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JAMA. 1927;88(21):1638. doi:10.1001/jama.1927.02680470024012.
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For some time, considerable attention has been devoted in this country to the therapeutic possibilities of prolonged fasting in the treatment of epilepsy. Favorable results so far as the suppression of the characteristic epileptic attacks is concerned were reported in 1921 by Geyelin.1 Obviously the withholding of food can at best become only a transient method of treatment; consequently efforts have been directed to ascertain what changes in the organism incident to inanition might account for its effect in ameliorating the symptoms of epilepsy. One of the metabolic peculiarities accompanying fasting is the accumulation and excretion of aceto-acetic acid and its products, beta-hydroxybutyric acid and acetone. A similar ketosis occurs in diabetes when the oxidation of sugar is sufficiently depressed, and may be provoked in nondiabetic subjects by diets in which the proportion of carbohydrate and protein are sufficiently restricted. Wilder 2 suggested that such diets might offer a


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