Underage drinking is a major public health concern, showing disproportionately harmful effects on African Americans. Despite the fact that African-American youth exhibit higher rates of abstinence and lower rates of binge drinking, African-American drinkers experience more negative consequences from drinking such as more negative family and interpersonal problems, legal problems, alcohol-related injuries and diseases, and alcohol dependence symptoms. In addition, once developed, alcohol problems are more likely to persist in African American drinkers than in other racial groups. To reduce these troubling alcohol-related health disparities, it is essential to better understand the risk pathways involved in escalations of alcohol use and negative drinking consequences (e.g., academic failure, involvement with the criminal justice system, substance use, and risky sexual behaviors) among African Americans. Mid-adolescence is the optimal period to observe escalations of alcohol use and negative drinking consequences and their risk processes, because alcohol initiation peaks at ages 12/13 and alcohol use disorders peaks at age 18. In the dynamic interactionism perspective, individuals develop through the ongoing reciprocal interplay with their social environment. Although a wide range of individual and social environmental risk factors have been identified, it is unknown how these factors reciprocally affect each other and shape changes in alcohol use and negative drinking consequences among African-American youth over time. Using a genetically-informed 2-wave longitudinal study design, this proposed research aims to model two pathways (i.e., self-selection and gene- environment interaction), by which individual factors interplay with social environmental factors and affect increases in alcohol use and consequences among urban African American youth. First, individual factors (e.g., prior drinking, impulsivity, intention to drink, and the DRD4 rs1800955) that determine the extent to which youth select into high-risk environments (e.g., heavy-drinking peers, and easy alcohol accessibility) will be identified. Second, the extent to which genotypes (the 5-HTTLPR, the DRD4 VNTR, the DRD4 rs1800955, and the ADH1B*3) modulate environmental influences on changes in alcohol use and consequences over time will be tested. The two processes of self-selection and gene-environment interactions will elucidate critical pathways by which alcohol use and consequences are exacerbated over time. The enhanced knowledge about the risk pathways among African American youth will improve public health by informing the development of ethnically and developmentally sensitive prevention and intervention strategies designed to reduce health disparities related to alcohol among African American youth.
This study aims to identify individual and social environmental risk factors for alcohol use and consequences among Black/African American youth. Results from this study will inform ethnically-sensitive prevention and treatment strategies to reduce alcohol use and related negative consequences among Black/African American youth.
