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BACKGROUND AND PURPOSE Elevated C-reactive protein (CRP) is associated with an increased risk of ischaemic stroke (IS). However, the causality of this association is uncertain. The aim is to investigate whether genetically raised plasma CRP concentration levels are associated with IS on the basis of the Mendelian randomization method. METHODS Based on the National Center for Biotechnology Information single nucleotide polymorphism (SNP) database, the Chinese online genetic database as well as previously published studies, four CRP-associated SNP alleles (rs1130864, rs1205, rs876537 and rs3093059) with minor allele frequency ≥0.15 were selected and the concentration levels of CRP were measured in 378 first-ever IS patients and 613 healthy controls. RESULTS Three SNPs were chosen and used as instrumental variables. The adjusted odds ratios (ORs) [95% confidence interval (95% CI)] of IS per addition of the modelled allele were 1.07 (0.79-1.45) for rs876537, 0.99 (0.73-1.35) for rs1205 and 1.08 (0.71-1.65) for rs3093059. The OR (95% CI) of IS for plasma CRP ≥2.0 mg/l was 2.19 (1.06-4.53) compared with

Background & aims Although evidence indicates that visceral adipose tissue is associated with nonalcoholic fatty liver disease (NAFLD), it is unclear whether the visceral adiposity index (VAI) can predict the onset of NAFLD. This study aimed to determine whether the VAI is an independent risk factor of NAFLD and whether there is a dose-response relationship. Methods We explored the relationship between VAI levels and NAFLD in a health check-up cohort established in 2012. There were 4809 subjects with baseline data and results from 4 follow-up examinations. The diagnosis of NAFLD was established by demonstration of increased hepatic echogenicity with ultrasound and exclusion of alcohol overconsumption with questionnaires. We divided the subjects into 4 groups according to baseline VAI levels and used the Cox hazard regression model to estimate NAFLD risk by VAI quartile at baseline by adjusting for potential confounding factors. A Kaplan-Meier survival analysis was used to compare the risk of NAFLD incidence among individuals in each VAI quartile. Results The 4-year cumulative incidence of NAFLD in this cohort was 13.9%. The hazard ratios (95% confidence intervals, 95% CI) for NAFLD in the second, third and fourth VAI quartiles compared with the first quartile were 1.42 (95% CI: 1.24-1.64), 1.73 (95% CI: 1.51-1.99) and 2.13(95% CI: 1.86-2.45) respectively. The Kaplan-Meier survival analysis suggested that higher VAI levels predict higher incidences of NAFLD in a dose-dependent relationship. Conclusions Our findings suggest that the VAI level is an independent risk factor of NAFLD and there is a dose-response relationship between VAI level and NAFLD risk.