Evidence map›Paper›PMID 40186783›Full record

SynthesisEuropean journal of nutrition2025

Assessing the genetic estimates of the association between plasma caffeine and cancer risk through Mendelian randomization.

Hao Wang, Keru Ma, Ming Shan, Guoqiang Zhang

Abstract readMeta-Analysis
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In one paragraph

Synthesis in European journal of nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

2 citing papers in PubMed.

  1. Caffeine-mediated CD39Frontiers in immunology · 2026
    Article
  2. Article
4 · The record

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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

4 authors.

Hao Wang *Department of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Keru Ma *Department of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China.
Ming ShanDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China. shanming@ems.hrbmu.edu.cn.
Guoqiang ZhangDepartment of Breast Surgery, Harbin Medical University Cancer Hospital, Harbin, China. zhangguoqiang@hrbmu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundObservational studies still cannot establish a causal relationship between plasma caffeine levels and cancer risk. This study aimed to investigate the genetic effects of plasma caffeine levels on cancer risk through Mendelian randomization (MR).

methodsPlasma caffeine's genome-wide association study (GWAS) data were derived from a meta-analysis of 9,876 individuals of European ancestry. We selected 8 single nucleotide polymorphisms (SNPs) closely associated with plasma caffeine levels as instrumental variables (IVs). The GWAS data for cancer outcomes were obtained from genotype data in the Finnish Biobank and digital health record data from the Finnish National Institute for Health and Welfare, specifically the R10 version released on December 18, 2023. The risk effects of genetic variations were assessed using the inverse variance-weighted (IVW) method and the wald ratio method.

resultsAfter correction, genetically predicted higher levels of plasma caffeine were significantly associated with an increased risk of lung cancer (OR = 1.54, 95%CI: 1.33-1.78, P_FDR < 0.001). In cancer subtype analysis, genetically predicted higher levels of plasma caffeine were significantly associated with the risk of lung squamous cell carcinoma (OR = 1.60, 95%CI: 1.16-2.19, P_FDR = 0.037) and non-small cell lung cancer (OR = 1.51, 95%CI: 1.21-1.89, P_FDR = 0.003) after correction.

conclusionThe current MR results indicate that long-term higher levels of plasma caffeine are associated with an increased risk of lung cancer. These findings merit further exploration to understand whether caffeine intake, supplementation, or cessation could have clinically relevant therapeutic or preventive effects.

Indexed as

CaffeineLung NeoplasmsMendelian Randomization AnalysisNeoplasmsFemaleFinlandGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansMalePolymorphism, Single NucleotideRisk FactorsCaffeineCaffeineCancer riskCoffee consumptionMendelian randomization

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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.