• Log in with Facebook Log in with Twitter Log In with Google      Sign In    
  • Create Account
  LongeCity
              Advocacy & Research for Unlimited Lifespans

Photo
* * * * * 11 votes

David Sinclair strikes again

aging aging theories david sinclair mitochondria nad sinclair niagen nmn nicotinamide riboside

  • Please log in to reply
529 replies to this topic

#211 mikeinnaples

  • Guest
  • 1,907 posts
  • 296
  • Location:Florida

Posted 13 March 2014 - 03:54 PM

Have you considered giving her C60 in olive oil?

Slightly off topic and can be moved if there is enough interest, but does anyone have an opinion on how Niagen might affect a 17 year old dog and what the dosage might be for a body weight of 16 lbs?

Her deterioration is becoming more rapid and due to her advanced age I'm looking for a slightly more aggressive approach than my own dose of 250mg every morning. She's also currently on C60 so it's something to take into account.

Thanks in advance!


The answer to your question in bold.
  • like x 1
  • dislike x 1

#212 APBT

  • Guest
  • 906 posts
  • 389

Posted 13 March 2014 - 09:43 PM

Food sources of anthocyanins, in addition to those listed in previous posts:

http://en.wikipedia....iki/Anthocyanin

Plants rich in anthocyanins are Vaccinium species, such as blueberry, cranberry, and bilberry; Rubus berries, including black raspberry, red raspberry, and blackberry; blackcurrant, cherry, eggplant peel, black rice, Concord grape, muscadine grape, red cabbage, and violet petals. Anthocyanins are less abundant in banana, asparagus, pea, fennel, pear, and potato, and may be totally absent in certain cultivars of green gooseberries.[8] Red-fleshed peaches are rich in anthocyanins.[13]

The highest recorded amount appears to be specifically in the seed coat of black soybean (Glycine max L. Merr.) containing some 2,000 mg per 100 g[14] and in skins and pulp of black chokeberry (Aronia melanocarpa L.) (table). However, the Amazonian palmberry, a�a�, having about 320 mg per 100 g[15] of which cyanidin-3-glucoside is the most prevalent individual anthocyanin (approximately 10 mg per 100 g),[16] is also a high-content source for which only a small fraction of total anthocyanins has been determined to date. Due to critical differences in sample origin, preparation and extraction methods determining anthocyanin content,[17][18] the values presented in the adjoining table are not directly comparable.

Nature, traditional agriculture, and plant breeding have produced various uncommon crops containing anthocyanins, including blue- or red-flesh potatoes and purple or red broccoli, cabbage, cauliflower, carrots, and corn. Tomatoes have been bred conventionally for high anthocyanin content by crossing wild relatives with the common tomato to transfer a gene called the anthocyanin fruit tomato (aft) gene into a larger and more palatable fruit.[19]

Tomatoes have also been genetically modified with transcription factors from snapdragons to produce high levels of anthocyanins in the fruits.[20][21][22] Anthocyanins can also be found in naturally ripened olives,[23][24] and are partly responsible for the red and purple colors of some olives.[23]
  • dislike x 1
  • like x 1

sponsored ad

  • Advert
Click HERE to rent this advertising spot for SUPPLEMENTS (in thread) to support LongeCity (this will replace the google ad above).

#213 PWAIN

  • Topic Starter
  • Guest
  • 1,288 posts
  • 241
  • Location:Melbourne

Posted 13 March 2014 - 10:12 PM

The answer to your question in bold.

Doh!! :)

#214 APBT

  • Guest
  • 906 posts
  • 389

Posted 13 March 2014 - 10:50 PM

Earlier in the thread, tryptophan was mentioned as a potential means of increasing NAD concentrations. Any thoughts on this? Dosage?
See figure 2 on page 4: http://jcb.rupress.o...2/205.full.pdfhtml
  • dislike x 1
  • like x 1

#215 Ukko

  • Guest
  • 190 posts
  • 47
  • Location:In the Multiverse

Posted 14 March 2014 - 02:26 AM

Earlier in the thread, tryptophan was mentioned as a potential means of increasing NAD concentrations. Any thoughts on this? Dosage?
See figure 2 on page 4: http://jcb.rupress.o...2/205.full.pdfhtml


Well, that pathway is phenomenally inefficient. Like 60mg of tryptophan yielding a mere 1mg of NAD+. And a metabolite along the path is quinolinic acid, a notorious excitotoxin and NMDA receptor agonist. No simple thing. And a strong anti-nootropic.

'Toxicity[edit]

Quinolinic acid is an excitotoxin in the CNS. It reaches pathological levels in response to inflammation in the brain, which activates resident microglia and macrophages. High levels of quinolinic acid can lead to hindered neuronal function or even apoptotic death.[9] Quinolinic acid produces its toxic effect through several mechanisms, primarily as its function as an NMDA receptor agonist, which triggers a chain of deleterious effects, but also through lipid peroxidation, and cytoskeletal destabilization.[9] The gliotoxic effects of quinolinic acid further amplify the inflammatory response. Quinolinic acid affects neurons located mainly in the hippocampus, striatum, and neocortex, due to the selectivity toward quinolinic acid by the specific NMDA receptors residing in those regions.[9]

When inflammation occurs, quinolinic acid is produced in excessive levels through the kynurenine pathway. This leads to over excitation of the NMDA receptor, which results in an influx of Ca2+ into the neuron. High levels of Ca2+ in the neuron trigger an activation of destructive enzymatic pathways including protein kinases, phospholipases, NO synthase, and proteases.[12] These enzymes will degenerate crucial proteins in the cell and increase NO levels, leading to an apoptotic response by the cell, which results in cell death.

In normal cell conditions, astrocytes in the neuron will provide a glutamate-glutamine cycle, which results in reuptake of glutamate from the synapse into the pre-synaptic cell to be recycled, keeping glutamate from accumulating to lethal levels inside the synapse. At high concentrations, quinolinic acid inhibits glutamine synthetase, a critical enzyme in the glutamate-glutamine cycle. In addition, It can also promote glutamate release and block its reuptake by astrocytes. All three of these actions result in increased levels of glutamate activity that could be neurotoxic.[9]

This results in a loss of function of the cycle, and results in an accumulation of glutamate. This glutamate further stimulates the NMDA receptors, thus acting synergistically with quinolinic acid to increase its neurotoxic effect by increasing the levels of glutamate, as well as inhibiting its uptake. In this way, quinolinic acid self-potentiates its own toxicity.[9] Furthermore, quinolinic acid results in changes of the biochemistry and structure of the astrocytes themselves, resulting in an apoptotic response. A loss of astrocytes results in a pro-inflammatory effect, further increasing the initial inflammatory response which initiates quinolinic acid production.[9]

Quinolinic acid can also exert neurotoxicity through lipid peroxidation, as a result of its pro-oxidant properties. Quinolinic acid can interact with Fe(II) to form a complex that induces a reactive oxygen and nitrogen species (ROS/RNS), notably the hydroxyl radical •OH. This free radical causes oxidative stress by further increasing glutamate release and inhibiting its reuptake, and results in the breakdown of DNA in addition to lipid peroxidation.[12] Quinolinic acid has also been noted to increase phosphorylation of proteins involved in cell structure, leading to destabilization of the cytoskeleton.[9]

Edited by Ukko, 14 March 2014 - 02:28 AM.

  • like x 1

#216 Ukko

  • Guest
  • 190 posts
  • 47
  • Location:In the Multiverse

Posted 14 March 2014 - 02:58 AM

Above I mentioned that melatonin is related to NAD. And melatonin is related to the circadian rhythm. It was known that metabolism and SIRT1 expression oscillates depending on the time of the day. And guess what causes that? Well it seems that it may be because NAD oscillates in a circadian rhythm. I say this all is highly impacted by sleep, light/darkness, melatonin etc. And probably supplemental NAD precursors are best taken in alignment with this rhythm. Same with CD38 blockers.

http://symposium.csh...tent/76/31.full

Edited by Ukko, 14 March 2014 - 02:59 AM.


#217 Ukko

  • Guest
  • 190 posts
  • 47
  • Location:In the Multiverse

Posted 14 March 2014 - 03:10 AM

See these too. For some reason I have already for a while been intuitively looking into melatonin/NAD+ and been wondering about how to time the NAD+ precursors and CD38 blockers I take. Turns out my intuition was right and I guess timing those wrong could even be counterproductive. You do not, repeat not, want to put your circadian clock out of sync.

Circadian Clock NAD+ Cycle Drives Mitochondrial Oxidative Metabolism in Mice

http://www.sciencema...42/6158/1243417

Circadian clock feedback cycle through NAMPT-mediated NAD+ biosynthesis

http://www.ncbi.nlm....pubmed/19299583

Rhythmic Respiration

https://www.sciencem...158/570.summary

Circadian Control of the NAD+ Salvage Pathway by CLOCK-SIRT1

http://www.sciencema...pe2=tf_ipsecsha

Edited by Ukko, 14 March 2014 - 03:15 AM.

  • like x 2

#218 Ukko

  • Guest
  • 190 posts
  • 47
  • Location:In the Multiverse

Posted 14 March 2014 - 03:17 AM

More. Exactly as I assumed, logical. Don't mess with NAD+ by timing your precursors or CD38 blockers wrong.

Altered behavioral and metabolic circadian rhythms in mice with disrupted NAD+ oscillation

http://www.ncbi.nlm....les/PMC3184980/

In a nutshell, messing up the circadian rhythm through wrongly timed NAD+ precursors or CD38 blockers can cause chronic fatigue, runaway metabolism and, for all us nootropic users ... drum roll...mess up your neurotransmitters. This all again reinforces, from yet another angle, that taking sustained release niacin and maybe also niacinamide is a dumb idea

"An intriguing speculation relates to the notion that amino acids and their metabolites can also function as neurotransmitters or their precursors. Glutamate, aspartate, glycine and γ-amino butyric acid (GABA) are neurotransmitters. Tryptophan is a precursor for serotonin, whereas tyrosine is a precursor for catecholamines, such as dopamine, epinephrine and norepinephrine. An imbalance in these amino acids can potentially change the concentration of certain neurotransmitters in the brain. Further studies will establish whether changes in these neurotransmitters are responsible for alterations in the rest/activity rhythms and locomotor activity in the CD38-null mice.
In conclusion, our results reveal a role for NAD+ homeostasis and SIRT1 activity in circadian regulation of behavioral and metabolic rhythms. Increased NAD+ levels and concomitant activation of SIRT1 might lead to reduction in several amino acids, which activates the AAR pathway in CD38-null mice. Our findings underscore the importance of circadian control in amino acid metabolism."

Edited by Ukko, 14 March 2014 - 03:26 AM.


#219 Kevnzworld

  • Guest
  • 885 posts
  • 306
  • Location:Los Angeles

Posted 14 March 2014 - 04:29 AM

More. Exactly as I assumed, logical. Don't mess with NAD+ by timing your precursors or CD38 blockers wrong.

Altered behavioral and metabolic circadian rhythms in mice with disrupted NAD+ oscillation


So what would be the best way to take NR, CD38 inhibitors? Niagen recommends taking NR in the morning. I take 3 in divided doses throughout the day, but before 6pm. I do take melatonin at night . I've reduced my Metformin dose by half given that it inhibits NAD. DHEA, which I also take upregulates NAD.
I think one can over think this. Everything we do and eat up regulates, expends or inhibits NAD.

#220 Ukko

  • Guest
  • 190 posts
  • 47
  • Location:In the Multiverse

Posted 14 March 2014 - 04:39 AM

More. Exactly as I assumed, logical. Don't mess with NAD+ by timing your precursors or CD38 blockers wrong.

Altered behavioral and metabolic circadian rhythms in mice with disrupted NAD+ oscillation


So what would be the best way to take NR, CD38 inhibitors? Niagen recommends taking NR in the morning. I take 3 in divided doses throughout the day, but before 6pm. I do take melatonin at night . I've reduced my Metformin dose by half given that it inhibits NAD. DHEA, which I also take upregulates NAD.
I think one can over think this. Everything we do and eat up regulates, expends or inhibits NAD.


Still looking into it, but the time between early afternoon and like 9pm seems best for eating in general. The ideal window for NAD precursor supplementation and CD38 blockers is likely from around noon to 6pm. Late at night is not good. First thing upon waking up seems bad also, though I know what the recommendation for Niagen is. Also, buffered forms of niacin seem like a dumb idea. Melatonin and DHeA seem good.

#221 hav

  • Guest
  • 1,089 posts
  • 219
  • Location:Cape Cod, MA
  • NO

Posted 14 March 2014 - 03:27 PM

More. Exactly as I assumed, logical. Don't mess with NAD+ by timing your precursors or CD38 blockers wrong.

Altered behavioral and metabolic circadian rhythms in mice with disrupted NAD+ oscillation

http://www.ncbi.nlm....les/PMC3184980/

In a nutshell, messing up the circadian rhythm through wrongly timed NAD+ precursors or CD38 blockers can cause chronic fatigue, runaway metabolism and, for all us nootropic users ... drum roll...mess up your neurotransmitters. This all again reinforces, from yet another angle, that taking sustained release niacin and maybe also niacinamide is a dumb idea


Sounds like its pretty easy to tell if supplementing with a CD38 blocker rises to the levels observed with CD38 knockout mice. Look how they behaved night and day compared to the normal WT mice:

Altered rest/activity rhythms in the CD38-null mice. While monitoring locomotor activity of the WT and CD38-KO mice, we noticed a marked difference in their rest/activity patterns. The WT mice displayed a significant break from activity during the middle of the night; however, CD38-null mice did not appear to take this break (Fig. 2C, area over the striped bar). Instead, CD38-KO mice appeared to take multiple breaks, randomly spread throughout the day. Quantitation of this difference in activity revealed that while WT mice decrease their locomotor activity significantly between ZT20 and ZT22, CD38-null mice maintained almost constant levels of activity throughout the night (Fig. 2D).


Makes me wonder if Thomas Edison lacked a CD38 gene.

Would not getting this effect suggest no NAD+ effect from a supplement? That would kind of be the converse of what this study showed.

Howard

#222 cudBwrong

  • Guest
  • 106 posts
  • 31
  • Location:New York

Posted 14 March 2014 - 05:05 PM

http://www.ncbi.nlm....les/PMC3184980/
Altered behavioral and metabolic circadian rhythms in mice with disrupted NAD+ oscillation

The title is a little misleading. Yes the oscillation was disrupted, but so were the absolute levels.
NAD+ was way up because these mice have no CD38 at all. You can live without it (the mice are viable,) but not well.

The goal is not to eliminate CD38 entirely but to downregulate it somewhat, especially in older people, to bring NAD+ back into balance. CD38 is there for a reason.

So I think the timing is less of an issue here. I don't say it's irrelevant, but it may just work itself out. The pathways are complex, and many components can be quite persistent. Results can take a long time to have their full effect. Take it one step at a time and be patient.

Edited by cudBwrong, 14 March 2014 - 05:10 PM.


#223 Ukko

  • Guest
  • 190 posts
  • 47
  • Location:In the Multiverse

Posted 14 March 2014 - 05:13 PM

http://www.ncbi.nlm....les/PMC3184980/
Altered behavioral and metabolic circadian rhythms in mice with disrupted NAD+ oscillation

The title is a little misleading. Yes the oscillation was disrupted, but so were the absolute levels.
NAD+ was way up because these mice have no CD38 at all. You can live without it (the mice are viable,) but not well.

The goal is not to eliminate CD38 entirely but to downregulate it somewhat, especially in older people, to bring NAD+ back into balance. CD38 is there for a reason.

So I think the timing is less of an issue here.


Agreed, but totally does seem to be the case that there are times of the day when NAD+ precursors and CD38 blockers would be supportive of the circadian metabolic rhythm and also a time when they would seem to risk disturbing it. And you really should not try to disturb it. Basically what I am saying is that you will likely get a far better bang for buck from your supplements by timing it right. Human species is ancient. Fighting evolution is a bad idea, cheating a little with supplementation in alignment with the natural circadian rhythm of the body is likely to work far better.


Makes me wonder if Thomas Edison lacked a CD38 gene.

Would not getting this effect suggest no NAD+ effect from a supplement? That would kind of be the converse of what this study showed.

Howard


Not at all. Timing NAD+ precursors and CD38 blockers right...likely mainly sometime right after noon...could actually not just support metabolism, but also be supportive of resetting the circadian rhythm of metabolism.

#224 to age or not to age

  • Guest
  • 151 posts
  • 93
  • Location:NY

Posted 14 March 2014 - 07:04 PM

This is slightly off topic but I am posting part 2 of my interview with Dr David Sinclair. David thinks
deeply about this subject, both on a scientific and societial level. The clip runs 4 minutes.
:
  • like x 4

#225 APBT

  • Guest
  • 906 posts
  • 389

Posted 15 March 2014 - 10:40 PM

Is the full David Sinclair paper from "Cell" available as a free download anywhere?

Edited by APBT, 15 March 2014 - 10:40 PM.


#226 APBT

  • Guest
  • 906 posts
  • 389

Posted 16 March 2014 - 12:13 AM

Present Knowledge in Nutrition:
http://books.google....iboside&f=false

#227 Kevnzworld

  • Guest
  • 885 posts
  • 306
  • Location:Los Angeles

Posted 16 March 2014 - 12:32 AM

Is the full David Sinclair paper from "Cell" available as a free download anywhere?


You can purchase it.
http://www.cell.com/...092867413015213

#228 trance

  • Guest
  • 335 posts
  • 112
  • Location:Dallas, Tx

Posted 16 March 2014 - 12:40 AM

Is the full David Sinclair paper from "Cell" available as a free download anywhere?


You can purchase it.
http://www.cell.com/...092867413015213



Here you go: http://www.cnd.mcgil...ng-compound.pdf
  • like x 4

#229 APBT

  • Guest
  • 906 posts
  • 389

Posted 16 March 2014 - 12:52 AM

Is the full David Sinclair paper from "Cell" available as a free download anywhere?


You can purchase it.
http://www.cell.com/...092867413015213



Here you go: http://www.cnd.mcgil...ng-compound.pdf

Many thanks, sir!

#230 1thoughtMaze1

  • Guest
  • 335 posts
  • -127
  • Location:Toronto

Posted 16 March 2014 - 04:55 AM

Hey guys sorry so what's the deal? Why are we not just supplementing with with NADH again?

What is the best way to increase NAD levels?

#231 1thoughtMaze1

  • Guest
  • 335 posts
  • -127
  • Location:Toronto

Posted 16 March 2014 - 05:14 AM

I mean, that is, in till we all fork out 475.

#232 Kevnzworld

  • Guest
  • 885 posts
  • 306
  • Location:Los Angeles

Posted 16 March 2014 - 05:32 PM

Hey guys sorry so what's the deal? Why are we not just supplementing with with NADH again?

What is the best way to increase NAD levels?


Nicotinamide Riboside
http://www.cell.com/...550413112001921
  • like x 1

#233 1thoughtMaze1

  • Guest
  • 335 posts
  • -127
  • Location:Toronto

Posted 16 March 2014 - 06:20 PM

Hey guys sorry so what's the deal? Why are we not just supplementing with with NADH again?

What is the best way to increase NAD levels?


Nicotinamide Riboside
http://www.cell.com/...550413112001921


shit on me,

got it.

Thanks world
  • dislike x 3

#234 Ukko

  • Guest
  • 190 posts
  • 47
  • Location:In the Multiverse

Posted 17 March 2014 - 01:36 AM

Just added 20g of L-Glutamine to my daily regimen after learning that it is more rate limiting than the substrate for the final step in NAD+ synthesis from nicotinic acid. Have always reacted great to the good old, glutamine.
"How could a deficiency in the Krebs cycle cause apoptosis? This cycle has two main functions: to supply NADH and FADH for oxidative phosphorylation by reducing FAD+ and NAD+ and to link multiple metabolic pathways (Fig. 9 B). Although we found that a deficiency in oxidative phosphorylation does not cause apoptosis in our system, a change in the mitochondrial NADH/NAD+ and FADH/FAD+ ratios, which we did not measure, could affect other processes, including regulation of gene transcription (for review see Ladurner, 2006) and mitochondrial permeability (Jonas et al., 2004). Therefore, glutamine might support cell viability not by providing biosynthetic precursors, but by enabling the Krebs cycle to function as a catalyst of redox reactions (Kovacevic, 1972; Baggetto, 1992). This hypothesis is consistent with the observation that only a few percent of consumed glutamine is used by proliferating cells for biosynthesis (Newsholme et al., 1985)."

#235 Ukko

  • Guest
  • 190 posts
  • 47
  • Location:In the Multiverse

Posted 17 March 2014 - 01:42 AM

My Medline intuition has been near,perfect lately . All intuited things backed by old science. Must be the higher NAD+ levels :) http://www.jbc.org/c.../33395.full.pdf
  • like x 1

#236 trance

  • Guest
  • 335 posts
  • 112
  • Location:Dallas, Tx

Posted 17 March 2014 - 02:39 AM

My Medline intuition has been near,perfect lately . All intuited things backed by old science. Must be the higher NAD+ levels :) http://www.jbc.org/c.../33395.full.pdf


Are you actually doing your sublingual administration correctly now by placing the NR powder -- without the capsule -- under your tongue (not between gum & teeth still in the capsule like you were) ?

http://www.ijppsjour...Suppl2/1092.pdf
  • like x 1

#237 Ukko

  • Guest
  • 190 posts
  • 47
  • Location:In the Multiverse

Posted 17 March 2014 - 04:12 AM

My Medline intuition has been near,perfect lately . All intuited things backed by old science. Must be the higher NAD+ levels :) http://www.jbc.org/c.../33395.full.pdf


Are you actually doing your sublingual administration correctly now by placing the NR powder -- without the capsule -- under your tongue (not between gum & teeth still in the capsule like you were) ?

http://www.ijppsjour...Suppl2/1092.pdf

Yes. Thanks for pointing that out earlier. This was also pretty interesting. Resveratrol boosts glutamine synthetase which boosts glutamine which boosts NAD+.
http://www.ncbi.nlm....pubmed/16904623
  • like x 2

#238 to age or not to age

  • Guest
  • 151 posts
  • 93
  • Location:NY

Posted 17 March 2014 - 04:02 PM

I will publish an excerpt from my video taped interview (conducted on January 22, 2014) with Dr. Leonard Guarente
at MIT. In it, he explains that both NMN and NR raise NAD levels, either of these will do the job; they don't have
to be taken together. The effect of taking them with resveratrol is greater than additive, rather, it is multiplied. This
is new research and certain things are still being worked out this year. Could negative information come out?
Possibly, but it's looking good.
  • like x 1

#239 APBT

  • Guest
  • 906 posts
  • 389

Posted 17 March 2014 - 09:38 PM

http://www.buy-nicot...e-riboside.com/


Summary:

Preliminary evidence suggests Nicotinamide mononucleotide (NMN) help reverse one important aspect of aging by raising cellular NAD+ levels. Low levels of NAD+ seem to trigger a cascade a processes which lock our cells into a suboptimal state, "psuedohypoxia". Increasing NAD+ levels seems to reverse this suboptimal function, thereby leading to more youthful cellular function. [1]

The NAD+ Theory of Aging:

The decline in mitochondrial function has long been thought to play a critical role in aging. The cause of this malfunction is still a matter of debate and exploration. But one new prominent hypothesis is the decline is caused by impaired mitochondrial regulation brought about by impaired sirt1 expression. Sirt1 expression has been implicated as a major contributor to the beneficial effects of calorie restriction on longevity. [2] Deliberate over-expression of Sirt1 seems to have protective effects [3]

Sirt1 however, is an NAD+ dependent deacetylase, which means that the age-related decline of NAD+ levels can actually inhibit its activity. Since Sirt1 expression seems to be a protective factor in aging, inadequate NAD+ levels would be expected to accelerate aging.




Interestingly, in a recent study overseen by David Sinclair at Harvard University, supplementing NAD+ levels in mice with Nicotinamide mononucleotide (NMN) was shown to reverse a number of important bio-markers of aging. In aged mice supplemented with the NAD+ precursor, the accumulation of HIF-1alpha, lactate levels and markers of muscle wasting were reversed, while increasing ATP levels, COX activity, and mitochondrially encoded OXPHOS transcripts. An apparent reversal of age-related "pseudohypoxia".[1]

Practical Enhancement of NAD+ levels:

In the recent study by David Sinclair's Lab, nicotinamide mononucleotide was used to increase NAD+ levels in mice. Unfortunately, nicotinamide mononucleotide (NMN) may cost close to $1800 per gram for the foreseeable future.

There is good news however, nicotinamide mononucleotide (NMN) doesn't seem to be the only bio-available NAD+ precursor. Nicotinamide riboside is another bio-available precursor to both nicotinamide mononucleotide (NMN) and NAD+ and is therefore very likely to have the similar benefits while also not being extremely expensive and not requiring intravenous administration. [4] Also, and very importantly, nicotinamide riboside has already been shown to have similar effects through raising sirt1 and sirt3 expression in mammals, [4] unlike plain nicotinamide which has been shown to suppress sirt1. [5] Extrapolation from animal studies yields a human equivalent of 52 mg/kg or a dose of about 3.5 grams per day for one week for a 70kg individual.








<img src="http://static.square...AD decline.png" alt="NAD decline.png" />

Edited by APBT, 17 March 2014 - 10:00 PM.

  • like x 1

sponsored ad

  • Advert
Click HERE to rent this advertising spot for SUPPLEMENTS (in thread) to support LongeCity (this will replace the google ad above).

#240 APBT

  • Guest
  • 906 posts
  • 389

Posted 17 March 2014 - 09:43 PM

NMN: Nicotinamide Mononucleotide Lowers Blood Glucose in Mice
http://www.decodedsc...se-in-mice/3616





Also tagged with one or more of these keywords: aging, aging theories, david sinclair, mitochondria, nad, sinclair, niagen, nmn, nicotinamide riboside

2 user(s) are reading this topic

0 members, 2 guests, 0 anonymous users