Investigation of Neurobiological Reward Processing
Authors:   , Murray Helen Burton , Juarascio Adrienne S. 
Published: July 2021

Poor inhibition and high food reward sensitivity are linked with binge eating pathology, but few studies have examined whether these variables predict treatment outcome, especially with neuroimaging methods. We examined the relation of pre-treatment neurobiological correlates and neurocognitive measures of food-based reward inhibition to outcomes from a 7-session Cognitive-Behavioral Therapy guided self-help treatment for binge eating. Participants were 13 adults with clinically significant binge eating (69.2% female; body mass index M=34.68, SD=4.15). Pre-treatment, we measured prefrontal cortex (PFC) activation with a wearable neuroimaging tool, functional Near Infrared Spectroscopy, during a behavioral task with blocks of 5-second video clip trials. We created contrast values between two blocks (12 trials each) that instructed participants to either: cognitively "resist" palatable food videos versus "watch" neutral videos. We additionally measured reward inhibition by performance on a food-based stop-signal task (SST). We examined relation of PFC activity and SST performance to: (1) percent change in binge eating frequency pre-treatment to post-treatment; (2) change in Eating Disorder Examination (EDE) global scores pre- to post-treatment; and (3) percent change in binge eating frequency pre-treatment to 3-month follow-up. Due to the small sample, we reported relations of at least medium strength (r [greater than or equal to] .3). Greater activation in left ventromedial prefrontal cortex (region responsible for response inhibition) was significantly related to greater decreases pre- to post-treatment in EDE scores (r = .714, p = .047). Other PFC regions responsible for inhibition (left ventrolateral and bilateral ventromedial) showed similar relations with pre- to post-treatment percent changes in binge eating (r = .358 to .418) and changes in EDE scores (r= .500 to .583), at trend level. Greater reward inhibition performance (SST) also significantly related to greater decreases pre- to post-treatment in EDE scores (r = .764, p = .006) and at trend level, related to greater percent decreases pre- to post-treatment in binge eating (r = .469). However, relations between pre-treatment inhibition (neural correlates and inhibition performance) and pre-treatment to post-treatment binge eating change were not maintained by 3-month follow-up. In fact, greater percent increases pre-treatment to 3-month follow-up in binge eating frequency was associated with greater activation in the left ventromedial PFC (r = .345 to .633) and left superior frontal gyrus (r = .582), but all at trend level. Pre-treatment to 3-month follow-up binge frequency change was not related to other inhibition areas of the PFC or reward inhibition performance (SST). We found that there was variability in participant changes in binge eating from post-treatment to 3-month follow-up, including two participants with large decreases in binge eating during treatment but relapses after treatment. Overall, our results extend previous food-based SST research and preliminarily support that food-based reward inhibition, evidenced by activation in specific inhibitory PFC regions and inhibition performance, may represent an important therapeutic target for binge eating during the course of treatment. Additional research is needed with larger samples, particularly for post-treatment follow-up time points.