Glucose is the body's primary energy source, but its role in longevity is complex. Chronically elevated blood glucose promotes non-enzymatic glycation and oxidative stress, leading to advanced glycation endproducts (AGEs) – a key aging mechanism. In model organisms (yeast, worms, mice), caloric restriction or glucose-lowering interventions extend lifespan via the insulin/IGF-1 signaling pathway. Human evidence is largely observational: longitudinal studies link good glycemic control with reduced age-related morbidity. Genetic variants affecting glucose metabolism (e.g., TCF7L2) are associated with type 2 diabetes, not directly with longevity. Direct-to-consumer genetic tests often overstate the predictive power of such SNPs for lifespan. In summary, glucose is essential, but chronically high levels accelerate aging. The evidence is mechanistic and observational, not from human randomized trials. Safety note: individuals with metabolic disorders should seek medical advice.
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