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Sci Rep. 2019 Jan 22;9(1):309. doi: 10.1038/s41598-018-36186-6.

Mendelian randomization provides support for obesity as a risk factor for meningioma.

Author information

1
Division of Genetics and Epidemiology, The Institute of Cancer Research, London, UK.
2
Division of Genetics and Epidemiology, The Institute of Cancer Research, London, UK. alex.cornish@icr.ac.uk.
3
School of Public Health, Yale University, New Haven, Connecticut, USA.
4
Division of Neuroepidemiology, Department of Neurological Surgery, University of California San Francisco, San Francisco, California, USA.
5
University of Bonn Medical School, Bonn, Germany.
6
Human Genomics Research Group, Department of Biomedicine, University of Basel, Basel, Switzerland.
7
Department of Genomics, Life & Brain Center, University of Bonn, Bonn, Germany.
8
Institute of Human Genetics, University of Bonn School of Medicine & University Hospital Bonn, Bonn, Germany.
9
Institute for Medical Informatics, Biometry and Epidemiology, University Hospital Essen, University of Duisburg-Essen, Essen, Germany.
10
Department of Public Health Sciences, University of Virginia, Charlottesville, Virginia, USA.
11
Department of Neurosurgery, Bethel Clinic, Bielefeld, Germany.
12
Section of Epidemiology and Population Sciences, Department of Medicine and Dan L., Duncan Comprehensive Cancer Center, Baylor College of Medicine, Houston, Texas, USA.
13
Institute for Human Genetics, University of California San Francisco, San Francisco, California, USA.
14
Department of Epidemiology and Biostatistics, University of California San Francisco, San Francisco, California, USA.
15
Department of Neurosurgery, Brigham and Women's Hospital, Boston, Massachusetts, USA.
16
William Harvey Research Institute, Queen Mary University, London, UK.
17
Guys and St. Thomas Foundation NHS Trust, Great Maze Pond, London, UK.

Abstract

Little is known about the causes of meningioma. Obesity and obesity-related traits have been reported in several epidemiological observational studies to be risk factors for meningioma. We performed an analysis of genetic variants associated with obesity-related traits to assess the relationship with meningioma risk using Mendelian randomization (MR), an approach unaffected by biases from temporal variability and reverse causation that might have affected earlier investigations. We considered 11 obesity-related traits, identified genetic instruments for these factors, and assessed their association with meningioma risk using data from a genome-wide association study comprising 1,606 meningioma patients and 9,823 controls. To evaluate the causal relationship between the obesity-related traits and meningioma risk, we consider the estimated odds ratio (OR) of meningioma for each genetic instrument. We identified positive associations between body mass index (odds ratio [ORSD] = 1.27, 95% confidence interval [CI] = 1.03-1.56, P = 0.028) and body fat percentage (ORSD = 1.28, 95% CI = 1.01-1.63, P = 0.042) with meningioma risk, albeit non-significant after correction for multiple testing. Associations for basal metabolic rate, diastolic blood pressure, fasting glucose, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, systolic blood pressure, total cholesterol, triglycerides and waist circumference with risk of meningioma were non-significant. Our analysis provides additional support for obesity being associated with an increased risk of meningioma.

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