FUNCTION 



claimed to be able to detect incipient hypovitaminosis by measuring 

 the B.B.S. in blood ; when the nutritional status was such that 11-4 % 

 of a test dose of aneurine was excreted, the B.B.S. were 7-8 mg. per 

 100 ml., whereas when the excretion fell to 3-6 % the B.B.S. had risen 

 to 13-4 mg. per 100 ml. Similarly, H. A. Harper and H. J. Deuel ® 

 found that during aneurine depletion the urinary excretion of pyruvate 

 increased, more in males than in females. The excretion was reduced 

 when optimal amounts of aneurine were given, although not when 

 amounts adequate for minimum growth were given. They did not 

 claim that the phenomenon could be used for diagnosing vitamin B^ 

 deficiency. Shils et al.}^ on the other hand, failed to observe any 

 increase in B.B.S. in the urine of subjects fed a vitamin Bi-deficient 

 diet. 



The method of assessing vitamin B^ deficiency by measuring the 

 bisulphite-binding substances in the blood never met with general 

 approval, however, and was explicitly rejected by Robinson et al.,^'^ 

 by Wortis et al.'^^ and by H. A. Davis and F. K. Bauer.^^ jj^g last- 

 named workers compared the blood pyruvic acid in various diseases 

 with that of controls. The normal level was 0-5 to 1-3 mg. per 100 

 ml., but in various hepatic disorders it increased up to 4-25 and in 

 toxic goitre to 3-5 mg. per 100 ml. No increase was observed in non- 

 toxic goitre or in renal disease, but an increase occurred in some malig- 

 nant diseases. It was estimated that half the cases of infection 

 examined also had increased pyruvic acid levels in the blood. Obvi- 

 ously, therefore, elevation of the blood pyruvic acid cannot be used 

 for the diagnosis and evaluation of vitamin B^ deficiency without 

 excluding other conditions that might equally well be responsible. 



M. K. Horwitt and O. Kreisler,^^'' however, claim that the levels of 

 lactate and p3mivate in the blood can be used to diagnose vitamin B^ 

 deficiency under the combined " metabolic load " of ingestion of 

 glucose and exercise, although quite useless in the fasting state. 



Methylglyoxal 



Another substance that was at one time implicated as the toxic 

 product responsible for the symptoms of vitamin B^ deficiency is 

 methylglyoxal (pyruvic aldehyde), CH3 . CO . CHO. The presence of 

 this substance in the urine of vitamin Bi-deficient infants was reported 

 by A. Geiger and A. Rosenberg,^* and in the milk of women with beri- 

 beri by several Japanese workers. ^^ 



Infantile beriberi is a condition in breast-fed infants first described 

 towards the end of last century by Japanese clinicians and, because 

 the infant recovered when removed from the breast, the condition was 

 attributed to a toxin in the milk. The presence of a toxin was, in 



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