Ss) 
17, 4 Sison: Experimental Starvation 419 
When the fast was broken, it fell to normal. The hemoglobin and the total 
quantity of blood remained constant. ; 
During the first days of the fast, more heat came from the glycogen that 
was burned than from the protein so used. Since glycogen burns most 
easily, it was rapidly drawn on and the available supply quickly depleted. 
From the first to the third day, from 10 to 16 per cent. of the heat was 
derived from glycogen. From the third to the thirteenth day, from 1 to 
3 per cent was so obtained. The combustion of glycogen ceased after this 
time. As one would expect, fat eventually becomes the chief source of heat. 
In normal catabolism, fat is burned completely the end products being carbon 
dioxid and water; but in some pathologic conditions and in inanition, fat 
combustion is defective, and certain partially oxidized substances known as 
acetone bodies are produced and excreted chiefly in the urine. The clinical 
significance of this phenomenon is well known. These acetone bodies were 
present in the urine throughout the latter part of the experiment. The 
concentration of alkali necessary for their combustion greatly exceeds 
that which can be tolerated by the body. 
Indicative of the so-called acidosis that occurs during starvation, besides 
the acetone bodies, the urine contains a large number of organic and inor- 
ganic acid radicals. Thus chlorin, phosphorus pentoxid, sulphur trioxid, 
and oxybutyric and other fatty acids are found. An albuminuria with 
hyaline and a few granular casts may also occur, but clears up after the 
fast is broken. 
From a study of the oxygen consumption, the carbon dioxid excretion, 
the pulse rate and the temperature, one may conclude that there is a paral- 
lelism between these activities and the metabolism, and that the body acts 
as a unit irrespective of its state of nutrition. 
With the foregoing results there are certain thoughts that 
force themselves as a corollary to our observations. Knowing 
the changes that occur after starvation, it is but logical to 
suppose that in certain diseases of long duration, mainly those 
on which the incidence of inanition is a necessary sequela or a 
concomitant condition that may arise therefrom, the train of 
pathological phenomena known as morbid anatomy of such dis- 
eases must be associated with those that are rather the effect 
of inanition. Now the question that suggests itself is: Are all 
of the physical findings on examination, ante- and post-mortem, 
the result of the disease per se, or are they accompanied by those 
that are produced by inanition, if it accompanies the disease? 
In spite of our knowledge of the morbid anatomy of many clinical 
entities, as well as their physical manifestations during their 
course, there still remains a little probability that this may have 
a part in the making up of some of the symptoms, physical 
findings, and morbid anatomy of many diseases in which there 
-is a greater or less degree of starvation accompanying the course 
of the disease. Going a little further, some of the complications 
and sequele, while not directly caused by starvation, might in- 
