Both NR and NMN have been shown to have beneficial effects in rodents.

Though they haven't been tested side by side, both precursors raise blood levels of NAD in people,

but similarly haven't been pitted head-to-head against one another. One potential advantage of

NMN over NR is that it may be more stable in the bloodstream, in mouse blood at least. Within an hour,

most NR is converted into NAM, whereas NMN levels remain steady. You could also argue that

NMN is better because it's a direct precursor of NAD, whereas

NR first has to be converted to NMN. So we might as well just take NMN in the first place.

Ironically, the exact opposite argument can also be made based on the inability of NMN

to pass through cell membranes. Structurally, NMN is just NR with a phosphate group attached to it.

The phosphate charge prevents NMN from passing in and out of cells.

So to get inside a cell, NMN first has to be converted into NR.

Then once inside, the N.R can turn back into NMN and make NAD. So if NMN first has to be

converted into NR for cell entry, the argument goes, maybe you might as well take NR to begin

with, because there's no NMN transporter. Or is there? An NMN transporter was recently

described, at least in mouse intestines,

so maybe NMN is able to skip the NR step and pass directly into cells to make NAD after

all. However, the evidence such an NMN transporter exists remains controversial.

NMN boasts a long list of rodent health span benefits, but, unlike NR, has yet

to demonstrate an extension of mammalian lifespan. What about in people? There have just

been a few human NMN studies published to date. One small study of healthy middle-aged men

found that various single doses had no apparent

effect on any of the measured variables, including retinal-eye functions, sleep quality, heart rate,

...