Assessment of the relationship between thyroid function and panic disorder: A mendelian randomization study

Abstract

Abstract Background Multiple observational studies have indicated a correlation between thyroid function and the risk of panic disorder (PD). Nevertheless, the causality surrounding this association remains unclear. Our objective was to evaluate the causality between thyroid function and the risk of PD by employing Mendelian randomization (MR). Methods We employed publicly available genome-wide association studies (GWAS) to select single nucleotide polymorphisms (SNPs) that are associated with various aspects of thyroid function (hyperthyroidism, hypothyroidism, FT4, TSH, TPOAb, and thyroid nodules). The statistical data on panic disorder were obtained from the FinnGen consortium. To assess causality, we utilized the inverse variance weighted (IVW) method, MR-Egger method and weighted median (WM) method for the MR estimates. Sensitivity analyses were conducted using Cochran’s Q test, MR-Egger intercept, MR-Pleiotropy Residual Sum and Outlier method, leave-one-out analysis, and funnel plot. Results The genetically predicted presence of hyperthyroidism showed an inverse association with PD as evident from the IVW OR of 0.93 (95% CI: 0.87–0.98; P = 0.01).However, our findings did not indicate any causal effects of variation in FT4 (OR: 0.78, 95%CI: 0.78–1.27; P = 1)、TSH (OR: 1.03, 95%CI: 0.83–1.28; P = 0.77)、TPOAb (OR: 0.9, 95%CI: 0.47–1.72; P = 0.75)、hypothyroidism (OR: 0.57, 95%CI: 0.01–50.54; P = 0.81) and thyroid nodules (OR: 1.02, 95%CI: 0.91–1.14; P = 0.76) on PD risk. Conclusions In summary, Our findings indicated a significant inverse correlation between hyperthyroidism and PD risk, with no discernible causal impacts of alterations in FT4、TSH、TPOAb、hypothyroidism and thyroid nodules on PD risk. It may suggest that most thyroid function may not be the etiological factor of PD, further studies are needed to verify our results in the real world.