Long-Term Obesity Associated With Accelerated Biological Aging in Young Adults

Paulina Correa-Burrows, PhD

Courtesy of LinkedIn

A new study published in JAMA Network Open reports that persistent obesity from childhood or adolescence is associated with biochemical markers of accelerated aging in young adults aged 28 to 31 years.1

Researchers analyzed data from 205 participants in the Santiago Longitudinal Study, Chile’s oldest birth cohort, to examine the relationship between obesity duration and biological aging indicators. Participants were grouped according to body mass index (BMI) trajectory: those with a healthy BMI across the life course (n = 89), those with persistent obesity since adolescence (n = 43), and those with persistent obesity since childhood (n = 73).1

Findings showed that individuals with long-term obesity had DNA methylation–based ages that exceeded chronological age by a mean of 15% to 16%, with some participants showing differences up to 48%. For example, mean epigenetic age measured by the Horvath clock was 34.1 years for those with obesity since adolescence and 34.5 years for those with obesity since childhood, compared with 28.5 years in participants who maintained a healthy BMI (P < .001). Telomere length was also significantly shorter in the long-term obesity groups (7.42–7.46 kb) compared with the healthy BMI group (8.01 kb; P < .001).1

Markers of chronic inflammation and metabolic dysfunction were elevated in those with long-term obesity. High-sensitivity C-reactive protein levels averaged 3.67 mg/L in participants with obesity since adolescence and 4.24 mg/L in those with obesity since childhood, compared with 1.69 mg/L in the healthy BMI group (P < .001). Similarly, interleukin-6 levels were significantly higher in the long-term obesity groups (P < .001). These participants also had higher leptin and fibroblast growth factor 21 levels, as well as reduced insulinlike growth factor 1, consistent with disrupted nutrient sensing and mitochondrial stress.1

The study also confirmed that participants with long-term obesity displayed greater cardiometabolic dysfunction in adulthood, including higher waist circumference, insulin resistance, arterial stiffness, and risk of metabolic dysfunction–associated steatotic liver disease, compared with those who maintained a healthy BMI.1

Investigators concluded that obesity across the life course may accelerate primary hallmarks of aging, including telomere attrition and epigenetic modifications, as well as integrative hallmarks such as impaired intercellular communication and chronic inflammation. "In young adults, chronic health issues may emerge from accelerated biological aging associated with long-term obesity," they wrote.1

The authors noted limitations, including reliance on BMI as the primary exposure measure and the study’s focus on a Chilean cohort, which may limit generalizability. Nonetheless, the findings suggest that long-term obesity may be a model of accelerated aging and warrant further research into prevention strategies and interventions to mitigate early-onset chronic disease risk.1

In an accompanying editorial comment, Antonello Lorenzini, PhD, of the University of Bologna in Italy, wrote: The results speak for themselves...It is reasonable now to hypothesize that the excess calories that precede and accompany obesity, or obesity itself as a state of modified hormonal balance, or a combination of both these aspects, may accelerate the aging process."2

References:

1. Correa-Burrows P, Burrows R, Albala C, et al. Long-term obesity and biological aging in young adults. JAMA Netw Open. Published online July 1, 2025. doi: 10.1001/jamanetworkopen.2025.20011
2. Lorenzini A. Calorie restriction, obesity, and the aging process. JAMA Netw Open. Published online July 1, 2025. doi:10.1001/jamanetworkopen.2025.22387