On the etiology of rickets / by Edward Mellanby.

  • Mellanby, Edward, Sir, 1884-1955.
Date:
[1922?]
Catalogue details

Licence: In copyright

Credit: On the etiology of rickets / by Edward Mellanby. Source: Wellcome Collection.

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    to eat diets deficient in fat-soluble A and rich in pure carbo¬ hydrate such as starch, cane-sugar, or glucose. Nevertheless, the results obtained suggested that the carbohydrate in itself played some part in the production of rachitic symptoms. In view of my more recent experiments, however, it is difficult to believe that the rickets-producing effect of cereals is wholly due to their carbohydrate content, and I am at present engaged in finding the new factors involved. The most prominent fact brought out in the cereal experiments is that oatmeal has a greater rickets-producing effect under the conditions of these experiments than equal weights of flour, especially white flour, or rice. Since the amount of carbohydrate in oatmeal, wheaten flour, and rice is respectively of the order 65 per cent., 7.35 per cent., and 77 per cent.—that is to say, there is less carbohydrate in oatmeal than in the other cereals—it is manifest that the greater rickets-producing effect of oatmeal as compared with the other cereals cannot be due to its carbohydrate moiety. In some way the effect of cereals is no doubt related to their property of producing growth, both in the sense of producing longer and bigger bones and an actual increase in weight. This action of cereal is best illustrated by contrasting its effect on the metabolism with that of fat. Adding more cereal to a diet already adequate causes young animals to increase more rapidly in weight, to develop a deposit of fat which is undoubtedly formed from carbohydrate, and to become more lethargic. Under the same conditions the addition of fat makes no difference to the rate of increase in body weight, for it neither increases the laying down of tissue nor is it deposited subcutaneously as depot fat. It is burnt up and increases the metabolism. These opposite effects of cereal and fat on the metabolism of young animals are most striking and have probably not received the attention they deserve. Cereals, then, increase the laying down of fat and tissues generally, including the bones, and thereby make a greater demand on the calcification processes, so that any tendency to lag behind in this respect is increased by allowing the child or animal to eat a larger quantity of cereal. Increasing the bread, therefore, in a diet slightly^ rickets-producing only emphasizes the disease and causes the development of larger quantities of cartilage and osteoid tissue in the bones. This explanation, however, is not a complete one, for it does not satisfactorily explain the differences between oatmeal, white flour, and rice. In some series of experiments there was no obvious difference between the rates of growth or in the rates of putting on weight when oatmeal, white flour, and rice were the only variables, yet the rickets produced by oatmeal was much greater than that produced by equal quantities of the other cereals. Undoubtedly some other factor in oatmeal is at work which either prevents endochondral calcification or increases the formation of tissue at this point, thereby producing a relative lag in calcification at the ends of the bones. It does not appear to be the carbo¬ hydrate moiety, and as I pointed out in a previous Section the larger amounts of calcium and phosphorus in oatmeal discredit