Adolescent alcohol expectancies in offspring from families at high risk for developing alcoholism.

OBJECTIVE: The present study investigated alcohol expectancies derived from the Alcohol Expectancy Questionnaire (AEQ) in parents and their adolescent offspring. It was of interest to determine whether alcohol expectancies would differ by risk status, and whether those differences were influenced by parental beliefs. METHOD: Children/ adolescents aged 8 to 18, from families at high risk for developing alcoholism (n = 69; 37 males) and from low-risk control families (n = 46; 25 males), were evaluated annually. At every assessment, each child and one parent were administered the AEQ and interviewed to determine drinking status. Data for two time points approximately 3 years apart were analyzed. RESULTS: In early adolescence, high-risk offspring expected more improvement in social functioning when under the influence of alcohol than did low-risk controls. However, by age 16, risk group differences were not seen. Higher scores on two of the AEQ scales (Social Behavior and Relaxation) predicted the age of onset for regular drinking, whereas one scale (Social Behavior) predicted drinking behavior. In addition, high-risk offspring were found to have beliefs about the effects of alcohol that were similar to those of their parents, in contrast to low-risk offspring and their parents, who displayed significant negative correlations. CONCLUSIONS: This report confirms previous studies relating alcohol expectancies to drinking behavior (frequency, quantity per occasion, social consequences). Alcohol expectancies also were found to predict the age of onset to begin regular drinking in the combined group of adolescents studied, although risk differences in age of onset were not influenced by differing expectations concerning the effects of alcohol. These results suggest that the risk differences in expectancies that were seen in young adolescents (approximately age 13) may be due to the transmission of parental beliefs to their offspring. The absence of risk differences by late adolescence (approximately age 16) suggests that other factors (e.g., peer influences or experience drinking alcohol) also play a role.

Maternal smoking and drinking during pregnancy and the risk for child and adolescent psychiatric disorders.

OBJECTIVE: To examine the relative importance of prenatal exposure to cigarettes and alcohol and familial/genetic susceptibility for alcohol dependence in the etiology of childhood psychopathology. METHOD: A longitudinal prospective study of 150 children/adolescents (51.3% male), who were at either high or low risk for developing alcohol dependence because of their familial loading for alcoholism, provided multiple diagnostic assessments (N = 318) of these subjects. High-risk families were identified through the presence of two adult alcoholic sisters; low-risk control families were selected from the community. Annual assessments of offspring from these families included an in-depth psychiatric interview of each child and his/her parent to determine the presence or absence of childhood disorders. Mothers were interviewed concerning their prenatal use of substances, and information was gathered concerning their personal and familial loading for psychiatric disorders. RESULTS: Using conventional logistic regression analyses, internalizing and externalizing disorders were found to be associated with familial loading for alcoholism and prenatal exposure to cigarettes and alcohol. In addition, a specialized statistical analysis, a multivariate confounder score approach, was conducted using familial risk status and the child's exposure to maternal prenatal use of alcohol and cigarettes. This analysis demonstrated that only one relationship between a single variable and a childhood disorder was significant while controlling for the other two variables: Oppositional disorder remained significant in association with familial risk status. Three additional analyses were performed to evaluate the effects of familial risk status, prenatal alcohol exposure and prenatal cigarette exposure on childhood psychopathology while controlling for two known risk factors (SES and parental ASPD) for externalizing disorders. Results of these analyses revealed that the only childhood disorder that was elevated was ADHD, and that this was the result of the familial risk variable only. CONCLUSIONS: Familial loading for alcohol dependence is an important risk factor for the development of childhood psychopathology and may account for the previously reported associations between prenatal exposure to nicotine and alcohol. Studies of substance abuse/dependence etiology and childhood psychopathology need to include consideration of both prenatal exposures and familial loading for alcohol dependence and other psychiatric disorders.