■咖啡含有许多生物活性化合物,在观察性研究中已经报道了其与亚临床动脉粥样硬化的不一致关联。在孟德尔随机化研究中,我们调查了基因预测的咖啡消费是否与亚临床动脉粥样硬化有关,以及潜在中介的作用。
■我们首先进行了两个样本的孟德尔随机分析,以检查咖啡及其亚型对从冠状动脉钙化(CAC)推断的亚临床动脉粥样硬化的因果影响。接下来,使用另一个独立的数据集验证了显著结果.两步孟德尔随机化分析用于评估通过潜在介质从咖啡到亚临床动脉粥样硬化的因果途径。包括血压,血脂,身体质量指数,和糖化血红蛋白.孟德尔随机化分析采用乘性随机效应逆方差加权方法作为主要方法,其次是一系列的补充方法和敏感性分析。
■咖啡,过滤咖啡,和速溶咖啡与CAC风险相关(β=0.79,95%CI:0.12~1.47,p=0.022;β=0.66,95%CI:0.17~1.15,p=0.008;β=0.66,95%CI:0.20~1.13,p=0.005;分别)。而脱咖啡因咖啡与CAC之间没有显著的因果关系(β=-1.32,95%CI:-2.67至0.04,p=0.056)。在复制分析中验证了咖啡和CAC之间的关联(β=0.27,95%CI:0.07至0.48,p=0.009)。体重指数介导了咖啡对CAC影响的39.98%(95%CI:9.78至70.19%,p=0.009),和5.79%的速溶咖啡对CAC的影响(95%CI:0.54~11.04%,p=0.030)。
■我们的研究表明,除无咖啡因咖啡以外的咖啡会增加由CAC推断的亚临床动脉粥样硬化的风险。体重指数介导39.98和5.79%的咖啡和速溶咖啡对CAC的因果效应,分别。咖啡应该谨慎食用,尤其是在有心血管危险因素的个体中,脱咖啡因咖啡似乎是更安全的选择。
UNASSIGNED: Coffee contains many bioactive compounds, and its inconsistent association with subclinical atherosclerosis has been reported in observational studies. In this Mendelian randomization study, we investigated whether genetically predicted coffee consumption is associated with subclinical atherosclerosis, as well as the role of potential mediators.
UNASSIGNED: We first conducted a two-sample Mendelian randomization analysis to examine the causal effect of coffee and its subtypes on subclinical atherosclerosis inferred from coronary artery calcification (CAC). Next, the significant results were validated using another independent dataset. Two-step Mendelian randomization analyses were utilized to evaluate the causal pathway from coffee to subclinical atherosclerosis through potential mediators, including blood pressure, blood lipids, body mass index, and glycated hemoglobin. Mendelian randomization analyses were performed using the multiplicative random effects inverse-variance weighted method as the main approach, followed by a series of complementary methods and sensitivity analyses.
UNASSIGNED: Coffee, filtered coffee, and instant coffee were associated with the risk of CAC (β = 0.79, 95% CI: 0.12 to 1.47, p = 0.022; β = 0.66, 95% CI: 0.17 to 1.15, p = 0.008; β = 0.66, 95% CI: 0.20 to 1.13, p = 0.005; respectively). While no significant causal relationship was found between decaffeinated coffee and CAC (β = -1.32, 95% CI: -2.67 to 0.04, p = 0.056). The association between coffee and CAC was validated in the replication analysis (β = 0.27, 95% CI: 0.07 to 0.48, p = 0.009). Body mass index mediated 39.98% of the effect of coffee on CAC (95% CI: 9.78 to 70.19%, p = 0.009), and 5.79% of the effect of instant coffee on CAC (95% CI: 0.54 to 11.04%, p = 0.030).
UNASSIGNED: Our study suggests that coffee other than decaffeinated coffee increases the risk of subclinical atherosclerosis inferred from CAC. Body mass index mediated 39.98 and 5.79% of the causal effects of coffee and instant coffee on CAC, respectively. Coffee should be consumed with caution, especially in individuals with established cardiovascular risk factors, and decaffeinated coffee appears to be a safer choice.