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. 2025 Jul 1;8(7):e2520011.
doi: 10.1001/jamanetworkopen.2025.20011.

Long-Term Obesity and Biological Aging in Young Adults

Paulina Correa-Burrows  1   2 , Raquel Burrows  1 , Cecilia Albala  1   2 , Carlos Sepúlveda  3   4 , Felipe Salech  1   2   5 , Rodrigo Troncoso  1   6 , Daniel Bunout  1 , Christian Gonzalez-Billault  1   2   5   7   8
Affiliations

Long-Term Obesity and Biological Aging in Young Adults

Paulina Correa-Burrows et al. JAMA Netw Open. .

Abstract

Importance: It remains unclear whether obesity accelerates biological aging, potentially leading to early-onset chronic diseases.

Objective: To investigate the association between long-term obesity and the expression of biochemical aging markers in younger adults.

Design, setting, and participants: This multiple-events case-control study, conducted from April 5, 2022, to June 29, 2023, was embedded in the Santiago Longitudinal Study, a prospective Chilean birth cohort of adults aged 28 to 31 years among whom health and nutrition data were collected from September 1992 onward.

Exposure: Body mass index (BMI) trajectory across the life course, recorded multiple times since birth. Group 1 had healthy BMI across the life course, group 2 had persistent obesity since adolescence, and group 3 had persistent obesity since childhood.

Main outcomes and measures: Smoothed BMI trajectories (cubic polynomials) were used to estimate obesity duration. Primary outcomes were DNA methylation-based age and telomere length (TL). Secondary outcomes included levels of aging-related cytokines, growth factors, and adipomyokines.

Results: In the sample of 205 adults (mean [SD] age, 28.9 [0.6] years; 100 females [49%]), 89 (43%) were in group 1, 43 (21%) in group 2, and 73 (36%) in group 3. Mean (SD) obesity duration was 12.9 (4.8) years in group 2 and 26.6 (2.3) years in group 3. Long-term obesity was associated with adulthood expression of biomarkers denoting antagonistic and integrative aging hallmarks, including mean (SD) hs-CRP (1.69 [2.1] vs 3.67 vs 4.24 [2.4] mg/L; P < .001; f = 0.57 [95% CI, 0.44-0.70]) and IL-6 (log, 0.69 [0.5] vs 1.03 [0.4] vs 0.99 [0.4]; P < .001; f = 0.53 [95% CI, 0.41-0.62]), as well as FGF-21, IGF-1, IGF-2, apelin, and irisin. Cohen f coefficient indicated a large effect size for the association of long-term obesity with adulthood expression of these markers.

Conclusions and relevance: In this multiple-events case-control study, long-term obesity was associated with the expression of biochemical aging markers in adults aged 28 to 31 years, consistent with epigenetic alterations, telomere attrition, chronic inflammation, impaired nutrient sensing, mitochondrial stress, and compromised intercellular communication. In young adults, chronic health issues may emerge from accelerated biological aging associated with long-term obesity.

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Conflict of interest statement

Conflict of Interest Disclosures: None reported.

Figures

Figure.
Figure.. Data Visualization of Chronological vs Epigenetic Age in the Sample
Group 1 participants always had a body mass index in the healthy range, group 2 had obesity starting in adolescence and remaining into adulthood, and group 3 had obesity in early childhood and remaining into adulthood. A 2-tailed Pettitt test for homogeneity was used to detect change points in the data series. A, Pettitt test N = 5070. B, Pettitt test N = 5310. Horizontal dashed lines indicate the mean epigenetic age value for each of the 2 series identified by the Pettitt test.
See this image and copyright information in PMC

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