Beyond BMI: visceral adiposity assessed by the lipid accumulation product index shows independent associations with IL-5 and TNF-β in older adults

Visceral adiposity contributes to inflammaging, but body mass index (BMI) may poorly reflect fat redistribution in late life. The lipid accumulation product (LAP) index is a surrogate of visceral adiposity; its immune correlates in older adults remain incompletely defined. In this cross-sectional study, we analyzed 206 community-dwelling older adults (mean age 75.9 ± 7.5 years; 57.3% women). Clinical, functional, anthropometric, metabolic, and biochemical data were collected with circulating cytokine and chemokine concentrations. Associations between LAP and immune mediators were explored using correlation analyses and progressively adjusted multivariable linear regression models. LAP did not differ by sex (p = 0.825). Women showed lower IL-10 (p = 0.011), IL-12p70 (p = 0.004), IL-3 (p = 0.017), IL-4 (p = 0.006), IL-15 (p = 0.013), and higher RANTES/CCL5 (p = 0.029). In the overall cohort, LAP correlated with BMI (p < 0.001) and glycaemia (p < 0.001), and inversely with HDL-C (p < 0.001). LAP was correlated with eotaxin (p = 0.029), MCP-1 (p = 0.038), IL-5 (p = 0.016), and TNF-β (p = 0.007) after age/sex adjustment. In fully adjusted regression models, IL-5 (p = 0.023) and TNF-β (p = 0.002) remained independently inversely associated with LAP, whereas MCP-1 and eotaxin lost significance after BMI adjustment. Associations between IL-5, TNF-β and other conventional measure of central adiposity ( waist-to-hip ratio) were weaker and less consistent than those observed for LAP index. In older adults, LAP index may capture an immunometabolic phenotype not fully explained by BMI alone. Higher LAP index is independently associated with lower IL-5 and TNF-β, suggesting a potential selective impairment of regulatory immune signaling with increasing visceral lipid accumulation.