Ok, I think I've figured out why NMN (nicotinamide mononucleotide) is preferred vs NR (nicotinamide riboside)..
It's a guess, based on the article below's guess:
NAD (specifically the NadR protein) regulates the addition of phosphate to NR (which creates NMN).. so if the cell isn't function great, with lower levels of NadR proteins, then presumably less phosphate binding occurs to NR to create NMN (..which then binds together to create NAD).
-basically a cyclical effect that is decaying.
Dumping more NR into the cell may not substantially increase NMN levels with particularly damaged cells; the NR is there at a much higher supply (due to the supplement) to be converted to NMN, but the NadR protein doesn't have the "demand" to match NR's supply.
There are probably cell's in various stages of decline. The more "healthy" the cell (up to a point), the better the "demand" of NadR matches the supply of NR to produce NMN (..and thereby NAD). I think this is why NAD levels seem to change in these sorts of studies - some cells (and organisms) are "healthier" overall (..though not "healthy) and just accept NR more readily, showing a rapid increase in NAD - resulting in a "rejuvenated" cell.
Now, IF you can bypass this portion of protein signaling (which is likely not working particularly well in the really "UNhealthy" cells), then you should end-up with higher levels of NAD within those really "UNhealthy" cells - hopefully precluding further decline/mutation.
My guess is that this sort of "supplement" isn't required on a typical "supplemental" basis. Basically intermittent (monthly, 3 months, 6 months?) short-period (maybe a few days, or even a week?) "dosing" to get cells to better accept an NR supplement (with enough NadR protein to now "demand" that added supply). The occasional "booster" shot (..or series of injections).
Again, it's a guess.
btw, there are mutations (transporter mutations) that allow NMN to pass into the cell without conversion into NR due to the cell membrane's periplasmic acid phosphatase process.
My guess is that the corporate-side of this research is focused on synthesizing a particularly beneficial transporter mutation (at a reasonable cost) that accomplishes this process better than the natural acid phosphatase process imposes on "standard" NMN (..which is NMN to NR - to get into the cell).
-as for why the cell membrane's periplasimic layer acts as a gate-keeper with respect to NMN blocking transportation to the cell, it's function apparently has more to due with keeping NMN from LEAVING the cell (..so it can bind together to create NAD).
Edited by Simi, 01 April 2017 - 09:31 PM.