Pathological Overeating: Emerging Evidence for a Compulsivity Construct

Abstract

Compulsive eating behavior is a transdiagnostic construct that is characteristic of medical and psychiatric conditions such as forms of obesity and eating disorders. Although feeding research is moving toward a better understanding of the proposed addictive properties of food, the components and the mechanisms contributing to compulsive eating are not yet clearly defined or understood. Current understanding highlights three elements of compulsive behavior as it applies to pathological overeating: (1) habitual overeating; (2) overeating to relieve a negative emotional state; and (3) overeating despite aversive consequences. These elements emerge through mechanisms involving pathological habit formation through an aberrant learning process, the emergence of a negative emotional state, and dysfunctions in behavioral control. Dysfunctions in systems within neurocircuitries that comprise the basal ganglia, the extended amygdala, and the prefrontal cortex result in compulsive eating behaviors. Here, we present evidence to relate compulsive eating behavior and addiction and to characterize their underlying neurobiological mechanisms. A major need to improve understanding of compulsive eating through the integration of complex motivational, emotional, and cognitive constructs is warranted.

Figure 1

Neurobiology of the elements of compulsive overeating. The key systems that underlie the elements of compulsive eating are: (1) the basal ganglia, (2) the extended amygdala, and (3) the prefrontal cortex. The basal ganglia (shown in blue) consist of multiple subcortical nuclei, such as the nucleus accumbens (NAc), which is involved in the rewarding and reinforcing effects of food, and the dorsal striatum, which is involved in instrumental learning and habitual behavior. The basal ganglia contribute to habitual overeating that can arise from maladaptive habit formation processes. The extended amygdala (shown in red) is a basal forebrain composite structure encompassing the central nucleus of the amygdala (CeA), the bed nucleus of the stria terminalis (BNST), and a transition area in the medial and caudal portions of the NAc. The brain stress systems in the extended amygdala mediate overeating to relieve a negative emotional state that emerges from withdrawal processes. Prefronto-cortical regions (shown in green) include the medial prefrontal (mPFC, comprised of dorsolateral (dlPFC) and ventromedial (vmPFC) regions), anterior cingulate (ACC), and orbitofrontal (OFC) cortices; these areas control cognitive functions such as decision-making and response inhibition through interactions with subcortical structures such as the basal ganglia and the extended amygdala. Dysfunctions in the PFC are hypothesized to underlie overeating despite aversive consequences, reflecting failures in inhibitory control over behavior. Figure modified from Koob GF, Arends MA, Le Moal M. Drugs, Addiction, and the Brain. Academic Press, San Diego, 2014. A full color version of this figure is available at the Neuropsychopharmacology journal online.