Neural and Mobile Assessment of Behavior Change Among Problem Drinkers

对问题饮酒者行为变化的神经和移动评估

• 批准号: 10321942
• 负责人: JON MORGENSTERN
• 金额: $ 52.71万
• 依托单位: COLUMBIA UNIV NEW YORK MORNINGSIDE
• 依托单位国家: 美国
• 财政年份: 2017
• 资助国家: 美国
• 起止时间: 2017-01-06 至 2023-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/10321942
• 关键词: Address; Adult; Alcohol abuse; Alcohol consumption; Alcoholic beverage heavy drinker; Alcohols; Behavior; Behavioral; Brain; Cognitive; Cues; DSM-V; Divorce; Ecological momentary assessment; Environment; Feedback; Functional Magnetic Resonance Imaging; Grant; Heavy Drinking; Impairment; Incentives; Individual Differences; Intervention; Knowledge; Laboratories; Life; Literature; Measures; Mediating; Motivation; Neurophysiology - biologic function; Outcome; Outcome Measure; Participant; Patient Self-Report; Play; Population; Prefrontal Cortex; Process; Protocols documentation; Randomized; Regulation; Reporting; Role; Substance Use Disorder; System; Testing; Thinking; Ventral Striatum; affective neuroscience; aged; alcohol consequences; alcohol craving; alcohol cue; alcohol use disorder; behavior change; brief intervention; cognitive control; cognitive neuroscience; cognitive system; comorbidity; craving; cue reactivity; disability; drinking; drinking behavior; functional MRI scan; group intervention; incentive salience; indexing; motivational processes; neural correlate; neuroimaging; neuromechanism; preventable death; problem drinker; recruit; relating to nervous system; response; smartphone based assessment; social

Heavy drinking is the third leading cause of preventable death in the U.S. and is the second leading cause of disability among adults aged 24-44, however, there are two important gaps in current knowledge: 1) the mechanisms underlying less severe forms of AUD, like problem drinking (PD), are poorly understood, as are 2) the mechanisms underlying behavior change in PD, including both spontaneous (non-treatment) behavior change and behavior change that results from brief interventions (BI), which are particularly effective in PD . Here, we address the first gap by positing that PD have heightened incentive salience to alcohol cues (reactivity) and impaired ability to regulate incentive salience (regulation), compared to social drinkers (SD). We will test this hypothesis at a neural and behavioral level in the lab using functional MRI (fMRI) and in the natural environment ecological momentary assessment (EMA). We address the second gap by positing that whereas spontaneous behavior change in PD depends primarily upon the reactivity processes, behavior change in response to a BI depends primarily upon regulation processes. To these ends, we will recruit 100 PDs and 50 social drinkers (SD). At baseline, all participants will complete two weeks of EMA, perform an alcohol regulation of craving (ROC) task during fMRI scanning, and then complete 3 more weeks of EMA. The ROC task provides behavioral and fMRI measures of reactivity (e.g. increased ventral striatum activity and reports of cue-induced alcohol craving) regulation (e.g. control-related prefrontal activity and diminished craving). The analyses will test for group differences in baseline neural and environmental measures of reactivity and regulation. Next, PDs will be randomized to receive either a BI immediately or to receive the BI after 6 months, after outcomes are measured (the delayed intervention control, or DIC group). Both BI and DIC groups will complete an EMA protocol for the three weeks following assignment. Drinking outcomes will be assessed at 3 and 6 months. We expect that relative to SDs, PDs will show heightened neural measures of reactivity (e.g. elevated ventral striatum (VS) activation to alcohol cues in passive viewing conditions), and reduced neural measures of regulation (e.g. reduced activity in prefrontal control regions during regulation conditions) (Aim 1). In parallel, PDs will report higher levels of reactivity and lower levels of regulation in EMA measures, compared to SD, which will be correlated with fMRI measures (Aim 2). We predict that in the BI group, reduction in alcohol use will be moderated by the functioning of neural systems for regulation (e.g. dorsolateral PFC), whereas in the DIC group a persistence of alcohol use will be moderated by the functioning of neural systems for reactivity (e.g. VS) (Aim 3). Finally, we predict that in the BI group, changes in alcohol use will be mediated by changes in EMA measures of regulation and predicted by pre-treatment indices of regulation in the ROC task, whereas in the DIC group, changes in alcohol use will be mediated by changes in EMA measures of reactivity and predicted by pre-treatment measures of reactivity in the ROC task (Aim 4).

酗酒是美国可预防死亡的第三大原因，也是导致死亡的第二大原因 然而，24-44 岁成年人的残疾，目前的知识存在两个重要差距：1) 不太严重的 AUD 形式（例如酗酒 (PD)）背后的机制尚不清楚，如 2) PD 行为改变的机制，包括自发（非治疗）行为 短暂干预（BI）导致的改变和行为改变，这对帕金森病特别有效。 在这里，我们通过假设 PD 提高了对酒精线索的激励显着性来解决第一个差距 与社交饮酒者（SD）相比，（反应性）和调节激励显着性（调节）的能力受损。 我们将在实验室中使用功能性 MRI (fMRI) 和在实验室中在神经和行为层面上测试这一假设。 自然环境生态瞬时评价（EMA）。我们通过假设来解决第二个差距 而 PD 中的自发行为变化主要取决于反应过程、行为 对 BI 的响应变化主要取决于监管流程。为此，我们将招募100名 PD 和 50 名社交饮酒者 (SD)。在基线时，所有参与者将完成两周的 EMA，执行 在 fMRI 扫描期间进行酒精渴望调节 (ROC) 任务，然后再完成 3 周的 EMA。这 ROC 任务提供反应性的行为和功能磁共振成像测量（例如腹侧纹状体活动增加和 关于提示诱发的酒精渴望的报告）调节（例如与控制相关的前额叶活动和减少） 渴望）。该分析将测试基线神经和环境测量的群体差异 反应性和调节性。接下来，PD 将被随机分配为立即接收 BI 或接收 BI 6 个月后，测量结果后（延迟干预对照组，或 DIC 组）。 BI 和 DIC 小组将在分配后的三周内完成 EMA 协议。饮酒的结果将是 3个月和6个月时进行评估。我们预计，相对于 SD，PD 将表现出更强的神经测量 反应性（例如，在被动观看条件下，腹侧纹状体（VS）对酒精线索的激活升高），以及 调节的神经测量减少（例如，调节期间前额叶控制区域的活动减少 条件）（目标 1）。与此同时，PD 将报告 EMA 中更高水平的反应性和更低水平的监管 与 SD 相比，这将与 fMRI 测量相关（目标 2）。我们预测在 BI 中 组中，酒精使用的减少将通过神经系统的调节功能来调节（例如， 背外侧 PFC），而在 DIC 组中，持续饮酒将受到功能性调节 神经系统的反应性（例如 VS）（目标 3）。最后，我们预测在 BI 组中，酒精含量的变化 使用将通过 EMA 监管措施的变化来调节，并通过预处理指数进行预测 ROC 任务中的调节，而在 DIC 组中，酒精使用的变化将由 EMA 测量反应性并通过 ROC 任务（目标 4）中的预处理反应性测量进行预测。