ADOLESCENT CHILDREN OF ALCOHOLICS--TWIN FAMILY STUDY

该项目似乎描述了遗传和家庭环境对酗酒和共病精神病理的发展和过程的影响，重点关注酗酒母亲的后代在青春期的后果。采用队列序列设计，我们将对澳大利亚酗酒母亲和对照母亲及其双胞胎姐妹的青少年后代（13-21岁）进行前瞻性随访。拟议的研究建立在对澳大利亚双胞胎登记处1981年队列双胞胎（N=6000）及其配偶或伴侣（N=3700；最终N=4000）完成的诊断评估的基础上。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基因，异卵双胞胎共享一半基因，这样遗传对酗酒的影响就得到了控制。第一个目标是通过结构化访谈和调查问卷来确定虐待是否和扩大到何种程度、精神病理、学业成就、一般社会心理能力以及家庭和其他社会关系。其次，将检查母亲共病精神病理学作为青少年结局的限定条件的作用，以及怀孕期间母亲物质使用（自我和线人报告）。第三，父亲酗酒和其他精神病理（即通过选择性交配增加的遗传风险，以及父亲酗酒的环境后果）的贡献将被检查和控制。双胞胎家庭设计的全部潜力将用于测试酒精中毒风险的三种主要中介模型：异常社会化，负面影响调节和药理学脆弱性。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，异常社会化和接触异常和使用物质的同伴（异常社会化模型），（ii）父母缺乏温暖，社会关系受损，创伤性事件暴露增加和抑郁风险增加，以及（iii）饮酒增强和应对动机的环境传播，以及相关的酒精预期。每一项研究都将扩展到遗传和环境影响的相互作用模型，以确定酒精风险的差异。

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.