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

Abstract

Obesity and aging are characterized by chronic low-grade inflammation, which contributes to the onset of degenerative processes. The objective was to comprehensively analyze the prevalence of premature aging in obesity and identify metabolic factors influencing aging. In this prospective cohort study, the telomere length, 8-Oxo-2'-deoxyguanosine DNA damage, interleukin-6 (IL-6), metabolic age and cognitive functions were evaluated in the patients with severe obesity (study group (SG), defined as BMI ≥ 40 kg/m2 or ≥ 35 kg/m2 with comorbidities, n=100) and the healthy volunteers (control group (CG), defined as BMI 18.5 - 24.9 kg/m2, n=33). SG was further divided into two subgroups: study group 1 (SG1) - subjects with BMI≥ 50 kg/m2and study group 2 (SG2) with BMI < 50 kg/m2. Our findings revealed that individuals in the SG exhibited shorter telomeres, higher levels of inflammation, and more advanced metabolic age compared to those in the CG. However, no significant differences in DNA damage or cognitive function abilities were observed between the SG and CG. Notably, SG1 displayed elevated IL-6 levels compared to SG2. Furthermore, IL-6 levels decreased significantly with increasing body fat, and individuals with higher visceral fat levels had longer telomeres. Premature aging manifests in obesity concerning telomere length, inflammation levels and metabolic age. Aging in obesity should be considered as a non-linear process.