The link between salt intake and the risk of gastric cancer remains uncertain, and a causal relationship has not been established. Therefore, clarifying the causal effect of salt intake on the risk of gastric cancer using reliable causal inference methods is necessary. The aim of this study was to assess the causal association between salt intake and cancer by integrating summary-level genome-wide association study (GWAS) data. Two-sample Mendelian randomization (MR) analyses were performed using summary statistics from a GWAS. Inverse-variance weighted (IVW) regression, Mendelian randomization-Egger (MR-Egger) regression, and weighted median analyses were used to evaluate the causal relationship between salt intake and gastric cancer. Moreover, Mendelian Randomization Pleiotropy RESidual Sum of Squares and Outliers and MR-Egger analyses were used to evaluate the level of multipotency, and "leave-one-out" sensitivity analysis was assessed. The IVW method estimate indicated that salt intake was not correlated with gastric cancer incidence. The IVW (β = 0.1008, standard error SE = 0.1510, odds ratio OR = 1.1061, 95% confidence interval CI, 0.82-1.48, P = .5042), MR-Egger regression (β = 0.059, SE = 0.5318, OR = 1.0612, 95% CI, 0.37-3.01, P = .9111), and weighted median (β = 0.2639, SE = 0.2298, OR = 1.3020, 95% CI, 0.82-2.04, P = .2508) analyses revealed no causal relationship between salt intake and gastric cancer risk (P > .05). In addition, the funnel plot and MR-Egger analysis (P = .6694 > .05) did not indicate horizontal pleiotropy or heterogeneity. GWAS data from public databases were used in this study, and the causal relationship between salt intake and gastric cancer risk was analyzed via a two-sample MR method. The results revealed no genetic causal relationship between salt intake and gastric cancer.
Li et al. (Fri,) studied this question.