The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
there's a debate it's not earth shattering it's very academic but you're debating in the field about which molecule gets transported and which one doesn't and n are definitely has transported the question is does any n MN getting transported
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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
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my guess is if you take a nicotinamide RIE beside supplement you are absorbing the NR in tact and if you take a nicotinamide mononucleotide supplement and and then you are probably digesting that down to NR or nicotinamide and absorbing them
so in an ideal world if you could wave a magic wand you would presumably want more nad inside your mitochondria tell us why that magic wand doesn't exist in why can't you just eat nad in other words I wouldn't say it doesn't exist but it's questionable how powerful of a wand this is
but i think that reflects a bigger problem with the nad precursor field which is that you know there's a lot of controversy even among the two camps so i mean it's sort of funny right because there's an nr camp of researchers who really you know think nr is the the tool that we should use and then there's an nmn camp and they both you know say that the other camp that their molecule doesn't work right because it's not biologically available or you know all sorts of reasons right so there's a lot of lack of clarity around biological availability and efficacy with these molecules in the pre-clinical literature
there's a lot of controversy even among the two camps so i mean it's sort of funny right because there's an nr camp of researchers who really you know think nr is the the tool that we should use and then there's an nmn camp and they both you know say that the other camp that their molecule doesn't work right because it's not biologically available or you know all sorts of reasons right so there's a lot of lack of clarity around biological availability and efficacy with these molecules in the pre-clinical literature
so i think the majority of efforts to increase intracellular nad are done through oral uh precursors and the two are nr and nmn which as you said are pretty similar and are you aware of a more convincing argument for why one might be a more preferred substrate i i haven't particularly seen arguments that one is superior than the other
the bioavailability of either nicotinamide rai beside or nicotinamide mononucleotide the important point to address is whether nicotinamide right beside or nicotinamide mononucleotide can reach other tissues intact and directly form nad without going through that nad recycling pathway that I mentioned earlier called the salvage pathway