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Computer Graphics	General Models of Feeding It is not possible yet to specify which signals are the critical ones controlling feeding. Indeed, for the reason stated above, there might not be one critical signal. Nevertheless, there is good evidence that information detected by gustatory, visceral, and brain receptors constitute the major factors in the control of feeding. The idea that there is an integration of a variety of signals and that all of them play some role in feeding control has not, until recently, been a popular notion. In the past, what has been dominant has been homeostatic or set-point theories, both of which give a more prominent place in control to internal events while relegating external factors to a modulatory role. In contrast, incentive models assume that external stimuli (the incentives) have a primary role in eliciting and directing feeding behavior, and internal events "gate" these primary controls. What is dissatisfying about homeostatic and set-point models as well as incentive models is that they create artificial and perhaps misleading distinctions between the various controlling conditions. In the case of homeostatic models, the basic controls are internal events (e.g., glucose availability, fat storage, hormone levels), whereas food palatability, for example, would be considered a modulating condition. The most reasonable supposition is that palatability cues are as critical a factor in controlling food intake as any so-called internal or homeostatic variable, but not more so, as incentive models would argue. If there is a real physiological set point against which current conditions are continuously compared, gustatory cues have been shown experimentally to exert powerful effects on where this reference point is established. Thus, until evidence to the contrary is presented, it is best to consider food intake as jointly and interactively controlled by both internal and external factors. For a more extensive review of these arguments, refer to Toates' excellent theoretical paper on hunger models. Historically, if not logically, the stomach is a good place to start when considering the origin of signals and neural substrates that might control or modulate food intake. Cannon, early in this century, developed the first systematic and empirically based theory of hunger. In his formulation, the empty stomach displayed strong contractions, and these were the basic hunger stimuli. The ingestion of a meal reduced these contractions, and the resultant stomach quiesence was the signal of satiety. Later theorists made assumptions that these signals were neural in origin and likely traveled to the brain over the vagus nerves. The reasons for the ultimate replacement of this theory are more fully outlined in another paper, but primarily it was that newer theories seemed to account for a greater variety of the facts with fewer assumptions and contradictions. The next major step in the neural modeling of feeding control was the "dual center" hypothesis. In this formulation, the hypothalamus exercised the primary control over feeding. More specifically, there was the ventro-medial hypothalamic nuclei (VMH) that acted as a satiety center inhibiting a lateral hypothalamic area (LHA) feeding center. This theory grew primarily from lesion work on rats and other animals and in part by observation of human cases of naturally occurring brain damage. Initial observations of experimental lesions in rats and other animals appeared to demonstrate that after VMH lesions, animals would overeat and, as a consequence, become obese. Thus came the notion of the VMH as a satiety center. In contrast, destruction of the LHA resulted in aphagia, in some cases so severe that the animal might starve to death. On the basis of the observation that the effect of destruction of both areas was most like the destruction of the LHA, it was hypothesized that the VMH satiety center operated by inhibiting the LHA. Studies of the effects of electrical stimulation of the brain in behaving animals provided additional and powerful support for the dual center hypothesis. Stimulation of the LHA resulted in increased feeding and hunger motivation, whereas VMH stimulation suppressed food intake. In so far as one would assume that stimulation should have the opposite effects of destruction of the brain area, these results provide powerful support for the theory. For more than a decade this was the leading theory of the neural control of food intake, probably because it was powerful and parsimonious, that is, it made many testable predictions with relatively few assumptions. However good the dual center theory was, it seemed there were always facts that could not easily fit into this theoretical framework. It was always assumed that the metabolic effects of the lesions, especially those following VMH destruction, were secondary to the feeding effects of the lesion. However, there were data showing that there were metabolic effects of the lesion that were primary and independent of the altered feeding. In addition, it was demonstrated that if the animal was made to either gain or lose substantial amounts of weight prior to the production of the lesions, the feeding effects of the lesions were substantially reduced or eliminated. These observations led to the more currently popular set-point theory. In this theory there is a predetermined level of body weight, or more specifically adiposity, and a way of measuring deviations from that. Those deviations from a set point activate mechanisms designed to restore conditions as close as possible to the pre-set value. In this scheme, the VMH and LHA do not control food intake directly, rather they set the upper and lower limits, respectively, for body weight (adiposity). Thus, when they are destroyed, new, more extreme levels of body weight are maintained. The neural and hormonal mechanisms that are presumed to operate in this scheme have not been fully worked out, but one prominent mechanism certainly involves the pancreatic hormones, especially insulin. In this formulation, VMH lesions disinhibit the parasympathetic excitation of the beta cell, and insulin secretion is increased, leading to enhanced lipogenesis. The increased demand for lipid storage can ultimately be met only by increased nutrient intake until a new level of adiposity is achieved. The set-point theory accounts for many new and old observations not compatible with the notion that these hypothalamic structures had as their primary role the direct control of feeding behavior. Recently, incentive models have become popular. In this model of feeding, behavior is not driven by an internal state or need, but rather is stimulated by certain external signals whose strength is modulated by internal states and prior experience with the external signals. In this scheme, such stimuli as the sight, smell, and taste of food become the cause for ingestion. The effectiveness of these stimuli is facilitated or inhibited by past experience with those particular stimuli and gated by concurrent internal states such as stomach distention and glucose availability. Thus, Booth ( 1977) showed that flavors associated with a calorically concentrated nutrient are preferred early in a meal, well before repletion occurs. In contrast, nearing repletion preferences switch to a flavor previously associated with a calorically diluted nutrient. Incentive theorists have quite rightly criticized homeostatic models for not taking into account the important effects external factors have in the control of food intake. However, incentive theorists overlook the powerful and direct effects that internal states have in the control of ingestion. With all other conditions held constant, the longer the food deprivation, the stronger is the hunger drive. It would seem hard to argue that this was not the effect of an internal state. Furthermore, Louis-Sylvestre and Le Magnen have demonstrated that in the relatively undisturbed, ad-libitum feeding rat, every meal was preceded by a small but consistent decrease in blood glucose level, and no such change in internal state occurred without being followed by a spontaneous meal. These data suggest that the internal state, whatever the external stimulation, can be the direct cause of feeding. That is, the external food incentive was present at all times, and this did not predict whether or not the animal would initiate a meal. However, the internal state, namely a fall in the glycemic level, did predict this. Another issue is that it seems odd to build a theory in which gustatory chemoreceptors are considered to be detecting external stimuli, whereas gastric and gut receptors are monitoring internal events. Both homeostatic and incentive models commit this error. From a topological sense, and more directly in consideration of the embryological origins of these tissues, this distinction is difficult to justify. The alimentary canal is a continuous tube in direct contact with the outside world. At the moment there is no evidence to make one elevate external factors above internal ones or vice versa in their importance for feeding control. Indeed, in some cases as mentioned above, the distinction might not even be particularly useful or even valid. Other theories have focussed more narrowly on one or a few aspects of the control of food intake. There have been theories emphasizing one organ, such as stomach, gut, or liver. Other hypotheses have concentrated on the signals that might drive food intake. This has resulted in glucostatic, lipostatic, aminostatic, and caloriestatic theories. Still other formulations emphasize the neurotransmitters involved, such as catecholamines or peptides or humoral agents that themselves act as signals, such as insulin or cholecystokinin. There can be no question that there must be initiating signals capable of activating organs that are differentially sensitive to them. Also, there must be a message system transmitting this information using either humoral agents, the nervous system with its attendant neurotransmitters, or both. It is difficult to formulate a grand theory to encompass these observations because there seem to be no necessary links in the causal chain connecting the initiating signals to the act of ingestion. Thus, the elimination of some presumed important factor has often given small or confusing results. One way to understand this is to recognize that the control of feeding is probably multifactorial and redundant. The multitude of controls may be, in part, due to the nature of the goal object. Unlike thirst, in which the goal object is the intake of water, however it might be mixed with other substances, there is no one substance the ingestion of which is uniquely connected to a hunger drive. Any one of a number of macro- and micronutrients may or may not satiate, depending on a variety of as yet largely unknown variables. Redundancy may partly arise from the complex nature of the ingested material but is probably also derived from the safety factor it provides by having parallel channels of control or modulation of this vital function.