Are patients with severe obesity aging faster? Impact of severe obesity on different aspects of biological age.

Introduction: Obesity and aging are characterized by chronic low‑grade inflammation, which contributes to the onset of degenerative processes.

Objectives: Our objective was to comprehensively analyze the prevalence of premature aging in patients with obesity and identify metabolic factors influencing aging.

Patients And Methods: In this prospective cohort study, telomere length, DNA damage, interleukin 6 (IL‑6) level, metabolic age, and cognitive functions were evaluated in patients with severe obesity (study group [SG], defined as body mass index [BMI] equal to or above 40 kg/m2 or equal to or above 35 kg/m2 with comorbidities; n = 100) and healthy volunteers (control group [CG], defined as BMI 18.5-24.9 kg/m2; n = 33). The SG was further divided into 2 subgroups, SG1 comprising patients with BMI equal to or above 50 kg/m2 and SG2 with BMI below 50 kg/m2.

Results: Our findings showed that individuals in the SG had shorter telomeres, higher levels of inflammation, and more advanced metabolic age than those in the CG. However, no significant differences in DNA damage or cognitive function abilities were observed between the groups. Notably, the SG1 displayed elevated IL‑6 levels as compared with the SG2. Furthermore, IL‑6 levels decreased significantly with increasing body fat, and the individuals with higher visceral fat levels had longer telomeres.

Conclusions: Premature aging manifests in obesity through telomere length, inflammation levels, and metabolic age. Aging in obesity should be considered as a nonlinear process.