On deficiency diseases, with special reference to rickets / by Edward Mellanby.

  • Mellanby, Edward, Sir, 1884-1955.
Date:
1924
Catalogue details

Licence: In copyright

Credit: On deficiency diseases, with special reference to rickets / by Edward Mellanby. Source: Wellcome Collection.

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    of children in this country develop carious teeth. It is true that, according to present standards, the temporary teeth of children on naked-eye examination seem well formed, but examined microscopically these teeth show quite a different picture. In fact, of 302 teeth examined microscopically by M. Mellanby after being ground down, as many as 85 per cent, were defectively formed, whereas the dentists supply¬ ing them reported that only 2 to 3 per cent, were hypo¬ plastic. Of 226 temporary human molar teeth examined only one was perfectly formed and quite free from caries. It seems clear therefore that, generally speaking, more per¬ fectly formed teeth are more free from caries. For excep¬ tions to this rule the original papers ought to be consulted. If this be true the first method to be employed to reduce the scourge of tooth defect in this country is to improve the formation of children’s teeth by better feeding of the mother during pregnancy and lactation and of the children so long as the teeth are being calcified—that is, for the first eighteen years. Better feeding means the greater consumption of such foodstuffs as promote good teeth formation and the diminished consumption of foodstuff antagonizing this development. These experimental results have completely changed the point of view as to the causation of dental defect, for previously all attention has been directed to the action of bacteria and their end-products externally on the teeth, and the toothbrush has been the great stand-by. It has proved but a bruised reed. It will be realized from this brief account how very important, even considered from the point of view of teeth alone, are the calcifying vitamin and the substances with which it reacts. \ Fat-soluble Vitamins and Muscle Structure and Function, So far attention has been confined to the effect of the fat-soluble vitamin on processes of calcification. But in rickets other organs besides the bones are abnormal, and among these probably the most noticeable is the condition of the muscles, as evidenced by the flabbiness and lethargy of the average child suffering from this disease in an active form. Recently a more detailed study has been made into the j effect of diet upon the muscles, and the preliminary results described to the Physiological Society (1923) by Clifford, Surie, and myself. Degenerative changes in muscles of animals suffering from scurvy have also been described (Hayem,4 Aschoff and Koch,5 Hart and Lessing6). Our results are, briefly, that those dietetic changes which are responsible for rachitic changes in bones are also, on the whole, responsible for certain defects in muscle. These defects, besides being evident from the weakness of the muscles, can also be determined and analysed by their microscopic structure and alteration of their chemical con¬ stituents. Fat-soluble vitamin, again, plays a dominant part in controlling the muscular structure and function, and is opposed in its work by the cereal portion of the diet, as described above in the case of bone structure. A diet deficient in fat-soluble vitamin and containing excess of cereal is capable of producing muscles which are extra¬ ordinarily defective in structure, and have the appearance of pseudo-hypertrophic muscular dystrophy. In the case of puppies it is possible, by slight alterations in feeding, to produce all degrees of muscle change, so that the animals j may show the greatest activity or all grades of abnormality down to absolute paralysis. Results of this type demon¬ strate clearly the dominant position held by diet over muscular activity, and show that, given a normal young animal, its activity can be controlled by its diet rather than by the space allowed it in which to move about. It is interesting also to note that Nature has so arranged matters that a strong active muscle is developed along with a well calcified bone, and a weak muscle with a defectively calcified bone. Teleologically this arrangement would be expected. I have described from an experimental point of view •~a number of tiv nes of the body whose structure and function are confi oiled by a few dietetic factors—factors which there is season to believe bring about the same defects in corresponding human tissues in a widespread manner. Other physiological functions are undoubtedly interfered with by the same apparently small dietetic abnormalities, and these are gradually coming to light. On the other hand, it is equally certain that other dietetic elements not dealt with here are fundamentally responsible for many pathological conditions, and that these will also be unfolded gradually by investigation. Before attempting to show how the experimental results are being applied to clinical problems, I shall first discuss briefly the recent work on light treatment, and give the evidence which indicates that the influence of light, as regards some physiological processes at least, is closely bound up with the dietetic factors, the fat-soluble vitamins and cereals. The Relation of Light Radiations to Deficiency Disease„ Although the therapeutic influence of light radiations has been long recognized, more particularly in respect to bone tuberculosis, it is only in the last two years that the subject has been put upon an experimental basis. The experi¬ mental work already done has led to the discovery of interesting facts, so that it can now be claimed that light therapy has been raised from a position of empiricism to one with some scientific foundation. It is true that the foundation is as yet fragile, but this drawback will un¬ doubtedly rapidly disappear in view of the many investi¬ gations now being made on the subject. I do not propose to deal here with the great pioneer work carried out by various clinicians on this subject, but will simply mention the more recent results which are germane to the subject of deficiency diseases, and which have brought it under the scrutiny of the investigator both in the laboratory and the hospital. In 1919 Huldschinsky described the curative effect of exposures to the ultra-violet rays of a mercury- vapour lamp on rickets in children. These observations have been abundantly confirmed both as regards children (Chick, Dalyell, et al.) and in the case of experimental rickets in rats (Hess, Unger and Pappenheimer, Shipley, Park, Powers, et al.), and in puppies by myself. Before and throughout the period during which the effect of light on rickets was being investigated, the above described results dealing with the influence of antirachitic vitamin on bone calcification were also being widely discussed, and it soon happened that the two influences became associated in the minds of those investigating the diseases. It was found that the effect of the ultra-violet rays striking the skin was a more general one than at first imagined. Huldschinsky, for instance, described cases of latent and actual tetany cured by exposure to these rays, whereas Powers, Park, Shipley, McCollum, and Simmonds found that sunlight brought about a greater consumption of food in rats, stimulated their activity, improved their appearance, and increased their reproductive capacity when fed on vitamin-deficient diets. In general, exposure of animals to ultra-violet rays acted in many respects like adding fat-soluble vitamin to their diet when devoid of or deficient in this substance. Of the two hypotheses, then, suggested as to the mode of action of the radiations— namely, (1) the possible synthesis of the vitamin, or (2) the activation of the fat-soluble vitamin already stored in the body, it is now known that the second is the true one. ■ The establishment of this hypothesis rests largely upon the experiments published respectively and simultaneously by Hume (1922) and Goldblatt and Soames (1922). It will be remembered that both these investigations dealt with the effect of exposure to ultra-violet radiations on the growth of rats, and the results were in close agreement. When young rats were fed on a diet devoid of vitamin A, and exposed at the same time to the ultra-violet rays, they were stimulated to grow at the normal rate for a period if the rays were applied at an early stage of the diet. In course of time—that is, after about eight weeks—all growth ceased, presumably because the vitamin A supplies of the body were exhausted. This cessation of growth took place in spite of the continued application of the radiations. Other evidence pointing to this conclusion was that the longer the period on vitamin A-deficient diet before the rays were applied, the less was the effect on growth pro¬ duced by the exposure, so that, after a period of eight