Asthma and obesity remain two of the most common chronic conditions in children and adults. Although widely recognized to coexist in patients across the age spectrum, the causal and pathobiologic relationship between asthma and obesity remains incompletely understood. Forno and colleagues showed that being overweight or obese in a pediatric nonasthmatic cohort was related to dysanapsis (disproportionate growth between lung size and airway caliber) and therefore had a reduced FEV1/FVC ratio characteristic of obstructive airway diseases (1). Those with asthma who showed evidence of dysanapsis had more severe disease. Connecting these findings with metabolic abnormalities often associated with obesity, an analysis of adolescents in the cross-sectional 2010 National Health and Nutrition Examination Survey (2) showed more airflow obstruction in those with asthma and metabolic syndrome than in either characteristic alone. A recent analysis of data from the SARP-3 (Severe Asthma Research Program)(3) showed that adult patients with asthma with insulin resistance had lower FEV1 and FVC not attributable to obesity, with reduced response to medications. Furthermore, patients with insulin resistance were more likely to have a decline in lung function over time. Taken together, these data suggest that obesity, metabolic syndrome, and insulin resistance may influence lung function in patients with asthma. The developmental origins of these associations have not been elucidated. We recently showed that elevated insulin concentrations in early childhood predicted subsequent development of asthma in two longitudinal birth cohorts, the TCRS (Tucson Childrenes Respiratory Study) and the Avon Longitudinal Study of Adults and Children, irrespective of body mass index (BMI)(4). Here, we hypothesized that among individuals with asthma, elevated insulin in early childhood may be a risk factor for subsequent reduction in lung function.

TCRS is a longitudinal, nonselected birth cohort designed to study early life risk factors for chronic lung disease. This cohort enrolled 1,246 participants between 1980 and 1984 with continuous follow-up to the present time (5). Lung function was measured every 4-6 years by spirometry according to American Thoracic Society guidelines. Active asthma was recorded at each visit and defined as physician-diagnosed asthma with reports of asthma symptoms in the