http://www.vrp.com/a...T...id=&zTYPE=2
I've been using 1000mg Niacinamide and 50mg NAD+ and I like it. I would assume most of the niacinamide, given the timing would be a used in this krebs cycle pathway. Again, I've found this to be pretty good and would like to continue it... I am merely using it to push the NAD pathway.
My understanding is that niacinamide is directly incorparated into NAD which acts as an enzyme in both glycolysis and the krebs cycle, so it will be actively recycled and will not be "used" like glucose or pyruvate is "used" in the cycle, if that was what you were thinking. A dose of 1000mg is huge and will probably be on board for quite a while.
If you are concerned about inhibition of SIRT, a recent article (PMID: 17725178) lists a plasma half life of 4.3 hours for niacinamide, but I am not sure how relevant a plasma half life would be as far as inhibition of SIRT goes. Certainly a lot of niacinamide would be taken up in various tissue compartments where it would increase intracellular levels and affect SIRT for who knows how long.
The same article deals with the conversion of oral niacin to niacinamide and other metabolites, so I don't think switching to niacin will avoid all of these concerns.
Here is the abstract:
Int J Clin Pharmacol Ther. 2007 Aug;45(8):448-54.
Plasma and urine pharmacokinetics of niacin and its metabolites from an extended-release niacin formulation.
Menon RM, Adams MH, González MA, Tolbert DS, Leu JH, Cefali EA.
OBJECTIVE: To characterize plasma and urine pharmacokinetics of niacin and its metabolites after oral administration of 2,000 mg of extended-release (ER) niacin in healthy male volunteers. METHODS: Niacin ER was administered to 12 healthy male subjects following a low-fat snack. Plasma was collected for 12 h post dose and was analyzed for niacin, nicotinuric acid (NUA), nicotinamide (NAM) and nicotinamide-N-oxide (NNO). Urine was collected for 96 h post dose and analyzed for niacin and its metabolites, NUA, NAM, NNO, N-methylnicotinamide (MNA) and N-methyl-2-pyridone-5-carboxamide (2PY). RESULTS: Mean niacin Cmax and AUC(0-t) values were 9.3 microg/ml and 26.2 microg x h/ml and were the highest of all analytes measured. Peak niacin and NUA levels occurred at 4.6 h (median) while tmax for NAM and NNO were 8.6 and 11.1 h, respectively. The mean plasma terminal half-life for niacin (0.9 h) and NUA (1.3 h) was shorter as compared to NAM (4.3 h). Urine recovery of niacin and metabolites accounted for 69.5% of the administered dose; only 3.2% was excreted as niacin. The highest recovery was for 2PY (37.9%), followed by MNA (16.0%) and NUA (11.6%). Mean half-lives for 2PY and MNA calculated in urine were 12.6 and 12.8 h, respectively. CONCLUSIONS: Niacin was extensively metabolized following oral administration, and about 70% of the administered dose is recovered in urine in 96 h as niacin, NUA, MNA, NNO, NAM and 2PY. The plasma levels of the parent niacin were higher than its metabolites though only about 3% of the unchanged drug is recovered in urine.
PMID: 17725178