Abnormally intense hunger sensation has been termed bulimia. Some authors do, others do not, distinguish between bulimia and polyphagia. When distinctions are made, the term polyphagia is used to denote the condition of excessive ingestion of food, that is, an absence of satiety or sensation of fulness, rather than an abnormally intense hunger sensation. Bulimia may be temporary or chronic. It is characterized by the fact that hunger comes on shortly after eating, and if it is not appeased by food there follow headache, weakness, and prostration, just as in normal hunger in many persons, only to a much greater degree. Very small quantities of food may appease this hunger temporarily. This sensation of hunger may arise before the stomach is empty, although in many cases of bulimia, the food leaves the stomach more rapidly than in normal persons (Ewald, Perthes, Sick, Leo, Boas). Nicolai concluded that bulimia is due to hyperexcitability of the afferent hunger nerves in the stomach and esophagus. Ploenius insists that bulimia is an augmentation of normal hunger, and appears only when the stomach is empty; and that it invariably indicates organic lesions in the stomach, such as local destruction of the mucosa with pepsin-HCl corrosion of the deep tissues. According to Leo, bulimia may occur in exophthalmic goitre, in gastric and duodenal ulcer, with hyperacidity, in chronic gastritis, diarrhoea, tapeworms, pregnancy, excessive menstruation (hemorrhage), and even in cancer and in dilation of the stomach. Ewald records bulimia associated with Addison's disease, syphilis, uterine diseases, and brain injuries (tumors, emboli, trauma). Meyer states that excessive hunger or bulimia may appear in all types of neurosis.
This hunger has usually a very sudden onset, and is satisfied or even turned into nausea by very small quantities of food. Meyer describes another type of intense hunger accompanied by headache, in which neither the hunger nor the headache is relieved by eating, and the ingestion of food does not lead to the sensation of fulness or satiety. But in these patients there was evidence of other cerebral disturbances. Meyer argues that in cases where the intense hunger is satisfied or even turned to nausea with a few mouthfuls of food we cannot be dealing with the mere augmentation of true hunger. This position is not tenable. There may be increased excitability of the inhibitory reflexes from the mouth and the gastric mucosa, and hyperexcitability of the mucosa nerve-endings would lead to nausea after ingestion of even small quantities of food. Meyer also reports excessive hunger in certain persons past middle life with tendency to adiposity. Perthes reports bulimia in persons with patent pylorus. In some of Perthes's patients the hunger was intense enough to wake them up from sleep every two hours during the night. Boas assumes a type of "idiopathic" bulimia, not accompanied by any other functional or organic disturbances.
The excessive hunger in pregnancy is in all probability a normal physiological effect of the increased metabolism due to the growing fetus. The peculiar fluctuation in the appetite or desire for certain kinds of food that may occur in pregnancy involves more complex factors.
The bulimia of hypochondriacs, and other types of neurotics, may be a subjective exaggeration of normal hunger impulses.
The gastric pains that appear in the empty stomach or a few hours after ingestion of a meal in persons with gastric or duodenal ulcers, or with gall-bladder disease are designated by Moynihan, Hertz, and others as "hunger pains." In normal persons the hunger sensation, if sufficiently strong, is painful.
The patients with ulcer or hypersecretion describe these hunger pains in part as continuous or persistent, in part as variable or "gnawing" precisely like the normal pangs of hunger, except that they are more intense or painful. Like the normal pangs of hunger the pathological hunger pains are allayed by the ingestion of food. Most of the German authors do not differentiate between bulimia and the hunger pains of gastric and duodenal ulcers.
Following Moynihan, many clinicians regard the hunger pains in ulcers as caused by hydrochloric acid stimulation of the raw surfaces of the ulcer. In support of this view they cite the fact that the pains are temporarily relieved by giving alkalies by mouth. Hertz has shown, however, that giving strong acids by mouth to ulcer patients does not cause or increase the hunger pains. If the acid stimulation of the ulcer gives rise to these hunger pains in ulcer patients, they have a different origin from the normal hunger pains, as the latter are caused by strong contractions of the stomach, especially of the fundic and cardiac regions. The gnawing or rhythmical character of the hunger pains in ulcer cases appears to the author to show that they are due to contractions. If they were caused by chemical stimulation of the sensory nerves directly we should expect them to be continuous. Hertz has pointed out additional facts that support the mechanical or contraction origin of the pains, such as the patency of the pylorus, the rapid emptying of the stomach, the hypertonicity and hyper-peristalsis of the stomach, etc., in both duodenal and gastric ulcer. Moreover, hypersecretion and hyperacidity is not a constant factor in ulcers (Hardt), and the hunger pains in ulcers may closely simulate the gastric pain in cases of gallstones, appendicitis, gasteroptosis, etc., where there is no raw mucous surface to be stimulated chemically, either in the stomach or the duodenum.
Edelmann states that the gastric digestion peristalsis is directly dependent on the acidity of the gastric juice. But according to Eisner the condition of achylia gastrica in man has per se no effect on the digestion movements. The emptying time of the stomach in achylia may be normal, less than normal, or greater than normal.