NMN (Nicotinamide Mononucleotide)
Direct precursor to nicotinamide adenine dinucleotide (NAD+) via the salvage pathway enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT). Bypasses the rate-limiting NAMPT step when administered exogenously. Restores NAD+ levels that decline approximately 50% between ages 40 and 60. Elevated NAD+ activates SIRT1/3 deacetylases and PARP1 DNA repair enzymes, improves mitochondrial function, and enhances cellular energy metabolism.
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- fasting-glucose
- hba1c
- fasting-insulin
- lipid-panel
- alt
- ast
- homocysteine
- hs-crp
- active-cancer-uncontrolled
- concurrent-nicotinamide-high-dose
- pregnancy
- PMID:27127236Long-term administration of nicotinamide mononucleotide mitigates age-associated physiological decline in mice — Cell Metab, 2016
- PMID:31471192NMN supplementation increases NAD+ levels in healthy humans — Endocr J, 2020
- PMID:35927255NMN increases muscle insulin sensitivity in prediabetic women — Science, 2021
- PMID:36482258MIB-626 (NMN formulation) in overweight adults: a randomized clinical trial — J Clin Endocrinol Metab, 2023
NMN is the NAD+ precursor that David Sinclair put on the map, for better and worse. The science is real — NAD+ declines with age, NMN restores it, and elevated NAD+ activates sirtuins and PARPs that are critical for DNA repair and mitochondrial function. The first human RCT data from Washington University showed insulin sensitivity improvements in prediabetic women. The MIB-626 trial confirmed dose-dependent NAD+ elevation. What the data does not yet show is whether taking NMN for 20 years extends human lifespan. The mouse data is compelling. The human translation is still in its first chapter. Also appears in the supplements category because the regulatory classification remains contested.
This is not medical advice
Discuss with a licensed clinician before starting, stopping, or changing any compound. This page documents what the research literature describes — it is not a prescription.
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