NR and NMN seem to be more promising NAD precursors than N-A or NAM, since they don't cause flushing,

nor do they directly inhibit surtoins. In mice, N-R and NMNN both raised liver NAD levels, but of the two, only

NR significantly raised NAD in the muscles. Also, NR is so far the only NAD booster

shown to prolong the lifespan of mice. There have been at least 10 clinical trials of NR,

most showing it can boost human blood levels of NAD by up to

168 percent. Note, though, that most doses used exceeded 300 milligrams, which the daily

dose approved as safe by the U.S. Food and Drug Administration and the European Food Safety Authority.

At the approved dose, blood NAD has boosted more on the order of 50 to 60 percent,

but no dose was found to affect NAD levels in human muscle compared to placebo.

The greater preponderance of human bioavailability and safety data for NR compared to NMN

has led some to proclaim NR as the preferred

NAD precursor, and by some, I mean, employees of a chemical company that produces NR for supplements.

The question, after all these human NR trials, is, have any of them shown clinical benefit? Sadly, no.

Let's go through the alphabet.

After accounting for multiple testing, randomized, double-blank, placebo-controlled trials

of NR and middle-aged or older adults failed,

defined any significant benefit over placebo for artery stiffness or artery function, bat activation,

blood pressure, blood sugar control, body weight, cardiac energy or ejection fraction,

fat burning, fatty liver, exercise capacity, fatigue, insulin sensitivity, metabolic flexibility,

metabolic health, metabolic rate, mitochondrial function or biogenesis, muscle blood flow,

upper or lower body muscle strength, pancreatic function or the release of metabolic

hormones, the treatment of Parkinson's disease symptoms, or physical performance.

...