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Mendelian randomisation supports causal link between obesity and asthma
  1. Diana A van der Plaat
  1. National Heart and Lung Institute, Imperial College London, London, UK
  1. Correspondence to Dr Diana A van der Plaat, National Heart and Lung Institute, Imperial College London, London SW3 6LR, UK; d.van-der-plaat{at}imperial.ac.uk

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Over the last few decades the prevalence of both obesity and asthma has increased substantially in many parts of the world. A clear link between obesity and asthma incidence and severity has been shown in both children and adults in observational studies.1 2 The biological mechanisms underlying this relationship are not fully understood. Hypotheses to explain the association include mechanisms related to one or more factors, including systemic inflammation, endocrine factors, oxidative stress, decreased lung volumes and comorbidities (type 2 diabetes, obstructive sleep apnoea and gastro-oesophageal reflux disease).3–6 The systemic inflammation pathway has gained particular traction, as both obese subjects and asthmatics have high inflammatory burdens. In addition, obese patients with asthma present with a different type of airway inflammation, tending to be more neutrophilic than eosinophilic.3 Controversy exists over whether obesity has a different effect on asthma in males and females, as studies in children show mixed results while some studies in adults suggest stronger effects in females.4 5 Furthermore, there has been a concern that the body mass index (BMI)–asthma association is due to reverse causation; that is, that people with asthma become obese due to the impact of asthma on their ability to remain active or perhaps even due to medications. Overall, findings by observational studies are susceptible to bias (confounding) and cannot elucidate the directionality of the relationship between obesity and asthma.

The Mendelian randomisation (MR) approach is increasingly used to assess causal relationships and can be regarded as a ‘natural’ randomised controlled trial. MR uses genetic variants (single nucleotide polymorphisms; SNP), which were randomly assigned at conception, as proxies (‘instrumental variables’) for an exposure of interest.7 Indirect evidence of a causal effect of the exposure on the outcome is provided when the SNPs that are known to modify the exposure …

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Footnotes

  • Contributors DAvdP was responsible for writing the editorial.

  • Funding DAvdP has received funding from the European Respiratory Society and the European Union’s H2020 research and innovation programme under the Marie Sklodowska-Curie grant agreement number 713406.

  • Competing interests None declared.

  • Patient consent for publication Not required.

  • Provenance and peer review Commissioned; externally peer reviewed.

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