A longitudinal examination of reward, eating expectancies, and inhibitory control in the progression of loss of control eating PROJECT SUMMARY/ABSTRACT Binge eating (BE) is a transdiagnostic symptom of bulimic spectrum disorders, and is associated with weight gain, obesity, psychosocial impairment, and increased risk for medical comorbidity. Current interventions for BE are limited in their efficacy, suggesting the need for improved prevention and treatment approaches which directly target mechanisms of BE onset and maintenance. Theory suggests that positive eating expectancies (i.e., beliefs about the reinforcing consequences of food consumption) may be a key mechanism relating a history of reinforcement from eating and risk for BE symptoms. While evidence indicates that eating expectancies are a robust predictor of BE, limited work has examined the hypothesis that reinforcement history shapes eating expectancies. Further, evidence suggests that abnormalities in reward processing and inhibitory control may compound risk for BE, however, no study to date has examined the prospective relationships between these constructs within a comprehensive theoretical model using multi-modal assessment. Therefore, the current application seeks to examine an etiological model of BE symptom progression, which incorporates observed abnormalities in reward processing and inhibitory control within an expectancy-based framework among individuals demonstrating symptoms of BE (i.e., loss of control eating, LOC) using a longitudinal design. More specifically, the project will test a moderated mediation model hypothesizing that greater reinforcement from LOC eating episodes at baseline (i.e., reductions in negative affect and increases in positive affect as assessed by ecological momentary assessment) will lead to increases in eating expectancies at 3-month follow-up (i.e., expectancies that eating reduces negative emotions and increases feelings of pleasantness/reward), which will subsequently lead to increased frequency of LOC eating and progression to BE at 6-month follow-up. It is further hypothesized that higher reward responsiveness (e.g., reward sensitivity, preference for immediate rewards) will amplify the relationship between eating reinforcement history and eating expectancies, while decreased inhibitory control is hypothesized to amplify the relationship between eating expectancies and BE symptoms. Given this project’s focus on identifying mechanisms of BE symptom progression, findings from the current project would help to identify malleable maintenance factors for LOC eating and risk factors for BE, which could be targeted in treatment and prevention efforts.