Characterizing Low Alcohol Sensitivity in Laboratory and Real-World Contexts

对酒精急性效应的敏感性不同，特别是镇静样效应降低， 刺激样效应（这里简化为“低敏感性”; LS）是已知的酒精的潜在风险因素 滥用、依赖和饮酒相关的不良后果。然而，目前相对较少 关于LS促进问题饮酒的具体心理机制，我们已经知道。 本文提出的研究旨在验证一个新的翻译假设， 成瘾的敏化理论，将LS与特定的心理和神经生物学过程联系起来， 促进对酒精的渴望和动机，并促进大量饮酒。该研究将使用一个 结合实验室为基础的措施，以衡量注意，动机，和激励价值的酒精- 相关线索（酒精线索反应性; ACR）和“现实世界”的生态瞬时评估（EMA） 饮酒及相关经历参与者将是从美国加州大学洛杉矶分校招募的年轻饮酒者（18-20岁）。 社区，允许调查一个新的，理论驱动的模型的风险，有问题的饮酒期间， 酒精参与的关键发育期（成年期）。利用各种招聘 渠道，我们将筛选潜在的参与者，以获得有关他们的酒精敏感性水平的信息（如 使用经验证的问卷调查确定）和饮酒模式。420名新生儿（70 三个灵敏度Terciles中的每一个中的70名男性和女性）将被邀请参加实验室会议 在此期间，将使用四个任务来评估ACR：（1）视觉点探针检测任务，评估 （2）酒精接近-回避任务评估内隐注意力; 酒精提示诱发的P3事件相关电位的幅值， 评估酒精的激励价值;（4）嗅觉线索暴露任务，测量自我报告的渴望 因为酒精在该实验室课程之后，参与者将开始为期21天的EMA期，在此期间，他们将 使用智能手机应用程序记录酒精提示暴露，酒精渴望，饮酒行为和不良反应。 在自然环境中饮酒的后果。参与者将完成在线跟踪调查 实验室会议后一年。这项研究将使我们能够（a）描述个体差异如何 在酒精敏感性与神经行为和自我报告措施激励敏感化过程; (b)研究LS如何与饮酒行为、ACR、渴望和年轻饮酒者的自然问题有关。 环境;以及（c）评估酒精敏感性，实验室内表型， 经过生态评估的饮酒经历和有问题的饮酒结果。这种方法将产生一个 独特而丰富的数据集，从中发现的结果将有助于填补有关病因学的现有知识的关键空白。 澳元的LS相关风险。

Differential sensitivity to the acute effects of alcohol, particularly reduced sedation-like effects and enhanced stimulation-like effects (here simplified as “low sensitivity;” LS), is known to be a potent risk factor for alcohol abuse, dependence, and drinking-contingent adverse consequences. However, at present relatively little is known concerning the specific psychological mechanisms through which LS promotes problematic drinking. The research proposed here is aimed at testing a novel translational hypothesis, based in the incentive sensitization theory of addiction, linking LS with specific psychological and neurobiological processes that both promote craving and motivation for alcohol and facilitate heavy drinking. The proposed research will use a combination of laboratory-based measures to gauge attention to, motivation for, and incentive value of alcohol- related cues (alcohol cue-reactivity; ACR) and ecological momentary assessments (EMA) of ‘real-world’ drinking and related experiences. Participants will be young drinkers (ages 18-20 years) recruited from the community, permitting investigation of a novel, theory-driven model of risk for problematic drinking during a critical developmental period for alcohol involvement (emerging adulthood). Using a variety of recruitment channels, we will screen potential participants to obtain information about their level of alcohol sensitivity (as determined using validated questionnaires) and drinking patterns. A target sample of 420 emerging adults (70 males and 70 females in each of three sensitivity terciles) will be invited to participate in a laboratory session during which four tasks will be used to evaluate ACR: (1) a visual dot-probe detection task assessing involuntary capture of attention by alcohol cues; (2) an alcohol approach-avoidance task evaluating implicit approach bias elicited by alcohol cues; (3) amplitude of the P3 event-related potential elicited by alcohol cues, assessing incentive value for alcohol; and (4) an olfactory cue exposure task measuring self-reported craving for alcohol. Following this laboratory session, participants will begin a 21-day EMA period during which they will use a smartphone app to record alcohol cue exposure, alcohol craving, drinking behaviors, and adverse consequences of drinking in their natural environments. Participants will complete an online follow-up survey one year after the laboratory session. The research will permit us to (a) characterize how individual differences in alcohol sensitivity relate to neurobehavioral and self-report measures of incentive sensitization processes; (b) investigate how LS relates to drinking behavior, ACR, craving, and problems in young drinkers' natural environments; and (c) evaluate empirical associations among alcohol sensitivity, laboratory endophenotypes, ecologically assessed drinking experiences, and problematic drinking outcomes. This approach will produce a unique and rich dataset, findings from which will help fill critical gaps in extant knowledge about the etiology of LS-related risk for AUD.