Hoist and Frohlich, studying experimental scurvy in guinea pigs, find that some foods such as cabbage show a marked loss of antiscorbutic power as the result of simple heating or slow drying, while others (grains) develop antiscorbutic value in sprouting. In neither of these cases is the relation of acid-forming to base-forming elements altered and these authors therefore consider that they have entirely disproven the acidosis theory of Wright and that antiscorbutic properties of foods have no connection with their ash constituents but are due to the presence of small quantities of a specific organic substance or substances, of undetermined chemical nature, and (in most cases at least) very readily destroyed by heat. . Guinea pigs fed exclusively on bread or grain developed symptoms which Hoist and Frohlich considered to be "identical in all essentials with those of human scurvy." Since one of these symptoms is loss in weight and since animals may fail to eat enough of a one-sided diet to meet the energy requirement, special experiments were made to establish the distinction between the effects of scurvy and those of starvation or undernutrition. It was found that guinea pigs kept on an exclusive diet of fresh raw cabbage, dandelion greens, or even carrots may die of starvation; but they do not become scorbutic. Those kept on grain alone regularly became scorbutic. Those fed grain plus a moderate allowance of cabbage, dandelion, carrot, potato, or other fresh vegetable remained normal. The antiscorbutic properties of other foods were then tested by adding them to a bread or grain diet and observing whether the guinea pigs developed symptoms of scurvy or not.

Raw cabbage, dandelion greens, lettuce, endive, sorrel, potatoes, carrots, bananas, apples, and cloudberries all showed antiscorbutic properties - apparently in varying degrees. Apples and bananas were thought to be somewhat less effective than the potatoes, lettuce, greens, and berries. Cabbage and dandelion juices seem to lose their antiscorbutic properties more rapidly than the vegetables themselves. Fruit juices and sorrel juice on the other hand retain their efficacy as antiscorbutics remarkably well. Raspberry juice seemed but little injured by heating for 1 hour at 100° or even no°. Acidulated cabbage or dandelion juice retained its antiscorbutic property much better than the natural juice of these vegetables. If, as these experiments indicate, the antiscorbutic property is due to the presence of some unstable substance, the latter would appear to be much more stable in an acid than in a neutral or alkaline medium.

The effect of cooking was studied in the case of several different foods with the following results: Cabbage cooked at 100° for ½ to 1 hour was still a good antiscorbutic. Carrots cooked at 100° for 1 hour showed a great diminution in antiscorbutic power. Cooking for ½ hour at the same temperature showed a less serious injury to the antiscorbutic property. Cauliflower was much injured by cooking for 1 hour at 100°; when cooked only ½ hour it was a much better antiscorbutic. Dandelion leaves lost much of their antiscorbutic property when cooked for 1 hour at 100°. Potatoes cooked at 100° "in the usual way" (½ hour) had excellent antiscorbutic properties.

Turnips and kohlrabi cooked at 100° had antiscorbutic power similar to cooked potatoes. Cloudberries retained their efficiency after cooking to a very marked degree. When cooked at 100° as usual they were still excellent antiscorbutics and were shown to retain this property when kept for at least 3 months after cooking. From this it would appear that canned fruit which has been sterilized at temperature of boiling water and then kept in a cool place ought to be a good antiscorbutic even after many months, and in general that ordinary cooking of vegetables (or low temperature pasteurization of milk) destroys only a part of the antiscorbutic substance, and so the food still possesses antiscorbutic properties though not in as high degree as when raw.

The results of several recent investigations are, however, not entirely consistent with the findings of Hoist and Frohlich.

Funk, who had been a prominent advocate of the theory that scurvy is due to deficiency of a specific unidentified substance, has recently concluded that the disease produced in guinea pigs by a diet of oats (Hoist and Frohlich's experimental scurvy) may be due to acidosis. It has also been found independently by Jackson and by McCollum that guinea pigs are so susceptible to nutritive disorders with scurvy symptoms when placed upon experimental diets as to make the interpretation of such experiments exceedingly difficult. Jackson finds in the scorbutic tissues of the experimental animals bacteria of the Dip-lococcus type which appear to be specific to the scurvy lesions and pathogenic when inoculated into other guinea pigs. The results of such inoculation depend largely upon the diet; guinea pigs fed on carrots, cabbage, and hay appear relatively immune, while those fed on grain or bread diet are much more susceptible. According to McCollum the physical character of the diet and of the resultant intestinal residues is responsible for guinea pig scurvy. His examinations of guinea pigs dying with scurvy symptoms reveal characteristically an abnormal accumulation of fecal material in the caecum. McCollum holds that the guinea pig will have scurvy on any diet which does not contain a succulent vegetable and that this is due to the anatomical character of the digestive tract, the caecum being relatively large and delicate in this species and especially liable to the accumulation of fecal residues when the food is not of suitable physical character. His guinea pigs showing typical scurvy symptoms recovered after liberal doses of petroleum oil. He therefore holds that guinea pig scurvy, although "referable to faulty diet," is not a deficiency disease, the fault lying rather in the unsatisfactory physical character of the diet which leads to an injurious accumulation of material in the caecum. The immediate cause of the pathological symptoms of scurvy is not known. It may perhaps be due to absorption of toxic substances resulting from bacterial action in the caecum or to invasion of bacteria through an injured intestinal wall. In view of these results so recently reported by McCollum it becomes extremely difficult to interpret the work of Hoist and Frohlich, who apparently failed to realize the part played by such digestive disorders.

It also remains an open question whether guinea pig scurvy and human scurvy are referable to the same causes.

Recently, as a result of war conditions, there has been renewed interest in human scurvy and a tendency toward the view that this may be a disease in which two factors, a nutritional condition and an infection, may both be involved.

It also seems probable that the term "scurvy" may have been applied to more than one disease in man.