Experimental Rickets as a Phosphorus Deficiency Disease

Abstract

ALTHOUGH both prophylactic and curative technique against rickets is now highly developed, the pathogenesis of the disease is still far from being adequately understood. Recent experimental findings—some having already been published¹, others to be published shortly—are briefly summarised here since they afford, it would seem, strong support for the view that, whilst other factors play a part, and it would be idle to endeavour to dissociate phosphorus from calcium metabolism, yet nevertheless a chronic defect of phosphorus uptake from the diet is the most important single factor in the production of experimental rickets in rats. This is very probably true in a large proportion of cases of human rickets also, vitamin D being of importance in the rat or human dietary only in so far as its presence enables the organism to increase the net intestinal absorption of phosphorus from the food. Our findings also throw a little light, it is believed, on the part played by the bone enzyme in this disease.