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Nicotinamide Riboside Current News and Updates

niagen nad booster charles brenner david sinclair nicotinamide riboside nad nicotinamide ribo nad news leonard guarente

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#301 Asor

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Posted 16 August 2015 - 02:34 AM

 

But the study seems to imply that a few grams per day might be useful in ameliorating Alzheimer's pathology.

 

i dont know about Alzheimer, but my sources say that for the NR study on Mitochodrial diseases the dosage will be in the ballpark of 2 grams / day.

 

My source: researcher from Cambridge University who worked on the study on rats already mentioned in this thread and he's now working on the study on human patients with Mitochondrial diseases.

 

Just got word a couple days ago that they made some important improvements to get the study started and "we are almost there".

They were also waiting for the Chromadex study that was posted couple days ago.



#302 Bryan_S

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Posted 16 August 2015 - 03:48 AM

So I take it that you would agree that raising NAD+ a reasonable first step towards retarding the aging process, with sirtuin activation being a logical second step. If that's the case, I would agree, but I'm not sure that you should be looking to pterostilbene for SIRT1 activation: "Neither resveratrol nor pterostilbene increased sirtuin 1 (SIRT1) expression or downstream markers of sirtuin 1 activation." -- at least, in this case, in which it was hypothesized that PPARa was responsible for pterostilbene's benefits. I stopped taking 250 mg/d several months ago, and didn't notice anything. But the study seems to imply that a few grams per day might be useful in ameliorating Alzheimer's pathology. So thanks for your interjection about this substance; perhaps I'll do a megadose microtrial in the future. (Lurkers, be warned: pterostilbene can drop your blood sugar like a rock, and although it has GRAS status, it's generally produced with toxic solvents, so in massive quantities this could be a problem.)

 

SIRT3 seems to be activated by honokiol (see Brian's previous posts). For that matter, I also seem to recall that Longvida lipidated curcumin hits SIRT2. As to SIRT4-7, I don't know how to enable them, except, perhaps, for fasting.

 

Anyway nice blog. You might want to share it in one of the various pterostilbene threads.

 

Quercetin is a SIRT1 activator but I tried that for a week and felt rather poor while taking it and discontinued its use. I did some further reading and it suggested it only worked only under certain circumstances. Their was also bit of conversation on Quercetin in the senolytics forum thats worth reading. Pterostilbene's claim to fame is SIRT1 activation but I've also read some contradictory findings, I think that is the same study you noted. A new study was published, "Effects of pterostilbene and resveratrol on brain and behavior." I don't hold a ScienceDirect subscription and the abstract tells us nothing. So I'm not completely sold on Pterostilbene either but I'm giving it a try.

 

Where are we hosting a forum on sirtuins anyway? I find a smattering of posts touching on them but not a dedicated forum. I suspect there will be some growing interest because this could be a synergistic topic to NAD boosting. For now I'll include what I find on this forum and if it gets distractive we'll move that conversation to another room.


Edited by Bryan_S, 16 August 2015 - 03:49 AM.


#303 follies

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Posted 16 August 2015 - 03:48 AM

Anti aging firewall theory is that it will go down to the original level)

?


Anti aging firewall theory is that it will go down even if you continue supplementation. I would like to know if you stop does it go below normal levels? These should be easy questions to answer.

#304 resveratrol_guy

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Posted 16 August 2015 - 04:09 AM

 


i dont know about Alzheimer, but my sources say that for the NR study on Mitochodrial diseases the dosage will be in the ballpark of 2 grams / day.

 

My source: researcher from Cambridge University who worked on the study on rats already mentioned in this thread and he's now working on the study on human patients with Mitochondrial diseases.

 

Just got word a couple days ago that they made some important improvements to get the study started and "we are almost there".

They were also waiting for the Chromadex study that was posted couple days ago.

 

 

Very interesting. Was this just in the context of your conversation with the researcher, or is there something published or written which you could provide?

 

Obviously combining pterostilbene with NR would be the next most compelling idea...
 



#305 resveratrol_guy

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Posted 16 August 2015 - 04:14 AM


Quercetin is a SIRT1 activator but I tried that for a week and felt rather poor while taking it and discontinued its use. I did some further reading and it suggested it only worked only under certain circumstances. Their was also bit of conversation on Quercetin in the senolytics forum thats worth reading. Pterostilbene's claim to fame is SIRT1 activation but I've also read some contradictory findings, I think that is the same study you noted. A new study was published, "Effects of pterostilbene and resveratrol on brain and behavior." I don't hold a ScienceDirect subscription and the abstract tells us nothing. So I'm not completely sold on Pterostilbene either but I'm giving it a try.

 

Where are we hosting a forum on sirtuins anyway? I find a smattering of posts touching on them but not a dedicated forum. I suspect there will be some growing interest because this could be a synergistic topic to NAD boosting. For now I'll include what I find on this forum and if it gets distractive we'll move that conversation to another room.

 

 

For the record, quercetin is supposedly not very bioavailable, as discussed in the senolytics thread you linked. (Liposomal quercetin is an interesting concept for this reason.)

 

In this case, I wouldn't recommend creating another thread, because the discussion of how to power repair processes (NAD+) is inseparable from the levers which control said processes (sirtuins etc).

 

"In this review, we summarize the current knowledge on the role of resveratrol and pterostilbene in improving brain health during aging, with specific focus on antioxidant and anti-inflammatory signaling and behavioral outcomes." -- Sounds like a metastudy to me, which means that a Pubmed scan should provide most of their source material.


Edited by resveratrol_guy, 16 August 2015 - 04:16 AM.


#306 Bryan_S

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Posted 16 August 2015 - 04:18 AM

And more than all: is this will be enough to really stop aging ? Does nad+ is increased in ALL cells ?

 

I don't want to write a dissertation but I believe as far as "NAD supplementation" is concerned, once the original cellular damage is done your going to continue to carry that forward. Now thats not to say that you can't improve your condition and increase cellular repair and boost the immune system. For instance the mitochondria can increase in number but I don't think they will work as well as when you were a child. So in some respects yes but in many respects no.

 

Not all cells respond equally to the NAD precursors, we touched on that in this post



#307 Iporuru

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Posted 16 August 2015 - 07:57 AM

 

 


i dont know about Alzheimer, but my sources say that for the NR study on Mitochodrial diseases the dosage will be in the ballpark of 2 grams / day.

 

My source: researcher from Cambridge University who worked on the study on rats already mentioned in this thread and he's now working on the study on human patients with Mitochondrial diseases.

 

Just got word a couple days ago that they made some important improvements to get the study started and "we are almost there".

They were also waiting for the Chromadex study that was posted couple days ago.

 

 

Very interesting. Was this just in the context of your conversation with the researcher, or is there something published or written which you could provide?

 

Obviously combining pterostilbene with NR would be the next most compelling idea...
 

 

 

This is what Leonard Guarante and the Elysium team have come up with: http://www.elysiumhe...upplement-facts
 



#308 Tom Andre F. (ex shinobi)

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Posted 16 August 2015 - 08:19 AM

So I take it that you would agree that raising NAD+ a reasonable first step towards retarding the aging process, with sirtuin activation being a logical second step. If that's the case, I would agree, but I'm not sure that you should be looking to pterostilbene for SIRT1 activation: "Neither resveratrol nor pterostilbene increased sirtuin 1 (SIRT1) expression or downstream markers of sirtuin 1 activation." -- at least, in this case, in which it was hypothesized that PPARa was responsible for pterostilbene's benefits. I stopped taking 250 mg/d several months ago, and didn't notice anything. But the study seems to imply that a few grams per day might be useful in ameliorating Alzheimer's pathology. So thanks for your interjection about this substance; perhaps I'll do a megadose microtrial in the future. (Lurkers, be warned: pterostilbene can drop your blood sugar like a rock, and although it has GRAS status, it's generally produced with toxic solvents, so in massive quantities this could be a problem.)

SIRT3 seems to be activated by honokiol (see Brian's previous posts). For that matter, I also seem to recall that Longvida lipidated curcumin hits SIRT2. As to SIRT4-7, I don't know how to enable them, except, perhaps, for fasting.

Anyway nice blog. You might want to share it in one of the various pterostilbene threads.

Thanks for the study, does anyone have access to the full study please ?
Anyway i will contact them.
Did you read my article here : http://www.pterostil...irt1-activator/ ?
They used a different protocol and pterostilbene was a more potent activator of sirt1 than resveratrol and quercetin has a negative impact on sirt 1 !
For too high dosage of nr problem is the conversion into nicotinamide wich is also anti sirt1 and pro homocysteine (= 3 times more telomere shortening rate)

#309 Tom Andre F. (ex shinobi)

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Posted 16 August 2015 - 08:41 AM

And more than all: is this will be enough to really stop aging ? Does nad+ is increased in ALL cells ?


I don't want to write a dissertation but I believe as far as "NAD supplementation" is concerned, once the original cellular damage is done your going to continue to carry that forward. Now thats not to say that you can't improve your condition and increase cellular repair and boost the immune system. For instance the mitochondria can increase in number but I don't think they will work as well as when you were a child. So in some respects yes but in many respects no.

Not all cells respond equally to the NAD precursors, we touched on that in this post.
Well we also have the sinclair study on mice where he state he rejuveneted the mice muscles

#310 stefan_001

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Posted 16 August 2015 - 01:26 PM

 

Now maybe a little off topic but I'm seeing something happen I didn't expect and I'm trying to figure this one out. I have as many men in their 50's Benign prostatic hyperplasia. Its not a big problem, maybe an inconvenience at best. I've been very busy at the studio for the last couple of weeks without much time off to take care of the small things and haven't had a chance to renew my prescriptions for my BPH medication. The thing is, I'm not having a problem voiding and I have to question why I'm back to normal at the moment?

 

With so many new supplements, to what can I attribute this unexpected relief? I'm going to give this a bit longer without my medication to be sure but I was totally taken off guard.

 

I did a google search an unexpectedly turned up something with the search tag "Honokiol Benign prostatic hyperplasia" so nothing conclusive on the Honokiol as the cause because I'm taking multiple things but its worth digging deeper into because so many of us are effected.

 

 

Hello Brian,

 

I am new to this forum and have been reading this discussion with high interest. I am 45 years old. Never used any supplements except some vitamins. Mid April I started to use NR and Pterostilbene. Dosage:

- in the morning 125mg NR and 50mg Pterostilbene

- in the evening 125mg NR and 50mg Pterostilbene

(never understand the once a day boost as I think a day is just an arbritary time, I figured as it stays not very long in the blood, two spikes is better than one).I use nothing else. The other topic to mention is that without doing it on purpose I would say my eating pattern is somewhat CR like. It may be I hardly eat anything for the entire day except a very late noght dinner. Exercise I do as well.

 

I started using pTero/NR as i was seeing typical signs of aging growing. I saw a simlar pattern when I just passed 40 but that stopped when I added weights to the exercising. I understand that has effect on hormon release.

 

While not an expert, learning about this, I think I could be a relatively clean experience source. In general I am very happy about the effects. Now as too blatter function, I am pretty certain this improved. Amount of bathroom visits has gone down and volume up.

 

Stefan

 

 


Edited by stefan_001, 16 August 2015 - 01:51 PM.


#311 Bryan_S

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Posted 16 August 2015 - 03:17 PM

PINK1 protein crucial for removing broken-down energy reactors

Another piece of the puzzle.

pink1protein.jpg

http://medicalxpress...own-energy.html

 

"When PINK1 accumulates on the surface of defective mitochondria, it alters a molecule called ubiquitin. The modified ubiquitin then recruits autophagy receptors as well as Parkin. Parkin promotes mitophagy by bringing more ubiquitin to the mitochondria to form long chains that flag damaged mitochondria for removal. Since PINK1 is needed to start building these ubiquitin chains, Dr. Youle's work suggests a new avenue for creating drugs that treat disease by boosting the disposal of damaged mitochondria."

 

"A number of companies are trying to develop drugs to activate this pathway," Dr. Youle said. "Some of them are trying to find drugs that activate Parkin, but this new model might suggest a different strategy. It may not be so important to activate Parkin; it may be more important to activate PINK1."


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#312 Bryan_S

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Posted 16 August 2015 - 03:40 PM

 

 

Well we also have the sinclair study on mice where he state he rejuveneted the mice muscles 

 

There is more and more data accumulating that suggests NMN is cleaved to NR at the cell membrane and reassembled within the cell.  "Our results demonstrate that, besides nicotinamide and nicotinic acid, only the corresponding nucleosides readily enter the cells. Nucleotides (e.g. NAD and NMN) undergo extracellular degradation resulting in the formation of permeable precursors.This takes nothing away from his results because he raised NAD levels.

 

 

 

This is what Leonard Guarante and the Elysium team have come up with

 

I'm trialling pterostilbene with NR now. Basis is also incredibly expensive. Both ingredients can be purchased separately for much less. So far I haven't noticed any benefits from pterostilbene. But I'll be fair and give it a few months.

 

 

 

In general I am very happy about the effects. Now as too blatter function, I am pretty certain this improved. Amount of bathroom visits has gone down and volume up.

 

That's encouraging. I'm still trying to figure out from which supplement I'm getting the voiding benefit. 



#313 APBT

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Posted 16 August 2015 - 04:47 PM

 

So I take it that you would agree that raising NAD+ a reasonable first step towards retarding the aging process, with sirtuin activation being a logical second step. If that's the case, I would agree, but I'm not sure that you should be looking to pterostilbene for SIRT1 activation: "Neither resveratrol nor pterostilbene increased sirtuin 1 (SIRT1) expression or downstream markers of sirtuin 1 activation." -- at least, in this case, in which it was hypothesized that PPARa was responsible for pterostilbene's benefits. I stopped taking 250 mg/d several months ago, and didn't notice anything. But the study seems to imply that a few grams per day might be useful in ameliorating Alzheimer's pathology. So thanks for your interjection about this substance; perhaps I'll do a megadose microtrial in the future. (Lurkers, be warned: pterostilbene can drop your blood sugar like a rock, and although it has GRAS status, it's generally produced with toxic solvents, so in massive quantities this could be a problem.)

SIRT3 seems to be activated by honokiol (see Brian's previous posts). For that matter, I also seem to recall that Longvida lipidated curcumin hits SIRT2. As to SIRT4-7, I don't know how to enable them, except, perhaps, for fasting.

Anyway nice blog. You might want to share it in one of the various pterostilbene threads.

Thanks for the study, does anyone have access to the full study please ?

 

 

FULL TEXT:


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#314 stefan_001

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Posted 16 August 2015 - 07:24 PM

In general I am very happy about the effects. Now as too blatter function, I am pretty certain this improved. Amount of bathroom visits has gone down and volume up.

That's encouraging. I'm still trying to figure out from which supplement I'm getting the voiding benefit.
Brian I think I read somewhere that you somewhat recent also changed the dosing pattern for NR, so more frequent during the day. Perhaps that has an influence? If something should improve I guess it only happens when there is a NR boost. With a single boost a day there is limited time for "repairs" and the rest of the day is still mostly as usual. Multiple boosts increase periods of "repair" time - till a point comes that repairs are more than normal detoriation?

Stefan

Ps asked the same question also in BHP thread, but thought its relevant for this discussion also.

Edited by stefan_001, 16 August 2015 - 07:25 PM.


#315 Tom Andre F. (ex shinobi)

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Posted 16 August 2015 - 07:45 PM

 

 

So I take it that you would agree that raising NAD+ a reasonable first step towards retarding the aging process, with sirtuin activation being a logical second step. If that's the case, I would agree, but I'm not sure that you should be looking to pterostilbene for SIRT1 activation: "Neither resveratrol nor pterostilbene increased sirtuin 1 (SIRT1) expression or downstream markers of sirtuin 1 activation." -- at least, in this case, in which it was hypothesized that PPARa was responsible for pterostilbene's benefits. I stopped taking 250 mg/d several months ago, and didn't notice anything. But the study seems to imply that a few grams per day might be useful in ameliorating Alzheimer's pathology. So thanks for your interjection about this substance; perhaps I'll do a megadose microtrial in the future. (Lurkers, be warned: pterostilbene can drop your blood sugar like a rock, and although it has GRAS status, it's generally produced with toxic solvents, so in massive quantities this could be a problem.)

SIRT3 seems to be activated by honokiol (see Brian's previous posts). For that matter, I also seem to recall that Longvida lipidated curcumin hits SIRT2. As to SIRT4-7, I don't know how to enable them, except, perhaps, for fasting.

Anyway nice blog. You might want to share it in one of the various pterostilbene threads.

Thanks for the study, does anyone have access to the full study please ?

 

 

FULL TEXT:

 

 

thanks a lot !

 



#316 Asor

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Posted 16 August 2015 - 09:54 PM

 

 


i dont know about Alzheimer, but my sources say that for the NR study on Mitochodrial diseases the dosage will be in the ballpark of 2 grams / day.

 

My source: researcher from Cambridge University who worked on the study on rats already mentioned in this thread and he's now working on the study on human patients with Mitochondrial diseases.

 

Just got word a couple days ago that they made some important improvements to get the study started and "we are almost there".

They were also waiting for the Chromadex study that was posted couple days ago.

 

 

Very interesting. Was this just in the context of your conversation with the researcher, or is there something published or written which you could provide?

 

 

 

 

I exchanged about a dozen emails with the researcher (who's interested in my case because i fit the type of patient they need in the study due to my genetic mutation) and direct convo with my own neurologist (specialized in MITO), who is involved in the study as well.

 

My doctor told me after the study on mice they did other experiments on "larger animal models", came to conclusion that NR dosage to be effective on mitochondrial patients should be around 2 grams / day (which is a lot, obviously).

 

I asked whether there is any link between theirs and with David Sinclair and Guarente's work, my doctor didnt give me a direct answer but from what she told me for "normal" persons the 2grams dosage is not necessary, even less is beneficial.

 

It was a very quick answer and it's very hard to get info from them, they're obviously very cautious in divulging information for different reasons.

 

There is nothing published regarding study on humans because they haven't done any yet, there are different ones in this field being organized from few research institutions, the first step was to make sure that such dosages arent toxic, the results just released by Chromadex are promising in this aspect.

 

In fact there were other drugs that were tried in these kind of studies (some drug already used for diabetes) that turned out to be toxic in the dosages needed to be beneficial for mito patients.

 

From my own perception: little is know about "this stuff", but sounds very important. Heard about Nobel Prize potential regarding the studies involved in these mechanisms.... mitochondrial health, communication pathways between cells and mitochondria, etc.etc... fascinating stuff.

 

 

 

 

 


 


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#317 ironfistx

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Posted 17 August 2015 - 07:45 PM

So if you quit taking nicotinamide robisode the effects go back to worse than before you started?


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#318 Bryan_S

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Posted 18 August 2015 - 06:28 PM

Mechanism of Inhibition of the Human Sirtuin Enzyme SIRT3 by Nicotinamide: Computational and Experimental Studies

http://journals.plos...al.pone.0107729

http://www.pmc-at.co...IRT3 Enzyme.pdf

 

If everyone is interested in how the NAD / Nicotinamide / Sirtuin feedback mechanisms work, this recent article is about as up-to-date as its gets. It appeared on my radar today because they posted a Correction.

 

Attached File  Nicotinamide_Binding_Pockets.jpg   205.61KB   3 downloads

Of special interest are the newly discovered Nicotinamide binding pockets. These pockets aid in enabling or disabling the enzymes as part of the feedback loop. It is all based on the relative concentrations. Now not mentioned in this article, think about the pocket concept as a lock waiting for a proper key molecule to fit in. Now what do you think will happen when a Nicotinamide Riboside molecule tries to fit into a Nicotinamide binding pocket. The Riboside portion of the molecule doesn't fit. So here is an indicator of why the Nicotinamide Riboside molecule could be better at raising NAD levels because it isn't initially blocked by these receptor binding sites. 

 

 

We can all sit around thinking; "Oh maybe we should't tamper with this because we'll be worse off than before," but where's the data to support that notion? If NAD boosting increases mitochondrial biogenesis, creating more sites/capacity for NAD production and this higher NAD pool encourages the NAD consuming cellular maintenance enzymes like PARPs and Sirtuins. How could we be worse off?

 

All I can say guys is read, read, read! Anything you can do to enhance and maintain your cellular Respiration Redox State "The Krebs cycle" the better equipped you'll be at defending against cellular insults as you creep into old age. Also let's not neglect mentioning our brain, as it will be better protected against physical or chemical insult.

 

14A.jpg


Edited by Bryan_S, 18 August 2015 - 06:49 PM.

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#319 Bryan_S

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Posted 18 August 2015 - 09:22 PM

In the previous post I meant to say; "So here is an indicator of why the Nicotinamide Riboside molecule could be better at raising NAD levels and activating sirtuins because it isn't initially blocked by these receptor binding sites" In the end its NAD that activates the sirtuins. So that edit feature only lasts so long as I've just seen.



#320 cudBwrong

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Posted 19 August 2015 - 03:30 AM

For the record, quercetin is supposedly not very bioavailable, as discussed in the senolytics thread you linked. (Liposomal quercetin is an interesting concept for this reason.)

 

 

There is some evidence that quercetin bioavailability actually is not so bad. These levels are more or less in the range of what was tested in a variety of animal studies.

 

http://www.ncbi.nlm....pubmed/23094941

 

 

 

J Food Sci. 2012 Nov;77(11):H231-8. doi: 10.1111/j.1750-3841.2012.02934.x. Epub 2012 Oct 24.
Comparison of quercetin pharmacokinetics following oral supplementation in humans. Abstract

The objective of the study was to investigate the absorption of quercetin aglycone in 18 healthy human subjects administered via the following oral carrier systems: suspension of quercetin (quercetin QU995 powder in Tang(®) and spring water), nutritional bars (First Strike™), and chews (RealFX™ Q-Plus™). Subjects were divided into 3 groups of 6 individuals each receiving 500 mg quercetin in one of the aforementioned formulations. Blood levels were monitored immediately pre- and for 32 h postadministration. The concentration of total quercetin in blood samples was determined by solid phase extraction followed by high-performance liquid chromatography analysis. Pharmacokinetic parameters were determined by noncompartmental modeling using Kinetica software. The C(max) of quercetin was highest with RealFX™ Q-Plus™ Chews (1051.9 ± 393.1 μg/L) achieved within 3.3 h as compared to that for First Strike™ Bars (698.1 ± 189.5 μg/L in 2.3 h) and Tang(®) suspension (354.4 ± 87.6 μg/L in 4.7 h). The results showed no statistically significant difference in quercetin absorption among groups due to high variability within groups receiving quercetin from same dosage form. This study represents the first comprehensive evaluation of quercetin absorption from quercetin fortified oral food products at doses commonly used for quercetin supplementation.

PRACTICAL APPLICATION:

The current study describes for the first time, comprehensive evaluation of quercetin PK in humans from quercetin fortified oral food products at doses commonly used for quercetin supplementation. Owing to quercetin's potent antioxidant and anti-inflammatory actions, quercetin is widely being used as a nutritional supplement. In order to maximize the bioavailability of quercetin for its use in efficacy studies, it is important to determine its ideal oral carrier system and route for its delivery. The current research unveils vital information about quercetin supplementation to the international community, especially to soldiers, athletes, and the dietary supplement industry.

 

 

Off topic, but just an enormous expression of thanks to Bryan_S and all the contributors on this challenging topic.  Trying to preserve my eyesight (Mactel Type 2) and I'm actively researching why neurons and glia get sick and what might keep them going.  A very useful thread, thanks so much.


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#321 Bryan_S

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Posted 19 August 2015 - 03:00 PM

ChromaDex to Host Investor Call on Wednesday, August 19th at 11am EDT

 

 
 

IRVINE, Calif., Aug. 18, 2015 (GLOBE NEWSWIRE) -- ChromaDex Corp. (OTCQX:CDXC), an innovator of proprietary health, wellness, and nutritional ingredients that creates science-based solutions for dietary supplements, food and beverage, skin care, sports nutrition, and pharmaceutical products will host an investor conference call to discuss the 2015 second quarter results and provide a general business update on Wednesday, August 19th, at 11am EDT.

Participants should call in at least 10 minutes prior to the call. The dial-in information is as follows:
U.S. toll free: 1-866-327-8118
Outside the U.S.: 1-678-509-7526
Conference ID for this call is: 98596925

A webcast replay will be available on the Investor Relations section of the Company website, www.chromadex.com.

 

I'm at the office today so take notes. If you miss the call they will post a replay. I would expect we will get more information on this call from the clinical study.

 



#322 resveratrol_guy

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Posted 19 August 2015 - 04:48 PM

There is too much to digest in this brilliant thread. But to hit a few salient points:

 

Bryan said "AICAR might be the answer but it is to early to say." But Asor said above on 6/26/2015, "[C. Lamperti] told me AICAR (which is already used for diabetes treatments) resulted to be toxic to be used in dosages useful for mitochondrial diseases". Fortunately bitter guord activates AMPK as well, although i don't know if this is due to AICAR content or something else. Bitter gourd is widely available in Asia and Asian specialty stores. You can also buy it in the form of a drink, powder, or capsules on Amazon, which is convenient for controlled dosing. Just be advised of the potential side effects, for example urinary incontinence, as discussed the Wiki article.

 

Bryan commented above that "For instance the mitochondria can increase in number but I don't think they will work as well as when you were a child." While there is some evidence that this can be overcome using (epi)genetic error correction with modern iPSC techniques, why bet on that? Save your stem cells, like I did, with Neostem or similar companies. On the plus side, because most of the damage occurs late in life, this can be a prudent undertaking even for senior citizens.

 

Tom Andre said "nicotinamide wich is also anti sirt1 and pro homocysteine " -- that's counterintuitive, to put it mildly, because this sounds like "nicotinamide causes aging acceleration and heart attacks". Can anyone substantiate this? Does it occur to any meaningful extent in realistic nicotinamide dosing ranges?

 

APBT posted the resveratrol/ptereostilbene study above. Looking at the graphs, it seems that pterostilbene reduces both phosphotau and phosphoJNK, and the water maze results show remarkable cognitive improvements (but these were young and more repairable rodents). It's also astonishing that they were able to obtain their impressive HPLC results with a dose of 120 mg per kilogram of diet. So for a human, that's what -- 100 or 200 mg of pterostilbene daily? This might be overstated because I didn't adjust for our lower metabolic rate. But, then, even pterostilbene is only 10X as bioavailable as resveratrol, which amounts to like 2 hours of half life. So the upshot of all this, in my view, is that megadose pterostilbene might be a reasonable approach to dissolving brain plaque, considering its GRAS status.

 

For the record, I'm still a strong proponent of using hepatoprotective supplements such as Longvida to allow ourselves to exceed the usual upper intake levels of all 3 NAD+ precursors. Perhaps I'll be the first to attempt this.

 


Edited by resveratrol_guy, 19 August 2015 - 04:55 PM.


#323 stefan_001

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Posted 19 August 2015 - 07:13 PM


ChromaDex to Host Investor Call on Wednesday, August 19th at 11am EDT






IRVINE, Calif., Aug. 18, 2015 (GLOBE NEWSWIRE) -- ChromaDex Corp. (OTCQX:CDXC), an innovator of proprietary health, wellness, and nutritional ingredients that creates science-based solutions for dietary supplements, food and beverage, skin care, sports nutrition, and pharmaceutical products will host an investor conference call to discuss the 2015 second quarter results and provide a general business update on Wednesday, August 19th, at 11am EDT.

Participants should call in at least 10 minutes prior to the call. The dial-in information is as follows:
U.S. toll free: 1-866-327-8118
Outside the U.S.: 1-678-509-7526
Conference ID for this call is: 98596925

A webcast replay will be available on the Investor Relations section of the Company website, www.chromadex.com.


I'm at the office today so take notes. If you miss the call they will post a replay. I would expect we will get more information on this call from the clinical study.


I listened to the call but there was not anything new except that larger parties see potential benefits and we may see niagen included in food product etc in coming months. I could imagine that a scale up in volume would help lower the price. In that sense good news.
  • Agree x 1

#324 rlb373

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Posted 19 August 2015 - 11:44 PM

I have ChromaDex on my iPhone stock watch list. Pretty volatile to say the least. On Tues, pre call, it was down about 8.5%, today it was back up by 5.2%. Some other stats: 1 yr high 1.72, low 0.80, close today 1.21. It's total market cap is $130M and average volume about 100K. I don't own any shares and don't intend to, I just find it interesting to follow its fortunes.



#325 Bryan_S

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Posted 20 August 2015 - 05:59 AM

Thanks I follow them as well and almost jumped in at $1.08 per share. My only reservation is that its very thinly traded at this time and I'm not currently interested in OTC stocks.

 

I'm combing thought the conference call looking for the jewels to add to our update thread. http://edge.media-se...ofd5ndv8/lan/en

 

I pulled a few of Frank Jaksch's comments;

 

"We are preparing to start our second human study on nicotinamide riboside. The first study was a single dose administration which demonstrated that even a single dose of NIAGEN or NR was enough to show an increase of NAD. The second study will have a larger patient population and will be held over a longer period of time. Again monitoring not only the effects of nicotinamide riboside as an NAD or an effective NAD precursor, but will also be looking at several therapeutic end points that may result from increasing NAD with NR.
 

In Q2 we also announced a collaborative study, a human clinical study on NIAGEN with the University of Colorado in Boulder. Dr. Doug Seals will investigate the effects of NIAGEN on physical function of metabolism and healthy adults aged 45 to 79 years old. This placebo controlled double blind randomized crossover study will assess the potential benefits of daily NIAGEN supplementation over a course of six weeks. End points that will be assessed in the study include physical function, cardiorespiratory fitness and overall metabolism.

 
ChromaDex providing the NIAGEN supplements for the study along with the match placebo pills or control pills and ChromaDex is awarded a $100,000 research to Dr. Martin's postdoc research at Seals, Dr. Seal's lab, which will fund approximately 25% of the cost of the study." . . .
 
"We have seen an increased interest from multiple sources from the media regarding NR. We've also seen an increased interest in media attention to high profile published research studies. To highlight a couple of recent examples of that, Scientific American recently published an article by David Stipp  who is actually a former Wall Street Journal writer. The article brought attention to the importance of NAD and the importance of both NR and pterostilbene essentially to NAD metabolism." . . . LongeCity Post Beyond Resveratrol: The Anti-Aging NAD Fad
 

"NAD is a lynch pin of energy metabolism among other roles and it's . . . its diminishing level with age is been implicated in mitochondrial deterioration. Supplements containing nicotinamide riboside, a precursor to NAD might be able to boost NAD levels and the article highlighted that point, which is important for us.

 

The article also reasserted ChromaDex's firstcomer status in the NAD game, by announcing that it conducted a clinical trial demonstrating a single dose of NR resulted in statistically significant increases of NAD. And it was also sorted as one would say, a sidebar important piece but the article also highlighted pterostilbene which is our first ingredient.

 

David Stipp has a fairly extensive background writing on science, medicine and aging since 1982 for Scientific American, the Wall Street Journal, Fortune, New York Times and many other publications as well. In 2014, he won an award for American Aging Associations Excellence in Journalism award. So having an article, a high profile article come out not only in Scientific American but from such a high profile author that had a previous history in writing about aging was important for ChromaDex. And we expect that type of pick up in the future as well."

 
"Cockayne syndrome for those of you know may not know what it is, it's a rare pediatric orphan disease, these kids suffer from a genetic abnormality that causes this accelerated aging condition. The researchers concluded that NR promise it's potential therapy for the disease as well as for other age related nerve generative conditions. We believe there is an immediate opportunity for pursue NR as a pharmaceutical therapy for treating Cockayne syndrome. We are currently preparing to file applications for both IND any orphan designation with the FDA."
 
They went into pTeroPure pterostilbene and something called anthocyanins which are plant pigments which they are making cheaply from a special variety of corn.
 
Then they went into the stock analyst questions. I thought there might be some questions related to the recent clinical study but there were none. 
 
There was one guy who asked about inflammation and NR, an analyst with Kay Associates. He asked "Have there been studies that showed that NR has anti-inflammatory effects?" I thought the question might be handled by Frank Jaksch or someone more associated with the comparative B3 research but the question was taken by the companies Chief Financial Officer who said; "Well, we haven't focused on the anti-inflammatory side of things, there is some evidence that shows that there is some impact potentially on inflammation but that’s not a primary focus for us." 
 
I don't want to say they missed the boat on inflammation but since B3's other cousin NAM has been heavily studied in this regard they could have been more enthusiastic in at least saying it warranted further investigation. But instead they said its; "not a primary focus for us." I get the feeling they want to push the things that are unique to this B3 analog, not what it has in common with its cousin. 
 
They are doing better quarter by quarter but still maintain considerable debt. They got called out on their employee stock option plan but more and more companies are going this direction, awarding these incentives to hold employees. I will not get into the quarterly numbers as we are not concentrating on this companies stock but rather its sustainability in future to provide us product and published medical details. Both seem to be in the future cards.
 
That's my short take on the conference call, wished I could have asked a few questions myself but I'd already hit the road for the office by the time they got to those and I'm not a stock analyst.

 


Edited by Bryan_S, 20 August 2015 - 06:21 AM.


#326 Bryan_S

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Posted 20 August 2015 - 06:44 AM

Genetic Ablation of CD38 Protects against Western Diet-Induced Exercise Intolerance and Metabolic Inflexibility

Shian-Huey Chiang , W. Wallace Harrington, Guizhen Luo, Naphtali O. Milliken, John C. Ulrich, Jing Chen, Deepak K. Rajpal, Ying Qian, Tiffany Carpenter, Rusty Murray, Robert S. Geske, Stephen A. Stimpson, Henning F. Kramer,  [ ... ], Andrew N. Billin [ view all ]  Published: August 19, 2015DOI: 10.1371/journal.pone.0134927

 

http://journals.plos...al.pone.0134927



#327 Bryan_S

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Posted 20 August 2015 - 03:22 PM

Six Scientists From Top Academic And Medical Centers Join Elysium Health's™ Scientific Advisory Board, Composed Of More Than 35 Members, Including Six Nobel Laureates, To Help Pursue The Study Of Natural Compounds For Consumer Health

 

Elysium Health plans to initiate a clinical trial on its first product BASIS™, which targets DNA repair, cellular detoxification, energy production and protein function

 

http://www.prnewswir...-300131170.html


Edited by Bryan_S, 20 August 2015 - 03:22 PM.


#328 Bryan_S

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Posted 20 August 2015 - 03:44 PM

Expression of Nicotinamide Phosphoribosyltransferase-Influenced Genes Predicts Recurrence-Free Survival in Lung and Breast Cancers
Tong Zhou, Ting Wang & Joe G. N. Garcia
Scientific Reports 4, Article number: 6107 (2014)
doi:10.1038/srep06107
 
Biomarker research | Cancer Received: 06 May 2014 Accepted: 30 July 2014 Published online: 22 August 2014
 
 
 


#329 Bryan_S

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Posted 20 August 2015 - 03:52 PM

Local axonal protection by WldS as revealed by conditional regulation of protein stability
 


#330 Bryan_S

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Posted 20 August 2015 - 06:47 PM

There is too much to digest in this brilliant thread. But to hit a few salient points:

 

Bryan said "AICAR might be the answer but it is to early to say." But Asor said above on 6/26/2015, "[C. Lamperti] told me AICAR (which is already used for diabetes treatments) resulted to be toxic to be used in dosages useful for mitochondrial diseases". Fortunately bitter guord activates AMPK

 

Bryan commented above that "For instance the mitochondria can increase in number but I don't think they will work as well as when you were a child."

 

I frequently comb back thru the thread as well and 2 articles have stuck in my mind.

 

Scientists reverse aging in human cell lines and give theory of aging a new lease of life

http://www.scienceda...50526085138.htm

Interesting article about glycine.

 

Repression of the Heat Shock Response Is a Programmed Event at the Onset of Reproduction

http://www.longecity...e-9#entry737774

Simple flip of genetic switch determines aging or longevity in animals. Seems like we need to learn how to switch the maintinace program back on.

 

 

I personally like it when researchers upset the theory of mitochondrial aging. Here are 2 articles that offer other causes and targets for intervention. Now this is not to say that the mitochondria do not become damaged with age but there may be programing or lack there of that initiates our decline that gets turned off. The epigenome and programing related to cellular maintenance seem to underlie everything.  


Edited by Bryan_S, 20 August 2015 - 07:31 PM.

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