Background The association between triglyceride and prostate cancer (PCa) has been reported in observational studies. However, the causality from triglyceride on PCa remained unknown. Method Two-sample Mendelian randomization (MR) was performed with triglyceride genome-wide association study (GWAS) data from 177,861 individuals and GWAS summary statistics of PCa from 463,010 individuals. Then, 48 single nucleotide polymorphisms (SNPs) of triglyceride were used as instrumental variables (IVs) to conduct MR analysis on PCa. Inverse‐variance weighted (IVW), Weighted median, MR‐Egger regression, Simple mode and Weighted mode were used for MR analysis. To verify the sensitivity of the data, heterogeneity test, pleiotropy test and leave-one-out sensitivity test were performed. Results Association for an effect of triglyceride on PCa risk was found in IVW (odds ratio [OR]: 1.002, 95% confidence interval (CI): 1.000–1.004, p = 0.016). However, opposing results were observed using the weighted median (OR: 1.001, 95% CI: 0.999–1.003, p = 0.499) and MR‐Egger (OR: 0.999, 95% CI: 0.995–1.002, p = 0.401) approach. After MRPRESSO, the same result was obtained by using IVW method (OR: 1.002, 95% CI: 1.001–1.004, p = 0.004). Conclusions The large MR analysis indicated that the potential causal effect of triglyceride on PCa. The odds of PCa would increase with high levels of triglyceride.

Background Risk factors for urolithiasis have not been identified. Here, we aimed to identify potentially causal risk factors driving the risk of urolithiasis. Methods Two sets of instrumental variables were used for analysis, derived from publicly available databases. Summary-level statistical data for urolithiasis were obtained from the MRC-IEU Consortium and UK biobank (Neale Lab). Mendelian randomization (MR) was conducted to identify causal risk of urolithiasis. Finally, the results of the two databases were combined and a meta-analysis was performed. Results In the MRC-IEU consortium, the odds of urolithiasis increased per 1-SD increase of body mass index (BMI) (OR = 1.0016, 95% CI:1.0004–1.0029, p = 0.010), triglycerides (OR = 1.0016, 95% CI:1.0003–1.0029, p = 0.017), adiponectin (OR = 1.0027, 95% CI:1.0003–1.0050, p = 0.024), and body fat percentage (OR = 1.008, 95% CI:1.0001–1.0161, p = 0.047). In addition, alcohol intake also increased the incidence of urolithiasis (OR = 1.0030, 95% CI:1.0009–1.0051, p = 0.005). In the UK biobank, the odds of urolithiasis increased per 1-SD increase of waist circumference (OR = 1.0215, 95% CI:1.0061–1.0372, p = 0.008) and body fat percentage (OR = 1.0239, 95% CI:1.0043–1.0440, p = 0.020). Surprisingly, we found that the risk of urolithiasis decreased with increasing hip circumference (OR = 0.9954, 95% CI:0.9915–0.9992, p = 0.017). In a meta-analysis of MR results, higher BMI (OR = 1.0016, 95% CI:1.0004–1.0027, p = 0.009), waist circumference (OR = 1.0073, 95% CI:1.0020–1.0126, p = 0.007), adiponectin (OR = 1.0026, 95% CI:1.0008–1.0043, p = 0.004), triglycerides (OR = 1.0015, 95% CI:1.0004–1.0026, p = 0.008) and body fat percentage (OR = 1.0104, 95% CI:1.0030–1.0178, p = 0.006) increased the risk of urolithiasis. Furthermore, alcohol intake also increased the incidence of urolithiasis (OR = 1.0033, 95% CI:1.0012–1.0053, p = 0.002). Conclusions Our MR study found that higher BMI, triglycerides, waist circumference, adiponectin, body fat percentage, and alcohol intake increased the risk of urolithiasis.