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).

大量饮酒是美国可预防死亡的第三大原因，是导致的第二大主要原因 然而，在24-44岁的成年人中的残疾，当前知识中有两个重要差距：1） 不太严重的AUD（例如饮用问题（PD））的机制对2的理解很差，2） PD行为的潜在机制，包括自发（非处理）行为 由简短干预措施（BI）导致的变化和行为改变，这在PD中特别有效。 在这里，我们通过认为PD对酒精提示提高了激励性显着性来解决第一个差距 （反应性）和与社会饮酒者（SD）相比，调节激励显着性（调节）的能力受损。 我们将使用功能性MRI（fMRI）和在实验室中的神经和行为层面测试该假设 自然环境生态瞬时评估（EMA）。我们通过认为 PD的自发行为变化主要取决于反应性过程，而行为 对BI的响应变化主要取决于调节过程。到这些目的，我们将招募100 PDS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 fMRI扫描期间渴望（ROC）任务的酒精调节，然后再完成3周的EMA。这 ROC任务提供了反应性的行为和功能磁共振成像措施（例如，腹侧纹状体活性增加和 提示诱导酒精渴望的报告）调节（例如，与对照相关的前额叶活性并减少 渴望）。分析将测试基线神经和环境度量的群体差异 反应性和调节。接下来，PD将随机分配以立即接收BI或接收BI 6个月后，测量结果后（延迟干预控制或DIC组）。 BI和DIC 分配后的三个星期，小组将完成EMA协议。饮酒结果将是 在3个月和6个月时进行评估。我们希望相对于SD，PDS将显示出更高的神经测量 反应性（例如，在被动观看条件下腹侧纹状体（VS）激活到酒精提示），并且 调节的神经测量降低（例如，调节期间前额叶控制区的活性降低 条件）（目标1）。同时，PDS将报告EMA的反应性水平较高和调节水平较低 与SD相比，措施将与功能磁共振成像措施相关（AIM 2）。我们预测在BI中 群体的减少将通过调节神经系统的功能来减少酒精的使用（例如 背外侧PFC），而在DIC组中，饮酒的持久性将受到功能的主持 反应性神经系统（例如VS）（AIM 3）。最后，我们预测在BI组中，酒精的变化 EMA调节测量的变化将介导使用，并通过 ROC任务中的调节，而在DIC组中，酒精使用的变化将由变化介导 EMA的反应性测量，并通过ROC任务中反应性的预处理测量进行预测（AIM 4）。