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美国老年人中饮酒与痴呆症之间的孟德尔随机化研究关系

Relationship between alcohol consumption and dementia with Mendelian randomization approaches among older adults in the United States.

作者信息

Campbell Kyle A, Fu Mingzhou, MacDonald Elizabeth, Zawistowski Matthew, Bakulski Kelly M, Ware Erin B

机构信息

Department of Epidemiology University of Michigan School of Public Health Ann Arbor Michigan USA.

Department of Biostatistics University of Michigan School of Public Health Ann Arbor Michigan USA.

出版信息

Alzheimers Dement (Amst). 2024 Jun 20;16(2):e12598. doi: 10.1002/dad2.12598. eCollection 2024 Apr-Jun.

Abstract

INTRODUCTION

In observational studies, the association between alcohol consumption and dementia is mixed.

METHODS

We performed two-sample Mendelian randomization (MR) using summary statistics from genome-wide association studies of weekly alcohol consumption and late-onset Alzheimer's disease and one-sample MR in the Health and Retirement Study (HRS), wave 2012. Inverse variance weighted two-stage regression provided odds ratios of association between alcohol exposure and dementia or cognitively impaired, non-dementia relative to cognitively normal.

RESULTS

Alcohol consumption was not associated with late-onset Alzheimer's disease using two-sample MR (odds ratio [OR] = 1.15, 95% confidence interval [CI]: [0.78, 1.72]). In HRS, doubling weekly alcohol consumption was not associated with dementia (African ancestries,  = 1,322, OR = 1.00, 95% CI [0.45, 2.25]; European ancestries,  = 7,160, OR = 1.37, 95% CI [0.53, 3.51]) or cognitively impaired, non-dementia (African ancestries,  = 1,322, OR = 1.17, 95% CI [0.69, 1.98]; European ancestries,  = 7,160, OR = 0.75, 95% CI [0.47, 1.22]).

DISCUSSION

Alcohol consumption was not associated with cognitively impaired, non-dementia or dementia status.

HIGHLIGHTS

Cross-sectionally in a large, diverse sample, alcohol appears protective for dementia.We apply two- and one-sample Mendelian randomization to test inferred causality.Mendelian randomization approaches show no association with alcohol and dementia.We conclude that alcohol consumption should not be considered protective.

摘要

引言

在观察性研究中,饮酒与痴呆症之间的关联并不一致。

方法

我们使用每周饮酒量和晚发性阿尔茨海默病的全基因组关联研究的汇总统计数据进行了两样本孟德尔随机化(MR),并在2012年第20波健康与退休研究(HRS)中进行了单样本MR。逆方差加权两阶段回归提供了饮酒暴露与痴呆症或认知障碍、非痴呆症(相对于认知正常)之间关联的优势比。

结果

使用两样本MR,饮酒与晚发性阿尔茨海默病无关(优势比[OR]=1.15,95%置信区间[CI]:[0.78,1.72])。在HRS中,每周饮酒量翻倍与痴呆症无关(非洲血统,n=1322,OR=1.00,95%CI[0.45,2.25];欧洲血统,n=7160,OR=1.37,95%CI[0.53,3.51])或认知障碍、非痴呆症(非洲血统,n=1322,OR=1.17,95%CI[0.69,1.98];欧洲血统,n=7160,OR=0.75,95%CI[0.47,1.22])。

讨论

饮酒与认知障碍、非痴呆症或痴呆症状态无关。

要点

在一个大型、多样化的样本中进行横断面研究,酒精似乎对痴呆症有保护作用。我们应用两样本和单样本孟德尔随机化来检验推断的因果关系。孟德尔随机化方法显示饮酒与痴呆症之间无关联。我们得出结论,不应将饮酒视为有保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9941/11187745/2e97db490f2d/DAD2-16-e12598-g001.jpg

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