Strategies to investigate and mitigate collider bias in genetic and Mendelian randomization studies of disease progression
Mitchell, R. E.; Hartley, A. E.; Walker, V.; Gkatzionis, A.; Yarmolinsky, J.; Bell, J. A.; Chong, A. H. W.; Paternoster, L.; Tilling, K.; Davey Smith, G.
Show abstract
Genetic studies of disease progression can be used to identify factors that may influence survival or prognosis, which may differ from factors which influence on disease susceptibility. Studies of disease progression feed directly into therapeutics for disease, whereas studies of incidence inform prevention strategies. However, studies of disease progression are known to be affected by collider (also known as "index event") bias since the disease progression phenotype can only be observed for individuals who have the disease. This applies equally to observational and genetic studies, including genome-wide association studies and Mendelian randomization analyses. In this paper, our aim is to review several statistical methods that can be used to detect and adjust for index event bias in studies of disease progression, and how they apply to genetic and Mendelian Randomization studies using both individual and summary-level data. Methods to detect the presence of index event bias include the use of negative controls, a comparison of associations between risk factors for incidence in individuals with and without the disease, and an inspection of Miami plots. Methods to adjust for the bias include inverse probability weighting (with individual-level data), or Slope-hunter and Dudbridges index event bias adjustment (when only summary-level data are available). We also outline two approaches for sensitivity analysis. We then illustrate how three methods to minimise bias can be used in practice with two applied examples. Our first example investigates the effects of blood lipid traits on mortality from coronary heart disease, whilst our second example investigates genetic associations with breast cancer mortality.
Matching journals
The top 5 journals account for 50% of the predicted probability mass.
Similar papers in this journal
- An empirical investigation into the impact of winner's curse on estimates from Mendelian randomization 97%
- Educational attainment as a modifier of the effect of polygenic scores for cardiovascular risk factors: cross-sectional and prospective analysis of UK Biobank 95%
- Bias in two-sample Mendelian randomization when using heritable covariable-adjusted summary associations 94%
Similar papers in this journal
- Causal relationships between obesity and the leading causes of death in women and men 93%
- Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19 93%
- Relaxing parametric assumptions for non-linear Mendelian randomization using a doubly-ranked stratification method 93%
Similar papers in this journal
- Evaluating and implementing block jackknife resampling Mendelian randomization to mitigate bias induced by overlapping samples 94%
- The impact of fatty acids biosynthesis on the risk of cardiovascular diseases in Europeans and East Asians: A Mendelian randomization study 94%
- Imputed Gene Expression Risk Scores: A Functionally Informed Component of Polygenic Risk 93%
Similar papers in this journal
Similar papers in this journal
- Actionable absolute risk prediction of atherosclerotic cardiovascular disease: a behavior-management approach based on data from 464,547 UK Biobank participants 95%
- Genetic loci associated with prevalent and incident myocardial infarction and coronary heart disease in the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium 93%
- Coffee consumption and risk of breast cancer: a Mendelian Randomization study 93%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.