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Testosterone and lung function: bigger lungs, slower decline or some combination of both?
  1. Stephen Milne1,2,3
  1. 1 Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia
  2. 2 Ludwig Engel Centre for Respiratory Research, Westmead Institute for Medical Research, Westmead, New South Wales, Australia
  3. 3 Department of Respiratory and Sleep Medicine, Westmead Hospital, Western Sydney Local Health District, Westmead, New South Wales, Australia
  1. Correspondence to Dr Stephen Milne, Department of Respiratory and Sleep Medicine, Westmead Hospital, Western Sydney Local Health District, Westmead, New South Wales, Australia; stephen.milne{at}sydney.edu.au

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In healthy adults, 70%–80% of our vital capacity can be exhaled in a single second when measured by spirometry. This is made possible by the combination of a highly elastic lung, a low-resistance airway tree and recruitable respiratory muscles. Reduced spirometric values do not necessarily indicate disease, however, since forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and the ratio of FEV1/FVC all decrease as part of normal ageing. Much of lung function is determined by genetics: approximately 40% of lung function can be explained by familial heritability,1 and genome-wide association studies have identified hundreds of genetic variants associated with lung function that, when combined, account for around 6%–12% of this heritability.2 Understanding the genetic control of lung function can give vital insights into the nature of disease and ultimately help us develop preventative treatments.

Mendelian randomisation (MR) is a statistical construct that exploits the relationship between genetic variants and biological features to identify causal associations. In what is known as instrumental variable analysis, the effect of a genetic variant on an exposure (eg, a blood protein) and an outcome (eg, a phenotype or disease) is used to determine the effect of the exposure on the outcome. The ‘randomisation’ element comes from the random allocation of alleles during meiosis: this allows comparison between two groups who differ only by the level of the exposure—akin to treatment arms in a randomised controlled trial—and hence a causal inference can be made. For an easy-to-understand description of …

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Footnotes

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  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests SM has received research funding from Michael Smith Health Research BC and Mitacs; honoraria from Chiesi Australia, The Limbic and Research Review Australia; and travel support from Sanofi Australia. He is a member of the Executive of the Thoracic Society of Australia and New Zealand (NSW/ACT branch).

  • Provenance and peer review Commissioned; internally peer reviewed.

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