Decision making deficits in relation to food cues influence obesity: A triadic neural model of problematic eating

In this review article we propose a model of the brain systems, the deficiency of which may underlie problematic eating. This integrative model is based on studies that have focused on discrete brain components involved in problematic eating, combined with insights from studies on the neurocognitive basis of other addictive and problematic behaviors. The model includes: (a) a hyper-functioning reward anticipation and processing system (amygdala-striatum dependent) in response to food-related cues; (b) a hypo-functioning reflective and inhibitory control system (prefrontal cortex dependent), that fails to anticipate and properly weigh future outcomes; and (c) an altered interoceptive awareness system (insular cortex dependent) that translates homeostatic violation signals into a strong consumption desire that hijacks the inhibitory system and excites the reward system. We posit that when the abovementioned systems are imbalanced in such a way that the dopamine axis is hyperactive in relation to food cues and the inhibitory system is weak, and this is further aggravated by an altered interoceptive awareness system, people may experience loss of control or inability to resist tempting/rewarding foods. This loss of control over food consumption can explain, at least in part, the development of excess weight and contribute to the obesity epidemic.