Limited overlap between genetic effects on disease susceptibility and disease survival
Zhiyu YangiD, Fanny‐Dhelia PajusteiD, Kristina ZguroiD, Yipeng ChengiD, Danielle E. Kurant, Andrea EoliiD, Julian S. WanneriD, Bradley S. JermyiD, Joel T RämöiD, FinnGeniD, Stavroula KanoniiD, David A. van HeeliD, Caroline HaywardiD, Riccardo Emilio MarioniiD, Daniel L. McCartneyiD, Alessandra RenieriiD, Simone FuriniiD, Reedik MägiiD, Alexander GuseviD, Petros Drineas BiD, Peristera PaschouiD, Henrike HeyneiD, Samuli RipattiiD, Nina MarsiD, Andrea GannaiD
Abstract
Understanding disease progression is of a high biological and clinical interest. Unlike disease susceptibility whose genetic basis has been abundantly studied, less is known about the genetics of disease progression and its overlap with disease susceptibility. Considering ten common diseases (N cases ranging from 17,152 to 99,666) across seven biobanks, we systematically compared the genetic architecture of susceptibility and progression, defined as disease-specific mortality. We identified only one locus significantly associated with disease-specific mortality and show that, at a similar sample size, more genome-wide significant loci can be identified in a GWAS of disease susceptibility. Variants that were significantly affecting disease susceptibility were weakly or not associated with disease-specific mortality. Moreover, susceptibility polygenic scores (PGSs) were weak predictor of disease-specific mortality while a PGS for general lifespan was significantly associated with disease-specific mortality for five out of ten diseases. We used theoretical derivation and simulation to propose plausible explanations for our empirical observations and account for potential index-event bias. Overall, our findings point to little similarity in genetic effects between disease susceptibility and disease-specific mortality and suggest that either larger sample sizes or different measures of progression are needed to identify the genetic underpinning of disease progression.
02 /Specification & Classification
Click any tag to browse matching papers- Citations
- 27
- FWCI
- 14.04
- Field percentile
- top 1%
- Organism
- Assay
- Research Focus
- Approach
Reproducibility ledger
Nobody has reported trying to reproduce this paper yet. Did you replicate an experiment or run the code? Your report saves the next lab a week.
Sign in to file a reproducibility report.
Related papers
- Biases in GWAS - the dog that did not bark
Catherine Mary Schooling·bioRxiv·Jul 20, 2019
- Positive-control Mendelian randomization highlights power constraints in disease-mortality GWAS
Chen-Yang Su, Guillaume Butler‐Laporte·medRxiv·Jun 1, 2026
- Genetic predisposition to longer lifespan, lifestyle factors, and all-cause mortality: a 17-year prospective cohort study
Niko Paavo Tynkkynen, Laura Joensuu, … Elina Sillanpää·GeroSciencePeer-reviewed·Jul 25, 2026
- Why do we get sick? Genetic evidence for evolutionary trade-offs between fertility, longevity, and disease
Eva Brigos-Barril, Claudia Vasallo, … Gerard Muntané·medRxiv·Jun 18, 2025
- Phenome-derived polygenic scores and social determinants jointly shape context-dependent disease risk
Ying Wang, Buu Minh Thanh Truong, … Alicia R. Martin·medRxiv·Apr 18, 2026
- Findings and insights from the genetic investigation of age of first reported occurrence for complex disorders in the UK Biobank and FinnGen
Yen‐Chen Anne Feng, Tian Ge, … Benjamin M. Neale·medRxiv·Nov 20, 2020