's iron status. Iron deficiency and effects of nutrient depletion probable with extended use; adverse effect improbable with short-term or topical use. Caution warranted regarding supplementation during infection.Iron supplementation with iron or other appropriate nutrients may be appropriate with extended therapy, but caution warranted regarding iron, even with established depletion; separate intake by several hours.
Oral contraceptives (OCs)
OCs may support iron status and reduce need for supplementation by reducing menstrual blood loss. Serum ferritin, serum transferrin, serum iron, TIBC, MCH, and MCHC levels may be greater, but RBC and hematocrit levels often lower in OC users. Systemic implications of exogenous hormones, in diverse formulations and with chronic administration, on multiple levels of iron metabolism and storage not fully elucidated. Continued research into responses among variable individuals to these complex medications is warranted.Women using OCs may have reduced need for iron supplementation, although possibly higher needs for folate and vitamins B12and B6. Individual evaluation of safe and effective hormone dosage levels necessary. Periodic assessment of serum ferritin, ferritin saturation, and/or serum transferrin receptor levels may be warranted.
/ / /
Penicillamine is a chelating agent applied to treat overload and intoxification involving copper, iron, and other metals. It binds to iron and increases iron excretion. Intake of iron (supplemental or as iron-rich foods) can bind medication doses when ingested concurrently. However, abrupt discontinuation of ongoing iron intake may lead to rapid elevation in circulating penicillamine levels and resultant nephrotoxicity. Iron intake may also be contraindicated, as opposed to the therapeutic intent, i.e., copper chelation.Avoid concurrent iron and dietary intake; tapered reduction needed in discontinuing supplemental iron. Close supervision and monitoring necessary. Supplementation with iron and other nutrients may be appropriate with extended therapy if depletion detected; separate intake by several hours.
/ /
When ingested concurrently, iron can bind to sulfasalazine, interfering with its breakdown into 5-aminosalicylic acid (5ASA) and sulfapyridine. This pharmacokinetic interaction can reduce absorption, bioavailability, and therapeutic activity of the prodrug, its constituents, and the nutrient, but can be minimized by separation of intake. Iron depletion possible with extended use, particularly in patient population with ulceration and GI bleeding, but not established.Separate intake by several hours to avoid binding and interference. Iron supplementation may be warranted if bleeding, anemia, and/or iron depletion established, but caution is appropriate to avoid aggravating inflammation.
Tetracycline antibiotics
/ /
Chelation between iron and tetracycline-class antibiotics and impaired absorption of both to clinically significant degree probable with concurrent intake. Iron intake, even small amounts, can significantly impair antimicrobial activity. General consensus despite minimal direct evidence. Iron depletion with extended tetracycline use but evidence lacking. Caution warranted regarding supplementation during infection.Discontinue iron (including iron-rich foods) or separate intake during short-term therapy. Iron supplementation may be appropriate with extended therapy, but caution warranted, even with established depletion; separate intake by several hours.
/ / /
Trientine is a chelating agent applied to treat copper overload and toxicity, particularly in Wilson's disease. Simultaneous ingestion with iron likely to bind to form poorly soluble chelate complex and thereby impair absorption and bioavailability of both agents. Anemia is common adverse effect of trientine due to increased iron excretion, as well as decreased iron absorption, with children, menstruating women, and pregnant women at greatest risk.Separate intake by several hours to avoid binding and interference. Iron supplementation may be warranted if anemia and/or iron depletion established; separate intake by several hours.
NO, Nitric oxide; IV , intravenous, GERD , gastroesophageal reflux disease; EPO , erthyropoietin; TSH , thyroid-stimulating hormone; TIBC , total iron-binding capacity; MCH , mean corpuscular hemoglobin; MCHC , MCH concentration; RBC , red blood cell.
nutrient description

Chemistry and Forms

  • Oxidation states: Ferric (Fe3+) iron, ferrous (Fe2+) iron.
  • Heme and nonheme.

Physiology and Function

Iron is an essential mineral that plays a vital role in numerous essential biochemical pathways. The principal functions of iron involve DNA synthesis and cell formation, oxygen sensing and cellular uptake, oxygen transport and storage within blood and muscle, electron transfer and the conversion of glucose to adenosine triphosphate (ATP), both antioxidant and beneficial pro-oxidant functions, and regulation of intracellular iron. Within the human body, iron occurs primarily in functional forms, such as proteins, particularly hemoglobin and myoglobin, and in transport and storage forms, such as transferrin, ferritin, and hemosiderin. Iron is also a constituent of numerous enzymes, amino acids, hormones, and neurotransmitters. Iron is a key component of enzymes responsible for oxidative phosphorylation and ATP generation in the mitochondria and for synthesis of serotonin and dopamine. Iron is essential for the synthesis of carnitine, a critical compound in fatty acid metabolism, and for the operation of the cytochrome P450 system and other cytochromes. It also acts as a cofactor in the synthesis of collagen and elastin.

Iron absorption is highly dependent on maintenance of the normal biochemical environment and coordination of upper gastrointestinal (GI) function. Iron must be in ferrous form to be absorbed. When iron is found in meat, it is in the heme form. When the source of iron is from plants or from animal products such as milk, eggs, and cheese, it is referred to as nonheme iron. In the heme form, once it is cleaved from the food, iron may be converted to hemin (Fe3+), which can be directly absorbed intact by the mucosal cell into the blood. Absorption of heme iron is about 10 times that of nonheme iron, depending on whether body stores are replete. In the nonheme form, iron must be cleaved from its food source, then reduced from the ferric to the ferrous form, facilitated by gastric hydrochloric acid, before it can be absorbed. Likewise, ascorbic acid, found in foods and supplements, increases absorption by keeping the ferrous form from oxidizing to ferric in the gastric environment. Iron absorption is a slow process, taking between 2 and 4 hours, and occurring principally in the duodenum and proximal jejunum. Iron is absorbed from the small intestine in different forms at 5% to 15% of intake. Absorption percentages, as opposed to excretion, are largely responsible for regulation of body iron content and respond to levels of body iron stores. Thus, low body iron levels lead to improved absorption.

Iron is oxidized back to ferric state for transport and then transported within the mucosal cell and in the blood bound to the protein transferrin. Transferrin is usually saturated to about one-third its total iron-binding capacity (TIBC). If no iron is needed, transferrin remains saturated and less is absorbed from the intestinal mucosal cells. The transferrin that remains in the cells eventually is sloughed away with the mucosal cells at the end of their 2- to 3-day life cycle. If iron is needed, the transferrin is less saturated when it reaches the intestinal mucosal cells, and more iron passes from the mucosal cell to the transferrin. Thus, the degree of saturation of transferrin is also used as a measurement of body stores of iron. Iron is stored in the liver, spleen, and bone marrow as ferritin and hemosiderin. The normal human body contains 3 to 4 grams of iron (40-50 mg/kg body weight), 75% of which (∼36 mg/kg) is present in metabolically active compounds. A storage pool maintains the remaining 25% (∼10 mg/kg in men and ∼ 5 mg/kg in menstruating women) in a form that is readily available for use if metabolically active iron is depleted for any reason.

The body's capacity to eliminate iron is limited and, once absorbed, largely occurs through blood loss. Under normal conditions, the largest loss of iron is through bleeding in menstruating women; although considerably greater than other channels, these iron losses vary widely from individual to individual. Very small amounts of iron are also excreted through sweat and normal exfoliation of hair, skin, and nails. Most iron expelled in the feces is nonabsorbed iron from dietary intake.

Hemoglobin and myoglobin are proteins involved in the transport and storage of oxygen that contain heme, an iron-based compound. Hemoglobin is the primary protein responsible for oxygen transport in red blood cells (RBCs) and constitutes approximately two thirds of the iron in the human body. Hemoglobin functions to acquire oxygen efficiently and rapidly during its short contact in oxygenated lung tissue, transporting that oxygen from the lungs throughout the circulatory system and releasing it as needed into the target tissues. Myoglobin is the primary protein responsible for oxygen transport and regulation of short-term oxygen storage within myocytes and for the coordination of oxygen influx with the physiological demands of muscle function. Iron's ability to shift between its ferrous or reduced state (Fe2+) and its oxidized ferric state (Fe3+) enables it to hold or release oxygen and empowers its functional activity in electron transport and energy production.

Iron plays a critical role in the body's ability to sense oxygen and dynamically respond to variable conditions. Prolyl hydroxylase is an iron-dependent enzyme that participates in regulating the body's response to hypoxic conditions, such as high altitude or impaired function caused by lung disease. In particular, hypoxia inducible factors (HIFs) are transcription factors that respond to decreases in cellular oxygen tension characteristic of hypoxic conditions, by binding to genetic response elements that encode various proteins involved in compensatory responses to hypoxia, and increase their synthesis. Thus, in response to cellular oxygen tension, prolyl hydroxylase will either rapidly degrade HIF-alpha subunits or bind them to HIF-beta subunits to create an active transcription factor capable of entering the nucleus and binding to specific response elements on genes.

Iron, in both heme and nonheme forms, is part of several enzymes involved in electron transport, cellular energy production, and cellular detoxification. Cytochromes are heme-containing compounds critical to mitochondrial electron transport in the synthesis of ATP. In the liver the cytochrome P450 family of enzymes, in particular, metabolizes a wide range of biological molecules and exogenous toxins, including detoxification and metabolism of pharmaceuticals. NADH dehydrogenase and succinate dehydrogenase are among several enzymes containing nonheme iron involved in energy metabolism. Iron is also prominent in the synthesis of carnitine, an amino acid that plays an essential role in the metabolism of fatty acids. Thus, in a state of iron deficiency, an individual will fatigue more readily because of inadequate accessible oxygen and impaired synthesis of ATP.

Iron is well known for its tendency to cause oxidative damage, but it is also part of the antioxidant enzymes catalase and peroxidase, which serve to quench potentially damaging reactive oxygen species (ROS). These heme-containing enzymes catalyze the conversion of hydrogen peroxide to water and oxygen and thus prevent its buildup within cells. Myeloperoxidase, another heme-containing enzyme, catalyzes neutrophils to synthesize hypochlorous acid, an ROS, to be used within the immune system's response to pathogenic bacteria.

Iron is intimately involved in a number of other physiological and biochemical processes at cellular and systemic levels. DNA synthesis requires the activities of ribonucleotide reductase, an iron-dependent enzyme. Iron storage and metabolism are managed by key proteins within self-regulatory processes coded by short sequences of nucleotides found in the messenger RNA (mRNA), known as “iron response elements,” in response to changing iron storage levels. In particular, iron regulatory proteins (IRPs) can bind to iron response elements and affect mRNA translation, thereby regulating the synthesis of specific proteins. Thus, iron binds to IRPs to a greater or lesser degree, depending on iron supply to influence relative levels of ferritin, the central iron storage protein; translation of mRNA that regulates enzymatic control of heme synthesis in immature RBCs; and synthesis of transferrin receptors. Iron is also a constituent of the enzymes that initiate the synthesis of serotonin and dopamine. Lastly, iron is essential in the synthesis of collagen and elastin.

nutrient in clinical practice

Known or Potential Therapeutic Uses

Treatment of iron deficiency anemia constitutes the dominant use of supplemental iron within conventional medicine. Standard practice recognizes the increased risks of iron depletion associated with menstrual blood loss but typically responds only reactively and in the narrowest sense of anemia. Modern schools of natural medicine more often recognize the potential value of iron-rich foods and botanical preparations as a tonic therapy within a comprehensive strategy.

Historical/Ethnomedicine Precedent

In the classical medical tradition of Western culture, iron was considered the metal of Mars, and associated with vitality, the qualities of heat and fire, the blood, and inflammatory processes. Historically, traditions of natural medicine have emphasized enhancement of iron intake as part of a broader approach toward enriching the blood through provision of multiple minerals within the context of single herbs, herbal formulae, and nutrient-rich foods. Herbal formulae that “build the blood” have played central roles within many classical and folk herbal traditions around the world, especially in conjunction with strategies to regulate the menstrual cycle and improve hormonal balance, treat or prevent fatigue, and improve stamina and fertility.

Possible Uses

Alzheimer's disease, anemia, athletic performance (with deficiency only), attention deficit–hyperactivity disorder (ADHD), canker sores, celiac disease (with deficiency only), childhood cognitive development (with deficiency), cough, depression (with deficiency), dermatitis herpetiformis, human immunodeficiency virus (HIV) support, infertility (female) (with deficiency only), iron deficiency anemia, lactation support, menorrhagia (heavy menstruation) (with deficiency only), presurgery and postsurgery support (with deficiency, or after major surgery), pregnancy and postpartum support, restless legs syndrome (with deficiency).

Deficiency Symptoms

Iron deficiency is the most common nutrient deficiency in the United States (U.S.) and the world. Mild degrees of iron deficiency are common in U.S. toddlers, teenage girls, and women of childbearing age, although full-fledged iron deficiency anemia remains rare. 1 Most cases of iron deficiency appear according to well-known patterns of susceptibility, malnutrition, depletion, and exacerbation. Nevertheless, because of the numerous risk factors associated with excess iron intake, use of supplemental iron to prevent or treat any of these patterns associated with iron deficiency must be assessed based on individual characteristics, needs, and susceptibilities.

Although iron deficiency is the primary nutritional disorder among humans and perhaps the most studied form of nutritional deficit within conventional medicine, a comprehensive and coherent understanding of its effects and influences, both frank and subtle, immediate and long-term, is just beginning to emerge into a coherent and comprehensive model. Iron deficiency anemia is the most overt and well-known symptom of iron deficiency. However, several gradations of iron depletion, including stages below the threshold and before the appearance of overt pathology, may contribute to physiological dysfunction and adversely affect quality of life. Thus, contrary to common assumptions, an individual does not have to be anemic to be iron deficient. 2 Furthermore, it is also critical to remember that iron deficiency anemia is not the only form of anemia, that other forms of anemia tend to appear in the same population(s), and that factors other than iron status contribute to iron deficiency anemia. In particular, folate and vitamin B12status, as well as confounding factors such as drug-induced depletion patterns, must be considered to adequately diagnose suspected anemia.

Cellular responses to iron deprivation are poorly understood. Emerging evidence indicates that iron deficiency reprograms cellular genetic expression. Puig, Askeland, and Thiele 3 found that a deficiency of iron altered the expression of more than 80 genes in Saccharomyces cerevisiae (yeast) cells, which were chosen because of the similarity of their genome to that of humans. They observed that Cth2, a protein overproduced by iron-deficient cells, binds to the mRNA of over 80 genes and targets it for degradation or destruction by specifically downregulating mRNAs encoding proteins that participate in many iron-dependent processes. Through this proposed mechanism, iron deficiency controls a posttranscriptional regulatory process that coordinately drives widespread metabolic reprogramming. The authors concluded: “We discovered that iron deprivation actually reprograms the metabolism of the entire cell. Literally hundreds of proteins require iron to carry out their proper function, so without this nutrient, there is a complete reorganization of how cellular processes occur.” 3

Iron deficiency may be modeled in the following three levels of increasing severity 4,5

  1. Storage iron depletion. Tissue iron stores are depleted, but the functional iron supply is not limited.
  2. Early functional iron deficiency. The supply of functional iron is low enough to impair RBC formation, but not sufficiently low to cause measurable anemia.
  3. Iron deficiency anemia. Available iron is insufficient to support normal RBC formation, resulting in the microcytic and hypochromic anemia characteristic of iron deficiency. Both inadequate oxygen delivery due to anemia and suboptimal function of iron-dependent enzymes can produce symptoms at this more severe stage of iron deficiency.
  4. Most of symptoms associated with iron deficiency result from the associated anemia; these include fatigue, weakness, pallor, tachycardia, palpitations, dyspnea on exertion, decreased endurance, and excess lactic acid production. Reduced hemoglobin and myoglobin levels associated with iron deficiency will impair physical exertion capacity and athletic performance by limiting oxygen delivery to tissues, reducing oxidative metabolism in mitochondria, diminishing mitochondrial content of cytochromes and other iron-dependent enzymes, and undercutting electron transport and ATP synthesis. Nonhematological effects resulting from iron deficiency include glossitis, taste bud atrophy, canker sores, nail spooning (koilonychia), brittle nails, hair loss, diminished immune function and increased susceptibility to infection, impaired intellectual performance, neurological dysfunction, and increased sensitivity to chill. Plummer-Vinson syndrome, characterized by the formation of webs of tissue in the throat and esophagus and difficulty swallowing, can occur in some advanced cases, possibly corresponding to a genetic predisposition. Children may also manifest behavioral disturbances such as attention deficit–hyperactivity disorder (ADHD) and breath-holding spells. Restless legs syndrome, initial seizure, pica, and pagophagia (excessive ice consumption, characterized in particular by chewing of ice) have also been associated with iron deficiency. Fatigue, weakness, anorexia, and pica may be caused by tissue depletion of iron-containing enzymes and not by decreased levels of blood hemoglobin.

    Conditions contributing to iron deficiency, particularly from blood loss or malabsorption, include diarrhea, ulcers, ulcerative colitis, Crohn's disease, celiac disease, parasitic infections, hemorrhoids, GI cancers, menorrhagia, accidents, injuries, and surgery. Other factors influencing iron absorption and deficiency include hydrochloric acid secretion and gastric pH, decreased dietary intake, blood loss (both internal and external, as in menorrhagia), calcium intake, caffeine intake, high–phytic acid fiber foods, vitamin A, genetic variability, and iron storage levels.

    Populations particularly at risk for compromised iron status include infants and children, age 6 months to 4 years, especially those living in inner cities or other impoverished circumstances; rapidly growing adolescents, especially females after menarche; pregnant women; individuals with acute or chronic blood loss due to medication-induced ulcers or intestinal parasites; frequent blood donors; individuals, especially children, with Helicobacter pylori infection (even without GI bleeding); populations exposed to environmental contaminants, especially lead; and individuals who engage in regular, intense exercise, particularly daily endurance training. All these factors are exacerbated in the context of ongoing menstrual cycles; menstruating women require approximately twice as much iron intake as men to replace their monthly losses due to menses. Although iron deficiency is not usually caused by a lack of iron in the diet alone, vegan or vegetarian diet or dietary intake may increase the risk of deficiency because of less relative bioavailability of iron from plant versus animal sources, at least in some individuals. Nutriture status of all nutrients, including iron, is compromised with poverty or lifestyle choices characterized by high intake of processed and refined foods or other forms of malnutrition.

    Dietary Sources

    The hemoglobin and myoglobin consumed within meat, poultry, oysters, and fish are the primary sources of heme iron in the diet. Approximately 40% of the iron in animal foods is heme iron and 60% is nonheme iron. Heme iron provides up to one third of total absorbed dietary iron, even though it accounts for only 10% to 15% of the iron potentially available in the diet. Nonheme iron is an inorganic compound, less easily absorbed, and derived from plant foods, dairy products, dried fruit, molasses, leafy green vegetables, and wine. Overall, absorption of heme iron can be up to 10 times that of nonheme iron, depending on whether body stores are replete. In the U.S., most grain products are fortified with iron. Iron fortification of cereal, using microencapsulated ferrous fumarate flakes, appears to achieve high iron bioavailability and can serve as an effective means of enhancing hemoglobin nutriture for infants and children. 6

    Many foods, beverages, and supplements have been shown to affect the bioavailability and absorption of iron. Foods that contain heme iron usually also provide nonheme iron, and the presence of the heme iron will enhance absorption of nonheme iron within the same foods or from foods consumed concurrently. In contrast to heme iron, the absorption of which is influenced less by other dietary factors, the absorption of nonheme iron is strongly influenced by enhancers and inhibitors ingested at the same time. Iron absorption, especially nonheme iron, can be inhibited by concomitant intake of phytate (phytic acid, as found in unleavened wheat products, whole-wheat bran, wheat germ, oats, some rye crackers, nuts, beans, cacao powder, vanilla extract, and many other high-fiber foods), tannins (found in tea and coffee), polyphenols (as in green tea, rosemary, and red wine), calcium-rich foods, soy protein, and egg yolk. Conversely, the absorption of nonheme iron is also enhanced by concurrent ingestion of various organic acids, particularly ascorbic acid, but also citric, malic, tartaric, and lactic acids. Certain soy-containing foods (e.g., tofu, miso, tempeh), some soy sauces, vitamin A, and alcohol (other than red wine) can also increase iron absorption. In general, iron absorption from all forms may be influenced most by relative iron nutriture and storage status.

    Ferrous salts are more efficiently absorbed than ferric salts. Acidic foods (e.g., tomato sauce) cooked in iron cookware may also provide a source of dietary iron, although not necessarily the optimal form. Alcohol, but not red wine, can increase the absorption of ferric, but not ferrous, iron.

    Nutrient Preparations Available

    Ferrous citrate, ferrous fumarate, ferrous gluconate, ferrous glutamate, ferrous glycinate, ferrous glycine sulfate, ferrous lactate, ferrous picolinate, ferrous succinate, ferrous sulfate; carbonyl iron; ferric sulfate.

    A number of supplemental iron preparations are available, and different forms provide different proportions of elemental iron, with differing bioavailability characteristics. Ferrous fumarate is 33% elemental iron, ferrous sulfate (monohydrate) 33%, ferrous sulfate (heptahydrate) 23%, and ferrous gluconate 12% elemental iron. In general, absorption of elemental iron is very poor. Ferrous iron is much better absorbed than ferric iron. Heme iron is far better absorbed than nonheme. Absorption of organic chelates is probably the next highest, followed by organic salts (e.g., ferrous gluconate). Inorganic salts (e.g., ferrous sulfate) are the least well absorbed.

    Diverse users absorb, tolerate, and respond to the various forms of iron to varying degrees and with differential responses. Iron supplements can be challenging to those who need to take them because when isolated, the nutrient is not easy to digest and can readily lead to nausea, constipation, or both. Nonheme iron is the predominant type of iron present in nutritional supplements. Ferrous forms (usually as the sulfate, gluconate, or fumarate salt) are readily absorbed without the need for acid. Although ferrous sulfate is the form of nonheme iron used most frequently, ferrous succinate is more often recommended. Ferrous fumarate and iron-EDTA may be more bioavailable than ferrous sulfate, particularly in individuals with low (or impaired) gastric acidity. Enteric coating is sometimes used with ferrous sulfate to delay tablet dissolution and moderate adverse effects, but bioavailability may be compromised. Combining iron with certain mineral-rich herbs, such as yellow dock (Rumex crispus), dandelion root (Taraxacum officinale), alfalfa leaf (Medicago sativa), and nettles tops (Urtica dioica), may enhance absorption, buffer irritant effects, and expand the nutritive effect beyond iron alone.

    Dosage Forms Available

    • Capsule; capsule, time-release; liquid; tablet.
    • Intravenous (IV) iron forms: Iron dextran (DexFerrum, Imferon), iron sucrose (Venofer), sodium ferric gluconate (Ferrlecit).

    Source Materials for Nutrient Preparations

    Most are inorganic and organic salts, chelates, and synthetic polymeric matrices. Botanical extracts of iron-rich plants. Some heme iron concentrates have been used in clinical trials, but generally are not commercially available.

    Dosage Range

    The doses of iron discussed in this monograph represent elemental iron unless stated otherwise.


    Dietary: In the U.S. the average adult daily diet of premenopausal and postmenopausal women provides 12 mg/day and of pregnant women about 15 mg/day. In the United Kingdom (U.K.) the average daily dietary intake for adult women is 12.9 mg/day. For men in the U.S. the average adult daily diet provides 16 to 18 mg elemental iron daily; in the U.K., 14.5 mg.


    • Men: 8 mg/day
    • Women, nonpregnant, nonlactating, age 19 to 50 years: 18 mg/day
    • Women, age 19 to 51 and older: 8 mg/day

    During pregnancy, the metabolic needs of the developing fetus and placenta, as well as a significant expansion of blood volume, increase iron utilization. Conversely, iron requirements are potentially reduced during pregnancy by cessation of menstruation and increased efficiency of absorption. Consequently, iron intake may not need to be any greater than for other adult women, and routine iron supplementation is not necessarily required in pregnancy. Nevertheless, within context of care by a qualified health care professional, pregnant women may benefit from iron supplementation during the last 3 to 6 months of pregnancy. In particular, prenatal prophylactic iron supplementation before 20 weeks’ gestation may help pregnant women increase the birth weight of their infants. 7 Iron status should be monitored in all pregnant women.

    In general, routine supplementation of iron on a daily basis is not recommended. It is generally advised that use of iron supplements be avoided unless clinically indicated, such as low serum ferritin or microcytic, hypochromic anemia. Excess iron has been implicated in free-radical damage. These cautions do not extend consumption of iron-rich foods in moderation for most individuals. Notably, the dietary iron intake of the majority of premenopausal and pregnant women in the U.S. is lower than the recommended dietary allowance (RDA) and the dietary intake of many men is greater than the RDA. Many multivitamin-mineral preparations contain 18 mg of iron, which may result in excessive iron intake for certain individuals.

    Pharmacological/Therapeutic: 10 to 200 mg/day.

    In treatment of iron deficiency, 100 mg/day is a common recommended amount for an adult; dosage is generally reduced after the frank deficiency is corrected. Administration of therapeutic levels is generally recommended for 3 to 4 months after correction of iron deficiency anemia, to replace iron stores.

    Toxic: 100 mg/day (in absence of iron deficiency).

    The tolerable upper intake level (UL) for iron is 45 mg/day for non-iron-deficient adolescents and adults over age 14 years, including pregnant and breastfeeding women, according to standards set by the Food and Nutrition Board (FNB) of the U.S. Institute of Medicine. This UL is based on the prevention of GI distress and is generally understood not to apply to individuals being treated with iron under supervision of a qualified health care professional.

    Pediatric (<18 Years)

    Dietary (AI, adequate intake):

    • Infants, birth to 6 months: 0.27 mg/day (AI, adequate intake)
    • Infants, 7 to 12 months: 11 mg/day (AI)
    • Children, 1 to 3 years: 7 mg/day (AI)
    • Children, 4 to 8 years: 10 mg/day (AI)
    • Children, 9 to 13 years: 8 mg/day (AI)
    • Adolescents, 14 to 18 years: 15 mg/day (for females); 11 mg/day (for males)

    Supplemental/Maintenance: Otherwise-healthy infants born without iron deficiency benefit from iron supplementation, according to the findings of an intervention trial. 8

    Pharmacological/Therapeutic: 10 to 50 mg/day, depending on body weight, condition, and other individual factors, under medical supervision.

    Toxic: 2.0 to 2.5 g can be lethal in a 10-kg child. Deaths in children have occurred from ingesting as little as 200 mg to as much as 5.85 g of iron. 9

    Laboratory Values

    Current diagnostic markers for iron deficiency are not highly sensitive, unless the deficiency is severe. Bone marrow iron is often considered the “gold standard” of iron stores but is rarely practical in most clinical situations. Serum ferritin concentration provides the most accurate diagnostic method to assess iron stores and confirm iron deficiency, but only if the values are low. Iron deficiency can accompany elevated serum ferritin levels when acute or chronic inflammatory states are present, because ferritin is one of the acute-phase reactants.

    One can traditionally obtain a serum iron and serum iron-binding capacity and divide the former by the latter to determine the transferrin saturation. If iron/iron-binding capacity is less than 10%, there is a probability of iron deficiency. A more modern approach to this diagnosis is to measure the serum ferritin; iron deficiency can usually be excluded as a diagnosis if serum ferritin is more than 220 µg/L. However, if it is less than 220, it is judicious to obtain a serum transferrin receptor (sTfR) level. This measures the soluble receptors of transferrin in the circulation, receptors that bind to the available iron. If this value is 28 mg/L or higher, there is a significant probability of iron deficiency. 10 Ongoing developments in knowledge of how iron deficiency influences cellular genetic expression may soon provide diagnostic markers of increased sensitivity by pinpointing the genes affected by iron deprivation to provide a genetic fingerprint of how varying levels of iron deprivation are expressed in different patients. 3

    It is often necessary to assess ferritin, percentage transferrin saturation, and sTfR levels for an accurate assessment of iron status, because ferritin can be falsely elevated by a number of conditions, including pregnancy, inflammatory conditions (e.g., arthritis), malignancy, skin conditions, irritable bowel disease, and acute/chronic infections, both viral and bacterial.

    Areas to exclude as causes of anemia include iron deficiency anemia, nutritional anemias due to B12and folic acid deficiency, drug-induced anemia, alcohol-induced bone marrow toxicity, acute and chronic hemolysis, other illnesses affecting RBC production, and malignant infiltration of the bone marrow.

    Serum Ferritin

    Normal: 12 to 200 µg/L.

    Serum ferritin is the measure of iron status that provides the most accurate indicator of tissue stores and can serve as an effective screening tool. However, it can be elevated with inflammation or infection independent of iron status. Serum ferritin greater than 225 µg/L can generally be interpreted as ruling out iron deficiency anemia. When serum ferritin is less than 220 µg/L, the soluble transferrin receptor (sTfR) level can be used to determine if the patient has upregulated transferrin receptors. Some practitioners of natural therapeutics recommend that males ideally should not have a ferritin level much more than 80 µg/L, unless they are actively engaged in strenuous athletic training or exercise regimens, to minimize iron-catalyzed oxidative stress.

    Serum Iron

    Normal: 9 to 29 mmol/L.

    Serum iron provides an insensitive indicator of iron status, declining only after tissue stores are completely exhausted.

    Transferrin Saturation

    Transferrin saturation of less than 16% of available binding sites indicates iron deficiency.

    Some practitioners of natural therapeutics recommend that transferrin saturation not be greater than 45%, especially with a history of heart disease, diabetes, or cancer. Transferrin saturations greater than 60% are highly suggestive of hereditary hemochromatosis, or another form of iron overload, and should be thoroughly investigated with genotyping and/or liver biopsy to assess hepatic iron stores.

    Serum Transferrin Receptor

    Also known as soluble transferrin receptor (sTfR). Levels greater than 8 mg/L indicate deficiency in standard diagnostic usage. However, some experienced practitioners of nutritional therapeutics use 28 mg/L as the level for demarcating iron deficiency. Values greater than 28 mg/L are also consistent with iron deficiency with corrections for altitude.

    Measurement of serum transferrin receptor is a new marker of iron metabolism that reflects body iron stores and total erythropoiesis. Unlike serum ferritin, the sTfR is not an acute-phase reactant, so it is not elevated in response to acute or chronic inflammatory disease. 10 Thus, it serves as a reliable marker of iron status when iron deficiency is associated with chronic disorders, such as inflammation, infection, or malignancy. In situations of iron deficiency, the avidity and number of soluble transferrin receptors (i.e., sTfR) increases in proportion to tissue iron deficit. Thus, soluble TfR levels are decreased in situations characterized by diminished erythropoietic activity and are increased when erythropoiesis is stimulated by hemolysis or ineffective erythropoiesis. Measurements of sTfR are very helpful in investigating the pathophysiology of anemia, quantitatively evaluating the absolute rate of erythropoiesis and the adequacy of marrow proliferative capacity for any given degree of anemia, and to monitor the erythropoietic response to various forms of therapy, in particular allowing one to predict the response early, when changes in hemoglobin are not yet apparent. Iron status also influences sTfR levels, which are considerably elevated in iron deficiency anemia but remain normal in the anemia of inflammation, and thus may be particularly valuable in the differential diagnosis of microcytic anemia, especially when identifying concomitant iron deficiency in a patient with inflammation, because ferritin values are then generally normal. Elevated sTfR levels are also the characteristic feature of functional iron deficiency, a situation defined by tissue iron deficiency despite adequate iron stores. The sTfR/ferritin ratio can thus describe iron availability over a wide range of iron stores. With the exception of chronic lymphocytic leukemia (CLL), high-grade non-Hodgkin's lymphoma, and possibly hepatocellular carcinoma, sTfR levels are not increased independent of iron status in patients with malignancies. 11

    Erythrocyte Protoporphyrin

    Recent research indicates that erythrocyte protoporphyrin (EP) can provide a useful screening tool for determining iron deficiency. Using the receiver operating characteristic (ROC) curve to characterize the sensitivity and specificity of hemoglobin and EP measurements in screening for iron deficiency, Mei et al. 12 found EP “consistently better than measurements of hemoglobin for detecting iron deficiency” in preschool children, age 1 to 5 years. However, in nonpregnant women, they found “no significant difference between EP and hemoglobin in ROC performance for detecting iron deficiency.”

safety profile


Adverse effects resulting from ingestion of iron supplements occur frequently and often manifest with common dosage levels. However, iron toxicity is relatively rare and predominantly occurs acutely as a result of overdose. In the U.S., iron is the leading cause of accidental poisonings in children. In response, child-resistant safety packaging is legally required for all iron-containing products. Even so, the incidence of iron poisonings in young children increased dramatically in 1986. Many of these children obtained the iron from a child-resistant container opened by themselves or another child, or left open or improperly closed by an adult. 13

Nutrient Adverse Effects

General Adverse Effects

In adults, early symptoms of supplemental iron toxicity include GI irritation, nausea, vomiting, and abdominal pain. Constipation is the most frequently reported adverse effect associated with some forms of iron, even when therapeutically indicated, and may lead to fecal impaction, particularly in the elderly. Conversely, an exacerbation of diarrhea can occur in individuals with inflammatory bowel disease and may be accompanied by bleeding. Liquid iron preparations may blacken the teeth. Signs and symptoms of overload include grayish skin, headache, shortness of breath, fatigue, dizziness, and weight loss. More advanced toxic effects associated with acute excessive iron intake include weakness, fatigue, pallor, arrhythmia, tachycardia, cardiovascular collapse, cyanosis, seizures, and coma.

Intravenous iron, administered in some cases of severe anemia in an inpatient setting, can lead to headache, fever, lymphadenopathy, joint pain and inflammation, hives, exacerbation of rheumatoid arthritis, hemolytic reactions (often associated with acute back pain and renal injury), and (rarely) anaphylaxis.

Adverse Effects Among Specific Populations

Individuals with insulin resistance syndrome, diabetes, or hepatitis C may be particularly susceptible to iron overload. Iron overload triples mortality in people with elevated transferrin saturation. 14

Supplementing iron can be quite dangerous for individuals with hereditary hemochromatosis, hemosiderosis, polycythemia, iron-loading anemias, and other conditions involving excessive storage of iron. Excessive absorption of iron from dietary sources may occur in response to excessive formation of red blood cells. Hereditary hemochromatosis (HH) is a genetic disorder that affects up to 1 in 200 individuals of northern European descent and is characterized by increased intestinal absorption of iron leading to progressive deposition of iron-containing pigments in the liver and other tissues. If untreated, tissue iron accumulation may lead to bronzing of skin, cirrhosis, cardiomyopathies, diabetes, conduction irregularities, testicular atrophy, and arthritis. The HFE gene and the mutation resulting in HH were identified in 1996, but the precise role of the protein encoded by the HFE gene in intestinal iron absorption has yet to be fully elucidated. 15,16Supplemental iron is generally contraindicated in individuals with HH, but they are usually not advised to avoid iron-rich foods, depending on their degree of iron overload at diagnosis and their response to iron unloading on repeated phlebotomies. Sub-Saharan African hemochromatosis is a variant that appears to require both high iron intake and an as-yet unidentified genetic factor. 17

Hemosiderosis is characterized by excessive iron deposits in hemosiderin, the normal iron storage protein. Long-term use of iron at high dosage levels can cause hemosiderosis that clinically resembles hemochromatosis.

Patients with sideroblastic anemia, pyruvate kinase deficiency, thalassemia major, and similar conditions are particularly at risk of iron overload when treated for anemia with numerous transfusions. Iron overload is significantly less common in individuals with hereditary spherocytosis and thalassemia minor, unless they are administered excessive amounts of iron after being misdiagnosed as iron deficient. Emerging information suggests the existence of a Mediterranean form of hemochromatosis, not involving the HFE gene, and with a genetic association unknown at this time, distinct from HH and thalassemias. Treatment for iron overload is by phlebotomy, typically weekly removal of 500 mL of blood until mild iron deficiency is induced. Transfusion-dependent states, however, require iron chelation, generally with regular overnight subcutaneous infusions of deferoxamine mesylate (Desferal).

In a randomized, placebo-controlled trial involving children age 1 to 35 months living in Zanzibar, Sazawal et al. 18 found that “supplementation with iron and folic acid in preschool children in a population with high rates of malaria can result in an increased risk of severe illness and death.” Routine prophylactic iron supplementation in such situations should be avoided pending further research. However, within the context of an active program “to detect and treat malaria and other infections, iron-deficient and anaemic children can benefit from supplementation.”

Pregnancy and Nursing

Low-dose iron supplements are generally safe and effective in pregnancy. 19 Iron supplementation during pregnancy and lactation should be undertaken only under the supervision of a health care professional trained and experienced in nutritional therapeutics.

Infants and Children

Infants and children are especially vulnerable to iron toxicity. Doses as low as 60 mg/kg can be fatal.


Iron preparations are generally contraindicated for individuals diagnosed with a variety of conditions, including hemochromatosis, hemosiderosis, transfusion-dependent thalassemia or other transfusion-dependent states, other conditions associated with iron overload, peptic ulcer, inflammatory bowel disease or other GI disease, diverticulitis, and intestinal stricture. Patients receiving hemodialysis for end-stage renal disease (ESRD) are particularly susceptible to oxidative stress and carotid artery intima media thickening as a result of iron administration, especially without concomitant vitamin E. 20,21

Prophylactic iron (and folic acid) may be contraindicated for children in malarial environments. 18

Iron supplements are generally inappropriate for individuals with a history of any unusual or allergic reaction to iron, or medicines, foods, dyes, or preservatives containing iron.

Precautions and Warnings

Conservative principles of practice suggest that regular iron supplementation be avoided in any individual who has not demonstrated iron deficiency anemia or low iron stores. Such caution is warranted because of the frequency of undetected HH, the pervasive pathophysiology of inflammation and oxidative stress, and emerging concerns about the more subtle effects of chronic excess iron intake. Chronic iron administration increases vascular oxidative stress and accelerates arterial thrombosis. 22 Thus, for example, iron supplementation appears particularly to increase risks of vascular disease and thrombosis for smokers with hypercholesterolemia. 23

Some patients have a serious allergic reaction to IV iron dextran (Imferon), and therefore patients must be monitored especially closely during the first two Imferon administrations using a test dose of 25 mg for each session. After the second test dose is given, the administered dose can be increased to 100 mg. Intravenous sodium ferric gluconate (Ferrlecit) does not contain dextran, and this significant concern regarding anaphylactic reactions is essentially negligible.

Numerous researchers and reviewers have proposed, and sometimes proved, links between excess iron and the development or exacerbation of numerous pathological conditions, including increased risk of infection and inflammatory processes (e.g., pulmonary tuberculosis, pelvic endometriosis), heart disease (e.g., carotid atherosclerosis, coronary disease, myocardial infarction), autoimmune processes (e.g., diabetes, rheumatoid arthritis, systemic lupus erythematosus), neurodegenerative diseases (e.g., Alzheimer's disease, Parkinson's disease, Huntington's disease), and cancer (especially hepatocellular carcinoma and colorectal cancer). 23-46Most of these associations are not conclusively supported by a review of well-done human studies, and some have been disproved, but many are consistent with known patterns of physiology, epidemiology, and pathogenesis. This important area of conflicting data, experience, and opinions will undoubtedly continue to be the subject of clinical trials and meta-analyses.

interactions review

Strategic Considerations

Iron deficiency is the most common micronutrient deficiency in the world, and iron is the nutrient most often prescribed by conventional physicians as an active therapeutic intervention. However, the principles underlying and clinical practices framing such administration have not yet matured into a comprehensive and coherent approach for safe and effective prescribing in daily clinical practice. As with the inflammation it can induce and the free radicals it often generates, the classical metaphor of iron as a “hot” mineral can be applied therapeutically, serving well in suitable circumstances at the appropriate amounts, but just as easily causing a ripple of multiple adverse effects when insufficient, excessive, or simply inappropriately situated. Given the risks of iron depletion and iron overload and the multiple interaction patterns involving iron, deeper analysis of the research data and clinical practices reveals that universal declarations of efficacy, risk, and response patterns do not adequately convey the complexity of individual variability, patient subgroups, and conflicting needs. Thus, iron exemplifies the need for personalized and evolving therapeutic strategies within an integrative model when multiple therapies and coordinated care among various health care providers are involved.

Iron might be seen as a warrior whose sword cuts both ways. It produces heat, agitation, and invigoration, which can convey vitality, sustain activity, and embody vigor, but also carries the risk of oxidative stress, irritation, inflammation, and infection. Although iron depletion is common and has been given more attention than any other nutrient deficiency in conventional medical practice, the methods of evaluation and the standards for augmentation (or reduction) remain controversial. Depleted tissue iron stores are often missed in susceptible individuals because the clinical focus almost exclusively centers on frank iron deficiency anemia rather than functional parameters. Conversely, iron excess or overload, or even inappropriately timed administration, will tend to increase susceptibility to, or aggravate inflammatory processes and promote an environment favorable to, pathogenic microorganisms. The physiological response to infection and neoplasm is to make iron as unavailable as possible to the invading cells, which results in the functional iron deficiency, often seen with acute or chronic infections, and malignancies. Although not rigorously investigated with careful clinical research, much clinical experience suggests that it is often unwise to override this physiological adaptation with oral, and particularly parenteral, iron administration.

Accurate laboratory evaluation of iron status is multifactorial, often making it difficult and elusive to assess functional iron levels, metabolic processes, and depletion and overload states. It is often necessary to assess ferritin, percentage transferrin saturation, and sTfR levels for an accurate assessment of iron status, because ferritin can be falsely elevated by a number of conditions, including pregnancy, inflammatory conditions (e.g., arthritis), malignancy, skin conditions, irritable bowel disease, and chronic infections, both viral and bacterial.

Many minerals and metals are known to bind with a wide range of medications to form insoluble complexes that impair absorption and bioavailability, but with no other common nutrient as much as with the iron salts. Although this phenomenon has been studied widely, the body of evidence indicates that adverse effects on therapeutic efficacy of either agent involved can usually be effectively avoided by separating oral intake by at least 2 hours. Nevertheless, direct inquiry and frank discussion with patients regarding supplement use is critical because simultaneous intake over an extended period could adversely impact therapeutic action and confuse monitoring. Further, unsupervised alterations in intake habits, especially sudden discontinuation of iron that had been taken simultaneously, could result in a rapid elevation in effective dose levels of other agents, thus creating unintended consequences. As always, physician-patient communication, interdisciplinary collaboration, and reinforcement of trust, honesty, and respect for patient choices will always enhance the therapeutic process and support positive clinical outcomes.

The volatility of iron within human physiology, its complex interactions with a wide range of medications and nutrients, and the adverse implications of not maintaining dynamic equilibrium all attest to the critical importance of attentiveness to the changing needs of the individual patient whenever dealing with iron, its intake, and reverberations throughout the economy of the organism.

nutrient-drug interactions
Acetylsalicylic Acid (Aspirin)
Angiotensin-Converting Enzyme (ACE) Inhibitors
Antacids and Gastric Acid–Suppressive Medications
Bile Acid Sequestrants
Carbidopa, Levodopa, and Related Antiparkinsonian Medications
Cefdinir and Related Cephalosporin Antibiotics
Erythropoiesis-Stimulating Agents
Fluoroquinolone (4-Quinolone) Antibiotics
Indomethacin and Related Nonsteroidal Anti-Inflammatory Drugs (NSAIDS)
Interferon Alpha
Levothyroxine and Related Thyroid Hormones
Oral Contraceptives: Monophasic, Biphasic, and Triphasic Estrogen Preparations (Synthetic Estrogen and Progesterone Analogs)
Tetracycline Antibiotics
theoretical, speculative, and preliminary interactions research, including overstated interactions claims
Amphetamines and Related Stimulant Medications
nutrient-nutrient interactions
Pancreatic Enzymes
Phosphorus/Phosphate Supplements
Vitamin A
Vitamin C (Ascorbic Acid)
Vitamin E
herb-nutrient interactions
Herbs Containing Tannins And Polyphenols
Citations and Reference Literature
  • 1.Iron deficiency—United States, 1999-2000. MMWR Morb Mortal Wkly Rep 2002;51:897-899.
  • 2.Brownlie T, Utermohlen V, Hinton PS et al. Marginal iron deficiency without anemia impairs aerobic adaptation among previously untrained women. Am J Clin Nutr 2002;75:734-742.
  • 3.Puig S, Askeland E, Thiele DJ. Coordinated remodeling of cellular metabolism during iron deficiency through targeted mRNA degradation. Cell 2005;120:99-110.
  • 4.Yip R, Dallman PR. Iron. In: Ziegler EE, Filer LJ, eds. Present Knowledge in Nutrition. 7th ed. Washington, DC: ILSI Press; 1996:277-292.
  • 5.Lee GR. Disorders of iron metabolism and heme synthesis. In: Lee GR, Foerster J, Paraskevas F et al, eds. Wintrobe’s Clinical Hematology. 10th ed. Baltimore: Williams & Wilkins; 1999:979-1070.
  • 6.Zlotkin S, Arthur P, Antwi KY, Yeung G. Treatment of anemia with microencapsulated ferrous fumarate plus ascorbic acid supplied as sprinkles to complementary (weaning) foods. Am J Clin Nutr 2001;74:791-795.View Abstract
  • 7.Cogswell ME, Parvanta I, Ickes L et al. Iron supplementation during pregnancy, anemia, and birth weight: a randomized controlled trial. Am J Clin Nutr 2003;78:773-781.
  • 8.Lozoff B, De Andraca I, Castillo M et al. Behavioral and developmental effects of preventing iron-deficiency anemia in healthy full-term infants. Pediatrics 2003;112:846-854.View Abstract
  • 9.Mills KC, Curry SC. Acute iron poisoning. Emerg Med Clin North Am 1994;12:397-413.View Abstract
  • 10.Baillie FJ, Morrison AE, Fergus I. Soluble transferrin receptor: a discriminating assay for iron deficiency. Clin Lab Haematol 2003;25:353-357.View Abstract
  • 11.Beguin Y. Soluble transferrin receptor for the evaluation of erythropoiesis and iron status. Clin Chim Acta 2003;329:9-22.View Abstract
  • 12.Mei Z, Parvanta I, Cogswell ME et al. Erythrocyte protoporphyrin or hemoglobin: which is a better screening test for iron deficiency in children and women? Am J Clin Nutr 2003;77:1229-1233.
  • 13.Morris CC. Pediatric iron poisonings in the United States. South Med J 2000;93:352-358.View Abstract
  • 14.Mainous AG 3rd, Gill JM, Carek PJ. Elevated serum transferrin saturation and mortality. Ann Fam Med 2004;2:133-138.View Abstract
  • 15.Feder JN, Gnirke A, Thomas W et al. A novel MHC class I–like gene is mutated in patients with hereditary haemochromatosis. Nat Genet 1996;13:399-408.View Abstract
  • 16.Anderson GJ, Powell LW. Of metals, mice, and men: what animal models can teach us about body iron loading. J Clin Invest 2000;105:1185-1186.View Abstract
  • 17.Walker AR, Segal I. Iron overload in Sub-Saharan Africa: to what extent is it a public health problem? Br J Nutr 1999;81:427-434.
  • 18.Sazawal S, Black RE, Ramsan M et al. Effects of routine prophylactic supplementation with iron and folic acid on admission to hospital and mortality in preschool children in a high malaria transmission setting: community-based, randomised, placebo-controlled trial. Lancet 2006;367:133-152.View Abstract
  • 19.Makrides M, Crowther CA, Gibson RA et al. Efficacy and tolerability of low-dose iron supplements during pregnancy: a randomized controlled trial. Am J Clin Nutr 2003;78:145-153.
  • 20.Roob JM, Khoschsorur G, Tiran A et al. Vitamin E attenuates oxidative stress induced by intravenous iron in patients on hemodialysis. J Am Soc Nephrol 2000;11:539-549.View Abstract
  • 21.Drueke T, Witko-Sarsat V, Massy Z et al. Iron therapy, advanced oxidation protein products, and carotid artery intima-media thickness in end-stage renal disease. Circulation 2002;106:2212-2217.View Abstract
  • 22.Day SM, Duquaine D, Mundada LV et al. Chronic iron administration increases vascular oxidative stress and accelerates arterial thrombosis. Circulation 2003;107:2601-2606.View Abstract
  • 23.Klipstein-Grobusch K, Grobbee DE, den Breeijen JH et al. Dietary iron and risk of myocardial infarction in the Rotterdam Study. Am J Epidemiol 1999;149:421-428.View Abstract
  • 24.Weinberg ED. Iron withholding: a defense against infection and neoplasia. Physiol Rev 1984;64:65-102.View Abstract
  • 25.Cutler P. Deferoxamine therapy in high-ferritin diabetes. Diabetes 1989;38:1207-1210.View Abstract
  • 26.Salonen JT, Nyyssonen K, Korpela H et al. High stored iron levels are associated with excess risk of myocardial infarction in eastern Finnish men. Circulation 1992;86:803-811.View Abstract
  • 27.Oh VM. Iron dextran and systemic lupus erythematosus. BMJ 1992;305:1000.View Abstract
  • 28.Dabbagh AJ, Trenam CW, Morris CJ, Blake DR. Iron in joint inflammation. Ann Rheum Dis 1993;52:67-73.View Abstract
  • 29.Ascherio A, Willett WC, Rimm EB et al. Dietary iron intake and risk of coronary disease among men. Circulation 1994;89:969-974.
  • 30.Stevens RG, Graubard BI, Micozzi MS et al. Moderate elevation of body iron level and increased risk of cancer occurrence and death. Int J Cancer 1994;56:364-369.View Abstract
  • 31.Wurzelmann JI, Silver A, Schreinemachers DM et al. Iron intake and the risk of colorectal cancer. Cancer Epidemiol Biomarkers Prev 1996;5:503-507.View Abstract
  • 32.Kiechl S, Willeit J, Egger G et al. Body iron stores and the risk of carotid atherosclerosis: prospective results from the Bruneck study. Circulation 1997;96:3300-3307.View Abstract
  • 33.Tzonou A, Lagiou P, Trichopoulou A et al. Dietary iron and coronary heart disease risk: a study from Greece. Am J Epidemiol 1998;147:161-166.View Abstract
  • 34.De Valk B, Marx JJ. Iron, atherosclerosis, and ischemic heart disease. Arch Intern Med 1999;159:1542-1548.View Abstract
  • 35.Bartzokis G, Cummings J, Perlman S et al. Increased basal ganglia iron levels in Huntington disease. Arch Neurol 1999;56:569-574.View Abstract
  • 36.Danesh J, Appleby P. Coronary heart disease and iron status: meta-analyses of prospective studies. Circulation 1999;99:852-854.View Abstract
  • 37.Kato I, Dnistrian AM, Schwartz M et al. Iron intake, body iron stores and colorectal cancer risk in women: a nested case-control study. Int J Cancer 1999;80:693-698.View Abstract
  • 38.Pinero DJ, Hu J, Connor JR. Alterations in the interaction between iron regulatory proteins and their iron responsive element in normal and Alzheimer’s diseased brains. Cell Mol Biol (Noisy-le-grand) 2000;46:761-776.
  • 39.Sayre LM, Perry G, Atwood CS, Smith MA. The role of metals in neurodegenerative diseases. Cell Mol Biol (Noisy-le-grand) 2000;46:731-741.View Abstract
  • 40.Gangaidzo IT, Moyo VM, Mvundura E et al. Association of pulmonary tuberculosis with increased dietary iron. J Infect Dis 2001;184:936-939.View Abstract
  • 41.Van Langendonckt A, Casanas-Roux F, Donnez J. Iron overload in the peritoneal cavity of women with pelvic endometriosis. Fertil Steril 2002;78:712-718.View Abstract
  • 42.Powers KM, Smith-Weller T, Franklin GM et al. Parkinson’s disease risks associated with dietary iron, manganese, and other nutrient intakes. Neurology 2003;60:1761-1766.
  • 43.Lee DH, Anderson KE, Harnack LJ et al. Heme iron, zinc, alcohol consumption, and colon cancer: Iowa Women’s Health Study. J Natl Cancer Inst 2004;96:403-407.
  • 44.Jiang R, Manson JE, Meigs JB et al. Body iron stores in relation to risk of type 2 diabetes in apparently healthy women. JAMA 2004;291:711-717.View Abstract
  • 45.Gotz ME, Double K, Gerlach M et al. The relevance of iron in the pathogenesis of Parkinson’s disease. Ann N Y Acad Sci 2004;1012:193-208.
  • 46.Zecca L, Youdim MB, Riederer P et al. Iron, brain ageing and neurodegenerative disorders. Nat Rev Neurosci 2004;5:863-873.View Abstract
  • 47.Leonards JR, Levy G, Niemczura R. Gastrointestinal blood loss during prolonged aspirin administration. N Engl J Med 1973;289:1020-1022.
  • 48.Palme G, Koeppe P. [Comparative experimental studies in animals and humans on gastrointestinal blood loss following antirheumatic pharmacotherapy] (author’s translation). Arzneimittelforschung 1978;28:426-428.
  • 49.Campbell NR, Hasinoff BB. Iron supplements: a common cause of drug interactions. Br J Clin Pharmacol 1991;31:251-255.View Abstract
  • 49a.Schaefer JP, Tam Y, Hasinoff BB, et al. Ferrous sulphate interacts with captopril. Br J Clin Pharmacol 1998;46(4):377-381
  • 50.Lee SC, Park SW, Kim DK et al. Iron supplementation inhibits cough associated with ACE inhibitors. Hypertension 2001;38:166-170.View Abstract
  • 51.Wong KC, Woo KS, Lam WK et al. A comparison of the effect of enalapril and metoprolol on renal function, potassium balance, lipid profile, cardiac function, exercise tolerance and quality of life in hypertensive dialysis patients. Int J Artif Organs 1995;18:757-762.View Abstract
  • 52.Ozbek N, Ozen S, Saatci U. Enalapril-induced anemia in a renal transplant patient. Acta Paediatr Jpn 1997;39:626-627.View Abstract
  • 53.Incalzi RA, Gemma A, Carbonin P. ACE inhibitors: a possible cause of unexplained anemia. J Am Geriatr Soc 1998;46:117-118.View Abstract
  • 54.Albitar S, Genin R, Fen-Chong M et al. High dose enalapril impairs the response to erythropoietin treatment in haemodialysis patients. Nephrol Dial Transplant 1998;13:1206-1210.View Abstract
  • 55.Gossmann J, Thurmann P, Bachmann T et al. Mechanism of angiotensin converting enzyme inhibitor–related anemia in renal transplant recipients. Kidney Int 1996;50:973-978.View Abstract
  • 56.Rolla G, Bucca C, Brussino L. Systemic reactions to intravenous iron therapy in patients receiving angiotensin converting enzyme inhibitor. J Allergy Clin Immunol 1994;93:1074-1075.View Abstract
  • 57.Coste JF, DeBari VA, Keil LB, Needle MA. In-vitro interactions of oral hematinics and antacid suspensions. Curr Ther Res 1977;22:205-215.
  • 58.Benjamin BI, Cortell S, Conrad ME. Bicarbonate-induced iron complexes and iron absorption: one effect of pancreatic secretions. Gastroenterology 1967;35:389-396.
  • 59.Hall GJ, Davis AE. Inhibition of iron absorption by magnesium trisilicate. Med J Aust 1969;2:95-96.View Abstract
  • 60.Aymard JP, Aymard B, Netter P et al. Haematological adverse effects of histamine H2-receptor antagonists. Med Toxicol Adverse Drug Exp 1988;3:430-448.View Abstract
  • 61.Campbell NR, Hasinoff BB, Meddings JB et al. Ferrous sulfate reduces cimetidine absorption. Dig Dis Sci 1993;38:950-954.View Abstract
  • 62.Conrad ME, Schade SG. Ascorbic acid chelates in iron absorption: a role for hydrochloric acid and bile. Gastroenterology 1968;55:35-45.View Abstract
  • 63.Hathcock JN. Metabolic mechanisms of drug-nutrient interactions. Fed Proc 1985;44:124-129.View Abstract
  • 64.D’Arcy PF, McElnay JC. Drug interactions in the gut involving metal ions. Rev Drug Metab Drug Interact 1985;5:83-112.
  • 65.Champagne ET. Low gastric hydrochloric acid secretion and mineral bioavailability. Adv Exp Med Biol 1989;249:173-184.View Abstract
  • 66.Sturniolo GC, Montino MC, Rossetto L et al. Inhibition of gastric acid secretion reduces zinc absorption in man. J Am Coll Nutr 1991;10:372-375.View Abstract
  • 67.Lambat Z, Limson JL, Daya S. Cimetidine: antioxidant and metal-binding properties. J Pharm Pharmacol 2002;54:1681-1686.View Abstract
  • 68.Rastogi SP, Padilla F, Boyd CM. Effect of aluminum hydroxide on iron absorption. J Ark Med Soc 1976;73:133-134.View Abstract
  • 69.Ekenved G, Halvorsen L, Solvell L. Influence of a liquid antacid on the absorption of different iron salts. Scand J Haematol Suppl 1976;28:65-77.View Abstract
  • 70.O’Neil-Cutting MA, Crosby WH. The effect of antacids on the absorption of simultaneously ingested iron. JAMA 1986;255:1468-1470.
  • 71.Snyder BK, Clark RF. Effect of magnesium hydroxide administration on iron absorption after a supratherapeutic dose of ferrous sulfate in human volunteers: a randomized controlled trial. Ann Emerg Med 1999;33:400-405.View Abstract
  • 72.Wallace KL, Curry SC, LoVecchio F, Raschke RA. Effect of magnesium hydroxide on iron absorption after ferrous sulfate. Ann Emerg Med 1999;34:685-687.View Abstract
  • 73.Macdougall BR, Bailey RJ, Williams R. H2-receptor antagonists and antacids in the prevention of acute gastrointestinal haemorrhage in fulminant hepatic failure: two controlled trials. Lancet 1977;1:617-619.View Abstract
  • 74.Bianchi FM, Cavassini GB, Leo P. Iron protein succynilate in the treatment of iron deficiency: potential interaction with H2-receptor antagonists. Int J Clin Pharmacol Ther Toxicol 1993;31:209-217.View Abstract
  • 75.Partlow ES, Chan SC, Pap KM et al. The effect of ferrous sulfate on famotidine serum levels in healthy patients. Clin Invest Med 1994;17:B15.
  • 76.Partlow ES, Campbell NR, Chan SC et al. Ferrous sulfate does not reduce serum levels of famotidine or cimetidine after concurrent ingestion. Clin Pharmacol Ther 1996;59:389-393.
  • 77.Stockley IH. Drug Interactions. 6th ed. London: Pharmaceutical Press; 2002.
  • 78.Esposito R. Cimetidine and iron-deficiency anaemia. Lancet 1977;2:1132.View Abstract
  • 79.Rosner F. Cimetidine and iron absorption. Lancet 1978;1:95.
  • 80.Drasar BS, Shiner M, McLeod GM. Studies on the intestinal flora. I. The bacterial flora of the gastrointestinal tract in healthy and achlorhydric persons. Gastroenterology 1969;56:71-79.View Abstract
  • 81.Drasar BS, Shiner M. Studies on the intestinal flora. II. Bacterial flora of the small intestine in patients with gastrointestinal disorders. Gut 1969;10:812-819.View Abstract
  • 82.Giannella RA, Broitman SA, Zamcheck N. Influence of gastric acidity on bacterial and parasitic enteric infections: a perspective. Ann Intern Med 1973;78:271-276.View Abstract
  • 83.Walker WA, Isselbacher KJ. Uptake and transport of macromolecules by the intestine: possible role in clinical disorders. Gastroenterology 1974;67:531-550.View Abstract
  • 84.Mayron LW. Portals of entry—a review. Ann Allergy 1978;40:399-405.View Abstract
  • 85.Russell RM, Krasinski SD, Samloff IM. Correction of impaired folic acid (Pte Glu) absorption by orally administered HCl in subjects with gastric atrophy. Am J Clin Nutr 1984;39:656.
  • 86.Laheij RJ, Sturkenboom MC, Hassing RJ et al. Risk of community-acquired pneumonia and use of gastric acid-suppressive drugs. JAMA 2004;292:1955-1960.View Abstract
  • 87.Leonard JP, Desager JP, Beckers C, Harvengt C. In vitro binding of various biological substances by two hypocholesterolaemic resins: cholestyramine and colestipol. Arzneimittelforschung 1979;29:979-981.
  • 88.Watkins DW, Khalafi R, Cassidy MM, Vahouny GV. Alterations in calcium, magnesium, iron, and zinc metabolism by dietary cholestyramine. Dig Dis Sci 1985;30:477-482.View Abstract
  • 89.Torkos S. Drug-nutrient interactions: a focus on cholesterol-lowering agents. Int J Integr Med 2000;2:9-13.
  • 90.Thomas FB, McCullough FS, Greenberger NJ. Inhibition of the intestinal absorption of inorganic and hemoglobin iron by cholestyramine. J Lab Clin Med 1971;78:70-80.View Abstract
  • 91.Thomas FB, Salsburey D, Greenberger NJ. Inhibition of iron absorption by cholestyramine: demonstration of diminished iron stores following prolonged administration. Am J Dig Dis 1972;17:263-269.View Abstract
  • 92.Schlierf G, Vogel G, Kohlmeier M et al. [Long-term therapy of familial hypercholesterolemia in young patients with colestipol: availability of minerals and vitamins]. Klin Wochenschr 1985;63:802-806.View Abstract
  • 93.Russell RG, Rogers MJ, Frith JC et al. The pharmacology of bisphosphonates and new insights into their mechanisms of action. J Bone Miner Res 1999;14 Suppl 2:53-65.View Abstract
  • 94.Fleisch H. Bisphosphonates: mechanisms of action. Endocr Rev 1998;19:80-100.View Abstract
  • 95.Campbell NR, Hasinoff B. Ferrous sulfate reduces levodopa bioavailability: chelation as a possible mechanism. Clin Pharmacol Ther 1989;45:220-225.View Abstract
  • 96.Greene RJ, Hall AD, Hider RC. The interaction of orally administered iron with levodopa and methyldopa therapy. J Pharm Pharmacol 1990;42:502-504.View Abstract
  • 97.Campbell NR, Rankine D, Goodridge AE et al. Sinemet-ferrous sulphate interaction in patients with Parkinson’s disease. Br J Clin Pharmacol 1990;30:599-605.
  • 98.Campbell RR, Hasinoff B, Chernenko G et al. The effect of ferrous sulfate and pH on I-dopa absorption. Can J Physiol Pharmacol 1990;68:603-607.View Abstract
  • 99.Zhou B, Westaway SK, Levinson B et al. A novel pantothenate kinase gene (PANK2) is defective in Hallervorden-Spatz syndrome. Nat Genet 2001;28:345-349.
  • 100.Bharath S, Hsu M, Kaur D et al. Glutathione, iron and Parkinson’s disease. Biochem Pharmacol 2002;64:1037-1048.
  • 101.Youdim MB, Stephenson G, Ben Shachar D. Ironing iron out in Parkinson’s disease and other neurodegenerative diseases with iron chelators: a lesson from 6-hydroxydopamine and iron chelators, desferal and VK-28. Ann NY Acad Sci 2004;1012:306-325.
  • 102.Shachar DB, Kahana N, Kampel V et al. Neuroprotection by a novel brain permeable iron chelator, VK-28, against 6-hydroxydopamine lesion in rats. Neuropharmacology 2004;46:254-263.
  • 103.Ueno K, Tanaka K, Tsujimura K et al. Impairment of cefdinir absorption by iron ion. Clin Pharmacol Ther 1993;54:473-475.View Abstract
  • 104.Cefdinir—a new oral cephalosporin. Med Lett Drugs Ther 1998;40:85-87.
  • 105.Kato R, Ooi K, Takeda K et al. Lack of interaction between cefdinir and calcium polycarbophil: in vitro and in vivo studies. Drug Metab Pharmacokinet 2002;17:363-366.
  • 106.Rigdon RH, Crass G, Martin N. Anemia produced by chloramphenicol (chloromycetin) in the duck. AMA Arch Pathol 1954;58:85-93.View Abstract
  • 107.Saidi P, Wallerstein RO, Aggeler PM. Effect of chloramphenicol on erythropoiesis. J Lab Clin Med 1961;57:247-256.View Abstract
  • 108.McCurdy PR. Chloramphenicol bone marrow toxicity. JAMA 1961;176:588-593.
  • 109.Jiji RM, Gangarosa EJ, de la Macorra F. Chloramphenicol and its sulfamoyl analogue: report of reversible erythropoietic toxicity in healthy volunteers. Arch Intern Med 1963;111:116-128.
  • 110.Scott JL, Finegold SM, Belkin GA, Lawrence JS. A controlled double-blind study of the hematologic toxicity of chloramphenicol. N Engl J Med 1965;272:1137-1142.View Abstract
  • 111.Warner RR, Myers MC, Burns J, Mitra S. Analytical electron microscopy of chlorhexidine-induced tooth stain in humans: direct evidence for metal-induced stain. J Periodont Res 1993;28:255-265.View Abstract
  • 112.Powanda MC, Blackburn BS, Bostian KA et al. Clofibrate-induced alterations in zinc, iron and copper metabolism. Biochem Pharmacol 1978;27:125-127.View Abstract
  • 113.Hettiarachchi M, Hilmers DC, Liyanage C, Abrams SA. Na2EDTA enhances the absorption of iron and zinc from fortified rice flour in Sri Lankan children. J Nutr 2004;134:3031-3036.
  • 114.Davidsson L, Ziegler E, Zeder C et al. Sodium iron EDTA [NaFe(III)EDTA] as a food fortificant: erythrocyte incorporation of iron and apparent absorption of zinc, copper, calcium, and magnesium from a complementary food based on wheat and soy in healthy infants. Am J Clin Nutr 2005;81:104-109.View Abstract
  • 115.Aapro M, San Miguel J. Evolving treatment strategies for anaemia in cancer: experience with epoetin beta. Oncology 2004;67 Suppl 1:17-22.View Abstract
  • 116.Beguin Y. Prediction of response and other improvements on the limitations of recombinant human erythropoietin therapy in anemic cancer patients. Haematologica 2002;87:1209-1221.View Abstract
  • 117.Rizzo JD, Lichtin AE, Woolf SH et al. Use of epoetin in patients with cancer: evidence-based clinical practice guidelines of the American Society of Clinical Oncology and the American Society of Hematology. J Clin Oncol 2002;20:4083-4107.View Abstract
  • 118.Henry DH. Supplemental iron: a key to optimizing the response of cancer-related anemia to rHuEPO? Oncologist 1998;3:275-278.
  • 119.Markowitz GS, Kahn GA, Feingold RE et al. An evaluation of the effectiveness of oral iron therapy in hemodialysis patients receiving recombinant human erythropoietin. Clin Nephrol 1997;48:34-40.View Abstract
  • 120.Coyne DW, Adkinson NF, Nissenson AR et al. Sodium ferric gluconate complex in hemodialysis patients. II. Adverse reactions in iron dextran-sensitive and dextran-tolerant patients. Kidney Int 2003;63:217-224.View Abstract
  • 121.Kooistra MP, Niemantsverdriet EC, van Es A et al. Iron absorption in erythropoietin-treated haemodialysis patients: effects of iron availability, inflammation and aluminium. Nephrol Dial Transplant 1998;13:82-88.View Abstract
  • 122.Auerbach M, Winchester J, Wahab A et al. A randomized trial of three iron dextran infusion methods for anemia in EPO-treated dialysis patients. Am J Kidney Dis 1998;31:81-86.View Abstract
  • 123.Vankova S, Safarova R, Horackova M et al. [Clinical and economic significance of iron replacement in anemia treated with recombinant human erythropoietin in patients on hemodialysis]. Cas Lek Cesk 2001;140:209-213.View Abstract
  • 124.Chang CH, Chang CC, Chiang SS. Reduction in erythropoietin doses by the use of chronic intravenous iron supplementation in iron-replete hemodialysis patients. Clin Nephrol 2002;57:136-141.View Abstract
  • 125.Nissenson AR, Berns JS, Sakiewicz P et al. Clinical evaluation of heme iron polypeptide: sustaining a response to rHuEPO in hemodialysis patients. Am J Kidney Dis 2003;42:325-330.View Abstract
  • 126.Auerbach M, Ballard H, Trout JR et al. Intravenous iron optimizes the response to recombinant human erythropoietin in cancer patients with chemotherapy-related anemia: a multicenter, open-label, randomized trial. J Clin Oncol 2004;22:1301-1307.View Abstract
  • 127.Pedrazzoli P, Tullio C, Cerea G, Siena S. Iron supplement in cancer patients receiving erythropoietin. J Clin Oncol 2004;22:4428; author reply 4428-4429.View Abstract
  • 128.Henke M, Laszig R, Rube C et al. Erythropoietin to treat head and neck cancer patients with anaemia undergoing radiotherapy: randomised, double-blind, placebo-controlled trial. Lancet 2003;362:1255-1260.View Abstract
  • 129.Andrews NC. Anemia of inflammation: the cytokine-hepcidin link. J Clin Invest 2004;113:1251-1253.View Abstract
  • 130.Nemeth E, Rivera S, Gabayan V et al. IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. J Clin Invest 2004;113:1271-1276.View Abstract
  • 131.Arndt U, Kaltwasser JP, Gottschalk R et al. Correction of iron-deficient erythropoiesis in the treatment of anemia of chronic disease with recombinant human erythropoietin. Ann Hematol 2005;84(3):159-166.View Abstract
  • 132.Goodnough LT, Skikne B, Brugnara C. Erythropoietin, iron, and erythropoiesis. Blood 2000;96:823-833.View Abstract
  • 133.Polk RE, Healy DP, Sahai J et al. Effect of ferrous sulfate and multivitamins with zinc on absorption of ciprofloxacin in normal volunteers. Antimicrob Agents Chemother 1989;33:1841-1844.View Abstract
  • 134.Okhamafe AO, Akerele JO, Chukuka CS. Pharmacokinetic interactions of norfloxacin with some metallic agents. Int J Pharmaceutics 1991;68:11-16.
  • 135.Kara M, Hasinoff BB, McKay DW, Campbell NR. Clinical and chemical interactions between iron preparations and ciprofloxacin. Br J Clin Pharmacol 1991;31:257-261.
  • 136.Akerele JO, Okhamafe AO. Influence of oral co-administered metallic drugs on ofloxacin pharmacokinetics. J Antimicrob Chemother 1991;28:87-94.View Abstract
  • 137.Brouwers JR. Drug interactions with quinolone antibacterials. Drug Saf 1992;7:268-281.View Abstract
  • 138.Lehto P, Kivisto KT, Neuvonen PJ. The effect of ferrous sulphate on the absorption of norfloxacin, ciprofloxacin and ofloxacin. Br J Clin Pharmacol 1994;37:82-85.View Abstract
  • 139.Wallis SC, Gahan LR, Charles BG et al. Copper(II) complexes of the fluoroquinolone antimicrobial ciprofloxacin: synthesis, X-ray structural characterization, and potentiometric study. J Inorg Biochem 1996;62:1-16.View Abstract
  • 140.Balfour JA, Wiseman LR. Moxifloxacin. Drugs 1999;57:363-373; discussion 374.View Abstract
  • 141.Li RC, Lo KN, Lam JS, Lau PY. Effects of order of magnesium exposure on the postantibiotic effect and bactericidal activity of ciprofloxacin. J Chemother 1999;11:243-247.View Abstract
  • 142.Sirtori CR, Barbi S, Dorigotti F et al. Iron-ovotransferrin preparation does not interfere with fluoroquinolone absorption. Therapie 1995;50(Suppl):Abstract 500.
  • 143.Pazzucconi F, Barbi S, Baldassarre D et al. Iron-ovotransferrin preparation does not interfere with ciprofloxacin absorption. Clin Pharmacol Ther 1996;59:418-422.
  • 144.Wong PY, Zhu M, Li RC. Pharmacokinetic and pharmacodynamic interactions between intravenous ciprofloxacin and oral ferrous sulfate. J Chemother 2000;12:286-293.
  • 145.LePennec MP, Kitzis MD, Terdjman M et al. Possible interaction of ciprofloxacin with ferrous sulphate. J Antimicrob Chemother 1990;25:184-185.View Abstract
  • 146.Lode H, Stuhlert P, Deppermann KH et al. Pharmacokinetic interactions between oral ciprofloxacin (CIP)/ofloxacin (OFL) and ferro-salts. Intersci Conf Antimicrob Agents Chemother 1989;29:136.
  • 147.Brouwers JR, Van der Kam HJ, Sijtsma J, Proost JH. Decreased ciprofloxacin absorption with concomitant administration of ferrous fumarate. Pharm Weekbl Sci 1990;12:182-183.View Abstract
  • 148.Sorgel F, Naber KG, Kinzig M et al. Effect of ferrous sulfate on fleroxacin analyzed by the confidence interval (CI) approach. Pharm Res 1995;12(9 Suppl):S-422.
  • 149.Shiba K, Kusajima H, Momo K. The effects of aluminum hydroxide, cimetidine, ferrous sulfate, green tea and milk on pharmacokinetics of gatifloxacin in healthy humans. J Antimicrob Chemother 1999;44(Suppl A):141.
  • 150.Allen A, Bygate E, Faessel H et al. The effect of ferrous sulphate and sucralfate on the bioavailability of oral gemifloxacin in healthy volunteers. Int J Antimicrob Agents 2000;15:283-289.View Abstract
  • 151.Shiba K, Okazaki O, Aoki H et al. Inhibition of DR-3355 absorption by metal ions. Intersci Conf Antimicrob Agents Chemother 1991;31:198.
  • 152.Lehto P, Kivisto KT. Different effects of products containing metal ions on the absorption of lomefloxacin. Clin Pharmacol Ther 1994;56:477-482.View Abstract
  • 153.Campbell NR, Kara M, Hasinoff BB et al. Norfloxacin interaction with antacids and minerals. Br J Clin Pharmacol 1992;33:115-116.View Abstract
  • 154.Kanemitsu K, Hori S, Yanagawa A, Shimada J. Effect of ferrous sulfate on the absorption of sparfloxacin in healthy volunteers and rats. Drugs 1995;49 Suppl 2:352-356.View Abstract
  • 155.Kanemitsu K, Hori S, Yanagawa A, Shimada J. Effect of ferrous sulfate on the pharmacokinetics of sparfloxacin. Chemotherapy (Japan) 1994;42:6-13.
  • 156.Martinez Cabarga M, Sanchez Navarro A, Colino Gandarillas CI, Dominguez-Gil A. Effects of two cations on gastrointestinal absorption of ofloxacin. Antimicrob Agents Chemother 1991;35:2102-2105.View Abstract
  • 157.Orrego-Matte H, Fernandez O, Mena I. Effect of anticholinergic agents on the intestinal absorption of 59 Fe ferrous citrate. Am J Dig Dis 1971;16:789-795.View Abstract
  • 158.Bjarnason I, Macpherson AJ. Intestinal toxicity of non-steroidal anti-inflammatory drugs. Pharmacol Ther 1994;62:145-157.View Abstract
  • 159.Davies NM. Toxicity of nonsteroidal anti-inflammatory drugs in the large intestine. Dis Colon Rectum 1995;38:1311-1321.View Abstract
  • 160.Bertschinger P, Zala GF, Fried M. [Effect of non-steroidal antirheumatic agents on the gastrointestinal tract: clinical aspects and pathophysiology]. Schweiz Med Wochenschr 1996;126:1566-1568.View Abstract
  • 161.Battistella M, Mamdami MM, Juurlink DN et al. Risk of upper gastrointestinal hemorrhage in warfarin users treated with nonselective NSAIDs or COX-2 inhibitors. Arch Intern Med 2005;165:189-192.View Abstract
  • 162.Giglio MJ, Bozzini CE. Effect of indomethacin on red cell volume, iron kinetics and red cell survival in mice. Exp Hematol 1982;10:487-492.View Abstract
  • 163.Ganchev T, Negrev N, Mileva V. Effects of indomethacin on erythropoiesis and plasma iron in rats. Acta Physiol Pharmacol Bulg 1989;15:53-57.View Abstract
  • 164.Burghuber O. [Aplastic anemia following indomethacin therapy]. Acta Med Austriaca Suppl 1979;6:384-386.View Abstract
  • 165.Schattner A, Shtalrid M, Levy R, Berrebi A. Fatal aplastic anemia due to indomethacin: lymphocyte transformation tests in vitro. Isr J Med Sci 1981;17:433-436.View Abstract
  • 166.Risks of agranulocytosis and aplastic anemia: a first report of their relation to drug use with special reference to analgesics. The International Agranulocytosis and Aplastic Anemia Study. JAMA 1986;256:1749-1757.
  • 167.Troost FJ, Brummer R-JM, Saris WHM. The effect of chronic iron therapy and indomethacin challenge on intestinal permeability in iron deficient women. Dig Dis Week 2001; May 20.
  • 168.Troost FJ, Saris WH, Brummer RJ. Recombinant human lactoferrin ingestion attenuates indomethacin-induced enteropathy in vivo in healthy volunteers. Eur J Clin Nutr 2003;57:1579-1585.View Abstract
  • 169.Blumberg BS, Lustbader ED, Whitford PL. Changes in serum iron levels due to infection with hepatitis B virus. Proc Natl Acad Sci USA 1981;78:3222-3224.View Abstract
  • 170.Van Thiel DH, Friedlander L, Fagiuoli S et al. Response to interferon alpha therapy is influenced by the iron content of the liver. J Hepatol 1994;20:410-415.View Abstract
  • 171.Fargion S, Fracanzani AL, Sampietro M et al. Liver iron influences the response to interferon alpha therapy in chronic hepatitis C. Eur J Gastroenterol Hepatol 1997;9:497-503.View Abstract
  • 172.Hayashi H, Takikawa T, Nishimura N et al. Improvement of serum aminotransferase levels after phlebotomy in patients with chronic active hepatitis C and excess hepatic iron. Am J Gastroenterol 1994;89:986-988.View Abstract
  • 173.Fong TL, Han SH, Tsai NC et al. A pilot randomized, controlled trial of the effect of iron depletion on long-term response to alpha-interferon in patients with chronic hepatitis C. J Hepatol 1998;28:369-374.View Abstract
  • 174.Fontana RJ, Israel J, LeClair P et al. Iron reduction before and during interferon therapy of chronic hepatitis C: results of a multicenter, randomized, controlled trial. Hepatology 2000;31:730-736.
  • 175.Di Bisceglie AM, Bonkovsky HL, Chopra S et al. Iron reduction as an adjuvant to interferon therapy in patients with chronic hepatitis C who have previously not responded to interferon: a multicenter, prospective, randomized, controlled trial. Hepatology 2000;32:135-138.View Abstract
  • 176.Fargion S, Fracanzani AL, Rossini A et al. Iron reduction and sustained response to interferon-alpha therapy in patients with chronic hepatitis C: results of an Italian multicenter randomized study. Am J Gastroenterol 2002;97:1204-1210.View Abstract
  • 177.Tandon N, Thakur V, Guptan RK, Sarin SK. Beneficial influence of an indigenous low-iron diet on serum indicators of iron status in patients with chronic liver disease. Br J Nutr 2000;83:235-239.View Abstract
  • 178.Tanaka K, Ikeda M, Nozaki A et al. Lactoferrin inhibits hepatitis C virus viremia in patients with chronic hepatitis C: a pilot study. Jpn J Cancer Res 1999;90:367-371.View Abstract
  • 179.Campbell NR, Hasinoff BB, Stalts H et al. Ferrous sulfate reduces thyroxine efficacy in patients with hypothyroidism. Ann Intern Med 1992;117:1010-1013.View Abstract
  • 180.Beard JL, Borel MJ, Derr J. Impaired thermoregulation and thyroid function in iron-deficiency anemia. Am J Clin Nutr 1990;52:813-819.View Abstract
  • 181.Campbell NR, Wong NC, Hasinoff BB et al. Ferrous sulfate reduces thyroxine efficacy. Clin Pharmacol Ther 1992:165.View Abstract
  • 182.Beard J, Borel M, Peterson FJ. Changes in iron status during weight loss with very-low-energy diets. Am J Clin Nutr 1997;66:104-110.
  • 183.Beard JL, Brigham DE, Kelley SK, Green MH. Plasma thyroid hormone kinetics are altered in iron-deficient rats. J Nutr 1998;128:1401-1408.View Abstract
  • 184.Schlienger JL. [Increased need for thyroxine induced by iron sulfate]. Presse Med 1994;23:492.View Abstract
  • 184a.Shakir KM, Chute JP, Aprill BS, Lazarus AA. Ferrous sulfate-induced increase in requirement for thyroxine in a patient with primary hypothyroidism. South Med J 1997;90(6):637-639.
  • 185.Campbell NR, Campbell RR, Hasinoff BB. Ferrous sulfate reduces methyldopa absorption: methyldopa:iron complex formation as a likely mechanism. Clin Invest Med 1990;13:329-332.View Abstract
  • 186.Campbell N, Paddock V, Sundaram R. Alteration of methyldopa absorption, metabolism, and blood pressure control caused by ferrous sulfate and ferrous gluconate. Clin Pharmacol Ther 1988;43:381-386.View Abstract
  • 187.Roe DA. Drug-Induced Nutritional Deficiencies. 2nd ed. Westport, Conn: Avi Publishing; 1985.
  • 188.Jacobson ED, Chodos RB, Faloon WW. An experimental malabsorption syndrome induced by neomycin. Am J Med 1960;28:524-533.View Abstract
  • 189.Miale JB, Kent JW. The effects of oral contraceptives on the results of laboratory tests. Am J Obstet Gynecol 1974;120:264-272.View Abstract
  • 190.Worthington BS. Nutrition during pregnancy, lactation, and oral contraception. Nurs Clin North Am 1979;14:269-283.
  • 191.Webb JL. Nutritional effects of oral contraceptive use: a review. J Reprod Med 1980;25:150-156.View Abstract
  • 192.Tyrer LB. Nutrition and the pill. J Reprod Med 1984;29:547-550.View Abstract
  • 193.Frassinelli-Gunderson EP, Margen S, Brown JR. Iron stores in users of oral contraceptive agents. Am J Clin Nutr 1985;41:703-712.View Abstract
  • 194.Palomo I, Grebe G, Valladares G et al. [Hemoglobin, serum iron and transferrin saturation among users of intrauterine devices and oral contraceptive agents]. Rev Med Chil 1990;118:506-511.
  • 195.Masse PG, Roberge AG. Long-term effect of low-dose combined steroid contraceptives on body iron status. Contraception 1992;46:243-252.View Abstract
  • 196.Steegers-Theunissen RP, Van Rossum JM, Steegers EA et al. Sub-50 oral contraceptives affect folate kinetics. Gynecol Obstet Invest 1993;36:230-233.View Abstract
  • 197.Mooij PN, Thomas CM, Doesburg WH, Eskes TK. The effects of oral contraceptives and multivitamin supplementation on serum ferritin and hematological parameters. Int J Clin Pharmacol Ther Toxicol 1992;30:57-62.View Abstract
  • 198.Jensen JT, Speroff L. Health benefits of oral contraceptives. Obstet Gynecol Clin North Am 2000;27:705-721.View Abstract
  • 199.Dayal M, Barnhart KT. Noncontraceptive benefits and therapeutic uses of the oral contraceptive pill. Semin Reprod Med 2001;19:295-303.View Abstract
  • 200.Miscellaneous products, Penicillamine. In: Threlkeld DS, ed. Facts and Comparisons Drug Information. St Louis: Facts and Comparisons; August 1996:714-716b.
  • 201.Osman MA, Patel RB, Schuna A et al. Reduction in oral penicillamine absorption by food, antacid, and ferrous sulfate. Clin Pharmacol Ther 1983;33:465-470.View Abstract
  • 202.Harkness JA, Blake DR. Penicillamine nephropathy and iron. Lancet 1982;2:1368-1369.View Abstract
  • 203.Dukes GE Jr, Duncan BS. Inflammatory bowel disease. Applied Therapeutics: the Clinical Use of Drugs. 6th ed. Vancouver, Wash: Applied Therapeutics; 1995:24-27.
  • 204.Neuvonen PJ. Interactions with the absorption of tetracyclines. Drugs 1976;11:45-54.View Abstract
  • 205.Machado FC, Demicheli C, Garnier-Suillerot A, Beraldo H. Metal complexes of anhydrotetracycline. 2. Absorption and circular dichroism study of Mg(II), Al(III), and Fe(III) complexes: possible influence of the Mg(II) complex on the toxic side effects of tetracycline. J Inorg Biochem 1995;60:163-173.View Abstract
  • 206.Howitz PF. The effect of Apurin (allopurinol) on liver function and serum iron. Dan Med Bull 1970;17:203-205.View Abstract
  • 207.Houze P, Rouach H, Gentil M et al. Effect of allopurinol on the hepatic and cerebellar iron, selenium, zinc and copper status following acute ethanol administration to rats. Free Radic Res Commun 1991;12-13 Pt 2:663-668.View Abstract
  • 208.Minerals. In: Threlkeld DS, ed. Facts and Comparisons Drug Information. St Louis: Facts and Comparisons; 2000:27-51.
  • 209.Hendler SS, Rorvik DR. PDR for Nutritional Supplements. Montvale, NJ: Medical Economics Company; 2001.
  • 210.Powers RH, Stadnicka A, Kalbfleish JH, Skibba JL. Involvement of xanthine oxidase in oxidative stress and iron release during hyperthermic rat liver perfusion. Cancer Res 1992;52:1699-1703.
  • 211.Konofal E, Lecendreux M, Arnulf I, Mouren MC. Iron deficiency in children with attention-deficit/hyperactivity disorder. Arch Pediatr Adolesc Med 2004;158:1113-1115.View Abstract
  • 212.De la Cruz JP, Garcia PJ, Sanchez de la Cuesta F. Dipyridamole inhibits platelet aggregation induced by oxygen-derived free radicals. Thromb Res 1992;66:277-285.View Abstract
  • 213.Central nervous system drugs, Antipsychotic agents. In: Threlkeld DS, ed. Facts and Comparisons Drug Information. St Louis: Facts and Comparisons; May 1998:266k-266m.
  • 214.Ben-Shachar D, Youdim MB. Neuroleptic-induced supersensitivity and brain iron. I. Iron deficiency and neuroleptic-induced dopamine D2 receptor supersensitivity. J Neurochem 1990;54:1136-1141.View Abstract
  • 215.Hamilton SF, Campbell NR, Kara M et al. The effect of ingestion of ferrous sulfate on the absorption of oral methotrexate in patients with rheumatoid arthritis. J Rheumatol 2003;30:1948-1950.View Abstract
  • 216.Verhoef H, West CE, Nzyuko SM et al. Intermittent administration of iron and sulfadoxine-pyrimethamine to control anaemia in Kenyan children: a randomised controlled trial. Lancet 2002;360:908-914.View Abstract
  • 217.Desai MR, Mei JV, Kariuki SK et al. Randomized, controlled trial of daily iron supplementation and intermittent sulfadoxine-pyrimethamine for the treatment of mild childhood anemia in western Kenya. J Infect Dis 2003;187:658-666.View Abstract
  • 218.Desai MR, Dhar R, Rosen DH et al. Daily iron supplementation is more efficacious than twice weekly iron supplementation for the treatment of childhood anemia in western Kenya. J Nutr 2004;134:1167-1174.View Abstract
  • 219.Taberner DA. Iron deficiency and stanozol therapy. Lancet 1983;1:648.View Abstract
  • 220.Pinto JT. The pharmacokinetic and pharmacodynamic interactions of foods and drugs. Top Clin Nutr 1991;6:14-33.
  • 221.Dawson-Hughes B, Seligson FH, Hughes VA. Effects of calcium carbonate and hydroxyapatite on zinc and iron retention in postmenopausal women. Am J Clin Nutr 1986;44:83-88.View Abstract
  • 222.Cook JD, Dassenko SA, Whittaker P. Calcium supplementation: effect on iron absorption. Am J Clin Nutr 1991;53:106-111.View Abstract
  • 223.Hallberg L, Brune M, Erlandsson M et al. Calcium: effect of different amounts on nonheme- and heme-iron absorption in humans. Am J Clin Nutr 1991;53:112-119.View Abstract
  • 224.Hallberg L, Rossander-Hulten L, Brune M, Gleerup A. Inhibition of haem-iron absorption in man by calcium. Br J Nutr 1992:533-540.
  • 225.Hallberg L, Rossander-Hulten L, Brune M, Gleerup A. Calcium and iron absorption: mechanism of action and nutritional importance. Eur J Clin Nutr 1992;46:317-327.View Abstract
  • 226.Hallberg L. Does calcium interfere with iron absorption? Am J Clin Nutr 1998;68:3-4.
  • 227.Sokoll LJ, Dawson-Hughes B. Calcium supplementation and plasma ferritin concentrations in premenopausal women. Am J Clin Nutr 1992;56:1045-1048.View Abstract
  • 228.Lynch SR. Interaction of iron with other nutrients. Nutr Rev 1997;55:102-110.View Abstract
  • 229.Panel on Dietary Antioxidants and Related Compounds, Food and Nutrition Board, Institute of Medicine. Dietary Reference Intakes for Vitamin A, Vitamin K, Arsenic, Boron, Chromium, Copper, Iodine, Iron, Manganese, Molybdenum, Nickel, Silicon, Vanadium, and Zinc. Washington, DC: National Academy Press; 2001:290-293.
  • 230.Thompson JR, Gerald PF, Willoughby ML, Armstrong BK. Maternal folate supplementation in pregnancy and protection against acute lymphoblastic leukaemia in childhood: a case-control study. Lancet 2001;358:1935-1940.View Abstract
  • 231.Davis CD, Malecki EA, Greger JL. Interactions among dietary manganese, heme iron, and nonheme iron in women. Am J Clin Nutr 1992;56:926-932.
  • 232.Finley JW. Manganese absorption and retention by young women is associated with serum ferritin concentration. Am J Clin Nutr 1999;70:37-43.View Abstract
  • 233.Freeland-Graves JH. Manganese: an essential nutrient for humans. Nutr Today 1989;23:10-13.
  • 234.Sirdah MM, El-Agouza IM, Abu Shahla AN. Possible ameliorative effect of taurine in the treatment of iron-deficiency anaemia in female university students of Gaza, Palestine. Eur J Haematol 2002;69:236-242.View Abstract
  • 235.Semba RD, Muhilal, West KPJ et al. Impact of vitamin A supplementation on hematological indicators of iron metabolism and protein status in children. Nutr Res 1992;12:469-478.
  • 236.Suharno D, West CE, Muhilal et al. Supplementation with vitamin A and iron for nutritional anaemia in pregnant women in West Java, Indonesia. Lancet 1993;342:1325-1328.View Abstract
  • 237.Muñoz EC, Rosado JL, Lopez P et al. Iron and zinc supplementation improves indicators of vitamin A status of Mexican preschoolers. Am J Clin Nutr 2000;71:789-794.
  • 237a.Zadik Z, Sinai T, Zung A, Reifen R. Vitamin A and iron supplementation is as efficient as hormonal therapy in constitutionally delayed children. Clin Endocrinol (Oxf) 2004;60(6):682-687
  • 238.Brise H, Hallberg L. Effect of ascorbic acid on iron absorption. Acta Med Scand 1962;171(Suppl 376):51-58.View Abstract
  • 239.Lynch SR, Cook JD. Interaction of vitamin C and iron. Ann NY Acad Sci 1980;355:32-44.View Abstract
  • 240.Hallberg L, Brune M, Rossander L. Effect of ascorbic acid on iron absorption from different types of meals: studies with ascorbic-acid-rich foods and synthetic ascorbic acid given in different amounts with different meals. Hum Nutr Appl Nutr 1986;40:97-113.View Abstract
  • 241.Hallberg L, Brune M, Rossander L. The role of vitamin C in iron absorption. Int J Vitam Nutr Res Suppl 1989;30:103-108.View Abstract
  • 242.Hallberg L, Brune M, Rossander L. Iron absorption in man: ascorbic acid and dose-dependent inhibition by phytate. Am J Clin Nutr 1989;49:140-144.View Abstract
  • 243.Hunt JR, Gallagher SK, Johnson LK. Effect of ascorbic acid on apparent iron absorption by women with low iron stores. Am J Clin Nutr 1994;59:1381-1385.View Abstract
  • 244.Siegenberg D, Baynes RD, Bothwell TH et al. Ascorbic acid prevents the dose-dependent inhibitory effects of polyphenols and phytates on nonheme-iron absorption. Am J Clin Nutr 1991;53:537-541.View Abstract
  • 245.Hoffman KE, Yanelli K, Bridges KR. Ascorbic acid and iron metabolism: alterations in lysosomal function. Am J Clin Nutr 1991;54:1188S-1192S.View Abstract
  • 246.Melhorn DK, Gross S. Relationships between iron-dextran and vitamin E in iron deficiency anemia in children. J Lab Clin Med 1969;74:789-802.
  • 247.Zago MP, Oteiza PI. The antioxidant properties of zinc: interactions with iron and antioxidants. Free Radic Biol Med 2001;31:266-274.View Abstract
  • 248.Hurrell RF, Reddy M, Cook JD. Inhibition of non-haem iron absorption in man by polyphenolic-containing beverages. Br J Nutr 1999;81:289-295.View Abstract
  • 249.Morck TA, Lynch SR, Cook JD. Inhibition of food iron absorption by coffee. Am J Clin Nutr 1983;37:416-420.View Abstract
  • 250.Muñoz LM, Lonnerdal B, Keen CL, Dewey KG. Coffee consumption as a factor in iron deficiency anemia among pregnant women and their infants in Costa Rica. Am J Clin Nutr 1988;48:645-651.
  • 251.Merhav H, Amitai Y, Palti H, Godfrey S. Tea drinking and microcytic anemia in infants. Am J Clin Nutr 1985;41(6):1210-1213.View Abstract
  • 252.Koren G, Boichis H, Keren G. Effects of tea on the absorption of pharmacological doses of an oral iron preparation. Sci Meet Israel 1982;18:547.
  • 253.Samman S, Sandstrom B, Toft MB et al. Green tea or rosemary extract added to foods reduces nonheme-iron absorption. Am J Clin Nutr 2001;73:607-612.View Abstract
  • .[No authors listed.] Infect Dis News June;1990:17.
  • .[No authors listed.] Iron deficiency: United States, 1999-2000. MMWR Morb Mortal Wkly Rep 2002;51(40):897-899.
  • .[No authors listed.] Product information: Actonel, risedronate. Cincinnati: Procter & Gamble Pharmaceuticals, Inc;1998.
  • .[No authors listed.] Product information: Prilosec, omeprazole. Wayne, PA: Astra Merck Inc;1995.
  • .[No authors listed.] Product information: Skelid, tiludronate. New York: Sanofi Pharmaceuticals, Inc;1998.
  • .[No authors listed.] Product information: Syprine, trientine hydrochloride. West Point, PA: Merck & Co, Inc;1997.
  • .[No authors listed.] The Food and Nutrition Information Center: National Agricultural Library (NAL), United States Department of Agriculture’s (USDA) Agricultural Research Service (ARS). Available at March 18, 1999.
  • .Ahluwalia N, Sun J, Krause D, et al. Immune function is impaired in iron-deficient, homebound, older women. Am J Clin Nutr 2004;79(3):516-521.
  • .Allen J, Backstrom KR, Cooper JA, et al. Measurement of soluble transferrin receptor in serum of healthy adults. Clin Chem 1998;44(1):35-39.
  • .Allen RP, Barker PB, Wehrl F, et al. MRI measurement of brain iron in patients with restless legs syndrome. Neurology 2001;56(2):263-265.
  • .Ames BN. DNA damage from micronutrient deficiencies is likely to be a major cause of cancer. Mutat Res 2001;475(1-2):7-20. (Review)
  • .Ames BN, Elson-Schwab I, Silver EA. High-dose vitamin therapy stimulates variant enzymes with decreased coenzyme binding affinity (increased K(m)): relevance to genetic disease and polymorphisms. Am J Clin Nutr 2002;75(4):616-658. (Review)
  • .Anderson GJ, Powell LW. Of metals, mice, and men: what animal models can teach us about body iron loading. J Clin Invest 2000;105(9):1185-1186.
  • .Arvidsson B, Ekenved G, Rybo G, et al. Iron prophylaxis in menorrhagia. Acta Obstet Gynecol Scand 1981;60(2):157-160.
  • .Atamna H. Heme, iron, and the mitochondrial decay of ageing. Ageing Res Rev 2004;3(3):303-318.
  • .Atamna H, Frey WH II. A role for heme in Alzheimer’s disease: heme binds amyloid beta and has altered metabolism. Proc Natl Acad Sci U S A 2004;101(30):11153-11158.
  • .Atamna H, Killilea DW, Killilea AN, et al. Heme deficiency may be a factor in the mitochondrial and neuronal decay of aging. Proc Natl Acad Sci U S A 2002;99(23):14807-14812.
  • .Atamna H, Walter PB, Ames BN. The role of heme and iron-sulfur clusters in mitochondrial biogenesis, maintenance, and decay with age. Arch Biochem Biophys 2002;397(2):345-353. (Review)
  • .Bastani B, Jain A, Pandurangan G. Incidence of side-effects associated with high-dose ferric gluconate in patients with severe chronic renal failure. Nephrology (Carlton) 2003;8(1):8-10.
  • .Basu TK, Donaldson D. Intestinal absorption in health and disease: micronutrients. Best Pract Res Clin Gastroenterol 2003;17(6):957-979.
  • .Baumgaertel A. Alternative and controversial treatments for attention-deficit/hyperactivity disorder. Pediatr Clin North Am 1999;46(5):977-992.
  • .Baynes RD, Macfarlane BJ, Bothwell TH, et al. The promotive effect of soy sauce on iron absorption in human subjects. Eur J Clin Nutr 1990;44:419-424.
  • .Bays HE, Dujovne CA. Drug interactions of lipid-altering drugs. Drug Saf 1998;19(5):355-371. (Review)
  • .Beard JL. Effectiveness and strategies of iron supplementation during pregnancy. Am J Clin Nutr 2000;71(Suppl):1288S-1294S. (Review)
  • .Beard JL. Iron biology in immune function, muscle metabolism and neuronal functioning. J Nutr 2001;131(2S-2):568S-579S. (Review)
  • .Beard JL, Dawson HD. Iron. In: O’Dell BL, Sunde RA, eds. Handbook of nutritionally essential minerals. New York: Marcel Dekker, Inc; 1997:275-334.
  • .Belton N. Iron deficiency in infants and young children. Professional Care Mother Child 1995;5:69-71.
  • .Bender-Gotze C. Therapy of juvenile iron deficiency with bivalent iron dragees (Fe2-fumarate, succinate, sulfate): controlled double-blind study. Fortschr Med 1980;98:590-593. [German]
  • .Bendich A, Cohen M. Ascorbic acid safety: analysis of factors affecting iron absorption. Toxicol Lett 1990;51:189-201.
  • .Bergmann RL, Gravens-Muller L, Hertwig K, et al. Iron deficiency is prevalent in a sample of pregnant women at delivery in Germany. Eur J Obstet Gynecol Reprod Biol 2002;102(2):155-160.
  • .Bezwoda WR, Torrance JD, Bothwell TH, et al. Iron absorption from red and white wines. Scand J Haematol 1985;34:121-127.
  • .Bhatia MS, Singhal PK, Dhar NK, et al. Breath holding spells: an analysis of 50 cases. Indian Pediatr 1990;27:1073-1079.
  • .Bienfait HF, Van Del Briel ML. Rapid mobilization of ferritin iron by ascorbate in the presence of oxygen. Biochim Biophys Acta 1980;631:507-510.
  • .Bjorn-Rasmussen E, Hallberg L. Effect of animal proteins on the absorption of food iron in man. Nutr Metab 1979;23:192-202.
  • .Blanck HM, Cogswell ME, Gillespie C, et al. Iron supplement use and iron status among US adults: results from the third National Health and Nutrition Examination Survey. Am J Clin Nutr 2005;82:1024-1031.
  • .Bostick R. Diet and nutrition in the prevention of colon cancer. In: Bendich A, Deckelbaum RJ, eds. Preventive nutrition: the comprehensive guide for health professionals. 2nd ed. Totowa: Humana Press, Inc; 2001:57-95.
  • .Bothwell TH. Iron in the soul. Proc R Coll Physicians Edinb 1991;21(1):72-81.
  • .Bothwell TH, Bradlow BA, Jacobs P, et al. Iron metabolism in scurvy with special reference to erythropoiesis. Br J Haematol 1964;10:50-58.
  • .Bradman A, Eskenazi B, Sutton P, et al. Iron deficiency associated with higher blood lead in children living in contaminated environments. Environ Health Perspect 2001;109(10):1079-1084.
  • .Bridge EM, Livingston S, Tietze C. Breath-holding spells: their relationship to syncope, convulsions and other phenomena. J Pediatr 1943;23:539-561.
  • .Brise H. Influence of meals on iron absorption in oral iron therapy. Acta Med Scand 1962;171(Suppl 376):39-45.
  • .Brody T. Nutritional biochemistry. 2nd ed. San Diego: Academic Press; 1999.
  • .Brotanek JM, Halterman JS, Auinger P, et al. Iron deficiency, prolonged bottle-feeding, and racial/ethnic disparities in young children. Arch Pediatr Adolesc Med 2005;159(11):1038-1042.
  • .Brutsaert TD, Hernandez-Cordero S, Rivera J, et al. Iron supplementation improves progressive fatigue resistance during dynamic knee extensor exercise in iron-depleted, nonanemic women. Am J Clin Nutr 2003;77:441-448.
  • .Calabrese V, Butterfield DA, Stella AM. Nutritional antioxidants and the heme oxygenase pathway of stress tolerance: novel targets for neuroprotection in Alzheimer’s disease. Ital J Biochem 2003;52(4):177-181. (Review)
  • .Calvo E, Hertrampf E, de Pablo S, et al. Haemoglobin-fortified cereal: an alternative weaning food with high iron bioavailability. Eur J Clin Nutr 1989;43:237-243. (Review)
  • .Campbell NR, Hasinoff BB. Iron supplements: a common cause of drug interactions. Br J Clin Pharmacol 1991;31(3):251-255. (Review)
  • .Campbell NR, Paddock V, Sundaram R. Alteration of methyldopa absorption, metabolism, and blood pressure control caused by ferrous sulfate and ferrous gluconate. Clin Pharmacol Ther 1988;43(4):381-386.
  • .Canonne-Hergaux F, Gruenheid S, Ponka P, et al. Cellular and subcellular localization of the Nramp2 iron transporter in the intestinal brush border and regulation by dietary iron. Blood 1999;93(12):4406-4417.
  • .Casparis D, Del Carlo P, Branconi F, et al. Effectiveness and tolerability of oral liquid ferrous gluconate in iron-deficiency anemia in pregnancy and in the immediate post-partum period: comparison with other liquid or solid formulations containing bivalent or trivalent iron. Minerva Ginecol 1996;48:511-518. [Italian]
  • .Castaldo A, Tarallo L, Palomba E, et al. Iron deficiency and intestinal malabsorption in HIV disease. J Pediatr Gastroenterol Nutr 1996;22:359-363.
  • .Caulfield LE, Richard SA, Black RE. Undernutrition as an underlying cause of malaria morbidity and mortality in children less than five years old. Am J Trop Med Hyg 2004;71(2 Suppl):55-63. (Review)
  • .Celsing F, Blomstrand E, Werner B, et al. Effects of iron deficiency on endurance and muscle enzyme activity in man. Med Sci Sports Exerc 1986;18:156-161.
  • .Centers for Disease Control and Prevention. Recommendations to prevent and control iron deficiency in the United States. Morbid Mortal Wkly Rep 1998;47(RR-3):1-29.
  • .Charlton RW, Jacobs P, Seftel H, et al. Effect of alcohol on iron absorption. Br Med J 1964;5422:1427-1429.
  • .Chavarro JE, Rich-Edwards JW, Rosner BA, et al. Iron intake and risk of ovulatory infertility. Obstet Gynecol 2006;108(5):1145-1152.
  • .Chen WT, Lin YF, Yu FC, et al. Effect of ascorbic acid administration in hemodialysis patients on in vitro oxidative stress parameters: influence of serum ferritin levels. Am J Kidney Dis 2003;42(1):158-166.
  • .Chiang WC, Tsai TJ, Chen YM, et al. Serum soluble transferrin receptor reflects erythropoiesis but not iron availability in erythropoietin-treated chronic hemodialysis patients. Clin Nephrol 2002;58(5):363-369.
  • .Chin TF, Lach JL. Drug diffusion and bioavailability: tetracycline metallic chelation. Am J Hosp Pharm 1975;32(6):625-629.
  • .Christen Y. Oxidative stress and Alzheimer disease. Am J Clin Nutr 2000;71(Suppl):621S-629S.
  • .Christian P, Khatry SK, Katz J, et al. Effects of alternative maternal micronutrient supplements on low birth weight in rural Nepal: double blind randomised community trial. BMJ 2003;326(7389):571.
  • .Chuang CL, Liu RS, Wei YH, et al. Early prediction of response to intravenous iron supplementation by reticulocyte haemoglobin content and high-fluorescence reticulocyte count in haemodialysis patients. Nephrol Dial Transplant 2003;18(2):370-377.
  • .Cogswell ME, Kettel-Khan L, Ramakrishnan U. Iron supplement use among women in the United States: science, policy and practice. J Nutr 2003;133(6):1974S-1977S.
  • .Cogswell ME, Parvanta I, Ickes L, et al. Iron supplementation during pregnancy, anemia, and birth weight: a randomized controlled trial. Am J Clin Nutr 2003;78(4):773-781.
  • .Colina KF, Abelson HT. Resolution of breath-holding spells with treatment of concomitant anemia. J Pediatr 1995;126:395-397.
  • .Cook JD. Iron-deficiency anaemia. Baillieres Clin Haematol 1994;7(4):787-804. (Review)
  • .Cook JD, Monsen ER. Food iron absorption in human subjects:III: comparison of the effect of animal proteins on nonheme iron absorption. Am J Clin Nutr 1976;29:859-867.
  • .Cook JD, Morck TA, Lynch SR. The inhibitory effect of soy products on nonheme iron absorption in man. Am J Clin Nutr 1981;34:2622-2629.
  • .Cook JD, Reddy MB, Hurrell RF. The effect of red and white wines on nonheme-iron absorption in humans. Am J Clin Nutr 1995;61:800-804.
  • .Dallman PR. Manifestations of iron deficiency. Semin Hematol 1982;19(1):19-30. (Review)
  • .Danesh J, Appleby P. Coronary heart disease and iron status: meta-analyses of prospective studies. Circulation 1999;99:852-854.
  • .Daoud AS, Batieha A, Abu-Ekteish F, et al. Iron status: a possible risk factor for the first febrile seizure. Epilepsia 2002;43(7):740-743.
  • .Daoud AS, Batieha A, al-Sheyyab M, et al. Effectiveness of iron therapy on breath-holding spells. J Pediatr 1997;130(4):547-550.
  • .D’Arcy PF, McElnay JC. Drug interactions in the gut involving metal ions. Rev Drug Metabol Drug Interact 1985;5(2-3):83.
  • .D’Souza RF, Feakins R, Mears L, et al. Relationship between serum ferritin, hepatic iron staining, diabetes mellitus and fibrosis progression in patients with chronic hepatitis C. Aliment Pharmacol Ther 2005;21(5):519-524.
  • .Das KM, Eastwood MA. Effect of iron and calcium on salicylazosulphapyridine metabolism. Scand Med J 1973;18:45-50.
  • .Davolos A, Castillo J, Marrugat J, et al. Body iron stores and early neurologic deterioration in acute cerebral infarction. Neurology 2000;54:1568-1574.
  • .Davidsson L, Kastenmayer P, Szajewska H, et al. Iron bioavailability in infants from an infant cereal fortified with ferric pyrophosphate or ferrous fumarate. Am J Clin Nutr 2000;71:1597-1602.
  • .Davila-Hicks P, Theil EC, Lonnerdal B. Iron in ferritin or in salts (ferrous sulfate) is equally bioavailable in nonanemic women. Am J Clin Nutr 2004;80:936-940.
  • .Day SM, Duquaine D, Mundada LV, et al. Chronic iron administration increases vascular oxidative stress and accelerates arterial thrombosis. Circulation 2003;107:2601-2606.
  • .De Block CE, Van Campenhout CM, De Leeuw IH, et al. Soluble transferrin receptor level: a new marker of iron deficiency anemia, a common manifestation of gastric autoimmunity in type 1 diabetes. Diabetes Care 2000;23(9):1384-1388.
  • .de Valk B, Marx MMJ. Iron, atherosclerosis, and ischemic heart disease. Arch Intern Med 1999;159:1542-1548. (Review)
  • .Deira J, Diego J, Martinez R, et al. Comparative study of intravenous ascorbic acid versus low-dose desferroxamine in patients on hemodialysis with hyperferritinemia. J Nephrol 2003;16(5):703-709.
  • .Derman D, Sayers M, Lynch SR, et al. Iron absorption from a cereal-based meal containing cane sugar fortified with ascorbic acid. Br J Nutr 1977;38:261-269.
  • .Dewey KG, Domellof M, Cohen RJ, et al. Iron supplementation affects growth and morbidity of breast-fed infants: results of a randomized trial in Sweden and Honduras. J Nutr 2002;132(11):3249-3255.
  • .Dewey KG, Romero-Abal ME, Quan de Serrano J, et al. A randomized intervention study of the effects of discontinuing coffee intake on growth and morbidity of iron-deficient Guatemalan toddlers. J Nutr 1997;127(2):306-313.
  • .Dietzfelbinger H. Bioavailability of bi- and trivalent oral iron preparations: investigations of iron absorption by postabsorption serum iron concentrations curves. Arzneimittelforschung 1987;37:107-112. (Review)
  • .Dimitriou H, Stiakaki E, Markaki EA, et al. Soluble transferrin receptor levels and soluble transferrin receptor/log ferritin index in the evaluation of erythropoietic status in childhood infections and malignancy. Acta Paediatr 2000;89(10):1169-1173.
  • .Diplock AT. Safety of antioxidant vitamins and beta-carotene. Am J Clin Nutr 1995;62(Suppl 6):1510S-1516S.
  • .Disler PB, Lynch SR, Charlton RW, et al. The effect of tea on iron absorption. Gut 1975;16:193-200.
  • .Domellof M, Dewey KG, Lonnerdal B, et al. The diagnostic criteria for iron deficiency in infants should be reevaluated. J Nutr 2002;132(12):3680-3686.
  • .Domellof M, Lonnerdal B, Abrams SA, et al. Iron absorption in breast-fed infants: effects of age, iron status, iron supplements, and complementary foods. Am J Clin Nutr 2002;76(1):198-204.
  • .Domellof M, Lonnerdal B, Dewey KG, et al. Sex differences in iron status during infancy. Pediatrics 2002;110(3):545-552.
  • .Doyle W. The association between maternal diet and birth dimensions. J Nutr Med 1990;1:9-17.
  • .Duffy SJ, Biegelsen ES, Holbrook M, et al. Iron chelation improves endothelial function in patients with coronary artery disease. Circulation 2001;103(23):2799-2804.
  • .Earley CJ, Connor JR, Beard JL, et al. Abnormalities in CSF concentrations of ferritin and transferrin in restless legs syndrome. Neurology 2000;54(8):1698-1700.
  • .Engle PL, VasDias T, Howard I, et al. Effects of discontinuing coffee intake on iron deficient Guatemalan toddlers’ cognitive development and sleep. Early Hum Dev 1999;53(3):251-269.
  • .Ezzati M, Lopez AD, Rodgers A, et al. Selected major risk factors and global and regional burden of disease. Lancet 2002;360(9343):1347-1360.
  • .Fairbanks VF. Iron in medicine and nutrition. In: Shils M, Olson JA, Shike M, et al, eds. Nutrition in health and disease. 9th ed. Baltimore: Williams & Wilkins; 1999:223-239.
  • .Farmer JA, Gotto AM Jr. Antihyperlipidaemic agents: drug interactions of clinical significance. Drug Saf 1994;11(5):301-309.
  • .Farmer JA, Gotto AM Jr. Choosing the right lipid-regulating agent: aguide to selection. Drugs 1996;52(5):649-661.
  • .Fernandez-Real JM, Penarroja G, Castro A, et al. Blood letting in high-ferritin type 2 diabetes: effects on vascular reactivity. Diabetes Care 2002;25(12):2249-2255.
  • .Ferrennini E. Insulin resistance, iron, and the liver. Lancet 2000;355:2181-2182.(Letter)
  • .Finch CA, Huebers H. Perspectives in iron metabolism. N Engl J Med 1982;306(25):1520-1528. (Review)
  • .Fischer Walker C, Kordas K, Stoltzfus RJ, et al. Interactive effects of iron and zinc on biochemical and functional outcomes in supplementation trials. Am J Clin Nutr 2005;82(1):5-12. (Review)
  • .Fleming DJ, Jacques PF, Dallal GE, et al. Dietary determinants of iron stores in a free-living elderly population: the Framingham Heart Study. Am J Clin Nutr 1998;67:722-733.
  • .Fleming DJ, Jacques PF, Tucker KL, et al. Iron status of the free-living, elderly Framingham Heart Study cohort: an iron-replete population with a high prevalence of elevated iron stores. Am J Clin Nutr 2001;73(3):638-646.
  • .Ford PA, Ford JM. Strategies to optimize the use of erythropoietin and iron therapy in oncology patients. Transfusion 2004;44(12 Suppl):15S-25S.
  • .Fox TE, Eagles J, Fairweather-Tait SJ. Bioavailability of iron glycine as a fortificant in infant foods. Am J Clin Nutr 1998;67:664-668.
  • .Freeland-Graves JH. Manganese: an essential nutrient for humans. Nutr Today 1989;23:10-13. (Review)
  • .Freeland-Graves J. Mineral adequacy of vegetarian diets. Am J Clin Nutr 1988;48(3 Suppl):859-862. (Review)
  • .Friedmann B, Weller E, Mairbaurl H, et al. Effects of iron repletion on blood volume and performance capacity in young athletes. Med Sci Sports Exerc 2001;33:741-746.
  • .Friel JK, Andrews WL, Aziz K, et al. A randomized trial of two levels of iron supplementation and developmental outcome in low birth weight infants. J Pediatr 2001;139(2):254-260.
  • .Frykman E, Bystrom M, Jansson U, et al. Side effects of iron supplements in blood donors: superior tolerance of heme iron. J Lab Clin Med 1994;123:561-564.
  • .Galan P, Yoon HC, Preziosi P, et al. Determining factors in the iron status of adult women in the SU.VI.MAX study:SUpplementation en VItamines et Mineraux AntioXydants. Eur J Clin Nutr 1998;52(6):383-388.
  • .Galloway R, Dusch E, Elder L, et al. Women’s perceptions of iron deficiency and anemia prevention and control in eight developing countries. Soc Sci Med 2002;55(4):529-544.
  • .Galloway R, McGuire J. Determinants of compliance with iron supplementation: supplies, side effects, or psychology? Soc Sci Med 1994;39(3):381-390. (Review)
  • .Gastaldello K, Vereerstraeten A, Nzame-Nze T, et al. Resistance to erythropoietin in iron-overloaded haemodialysis patients can be overcome by ascorbic acid administration. Nephrol Dial Transplant 1995;10(Suppl 6):44-47.
  • .Geerligs PD, Brabin BJ, Omari AA. Food prepared in iron cooking pots as an intervention for reducing iron deficiency anaemia in developing countries: a systematic review. J Hum Nutr Diet 2003;16(4):275-281.
  • .Gera T, Sachdev HP. Effect of iron supplementation on incidence of infectious illness in children: systematic review. BMJ 2002;325(7373):1142. (Review)
  • .Giancaspro V, Nuzziello M, Pallotta G, et al. Intravenous ascorbic acid in hemodialysis patients with functional iron deficiency: a clinical trial. J Nephrol 2000;13(6):444-449.
  • .Gibbs MA. Ascorbic acid use in hyporesponders to Epoetin alfa. Nephrol Nurs J 2000;27(4):413-415.
  • .Gibson RS. Strategies for preventing micronutrient deficiencies in developing countries. Asia Pac J Clin Nutr 2004;13(Suppl):S23.
  • .Goldberg A. The enzymic formation of haem by the incorporation of iron into protoporphyrin: importance of ascorbic acid, ergothioneine and glutathione. Br J Haematol 1959;5:150-157.
  • .Gordon N. Iron deficiency and the intellect. Brain Dev 2003;25(1):3-8. (Review)
  • .Grantham-McGregor S, Ani C. A review of studies on the effect of iron deficiency on cognitive development in children. J Nutr 2001;131(2S-2):649S-666S. (Review)
  • .Gunnarsson BS, Thorsdottir I, Palsson G. Iron status in 2-year-old Icelandic children and associations with dietary intake and growth. Eur J Clin Nutr 2004;58(6):901-906.
  • .Hallberg L. Bioavailability of dietary iron in man. Annu Rev Nutr 1981;1:123-147. (Review)
  • .Hallberg L. Combating iron deficiency: daily administration of iron is far superior to weekly administration. Am J Clin Nutr 1998;68(2):213-217.
  • .Hallberg L, Hulthen L. Prediction of dietary iron absorption: an algorithm for calculating absorption and bioavailability of dietary iron. Am J Clin Nutr 2000;71:1147-1160.
  • .Hallberg L, Rossander L. Effect of different drinks on the absorption of non-heme iron from composite meals. Hum Nutr Appl Nutr 1982;36:116-123.
  • .Hallberg L, Rossander L. Effect of soy protein on nonheme iron absorption in man. Am J Clin Nutr 1982;36:514-520.
  • .Hallberg L, Rossander L. Improvement of iron nutrition in developing countries: comparison of adding meat, soy protein, ascorbic acid, citric acid, and ferrous sulphate on iron absorption from a simple Latin American-type of meal. Am J Clin Nutr 1984;39:577-583.
  • .Hallberg L, Rossander L, Skanberg AB. Phytates and the inhibitory effect of bran on iron absorption in man. Am J Clin Nutr 1987;45(5):988-996.
  • .Halterman JS, Kaczorowski JM, Aligne CA, et al. Iron deficiency and cognitive achievement among school-aged children and adolescents in the United States. Pediatrics 2001;107(6):1381-1386.
  • .Hansen CM. Oral iron supplements. Am Pharm 1994;NS34:66-71. (Review)
  • .Harju E. Clinical pharmacokinetics of iron preparations. Clin Pharmacokinet 1989;17:69-89. (Review)
  • .Harvey LJ, Dainty JR, Hollands WJ, et al. Effect of high-dose iron supplements on fractional zinc absorption and status in pregnant women. Am J Clin Nutr 2007;85(1):131-136.
  • .Haschke F, Ziegler EE, Edwards BB, et al. Effect of iron fortification of infant formula on trace mineral absorption. J Pediatr Gastroenterol Nutr 1986;5:768-773.
  • .Hathcock JN. Metabolic mechanisms of drug-nutrient interactions. Fed Proc 1985;44(1 Pt 1):124-129. (Review)
  • .Heinrich HC, Oppitz KH, Gabbe EE. Inhibition of iron absorption in man by tetracycline. Klin Wochenschr 1974;52:493-498. [German]
  • .Hendler SS, Rorvik DR, eds. PDR for nutritional supplements. Montvale, NJ: Medical Economics Company, Inc; 2001.
  • .Hercberg S, Preziosi P, Galan P. Iron deficiency in Europe. Public Health Nutr 2001;4(2B):537-545.
  • .Hertrampf E, Olivares M, Pizarro F, et al. Haemoglobin fortified cereal: a source of available iron to breast-fed infants. Eur J Clin Nutr 1990;44:793-798.
  • .Hines Burnham T, et al, eds. Drug facts and comparisons. St Louis: Facts and Comparisons; 2000:1294.
  • .Hinton PS, Giordano C, Brownlie T, et al. Iron supplementation improves endurance after training in iron depleted, nonanemic women. J Appl Physiol 2000;88(3):1103-1111.
  • .Hoffbrand AV, Wonke B. Iron chelation therapy. J Intern Med Suppl 1997;740:37-41.
  • .Hoffbrand AV. Prospects for oral iron chelation therapy. J Lab Clin Med 1994;123(4):492-494. (Review)
  • .Holowach J, Thurston DL. Breath-holding spells and anemia. N Engl J Med 1963;268:21-23.
  • .Holt GA. Food and drug interactions. Chicago: Precept Press;1998. (Review)
  • .Hua NW, Stoohs RA, Facchini FS. Low iron status and enhanced insulin sensitivity in lacto-ovo vegetarians. Br J Nutr 2001;86(4):515-519.
  • .Hurrell RF, Furniss DE, Burri J, et al. Iron fortification of infant cereals: a proposal for the use of ferrous fumarate or ferrous succinate. Am J Clin Nutr 1989;49:1274-1282.
  • .Hurtado EK, Claussen AH, Scott KG. Early childhood anemia and mild or moderate mental retardation. Am J Clin Nutr 1999;69:115-119.
  • .Hussain MA, Green N, Flynn DM, et al. Effect of dose, time, and ascorbate on iron excretion after subcutaneous desferrioxamine. Lancet 1977;1(8019):977-979.
  • .Iannotti LL, Tielsch JM, Black MM, et al. Iron supplementation in early childhood: health benefits and risks. Am J Clin Nutr 2006;84(6):1261-1276. (Review)
  • .Imagawa M, Naruse S, Tsuji S, et al. Coenzyme Q10, iron, and vitamin B6 in genetically-confirmed Alzheimer’s disease. Lancet 1992;340(8820):671.
  • .Ivan M, Kondo K, Yang H, et al. HIFalpha targeted for VHL-mediated destruction by proline hydroxylation: implications for O2 sensing. Science 2001;292(5516):464-468.
  • .Iwasa M, Iwata K, Kaito M, et al. Efficacy of long-term dietary restriction of total calories, fat, iron, and protein in patients with chronic hepatitis C virus. Nutrition 2004;20(4):368-371.
  • .Jaakkola P, Mole DR, Tian YM, et al. Targeting of HIF-alpha to the von Hippel-Lindau ubiquitylation complex by O2-regulated prolyl hydroxylation. Science 2001;292(5516):468-472.
  • .Jiang R, Ma J, Ascherio A, et al. Dietary iron intake and blood donations in relation to risk of type 2 diabetes in men: a prospective cohort study. Am J Clin Nutr 2004;79(1):70-75.
  • .Kahn JL, Binns HJ, Chen T, et al. Persistence and emergence of anemia in children during participation in the Special Supplemental Nutrition Program for Women, Infants, and Children. Arch Pediatr Adolesc Med 2002;156(10):1028-1032.
  • .Kaltwasser JP, Werner E, Schalk K, et al. Clinical trial on the effect of regular tea drinking on iron accumulation in genetic haemochromatosis. Gut 1998;43:699-704.
  • .Kato I, Dnistrian AM, Schwartz M, et al. Iron intake, body iron stores and colorectal cancer risk in women: a nested case-control study. Int J Cancer 1999;80(5):693-698.
  • .Keven K, Kutlay S, Nergizoglu G, et al. Randomized, crossover study of the effect of vitamin C on EPO response in hemodialysis patients. Am J Kidney Dis 2003;41(6):1233-1239.
  • .Kiechl S, Willeit J, Egger G, et al. Body iron stores and the risk of carotid atherosclerosis: prospective results from the Bruneck study. Circulation 1997;96(10):3300-3307.
  • .Klausner RD, Rouault TA, Harford JB. Regulating the fate of mRNA: the control of cellular iron metabolism. Cell 1993;72(1):19-28. (Review)
  • .Klingshirn LA, Pate RR, Bourque SP, et al. Effect of iron supplementation on endurance capacity in iron-depleted female runners. Med Sci Sports Exerc 1992;24:819-824.
  • .Klipstein-Grobusch K, Grobbee DE, den Breeijen JH, et al. Dietary iron and risk of myocardial infarction in the Rotterdam Study. Am J Epidemiol 1999;149(5):421-428.
  • .Klipstein-Grobusch K, Koster JF, Grobbee DE, et al. Serum ferritin and risk of myocardial infarction in the elderly: the Rotterdam Study. Am J Clin Nutr 1999;69:1231-1236.
  • .Knodel LC, Talbert RL. Adverse effects of hypolipidaemic drugs. Med Toxicol 1987;2(1):10-32.
  • .Kohgo Y, Torimoto Y, Kato J. Transferrin receptor in tissue and serum: updated clinical significance of soluble receptor. Int J Hematol 2002;76(3):213-218.
  • .Koop H. Review article: metabolic consequences of long-term inhibition of acid secretion by omeprazole. Aliment Pharmacol Ther 1992;6(4):399-406. (Review)
  • .Koop H, Bachem MG. Serum iron, ferritin, and vitamin B12 during prolonged omeprazole therapy. J Clin Gastroenterol 1992;14(4):288-292.
  • .Kosch M, Schaefer RM. Iron management in renal failure patients: how do we achieve the best results? EDTNA ERCA J 2002;28:182-184.
  • .Krezenlok EP, Hoff JV. Accidental iron poisoning: aproblem of marketing and labeling. Pediatrics 1979;63:591-596.
  • .LaManca JJ, Haymes EM. Effects of iron repletion on VO2max, endurance, and blood lactate in women. Med Sci Sports Exerc 1993;25:1386-1392.
  • .Lao TT, Tam K, Chan LY. Third trimester iron status and pregnancy outcome in non-anaemic women; pregnancy unfavourably affected by maternal iron excess. Hum Reprod 2000;15:1843-1848.
  • .Layrisse M, Martinez-Torres C, Roche M. Effect of interaction of various foods on iron absorption. Am J Clin Nutr 1968;21:1175-1183.
  • .Lee DH, Anderson KE, Harnack LJ, et al. Heme iron, zinc, alcohol consumption, and colon cancer: Iowa Women’s Health Study. J Natl Cancer Inst 2004;96(5):403-407.
  • .Lee GR. Disorders of iron metabolism and heme synthesis. In: Lee GR, Foerster J, Paraskevas F, et al, eds. Wintrobe’s clinical hematology. 10th ed. Baltimore: Williams and Wilkins; 1999:979-1070.
  • .Leng S, Chaves P, Koenig K, et al. Serum interleukin-6 and hemoglobin as physiological correlates in the geriatric syndrome of frailty: a pilot study. J Am Geriatr Soc 2002;50(7):1268-1271.
  • .Leonards JR, Levy G, Niemczura R. Gastrointestinal blood loss during prolonged aspirin administration. N Engl J Med. 1973;289(19):1020-1022.
  • .Leyden JJ. Absorption of minocycline hydrochloride and tetracycline hydrochloride: effect of food, milk, and iron. J Am Acad Dermatol 1985;12(2 Pt 1):308-312.
  • .Li CL, Werner P, Cohen G. Lipid peroxidation in brain: interactions of L-DOPA/dopamine with ascorbate and iron. Neurodegeneration 1995;4(2):147-153. Erratum in Neurodegeneration 1995;4(3):347.
  • .Liehr JG, Jones JS. Role of iron in estrogen-induced cancer. Curr Med Chem 2001;8(7):839-849.
  • .Lih-Brody L, Powell Sr, Collier KP, et al. Increased oxidative stress and decreased antioxidant defenses in mucosa of inflammatory bowel disease. Dig Dis Sci 1996;41(10):2078-2086.
  • .Lim, D, McKay, M. Food-drug interactions. Drug Information Bull 1995;15(2). (Review)
  • .Lin CL, Hsu PY, Yang HY, et al. Low dose intravenous ascorbic acid for erythropoietin-hyporesponsive anemia in diabetic hemodialysis patients with iron overload. Ren Fail 2003;25(3):445-453.
  • .Lin YW, Okazaki S, Hamahata K, et al. Acute pure red cell aplasia associated with allopurinol therapy. Am J Hematol 1999;61(3):209-211.
  • .Lind T, Hernell O, Lonnerdal B, et al. Dietary iron intake is positively associated with hemoglobin concentration during infancy but not during the second year of life. J Nutr 2004;134(5):1064-1070.
  • .Lochhead AC, Goldberg A. Transfer of iron to protoporphyrin for haem biosynthesis: role of ascorbic acid and glutathione. Lancet 1959;2:271-272.
  • .Logan EC, Yates JM, Stewart RM, et al. Investigation and management of iron deficiency anaemia in general practice: a cluster randomised controlled trial of a simple management prompt. Postgrad Med J 2002;78(923):533-537.
  • .Lönnerdal B, Bryant A. Absorption of iron from recombinant human lactoferrin in young US women. Am J Clin Nutr 2006;83:305-309.
  • .Lozoff B, De Andraca I, Castillo M, et al. Behavioral and developmental effects of preventing iron-deficiency anemia in healthy full-term infants. Pediatrics 2003;112(4):846-854. Erratum in Pediatrics 2004;113(6):1853.
  • .Lukaski HC, Bolonchuk WW, Klevay LM, et al. Interactions among dietary fat, mineral status, and performance of endurance athletes: a case study. Int J Sport Nutr Exerc Metab 2001;11(2):186-198.
  • .Lyle WH. Penicillamine and iron. Lancet 1976;2(7982):420. (Letter)
  • .Lynch SR. Interaction of iron with other nutrients. Nutr Rev 1997;55(4):102-110. (Review)
  • .Macfarlane BJ, van der Riet WB, Bothwell TH, et al. Effect of traditional oriental soy products on iron absorption. Am J Clin Nutr 1990;51:873-880.
  • .Mainous AG III, Gill JM, Carek PJ. Elevated serum transferrin saturation and mortality. Ann Fam Med 2004;2(2):133-138.
  • .Mainous AG III, Gill JM, Everett CJ. Transferrin saturation, dietary iron intake, and risk of cancer. Ann Fam Med 2005;3:131-137.
  • .Mainous AG III, Wells BJ, Koopman RJ, et al. Iron, lipids, and risk of cancer in the Framingham Offspring cohort. Am J Epidemiol 2005;161(12):1115-1122.
  • .Makoff R. Vitamin replacement therapy in renal failure patients. Miner Electrolyte Metab 1999;25(4-6):349-351. (Review)
  • .Marchal C, Spaeth D, Casadevall N, et al. Comite d’organisation des Standards, Options and Recommendations. [Standards, options and recommendations for the use of recombinant erythropoietin (epoietin alpha and beta darbepoietin-alpha, EPO) in the management of anaemia in oncology for patient undergoing radiotherapy-update 2003.] Cancer Radiother 2004;8(3):197-206. [French]
  • .Martin TJ, Grill V. Bisphosphonates: mechanisms of action. Aust Prescr 2000;23:130-132. (Review)
  • .Martinez C, Fox T, Eagles J, et al. Evaluation of iron bioavailability in infant weaning foods fortified with haem concentrate. J Pediatr Gastroenterol Nutr 1998;27:419-424.
  • .Marz R. Medical nutrition from Marz. 2nd ed. Portland, OR: Omni Press; 1997. (Review)
  • .Maskos Z, Koppenol WH. Oxyradicals and multivitamin tablets. Free Radic Biol Med 1991;11:609-610.
  • .Mason P. Nutrition and dietary advice in the pharmacy. Oxford, UK: Blackwell Scientific; 1994:234-235. (Review)
  • .Mebrahtu T, Stoltzfus RJ, Chwaya HM, et al. Low-dose daily iron supplementation for 12 months does not increase the prevalence of malarial infection or density of parasites in young Zanzibari children. J Nutr 2004;134(11):3037-3041.
  • .Menendez C, Schellenberg D, Quinto L, et al. The effects of short-term iron supplementation on iron status in infants in malaria-endemic areas. Am J Trop Med Hyg 2004;71(4):434-440.
  • .Michael B, Coyne DW, Fishbane S, et al. For the Ferrlecit Publication Committee: sodium ferric gluconate complex in hemodialysis patients: adverse reactions when compared to placebo and iron dextran. Kidney Int 2002;61:1830-1839.
  • .Mills KC, Curry SC. Acute iron poisoning. Emerg Med Clin NorthAm 1994;12;397-413.
  • .Miret S, Simpson RJ, McKie AT. Physiology and molecular biology of dietary iron absorption. Annu Rev Nutr 2003;23:283-301. (Review)
  • .Mocan H, Yildiran A, Orhan F, et al. Breath holding spells in 91 children and response to treatment with iron. Arch Dis Child 1999;81:261-262.
  • .Morley R, Abbott R, Fairweather-Tait S, et al. Iron fortified follow on formula from 9 to 18 months improves iron status but not development or growth: a randomised trial. Arch Dis Child 1999;81:247-252.
  • .Murray-Kolb LE, Beard JL, Joseph LJ, et al. Resistance training affects iron status in older men and women. Int J Sport Nutr Exerc Metab 2001;11(3):287-298.
  • .Murray-Kolb LE, Welch R, Theil EC, et al. Women with low iron stores absorb iron from soybeans. Am J Clin Nutr 2003;77(1):180-184.
  • .Nagral A, Mehta AB, Gomes AT, et al. Serum soluble transferrin receptor in the diagnosis of iron deficiency in chronic liver disease. Clin Lab Haematol 1999;21(2):93-97.
  • .National Heart Lung, and Blood Institute Working Group on Restless Legs Syndrome. Restless legs syndrome: detection and management in primary care. Am Fam Physician 2000;62(1):108-114.
  • .Nead KG, Halterman JS, Kaczorowski JM, et al. Overweight children and adolescents: a risk group for iron deficiency. Pediatrics 2004;114(1):104-108.
  • .Nelson M, Ash R, Mulvhill C, et al. Iron status, diet and cognitive function in British adolescent girls. Poster presented at The Nutrition Society’s Nutrition 2000: Research Themes for the New Millenium.Cork, Ireland, Jun 26, 2000.
  • .Newhouse IJ, Clement DB, Lai C. Effects of iron supplementation and discontinuation on serum copper, zinc, calcium, and magnesium levels in women. Med Sci Sports Exerc 1993;25(5):562-571.
  • .Nightingale SL. Action to prevent accidental iron poisoning in children. JAMA 1997;27:1343.
  • .Nyakeriga AM, Troye-Blomberg M, Dorfman JR, et al. Iron deficiency and malaria among children living on the coast of Kenya. J Infect Dis 2004;190(3):439-447.
  • .O’Keeffe ST, Gavin K, Lavan JN. Iron status and restless legs syndrome in the elderly. Age Ageing 1994;23(3):200-203.
  • .Ogi M, Horiuchi T, Abe R, et al. [Comparison of intravenous ascorbic acid versus intravenous iron for functional iron deficiency in hemodialysis patients.] Nippon Jinzo Gakkai Shi 2004;46(8):804-809. [Japanese]
  • .Oppenheimer SJ. Iron and its relation to immunity and infectious disease. J Nutr 2001;131(2S-2):616S-633S.
  • .Papapoulos SE. The role of bisphosphonates in the prevention and treatment of osteoporosis. Am J Med 1993;95(Suppl 5A):48S-52S. (Review)
  • .Perez EM, Hendricks MK, Beard JL, et al. Mother-infant interactions and infant development are altered by maternal iron deficiency anemia. J Nutr 2005;135(4):850-855.
  • .Peterson DA, Gerrard JM, Rao GH, et al. Inhibition of ferrous iron induced oxidation of arachidonic acid by indomethacin. Prostaglandins Med 1979;2(2):97-108.
  • .Picciano MF. Pregnancy and lactation: physiological adjustments, nutritional requirements and the role of dietary supplements. J Nutr 2003;133(6):1997S-2002S. (Review)
  • .Pietrangelo A. Hemochromatosis 1998: is one gene enough? J Hepatol 1998;29(3):502-509.
  • .Pietrangelo A. Hereditary hemochromatosis: a new look at an old disease. N Engl J Med 2004;350(23):2383-2397. (Review)
  • .Pineda O, Ashmead HD, Perez JM, et al. Effectiveness of iron amino acid chelate on the treatment of iron deficiency anemia in adolescents. J Appl Nutr 1994;46:2-13.
  • .Pinto JT. The pharmacokinetic and pharmacodynamic interactions of foods and drugs. Top Clin Nutr 1991;6(3):14-33. (Review)
  • .Piperno A, Trombini P, Gelosa M, et al. Increased serum ferritin is common in men with essential hypertension. J Hypertens 2002;20(8):1513-1518.
  • .Polk RE. Drug-drug interactions with ciprofloxacin and other fluoroquinolones. Am J Med 1989;87(5A):76S-81S. (Review)
  • .Pollitt E. Poverty and child development: relevance of research in developing countries to the United States. Child Dev 1994;65(2 Spec No.):283-295.
  • .Ponka P. Tissue-specific regulation of iron metabolism and heme synthesis: distinct control mechanisms in erythroid cells. Blood 1997;89(1):1-25. (Review)
  • .Powanda MC, Blackburn BS, Bostian KA, et al. Clofibrate-induced alterations in zinc, iron and copper metabolism. Biochem Pharmacol 1978;27(1):125-127.
  • .Powers KM, Smith-Weller T, Franklin GM, et al. Parkinson’s disease risks associated with dietary iron, manganese, and other nutrient intakes. Neurology 2003;60(11):1761-1766.
  • .Ramakrishnan U. Nutrition and low birth weight: from research to practice. Am J Clin Nutr 2004;79(1):17-21. (Review)
  • .Ramakrishnan U, Gonzalez-Cossio T, Neufeld LM, et al. Multiple micronutrient supplementation during pregnancy does not lead to greater infant birth size than does iron-only supplementation: a randomized controlled trial in a semirural community in Mexico. Am J Clin Nutr 2003;77(3):720-725.
  • .Rasmussen K. Is there a causal relationship between iron deficiency or iron-deficiency anemia and weight at birth, length of gestation and perinatal mortality? J Nutr 2001;131(2S-2):590S-601S.
  • .Richardson DR, Ponka P. The molecular mechanisms of the metabolism and transport of iron in normal and neoplastic cells. Biochim Biophys Acta 1997;1331(1):1-40. (Review)
  • .Ricketts CD. Iron bioavailability from controlled-release and conventional iron supplements. J Appl Nutr 1993;45:13-19.
  • .Riedel MK, Morgenstern T. [Iron replacement in hemodialysis patients with a normal serum ferritin level.] Dtsch Med Wochenschr 2004;129(36):1849-1853. [German]
  • .Rimon E, Kagansky N, Kagansky M, et al. Are we giving too much iron? Low-dose iron therapy is effective in octogenarians. Am J Med 2005;118(10):1142-1147. 
  • .Roe DA. Drug and nutrient interactions in the elderly diabetic. Drug Nutr Interact 1988;5(4):195-203. (Review)
  • .Roe DA. Drug-induced nutritional deficiencies. 2nd ed. Westport, CT: Avi Publishing;1985. (Review)
  • .Roe DA. Risk factors in drug-induced nutritional deficiencies. In: Roe DA, Campbell T, eds. Drugs and nutrients: the interactive effects. New York: Marcel Decker;1984. (Review)
  • .Roncagliolo M, Garrido M, Walter T, et al. Evidence of altered central nervous system development in infants with iron deficiency anemia at 6 mo: delayed maturation of auditory brainstem responses. Am J Clin Nutr 1998;68:683-690.
  • .Rossander L, Hallberg L, Bjorn-Rasmussen E. Absorption of iron from breakfast meals. Am J Clin Nutr 1979;32:2484-249.
  • .Rowland TW, Deisroth MB, Green GM, et al. The effect of iron therapy on the exercise capacity of nonanemic iron-deficient adolescent runners. Am J Dis Child 1988;142:165-169.
  • .Rudinskas L, Paton TW, Walker SE. Poor clinical response to enteric-coated iron preparations. Can Med Assoc J 1989;141:565-566.
  • .Sakagami H, Satoh K, Fukuchi K, et al. Effect on an iron-chelator on ascorbate-induced cytotoxicity. Free Radic Biol Med 1997;23(2):260-270.
  • .Salahudeen AK, Fleischmann E, Ahmed A, et al. Anemia and iron target realization in 1998: clinical management of anemia in 1,639 patients on hemodialysis. ASAIO J 2001;47(5):511-515.
  • .Salonen JT, Nyyssonen K, Korpela H, et al. High stored iron levels associated with excess risk of myocardial infarction in western Finnish men. Circulation 1992;86(3):803-811.
  • .Sandberg AS, Brune M, Carlsson NG, et al. Inositol phosphates with different numbers of phosphate groups influence iron absorption in humans. Am J Clin Nutr 1999;70:240-246.
  • .Sandstrom B, Davidsson L, Cederblad A, et al. Oral iron, dietary ligands and zinc absorption. J Nutr 1985;115(3):411-414.
  • .Say AE, Gursurer M, Yazicioglu MV, et al. Impact of body iron status on myocardial perfusion, left ventricular function, and angiographic morphologic features in patients with hypercholesterolemia. Am Heart J 2002;143(2):257-264.
  • .Schaefer JP, Tam Y, Hasinoff BB, et al. Ferrous sulphate interacts with captopril. Br J Clin Pharmacol 1998;46(4):377-381.
  • .Schaible UE, Collins HL, Priem F, et al. Correction of the iron overload defect in beta-2-microglobulin knockout mice by lactoferrin abolishes their increased susceptibility to tuberculosis. J Exp Med 2002;196(11):1507-1513.
  • .Sempos C, Looker AC, Gillum RE, et al. Serum ferritin and death from all causes of cardiovascular disease: the NHANES II Mortality Study. Ann Epidemiol 2000;10(7):441-448.
  • .Seo JK, Ko JS, Choi KD. Serum ferritin and Helicobacter pylori infection in children: a sero-epidemiologic study in Korea. J Gastroenterol Hepatol 2002;17(7):754-757.
  • .Sever Y, Ashkenazi A, Tyano S, et al. Iron treatment in children with attention deficit hyperactivity disorder: a preliminary report. Neuropsychobiology 1997;35:178-180.
  • .Shah BK, Gupta P. Weekly vs daily iron and folic acid supplementation in adolescent Nepalese girls. Arch Pediatr Adolesc Med 2002;156(2):131-135.
  • .Shakir KM, Chute JP, Aprill BS, et al. Ferrous sulfate-induced increase in requirement for thyroxine in a patient with primary hypothyroidism. South Med J 1997;90(6):637-639.
  • .Sherman PM, Macarthur C. Current controversies associated with Helicobacter pylori infection in the pediatric population. Front Biosci 2001;6:E187-192.
  • .Shils ME, Olson JA, Shike M, eds. Modern nutrition in health and disease. 9th ed. Baltimore: Williams & Wilkins; 1999:210,860,1422,1424,1772.
  • .Siega-Riz AM, Hartzema AG, Turnbull C, et al. The effects of prophylactic iron given in prenatal supplements on iron status and birth outcomes: a randomized controlled trial. Am J Obstet Gynecol 2006;194(2):512-519.
  • .Silber MH, Richardson JW. Multiple blood donations associated with iron deficiency in patients with restless legs syndrome. Mayo Clin Proc 2003;78(1):52-54.
  • .Simmons WK, Cook JD, Bingham KC, et al. Evaluation of a gastric delivery system for iron supplementation in pregnancy. Am J Clin Nutr 1993;58:622-626.
  • .Simonart T, Boelaert JR, Mosselmans R, et al. Antiproliferative and apoptotic effects of iron chelators on human cervical carcinoma cells. Gynecol Oncol 2002;85(1):95-102.
  • .Simpson KM, Morris ER, Cook JD. The inhibitory effect of bran on iron absorption. Am J Clin Nutr 1981;34:1469-1478.
  • .Singh NP, Lai H. Selective toxicity of dihydroartemisinin and holotransferrin toward human breast cancer cells. Life Sci 2001;70(1):49-56.
  • .Skaar EP, Humayun M, Bae T, et al. Iron-source preference of Staphylococcus aureus infections. Science 2004;305(5690):1626-1628.
  • .Smythies J. The neurotoxicity of glutamate, dopamine, iron and reactive oxygen species: functional interrelationships in health and disease: a review-discussion. NeurotoxicolRes 1999;1(1):27-39. (Review)
  • .Spaeth D, Casadevall N, Daouphars M, et al; Standards, Options and Recommendations project. [Summary version of the Standards, Options and Recommendations for the use of recombinant erythropoietin (epoietin-alpha and beta, darbepoietin-alpha, EPO) in the management of anaemia in oncology: update 2003.] Bull Cancer 2004;91(2):179-188. [French]
  • .Srigiridhar K, Nair KM. Supplementation with alpha-tocopherol or a combination of alpha-tocopherol and ascorbic acid protects the gastrointestinal tract of iron-deficient rats against iron-induced oxidative damage during iron repletion. Br J Nutr 2000;84(2):165-173.
  • .Stewart CA, Termanini B, Sutliff VE, et al. Iron absorption in patients with Zollinger-Ellison syndrome treated with long-term gastric acid antisecretory therapy. Aliment Pharmacol Ther 1998;12(1):83-98.
  • .Sturniolo GC, Mestriner C, Lecis PE, et al. Altered plasma and mucosal concentrations of trace elements and antioxidants in active ulcerative colitis. Scand J Gastroenterol 1998;33:644-649.
  • .Sullivan JL. Stored iron and ischemic heart disease. Circulation 1992;86:1036. (Editorial)
  • .Sun ER, Chen CA, Ho G, et al. Iron and the restless legs syndrome. Sleep 1998;21:371-377.
  • .Tarng DC, Huang TP. A parallel, comparative study of intravenous iron versus intravenous ascorbic acid for erythropoietin-hyporesponsive anaemia in haemodialysis patients with iron overload. Nephrol Dial Transplant 1998;13: 2867-2872.
  • .Tarng DC, Huang TP, Chen TW. Mathematical approach for estimating iron needs in hemodialysis patients on erythropoietin therapy. Am J Nephrol 1997;17(2):158-164.
  • .Tarng DC, Huang TP, Chen TW, et al. Erythropoietin hyporesponsiveness: from iron deficiency to iron overload. Kidney Int Suppl 1999;69:S107-S118. (Review)
  • .Tarng DC, Hung SC, Huang TP. Effect of intravenous ascorbic acid medication on serum levels of soluble transferrin receptor in hemodialysis patients. J Am Soc Nephrol 2004;15(9):2486-2493.
  • .Tarng DC, Huang T-P, Wei YH. Erythropoietin and iron: the role of ascorbic acid. Nephrol Dial Transplant 2001;16(Suppl 5):35-39. (Review)
  • .Tarng DC, Wei YH, Huang TP, et al. Intravenous ascorbic acid as an adjuvant therapy for recombinant erythropoietin in hemodialysis patients with hyperferritinemia. Kidney Int 1999;55:2477-2486.
  • .Taylor RT, Huskisson EC, Whitehouse GH, et al. Gastric ulceration occurring during indomethacin therapy. Br Med J 1968;4(633):734-737.
  • .Taymor ML, Sturgis SH, Yahia C. The etiological role of chronic iron deficiency in production of menorrhagia. JAMA 1964;187:323-327.
  • .Threlkeld DS, ed. Hormones, thyroid hormones. In: Facts and comparisons drug information. St Louis: Facts and Comparisons;1991. (Review)
  • .Threlkeld DS, ed. Miscellaneous products, penicillamine. In: Facts and comparisons drug information. St Louis: Facts and Comparisons;1996. (Review)
  • .Toth I, Bridges KR: Ascorbic acid enhances ferritin mRNA translation by an IRP/Aconitase switch. J Biol Chem 1995;270:19540-19544.
  • .Troost FJ, Saris WH, Haenen GR, et al. New method to study oxidative damage and antioxidants in the human small bowel: effects of iron application. Am J Physiol Gastrointest Liver Physiol 2003;285(2):G354-359.
  • .Trovato A, Nuhlicek DN, Midtling JE. Drug-nutrient interactions. Am Fam Physician 1991;44(5):1651-1658. (Review)
  • .Turnlund JR. Copper. In: Shils M, Olson JA, Shike M, et al, eds. Nutrition in health and disease. 9th ed. Baltimore: Williams & Wilkins; 1999. (Review)
  • .Tzonou A, Lagiou P, Trichopoulou A, et al. Dietary iron and coronary heart disease risk: a study from Greece. Am J Epidemiol 1998;147(2):161-166.
  • .USDA: Composition of foods:USDA Handbook #8. Washington DC:ARS, USDA;1976-1986.
  • .US Food and Drug Administration. FDA Medical Bulletin, US Government Printing Office. Document number 386-942/00002. February 6, 1995.
  • .Van Belle SJ, Cocquyt V. Impact of haemoglobin levels on the outcome of cancers treated with chemotherapy. Crit Rev Oncol Hematol 2003;47(1):1-11.
  • .van den Broek N. Anaemia and micronutrient deficiencies. Br Med Bull 2003;67:149-160. PMID:14711761. (Review)
  • .van der A DL, Peeters PH, Grobbee DE, et al. Dietary haem iron and coronary heart disease in women. Eur Heart J 2005;26(3):257-262.
  • .van Zyl-Smit R, Halkett JA. Experience with the use of an iron polymaltose (dextrin) complex given by single total dose infusion to stable chronic haemodialysis patients. Nephron 2002;92(2):316-323.
  • .Verdon F, Burnand B, Fallab Stubi C-L, et al. Iron supplementation for unexplained fatigue in non-anaemic women: double blind randomised placebo controlled trial. BMJ 2003;326:1124-1127.
  • .Vernet M, Doyen C. Assessment of iron status with a new fully automated assay for transferrin receptor in human serum. Clin Chem Lab Med 2000;38(5):437-442.
  • .Vulpe CD, Kuo YM, Murphy TL, et al. Hephaestin, a ceruloplasmin homologue implicated in intestinal iron transport, is defective in the sla mouse. Nat Genet 1999;21(2):195-199.
  • .Walker SE, Paton TW, Cowan DH, et al. Bioavailability of iron in oral ferrous sulfate preparations in healthy volunteers. Can Med Assoc J 1989;141:543-547.
  • .Wang X, Wiesinger J, Beard J, et al. Thy1 expression in the brain is affected by iron and is decreased in restless legs syndrome. J Neurol Sci 2004;220(1-2):59-66.
  • .Weinreb O, Mandel S, Amit T, et al. Neurological mechanisms of green tea polyphenols in Alzheimer’s and Parkinson’s diseases. J Nutr Biochem 2004;15(9):506-516.
  • .Welch KM, Nagesh V, Aurora SK, et al. Periaqueductal gray matter dysfunction in migraine: cause or the burden of illness? Headache 2001;41(7):629-637.
  • .Werbach MR. Foundations of nutritional medicine. Tarzana, CA: Third Line Press;1997:57-59,221-222. (Review)
  • .Willeit J, Kiechl S, Oberhollenzer F, et al. Distinct risk profiles of early and advanced atherosclerosis: prospective results from the Bruneck Study. Arterioscler Thromb Vasc Biol 2000;20(2):529-537.
  • .Williams J, Wolff A, Daly A, et al. Iron supplemented formula milk related to reduction in psychomotor decline in infants from inner city areas: randomised study. BMJ 1999;318:693-697.
  • .Wright RO. The role of iron therapy in childhood plumbism. Curr Opin Pediatr 1999;11(3):255-258.
  • .Wurapa RK, Gordeuk VR, Brittenham GM, et al. Primary iron overload in African Americans. Am J Med 1996;101(1):9-18.
  • .Wurzelmann JI, Silver A, Schreinemachers DM, et al. Iron intake and the risk of colorectal cancer. Cancer Epidemiol Biomarkers Prev 1996;5(7):503-507.
  • .Yeung CK, Glahn RP, Miller DD. Inhibition of iron uptake from iron salts and chelates by divalent metal cations in intestinal epithelial cells. J Agric Food Chem 2005;53(1):132-136.
  • .Yip R, Dallman PR. Iron. In: Ziegler EE, Filer LJ, eds. Present knowledge in nutrition. 7th ed. Washington,DC: ILSI Press; 1996:277-292. (Review)
  • .Yip R. Significance of an abnormally low or high hemoglobin concentration during pregnancy: special consideration of iron nutrition. Am J Clin Nutr 2000;72(1 Suppl):272S-279S.
  • .Young IS, Trouton TG, Torney JJ, et al. Antioxidant status and lipid peroxidation in hereditary haemochromatosis. Free Radic Biol Med 1994;16:393-397.
  • .Zadik Z, Sinai T, Zung A, et al. Vitamin A and iron supplementation is as efficient as hormonal therapy in constitutionally delayed children. Clin Endocrinol (Oxf) 2004;60(6):682-687.
  • .Zhou JR, Erdman JW Jr. Phytic acid in health and disease. Crit Rev Food Sci Nutr 1995;35(6):495-508. (Review)
  • .Zimmermann MB, Molinari L, Staubli-Asobayire F, et al. Serum transferrin receptor and zinc protoporphyrin as indicators of iron status in African children. Am J Clin Nutr 2005;81:615-623.