NMN → NAD+ via the enzyme NMNAT (nicotinamide mononucleotide adenylyltransferase) in a single enzymatic step. This is the most direct precursor pathway to NAD+. Once NAD+ is restored: (1) sirtuins (SIRT1-7) are activated — deacetylases that regulate gene expression, mitochondrial function, and DNA repair; (2) PARPs (DNA repair enzymes) function more efficiently; (3) CD38 (NAD+ consumer that increases with age and inflammation) is counteracted; (4) mitochondrial electron transport chain efficiency improves (NAD+/NADH ratio). The age-related NAD+ decline is driven by: increasing CD38 expression (inflammatory NAD+ consumption), decreasing NAMPT expression (NAD+ synthesis enzyme), and accumulating DNA damage (PARP consumption).
No critical interactions identified.
Independently graded against 173,636 indexed supplements with 177 published clinical interactions, sourced from PubMed, FDA CAERS, openFDA, and NIH DSLD | Last updated:
Not medical advice. Based on published clinical research and systematic reviews.