Even though iron is a mineral that is essential to human health, the human body contains only 3 - 4 grams. The total quantity of iron in the body varies with weight, hemoglobin concentration, sex, and storage compartment size.
Average daily intake of iron in North America and Europe is between 10 and 30 mg, about 5 to 7 mg of iron per 1000 calories.
Iron deficiency is the most common nutritional deficiency in the U.S. It affects 30-50% of infants under the age of two, teenage girls, pregnant women, and the elderly, who are at higher risk for iron deficiency.
There are two forms of dietary iron: heme and non-heme iron. Heme iron, found primarily in animal products, is bound to hemoglobin and myoglobin and is the most efficiently absorbed form of iron. The process of absorption of heme iron is poorly understood. Non-heme iron, found in plant foods, is poorly absorbed compared to heme iron.
Healthy individuals absorb 5 - 10 % of dietary iron, whereas those who are iron deficient absorb 10-20 %. Absorption of iron mainly occurs in duodenum of the small intestine.1
Iron supplements are mainly in the ferrous (Fe II) form. Some iron supplements are in the ferric (Fe III) form and are reduced to the ferrous form.
Redox cycle between ferrous and ferric form can produce the highly reactive oxygen species, which can damage lipids, DNA and proteins.
Serum ferritin concentrations accurately mirror the concentration of ferritin in tissues. Decreased serum ferritin concentration is the earliest sign of iron deficiency.
Tea and coffee reduce the absorption of iron by 60%
and 40% respectively, by forming insoluble complexes.
Iron is necessary for function and synthesis of hemoglobin, which transports oxygen through the circulatory system to all tissues of the body.
Iron also has a fundamental role in energy production, specifically for oxidation-reduction reactions. It is necessary for production and function of cytochromes in the electron transport chain, as well as for activating enzymes in the Krebs cycle.
Iron is involved in synthesis of DNA, and plays a role in immune function.
Iron is a necessary component in brain development and function, and is needed to synthesize certain neurotransmitters (serotonin, dopamine, norepinephrine) and collagen.
Iron deficiency may cause learning problems in
children and adolescents, probably because iron has a role in synthesizing
neurotransmitters.
* Values are Adequate Intakes (AI), others are RDA.
Iron supplementation is strongly recommended when a true deficiency is present, especially in certain populations. Iron deficiency can be evaluated by 3 different measurements: 3
Measurement:
Iron Deficiency:
1) Plasma Ferritin
<10 mcg/L
2) Transferrin Saturation
<15%
3) *Hgb
<10 g/dl - females** <12 g/dl - males
4) Hct
<31% -- females** <37% -- males
*Hemoglobin (Hgb) concentration is
unsuitable as a diagnostic tool of iron deficiency anemia by itself, because:»
it is affected only late in the disease» it does not separate iron deficiency
from other anemias» the values of normal individuals vary widely**In pregnancy:
Hgb <9.5 g/dl in the 2nd trimester, Hgb <9.0 g/dl in the 3rd trimester;
Hct <30% in the 2nd and 3rd trimesters
Iron deficiency can lead to anemia*, excessive menstrual loss, learning disabilities, impaired immune function, and decreased energy levels and physical performance. Symptoms of iron-deficiency anemia include pale skin and mucous membranes, fatigue, dizziness, sensitivity to cold, shortness of breath, rapid heartbeat and a tingling sensation in the extremities. [*Anemia is the 3rd stage of iron deficiency, in which blood is deficient in the hemoglobin (iron-containing) portion of red blood cells. It is preceded by iron depletion and iron deficiency without anemia.]
Iron deficiency is second only to hunger as a major nutritional problem in the world, affecting almost 40% of the world's population (nearly two billion people). Iron deficiency is also the second most common nutritional problem in the United States. Infants, children, young women, pregnant or postpartum women and the elderly are at risk for iron deficiency. Poverty is the greatest risk factor for iron deficiency and anemia.
Iron deficiency may lead to anemia (reduction in blood cells). However, inadequate dietary iron can also cause other symptoms, such as weakness, impaired cognition, decreased athletic performance and lack of endurance. Infants born to anemic mothers are more likely to develop anemia in the first year. These infants may also have an increased risk for mental retardation.
Other conditions associated with increased risk for iron deficiency are: Hemorrhage Anemia Nephrosis Infection Achlorhydria Steatorrhea Malabsorption Parasites Protein-calorie malnutrition Decreased GI transit time
Iron supplements can be extremely toxic to small children. Doses of 3 to 10 grams can be fatal in children. Iron can cause irritation to the mucosa with ulceration and bleeding, hypoxia, metabolic acidosis, liver damage and renal failure. Death can occur in 12 to 48 hours.
Iron should be used with caution in those with a history of gastrointestinal (GI) bleeding, peptic ulcer disease or gastritis.
Patients with hemochromatosis or hemosiderosis should not use iron supplements.
Other persons who are at particularly high risk for iron overload are those with the iron-loading anemias, thalassemia and sideroblastic anemia. Elevated erythropoiesis in individuals causes an increased absorption of iron.
A study examined premenopausal and postmenopausal
middle-aged women with a high prevalence of nutritional supplementation, and
results indicated that iron overload in middle-aged women seems unlikely from
both diet and nutrition supplement.
Food iron is presented to the body either as heme iron, found only in animal products or as nonheme iron, which is in plant foods and about 60% in animals. Whether the iron in food is heme or nonheme iron has a major influence on the amount of the mineral absorbed. The nonheme iron is not as well absorbed as heme iron.
The best dietary sources of iron are dark- vegetables and legumes. Good dietary sources of iron are kelp, brewer's yeast, blackstrap molasses, clams, oysters, wheat bran, nuts and seeds, dried fruits, and beef liver.
Although (non-heme) iron is found in some breads and cereals in the American diet, much of the iron is not well absorbed.
The iron in many foods is not readily available to the human body. Iron absorption is decreased by:4 fiber phytates phenolic compounds soy proteins coffee tea Iron absorption is enhanced by: vitamin C body's need for
iron
The prevalence of iron deficiency among adolescents is high, especially among girls. A published study using the NHANES III data to examine the iron status of a sample of school-aged children in the U.S., found that iron deficiency was most prevalent among adolescent girls. 5
One study examined vegetarians who had sufficient iron intake higher than recommended daily allowance, but vegetarians were found to have impaired iron status, due to the limited bioavailability of (non-heme) iron, particularly in women. 1
It has been suggested that demands for iron are the
highest in the third trimester of pregnancy, in order to support fetal
erythropoiesis and placental iron accumulation.6
Antacids may reduce GI absorption of iron. Administration of these agents should be as far apart as possible.
Ascorbic acid at doses >200 mg has been shown to enhance absorption of iron by >30%. However, preparations containing iron and ascorbic acids may not have a sufficient amount to substantially affect iron absorption.
Chloramphenicol [Chloromycetinâ], an antibiotic agent, may delay responses to iron therapy. Patients with iron-deficient anemia receiving iron therapy should avoid chloramphenicol therapy.
Cimetidine [Tagametâ], an H2 blocker, may reduce GI absorption of iron. If possible, cimetidine should be either separated from or avoided with iron therapy.
Absorption of methyldopa [Aldometâ], a hypertension medication, may be decreased with concomitant iron therapy, possibly resulting in decreased efficacy and increased urinary excretion of the sulfate conjugate of the drug. Levodopa appears to form chelates with iron salts, decreasing absorption and serum concentrations. Patients receiving chronic methyldopa therapy (250 mg 1 to 3 times daily, or 500 mg 3 times daily) with oral ferrous sulfate therapy may experience an increase in blood pressure during concomitant therapy and a decrease in blood pressure when iron preparation was discontinued. Patients who have to use this concomitant therapy should consult a physician for a decreased hypotensive effect of methyldopa.
Efficacy of levothyroxine [Synthroidâ], a thyroid agent, may be decreased with concomitant administration of iron, resulting in hypothyroidism. If concomitant administration of iron and thyroxine therapy is necessary, the agents should be administered at least 2 hours apart, and thyroid function should be monitored.
Gastrointestinal absorption of penicillamine [Cuprimineâ], used for copper toxicity, may be reduced due to its chelation of iron molecules. Administration of the drug and iron therapy should be at least 2 hours apart.
Gastrointestinal absorption of quinolones or antibiotics may be decreased because of formation of ferric ion-quinolone complex. Oral preparations containing iron should not be administered within 2 hours of oral quinolones.
Concomitant use within two hours of iron and a tetracycline antibiotic may decrease absorption and serum iron concentrations. Absorption of iron salts may also be decreased. If concomitant therapy is necessary, patients should take the drug 2 hours before or 4 hours after oral iron administration.
Iron supplements can interfere with the absorption of catopril [Capotenâ], angiotensin-converting enzyme (ACE) inhibitor, used for hypertension, and other ACE inhibitors. It is recommended that iron supplements and ACE inhibitors be taken at least 2 to 3 hours apart.
Dairy products or calcium supplementation may
interfere with iron absorption. Coffee and tea consumed with a meal or within
1 hour after a meal may inhibit absorption of dietary iron. Iron supplements
should be taken between meals.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Pregnancy: Iron supplementation during pregnancy has consistently demonstrated positive effects on maternal status at delivery.7 Future research should focus on determining the appropriate window during pregnancy in which iron supplementation would have maximum effects.
One randomized, double-blind, placebo-controlled study of a small sample size of 31 did find that iron supplementation (27 mg elemental iron) with a heme component given in the 2nd half of pregnancy prevented depletion of iron stores after birth in most women.8
Another study on Peruvian women receiving 60 mg of iron or a placebo from a prenatal supplement from 10 to 24 weeks gestation to delivery, found that maternal serum ferritin and folate concentrations were significantly influenced by prenatal supplementation. Serum iron concentrations were significantly higher in those taking just iron, versus either iron and zinc or placebo groups.6
In another randomized, double blind trial, pregnant women supplemented weekly with 120 mg iron, along with folic acid (500 mcg) and vitamin A improved hemoglobin concentrations near term, whereas those receiving iron supplementation alone did not. Weekly iron supplementation along with vitamin A during pregnancy enhanced iron's use for erythropoiesis.9
A review noted that iron in breast-fed milk is
preferred to formula in terms of risk for infectious morbidity, especially in
deprived communities. 9
Heart Disease: Researchers have debated the role of iron in development of atherosclerosis and ischemic heart disease, however, no clear answer concerning the role of iron in these disorders has been established.10
A review of numerous studies has suggested that iron is an important factor in the development process of atherosclerosis.10
A prospective cohort study as part of NHANES II mortality study, measured the relative risk of death from serum ferritin concentrations in black and Caucasian men and women. Results from the study did not support positive iron stores as a risk factor for CVD, CHD, or myocardial infarction death or for serum ferritin concentrations and all causes mortality.11
One study found that serum ferritin concentrations >200 mcg/l were strongly associated with a 2.2 fold risk of acute myocardial infarction in men with elevated (193 mg/dl) serum LDL cholesterol concentrations.12
A longitudinal and cross-sectional study, investigated the influence of heme, non-heme, and iron supplementation on iron stores (serum ferritin concentration) of healthy men and women. No association between heme iron intake and iron stores was found in either study, except in the women, where age and iron intake from supplements was associated with increased iron stores. Therefore, elderly persons who consume a balanced diet should not take iron supplements, unless recommended by a physician or to correct anemia. 13
The Rotterdam prospective cohort study found a positive association with heme iron intake and risk for myocardial infarction, especially in those with risk factors (cigarette smoking, diabetes, hypercholesterolemia, or hypertension). However, there was no evidence of a positive association between total iron intake and risk for myocardial infarction. 14
The Framingham Heart Study Cohort analyzed the iron
status of non-institutionalized elderly subjects in the U.S. Iron deficiency
was not prevalent in the elderly and only a small percentage had elevated iron
stores. In addition, elevated iron stores (serum ferritin concentration) was
not likely attributable to onset of disease. Due to the equivocal evidence on
high iron stores and risk of disease, iron supplementation in free-living
elderly white Americans is not recommended. 15
Physical Performance: The incidence of iron depletion is reported to be between 30 - 50 %, particularly among female athletes and male and female athletes in endurance sports.16
Physical training can reduce iron stores (ferritin) and create a negative iron balance, especially in female athletes and athletes in certain sports. Serum ferritin concentration is a good indicator of prelatent iron deficiency, and may also prove valuable as an indicator for treatment. 17
A randomized experimental study on 31 healthy, inactive women with normal iron stores, showed that after 12 weeks of moderate endurance exercise, serum ferritin concentrations did not change significantly.18
A study done on the effects of iron supplementation on endurance training at a moderate altitude, does not seem to lead to a depletion in total body Hgb in athletes, with or without iron supplementation. 19
It has been established that iron deficiency anemia
can impair physical performance and iron supplementation is recommended when a
deficiency is present. However, the benefit of iron supplements in non-anemic
athletes is unclear. 20
Cognitive Function: Iron depletion or deficiency can contribute to neurological impairment. 21
In a study of non-anemic iron deficient adolescent girls, daily iron supplementation increased serum iron concentrations, while showing a significant improvement in their performance on verbal learning and memory tests.22
A study on the effects of dieting on iron status and
cognitive function in obese women demonstrated that impaired iron status, caused
by dieting, may reduce attention span. 23
Diabetes: Earlier research has suggested that elevated body iron stores can contribute to the etiology of diabetes, particularly since iron can act as a catalyst of free radical formation.24 A prospective 4-year randomized follow-up study in Finland, examined men with a high incidence of NIDDM. Men with high iron stores had a 2.5 fold risk for NIDDM than men with lower iron stores. This is the first study showing that body iron stores may contribute to the development of non-insulin dependent diabetes mellitus, however, further studies are warranted. 25
Immunity: Numerous studies have been conducted on iron deficiency and immune function. However, the severity and relevance of these studies is questioned due to the impact of other factors on immune function such as: age, past immune experience, diet and cooking practice, and common inherited disorders of globin genes. Therefore, a clear relationship between states of iron deficiency and susceptibility to infections cannot be firmly established and remains controversial.9
Cancer: Iron has many essential
functions in the body. It can also have deleterious side effects by increasing
oxidative damage, particularly in the colon. A paper reviewed 33 studies on iron
and cancer risk. Many of the larger studies supported the association of iron
with colorectal cancer risk.26 Although iron supplementation is necessary
and beneficial to certain groups, it has been suggested that long-term iron
supplementation may pose a risk for colorectal cancer.
The dietary supplement information contained on this site has been compiled from published sources thought to be reliable, but it cannot be guaranteed. Efforts have been made to assure this information is accurate and current. However, some of this information may be purported or outdated due to ongoing research or discoveries. The authors, editors and publishers cannot accept responsibility for errors or omissions or for any consequences from applications of the information in this site and make no warranty, expressed or implied, with respect to the contents herein.
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