Vitamin B3 Blocks FFA Elevation Caused By Caffeine

[haidut]

post 114146

post 114092

post 114013

post 104309

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?

Been 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.
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."

Please share if you get a copy of the study. Looks really informative.

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.

 

[NathanK]

post 114554

post 114146

post 114092

post 114013

post 104309

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?

Been 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.
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."

Please share if you get a copy of the study. Looks really informative.

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.

It was in the original suppversity article I posted, which is why I said it would be nice to see the whole study. Check out figure 4 in the article.
"And while both nicotinic acid (niacin) and niacinamide led to improvements in insulin sensitivity (= reduced HOMA-IR), the latter lead to significant increases in triglycerides which stand in contrast to the triglyceride lowering effects of nicotinic acid."

I'm not sure how corollary NEFA is with TG

 

[haidut]

post 114569

post 114554

post 114146

post 114092

post 114013

post 104309

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?

Been 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.
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."

Please share if you get a copy of the study. Looks really informative.

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.

It was in the original suppversity article I posted, which is why I said it would be nice to see the whole study. Check out figure 4 in the article.
"And while both nicotinic acid (niacin) and niacinamide led to improvements in insulin sensitivity (= reduced HOMA-IR), the latter lead to significant increases in triglycerides which stand in contrast to the triglyceride lowering effects of nicotinic acid."

I'm not sure how corollary NEFA is with TG

Maybe the NEFA that niacinamide inhibited got turned into trigs. Btw, this study found quite beneficial effects on liver and the SuppVesity one also said niacinamide was highly beneficial for glucose control, so I doubt the liver was affected in any negative way.
viewtopic.php?f=124&t=8146

Also, the trigs are relatively safe as they are the "storage" form of fat. It is the NEFA that wreaks havoc. High trigs usually mean either high fat diet or the liver is having problem converting glucose into glycogen, so some of the sugar is converted into fat. I guess lowering NEFA may also lead to increased trigs as the body's way of storing the fat that is not oxidized. Interesting find for sure. The other interesting part is that the niacinamide dose used in the human studied mention by your post was 500mg x 3 a day and that matches perfectly the rodent dose used in this study for reversing insulin resistance and diabetes.
viewtopic.php?f=124&t=4948

 

[NathanK]

It was in the original suppversity article I posted, which is why I said it would be nice to see the whole study. Check out figure 4 in the article.
"And while both nicotinic acid (niacin) and niacinamide led to improvements in insulin sensitivity (= reduced HOMA-IR), the latter lead to significant increases in triglycerides which stand in contrast to the triglyceride lowering effects of nicotinic acid."

I'm not sure how corollary NEFA is with TG

Maybe the NEFA that niacinamide inhibited got turned into trigs. Btw, this study found quite beneficial effects on liver and the SuppVesity one also said niacinamide was highly beneficial for glucose control, so I doubt the liver was affected in any negative way.
viewtopic.php?f=124&t=8146

Also, the trigs are relatively safe as they are the "storage" form of fat. It is the NEFA that wreaks havoc. High trigs usually mean either high fat diet or the liver is having problem converting glucose into glycogen, so some of the sugar is converted into fat. I guess lowering NEFA may also lead to increased trigs as the body's way of storing the fat that is not oxidized. Interesting find for sure. The other interesting part is that the niacinamide dose used in the human studied mention by your post was 500mg x 3 a day and that matches perfectly the rodent dose used in this study for reversing insulin resistance and diabetes.
viewtopic.php?f=124&t=4948

Yes, I wondered if suppressing FFA caused more to be stored as TG especially if liver health hasn't caught up to properly metabolize them. We just hope that the body/liver does catch up over time while FFA suppression gives the body a break.

I think you'll find this paper interesting. I read it a while ago, but never posted. Too many good points to quote. There were things a little over my head, but still educational. They explain more the relationship between FFA and TG, obesity and FFA, eating fat and FFA, increased glycerols, gluconeogenesis, baseline FFA regulation in insulin resistance, and of particular interest a "spillover effect" of FFA from TG. The latter I'm not sure of the weight of importance in context.
http://m.diabetes.diabetesjournals.org/ ... 41.extract

Ironically, I think I've gotten better results from lower dose niacinamide closer to the range Ray recommends. Not more than a gram/day, but I also take biotin and aspirin with frequent feedings. Any more niacinamide tended to make my brain feel "floaty" though I haven't discerned yet if that was the niacinamide or biotin.

I've noticed over the past year or two that my bf% is correlated more to FFA than any estrogen retaining water (AI like supps never moved the scale). It's more a guess because after certain supplements or exercise my bf% would drop substantially and days later will revert back to the mean. On lower dose niacinamide my bf% has remained more stable than I can ever remember, which I'm taking as a very good thing.

 

[haidut]

post 114686

It was in the original suppversity article I posted, which is why I said it would be nice to see the whole study. Check out figure 4 in the article.
"And while both nicotinic acid (niacin) and niacinamide led to improvements in insulin sensitivity (= reduced HOMA-IR), the latter lead to significant increases in triglycerides which stand in contrast to the triglyceride lowering effects of nicotinic acid."

I'm not sure how corollary NEFA is with TG

Maybe the NEFA that niacinamide inhibited got turned into trigs. Btw, this study found quite beneficial effects on liver and the SuppVesity one also said niacinamide was highly beneficial for glucose control, so I doubt the liver was affected in any negative way.
viewtopic.php?f=124&t=8146

Also, the trigs are relatively safe as they are the "storage" form of fat. It is the NEFA that wreaks havoc. High trigs usually mean either high fat diet or the liver is having problem converting glucose into glycogen, so some of the sugar is converted into fat. I guess lowering NEFA may also lead to increased trigs as the body's way of storing the fat that is not oxidized. Interesting find for sure. The other interesting part is that the niacinamide dose used in the human studied mention by your post was 500mg x 3 a day and that matches perfectly the rodent dose used in this study for reversing insulin resistance and diabetes.
viewtopic.php?f=124&t=4948

Yes, I wondered if suppressing FFA caused more to be stored as TG especially if liver health hasn't caught up to properly metabolize them. We just hope that the body/liver does catch up over time while FFA suppression gives the body a break.

I think you'll find this paper interesting. I read it a while ago, but never posted. Too many good points to quote. There were things a little over my head, but still educational. They explain more the relationship between FFA and TG, obesity and FFA, eating fat and FFA, increased glycerols, gluconeogenesis, baseline FFA regulation in insulin resistance, and of particular interest a "spillover effect" of FFA from TG. The latter I'm not sure of the weight of importance in context.
http://m.diabetes.diabetesjournals.org/ ... 41.extract

Ironically, I think I've gotten better results from lower dose niacinamide closer to the range Ray recommends. Not more than a gram/day, but I also take biotin and aspirin with frequent feedings. Any more niacinamide tended to make my brain feel "floaty" though I haven't discerned yet if that was the niacinamide or biotin.

I've noticed over the past year or two that my bf% is correlated more to FFA than any estrogen retaining water (AI like supps never moved the scale). It's more a guess because after certain supplements or exercise my bf% would drop substantially and days later will revert back to the mean. On lower dose niacinamide my bf% has remained more stable than I can ever remember, which I'm taking as a very good thing.

That is a very good find, thanks for sharing. I suspect that the higher doses niacinamide would be more beneficial in someone with really low NAD/NADH ratio such as "autoimmune" conditions or dementias. Higher dose niacinamid seems to help these issues a lot. For the rest of us, Ray's recommended doses are probably optimal.

 

[jaa]

That is a very good find, thanks for sharing. I suspect that the higher doses niacinamide would be more beneficial in someone with really low NAD/NADH ratio such as "autoimmune" conditions or dementias. Higher dose niacinamid seems to help these issues a lot. For the rest of us, Ray's recommended doses are probably optimal.

How high a dose are you talking? 3x500mg or greater?

 

[HealthisWealth]

How many milligram a day ray peat recommend taking niacin?

 

[tara]

How many milligram a day ray peat recommend taking niacin?

Niacinamide (not niacin), 50 - 100mg, 3+ times a day.

 

[HealthisWealth]

Niacinamide (not niacin), 50 - 100mg, 3+ times a day.

Tara whats wrong with niacin? Its the only available in my country health vitamin store. 100mg and 500mg

 

[DaveFoster]

Tara whats wrong with niacin? Its the only available in my country health vitamin store. 100mg and 500mg

It promotes prostaglandin synthesis.

 

[HealthisWealth]

It promotes prostaglandin synthesis.

So in layman's term it promotes inflamation? I read i another thread about Dr Hoffman using niacin. I forgot what thread.

Edit I found the thread im referring

Renky,

I am coming in late to this, but if you haven't already considered it, you might think about supplementing with Niacin, aka Vitamin B3. I will probably be criticised for throwing yet another supplement at you, but anyway, please bear with me for a moment and read on.

Before you actually take it, I'd suggest trying to read something by the late Dr Abram Hoffer (e.g. "Niacin: The Real Story"), and then make up your own mind.

However, you will find that Niacin/vitamin B3 comes in several forms. The basic one, simplest and probably cheapest, is nicotinic acid, which you can get in capsule form from, e.g. Solgar. This is the one that Hoffer recommended in most cases, provided that the person can tolerate the "flush", which can be alarming at first, but I can verify that you do get used to it, and in fact, if you take it regularly, it usually stops occurring.

Hoffer was a contemporary of Pauling's, and they did interact to some extent; I think Pauling partly credits Hoffer with the idea of vitamin megadosing, and by the way, Hoffer suggested taking niacin with vitamin C.

Niacin seems to have a lot of benefits, but one of them is normalising blood lipid levels, i.e. reducing total cholesterol, and improving the HDL to LDL ratio, and I think reducing triglycerides.

I think that Ray Peat has respect for the work of both Hoffer and Pauling, and I think I have read that he thinks that as well as normalising blood lipid levels, it is doing something to strengthen the health of the blood vessels.

I have noticed people here recommending the niacinamide (non-flushing) form of vitamin B3 in preference to nicotinic acid. However, according to ""Niacin: the real story" (Abram Hoffer) niacinamide has no beneficial effect on blood lipids. If you want a no-flush form of vitamin B3 which does have beneficial effects, you could try Inositol Hexaniacinate.
however, Hoffer says that it's not as effective as nicotinic acid, and I think it's more expensive.


@Renky: I think nicotinic acid is something worth trying in your case, since as you say, your levels were so high, even if it is supposedly not ideal from a Peat point of view. I've seen the comment made that niacin causes PUFAs to be released in the blood. Well, that's a risk I suppose, but presumably you have already taken steps to remove PUFAs from your diet (if they were in it to begin with).

And take it with vitamin C...but ideally read what Hoffer has to say about it first.

 

[DaveFoster]

You'll find that Ray opposes Pauling and Hoffman on many points. Niacin and vitamin C being the most prominent.

 

[HealthisWealth]

You'll find that Ray opposes Pauling and Hoffman on many points. Niacin and vitamin C being the most prominent.

Ok i will return the niacin i bought. They dont sell niacinamide. What B vitamins do i exchange this? B1? B2? B5? Taurine?

Right now i found the combination to help temporarily for my sleep. Rivotril and atenolol and fufang danshen pian(chinese herb i think for the heart) My symptoms primarily is irregular hearbeat like fluttering, shortness of breath, racing that made me not to sleep. Last night was the best sleep i had when i took for the first time fufang danshen pian. I really want to weaned of the rivotril 1mg.

Before when i was taking only the rivotril i only slept 3 to 4 hours woke up again and hard time to go back to sleep. When i combined with atenolol it helped. But with this fufang danshen pian it really help. The feeling when i took it my head feels like blood is flowing.

What do your recommend to exchange this niacin because they dont sell niacinamide. They have B50 B100 complex but it has inositol and other that ray peat dont recommend.

 

[dookie]

Even though it is a logical finding knowing how niacinamide works, I still wanted to post this since it is one of the few studies looking at the combined effects of Peat substances like niacinamide and caffeine. I guess for simplicity you can assume that taking as much niacinamide as caffeine (in mg) will be enough to block the FFA elevating effects of caffeine.

http://jpet.aspetjournals.org/content/1 ... 8.abstract

"...When caffeinesodium bensoate plus nicotinic acid was given concomitantly, the FFA-lowering effect of nicotinic acid prevailed. However, maximum lowering of FFA levels did not appear during the first hour. These findings were believed to be of interest in two respects. 1) Nicotinic acid was able to completely abolish caffeine-induced rises in FFA; caffeine, in turn, seemed to attenuate, but could not prevent, the FFA-lowering effect of nicotinic acid 2) By increasing the doses of nicotinic acid administered, rebound of FFA above base-line values, reported by others, could be abolished for at least four hours. It is thus conceivable that FFA rebound can be completely blocked by administering appropriate doses of nicotinic acid at adequately spaced intervals."

This whole study was done with nicotinic acid - the same type of niacin that Max Gerson (in his Gerson therapy) used for treating terminally ill cancer patients, and which other practitioners, such as Abram Hoffer, used.

So while it probably has some drawbacks (eg increasing prostaglandins temporarily), maybe the benefits outweigh the risks of nicotinic acid? Maybe it even has some benefits over niacinamide?

 

[HealthisWealth]

This whole study was done with nicotinic acid - the same type of niacin that Max Gerson (in his Gerson therapy) used for treating terminally ill cancer patients, and which other practitioners, such as Abram Hoffer, used.

So while it probably has some drawbacks (eg increasing prostaglandins temporarily), maybe the benefits outweigh the risks of nicotinic acid? Maybe it even has some benefits over niacinamide?

In layman's terms what happens/symptoms if prostaglandins increases?

-

 

[dookie]

In layman's terms what happens/symptoms if prostaglandins increases?

-

I think those are partially responsible for the short-lived "niacin flush", ie reddening/itchiness of the skin, which occurs shortly after taking a high dose of nicotinic acid. I've never experienced it though with 100 mg doses..

The mechanism and mitigation of niacin-induced flushing

 

[NathanK]

I think those are partially responsible for the short-lived "niacin flush", ie reddening/itchiness of the skin, which occurs shortly after taking a high dose of nicotinic acid. I've never experienced it though with 100 mg doses..

The mechanism and mitigation of niacin-induced flushing

I didn't realize this, thanks.
"...Niacin induces flushing through dermal Langerhans cells where the activation of G protein-coupled receptor 109A (GPR109A) increases arachidonic acid and prostaglandins, such as prostaglandin D2 (PGD2) and prostaglandin E2 (PGE2), subsequently activating prostaglandin D2 receptor (DP1), prostaglandin E2 receptor (EP2) and prostaglandin E receptor 4 (EP4) in capillaries and causing cutaneous vasodilatation..."

Been 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.
Niacin (B3) & Glucose Management | Part V of the "There is More To Glucose Control Than Carbohydrates"-Series. Plus: Can You Use Niacin to Ramp Up Fat Burning During Fasts? - SuppVersity: Nutrition and Exercise Science for Everyone
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: Preferential increase in high-molecular weight adiponectin after niacin. - PubMed - NCBI

Here's the second study I finally got my hands on. Very interesting.
"...This study aimed to clarify further our recent observation that while niacin raises adiponectin markedly, it nevertheless reduces insulin sensitivity. The major findings are, first, that among the adiponectin fractions HMW adiponectin is increased preferentially, and second, that this increase is more pronounced in patients with lower BMI. However, even this subgroup was not protected from the deterioration of insulin sensitivity..."

 

[HealthisWealth]

I didn't realize this, thanks.
"...Niacin induces flushing through dermal Langerhans cells where the activation of G protein-coupled receptor 109A (GPR109A) increases arachidonic acid and prostaglandins, such as prostaglandin D2 (PGD2) and prostaglandin E2 (PGE2), subsequently activating prostaglandin D2 receptor (DP1), prostaglandin E2 receptor (EP2) and prostaglandin E receptor 4 (EP4) in capillaries and causing cutaneous vasodilatation..."


Here's the second study I finally got my hands on. Very interesting.
"...This study aimed to clarify further our recent observation that while niacin raises adiponectin markedly, it nevertheless reduces insulin sensitivity. The major findings are, first, that among the adiponectin fractions HMW adiponectin is increased preferentially, and second, that this increase is more pronounced in patients with lower BMI. However, even this subgroup was not protected from the deterioration of insulin sensitivity..."

So in layman's term niacin is beneficial with patients with lower body mass index?

 

[success23]

But if niacinamide doesn't interact with the GPR109A receptor it mean it doesn't lower free fatty acids.. Am i missing something?

 

[deliciousfruit]

Wait, the study was on nicotinic acid, not niacinamide, right?
What am I missing?