NAD+
Essential cellular cofactor central to redox reactions, energy metabolism, DNA-repair signalling and mitochondrial biology.
Mechanism & research rationale
NAD+ (nicotinamide adenine dinucleotide) cycles between oxidized and reduced states in core metabolic pathways and also serves as a substrate for enzymes including sirtuins, PARPs and CD38-related pathways. Ageing and disease-related changes in NAD metabolism are an active research field.
Human evidence
Most modern human intervention evidence concerns NAD+-boosting precursors such as nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN), not direct administration of NAD+ itself. Reviews find that precursor supplementation can raise NAD-related metabolites, but consistent improvements in clinical function or “anti-ageing” outcomes have not been established across populations. A 2025 Nature Metabolism review describes human efficacy as limited and tissue-specific evidence as sparse.
Preclinical / translational evidence
Rodent and cell studies report broad metabolic, mitochondrial, inflammatory and stress-response effects from manipulating NAD metabolism. Translation is complicated because different precursors, tissues and disease states produce different responses.
Key limitations
- Do not treat NR/NMN trial results as direct evidence for an NAD+ research preparation.
- “Anti-ageing” claims run ahead of the current clinical evidence.
- Optimal route, exposure, long-term safety and clinically meaningful endpoints remain active research questions.