Educational attainment, brain cortical structure, and sarcopenia: a Mendelian randomization study.

IF 3 3区医学 Q2 PUBLIC, ENVIRONMENTAL & OCCUPATIONAL HEALTH

Frontiers in Public Health Pub Date : 2024-10-23 eCollection Date: 2024-01-01 DOI:10.3389/fpubh.2024.1415343

Yunqing Zhang, Ruideng Wang, Zhengyang Chen, Fang Zhou, Shilong Su

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引用次数: 0

Abstract

Background: Previous observational studies have suggested associations between high-level educational attainment (EA) and a lower risk of sarcopenia. However, the causality inferred from those studies was subjected to residual confounding and reverse causation. The protective effect of EA on sarcopenia may be mediated via changes in brain cortical structure. The aim of this study was to use a two-step Mendelian randomization (MR) analysis to illustrate the causal relationship between EA, brain cortical structure, and sarcopenia.

Methods: Instrumental variables at the genome-wide significance level were obtained from publicly available datasets, and inverse variance weighted as the primary method was used for MR analysis. We perform several sensitivity analyses, including Cochran Q test, MR-Egger intercept test, leave-one-out analyses, and MR Pleiotropy Residual Sum and Outlier to evaluate the reliability of the results.

Results: EA was causally associated with increased appendicular lean mass (β = 0.25, 95% confidence interval (CI): 0.19 to 0.31, p = 2.25 × 10^-15), hand grip strength (left: β = 0.042, 95% CI: 0.013 to 0.071, p = 4.77 × 10^-3 and right: β = 0.050, 95% CI: 0.022 to 0.079, p = 5.17 × 10^-4), and usual walking pace (β = 0.20, 95% CI: 0.18 to 0.22, p = 6.16 × 10^-83). In addition, EA was associated with increased brain cortical surface area (β = 4082.36, 95% CI: 2513.35 to 5681.38, p = 3.40 × 10^-7) and cortical thickness (TH) (β = 0.014, 95% CI: 0.0045 to 0.023, p = 3.45 × 10^-3). Regarding the causal effect of EA on usual walking pace, the mediatory effect of TH was 0.0069 and the proportion of mediation by TH was 3.43%.

Conclusion: The study will have revealed the protective causal effect of EA on sarcopenia, which provides a reference for the prevention of sarcopenia at the public health level. We also will have found EA could affect the brain cortical structure, and the brain cortical structure could mediate the protective effect of EA against sarcopenia risk.

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教育程度、大脑皮层结构和肌肉疏松症：孟德尔随机研究。

背景：以往的观察性研究表明，高教育程度（EA）与较低的肌肉疏松症风险之间存在关联。然而，从这些研究中推断出的因果关系受到残余混杂因素和反向因果关系的影响。EA对肌肉疏松症的保护作用可能是通过大脑皮层结构的变化来实现的。本研究旨在使用两步孟德尔随机分析法（MR）来说明EA、大脑皮质结构和肌肉疏松症之间的因果关系：从公开数据集中获取全基因组显著性水平的工具变量，并采用反方差加权作为 MR 分析的主要方法。我们进行了多项敏感性分析，包括Cochran Q检验、MR-Egger截距检验、leave-one-out分析以及MR褶皱残差和离群值分析，以评估结果的可靠性：EA与阑尾瘦肉质量增加（β = 0.25，95% 置信区间（CI）：0.19 至 0.31，p = 2.25 × 10-15）、手握力（左：β = 0.042，95% CI：0.013 至 0.071，p = 4.77 × 10-3；右：β = 0.050，95% CI：0.022 至 0.079，p = 5.17 × 10-4），以及通常的步行速度（β = 0.20，95% CI：0.18 至 0.22，p = 6.16 × 10-83）。此外，EA 与大脑皮质表面积（β = 4082.36，95% CI：2513.35 至 5681.38，p = 3.40 × 10-7）和皮质厚度（TH）（β = 0.014，95% CI：0.0045 至 0.023，p = 3.45 × 10-3）的增加有关。关于 EA 对通常步行速度的因果效应，TH 的中介效应为 0.0069，TH 的中介比例为 3.43%：本研究将揭示 EA 对肌肉疏松症的保护性因果效应，为在公共卫生层面预防肌肉疏松症提供参考。我们还将发现 EA 可影响大脑皮层结构，而大脑皮层结构可介导 EA 对肌肉疏松症风险的保护作用。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Frontiers in Public Health Medicine-Public Health, Environmental and Occupational Health

CiteScore

4.80

自引率

7.70%

发文量

4469

审稿时长

14 weeks

期刊介绍： Frontiers in Public Health is a multidisciplinary open-access journal which publishes rigorously peer-reviewed research and is at the forefront of disseminating and communicating scientific knowledge and impactful discoveries to researchers, academics, clinicians, policy makers and the public worldwide. The journal aims at overcoming current fragmentation in research and publication, promoting consistency in pursuing relevant scientific themes, and supporting finding dissemination and translation into practice. Frontiers in Public Health is organized into Specialty Sections that cover different areas of research in the field. Please refer to the author guidelines for details on article types and the submission process.