Endocrine Abstracts

Background: Obesity poses a considerable threat to health, increasing the likelihood of accompanying conditions such as type 2 diabetes, hypertension, dyslipidemia, and cancer. Ageing results in the accumulation of damaging factors leading to the development of chronic diseases. Inflammation levels, telomere length, level of neurocognitive function, metabolic age serve as acknowledged indicators of biological aging. The prevalence of premature ageing in obesity has been evidenced. The precise factors driving this premature aging in obese individuals remain uncertain.

Objectives: The aim of the study was to assess the impact of comorbidity on premature ageing in obesity.

Methods: In this prospective cohort study the interleukin-6 (IL-6), C-reactive protein (CRP), telomere length (TL), speed of attention in Colour Trailed Test and metabolic age were evaluated in patients with severe obesity (SG, BMI ≥ 40 kg/m² or ≥35 kg/m² with obesity comorbidities, n=100) and the healthy volunteers (CG, BMI 18.5 - 24.9 kg/m², n=30). SG was divided into two subgroups: subjects with comorbidities (n=78) and subjects without comorbidities (n=21). The regression model tested the effect of dyslipidaemia, hypertension, diabetes and pre-diabetes on markers of ageing.

Results: Our results demonstrated that both SG subgroups presented higher levels of IL-6 (4.75 vs 3,96 vs 1.13 pg/ml), CRP (22.45 vs 17.8 vs 0.43 pg/ml); shorter TL (4002 vs 3809 vs 5353 bp) than never-obese subjects (P<0.05). However, there were no differences between patients with obesity and comorbidities and without comorbidities. The effect of BMI on increased inflammation has been demonstrated. The effect of the presence of hypertension on cognitive decline was observed.

Conclusions: Our study showed that obesity regardless of comorbidity causes premature ageing. An interesting point is the association of hypertenstion with cognitive function decline.