ArticleNature communications2026
Preventing premature deaths through polygenic risk scores.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Modifying genetic susceptibility to coronary heart disease through an integrated plant-based diet-lifestyle.The Lancet regional health. Europe · 2026Article
- Predictive Biomarkers for Asymptomatic Adults: Opportunities, Risks, and Guidance for General Practice.Diagnostics (Basel, Switzerland) · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Polygenic risk scores (PRS) have demonstrated predictive validity across a range of cohorts and diseases, but quantifying their clinical utility remains a challenge. As PRS can be derived from a single biological sample and remains stable throughout life, we explore the potential of PRS to optimize existing screening programs. Via an integrated modelling approach, we quantify the potential clinical benefits arising from a knowledge of PRS across seven diseases with existing screening programs (abdominal aortic aneurysm, breast cancer, colorectal cancer, coronary artery disease, hypertension, prostate cancer, and type 2 diabetes). We identify individuals at high genetic risk (PRS OR>2) and very high genetic risk (PRS OR>3) and estimate the optimal screening ages for these genetically high-risk individuals, based on the equivalent risk to population-level risk at recommended screening ages. We then leverage published data on differential mortality and other outcomes, with and without screening-based interventions, to assess the potential benefits of tailoring screening age based on genetic risk. Very high risk individuals reach the risk level associated with usual starting screening age on average 10.8 years earlier, high risk individuals 8.9 years earlier and reduced risk individuals (OR<0.5) 16.8 years later. During this time, case enrichment (the ratio of the percentage of cases in the high PRS risk group and in the total population) in the high risk group is between 1.7 and 3.0, depending on the disease. Across all seven diseases, appropriate interventions following PRS-guided screening could reduce premature deaths in high-risk individuals by 23.3%. Knowledge of genetic risk, measured using PRS, has the potential to deliver substantial public health benefits when aggregated across conditions, and could reduce premature mortality by tailoring existing screening programs.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.