Causal relationship between smoking and level of C-reactive protein:a two-sample Mendelian randomization study
Background Previous investigations have illuminated the correlation between smoking and C-reactive protein(CRP),but previous research findings may be influenced by other confounding factors.The causal relationship of CRP in smoking-related pathological process requires further exploration.Objective To investigate the causal relationship between smoking behavior and CRP by utilizing the cumulative statistical data from existing genome-wide association studies(GWAS),so as to provide references for formulating relevant public health policies and smoking intervention measures.Methods This research utilized the GWAS summary statistics for CRP and four smoking phenotypes:age of initiation of regular smoking,smoking initiation,smoking cessation and cigarettes per day-selecting independent genetic loci correlated with smoking and CRP as instrumental variables.The study employed the inverse variance weighted method(IVW)and the weighted median approach for two-sample Mendelian randomization(MR)analysis to explore the bidirectional causal relationship between smoking and CRP.The Cochran's Q test was applied to assess heterogeneity among single nucleotide polymorphisms(SNPs).MR pleiotropy residual sum and outlier was used to detect SNP outliers.MR-Egger intercept test examined the horizontal pleiotropy of SNPs.Leave-one-out sensitivity analysis assessed the impact of individual SNP on the Mendelian randomization results.Results The MR analysis revealed a bidirectional causal relationship between CRP and smoking initiation(β=0.170,P=0.01)(with smoking initiationas the exposure),(β=0.040,P=0.001)(with CRP as the exposure).Conclusion Smoking may lead to alterations in CRP levels,while changes in CRP levels could also influence individual's propensity to initiate smoking.
SmokingC-reactive proteinGenome-wide association studiesMendelian randomization
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