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Also indexed as: Hemolytic Anaemia, Low Hematocrit, Low Haemoglobin, Low Red Blood Cell Count, Sideroblastic Anaemia, Thallasaemia 
Boost your red blood cell count to a normal level by replenishing what your body may be missing. According to research or other evidence, the following self-care steps may help you treat your specific type of anaemia: |
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| Science Ratings | Nutritional Supplements | Herbs |
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Copper (if deficient) Iron (when iron deficiency is diagnosed) Vitamin A (if deficient) Vitamin B1 (for genetic thiamine-responsive anaemia) Vitamin B12 (if deficient) Vitamin B2 (if deficient) Vitamin B6 (if deficient and for genetic vitamin B6-responsive anaemia) Vitamin C (if deficient) Vitamin E (if deficient) |
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Folic acid (for thallasaemia if deficient) L-carnitine(for thallasaemia) Magnesium(for thallasaemia) Taurine (if deficient in iron) Vitamin B12 (for thallasaemia if deficient) Vitamin E (injections for thallasaemia, orally for glucose-6-phosphate dehydrogenase deficiency [G6PD] anaemia and anaemia caused by kidney dialysis) Zinc (for thallasaemia if deficient) |
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Antioxidants (for thallasaemia) Vitamin C (for thallasaemia if deficient) |
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| Reliable
and relatively consistent scientific data showing a substantial health benefit. Contradictory, insufficient, or preliminary studies
suggesting a health benefit or minimal health benefit. For a herb, supported by traditional use but minimal
or no scientific evidence. For a supplement, little scientific support and/or minimal health
benefit. |
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What are the symptoms?
Some common symptoms of anaemia include fatigue, lethargy, weakness, poor concentration, and frequent colds. A peculiar symptom of iron-deficiency anaemia, called pica, is the desire to eat unusual things, such as ice, clay, cardboard, paint, or starch. Advanced anaemia may also result in lightheadedness, headaches, ringing in the ears (tinnitus), irritability, pale skin, unpleasant sensations in the legs with an uncontrollable urge to move them, and getting out of breath easily.
Medical options
Over the counter treatment of anaemia includes iron (Feosol®, Fergon®), vitamin B12, and folic acid, though a correct diagnosis is necessary to determine which nutrient is deficient.
Medications requiring a prescription include injectable forms of iron (InFeD®, Ferrlecit®), vitamin B12, and folic acid, as well as a high dose oral form of folic acid. Individuals with non-nutrient-deficient anaemia may be prescribed epoetin (Epogen®, Procrit®).
Blood transfusions may be required to treat severe anaemia.
Dietary changes that may be helpful
Severe protein deficiency can cause anaemia because protein is required for normal production of haemoglobin and red blood cells.2 However, this deficiency is uncommon in healthy people living in developed countries.
Thallasaemia is an inherited type of anaemia that is most common in people of Mediterranean descent. Children with severe thallasaemia often have reduced growth rates that may be partially due to inadequate diets. This problem is primarily found in developing countries.3
Vitamins that may be helpful
Deficiencies of iron, vitamin B12, and folic acid are the most common nutritional causes of anaemia.4 Although rare, severe deficiencies of several other vitamins and minerals, including vitamin A,5 6 vitamin B2,7 vitamin B6,8 9 vitamin C,10 and copper,11 12 can also cause anaemia by various mechanisms. Rare genetic disorders can cause anaemias that may improve with large amounts of supplements such as vitamin B1.13 14
Taurine has been shown, in a double-blind study, to improve the response to iron therapy in young women with iron-deficiency anaemia.15 The amount of taurine used was 1,000 mg per day for 20 weeks, given in addition to iron therapy, but at a different time of the day. The mechanism by which taurine improves iron utilization is not known.
Hemolytic anaemia refers to a category of anaemia in which red blood cells become fragile and undergo premature death. Vitamin E deficiency, though quite rare, can cause hemolytic anaemia because vitamin E protects the red blood cell membrane from oxidative damage. Vitamin E deficiency anaemia usually affects only premature infants and children with cystic fibrosis.16 17 Preliminary studies have reported that large amounts (typically 800 IU per day) of vitamin E improve hemolytic anaemia caused by a genetic deficiency of the enzyme glucose-6-phosphate dehydrogenase (G6PD)18 19 20 and anaemia caused by kidney dialysis.21 22
People with severe thallasaemia who receive regular blood transfusions become overloaded with iron, which increases damaging free radical activity and lowers antioxidant levels in their bodies.23 24 25 26 Some people with milder forms of thallasaemia may also have iron overload.27 Iron supplements should be avoided by people with thallasaemia unless iron deficiency is diagnosed. Preliminary studies have found that oral supplements of 200 to 600 IU per day of vitamin E reduce free radical damage to red blood cells in thallasaemia patients.28 29 30 However, only injections of vitamin E have reduced the need for blood transfusions caused by thallasaemia.31 32
Test tube studies have shown that propionyl-L-carnitine (a form of L-carnitine) protects red blood cells of people with thallasaemia against free radical damage.33 In a preliminary study, children with beta thallasaemia major who took 100 mg of L-carnitine per 2.2 pounds of body weight per day for three months had a significantly decreased need for blood transfusions.34 Some studies have found people with thallasaemia to be frequently deficient in folic acid, vitamin B12,35 and zinc.36 37 Researchers have reported improved growth rates in zinc-deficient thalassemic children who were given zinc supplements of 22.5 to 90 mg per day, depending on age.38 39 Magnesium has been reported to be low in thallasaemia patients in some,40 41 but not all,42 studies. A small, preliminary study reported that oral supplements of magnesium, 7.2 mg per 2.2 pounds of body weight per day, improved some red blood cell abnormalities in thallasaemia patients.43
Sideroblastic anaemia refers to a category of anaemia featuring a build-up of iron-containing immature red blood cells (sideroblasts). One type of sideroblastic anaemia is due to a genetic defect in an enzyme that uses vitamin B6 as a cofactor.44 45 Vitamin B6 supplements of 50 to 200 mg per day partially correct the anaemia, but must be taken for life.46
References
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1. Smith JA. Exercise, training and red blood cell turnover. Sports Med 1995;19:9–31 [review].
2. Torun B, Chew F. Protein-energy malnutrition. In Shils ME, Olsen JA, Shike M, Ross AC, eds. Modern Nutrition in Health and Disease, 9th ed. Baltimore: Williams & Wilkins, 1999, 963–88 [review].
3. Fuchs GJ, Tienboon P, Linpisarn S, et al. Nutritional factors and thalassaemia major. Arch Dis Child 1996;74:224–7.
4. Little DR. Ambulatory management of common forms of anemia. Am Fam Physician 1999;59:1598–604 [review].
5. Hodges RE, Sauberlich HE, Canham JE, et al. Hematopoietic studies in vitamin A deficiency. Am J Clin Nutr 1978;31:876–85 [review].
6. Bloem MW. Interdependence of vitamin A and iron: an important association for programmes of anaemia control. Proc Nutr Soc 1995;54:501–8 [review].
7. Lane M, Alfrey CP. The anemia of human riboflavin deficiency. Blood 1965;25:432–42.
8. Orehek AJ, Kollas CD. Refractory postpartum anemia due to vitamin B6 deficiency. Ann Intern Med 1997;126(10):834–5 [letter].
9. Iwama H, Iwase O, Hayashi S, et al. Macrocytic anemia with anisocytosis due to alcohol abuse and vitamin B6 deficiency. Rinsho Ketsueki 1998;39:1127–30 [in Japanese].
10. Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol 1999;41:895–906 [review].
11. Summerfield AL, Steinberg FU, Gonzalez JG. Morphologic findings in bone marrow precursor cells in zinc-induced copper deficiency anemia. Am J Clin Pathol 1992;97:665–8.
12. Freycon F, Pouyau G. Rare nutritional deficiency anemia: deficiency of copper and vitamin E. Sem Hop 1983;59:488–93 [review] [in French].
13. Borgna-Pignatti C, Marradi P, Pinelli L, et al. Thiamine-responsive anemia in DIDMOAD syndrome. J Pediatr 1989;114:405–10.
14. Neufeld EJ, Mandel H, Raz T, et al. Localization of the gene for thiamine-responsive megaloblastic anemia syndrome, on the long arm of chromosome 1, by homozygosity mapping. Am J Hum Genet 1997;61:1335–41.
15. Sirdah MM, El-Agouza IMA, Abu Shahla ANK. Possible ameliorative effect of taurine in the treatment of iron-deficiency anaemia in female university students of Gaza, Palestine. Eur J Haematol 2002;69:236–2.
16. Mino M. Clinical uses and abuses of vitamin E in children. Proc Soc Exp Biol Med 1992;200:266–70 [review].
17. Swann IL, Kendra JR. Anaemia, vitamin E deficiency and failure to thrive in an infant. Clin Lab Haematol 1998;20:61–3.
18. Hafez M, Amar ES, Zedan M, et al. Improved erythrocyte survival with combined vitamin E and selenium therapy in children with glucose-6-phosphate dehydrogenase deficiency and mild chronic hemolysis. J Pediatr 1986;108:558–61.
19. Corash L, Spielberg S, Bartsocas C, et al. Reduced chronic hemolysis during high-dose vitamin E administration in Mediterranean-type glucose-6-phosphate dehydrogenase deficiency. N Engl J Med 1980;303:416–20.
20. Eldamhougy S, Elhelw Z, Yamamah G, et al. The vitamin E status among glucose-6 phosphate dehydrogenase deficient patients and effectiveness of oral vitamin E. Int J Vitam Nutr Res 1988;58:184–8.
21. Ono K. Reduction of osmotic haemolysis and anaemia by high dose vitamin E supplementation in regular haemodialysis patients. Proc Eur Dial Transplant Assoc Eur Ren Assoc 1985;21:296–9.
22. Ono K. Effects of large dose vitamin E supplementation on anemia in hemodialysis patients. Nephron 1985;40:440–5.
23. Livrea MA, Tesoriere L, Pintaudi AM, et al. Oxidative stress and antioxidant status in beta-thalassemia major: iron overload and depletion of lipid-soluble antioxidants. Blood 1996;88:3608–14.
24. Loebstein R, Lehotay DC, Luo X, et al. Diabetic nephropathy in hypertransfused patients with beta-thalassemia. The role of oxidative stress. Diabetes Care 1998;21:1306–9.
25. Livrea MA, Tesoriere L, Maggio A, et al. Oxidative modification of low-density lipoprotein and atherogenetic risk in beta-thalassemia. Blood 1998;92:3936–42.
26. De Luca C, Filosa A, Grandinetti M, et al. Blood antioxidant status and urinary levels of catecholamine metabolites in beta-thalassemia. Free Radic Res 1999;30:453–62.
27. Da Fonseca SF, Kimura EY, Kerbauy J. Assessment of iron status in individuals with heterozygotic beta-thalassemia. Rev Assoc Med Bras 1995;41:203–6 [in Portuguese].
28. Miniero R, Canducci E, Ghigo D, et al. Vitamin E in beta-thalassemia. Acta Vitaminol Enzymol 1982;4:21–5.
29. Giardini O, Cantani A, Donfrancesco A, et al. Biochemical and clinical effects of vitamin E administration in homozygous beta-thalassemia. Acta Vitaminol Enzymol 1985;7:55–60.
30. Suthutvoravut U, Hathirat P, Sirichakwal P, et al. Vitamin E status, glutathione peroxidase activity and the effect of vitamin E supplementation in children with thalassemia. J Med Assoc Thai 1993;76 Suppl 2:146–52.
31. Giardini O, Cantani A, Donfrancesco A, et al. Biochemical and clinical effects of vitamin E administration in homozygous beta-thalassemia. Acta Vitaminol Enzymol 1985;7:55–60.
32. Miniero R, Canducci E, Ghigo D, et al. Vitamin E in beta-thalassemia. Acta Vitaminol Enzymol 1982;4:21–5.
33. Palmieri L, Ronca F, Malengo S, Bertelli A. Protection of beta-thalassaemic erythrocytes from oxidative stress by propionyl carnitine. Int J Tissue React 1994;16:121–9.
34. Yesilipek MA, Hazar V, Yegin O. L-Carnitine treatment in beta thalassemia major. Acta Haematol 1998;100:162–3.
35. Saraya AK, Kumar R, Kailash S, Sehgal AK. Vitamin B12 and folic acid deficiency in b-heterozygous thalassemia. Indian J Med Res 1984;79:783–8.
36. Silprasert A, Laokuldilok T, Kulapongs P. Zinc deficiency in b-thalassemic children. In Fucharoen S, Rowley PT, Paul NW, eds. Thalassemia: pathophysiology and management, part A. New York: Alan R Liss, 1988 [review].
37. Bashir NA. Serum zinc and copper levels in sickle cell anaemia and beta-thalassaemia in North Jordan. Ann Trop Paediatr 1995;15:291–3.
38. Arcasoy A, Cavdar AO, Cin S, et al. Effects of zinc supplementation on linear growth in beta thalassemia. Am J Hematol 1987;24:127–36.
39. Akar N, Berberoglu M, Arcasoy A. Effects of zinc supplementation on somatomedin-C level, in beta-thalassemia. Am J Hematol 1992;41:142–3 [letter].
40. Cohen L, Bitterman H, Froom P, Aghai E. Decreased bone magnesium in beta thalassemia with spinal osteoporosis. Magnesium 1986;5:43–6.
41. Hyman CB, Ortega JA, Costin G, Takahashi M. The clinical significance of magnesium depletion in thalassemia. Ann N Y Acad Sci 1980;344:436–43.
42. Arcasoy A, Cavdar AO. Changes of trace minerals (serum iron, zinc, copper and magnesium) in thalassemia. Acta Haematol 1975;53:341–6.
43. De Franceschi L, Cappellini MD, Graziadei G, et al. The effect of dietary magnesium supplementation on the cellular abnormalities of erythrocytes in patients with beta thalassemia intermedia. Haematologica 1998;83:118–25.
44. May A, Bishop DF. The molecular biology and pyridoxine responsiveness of X-linked sideroblastic anaemia. Haematologica 1998;83:56–70 [review].
45. May A, Fitzsimons E. Sideroblastic anaemia. Baillieres Clin Haematol 1994;7:851–79 [review].
46. Kasdan TS. Medical nutrition therapy for anemia. In Mahan LK, Escott-Stump S, eds. Krause’s Food, Nutrition & Diet Therapy, 10th ed. Philadelphia: W.B. Saunders, 2000, 796–7.
Copyright © 2006 Healthnotes, Inc. All rights reserved. www.healthnotes.com
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The information presented in Healthnotes is for informational purposes only. It is based on scientific studies (human, animal, or in vitro), clinical experience, or traditional usage as cited in each article. The results reported may not necessarily occur in all individuals. For many of the conditions discussed, treatment with prescription or over the counter medication is also available. Consult your doctor, practitioner, and/or chemist for any health problem and before using any supplements or before making any changes in prescribed medications. Information expires March 2007.
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