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RF4 ‘Common versus specific liability for substance abuse in early adulthood: a genetically informed approach’
  1. E Iob1,
  2. T Schoeler2,
  3. J Pingault2
  1. 1Department of Epidemiology and Public Health, University College London, London, UK
  2. 2Department of Clinical, Educational and Health Psychology, University College London, London, UK


Background Young people experiencing psychological or behavioural problems are more likely to engage in poly-substance use. The common liability theory posits a common liability to all substance addictions. Such shared risk factors may therefore explain the observed patterns of comorbid substance use, where a common genetic susceptibility could underlie this co-occurrence. However, to date most research has failed to measure the aforementioned common liability, and the first genome-wide association studies (GWAS) have identified genetic variants specific to each substance rather than common ones. Therefore, the aim of this project is two-fold: firstly, to construct a new longitudinal measurement model of common liability to substance use; secondly, to investigate specific versus common genetic influences on substance use applying polygenic scoring.

Methods The sample includes 6399 young adults from the Avon Longitudinal Study of Parents and Children. Self-reported data on substance use (i.e. tobacco, alcohol, marijuana, and other illicit drugs) was collected at age 17.5, 20, and 22 with validated questionnaires. A Trait-State-Occasion model applied within Structural Equation Modelling (SEM) was used to identify a common trait factor for substance use across the three time points, as well as occasion- and drug-specific latent factors. Polygenic scores were calculated using GWAS results on substance use and related psychopathological, behavioural, and cognitive phenotypes. All analyses were conducted using R and PRSice software.

Results In Study 1, the Trait-State-Occasion model was tested using Robust Maximum Likelihood Estimation, which accounted for the non-normal distribution of the substance abuse measures. The model fitted the data well, χ2 (33)=100.572, p<0.001, CFI=0.987, RMSEA=0.018, SRMR=0.027. The variance of the trait factor was 0.155 [95% CI 0.124; 0.185]. On average, the model R-Squared was 70%, with residuals being 30%. The total variance explained by the model was further decomposed into trait, occasion, and drug-specific variance, which was equal to 16%, 11%, and 44% respectively. Study 2 (ongoing) will test a full SEM model by regressing the polygenic scores on both the common trait and drug-specific factors.

Conclusion The results of Study 1 provided evidence for a common liability to substance use, which is partly shared across different drugs and stable over time. This therefore suggests that both common and drug-specific susceptibility should be considered where examining genetic and environmental risk factors for substance use. Study 2 will reveal the influence of genetic variants associated with various psychopathology related-traits on both common and drug-specific dimensions of substance use.

  • Substance Use
  • Common Liability
  • Polygenic Risk

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