Persistent obesity since childhood or adolescence accelerates biological aging in young adults from Chile's oldest birth cohort

Aging and obesity are primary risk factors for chronic conditions such as hypertension and diabetes. However, a mechanistic correlation between these risk factors has not been fully established. Using a historical birth cohort from Chile, we delve into the relationship between obesity and accelerated aging, spanning cellular to systemic levels. The cohort, comprising men and women in their late 20s, had their BMI recorded since birth, with 57% having obesity since childhood or adolescence. Our aim was to investigate if persistent obesity since childhood or adolescence leads to the display of molecular aging features in young adulthood. We also sought to determine whether cardiometabolic health issues accompanied this early aging phenotype. We used inferential statistics and data mining for analysis. Results show that persistent obesity since childhood or adolescence leads to epigenetic changes, telomere shortening, chronic inflammation, impaired nutrient sensing, mitochondrial stress, and diminished intercellular communication, resembling a compound network of interactions. This obesity-induced accelerated aging phenotype coincided with persistent decline of the cardiometabolic profile. Implications of our findings are significant and suggest that integrating molecular markers with clinical and epidemiological data could be valuable in identifying individuals at increased disease risk due to accelerated aging.