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饮食影响炎性关节炎:一项关于30种与炎性关节炎有因果关联的饮食模式的孟德尔随机化研究。

Diet affects inflammatory arthritis: a Mendelian randomization study of 30 dietary patterns causally associated with inflammatory arthritis.

作者信息

Wang Haiyang, Wu Qinglin, Qu Pengda, Wang Shiqi, Du Shiyu, Peng Zhaorong, Tao Licheng, Wang Wuxia, Tang Xiaohu

机构信息

The First Clinical of Medicine College, Yunnan University of Chinese Medicine, Kunming, China.

Department of Rheumatology, Yunnan Provincial Hospital of Traditional Chinese Medicine, Kunming, China.

出版信息

Front Nutr. 2024 Jul 17;11:1426125. doi: 10.3389/fnut.2024.1426125. eCollection 2024.

DOI:10.3389/fnut.2024.1426125
PMID:39086544
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11289845/
Abstract

BACKGROUND

The causal associations between dietary intake and the risk and severity of Inflammatory Arthritis (IA) are currently unknown.

OBJECTIVE

In this study, we aimed to investigate the causal relationship between nine dietary categories (30 types of diet) and IA using Mendelian randomization (MR).

METHODS

We analyzed data from 30 diets and IA in a genome-wide association study (GWAS). Single nucleotide polymorphisms (SNPs) that could influence the results of MR analyses were screened out through the Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO) test. SNPs were analyzed through two-sample bidirectional MR using inverse variance weighting, MR-Egger regression, and weighted median method. The multiplicity and heterogeneity of SNPs were assessed using MR-Egger intercept term tests and Cochran's tests. FDR correction was used to correct the -values.

RESULTS

IVW results showed that Beef intake [Odds ratio (OR) = 2.862; 95% confidence interval (CI), 1.360-6.021,  = 0.006,  < 0.05] was positively associated with rheumatoid arthritis(RA); Dried fruit intake (OR = 0.522; 95% CI, 0.349-0.781,  = 0.002,  < 0.05), and Iron intake (OR = 0.864; 95%CI, 0.777-0.960,  = 0.007, r < 0.05) were negatively associated with RA, all of which were evidence of significance. Fresh fruit intake (OR = 2.528. 95% CI, 1.063-6.011,  = 0.036,  > 0.05) was positively associated with psoriatic arthritis (PsA); Cheese intake (OR = 0.579; 95% CI, 0.367-0.914,  = 0.019,  > 0.05) was negatively associated with PsA; both were suggestive evidence. Processed meat intake (OR = 0.238; 95% CI, 0.100-0.565,  = 0.001,  < 0.05) was negatively associated with reactive arthritis (ReA), a protective factor, and significant evidence. All exposure data passed the heterogeneity check (Cochrane's test  > 0.05) and no directional pleiotropy was detected. Leave-one-out analyses demonstrated the robustness of the causal relationship in the positive results.

CONCLUSION

Our study presents genetic evidence supporting a causal relationship between diet and an increased risk of IA. It also identifies a causal relationship between various dietary modalities and different types of IA. These findings have significant implications for the prevention and management of IA through dietary modifications.

摘要

背景

目前尚不清楚饮食摄入与炎症性关节炎(IA)的风险和严重程度之间的因果关系。

目的

在本研究中,我们旨在使用孟德尔随机化(MR)研究九种饮食类别(30种饮食类型)与IA之间的因果关系。

方法

我们在全基因组关联研究(GWAS)中分析了30种饮食和IA的数据。通过孟德尔随机化多效性残差和离群值(MR-PRESSO)检验筛选出可能影响MR分析结果的单核苷酸多态性(SNP)。使用逆方差加权、MR-Egger回归和加权中位数方法通过两样本双向MR分析SNP。使用MR-Egger截距检验和 Cochr an检验评估SNP的多重性和异质性。使用FDR校正来校正P值。

结果

IVW结果显示,牛肉摄入量[比值比(OR)=2.862;95%置信区间(CI),1.360 - 6.021,P = 0.006,P < 0.05]与类风湿性关节炎(RA)呈正相关;干果摄入量(OR = 0.522;95%CI,0.349 - 0.781,P = 0.002,P < 0.05)和铁摄入量(OR = 0.864;95%CI,0.777 - 0.960,P = 0.007,r < 0.05)与RA呈负相关,所有这些均具有显著意义。新鲜水果摄入量(OR = 2.528,95%CI,1.063 - 6.011,P = 0.036,P > 0.05)与银屑病关节炎(PsA)呈正相关;奶酪摄入量(OR = 0.579;95%CI,0.367 - 0.914,P = 0.019,P > 0.05)与PsA呈负相关;两者均为提示性证据。加工肉类摄入量(OR = 0.238;95%CI,0.100 - 0.565,P = 0.001,P < 0.05)与反应性关节炎(ReA)呈负相关,是一个保护因素,且具有显著证据。所有暴露数据均通过异质性检验( Cochr an检验P > 0.05),未检测到定向多效性。留一法分析证明了阳性结果中因果关系的稳健性。

结论

我们的研究提供了遗传证据,支持饮食与IA风险增加之间的因果关系。它还确定了各种饮食方式与不同类型IA之间的因果关系。这些发现对于通过饮食调整预防和管理IA具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87a3/11289845/389658b5f2f1/fnut-11-1426125-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87a3/11289845/66f151f621a8/fnut-11-1426125-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87a3/11289845/145382ec7dbb/fnut-11-1426125-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87a3/11289845/24dc05df14d1/fnut-11-1426125-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87a3/11289845/e93a6d8e684e/fnut-11-1426125-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87a3/11289845/389658b5f2f1/fnut-11-1426125-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87a3/11289845/66f151f621a8/fnut-11-1426125-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87a3/11289845/145382ec7dbb/fnut-11-1426125-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87a3/11289845/24dc05df14d1/fnut-11-1426125-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87a3/11289845/e93a6d8e684e/fnut-11-1426125-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/87a3/11289845/389658b5f2f1/fnut-11-1426125-g005.jpg

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