Department of Psychology, University of Southern California, Los Angeles, California 90089-1061, USA.
Alcohol Clin Exp Res. 2012 Apr;36(4):693-704. doi: 10.1111/j.1530-0277.2011.01630.x. Epub 2011 Sep 6.
A study by Dawson and colleagues (Alcohol Clin Exp Res 2007; 31:69) using data from National Epidemiologic Survey on Alcohol and Related Condition found earlier drinking onset age, and higher levels of past-year stressful life events (SLE) were associated with higher past-year alcohol consumption. The aims of our study were as follows: (i) to attempt to replicate this interaction; (ii) to extend it by examining sex and event dependence as potential moderators of the effect; and (iii) to estimate the roles of genetic and environmental factors in mediating the overlap of early drinking onset and SLE in their relations with alcohol consumption.
Data were from 1,382 female and 2,218 male drinkers interviewed as part of the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders. Regression models were used to evaluate the main and interactive effects of early drinking onset and moderate or severe past-year SLE on past-year drinking density (PYDD), a weighted quantity-frequency measure of alcohol consumption. Analyses adjusted for demographic covariates and were stratified by sex and whether SLE were independent or dependent on the person's actions, as rated by interviewers. Structural twin models were used to estimate the degree to which early drinking onset, SLE, and their interaction accounted for additive genetic, common environmental and individual-specific variance in PYDD.
We replicated the prior finding of a main effect of higher alcohol consumption among individuals reporting earlier drinking onset. Age at drinking onset accounted for about 5% of the variation in PYDD, and this association was mostly attributable to overlapping genetic influences. Evidence for an interaction between onset age and SLE was generally weak, possibly because of lower power and other methodological differences from Dawson and colleagues' study. However, there was some evidence consistent with an interaction of higher PYDD among early drinking men who experienced independent SLE and early drinking women with dependent SLE.
We confirmed prior findings of an association between early age at drinking onset with higher past-year drinking among young- and middle-aged adults and found limited evidence supporting a replication for higher stress-related drinking among early-onset drinkers. The association is consistent with early onset and stress-related drinking being attributable to overlapping genetic liability. Among early drinkers, our results suggest sex differences in consumption with regard to event dependence.
道森等人（Alcohol Clin Exp Res 2007; 31:69）使用来自国家酒精相关状况流行病学调查的数据进行的一项研究发现，饮酒起始年龄较早，以及过去一年中经历较多的压力生活事件（SLE）与过去一年的饮酒量较高有关。我们研究的目的如下：（i）尝试复制这种相互作用；（ii）通过检查性别和事件依赖性作为潜在的调节因素来扩展它；（iii）估计遗传和环境因素在调节早期饮酒开始和 SLE 与其与饮酒的关系重叠中的作用。
数据来自作为弗吉尼亚成人双生子精神和物质使用障碍研究的一部分接受采访的 1382 名女性和 2218 名男性饮酒者。回归模型用于评估早期饮酒开始和中度或重度过去一年 SLE 对过去一年饮酒密度（PYDD）的主要和交互作用，PYDD 是一种衡量饮酒量的加权数量频率测量值。分析调整了人口统计学协变量，并按性别和 SLE 是否独立于或依赖于受访者对个人行为的评估进行分层。结构双胞胎模型用于估计早期饮酒开始、SLE 及其相互作用在 PYDD 的加性遗传、共同环境和个体特异性方差中的程度。
我们复制了先前的发现，即报告较早饮酒开始的个体的饮酒量较高。饮酒起始年龄占 PYDD 变异的约 5%，这种关联主要归因于重叠的遗传影响。起始年龄和 SLE 之间的相互作用的证据通常较弱，这可能是由于与道森等人的研究相比，功率较低和其他方法学差异所致。然而，有一些证据与独立 SLE 经历的早期饮酒男性和依赖 SLE 的早期饮酒女性的较高 PYDD 相互作用一致。
我们证实了先前的发现，即饮酒起始年龄较早与年轻和中年成年人过去一年的饮酒量较高有关，并发现了一些支持早期饮酒者与压力相关的饮酒量较高的复制证据有限。这种关联与早期发病和与压力相关的饮酒归因于重叠的遗传易感性一致。在早期饮酒者中，我们的结果表明与事件依赖性有关的性别差异。
