VITAMIN B (B,) 81 



but the more alkali-stable vitamin G. This was confirmed by Hartwell 

 (1928), and indirectly by Kon (1929). 



Sherman and Gloy (1927) found no differences in the outcome of 

 vitamin B experiments for the age period covered in the usual tests 

 for vitamin B in foods when the protein of the standard basal ration 

 was varied from 12 to 54 per cent. 



Stucky and Rose (1929) reported that the blood sugar of vitamin 

 B deficient dogs remained normal, while the blood chloride fell some- 

 times to a marked extent ; anhydremia developed accompanied by an 

 increase in the hemoglobin content of the blood. Sure and Smith 

 (1929a) reported a rise in the reducing non-sugars of the blood of 

 the rat. 



Peters (1929) suggests that vitamin B may be concerned with the 

 removal of lactic acid. The symptom of opisthotonus in pigeons appears 

 to be due to excess of lactic acid in the brain and is cured most quickly 

 by injecting concentrated preparations of torulin locally. Absence of 

 another vitamin B fraction apparently leads to heart block and a re- 

 markably slow pulse, and the puzzling question of edema (wet and 

 dry beriberi) may be due to another fraction which in conjunction 

 with torulin regulates distribution of water in the body. 



Kinnersley and Peters (1929) found that increased lactic acid in 

 the brain is a concomitant of the symptoms in avitaminosis Bi and dis- 

 appears within a short time after the administration of torulin. 



"A forcibly fed bird suffering from lack of vitamin Bj has a per- 

 manent hyperglycaemia, so that the tissue cells are being continually 

 bathed with an abnormal concentration of blood sugar. The animal 

 which feeds normally doubtless does not eat so much in the later stages 

 and is often found to have practically normal blood-sugar. It is not 

 improbable that the lack of appetite is correlated with an adjustment 

 of the blood-sugar." 



Continuing this investigation, Kinnersley and Peters (1930, 1930a) 

 have reported very recently that the abnormal amounts of lactic acid 

 found in the brains of vitamin Bi-deficient pigeons are unevenly dis- 

 tributed, the increase being especially marked in the lower parts of the 

 brain. These findings are thought to furnish convincing proof of the 

 theory so often advanced that vitamin Bi is associated with inter- 

 mediary metabolism of carbohydrate. Kinnersley and Peters go so far 

 as to suggest that vitamin Bi is concerned with the oxidative removal 

 of lactic acid, though admitting that a substantive proof of this is at 

 present lacking. 



A new approach to the question of the relation of vitamin Bi to 



