Smoking as a product of gene-environment interaction.
A strong hereditary influence on smoking has been demonstrated. As one of the candidate genes in relation to smoking, the serotonin transporter gene (5-HTTLPR) has been suggested, however with conflicting results. In recent studies, it has been shown that genotypic and environmental (G*E) factors interact in the shaping of a variety of phenotypic expressions. The objective of the present study was to investigate the interaction between a variation in the 5-HTTLPR and family environment in relation to smoking habits, nicotine dependence, and nicotine and cotinine levels in hair samples. A random Swedish adolescent population sample (n = 785), from which 200 individuals were stratified regarding behaviour, was genotyped for 5-HTTLPR and assessed with semi-structured interviews, a questionnaire, and hair analyses of nicotine and cotinine. The 5-HTTLPR gene interacted with a poor family environment to predict smoking habits, as well as nicotine and cotinine levels. The risk of being a smoker was increased 13 times for an individual with a combination of the 5-HTTLPR LS genotype and a poor family environment in comparison with the Homozygous Long-Long (LL) genotype and a good family environment.
Nilsson
Kent W
KW
Centre for Clinical Research, Uppsala University, Central Hospital, Västerås, Sweden. kent.nilsson@ltv.se
Oreland
Lars
L
Kronstrand
Robert
R
Leppert
Jerzy
J
D000293:Adolescent; D000328:Adult; D003367:Cotinine / Q000032:analysis; D004777:Environment; D005190:Family; D020022:Genetic Predisposition to Disease; D006197:Hair / Q000737:chemistry; D006801:Humans; D009538:Nicotine / Q000032:analysis; D016133:Polymerase Chain Reaction; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics; D012907:Smoking / Q000235:genetics*; D011795:Surveys and Questionnaires
D050486:Serotonin Plasma Membrane Transport Proteins; D009538:Nicotine; D003367:Cotinine