Evidence map›Paper›PMID 35000008›Full record

ArticleClinical rheumatology2022

Mendelian randomization study on the causal effects of omega-3 fatty acids on rheumatoid arthritis.

Gaizhi Zhu, Shan Zhou, Yaqi Xu, Ran Gao, Huan Li, Bing Zhai, Xiaoling Liu, Youdi He, Xiaoqian Wang, Gencheng Han and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Clinical rheumatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
7.5field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 60 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 2 countries.

Gaizhi Zhu *Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No.10 Xitoutiao, You An Men, Beijing, 100069, China.
Shan Zhou *Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No.10 Xitoutiao, You An Men, Beijing, 100069, China.
Yaqi XuBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No.10 Xitoutiao, You An Men, Beijing, 100069, China.
Ran GaoBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No.10 Xitoutiao, You An Men, Beijing, 100069, China.
Huan LiBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No.10 Xitoutiao, You An Men, Beijing, 100069, China.
Bing ZhaiDepartment of Geriatric Hematology, Chinese PLA General Hospital, Beijing, 100853, China.
Xiaoling LiuDepartment of Dermatology, First Medical Centre of Chinese, PLA General Hospital, Beijing, 100853, China.
Youdi HeDepartment of Neurology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, 100020, China.
Xiaoqian WangStaidson (Beijing) Biopharmaceuticals Co., Ltd, Beijing, 100176, China.
Gencheng HanDepartment of Neuroimmune and Antibody Engineering, Beijing Institute of Basic Medical Sciences, Box 130 (3), Taiping Road #27, Beijing, 100850, China. genchenghan@163.com.
Wenting SuBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No.10 Xitoutiao, You An Men, Beijing, 100069, China. wtsu@ccmu.edu.cn.
Renxi WangBeijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University, No.10 Xitoutiao, You An Men, Beijing, 100069, China. renxi_wang@ccmu.edu.cn.ORCID http://orcid.org/0000-0003-4130-3334
Capital Medical University · CNChinese PLA General Hospital · CNBeijing Biocytogen (China) · CNBeijing Institute of Education · CN

Funding

Beijing Municipal Commission of Education KM201710025014National Natural Science Foundation of China 31770956National Natural Science Foundation of China 81704151National Natural Science Foundation of China 82071758Postdoctoral Research Foundation of China 2019M664000
6 · The paper itself

Abstract

objectivesTo resolve the ongoing debate on the role of plasma omega-3 fatty acids in rheumatoid arthritis (RA), we attempted to identify the association between omega-3 intake and the risk of RA.

methodsWe analyzed data from the largest genome-wide association study (GWAS) for omega-3 fatty acids (N = 114,999 of European ancestry) and RA (14,361 cases and 43,923 controls of European ancestry). Mendelian randomization-egger_intercept, MR-PRESSO, and Cochran's Q test were used to determine pleiotropy and heterogeneity. Egger, weighted median, inverse variance weighted (IVW), simple mode, and weighted mode were used to evaluate the causal association of plasma omega-3 levels on RA.

resultsWe found no significant pleiotropy, heterogeneity, and bias among the omega-3 genetic instrumental variables (IVs) in RA GWAS datasets. MR analysis demonstrated that as omega-3 levels genetically increased, the risk of MS increased using MR-egger (Beta = 0.137, p = 0.037; OR = 1.146, 95% CI: [1.014, 1.296]), weighted median (Beta = 0.162, p = 0.001; OR = 1.176, 95% CI: [1.070, 1.292]), IVW (Beta = 0.102, p = 0.025; OR = 1.108, 95% CI: [1.013, 1.211]), simple mode (Beta = 0.219, p = 0.149; OR = 1.245, 95% CI: [0.931, 1.665]), and weighted mode (Beta = 0.146, p = 0.006; OR = 1.157, 95% CI: [1.051, 1.274]).

conclusionsOur analysis suggested a causal association between genetically increased plasma omega-3 levels and the increased risk of RA in populations with European ancestry. Thus, to reduce the risk of RA, those of European descent should reduce omega-3 intake. Key Points • No significant pleiotropy or heterogeneity among the omega-3 genetic IVs in RA GWAS datasets. • Genetically increased plasma omega-3 levels enhanced the risk of RA in European lineages.

Indexed as

Arthritis, RheumatoidFatty Acids, Omega-3Genome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single NucleotideFatty Acids, Omega-3Genome-wide association studyMendelian randomizationOmega-3Rheumatoid arthritis

Identifiers

PMID35000008
OpenAlexW4206234958

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.