1915] Casimir Funk 311 



FoodstuSFs Amount necessary for prevention 



Wet (natural) Dry 



grams grams 



Ox cerebrum 6 1.2 



Ox cerebellum 12 2.4 



Ox liver 3 0.9 



Cow milk > 35 > 3-5 



Nuts (husked filberts) — 2.0 



Cheese > 8 > 5-6 



son (13) finds that human milk is less protective than cow 

 milk; also, that compensated salt mixtures (often o£ calcium and 

 sodium tartrate) delayed the onset of Symptoms and rendered the 

 degeneration of nerves less pronounced. Ohler (14) and Weill and 

 Mouriquand (15) confirmed the findings of Hill and Flack (16) 

 who found that altho white bread caused beriberi in fowls, tk3 latter 

 remained healthy on whole wheat bread. Ohler finds, also, that 

 fowls remain well on whole corn but not on hominy (the inside of 

 the corn kernel) ; in the latter case they develop the same condition 

 as that on white bread, a very interesting Observation to be discussed 

 further under pellagra. Merklen (17) describes a peculiar disease 

 in ducklings (3-4 weeks old) with Symptoms of cramps and paral- 

 ysis of the legs. These Symptoms disappeared when the diet was 

 variable. Possibly the disease was beriberi. 



AUeged beriberi and beriberi-like diseases in other animals, 

 especially mammals. The question whether other animals than 

 birds and man are suitable for the study of beriberi is still open to 

 discussion. It is undoubtedly true that no animal is able to live on 

 polished rice or any vitamine-free food, but it seems probable that 

 the condition described in monkeys, dogs, mice, rats, rabbits and 

 guinea-pigs is either scurvy or a condition of general weakness. 

 None of the conditions described (even the fatty degeneration of 

 nerves) classifies the disease as beriberi. The symptom usually ob- 

 served is a peculiar weakness of the bind legs which can hardly be 

 interpreted as beriberi. Schnyder (9) found that the disease in mice, 

 dogs and cats is etiologically and chemically the same as in birds, 

 but not pathologically, for there is very little nerve degeneration. 

 Empirically, I have divided animals into two groups : those in which 

 the terminal purin metabolism results in allantoin; those in which 

 uric acid is the final product. In the first group are monkeys, 



