In this narrative translational review, we propose that obesity and aging are not merely parallel epidemics, but biologically convergent processes with shared metabolic and molecular substrates. We introduce the Obesity-Accelerated Aging (ObAGE) framework, arguing that excess adiposity functions as a clinically relevant accelerator of biological aging trajectories. Because much of the supporting human evidence is observational, we use acceleration to indicate earlier appearance or increases in aging-related biological signatures and clinical phenotypes, while recognizing that causal strength varies across aging pathways and study designs. By prematurely engaging core aging hallmarks, including dysregulated nutrient sensing, chronic low-grade inflammation, cellular senescence, and epigenetic drift, obesity may intensify aging-related decline without replacing the underlying aging process, progressively eroding physiological resilience before overt cardiometabolic disease becomes clinically manifest. This convergence helps explain why obesity does not simply increase risk for isolated non-communicable diseases but is associated with earlier multimorbidity and functional impairment. Importantly, this biological embedding begins during sensitive life-course windows. Yet, converging evidence from human studies (from lifestyle interventions to incretin-based pharmacotherapy) suggests that several aging-related signatures remain at least partially modifiable through metabolic optimization. Framing obesity within a geroscience paradigm positions metabolic treatment not only as disease management but also as a strategy to preserve physiological capacity and delay aging-related decline.
