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.