Goat's Milk Anemia *

That infants fed a diet comprised chiefly of goat's milk may develop an anemia has been observed by many investigators (see Alt', Davidson and Leitch6, and Kronacher et al.9), particularly in Continental Europe where this kind of milk has been employed extensively in infant feeding. Although there is some difference of opinion, the balance of clinical evidence seems to indicate that goat's milk anemia is usually the hyperchromic type and is more severe than is cow's milk anemia (Davidson and Leitch6). Several hypotheses have been advanced to explain the anemia-producing effect of goat's milk. One of these postulates the presence of toxic substances in the milk, perhaps certain types of fatty acids in the milk fat (see Brouwer4, Davidson and Leitch6, de Rudder"5, Rominger, Meyer and Bomskov12, and Stoltzner17), which promote an increased rate of erythrocyte destruction and thus cause an anemia. However, the fact that the administration of relatively large amounts of fatty acids prepared from goat's milk or mixtures of pure fatty acids to animals receiving either a mixed ration or a goat's milk diet had no noticeable effect on the composition of the blood (Bomskov and Auffarth3) seems to preclude the possibility of the presence of a hemolytic agent in the fat of goat's milk. Other recent work, to be discussed later, likewise lends no support to the "toxic theory" of the etiology of goat's milk anemia. Another explanation of the cause of goat's milk anemia is that this type of milk is deficient in some necessary hematogenic substance, such as iron (Brouwer5) or, as has been recently suggested (Rominger et al.12, , 14, Gyorgy7), an essential organic substance perhaps related to the "extrinsic factor" said to be needed for the prevention of pernicious anemia in man. The evidence upon which the latter view is based was obtained chiefly from experiments on young albino rats fed an exclusive goat's milk diet. A severe hyperchromic anemia developed and the condition was not cured by iron and copper, by vitamins A, B1, or B4 (Rominger et al."2 13 14), or