250–1,000 mg/day in studies.
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Nicotinamide mononucleotide (NMN) is a precursor molecule for the biosynthesis of nicotinamide adenine dinucleotide, or NAD+, a coenzyme that takes part in cellular energy production and DNA repair; NAD+ can also be synthesized from other precursors such as nicotinamide, nicotinic acid, and nicotinamide riboside, which are collectively called niacin or vitamin B3, and also from tryptophan, an amino acid obtained from the diet.
NMN is present in several foods such as broccoli, avocado, and beef, and acts as an intermediate in the NAD+ salvage pathway; NAD+ depletion, which occurs with age, has been implicated in the progression of multiple aging-related conditions such as metabolic dysfunction and neurodegenerative diseases, and boosting NAD+ levels through precursors such as NMN has shown therapeutic potential in multiple animal models of aging and age-related diseases.
In mouse models of diet-induced diabetes, injection of 500 mg/kg of NMN for 7 days improved insulin sensitivity and glucose tolerance; in old mice aged 26-28 months fed 300 mg/kg for 8 weeks, age-related arterial dysfunction and oxidative stress were reversed; and in a cardiomyopathy model, NMN injection for 6 weeks improved cardiac contractility compared with untreated mice.
For neurodegeneration, rats injected with 500 mg/kg of NMN daily for 10 days showed sustained improvements in cognitive function and attenuation of neuronal cell death; in mice predisposed to developing Alzheimer's, 100 mg/kg daily for 28 days produced substantial improvements in behavioral measures of cognitive decline and significantly reduced the production of beta-amyloid and the inflammatory responses that drive disease progression.
One controversial aspect of NMN is its relationship with cancer: the enzyme NAMPT, which converts nicotinamide into NMN as the first step of the NAD+ salvage pathway, may have pro-angiogenic activity that supports the growth of some types of cancer; in a mouse model of pancreatic cancer, NMN injection for 13 days showed significant increases in precancerous and cancerous lesions, which suggests that NMN supplementation might need to be administered with precision to balance its anti-aging effects against possible pro-tumorigenic effects.
As for oral availability in humans, studies in mice show that orally administered NMN at high doses can effectively raise NAD+ levels in multiple tissues within 10-30 minutes of administration; however, at low doses almost all NMN-derived NAD+ comes from the salvage pathway and not directly from NMN, which makes it subject to feedback inhibition and limits how far tissue NAD+ levels can be raised.
Information, not medical advice. Scientific evidence reflects the quality of the studies.