• J R Drake and C D Fitch.
• Am. J. Clin. Nutr. 1980 Nov 1; 33 (11): 2386-93.

AbstractThere is now convincing evidence that vitamin E is a specific erythropoietic factor for nonhuman primates and swine. There is no evidence, however, that vitamin E is normally required as an erythropoietic factor for humans and many species of animals. We propose that the lack of a requirement for vitamin E in erythropoiesis in humans is due to a metabolic adaptation that circumvents the need for the role that the vitamin otherwise would serve. There is reason to believe that this metabolic adaptation is deranged in patients with protein-calorie malnutrition. These patients respond with reticulocytosis and a limited increase in hemoglobin concentration when vitamin E is given before their metabolic derangement is reversed by correcting their other nutritional deficiencies. Given this information, we may predict that other acquired or congenital abnormalities of metabolism could impair the adaptation that circumvents the role of vitamin E in erythropoiesis. Therefore, vitamin E should be viewed as a potential erythropoietic factor for humans, and it should receive further carefully controlled therapeutic trials in patients with anemia of obscure etiology, particularly in those with erythroid hyperplasia and unexplained ineffective erythropoiesis.

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