A decline in asthma prevalence from 2000 to 2005 was reported previously. The objective is to examine the temporal trends for the prevalence of obesity and other childhood disorders and consider the extent to which associations between asthma and other co-morbidities can be accounted for by body mass index.
Serial cross-sectional surveys of primary school entrants (n = 18,999) in the Australian Capital Territory between 2001 and 2005 were used. Asthma, recent respiratory symptoms and diabetes data were extracted from parental reports. Anthropometric measurements were obtained from health assessments by school nurses. Child obesity was defined using the age and sex-specific Cole criteria. Time trends for the prevalence of obesity and other disorders, and the association between 'current asthma' and co-morbidities were analysed using multiple logistic regression and other analyses.
Obesity prevalence was 5.24% in 2001 decreasing to 3.60% in 2005 (test of linear trend P = 0.02). Overweight (adjusted odds ratio (AOR) 1.30 (95% confidence interval (CI) 1.16, 1.46), P < 0.001) and obese (AOR 1.36 (95% CI 1.13, 1.62), P = 0.001) children were more likely to report 'asthma ever'. Children with diabetes (AOR 9.35 (95% CI 3.11, 28.12, P < 0.001)) and attention deficit (AOR 3.39 (95% CI 2.04, 5.64), P < 0.001) were more likely to report 'current asthma'.
The pattern of association with co-morbidities was different for asthma and obesity. The temporal decline/plateau effect in 'current asthma' could not be explained by concurrent body mass index changes. The decline in obesity was largely driven by the 2005 findings. Longer term trends need to be evaluated further.
"the mean asthma prevalence across the 7 years included in the present analysis was 11 %, with a higher prevalence evident in boys and overweight/obese participants relative to girls and normal weight participants, respectively. this association between obesity and asthma is in accord with previous studies (Black et al. 2012; Figueroa-Muñoz et al. 2001; gennuso et al. 1998; luder et al. 1998), as is the gender difference (Anthracopoulos et al. 2011; Hansen et al. 2013; James et al. 2013). the maturation status of the children is important when comparing studies regarding the prevalence of asthma, as the predominance tends to reverse in adolescence and adulthood towards asthma being more prevalent Fig. 1 Influence of asthma and BMI percentile on shuttle run performance when age and gender are accounted for as covariates. "
[Show abstract][Hide abstract] ABSTRACT: To assess the relationship between asthma, body mass index (BMI) and aerobic performance, as indicated by a shuttle test.
20,577 participants (10,413 boys) from the SportsLinx serial cross-sectional study participated. Parental reports of asthma status and home postcode data were gathered from consent forms. Stature, sitting stature and body mass were measured and BMI, somatic maturity and indices of multiple deprivation scores (IMD) were derived. Performance on the 20 m multi-stage shuttle runs test (20mSRT) was used to estimate cardiorespiratory fitness (CRF).
Asthma [F (1, 17,015) = 82.26, P < 0.01] and gender [F (1, 17,015) = 678.491, P < 0.001] significantly influenced 20mSRT. The addition of BMI, maturity and IMD to the model did not alter these significant effects. There was a significant interaction between 20mSRT and BMI [F (1, 16,723) = 132.80, P < 0.01], with a significant decrease in 20mSRT from the 50th BMI percentile upwards [t (16,699) = 36.88, P < 0.01]. Binary logistic regression revealed gender and 20mSRT to be significant predictors of asthma occurrence; BMI SDS just reached significance whilst maturity and IMD were not significant contributors to the model.
This study demonstrates the negative influences of low CRF and high BMI on the risk of asthma occurrence in pre-pubertal children. Furthermore, it highlights the significant influence of BMI on CRF, revealing these effects to be manifest considerably below those BMI percentiles conventionally associated with being overweight or obese.
[Show abstract][Hide abstract] ABSTRACT: Obesity and asthma are chronic conditions affecting millions of people worldwide. The two conditions also appear to be linked with an increased risk of asthma in people who are obese. The purpose of this review is to describe mechanism(s) that may explain the association between asthma and obesity.
Current evidence suggests that the association between asthma and obesity is linked by two major phenotypes and three important pathways of obesity-related asthma: one phenotype with primary (often atopic) asthma that is aggravated by obesity and a second phenotype with late-onset nonatopic asthma, which predominantly affects women and primarily seems to be associated with neutrophilic inflammation. Proposed pathways include the mechanical effects of obesity (fewer deep inspirations leading to increased airway hyperresponsiveness), an inflammatory pathway driven by obesity-related cytokines (adipokines), and finally environment and lifestyle changes that have led to an increasing prevalence of obesity over the past 50 years (including exposures in utero, physical activity, and diet) may also result in asthma in predisposed individuals. How these environmental changes influence the occurrence and expression of asthma may depend on the age of exposure and on interactions with genetic susceptibilities.
Future research should be directed to shed light on the associations between obesity and asthma phenotypes, modern lifestyles and environmental exposures and genetic susceptibilities.
see the video supplementary digital content (http://links.lww.com/COAI/A6).
Current Opinion in Allergy and Clinical Immunology 12/2013; 14(1). DOI:10.1097/ACI.0000000000000024 · 3.57 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.