Individuals with Sjögren's syndrome (SS) frequently experience insomnia, which may indicate a potential connection between the two conditions. Nonetheless, the exact causal relationship between insomnia and SS, including its direction, isn't fully understood.

We conducted a bidirectional Mendelian randomization (MR) study to see if a genetic link exists. Within our research, we retrieved data from two sources: the IEU database, which provided information on 1,402 individuals with insomnia and 485,225 controls, and the FinnGen database, which included data on 1,290 patients with SS and 213,145 controls. We mainly used the inverse variance weighted (IVW) method along with four additional approaches to analyze the two-way causal relationship between insomnia and SS. To assess the results' stability and reliability, we conducted heterogeneity and sensitivity analyses using Cochran's Q test, the leave-one-out method, and other relevant techniques.

A total of 13 single nucleotide polymorphisms (SNPs) related to SS were screened out, with 12 included in the analysis for SS; 5 SNPs related to insomnia were identified, with 4 included in the analysis for insomnia. The findings from the MR analysis suggested that insomnia does not have a significant causal impact on SS, with an IVW odds ratio (OR) of 1.0373; 95% confidence interval (CI): 0.8777-1.2260; P = 0.667. Similarly, the reverse MR analysis also indicated that SS has no significant influence on insomnia with an IVW OR of 0.9960; 95%CI: 0.9272-1.0698; P = 0.912. The results from the other four analytical methods aligned with these conclusions (P > 0.05). No significant pleiotropy was observed in the association between insomnia and SS. Furthermore, the random effects model revealed heterogeneity in the effect of insomnia on SS, but not in the reverse direction.

We found no significant causal connection between insomnia and the risk of SS. Thus, it is necessary to conduct large-scale studies to further explore the potential causal relationship and the exact underlying mechanisms.