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Benefits of Niacin for longevity?

niacin antioxidants

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#1 albedo

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Posted 19 October 2013 - 06:53 PM


"Niacin, the fountain of youth"

"The vitamin niacin has a life-prolonging effect, as Michael Ristow has demonstrated in roundworms. From his study, the ETH-Zurich professor also concludes that so-called reactive oxygen species are healthy, not only disagreeing with the general consensus, but also many of his peers."

http://www.ethlife.e...cin_fb/index_EN

Our good friend for its cholesterol lowering effects seems to have other befits. Interesting the point of not abusing with antioxidants too!

See also this: http://www.nature.co...embio.1352.html

I think this discussion has been going on for sometime already here. I wonder about your thoughts to the light of these new results.
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#2 xEva

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Posted 20 October 2013 - 02:04 PM

The article in Nature speaks of nicotinamide, while you speak of niacin. Even thought both are 'vit B3' they are different substances with different effects. I would be careful with niacin, especially when on certain diets, for 100 mg can sequester FFAs from the bloodstream for several hours -- which could be a good thing or a bad thing, depending on the circumstance and application.
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#3 RJ23_1989

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Posted 20 October 2013 - 02:09 PM

More on the role of nicotinamide:

http://www.ncbi.nlm....les/PMC3764375/

Sent from my SAMSUNG-SM-N900A using Tapatalk



Edited by PatrickM500, 20 October 2013 - 02:44 PM.


#4 Hebbeh

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Posted 20 October 2013 - 03:14 PM

An interesting study Turnbuckle posted on another thread:

http://www.ncbi.nlm....les/PMC2874142/

When I tried 500+ mg of nicotinamide (several different trials on several occasions) due to a similar discussion on another thread, It always resulted in miserable and insatiable hunger and I was unable to continue.

edit: and I know of one other person who had similar or identical uncontrollable hunger from higher dose nicotinamide.

Edited by Hebbeh, 20 October 2013 - 03:17 PM.


#5 rberezews

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Posted 22 October 2013 - 12:32 AM

The article in Nature speaks of nicotinamide, while you speak of niacin. Even thought both are 'vit B3' they are different substances with different effects. I would be careful with niacin, especially when on certain diets, for 100 mg can sequester FFAs from the bloodstream for several hours -- which could be a good thing or a bad thing, depending on the circumstance and application.


Hi there, I am a newbie here and well unfortunately not familiar wit niacin; I really would like to know more on this. Would you care to elaborate more? Thanks

#6 Heh

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Posted 22 October 2013 - 10:48 AM

Yea, I think niacin is good for this. You can also read the Abram Hoffer research. You should take niacin with equal amounts (or more) vitamin C, and an amount of vitamin B5 equal to 1/3rd the dosage of niacin (or more).
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#7 niner

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Posted 22 October 2013 - 12:55 PM

Yea, I think niacin is good for this. You can also read the Abram Hoffer research. You should take niacin with equal amounts (or more) vitamin C, and an amount of vitamin B5 equal to 1/3rd the dosage of niacin (or more).


What's the rationale for the C and B5?

#8 Turnbuckle

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Posted 22 October 2013 - 01:31 PM

An interesting study Turnbuckle posted on another thread:

http://www.ncbi.nlm....les/PMC2874142/

When I tried 500+ mg of nicotinamide (several different trials on several occasions) due to a similar discussion on another thread, It always resulted in miserable and insatiable hunger and I was unable to continue.

edit: and I know of one other person who had similar or identical uncontrollable hunger from higher dose nicotinamide.



Looking at the plots of a subsequent study, the amounts that might cause obesity in adults are very small, ranging up to 30 mg. But there is a time lag of 20-30 years, which makes me doubt any causal relationship.

Looking at FDA reports on ehealthme.com, it seems that niacin more often decreases appetite among adults--

On Oct, 22, 2013: 5,261 people reported to have side effects when taking Niacin. Among them, 126 people (2.39%) have Decreased Appetite.

On Sep, 23, 2013: 5,261 people reported to have side effects when taking Niacin. Among them, 9 people (0.17%) have Excessive Hunger.
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#9 Hebbeh

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Posted 22 October 2013 - 03:08 PM

I wonder if the hunger thing can be related to either diet, body composition (leanness), or insulin sensitivity? The other individual and myself both eat a moderate lowish carb diet, are both quite lean, and both fit with good insulin sensitivity and lower blood glucose values. The hunger certainly seemed to be driven by a sense of low blood sugar but I never measured blood glucose at the time. I usually don't have issues with blood glucose except some supplements tend to cause my blood sugar to dip lower than optimal.
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#10 Heh

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Posted 22 October 2013 - 03:48 PM

Yea, I think niacin is good for this. You can also read the Abram Hoffer research. You should take niacin with equal amounts (or more) vitamin C, and an amount of vitamin B5 equal to 1/3rd the dosage of niacin (or more).


What's the rationale for the C and B5?

At higher dosages (regular) niacin can cause liver damage. You take the right ratio of vitamin C and vitamin B5 to prevent that problem. It also does other things, but I don't remember what.
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#11 8bitmore

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Posted 22 October 2013 - 04:14 PM

I wonder if the hunger thing can be related to either diet, body composition (leanness), or insulin sensitivity? The other individual and myself both eat a moderate lowish carb diet, are both quite lean, and both fit with good insulin sensitivity and lower blood glucose values. The hunger certainly seemed to be driven by a sense of low blood sugar but I never measured blood glucose at the time. I usually don't have issues with blood glucose except some supplements tend to cause my blood sugar to dip lower than optimal.


I think this point contextualizes the data Turnbuckle posted from FDA nicely, in general people's blood glucose is far above what it should be - but this is probably hardly the case for many of the longecity users and hence a key "helping" factor of niacin (-amide) is effectively cancelled out.

#12 xEva

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Posted 23 October 2013 - 12:25 AM

The thing with niacin, in my view, is exactly its ability to sequester FFAs from the bloodstream for several hours. Citing from memory, the first studies of this sort were done in 1980s: 100mg cleared the bloodstream of healthy fasted people of FFAs (they fasted for 16-36 h before niacin administration, depending on a study).

Re hunger or lack of appetite, it depends on the circumstance. If you you're fasting or on a low-carb diet (with low calories), this means that you're running on fat. In this case, sudden clearance of FFAs from the bloodstream will result in insane hunger -- and will greatly upregulate autophagy. For example, I'm afraid of trying niacin during a fast, even though I'm very curious to experiment, because I'm not certain what will my body eat when glucose is low and FFAs are suddenly not available.

Then there are circumstances of 'insulin resistance', which may happen after a fast or a carb-load on a low-carb diet. In this case, high FFAs lingering after a fast will interfere with skeletal muscle taking up glucose coming from a meal. In this case, taking niacin ~20 min before a carb meal, will force the body to mop up glucose quickly -- because the FFAs will not be there to interfere.

In an average case, I believe, nothing much will happen with niacin. People on normal diets usually have enough BG or glycogen stores to sustain their needs while FFAs are low for whatever reason.

Edited by xEva, 23 October 2013 - 12:28 AM.

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#13 Hebbeh

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Posted 23 October 2013 - 01:34 AM

Re hunger or lack of appetite, it depends on the circumstance. If you you're fasting or on a low-carb diet (with low calories), this means that you're running on fat. In this case, sudden clearance of FFAs from the bloodstream will result in insane hunger -- and will greatly upregulate autophagy. For example, I'm afraid of trying niacin during a fast, even though I'm very curious to experiment, because I'm not certain what will my body eat when glucose is low and FFAs are suddenly not available.


That may very well be the case. I tend towards moderate carb lower calorie maintenance diet and I simply cannot tolerate the insatiable hunger brought on by higher doses of niacinamide.

#14 xEva

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Posted 23 October 2013 - 04:04 AM

oh so it's niacinamide that makes you hungry. but it is niacin --aka nicotinic acid proper-- that sequesters FFAs while its amide form does not have this particular effect (but of course it has other effects on cell metabolism and the two are supposed to be interchangeable -?)

The other thing I forgot to mention about niacin administration is that FFAs level rebounds after it is metabolized; i.e. first FFAs practically disappear and then flood the sys.

So I'm curious as to when this hunger thing happens to you after 500mg of niacinamide and when do you take it relative to meals.

Edited by xEva, 23 October 2013 - 04:05 AM.


#15 Hebbeh

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Posted 23 October 2013 - 04:14 AM

I experimented with different dosing amounts and schemes using either 500mg IR or 1500mg time release versions of niacinamide but it didn't matter when I took the niacinmide...I'd have ravenous hunger all day. I thought if I would take it at bedtime, I would get the benefits while I slept and the hunger sides would wear off by morning...but no such luck...the entire next morning I would always have insatiable hunger that would only slowly fade in the afternoon...all from a single dose of either the 500mg IR or the 1500mg TR at bedtime.

Edited by Hebbeh, 23 October 2013 - 04:16 AM.

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#16 timar

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Posted 30 October 2013 - 05:01 PM

The co-author of that paper is actually a friend of mine (now I know why he has been so busy since he went to Zürich :happy:). I'm going to meet him soon and of course, I will discuss that paper with him. If you have questions regarding the paper, maybe I can ask for you.

Edited by timar, 30 October 2013 - 05:02 PM.

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#17 Darryl

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Posted 31 October 2013 - 10:06 AM

I take 500 mg nicotinic acid (full flush niacin) nightly to for its blood lipid benefits (It helps me get below the 150 mg/dl TC threshold from Framingham). I'd avoid the flush free niacins (inositol hexanicotinate) for this purpose, as it likely have no benefits. Persist a week and your skin stores of prostaglandin E2 and D2 will deplete enough that flushing becomes a mild warming cue that its bedtime.

However this paper did not go unnoticed:

Canner, Paul L., et al. "Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin." Journal of the American College of Cardiology 8.6 (1986): 1245-1255.

The Coronary Drug Project was conducted between 1966 and 1975 to assess the long-term efficacy and safety of five lipid-influencing drugs in 8,341 men aged 30 to 64 years with electrocardiogram-documented previous myocardial infarction.

Niacin treatment showed modest benefit in decreasing definite nonfatal recurrent myocardial infarction but did not decrease total mortality. With a mean follow-up of 15 years, nearly 9 years after termination of the trial, mortality from all causes in each of the drug groups, except for niacin, was similar to that in the placebo group. Mortality in the niacin group was 11% lower than in the placebo group (52.0 versus 58.2%; p = 0.0004).


Edited by Darryl, 31 October 2013 - 10:17 AM.

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#18 Turnbuckle

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Posted 31 October 2013 - 12:38 PM

I take 500 mg nicotinic acid (full flush niacin) nightly to for its blood lipid benefits (It helps me get below the 150 mg/dl TC threshold from Framingham). I'd avoid the flush free niacins (inositol hexanicotinate) for this purpose, as it likely have no benefits. Persist a week and your skin stores of prostaglandin E2 and D2 will deplete enough that flushing becomes a mild warming cue that its bedtime.

However this paper did not go unnoticed:

Canner, Paul L., et al. "Fifteen year mortality in Coronary Drug Project patients: long-term benefit with niacin." Journal of the American College of Cardiology 8.6 (1986): 1245-1255.

The Coronary Drug Project was conducted between 1966 and 1975 to assess the long-term efficacy and safety of five lipid-influencing drugs in 8,341 men aged 30 to 64 years with electrocardiogram-documented previous myocardial infarction.

Niacin treatment showed modest benefit in decreasing definite nonfatal recurrent myocardial infarction but did not decrease total mortality. With a mean follow-up of 15 years, nearly 9 years after termination of the trial, mortality from all causes in each of the drug groups, except for niacin, was similar to that in the placebo group. Mortality in the niacin group was 11% lower than in the placebo group (52.0 versus 58.2%; p = 0.0004).



The whole cholesterol story is a scam. But niacin has other, equally important benefits. For instance, with AD.

Much attention has been focused on the relation between
dementia and other B vitamins, particularly vitamin B12,
vitamin B6 and folate. There has been little previous
examination of dietary niacin and AD, although niacin has
been administered to older people to prevent confusional
states, and there have been several published clinical trials of
medications for this indication. In this prospective study,
we observed a protective association of niacin against the
development of AD and cognitive decline within normal
levels of dietary intake, which could have substantial public
health implications for disease prevention if confirmed by
further research.
http://www.ncbi.nlm..../v075p01093.pdf

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#19 blood

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Posted 01 November 2013 - 03:09 AM

The co-author of that paper is actually a friend of mine (now I know why he has been so busy since he went to Zürich :happy:). I'm going to meet him soon and of course, I will discuss that paper with him. If you have questions regarding the paper, maybe I can ask for you.


I have a question for the professor. Could direct supplementation with 1-methyl-nicotinamide have health or life extension benefits in humans?

(Pro: bypass/obviate the need to bump up sirtuin levels? Con: maybe it could produce an excess of ROS?)

It seems that until recently 1-methylnicotinamide has been thought of as an inactive metabolite of niacin. But there is at least some research indicating it might have promise as a supplement:

http://www.ncbi.nlm....les/PMC1978255/

1-Methylnicotinamide (MNA), a primary metabolite of nicotinamide, exerts anti-thrombotic activity mediated by a cyclooxygenase-2/prostacyclin pathway


S Chlopicki,1,* J Swies,1 A Mogielnicki,2 W Buczko,2 M Bartus,1 M Lomnicka,1 J Adamus,3 and J Gebicki3,*

Author information ► Article notes ► Copyright and License information ►


Go to:


Abstract



Background and purpose:

1-methylnicotinamide (MNA) has been considered to be an inactive metabolite of nicotinamide. Here we assessed the anti-thrombotic activity of MNA in vivo.

Experimental approach:

Antithrombotic action of MNA was studied in normotensive rats with extracorporeal thrombus formation (thrombolysis), in renovascular hypertensive rats with intraarterial thrombus formation (arterial thrombosis) and in a venous thrombosis model in rats (venous thrombosis).

Key results:

MNA (3-100 mg kg−1) induced a dose-dependent and sustained thrombolytic response, associated with a rise in 6-keto-PGF1α in blood. Various compounds structurally related to MNA were either inactive or weaker thrombolytics. Rofecoxib (0.01-1 mg kg−1), dose-dependently inhibited the thrombolytic response of MNA, indomethacin (5 mg kg−1) abolished it, while L-NAME (5 mg kg−1) were without effect. MNA (3–30 mg kg−1) also reduced arterial thrombosis and this effect was abrogated by indomethacin (2.5 mg kg−1) as well as by rofecoxib (1Posted Imagemg kg−1). MNA, however, did not affect venous thrombosis. In vitro MNA did not modify platelet aggregation nor induce vasodilation.

Conclusions and implications:

MNA displayed a profile of anti-thrombotic activity in vivo that surpasses that of closely related compounds. MNA inhibited platelet-dependent thrombosis by a mechanism involving cyclooxygenase-2 and prostacyclin. Our findings suggest that endogenous MNA, produced in the liver by nicotinamide N-methyltransferase, could be an endogenous activator of prostacyclin production and thus may regulate thrombotic as well as inflammatory processes in the cardiovascular system.
Keywords: 1-methylnicotinamide, thrombolysis, thrombosis, PGI2, COX-2, platelets





From the discussion section of the above paper:

... it was quite surprising that, among the various structurally modified MNA analogues, we have not found a compound with better thrombolytic activity than MNA itself. Only the replacement of the amide group at the three-position of the pyridine ring by an acetyl group, as in the case of MAP, resulted in the retention of sustained dose-dependent thrombolysis (3–30Posted ImagemgPosted Imagekg−1) with a concomitant rise in 6-keto-PGF1α in blood. Other tested compounds were inactive or much weaker thrombolytic agents. For example, 6-amino nicotinamide—an inhibitor of pentose phosphate pathway (PPP) (Gupte et al., 2003) and 1-ribosylnicotinamide—a newly discovered precursor of NAD+ (Bieganowski and Brenner, 2004)—were virtually inactive as thrombolytics. Thus the mechanism of MNA-induced thrombolysis would seem independent of PPP activity or of intracellular NAD+. Nicotinic acid and trigonelline were also ineffective thrombolytically, even though nicotinic acid, at very high doses, has previously been shown to induce a remarkable thrombolytic response in cats that was attributed to the release of PGI2 (Swies and Dabrowski, 1984). In turn, the nicotinamide-induced response was substantially weaker than that of MNA. The observed weak anti-thrombotic activity of nicotinamide may be explained by the fact that only a minor part of nicotinamide is transformed to MNA by liver nicotinamide-N-methyltransferase upon direct intravascular administration, while the different magnitude of the response to nicotinic acid in cats vs rats may underline species differences known to mark the selective biological response to nicotinic acid (Declercq et al., 2005).

It is of note that in patients with peripheral artery disease the drugs with the nicotinic acid moiety such as β-pyridylcarbinol (Ronicol) or xanthinol nicotinate (Sadamin) exert their antiplatelet actions through the release of endothelial PGI2 (Dembinska-Kiec et al., 1983; Bieron et al., 1998), while nicotinic acid-induced flushing is mediated by a stimulation of the GPR109A receptor and the subsequent release of PGD2 and PGE2 from COX-1 (Benyo et al., 2005; Pike, 2005). It remains to be tested whether the MNA-induced release of PGI2 from COX-2 involves this vascular nicotinic acid-like receptor or other mechanisms.

There is overwhelming evidence that COX-2 derived PGI2 affords vasculoprotective, cardioprotective and anti-atherogenic activity (Gryglewski, 1980; Dowd et al., 2001; Grosser et al., 2006). The biological importance of the vascular COX-2/PGI2 pathway has recently been emphasized by the increased risk of myocardial infarction and stroke reported in patients treated with selective COX-2 inhibitors (Grosser et al., 2006). It is clear today that the long-term use of drugs known to inhibit COX and subsequently to depress PGI2 production proved to be harmful, while pharmacological stimulation of PGI2 in vivo with the use of MNA might be beneficial in vascular diseases. Indeed MNA, being a stable and non-toxic molecule, seems to be a good candidate for a drug to boost the endogenous COX-2/PGI2 pathway. So far, PGI2 or its stable analogues have been widely used in the treatment of pulmonary hypertension (Wise and Jones, 1996) and have been proven effective in cases of peripheral arterial disease (Gryglewski, 1980) or liver injury (Ohta et al., 2005). It will be important to test the therapeutic effectiveness of MNA.

It is important to note that in our experiments, MNA afforded anti-thrombotic action, not only in normotensive rats, but also in rats with renovascular hypertension (2K-1C hypertension). Hypertension is one of the most important risk factors of arterial thrombosis and its clinical consequences such as acute coronary syndrome or ischaemic stroke. Therefore studying thrombosis in hypertensive rats more closely resembles a clinically relevant situation. In various cardiovascular pathologies, including hypertension, endothelial dysfunction develops that is characterized by an impaired production of NO, an impairment of basal PGI2 production (Gryglewski, 1980; Frein et al., 2005) and a compensatory increase in PGI2 formation by COX-2 (FitzGerald et al., 2000). Our results suggest that in the setting of impaired NO-dependent function, the COX-2/PGI2 pathway is able to be stimulated pharmacologically with MNA. These findings have important therapeutic implications.

Finally, the demonstration of biological activity of MNA may bring a new understanding of the mechanism of the pharmacological activities of nicotinamide. Indeed, the anti-diabetic, neuroprotective (Satoh et al., 1999; Gosteli, 2005) as well as anti-inflammatory action of nicotinamide, at least in part, may be mediated by a MNA-COX-2/PGI2 pathway, as outlined here.

Summing up, we demonstrate here—to our knowledge for the first time—the novel biological activity of MNA in vivo that greatly surpasses that of closely related compounds. MNA appears as an anti-thrombotic agent that limits platelet-dependent experimental thrombosis by a mechanism dependent on the COX-2/PGI2 pathway. Although our study focused on exogenously applied MNA, our results could imply that endogenous MNA formed in the liver by nicotinamide N-methyltrasferase is an endogenous activator of the COX-2/PGI2 pathway and may play an important regulatory role in limiting thrombosis, as well as inflammatory processes in the cardiovascular system. Our findings of novel in vivo biological activity of MNA may have potentially important physiological, biochemical as well as therapeutic implications and warrant further studies.


Edited by blood, 01 November 2013 - 04:04 AM.


#20 blood

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Posted 01 November 2013 - 06:04 AM

Link: http://www.food.gov....a/pdfs/1mna.pdf

APPLICATION FOR THE APPROVAL OF
1- METHYLNICOTINAMIDE CHLORIDE (1 - MNA)
AS A NOVEL FOOD INGREDIENT FOR USE IN THE MANUFACTURE OF FOOD SUPPLEMENTS PURSUANT TO EU NOVEL FOODS REGULATION (EC) 258/97






2. EXECUTIVE SUMMARY
Introduction of synthetic 1-Methylnicotinamide (1-MNA) on the market as a novel food ingredient in the EU as a physiologically active ingredient in food supplements is proposed by Pharmena S.A.

1-MNA is a vitamin-based substance which is formed in the body from vitamin PP, as a result of the nicotinamide N-methyltransferase activity and then it is metabolized to the corresponding pyridines. 1-MNA is present naturally in human body as a normal product of niacin metabolism. It is excreted from the body in urine.




1-MNA is intended for consumption in the form of a powder in several different final formats (gelatine capsules, tablets and possible other). It is supposed to be consumed as dietary supplement, either in a short-term or in a prolonged manner. Proposed use levels 125 mg/single dose and 250 mg/day.

It is expected that the product would be consumed by adult population and elderly people. The final product containing 1-MNA will be designated to maintain circulatory system health because this substance protects normal function of endothelium, lowers risk of vascular impairment induced by postprandial hypertriglyceridemia and stimulates endothelium-dependent repair response or/and organ protection. Positive effect may be expected also in different situations with involvement of endothelial vasoprotective mechanisms not related to cardiovascular system. 1- MNA is already used topically in cosmetology as an anti-irritation component and also as compound which stimulates the processes of repair and regeneration of skin.

Pharmacokinetic studies performed in animal and human models are discussed in details in the dossier. Toxicity of 1-MNA was studied in several animal studies assessing acute toxicity after oral administration, acute skin and eye irritation, allergenic effects on skin, subacute toxicity and genotoxicity (including OECD471 and OECD487 tests). 1-MNA has demonstrated very low toxicity in mice and rats models at doses exceeding those expected to be used in humans. Based on 28- day toxicity study in rats the dose of 1000 mg/kg/day 1-MNA can be considered a no-observed- adverse-effect level (NOAEL) following 1-MNA oral administration. Safety and efficacy aspects of 1-MNA were also studied in randomized placebo-controlled double-blind trial (phase II) in humans.



#21 albedo

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Posted 02 November 2013 - 08:12 PM

With reference to the reactive oxygen species in the article, I find the all "antioxidants" area complex and full of diverging opinions. Even Aubrey de Grey mentions the issue of attacking the problem where it matters most (mitochondria) and the failure of general "souped-up" approaches (I recollected this from his book "Ending Age", which I heartily recommend, and I could find one page (38/39) extract HERE). He even mentions the necessity of free-radicals.

#22 Heh

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Posted 05 November 2013 - 11:03 AM

Yea, I think niacin is good for this. You can also read the Abram Hoffer research. You should take niacin with equal amounts (or more) vitamin C, and an amount of vitamin B5 equal to 1/3rd the dosage of niacin (or more).


Yea, I think niacin is good for this. You can also read the Abram Hoffer research. You should take niacin with equal amounts (or more) vitamin C, and an amount of vitamin B5 equal to 1/3rd the dosage of niacin (or more).


What's the rationale for the C and B5?

At higher dosages (regular) niacin can cause liver damage. You take the right ratio of vitamin C and vitamin B5 to prevent that problem. It also does other things, but I don't remember what.

Why are my posts being downvoted again? Abram Hoffer mentions life extension in addition to his main topic. And anyway, at higher doses (regular) niacin raises liver enzymes, which is the reason for the B5 and vitamin C. If the raised enzymes goes unchecked, then they could become the liver damage they normally represent.

http://www.ncbi.nlm....les/PMC2874142/ says, "The appetite-stimulating effect of nicotinamide appears to involve oxidative stress," so maybe your problem is being experienced exactly because you aren't supplementing with vitamin C and vitamin B5. Also, (regular) niacin raises blood sugar, but that's only temporary, and goes away as you keep taking the supplement.

Edited by Joel, 05 November 2013 - 11:44 AM.

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#23 ta5

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Posted 07 December 2013 - 04:56 PM

A new study:

J Appl Physiol (1985). 2013 Dec 5. [Epub ahead of print]

Vascular Endothelial Function and Oxidative Stress are Related to Dietary Niacin Intake Among Healthy Middle-Aged and Older Adults.

Kaplon RE, Gano LB, Seals DR. University of Colorado.

Abstract
We tested the hypothesis that vascular endothelial function and oxidative stress are related to dietary niacin intake among healthy middle-aged and older adults. In 127 men and women aged 48-77 years, brachial artery flow-mediated dilation (FMD) was positively related to dietary niacin intake (%Δ: r=0.20, P<0.05; mmΔ: r=0.25, P<0.01). In subjects with above-average dietary niacin intake (≥22mg/day, NHANES III), FMD was 25% greater than in subjects with below-average intake (P<0.05). Stepwise linear regression revealed that dietary niacin intake (above- vs. below-average) was an independent predictor of FMD (%Δ: β=1.8; mmΔ: β=0.05, both P<0.05). Plasma oxidized low-density lipoprotein, a marker of systemic oxidative stress, was inversely related to niacin intake (r=-0.23, P<0.05) and was lower in subjects with above- vs. below-average niacin intake (48±2 vs. 57±2 mg/dL, P<0.01). Intravenous infusion of the antioxidant vitamin C improved brachial FMD in subjects with below-average niacin intake (P<0.001, n=33), but not above-average (P>0.05, n=20). In endothelial cells sampled from the brachial artery of a subgroup, dietary niacin intake was inversely related to nitrotyrosine, a marker of peroxynitrite-mediated oxidative damage (r=-0.30, P<0.05, n=55), and expression of the pro-oxidant enzyme, NADPH oxidase (r=-0.44, p<0.01, n=37), and these markers were lower in subjects with above- vs. below-average niacin intake (nitrotyrosine: 0.39±0.05 vs. 0.56±0.07; NADPH oxidase: 0.38±0.05 vs. 0.53±0.05 [ratio to HUVEC control], both P<0.05). Our findings support the hypothesis that higher dietary niacin intake is associated with greater vascular endothelial function related to lower systemic and vascular oxidative stress among healthy middle-aged and older adults.
PMID: 24311750


Edited by ta5, 07 December 2013 - 04:57 PM.






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