When Hopkins pointed out in 1912 that the addition of small amounts of milk to a diet of purified food substances would lead to growth, whereas without such addition the animals failed, and on the basis of this observation conceived the idea that certain "accessory" food substances are necessary in the diet, he had no comprehension, apparently, of the number or specificity of these substances. This view did not become appreciated until Funk attributed to specific deficiency a number of diseases, especially beri-beri, scurvy, pellagra, rickets and sprue, and expressed the belief that a special "vitamin" for growth was essential. The view that there were two unidentified substances essential in the diet did not become established on experimental evidence until McCollum and Davis (5) in 1915 published their paper on the essential factors in the diet during growth.

278. Osborne And Mendel Describe Ophthalmia In Their Experimental Rats

In 1913 Osborne and Mendel (15) called attention to the prevalence of an inflammation of the eyes of their rats restricted to a diet of purified proteins, "protein-free milk," lard and starch. They referred to this as a "type of nutritive deficiency exemplified in the form of an infectious eye disease prevalent in animals inappropriately fed," and stated that the condition was speedily alleviated by the introduction of butter-fat into the diet.

279. Mccollum And Simnionds Prove Xerophthalmia To Be Due Specifically To Lack Of Fat-Soluble A

McCollum and Simmonds had repeatedly observed the development of this peculiar form of ophthalmia in animals subjected to their experimental diets. They, however, did not feel convinced until they had collected numerous observations, all of which pointed to the belief that the eye disease in question is non-infectious, that it could more satisfactorily be explained on the basis of specific starvation for fat-soluble A, than on any other. Many groups of rats in various degrees of enfeeblement or arrested development resulting from restriction to faulty diets of various types, failed to develop the disease, when others in adjacent cages were suffering from it. They found it to occur only in those animals whose diets were faulty in the content of fat-soluble A. McCollum and Simmonds (16) correlated these observations on rats with those reported by Bloch and by Mori, and came to the conclusion that the xerophthalmia or keratomalacia produced experimentally in animals is the analogue of the condition which these authors have reported in man. It was on evidence of that nature that they formulated the view that this type of xerophthalmia is a deficiency disease in the same sense as beriberi, and that it is due specifically to lack of fat-soluble A.