Uncoupling Systemic Inflammation from Body Mass Index: The Unseen Role of Visceral Adiposity and Metabolic Phenotypes-A Subgroup Analysis of the Nationwide OBREDI-TR Cohort.

Objectives

Although obesity is known to cause low-grade chronic inflammation, the extent to which body mass index (BMI) reflects this remains questionable. To investigate this, we classified a national obesity cohort by BMI and evaluated its association with complete blood count (CBC)-derived systemic inflammatory indices.

Methods

This retrospective, multi-center study included 6499 adults from the OBREDI-TR cohort with available laboratory data. Patients were categorized by BMI into Class I (30.0-34.9 kg/m2, n = 2751), Class II (35.0-39.9 kg/m2, n = 1804), and Class III (≥40.0 kg/m2, n = 1944) obesity. We compared demographic, clinical, and laboratory parameters, especially in terms of CBC-derived inflammation parameters: neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), lymphocyte-to-monocyte ratio (LMR), systemic immune-inflammation index (SII), and systemic inflammation response index (SIRI).

Results

The Class III group was younger (42.73 ± 13.21 vs. 45.14 ± 14.12 in Class I) and predominantly female (p < 0.001 for both). None of the evaluated inflammatory indices showed significant differences across the groups (NLR, p = 0.435; PLR, p = 0.141; LMR, p = 0.520; SII, p = 0.326; SIRI, p = 0.459). Interestingly, hypertension was less common in the Class III obesity group (49.0% vs. 53.5% in Class I, p = 0.009).

Conclusions

The failure of increasing inflammatory indices to parallel BMI, creating a "ceiling effect," reflects the inadequacy of BMI in determining inflammatory burden. Evaluating the inflammatory burden of obesity through visceral adiposity and metabolic phenotyping (metabolically healthy (MHO) vs. metabolically unhealthy obesity (MUO) rather than BMI will provide a more accurate basis for objective clinical evaluation and personalized treatment.