Gene-environment transactions between peer tobacco use, parental supervision, and Chinese adolescent tobacco initiation

Introduction: Tobacco use continues to cause preventable disease and death that stresses healthcare systems globally. Tobacco initiation in adolescence can increase the risk for tobacco use maintenance and abuse of other substances in later life. Low parental supervision (PS) and high peer tobacco use (PTU) are risk factors for adolescent tobacco initiation (ATI). Twin research has suggested a shared genetic etiology between PS, PTU, and ATI, yet few studies have explored these factors concurrently. Extant research primarily focuses on Western populations, with scant studies examining Chinese twins. This study explored gene-environment interactions (G×E) and correlations (rGE) involving PS and PTU with ATI in a large sample of Chinese twins observed from early to mid-adolescence. We hypothesized that: 1) shared environmental influences on ATI would be larger in Chinese adolescent twins than in Western populations; 2) rGE between ATI, PTU, and PS would show common genetic factors partially explaining the links between them; and 3) PS and PTU could moderate genetic influences on ATI in Chinese adolescents, where higher levels of supervision would suppress, while high levels of PTU would magnify genetic influences on ATI. Methods: 602 Chinese twin pairs (52% female) were assessed at 2 time points (Mage = 12 and 15 years). Participants reported lifetime tobacco use, parental supervision, and peer tobacco use via paper-pencil questionnaires at each timepoint. Univariate biometric models decomposed the phenotypic variances of each variable into genetic (A), shared (C), and non-shared (E) environmental components. Bivariate biometric models examined both phenotypical associations as well as the extent to which common genetic and environmental factors influenced the links between ATI, PS, and PTU. To examine G×E, bivariate moderation modelling was implemented to explore the moderating effects of PS and PTU on both genetic and environmental influences on ATI. Results: Univariate modelling indicated that genetic influences on ATI increased over time, while both shared and non-shared environmental influences decreased. Bivariate modelling showed that at both timepoints, the phenotypic correlations between PTU and ATI were larger than those between PS and ATI. There was a significant negative genetic correlation between PS and ATI at time 2, while all other common genetic or environmental correlations at each timepoint were nonsignificant. PTU moderated the unique genetic contributions to ATI only at time 2, such that genetic influences on ATI increased at higher levels of PTU. Conclusion: The amplifying effects of PTU on the genetic influences of ATI is consistent with the diathesis stress model. Peers appear to exert larger influences on ATI than parents. Peer influences are often conceptualized primarily as social processes; however, the current findings also illustrate their role in modulating biological mechanisms of behavioural development. The significant G×E of PTU at time 2 but not time 1 is noteworthy as this suggests G×E ×development, wherein G×E between PTU and ATI is contingent upon an individual’s current developmental stage, thus offering a potential window for prevention.