Nicotinamide Mononucleotide (NMN)

What is NMN? The age-defying solution of the century?

Nicotinamide Mononucleotide (NMN) is the latest groundbreaking life science discovery and proven a precursor of NAD+ , meaning that it serves as a “building block” to make the NAD+ molecule for preventing genetic changes in aging process.

2013 – The Discovery of Significant Anti-aging Results of NMN¹ by Harvard University
- Dr. David Sinclair, A tenured Professor in the Department of Genetics and co-Director of the Paul F. Glenn Center for the Biology of Aging at Harvard Medical School. He made a breakthrough in anti-aging research.
  - Time: One Week
  - Administering NMN in normal drinking water to older mice
  - NAD+ levels were restored to levels seen in younger control mice
  - Restored muscle mitochondrial function to levels seen in younger control mice
  - Strong correction in age-associated metabolic dysfunction
  Before Taking NMN

2016 – Oral Administration of NMN on Improving Age-associated Dysfunctions²

How does NMN work for age defense?

Shinichiro Imai, a Japanese professor at the University of Washington in the United States, has made the major discovery, marking a historic breakthrough in the development of global anti-aging research:

The oral administration of a small molecular weight of NMN increases the amount of nicotinamide adenine dinucleotide (NAD+) in various organs and restore ATP (energy molecules synthesized by mitochondrial cells). It appears in the bloodstream in less than three minutes and is quickly converted to NAD in multiple tissues. It rewrites the aging process by improving age-associated functional decline and disease conditions in animals.

The researchers found a variety of beneficial effects of NMN supplementation, including in skeletal muscle, liver function, bone density, eye function, insulin sensitivity, immune function, body weight and physical activity levels.

NAD+ level increases after taking NMN for 30 minutes


Lean Energetic Increase Insulin sensitivity & Lipid metabolism Decrease chances of diabetes Better eye function Higher bone density Better immunity	Weight gain Decrease energy metabolism Increase chances of diabetes

2017 – Oral Administration of NMN on DNA Repair³
- Team of Dr. David Sinclair administered NMN to the 2-year-old mice (roughly equivalent to a 70-year-old human) and their following functions have returned to the level as those of 4-month-old mice (like a 25-year-old adult):
  - DNA Repair Capacities
  - Sample Tissues
  - Muscle Endurance
  - Extend Life span by 20%

How safe is NMN?
2017 – Recognized by NASA on Protecting Astronauts from Serious Aging
- With the benefit of NMN in DNA repair effect, The National Aeronautics and Space Administration (NASA) has begun the research of taking NMN to protect astronauts from cosmic rays in the outer space.
  
  NMN is expected to become the resolution of aging challenges for astronauts caused by the space missions. Previous studies have shown that after a four-year round trip to Mars, the DNA damage to astronauts caused by high-energy particle radiation in space would increase the death rate of body cells by 5% and cell mutation by almost 100% which lead to significant aging.

2016-2018 – Awarded by NASA Twice
- Due to the role of NMN in protecting against DNA damage caused by space ionizing radiation and restoring the loss of skeletal muscle under weightlessness, a panel of judges from NASA recognize NMN as one of the top three innovations for of NASA iTech in 2016 and 2018.

2018 – “Times” Health Person of the Year 2018
- David himself was awarded the Australian Medal and 50 people of “Times” Health Person of the Year 2018 for his contribution in the field of anti-aging

2019 – NMN Is Clinically Proven Safe for Human Use⁴
- Since 2016, The Keio University research team has conducted a clinical trial study to investigate the safety of single administration of NMN in healthy men. It has confirmed NMN can be safely administered that it is effectively metabolized in the body. The results of this research were published in Endocrine Journal on November 2, 2019.

引文

Gomes, A. P., Price, N. L., Ling, A. J., Moslehi, J. J., Montgomery, M. K., Rajman, L., White, J. P., Teodoro, J. S., Wrann, C. D., Hubbard, B. P., Mercken, E. M., Palmeira, C. M., de Cabo, R., Rolo, A. P., Turner, N., Bell, E. L., & Sinclair, D. A. (2013). Declining NAD(+) induces a pseudohypoxic state disrupting nuclear-mitochondrial communication during aging. Cell, 155(7), 1624–1638. https://doi.org/10.1016/j.cell.2013.11.037
Mills, K. F., Yoshida, S., Stein, L. R., Grozio, A., Kubota, S., Sasaki, Y., Redpath, P., Migaud, M. E., Apte, R. S., Uchida, K., Yoshino, J., & Imai, S. I. (2016). Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell metabolism, 24(6), 795–806. https://doi.org/10.1016/j.cmet.2016.09.013
Li, J., Bonkowski, M. S., Moniot, S., Zhang, D., Hubbard, B. P., Ling, A. J., Rajman, L. A., Qin, B., Lou, Z., Gorbunova, V., Aravind, L., Steegborn, C., & Sinclair, D. A. (2017). A conserved NAD+ binding pocket that regulates protein-protein interactions during aging. Science (New York, N.Y.), 355(6331), 1312–1317. https://doi.org/10.1126/science.aad8242
Irie, J., Inagaki, E., Fujita, M., Nakaya, H., Mitsuishi, M., Yamaguchi, S., Yamashita, K., Shigaki, S., Ono, T., Yukioka, H., Okano, H., Nabeshima, Y. I., Imai, S. I., Yasui, M., Tsubota, K., & Itoh, H. (2020). Effect of oral administration of nicotinamide mononucleotide on clinical parameters and nicotinamide metabolite levels in healthy Japanese men. Endocrine journal, 67(2), 153–160. https://doi.org/10.1507/endocrj.EJ19-0313
Das, A., Huang, G. X., Bonkowski, M. S., Longchamp, A., Li, C., Schultz, M. B., Kim, L. J., Osborne, B., Joshi, S., Lu, Y., Treviño-Villarreal, J. H., Kang, M. J., Hung, T. T., Lee, B., Williams, E. O., Igarashi, M., Mitchell, J. R., Wu, L. E., Turner, N., Arany, Z., … Sinclair, D. A. (2018). Impairment of an Endothelial NAD+-H2S Signaling Network Is a Reversible Cause of Vascular Aging. Cell, 173(1), 74–89.e20. https://doi.org/10.1016/j.cell.2018.02.008

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