Cognitive Brain Research Unit, Institute of Behavioural Sciences, University of Helsinki, Helsinki, Finland.
Alcohol Clin Exp Res. 2011 Jul;35(7):1339-50. doi: 10.1111/j.1530-0277.2011.01470.x. Epub 2011 Apr 4.
Long-term functional brain effects of adolescent alcohol abuse remain uncertain, partially because of difficulties in distinguishing inherited deficits from neuronal effects of ethanol and by confounds associated with alcohol abuse, especially nicotine exposure. We conducted a longitudinal twin study to determine neurocognitive effects of adolescent alcohol abuse, as measured with the auditory event-related potential (ERP) component P3, a putative marker of genetic vulnerability to alcoholism.
Twin pairs (N=177; 150 selected for intrapair concordance/discordance for alcohol-related problems at age 18½) were recruited from ongoing studies of twins born 1975-1979 in Finland. Alcohol and tobacco use were assessed with questionnaires at ages 16, 17, 18½, and ~25, and by a structured psychiatric interview concurrent with the ERP testing at mean age 25.8. During ERP recordings, subjects were instructed to detect target tones within a train of frequent "standards" and to ignore occasional "novel" sounds. To distinguish familial factors from ethanol effects, ERP and self-reported alcohol use measures were incorporated into hierarchical multiple regression (HMR) analysis, and intrapair differences in ERP were associated with intra-pair differences in alcohol variables.
Novel-sound P3 amplitude correlated negatively with self-reported alcohol use in both between- and within-family analyses. No similar effect was observed for target-tone P3. HMR results suggest that twins' similarity for novel-sound P3 amplitude is modulated by their alcohol use, and this effect of alcohol use is influenced by genetic factors.
Our results, from a large sample of twins selected from a population-based registry for pairwise concordance/discordance for alcohol problems at 18½, demonstrate that adolescent alcohol abuse is associated with subtle neurophysiological changes in attention and orienting. The changes are reflected in decreased novel-sound P3 amplitude and may be modified by genetic factors.
青少年酗酒对大脑的长期功能影响仍不确定，部分原因是难以区分遗传缺陷与乙醇对神经元的影响，以及与酗酒相关的混杂因素，尤其是尼古丁暴露。我们进行了一项纵向双胞胎研究，以确定青少年酗酒的神经认知效应，方法是测量听觉事件相关电位（ERP）成分 P3，这是一种对酒精中毒遗传易感性的假定标志物。
双胞胎对（N=177；150 对根据 18 岁半时与酒精相关问题的同卵对/异卵对的一致性/不一致性选择）从芬兰 1975-1979 年出生的双胞胎的正在进行的研究中招募。酒精和烟草使用情况在 16、17、18 岁半和~25 岁时通过问卷进行评估，并在平均年龄 25.8 岁时通过与 ERP 测试同时进行的结构化精神病学访谈进行评估。在 ERP 记录期间，要求受试者在一系列频繁的“标准”音中检测目标音，并忽略偶尔出现的“新颖”声音。为了将家族因素与乙醇效应区分开来，将 ERP 和自我报告的酒精使用量纳入分层多重回归（HMR）分析中，并将 ERP 中的个体内差异与个体内的酒精变量差异相关联。
新颖声音 P3 幅度与自我报告的酒精使用量在双生子和家族内分析中呈负相关。对于目标音 P3 则没有观察到类似的效果。HMR 结果表明，双胞胎对新颖声音 P3 幅度的相似性受到他们的酒精使用的调节，而这种酒精使用的影响受到遗传因素的影响。
我们从一个基于人群的登记处选择的大样本双胞胎中得出的结果，这些双胞胎在 18 岁半时对酒精问题进行了成对的一致性/不一致性选择，证明青少年酗酒与注意力和定向的神经生理变化有关。这些变化反映在新颖声音 P3 幅度降低上，并且可能受到遗传因素的影响。
