Evidence map›Paper›PMID 34523676›Full record

SynthesisHuman molecular genetics2022

Blood copper and risk of cardiometabolic diseases: a Mendelian randomization study.

Susanne Jäger, Maria Cabral, Johannes F Kopp, Per Hoffmann, Esther Ng, John B Whitfield, Andrew P Morris, Lars Lind, Tanja Schwerdtle, Matthias B Schulze

Open access · bronzeAbstract readMeta-Analysis
In one paragraph

Synthesis in Human molecular genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
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

19 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Association of Copper with Atherosclerosis and Treatment Strategies.Journal of cardiovascular translational research · 2025
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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

10 authors at 7 institutions in 5 countries.

Susanne JägerDepartment of Molecular Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal 14558, Germany.ORCID 0000-0001-6619-0861
Maria CabralDepartment of Molecular Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal 14558, Germany.
Johannes F KoppTraceAge-DFG Research Unit on Interactions of Essential Trace Elements in Healthy and Diseased Elderly, Potsdam-Berlin-Jena, Germany.
Per HoffmannHuman Genomics Research Group, Department of Biomedicine, University of Basel, Basel 4031, Switzerland.
Esther NgWellcome Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK.
John B WhitfieldQIMR Berghofer Medical Research Institute, Brisbane, Queensland 4029, Australia.
Andrew P MorrisCentre for Genetics and Genomics Versus Arthritis, Centre for Musculoskeletal Research, The University of Manchester, Manchester M13 9PL, UK.ORCID 0000-0002-6805-6014
Lars LindDepartment of Medical Sciences, Cardiovascular Epidemiology, Uppsala University, Uppsala 75185, Sweden.
Tanja SchwerdtleTraceAge-DFG Research Unit on Interactions of Essential Trace Elements in Healthy and Diseased Elderly, Potsdam-Berlin-Jena, Germany.
Matthias B SchulzeDepartment of Molecular Epidemiology, German Institute of Human Nutrition Potsdam-Rehbruecke, Nuthetal 14558, Germany.
University of Potsdam · DEDeutsches Diabetes-Zentrum e.V. · DECentre for Human Genetics · GBQIMR Berghofer Medical Research Institute · AUUniversity of Basel · CHUniversity of Manchester · GBUppsala University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Observational evidence links higher blood levels of copper with higher risk of cardiovascular diseases. However, whether those associations reflect causal links or can be attributed to confounding is still not fully clear. We investigated causal effects of copper on the risk of cardiometabolic endpoints (stroke, coronary artery disease [CAD] and type 2 diabetes) and cardiometabolic risk factors in two-sample Mendelian randomization (MR) studies. The selection of genetic instruments for blood copper levels relied on meta-analysis of genome-wide association studies in three independent studies (European Prospective Investigation into Cancer and Nutrition-Potsdam study, Prospective investigation of the Vasculature in Uppsala Seniors study, Queensland Institute of Medical Research studies). For the selected instruments, outcome associations were drawn from large public genetic consortia on the respective disease endpoints (MEGASTROKE, Cardiogram, DIAGRAM) and cardiometabolic risk factors. MR results indicate an inverse association for genetically higher copper levels with risk of CAD (odds ratio [95% confidence interval] = 0.92 [0.86-0.99], P = 0.022) and systolic blood pressure (beta [standard error (SE)] = -0.238 [0.121]; P = 0.049). Multivariable MR incorporating copper and systolic blood pressure into one model suggested systolic blood pressure as mediating factor between copper and CAD risk. In contrast to previous observational evidence establishing higher blood copper levels as risk-increasing factor for cardiometabolic diseases, this study suggests that higher levels of genetically predicted copper might play a protective role for the development of CAD and systolic blood pressure.

Indexed as

Cardiovascular DiseasesCoronary Artery DiseaseDiabetes Mellitus, Type 2CopperGenome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single NucleotideProspective StudiesRisk FactorsCopper

Identifiers

PMID34523676
PMCPMC8895748
OpenAlexW3201390337

What OpenQuestion holds

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LicenceCC BY-NC
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 OpenQuestion graph.