Methods: Data on sociodemograhics, childhood-onset drinking, pro-alcohol social context (e.g., parental alcohol drinking), and AEs were ascertained from 2630 primary school-attending children (aged 10-12) in the academic year of 2006 (response rate = 60.1%); two waves of assessment were conducted annually (follow-up rates > 80%). AEs covered three positive: Global Positive Transformation [GPT], Enhanced Social Behaviors [ESB], and Promoting Relaxation or Tension Reduction [PRTR]; one negative: Deteriorated cognitive and behavioral function [DCBF] (all cronbach’s alpha > 0.7). 1084 had provided saliva for DNA retrieval (response rate: 58.4%wt) and the polymorphisms of DRD2 (rs1799978, rs6277), DRD3 (rs6280), and DRD4 (rs1800955) were genotyped. Using the dopaminergic polygenic risk scores, a proxy for additive effects of alleles, we performed the Generalized Linear Model to estimate the connection linking dopaminergic markers with endorsed AEs, with stratified by childhood-onset drinking.
Results: At baseline, a total of 381 (36.0% wt) children had tried alcohol, and three domains of positive AEs for the alcohol experienced were significantly greater than the alcohol naïve (p<0.01). During the two-year follow-up, 24.9% wt initiated alcohol drinking and the change in positive AEs was particularly prominent for the ESB (mean= 0.21). With statistical adjustment for sociodemographics and pro-alcohol social contexts, having higher dopaminergic genetic scores was manifested in negative AE (DCBF: βwt = -1.80; 95% CI = -3.45, -0.16) for those alcohol experienced (both childhood- and adolescence-onset).
Conclusion: The association linking dopamine receptor phenotype with negative alcohol expectancies varied by childhood-onset drinking. Our results indicated that prevention/intervention programs reducing underage drinking problems should better understand the role of genetics while developing strategies tackling cognitive pathways.