title: Cognitive and neuronal systems underlying obesity.
abstract: Since the late 1970s obesity prevalence and per capita food intake in the USA have increased dramatically. Understanding the mechanisms underlying the hyperphagia that drives obesity requires focus on the cognitive processes and neuronal systems controlling feeding that occurs in the absence of metabolic need (i.e., "non-homeostatic" intake). Given that a portion of the increased caloric intake per capita since the late 1970s is attributed to increased meal and snack frequency, and given the increased pervasiveness of environmental cues associated with energy dense, yet nutritionally depleted foods, there's a need to examine the mechanisms through which food-related cues stimulate excessive energy intake. Here, learning and memory principles and their underlying neuronal substrates are discussed with regard to stimulus-driven food intake and excessive energy consumption. Particular focus is given to the hippocampus, a brain structure that utilizes interoceptive cues relevant to energy status (e.g., neurohormonal signals such as leptin) to modulate stimulus-driven food procurement and consumption. This type of hippocampal-dependent modulatory control of feeding behavior is compromised by consumption of foods common to Western diets, including saturated fats and simple carbohydrates. The development of more effective treatments for obesity will benefit from a more complete understanding of the complex interaction between dietary, environmental, cognitive, and neurophysiological mechanisms contributing to excessive food intake.
authors.affiliation: University of Pennsylvania, Department of Psychology, Philadelphia, PA 19104, United States. kanoski@sas.upenn.edu
authors.forename: Scott E
authors.initials: SE
authors.lastname: Kanoski
mesh_terms: D000818:Animals; D001921:Brain / Q000473:pathology*; D003072:Cognition Disorders / Q000209:etiology*; D004435:Eating / Q000502:physiology; D006801:Humans; D009474:Neurons / Q000473:pathology*; D009765:Obesity / Q000150:complications / Q000453:epidemiology / Q000473:pathology