Nutrition in relation to bone growth and the nervous system / by Sir Edward Mellanby.
- Edward Mellanby
- Date:
- [1944?]
Licence: In copyright
Credit: Nutrition in relation to bone growth and the nervous system / by Sir Edward Mellanby. Source: Wellcome Collection.
2/30
![0 Nutrition in relation to bone growth and the nervous system By Sir Edward Mellanby, K.C.B., F.R.S. (Delivered 15 July 1943.—Received 22 September 1943) [Plates 1-9] The problem to be discussed was presented as long ago as 1918 when, at the request of the Medical Research Committee (now Council), I was engaged on an investiga¬ tion to discover the cause of rickets. It was noticed that some of the experimental animals became very incoordinated in their movements and that this disability might develop with or without rickets. The independence of the two syndromes thus experimentally produced and the fact that incoordination of movement does not form a part of the usual clinical picture in rachitic children suggested that the cause of the incoordination in the animals was independent of but related to that of rickets. The main result of the earlier work was to establish the fact that rickets was due primarily to a deficiency in the diet of an antirachitic vitamin which was fat-soluble and was either vitamin A or a substance closely allied to it in properties and distribution (1919, 1921). At that time vitamin A, discovered 5 years earlier by McCollum & Davis (1913), was the only recognized fat-soluble vitamin. But little was known of its chemistry in 1918 and it was identified by two biological tests: (1) its power to promote growth in young rats when added to diets previously deficient in it, (2) the fact that when it was absent from the diet animals developed xerophthalmia, which could then be cured if substances containing it were administered. It was found later that the vitamin A of those days was really a mixture of two fat-soluble vitamins—one of which retained the designation vitamin A and the second, the calcifying or anti- i rachitic vitamin, was called vitamin D. Looking back, it is of interest to note that, of the two biological properties of the j original vitamin A complex—growth promotion and antixerophthalmic action in rats—the former was due more to its vitamin D than to the vitamin A moiety. It i is true that the absence of vitamin A, as we now know it, causes young rats to stop • growing, but this is largely because, unlike other young experimental animals, rats4 develop infective foci in many places—middle ear, kidney, lung, mouth, indeed 9 almost anywhere—and they stop growing primarily for this reason. Vitamin A prevents or often cures these infections and thereby allows growth to proceed. | But vitamin D, the other part of the original vitamin A complex, is a real growth h promoter in the sense that, in its absence, bones cease to grow normally in length Ij because calcium metabolism, including that at the bony epiphyses, stops func- j tioning. Thus, there was no more reason why the name vitamin A should not have (J](https://iiif.wellcomecollection.org/image/b30632043_0002.jp2/full/800%2C/0/default.jpg)
