Anemia

Also indexed as: Hemolytic Anemia, Low Hematocrit, Low Hemoglobin, Low Red Blood Cell Count, Sideroblastic Anemia, Thalassemia

Anemia is a general term for a category of blood conditions that affects the red blood cells or the oxygen-carrying hemoglobin they contain. In anemia, there is either a reduction in the number of red blood cells in circulation or a decrease in the amount or quality of hemoglobin. There are many causes of anemia, including severe blood loss, genetic disorders, and serious diseases. (See iron deficiency anemia, pernicious anemia [vitamin B12-related], and sickle cell anemia.) Anyone with unexplained anemia should have the cause determined by a qualified doctor.

Some athletes appear to have anemia when their blood is tested, but this may be a normal adaptation to the stress of exercise,1 which does not need treatment. Further evaluation by a qualified doctor is necessary.

Checklist for Anemia

Rating Nutritional Supplements Herbs
3Stars Copper (if deficient)
Iron (when iron deficiency is diagnosed)
Vitamin A (if deficient)
Vitamin B1 (for genetic thiamine-responsive anemia)
Vitamin B12 (if deficient)
Vitamin B2 (if deficient)
Vitamin B6 (if deficient and for genetic vitamin B6-responsive anemia)
Vitamin C (if deficient)
Vitamin E (if deficient)		  
2Stars Folic acid (for thalassemia if deficient)
L-carnitine(for thalassemia)
Magnesium(for thalassemia)
Vitamin B12 (for thalassemia if deficient)
Vitamin E (injections for thalassemia, orally for glucose-6-phosphate dehydrogenase deficiency [G6PD] anemia and anemia caused by kidney dialysis)
Zinc (for thalassemia if deficient)		  
1Star Antioxidants (for thalassemia)
Vitamin C (for thalassemia if deficient)		  
3Stars Reliable and relatively consistent scientific data showing a substantial health benefit.
2Stars Contradictory, insufficient, or preliminary studies suggesting a health benefit or minimal health benefit.
1Star An herb is primarily supported by traditional use, or the herb or supplement has little scientific support and/or minimal health benefit.

What are the symptoms of anemia? Some common symptoms of anemia include fatigue, lethargy, weakness, poor concentration, and frequent colds. A peculiar symptom of iron-deficiency anemia, called pica, is the desire to eat unusual things, such as ice, clay, cardboard, paint, or starch. Advanced anemia 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.

How is it treated? Conventional therapy for anemia involves treating the cause of anemia and may include blood transfusions or supplementation with iron, vitamin B12, folic acid, or erythropoietin (EPO), a blood-building hormone.

Dietary changes that may be helpful: Severe protein deficiency can cause anemia because protein is required for normal production of hemoglobin and red blood cells.2 However, this deficiency is uncommon in healthy people living in developed countries.

Thalassemia is an inherited type of anemia that is most common in people of Mediterranean descent. Children with severe thalassemia often have reduced growth rates that may be partially due to inadequate diets. This problem is primarily found in developing countries.3

Nutritional supplements that may be helpful: Deficiencies of iron, vitamin B12, and folic acid are the most common nutritional causes of anemia.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 anemia by various mechanisms. Rare genetic disorders can cause anemias that may improve with large amounts of supplements such as vitamin B1.13 14

Hemolytic anemia refers to a category of anemia in which red blood cells become fragile and undergo premature death. Vitamin E deficiency, though quite rare, can cause hemolytic anemia because vitamin E protects the red blood cell membrane from oxidative damage. Vitamin E deficiency anemia usually affects only premature infants and children with cystic fibrosis.15 16 Preliminary studies have reported that large amounts (typically 800 IU per day) of vitamin E improve hemolytic anemia caused by a genetic deficiency of the enzyme glucose-6-phosphate dehydrogenase (G6PD)17 18 19 and anemia caused by kidney dialysis.20 21

People with severe thalassemia who receive regular blood transfusions become overloaded with iron, which increases damaging free radical activity and lowers antioxidant levels in their bodies.22 23 24 25 Some people with milder forms of thalassemia may also have iron overload.26 Iron supplements should be avoided by people with thalassemia 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 thalassemia patients.27 28 29 However, only injections of vitamin E have reduced the need for blood transfusions caused by thalassemia.30 31

Test tube studies have shown that propionyl-L-carnitine (a form of L-carnitine) protects red blood cells of people with thalassemia against free radical damage.32 In a preliminary study, children with beta thalassemia 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.33 Some studies have found people with thalassemia to be frequently deficient in folic acid, vitamin B12,34 and zinc.35 36 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.37 38 Magnesium has been reported to be low in thalassemia patients in some,39 40 but not all,41 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 thalassemia patients.42

Sideroblastic anemia refers to a category of anemia featuring a buildup of iron-containing immature red blood cells (sideroblasts). One type of sideroblastic anemia is due to a genetic defect in an enzyme that uses vitamin B6 as a cofactor.43 44 Vitamin B6 supplements of 50 to 200 mg per day partially correct the anemia, but must be taken for life.45

Are there any side effects or interactions? Refer to the individual supplement for information about any side effects or interactions.

References:

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].

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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. Mino M. Clinical uses and abuses of vitamin E in children. Proc Soc Exp Biol Med 1992;200:266–70 [review].

16. Swann IL, Kendra JR. Anaemia, vitamin E deficiency and failure to thrive in an infant. Clin Lab Haematol 1998;20:61–3.

17. 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.

18. 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.

19. 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.

20. 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.

21. Ono K. Effects of large dose vitamin E supplementation on anemia in hemodialysis patients. Nephron 1985;40:440–5.

22. 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.

23. 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.

24. 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.

25. 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.

26. 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].

27. Miniero R, Canducci E, Ghigo D, et al. Vitamin E in beta-thalassemia. Acta Vitaminol Enzymol 1982;4:21–5.

28. 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.

29. 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.

30. 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.

31. Miniero R, Canducci E, Ghigo D, et al. Vitamin E in beta-thalassemia. Acta Vitaminol Enzymol 1982;4:21–5.

32. 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.

33. Yesilipek MA, Hazar V, Yegin O. L-Carnitine treatment in beta thalassemia major. Acta Haematol 1998;100:162–3.

34. 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.

35. 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].

36. Bashir NA. Serum zinc and copper levels in sickle cell anaemia and beta-thalassaemia in North Jordan. Ann Trop Paediatr 1995;15:291–3.

37. 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.

38. 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].

39. Cohen L, Bitterman H, Froom P, Aghai E. Decreased bone magnesium in beta thalassemia with spinal osteoporosis. Magnesium 1986;5:43–6.

40. 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.

41. Arcasoy A, Cavdar AO. Changes of trace minerals (serum iron, zinc, copper and magnesium) in thalassemia. Acta Haematol 1975;53:341–6.

42. 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.

43. May A, Bishop DF. The molecular biology and pyridoxine responsiveness of X-linked sideroblastic anaemia. Haematologica 1998;83:56–70 [review].

44. May A, Fitzsimons E. Sideroblastic anaemia. Baillieres Clin Haematol 1994;7:851–79 [review].

45. 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.