Anemia (Holistic)

Anemia (Holistic)

About This Condition

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 be helpful.
  • Replace needed nutrients

    Prevent and treat anemia with supplemental iron, vitamin B12, and folic acid; you should not take iron unless a blood test has revealed a deficiency

  • Get a checkup

    Visit your healthcare provider for a test to determine the cause

  • Add L-carnitine to your routine

    If you have thalassemia, take 100 mg of this nutritional supplement per 2.2 pounds of body weight each day to reduce the need for blood transfusions

About

About This Condition

Anemia is a general term for a category of blood conditions that affect 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.

Symptoms

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.

Supplements

What Are "Star" Ratings?

Our proprietary “Star-Rating” system was developed to help you easily understand the amount of scientific support behind each supplement in relation to a specific health condition. While there is no way to predict whether a vitamin, mineral, or herb will successfully treat or prevent associated health conditions, our unique ratings tell you how well these supplements are understood by the medical community, and whether studies have found them to be effective for other people.

For over a decade, our team has combed through thousands of research articles published in reputable journals. To help you make educated decisions, and to better understand controversial or confusing supplements, our medical experts have digested the science into these three easy-to-follow ratings. We hope this provides you with a helpful resource to make informed decisions towards your health and well-being.

3 Stars Reliable and relatively consistent scientific data showing a substantial health benefit.

2 Stars Contradictory, insufficient, or preliminary studies suggesting a health benefit or minimal health benefit.

1 Star For an herb, supported by traditional use but minimal or no scientific evidence. For a supplement, little scientific support.

Supplement Why
3 Stars
Vitamin A
10,000 to 25,000 IU daily
Vitamin A deficiency can contribute to anemia, supplementing with this vitamin may restore levels and improve symptoms.

Deficiencies of iron, vitamin B12, and folic acid are the most common nutritional causes of anemia.2 Although rare, severe deficiencies of several other vitamins and minerals, including vitamin A,3 , 4 vitamin B2,5 vitamin B6,6 , 7 vitamin C,8 and copper,9 , 10 can also cause anemia by various mechanisms. Rare genetic disorders can cause anemias that may improve with large amounts of supplements such as vitamin B1.11 , 12
3 Stars
Vitamin B12 (Vitamin B12 Deficiency)
600 to 1,000 mcg daily
Taking vitamin B12 may help prevent and treat anemia. Deficiencies of iron, vitamin B12, and folic acid are the most common nutritional causes of anemia.

Deficiencies of iron, vitamin B12, and folic acid are the most common nutritional causes of anemia.13 Although rare, severe deficiencies of several other vitamins and minerals, including vitamin A,14 , 15 vitamin B2,16 vitamin B6,17 , 18 vitamin C,19 and copper,20 , 21 can also cause anemia by various mechanisms. Rare genetic disorders can cause anemias that may improve with large amounts of supplements such as vitamin B1.22 , 23
3 Stars
Vitamin B2
5 to 30 mg daily in divided doses
Vitamin B2 deficiency can contribute to anemia, supplementing with this vitamin may restore levels and improve symptoms.

Deficiencies of iron, vitamin B12, and folic acid are the most common nutritional causes of anemia.24 Although rare, severe deficiencies of several other vitamins and minerals, including vitamin A,25 , 26 vitamin B2,27 vitamin B6,28 , 29 vitamin C,30 and copper,31 , 32 can also cause anemia by various mechanisms. Rare genetic disorders can cause anemias that may improve with large amounts of supplements such as vitamin B1.33 , 34
3 Stars
Vitamin B6 (Genetic Vitamin B6-Responsive Anemia)
50 to 200 mg per day
Taking vitamin B6 may partially correct sideroblastic anemia, although they must be taken for life.

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.35 , 36 Vitamin B6 supplements of 50 to 200 mg per day partially correct the anemia, but must be taken for life.37
3 Stars
Vitamin B6
2.5 to 25 mg daily for three weeks, then 1.5 to 2.5 mg per day as maintenance therapy
Vitamin B6 deficiency can contribute to anemia, supplementing with this vitamin may restore levels and improve symptoms.

Deficiencies of iron, vitamin B12, and folic acid are the most common nutritional causes of anemia.38 Although rare, severe deficiencies of several other vitamins and minerals, including vitamin A,39 , 40 vitamin B2,41 vitamin B6,42 , 43 vitamin C,44 and copper,45 , 46 can also cause anemia by various mechanisms. Rare genetic disorders can cause anemias that may improve with large amounts of supplements such as vitamin B1.47 , 48
3 Stars
Vitamin C
100 to 250 mg once or twice per day
Vitamin C deficiency can contribute to anemia, supplementing with this vitamin may restore levels and improve symptoms.

Deficiencies of iron, vitamin B12, and folic acid are the most common nutritional causes of anemia.49 Although rare, severe deficiencies of several other vitamins and minerals, including vitamin A,50 , 51 vitamin B2,52 vitamin B6,53 , 54 vitamin C,55 and copper,56 , 57 can also cause anemia by various mechanisms. Rare genetic disorders can cause anemias that may improve with large amounts of supplements such as vitamin B1.58 , 59
3 Stars
Vitamin E
60 to 75 IU per day
Supplementing with vitamin E may improve anemia in cases of vitamin E deficiency.

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.60 , 61 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)62 , 63 , 64 and anemia caused by kidney dialysis.65 , 66
3 Stars
Vitamin E Oral
800 IU daily
Studies have reported that large amounts of vitamin E improve hemolytic anemia caused by a genetic deficiency of the enzyme glucose-6-phosphate dehydrogenase (G6PD).

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.67 , 68 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)69 , 70 , 71 and anemia caused by kidney dialysis.72 , 73
2 Stars
Copper
If deficient: 2 to 3 mg daily
Copper deficiency can contribute to anemia, supplementing with this mineral may restore levels and improve symptoms.

Deficiencies of iron, vitamin B12, and folic acid are the most common nutritional causes of anemia.74 Although rare, severe deficiencies of several other vitamins and minerals, including vitamin A,75 , 76 vitamin B2,77 vitamin B6,78 , 79 vitamin C,80 and copper,81 , 82 can also cause anemia by various mechanisms. Rare genetic disorders can cause anemias that may improve with large amounts of supplements such as vitamin B1.83 , 84
2 Stars
Vitamin B1 (Genetic Thiamine-Responsive Anemia)
10 to 20 mg daily
Rare genetic disorders can cause anemias that may improve with large amounts of supplements such as vitamin B1.

Deficiencies of iron, vitamin B12, and folic acid are the most common nutritional causes of anemia.85 Although rare, severe deficiencies of several other vitamins and minerals, including vitamin A,86 , 87 vitamin B2,88 vitamin B6,89 , 90 vitamin C,91 and copper,92 , 93 can also cause anemia by various mechanisms. Rare genetic disorders can cause anemias that may improve with large amounts of supplements such as vitamin B1.94 , 95
2 Stars
Vitamin E Oral (Kidney Dialysis)
800 IU daily
Studies have reported that large amounts of vitamin E improve anemia caused by kidney dialysis.

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.96 , 97 , 98 , 99 Some people with milder forms of thalassemia may also have iron overload.100 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.101 , 102 , 103 However, only injections of vitamin E have reduced the need for blood transfusions caused by thalassemia.104 , 105
1 Star
Açaí
Refer to label instructions
Açaí, which contains small amounts of iron, has been traditionally used to help treat anemia.

Açaí contains iron (approximately 1.5 to 5 mg per 3.5 ounces of fruit).106 Although it has been traditionally used to help treat anemia, the amount of iron in açaí is not likely to be abundant or absorbable enough to have a significant effect.

Related Information

Anemia
  1. Find Drug Interaction Information

References

1. Smith JA. Exercise, training and red blood cell turnover. Sports Med 1995;19:9–31 [review].

2. Little DR. Ambulatory management of common forms of anemia. Am Fam Physician 1999;59:1598–604 [review].

3. Hodges RE, Sauberlich HE, Canham JE, et al. Hematopoietic studies in vitamin A deficiency. Am J Clin Nutr 1978;31:876–85 [review].

4. Bloem MW. Interdependence of vitamin A and iron: an important association for programmes of anaemia control. Proc Nutr Soc 1995;54:501–8 [review].

5. Lane M, Alfrey CP. The anemia of human riboflavin deficiency. Blood 1965;25:432–42.

6. Orehek AJ, Kollas CD. Refractory postpartum anemia due to vitamin B6 deficiency. Ann Intern Med 1997;126(10):834–5 [letter].

7. 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].

8. Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol 1999;41:895–906 [review].

9. 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.

10. Freycon F, Pouyau G. Rare nutritional deficiency anemia: deficiency of copper and vitamin E. Sem Hop 1983;59:488–93 [review] [in French].

11. Borgna-Pignatti C, Marradi P, Pinelli L, et al. Thiamine-responsive anemia in DIDMOAD syndrome. J Pediatr 1989;114:405–10.

12. 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.

13. Little DR. Ambulatory management of common forms of anemia. Am Fam Physician 1999;59:1598–604 [review].

14. Hodges RE, Sauberlich HE, Canham JE, et al. Hematopoietic studies in vitamin A deficiency. Am J Clin Nutr 1978;31:876–85 [review].

15. Bloem MW. Interdependence of vitamin A and iron: an important association for programmes of anaemia control. Proc Nutr Soc 1995;54:501–8 [review].

16. Lane M, Alfrey CP. The anemia of human riboflavin deficiency. Blood 1965;25:432–42.

17. Orehek AJ, Kollas CD. Refractory postpartum anemia due to vitamin B6 deficiency. Ann Intern Med 1997;126(10):834–5 [letter].

18. 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].

19. Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol 1999;41:895–906 [review].

20. 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.

21. Freycon F, Pouyau G. Rare nutritional deficiency anemia: deficiency of copper and vitamin E. Sem Hop 1983;59:488–93 [review] [in French].

22. Borgna-Pignatti C, Marradi P, Pinelli L, et al. Thiamine-responsive anemia in DIDMOAD syndrome. J Pediatr 1989;114:405–10.

23. 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.

24. Little DR. Ambulatory management of common forms of anemia. Am Fam Physician 1999;59:1598–604 [review].

25. Hodges RE, Sauberlich HE, Canham JE, et al. Hematopoietic studies in vitamin A deficiency. Am J Clin Nutr 1978;31:876–85 [review].

26. Bloem MW. Interdependence of vitamin A and iron: an important association for programmes of anaemia control. Proc Nutr Soc 1995;54:501–8 [review].

27. Lane M, Alfrey CP. The anemia of human riboflavin deficiency. Blood 1965;25:432–42.

28. Orehek AJ, Kollas CD. Refractory postpartum anemia due to vitamin B6 deficiency. Ann Intern Med 1997;126(10):834–5 [letter].

29. 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].

30. Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol 1999;41:895–906 [review].

31. 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.

32. Freycon F, Pouyau G. Rare nutritional deficiency anemia: deficiency of copper and vitamin E. Sem Hop 1983;59:488–93 [review] [in French].

33. Borgna-Pignatti C, Marradi P, Pinelli L, et al. Thiamine-responsive anemia in DIDMOAD syndrome. J Pediatr 1989;114:405–10.

34. 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.

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

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

37. 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.

38. Little DR. Ambulatory management of common forms of anemia. Am Fam Physician 1999;59:1598–604 [review].

39. Hodges RE, Sauberlich HE, Canham JE, et al. Hematopoietic studies in vitamin A deficiency. Am J Clin Nutr 1978;31:876–85 [review].

40. Bloem MW. Interdependence of vitamin A and iron: an important association for programmes of anaemia control. Proc Nutr Soc 1995;54:501–8 [review].

41. Lane M, Alfrey CP. The anemia of human riboflavin deficiency. Blood 1965;25:432–42.

42. Orehek AJ, Kollas CD. Refractory postpartum anemia due to vitamin B6 deficiency. Ann Intern Med 1997;126(10):834–5 [letter].

43. 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].

44. Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol 1999;41:895–906 [review].

45. 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.

46. Freycon F, Pouyau G. Rare nutritional deficiency anemia: deficiency of copper and vitamin E. Sem Hop 1983;59:488–93 [review] [in French].

47. Borgna-Pignatti C, Marradi P, Pinelli L, et al. Thiamine-responsive anemia in DIDMOAD syndrome. J Pediatr 1989;114:405–10.

48. 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.

49. Little DR. Ambulatory management of common forms of anemia. Am Fam Physician 1999;59:1598–604 [review].

50. Hodges RE, Sauberlich HE, Canham JE, et al. Hematopoietic studies in vitamin A deficiency. Am J Clin Nutr 1978;31:876–85 [review].

51. Bloem MW. Interdependence of vitamin A and iron: an important association for programmes of anaemia control. Proc Nutr Soc 1995;54:501–8 [review].

52. Lane M, Alfrey CP. The anemia of human riboflavin deficiency. Blood 1965;25:432–42.

53. Orehek AJ, Kollas CD. Refractory postpartum anemia due to vitamin B6 deficiency. Ann Intern Med 1997;126(10):834–5 [letter].

54. 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].

55. Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol 1999;41:895–906 [review].

56. 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.

57. Freycon F, Pouyau G. Rare nutritional deficiency anemia: deficiency of copper and vitamin E. Sem Hop 1983;59:488–93 [review] [in French].

58. Borgna-Pignatti C, Marradi P, Pinelli L, et al. Thiamine-responsive anemia in DIDMOAD syndrome. J Pediatr 1989;114:405–10.

59. 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.

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

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

62. 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.

63. 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.

64. 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.

65. 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.

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

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

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

69. 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.

70. 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.

71. 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.

72. 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.

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

74. Little DR. Ambulatory management of common forms of anemia. Am Fam Physician 1999;59:1598–604 [review].

75. Hodges RE, Sauberlich HE, Canham JE, et al. Hematopoietic studies in vitamin A deficiency. Am J Clin Nutr 1978;31:876–85 [review].

76. Bloem MW. Interdependence of vitamin A and iron: an important association for programmes of anaemia control. Proc Nutr Soc 1995;54:501–8 [review].

77. Lane M, Alfrey CP. The anemia of human riboflavin deficiency. Blood 1965;25:432–42.

78. Orehek AJ, Kollas CD. Refractory postpartum anemia due to vitamin B6 deficiency. Ann Intern Med 1997;126(10):834–5 [letter].

79. 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].

80. Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol 1999;41:895–906 [review].

81. 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.

82. Freycon F, Pouyau G. Rare nutritional deficiency anemia: deficiency of copper and vitamin E. Sem Hop 1983;59:488–93 [review] [in French].

83. Borgna-Pignatti C, Marradi P, Pinelli L, et al. Thiamine-responsive anemia in DIDMOAD syndrome. J Pediatr 1989;114:405–10.

84. 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.

85. Little DR. Ambulatory management of common forms of anemia. Am Fam Physician 1999;59:1598–604 [review].

86. Hodges RE, Sauberlich HE, Canham JE, et al. Hematopoietic studies in vitamin A deficiency. Am J Clin Nutr 1978;31:876–85 [review].

87. Bloem MW. Interdependence of vitamin A and iron: an important association for programmes of anaemia control. Proc Nutr Soc 1995;54:501–8 [review].

88. Lane M, Alfrey CP. The anemia of human riboflavin deficiency. Blood 1965;25:432–42.

89. Orehek AJ, Kollas CD. Refractory postpartum anemia due to vitamin B6 deficiency. Ann Intern Med 1997;126(10):834–5 [letter].

90. 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].

91. Hirschmann JV, Raugi GJ. Adult scurvy. J Am Acad Dermatol 1999;41:895–906 [review].

92. 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.

93. Freycon F, Pouyau G. Rare nutritional deficiency anemia: deficiency of copper and vitamin E. Sem Hop 1983;59:488–93 [review] [in French].

94. Borgna-Pignatti C, Marradi P, Pinelli L, et al. Thiamine-responsive anemia in DIDMOAD syndrome. J Pediatr 1989;114:405–10.

95. 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.

96. 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.

97. 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.

98. 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.

99. 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.

100. 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].

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

102. 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.

103. 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.

104. 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.

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

106. Yuyama LKO, Dias RR, Nagahama D, et al. Acai ( Euterpe oleracea Mart.) and camu-camu (Myrciaria dubia (H.B.K.) Mc Vaugh), do they possess anti-anemic action? Acta Amazonica2002;32:625–33.

Last Review: 11-07-2012

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The information presented in Aisle7 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. Self-treatment is not recommended for life-threatening conditions that require medical treatment under a doctor's care. For many of the conditions discussed, treatment with prescription or over the counter medication is also available. Consult your doctor, practitioner, and/or pharmacist for any health problem and before using any supplements or before making any changes in prescribed medications. Information expires June 2013.
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