Rapid adiposity growth increases risks of new-onset asthma and airway inflammation in children.
prospective_cohort · Level II
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- Record sourced from PubMed, PMID 28286341.
- Also identified by DOI 10.1038/ijo.2017.67.
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Abstract
We aim to (1) examine the influence of long-term adiposity status/short-term adiposity changes on asthma with high or low fractional exhaled nitric oxide (Fe<sub>NO</sub>), and (2) to determine the differences in long-term adiposity status/short-term adiposity changes on atopy, airway inflammation and pulmonary function. We recruited 2450 fourth- to sixth-grade children from the nationwide Taiwan Children Health Study. Data regarding various adiposity indicators, atopic status, pulmonary function tests and asthma outcomes were collected annually. New-onset asthma was stratified by airway inflammation status using Fe<sub>NO</sub>. The generalized estimating equation was used for analyzing longitudinal relationships between long-term adiposity status/short-term adiposity changes and new-onset asthma. Individual adiposity growth slopes were obtained using a hierarchical linear model to establish the relationships between short-term adiposity changes and asthma among children with high airway inflammation. We found long-term adiposity status predicted childhood asthma with low Fe<sub>NO</sub>, whereas short-term adiposity changes may increase risks of childhood asthma with high Fe<sub>NO</sub>. Long-term adiposity status reduced pulmonary function, whereas short-term adiposity increase were associated with atopic diseases and airway inflammation. Obesity-induced asthma could be mediated by high or low airway inflammation, depending on the velocity of increase in adiposity. Rapid adiposity growth may increase risks of childhood asthma and airway inflammation.
Medical subject headings
- Adiposity
- Asthma
- Inflammation
- Pediatric Obesity