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饮食中添加盐与欧洲血统人群痴呆症的关联:一项孟德尔随机化研究。

Association between adding salt in food and dementia in European descent: A mendelian randomization study.

机构信息

Department of Anesthesiology, The Ninth People's Hospital of Shanghai, Jiao Tong University School of Medicine, Shanghai, P. R. China.

出版信息

Brain Behav. 2024 May;14(5):e3516. doi: 10.1002/brb3.3516.

Abstract

BACKGROUND

High salt intake has been proposed as a risk factor for dementia. However, causal relationship between salt intake and dementia remains uncertain.

PURPOSE

The aim of this study was to employ a mendelian randomization (MR) design to investigate the causal impact of salt intake on the risk of dementia.

METHODS

Genome-wide association study (GWAS) data of exposures and outcomes (any dementia, cognitive performance, different types of dementia, Alzheimer's disease [AD], and Parkinson's disease) were obtained from the IEU database. MR estimates were generated though inverse-variance weighted model. MR-Egger, weighted median, and MR-Pleiotropy Residual Sum and Outlier (MR-PRESSO) method also used in our study. Sensitivity analyses included Cochran's Q test, MR-Egger intercept, MR-PRESSO global test and outlier test, leave-one-out analysis, and funnel plot assessment.

RESULTS

Our MR analysis provided evidence of a causal association between high salt added to food and dementia (odds ratio [OR] = 1.73, 95% confidence interval [CI]: 1.21-2.49, and p = .003), dementia in AD (OR = 2.10, 95% CI: 1.15-3.83, and p = .015), and undefined dementia (OR = 2.61, 95% CI: 1.26-5.39, and p = .009). Higher salt added was also associated with increased risk of AD (OR = 1.80, 95% CI: 1.12-2.87, and p = .014) and lower cognitive performance (β = -.133, 95% CI: -.229 to -.038, and p = .006).

CONCLUSION

This study provides evidence suggesting that high salt intake is causally associated with an increased risk of developing dementia, including AD and undefined dementia, highlighting the potential importance of reducing salt consumption as a preventive measure.

摘要

背景

高盐摄入量被认为是痴呆的危险因素。然而,盐摄入量与痴呆之间的因果关系仍不确定。

目的

本研究旨在采用孟德尔随机化(MR)设计,研究盐摄入量对痴呆风险的因果影响。

方法

从 IEU 数据库中获取暴露和结局(任何类型的痴呆、认知表现、不同类型的痴呆、阿尔茨海默病[AD]和帕金森病)的全基因组关联研究(GWAS)数据。通过逆方差加权模型生成 MR 估计值。我们的研究还使用了 MR-Egger、加权中位数和 MR-Pleiotropy Residual Sum and Outlier(MR-PRESSO)方法。敏感性分析包括 Cochrane's Q 检验、MR-Egger 截距、MR-PRESSO 全局检验和异常值检验、逐一剔除分析和漏斗图评估。

结果

我们的 MR 分析提供了证据表明,食物中添加的高盐与痴呆(比值比[OR] = 1.73,95%置信区间[CI]:1.21-2.49,p = 0.003)、AD 痴呆(OR = 2.10,95%CI:1.15-3.83,p = 0.015)和未定义的痴呆(OR = 2.61,95%CI:1.26-5.39,p = 0.009)之间存在因果关系。添加的盐量较高也与 AD 的风险增加(OR = 1.80,95%CI:1.12-2.87,p = 0.014)和认知表现下降(β = -.133,95%CI:-.229 至 -.038,p = 0.006)相关。

结论

本研究提供了证据表明,高盐摄入量与痴呆(包括 AD 和未定义的痴呆)的发病风险增加存在因果关系,强调了减少盐摄入量作为预防措施的潜在重要性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9798/11069030/bab23dc49af3/BRB3-14-e3516-g002.jpg

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