This study investigates the causal relationship between the duration of mobile phone use (DMPU) and risk of stroke using Mendelian randomization (MR) analysis. Independent single nucleotide polymorphisms from genome-wide association study datasets were employed as instrumental variables to estimate the effects of DMPU on the risk of stroke, intracerebral hemorrhage, ischemic stroke, and its subtypes (cardioembolic infarction, small-vessel disease, large artery atherosclerosis LAAS). Inverse-variance weighting was utilized as the primary MR method and sensitivity analyses were performed. Ninety single nucleotide polymorphisms associated with stroke from genome-wide association study datasets were selected as instrumental variables. Inverse-variance weighted analysis showed a significant causality between DMPU and an increased risk of LAAS (odds ratio OR = 1.120; 95% confidence interval CI = 1.005–1.248; P = .040). No genetic association was found for stroke (OR = 1.000; 95% CI = 0.999–1.001, P = .677), intracerebral hemorrhage (OR = 1.020; 95% CI = 0.912–1.140, P = .734), ischemic stroke (OR = 1.020; 95% CI = 0.979–1.062, P = .344), cardioembolic infarction (OR = 1.066; 95% CI = 0.974–1.166, P = .166), and small-vessel disease (OR = 1.052; 95% CI = 0.944–1.173, P = .356). MR-Egger regression (intercept = 2.75 × 10⁻ 3 ; P = .888) suggested multidimensionality was unlikely to bias the results; Cochran Q test and funnel plot showed no heterogeneity or asymmetry, indicating the robustness of present findings. The current investigation confirmed a causal relationship between DMPU and an increased risk of LAAS, suggesting significant implications for public health initiatives and policy development.
Jin et al. (Fri,) studied this question.