Aug 2026· Medicine· Vol 105, pp. e50075· 0 citations· 48 references
Medicine
TL;DR
Evidence is provided of a potential causal relationship between other cataract and anxiety, though findings were method-dependent and no significant associations were observed for senile cataract or most psychiatric disorders.
Abstract
This study aimed to investigate the genetic causality between cataract (senile and other types) and psychiatric disorders using Mendelian randomization (MR). We performed a bidirectional 2-sample MR analysis using genome-wide association studies summary data. Primary analysis employed inverse-variance weighted, MR-Egger, weighted median, and weighted mode methods. Sensitivity analyses included Cochran Q, MR-pleiotropy residual sum and outlier, MR-Egger intercept, and leave-one-out tests to assess heterogeneity and pleiotropy. Forward MR analysis revealed a suggestive causal effect of other cataract on anxiety (inverse-variance weighted odds ratio [OR] = 0.99, 95% confidence interval: 0.98–1.00, P = .043), though unsupported by other methods. MR-Egger and weighted median suggested potential associations between other cataract and bipolar disorder (P < .05). No significant links were found between senile cataract and psychiatric disorders. Reverse MR analysis showed no consistent causal effects, except for anxiety disorder on other cataract (MR-Egger OR = 8.04, P = .040; weighted median OR = 2.99, P = .047). Sensitivity analyses confirmed robustness despite heterogeneity. This study provides evidence of a potential causal relationship between other cataract and anxiety, though findings were method-dependent. No significant associations were observed for senile cataract or most psychiatric disorders.
Genetic evidence supporting a causal role for depression in the etiology of late-onset AD is provided, a link not observed for other major psychiatric disorders tested and highlighted the specific importance of managing depression as a potential strategy for mitigating AD risk.
Objective This study used two-sample Mendelian Randomization to investigate the causal link between multiple biological aging indicators and vascular disease. Methods Summary genetic data was obtained from genome-wide association studies (GWAS) focusing on aging-related exposures and various vascular disease outcomes. The exposures included granulocyte proportions, PAI-1 (plasminogen activator inhibitor-1), telomere lengths, and the Frailty Index. The primary analysis employed the Inverse Variance Weighted (IVW) method to estimate causal relationships, supported by MR-Egger, weighted median, and weighted mode methods. Sensitivity analyses, including Cochran’s Q test, MR-Egger regression, leave-one-out test, and the MR Pleiotropy Residual Sum and Outlier (MR-PRESSO) test, were conducted to evaluate heterogeneity and pleiotropy. Results The analysis revealed distinct pathways after sensitivity adjustments. A higher genetically predicted Frailty Index was associated with an increased risk of abdominal aortic aneurysm (OR=2.5935, 95% CI: 1.3936–4.8268, P=0.0026, false discovery rate (FDR)=0.0475), atherosclerosis excluding cerebral and coronary sclerosis (OR=2.0262, 95% CI:1.5179–2.705, P=1.66×10-6, FDR=1×10-4), and arterial thromboembolic events (OR = 4.0306, 95% CI: 1.7133–9.4818, P = 0.0014, FDR = 0.0337). Conversely, longer telomere length demonstrated a strong, specific protective effect against abdominal aortic aneurysm (OR=0.5008, 95% CI:0.4111–0.6100, P=6.42×10-12, FDR=9.25×10-10), indicating that shorter telomere length is associated with an increased risk of AAA. Furthermore, a lower granulocyte proportion was causally linked to an increased risk of thoracic aortic aneurysm (OR=0.0181, 95% CI: 0.0014–0.2376, P=0.0023, FDR=0.0465). Conclusion This study identifies three genetic pathways linking biological aging to vascular disease, offering new molecular targets for its prevention and treatment.
Hao Yan, Shang Wei, Hui Hui et al.· Clinical and applied thrombo...· 0 citations
Evidence is provided supporting a causal effect of PMR on the risk of hypothyroidism and suggesting that hypothyroidism-induced myopathic changes may mimic or exacerbate PMR symptoms, potentially leading to misdiagnosis or overtreatment with corticosteroids.
Kaige Gao, Xin Yang, Zhenyu Wang et al.· Current Rheumatology Reviews· 0 citations
It is suggested that sleep disturbances may represent potential modifiable factors associated with mental health outcomes and highlight the importance of sleep-related interventions in psychiatric disease prevention and management.
Xin Wu, Mei Chang, Bingyi Song et al.· Frontiers in Psychiatry· 0 citations
The potential causal relationship between hip osteoarthritis (HOA) and pancreatic cancer (PC) is not well understood. To investigate this, our study utilized a two-sample Mendelian randomization (MR) method to examine a possible causal link between HOA and an increased risk of PC. Genome-wide association study summary data for both HOA and PC were sourced from the Integrative Epidemiology Unit OpenGWAS database (https://gwas.mrcieu.ac.uk/datasets/). The single-nucleotide polymorphisms associated with these conditions at a statistically significant level (P value <5 × 10−8) were identified as instrumental variables for subsequent analysis. We conducted bidirectional two-sample MR analyses employing inverse-variance weighting (IVW), weighted median, MR-Egger regression, and weighted mode methods. The robustness of the findings was assessed through sensitivity testing. The IVW analysis indicated that HOA elevated the risk of PC (odds ratio = 1.788; 95% confidence interval: 1.166–2.742; P = .008). Conversely, in the reverse MR analysis, the IVW analysis provided no evidence that PC increased the risk of HOA (odds ratio = 1.016; 95% confidence interval: 0.973–1.060; P = .475). In addition, the weighted mode, weighted median, and MR-Egger regression methods did not uncover a causal relationship. There was no heterogeneity or horizontal pleiotropy among the instrumental variables. The “leave-one-out” analysis revealed that no single-nucleotide polymorphism significantly influenced the overall results. Genetically predicted HOA is significantly associated with an increased risk of PC. However, we found no evidence that PC leads to an increased risk of HOA.
