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EPA-1747 – Investigation of the Interplay Between Genetic and Environmental Risk Factors for Smoking Behaviour
- J. Strohmaier, J. Treutlein, J. Frank, T. Mühleisen, F. Degenhardt, S.H. Witt, S. Cichon, T.G. Schulze, M.M. Nöthen, M. Rietschel
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- Journal:
- European Psychiatry / Volume 29 / Issue S1 / 2014
- Published online by Cambridge University Press:
- 15 April 2020, p. 1
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Smoking-behaviour is influenced by environmental and genetic risk factors. Established epidemiological risk factors include early age at onset (AaO), depression, positive family history (FH+) of depression/alcohol-dependence, low education, older birth cohort, and male gender. Genomewide-association-studies (GWAS) have identified genetic risk variants for smoking-behaviour. In the present study we investigated correlations between these epidemiological and genetic risk factors and smoking-behaviour in a large population-based German sample. Genetic risk was defined in terms of a polygenic score – the accumulated effect of seven independent genetic risk markers for smoking-behaviour identified through GWAS.
The sample comprised 1736 individuals (815 males, 921 females). Dependent variables were: smoking-duration, nicotine-dependence, cigarettes–per-day, ever-smoking, and smoking-cessation. The effect of the epidemiological risk factors, the polygenic risk score, and their combined effect on the smoking-behaviours was tested via linear or logistic regression analyses.
The following associations were detected: AaO and birth cohort with smoking-duration (p=0.004; p<0.001); AaO, education and FH+ depression with nicotine-dependence (p=0.002; p=0.092); sex and AaO with cigarettes–per-day (p=0.020; p<0.001); FH+ alcohol dependence with eversmoking (p=0.049); and birth cohort and education with smoking-cessation (p=0.001; p=0.029). The polygenic risk score showed a trend towards association with nicotine-dependence (p=0.113) and cigarettes–per-day (p=0.109). In the combined analyses, the polygenic risk score improved the regression model for nicotine-dependence, cigarettes–per-day, and smoking-cessation.
The addition of GWAS information concerning genetic risk factors explained an increased fraction of the smoking behaviours nicotine dependence, CPD, and smoking cessation. Future studies are warranted to elucidate the biological correlates of these genetic risk factors.
Genome-wide association study of pathological gambling
- M. Lang, T. Leménager, F. Streit, M. Fauth-Bühler, J. Frank, D. Juraeva, S.H. Witt, F. Degenhardt, A. Hofmann, S. Heilmann-Heimbach, F. Kiefer, B. Brors, H.-J. Grabe, U. John, A. Bischof, G. Bischof, U. Völker, G. Homuth, M. Beutel, P.A. Lind, S.E. Medland, W.S. Slutske, N.G. Martin, H. Völzke, M.M. Nöthen, C. Meyer, H.-J. Rumpf, F.M. Wurst, M. Rietschel, K.F. Mann
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- Journal:
- European Psychiatry / Volume 36 / August 2016
- Published online by Cambridge University Press:
- 23 March 2020, pp. 38-46
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Background
Pathological gambling is a behavioural addiction with negative economic, social, and psychological consequences. Identification of contributing genes and pathways may improve understanding of aetiology and facilitate therapy and prevention. Here, we report the first genome-wide association study of pathological gambling. Our aims were to identify pathways involved in pathological gambling, and examine whether there is a genetic overlap between pathological gambling and alcohol dependence.
MethodsFour hundred and forty-five individuals with a diagnosis of pathological gambling according to the Diagnostic and Statistical Manual of Mental Disorders were recruited in Germany, and 986 controls were drawn from a German general population sample. A genome-wide association study of pathological gambling comprising single marker, gene-based, and pathway analyses, was performed. Polygenic risk scores were generated using data from a German genome-wide association study of alcohol dependence.
ResultsNo genome-wide significant association with pathological gambling was found for single markers or genes. Pathways for Huntington's disease (P-value = 6.63 × 10−3); 5′-adenosine monophosphate-activated protein kinase signalling (P-value = 9.57 × 10−3); and apoptosis (P-value = 1.75 × 10−2) were significant. Polygenic risk score analysis of the alcohol dependence dataset yielded a one-sided nominal significant P-value in subjects with pathological gambling, irrespective of comorbid alcohol dependence status.
ConclusionsThe present results accord with previous quantitative formal genetic studies which showed genetic overlap between non-substance- and substance-related addictions. Furthermore, pathway analysis suggests shared pathology between Huntington's disease and pathological gambling. This finding is consistent with previous imaging studies.