Obesity is not just a problem of excess weight; it significantly increases the risk of chronic diseases such as diabetes, atherosclerosis, and musculoskeletal disorders. However, recent research by a group of Chilean scientists reveals that obesity may pose an even greater threat: it accelerates biological aging, even in young adults. In a comprehensive study involving 205 participants, researchers found that long-term obesity, starting in childhood or adolescence, leads to premature biological aging.
How Is Obesity Linked to Aging?
Aging and obesity share many common traits, including systemic inflammation (inflammaging), telomere shortening, impaired intercellular communication, cellular senescence, and changes in DNA methylation. Researchers hypothesized that obesity could trigger these processes prematurely, even in young individuals. To test this hypothesis, they conducted a detailed study analyzing epigenetic age, telomere length, and biochemical markers of participants.
Study Design and Methodology
The study was part of the Santiago Longitudinal Study (SLS), which investigates the impact of nutrition on children's health. The participants included 205 individuals aged 28 to 31:
• Group 1 (89 individuals): Maintained a healthy body mass index (BMI) throughout their lives.
• Group 2 (43 individuals): Developed obesity during adolescence (average onset at 15.8 years). Average duration of obesity was 12.9 years.
• Group 3 (73 individuals): Developed obesity during childhood (average onset at 1.9 years). Average duration of obesity was 26.6 years.
Participants underwent clinical, physiological, and biochemical evaluations, and blood samples were analyzed between April 2022 and June 2023.
• Group 1 (89 individuals): Maintained a healthy body mass index (BMI) throughout their lives.
• Group 2 (43 individuals): Developed obesity during adolescence (average onset at 15.8 years). Average duration of obesity was 12.9 years.
• Group 3 (73 individuals): Developed obesity during childhood (average onset at 1.9 years). Average duration of obesity was 26.6 years.
Participants underwent clinical, physiological, and biochemical evaluations, and blood samples were analyzed between April 2022 and June 2023.
Study Results
Epigenetic Age and Telomere Length
The primary endpoints of the study were epigenetic age (calculated using Horvath’s and GrimAge epigenetic clocks) and leukocyte telomere length. The results were striking:
Thus, participants with obesity had an epigenetic age 4.4–4.7 years higher than their peers with a healthy BMI. In some cases, the difference reached up to 48%.
- In Group 1 (healthy BMI), epigenetic age closely matched chronological age: 28.5 years according to Horvath’s clock and 26.3 years according to GrimAge. Telomere length was 8.01 kilobases (kb).
- In Group 2 (adolescent-onset obesity), epigenetic age was significantly higher: 34.1 years (Horvath) and 31.6 years (GrimAge). Telomere length decreased to 7.46 kb.
- In Group 3 (childhood-onset obesity), the gap was even larger: 34.5 years (Horvath), 32.5 years (GrimAge), and telomere length was only 7.42 kb.
Thus, participants with obesity had an epigenetic age 4.4–4.7 years higher than their peers with a healthy BMI. In some cases, the difference reached up to 48%.
Secondary Markers of Aging
Analysis of secondary endpoints revealed signs of systemic inflammation (inflammaging) in Groups 2 and 3:
Conversely, levels of insulin-like growth factors IGF-1 and IGF-2 were reduced, indicating impaired nutrient absorption.
- Levels of high-sensitivity C-reactive protein (hs-CRP) and interleukins IL-6, IL-2, and IL-10 were significantly elevated.
- Growth differentiation factor 15 (GDF-15), a marker of mitochondrial stress, was also increased.
- Levels of fibroblast growth factor 21 (FGF-21) and leptin hormone were higher compared to Group 1.
Conversely, levels of insulin-like growth factors IGF-1 and IGF-2 were reduced, indicating impaired nutrient absorption.
Impaired Intercellular Communication
Researchers found that myokine levels (apelin, oncostatin, myostatin, and musclin) were significantly lower in participants with obesity compared to those with a healthy BMI. This suggests impaired signaling pathways and intercellular communication, likely linked to heightened systemic inflammation.
Conclusion
Long-term obesity, even in young adults, leads to premature biological aging. This manifests as increased epigenetic age, shortened telomeres, chronic inflammation, impaired nutrient absorption, elevated mitochondrial stress, and disrupted intercellular communication. These findings highlight the importance of preventing obesity from an early age and developing new approaches to mitigate its consequences.
Publication date: 17.07.2025
Source:
Correa-Burrows P. et al. Long-Term Obesity and Biological Aging in Young Adults. JAMA Netw Open. 2025 Jul 1;8(7):e2520011. doi: 10.1001/jamanetworkopen.2025.20011. PMID: 40643913; PMCID: PMC12254895.
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2836386
Source:
Correa-Burrows P. et al. Long-Term Obesity and Biological Aging in Young Adults. JAMA Netw Open. 2025 Jul 1;8(7):e2520011. doi: 10.1001/jamanetworkopen.2025.20011. PMID: 40643913; PMCID: PMC12254895.
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2836386