Pulsed Reductive Impulses via Exogenous Reducing Equivalents: A Novel Paradigm for Anti-Cancer and Anti-Aging Metabolic Therapy

Nicotinamide adenine dinucleotide (NAD⁺/NADH) metabolism occupies a central position in both tumour pathogenesis and cellular aging. Current therapeutic strategies pursue apparently contradictory objectives: oncology seeks to deplete NAD⁺ in cancer cells, while anti-aging practice administers NAD⁺ intravenously to restore levels that decline with age. This work proposes the pulsed administration of exogenous reducing equivalents as an integrated anti-cancer and anti-aging strategy. The core proposition concerns the principle of pulsed redox perturbation rather than any specific molecular vehicle: NADH is discussed as the illustrative first-line candidate because it is the native substrate of the respiratory chain and has an existing clinical precedent for intravenous administration, but it is explicitly not the ideal vehicle, being limited by molecular instability, restricted membrane permeability and stoichiometric consumption. Selectivity is proposed to arise from differential redox buffering capacity between healthy and transformed cells, through two complementary mechanisms operating at opposite ends of the axis of residual mitochondrial competence: reverse electron transport at Complex I in cells retaining proton-pumping capacity, and NAD⁺ depletion with consequent arrest of glycolysis and mitochondrial substrate-level phosphorylation in cells that cannot re-oxidise NADH. Healthy cells are proposed to escape both by possessing simultaneously the respiratory reserve to dispose of the imposed load and the ATP turnover required to discharge the accumulated proton gradient. A protocol of brief, intense pulses followed by recovery phases (redox press-pulse) is proposed, in combination with glucose restriction and optimisation of intracellular magnesium. The framework generates dissociable experimental signatures, an explicitly predicted zone of resistance, and a candidate predictive biomarker. Principal limitations, including cytosolic lactate dehydrogenase as an escape route and the vulnerability of cardiac and neural tissue to the same reverse-electron-transport mechanism, are stated explicitly. A speculative appendix considers coherence times in future engineered electron-delivery vehicles.