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Polygenic risk scores for nicotine use and family history of smoking are associated with smoking behaviour. | LitMetric

Polygenic risk scores for nicotine use and family history of smoking are associated with smoking behaviour.

Drug Alcohol Depend

Department of Genetic Epidemiology in Psychiatry, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim,  Germany; German Center for Mental Health (DZPG), partner site Mannheim/Heidelberg/Ulm, Germany. Electronic address:

Published: October 2024

AI Article Synopsis

  • Research suggests that genetic factors significantly influence smoking behavior, and investigating this on a molecular level could provide better understanding of why people smoke.
  • A study used genetic data to calculate polygenic risk scores in about 2200 individuals, examining how these scores relate to smoking initiation and dependence while also considering the impact of parental smoking.
  • The findings indicate that genetic factors explain a notable portion of smoking behaviors, indicating the value of combining genetic and familial risk assessments to improve smoking prevention efforts.

Article Abstract

Introduction: Formal genetics studies show that smoking is influenced by genetic factors; exploring this on the molecular level can offer deeper insight into the etiology of smoking behaviours.

Methods: Summary statistics from the latest wave of the GWAS and Sequencing Consortium of Alcohol and Nicotine (GSCAN) were used to calculate polygenic risk scores (PRS) in a sample of ~2200 individuals who smoke/individuals who never smoked. The associations of smoking status with PRS for Smoking Initiation (i.e., Lifetime Smoking; SI-PRS), and Fagerström Test for Nicotine Dependence (FTND) score with PRS for Cigarettes per Day (CpD-PRS) were examined, as were distinct/additive effects of parental smoking on smoking status.

Results: SI-PRS explained 10.56% of variance (Nagelkerke-R) in smoking status (p=6.45x10). In individuals who smoke, CpD-PRS was associated with FTND score (R=5.03%, p=1.88x10). Parental smoking alone explained R=3.06% (p=2.43×10) of smoking status, and 0.96% when added to the most informative SI-PRS model (total R²=11.52%).

Conclusion: These results show the potential utility of molecular genetic data for research investigating smoking prevention. The fact that PRS explains more variance than family history highlights progress from formal to molecular genetics; the partial overlap and increased predictive value when using both suggests the importance of combining these approaches.

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Source
http://dx.doi.org/10.1016/j.drugalcdep.2024.112415DOI Listing

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