Mediating mechanisms from central obesity to childhood asthma
Date Issued
2014
Date
2014
Author(s)
Chih, An-Hsuan
Abstract
Background
There was abundant evidence supporting a strong correlation between obesity and childhood asthma. Several possible mediators had been proposed to explain the association. However, these mediators were never discussed and compared in a longitudinal cohort.
Objectives
We aimed to investigate the mediating mechanisms and search for the most prominent pathological pathway from central obesity to childhood asthma.
Methods
The TCHS was a longitudinal study of a nationwide, schoolchildren-based cohort. A questionnaire was distributed to parents of the participants to assess children atopic conditions and asthma. Data regarding parents’ questionnaire, obesity measures, and pulmonary function tests were collected annually for three years from 2010 to 2012. Fractional exhaled nitric oxide was recorded in the 2012 survey. Generalized estimating equations (GEE) and general linear models (GLM) were used to examine the associations amongst central obesity, possible mediators, and the respiratory outcomes (active asthma and lifetime wheeze). Structural equation models (SEM) were applied to explore the mechanisms, which mediate the link between central obesity and the respiratory outcomes.
Measurements and Main Results
Central obesity (waist-to-hip ratio) predicted active asthma most accurately. Atopy, airway inflammation, and reduction in pulmonary function were all significant mediators in the pathways from central obesity to active asthma and lifetime wheeze. The percentage of mediation of pulmonary function was greater than that of atopy and airway inflammation in both models for active asthma and lifetime wheeze.
Conclusions
Decrease in pulmonary function was the most important pathological pathway in childhood asthma caused by central obesity. Future studies should aim to elucidate the pathogenesis in other phenotypes of childhood asthma.
Subjects
中央型肥胖
氣喘
過敏
呼吸道發炎
肺功能
SDGs
Type
thesis
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