Hi Bryan,
Na has an RDA that can be increased accordingly to get it as a good NAD+ precursor, and I think I showed enough data to believe it is a much better precursor than NR (more complete). NR however is more marketed.. But important is scientific evidence. The flush effect people can get is actually a good thing according to data (see the corresponding thread), the fact that people dont get it using NR doesnt mean its more safe in large dose too. Actually this is even a more silent risk. However, in the dosage of NR you have to remove the Ribose part in the calculation that count for half its weight (255gmol versus 122). Im now questioning why such hype for NR ?
State your case Tom. Evidently as I see in your dosage you feel 50mg of Niacin to be superior to (NR). "Currently I switched NR for Na (50mg) for instance" Everyone here is initialed to their opinions on this forum but we want to see some research documentation to back up our claims here. I've taken Niacin and can tell you small amounts are more than I can stand. I'm not alone in this sensitivity, I'm also part of a segment of rosacea suffer's who are already severely flushed before taking the first milligram of Niacin and adding it to my regiment worsens my skin condition. I don't deny that Niacin raises NAD+ levels but I take 1000mg's of NR a day, how could 20 times less of the NAD+ precursor (Na) do more than my (NR)? What are we chasing here Tom, the flush feeling, telling you its working, Increased NAD levels or maybe we are worried about cholesterol. If its price alone I'll accept that as well but 50mg isn't getting you into a therapeutic range at all and your NAD+ needle isn't going to move that much because of the dosage.
"Hyperlipidemia.
For a long time, patients with hyperlipidemia have been treated with niacin (Altschul et al., 1955), often in combination with statins to lower cholesterol biosynthesis. Although the G protein–coupled receptor GPR109A was linked to the effects of niacin (Tunaru et al., 2003), an increase in NAD+ could also contribute, especially considering the central role of sirtuin enzymes in lipid metabolism (Schug and Li, 2011; Houtkooper et al., 2012). Arguing in favor of the latter hypothesis is the fact that high doses of niacin (grams/day) are required for lipid lowering, while the EC50 for GPR109A (i.e., concentration to activate 50% of the receptor; ∼250 nmol/L) is rather low (Wise et al., 2003). Interestingly, supplementation with NR decreased the LDL/HDL ratio in mice without activating GPR109A, suggesting that this may be true (Cantó et al., 2012). This would circumvent the GPR109A-mediated adverse effects, such as flushing, observed upon high-level niacin intake (Cantó et al., 2012). Further mechanistic studies with other NAD-centered approaches leading to sirtuin activation are required to establish the potential of the NAD+/sirtuin axis for lipid lowering." http://jcb.rupress.o.../199/2/205.full
"many of the beneficial effects of niacin, such as the lipid-lowering effects (Kamanna and Kashyap, 2008), take place at concentrations higher than those required for GPR109A activation but lead to intracellular NAD+ accumulation (Jackson et al., 1995). It is therefore tempting to speculate that some of the effects promoted by niacin might be achieved through an NAD+-induced activation of SIRT1 and the consequent deacetylation of the multiple SIRT1 targets that act as critical regulators of fatty acid, lipid and sterol homeostasis in eukaryotes, such as PGC-1α, FOXOs, LXR, or SREBP-1c (described in section II.C)." http://pharmrev.aspe...t/64/1/166.full
So the lipid-lowering effects don't appear to be the result of GPR109A activation and higher levels are required than those needed for simple GPR109A activation, so just the flushing alone doesn't mean its working. So simply the fact of raising NAD+ might be how the lipid-lowering effects work through SIRT1 targets with Niacin anyway. So we don't need the flush, correct, just higher NAD+ levels.
So again no argument about lipid-lowering effects of Niacin but it seems to be tied to raising your NAD levels and most studies put that dose at a gram of higher.
"The doses of niacin used in the therapy of hyperlipidemia are far higher than the RDA and are generally in the range of 1 to 6 grams daily. When given at these doses, niacin has been shown to increase HDL and lower LDL cholesterol levels and to decrease rates of cardiovascular events in high risk individuals." http://livertox.nih.gov/Niacin.htm
So the RDA isn't moving NAD levels much.
Do you remember reading "nicotinamide riboside may be the only vitamin precursor that supports neuronal NAD+ synthesis" I do and we chased that down some months ago in something called the "Expression Atlas." I found several sources of information depicting which tissues of the human anatomy were equipped to utilize Nicotinamide Riboside (NR) and each database shared similar research links backing up their data.
So what we find are some tissues are better at assimilating (NR) than others precursors and the ability of brain cells to utilize (NA) far from the cell nucleus along axons and dendrites might be the reason why. Data seems limited in this regard but our Neuroglia seem to responsible for many of the enzymatic reactions needed for neuronal NAD maintenance. I'd like to see an expression map for this one cell type.
So Tom, more to the point show us how Niacin is better with the GPR109A activation and flushing. I know it will raise NAD+ levels but if I don't have to feel the pain after taking a gram or more to get the benefits why should I? Plus how is 50mg "much better."
Edited by Bryan_S, 27 June 2016 - 09:18 AM.
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