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Mendelian randomisation study of the relationship between vitamin D and risk of glioma

Abstract:
Background The etiological basis of glioma is poorly understood. We have used genetic markers in a Mendelian randomization (MR) framework to examine if lifestyle, cardiometabolic, and inflammatory factors influence the risk of glioma. This methodology reduces bias from confounding and is not affected by reverse causation.Methods We identified genetic instruments for 37 potentially modifiable risk factors and evaluated their association with glioma risk using data from a genome-wide association study of 12 488 glioma patients and 18 169 controls. We used the estimated odds ratio of glioma associated with each of the genetically defined traits to infer evidence for a causal relationship with the following exposures:Lifestyle and dietary factors-height, plasma insulin-like growth factor 1, blood carnitine, blood methionine, blood selenium, blood zinc, circulating adiponectin, circulating carotenoids, iron status, serum calcium, vitamins (A1, B12, B6, E, and 25-hydroxyvitamin D), fatty acid levels (monounsaturated, omega-3, and omega-6) and circulating fetuin-A;Cardiometabolic factors-birth weight, high density lipoprotein cholesterol, low density lipoprotein cholesterol, total cholesterol, total triglycerides, basal metabolic rate, body fat percentage, body mass index, fasting glucose, fasting proinsulin, glycated hemoglobin levels, diastolic and systolic blood pressure, waist circumference, waist-to-hip ratio; andInflammatory factors- C-reactive protein, plasma interleukin-6 receptor subunit alpha and serum immunoglobulin E.Results After correction for the testing of multiple potential risk factors and excluding associations driven by one single nucleotide polymorphism, no significant association with glioma risk was observed (ie, PCorrected > 0.05).Conclusions This study did not provide evidence supporting any of the 37 factors examined as having a significant influence on glioma risk
Publication status:
Published
Peer review status:
Peer reviewed

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Publisher copy:
10.1038/s41598-018-20844-w

Authors

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Role:
Author
ORCID:
0000-0002-3966-3501
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Institution:
University of Oxford
Role:
Author
ORCID:
0000-0002-6133-0164
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Role:
Author
ORCID:
0000-0001-9663-4611
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Role:
Author
ORCID:
0000-0003-1783-6296


Publisher:
Nature Research
Journal:
Scientific Reports More from this journal
Volume:
8
Issue:
1
Pages:
2339-2339
Publication date:
2018-02-05
DOI:
EISSN:
2045-2322
ISSN:
2045-2322


Language:
English
Keywords:
Pubs id:
2063263
Local pid:
pubs:2063263
Source identifiers:
W2794051840
Deposit date:
2025-12-19
ARK identifier:
This ORA record was generated from metadata provided by an external service. It has not been edited by the ORA Team.

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