Advanced NMN: Nicotinamide Mononucleotide - 10 Grams
10 Grams - Each scoop serving contains 170mg NMN. Nicotinamide Mononucleotide Was Used by David Sinclair To Rejuvenate Animals*. RevGenetics has made this available as a dietary supplement and precursor to NAD+ which activates SIRT and allows low energy cells (low ATP) to help restore their youthful energy. This powder product is not covered by our 30 day guarantee. Our NMN capsules are covered by our 30 day guarantee.
In a study by David Sinclair, Mice taking Nicotinamide Mononucleotide increased lifespan*. NMN is a 1 Step NAD Precursor and does not require ATP to convert itself into NAD. We feel NMN is better suited for older folks with older cells that produce low amounts of ATP (cell energy) and may not be able to efficiently convert normal food vitamins into energy (NAD). For older people with low ATP cells, NMN is a great choice to energize depleted ATP cells and maintain a healthy lifestyle as you age.
If you have seen a decline of benefits over time with your current supplements, it may be that your cell ATP (energy) is low and may need to be restored. Try NMN today with your supplements, to see if the synergy boosts your energy and quality of life. More on (ATP and the Heart is available here) More on (ATP Depletion is available here). NMN is a dietary supplement. *These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease.
Will this Nicotinamide Mononucleotide Supplement work on people? There are no clinical studies on longevity using NMN. We cannot answer if it will work in people as it did in mice at this time. We simply make it available so that you can study and research the product for yourself.
The Nicotinamide Mononucleotide Supplement product is available? We now have the product and it will start shipping.
Thank you for purchasing the NMN product. We believe it will be perfect for those that have seen a decline in benefits from various supplements over the course of 5-10 years. It may be that the low NAD which is caused by aging cells is causing any Sirtuin activation benefits to decline. Since NMN has been shown to restore NAD, we feel it is the perfect addition to your daily supplement intake.
Can't I just take NAD+ instead of NMN? No, NAD is too large to pass through the cell membrane. NMN can easily pass into the cell membrane and then join other NMN to form NAD within the cells.
When will the Nicotinamide Mononucleotide Supplement product be available? We are shipping now while supplies last.
What are the supplements you suggest to take with NMN? We suggest taking micronized resveratrol and MetaCurcumin if possible. We have verified that both of these activate all 7 sirtuins in human immune cells. We believe NMN would only boost any benefits as NAD restoration and cell ATP is necessary for Sirtuins to function properly as you get older.
Can I see the study? The full study is copyrighted and we only link to the abstract below. You can view it on PubMed (Link) and you can directly order the full published study here (Link).
Study Abstract: SIRT2 induces the checkpoint kinase BubR1 to increase lifespan. Mice overexpressing the mitotic checkpoint kinase gene BubR1 live longer, whereas mice hypomorphic for BubR1 (BubR1(H/H)) live shorter and show signs of accelerated aging. As wild-type mice age, BubR1 levels decline in many tissues, a process that is proposed to underlie normal aging and age-related diseases. Understanding why BubR1 declines with age and how to slow this process is therefore of considerable interest. The sirtuins (SIRT1-7) are a family of NAD(+)-dependent deacetylases that can delay age-related diseases. Here, we show that the loss of BubR1 levels with age is due to a decline in NAD(+) and the ability of SIRT2 to maintain lysine-668 of BubR1 in a deacetylated state, which is counteracted by the acetyltransferase CBP. Overexpression of SIRT2 or treatment of mice with the NAD(+) precursor nicotinamide mononucleotide (NMN) increases BubR1 abundance in vivo. Overexpression of SIRT2 in BubR1(H/H) animals increases median lifespan, with a greater effect in male mice. Together, these data indicate that further exploration of the potential of SIRT2 and NAD(+) to delay diseases of aging in mammals is warranted.
Can you provide a COA to know this is real NMN? Yes we can: