ADOLESCENT CHILDREN OF ALCOHOLICS--TWIN FAMILY STUDY

这个项目似乎特点的遗传和家庭环境的影响，在发展和过程中的酗酒和共病的精神病理学，重点是在青春期的酒精母亲的后代的结果。采用队列序贯设计，我们将前瞻性地跟踪澳大利亚酗酒母亲和对照母亲及其双胞胎姐妹篇的青少年后代（13-21岁）。拟议的研究建立在澳大利亚双胞胎登记'1981年队列'双胞胎（N=6000）和他们的配偶或合作伙伴（N=3700;最终N=4000）完成的诊断评估。双胞胎家庭研究提供了重要的设计优势：同卵双胞胎共享所有的基因，异卵双胞胎共享一半，这样对酒精中毒发病的遗传贡献就得到了控制。第一个目标是确定是否以及在多大程度上存在虐待、精神病理学、学业成绩、一般心理社会能力以及家庭和其他社会关系，并通过结构化访谈和问卷进行评估。第二，母亲共病精神病理学作为青少年结局的限定词的作用，以及母亲在怀孕期间使用的物质（自我和线人报告）将被检查。第三，将检查和控制父亲酗酒和其他精神病理学（即通过强迫交配增加遗传风险，以及父亲酗酒的环境后果）的贡献。双胞胎家庭设计的全部潜力将被用于测试酗酒风险的三个主要中介模型：越轨社会化，负面情绪调节和药理脆弱性。将对酗酒风险环境传播的强社会学习理论模型进行测试，重点是（i）父母控制不良，异常社会化以及暴露于异常和物质使用同伴（偏差社会化模型），（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）饮酒的增强和应对动机的环境传播，以及相关的酒精预期。这些都将被扩展到模型的相互作用，遗传和环境的影响，在确定不同的差异，酒精风险。

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.