Some Effects Produced by Long-Continued Subminimal Intakes of Vitamin B1 *

The earlier literature on the pathology produced experimentally with diets lacking vitamin B (for the most part the undifferentiated vitamin B complex) has been reviewed by Zimmerman and Burack.'5 Their review may be summed up briefly as follows: Myelin degeneration in peripheral nerves, and sometimes in the spinal cord, has been described by many workers as occurring in several species of laboratory animals. In most cases the diets used were deficient with respect to the entire vitamin B complex. Stern and Findlay12 studied the nervous systems of rats maintained on a diet lacking vitamin B1, but containing the heat-stable portion of the B complex. In these animals early degeneration of the myelin was observed in peripheral nerves, but no myelin destruction was noted in the cord. Zimmerman and Burack, in the paper mentioned above, reported extensive myelin destruction in the peripheral nerves, but none in the spinal cords, of their dogs fed a diet lacking vitamin B1. These animals subsisted for from 37 to 109 days on the experimental ration. Recently, Prickett' studied the nervous systems of rats which were given a diet devoid of vitamin B1 and drew the rather surprising conclusion that the site of the lesion responsible for the symptoms associated with a lack of vitamin B in the rat is the central rather than the peripheral nervous system. There were cellular changes in the brain; the spinal cords and peripheral nerves of the experimental animals appeared to be no different from those of the controls. More recently, Engel and Phillips8 reported the results of their studies of the nervous systems of rats and chicks maintained on diets believed to contain optimal amounts of all dietary essentials except vitamin B1. No pathology was observed in these animals. From this the authors drew the conclusion that "uncomplicated beriberi is