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Observational studies have found that coffee consumption is inversely associated with risk of incident gout but inconsistently with serum uric acid concentrations.1–3 The causality of the associations is, however, uncertain since observational studies are susceptible to confounding and reverse causation bias. Genetic variants with an explicit impact on a modifiable exposure, such as a biomarker or habitual behaviour like coffee consumption, can be used as instrumental variables (proxies) for the exposure to improve causal inference.4 This method, known as Mendelian randomisation, builds on Mendel’s second law and the fact that genetic variants are randomly assorted during meiosis. Therefore, results from Mendelian randomisation studies are less prone to bias due to confounding and reverse causality. We used the Mendelian randomisation approach to examine whether coffee consumption is associated with gout and whether the association may be mediated by serum uric acid concentrations.
A genome-wide association study from the Coffee and Caffeine Genetics Consortium identified 10 single-nucleotide polymorphisms (SNPs), at eight loci, associated with coffee …
Handling editor Josef S Smolen
Contributors SCL: conception and design of the work, analysis and interpretation of data, drafting the work and final approval. MC: conception and design of the work, interpretation of data and final approval.
Funding This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
Data sharing statement No additional data to share. All data are publicly available and also provided in Figure 1 and Table S1.
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