Boscoejean Excellent Question!! Does this mean that NADH is a better supplement?
According to the figure, I would say yes - especially, if the real target is Mitochondrial ETC. But, has NADH been tested? Will it cross the blood brain barrier? Maybe not if DNA repair (with PARP-1) or Ca regulation is the main objection.
A total of 30 individuals with early Parkinson’s disease received either 1000mg NR or placebo for a total of 30 days. The study showed that NR supplements significantly increased NAD levels in the patient brain, longevity.technology/key-to...
"Taken orally, NMN is rapidly absorbed and converted to NAD+. In numerous studies, supplementation with NMN has increased NAD+ biosynthesis"ncbi.nlm.nih.gov/pmc/articl...
Yes, it is well known that NMN needs fewer steps to create an increase in NAD+, but the net result is the same. However, NMN has a longer shelf life and can be bought far cheaper than Niagen if purchased in powder form. I stick with the more expensive Niagen because of the convenience of the pill and the fact that the existing Clinical Trials related to NAD+ production for treatment of neurological disorders have all to this date used NR and not NMN. NMN would likely have had the same results, but there it is. Click on my avatar and you will see that I have promoted NR for many, many years and take 1.5 g daily myself. (Along with a host of other supplements as well). Joe in NY
Several of the supplements that I take enhance methylation including Avmacol and pterostilbene. I'm sure you have studied this as well, but just to be certain - you are aware that Niacin inhibits Sirtuin activity which is generally not favorable to neurological disorders? I am sure you have well thought out reasons for taking Niacin, so I am not knocking that choice. I'm simply wanting to share knowledge that you may or may not already have.
Also, I update information on what and why I do what I do here:
P.S. I turn 56 on Monday and that will mark 6 years with little to no progression for me. I do not have Parkinsons but rather something called Spinocerebellar Ataxia Type 1 or SCA1. The root cause is a protein that is produced in the brain that forms a harmful oligomer and is not cleared from the brain thru normal autophagy. I began posting on the Parkinson's forum years ago because I believe some forms of Parkinsons are primarily due to the formation of a harmful oligomer as well. However, my non-scientist hunch is that Parkinson disease is not one but actually many different diseases so what works for some may not work for others.
Thank you for your thought provoking response and link to your additional info. I am concerned about inhibiting sirtuins activity. It is my hope that trans Resveratrol helps offset this. I use the NMN to hopefully increase NAD levels and the niacin based on the PD trial in Augusta, GA.
You have spurred me in to revisiting these choices and to seek out info on Avmacol and Pterostilbene. Thank you!
I’ve been reading about niacin’s effect on sirtuins. In this video (and others) David Sinclair mentions this. But, where I’m confused is, niacin does but to what extent does NR or NMN?
Resveratrol , Pterostilbene and Citicoline should offset this but to what extent I do not know.
I noticed you don’t take Citicoline. Would you mind sharing your thoughts on it?
I’ve been researching it a lot and although it is “safe” is it? Wondering about its role in Glutamate Excitotoxicity
Hello Joe, you got my attention with the Niacin inhibiting sirtuin activity comment. I spent the last hour poking around. Nothing is very clear, but the impression I get is Nicotinic acid supresses sirt1, but then the Nicotinic acid also boosts NAD+, and NAD+ boosts sirt1, so in the end, it might be a wash.
(I have an interest as I take 250 mg of NA Time Released every day)
because they are very different in their pharmacokinetics . In their absorption and passage through the body they have many different effects that go well beyond the concentration of NAD + in the blood which among other things reaches a saturation point after a few days and does not go beyond. So it is easy to infer, in my opinion, that continuous high doses could be a waste.
Looks like the relationships are complex. Hard to predict the ultimate result of all this:
"Nicotinamidase is an enzyme that cleaves nicotinamide making nicotinic acid. Since nicotinamide is the primary starting material for NAD synthesis [12], cleavage of nicotinamide may decrease tissue NAD levels. In addition, nicotinamide is an inhibitor of sirtuins [4]. Cleavage of nicotinamide, to nicotinic acid, may activate sirtuins. NAD is synthesized by nicotinamide phosphoribosyl transferase and NMN adenyl transferase. NMN is nicotinamide mononucleotide."
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Hot off the press. Randomized, double-blind safety trial of high dose nicotinamide riboside in Parkinson’s disease.
SoPD blog post from Simon on the recent results from the NADPARK trial of nicotinamide riboside (Niagen)
Nicotinamide supplement
Nicotinamide Riboside supplement 
NADH instead of NR, NMN, or niacin? 
