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Long-term obesity accelerates aging in young adults, increasing risks for cardiovascular diseases and metabolic dysfunction.
New study findings published by investigators in JAMA Network found that long-term obesity is related to the expression of biochemical aging markers in adults aged 28 to 31 years. The study authors noted that the findings suggest that long-term obesity may trigger aging-related molecular signals in young adults, which is consistent with epigenetic alterations, telomere attrition, chronic inflammation, impaired nutrient sensing, mitochondrial stress, and compromised intercellular communication.1,2
Image credit: Protsenko Dmitriy | stock.adobe.com
Obesity is a serious medical problem that increases the risk of many diseases, including heart disease, diabetes, high blood pressure, high cholesterol, liver disease, sleep apnea, and certain cancers. Obesity is defined as a body mass index (BMI) of 30.0 and higher. The study authors noted that an estimated 1 billion individuals are expected to have obesity by 2030.1,3
Previous research has demonstrated that obesity reduces health span and life expectancy due to the increased risk of these cardiometabolic, neoplastic, and musculoskeletal diseases. However, in each of these conditions, aging is the most common risk factor, and these health issues have alarmingly increased in young individuals, suggesting signs of accelerated aging. Research on the connection between obesity and lifespans is limited, emphasizing the need to better understand their molecular pathways and mechanisms, as both share many traits, including systemic inflammation, telomere attrition, gut microbiome imbalance, mitochondrial dysfunction, impaired nutrient sensing, poor intercellular communication, altered proteostasis, cellular senescence, and age-related DNA hypomethylation.1,3
Researchers conducted a prospective multiple-events, case-control, cohort study of males and females that were born in Chile in the 1990s to assess how obesity accelerates aging. The study began in April 2022 and ended in June 2023. A total of 205 adults aged 28 to 31 years (mean age: 28.6 years) were included, with 89 participants in group 1, 43 in group 2, and 73 in group 3. The BMI of the included individuals was recorded various times since birth, as group 1 had a healthy BMI, group 2 had persistent obesity since adolescence, and group 3 had persistent obesity since childhood.1
To estimate obesity duration, researchers used cubic polynomials, or smoothed BMI trajectories, across all participants life courses. Following, they estimated the timing of obesity onset and the duration of individuals with obesity. They found that the mean obesity duration was about 12.9 years in group 2 and 26.6 years in group 3.1
Among the 205 individuals divided into the 3 groups, obesity onset was significantly earlier for those with childhood obesity compared with adolescent obesity, leading to a longer duration of obesity for the childhood-onset group. Sex was not found to be linked with either BMI trajectory or age.1
The results demonstrated that individuals who maintained a healthy BMI had better cardiometabolic markers—including lower waist circumference, systolic blood pressure, insulin levels, and metabolic syndrome severity—compared to those who had adolescent or childhood obesity. While fasting glucose remained at normal levels across all groups, individuals with obesity displayed elevated insulin levels and insulin resistance. In both groups that experienced obesity, a high risk of metabolic dysfunction-associated steatotic liver disease was reported, regardless of the age of obesity onset.1
The findings suggest that long-term obesity is connected with a greater negative impact on cardiometabolic health, which could lead to early-onset cardiometabolic diseases.1,2
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