For the purposes of this discussion, we use a simplified but useful definition of food addiction as “a loss of control over food intake.” Using drugs of abuse as a model, we compare the neuronal regulation of food intake to drug consumption and discuss the potential for food to be considered addictive. Given the requirement of food for life, much debate has centered on defining the term food addiction. In contrast to addiction to drugs of abuse, much less is known about the behavioral and neurobiological consequences of repeated exposure to highly palatable foods. Although the concept of food addiction has received considerable attention from the popular media in recent years, there is not actually a diagnosis for food addiction in medical science. Within the field of medicine, the term addiction is applied only to drugs of abuse such as alcohol and cocaine. Finally, we discuss the clinical implications of these neuronal adaptations in the context of obesity and neuropsychiatric syndromes such as bulimia nervosa and Prader-Willi syndrome. Next, we discuss the normal homeostatic regulation of food intake, which is a unique aspect of food addiction. We then compare our current understanding of drug-induced changes in neuronal reward circuitry with what is known about the consequences of repeated consumption of highly palatable foods such as high-fat and high-sugar diets. In this article we review the extensive research that has identified several mechanisms by which repeated exposure to drugs of abuse alters neuronal function and increases the motivational incentive to obtain and use these substances. In contrast to the consumption of food, the motivation to use drugs of abuse is mediated only by the reward pathway.
In contrast, hedonic or reward-based regulation can override the homeostatic pathway during periods of relative energy abundance by increasing the desire to consume foods that are highly palatable. The homeostatic pathway controls energy balance by increasing the motivation to eat following depletion of energy stores. Food intake is regulated by 2 complementary drives: the homeostatic and hedonic pathways.