There 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.