Beer and Alcoholic Beverages.—For generations beer has been highly regarded as an antiscorbutic. Captain Cook prized it greatly and always supplied his men with a freshly-made infusion of malt called “sweetwort.” Lind writes: “Beer and fermented liquors of any sort will be found the best antiscorbutic remedies” ([p. 76]). He refers at different times to the value of spruce beer, ale, wine and other vinous liquors. In his excellent book on “Military Hygiene,” Munson writes: “Good beer and wine have decided value, also vinegar.” On the other hand, recent scientific experiment has shown that beer has practically no antiscorbutic value. There is but one study on this subject, that of Harden and Zilva, which is quite convincing. They found that guinea-pigs and monkeys developed scurvy in spite of the fact that they received, respectively, 50 c.c. and 180 c.c. of beer daily. They conclude, as a result of their experiments, that “bottled ale and stout and fined beer as brought on to the market, are lacking both in antineuritic and antiscorbutic accessory factors, and that kilned material is also wanting in these two principles.” The apparent contradiction between practical experience and laboratory investigation in regard to beer is due to a difference in the process of brewing. Cook and Lind and the older authors refer to freshly-made beer, whereas the modern beer which was tested in the laboratory was made from “high-dried” material. The antiscorbutic potency of beer as formerly used was due to its preparation from freshly-germinated grain and its consumption shortly after brewing. Dyke tells us of an interesting incident illustrating the importance of this distinction. In the recent war an outbreak of scurvy occurred among the Kaffir labor battalion in France. At home these natives consume a large amount, as much as three gallons a day, of Kaffir beer, which is made from freshly-germinated corn, and is consumed shortly after it is made. The French prepared a similar fermented beverage for their South African laborers, the sole difference in preparation being that the process of germination had been omitted for reasons of convenience. Scurvy resulted, a disorder which is practically unknown among the natives at home.
Miscellaneous Foodstuffs.—During the past few years a great many different kinds of foods have been tested in the laboratory for their antiscorbutic value. It will be well for completeness’ sake to say a word about them, although they have been found to possess little or no antiscorbutic properties. The studies of Holst and Froelich showed definitely that all the cereals—oat, barley, rye, maize, and preparations made from the bran or from the endosperm—are devoid of antiscorbutic vitamine. Cohen and Mendel added 3 per cent. of calcium lactate or sodium chloride, or 5 per cent. of butter, without enhancing the value of oats in this respect.
Fig. 14.—Failure of yeast as a prophylactic; latent scurvy promptly yielding to orange juice.
As is well known, yeast possesses the water-soluble vitamine in marked concentration. It is natural, therefore, that its antiscorbutic power was put to the test, especially as it has been accorded therapeutic value. Hess and Unger showed that autolyzed yeast was of no value in the cure of infantile scurvy (Fig. 14); Chick and Hume (1917) and Cohen and Mendel (1918) came to the same conclusion in regard to guinea-pig scurvy, making use of autolyzed yeast, yeast extract and dried brewers’ yeast.
In view of the fact that cod liver oil is practically a specific for human rickets, Hess and Unger tried the effect of this oil both in infantile scurvy and in that of guinea-pigs. It proved to have no protective or curative value. The animal experiments were confirmed by Cohen and Mendel. The use of olive oil also proved futile.
Pitz in 1918 reported that in animal experiments he had found that lactose was able to protect against scurvy, and attributed this result to its power to alter the intestinal flora. We shall not enter into a detailed discussion of this question, as the study was carried out on a ration embodying unlimited and uncontrolled amounts of milk, and it has since been shown that the apparent cure was due to an increased consumption of milk by the animals in the progress of the experiment. Cohen and Mendel, Harden and Zilva, Hart, Steenbock and Smith (1919) all failed to protect or to cure their animals with lactose when they were placed on a ration which was definitely measured and limited. Hess and Unger failed to cure infantile scurvy by means of lactose.
It has been suggested that scurvy is due to a lack of secretion of the endocrine glands, a question which will be referred to again in considering the relation of scurvy to other “deficiency diseases.” With this idea Ingier added thyroid, hypophysis, thymus and parathyroid to the food of guinea-pigs, or gave it parenterally. She was unable to observe any beneficial results. Jackson and Moore met with the same result on feeding desiccated thyroid gland. We may add that we gave dried thyroid and also parathyroid glands in the treatment of infantile scurvy without effect.