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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 …
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