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

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Abstract

Nicotinamide adenine dinucleotide (NAD+/NADH) metabolism holds a central position in both tumor pathogenesis and cellular aging processes. Current therapeutic strategies pursue apparently contradictory objectives: oncology aims to deplete NAD+ in cancer cells, while anti-aging medicine administers NAD+ intravenously to restore levels that decline with age. This work proposes a paradigm shift: the pulsed administration of exogenous reducing equivalents — with NADH (the reduced form of the coenzyme) as the primary but not exclusive vehicle — as an integrated anti-cancer and anti-aging strategy. The rationale is based on intrinsic metabolic selectivity: cancer cells, characterized by mitochondrial dysfunction and dependence on fermentative glycolysis (Warburg effect), are unable to dispose of an acute excess of NADH through the electron transport chain, thereby suffering selectively lethal reductive stress. Healthy cells, endowed with functional mitochondria, can manage the reductive overload by oxidizing excess NADH in the respiratory chain, with respiratory control mechanisms regulating the flux. A protocol of brief, intense pulses (redox press-pulse) followed by recovery phases is proposed, in synergistic combination with glucose restriction (ketogenic diet/fasting) and optimization of intracellular magnesium. This triad — reducing substrate, enzymatic structure, and environment — aims to restore respiratory chain efficiency in healthy cells and selectively destabilize cancer cell metabolism. The convergence between anti-cancer and anti-aging mechanisms mediated by cyclic reductive impulses is also discussed. A speculative appendix explores the implications of quantum biology for understanding the efficiency of mitochondrial electron transfer.

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