Evidence map›Paper›PMID 41615936›Full record

ArticlePloS one2026

Genetic insights into number of long-term conditions and their relationship with lifespan.

Youngjune Bhak, Bruce Guthrie, Albert Tenesa

Abstract read
In one paragraph

Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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2 · The registry

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3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

3 authors.

Youngjune BhakMRC Human Genetics Unit at the MRC Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom.ORCID https://orcid.org/0000-0002-9273-6984
Bruce GuthrieUsher Institute, University of Edinburgh, Edinburgh, United Kingdom.
Albert TenesaMRC Human Genetics Unit at the MRC Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Edinburgh, United Kingdom.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsRelationships between the genetic risk for long-term conditions (LTCs) and lifespan have been reported. However, the genetic factors underlying the total number of LTCs an individual has (LTC burden) and their association with lifespan have not been fully investigated. This study aims to investigate the genetics of LTC burden and evaluate its relationship with lifespan.

methodsA genome-wide association study (GWAS) and a genetic heritability test were conducted on LTC burden using data from 343,868 UK Biobank individuals. Global and local genetic correlations between the LTC burden and parental lifespan were estimated. A polygenic risk score (PRSLTC) for LTC burden was derived from a separate set of 34,339 UK Biobank individuals with records of age at death, who were not included in the GWAS analysis. The association between the PRSLTC and lifespan, as well as its ability to predict LTC burden, was assessed.

resultsLoci in the HLA region were the most significant among the 21 significant independent loci from the GWAS. The estimated SNP heritability of LTC burden was 0.0963 and significantly different from zero (se = 0.0034, p-value = 1.77 x 10-176). The global genetic correlation between LTC burden and parental lifespan exhibited a significant global genetic correlation of -0.7869 (se = 0.0419, p-value 9.57 x 10-79). Additionally, 44 loci showed significant local genetic correlations (p-value < 2.23 x 10-5). Individuals in the highest 10% PRSLTC had, on average, a 0.9-year shorter lifespan and 0.73 more LTCs than those in the lowest 10%.

conclusionsThis study identifies significant genetic factors associated with LTC burden and their association with lifespan, providing insights into the genetic underpinnings of both multiple LTCs and lifespan.

Indexed as

LongevityAgedFemaleGenetic Predisposition to DiseaseGenetic Risk ScoreGenome-Wide Association StudyHumansMaleMiddle AgedMultifactorial InheritancePolymorphism, Single NucleotideUK BiobankUnited Kingdom

Identifiers

PMID41615936
PMCPMC12857943

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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 OpenQuestion graph.