We believe all physicians will agree that the control of hunger and appetite is a very important factor in the control of disease, and especially of chronic disorders. The physiologist is therefore assured of the co-operation of the clinics in the investigation of the pathology of hunger and appetite. Such co-operation is a sine qua non for progress in this field, as the final verdict in the analysis of the pathology of hunger is the word and the reactions of the patient himself.
Conditions of disease in man, so far as they affect hunger, usually involve a decrease or absence of hunger and appetite sensations, as in fevers, anemias, cachexias, and neuroses of various origin. Certain pathological states such as diabetes, brain tumors, neuroses, etc., may be associated with abnormally strong hunger and appetite. In diseases of the stomach itself the hunger sensation may be decreased (atony, gastritis, constipation, etc.), increased (hypermotility, pyloric insufficiency, vagotonia, etc.), or altered in the direction of abnormal painfulness, as in gastric and duodenal ulcers.
From our analysis of the nature of the hunger mechanism, it is evident that depression or absence of the hunger sensation may theoretically be brought about in any one of the following ways: (i) direct failure or absence of the tonus and hunger contractions of the empty stomach; (2) prolonged reflex inhibition of the stomach; (3) interference with or depression of the central conduction paths; (4) direct depression of the cerebral or thalamic hunger centers; (5) interference with the central conduction of the hunger impulses by abnormal or unusually strong impulses from other proprioceptors. These various conditions may be caused by pathological changes in the blood, in the motor mechanism of the stomach itself, or in the central conduction paths and sensory centers. Pathological augmentation of hunger would result from the reversal of these conditions. The first question that must be settled in the physiological pathology of hunger is whether or not the abnormalities are due to changes in the gastric hunger mechanism itself. This can in every case be settled by direct tests on the patient, using our balloon method. When the pathological changes are in the central nervous system itself their analysis becomes much more difficult.