Chronic poisoning by tainted meat and fish was held responsible by Jackson and Harley25 a theory which found some acceptance when first promulgated, but the experimental evidence on which it was based has not been supported by later work and is itself susceptible of other interpretation.11

25 Jackson and Harley, Lano. 1900, i. 1184, Proc. Roy. Soc. 1900, 66, 250.

26 Hoist and Frolich, Z. f. Hyg. infekt 72,1, 1912.

The theory of bacterial origin 27 is refuted by the work of and Hoffman 28 who found that the blood of scorbutic guinea pigs is invariably sterile, regardless of the diet on which the disease is produced. No marked difference was found in the intestinal flora when smears and cultures were made from different parts of the intestinal tract of guinea pigs on a diet of oats alone, on oats plus 3 cc. of lemon juice daily, after scurvy developed, on soy cake diet, and on the same plus cabbage after the appearance of scurvy. The observations recorded as to the presence of bacterial infection in certain cases of scurvy can easily be explained by the susceptibility of animals in a poor condition of health to such infection.29 The faulty intestinal condition referred to by Steenbock 30 is also doubtless a result rather than the cause of the disease, and the same may be said of inanition.*1 The theory of McCollum and Pitz 32 relating scurvy with chronic constipation has been disproved by numerous investigators.

The argument is summed up by Cohen and Mendel.33

Fig. 10.

Fig. 11. - The upper chart shows the failure of skimmilk powder from summer-produced milk to protect against scurvy. The lower chart indicates a similar failure when using winter-produced milk.

Courtesy of Messrs. E. B. Hart, H. Steenbock, N. R. Ellis and Journal of Biological Chemistry (46, 311, 1921).

27 Coplans, TV. Epidemiol. 8oc. 23, i, 1004; Jackson and Moody, J. Infect. Dis. 19, 511, 1916.

28 Givens and Hoffman, Proc, Soc. Biol. Chem. J. Biol. Chem. 41, xxziii, 1920.

Fig. 12.

Fro. 13. - The upper chart shows the failure of a whole milk powder made by a spray process to protect against scurvy. An improvement is shown in the lower chart which records the results of feeding a larger proportion of the same milk powder. This powder still retained some of the antiscorbutic vitamin but not enough, even at this high level of feeding, to protect all individuals.

Courtesy of Messrs. E. B. Hart, H. Steenbock, N. R. Ellis and Journal of Biological Chemistry (46, 314, 1021).

29 See McCollum and Pitt, J. Biol. Chem. 31, 233, 1917; Abels, Wien. klin. Woch. 33, 899, 1930.

It is highly improbable, they observe, that constipation is the predisposing cause of scurvy, as can be seen from the results in feeding milk. A small amount ingested daily permitted the onset of symptoms of scurvy, while large quantities, which were not less constipating, caused the scorbutic symptoms to disappear. Moreover, aids to the ready elimination of feces, like differing amounts and kinds of roughage caused no corresponding change in the course of the disease. Contrary to the findings of McCollum and Pitz, other investigators, namely Hess and Unger,34 were unable to protect or cure animals with daily additions of mineral oil to a scurvy-producing diet. Neither were they able to induce active scurvy in a latent case by the production of marked constipation with morphine. Recently Hess and Unger reported the cure of scurvy by means of intra-venous injections of orange juice. This successful antiscorbutic effect apparently was not due to specific relief from constipation or its attendant intestinal complications.

Fig. 14. - This winter-produced skimmed milk, converted to a powder by a roll drying process, had lost in a considerable measure its antiscorbutic properties. In most cases the onset of scurvy was greatly delayed. The powder contained 0.35 per cent of fat.

Courtesy of Messrs. E. B. Hart, H. Steenbock, N. R. Ellis and Journal of Biological Chemistry (46, 317, 1921).

30 Sci. Mo. 7, 179, 1918. 31 Fiirit, Z. Hyg. 72, 121, 1912; Lewis and Karr, J. Biol. Chem. 28. 17, 1916-17; Cohen and Mendel, J. Biol. Chem. 35, 430, 1918.

32 McCollum and Pitz, J. Biol. Chem. 31, 229, 1917; Pitz, lb., 33, 471, 1918.

33 Cohen and Mendel, J. Biol. Chem. 35, 425, 1918.

34 Hess and Unger, Proc. Soc. Exp. Biol. Med. 15, 82, 1918.