The World Health Organization considers iron deficiency the number one nutritional disorder in the world.1 As many as 80% of the world's population may be iron deficient, while 30% may have iron deficiency anemia.2

Iron deficiency develops gradually and usually begins with a negative iron balance, when iron intake does not meet the daily need for dietary iron. This negative balance initially depletes the storage form of iron while the blood hemoglobin level, a marker of iron status, remains normal. Iron deficiency anemia is an advanced stage of iron depletion. It occurs when storage sites of iron are deficient and blood levels of iron cannot meet daily needs. Blood hemoglobin levels are below normal with iron deficiency anemia.3

Iron deficiency anemia can be associated with low dietary intake of iron, inadequate absorption of iron, or excessive blood loss.4  5  6 Women of childbearing age, pregnant women, preterm and low birth weight infants, older infants and toddlers, and teenage girls are at greatest risk of developing iron deficiency anemia because they have the greatest need for iron.7 Women with heavy menstrual losses can lose a significant amount of iron and are at considerable risk for iron deficiency.8 9 Adult men and post-menopausal women lose very little iron, and have a low risk of iron deficiency.

Individuals with kidney failure, especially those being treated with dialysis, are at high risk for developing iron deficiency anemia. This is because their kidneys cannot create enough erythropoietin, a hormone needed to make red blood cells. Both iron and erythropoietin can be lost during kidney dialysis. Individuals who receive routine dialysis treatments usually need extra iron and synthetic erythropoietin to prevent iron deficiency. 10 11 12

Vitamin A helps mobilize iron from its storage sites, so a deficiency of vitamin A limits the body's ability to use stored iron. This results in an "apparent" iron deficiency because hemoglobin levels are low even though the body can maintain normal amounts of stored iron.13 14 While uncommon in the U.S., this problem is seen in developing countries where vitamin A deficiency often occurs.

Chronic malabsorption can contribute to iron depletion and deficiency by limiting dietary iron absorption or by contributing to intestinal blood loss. Most iron is absorbed in the small intestines. Gastrointestinal disorders that result in inflammation of the small intestine may result in diarrhea, poor absorption of dietary iron, and iron depletion.15

Signs of iron deficiency anemia include:16 17 18 19 feeling tired and weak, decreased work and school performance, slow cognitive and social development during childhood, difficulty maintaining body temperature, decreased immune function, which increases susceptibility to infection, and glossitis (an inflamed tongue).

Eating nonnutritive substances such as dirt and clay, often referred to as pica or geophagia, is sometimes seen in persons with iron deficiency. There is disagreement about the cause of this association. Some researchers believe that these eating abnormalities may result in an iron deficiency. Other researchers believe that iron deficiency may somehow increase the likelihood of these eating problems.20 21

People with chronic infectious, inflammatory, or malignant disorders such as arthritis and cancer may become anemic. However, the anemia that occurs with inflammatory disorders differs from iron deficiency anemia and may not respond to iron supplements.22 23 24 Research suggests that inflammation may over-activate a protein involved in iron metabolism. This protein may inhibit iron absorption and reduce the amount of iron circulating in blood, resulting in anemia.25

Related Links: What is iron? | What foods provide iron? | How much iron do I need? | What happens if I do not get enough iron? | Do I need extra iron? | What are some of the current issues and controversies about iron? |

Disclaimer

Reasonable care has been taken in preparing this document and the information provided herein is believed to be accurate. However, this information is not intended to constitute an "authoritative statement" under Food and Drug Administration rules and regulations.

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The mission of the Office of Dietary Supplements (ODS) is to strengthen knowledge and understanding of dietary supplements by evaluating scientific information, stimulating and supporting research, disseminating research results, and educating the public to foster an enhanced quality of life and health for the U.S. population.

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The information is not intended to be a substitute for professional medical advice. It is important to seek the advice of a physician about any medical condition or symptom. It is also important to seek the advice of a physician, registered dietitian, pharmacist, or other qualified health professional about the appropriateness of taking dietary supplements and their potential interactions with medications.

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Footnotes

  1. CDC Recommendations to prevent and control iron deficiency in the United States. Centers for Disease Control and Prevention. MMWR Recomm Rep 1998;47:1-29. [↩]
  2. Stoltzfus RJ. Defining iron-deficiency anemia in public health terms: reexamining the nature and magnitude of the public health problem. J Nutr 2001;131:565S-7S. [↩]
  3. Institute of Medicine. Food and Nutrition Board. 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. [↩]
  4. Institute of Medicine. Food and Nutrition Board. 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. [↩]
  5. 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;59:1381-5. [PubMed abstract] [↩]
  6. Hallberg L. Prevention of iron deficiency. Baillieres Clin Haematol 1994;7:805-14. [PubMed abstract] [↩]
  7. CDC Recommendations to prevent and control iron deficiency in the United States. Centers for Disease Control and Prevention. MMWR Recomm Rep 1998;47:1-29. [↩]
  8. Institute of Medicine. Food and Nutrition Board. 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. [↩]
  9. Bothwell TH, Charlton RW, Cook JD, Finch CA. Iron Metabolism in Man. St. Louis: Oxford: Blackwell Scientific, 1979. [↩]
  10. Nissenson AR, Strobos J. Iron deficiency in patients with renal failure. Kidney Int Suppl 1999;69:S18-21. [PubMed abstract] [↩]
  11. Fishbane S, Mittal SK, Maesaka JK. Beneficial effects of iron therapy in renal failure patients on hemodialysis. Kidney Int Suppl 1999;69:S67-70. [PubMed abstract] [↩]
  12. Drueke TB, Barany P, Cazzola M, Eschbach JW, Grutzmacher P, Kaltwasser JP, MacDougall IC, Pippard MJ, Shaldon S, van Wyck D. Management of iron deficiency in renal anemia: guidelines for the optimal therapeutic approach in erythropoietin-treated patients. Clin Nephrol 1997;48:1-8. [PubMed abstract] [↩]
  13. Kolsteren P, Rahman SR, Hilderbrand K, Diniz A. Treatment for iron deficiency anaemia with a combined supplementation of iron, vitamin A and zinc in women of Dinajpur, Bangladesh. Eur J Clin Nutr 1999;53:102-6. [PubMed abstract] [↩]
  14. van Stuijvenberg ME, Kruger M, Badenhorst CJ, Mansvelt EP, Laubscher JA. Response to an iron fortification programme in relation to vitamin A status in 6-12-year-old school children. Int J Food Sci Nutr 1997;48:41-9. [PubMed abstract] [↩]
  15. Annibale B, Capurso G, Chistolini A, D'Ambra G, DiGiulio E, Monarca B, DelleFave G. Gastrointestinal causes of refractory iron deficiency anemia in patients without gastrointestinal symptoms. Am J Med 2001;111:439-45. [PubMed abstract] [↩]
  16. Institute of Medicine. Food and Nutrition Board. 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. [↩]
  17. Haas JD, Brownlie T 4th. Iron deficiency and reduced work capacity: a critical review of the research to determine a causal relationship. J Nutr 2001;131:691S-6S. [PubMed abstract] [↩]
  18. Bhaskaram P. Immunobiology of mild micronutrient deficiencies. Br J Nutr 2001;85:S75-80. [PubMed abstract] [↩]
  19. Allen LH, Iron supplements: scientific issues concerning efficacy and implications for research and programs. J Nutr 2002;132:813S-9S. [PubMed abstract] [↩]
  20. Rose EA, Porcerelli JH, Neale AV. Pica: common but commonly missed. J Am Board Fam Pract 2000;13:353-8. [PubMed abstract] [↩]
  21. Singhi S, Ravishanker R, Singhi P, Nath R. Low plasma zinc and iron in pica. Indian J Pediatr 2003;70:139-43. [PubMed abstract] [↩]
  22. Jurado RL. Iron, infections, and anemia of inflammation. Clin Infect Dis 1997;25:888-95. [PubMed abstract] [↩]
  23. Abramson SD, Abramson N. 'Common' uncommon anemias. Am Fam Physician 1999;59:851-8. [PubMed abstract] [↩]
  24. Spivak JL. Iron and the anemia of chronic disease. Oncology (Huntingt) 2002;16:25-33. [PubMed abstract] [↩]
  25. Leong W and Lonnerdal B. Hepcidin, the recently identified peptide that appears to regulate iron absorption. J Nutr 2004;134:1-4. [PubMed abstract] [↩]

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