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Asthma
Original research
Adiposity and asthma in adults: a bidirectional Mendelian randomisation analysis of The HUNT Study
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  1. Yi-Qian Sun1,2,3,
  2. Ben Michael Brumpton4,5,6,
  3. Arnulf Langhammer7,
  4. Yue Chen8,
  5. Kirsti Kvaløy7,
  6. Xiao-Mei Mai7
  1. 1 Department of Clinical and Molecular Medicine, Norwegian University of Science and Technology, Trondheim, Norway
  2. 2 Department of Pathology, Clinic of Laboratory Medicine, St Olavs Hospital, University Hospital in Trondheim, Trondheim, Norway
  3. 3 Center for Oral Health Services and Research Mid-Norway (TkMidt), Trondheim, Norway
  4. 4 KG Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway
  5. 5 Department of Thoracic Medicine, St Olavs Hospital, University Hospital in Trondheim, Trondheim, Norway
  6. 6 MRC Integrative Epidemiology Unit, School of Social and Community Medicine, University of Bristol, Bristol, UK
  7. 7 Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway
  8. 8 Faculty of Medicine, School of Epidemiology and Public Health, University of Ottawa, Ottawa, Ontario, Canada
  1. Correspondence to Dr Xiao-Mei Mai, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim 7491, Norway; xiao-mei.mai{at}ntnu.no

Abstract

Background We aimed to investigate the potential causal associations of adiposity with asthma overall, asthma by atopic status or by levels of symptom control in a large adult population and stratified by sex. We also investigated the potential for reverse causation between asthma and risk of adiposity.

Methods We performed a bidirectional one-sample Mendelian randomisation (MR) study using the Norwegian Nord-Trøndelag Health Study population including 56 105 adults. 73 and 47 genetic variants were included as instrumental variables for body mass index (BMI) and waist-to-hip ratio (WHR), respectively. Asthma was defined as ever asthma, doctor-diagnosed asthma and doctor-diagnosed active asthma, and was further classified by atopic status or levels of symptom control. Causal OR was calculated with the Wald method.

Results The ORs per 1 SD (4.1 kg/m2) increase in genetically determined BMI were ranged from 1.36 to 1.49 for the three asthma definitions and similar for women and men. The corresponding ORs for non-atopic asthma (range 1.42–1.72) appeared stronger than those for the atopic asthma (range 1.18–1.26), but they were similar for controlled versus partly controlled doctor-diagnosed active asthma (1.43 vs 1.44). There was no clear association between genetically predicted WHR and asthma risk or between genetically predicted asthma and the adiposity markers.

Conclusions Our MR study provided evidence of a causal association of BMI with asthma in adults, particularly with non-atopic asthma. There was no clear evidence of a causal link between WHR and asthma or of reverse causation.

  • adiposity
  • asthma
  • symptom control
  • atopy
  • bidirectional association
  • body mass index
  • Mendelian randomisation
  • obesity
  • single-nucleotide polymorphisms
  • waist-hip ratio

https://doi.org/10.1136/thoraxjnl-2019-213678

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    Footnotes

    • Contributors YQS, BMB, AL, YC, KK and XMM contributed to the study design. YQS conducted statistical analyses. YQS and XMM wrote the initial draft of the manuscript. AL is the leader of the HUNT Lung Study and contributed to data collection. All authors participated in the data interpretation and contributed to the final draft of the manuscript with intellectual importance.

    • Funding YQS was supported by the Norwegian Cancer Society (project ID 5769155-2015) and The Research Council of Norway 'Gaveforsterkning', as well as by a research grant from The Liaison Committee for Education, Research and Innovation in Central Norway. BMB was supported by a research grant (No 46055500-10) from The Liaison Committee for Education, Research and Innovation in Central Norway. The KG Jebsen Center for Genetic Epidemiology is financed by Stiftelsen Kristian Gerhard Jebsen, Faculty of Medicine and Health Sciences, Norwegian University of Science and Technology (NTNU), Central Norway Regional Health Authority, and the Medical Research Council Integrative Epidemiology Unit at the University of Bristol.

    • Competing interests None declared.

    • Patient consent for publication Not required.

    • Ethics approval The current study was approved by the Norwegian Regional Committees for Medical and Health Research Ethics. All participants gave their informed consent for participation in HUNT.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Data availability statement Data from the HUNT Study that is used in research projects will, when reasonably requested by others, be made available on request to the HUNT Data Access Committee (hunt@medisin.ntnu.no). The HUNT data access information describes the policy regarding data availability (https://www.ntnu.edu/hunt/data https://www.ntnu.edu/hunt/data).

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