Background: The parallel global increase in the prevalence of obesity and bronchial asthma has highlighted a significant comorbidity. Evidence suggests obesity is a major risk factor for asthma development and a distinct phenotype modifier, leading to more severe disease and reduced treatment responsiveness.
Objective: To systematically review and synthesize current evidence on the pathophysiological mechanisms linking obesity to asthma and its impact on the clinical presentation and management of the disease.
Methods: A systematic search of PubMed/MEDLINE, Scopus, and Web of Science was conducted for studies published from inception to May 2024. The search strategy utilized keywords and MeSH terms related to "asthma," "obesity," "pathogenesis," "phenotype," and "clinical course." Observational studies, clinical trials, and reviews investigating the obesity-asthma relationship in humans were included. Study selection followed PRISMA guidelines, and quality was assessed using appropriate tools (e.g., Newcastle-Ottawa Scale).
Results: Of 3,250 identified records, 68 studies were included. Obesity influences asthma through: 1) Systemic Inflammation: Adipose tissue-derived mediators (leptin, resistin, IL-6) create a pro-inflammatory state, while adiponectin is reduced. This non-Th2 inflammation is often associated with neutrophilic or paucigranulocytic airway infiltration. 2) Mechanical Effects: Truncal adiposity reduces lung volumes (FRC, ERV), leading to airway narrowing and heightened hyperresponsiveness. 3) Comorbidities: High prevalence of OSA and GERD further exacerbates asthma control. Clinically, the "obese asthma" phenotype is characterized by increased symptoms, frequent exacerbations, accelerated lung function decline, and impaired response to inhaled corticosteroids.
Conclusion: Obesity fundamentally alters asthma pathogenesis, driving a complex phenotype that is often more severe and difficult to treat. Management should extend beyond conventional asthma therapy to include integrated strategies such as weight loss, which has demonstrated efficacy in improving asthma control and quality of life in this population.

Asthma, Obesity, Phenotype, Pathogenesis, Systemic Inflammation, Leptin, Adiponectin, Corticosteroid Resistance.

Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 2024.

World Health Organization. Obesity and Overweight Fact Sheet, 2024.

Peters U, et al. Curr Opin Allergy Clin Immunol. 2018;18(1):42-49.

Beuther DA, Sutherland ER. Am J Respir Crit Care Med. 2007;175(7):661-666.

Peters MC, et al. J Allergy Clin Immunol. 2018;141(5):1790-1794.

Haldar P, et al. Am J Respir Crit Care Med. 2008;178(5):469-475.

Sutherland ER, et al. J Allergy Clin Immunol. 2008;122(5):927-934.

Page MJ, et al. BMJ. 2021;372:n71.

Fantuzzi G. J Allergy Clin Immunol. 2005;115(5):911-919.

Shore SA. J Allergy Clin Immunol. 2015;136(1):92-99.

Shore SA, et al. J Allergy Clin Immunol. 2010;126(6):1093-1099.

Telenga ED, et al. Allergy. 2014;69(10):1301-1311.

Salome CM, et al. Thorax. 2010;65(2):101-107.

Sutherland TJ, et al. Am J Respir Crit Care Med. 2008;178(5):469-475.

Julien JY, et al. Chest. 2009;135(5):1125-1129.

Harding SM. J Allergy Clin Immunol. 2003;111(5):997-1003.

Taylor B, et al. Thorax. 2008;63(1):14-20.

Boulet LP, Franssen E. Respir Med. 2007;101(5):1040-1048.

Chen Y, et al. Ann Am Thorac Soc. 2015;12(8):1158-1164.

Dias-Júnior SA, et al. Chest. 2014;145(2):232-238.

Dixon AE, et al. J Allergy Clin Immunol. 2011;128(3):508-515.