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• W4387496931 abstract "Smoking is associated with diseases like cancer, COPD, and heart disease. Nevertheless, the number of smokers worldwide is increasing, leading to smoking-related illnesses and preventable deaths. Understanding genetic influences on smoking behavior can inform prevention measures. Polygenic risk scores (PRS) combine genetic variants known to be associated with a specific phenotype to assess susceptibility. Although PRS partially capture disease risk, their predictive ability is still limited. Another measure of genetic risk is family history (FH), e.g. the incidence of a certain trait in relatives. However, FH does not only capture genetic risk, but also environmental influences. While both PRS and FH reflect genetic risk, they capture different aspects of genetic risk, showing different predictive abilities. Therefore, the measures can be complementary and may improve risk prediction when combined. The present study aimed to examine and compare the predictive power of nicotine use PRS and FH of for smoking behavior. Data from the German multi-center study “Genetics of Nicotine Dependence and Neurobiological Phenotypes” was used. Smokers (n=1,116) and never-smokers (n=1,280) from 18 to 65 years were recruited. Smoking was assessed with the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV), the Structured Clinical Interview (SCID), and the Fagerström Test for Nicotine Dependence (FTND). For FH, parental smoking was assessed in a questionnaire. Genetic data was available from 2,312 individuals. After quality control, the final dataset for PRS analysis included 2,169 individuals and 652,021 single nucleotide polymorphisms (SNPs). PRS were based on GWAS meta-analysis summary statistics from the GWAS and Sequencing Consortium of Alcohol and Nicotine (GSCAN) for smoking initiation (SI), cigarettes per day (CpD), and smoking cessation (SC). PRS were calculated using PRSice 2, and regression analyses were used to test associations between PRS (SI, CpD, SC), parental FH of smoking and smoking phenotypes using R 3.6.3. PRS for SI explained 6.65% of variance in SI (Pt=0.5, p=1.71 × 10-24), while parental FH alone explained 3.06% (p=2.43 × 10-12). Parental FH explained 3.60% of variance in PRS for SI (Pt=0.05, p = 1.6 × 10-18). Parental FH added 1.39% to the variance explained in SI independently in a combined model with PRS for SI (p=1.2 × 10-6), resulting in a total R² of 8.04%. PRS for CpD (Pt=0.2, R2=3.15% p=1.82 × 10-8) and SC (Pt=0.01, R2=2.01% p=7.18 × 10-6) were associated with FTND scores in smokers. This study highlights the predictive utility of PRS for disease risk, particularly in smoking behaviors. PRS for smoking were associated with SI and FTND scores, suggesting their relevance in smoking research. The results indicate both independent and overlapping contributions of PRS and parental FH of smoking. PRS for SI can aid in risk prediction and inform prevention strategies, especially when combined with family history. PRS for CpD and SC were associated with FTND scores, indicating their potential for identifying high-risk individuals and treatment responsiveness. These findings serve as a proof of concept with the potential for further discoveries as sample sizes increase. For the congress, the calculations will be updated with the most recent GWAS data available." @default.
• W4387496931 created "2023-10-11" @default.
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• W4387496931 date "2023-10-01" @default.
• W4387496931 modified "2023-10-12" @default.
• W4387496931 title "W100. ASSOCIATIONS OF SMOKING BEHAVIOR WITH POLYGENIC RISK SCORES FOR NICOTINE USE AND PARENTAL FAMILY HISTORY OF SMOKING" @default.
• W4387496931 doi "https://doi.org/10.1016/j.euroneuro.2023.08.286" @default.
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