NathanK said:post 114146Please share if you get a copy of the study. Looks really informative.haidut said:post 114092NathanK said:post 114013Been trying to find this answer for a while and would be curious about aspirin and biotin, but niacinamide does NOT have any FFA rebound effect.haidut said:post 104309paymanz said:post 104302 haidut have you read about rebound of plasma free fatty acid level after initial fall with niacinamide use?
Not really. Do you have some references?
http://suppversity.blogspot.com/2014/03/niacin-b3-glucose-management-part-v-of.html
Unlike ET and "flush" niacin, nicotinamide does not interact with the GPR109A receptor (Soga. 2003; Tunaru. 2003; Wise. 2003) and will thus neither produce free fatty acid rebounds nor will it raise your HDL, adiponectin and leptin levels (Westphal. 2006 & 2007; see Figure 5).
Here's the study. If someone can get the full text I'd appreciate it: http://www.ncbi.nlm.nih.gov/pmc/article ... 8-0S77.pdf
The FFA rebound would explain the lowered insulin sensitivity of high dose niacin: http://www.ncbi.nlm.nih.gov/pubmed/17996241
That is a great find for also another reason - it explains why niacin raises HDL. Given the flush of FFA, most of which are likely PUFA, niacin caused in the bloodstream makes the liver produce this extra HDL to carry the poison to the liver for excretion. This is also probably why niacin can paradoxically fatten up your liver (as it is well known to do in high doses) since it makes the liver absorb a LOT of that liberated fat and it is mostly PUFA.
So, once again, HDL is more of a "bad" biomarker when elevated meaning you are struggling with toxin of some sort. However, not producing enough can also be an issue since it means you cannot detoxify. Maybe that is why HDL by itself is not a very good predictor of CVD and metabolic health.
https://en.wikipedia.org/wiki/High-density_lipoprotein
"... Unlike the larger lipoprotein particles which deliver fat molecules to cells, HDL particles remove fat molecules from cells which want to export fat molecules. The fats carried include cholesterol, phospholipids, and triglycerides; amounts of each quite variable."
"...HDL particles (though vastly different from just cholesterol and other fat molecules per-se) are sometimes referred to as good cholesterol because they can transport fat molecules (including cholesterol, triglycerides, etc.) out of artery walls, reduce macrophage accumulation, and thus help prevent, even regress atherosclerosis over weeks, years, decades, thereby helping prevent cardiovascular disease, stroke(s) and other vascular disease complications body wide. In contrast, LDL particles (also far different from cholesterol per-se) are often called bad cholesterol or unhealthy cholesterol, because they deliver fat molecules to macrophages in the wall of arteries.[5] However, studies have shown that HDL lacking mice still have the ability to transport cholesterol to bile, suggesting that there are alternative mechanisms for cholesterol removal.[2] In addition to this another research group showed that transgenic mice retain the ability to metabolize bile and form gallstones in the absence of HDL.[3] This may also suggest that HDL is not as 'good' as popular belief claims."
It's funny how fish oil, niacin, and exercise are about the only things I can think of that are supposed to raise HDL....
It's good to know what "receptors" are associated with the FFA rebound. Means it probably be traced in other FFA lowering substances though it sounds isolated to niacin.
What are your thoughts on the possible mechanism that causes niacinamide to increase glucose tolerance while increasing triglycerides? Increases storage in the muscles/liver and the production of glycerols to "occupy" the excess FFA that can't be stored?
Where did you see that niacinamide increases trigs? The stuff I have seen says it lowers trigs. Peat recommends it in doses of 100mg a few times a day and in those doses it seems to reverse NAFLD as I posted in another thread. But I'd be interested in seeing counter evidence.
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