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模拟男性双胞胎中同伴群体偏差行为与大麻使用之间的遗传和环境关联。

Modeling the genetic and environmental association between peer group deviance and cannabis use in male twins.

作者信息

Gillespie Nathan A, Neale Michael C, Jacobson Kristen, Kendler Kenneth S

机构信息

Department of Psychiatry, Virginia Commonwealth University, Richmond, VA 23219-1534, USA.

出版信息

Addiction. 2009 Mar;104(3):420-9. doi: 10.1111/j.1360-0443.2008.02457.x.

Abstract

BACKGROUND

Peer group deviance (PGD) is linked strongly to liability to drug use, including cannabis. Our aim was to model the genetic and environmental association, including direction of causation, between PGD and cannabis use (CU).

METHOD

Results were based on 1736 to 1765 adult males from the Mid-Atlantic Twin Registry with complete CU and PGD data measured retrospectively at three time-intervals between 15 and 25 years using a life-history calendar.

RESULTS

At all ages, multivariate modeling showed that familial aggregation in PGD was explained by a combination of additive genetic and shared environmental effects. Moreover, the significant PGD-CU association was best explained by a CU-->PGD causal model in which large portions of the additive genetic (50-78%) and shared environmental variance (25-73%) in PGD were explained by CU.

CONCLUSIONS

Until recently PGD was assumed to be an environmental, upstream risk factor for CU. Our data are not consistent with this hypothesis. Rather, they suggest that the liability to affiliate with deviant peers is explained more clearly by a combination of genetic and environmental factors that are indexed by CU which sits as a 'risk indicator' in the causal pathway between genetic and environmental risks and the expression of PGD. This is consistent with a process of social selection by which the genetic and environmental risks in CU largely drive the propensity to affiliate with deviant peers.

摘要

背景

同伴群体偏差(PGD)与包括大麻在内的药物使用易感性密切相关。我们的目的是建立PGD与大麻使用(CU)之间的遗传和环境关联模型,包括因果关系方向。

方法

结果基于来自大西洋中部双胞胎登记处的1736至1765名成年男性,他们使用生活史日历在15至25岁之间的三个时间间隔进行回顾性测量,拥有完整的CU和PGD数据。

结果

在所有年龄段,多变量模型显示PGD中的家族聚集是由加性遗传和共享环境效应共同解释的。此外,显著的PGD-CU关联最好由CU→PGD因果模型解释,其中PGD中很大一部分加性遗传方差(50 - 78%)和共享环境方差(25 - 73%)由CU解释。

结论

直到最近,PGD一直被认为是CU的环境上游风险因素。我们的数据与这一假设不一致。相反,它们表明与偏差同伴交往的易感性更清楚地由遗传和环境因素共同解释,这些因素由CU作为指标,CU在遗传和环境风险与PGD表达之间的因果途径中作为“风险指标”。这与一种社会选择过程一致,即CU中的遗传和环境风险在很大程度上驱动了与偏差同伴交往的倾向。

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