American Journal of Clinical Nutrition, Vol 27, 1141-1151, Copyright © 1974 by The American Society for Clinical Nutrition, Inc.

Vitamin E deficiency anemia in Old and New World monkeys

¹ From the Department of Nutrition, Harvard School of Public Health, Boston Massachusetts 02115

In a study of vitamin E deficiency in two species of laboratory raised juvenile monkeys (12 cebus, 14 cynomolgus), diets containing 22% of the calories as coconut or stripped safflower oil with or without vitamin E were fed for 32 months. Signs of deficiency were recognized in the unsupplemented safflower oil-fed cebus monkeys after 12-13 months when severe anemia (hematocrit = 12-15), depressed appetite, weight loss, and plasma tocopherol concentrations less than 100 µg/dl were observed. Comparably treated cynomolgus monkeys became clinically ill after 2 years and developed moderate anemia (hematocrit = 25-30), anorexia, muscular weakness, and severe weight loss. Anemia in both species was macrocytic and was accompanied by reticulocytosis as high as 35% in some of the cebus monkeys. No monkeys fed coconut oil developed anemia. In vitro hemolysis tests paralleled the clinical findings in that red cells from the cebus hemolyzed earlier and to a greater degree than those from the cynomolgus. Vitamin E protected against the anemia and in vitro hemolysis. A higher percentage of polyunsaturated fatty acid in red blood cells from the cebus was thought to predispose them to hemolysis. In terms of the hematologic response to oral dosing with vitamin E, the minimal vitamin E requirement of three anemic cebus was 0.16 mg/kg per day and that of one cynomolgus was 0.10 mg/kg per day. Monkeys fed the coconut oil diet were calculated to have less than half the vitamin E requirement of those fed safflower oil. The precipitous decline in red cell number, the high percentage of reticulocytes, positive in vitro hemolysis tests, and observation of jaundice, splenomegaly, and hemosiderosis at necropsy indicated that the anemia was primarily hemolytic in nature. A dyspoietic hyporegenerative aspect of the anemia was accompanied by megaloblastic bone marrow changes that were interpreted in terms of intramedullary hemolysis and localized folate deficiency.