Olivares Emily L, Kendler Kenneth S, Neale Michael C, Gillespie Nathan A
Virginia Institute for Psychiatric and Behavior Genetics,Virginia Commonwealth University,Richmond,Virginia,USA.
Twin Res Hum Genet. 2016 Aug;19(4):297-305. doi: 10.1017/thg.2016.52.
Our aim was to test the direction of causation between self-report parental monitoring (PM) and the liability to illicit drug initiation (DI) as indicated by cannabis, cocaine, and stimulants. We fitted a multiple indicator model to test causal and non-causal models based on a large, genetically informative cross-sectional sample of male twins. The sample comprised 1,778 males aged 24-62 years from the Virginia Adult Twin Study of Psychiatric and Substance Use Disorders. Data came from self-report measures of lifetime cannabis, stimulants, and cocaine initiation, and retrospective assessment of PM between ages 8-17 years. Multivariate modeling showed that familial aggregation in PM and DI were both explained by a combination of additive genetic and shared environmental effects. Moreover, the significant association between PM and DI was best explained by a correlated liability model versus causal models. PM has typically been assumed to be an environmental, causal risk factor for drug use and has been shown to be among the more salient environmental risk factors for illicit DI. Our data were not consistent with this causal hypothesis. Instead, a correlated liability model in which PM and risk of DI share common genetic and environmental risks provided a better fit to the data.
我们的目的是检验自我报告的父母监督(PM)与大麻、可卡因和兴奋剂所表明的非法药物起始(DI)易感性之间的因果关系方向。我们基于一个大型的、具有遗传信息的男性双胞胎横断面样本,拟合了一个多指标模型来检验因果模型和非因果模型。该样本包括来自弗吉尼亚成人双胞胎精神疾病和物质使用障碍研究的1778名年龄在24至62岁之间的男性。数据来自终生大麻、兴奋剂和可卡因起始的自我报告测量,以及8至17岁之间父母监督的回顾性评估。多变量建模表明,父母监督和非法药物起始中的家族聚集性均由加性遗传效应和共同环境效应共同解释。此外,父母监督与非法药物起始之间的显著关联,用相关易感性模型比因果模型能得到更好的解释。父母监督通常被认为是药物使用的一个环境因果风险因素,并且已被证明是非法药物起始中较为突出的环境风险因素之一。我们的数据与这一因果假设不一致。相反,一个父母监督与非法药物起始风险共享共同遗传和环境风险的相关易感性模型与数据拟合得更好。