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NAD\u207a plays a central role in cellular energy metabolism, redox balance, and signaling pathways linked to aging, neurodegeneration, and metabolic health. Current evidence shows that oral NAD\u207a precursors such as nicotinamide riboside and nicotinamide mononucleotide can increase circulating NAD\u207a levels, although their clinical benefits remain variable and context-dependent. Intravenous NAD\u207a administration is less well characterized and lacks robust clinical validation. The modelling framework presented here highlights that NAD\u207a responses are nonlinear and influenced by factors such as dose, age, metabolic state, and route of administration. Rather than following a simple dose\u2013response relationship, NAD\u207a supplementation appears to operate within a complex regulatory system involving feedback mechanisms and biological saturation. 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