Asthma and lower airway disease
Obesity and asthma: An association modified by age of asthma onset

https://doi.org/10.1016/j.jaci.2011.03.036Get rights and content

Background

Studies of asthma phenotypes have identified obesity as a component of a group characterized by a high proportion of subjects with adult-onset asthma. However, whether age of asthma onset modifies the association between obesity and asthma is unknown.

Objectives

We sought to compare the associations between body mass index (BMI) categories with physiological, inflammatory, and clinical parameters across age of asthma onset phenotypes; and to compare the rate of BMI change in relation to asthma duration, by age of onset asthma phenotypes.

Methods

From the Severe Asthma Research Program, we defined age of asthma onset as early (<12 years of age) and late (≥12 years of age). Comparisons of BMI categories were done within age-of-onset groups, and obesity was also compared across these groups. Multivariable logistic regression analysis was done to evaluate the association between BMI categories with health care use and respiratory symptoms and multivariable linear regression for the association between duration of asthma and weight gain (BMI change per year). An interaction between obesity and age of asthma onset was included in the multivariable analyses.

Results

The study population consisted of 1049 subjects, and the median age for asthma onset was 10 years (interquartile range, 4-25 years); 48% had late-onset asthma (≥12 years of age), and 52% had early-onset asthma (<12 years of age). Compared with obese subjects with late-onset asthma, obese subjects with early-onset asthma had more airway obstruction, bronchial hyperresponsiveness, and higher odds ratios of ever having 3 or more previous oral steroid tapers per year or intensive care unit admissions for asthma per preceding year (interactions between obesity and age of asthma onset were P = .055 and P = .02, respectively). In subjects with early-onset asthma but not in subjects with late-onset asthma, there was a significant association between increasing BMI and duration of asthma after adjusting for confounders. The interaction between asthma duration and age of asthma onset was a P value of less than .01.

Conclusion

Asthmatic subjects are differentially affected by obesity based on whether they had asthma early (<12 years of age) or later in life. These results highlight the need to understand obesity as a comorbidity that affects specific clinical phenotypes and not all asthma subjects alike.

Section snippets

Study population

The study population consisted of participants aged 18 years or older from the multicenter SARP study that met the criteria for asthma, which included either a 12% increase in FEV1 after a short-acting bronchodilator or a 20% decrease in FEV1 after inhalation of methacholine (PC20, 25 mg/mL). The SARP study has been previously described in detail.15 Briefly, the study population consisted of subjects recruited at each of the SARP-participating academic centers through the use of local

Results

The study population consisted on 1049 adult subjects with asthma of whom 63% were female, 65% were white, 27% were African American, and 8% were of “other” race. The median age for asthma onset was 10 years (interquartile range [IQR], 4-24 years), 48% had late-onset asthma (25 years; range, 12-69 years), and 52% had early-onset asthma (4 years; range, 0-11 years). The median BMI was 28 kg/m2 (IQR, 23-34 kg/m2); 42% were obese, 27% were overweight, and 31% were lean. Within the late-onset

Discussion

Given its high prevalence in the general population, obesity is one of the most frequent comorbidities among subjects with asthma. Yet remarkably, the association between obesity and asthma severity has been inconsistent. This might be explained by a combination of factors, which include the fact that not every asthmatic subject is equally affected by increases in BMI and the fact that age of asthma onset might lead to differential weight-gain patterns. In other words, clinical or epidemiologic

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    Supported by National Institutes of Health grant HL-069174.

    Disclosure of potential conflict of interest: W. W. Busse has served on the advisory boards for Centocor and Merck; has consulted for AstraZeneca, Boehringer Ingelheim, Novartis, TEVA, GlaxoSmithKline, (GlaxoSmithKline) Amgen, Pfizer, MedImmune, and Genentech; and has received research support from the National Institutes of Health (NIH; National Institute of Allergy and Infectious Diseases [NIAID] and National Heart, Lung, and Blood Institute [NHLBI]), Novartis, AstraZeneca, GlaxoSmithKline, MedImmune, and Ception. M. Castro has consulted for Electrocore, NKTT, Schering, Asthmatx, and Cephalon; has served on an advisory board and given talks for Genentech; has given talks for AstraZeneca, Boehringer Ingelheim, Pfizer, Merck, and GlaxoSmithKline; has received research support from Asthmatx, Amgen, Ception, Genentech, MedImmune, Merck, Novartis, the NIH, and GlaxoSmithKline; and has received royalties from Elsevier. A. M Fitzpatrick has received research support from the NIH (NHLBI and National Institute of Nursing Research). B. Gaston has served on an advisory board for Gilead. E. Israel has consulted for Abbott, Amgen, Cowen & Co, GlaxoSmithKline, Icagen, MedImmune, Merck, NewMentor, NKT Therapeutics, Ono Pharmaceuticals US, Schering-Plough, and TEVA; has received research support from Aerovance, Amgen, Biota, Ception Therapeutics, Genentech, MedImmune, the NIH, and Novartis; and has provided legal consultation or expert witness testimony on the topic of asthma. N. N. Jarjour has consulted for Asthmatx and Genentech and has received research support from GlaxoSmithKline, Merck, Genentech, and MedImmune. S. P. Peters has received research support from the NIH (NHLBI). W. G. Teague has given talks for Merck and Genentech and has received research support from the NIH (NIAID and NHLBI) and the American Lung Association. The rest of the authors have declared that they have no conflict of interest.

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