34 THE POPULAR SCIENCE MONTHLY 



has been largely destroyed by fermentative bacteria introduces condi- 

 tions 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 putre- 

 faction, for it is true that in some intestinal infections in which we are 

 justified in assuming that the colon bacillus or B. cerogenes capsalatus 

 or both these organisms have extended in an upward direction toward 

 the stomach, the abundant presence of fermentable carbohydrate pabu- 

 lum 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. cerogenes capsulatus are capable of making an increased 

 attack upon the protein material. This increases intestinal putrefac- 

 tion. On the other hand, the irritation arising from organic acids 

 formed in the small intestine and stomach often leads to a fermenta- 

 tive diarrhoea. 



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 dis- 

 tinguish 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 putre- 

 factive decompositions are apt to take place. We should therefore 

 expect greater anti-putrefactive efficacy from the use of soured milk con- 

 taining 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 



