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通过共病症状和同伴犯罪行为,从内化和外化症状到青少年饮酒和酒精使用障碍的替代级联测试。

Testing alternative cascades from internalizing and externalizing symptoms to adolescent alcohol use and alcohol use disorder through co-occurring symptoms and peer delinquency.

机构信息

Department of Psychology, University of New Orleans, New Orleans, LA, USA.

Department of Psychology, University at Buffalo, The State University of New York, Buffalo, NY, USA.

出版信息

Dev Psychopathol. 2021 Feb;33(1):29-46. doi: 10.1017/S0954579419001512.

Abstract

Given the equivocal literature on the relationship between internalizing symptoms and early adolescent alcohol use (AU) and AU disorder (AUD), the present study took a developmental perspective to understand how internalizing and externalizing symptoms may operate together in the etiology of AU and AUD. We pit the delayed onset and rapid escalation hypothesis (Hussong et al., 2011) against a synthesis of the dual failure model and the stable co-occurring hypothesis (Capaldi, 1992; Colder et al., 2013, 2018) to test competing developmental pathways to adolescent AU and AUD involving problem behavior, peer delinquency, and early initiation of AU. A latent transactional and mediational framework was used to test pathways to AUD spanning developmental periods before AU initiation (Mage = 11) to early and high risk for AUD (Mage = 14-15 and Mage = 17-18). The results supported three pathways to AUD. The first started with "pure" externalizing symptoms in early childhood and involved multiple mediators, including the subsequent development of co-occurring symptoms and peer delinquency. The second pathway involved stable co-occurring symptoms. Interestingly, chronically elevated pure internalizing symptoms did not figure prominently in pathways to AUD. Selection and socialization effects between early AU and peer delinquency constituted a third pathway.

摘要

鉴于关于内化症状与青少年早期饮酒(AU)和 AU 障碍(AUD)之间关系的文献存在矛盾,本研究从发展的角度理解内化和外化症状如何共同作用于 AU 和 AUD 的病因。我们对延迟发作和快速升级假说(Hussong 等人,2011 年)与双重失效模型和稳定共存假说的综合(Capaldi,1992 年;Colder 等人,2013 年,2018 年)进行了比较,以检验涉及行为问题、同伴犯罪和 AU 早期开始的青少年 AU 和 AUD 的竞争发展途径。使用潜在的交易和中介框架来检验 AUD 的途径,这些途径跨越了 AU 开始前的发育阶段(Mage = 11)到 AUD 的早期和高风险阶段(Mage = 14-15 和 Mage = 17-18)。结果支持了 AUD 的三种途径。第一种途径始于幼儿期的“纯”外化症状,并涉及多个中介因素,包括随后出现的共病症状和同伴犯罪。第二种途径涉及稳定的共存症状。有趣的是,慢性升高的纯内化症状在 AUD 途径中并不突出。早期 AU 和同伴犯罪之间的选择和社会化效应构成了第三种途径。

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