ArticleNature communications2025
Assessing the potential causal effects of 1099 plasma metabolites on 2099 binary disease endpoints.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Gene-Environment Interaction Mendelian Randomization Reveals Statin-Dependent Associations Between Metabolites and Lipid Traits.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Fibroblast-derived HSD11B1 deficiency drives lung cancer in never-smokers through steroid metabolic imbalance.NPJ precision oncology · 2026Article
- Plasma multi-omics profiling unravels molecular alterations and biomarker panels during recovery from severe coronavirus disease 2019: a pilot study.BMC infectious diseases · 2026Article
- Widespread genetic effect heterogeneity impacts bias and power in nonlinear Mendelian randomization.medRxiv : the preprint server for health sciences · 2026Article
- Genetic Correlations and Causal Relationships Among Allergic Diseases: A Comprehensive Mendelian Randomization Study With Multiomic Mediation Analysis.Mediators of inflammation · 2026Article
- Novel Causal Evidence for the Role of Circulating Lipid Metabolites in Breast Cancer Risk: A Bidirectional Mendelian Randomization Analysis.Journal of nutrition and metabolism · 2025Article
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23 authors.
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Abstract
Metabolites are small molecules that are useful for estimating disease risk and elucidating disease biology. Here, we perform two-sample Mendelian randomization to systematically infer the potential causal effects of 1099 plasma metabolites measured in 6136 Finnish men from the METSIM study on risk of 2099 binary disease endpoints measured in 309,154 Finnish individuals from FinnGen. We find evidence for 282 putative causal effects of 70 metabolites on 183 disease endpoints. We also identify 25 metabolites with potential causal effects across multiple disease domains, including ascorbic acid 2-sulfate affecting 26 disease endpoints in 12 disease domains. Our study suggests that N-acetyl-2-aminooctanoate and glycocholenate sulfate affect risk of atrial fibrillation through two distinct metabolic pathways and that N-methylpipecolate may mediate the putative causal effect of N6,N6-dimethyllysine on anxious personality disorder.
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