VITAMIN D 299 



Sheets and Funk (1922) concluded that ultra-violet light had no 

 effect upon growth or the incidence of ophthalmia in animals on a 

 diet free from fat-soluble vitamins. 



Powers, Park and Simmonds (1923) found that the development 

 of pronounced xerophthalmia was delayed in those of their rats which 

 were exposed to sunlight. They concluded that, "Sunlight possibly ex- 

 erts no specific antixerophthalmic influence, but acts by raising the level 

 of cellular activity of the organism to a point where the onslaughts of 

 the disease are held in check or allowed to advance very slowly and 

 with relatively little disturbance. It may be true that the nearer the 

 animal to maturity the less vulnerable it is to the effects of a xero- 

 phthalmia-producing diet." . . . "Previous experiments have shown 

 that the unknown factor in cod liver oil which promotes normal forma- 

 tion of bone (and in that sense may be spoken of as antirachitic) has an 

 equivalent in sunlight. The experiments herein reported indicate that 

 sunlight does not contain at all or only to a very slight degree the 

 equivalent of the antixerophthalmic factor in cod liver oil." 



Hume (1922) found that, with rats of matched nutritional history, 

 the irradiated animals developed the typical symptoms of vitamin- A de- 

 ficiency with greater severity and greater rapidity than did control 

 animals, and that irradiation exerted no curative effect in animals which 

 had succumbed to xerophthalmia, but rather seemed to increase the 

 severity of the symptoms. She states that : "Early cessation of normal 

 growth followed by a long period of maintenance might almost be 

 regarded as a defense mechanism, which enabled the rat to tide over 

 a period of vitamin A famine, such as might easily be a danger in 

 the normal life of a rat. When irradiation is applied it would seem 

 as if, either the low level of vitamin A metabolism is rendered suffi- 

 cient, i.e., the vitamin is economized — or else the vitamin stores are 

 forced to yield up vitamin A at a rate sufficient to produce normal 

 growth until the stores are wholly exhausted. This effect can apparently 

 be produced at any time before the end of the period of slow growth, 

 and the amount of normal growth produced at any time would appear 

 to be roughly inversely proportional to the length of time any individual 

 rat has previously been on a deficient diet. Ultimately, when presumably 

 all the stores are exhausted, no normal growth can be evoked by irra- 

 diation. Hence it is clear that light can neither create or be substituted 

 for the vitamin; it appears only to act as an economiser or activator 

 when it is already present." 



Similar results were reported by Goldblatt and Soames (1922). 



Steenbock and Nelson (1923) commented on the paradox of light 



