For many patients, asthma symptoms are not driven by airway inflammation alone. Obesity can influence lung mechanics, systemic inflammation, medication response, and overall disease burden.

Asthma is a common chronic disease, affecting approximately 26 million people in the United States. Its economic burden is significant, with estimated annual costs of approximately $82 billion. Severe asthma is recognized as a complex clinical syndrome and often presents with multiple comorbidities associated with poorer outcomes. Treatable traits (TT)* may also contribute to persistent symptoms, and obesity is one important extra-pulmonary treatable trait.

Obesity can impair lung function and contribute to airway and systemic inflammation. It is also highly prevalent: more than 100 million people in the United States live with obesity, including 22 million with severe obesity. In 2019, the economic burden of obesity was estimated at $173 billion. Medical costs for adults with obesity were $1,861 higher than for adults with a healthy weight, and costs were even higher for patients with severe obesity, at approximately $3,097.

Obesity is a major public health issue and is both a risk factor and disease modifier for asthma. Individuals with obesity have a higher risk of developing asthma, and approximately 38.8% of people with asthma also have obesity. Patients with obesity-related asthma often experience more frequent symptoms, increased exacerbation frequency and severity, and lower quality of life. They may also have a reduced response to standard asthma medications, including inhaled corticosteroids (ICS) and ICS/LABA combination inhalers.

Obesity-related asthma is a complex syndrome. Excess adipose tissue can change lung physiology by compressing the lungs and reducing lung volume. These effects may be reflected in decreases in functional residual capacity (FRC), tidal volume (Vt), and expiratory reserve volume (ERV). Obesity also increases the collapsibility of the peripheral airways through mechanical compression, increasing the physical load of the respiratory system. Obesity is associated with increased airway resistance and altered airway reactance. Airway hyperresponsiveness (AHR) increases as body mass index (BMI) rises, making weight gain a risk factor for developing AHR. Weight loss of at least 5% has been shown to improve asthma control and spirometry values, with additional improvements reported in peak flow measurements and ERV. Although changes in AHR after weight loss are less clearly defined, airway reactivity may also improve.

Inflammation is a hallmark of both asthma and obesity. Asthma is often categorized as T2-high or T2-low based on the inflammatory cells and pathways present in the airways. T2-high asthma is predominantly eosinophilic, and several biomarkers are available to help assess it, including blood and sputum eosinophils and fractional exhaled nitric oxide (FeNO). Compared with T2-high asthma, T2-low asthma is less well characterized and has fewer validated biomarkers. FeNO and eosinophil counts can help exclude T2-high inflammation; however, there are currently no well-established biomarkers for T2-low asthma. T2-low inflammation is generally less responsive to inhaled corticosteroids (ICS), and symptoms may be driven by different inflammatory pathways, such as IL-17, IL-6, or IL-23. IL-6 is produced by macrophages in adipose tissue and is associated with metabolic health and asthma severity. Interestingly, not all patients with obesity-related asthma have elevated IL-6. Adipose tissue inflammation is also increased in people with asthma compared with non-asthmatic controls.

Because obesity-related asthma is not a single disease pattern, identifying phenotypes may help guide more targeted management. Obesity-related asthma includes a variety of phenotypes. A phenotype refers to a recognizable pattern of clinical characteristics, lung function, and inflammatory features.

• Earlier-onset asthma is often associated with more severe disease and higher T2 inflammation.
• Later-onset asthma is often seen in female patients and may be associated with lower airway inflammation but greater inflammation in adipose tissue.
• Neutrophilic inflammation, often seen in T2-low asthma, is another phenotype. Patients with neutrophilic asthma may experience improvement with weight loss.

Asthma can be difficult to diagnose accurately because many conditions mimic asthma symptoms. This is particularly important in patients with obesity, who may be at greater risk of misdiagnosis. A careful assessment of symptoms, lung function, inflammatory markers, comorbidities, and treatable traits can help guide more personalized and effective asthma management. Objective testing, including spirometry, FeNO, and methacholine challenge testing with Provocholine, can help distinguish asthma from asthma-like symptoms and support more individualized treatment decisions.

*Treatable Traits is discussed in the May 2026 Blog.

One-Size-Fits-All Or Treatable Traits? – Methapharm Respiratory

Author:

Heather Murgatroyd, BA, RRT, CPFT, AE-C 

Senior Clinical Specialist 

Methapharm Respiratory 

 References:

1. P.E. Pfeffer, H. Rupani, A. De Simoni. Bringing the treatable traits approach to primary care asthma management. Front Allergy. 2023;4:1240375.
2. P.J. McDowell, L.G. Heaney. Different endotypes and phenotypes drive the heterogeneity in severe asthma. Allergy. 2020;75:302-310.
3. U. Peter, A. Dixon, E. Forno. Obesity and asthma. J Allergy Clin Immunol. 2018;141(4):1169-1179.
4. Centers for Disease Control and Prevention. CDC. 2026.