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ABSTRACT The influence of friends and peers is theoretically one of the most consistent and important factors explaining adolescent alcohol use. However, not all adolescents are equally likely to be influenced by their friends' drinking behaviors. Genetic factors may underlie these inter-individual differences in susceptibility to the drinking behavior of friends. Because the long allele (≥ 7 repeats) of the dopamine D4 receptor ( DRD4) gene has been associated with susceptibility to alcohol and alcohol-related cues, we tested whether associations between best friend's and adolescent's alcohol use differed for DRD4 genotypes. A Dutch nationwide sample of 308 adolescents (age 13 at baseline) participated in a prospective, community-based study with five annual waves. A cross-lagged path analysis was carried out in Mplus to examine bi-directional relations between friends' and adolescents' weekly alcohol use (number of drinks). A multi-group approach was applied to test for moderation effects of a 48-base pair variable number of tandem repeats polymorphism in exon 3 of the DRD4 gene. Additionally, with latent growth curve models, it was examined whether the interaction between friends' drinking and DRD4 genotype predicted the development of adolescents' alcohol use. Results showed that both cross-sectionally and longitudinally higher levels of friends' alcohol use resulted in higher levels of adolescents' alcohol consumption over time (and vice versa). No significant moderation of DRD4 genotype was found: Associations between adolescents' and friends' drinking did not differ for adolescent carriers of the DRD4 long allele, when compared with adolescents without the DRD4 long allele. Because this is the first study to examine DRD4 × friends' drinking effects prospectively, replication is essential. Future longitudinal studies, possibly with observational or diary designs, are needed to increase our understanding of the interplay between genetic and environmental risk factors for adolescent alcohol use. [ABSTRACT FROM AUTHOR]

Drinking to cope (i.e., drinking to forget or alleviate negative feelings) has been found to be associated with adolescents' heavy drinking and alcohol-related problems. Additionally, it is widely accepted that genetic factors are involved in alcohol use and dependence. Studies are only beginning to reveal, however, which specific genotypes are related to drinking behaviors, and it is unknown whether they may interact with coping motives in predicting adolescents' risky drinking. The aim of this study was to examine relationships between the dopamine D2 receptor gene ( DRD2) Taq1A polymorphism (rs1800497), a serotonin transporter gene ( SLC6A4) polymorphism (5-HTTLPR), coping motives, and adolescents' binge drinking and alcohol-related problems. Participants in this cross-sectional study were 282 Dutch adolescents (mean age 17.4, 47% men) who had consumed alcohol at least once in their life. Coping motives were positively related to both binge drinking and alcohol-related problems, while DRD2 and SLC6A4 genotypes were not. DRD2, but not the SLC6A4 genotype, interacted with coping motives. The link between coping motives and alcohol outcomes was stronger among those carrying the DRD2 risk (A1) allele. This study extends the present literature by providing additional insight into the etiological factors of adolescent drinking behavior. An interaction between a vulnerability gene ( DRD2) and a cognitive factor (coping drinking) was found to be related to adolescents' binge drinking and alcohol-related problems. [ABSTRACT FROM AUTHOR]

Aim To discuss the current status of gene–environment interaction research with regard to alcohol use and dependence. Further, we highlight the difficulties concerning gene–environment studies. Methods Overview of the current evidence for gene–environment interactions in alcohol outcomes, and of the associated challenges in gene–environment studies. Results Attention to the causative roles of gene–environment interactions in alcohol use and dependence is increasing. Studies with twin designs are beginning to examine gene-shared environment effects, and animal studies have investigated gene–environment interaction effects on alcohol intake in primates. Thirteen studies incorporated gene–environment interactions in examining alcohol use or dependence in humans. These studies held a variety of candidate genes and environmental risk factors and their heterogeneity made it impossible to draw firm general conclusions. Conclusions Challenges for future gene–environment studies are abundant, and consist of, for example, the development of clear theoretical assumptions about neurobiological mechanisms and the recruitment of large longitudinal samples that already start in childhood. Replication is essential to prevent an overload of false-positive results. Despite the difficulties, it is crucial to include gene–environment interactions in future studies in order to unravel the aetiological factors of human alcohol outcomes. [ABSTRACT FROM AUTHOR]

Background: Transitions into heavy alcohol use often already take place during adolescence and are likely to be both genetically and environmentally determined. Therefore, in a 6-wave longitudinal study, we examined the effects of DRD2 Taq1A and OPRM1 A118G genotypes and the interaction with parental rule-setting on different groups of adolescent drinkers., Methods: Growth mixture modeling resulted in 3 distinct groups of adolescent drinkers: light drinkers (n = 346), moderate drinkers (n = 178), and heavy drinkers (n = 72)., Results: Multinomial regression showed that moderate drinkers carried the OPRM1 G allele and received lower levels of parental rule-setting significantly more often than the light drinking group. No other significant main effects of DRD2, OPRM1, and rule-setting were found. The interaction between OPRM1 genotype and parental rule-setting significantly distinguished the heavy drinkers from the light (p < 0.001) and moderate groups (p = 0.055): Particularly, the alcohol use of OPRM1 G allele carriers was affected by parental rule-setting, while AA genotype carriers remained largely unaffected by parental rules., Conclusions: Findings showed that different trajectories of adolescent drinking are preceded by a gene-parenting interaction. These results concur with Belsky's theory of plasticity (2009), as well as with Shanahan and Hofer's typology of a controlling and restricting gene-environment interaction (2005)., (Copyright © 2013 by the Research Society on Alcoholism.)