Genetic Epidemiology of Smoking Behaviour and Nicotine Dependence

Abstract

The public health significance of sustained smoking is overwhelming. The genetic epidemiology and architecture of smoking behaviour and nicotine dependence have been studied for several decades. Twin, family and adoption studies show consistent evidence for genetic effects on many aspects of smoking behaviour and nicotine dependence. Gene–environment interactions have been detected, such as parental monitoring moderating genetic vulnerability for smoking initiation. Molecular genetic analyses have only recently identified few genes consistently associated with amount smoked and nicotine dependence, whereas large genome‐wide association studies have identified only a handful of genes associated with nicotine dependence. The nicotinic receptor alpha 5 gene ( CHRNA5 ) variant associated with nicotine dependence in genetic association studies is functional. Further studies with more sophisticated phenotypes, larger sample sizes and better measures of the environment are needed. Key Concepts: Smoking behaviour and nicotine dependence aggregate in families. Genetic liability underlies this familial aggregation. The heritability of smoking behaviour is moderate, but varies between populations. The genetic architecture of nicotine dependence is poorly known. Large genome‐wide association studies have identified only a handful of genes associated with nicotine dependence. The nicotinic receptor alpha 5 gene variant associated with nicotine dependence in genetic association studies is functional. This functional variant affects nicotine intake in animal models. Gene–environment interactions have been detected for smoking behaviours, such as parental monitoring moderating genetic vulnerability in youth.

Health behaviours and psychosocial working conditions as predictors of disability pension due to different diagnoses: a population-based study

“…genetics and shared, mainly childhood, environment, on the associations. Based on the earlier twin studies, familial confounding was known to exist in psychological factors [28], smoking [30], alcohol consumption [31], sedentary physical activity [32], and DP [33,34]. However, due to limited number of discordant twin pairs (from 204 to 420), our results need to be interpreted with caution.…”

“…through psychological factors with genetic background [27][28][29]. It is also known that genetics play a role in health behaviours including smoking [30], alcohol consumption [31] and sedentary physical activity [32], and on the risk of DP [33,34]. Hence, twin studies provide a possibility to control familial factors and would be valuable when investigating the relations between psychosocial working conditions, health behaviours and DP.…”

Multiethnic Prediction of Nicotine Biomarkers and Association with Nicotine Dependence

“…[10][11][12] There are no heritability estimates of TNE. Heritability estimates of cigarettes per day (CPD), a less precise measure of consumption, are significant in twin and genome-wide approaches, [13][14][15] but lower . CC-BY-NC-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.…”

“…10–12 There are no heritability estimates of TNE. Heritability estimates of cigarettes per day (CPD), a less precise measure of consumption, are significant in twin and genome-wide approaches, 13–15 but lower than NMR estimates.…”