Epidemiology and Etiology

Research in the 1930s suggested that the distribution of convulsive and gangrenous ergotism was a function of the presence or absence of vitamin A in the diet. An analysis of the 1770 epidemic of gangrenous ergotism in Sologne and of convulsive ergotism in Hanover indicated that Sologne, on the left bank of the Rhine, was a dairy district that provided a diet rich in vitamin A, whereas Hanover, on the right bank, was unable to sustain a dairy economy. The striking difference in the effects of ergot on the two communities in close proximity caused researchers to study their differing experiences in a laboratory by feeding ergot to dogs along with different levels of vitamin A. The results confirmed the efficacy of vitamin A in mitigating the effects of ergotism.

Similarly, while some researchers believed that England's relative freedom from ergotism was due to the abundant ingestion of meat and potatoes, others demonstrated that the English diet, which was rich in milk and butter products, had enabled its inhabitants to remain relatively free from the convulsive effects of ergotized grain. In areas rich in dairy products, the phytase and the bowel bacteria broke down the poisonous phytates of the grain into the comparatively innocuous inorganic phosphates. Thus, the convulsive ergotism which had been common to nondairy areas was virtually absent in England and certain sections of France.

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