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Original research
A life course approach to elucidate the role of adiposity in asthma risk: evidence from a Mendelian randomisation study
  1. Shiu Lun Au Yeung1,
  2. Albert Martin Li2,
  3. C Mary Schooling1,3
  1. 1 School of Public Health, LKS Faculty of Medicine, University of Hong Kong, Hong Kong SAR, China
  2. 2 Department of Pediatrics, Faculty of Medicine, Chinese University of Hong Kong, Hong Kong SAR, China
  3. 3 City University of New York, Graduate School of Public Health and Health Policy, New York, USA
  1. Correspondence to Shiu Lun Au Yeung, School of Public Health, LKS Faculty of Medicine, The University of Hong Kong, 7 Sassoon Road, Pokfulam, Hong Kong SAR, China; ayslryan{at}hku.hk

Abstract

Background Adiposity is associated with asthma although studies do not usually explore the inter-related role of childhood and adult adiposity in asthma risk using a life course perspective.

Methods We conducted a Mendelian randomisation (MR) study using genetic instruments for childhood body mass index (BMI) (n=47 541), childhood obesity (n=29 822) and adult BMI (n=681 725) applied to the UK Biobank (n=401 837), with validation in a genome-wide association study of asthma (GABRIEL, n=5616). We used inverse variance weighting and other sensitivity analyses to examine the relationship between adiposity and asthma risk. We assessed mediation using multivariable Mendelian randomisation (MVMR) analysis.

Results Childhood BMI was related to asthma in the UK Biobank (OR 1.10 per SD increase, 95% CI 0.99 to 1.22). Adult BMI was associated with asthma risk (OR 1.33 per SD increase, 95% CI 1.25 to 1.43). Analyses in GABRIEL gave directionally consistent results but with wide CI. The relationship between childhood obesity and asthma risk was less clear in both data sources. MVMR suggested the relation of childhood BMI with asthma risk was largely mediated via adult BMI.

Conclusion Adiposity in childhood likely cause asthma, but the effect is primarily mediated via adult BMI.

  • Asthma
  • Obesity
  • Mendelian randomisation

https://doi.org/10.1136/jech-2020-213745

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    Footnotes

    • Twitter ShiuLunAuYeung @Ryan_Au_Yeung.

    • Contributors SLAY designed the study, wrote the analysis plan and interpreted the results. SLAY undertook analyses with feedback from CMS. SLAY wrote the first draft of the manuscript with critical feedback and revisions from AML and CMS. All authors gave final approval of the version to be published. SLAY is the guarantor of this study.

    • Funding This study was funded by the RAE 2020 Preparation URC Supplemental Funding for Faculties/Units of Assessment, The University of Hong Kong. The funder had no role in the design, analyses, interpretation of results or writing of the paper.

    • Competing interests None declared.

    • Patient consent for publication Not required.

    • Ethics approval The study only used publicly available data and hence no ethics approval was required.

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

    • Data availability statement All data relevant to the study are included in the article or uploaded as supplemental information.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.