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The genetic and environmental association between parental monitoring and risk of cannabis stimulants and cocaine initiation in a sample of male twins: Does parenting matter?

机译:父母监测与男性双胞胎样本中的大麻兴奋剂和可卡因引发风险之间的遗传和环境关联:父母育儿有关系吗?

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摘要

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 comprises 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. Multivariate modeling showed that familial aggregation in parental monitoring and drug initiation 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 amongst the more salient environmental risk factors for illicit drug initiation. 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.
机译:我们的目标是测试大麻,可卡因和兴奋剂表明自我报告父母监护(PM)与非法药物引发(DI)责任之间的因果关系。我们基于男性双胞胎的大量具有遗传学信息的横截面样本,拟合了多指标模型来测试因果模型和非因果模型。该样本包括1778名年龄在24-62岁的男性,来自弗吉尼亚精神病和物质使用障碍双生子研究。数据来自终生大麻,兴奋剂和可卡因起始的自我报告测量,以及对8-17岁之间PM的回顾性评估。多变量建模显示,父母遗传监测和药物起始中的家族聚集都是通过累加的遗传效应和共同的环境效应共同解释的。此外,PM和DI之间的显着关联最好通过相关责任模型与因果模型进行解释。 PM通常被认为是药物使用的环境,因果风险因素,并且已被证明是非法药物启动的重要环境风险因素之一。我们的数据与这种因果假设不一致。取而代之的是一种相关责任模型,其中PM和DI风险分担共同的遗传和环境风险,这使数据更适合。

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