Iron is an essential mineral crucial for human life. It is an important component of the hemoglobin molecule in red blood cells. It is critical for oxygen transportation from the lungs to the tissues of the body and for clearing carbon dioxide from the the tissues via the lungs. It also plays a key role in several biochemical reactions in energy production and metabolism, including DNA synthesis. 
The following foods have the highest concentration of iron. For a more expansive list on food sources of specific nutrients visit Health Canada's Dietary Reference Intakes for Elements or USDA's National Nutrient Database
- There are two forms of dietary iron, heme iron and non-heme iron. Heme iron is found in animal products and is bound to hemoglobin and myoglobin. It is absorbed much better as compared to non-heme sources typically found in plants.
Other food sources include:
- grains: wheat, millet, oats, brown rice
- protein sources: Liver, lean red meat (especially beef), oysters, poultry, dark red meat, pork, salmon, tuna, clam
- vegetables: broccoli, spinach, kale, collards, asparagus, dandelion greens
- fruit: Dried fruits, prunes, raisins, apricots
- Other sources include: kelp, blackstrap molasses
- Iron-Deficiency Anemia: In children, it is often due to inadequate diet; in adults, in can be caused by excessive bleeding and this cause must always be considered. Iron should be taken with vitamin C as this increases its absorption.
- Attention Deficit or Hyperactivity Disorder (ADD/ADHD): Iron supplementation has been shown to improve the severity of ADHD symptoms in boys aged 7-11 years, even if they did not have iron deficiency anemia. Iron plays a role in the synthesis of dopamine and possibly other important neurotransmitters. This extra iron in boys with ADHD may help with neurotransmitter synthesis and thus have a positive outcome in terms of behaviour.
- Restless Leg Syndrome: A study was done in geriatric patients with restless leg syndrome and it has been found that serum ferritin levels are inversely related to the severity of restless leg syndrome.
Iron deficiency is most common in infants under the age of 2 years, teenage girls, pregnant women, and the elderly. Deficiency may be caused by an increased need for iron, decreased dietary intake (especially seen in vegetarians and vegans), diminished iron absorption or utilization (chronic diarrhea or malabsoprtion, surgical removal of the stomach, and antacid use), blood loss, or a combination of factors. Requirements increase during growth and development in infancy and adolescence, and during pregnancy and lactation.
Iron deficiency can lead to:
- anemia (is the last stage of iron deficiency; usually presents as fatigue and is caused by decreased oxygen transportation to the tissue and increased build-up of carbon dioxide)
- excessive menstrual loss
- learning disabilities
- impaired immune function
- decreased energy levels
- decreased physical performance
Early symptoms of supplemental iron toxicity in adults includes:
Other symptoms of overload may include:
More advanced toxic effects associated with acute excessive iron intake include:
- muscle weakness
- cardiovascular collapse
- Cardiovascular Disease: Iron overload has been associated with cardiovascular disease and increased risk of heart attack, perhaps even being a better predictor than cholesterol or blood pressure of of one's risk. This may explain why premenopausal women are "safe" from coronary heart disease until they stop menstruating and why women on oral contraceptives, which decreases menstrual flow, have an increased risk. Vitamin E may be important in order to quench the free radical nature of iron.  *Mental Disease: Iron overload also has a connection to mental disease. Individuals with hemochromatosis have been found to have both psychiatric and neurological symptoms. Chelation may be needed in order to improve symptoms. Significant improvements have been shown for symptoms which have included: anxiety depression, obsessions, compulsions, and panic attacks. 
- Other conditions possibly associated with excess Iron: increase risk of infection and inflammatory processes, autoimmune processes, neurodegenerative diseases, and cancer. More research is needed in this area.
Best Specimens to Collect: 
- Serum ferritin - low result indicates deficiency
- Total Iron Binding Capacity - positive result is low
- Percent Saturation - positive result is low
- Heme iron is better absorbed than non-heme sources of iron such as ferrous sulfate and ferrous fumarate. Heme iron absorbs at a rate of 35% whereas non-heme iron absorbs at a rate of 2.9% on an empty stomach and 0.9% with food.
- Unbound non-heme iron is also more likely to lead to the production free radicals.
- The best form of non-heme iron is ferrous succinate 
- The recommended dosages varies based on age and health status. To determine what your specific requirements are talk to your naturopathic doctor or other trained medical professional.
- Infants: 6mg (under 6 months); 10mg (6-12 months)
- Child: 10 mg (1-10 years)
- Adolescent - Adult: 12mg (Males 11-18 years); 10mg (Males 19+ years); 15mg (Females 11-50 years); 10mg (Females 51+ years)
- Pregnancy: 30mg
- Lactation: 15mg
Generally speaking, supplementation with iron should also occur if there has been testing to verify a deficiency.
- Children: Infants and children are especially vulnerable to iron toxicity. Doses as low as 60mg/kg can be fatal.
- Adults and Seniors: Constipation is the most common adverse effect, especially in the elderly. Exacerbation of diarrhea may occur in individuals with inflammatory bowel disease and may be accompanied by bleeding.
- Pregnancy and Breastfeeding: Low-dose iron supplementation is safe in pregnancy; supplementation during both pregnancy and lactation should be undertaken under medical supervision.
- General adverse effects: IV iron given to severe anemics can lead to headaches, fever, lymphadenopathy, joint pain and inflammation, hives, exacerbation of rheumatoid arthritis, hemolytic reactions, and rarely anaphylaxis.
- Adverse effects in specific population: Individuals with insulin resistance, diabetes, or hepatitis C may be particularly susceptible to iron overload. 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.
- Contraindications: 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 are particularly susceptible to oxidative stress. May be contraindicated for children in malarial environments. Generally inappropriate for individuals with history of unusual or allergic reaction to iron, or medicine, foods, dyes, or preservatives containing iron.
- Drug Interactions include:
- Supportive or Beneficial:
- Levothyroxine and Related Thyroid Hormones - Thyroid therapy may be enhanced with iron co-administration. However, simultaneously ingested thyroxine and iron is likely to bind to form poorly soluble chelate complex and thereby impair absorption and bioavailability of both agents. Co-morbid conditions may require both agents. Separate intake by several hours to avoid interference.
- Addresses Drug-Induced Deficiency:
- Acetylsalicylic Acid (ASA, Aspirin) - Iron supplementation can reverse adverse hematological effects of ASA therapy. It also addresses the increased risk of iron-deficiency anemia.
- Antacids and Gastric Acid - Suppressive Medications - 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 this patient population. Some agents may bind with iron and impair absorption of either or both substances. Separate intake.
- Hyoscyamine - Drug can impair iron absorption. Potential for decreased therapeutic activity with simultaneous intake. Iron depletion and effects of iron depletion plausible with extended use. Iron supplementation with iron or other appropriate minerals may be appropriate with extended therapy. Separate intake by several hours.
- Indomethacin and Related 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. Separate intake.
- Carbidopa, Levodopa and Related Antiparkinsonian Medications - Simultaneous intake of these drugs and iron (especially ferric) may result in binding and reduced absorption due to formation of poorly absorbed chelate complexes. Medication may also autoxidize to ferric form. Iron may be contraindicated in this patient population. Separate intake if indicated.
- Desferoxamine - This drug is used as a chelating agent applied to treat overload and intoxication involving iron and other metals. Intake of iron (supplemental or iron-rich foods) is contraindicated and iron use should be discontinued.
- Dimercaprol - This drug is used as an antidote in arsenic, cadmium, lead, and mercury poisoning in inpatient settings. Iron intake during drug therapy may cause kidney damage but is often appropriate 24 hours after such treatment. Avoid supplemental iron during dimercaprol therapy.
- EDTA - EDTA is a chelating agent applied to treat overload and intoxication involving iron and other metals. Intake of iron (supplemental or iron-rich foods) is contraindicated and iron use should be discontinued. Supplementation with iron and other nutrients may be appropriate with extended therapy. Separate intake by several hours.
- 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. Avoid supplemental iron and recommend low-iron, vegetarian diet.
- Penicillamine - This drug is a chelating agent applied to treat overload and intoxication involving copper, iron, and other metals. Abrupt discontinuation of ongoing iron intake may lead to rapid elevation in circulating penicillamine levels and resultant nephrotoxicity. Avoid concurent iron and dietary intake; tapered reduction is needed in discontinuing supplemental iron. Supplementation may be necessary if depletion in detected in extended therapy.
- Separate Iron and Drug Intake:
- Angiotensin-Converting Enzyme (ACE) Inhibitors - Co-administration of iron can abolish cough induced by drug. However, iron and ACE medications may bind and reduce absorption of both agents. Separate intake by 3 or more hours.
- Bile Acid Sequestrants - Simultaneous intake of iron and drug may result in binding and reduced absorption due to formation of poorly absorbed chelate complexes. Drug action may be impaired with interaction. Low risk of significant interaction if oral intake is separated by at least 2 hours.
- Bisphosphonates - Binding may occur with simultaneous intake and inhibit absorption and bioavailability of both agents. Decreased therapeutic activity is probably with interaction; minimal effect with separation of intake (at least 2 hours).
- Cefdinir and Related Cephalosporin Antibiotics - Chelation between drug and iron is likely to impair absorption and bioavailability of both agents if ingested concurrently. Decreased therapeutic action with interaction; minimal effect with separation of intake. Iron depletion is plausible with extended use but not established. Caution is warranted regarding supplementation during infection. Discontinue iron or separate intake during short-term therapy. Mineral supplementation may be appropriate with extended therapy but caution is warranted.
- Chlorhexidine - Concurrent intake of drug and iron may stain teeth. Separate intake by at least 2 hours to avoid.
- Clofibrate - Chelation between clofibrate and iron is likely to impair absorption and bioavailability of both agents if ingested concurrently. Separate intake by 3 hours.
- Fluroquinolone (4-Quinolone) Antibiotics - Chelation between this class of antibiotics and iron is likely to impair absorption and bioavailability of both agents. 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 is warranted regarding iron, even with established depletion. Separate intake by several hours.
- Methyldopa - Simultaneously ingested methyldopa and iron is likely to bind to form poorly soluble chelate complex and thereby impair absorption and bioavailability of both agents. Medication may also cause autoxidation to the ferric form. Iron depletion and effects of iron depletion plausible with extended use, but not established. Separate intake by at least 2 hours when iron is indicated.
- Sulfasalazine - When ingested concurrently, iron can bind the drug and reduce its absorption, bioavailability and therapeutic action. This can be minimized with separation of intake by several hours. Iron supplementation may be warranted if bleeding anemia, and/or iron depletion is established but caution is appropriate to avoid aggravating inflammation.
- Trientine - This drug is a chelating agent applied to treat copper overload and toxicity. Simultaneous ingestion with iron is likely to bind to form poorly soluble chelate complex and thereby impair absorption and bioavailability of both agents. Anemia is a common adverse effect. Separate intake by several hours to avoid binding and interference. Iron supplementation may be warranted if anemia and/or depletion is established.
- Chloramphenicol - Drug can inhibit erythropoiesis and red cell maturation, thus delaying or impeding iron therapy; it can also cause aplastic anemia. Discontinuation of drug may be necessary if treating patients with anemia.
- Erythropoiesis-Stimulating Agents - Synergistic interaction is often used in treatment of oncology patients with functional iron deficiency or anemia but remains controversial. Co-administration may enhance epo-induced erythropoiesis, but risk of adverse effects is significant if applied prematurely. Iron administration in hemodialysis patients is often contraindicated, although oral heme iron may be effective.
- Neomycin - Drug is known to impair absorption of iron and many other nutrients; concurrent intake may alter drug activity. 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 may be necessary in extended therapy. Separate intake.
- Oral Contraceptives - may support iron status and reduce need for supplementation by reducing menstrual blood loss. Iron supplementation needs may be lower, but higher need for folate, vitamin B12, and vitamin B6 are possible.
- Tetracycline Antibiotics - Chelation between iron and antibiotic and impaired absorption of both to clinically significant degree probably with concurrent intake. Discontinue iron (including iron-rich foods) or separate intake during short-term therapy. Iron supplementation may be appropriate with extended therapy, but caution is warranted, even with established depletion. Separate intake by several hours.
- Nutrient Interactions include 
- Calcium - in foods or supplements may reduce absorption of iron, especially heme iron.
- Copper - Adequate copper nutriture appears necessary for normal iron absorption and metabolism, iron transport to the bone marrow, and RBC formation.
- Fiber - When consumed concurrently, fiber can reduce iron absorption (especially phytic acid-containing fiber such as cereal bran)
- Folic Acid - Iron and folate work together in many aspects of human physiology, particularly RBC formation and function.
- Manganese - When iron and manganese are ingested together, the absorption of manganese may be impaired.
- Pancreatic Enzymes - Iron absorption may potentially be reduced by concomitant use of pancreatic enzymes.
- Phosphorus/Phosphate Supplements - After oral administration, divalent cations, such as iron salts, can bind to orally administered phosphate in the GI tract, potentially reducing the absorption and bioavailability of phosphate supplements.
- Taurine - There has been a reported beneficial additive effect associated with co-administration of oral taurine and slow-release iron sulfate.
- Vitamin A - improves the absorption and utilization of iron, and vitamin A deficiency may exacerbate iron deficiency anemia.
- Vitamin C - supplemented or in vitamin C-rich foods can strongly enhance the absorption of nonheme iron in the GI tract.
- Vitamin E - Concomitant administration of vitamin E may diminish the therapeutic effects and mitigate the adverse effects of iron salts and attenuate oxidative stress.
- Zinc - When administer orally, at the same time, iron and zinc can mutually reduce absorption (particularly on an empty stomach).
When in excess, iron can behave as a heavy metal. The following may be helpful:
- Silybum marianum and EDTA may be effective in treatming iron overload.
- Drugs often used to treat iron overload include deferoxamine, deferiprone, pyridoxal isonicotyinoyl
- Murray Michael T (2005) Encyclopedia of Nutritional Supplements, The Essential Guide for Improving Your Health Naturally, Prima Publishing
- Medlineplus 
- Hoffer Abram, Prousky Jonathan (2006) Naturopathic Nutrition, A Guide to Nutrient-Rich Food & Nutritional Supplements for Optimum Health, CCNM Press
- Bralley J Alexander and Lord Richard S (2005) Laboratory Evaluations in Molecular Medicine, Nutrients, Toxicants, and Cell Regulators Institute for Advances in Molecular Medince, GA.
- Stargrove Mitchell Bebell, Treasure Jonathan, McKee Dwight L (2008) Herb, Nutrient, and Drug Interactions, Clinical Implications and Therapeutic Strategies. Mosby