Obesity alters lung function, can cause symptoms suggesting asthma, and may worsen preexisting asthma. The precise mechanisms on how obesity leads to or worsens asthma are not well elucidated. A combination of mechanical factors, adipose-released inflammatory mediators, and immune system activation appears likely responsible for the “obese-asthma” phenotype.
Pregnancy has a variable and unpredictable effect on asthma. Studies suggest maternal obesity may be a risk factor for the development of asthma in offspring.
In this chapter, we discuss the evidence linking asthma to obesity, review the proposed mechanisms, and discuss the clinical care of obese individuals with asthma (see Box 7-1 for key clinical points).
BOX 7-1 Key Clinical Points
Obesity is a risk factor for development of asthma, but the association is weak and needs further research.
Complex interactions between mechanical factors, inflammatory pathways, and adipokines are thought to contribute, but the exact mechanism of association is still unclear.
Asthma in obesity lacks cellular airway inflammation.
Obese individuals with asthma respond poorly to asthma controller medications.
Comorbidities, especially OSA, play a significant role in clinical presentation, while GERD (although common) does not play significant role.
Obese individuals with asthma have a poor quality of life, increased health care utilization, and increased symptoms despite lack of airway obstruction on lung function test.
Weight loss improves symptoms and physiological derangements, but its effect on inflammation is unclear.
Asthma in obesity has two clinical phenotypes (see Table 7-1 for details); understanding these is crucial to develop new treatment strategies in the future.
Maternal obesity and excessive weight gain during pregnancy may increase the risk of asthma in the offspring.
TABLE 7-1Characteristics of Asthma Phenotypes in Obesity |Favorite Table|Download (.pdf) TABLE 7-1 Characteristics of Asthma Phenotypes in Obesity
|Phenotype 1 ||Phenotype 2 |
|Asthma precedes obesity ||Obesity precedes asthma |
|Atopic ||Nonatopic |
|Early onset ||Late onset |
|Eosinophilic airway inflammation ||Lack of cellular inflammation |
|High serum IgE ||Low serum IgE |
|Severe airflow limitation ||Less airflow limitation |
|Male:Female unclear ||Predominantly female |
|Weight loss does not improve physiological and inflammatory derangements ||Weight loss can restore physiological and inflammatory derangements |
|Resistant to steroids ||Resistant to steroids |
|Comorbidities worsen asthma control ||Comorbidities may contribute to development of asthma |
LINKING ASTHMA AND OBESITY
Asthma prevalence has increased in parallel with obesity.1,2 Of US adults, 8% have asthma—an increase from the 1980 value of 3.1%.2 In the bariatric surgery population with body mass index (BMI) greater than 60 kg/m2, the asthma prevalence is estimated to be 33%.3
Obesity is defined as BMI greater than 30 kg/m2. While simple to calculate and commonly used, BMI is not the best measure of assessing body fat influence on respiratory diseases. BMI does not capture fat distribution patterns or assess metabolically active adipose. The android pattern (abdominal fat ...