Does genetic variation in a bitter taste receptor gene alter early smoking behaviours in adolescents and young adults?

Abstract

Variation in the TAS2R38 taste receptor gene alters the ability to taste bitter compounds. We tested whether TAS2R38 variation influences early smoking behaviours in adolescence, a critical period of acquisition when taste may influence the natural course of tobacco use. Observational study (Nicotine Dependence in Teens [NDIT]). Cox proportional hazards models were conducted using data from European ancestry adolescent participants who initiated smoking during follow-up (n = 219, i.e. incident smokers). In young adulthood, cross-sectional analyses were restricted to European ancestry self-reported current smokers at age 24 (n = 148). Montréal, Canada. In adolescents, the rates of attaining early smoking milestones were estimated for tasters {PAV diplotypes (i.e. PAV/PAV or PAV/AVI)} versus non-tasters {AVI diplotype (i.e. AVI/AVI)}. In young adults, associations between tasting status and a nicotine intake biomarker (cotinine + 3'hydroxycotinine) and past-week cigarette consumption were assessed. Among incident smokers, similar rates to first whole cigarette were found between the diplotype groups (hazard ratio [HR], 1.05; 95% confidence interval (CI), 0.75-1.48; P = 0.765). However, smokers with the PAV (vs AVI) diplotypes attained monthly smoking more rapidly (HR, 1.55; 95% CI, 1.04-2.32; P = 0.033) and had faster conversion to three different measures of tobacco dependence (International Classification of Diseases: HR,2.29; 95% CI, 0.99-5.28; P = 0.052; modified Fagerström Tolerance Questionnaire: HR, 3.02, 95% CI, 1.04-8.79; P = 0.043; Hooked on Nicotine Checklist: HR,1.87; 95% CI, 0.98-3.60; P = 0.059). At age 24, those with PAV (vs AVI) diplotypes had higher mean cotinine + 3'hydroxycotinine (197 vs 143 ng/mL; P = 0.053). Adolescents with a genetic variation increasing their ability to taste bitter compounds appear to escalate more quickly to monthly smoking and tobacco dependence during adolescence and have higher nicotine intake in young adulthood versus those without that genetic variation.