21 replies to this topic

[TheSimulation]

Nicotinamide is available for cheap pricing on ebay and other places like amazon... but it is not Nicotinamide Riboside.  So what exactly is it, if it does not contain the riboside portion? What is it bonded to if it's not riboside?

 

Anyone have any links to sites describing the disadvantages and advantages of taking plain Nicotinamide instead of the riboside one? 

The pricing for Nicotinamide is much much cheaper than for the riboside varieties..

 

From what I researched, Nicotinamide multivitamin that is not labeled as riboside does in fact release NAD into the cells and cause anti aging, however it says in some articles that if you take too much of it the effects can go into reverse and negate the effect of anti aging. I will try to find the web links to the studies that say this as I have misplaced them. If you can find them post them here.

 

So is it worth taking Nicotinamide since it is so cheap, compared to spending lots of money on riboside varieties?  What is the actual bond or chemical formula for Nicotinamide without riboside? I am wondering if it is bonded to something very similar and they are just using Nicotinamide to avoid paying royalties for the niagen name brand.. maybe it works just as good, or maybe not..

[TheSimulation]

"The darker side of niacin/niacinamide supplementation

Turning now to the darker side, there is unquestionable evidence that niacinamide inhibits the expression of SIRT1 and its multiple health and longevity benefits discussed in three recent blog posts ( SIRT1, mTOR, NF-kappaB and resveratrol, Visit with Leonard Guarante, and  SIRT1, the hypoxic response, autophagy and hormesis).  

The 2002 publication Inhibition of Silencing and Accelerated Aging by Nicotinamide, a Putative Negative Regulator of Yeast Sir2 and Human SIRT1 reported that in yeast at least nicotinamide inhibited Sir2 and decreased lifespan.  “We show here that nicotinamide strongly inhibits yeast silencing, increases rDNA recombination, and shortens replicative life span to that of asir2 mutant.”

 

http://www.anti-agin...od-or-bad-idea/

 

In the comments on that page:

 

"One must be careful when calling nicotinamide an “inhibitor” in this experiment. While it is true that our lab showed that nicotinamide is a direct inhibitor of SIRT1 enzyme, it is also a precursor of NAD+, and NAD+ is a co-substrate (i.e., activator) of SIRT1.

In vivo, there is an abundant enzyme called Nampt in cells and serum that initiates the conversion of nicotinamide to NAD+. Therefore we should entertain the possibility that nicotinamide is activating SIRT1 in vivo, not inhibiting it. This would fit with other papers showing that SIRT1 is neuroprotective."

Edited by TheSimulation, 22 July 2015 - 09:52 PM.

[Gerrans]

I am a fan of niacinamide, and the only thing I can find against it is this thing--played up on this website more than any other--that it might shorten one's life. I go a little steady with niacinamide on that account, but I take it for many reasons. For example, despite (and because of?) the association with SIRT1, it is also associated with many measures of health. I find it hard to see how it could shorten my life while improving various measures of my health. I have my own view, which is that we all possess mechanisms to ensure we do not live forever--in other words, we have built-in senescence--so maybe niacinamide is part of that system. After all, it is produced naturally in the body. All else being equal, I am banking that activation and inhibition of sirtuins are just normal balancing processes. I like the fact that some of the biggest proponents of niacinamide--Kaufman, Hoffer, and Pauling--lived to a ripe old age (and I get the impression they were shovelling it down the hatch with a grain scoop).

 

Niacinamide is not necessarily a supplement that gives you obvious effects, but I have noted one or two things from it. I have noticed that it can warm my fingers when they are cold, which is significant to me since I suffer from chilblains. I think it does this by dilating blood vessels at the periphery. I believe it helps with the heat too, which may contribute to my not getting sunburn. It does have a reputation for helping against sunburn and other skin stresses when taken internally; but it has also been used effectively as a topical skin treatment, for example for age spots. I have very few age spots, but I am thinking about seeing if I can fade them topically with some niacinamide. The science makes sense to me.

 

Niacinamide has been found to help ease arthritis, which suggests the same benefit to collagen as it has in skin. I also like what I have read about the effect of niacinamide on the brain, where it has been associated with cognitive benefits. I feel as if it supports my sleep.

 

There is a vast literature on niacinamide research, but here are a few papers bearing on my comments:

 

Green et al, "Nicotinamide restores cognition in Alzheimer's Disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotase", J Neurosci, 2008

 

Schmeisser, et al, "Role of sirtuins in lifespan regulation is linked to methylation of nicotinamide," Stroke, 2000

 

Yiasemides, et al, "Oral nicotinamide protects against ultraviolet radiation-induced immunosuppression in humans", Carcinogenesis, 2009

 

Hakozaki, et al, "The effect of niacinamide on reducing cutaneous pigmentation and suppression of melanosome transfer," Br J Dermatol, 2002

 

Kang, et al, "Nicotinamide extends replicative lifespan of human cells," Aging Cell, 2006

 

Jonas, et al, "The effect of niacinamide on osteoarthritis: a pilot study," Inflamm Res, 1996

Edited by Gerrans, 23 July 2015 - 11:09 AM.

[Bryan_S]

In the comments on that page:

 

"One must be careful when calling nicotinamide an “inhibitor” in this experiment. While it is true that our lab showed that nicotinamide is a direct inhibitor of SIRT1 enzyme, it is also a precursor of NAD+, and NAD+ is a co-substrate (i.e., activator) of SIRT1.

In vivo, there is an abundant enzyme called Nampt in cells and serum that initiates the conversion of nicotinamide to NAD+. Therefore we should entertain the possibility that nicotinamide is activating SIRT1 in vivo, not inhibiting it. This would fit with other papers showing that SIRT1 is neuroprotective."

 

True in vivo within a living system and in vitro in a test tube makes the SIRT1 difference. I also came across David Sinclair's post on this topic. Most arguments against Niacinamide AKA Nicotinamide (Nam) fail to make that distinction and in my opinion fuel its hate campaign. Niacinamide AKA Nicotinamide belongs to part of our natural NAD salvage cycle. You are constantly recycling it and it is a part of your everyday metabolism.

 

I take both but if I had enough money I would likely stick with only Nicotinamide Riboside (NR) because it is more bioactive. Also "because current data suggest that nicotinamide riboside may be the only vitamin precursor that supports neuronal NAD+ synthesis." As you study both of these you'll find each has a separate distinct path into the cell and some cells have a preference. Nicotinamide Riboside also seems to be the preferred NAD precursor for extracellular transport between tissues. Both paths for (NR and Nam) converge by building the NAD precursor Nicotinamide mononucleotide (NMN) which is converted to NAD.

 

Now all that aside you'll find 70-years of research on Niacinamide AKA Nicotinamide. In terms of safety its one of the most studied vitamins and very well tolerated. You said; "Niacinamide is not necessarily a supplement that gives you obvious effects," and I tend to agree because Vitamin B3 may also help prevent certain skin cancers among other things. So reading your post you don't seem to need any encouragement as you are already a fan.

 

So any good, yes. Can you do better, yes but if you cant afford better and are on a budget Niacinamide is a good fall back position.

[RWhigham]

I am a fan of niacinamide, and the only thing I can find against it is this thing--played up on this website more than any other--that it might shorten one's life.

 

Anti-aging Firewalls - James Watson, April 2015  Section 5:  "Conclusion: It is now clear that high concentrations nicotinamide are harmful to health. HIgh doses of dietary niacin probably produce the same effects, despite the many benefits of high dose niacin. With aging, nicotinamide levels already go up. Adding more nicotinamide is probably not going to “cure” aging. Adding a methyl donor to eliminate nicotinamide (such as betaine) may be a good thing."

• A healthspan argument can be made for supplementing niacin or niacinamide.
• Excessive niacin converts to niacinamide in vivo.
• Niacin/niacinamide RDA = 16 mg (male adults).
• I prefer to emphasize lifespan,  and therefore avoid excess niacinamide or niacin.
• The Jigsaw slow release B-complex which I take has 15 mg of niacinamide, and zero niacin.

 

Edited by RWhigham, 15 January 2017 - 10:17 PM.

[sthira]

Does it seem like there's some sloppy use of names going on around here? We have (1) Nicotinamide; (2) Niacinamide; (3) Niacin; (4) Nicotinic Acid; (5) vitamin B3; (6) Nicotinamide Mononucleotide
(7); and finally the holy grail of (8) Nicotinamide riboside. Have I missed any others?

I understand that niacin is nicotinic acid is vitamin B3 (same-same-same); that niacinamide is "flush-free niacin"; that Nicotinamide Mononucleotide the thing we want inside cells (presumably) but it isn't directly absorbed by cells, and requires conversion to NR before entry into cells; once inside cells it's evidently converted back again Nicotinamide Mononucleotide before being turned into NAD+. Or so says Brenner:

http://www.nature.co...les/ncomms12948

http://www.nature.co...les/ncomms13103

But what is Nicotinamide (sans riboside), and why when I search for it do I get a kinda bait and switch to niacinamide?

And why wouldn't I just take some nicotinamide with riboside together as two separate cheaper pills (assuming this stuff is worthwhile taking in megadoses like, what, 25 grams at a time?)

I realize this is an ongoing science project here, but really: what's up with the language here?

[RWhigham]

Does it seem like there's some sloppy use of names going on around here? We have (1) Nicotinamide; (2) Niacinamide; (3) Niacin; (4) Nicotinic Acid; (5) vitamin B3; (6) Nicotinamide Mononucleotide

(7); and finally the holy grail of (8) Nicotinamide riboside. Have I missed any others?

• (1) Nicotinamide (Nam)  and niacinamide (2) are different names for exactly the same thing. 
• (3) Niacin and nicotinic acid (4) (Na) are different names for exactly the same thing as well.
• (5) Vitamin B3 refers to niacin (nicotinic acid),  niacinamide (nicotinamide), or inositol hexanicotinate (IP6 aka phytic acid) all of which prevent the disease pellagra, but work somewhat differently in the body.
• (6) Nicotinamide Mononucleotide (NMN) is a precursor/substrate for NAD. NMN can be made from niacinamide with the rate-limiting enzyme NAMPT. Supplementary NMN can increase NAD and also supply B3.
• (7)(8) Nicotinamide Riboside (Nr) is another precursor/substrate for NAD.  Supplementary Nr can increase NAD and also supply B3.
• IP6 (phytic acid) is 1 molecule of inositol surrounded by 6 molecules of niacin. IP6 releases niacin into the bloodstream very slowly peaking about 10 hours after IP6 consumption. IP6 does not damage the liver like slow release niacin formulations. IP6 is about 70% absorbed.
• Niacin causes flushing, and reduces the liver's cholesterol production. Large doses of niacin are toxic to the liver, but the liver recovers ok if the doses are separated by 24 hours. Niacin does not inhibit SIRT1. However, extra niacin is converted to niacinamide. RDA = 16 mg. Muli-gram doses are used to reduce lipids.
• Niacinamide does not cause flushing, or lower cholesterol. Niacinamide, Nr, and NMN are all substrates for NAD+. We take Nr or NMN supplements to increase NAD+, but not niacinamide.
• NAD+ is a coenzyme for SIRT1. Increased SIRT1 may account for many of the benefits of raising NAD+. Although niacinamide is a substrate for NAD+, it is also the strongest known inhibitor of SIRT1.  Part 5 of the NAD world  James Watson May 2016

Edited by RWhigham, 16 January 2017 - 04:31 AM.

[TheSimulation]

To add more knowledge to this topic: There are two types of regular niacinimide/nicotinamide available. There is the prolonged release (delayed release) which is harder on the liver, but slowly releases the niacinimide into the body.   The other type is immediate release (the bottle of pills must not say prolonged release on it). The immediate release one is not as hard on the liver, but acts quicker so may be wasted. So best to alternate:. some days take the immediate release pill and other days take the prolonged release.

 

I'm skeptical about the whole riboside product and whether or not the regular cheap niacinimide has the same basic effects, because there is some evidence that riboside gets converted before it can even be used, unless you were to inject it directly as that substance... into your blood.

 

This whole niacinimide thing is actually ticking me off quite a bit, because it seems to be turning out the same as the Sinclair fiasco where he claimed that resveratrol was going to be the aging drug/supplement of the future. Turned out resveratrol was basically a scam or had the reverse effect if you took too much or too little (it is too picky and basically didn't work). Well not quite a scam, but, close to a scam... as basically these supplements are just like multi level marketing junk pills that make huge claims but don't actually do anything in reality.

 

Ultimately to me it seems we need to inject a substance into our blood or cells directly as the chemical gets broken down in our systems if taking it orally... and keeps converting back and forth into different forms.

 

Basically the whole niacinimide/nicotinamide research, IMO, is turning out exactly the same way as resveratol. Big claims, big hype, and basically no results... no success.. All the studies are all contradicting each other. One study says it works, others say it doesn't. Not the right quantity or dose.... Way too picky, it's not simple but a complicated joke. We know what happened to the resveratol, and now the same thing is happening to nicatinimide.... "it's a crap shoot". Or in other words, like a blind man hitting a pinyata.

 

http://media.gettyim...22755?s=170667a

 

http://www.urbandict...term=crap shoot

 

Yup a crap shoot.. No one really knows...

 

But looking on the positive side: is there any riboside injection therapy? injecting it into cells or blood? That would seem the best way to go, but even then you've got the dose amount issue to work out

 

 

[RWhigham]

To add more knowledge to this topic: There are two types of regular niacinimide/nicotinamide available. There is the prolonged release (delayed release) which is harder on the liver, but slowly releases the niacinimide into the body.   The other type is immediate release (the bottle of pills must not say prolonged release on it). 

You have conflated the quick and slow release formulations of niacin and niacinamide. 

 

Slow release niacin was formulated to suppress the liver's production of cholesterol on a more continuous basis to more effectively lower serum lipids. This was later discovered to damage the liver. (Slow release formulations are still available for the unwary). The liver needs up to 24 hr to recover between large doses of niacin. Slow release niacin may not give the liver enough time to recover, especially if take more than once/day. Depending on the dose and rate of release, once/day can be ok, but liver enzymes should be checked.

 

Slow release niacinamide is not "hard on the liver", and does not lower serum lipids.

 

Like all B-vitamins, niacinamide and niacin are water soluble and not stored in the body, making slow release formulations attractive. However, niacin is a much better substrate than niacinamide for raising NAD.  https://www.ncbi.nlm...pubmed/17604275

Edited by RWhigham, 16 January 2017 - 05:38 AM.

[TheSimulation]

 

To add more knowledge to this topic: There are two types of regular niacinimide/nicotinamide available. There is the prolonged release (delayed release) which is harder on the liver, but slowly releases the niacinimide into the body.   The other type is immediate release (the bottle of pills must not say prolonged release on it). 

You have conflated the quick and slow release formulations of niacin and niacinamide. 

 

No, I found research that found the prolonged slow release niacinimide/nicotinamide was hard on liver

 

I will reply back to this thread, if I can find the studies.... This research I did was almost a year ago or more, so I do not have the links handy right now.

 

I'm skeptical of anyone who has definite proclamations about this subject too... as this research is quite complex and does not have binary answers as in "it's definitely not hard on the liver"....  In this case, it's actually "wait until more research is done, it may in fact be"

 

It also depends on people's genetics. I believe I found some studies saying certain people were extremely sensitive to certain pills, when they were studying how b-vitamins helped mental illness (bipolar and schizophrenia) by mega dosing.

[RWhigham]

There is a feedback loop in which SIRT1 increases nicotinamide (Nam), and Nam then limits SIRT1 production. 

• Nam is a substrate for NAD+         Nam -> NAD+     (Nam is converted to NAD+, depleting Nam)
• NAD+ is a coenzyme for SIRT1     NAD+ -> SIRT1  (provided Nam is temporarily depleted)
• SIRT1 catalyzes NAD+ -> Nam     NAD+ -> Nam     (catalyzed by SIRT1)
• Nam now temporarily blocks the NAD+ to SIRT1 catalysis            

Edited by RWhigham, 16 January 2017 - 06:09 PM.

[RWhigham]

There is a feedback loop in which SIRT1 increases nicotinamide (Nam), and Nam then limits SIRT1 production. 

In another feedback loop, the key NAD+ biosynthetic enzyme NAMPT is deacetylated by SIRT1, allowing NAD+ to decline and further limiting the production of SIRT1.  What is the evolutionary reason for SIRT1 to be self-limiting?

 

Dark side of SIRT1 :

SIRT1 in adipose cells deacetylates iNAMPT (intracellular NAMPT).  Perhaps in other cells too, but in adipose cells the deacetylated NAMPT is excreted into the bloodstream where i'ts called eNAMPT (extracellular NAMPT).  eNAMPT is an endotoxin surrogate.  Macrophages treat eNAMPT as endotoxin/LPS and respond with massive inflammation. Chronic inflammation causes extensive damage, including cartilage and artery damage, rheumatoid arthritis, and diabetes. This is a connection between excess adipose tissue and the development of diabetes after yo-yo dieting. (Dieting ups SIRT1.) 

 

Speculation:

What is the evolutionary reason for adipose cells to create eNAMPT/inflamation?  SIRT1 is normally produced by food scarcity.  Perhaps during evolution well-fed people fasts were frequently due to illness. (Inflammation is needed for fighting illness). Whereas, skinny people fasts were usually caused by food scarcity instead.

 

Edited by RWhigham, 18 January 2017 - 03:15 AM.

[SearchHorizon]

 

There is a feedback loop in which SIRT1 increases nicotinamide (Nam), and Nam then limits SIRT1 production. 

• Nam is a substrate for NAD+         Nam -> NAD+     (Nam is converted to NAD+, depleting Nam)
• NAD+ is a coenzyme for SIRT1     NAD+ -> SIRT1  (provided Nam is temporarily depleted)
• SIRT1 catalyzes NAD+ -> Nam     NAD+ -> Nam     (catalyzed by SIRT1)
• Nam now temporarily blocks the NAD+ to SIRT1 catalysis            

 

1. Research shows that the conversion of NAM into NAD+ increases when melatonin production increases (at night). Increased melatonin level is accompanied by increased SIRT1 activation. It is interesting that melatonin production decreases with aging. Perhaps, the decreased level of NAMPT is driven by decrease in melatonin production.

 

2. NAM's 1/2 life fairly short. I seriously doubt it has a negative impact on SIRT1.

 

3. I believe that there is some evidence that constant over activation of SIRT1 is a bad thing. SIRT1 is not just activated by hunger. It appears to be a general "stress-response" gene. It make sense that its over activation leads to adverse effects - this is consistent with ill effects of chronic stress.

 

The temporary SIRT1 deactivation probably provides a "break" from translating stress into a physical response, which is probably a good thing.

 

4. I have been playing with niacin, niacinamide, and niacinamide for years (and with niacinamide ribside for 3 months). At appropriate dosages, each of these appears to have a different short term effect when ingested (initial 1-2 hours). Over a longer time frame (3-10) hours, their effects are identical or similar. They all raise body temperature, and appears to facilitate fat metabolism (over glycogen.  

[RSC]

Referencing this abstract dated Sept 2017 - https://www.ncbi.nlm...pubmed/28417163 - on Nicotinamide (NAM)

 

"NAM has been widely used as an inhibitor in the studies where SIRT1, a key member of sirtuins, may have a role in certain cell physiology. However, once administered to cells, NAM is rapidly converted to NAD+ and, therefore, the cellular concentration of NAM decreases rapidly while that of NAD+ increases. The result would be an inhibition of SIRT1 for a limited duration, followed by an increase in the activity. This possibility raises a concern on the validity of the interpretation of the results in the studies that use NAM as a SIRT1 inhibitor."

 

I am trying to figure out which is better and more economical to take "NAM" or "NR". Are there any recent studies disputing this abstract and indicating NAM inhibits SIRT1 to the point that there is no increase, or limited increase in NAD+,  in comparison to NR.

 

Thanks in advance for any replies...

[LawrenceW]

; that Nicotinamide Mononucleotide the thing we want inside cells (presumably) but it isn't directly absorbed by cells, and requires conversion to NR before entry into cells; once inside cells it's evidently converted back again Nicotinamide Mononucleotide before being turned into NAD+. Or so says Brenner:
 

 

The only part of this statement that is true is "Or so says Brenner:"

 

Brenner was debunked in January of this year by the publishing of this study:  https://www.nature.c...2255-018-0009-4

[RSC]

My limited understanding of all this is that we want to boost NAD+ and that NMN and NR do this but in somewhat different ways.

 

The question I want to clarify in my head is if taking NAM (Nicotinamide) will do the same thing as NMN and NR. I am aware that there is a debate that NAM may somewhat and briefly inhibit SIRT1. If such is the case and NAM only briefly inhibits SIRT1, as indicated in the aforementioned abstract I first posted, is it also a viable option for boosting NAD+. without having to take either NMN or NR. 

 

If I appear dense on this subject... it is because I am!

[Harkijn]

https://www.longecit...r-homocysteine/

[MikeDC]

My limited understanding of all this is that we want to boost NAD+ and that NMN and NR do this but in somewhat different ways.

The question I want to clarify in my head is if taking NAM (Nicotinamide) will do the same thing as NMN and NR. I am aware that there is a debate that NAM may somewhat and briefly inhibit SIRT1. If such is the case and NAMonly briefly inhibits SIRT1, as indicated in the aforementioned abstract I first posted, is it also a viable option for boosting NAD+. without having to take either NMN or NR.

If I appear dense on this subject... it is because I am!

NR and NMN definitely provide more benefits than NAM and Niacin. A recent mice study shows that if you delete NRK1 which converts NR to NMN and NAD+, liver health deteriorates. Even supplementing NAM does not help. So NR is an important precursor even without supplementation. Even though NR bioavailability is low, it can still increase baseline NR by a few hundreds percent. This is why NR has more health advantages than NAM. NAM has been shown to improve aspects of mice health, but not lifespan. NR has been shown to increase lifespan even late in life.

https://www.nestlehe...ng-liver-health

Dr Carles Canto, scientist at Nestlé and corresponding author of the study said, “This is the first paper suggesting a functional uniqueness of NR that cannot be mimicked by other precursors. This research highlights the opportunity for the development of dietary supplements and medical food products better tailored to specific states of NAD+ deficiency.”

Edited by MikeDC, 19 November 2019 - 11:36 PM.

[MikeDC]

So if NMN can get into cells directly, why is NRK1 critical? NMN might exist in higher concentration than NR in the blood. So there is really no need for NRK1 to exist.

[malbecman]

Many dermatologists, including mine at Kaiser, recommend nicotinamide for people who've had skin cancer like basal cell carcinomas. Its been shown to reduce reoccurrence based

on this study.

 

https://www.ncbi.nlm...les/PMC4570055/

 

Am Health Drug Benefits. 2015 Aug; 8(Spec Issue): 13–14.

 

PMCID: PMC4570055

PMID: 26380604

Oral Nicotinamide Prevents Common Skin Cancers in High-Risk Patients, Reduces Costs

Phoebe Starr

Copyright and License information Disclaimer

The prevention of common skin cancers and precancers is possible by taking an inexpensive, widely available, oral pill twice daily. The pill—the vitamin B₃ supplement called nicotinamide—cut the rate of new squamous-cell and basal-cell skin cancers by 23% compared with placebo after 1 year among patients at high risk for skin cancer. Nicotinamide also reduced the risk for developing actinic keratosis, a common precancer of the skin.

The results of the phase 3 ONTRAC skin cancer prevention study were presented at ASCO 2015.

These findings have the potential to lower healthcare costs. In the United States, skin cancer accounts for approximately $4.8 million annually.

The investigators emphasized that these results were achieved in individuals who previously had skin cancer and were thus at high risk for new skin cancers. The results do not apply to other patient populations.

In addition, the investigators emphasized that nicotinamide is the form of vitamin B₃ that should be taken for prevention—not other forms of vitamin B, such as niacin—and that continuous treatment is advised.

[MikeDC]

Cancer and age related diseases are mostly related to NAD+ depletion. The cellular machinery doesn’t work well when NAD+ is low. Werner Syndrome is a good example. Werner Syndrome patients have 40% lower NAD+ even at young age. Normal people starts to have accelerated aging after 40’s. Werner Syndrome patients starts much earlier. NR and NMN has been shown to limit this accelerated aging in worm models.

[Ames]

I realize exceptional results from niacinamide alone. The results feel mitochondrial in nature. The most palpable have been noticeably increased resistance to migraine triggers, less felt fatigue when engaging in bad sleep habits, easier sleep initiation, better respiratory function during exercise, and general stress resistance. In fact, I haven't yet added riboside because I'm attempting to first fully grasp and maximize the results I get just from niacinamide. 

 

The other part of this is that I take one niacinamide capsule per quarter (roughly every three months). I've repeated this three times to date. 

 

The philosophy behind this schedule was to 

 

1. give the results time to manifest. I find that they tend to kick in better after roughly one week from having taken the niacinamide. I disagree with daily dosing of niacinamide unless an individual has at first tried heavily spaced out dosing, in order to assure that they aren't limiting results through dosing that is too frequent (analgolous to lifting weights too frequently and therefore limiting muscle growth).

 

2. give the results time to fully develop, but also to get a grasp on the timing how the results build, level off, and diminish.

 

My experience is that this is at least a three month cycle, from beginning to end. Which probably just implies semi-permanent mitochondrial improvement, the results of which are diminished as I again accrue damage. 

 

I've been quite happy with the results so far, and don't want to risk limiting them. So, I will only change the schedule slowly and as needed. 

 

In the months after taking Niacinamide, I have noticed a difference in how (I would guess) my liver processes Excedrin. It isn't as effective as it always has been. I would guess that this could be due to a niacinamide inuduced change in my liver, perhaps in terms of enzyme function but I'm unsure. 

Edited by Ames, 09 September 2020 - 05:22 AM.