Evidence map›Paper›PMID 41865070›Full record

ArticleScientific reports2026

Genetic predisposition to coffee consumption and the association with the early risk of atherosclerosis.

Xiangyu Qiao, Vanessa William Toma, Jing Wang, Ángel Herraiz-Adillo, Simon Söderholm, Daniel Berglind, Susanna Calling, Bledar Daka, Mats Martinell, Frida Bergman and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

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

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

17 authors.

Xiangyu Qiao *Science for Life Laboratory, Department of Biomedical and Clinical Sciences, Division of Cell and Neurobiology, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
Vanessa William Toma *Science for Life Laboratory, Department of Biomedical and Clinical Sciences, Division of Cell and Neurobiology, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
Jing WangScience for Life Laboratory, Department of Biomedical and Clinical Sciences, Division of Cell and Neurobiology, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
Ángel Herraiz-AdilloDepartment of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden.
Simon SöderholmDepartment of Biomedical and Clinical Sciences, Division of Molecular and Virology, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
Daniel BerglindCentre for Epidemiology and Community Medicine, Region Stockholm, Stockholm, Sweden.
Susanna CallingCenter for Primary Health Care Research, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden.
Bledar DakaFamily Medicine, School of Public Health and Community Medicine, Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
Mats MartinellDepartment of Public Health and Caring Sciences, Uppsala University, Uppsala, Sweden.
Frida BergmanDepartment of Public Health and Clinical Medicine, Umeå University, Umeå, Sweden.
Pontus HenrikssonDepartment of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden.
Bijar GhafouriDepartment of Health, Medicine and Caring Sciences, Linköping University, Linköping, Sweden.
Martin UlanderScience for Life Laboratory, Department of Biomedical and Clinical Sciences, Division of Cell and Neurobiology, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
Carl Johan ÖstgrenPrimary Health Care Center, Department of Health, Medicine and Caring Sciences, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
Claudio CantùDepartment of Biomedical and Clinical Sciences, Division of Molecular and Virology, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden.
Wen ZhongScience for Life Laboratory, Department of Biomedical and Clinical Sciences, Division of Cell and Neurobiology, Faculty of Medicine and Health Sciences, Linköping University, Linköping, Sweden. wen.zhong@liu.se.
Fredrik IredahlWallenberg Centre for Molecular Medicine, Linköping University, Linköping, Sweden. fredrik.iredahl@liu.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The cardiovascular effects of coffee consumption remain debated, particularly regarding early-stage subclinical atherosclerosis. This study investigated the association between coffee intake, genetic predisposition, and the risk of subclinical coronary and carotid atherosclerosis in 24,835 participants from the Swedish CArdioPulmonary bioImage Study (SCAPIS). Coffee intake was assessed via self-reported questionnaires. Atherosclerosis was assessed via segment involvement score (SIS), coronary artery calcium score (CACS) and carotid plaque. Observational analysis showed no significant association between coffee consumption and SIS, CACS, or carotid plaques. However, both one-sample and two-sample (SCAPIS and UK Biobank) Mendelian randomization (MR) analyses showed an association between genetic predisposition to higher coffee consumption and increased SIS. Stratification analyses further explored differences in genetic associations across varying coffee consumption levels. Among individuals consuming coffee more than twice daily, two coffee consumption-associated single nucleotide polymorphisms (SNPs) in AHR and CYP1A1/CYP1A2 were correlated with SIS. Integrative metabolomics and proteomics analyses identified lipid-related metabolites (triglycerides, phospholipids, free cholesterol) and inflammation-related proteins (DLK1, IL1RL2, CCL17) associated with the genetic proxy of coffee consumption. These findings suggest that genetically influenced coffee consumption may be associated with coronary atherosclerosis risk in frequent coffee drinkers, although the underlying biological basis remains to be clarified.

Indexed as

AtherosclerosisCoffeeCoronary Artery DiseaseGenetic Predisposition to DiseaseAgedCytochrome P-450 CYP1A1Cytochrome P-450 CYP1A2FemaleHumansMaleMendelian Randomization AnalysisMiddle AgedPolymorphism, Single NucleotideReceptors, Aryl HydrocarbonRisk FactorsSwedenCoffeeCYP1A2 protein, humanCytochrome P-450 CYP1A1Cytochrome P-450 CYP1A2Receptors, Aryl HydrocarbonAtherosclerosisCoffee consumptionMendelian randomizationMulti-omics

Identifiers

PMID41865070
PMCPMC13009213

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.