The Obesity-Accelerated Aging (ObAGE) framework demonstrates that excess adiposity prematurely triggers core aging mechanisms including dysregulated nutrient sensing, chronic inflammation, cellular senescence, and epigenetic drift. Rather than simply increasing disease risk, obesity appears to accelerate the fundamental biological processes that drive aging itself. This convergence explains a puzzling clinical observation: why obese individuals don't just get more diseases, but experience earlier onset of multimorbidity and functional decline that typically characterizes much older adults. The framework represents a paradigm shift from viewing obesity as a risk factor to understanding it as an aging accelerator that erodes physiological resilience before overt disease appears. What makes this particularly compelling is the evidence that these aging signatures remain modifiable through metabolic interventions, from lifestyle changes to GLP-1 receptor agonists. This positions obesity treatment not merely as disease prevention but as a geroscience intervention that could preserve biological youth. However, the observational nature of much supporting evidence means causality remains to be definitively established across all proposed pathways.