Agrawal A, Lynskey M T, Bucholz K K, Martin N G, Madden P A F, Heath A C
Department of Psychiatry, Washington University School of Medicine, St Louis, MO 63110, USA.
Psychol Med. 2007 Jan;37(1):49-60. doi: 10.1017/S0033291706009287. Epub 2006 Nov 1.
The use of cannabis and other illicit drugs (OIDs) and their co-morbid misuse are frequently reported in the literature. Correlated vulnerabilities and causal or gateway influences have been implicated in this association. We investigated the source of this co-morbidity between cannabis use (experimentation, early and repeated use, and problems) and OID experimentation and problems using genetic models proposed by Neale and Kendler (American Journal of Human Genetics 1995, 57, 935-953).
In a sample of 4152 same-sex male and female adult Australian twin individuals, we fit 13 genetically informative models of co-morbidity to data on experimentation, early use, repeated use of cannabis and co-morbid OID experimentation, and to abuse/dependence (A/D) problems with cannabis and OIDs.
Model-fitting results suggest that common genetic, shared and unique environmental factors are responsible for the association between cannabis experimentation, early use, repeated use and A/D problems and OID experimentation or problems. The liability causation model, which is a reduced form of the correlated vulnerabilities model, also fit very well. In women, we found evidence for high-risk cannabis experimenters and repeated users to be at increased risk for OID experimentation, despite being below the risk threshold on the liability distribution for OID experimentation (extreme multiformity).
Co-morbid cannabis and OID use and misuse are due partly to a common predisposition to substance use disorders. Putative causal effects could not be ruled out. These models warrant further research, so that features of the correlated vulnerabilities model and the gateway models can be studied jointly in a single series of adaptive nested models.
大麻及其他非法药物（OIDs）的使用及其共病性滥用在文献中屡有报道。这种关联涉及相关的易感性以及因果或通路影响。我们使用尼尔和肯德勒提出的遗传模型（《美国人类遗传学杂志》1995年，第57卷，第935 - 953页），研究了大麻使用（尝试、早期及反复使用以及问题）与OID尝试及问题之间这种共病现象的根源。
在4152名澳大利亚成年同性双胞胎个体的样本中，我们将13个共病性的遗传信息模型应用于关于大麻尝试、早期使用、反复使用以及共病性OID尝试的数据，以及大麻和OIDs的滥用/依赖（A/D）问题的数据。
模型拟合结果表明，共同的遗传因素、共享和独特的环境因素导致了大麻尝试、早期使用、反复使用及A/D问题与OID尝试或问题之间的关联。责任因果模型作为相关易感性模型的简化形式，拟合效果也很好。在女性中，我们发现证据表明，尽管高风险大麻尝试者和反复使用者在OID尝试的责任分布上低于风险阈值（极端多态性），但他们进行OID尝试的风险有所增加。
大麻和OID的共病性使用及滥用部分归因于对物质使用障碍的共同易感性。不能排除假定的因果效应。这些模型值得进一步研究，以便在一系列单一的适应性嵌套模型中联合研究相关易感性模型和通路模型的特征。
