Vaillant G E
Harvard Medical School, Boston, MA.
Addiction. 1994 Sep;89(9):1049-57; discussion 1059-70. doi: 10.1111/j.1360-0443.1994.tb02776.x.
Studies supporting Cloninger's original Type 1/Type 2 hypothesis for classifying the genetic transmission of alcoholism have sometimes failed to control for important sources of potential bias. First, the environmental effects of parental alcoholism must be distinguished from the genetic effects of parental alcoholism. Secondly, antisocial personality disorder must be distinguished from alcohol dependence. Thirdly, to control for developmental effects a cohort of alcoholics should be followed into late mid-life. The present report, a 50-year prospective study of the development of alcoholism in two community samples of 456 disadvantaged youth and 204 Harvard graduates, addresses these three potential sources of bias. In this report the age of onset of alcoholism and the degree of antisocial symptomatology was correlated with disturbed family environment but was quite independent of the presence or absence of a heredity positive for alcoholism. The reasons why such findings threaten the validity of the Type 1/Type 2 hypothesis are discussed.
支持克洛宁格最初用于对酒精中毒遗传传递进行分类的1型/2型假说的研究有时未能控制潜在偏差的重要来源。首先，必须将父母酗酒的环境影响与父母酗酒的遗传影响区分开来。其次，必须将反社会人格障碍与酒精依赖区分开来。第三，为了控制发育影响，应该对一组酗酒者追踪到中年后期。本报告是一项对456名弱势青年和204名哈佛毕业生的两个社区样本中酒精中毒发展情况进行的50年前瞻性研究，探讨了这三个潜在的偏差来源。在本报告中，酒精中毒的发病年龄和反社会症状的程度与家庭环境紊乱相关，但与酗酒遗传阳性的有无相当独立。文中讨论了这些发现威胁1型/2型假说有效性的原因。
