Metformin activates AMPK and inhibits mTOR signaling while restoring autophagy, improving mitochondrial function, and reducing senescence-associated inflammatory responses at standard therapeutic doses. Large observational studies demonstrate reduced mortality and age-related disease incidence in both diabetic and non-diabetic populations, independent of blood sugar effects. This positions metformin as a potential breakthrough in geroscience — the first drug that could target aging itself rather than individual age-related diseases. The convergence of mechanistic plausibility with epidemiological evidence represents a paradigm shift from treating diseases of aging to intervening in the aging process directly. However, the findings aren't universally positive. Animal studies show metformin may actually accelerate aging in elderly subjects, highlighting the complexity of timing interventions. This contradiction underscores a critical gap in translating promising longevity research from laboratory to clinic. While metformin's safety profile spans decades, the optimal age to begin anti-aging therapy remains unclear, potentially determining whether it extends healthspan or paradoxically shortens it.