Asthma and Obesity Diet Versus Exercise

Obesity is recognized as a pro-inflammatory condition associated with multiple chronic diseases, including asthma. The specific mechanisms linking asthma and obesity remain hypothetical. Our primary hypothesis is that inflammatory SNPs may regulate the degree of the inflammatory response, with obesity modifying the severity of the disease. In this instance, asthma that develops in the context of obesity demonstrates the potential deleterious relationship between a specific proinflammatory state (obesity) and the genetic regulators of inflammation (SNPs). Our secondary hypothesis proposes that short-term (12-weeks) weight loss by diet alone, but not exercise alone, will reduce lung specific inflammation and diminish the pro-inflammatory responses in female African American obese adolescents with asthma compared to a waiting list control group who after their initial 12 weeks then receive a combined 12-week diet plus exercise program (waiting list control/combined). A third exploratory hypothesis proposes that the frequency of identified SNPs will be significantly related to the amount of fat loss through diet, exercise or combined program and will further be mediated by specific airway and, pro-and-anti-inflammatory markers.These hypotheses will be tested using the following Specific Aims: 1. To determine the frequency of single nucleotide polymorphisms and SNP haplotypes in pro- and anti-inflammatory genes in female African American obese and non-obese asthmatic and non-asthmatic adolescents, 13-19 years or age. 2. To examine the effects of diet or exercise on lung specific inflammation (exhaled nitric oxide, \[eNO\]) and pro-and-anti-inflammatory responses in female African-American obese asthmatic and non-asthmatic adolescents compared to a waiting list control/ combined group. In addition we will examine the following Exploratory Aim: To determine the effects of the inflammatory SNPs in the modulation of several inflammatory markers and lung specific inflammat