• Alicja Dudek, Barbara Zapała, Ilona Kawa, Piotr Tylec, Karol Ciszek, Katarzyna Cyranka, Michał Wysocki, and Piotr Major.
• Second Department of General Surgery, Jagiellonian University Medical College, Kraków, Poland. ala.ddudek@gmail.com
• Pol. Arch. Med. Wewn. 2024 Oct 30; 134 (10).

IntroductionObesity and aging are characterized by chronic low‑grade inflammation, which contributes to the onset of degenerative processes.ObjectivesOur objective was to comprehensively analyze the prevalence of premature aging in patients with obesity and identify metabolic factors influencing aging.Patients And MethodsIn 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.ResultsOur 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.ConclusionsPremature aging manifests in obesity through telomere length, inflammation levels, and metabolic age. Aging in obesity should be considered as a nonlinear process.

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