Liu Yang, Zhang Xinhong, Liu Yuehui, Zhang Dongwei
Second Department of Neurology, Affiliated Hospital of Inner Mongolia Minzu University, Tongliao, China.
Medicine (Baltimore). 2025 Sep 5;104(36):e44398. doi: 10.1097/MD.0000000000044398.
Observational studies have reported inconsistent links between tea intake and stroke risk. We applied two-sample Mendelian randomization (MR) to clarify whether the association is causal. Following STROBE-MR guidelines, we extracted genome-wide association study (GWAS) summary statistics for tea intake (UK Biobank, n = 447,485; GWAS ID ukb-b-6066) and stroke (UK Biobank, n = 462,933; GWAS ID ukb-b-6358), both of European ancestry. Thirty-six independent single-nucleotide polymorphisms (SNPs) meeting genome-wide significance (P < 5 × 10-8), linkage disequilibrium threshold r² < 0.001 (10,000 kb), and F > 10 were selected as instrumental variables (IVs). Causal estimates were calculated using inverse variance weighting (IVW) as the primary analysis and weighted median, MR-Egger, simple mode, and weighted mode as complementary methods. Heterogeneity (Cochran Q and Rücker Q), horizontal pleiotropy (MR-Egger intercept), and leave-one-out sensitivity analyses were performed to evaluate robustness. IVW indicated no causal effect of tea intake on stroke (odds ratio [OR] = 0.997, 95% confidence interval [CI]: 0.991-1.004, P = .381). Findings were consistent across MR-Egger (OR = 0.984, 95% CI: 0.953-1.015, P = .306), weighted median, simple mode, and weighted mode analyses. No significant heterogeneity was detected (Cochran Q P = .176; Rücker Q P = .181), and the MR-Egger intercept showed no evidence of horizontal pleiotropy (P = .386). Leave-one-out and funnel plot assessments confirmed result stability and minimal bias. Genetic evidence from this large, two-sample MR study does not support a causal relationship between habitual tea consumption and stroke risk. Public health strategies aimed at stroke prevention should therefore not rely on promoting tea intake alone.
观察性研究报告了茶摄入量与中风风险之间的关联并不一致。我们应用两样本孟德尔随机化（MR）来阐明这种关联是否具有因果关系。遵循STROBE-MR指南，我们提取了欧洲血统的茶摄入量（英国生物银行，n = 447,485；GWAS ID ukb-b-6066）和中风（英国生物银行，n = 462,933；GWAS ID ukb-b-6358）的全基因组关联研究（GWAS）汇总统计数据。选择36个符合全基因组显著性（P < 5×10-8）、连锁不平衡阈值r² < 0.001（10,000 kb）且F > 10的独立单核苷酸多态性（SNP）作为工具变量（IV）。使用逆方差加权（IVW）作为主要分析方法，并使用加权中位数、MR-Egger、简单模式和加权模式作为补充方法来计算因果估计值。进行异质性（Cochran Q和Rücker Q）、水平多效性（MR-Egger截距）和逐一剔除敏感性分析以评估稳健性。IVW表明茶摄入量对中风无因果效应（优势比[OR] = 0.997，95%置信区间[CI]：0.991 - 1.004，P = 0.381）。在MR-Egger（OR = 0.984，95% CI：0.953 - 1.015，P = 0.306）、加权中位数、简单模式和加权模式分析中，结果是一致的。未检测到显著的异质性（Cochran Q P = 0.176；Rücker Q P = 0.181），并且MR-Egger截距未显示水平多效性的证据（P = 0.386）。逐一剔除和漏斗图评估证实了结果的稳定性和最小偏差。这项大型两样本MR研究的遗传证据不支持习惯性饮茶与中风风险之间存在因果关系。因此，旨在预防中风的公共卫生策略不应仅依赖于促进茶的摄入量。
