The present study examined whether parental problem drinking affected parenting (i.e., behavioral control, support, rule-setting, alcohol-specific behavioral control), and whether parental problem drinking and parenting affected subsequent adolescent alcohol use over time. A total of 428 families, consisting of both parents and two adolescents (mean age 13.4 and 15.2 years at Time 1) participated in a three-wave longitudinal study with annual waves. A series of path analyses were conducted using a structural equation modeling program (Mplus). Results demonstrated that, unexpectedly, parental problem drinking was in general not associated with parenting. For the younger adolescents, higher levels of both parenting and parental problem drinking were related to lower engagement in drinking over time. This implies that shared environment factors (parenting and modeling effects) influence the development of alcohol use in young adolescents. When adolescents grow older, and move out of the initiation phase, their drinking behavior may be more affected by other factors, such as genetic susceptibility, and peer drinking.
Research suggests that people adapt their own drinking behavior to that of other people. According to a genetic-differences approach, some individuals may be more inclined than others to adapt their alcohol consumption level to that of other people. Using a 3 (drinking condition) x 2 (genotype) experimental design (N = 113), we tested whether susceptibility to alcohol-related cues (i.e., seeing someone drink) was related to the variable number of tandem repeats in exon 3 of the D4 dopamine receptor gene. A strong gene-environment interaction showed that participants carrying at least one copy of the 7-repeat allele consumed substantially more alcohol in the presence of a heavy-drinking individual than did participants without this allele. This study highlights that individual variability in sensitivity to other people's drinking behavior may be attributable to genetic differences. Carrying the 7-repeat allele may increase the risk for heavy alcohol use or abuse in the company of heavy-drinking peers.
Association studies investigating the link between the dopamine D2 receptor gene (DRD2) and alcohol (mis)use have shown inconsistent results. This may be due to lack of attention for environmental factors. High levels of parental rule-setting are associated with lower levels of adolescent alcohol use and delay of initiation of drinking. We tested whether DRD2 TaqI A (rs1800497) genotype interacts with alcohol-specific parenting practices in predicting the uptake of regular adolescent alcohol use. Non-regular drinkers were selected from a Dutch, nationwide sample of 428 adolescents (mean age 13.4 years at baseline) and participated in a prospective, community-based study with three annual waves. Parental rule-setting was directly and inversely related to adolescent alcohol use over time. For DRD2 genotype no significant main effect was found. DRD2 genotype interacted with parental rule-setting on adolescent alcohol use over time: adolescents, with parents highly permissive toward alcohol consumption and carrying a genotype with the DRD2 A1 (rs1800497T) allele, used significantly more alcohol over time than adolescents without these characteristics. The DRD2 genotype may pose an increased risk for alcohol use and abuse, depending on the presence of environmental risk factors, such as alcohol-specific parenting.
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