ADOLESCENT CHILDREN OF ALCOHOLICS--TWIN FAMILY STUDY

这个项目似乎刻画了在酒精中毒和共病精神病理学的发展和过程中遗传和家庭环境的影响，重点关注酗酒母亲的后代在青春期的结果。采用队列序贯设计，我们将前瞻性地跟踪澳大利亚酗酒者的青少年后代(年龄13-21岁)，并对照母亲及其双胞胎姐妹。这项拟议的研究建立在对澳大利亚双胞胎登记册1981年队列双胞胎(N=6000)及其配偶或伴侣(N=3700；最终N=4000)的完整诊断评估的基础上。双胞胎家族研究提供了重要的设计优势：同卵双胞胎共享所有基因，异卵双胞胎共享一半基因，从而控制了导致酗酒的遗传因素。第一个目标将通过结构化访谈和问卷调查，确定虐待、精神病理学、学业成就、一般心理社会能力以及家庭和其他社会关系是否以及在多大程度上。第二，母体共病的精神病理学作为青春期结局的限定符的作用，以及孕期母体物质的使用(自我和告密者报告)将被审查。第三，将审查和控制父亲酗酒和其他精神病理学的贡献(即通过分类交配增加遗传风险，以及父亲酗酒对环境的影响)。双胞胎家庭设计的全部潜力将被用来测试酒精中毒风险的三个主要中介模型：越轨社会化、负面影响调节和药物脆弱性。酒精中毒风险的环境传递的强有力的社会学习理论模型将被测试，重点是(I)父母控制不良，越轨社会化和暴露在越轨和使用同龄人的物质中(越轨社会化模式)，(Ii)父母缺乏温暖，社会关系受损，创伤事件暴露增加和抑郁风险增加，以及(Iii)增强和应对饮酒动机的环境传递，以及相关的饮酒期望。其中每一个都将被扩展到模型，在确定酒精风险的差异差异时，遗传和环境影响的相互作用。

This project seems to characterize genetic and family environmental influences in the development and course of alcoholism and co-morbid psychopathology, with a focus on outcomes in adolescence of offspring of alcoholic mothers. Using a cohort-sequential design, we will follow prospectively adolescent offspring (aged 13-21) of Australian alcoholic and control mothers and their twin sisters. The proposed study builds upon completed diagnostic assessments of Australian Twin Register '1981 cohort' twins (N=6000) and their spouses or partners (N=3700; final N=4000). Twin family studies afford important design advantages: identical twins share all their genes and fraternal twins share half so that genetic contributions to the onset of alcoholism are controlled. The first aim will determine whether and to what extend the abuse, psychopathology, academic achievement, general psychosocial competence and family and other social relationships, assessed by structured interviews and questionnaires. Second, the role of maternal comorbid psychopathology as a qualifier of adolescent outcomes, as well as maternal substance using during pregnancy (self- and informant report) will be examined. Third, the contributions of paternal alcoholism and other psychopathology (i.e. increased genetic risk through assortive mating, as well as environmental consequences of paternal alcoholism) will be examined and controlled for. The full potential of the twin- family design will be used to test three major mediation models of alcoholism risk: deviant socialization, negative affect regulation, and pharmacological vulnerability. Strong social learning theory models for the environment transmission of alcoholism risk will be tested, focused on (i) poor parental control, deviant socialization and exposure to deviant and substance using peers (deviant socialization model), (ii) parental lack of warmth, impaired social relationships, increased traumatic event exposure and increased risk of depression, and (iii) environmental transmission of enhancement and coping motives for drinking, and associated alcohol expectancies. Each of these will be extended to model the interplay of genetic and environmental influences in determining difference differences in alcohol risk.