A Longitudinal Examination of Reward, Eating Expectancies, and Inhibitory Control in the Progression of Loss of Control Eating

对进食过程中奖赏、进食期望和抑制控制的纵向研究 失控进食 项目摘要/摘要 暴饮暴食(BE)是暴食症谱系障碍的一种跨诊断症状，与体重有关 体重增加、肥胖、心理社会损害，以及增加患医学合并症的风险。当前的干预措施 BE的疗效有限，这表明需要改进预防和治疗方法， 直接针对BE的发病和维持机制。理论表明，积极的饮食预期 (即，对食物消费强化后果的信念)可能是一个关键机制，与 进食强化史和BE症状的风险。虽然有证据表明，吃东西 期望值是BE的可靠预测因子，有限的工作检验了强化历史的假设 形状吃期望值。此外，有证据表明，奖赏处理和抑制方面的异常 控制可能会增加BE的风险，然而，到目前为止还没有研究检查未来的关系 在这些结构之间建立了一个综合的理论模型，利用多模式进行评估。因此， 目前的申请寻求检查BE症状进展的病因学模型，该模型结合了 在基于期望的框架内观察到奖励处理和抑制控制的异常 在表现出BE症状(即，进食失控，LOC)的个体中，使用纵向 设计。更具体地说，该项目将测试一个缓和的调解模型，该模型假设 在基线水平上强化进食LOC事件(即减少负面影响和增加 通过生态瞬时评估评估的积极影响)将导致预期进食量的增加 在3个月的随访中(即，期望进食减少负面情绪并增加 愉悦/奖励)，这将导致进食LOC的频率增加，并进展为 进行为期6个月的随访。还假设较高的奖励响应性(例如，奖励敏感度， 对直接奖励的偏好)将放大进食强化史和进食之间的关系 预期，而减少抑制控制被假设为放大了进食之间的关系 期待和BE症状。鉴于本项目的重点是确定BE症状的机制 进展，当前项目的结果将有助于确定LOC的延展性维护因素 饮食和BE的危险因素，可作为治疗和预防工作的目标。

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.