Increased Asthma Risk and Asthma-Related Health Care Complications Associated With Childhood Obesity

Black, Maureen M.; Zhou, Hui; Takayanagi, Miwa; Jacobsen, Steven J.; Koebnick, Corinna

doi:10.1093/aje/kwt093

Cited by 110 publications

(94 citation statements)

References 34 publications

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“…11,30 Abnormal lung function may be further complicated by a decreased response to both corticosteroids and bronchodilators in overweight children. 31,32 Our study strengthens similar findings of poor control in obese patients with asthma in other studies [33][34][35] because it assesses a wider age range, uses chart review, and controls for asthma severity.…”

Section: Discussionsupporting

confidence: 86%

Impact of Obesity on Clinical Outcomes in Urban Children Hospitalized for Status Asthmaticus

Aragona

El-Magbri

Wang

et al. 2016

Hospital Pediatrics

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A B S T R A C T BACKGROUND AND OBJECTIVE:The prevalence of both childhood asthma and obesity remain at historically high levels and disproportionately affect urban children. Asthma is a common and costly cause for pediatric hospitalization. Our objective was to determine the effect of obesity on outcomes among urban children hospitalized with status asthmaticus. METHODS:A retrospective cohort study was performed by using billing system data and chart review to evaluate urban children admitted for asthma. Demographics, asthma severity, reported comorbidities, and outcomes were assessed. Obesity was defined by BMI percentile (lean ,85%, overweight 85%-95%, obese $95%). Outcomes were length of stay, hospitalization charges, ICU stay, repeat admissions, and subsequent emergency department (ED) visits. Bivariate analysis assessed for differences between overweight/obese and lean children. Multivariable regression assessed the relationship between overweight status and primary outcomes while controlling for other variables. Post hoc age-stratified analysis was also performed. RESULTS:The study included 333 subjects; 38% were overweight/obese. Overweight/obese children admitted with asthma were more likely than lean children to have subsequent ED visits (odds ratio 1.6, 95% confidence interval 1.0-2.6). When stratified by age, overweight/obese preschool-age children (,5 years) were .2 times as likely to have repeat ED visits than lean preschool-age children (odds ratio 2.3, 95% confidence interval 1.0-5.6). There were no differences in the other outcomes between overweight/obese and lean individuals within the entire cohort or within other age groups.

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Section: Discussionsupporting

confidence: 86%

Impact of Obesity on Clinical Outcomes in Urban Children Hospitalized for Status Asthmaticus

Aragona

El-Magbri

Wang

et al. 2016

Hospital Pediatrics

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“…In obese and overweight individuals, the prevalence of asthma (1)(2)(3) and the rate of new-onset asthma have increased (4)(5)(6). Obese patients with asthma also have increased severity of illness and reduced effectiveness of steroids compared with nonobese patients with asthma (1,6,7). The mechanisms by which obesity predisposes to asthma are unclear, limiting our ability to prevent and treat obesity-related asthma.…”

mentioning

confidence: 99%

Hyperinsulinemia Potentiates Airway Responsiveness to Parasympathetic Nerve Stimulation in Obese Rats

Nie

Jacoby

Fryer

2014

Am J Respir Cell Mol Biol

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Obesity is a substantial risk factor for developing asthma, but the molecular mechanisms underlying this relationship are unclear. We tested the role of insulin in airway responsiveness to nerve stimulation using rats genetically prone or resistant to diet-induced obesity. Airway response to vagus nerve stimulation and airway M 2 and M 3 muscarinic receptor function were measured in obeseprone and -resistant rats with high or low circulating insulin. The effects of insulin on nerve-mediated human airway smooth muscle contraction and human M 2 muscarinic receptor function were tested in vitro. Our data show that increased vagally mediated bronchoconstriction in obesity is associated with hyperinsulinemia and loss of inhibitory M 2 muscarinic receptor function on parasympathetic nerves. Obesity did not induce airway inflammation or increase airway wall thickness. Smooth muscle contraction to acetylcholine was not increased, indicating that hyperresponsiveness is mediated at the level of airway nerves. Reducing serum insulin with streptozotocin protected neuronal M 2 receptor function and prevented airway hyperresponsiveness to vagus nerve stimulation in obese rats. Replacing insulin restored dysfunction of neuronal M 2 receptors and airway hyperresponsiveness to vagus nerve stimulation in streptozotocintreated obese rats. Treatment with insulin caused loss of M 2 receptor function, resulting in airway hyperresponsiveness to vagus nerve stimulation in obese-resistant rats, and inhibited human neuronal M 2 receptor function in vitro. This study shows that it is not obesity per se but hyperinsulinemia accompanying obesity that potentiates vagally induced bronchoconstriction by inhibiting neuronal M 2 muscarinic receptors and increasing acetylcholine release from airway parasympathetic nerves.Keywords: hyperinsulinemia; obesity; asthma; airway responsiveness; neural M 2 muscarinic receptor Clinical RelevanceObesity-induced asthma does not respond well to traditional anti-inflammatory therapies, suggesting that it is a unique asthma phenotype. Here we show that hyperinsulinemia causes airway hyperresponsiveness to vagus nerve stimulation in obese rats. In human trachea and in rats, we demonstrate that insulin inhibits M 2 muscarinic receptors on airway parasympathetic nerves, resulting in increased acetylcholine release and increased airway contraction. Because hyperinsulinemia is greater and more prevalent in obese individuals, these data may explain why obese individuals are prone to asthma exacerbations and suggest that anticholinergic drugs may be effective in this specific phenotype of asthma.In the United States, 31% of adults and 15% of children are obese. In obese and overweight individuals, the prevalence of asthma (1-3) and the rate of new-onset asthma have increased (4-6). Obese patients with asthma also have increased severity of illness and reduced effectiveness of steroids compared with nonobese patients with asthma (1, 6, 7). The mechanisms by which obesity predisposes to asthma are unclear, limi...

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“…Increased prevalence of childhood obesity over the past three decades (1) has led to the identification of an epidemiologic association between obesity and pediatric pulmonary diseases (2)(3)(4). One of the proposed mechanisms for this association is obesity-mediated pulmonary function impairment (5).…”

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confidence: 99%

Association of Pulmonary Function with Adiposity and Metabolic Abnormalities in Urban Minority Adolescents

Rastogi

Bhalani²,

Hall³

et al. 2014

Annals ATS

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Rationale: Childhood obesity is a known risk factor for pulmonary diseases, likely due to obesity-mediated alteration of pulmonary function. Inflammation and mechanical fat load are two proposed causative mechanisms for altered pulmonary function among obese children; however, the association of metabolic abnormalities with pulmonary function among children is poorly understood.Objectives: We investigated the independent association of truncal and general adiposity and metabolic abnormalities with pulmonary function in a sample of urban minority adolescents.Methods: Spirometry and lung volume indices were compared between adolescents with general (body mass index [BMI] . 95th percentile) or truncal adiposity (waist circumference . 90th percentile) and normal-weight (BMI , 85th percentile or waist circumference < 90th percentile) and between those with metabolic abnormalities (homeostatic model assessment of insulin resistance [HOMA-IR] in the top quartile or high-density lipoprotein [HDL] , 40 mg/dl) and those with a normal metabolic profile.Measurements and Main Results: Obese adolescents had lower lung volumes, including residual volume (RV), RV/TLC ratio, expiratory reserve volume (ERV), and FRC, and higher inspiratory capacity (IC) than normal-weight adolescents, but did not differ in measures of lower airway obstruction, FEV 1 /FVC ratio, and mid-expiratory flow rate. Adolescents with high HOMA-IR had lower FEV 1 /FVC ratio, RV, RV/TLC ratio, ERV, and FRC and higher IC, whereas those with low HDL had lower FEV 1 /FVC and RV/TLC ratios. After adjusting for adiposity, HOMA-IR remained a predictor of ERV (b = 21.4; P = 0.02) and FEV 1 /FVC ratio (b = 20.5; P = 0.03), and HDL remained a predictor of FEV 1 /FVC ratio (b = 0.1; P = 0.01). General adiposity was a predictor of FRC (b = 20.5; P , 0.001), IC (b = 0.3; P , 0.001), RV (b = 20.8; P , 0.0001), and RV/TLC ratio (b = 20.2; P , 0.0001), and truncal adiposity was a predictor of RV (b = 220.3; P = 0.03) and FRC (b = 213.8; P = 0.004). Thus, adiposity and metabolic abnormalities were independent predictors of ERV, but only metabolic abnormalities independently predicted FEV 1 /FVC ratio. Although general adiposity predicted RV and RV/TLC ratio, truncal adiposity was predictive of RV and FRC, conferring additional risk above general adiposity. Conclusions:These results suggest that metabolic abnormalities and adiposity are independently associated with pulmonary function deficits among urban adolescents. Metabolic assessment of obese adolescents may identify those at risk of developing obesity-associated pulmonary morbidity.

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Increased Asthma Risk and Asthma-Related Health Care Complications Associated With Childhood Obesity

Cited by 110 publications

References 34 publications

Impact of Obesity on Clinical Outcomes in Urban Children Hospitalized for Status Asthmaticus

Impact of Obesity on Clinical Outcomes in Urban Children Hospitalized for Status Asthmaticus

Hyperinsulinemia Potentiates Airway Responsiveness to Parasympathetic Nerve Stimulation in Obese Rats

Association of Pulmonary Function with Adiposity and Metabolic Abnormalities in Urban Minority Adolescents

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