Page:Popular Science Monthly Volume 74.djvu/38

34 has been largely destroyed by fermentative bacteria introduces conditions unfavorable for intestinal fermentation. I consider that the diminution in fermentable material thus arising from the decrease in the parbohydrates of the milk is an important factor not merely in reducing intestinal fermentation, but also in reducing intestinal putrefaction, for it is true that in some intestinal infections in which we are justified in assuming that the colon bacillus or B. ærogenes capsalatus or both these organisms have extended in an upward direction toward the stomach, the abundant presence of fermentable carbohydrate pabulum leads to a great increase in these microorganisms. After the absorption of the acid produced in the course of this fermentation there may be established a neutral or even an alkaline reaction in the lower part of the small intestine and in the colon. In the absence of acid and indeed in the presence of a moderate amount of acid, the colon bacilli and B. ærogenes capsulatus are capable of making an increased attack upon the protein material. This increases intestinal putrefaction. On the other hand, the irritation arising from organic acids formed in the small intestine and stomach often leads to a fermentative diarrhœa.

Turning now to the effects attributable to the presence of lactic acid in the soured milk, it is at once apparent that we have to distinguish clearly between the action of such preformed lactic acid as may be introduced with the milk and such acid as may be formed in the course of further lactic acid fermentation after the soured milk has been ingested. The essential difference lies in the fact that such lactic acid as is preformed in fermented milk is liable to be absorbed from the upper part of the small intestine, whereas if lactic acid fermentation goes on within the digestive tract, the acid may be formed at any level of the intestine. In the former case the action of the acid is to be regarded as largely limited to the portion of the intestine in which putrefactive decompositions seldom occur; in the latter case there may be production of acid within the territory in which putrefactive decompositions are apt to take place. We should therefore expect greater anti-putrefactive efficacy from the use of soured milk containing living lactic acid producers than from the same milk after sterilization. Whether such a difference as this is actually discernible in practise I am unable to say, as I am not aware of the existence of satisfactory experiments made to test this point.

As to the efficacy of lactic acid as an anti-putrefactive agent it is necessary to speak with caution. It has been the practise of many physicians to employ lactic acid in the treatment of disorders of digestion, especially those of infancy. But I am unaware that we have adequate data for the establishment of the therapeutic anti-putrefactive value of lactic acid. Where the stomach secretes no free hydrochloric