ADOLESCENT CHILDREN OF ALCOHOLICS--TWIN FAMILY STUDY

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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.