Peterson J B, Pihl R O, Gianoulakis C, Conrod P, Finn P R, Stewart S H, LeMarquand D G, Bruce K R
Department of Psychology, Harvard University, Boston, Massachusetts, USA.
Alcohol Clin Exp Res. 1996 Dec;20(9):1542-52. doi: 10.1111/j.1530-0277.1996.tb01697.x.
Susceptibility to alcoholism varies with age, gender, and familial background. Youthful nonalcoholic males with multigenerational family histories of male alcoholism seem at particular risk. Previous investigations suggest that such males are characterized by abnormal psychophysiological response, while sober and alcohol-intoxicated; additional recent studies indicate that the endogenous opiate systems are involved in mediating ethanol reinforcement and modulating intake. We first compared cardiac response to alcohol administration among young (mean = 22.8 years), nonalcoholic men and women with multigenerational, unigenerational, and negative family histories of alcohol dependence and abuse. Then, we compared the ethanol-induced cardiac response of the males in these three groups to that of currently alcohol-dependent older males and age-matched nonalcoholic male controls. Finally, we examined ethanol-induced change in plasma beta-endorphin and cortisol levels among a subset of the nonalcoholic males, divided into those with high and low levels of postethanol administration heart-rate increase. Nonalcoholic males with multigenerational family histories of male alcoholism were characterized by significantly higher [t(301) = 5.70, p < 0.0001, Cohen's d = 0.73] levels of ethanol-induced heart-rate increase than nonalcoholics from all other comparison groups. The magnitude of their increase matched that of current male alcohol-dependents. Nonalcoholic males with high levels of ethanol-induced heart-rate increase also produced significantly more plasma beta-endorphin after consuming alcohol. Peak production of beta-endorphin was highly correlated (r = 0.861, p < 0.001) with magnitude of heart-rate increase. A subset of those at risk for alcoholism may be characterized by sensitivity to ethanol-induced reward, marked by heightened ethanol-induced, heart-rate increase, mediated by ethanol stimulation of endogenous opiate production. This subset might contain those who, once alcoholic, would differentially benefit from treatment with opiate antagonists.
酗酒易感性因年龄、性别和家族背景而异。有男性酗酒多代家族史的年轻非酗酒男性似乎尤其危险。先前的调查表明，这类男性的特点是在清醒和酒精中毒时心理生理反应异常；最近的其他研究表明，内源性阿片系统参与介导乙醇强化作用并调节摄入量。我们首先比较了有酒精依赖和滥用多代、单代及无家族史的年轻（平均年龄22.8岁）非酗酒男性和女性在饮酒后的心脏反应。然后，我们将这三组男性的乙醇诱导心脏反应与目前酒精依赖的老年男性及年龄匹配的非酗酒男性对照组进行比较。最后，我们检查了非酗酒男性亚组中乙醇诱导的血浆β-内啡肽和皮质醇水平变化，该亚组分为乙醇给药后心率增加水平高和低的两组。有男性酗酒多代家族史的非酗酒男性的特点是，乙醇诱导的心率增加水平显著高于所有其他比较组[t(301) = 5.70, p < 0.0001, 科恩d值 = 0.73]。其增加幅度与目前的男性酒精依赖者相当。乙醇诱导心率增加水平高的非酗酒男性在饮酒后产生的血浆β-内啡肽也显著更多。β-内啡肽的峰值产生与心率增加幅度高度相关（r = 0.861, p < 0.001）。一部分酗酒风险人群的特点可能是对乙醇诱导的奖赏敏感，表现为乙醇诱导的心率显著增加，这是由乙醇刺激内源性阿片产生介导的。这部分人群可能包括那些一旦酗酒，使用阿片拮抗剂治疗会有不同程度益处的人。
