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).

在美国，酗酒是可预防死亡的第三大原因，也是第二大原因 然而，在24-44岁的成年人中，目前的知识存在两个重要的缺口：1) 不那么严重的AUD的潜在机制，如问题饮酒(PD)，人们还不太清楚，2) 帕金森病患者行为改变的潜在机制，包括自发(非治疗)行为 由短暂干预(BI)导致的改变和行为改变，这对帕金森病特别有效。 在这里，我们通过假设帕金森病对酒精线索的激励显著增强来解决第一个差距 (反应性)和调节激励性显著的能力受损(调节)，与社交饮酒者(SD)相比。 我们将在实验室中使用功能磁共振成像(FMRI)在神经和行为水平上测试这一假设，并在 自然环境生态瞬时评价(EMA)。我们通过假设第二个缺口来解决 而帕金森病的自发行为改变主要取决于反应性过程，行为 对商业智能的反应变化主要取决于监管过程。为此，我们将招募100名 PDS和50名社交饮酒者(SD)。在基线上，所有参与者将完成为期两周的EMA，执行 在fMRI扫描过程中完成渴望的酒精调节(ROC)任务，然后完成3周以上的EMA。这个 ROC任务提供了反应性的行为和功能磁共振测量(例如，腹侧纹状体活动增加和 线索诱导的酒精渴求)调节的报告(例如，与控制相关的前额叶活动和减弱 渴望)。分析将测试基线神经和环境测量的组差异 反应性和调节性。接下来，将对PD进行随机化，以立即接收BI或接收BI 6个月后，测量结果(延迟干预对照组，或DIC组)。BI和DIC 小组将在作业后的三周内完成EMA方案。饮酒的结果将是 分别在3个月和6个月进行评估。我们预计，相对于SDS，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)对酒精刺激的激活)，以及 减少的神经调节措施(例如，调节期间前额叶控制区的活动减少 条件)(目标1)。同时，PDS将报告EMA中更高水平的反应性和更低水平的监管 测量，与SD相比，这将与fMRI测量相关(目标2)。我们预测，在商业智能中 在这一群体中，酒精使用的减少将受到神经系统调节功能的影响(例如 背外侧PFC)，而在DIC组，持续饮酒将受到功能的影响 神经系统的反应性(例如VS)(目标3)。最后，我们预测在BI组中，酒精的变化 使用将通过EMA监管措施的变化进行调节，并通过以下处理前指数进行预测 在ROC任务中的调节，而在DIC组中，酒精使用的变化将通过 EMA的反应性测量，并通过ROC任务中的反应性的预处理测量进行预测(目标4)。