The reader will recall from the review of the literature on hunger and appetite in chap, ii that most of the authors assume a chemical control of the hunger mechanism in the sense that starvation changes of the blood stimulate the conscious hunger center in the brain, the specific sensory nerves in the stomach, or sensory nerves in all the tissues. We know now that the hunger sensation is caused by strong contractions of the empty or nearly empty stomach. This fact modifies but does not eliminate the question of chemical control of the hunger mechanism. We must now determine whether starvation changes in the blood influence the motor side of the mechanism, while the earlier authors considered the influence of the blood only on the sensory side of the hunger apparatus.
Chemical changes in the blood may act in a positive way either on the vagi tonus centers in the brain or directly on the stomach motor tissues. The problem of chemical control of hunger is thus resolved into three main queries, namely: (i) Do chemical stimuli in the blood cause the increased gastric tonus of hunger ? (2) Do chemical stimuli in the blood initiate the individual gastric hunger contractions ? (3) Do chemical stimuli control the grouping of the hunger contractions into hunger periods, separated by periods of relative gastric quiescence, in species showing this grouping?
We must also consider the possibility of chemical blood changes that may depress or inhibit the hunger contractions.
The gastric hunger contractions are inhibited by mechanical and chemical stimulation of the nerve-endings in the mucous membrane of the mouth, the esophagus, and the stomach. This insures inhibition of the hunger contractions during mastication and gastric digestion. The gastric hunger mechanism receives motor or tonic innervation via the vagi, and the central connections of this tonus innervation appear to be practically isolated from all normal reflexes, while the inhibitory mechanism via the splanchnic nerves is very readily called into activity reflexly. The foregoing facts appear to have only two alternative explanations, viz: (i) The gastric hunger contractions are due to a specific automatism (vagi centers and stomach) primarily independent of afferent impulses as well as the conditions of the blood. Such an automatism would, of course, vary with the physiological condition of the automatic tissues; but if this is the mechanism we cannot speak of any physiological nervous control of the hunger apparatus, except in the way of inhibition. (2) The vagi and the gastric mechanism concerned in the genesis of the hunger contractions may be influenced in a positive way by physiological changes in the blood. If this is the case, we might expect such changes in the blood to be specially evident in the normal animal when starving.
Some of the facts already discussed seem to show that both of the factors named above are to be reckoned with. In man and dog the gastric hunger contractions usually appear as soon as the stomach is empty of food, that is, before intestinal digestion and absorption of the meal are completed. Under these conditions the initiation of the hunger contractions must be due to a primary automatism not opppsed by inhibitory reflexes rather than to any changes in the blood such as are presumably involved in starvation, for there is surely no auto-digestion of the body tissues or lack of pabulum in the body fluids while normal intestinal digestion and absorption are still in progress. In dogs with Pavlov stomach pouches we may also have hunger contractions in the main stomach while the Pavlov stomach is quiescent, or vice versa. Oh the other hand, excessive hemorrhage, prolonged starvation, and pancreatic diabetes, which is a type of starvation, lead to increased activity of the hunger mechanism, at least up to the point where the stomach becomes directly involved in the general debility and cachexia. The increased vigor of the hunger apparatus in normal, individuals as an after-effect of the greatly accelerated metabolism caused by physical exertion and cold, is a bit of evidence pointing in the same direction,
This augmentation of the hunger contractions in starvation may be due to (1) the appearance of substances in the blood stimulating the central tonus mechanism or the peripheral hunger apparatus; (2) the absence or diminution of inhibitory substances in the blood; (3) the absence or depression of inhibitory reflexes; (4) starvation changes in the tissues directly concerned in the hunger contraction.
If it is due to the presence of stimulating substances in the blood, it would seem that transfusion of the blood of starving animals into normal animals ought to augment the activity of the hunger mechanism, at least temporarily. This is actually the case.