Abstract
Since the Sendai City Hospital was founded, we always examined Arakawa's reaction of milk of all the lactating mothers who visited the Pediatric Dispensary with their diseased infants, and noticed accidentally that human milk of mothers would chnge from Arakawa-positive into Arakawa-negative-strongly negative*-in a large majority of the cases as a result of the onset of their new pregnancy, and the milk will cause dyspeptic symptoms in their infants. Furthermore, we were unable to make the negative Arakawa reaction into positive in spite of an administration of vitamin B in a relatively large amount, and thought that weaning is the only treatment to recover their infants from the dyspeptic symptoms. From this clinical experience we presumed an occurrence of a toxic substance in milk of lactating mothers as the result of the onset of new pregnancy, and injected some of the milk to mice. As was expected, such mice died very soon-between the 2nd day and the 7th day at the latest after injection of the milk, while the mice injected with non-pregnant mothers' milk survived for a long time. Then we investigated the milk under our hypothesis that the toxin (or at least one of the toxins) might be the methyl glyoxal like substance which was published by Takamatsu of our Laboratory, in 1934, to be contained in a larger amount in Arakawa-negative milk, and were able to identify the substance in a relatively large amount in pregnant mothers' milk. In the time of lactation, lactating mothers require a larger amount of vitamin B than in the time of non-lactation, and pregnant women require a larger amount of it than in the time of non-pregnancy. Then it may not be difficult to think how severe a state of avitaminosis B will affect lactating mothers in new pregnancy. A severe deficiency of oxidation will result in such mothers making them secrete milk rich in the methyl glyoxal like substance in a large amount.
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