Brain regulation of hunger and motivation: The case for integrating homeostatic and hedonic concepts and its implications for obesity and addiction.

Obesity and other eating disorders are marked by dysregulations to brain metabolic, hedonic, motivational, and sensory systems that control food intake. Classic approaches in hunger research have distinguished between hedonic and homeostatic processes, and have mostly treated these systems as independent. Hindbrain structures and a complex network of interconnected hypothalamic nuclei control metabolic processes, energy expenditure, and food intake while mesocorticolimbic structures are though to control hedonic and motivational processes associated with food reward. However, it is becoming increasingly clear that hedonic and homeostatic brain systems do not function in isolation, but rather interact as part of a larger network that regulates food intake. Incentive theories of motivation provide a useful route to explore these interactions. Adapting incentive theories of motivation can enable researchers to better understand how motivational systems dysfunction during disease. Obesity and addiction are associated with profound alterations to both hedonic and homeostatic brain systems that result in maladaptive patterns of consumption. A subset of individuals with obesity may experience pathological cravings for food due to incentive sensitization of brain systems that generate excessive 'wanting' to eat. Further progress in understanding how the brain regulates hunger and appetite may depend on merging traditional hedonic and homeostatic concepts of food reward and motivation.