ABSTRACT
BACKGROUND: Obesity is a risk factor for asthma. However, it is unclear if increased obesity prevalence contributed to rising childhood asthma prevalence. OBJECTIVE: To assess if population-level changes in weight status impacted asthma prevalence over time. METHODS: Using nationally representative 1988-2014 National Health and Nutrition Examination Survey data for 40 644 children aged 2-19 years, we analyzed asthma trends by weight status (body mass index age-specific percentiles determined using measured weight and height). Logistic regression and population attributable fraction were used to assess the association between obesity and asthma prevalence. RESULTS: Although obesity was a risk factor for asthma throughout the period, asthma prevalence increased only among children with normal weight; there was no interaction between weight status and time. The population attributable fraction for overweight/obesity rose from 8.5% in 1988-1994 to 11.9% in 2011-2014, but this increase was not significant (P = 0.44). CONCLUSIONS: Together, these data do not support a contribution of obesity trends to asthma prevalence trends.
Subject(s)
Asthma/epidemiology , Body Weight , Pediatric Obesity/complications , Adolescent , Adult , Asthma/etiology , Child , Child, Preschool , Cross-Sectional Studies , Female , Humans , Logistic Models , Male , Nutrition Surveys , Prevalence , Risk Factors , United States/epidemiology , Young AdultABSTRACT
We have used expression profiling and in vivo imaging to characterize Caenorhabditis elegans embryos as they transit from a developmentally plastic state to the onset of differentiation. Normally, this transition is accompanied by activation of developmental regulators and differentiation genes, downregulation of early-expressed genes, and large-scale reorganization of chromatin. We find that loss of plasticity and differentiation onset depends on the Polycomb complex protein mes-2/E(Z). mes-2 mutants display prolonged developmental plasticity in response to heterologous developmental regulators. Early-expressed genes remain active, differentiation genes fail to reach wild-type levels, and chromatin retains a decompacted morphology in mes-2 mutants. By contrast, loss of the developmental regulators pha-4/FoxA or end-1/GATA does not prolong plasticity. This study establishes a model by which to analyze developmental plasticity within an intact embryo. mes-2 orchestrates large-scale changes in chromatin organization and gene expression to promote the timely loss of developmental plasticity. Our findings indicate that loss of plasticity can be uncoupled from cell fate specification.
