A single, low dose niacinamide drops triglycerides by 75%

haidut

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Among the vitamin B3 analogs, niacin is perhaps the most famous for its ability to both raise "good" cholesterol (HDL) and also lower triglycerides. However, niacinamide, nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) are all effective precursors to NAD (as niacin is) and raising NAD levels is known to inhibit lipolysis and as such should result in lowering of blood lipids. Yet, mainstream medicine continues to claim that only the flush-inducing niacin has those effects and that other vitamin B3 analogs are ineffective in beneficially modifying these biomarkers of CVD. In reality, niacin has never been shown to beneficially affect the course of CVD in humans, and this is probably due to its pro-inflammatory effects of raising histamine and serotonin (hence the flush). In contrast, several studies have demonstrated improved biomarkers of CVD as a result of niacinamide and, more recently, NR (studies sponsored by the NR peddler ChromaDex), but so far a convincing mechanism of action for the beneficial effects of those vitamin B3 analogs has not been proposed. The study below is probably the first to confirm the anti-lipolysis effects of the non-flush vitamin B3 analogs in humans, which would be a plausible mechanism of action for the non-flush vitamin B3 analogs in CVD. It demonstrates that a single administration of just 300mg NMN resulted in a whopping 75%+ drop in triglycerides in the human volunteers, that drop was maintained for at least 3 hours, and the triglyceride levels were still below baseline at 5 hours post-administration (see Figure 2 in the link below).

Nicotinamide Mononucleotide Is Safely Metabolized and Significantly Reduces Blood Triglyceride Levels in Healthy Individuals

"...An increase in nicotinamide adenine dinucleotide (NAD+) levels alleviates age-related disease progression and promotes healthy life expectancy. Several studies have demonstrated that NAD+ levels can be efficiently replenished via nicotinamide mononucleotide (NMN) intake; additionally, the safety of its oral ingestion has been confirmed in recent clinical trials. However, the efficacy and safety of intravenous NMN administration in humans remain unclear. Therefore, we verified its safety in 10 healthy volunteers. Intravenous administration of NMN did not affect electrocardiograms, pulse, and blood pressure, nor did it affect metabolic markers in the liver, heart, pancreas, and kidneys. These results indicate that intravenous NMN administration is safe and beneficial in humans. Furthermore, NMN administration significantly increased blood NAD+ levels without damaging blood cells and significantly reduced blood triglyceride (TG) levels. "
 
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youngsinatra

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My triglycerides were very high back then, despite the daily usage of nicotinamide. (in doses of 1g+)
But I had very notable liver damage at that point in time, so I think my blood lipids were screwed for that reason.
 
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haidut

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Where did they use niacinamide?

They used nicotinamide mononucleotide (NMN). Several studies by the company ChromaDex peddling another analog called nicotinamide riboside (NR) showed that administering equal doses niacinamide, NR or NMN has the same effects on NAD levels. Btw, consuming NMN and NR results in their breakdown into the GI tract into niacinamide and other components, so the effects of NR and NMN on NAD levels are expected to be identital to taking niacinamide, which is what the studies showed. In any event, metabolically niacinamide, NMN and NR have been shown to be equivalent to each other in all studies so far that have compared them, but distinct in effects from niacin.
 
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@haidut because of that Do you think B3 is a good option to reverse gallstones? In this case it would be take with UCDA, vitamin C and Taurine. I am asking that because of its ability to reduce lipids. I have a aunt with gallstones who takes ucda, and I am looking for options to improve her treatment. English isn’t my first language
 
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Would taking one capsule of 300mg niacinamide a day halt fat loss?
 

DrJ

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Low dose for niacinamide is key IMO. I never take more than 250mg and typically less than 100mg if I can measure it out accurately...
 
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haidut

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Would taking one capsule of 300mg niacinamide a day halt fat loss?

According to this study below, quite the opposite:):
 
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According to this study below, quite the opposite:):
Ooo thats amazing! Thanks Haidut :D
 

aliml

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Unexpectedly, TG levels were significantly reduced after the intravenous administration of NMN without affecting low-density lipoprotein (LDL) levels in the blood. No reduction in TG levels was observed in previous clinical trials upon oral administration of NMN [9], suggesting that NMN may be metabolized via different pathways when administered orally and intravenously. This is thought to be caused by NMN being metabolized in cells throughout the body by avoiding the first passage through the liver via intravenous administration. A previous study reported that the increase in TG levels in the plasma and liver of mice deficient in adipocyte-specific NAMPT1, an enzyme that synthesizes NMN from NAM, indicates that increased intracellular NMN synthesis plays a critical role in decreasing TG levels [24]. We hypothesize that the SIRT1 activated by NAD+ synthesized via NAMPT in adipocytes regulates adiponectin expression through deacetylation of PPARγ (peroxisome proliferator-activated receptor gamma) (Figure 6). Adiponectin in adipocytes reduces the amount of free fatty acids (FFAs) released into the blood; subsequently, FFAs in the blood are taken up by the liver, and TG is synthesized [25]. The activation of PPARγ by NAMPT leads to the suppression of TG synthesis in the blood. The markedly elevated mRNA expression of NAMPT in blood cells in the present study suggests that similar phenomena may occur in adipocytes. It is extremely difficult to conclude that there was no change in blood cholesterol levels in the present study. The blood clearance of LDL requires the enhanced expression of LDL receptors on the cell membrane surface [26]. LDL protein expression might not have increased 5 h after the intravenous administration of NMN. Since the decrease in TG levels due to the intravenous administration of NMN is a very interesting phenomenon, we would like to investigate the detailed mechanism by conducting cell experiments in the future, including its relationship with LDL and HDL.
 
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Among the vitamin B3 analogs, niacin is perhaps the most famous for its ability to both raise "good" cholesterol (HDL) and also lower triglycerides. However, niacinamide, nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) are all effective precursors to NAD (as niacin is) and raising NAD levels is known to inhibit lipolysis and as such should result in lowering of blood lipids. Yet, mainstream medicine continues to claim that only the flush-inducing niacin has those effects and that other vitamin B3 analogs are ineffective in beneficially modifying these biomarkers of CVD. In reality, niacin has never been shown to beneficially affect the course of CVD in humans, and this is probably due to its pro-inflammatory effects of raising histamine and serotonin (hence the flush). In contrast, several studies have demonstrated improved biomarkers of CVD as a result of niacinamide and, more recently, NR (studies sponsored by the NR peddler ChromaDex), but so far a convincing mechanism of action for the beneficial effects of those vitamin B3 analogs has not been proposed. The study below is probably the first to confirm the anti-lipolysis effects of the non-flush vitamin B3 analogs in humans, which would be a plausible mechanism of action for the non-flush vitamin B3 analogs in CVD. It demonstrates that a single administration of just 300mg NMN resulted in a whopping 75%+ drop in triglycerides in the human volunteers, that drop was maintained for at least 3 hours, and the triglyceride levels were still below baseline at 5 hours post-administration (see Figure 2 in the link below).

Nicotinamide Mononucleotide Is Safely Metabolized and Significantly Reduces Blood Triglyceride Levels in Healthy Individuals

"...An increase in nicotinamide adenine dinucleotide (NAD+) levels alleviates age-related disease progression and promotes healthy life expectancy. Several studies have demonstrated that NAD+ levels can be efficiently replenished via nicotinamide mononucleotide (NMN) intake; additionally, the safety of its oral ingestion has been confirmed in recent clinical trials. However, the efficacy and safety of intravenous NMN administration in humans remain unclear. Therefore, we verified its safety in 10 healthy volunteers. Intravenous administration of NMN did not affect electrocardiograms, pulse, and blood pressure, nor did it affect metabolic markers in the liver, heart, pancreas, and kidneys. These results indicate that intravenous NMN administration is safe and beneficial in humans. Furthermore, NMN administration significantly increased blood NAD+ levels without damaging blood cells and significantly reduced blood triglyceride (TG) levels. "
Isn't this just confirming what we basically already knew, which is that Niacinamide blocks free fatty acids? And only temporarily. So I am not really sure what the significance is of this study. What benefit is there to only lowering it for a few hours? Also It looked like ALT and AST went up during that time too, which doesn't seem great. I have been taking it for a few months under the impression that it is good to lower free fatty acids but if so why are liver enzymes elevating? Could it be detrimental to block free fatty acids?
 

tommyg130

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Low dose for niacinamide is key IMO. I never take more than 250mg and typically less than 100mg if I can measure it out accurately...
How come its key in your opinion? I’ve heard this too? Does it have to do w methylation? Lowering other Bs? I do better low dose as well, and when I use riboflavin along w it
 

DrJ

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How come its key in your opinion? I’ve heard this too? Does it have to do w methylation? Lowering other Bs? I do better low dose as well, and when I use riboflavin along w it
Niacinamide depletes methyl donors which the liver needs for phase 2 detox of toxins. I don't think you want tons of methyl donors floating around but you don't want them going to zero.
 
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tommyg130

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Niacinamide depletes methyl donors which the liver needs for phase 2 detox of toxins. I don't think you want tons of methyl donors floating around but you don't want them going to zero.
Exactly what I thought too. Do take any other B’s w it?
 

cs3000

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The study below is probably the first to confirm the anti-lipolysis effects of the non-flush vitamin B3 analogs in humans, which would be a plausible mechanism of action for the non-flush vitamin B3 analogs in CVD. It demonstrates that a single administration of just 300mg NMN resulted in a whopping 75%+ drop in triglycerides in the human volunteers, that drop was maintained for at least 3 hours, and the triglyceride levels were still below baseline at 5 hours post-administration (see Figure 2 in the link below).

Nicotinamide Mononucleotide Is Safely Metabolized and Significantly Reduces Blood Triglyceride Levels in Healthy Individuals

"...An increase in nicotinamide adenine dinucleotide (NAD+) levels alleviates age-related disease progression and promotes healthy life expectancy. Several studies have demonstrated that NAD+ levels can be efficiently replenished via nicotinamide mononucleotide (NMN) intake; additionally, the safety of its oral ingestion has been confirmed in recent clinical trials. However, the efficacy and safety of intravenous NMN administration in humans remain unclear. Therefore, we verified its safety in 10 healthy volunteers. Intravenous administration of NMN did not affect electrocardiograms, pulse, and blood pressure, nor did it affect metabolic markers in the liver, heart, pancreas, and kidneys. These results indicate that intravenous NMN administration is safe and beneficial in humans. Furthermore, NMN administration significantly increased blood NAD+ levels without damaging blood cells and significantly reduced blood triglyceride (TG) levels. "

@haidut Ray peat talks about triglycerides being protective to the heart as the triglycerides synthesised by the liver are saturated , & not to lower them


View: https://www.youtube.com/watch?v=fHswGCXg_xU#t=28s



& also says they're shown to be protective against infective things / are anti-inflammatory (but i haven't found the studies)


View: https://www.youtube.com/watch?v=DYq-jrmZCpQ#t=10s


so that sounds like a negative effect from niacinimide (but doesn't work the same orally)
@aliml Unexpectedly, TG levels were significantly reduced after the intravenous administration of NMN without affecting low-density lipoprotein (LDL) levels in the blood. No reduction in TG levels was observed in previous clinical trials upon oral administration of NMN [9], suggesting that NMN may be metabolized via different pathways when administered orally and intravenously. This is thought to be caused by NMN being metabolized in cells throughout the body by avoiding the first passage through the liver via intravenous administration.

is there a benefit to lowering triglycerides?
 
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cs3000

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@haidut Ray peat talks about triglycerides being protective to the heart as the triglycerides synthesised by the liver are saturated , & not to lower them


View: https://www.youtube.com/watch?v=fHswGCXg_xU#t=28s



& also says they're shown to be protective against infective things / are anti-inflammatory (but i haven't found the studies)
]



This is the guy ray was talking about, ravnskov


"Most of the fatty acids in the diet and in the blood are bound to a type of alcohol called glycerol.
Usually each glycerol molecule is attached to three fatty acids, and this molecule complex is called a triglyceride. Often shortened to TG. As with cholesterol, high TG levels in the blood have been found to be associated with a higher risk of coronary heart disease. Does that mean that we should lover the level of TG in our blood?

To answer this question satisfactorily demands careful reading and a long explanation. However, if you understand the fallacy of the cholesterol hypothesis, then it will be easy for you to understand that you do not need to bother about your TG either because even the most zealous proponents of pharmaceutical intervention admit that the evidence for high TG causing atherosclerosis and cardiovascular disease, is weak, much weaker than for high cholesterol.

Thus, if it is weak or nonexistent for cholesterol, why bother about TG?
The TG level in the blood depends on many factors. Normally TGs go up after a meal. The more fats and carbohydrates you eat—and the more alcohol you drink—the higher your TG level becomes. Almost 12 hours must pass before the level returns to “normal.” An analysis of TG is therefore meaningless if the patient hasn’t been fasting the previous 12 hours.

***Furthermore, overweight people have higher levels of TG than thin people, smokers have more than non-smokers, diabetics have more than non-diabetics, people who lead a sedentary lifestyle have more than physically active people, and people under stress have more than people who are on ease. For instance, you could ask whether overweight, smoking, inactive and stressed diabetics with high TG are more at risk than overweight, smoking, inactive and stressed diabetics
with normal TG.

In addition, analysis of TG is highly inaccurate and the normal fasting levels are highly variable.
If a blood analysis finds 200 mg per deciliter, the true TG level may be anything between 100 and 300. To get a more reliable measure of your normal TG, it is therefore necessary to calculate the average of three measurements made at three different occasion, each time preceded by a 12-hour fast.

So, when researchers say that high TGs predict an increased risk for heart disease, the question is, whether this is caused by sedentary lifestyle, or smoking, or overweight, or mental stress, or diabetes, or a risk factor we don’t know about yet; or whether it is caused by a high TG.

And even if a 10-20 percent higher fasting value of TG is associated with an increased risk, it seems senseless to try to lower TG when TG rises after each meal to levels that can be several hundred present higher than the fasting state. All of us who eat three times a day and drink a glass of wine or whisky now and then simply have “too high” TG most of the time."


There's the big 300,000 person study that concluded triglycerides aren't a biomarker for heart disease when controlled for low or high HDL & that basically it should be scrapped


 
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Filosofy

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Recently did a bout with niacinamide and I honestly think it cleaned me too good (of triglycerides). My body feels less clogged, but hell, too "runny" isn't good either, right?
Niacinamide depletes methyl donors which the liver needs for phase 2 detox of toxins. I don't think you want tons of methyl donors floating around but you don't want them going to zero.

I was taking sunflower lecithin simulatenously. Choline is a methyl donor , I believe. Still, either the niacinamide or the choline seems to have messed with my sleep (waking up around 3 am, which signals liver issues).

I don't know. It always seems iffy to me to increase drastically the b3... it's such a orthomolecular and reductionistic perspective. The methylation will suffer eventually, and it will show differently in different persons, and we won't really know it is the methylation doing it.

Also, b3 is always accompanied with high amounts of the other b's (Except b12 at least in plants). Correct me if I am wrong here.
 

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