The Neurobiology of Appetite: Hunger as Addiction

Abstract

Obesity is caused by the consumption of excess calories. As such, it can be viewed as a failure of homeostatic systems that control body weight or, more appropriately, energy balance. The obese individual consumes excess calories in a non-homeostatic manner, as a result of excessive motivation or drive. A similar model has been proposed to explain drug addiction, in which hedonic homoestatic systems are dysregulated. There is considerable overlap between brain systems and neurotransmitters implicated in drug addiction and those known to control feeding behavior. Another way of looking at excess consumption of calories is that it is driven by pleasure, of food. It has been suggested that there are two parallel systems for driving food intake: a homeostatic one that responds to energy signals from the body, transmitted mainly via the circulation and the vagus nerve, and acting via the hypothalamus; and a hedonic one in which food cues (odors, thoughts, the sight of food) have the ability to stimulate appetite in the absence of metabolic need. It should be noted, however, that the addiction model provides a slightly different explanation of the effect of food cues, by viewing them as conditioned stimuli predictive of reward. This chapter reviews the evidence linking drug addiction and obesity, and a recent study that suggests homeostatic signals interact with hedonic and incentive signals to trigger food intake.