Beyond BMI: a three-dimensional integrative framework of morphology–metabolism-adipose inflammation for predicting obesity-related asthma

OBJECTIVE: Body mass index (BMI) fails to distinguish fat from lean mass, capture fat distribution, or reflect metabolic dysfunction and adipose inflammation, limiting its utility in obesity-related asthma. A framework integrating morphological, metabolic, and inflammatory indicators may offer a more biologically relevant approach. METHODS: We systematically searched PubMed, Embase, and Web of Science up to April 10, 2026, including population-based studies, imaging/body composition analyses, and mechanistic studies reporting asthma risk, phenotypes, lung function, control, or exacerbations. RESULTS: BMI alone insufficiently predicts asthma outcomes. Central and upper-body anthropometric indices (waist-to-height ratio, neck circumference, weight-adjusted waist index) show stronger, BMI-independent associations with asthma onset, poor control, and lung function decline. Body composition distinguishes fat versus lean mass effects; visceral adipose tissue and dysanapsis capture mechanical/developmental pathways. Metabolic abnormalities (dyslipidemia, small dense LDL, triglyceride-glucose index) correlate with airway resistance and exacerbation risk, often independent of total adiposity. Leptin is elevated and adiponectin (ADPN) reduced in asthma; the leptin/ADPN ratio and interleukin-6 identify a metabolically driven, non-type 2 phenotype poorly captured by BMI. These three dimensions offer complementary biomarkers for risk stratification, phenotyping, and monitoring treatment response. CONCLUSIONS: Assessing obesity-related asthma should move beyond a BMI-centered approach toward an integrated morphology-metabolism-inflammation framework, enhancing early identification, endotype-based stratification, and personalized management. Longitudinal studies are needed to validate multi-indicator scoring systems and establish standardized cutoffs.