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September 11, 1926


JAMA. 1926;87(11):852-853. doi:10.1001/jama.1926.02680110052020

The pathogenesis of the various conditions now commonly classed as avitaminoses is by no means clear as yet. For the most part, information is restricted to the description of symptoms that are characteristic of the disordered nutritive condition following a prolonged lack of any of the familiar vitamins. Xerophthalmia and the lesions of scurvy are illustrative of this statement. The studies of Wolbach and his co-workers at the Harvard Medical School1 have greatly advanced our knowledge of the tissue upsets that may arise when there is a deficiency of vitamin A and vitamin C, respectively, in the diet. The function of vitamin B remains more obscure, though there has not been a lack of hypothesis to account for the behavior of this more ubiquitous food factor. Thus, Cramer2 and his associates in London believe that vitamin B functions in a peculiarly specific manner to promote the activity of

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