X. EFFECTS OF DEFICIENCY 281 



Hawkins and liar!?ky"- attempted to piodncc deficiency of vitamin ]^6 in 

 an adull w ho subsisted for 55 days on a purified diet and i-eceived all neces- 

 sary known vitamins with the exception of vitamin He- The basal diet 

 consisted of a mixture of sucrose, corn oil, \'itamin-free casein, salt mixture, 

 cod li\(M- oil conccnli-ate, and all known watei'-soluble \itamins, except 

 pyridoxine. The unpalatability of the mixtuie made diflicult the in'i.estion 

 of a sufficient amount to supply the caloric needs of a moderately active 

 man. with the net result of a definite weight loss. At the level taken the 

 diet furnished 82.5 j>;. of protein and 50 m*;-. of iron daily. It is no wonder 

 that on such an experimental diet the subject toward the end of the experi- 

 mental period was complaining of "an unusual degree of depression and 

 mental confusion." It may be assumed that the noted beneficial effect of a 

 supplement of vitamin Be at this stage of the experiment was due more to a 

 psychological than nutritional-metabolic effect. The authors themselves 

 concluded that the experiment revealed no changes which could une([uivo- 

 cally be considered as resulting from a lack of \'itamin Be . Furthermore, 

 even on the animal experiments it may be definitely stated that the experi- 

 mental period of 55 days is too short to bring about deficiency of ^'itamin Be 

 in adult animals or man. 



More conclusive are the observations reported by Snyderman ct al.^*'^ 

 These authors administered a vitamin Be-deficient diet for therapeutic 

 reasons to two mentally defective infants for 76 and 130 days, respectively. 

 The first changes noted were of biochemical nature. P\n'idoxic acid dis- 

 appeared from the urine, and the total urinary pyridoxine was reduced to 

 extremely low values ranging from 0.2 to 2 7 per day. "Subsequently, lioth 

 infants lost the ability to convert trj^ptophan to nicotinic acid, an effect 

 which was desired in order to block a metabolic path for tryptophan 

 that might be competing with normal tissue synthesis. A plateauing of the 

 weight cur^'e occurred 33 and 73 days after the institution of the regime. 

 (3n the 76th day one subject developed a series of convulsions which were 

 promptly relieved by the administration of pyridoxine. The other subject 

 dexeloped a hypochromic anemia at approximately the 130th day. This 

 responded dramatically to pyridoxine; a rise of reticulocytes was noted 

 after 72 hours reaching a peak in 4 days after which red cell count and 

 hemoglobin rose to normal. Both subjects gained weight normally after 

 supplementation. In marked contrast to the excellent and prompt clinical 

 response to the administration of pyridoxine was a delay in the reappear- 

 ance in the ability to convert tryptophan to nicotinic acid." 



"2 W. W. Hawkins and .1. Har.sky, Science 108, 2S4 (1948). 



"••' 8. K. Siiydcrinaii, H. C'arretoro, and L. K. H<'It. .Jr., Federation Proc. 9, 371 

 (1950) . 



