Low-dose niacinamide has striking anti-obesity effects

[Lollipop2]

I always consult Dan Wich's Toxinless recommendations:

Directory of foods and supplements without questionable additives - Toxinless

Unfortunately he hasn’t been updating for like 4 years now. Not sure all the info is up to date.

 

[Mazzle]

Imo the best way to lose fat is low fat high carb + seafood and other low fat protein. It works especially with some walking, but will take 6-12 months maybe longer to lose your excess fat. I ate rice, fruit, potato, steamed vegetables and lean beef heart and shrimp for 6 months and lost about all fat possible while eating over 2000 calories per day walking a few miles every other day on average. I did my supplement anything else. I now supplement small amounts of niacinamide and methylene blue to increase NAD but in my case I don’t think it’s necessary for fat loss. I also eat more fat now without gaining fat.

Thank you Nebula. High carb + low fat protein is about the only combination I have not tried so I will give this a go.

 

[PowertothePeatple]

I am still very fat. This has not worked in the slightest for me. I have been taking 250mg in water (with asprin as it happens) as a divided dose three times a day since this post was put up.
Has anyone else had any results with this?

I think it would take more like 4-6 months to be comparative to the mouse study. Mice have a much shorter life span so they are showing the effects much sooner. My plan is to aim for 6 months or so and then see whether I think it worked.

 

[EvanHinkle]

I think it would take more like 4-6 months to be comparative to the mouse study. Mice have a much shorter life span so they are showing the effects much sooner. My plan is to aim for 6 months or so and then see whether I think it worked.

Agreed. I brought that point up up-thread. We live longer, so i ended up estimating somewhere between 6 months and 2 years honestly.

 

[Dr. B]

I think it would take more like 4-6 months to be comparative to the mouse study. Mice have a much shorter life span so they are showing the effects much sooner. My plan is to aim for 6 months or so and then see whether I think it worked.

what dosage is good for niacinamide? also wont it be depleting some other vitamins and methyl groups

 

[Waynish]

What is niacinamide made out of?

 

[TheCodez]

What is niacinamide made out of?

The usual suspects... carbon, hydrogen, nitrogen, oxygen and silicon (C9H14N2OSi)

 

[Dr. B]

The usual suspects... carbon, hydrogen, nitrogen, oxygen and silicon (C9H14N2OSi)

what are the supplements sourced from

 

[PowertothePeatple]

what dosage is good for niacinamide? also wont it be depleting some other vitamins and methyl groups

I settled on 250 mg dissolved in water and sipped slowly all day. And yes it can deplete certain nutrients. It appears to deplete methionine and possibly choline so it is important to eat enough protein and choline. There are so many PubMed studies about it if you want to see what the real life effects were on people and animals with supplemental niacinamide. And you can also see the various amounts that were administered.

 

[Dr. B]

I settled on 250 mg dissolved in water and sipped slowly all day. And yes it can deplete certain nutrients. It appears to deplete methionine and possibly choline so it is important to eat enough protein and choline. There are so many PubMed studies about it if you want to see what the real life effects were on people and animals with supplemental niacinamide. And you can also see the various amounts that were administered.

is dietary choline and methionine really enough to offset the effects of supplemental niacinamide though? wouldn't things be thrown off balance by supplementing if you do it long term?

 

[dreamcatcher]

A day or two after taking niacinamide (very small amounts) I usually notice more hair shedding for some reason.

 

[Waynish]

what are the supplements sourced from

Right, that is what I'm asking. Not theoretically the elements they believe exist. Rather what substance are they treating and processing with what in order to yield "niacinamide" ...?

 

[Dr. B]

A day or two after taking niacinamide (very small amounts) I usually notice more hair shedding for some reason.

is it related to it being a fatty acid oxidation inhibitor? have you tried other ones like aspirin?

Right, that is what I'm asking. Not theoretically the elements they believe exist. Rather what substance are they treating and processing with what in order to yield "niacinamide" ...?

some b vitamins are sourced from yeast, the risky ones i think are from molds or fungi. technically you could probably extract it from anything that had niacinamide but it wouldnt be economical to try to do it from something like meat.

 

[Mazzle]

I think it would take more like 4-6 months to be comparative to the mouse study. Mice have a much shorter life span so they are showing the effects much sooner. My plan is to aim for 6 months or so and then see whether I think it worked.

Ahh ok. But it’s been a month since post was made and I’ve been taking religiously since then. You would think some changes would be starting to show. Maybe it’s just me though. My Mum started two weeks ago and has lost 4lb with no other changes.

 

[Waynish]

is it related to it being a fatty acid oxidation inhibitor? have you tried other ones like aspirin?



some b vitamins are sourced from yeast, the risky ones i think are from molds or fungi. technically you could probably extract it from anything that had niacinamide but it wouldnt be economical to try to do it from something like meat.

Originally yes. But where is the evidence that any common ones we buy are not just synthetic?

 

[dreamcatcher]

is it related to it being a fatty acid oxidation inhibitor? have you tried other ones like aspirin?



some b vitamins are sourced from yeast, the risky ones i think are from molds or fungi. technically you could probably extract it from anything that had niacinamide but it wouldnt be economical to try to do it from something like meat.

@Dr. B
I have taken aspirin in the past hoping to restore hair growth but had to discontinue it unfortunately as it accelerated my hair shedding. It also made my eyebrows thin excessively. Later I learned that it can lower both estrogen and prostaglandins but don't know if these two are related to the hair loss.

 

[Dr. B]

@Dr. B
I have taken aspirin in the past hoping to restore hair growth but had to discontinue it unfortunately as it accelerated my hair shedding. It also made my eyebrows thin excessively. Later I learned that it can lower both estrogen and prostaglandins but don't know if these two are related to the hair loss.

i dont think the lowering estrogen is related to hair loss. it could be lowering prostaglandins or maybe related to the fatty acid oxidation inhibition?

 

[FocusedOnHealth]

It looks like the medical world has firmly set its sights on the bioenergetic wave/target, as the number of scientific papers focusing on niacinamide, NAD/NADH ratio and OXPHOS in general has been steadily climbing since 2010. That would be good news, despite the attempts of companies such as ChromaDex to fully "own" that market by claiming that their "patented" substances such as nicotinamide ribodise (NR) are the most effective intervention for reliably raising NAD levels (and thus the NAD/NADH ratio), and all others should be declared by the FDA to be "adulterated drugs". The presence of all these "bottom feeders" aside, the role of OXPHOS in various pathologies such as diabesity, CVD, and even cancer is becoming almost impossible to deny any longer. Speaking of diabesity, the study below presents some remarkable findings, that may send shivers down ChromaDex' spine. Namely, the administration of the cheap, unpatentable NAD precursor niacinamide (NAM), at low HED dose of 2.5mg/kg daily for 3 weeks, had striking anti-obesity effects in animals fed a high-fat diet. The low-dose NAM intervention reduced body fat by almost 50%, while also increasing lean muscle mass. In addition, NAM not only served as precursor to NAD but increased the activity of the enzyme NAMPT that synthesizes NAD. This increase in NAD also resulted in increased mitochondrial biogenesis, higher CO2 levels, improved insulin sensitivity, increased physical activity of the (formerly) obese animals back to control levels, and generally higher levels of OXPHOS. Finally, as another confirmation of the anti-obesity effects of this substance, NAM administration reduced the weight of not only the group that ate the high-fat diet, but also the weight of the group that ate the regular/normal diet.

Nicotinamide reprograms adipose cellular metabolism and increases mitochondrial biogenesis to ameliorate obesity

"...A three-week NAM supplementation significantly decreased the body weight in mice (Figure 1A). NAM also decreased fat mass by 47% as measured by magnetic resonance imaging (MRI) (9.39 ± 0.64 g fat mass of CTR group vs 2.94 ± 0.27 g of NAM group), while lean mass was increased by 1.4 fold (22.04 ± 0.46 g lean mass of CTR group vs 18.55 ± 1.35 g of NAM group) (Figure 1B). In addition, weights of subcutaneous adipose tissue (SCAT), epididymal adipose tissue (eWAT), brown adipose tissue (BAT) and liver were all significantly decreased (Figure 1C). Especially, the volume of SCAT and eWAT also declined (Figure 1D). Consistently, HE staining showed that NAM decreased hepatic lipid content and the size of adipocytes from several anatomical locations including SCAT, eWAT and BAT (Figure 1E). In addition, NAM supplementation lowered the glucose level at each time point over glucose tolerance test (GTT) (Figure S1A and S1B). Meanwhile, we observed carefully raw phenotype of the mice treated with NAM, and no symptoms including diarrhoea and vomiting were observed during NAM supplementation. In addition, we found hair color of NAM-treated mice looked black and glossy as control group mice did with less oil on the surface of hair induced by high fat diet than control group (Figure S1C). NAM-treated mice move as much as control group and showed similar day-night rhythm (Figure S1D). Food intakes were similar between mice treated with NAM and control (Figure S1E). In order to examine whether NAM supplementation induced injury of liver and heart, we checked the serum protein aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and creatine kinase (CK). We found that AST and CK were not changed (Figure S1F, G), and LDH were decreased by NAM treatment (Figure S1H), indicating NAM supplementation did not change significant injury of liver and heart. In addition, after measuring serum content of creatinine and uric acid by LC-MS/MS, we found that level of creatinine was not changed and uric acid even decreased (Figure S1I, J), so it can be concluded that NAM supplementation did not lead to injury of kidney. Furthermore, we examined the effects of NAM on 16-week C57BL/6J male mice fed a chow diet. NAM decreased body weight of mice fed a normal diet (Figure S1K). As obese mice, AST, ALP, CK or LDH were not increased by NAM supplementation, suggesting NAM supplementation did not induce injury of liver and heart (Figure S1L- O). The data indicated that NAM reduced fat content in DIO mice and improved glucose metabolism."

"...As shown in Figure 2C, glucose was consumed via glycolysis pathway to produce intermediate metabolites such as F16BP, 3PG and pyruvate, or pentose phosphate pathway (PPP) to produce 5-phosphoribosyl-1-pyrophosphate (PRPP). NAM treatment did not change the levels of F16P, and 3PG (Figure S2D, E), suggesting glycolysis was not altered in NAM treated cells while PRPP was decreased (Figure S2F). PRPP was used to synthesize NMN, which were converted into (m+5) and (m+10) NAD+, in which 22% and 55% of NAD+ were in (m+5) and (m+10) forms, respectively (Figure 2C). NAM treatment increased the labelling efficiency in both (m+5) and (m+10) forms (Figure 2D), suggesting that supplementary NAM enhanced NAD+ biosynthesis. Moreover, in 3T3L1 cells, both protein level and mRNA level of NAMPT were increased while NNMT was not changed as the dosage of NAM increased (Figure 2E, F). These data demonstrated that NAM increased NAMPT and enhance NAD+ synthesis."

"...We performed ingenuity pathway analysis (IPA) of these 154 DEPs to identify the biological pathways regulated by these DEPs. The results showed that NAM dramatically increased the abundance of proteins associated with oxidative phosphorylation (OXPHOS), fatty acid β-oxidation, TCA cycle and oxidative stress defense system (Figure 3B). To confirm that mitochondrial proteins were upregulated, western blot analysis was used to examine the expressions of COXIV and SOD2 and found that NAM upregulated both proteins (Figure 3C). Additionally, mRNA levels of mitochondrial genes such as COXIV, COX8b, SOD1, SOD2, ACADm, and ACADl were increased (Figure 3D). To confirm that NAM enhanced mitochondrial biogenesis, we performed qPCR on PPARα and PGC1α and found that both genes were upregulated in NMN-treated mice (Figure 3D)."

"...Herein, we reported that NAM supplementation ameliorated metabolic dysfunction in high fat diet induced obese (DIO) mice. We found that NAM strikingly decreased mass of SCAT, and boosted adipose NAD+, NADP, and N1-methylNAM, in which NAD+ was increased by 32 fold. The increase of lean mass partly contributed to the dramatic increase of NAD+ level. Interestingly, NAM also upregulated NAMPT expression, the rate limiting enzyme in NAD+ synthesis from NAM [38,39], and thus suggested that NAM reprogrammed NAD+ salvage pathway. The elevated NAD+ activated SIRTUINs. Consequently, protein acetylation was decreased in NAM-treated adipose tissue. Furthermore, the decreased acetylation intensity of SOD2 suggested that NAM improved the function of SIRT3, the major mitochondrial deacetylase to control mitochondrial biogenesis [33,35,40,41]. NAM-enhanced mitochondrial biogenesis was confirmed by proteomic analysis showing that mitochondrial proteins involved in fatty acid β oxidation, OXPHOS and TCA were all upregulated in adipose tissue. Consistently, NAM also increased O2 consumption, CO2 production, and adipose acylcarnitine levels by increasing expression of genes for carnitine biosynthesis in DIO mice."

"...In conclusion, our results provided a systemic perspective of effects of NAM on adipose tissue by reprogramming metabolic pathway to enhance mitochondrial biogenesis, and increased GSH production. These results suggested that NAM supplementation was an effective approach to increase fatty acid catabolism and to ameliorate obesity."

Thanks for posting this. What I do is take a 250mg. Niacinimide tablet and cut it into 4 parts, basically giving me about 62.5 mgs per dose spaced thrunout the day. I feel great taking it this way and I think it has increased my metabolism. I’m back down the 5 lbs I had gained without really changing my diet. Like some others have said in this thread, taking one tablet ( in my case a 250 mg one) made feel “off”. I think it was too much. Dividing it up and spreading it thruout the day seems to be what helped. I wouldn’t take it too close to bedtime though.

 

[FocusedOnHealth]

@haidut , the 2.5 mg HED dose seems awful small to be effective. Maybe I’m reading it wrong. Personally, I’m doing roughly 62 mgs. 4 x a day, and it seems fine for me. No side effects.

 

[Vinny]

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