Evidence map›Paper›PMID 31466528›Full record

Observational studyBMC medicine2019

Vitamin D and cause-specific vascular disease and mortality: a Mendelian randomisation study involving 99,012 Chinese and 106,911 European adults.

Tao Huang, Shoaib Afzal, Canqing Yu, Yu Guo, Zheng Bian, Ling Yang, Iona Y Millwood, Robin G Walters, Yiping Chen, Ningyu Chen and 9 more

Open access · goldAbstract readObservational Study
PubMed Full text at PMC Publisher
In one paragraph

Observational study in BMC medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 4 pooled it
5.4field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 4 syntheses or guidelines pooled it, 60 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 6 institutions in 4 countries.

Tao HuangDepartment of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100191, China.
Shoaib AfzalDepartment of Clinical Biochemistry and Copenhagen General Population Study, Copenhagen University Hospital, Herlev and Gentofte Hospital Copenhagen, Copenhagen, Denmark.
Canqing YuDepartment of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100191, China.
Yu GuoChinese Academy of Medical Sciences, Beijing, China.
Zheng BianChinese Academy of Medical Sciences, Beijing, China.
Ling YangClinical Trial Service Unit & Epidemiological Studies Unit (CTSU), Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Iona Y MillwoodClinical Trial Service Unit & Epidemiological Studies Unit (CTSU), Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Robin G WaltersClinical Trial Service Unit & Epidemiological Studies Unit (CTSU), Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Yiping ChenClinical Trial Service Unit & Epidemiological Studies Unit (CTSU), Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Ningyu ChenNCDs Prevention and Control Department, Liuzhou Center for Disease Control and Prevention, Liuzhou, China.
Ruqin GaoQingdao Center for Disease Control and Prevention, Qingdao, China.
Junshi ChenChina National Center for Food Safety Risk Assessment, Beijing, China.
Robert ClarkeClinical Trial Service Unit & Epidemiological Studies Unit (CTSU), Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Zhengming ChenClinical Trial Service Unit & Epidemiological Studies Unit (CTSU), Nuffield Department of Population Health, University of Oxford, Oxford, UK.
Christina EllervikDepartment of Clinical Biochemistry and Copenhagen General Population Study, Copenhagen University Hospital, Herlev and Gentofte Hospital Copenhagen, Copenhagen, Denmark.
Børge G NordestgaardDepartment of Clinical Biochemistry and Copenhagen General Population Study, Copenhagen University Hospital, Herlev and Gentofte Hospital Copenhagen, Copenhagen, Denmark.
Jun LvDepartment of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100191, China. epi.lvjun@vip.163.com.
Liming LiDepartment of Epidemiology and Biostatistics, School of Public Health, Peking University Health Science Center, 38 Xueyuan Road, Beijing, 100191, China. lmlee@vip.163.com.
China Kadoorie Biobank Collaborative Group
University of Oxford · GBChinese Academy of Medical Sciences & Peking Union Medical College · CNPeking University · CNUniversity of Copenhagen · DKChina National Center for Food Safety Risk Assessment · CNLiu Zhou Center for Disease Prevention and Control · CN

Funding

Medical Research Council MC_PC_13049Medical Research Council MC_PC_14135Medical Research Council MC_U137686851Medical Research Council MC_UU_00017/1Medical Research Council MC_UU_12026/2Wellcome Trust 088158/Z/09/ZWellcome Trust 104085/Z/14/ZWellcome Trust 202922/Z/16/ZWellcome Trust 212946/Z/18/Z
6 · The paper itself

Abstract

backgroundRandomised control trials and genetic analyses have demonstrated that vitamin D or 25-hydroxyvitamin D (25[OH]D) levels may not play a causal role in the development of cardiovascular disease. However, it is unclear if 25(OH)D is causally associated with cause-specific vascular disease and lipids. Therefore, we examined the causal association of 25(OH)D with myocardial infarction, stroke, ischaemic heart disease, ischaemic stroke, subarachnoid haemorrhage, intracerebral haemorrhage, and lipid levels among both Chinese and Europeans.

methodsWe used a Mendelian randomisation (MR) design in the China Kadoorie Biobank, the Copenhagen City Heart Study, and the Copenhagen General Population Study. The 25(OH)D-related genetic variants in the CYP2R1 and DCHR7 genes were genotyped in 99,012 Chinese adults and 106,911 Danish adults.

resultsIn Chinese adults, plasma 25(OH)D levels were not significantly associated with cause-specific vascular disease or mortality, with the exception of intracerebral haemorrhage (HR, 1.09 [95% CI, 1.01,1.18] per 25 nmol/L higher plasma 25(OH)D). In Europeans, plasma 25(OH)D levels were inversely associated with all types of vascular diseases and mortality. However, MR analysis did not demonstrate causal associations of genetically increased 25(OH)D levels with cause-specific vascular diseases, or mortality in both Chinese and European adults. In addition, each 25 nmol/L higher 25(OH)D was observationally associated with lower total cholesterol and low-density lipoprotein cholesterol levels, but higher high-density lipoprotein cholesterol levels. Likewise, MR analysis showed that 25(OH)D levels were not causally associated with lipids in both Chinese and European adults after Bonferroni correction.

conclusionsWe found no evidence to support that genetically increased 25(OH)D was associated with a lower risk of ischaemic stroke, intracerebral haemorrhage, subarachnoid haemorrhage, and lipid levels in both Chinese and European adults. These results suggest that the inverse associations of vitamin D with vascular disease could be the result of confounding.

Indexed as

AdultAgedAsian PeopleChinaFemaleGenotypeHumansLipidsMaleMendelian Randomization AnalysisMiddle AgedVascular DiseasesVitamin DWhite People25-hydroxyvitamin DLipidsVitamin DCardiovascular diseasesCausal effectLipidsMendelian randomisationVitamin D

Identifiers

PMID31466528
PMCPMC6716818
OpenAlexW2970762822

What OpenQuestion holds

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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.