HUNGER EDEMA 377 



we have already voiced our opinion, in the introduction to this chap- 

 ter, against the conception of a lack of protein as an etiological 

 factor in the development of hunger edema. By the addition of 

 casein, it is possible, first of all, that there might have been an 

 increase in appetite, with a consequently greater food and vitamine 

 intake. The considerable quantity of water not only diluted the 

 vitamine and protein content of this diet, but also caused great loss 

 by washing out. Kohman tried to get around these difficulties by 

 showing that on a synthetic diet prepared in the usual manner, a 

 small food intake, per se. is not followed by edema. However, since 

 the diet was properly constituted, in this case, the results cannot 

 be applied to the carrot diet. 



Another hypothesis deals with the role of the adrenals in the 

 development of edemas; this was formulated by McCarrison (I.e. 

 290 and 608). He showed that in beriberi, there was an increased 

 adrenaline output which was supposed to be responsible for the 

 development of edema. McCarrison held that butter, but not all 

 fats, contains a substance (apparently vitamine A) which is protec- 

 tive against edema. This idea was adopted by Bigland (1475), in 

 a practically unchanged form, who regarded an increased or de- 

 creased suprarenal activity as the causative factor in the explanation 

 of hunger edema and pellagra, respectively. Nixon (1476) assumed, 

 as the cause of edema, insufficient calories (fat?) and protein and 

 excess of water; adrenaline was also thought to play a part. In 

 conclusion, we shall mention the pathogenesis assumed by Schitten- 

 helm and Schlecht (I.e. 1443). They ascribed the cause to the 

 lack of protein and fat, the effect of cold and hard labor helping to 

 bring about the disease. They recognized that hunger edema occurs 

 on a diet rich in carbohydrates. The differentiation from beriberi 

 lies in the bradycardia; on the other hand, scurvy-like symptoms, 

 such as stomatitis and bleeding of the gums were observed. 

 Hemeralopia and xerosis of the eyes were also noted quite frequently. 

 Administration of vitamine B exerted no therapeutic effect. There 

 is a great analogy to "Mehlnahrschaden." 



Our presumption is that we are dealing here with a complication 

 of causes, although the disproportion between the individual dietary 

 constituents, as well as an inadequate diet in relationship with the 

 hard labor stands in the foreground. However, in this case too, 

 further work is necessary in order to arrive at an explanation of the 

 problem. 



