Common genetic vulnerability for pathological gambling and alcohol dependence in men

Common genetic vulnerability for pathological gambling and alcohol dependence in men
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DOI:
10.1001/archpsyc.57.7.666
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发表时间:
2000-07-01
影响因子:
--
通讯作者:
Tsuang, M
Tsuang, M
中科院分区:
其他
文献类型:
--
作者:
Slutske, WS;Eisen, S;Tsuang, M

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背景:与酒精依赖(AD)相比,人们对病理性赌博(PG)的原因知之甚少。考虑到PG和AD的高合并率,了解AD的原因可能有助于了解PG的原因。方法:研究对象为越南时代双胞胎登记处的成年男性双胞胎。通过结构化精神病学电话访谈评估PG和AD的终生病史。对PG责任连续性的有效性进行了测试,以确定亚临床PG或问题赌博的原因是否在数量或质量上与DSM-III-R PG障碍的原因不同。遗传模型拟合方法用于量化PG的遗传和环境风险可以用AD风险解释的程度。结果:PG连续性模型的检验均符合亚临床PG和DSM I-III-R PG障碍具有许多甚至全部相同的危险因素的假设,因此在数量上而非质量上存在差异。根据PG的定义,在12%之间;20%的遗传变异和3% - 8%的非共享环境变异是由AD风险引起的。结论:亚临床PG或问题赌博可能是PG的一种较轻的形式,而不是一种病因学上独特的综合征。在亚临床PG和DSM-III-R PG疾病的遗传和环境风险中,AD风险占显著但适度的比例。
Background: In comparison with alcohol dependence (AD), relatively little is known about the causes of pathological gambling (PG). Given the high rate of comorbidity between PG and AD, knowledge about the causes of AD may be applied to understanding those of PG.Methods: Subjects were adult male twin pairs from the Vietnam Era Twin Registry. Lifetime histories of PG and AD were assessed by structured psychiatric telephone interview. The validity of a continuum of PG liability was tested to determine whether the causes of subclinical PG, or problem gambling, are quantitatively or qualitatively distinct from those of DSM-III-R PG disorder. Genetic model-fitting methods were used to quantify the extent to which the genetic and environmental risk for PG could be explained by the risk for AD.Results: Tests of the continuity model of PG were all consistent with the hypothesis that subclinical PG and DSM I-III-R PG disorder have many, perhaps all, of the same risk factors and thus differ quantitatively rather than qualitatively . Depending on the PG definition, between 12%;, and 20% of the genetic variation and between 3% and 8% of the nonshared environmental variation in the risk for PG were accounted for by the risk for AD.Conclusions: Subclinical PG, or problem gambling, may be a milder form of PG, rather than an etiologically distinct syndrome. Risk for AD accounts for a significant but modest proportion of the genetic and environmental risk for subclinical PG and DSM-III-R PG disorder.