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The scientists said they switched youthful genes on and older genes off, using naturally occurring proteins and molecules.

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    @KickAssBrockSamson had to do a little bit of googling to find more info on exactly what NMN is and ran across this interview where he talks about it a little bit more at length.

    Also, here’s another article that talks a little bit more about NAD and SIRT1.

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      What brand is best to use for nmn???

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          @dan Thanks! I had no idea what NMN was as well. I am glad there are people like you to help shed some light on the subject. Thanks for the link!

          I was thinking about ordering some NAD+ for its longevity attributes. I will have to do some further investigation to see how much one should take and do a cost benefit analysis on the potential risks involved.

          Again thank you @dan!

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            Just an FYI: something to be aware of with respect to Sinclair’s work on resveratrol. Also… here’s a particularly colorful reddit rant on the subject. Some of this may color some of his other work somewhat as well.

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              @KickAssBrockSamson Check out my comment to programmer_ALi below regarding supplementation.

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              Does anyone know of the compound that Sinclair used to stimulate NAD in his research? It’s riddled in secrecy. @kickAssBrockSamson, @dan

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                @programmer_Ali @KickAssBrockSamson @dan The molecule that was used in this study is called nicotinamide mononucleotide (NMN) and it is a precursor of NAD, which regulates diverse biological processes, including, metabolism, aging, circadian rhythm, and axon survival. Actually, resveratrol (which Sinclair previously identified to extend lifespan, also increases NAD levels. Caloric restriction is another way to increase NAD levels and extend lifespan. I’m particularly interested in whether NMN cross the blood-brain barrier and if so, whether it gets converted into NAD. If it gets converted into NAD, this can repair damage to axons (GREAT) but if not it can cause axon degeneration. I think this is important to figure out before NMN supplementation.

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                  How would one know if NMN passes the BBB and if it gets converted? What would be the mechanism behind NMN causing axon degeneration?

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                    Niacinamide is transported across BBB but I’m not sure about supplemental NMN. When injected into rats, NMN causes Wallerian degeneration of axons but only when the enzyme that converts NMN to NAD+ is absent. I’m just not sure we know enough about supplemental NMN it terms of how much gets into the brain, what concentration saturates the NMNAT enzyme so that NMN begins to accumulate.

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                      :) What is the enzyme? Couldn’t one just simply inject a form of NAD? Or simply just simply IV NMN? My understanding of what you are saying is that there is good knowledge of injected NMN,

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                    @rhonda @KickAssBrockSamson @dan It looks like Sinclair is confident about no axon degeneration occurring from his research. He has already patented and is selling a commercial product of 250mg NMN named Niagen-> http://livecellresearch.com/niagen/ Furthermore other companies are already commercializing the stuff-> http://seekingalpha.com/instablog/10572281-secfilings-com/1990542-niagen-nicotinamide-riboside-offers-huge-potential-as-next-generation-niacin. Thoughts?

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                      NMN causing axon degeneration worries me. I know one can buy straight NAD+. That way you would not have to worry if the enzyme that converts NMN to NAD+ is absent. With that said I do not know how much one should take of NAD+ on a daily basis.

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                      Thanks!