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Given the concurrent worldwide epidemics of childhood obesity and asthma, it is perhaps not surprising that the two have been inextricably linked in the minds of many. Indeed, there is good evidence to suggest that adiposity in childhood is associated with an increased risk of developing asthma.1 2 Several longitudinal studies conducted in population-based cohorts have demonstrated that childhood obesity precedes incident asthma. One such study, from Taiwan, found that adiposity gain before age 6 years was good at predicting childhood-onset asthma, while adiposity gain during the prepubertal period was best at predicting young adult-onset asthma.3
More recently, however, we have seen rates of new asthma diagnoses in children and adolescents begin to fall in some countries, while childhood obesity continues to increase. This disconnect in asthma and obesity trends signals that there is likely a lot more to the relationship between obesity and asthma than initially meets the eye. There is, for instance, growing evidence of reverse causality, which is to say that children with asthma are more likely to become obese. This finding has been attributed to decreased physical activity and use of systemic corticosteroids for asthma symptom control.4 Studies have also shown that children who have asthma and are also obese tend to have more severe asthma and/or asthma that is less well controlled. It has also been suggested that the children with poorly controlled asthma might have higher fat mass and lower muscle mass than children whose asthma symptoms are well controlled.5 These findings and others all point to a complex relationship between obesity and asthma and suggest that there exists an obesity-related asthma phenotype (distinct from more usual T2-high atopic asthma phenotype) comprised of individuals in whom obesity either contributes to asthma risk or complicates existing asthma, as well as individuals …
Footnotes
Contributors ADM is the sole author of this work.
Funding The author has not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; externally peer reviewed.