A perspective on candidate neural underpinnings of Binge Eating Disorder: Reward and homeostatic systems

People with Binge Eating Disorder (BED) exhibit heightened sensitivity to rewarding stimuli and elevated activity in reward-related brain regions, including the orbitofrontal cortex (OFC), ventral striatum (VS) and insula, during food-cue exposure. BED has also been associated with altered patterns of functional connectivity during resting-state. Investigating neural connectivity in the absence of task stimuli provides knowledge about baseline communication patterns that may influence the behavioural and cognitive manifestation of BED. Elevated resting-state functional connectivity (rsFC) between reward-related brain regions may contribute to uncontrolled eating bouts observed in BED, through heightened food-cue sensitivity and food-craving. The impact of homeostatic state on rsFC of the reward system has not yet been investigated in people with BED. Homeostatic dysfunction is a key driver of excessive food consumption in obesity, whereby rsFC between rewardrelated brain regions does not attenuate during satiety. Future studies should investigate BED related differences in rsFC within the reward system during hunger and satiety, in order to determine whether individuals with BED display an abnormal neural response to changes in homeostatic state. This knowledge would further enhance current understandings of the mechanisms contributing to BED, potentially implicating both reward and homeostatic dysfunctions as drivers of BED.