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Since the discovery that ketone acids are produced in the body and accumulate in the blood to excess in severe diabetes, general opinion has held that the accumulation of these chemical compounds is responsible for the syndrome known as diabetic coma. The general application of the term acidosis to the condition is in itself sufficient evidence of the importance which is attached to this disorder of metabolism. Difference of opinion seems to have been restricted chiefly to the question of the relative parts played by the ketone bodies as such and by the reduction of blood alkali and diminution of pH which they caused. With the appearance and application of accurate and practical methods for the determination of blood bicarbonate and pH it has become increasingly apparent that alkali deficits of the magnitude found in diabetic acidosis, when they are produced experimentally or occur in the course of other diseases, are not necessarliy attended by a syndrome resembling that of diabetic acidosis. This has, perhaps, given more weight to the arguments of those who would hold that acetone and diacetic acid, by their anesthetic and poisonous effects, are responsible for the symptoms and fatalities. On the other hand there is but the scantiest positive quantitative evidence to support such a theory. The anesthetic actions of acetone and diacetic acid are notoriously slight, but hard to ascertain with certainty because of the ease with which normal animals excrete or oxidize these compounds. Ketosis unassociated with the other metabolic disorders of diabetes never attains so great an intensity. The most convenient experimental animals when rendered diabetic by pancreatectomy or phlorizin do not develop ketosis comparable in severity to that seen in humans with diabetic coma. Chemical analyses have demonstrated no exact correlation between the concentration of ketones in the blood and the profundity of coma in diabetic patients (20).

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