Background The causal inference between leisure sedentary behaviour (LSB) and rheumatoid arthritis (RA) is still controversial because of potential residual confounding and reverse causality. Methods The present study used publicly available large‐scale genome‐wide association studies (GWAS) of LSB (television watching, computer use, and driving) and RA to perform a two‐sample Mendelian randomization (MR) study to evaluate the causal effect of LSB on the risk of RA. We detected significant causal associations using the multiplicative random effects‐inverse variance weighted (MRE‐IVW) method, the maximum likelihood, robust adjusted profile scores, the weighted median, MR‐Egger regression, and several complementary sensitivity analyses. Risk factor analysis was also conducted to further investigate potential mediators linking causal inference. Results Increased genetic liability to leisure television watching was significantly associated with a higher risk of RA (MRE‐IVW method; OR = 2.46, 95% CI 1.77–3.41; p = 8.35 × 10−8). MR estimates indicated that prolonged leisure computer use was causally associated with a lower risk of RA (MRE‐IVW method; OR = 0.23, 95% CI 0.12–0.46; p = 2.19 × 10−5). However, we found no evidence for a causal effect of leisure driving on the risk of RA (MRE‐IVW method; OR = 0.59, 95% CI 0.10–3.41; p = 0.557). No pleiotropy was detected by the sensitivity analysis. Conclusions This study supports a causal association between prolonged leisure television watching and an increased risk of RA. Additionally, prolonged computer use might be a protective factor for RA.

Background It has been observed that cancer and venous thromboembolism (VTE) are associated, but anticancer therapy may violate the causality. Therefore, this study aimed to elucidate the causal relationship of various cancers to VTE using Mendelian randomization (MR). Methods Three MR methods were used to estimate causal effects: Inverse variance weighted (IVW), MR‐Egger and weighted median. Sensitivity analyses included Cochran's Q‐test, MR‐Egger intercept test and MR‐PRESSO. Gene ontology enrichment analysis was performed to elucidate the underlying mechanisms of VTE development in cancer patients. Results The primary IVW approach showed that non‐Hodgkin's lymphoma (NHL) might increase the risk of VTE (odds ratio [OR]: 1.20, 95% confidence interval [95% CI]: 1.00–1.44, p = 0.045), while melanoma possibly reduced the risk of VTE (OR: 0.89, 95% CI: 0.82–0.97, p = 0.006), although there was no significance after adjustment for multiple testing. No association was observed between VTE risk and other site‐specific cancers. Gene ontology enrichment analysis revealed that vitamin D played an important role in the development of VTE in cancer patients. Conclusions Our findings suggested that genetically predicted NHL was associated with higher VTE risk, whereas melanoma had lower VTE risk compared with other site‐specific cancers. Moreover, this study suggested that anticancer therapy and increased extensive examination might play a more important role in VTE development than the nature of cancer.