VITAMIN A-DEFICIENCY AND THE RETINA 159 



horses by increasing the carotene or vitamin A intake after 

 experimentally producing this condition by a vitamin A-defi- 

 cient diet. They give in tabular form the amounts necessary 

 to bring about night blindness, and the increased quantities 

 of either carotene or vitamin A required to restore normal 

 vision. It would be of interest to know, in the light of the 

 findings of Johnson and of Tansley, whether the primary 

 lesion which Hart and Guilbert obtained in sheep and cattle 

 may not have been in the retina, with the optic nerve in- 

 volved secondarily. In cases of greatly raised rod visual 

 thresholds in humans, where the return to normal does not 

 occur for many weeks and months, despite adequate diets 

 and supplementary vitamin A administration (Hecht and 

 Mandelbaum, 1939, 1940; McDonald and Adler, 1939), one 

 wonders whether there may not have been some structural 

 degeneration of the rods. If degenerative changes of the rod 

 outer segments occur in rats following prolonged deficiencies, 

 as has been shown by Johnson and by Tansley, there seems 

 to be no reason why this same condition might not occur in 

 man. Furthermore, in view of the fact that the rod outer 

 segments are capable of regeneration in rats, as has been 

 demonstrated by Johnson (op. cit.), it is not inconceivable 

 theoretically that the same may occur in humans, and thus 

 be a definite factor in the long period required by many 

 persons to recover normal vision after vitamin A-depletion. 

 At least it would seem pertinent for the ophthalmologists 

 to consider this possibility as a problem for further investi- 

 gation. 



