Testing relationship between tea intake and the risk of rheumatoid arthritis and systemic lupus erythematosus: a Mendelian randomization study.

BACKGROUND: We performed Mendelian randomization (MR) to assess the causal effect of tea intake on rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). METHODS: Genetic instruments for tea intake were obtained from a large genome-wide association study (GWAS) dataset of the UK Biobank. Genetic association estimates for RA (6236 cases and 147,221 controls) and SLE (538 cases and 213,145 controls) were obtained from the FinnGen study through the IEU GWAS database. RESULTS: MR analyses using the inverse-variance weighted method showed that tea intake was not associated with risk of RA [odds ratio (OR) per standard deviation increment in genetically predicted tea intake = 0.997, 95% confidence interval (CI) 0.658-1.511] and SLE (OR per standard deviation increment in genetically predicted tea intake = 0.961, 95% CI 0.299-3.092). Weighted median, weighted mode, MR-Egger, leave-one-out and multivariable MR controlling for several confounding factors including current tobacco smoking, coffee intake, and alcoholic drinks per week yielded completely consistent results. No evidence of heterogeneity and pleiotropy was found. CONCLUSION: Our MR study did not suggest a causal effect of genetically predicted tea intake on RA and SLE.

Testing relationship between tea intake and the risk of rheumatoid arthritis and systemic lupus erythematosus: a Mendelian randomization study

Abstract Background We performed Mendelian randomization (MR) to assess the causal effect of tea intake on rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Methods Genetic instruments for tea intake were obtained from a large genome-wide association study (GWAS) dataset of the UK Biobank. Genetic association estimates for RA (6236 cases and 147,221 controls) and SLE (538 cases and 213,145 controls) were obtained from the FinnGen study through the IEU GWAS database. Results MR analyses using the inverse-variance weighted method showed that tea intake was not associated with risk of RA [odds ratio (OR) per standard deviation increment in genetically predicted tea intake = 0.997, 95% confidence interval (CI) 0.658-1.511] and SLE (OR per standard deviation increment in genetically predicted tea intake = 0.961, 95% CI 0.299-3.092). Weighted median, weighted mode, MR-Egger, leave-one-out and multivariable MR controlling for several confounding factors including current tobacco smoking, coffee intake, and alcoholic drinks per week yielded completely consistent results. No evidence of heterogeneity and pleiotropy was found. Conclusion Our MR study did not suggest a causal effect of genetically predicted tea intake on RA and SLE.

Association of interleukin-1 gene polymorphisms with multiple sclerosis: a meta-analysis.

BACKGROUND: Dysregulated levels of interleukin-1 (IL-1) were observed in patients with multiple sclerosis (MS). Previous studies have provided conflicting evidence implicating the IL-1 gene polymorphisms in MS risk. METHODS: A meta-analysis of 16 case-control studies involving 3,482 cases and 3,528 controls was conducted to evaluate this association. RESULTS: No association was found between the IL-1α -889 (rs1800587), IL-1α +4,845 (rs17561), IL-1ß -511 (rs16944), IL-1ß +3,953 (rs1143634), IL-1ra variable number tandem repeat (VNTR) polymorphisms and MS risk. However, in subgroup analyses for the IL-1ra VNTR polymorphism, we found that individuals carrying the 2 allele had a 32 % increased risk for bout-onset MS (relapsing remitting and secondary progressive MS) when compared to the LL homozygotes (OR = 1.32, 95 % CI = 1.06-1.66, P (z) = 0.014). CONCLUSION: Common variants in the IL-1 region are not associated with MS risk but our data suggest that the IL-1ra VNTR polymorphism might be associated with bout-onset MS subtype.