Evidence map›Paper›PMID 34203356›Full record

ArticleNutrients2021

Coffee Consumption and Cardiovascular Diseases: A Mendelian Randomization Study.

Shuai Yuan, Paul Carter, Amy M Mason, Stephen Burgess, Susanna C Larsson

Abstract read
In one paragraph

Article in Nutrients, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 2 pooled it
–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

24 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

5 authors.

Shuai YuanUnit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, SE-171 77 Stockholm, Sweden.ORCID 0000-0001-5055-5627
Paul CarterDepartment of Medicine, University of Cambridge, Cambridge CB2 0QQ, UK.
Amy M MasonDepartment of Public Health and Primary Care, University of Cambridge, Cambridge CB1 8RN, UK.ORCID 0000-0002-8019-0777
Stephen BurgessDepartment of Public Health and Primary Care, University of Cambridge, Cambridge CB1 8RN, UK.
Susanna C LarssonUnit of Cardiovascular and Nutritional Epidemiology, Institute of Environmental Medicine, Karolinska Institutet, SE-171 77 Stockholm, Sweden.ORCID 0000-0003-0118-0341

Funding

British Heart Foundation CH/12/2/29428British Heart Foundation CH/1996001/9454British Heart Foundation RG/13/13/30194British Heart Foundation RG/18/13/33946EC-Innovative Medicines Initiative BigData@HeartForskningsrådet om Hälsa, Arbetsliv och Välfärd 2018-00123Karolinska Institutet 2020-01842Medical Research Council MC_PC_17228Medical Research Council MC_QA137853Medical Research Council MC_UU_00002/7Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society 204623/Z/16/ZSwedish Heart-Lung Foundation 20190247Vetenskapsrådet 2019-00977Wellcome Trust 204623/Z/16/Z
6 · The paper itself

Abstract

Coffee consumption has been linked to a lower risk of cardiovascular disease in observational studies, but whether the associations are causal is not known. We conducted a Mendelian randomization investigation to assess the potential causal role of coffee consumption in cardiovascular disease. Twelve independent genetic variants were used to proxy coffee consumption. Summary-level data for the relations between the 12 genetic variants and cardiovascular diseases were taken from the UK Biobank with up to 35,979 cases and the FinnGen consortium with up to 17,325 cases. Genetic predisposition to higher coffee consumption was not associated with any of the 15 studied cardiovascular outcomes in univariable MR analysis. The odds ratio per 50% increase in genetically predicted coffee consumption ranged from 0.97 (95% confidence interval (CI), 0.63, 1.50) for intracerebral hemorrhage to 1.26 (95% CI, 1.00, 1.58) for deep vein thrombosis in the UK Biobank and from 0.86 (95% CI, 0.50, 1.49) for subarachnoid hemorrhage to 1.34 (95% CI, 0.81, 2.22) for intracerebral hemorrhage in FinnGen. The null findings remained in multivariable Mendelian randomization analyses adjusted for genetically predicted body mass index and smoking initiation, except for a suggestive positive association for intracerebral hemorrhage (odds ratio 1.91; 95% CI, 1.03, 3.54) in FinnGen. This Mendelian randomization study showed limited evidence that coffee consumption affects the risk of developing cardiovascular disease, suggesting that previous observational studies may have been confounded.

Indexed as

Cardiovascular DiseasesCoffeeAdultAgedBody Mass IndexGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansMendelian Randomization AnalysisMiddle AgedOdds RatioPolymorphism, Single NucleotideRisk FactorsSmokingWhite PeopleCoffeecardiovascular diseasecoffeemendelian randomization analysis

Identifiers

PMID34203356
PMCPMC8308456

What OpenQuestion 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 OpenQuestion graph.