Abstract
Vitamin B1deficiency in man involves predominantly the nervous and circulatory systems. Clinical descriptions of the disturbances in these systems under the name beriberi date back to ancient Chinese medical writings. Although known to be widespread in the Orient and common in Newfoundland, beriberi has been considered rare in the United States of America1except for its occasional occurrence in epidemic form in penal institutions and insane asylums. During the past decade, however, it has been shown that beriberi is and has been endemic in the United States in characteristic form.2Alcoholic polyneuritis, the toxic polyneuritis of pregnancy, diabetic, biliary and gastrogenous polyneuritides, postinfectious polyneuritis, the Korsakoff syndrome and other similarly misleading names have concealed the true diagnosis of vitamin B1deficiency in the Western World. Clinically and pathologically identical to the Oriental disease, these polyneuritides differ only in the particular mechanism by which the deficiency