Observational research has indicated a potential link between dietary salt intake and susceptibility to dementia. However, it is important to note that these types of studies are prone to the issues of reverse causation and residual confounding. Therefore, we conducted a two-sample Mendelian randomization (MR) study to explore the causality. To explore the causal relationship between them, this Mendelian randomization (MR) study incorporated summary statistics of dietary salt intake and dementia. We estimated the causality between salt intake and the risk of overall dementia and various subtypes of dementia, including Alzheimer’s disease (AD), Vascular dementia (VaD), and Lewy body dementia (LBD). The inverse variance-weighted (IVW) method was the major MR analysis. To conduct sensitivity analyses, we employed various MR methods, the pleiotropy residual sum and outlier (MR-PRESSO) method, and the leave-one-out approach. The MR-Egger intercept and Cochran’s Q test were conducted to test pleiotropy and heterogeneity respectively. A suggestive association was observed for genetically predicted higher dietary salt intake and increased risk of overall dementia in the European ancestry [odds ratio (OR): 1.542; 95% confidence interval (95% CI): 1.095–2.169; P = 0.013]. The causal relationship between dietary salt intake and overall dementia is robust with respect to the choice of statistical methods and is validated through extensive sensitivity analyses that guard against various model assumption violations. Meanwhile, no clear heterogeneity or pleiotropy was identified. However, we failed to detect a causal effect of dietary salt intake on the risk of various dementia subtypes. The results of this research present strong evidence that established a significant association between dietary salt intake and the likelihood of developing dementia. These findings reinforce the notion that the amount of dietary salt intake plays a crucial role in determining the risk of acquiring this cognitive condition. By establishing a definitive correlation, this study highlights the importance of reducing salt consumption as a preventive measure against dementia.

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膳食盐摄入量与痴呆风险之间的因果关系：孟德尔随机研究

观察性研究表明膳食盐摄入量与痴呆症易感性之间存在潜在联系。然而，值得注意的是，这些类型的研究很容易出现反向因果关系和残留混杂的问题。因此，我们进行了两个样本的孟德尔随机化（MR）研究来探讨其中的因果关系。为了探索它们之间的因果关系，这项孟德尔随机化 (MR) 研究纳入了膳食盐摄入量和痴呆症的汇总统计数据。我们估计了盐摄入量与整体痴呆和各种痴呆亚型风险之间的因果关系，包括阿尔茨海默病 (AD)、血管性痴呆 (VaD) 和路易体痴呆 (LBD)。逆方差加权 (IVW) 方法是主要的 MR 分析。为了进行敏感性分析，我们采用了各种 MR 方法、多效性残差和离群值 (MR-PRESSO) 方法以及留一法。MR-Egger 截距和 Cochran's Q 检验分别用于检验多效性和异质性。在欧洲血统中，观察到基因预测较高膳食盐摄入量与整体痴呆风险增加之间存在暗示性关联[比值比 (OR)：1.542；95%置信区间（95% CI）：1.095–2.169；P = 0.013]。膳食盐摄入量与总体痴呆症之间的因果关系在统计方法的选择方面是稳健的，并通过广泛的敏感性分析进行了验证，以防止各种模型假设的违反。同时，没有发现明显的异质性或多效性。然而，我们未能发现膳食盐摄入量对各种痴呆亚型风险的因果影响。这项研究的结果提供了强有力的证据，证明膳食盐摄入量与患痴呆症的可能性之间存在显着关联。这些发现强化了这样的观点：饮食中盐的摄入量在确定罹患这种认知疾病的风险方面起着至关重要的作用。通过建立明确的相关性，这项研究强调了减少盐摄入量作为预防痴呆症的重要性。