By Dr Theron Hutton MD
Nicotinamide mononucleotide (NMN) and nicotinamide riboside (NR) are both precursors to nicotinamide adenine dinucleotide (NAD), a coenzyme that plays a crucial role in energy metabolism and a variety of other physiological processes.
NMN and NR are both converted into NAD in the body through a series of enzymatic reactions. NMN is formed from nicotinamide, a form of vitamin B3, and ATP, the primary energy currency of cells. NR is formed from nicotinamide and ribose, a sugar molecule.
NAD is involved in a wide range of physiological processes, including DNA repair, gene expression, and energy metabolism. It is also a substrate for a group of enzymes called sirtuins, which have been shown to have anti-aging effects in animal models.
Supplementation with NMN or NR has been shown to increase NAD levels in animal studies and may have potential therapeutic effects on a variety of age-related diseases. However, more research is needed to fully understand the effects and potential risks of NMN and NR supplementation in humans.
One study found that oral supplementation with NR increased NAD levels in healthy elderly subjects and improved markers of metabolic health (1). Another study found that NMN supplementation increased NAD levels and improved glucose metabolism in mice with type 2 diabetes (2).
It is important to note that the safety and effectiveness of NMN and NR supplements have not been fully established in humans and more research is needed to determine their potential risks and benefits. It is always best to speak with a healthcare provider before starting any new supplement regimen.
To learn more about if these are right for you get in touch with Mulberry Vitamin Infusion here.
References:
Canto, C., Houtkooper, R. H., Pirinen, E., Youn, D. H., Oosterveer, M. H., Cen, Y., … Auwerx, J. (2012). NAD(+) metabolism in aging: an integrated view. Trends in Endocrinology & Metabolism, 23(8), 439-447.
Hirschey, M. D., Shimazu, T., Huang, J., Verdin, E., & Driscoll, M. (2013). SIRT1 deacetylase protects against diet-induced metabolic disorders by regulating PPARγ coactivator 1α (PGC-1α). Nature Communications, 4, 1739.