2255 replies to this topic

[sthira]

I can honestly say I get lost in translation ...

...I am taking Basis at the moment and I started to take the r-lipoic acid but not fully understanding...

...so what would also mix with Basis?...

...Excuse my ignorance as I am slowly trying to understand all this.

The head-banger reality is: we're all trying to understand, we're all lost in translation, we're aging with cluelessness about how to slow aging, and I dislike seeing these stock-holder companies take advantage of innocence, of sickness, of unsolved ravages of aging, and selling promises at inflated costs. So if you want to chase the Basis pigeon (and who here doesn't want to reverse aging, who knows if the NR/pterostilbene combo does any longterm good for people) save your money, and buy the individual components most likely to encourage your belief placebo.

Or, as someone here is fond of repeating: hurry up and take it before it stops working.

I'm just glad the big picture is slowly dawning on some?

You mean longevity-seeking folks are finally recognizing the benefits of calorie restriction and fasting (which are free to everyone) and as close for now as anything we've got for slowing aging?

https://www.scienced...60614155722.htm

"The future of our research...

...We are also investigating the mechanisms...

"While further studies are needed, Dr. Chini believes..."

Edited by sthira, 16 June 2016 - 03:17 PM.

[normalizing]

so can i finally know after asking this for several pages in this thread, where do you guys buy your honokiol

 

 

http://www.swansonvi...-mg-30-veg-caps

Edited by Bryan_S, 16 June 2016 - 07:34 PM.
added link

[sthira]

so can i finally know after asking this for several pages in this thread, where do you guys buy your honokiol

https://www.amazon.c...onokiol extract

Edited by sthira, 16 June 2016 - 03:15 PM.

[normalizing]

just as i thought. no specifications for % honokiol. might as well brew the actual bark and believe you get any honokiol at all

[sthira]

just as i thought. no specifications for % honokiol. might as well brew the actual bark and believe you get any honokiol at all

Yep: blind faith.

[Harkijn]

https://www.scienced...60614155722.htm

"The future of our research will be to develop compounds that can inhibit the function of CD38 to increase NAD levels during aging," says Dr. Chini. "We are also investigating the mechanisms that lead to the increase in CD38 during the aging process."

 

 

Apparently, the jury is still out on whether it's useful to inhibit CD38 or not, or to some extend. There is the CD38 in inflammatory cells but also the CD38 that is essential for the production of oxytocin in the brain. Very confusing indeed.

Perhaps an important question is: why does CD38 use NAD so inefficiently? The study I linked in post #649 says that CD38 uses 100 NAD molecules to produce 1 cADPR.  Can this be influenced, perhaps by polyphenols?

 

 

Edited by harkijn, 16 June 2016 - 03:31 PM.

[Nate-2004]

Is honokiol being put forward as a CD38 inhibitor or something that's merely anti inflammatory? 

 

Sthira, I buy mine from Swanson, as they're the main distributor at the moment. I'd rather get it from a more reputable source if I could. It's fairly cheap though compared to most supplements, the only thing is the shipping cost which you'll have to make up for by buying several bottles.

 

Here it is:

 

 

See that big fat circle normalizing?....

[Ethic]

 

so can i finally know after asking this for several pages in this thread, where do you guys buy your honokiol

https://www.amazon.c...onokiol extract

 

 

 

That is no extract btw

 

 

just as i thought. no specifications for % honokiol. might as well brew the actual bark and believe you get any honokiol at all

 

 

search for "standardised magnolia bark" in google and you will find promising products ...

Edited by Ethic, 16 June 2016 - 03:38 PM.

[Hebbeh]

https://www.scienced...60614155722.htm

"The future of our research will be to develop compounds that can inhibit the function of CD38 to increase NAD levels during aging," says Dr. Chini. "We are also investigating the mechanisms that lead to the increase in CD38 during the aging process."

Apparently, the jury is still out on whether it's useful to inhibit CD38 or not, or to some extend. There is the CD38 in inflammatory cells but also the CD38 that is essential for the production of oxytocin in the brain. Very confusing indeed.
Perhaps an important question is: why does CD38 use NAD so inefficiently? The study I linked in post #649 says that CD38 uses 100 NAD molecules to produce 1 cADPR. Can this be influenced, perhaps by polyphenols?

Inhibiting CD38 doesn't mean we have to inhibit it into oblivion (not that would be even possible) but simply to the point of more youthful levels. Many of us do similar with other biological pathways already. I doubt the CD38 inhibitors already available will have any risk of inhibition to the point of levels lower than the minimum required.... I doubt they have that strength and our biology is too smart for that...it will seek homeostasis. Anyway researchers far more informed than most of us are leaning that way already.

[Nate-2004]

 

 

https://www.scienced...60614155722.htm

"The future of our research will be to develop compounds that can inhibit the function of CD38 to increase NAD levels during aging," says Dr. Chini. "We are also investigating the mechanisms that lead to the increase in CD38 during the aging process."

Apparently, the jury is still out on whether it's useful to inhibit CD38 or not, or to some extend. There is the CD38 in inflammatory cells but also the CD38 that is essential for the production of oxytocin in the brain. Very confusing indeed.
Perhaps an important question is: why does CD38 use NAD so inefficiently? The study I linked in post #649 says that CD38 uses 100 NAD molecules to produce 1 cADPR. Can this be influenced, perhaps by polyphenols?

Inhibiting CD38 doesn't mean we have to inhibit it into oblivion (not that would be even possible) but simply to the point of more youthful levels. Many of us do similar with other biological pathways already. I doubt the CD38 inhibitors already available will have any risk of inhibition to the point of levels lower than the minimum required.... I doubt they have that strength and our biology is too smart for that...it will seek homeostasis. Anyway researchers far more informed than most of us are leaning that way already.

 

 

The main problem is that CD38 levels rise considerably as NAD falls. I'm not sure to what degree something like apigenin inhibits the production of CD38 or to what degree it is lowered, but I doubt it results in total loss of CD38. It'd be nice if it were returned to the levels of a 25 year old.

[midas]

just as i thought. no specifications for % honokiol. might as well brew the actual bark and believe you get any honokiol at all

 

He/she linked the wrong one....90%

 

Standardized to minimum 90% honokiol

 

http://www.swansonvi...-mg-30-veg-caps

[sthira]

just as i thought. no specifications for % honokiol. might as well brew the actual bark and believe you get any honokiol at all

He/she linked the wrong one....90%

Standardized to minimum 90% honokiol

http://www.swansonvi...-mg-30-veg-caps

Thank you're right! Maybe that's why I've not had much effect from it. I'll try this one instead. Hope springs eternal, as they say, haha

[Bryan_S]

Flavonoid apigenin is an inhibitor of the NAD+ ase CD38: implications for cellular NAD+ metabolism, protein acetylation, and treatment of metabolic syndrome.

http://www.ncbi.nlm....pubmed/23172919

 

DARZALEX® (daratumumab) Approved by U.S. FDA: First Human Anti-CD38 Monoclonal Antibody Available for the Treatment of Multiple Myeloma

http://www.jnj.com/n...ultiple-Myeloma

 

Guys I'm not sure we want to kill the messenger. (signaling protein) While it is the single best candidate so far, nothing is understood about the mechanisms pushing CD38's levels higher. Listed above are 2 ways to go about reducing levels however inhibitors and antibodies treatments are difficult approaches long term. We still don't understand the upstream mechanism generating the increased levels. If we can understand that and address that we can reduce its production with the least number of consequences.

 

So being that this paper was just released and its such a pivotal insight lets see where this goes.

 

CD38 Dictates Age-Related NAD Decline and Mitochondrial Dysfunction through an SIRT3-Dependent Mechanism

http://www.cell.com/...4131(16)30224-8

 

Why NAD+ Declines during Aging: It’s Destroyed

http://www.cell.com/...4131(16)30244-3

 

So its one thing to discuss inhibiting it but as I read more CD38 is an important signaling protein and there could be consequences in crippling it, so let's keep reading and see where the research leads.

Edited by Bryan_S, 17 June 2016 - 07:31 AM.
Caution added

[stefan_001]

 

 

What we want is not to decrease CD38 or PARPs directly but via safer way: using anti inflammatory pathway and targeting TNFa like seems to also does the apigenin for instance. It also block p53 means will also increase PGC1a..  The indirect pathway is the solution. The question is then not if it inhibits CD38, but more how strong it will calm dalm the root of the inflammatory pathway.

 

@hebbeh, thank you also for the research. However I would like we look deeper into it since for instance quercetin was shown to decrease SIRT1 activity unlike pterostilnene or resveratrol : http://www.pterostil...irt1-activator/

 

I agree to this view, tamping down inflamation seems a smart thing to do. Personally I would not risk directly inhibiting CD38. A polyphenol cocktail may make sense.

 

I can honestly say I get lost in translation about a lot of what you, Bryan and Tom talk about at times; which is to say I am only understanding the peripheral at best. That being said though, what would (in your mind) be a good polyphenol cocktail. I am taking Basis at the moment and I started to take the r-lipoic acid but not fully understanding everything (even after my own research) and because of partial negative remarks herein I opted not to take it anymore, so what would also mix with Basis? Honokiol? (we that be part of your polyphenol coctail?)

 

Excuse my ignorance as I am slowly trying to understand all this.

 

Thank you.

 

 

There are a lot of them, flavonols, stilbenoids, curcuminoids, anthocyanins and most of them show anti-oxidant and anti -inflamation behavior as well as many other effects e.g. induce SIRTx's. Some of those are overlapping but also research suggest that each may have specific attributes of action. You already take basis which includes pterostilbene which is a stilbenoid others polyphenols often used are quercetin, honokiol, fisetin well and many more actually (just look at the topics in this forum). I dont think there is a silver bullet substance out there so that why I said cocktail or perhaps cycling. Honokiol is mentioned because of its SIRT3 activation and research indicating anti-cancer and prostate health. I have recommended it to my mom because of its inflamation dampening effect for osteoathritis.

 

 

[Logic]

 

I'm just glad the big picture is slowly dawning on some?

You mean longevity-seeking folks are finally recognizing the benefits of calorie restriction and fasting (which are free to everyone) and as close for now as anything we've got for slowing aging?

 

No; I mean what I said: Find the causes for inflammation and increased NF-kB etc and take steps to slow, stop and, in some cases, even reverse them.

Fasting is good, but there are plenty of accessible means to achieving the above without too much of it.
One has to live life too and when wine woman and song become too much for me I intend giving up singing!  

Some links here:
http://www.longecity...ndpost&p=775570

 

I think a group buy of some exotic chelators is in order!?

Edited by Logic, 16 June 2016 - 09:28 PM.

[normalizing]

Is honokiol being put forward as a CD38 inhibitor or something that's merely anti inflammatory? 

 

Sthira, I buy mine from Swanson, as they're the main distributor at the moment. I'd rather get it from a more reputable source if I could. It's fairly cheap though compared to most supplements, the only thing is the shipping cost which you'll have to make up for by buying several bottles.

 

Here it is:

 

 

See that big fat circle normalizing?....

 

 

oh yes but of course! he just urled me to some decoy trying to make a fool of me! ok listen nate, what do you feel from taking that one because i read it can help anxiety, does it help and have any sedative effect or no??
 

[Heisok]

At the risk of being thumbed down, this thread has died for me. Too much B.S. to wade through. I am sorry to add to it with this post.

 

Please delete some of the extra stuff including my post. If only for the less initiated to have a useful path to what could be great information. Semi abusive childish posts. Moderators please?

Edited by Heisok, 16 June 2016 - 11:10 PM.

[Black Fox]

Dear all,

it's looking some of us are getting carried away. I got limited knowledge in the field but after all my lurking/reading/ studying about it I got to one conclusion. All the published papers outthere, they agree one thing ...... Calorie Restriction increases life span.

It looks we are genetically engineered to pass down our DNA, die and let Darwin decides which ones are the fittest to survive, but when it comes to CR is like an employee stepping up to his big boss and making him come around.

Listen pal! We are going through a rough season, forget about reproducing and let's keep me fit for later till abundance gets back along with the right mate. Big boss listens upregulating these beautiful amigos called Sirtuins... So why on earth would we want to inhibit CD38 with quercetin and/or apigenin which are proven to silence SIRT1? It's like shooting yourself in the foot!!

NR+Ptero / resveratrol looks to me the right path, my will ain't strong enough to fast and I dunno if it'll extend my life but it'll definitely seem like it :P

It seems we know very little about CD38,..... What about upregulating its performance so we don't need a many of them and therefore the NAD consumption is lower and the job is done more efficiently ?in other words bringing it to younger levels. If Cd38 finally is responsible to metabolize NMN....if we are able to deliver more NMN with NR... It'll be definitely more than bueno!!

Sure thing , reducing inflammation , ROS, AGE's would help but we were exposed to those when we were kids and we still manage to grow and not to age ....

It's not about what we believe it's about what we know....

More studies are needed

[sthira]

he just urled me to some decoy trying to make a fool of me!

No! Haha, I'm sorry you feel that way, sir, I totally was not trying to make anyone look like a fool. I did not know about this extract because Amazon doesn't sell it, and I was too much of a ditz to look elsewhere. Making fools of people isn't in my nature, and I'm sorry you interpreted it that way!

I'll order this extract and see if it helps with my own deep anxiety issues. I suspect it wont do much of anything, though, because anxiety is a serious issue for me and so far nothing has worked for it except unconscious sleep.

[midas]

 

he just urled me to some decoy trying to make a fool of me!

I'll order this extract and see if it helps with my own deep anxiety issues. I suspect it wont do much of anything, though, because anxiety is a serious issue for me and so far nothing has worked for it except unconscious sleep.

 

 

I'm sorry to hear that, good luck finding something that helps..

[Yajerman]

 

 

 

What we want is not to decrease CD38 or PARPs directly but via safer way: using anti inflammatory pathway and targeting TNFa like seems to also does the apigenin for instance. It also block p53 means will also increase PGC1a..  The indirect pathway is the solution. The question is then not if it inhibits CD38, but more how strong it will calm dalm the root of the inflammatory pathway.

 

@hebbeh, thank you also for the research. However I would like we look deeper into it since for instance quercetin was shown to decrease SIRT1 activity unlike pterostilnene or resveratrol : http://www.pterostil...irt1-activator/

 

I agree to this view, tamping down inflamation seems a smart thing to do. Personally I would not risk directly inhibiting CD38. A polyphenol cocktail may make sense.

 

I can honestly say I get lost in translation about a lot of what you, Bryan and Tom talk about at times; which is to say I am only understanding the peripheral at best. That being said though, what would (in your mind) be a good polyphenol cocktail. I am taking Basis at the moment and I started to take the r-lipoic acid but not fully understanding everything (even after my own research) and because of partial negative remarks herein I opted not to take it anymore, so what would also mix with Basis? Honokiol? (we that be part of your polyphenol coctail?)

 

Excuse my ignorance as I am slowly trying to understand all this.

 

Thank you.

 

 

There are a lot of them, flavonols, stilbenoids, curcuminoids, anthocyanins and most of them show anti-oxidant and anti -inflamation behavior as well as many other effects e.g. induce SIRTx's. Some of those are overlapping but also research suggest that each may have specific attributes of action. You already take basis which includes pterostilbene which is a stilbenoid others polyphenols often used are quercetin, honokiol, fisetin well and many more actually (just look at the topics in this forum). I dont think there is a silver bullet substance out there so that why I said cocktail or perhaps cycling. Honokiol is mentioned because of its SIRT3 activation and research indicating anti-cancer and prostate health. I have recommended it to my mom because of its inflamation dampening effect for osteoathritis.

 

Thank you for the well thought response. I think i'll graph out the above term(s) and see where that takes me. I am pretty sure I am going to be taking Honokoil with my NR, im just going to see what other things I can use that have a direct benefit and perhaps a beneficial byproduct. 

[Bryan_S]

The resurgence of NAD+

Leonard Guarente

Science  17 Jun 2016:

http://science.scien...t/352/6292/1396

 

Summary

 

Interventions that can slow mammalian aging have been rare. On pages 1436 and 1474 of this issue, Zhang et al. (1) and Cambronne et al. (2), respectively, highlight nicotinamide adenine dinucleotide (NAD+) as a major intervention point to slow or ameliorate phenotypes of aging.

 

Restorative intervention.

In old mice, aging may trigger NAD+ loss by activating poly(ADP-ribose) polymerases (PARPs). NAD+ reduction lowers the activity of the antiaging proteins, sirtuins, leading to a feedforward cycle of aging. Nicotinamide riboside (NR) restores NAD+ amounts and reverses this cycle, resulting in better stem cell maintenance and tissue function. UPR, unfolded protein response.

Edited by Bryan_S, 17 June 2016 - 01:41 PM.

[Bryan_S]

NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice

Science  17 Jun 2016:

http://science.scien...t/352/6292/1436

 

A dietary supplement protects aging muscle

 

The oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) is critical for mitochondrial function, and its supplementation can lead to increased longevity. Zhang et al. found that feeding the NAD+ precursor nicotinamide riboside (NR) to aging mice protected them from muscle degeneration (see the Perspective by Guarente). NR treatment enhanced muscle function and also protected mice from the loss of muscle stem cells. The treatment was similarly protective of neural and melanocyte stem cells, which may have contributed to the extended life span of the NR-treated animals.

 

Abstract

 

Adult stem cells (SCs) are essential for tissue maintenance and regeneration yet are susceptible to senescence during aging. We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) and its effect on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence. Treatment with the NAD+ precursor nicotinamide riboside (NR) induced the mitochondrial unfolded protein response and synthesis of prohibitin proteins, and this rejuvenated MuSCs in aged mice. NR also prevented MuSC senescence in the mdx (C57BL/10ScSn-Dmdmdx/J) mouse model of muscular dystrophy. We furthermore demonstrate that NR delays senescence of neural SCs and melanocyte SCs and increases mouse life span. Strategies that conserve cellular NAD+ may reprogram dysfunctional SCs and improve life span in mammals.

Edited by Bryan_S, 17 June 2016 - 01:41 PM.

[Bryan_S]

Biosensor reveals multiple sources for mitochondrial NAD+

Science  17 Jun 2016:

Xiaolu A. Cambronne1,*, Melissa L. Stewart1, DongHo Kim1, Amber M. Jones-Brunette2, Rory K. Morgan3, David L. Farrens2, Michael S. Cohen3,*, Richard H. Goodman1

http://science.scien...t/352/6292/1474

 

Abstract

 

Nicotinamide adenine dinucleotide (NAD+) is an essential substrate for sirtuins and poly(adenosine diphosphate–ribose) polymerases (PARPs), which are NAD+-consuming enzymes localized in the nucleus, cytosol, and mitochondria. Fluctuations in NAD+ concentrations within these subcellular compartments are thought to regulate the activity of NAD+-consuming enzymes; however, the challenge in measuring compartmentalized NAD+ in cells has precluded direct evidence for this type of regulation. We describe the development of a genetically encoded fluorescent biosensor for directly monitoring free NAD+ concentrations in subcellular compartments. We found that the concentrations of free NAD+ in the nucleus, cytoplasm, and mitochondria approximate the Michaelis constants for sirtuins and PARPs in their respective compartments. Systematic depletion of enzymes that catalyze the final step of NAD+ biosynthesis revealed cell-specific mechanisms for maintaining mitochondrial NAD+ concentrations.

[Harkijn]

 

Biosensor reveals multiple sources for mitochondrial NAD+

Science  17 Jun 2016:

Xiaolu A. Cambronne1,*, Melissa L. Stewart1, DongHo Kim1, Amber M. Jones-Brunette2, Rory K. Morgan3, David L. Farrens2, Michael S. Cohen3,*, Richard H. Goodman1

http://science.scien...t/352/6292/1474

 

Abstract

 

Nicotinamide adenine dinucleotide (NAD+) is an essential substrate for sirtuins and poly(adenosine diphosphate–ribose) polymerases (PARPs), which are NAD+-consuming enzymes localized in the nucleus, cytosol, and mitochondria. Fluctuations in NAD+ concentrations within these subcellular compartments are thought to regulate the activity of NAD+-consuming enzymes; however, the challenge in measuring compartmentalized NAD+ in cells has precluded direct evidence for this type of regulation. We describe the development of a genetically encoded fluorescent biosensor for directly monitoring free NAD+ concentrations in subcellular compartments. We found that the concentrations of free NAD+ in the nucleus, cytoplasm, and mitochondria approximate the Michaelis constants for sirtuins and PARPs in their respective compartments. Systematic depletion of enzymes that catalyze the final step of NAD+ biosynthesis revealed cell-specific mechanisms for maintaining mitochondrial NAD+ concentrations.

 

Those who only read the abstracts of the studies posted by Bryan : this time read the full text. It contains photographs of NAD+. For me, being able to see it turns it from an abstraction to a reality...

I also learned from this research that every cell has three NAD+pools and that the mitochondrial pool can fall back on the cytoplasmic pool in case of shortage. The researchers do not know how the NAD is being transported from A to B. I hope this is discovered soon, because perhaps this process, too, can perhaps be tweaked to youthful functioning?

[Tom Andre F. (ex shinobi)]

 

NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice

Science  17 Jun 2016:

http://science.scien...t/352/6292/1436

 

A dietary supplement protects aging muscle

 

The oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) is critical for mitochondrial function, and its supplementation can lead to increased longevity. Zhang et al. found that feeding the NAD+ precursor nicotinamide riboside (NR) to aging mice protected them from muscle degeneration (see the Perspective by Guarente). NR treatment enhanced muscle function and also protected mice from the loss of muscle stem cells. The treatment was similarly protective of neural and melanocyte stem cells, which may have contributed to the extended life span of the NR-treated animals.

 

Abstract

 

Adult stem cells (SCs) are essential for tissue maintenance and regeneration yet are susceptible to senescence during aging. We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) and its effect on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence. Treatment with the NAD+ precursor nicotinamide riboside (NR) induced the mitochondrial unfolded protein response and synthesis of prohibitin proteins, and this rejuvenated MuSCs in aged mice. NR also prevented MuSC senescence in the mdx (C57BL/10ScSn-Dmdmdx/J) mouse model of muscular dystrophy. We furthermore demonstrate that NR delays senescence of neural SCs and melanocyte SCs and increases mouse life span. Strategies that conserve cellular NAD+ may reprogram dysfunctional SCs and improve life span in mammals.

 

 

This study was already posted and the lifespan increase in mean and maximum is a poor 4% over control. No CR group was tested
 

[Nate-2004]

 

 

NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice

Science  17 Jun 2016:

http://science.scien...t/352/6292/1436

 

A dietary supplement protects aging muscle

 

The oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) is critical for mitochondrial function, and its supplementation can lead to increased longevity. Zhang et al. found that feeding the NAD+ precursor nicotinamide riboside (NR) to aging mice protected them from muscle degeneration (see the Perspective by Guarente). NR treatment enhanced muscle function and also protected mice from the loss of muscle stem cells. The treatment was similarly protective of neural and melanocyte stem cells, which may have contributed to the extended life span of the NR-treated animals.

 

Abstract

 

Adult stem cells (SCs) are essential for tissue maintenance and regeneration yet are susceptible to senescence during aging. We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) and its effect on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence. Treatment with the NAD+ precursor nicotinamide riboside (NR) induced the mitochondrial unfolded protein response and synthesis of prohibitin proteins, and this rejuvenated MuSCs in aged mice. NR also prevented MuSC senescence in the mdx (C57BL/10ScSn-Dmdmdx/J) mouse model of muscular dystrophy. We furthermore demonstrate that NR delays senescence of neural SCs and melanocyte SCs and increases mouse life span. Strategies that conserve cellular NAD+ may reprogram dysfunctional SCs and improve life span in mammals.

 

 

This study was already posted and the lifespan increase in mean and maximum is a poor 4% over control. No CR group was tested
 

 

 

That sucks. I'm sure we'd all be ahead of you on this if it weren't for paywalls. I'm surprised they allowed it to be published in such a way that it implied a significant increase in the title/conclusion.

[Tom Andre F. (ex shinobi)]

Sure thing , reducing inflammation , ROS, AGE's would help but we were exposed to those when we were kids and we still manage to grow and not to age ....

It's not about what we believe it's about what we know....

More studies are needed

 

Not true, ROS, AGE, and general inflammation(actually there is a loop there) are increasing while we age due to accumulation. The more we age the more AGE stock, the more TGFb, the more IKK-β activity etc..

[Tom Andre F. (ex shinobi)]

 

 

 

NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice

Science  17 Jun 2016:

http://science.scien...t/352/6292/1436

 

A dietary supplement protects aging muscle

 

The oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) is critical for mitochondrial function, and its supplementation can lead to increased longevity. Zhang et al. found that feeding the NAD+ precursor nicotinamide riboside (NR) to aging mice protected them from muscle degeneration (see the Perspective by Guarente). NR treatment enhanced muscle function and also protected mice from the loss of muscle stem cells. The treatment was similarly protective of neural and melanocyte stem cells, which may have contributed to the extended life span of the NR-treated animals.

 

Abstract

 

Adult stem cells (SCs) are essential for tissue maintenance and regeneration yet are susceptible to senescence during aging. We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) and its effect on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence. Treatment with the NAD+ precursor nicotinamide riboside (NR) induced the mitochondrial unfolded protein response and synthesis of prohibitin proteins, and this rejuvenated MuSCs in aged mice. NR also prevented MuSC senescence in the mdx (C57BL/10ScSn-Dmdmdx/J) mouse model of muscular dystrophy. We furthermore demonstrate that NR delays senescence of neural SCs and melanocyte SCs and increases mouse life span. Strategies that conserve cellular NAD+ may reprogram dysfunctional SCs and improve life span in mammals.

 

 

This study was already posted and the lifespan increase in mean and maximum is a poor 4% over control. No CR group was tested
 

 

 

That sucks. I'm sure we'd all be ahead of you on this if it weren't for paywalls. I'm surprised they allowed it to be published in such a way that it implied a significant increase in the title/conclusion.

 

 

I already teached you how to manage with paywalls.. The 4% they dont even give in the study, its a calculation I made using their data. What sucks is to not use CR group too

 

[stefan_001]

 

 

 

 

NAD+ repletion improves mitochondrial and stem cell function and enhances life span in mice

Science  17 Jun 2016:

http://science.scien...t/352/6292/1436

 

A dietary supplement protects aging muscle

 

The oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) is critical for mitochondrial function, and its supplementation can lead to increased longevity. Zhang et al. found that feeding the NAD+ precursor nicotinamide riboside (NR) to aging mice protected them from muscle degeneration (see the Perspective by Guarente). NR treatment enhanced muscle function and also protected mice from the loss of muscle stem cells. The treatment was similarly protective of neural and melanocyte stem cells, which may have contributed to the extended life span of the NR-treated animals.

 

Abstract

 

Adult stem cells (SCs) are essential for tissue maintenance and regeneration yet are susceptible to senescence during aging. We demonstrate the importance of the amount of the oxidized form of cellular nicotinamide adenine dinucleotide (NAD+) and its effect on mitochondrial activity as a pivotal switch to modulate muscle SC (MuSC) senescence. Treatment with the NAD+ precursor nicotinamide riboside (NR) induced the mitochondrial unfolded protein response and synthesis of prohibitin proteins, and this rejuvenated MuSCs in aged mice. NR also prevented MuSC senescence in the mdx (C57BL/10ScSn-Dmdmdx/J) mouse model of muscular dystrophy. We furthermore demonstrate that NR delays senescence of neural SCs and melanocyte SCs and increases mouse life span. Strategies that conserve cellular NAD+ may reprogram dysfunctional SCs and improve life span in mammals.

 

 

This study was already posted and the lifespan increase in mean and maximum is a poor 4% over control. No CR group was tested
 

 

 

That sucks. I'm sure we'd all be ahead of you on this if it weren't for paywalls. I'm surprised they allowed it to be published in such a way that it implied a significant increase in the title/conclusion.

 

 

I already teached you how to manage with paywalls.. The 4% they dont even give in the study, its a calculation I made using their data. What sucks is to not use CR group too

 

 

 

I think this is a distortion of the study. The mice were fed for a period of 6 weeks with NR starting at an age of 24 months. The fact that this short treatment, at such late age results in life extension is quite impressive in my opinion.