Beriberi: Etiological and Clinical Considerations

Beriberi was recognised by the Chinese 3000 B.c. Tlhe etiology, however, remained obscure till 1870. In that year Eijkman, working in Java, notedl an epidemic of paralysis among fowls fed on polished rice. He found that this polyneuritis gallinarum could be cured if an extract of rice polishings were added to the diet. That polyneuritis gallinarum corresponded to human beriberi was shown by Frazer and Stanton in 1910. These' investigators produced beriberi in convicts by feeding them a diet consisting solely of overmilled rice. 'I'hey also succeeded in curing the disease by adding rice polishings to the diet. Frazer and Stanton concluded that the pericarp aleurone layers and the embryo of grain which are removed in the production of polished rice contained an anti-beriberi substance. The chemical composition of this substance was determined by Williams in 1935, and it was eventually synthesised by Williams and Spies in 1938. It was found to be a compound of pyrimidine and thiazole, to which Williams gave the name thiamin. Beriberi was therefore defined as a disease resulting from a metabolic disturbance caused by deficiency of the ante-neuritic vitamin B1, or thiamin. The minimal daily requirements of thiamin are in the region of 1 mg. or 333 I.U. Recently, however, it has been recognised that factors in addition to thiamin deficiency are concerned in the production of beriberi. It has been observed that beriberi is an uncommon complication of simple starvation. The disease was rarely seen among the starving populations of Europe during the war. Beriberi complicating anorexia nervosa has only once been recorded. The question of additional factors has been investigated by Cowgill in 1934 and by Williams and Spies in 1938. Cowgill as a result of his investigations came to the conclusion that the incidence of the disease was related to the ratio between the thiamin and the caloric value of the diet, rather than to the daily intake of thiamin. Williams and Spies attacked the problem by analysing typical Occidental and Oriental diets. 'T'hey found that the differences in thiamin value was insufficient to explain the rarity of the occurrence of beriberi in association with the former diet and its frequency in association with the latter. They noted that the chief difference in the diets was the greater fat-content of the American diet. From this they concluded that fat had a B1 sparing action. Analytically it was shown that the best index of the liability of a diet to produce beriberi was the relationship between the thiamin and the non-fat caloric value. This they express as the