Department of Psychiatry and Behavioral Sciences, University of Minnesota, USA.
VACT West Haven/Yale School of Medicine, USA.
Neuropsychologia. 2021 Oct 15;161:108009. doi: 10.1016/j.neuropsychologia.2021.108009. Epub 2021 Aug 26.
Negative Urgency (NU) is a prominent risk factor for hazardous alcohol use. While research has helped elucidate how NU relates to neurobiological functioning with respect to alcohol use, no known work has contextualized such functioning within existing neurobiological theories in addiction. Therefore, we elucidated mechanisms contributing to the NU-hazardous alcohol use relationship by combining NU theories with neurobiological dual models of addiction, which posit addiction is related to cognitive control and reinforcement processing. Fifty-five undergraduates self-reported NU and hazardous alcohol use. We recorded EEG while participants performed a reinforced flanker task. We measured cognitive control using N2 activation time-locked to the incongruent flanker stimulus, and we measured reinforcement processing using the feedback-related negativity (FRN) time-locked to better-than-expected negative reinforcement feedback. We modeled hazardous drinking using hierarchical regression, with NU, N2, and FRN plus their interactions as predictors. The regression model significantly predicted hazardous alcohol use, and the three-way interaction (NU × N2 × FRN) significantly improved model fit. In the context of inefficient processing (i.e., larger N2s and FRNs), NU demonstrated a strong relationship with hazardous alcohol use. In the context of efficient processing (i.e., smaller N2s and FRNs), NU was unrelated to hazardous alcohol use. Control analyses ruled out the potential impact of other impulsivity subscales, individual differences in dimensional negative affect or anxiety, and use of substances other than alcohol, and post hoc specificity analyses showed that this effect was driven primarily by heavy drinking, rather than frequency of drinking. This analysis provides preliminary evidence that brain mechanisms of cognitive control and reinforcement processing influence the relationship between NU and hazardous alcohol use, and confirms a specific influence of negative reinforcement processing. Future clinical research could leverage these neurobiological moderators for substance misuse treatment.
消极紧迫感 (NU) 是危险饮酒的一个突出风险因素。虽然研究已经帮助阐明了 NU 与酒精使用的神经生物学功能之间的关系,但目前尚无研究将这种功能置于成瘾的现有神经生物学理论中。因此,我们通过将 NU 理论与成瘾的神经生物学双重模型相结合,阐明了导致 NU-危险饮酒关系的机制,该模型假设成瘾与认知控制和强化处理有关。55 名本科生自我报告了 NU 和危险饮酒情况。我们在参与者执行强化侧抑制任务时记录了 EEG。我们使用与不一致侧抑制刺激定时的 N2 激活来衡量认知控制,使用与好于预期的负强化反馈定时的反馈相关负波 (FRN) 来衡量强化处理。我们使用分层回归来对危险饮酒进行建模,将 NU、N2 和 FRN 及其相互作用作为预测因子。回归模型显著预测了危险饮酒,并且 NU×N2×FRN 三向交互作用显著改善了模型拟合度。在处理效率低下的情况下(即更大的 N2 和 FRN),NU 与危险饮酒之间存在很强的关系。在处理效率高的情况下(即更小的 N2 和 FRN),NU 与危险饮酒无关。控制分析排除了其他冲动性分量表、维度负性情绪或焦虑的个体差异以及除酒精以外的物质使用的潜在影响,事后特异性分析表明,这种影响主要是由大量饮酒而不是饮酒频率驱动的。这项分析提供了初步证据,表明认知控制和强化处理的大脑机制影响了 NU 与危险饮酒之间的关系,并证实了负强化处理的特定影响。未来的临床研究可以利用这些神经生物学调节剂来治疗物质滥用。