Abstract
Studies of anemia in pregnancy1have directed attention to the hypothesis that the mother may not always have an adequate supply of blood-building material for both fetal and maternal demands and that the fetus may deplete the maternal stores regardless of the result to the mother.2More specifically, Wintrobe and Shumacker3suggested that a macrocytic anemia might develop during pregnancy if the fetus derived its supply of antianemic principle from the mother to the extent that a deficiency was caused to exist in the storage of maternal liver factor. If this assumption is correct, one should be able to influence embryonic and fetal erythropoiesis by supplying the mother with a superabundance of antianemic principle. Although Wintrobe and associates4were unable to influence the red cell count and the mean corpuscular volume of 21 and 23 day rabbit fetuses, they expressed the belief that this did not