471 replies to this topic

[BigLabRat]

Guys could you take your vender conversations to this venders thread? I for one find this offer suspect, 40 or 50% off, which is it? Many of you have brought these kinds of offers to threads not associated with LCR like the our HPN group buy thread. If you don't want to discuss it on their thread then take it to http://www.longecity...-and-discussion This is where we decide if something is legit or not.

 

I had no intention of discussing vendors, and I wasn't asking "What do you think of this offer?" I only mentioned the source because I realized that if I didn't, the immediate question would have been "From where?"

 

As I said, I thought a drop of NR price by half was news. There have been a lot of questions about when and if NR prices might decline. Isn't it news when the is an instance of a price falling by 50%?

 

I already bought 12 bottles, so I'm not just speculating. I have a USPS tracking number. I expect my order to arrive within the week, as USPS notified me that it shipped on Aug 7. If it isn't "legit" then I'll be contacting the Post Office about federal mail fraud charges. 

 

There is nothing "suspect" about the numbers. The offer was 40% off for 6 bottles or 50% off for 12 bottles. I didn't give details because my point wasn't about the specific offer--it was about the fact that prices seemed to be falling substantially for some reason.

 

If you want specifics, my previous price from this vendor was $45.50 per bottle, which is $6.07 per gram. My price this time for 12 bottles was $280, which is $23.33 per bottle. That's $3.11 a gram.

 

I'm now betting we will see the overall market prices decline significantly in the near future, which was my point.
 

[BigLabRat]

Has taking Enduramide been mentioned. (I'm sorry, but I haven't read every post in this thread.)
http://www.endur.com...ur-amide-500-mg

 

I found no safety issues, so I take 1,500 mg twice a day.

 

Enduramide is a pharmaceutial-grade sustained-release niacinamide that is being used in a study of Alzheimer's patients at UC Irvine.
https://clinicaltria...heimer's&rank=1

 

This human study was initiated after niacinamide resolved the mouse version of Alzheimer's and returned the mice's memory.
http://www.jneurosci.../11500.full.pdf

 

Since niacinamide only lasts about 90 minutes in the body, a true sustained-release version is a best option for people that don't want to take it every 90 minutes.

 

I also take high-dose NR.

 

Is there a reason not to take both?

 

I wasn't familiar with Enduramide. As I have made clear in discussions about Niacin, however, I am quite wary of sustained-release formulations.

 

As Bryan S has discussed at some length, Niacin, Nicotinamide, and NR have separate pathways to NAD with some overlap.

 

I think that supplementing with all 3 might be a good strategy. But I wouldn't be inclined to use sustained-release Niacin (such as Niaspan), which has demonstrated risks for the liver, or sustained-release Nicotinamide (such as Enduramide)--which strike me as likely to pose risks for the liver. (Notice that the UCI study is carefully monitoring liver function--so I guess they have same concern I do.) 

 

For that matter, when someone comes up with a sustained-release NR (count on it happening soon), I wouldn't be inclined to take that, either. At least not until someone demonstrates it has advantages an minimal risks.

[mikey]

 

Has taking Enduramide been mentioned. (I'm sorry, but I haven't read every post in this thread.)
http://www.endur.com...ur-amide-500-mg

 

I found no safety issues, so I take 1,500 mg twice a day.

 

Enduramide is a pharmaceutial-grade sustained-release niacinamide that is being used in a study of Alzheimer's patients at UC Irvine.
https://clinicaltria...heimer's&rank=1

 

This human study was initiated after niacinamide resolved the mouse version of Alzheimer's and returned the mice's memory.
http://www.jneurosci.../11500.full.pdf

 

Since niacinamide only lasts about 90 minutes in the body, a true sustained-release version is a best option for people that don't want to take it every 90 minutes.

 

I also take high-dose NR.

 

Is there a reason not to take both?

 

I wasn't familiar with Enduramide. As I have made clear in discussions about Niacin, however, I am quite wary of sustained-release formulations.

 

As Bryan S has discussed at some length, Niacin, Nicotinamide, and NR have separate pathways to NAD with some overlap.

 

I think that supplementing with all 3 might be a good strategy. But I wouldn't be inclined to use sustained-release Niacin (such as Niaspan), which has demonstrated risks for the liver, or sustained-release Nicotinamide (such as Enduramide)--which strike me as likely to pose risks for the liver. (Notice that the UCI study is carefully monitoring liver function--so I guess they have same concern I do.) 

 

For that matter, when someone comes up with a sustained-release NR (count on it happening soon), I wouldn't be inclined to take that, either. At least not until someone demonstrates it has advantages an minimal risks.

 

 

Niacinamide doesn't burden the liver the way niacin does.

 

However, the potential burden on the liver with niacin is exaggerated as there is no documented death from taking niacin, even high-dose sustained-release niacin.

 

The advantage to a true pharmaceutical-grade sustained-release niacinamide is that one can take it twice a day rather than every 90 minutes.

 

And niacinamide has been shown to produce no toxicity at doses below 3 g/day.

http://www.ncbi.nlm....pubmed/16596767

https://www.ncbi.nlm...pubmed/11126400

[BigLabRat]

Niacinamide doesn't burden the liver the way niacin does.

 

However, the potential burden on the liver with niacin is exaggerated as there is no documented death from taking niacin, even high-dose sustained-release niacin.

 

The advantage to a true pharmaceutical-grade sustained-release niacinamide is that one can take it twice a day rather than every 90 minutes.

 

And niacinamide has been shown to produce no toxicity at doses below 3 g/day.

http://www.ncbi.nlm....pubmed/16596767

https://www.ncbi.nlm...pubmed/11126400

 

 

Wow, your reference point for safety is that there is no documented death? You're hardcore, my man.

 

There are many documented cases of serious liver problems, extending to jaundice and hepatitis, associated with sustained-release niacin. These occur at daily dosages that are safe with non-sustained release niacin.

 

I'm familiar with the 3 g/d guideline on normal niacinamide (and quite a few people exceed it). But we have very little experience with it in a sustained-release form. Dosages shown to be safe with standard niacin were NOT safe with sustained-release niacin, so I'd be worried about sustained-release niacinamide as well.

 

In fact, some studies suggest that the body begins cutting back its own production of antioxidants when exposed to high sustained blood levels of ingested antioxidants. So I don't even take sustained-release Vitamin C anymore.

 

There is a prevailing medical paradigm that if something is beneficial, then high unvarying blood levels of it must be the most beneficial means of administration. There is virtually no evidence for this belief; it is simply assumed.

 

In any case, I agree--sustained-release niacinamide at reasonable doses probably won't actually kill you.
 

[resveratrol_guy]

This human study was initiated after niacinamide resolved the mouse version of Alzheimer's and returned the mice's memory.

 

The data isn't indicative of that, even though that's basically what they said in their conclusion. It looks more like they halfway reversed the deficits in mice with mild-to-moderate dementia.

 

Still, there's a lot more going on here than the mere amelioration of energy deficits, for example, the effects on amyloid and phosphotau. It's well worth a read. All in all, it sounds like we should consider the use of various NAD+ precursors for the prevention of cognitive decline. I definitely appreciate the liver risks, but I think we're much closer to treating those problems with drugs or stem cells, than we are to treating dementia.

[Bryan_S]

 

This human study was initiated after niacinamide resolved the mouse version of Alzheimer's and returned the mice's memory.

 

The data isn't indicative of that, even though that's basically what they said in their conclusion. It looks more like they halfway reversed the deficits in mice with mild-to-moderate dementia.

 

Still, there's a lot more going on here than the mere amelioration of energy deficits, for example, the effects on amyloid and phosphotau. It's well worth a read. All in all, it sounds like we should consider the use of various NAD+ precursors for the prevention of cognitive decline. I definitely appreciate the liver risks, but I think we're much closer to treating those problems with drugs or stem cells, than we are to treating dementia.

 

 

"sounds like we should consider the use of various NAD+ precursors for the prevention of cognitive decline" You also mention amyloid and phospho tau. They are also referred to as cellular highways or cellular scaffolding. Any problems with these structures prevents the normal binding and passage of motor proteins and this is very deeply rooted in the problem. Amazingly we have teams of motor proteins shuttling supplies and even entire cell organelles to and fro.

 

 

Do you guys remember the recent post on NAD+ and SIRT3 control microtubule dynamics and reduce susceptibility to antimicrotubule agents. I don't recall the other exact post on neurons but you should see how dynamic and busy a healthy nerve cell is all because of these microtuble highways. See video http://jama.jamanetw...mediaid=2522082

 

Now imagine a world were the cellular highways on which our mitochondria travel within our neurons as a tangled mess of proteins. Now the above article wasn't precisely about Alzheimer's but I think you get the thought. These protein folding problems are certainly a common cellular scaffolding theme among many diseases and we are beginning to find the mechanisms to protect and reinforce our cellular scaffolding.

 

Here is an article that caught my eye earlier this year LongeCity Posted 29 April 2015 - 01:36 PM. 

"Scripps Florida Scientists' 'Mad Cow' Discovery Points to Possible Neuron Killing Mechanism Behind Alzheimer’s and Parkinson’s Diseases"

 

What's the connection to this thread "Scripps Research Institute and ChromaDex® To Collaborate on Niagen™ Nicotinamide Riboside Research" They (Scipps) are working with NAD precursors on a number of studies and much of it has to do with re-energizing our underlying cellular maintenance.

 

​Now its doubtful even if you could get the cells to clear the tangled proteins that you'd completely restore a patient to their former self, considering the cell loss they may have already sustained. So finding preventive ways to keep neurons from dying in the first place and reinforcing their ability to self correct abnormalities should be priority one.

 

In this, early NAD boosting studies have already begun to show promise.     

 

Here was another related article Posted 25 May 2015 - 07:07 PM

http://www.longecity...e-7#entry729441

Edited by Bryan_S, 09 August 2015 - 06:04 AM.

[ceridwen]

That is why it is important to create new neurons that can be incorporated by the original for its use

[Bryan_S]

That is why it is important to create new neurons that can be incorporated by the original for its use

 

In the ischemia studies NAD boosting did increase post stem cell activation helping to replace lost neurons.

[Bryan_S]

Lycopene Pretreatment Ameliorates Acute Ethanol Induced NAD+ Depletion in Human Astroglial Cells

Received 15 February 2015; Revised 17 April 2015; Accepted 30 April 2015

Interesting and somewhat unexpected results. I'm sure there are a few of us who take a drink or 2 from time to time. Some of you may remember a study on nicotinamide and Fetal Alcohol Syndrome "Nicotinamide: A Way to Prevent Fetal Alcohol Syndrome" Also See "Vitamin B3 Variant Reverses Effects of Fetal Alcohol Syndrome in Mice" From these studies we can see niacinamide aka nicotinamide can help save of cell loss by raising NAD levels but it still isn't advisable to drink while pregnant.

 

OK so we know alcohol isn't good for the fetus. But we as adults can deal with a drink or 2, right? We also have some powerful antioxidants at our disposal that can fight any damage, well "yes and no." Here is a study looking at Lycopene which is one of the most powerful phytochemical antioxidants. In this study they got marginal protective effects from alcohol in a very narrow dose range. I wouldn't call this study a success where I felt I could binge and save off the deleterious effects but the data and insights are well worth a read.

http://www.hindawi.c...cl/2015/741612/

 

5. Conclusions

"In summary, results from this study indicate that acute ethanol exposure, at physiologically relevant concentrations, increases oxidative damage in U251 cells, resulting in upregulation of PARP activity and consequently a significant decrease in intracellular levels of its substrate NAD(H), a molecule critical for cellular health. A novel dose dependent relationship between ethanol exposure and reduced concentrations of the protective NAD+ dependent enzyme SIRT1 was also observed. Further investigation is required to determine if this effect was solely the consequence of reduced NAD+ availability. While data from this study suggests that exposure of the brain to alcohol at commonly observed blood concentrations may cause at least transitory oxidative damage, the novel finding that lycopene can prevent the ethanol induced reduction of astrocyte NAD(H) stores suggests that this naturally occurring carotenoid, if present in the brain at around 1 μM, may at least partly ameliorate ethanol mediated brain toxicity. Further research using mixed culture and murine models is required to confirm this hypothesis."

Edited by Bryan_S, 09 August 2015 - 05:15 PM.

[smithx]

The unfolded protein response is actually apoptosis (at least in normal UPR).

 

In fact, over-activation of the UPR is probably responsible for many diseases from diabetes to various forms of blindness. In some of these diseases, there are forms of the proteins which would fold properly given more time, but the UPR happens too quickly and triggers cell death.

 

One of my researcher friends works on this problem, and has some promising treatments in development which work in exactly this way: by inhibiting the UPR.

 

So if we were to activate the UPRmt in older cells which may need more time for proteins (albeit perhaps not perfect proteins) to finish folding, too many cells might die, and that could be bad. It's possible that UPRmt becomes less aggressive with aging specifically because there may be accumulated mutations causing the proteins to require longer to fold.

 

 

 

Do we need any more reasons to boost our NAD? Activating our UPRmt looks to be the Holy Grail. This is why I believe targeting the summit of our energy production and cellular respiration can have so many downstream health benefits.

 

[Bryan_S]

 

The unfolded protein response is actually apoptosis (at least in normal UPR).

 

In fact, over-activation of the UPR is probably responsible for many diseases from diabetes to various forms of blindness. In some of these diseases, there are forms of the proteins which would fold properly given more time, but the UPR happens too quickly and triggers cell death.

 

One of my researcher friends works on this problem, and has some promising treatments in development which work in exactly this way: by inhibiting the UPR.

 

So if we were to activate the UPRmt in older cells which may need more time for proteins (albeit perhaps not perfect proteins) to finish folding, too many cells might die, and that could be bad. It's possible that UPRmt becomes less aggressive with aging specifically because there may be accumulated mutations causing the proteins to require longer to fold.

 

 

 

Do we need any more reasons to boost our NAD? Activating our UPRmt looks to be the Holy Grail. This is why I believe targeting the summit of our energy production and cellular respiration can have so many downstream health benefits.

 

 

While what you say may be true, "In this context, the UPRmt senses the perturbations that overload its quality control network capacities, and activates the transcription of nuclearencoded protective genes in order to re-establish mitochondrial homeostasis (Haynes and Ron, 2010)."

 

"Moreover, treatment with NAD+ boosters, such as nicotinamide riboside (NR) and poly(ADP-ribose) polymerase inhibitors (PARPi), which stimulate mitochondrial biogenesis via the sirtuin 1 (SIRT1) pathway, also induced a mito-nuclear protein imbalance resulting in UPRmt in mammalian cells and in C. elegans (Mouchiroud et al., 2013). In line with the beneficial and protective effects of UPRmt, the stimulation of the SIRT1 pathway also increased worm lifespan (Mouchiroud et al., 2013). This suggests that UPRmt, triggered by different mitochondrial stresses, i.e. by increasing protein-folding workload during biogenesis or by mitonuclear proteostatic imbalance, could be the underlying mechanism leading to increased longevity. These results highlight the importance of UPRmt in the control of mitochondrial function across multiple species. Furthermore, if the C. elegans data can be extended to mammals, one can speculate that health and lifespan may be improved by using pharmacological agents to activate UPRmt."

 

"While these outstanding issues are being addressed, we should not forget that this pathway could provide therapeutic opportunities that may help us to manage some of the most pervasive diseases that are associated with aging, such as metabolic diseases, cancer and neurodegenerative diseases. Drawing parallels with the beneficial impact of UPRmt in C. elegans, targeting this pathway via nutritional and/or pharmaceutical approaches could hence also improve health and lifespan in higher organisms and eventually help to manage some of the common age-related diseases."

 

I agree they are only beginning to grasp this pathway but NAD boosting in this context produced protective effects which I don't think went as far as over-activation.

http://jeb.biologist.../1/137.full.pdf

[Bryan_S]

Major Pathway Identified in Nerve Cell Death Offers Hope for Therapies

Released: 21-Apr-2015 2:05 PM EDT 
Source Newsroom: Washington University in St. Louis

 

http://www.newswise....es/view/633076/

 

 

Major Pathway Identified in Nerve Cell Death Offers Hope for Therapies

http://neurosciencen...thy-sarm1-1987/

4 days ago in Neuroscience News

Axon degeneration (top), caused by nerve injury or disease, depletes the energy supply within axons, shutting down communication between nerve cells. Washington University scientists blocked axon degeneration by supplementing neurons with a chemical called nicotinamide riboside, which kept the axons energized and healthy (bottom). The image is for illustrative purposes only. Image credit: Milbrandt lab.

 

“When a nerve is diseased or injured, SARM1 becomes more active, initiating a series of events that quickly causes an energetic catastrophe within the axon, and the axon undergoes self-destruction,” said first author Josiah Gerdts, an MD/PhD student in Milbrandt’s laboratory.

Working in neurons in which SARM1 was activated, the researchers showed they could completely block axon degeneration and neuron cell death by supplementing the cells with a precursor to NAD, a chemical called nicotinamide riboside. The neurons were able to use nicotinamide riboside to keep the axons energized and healthy.

Nicotinamide riboside has been linked in animal studies to good health and longevity, but its benefits have not been shown in people. The researchers said much more research is needed to know whether the chemical could slow or halt axon degeneration in the body.

“We are encouraged by the findings and think that identifying a class of drugs that block SARM1 activity has therapeutic potential in neurological disorders,” Milbrandt said. “The molecular details this pathway provides give us a number of therapeutic avenues to attack.”

[Bryan_S]

Results from First Human Clinical Study Demonstrate ChromaDex's NIAGEN® Nicotinamide Riboside Effectively Increases the Co-enzyme NAD+ and is Safe

http://investors.chr...icle&ID=2078998

 

 

Results from First Human Clinical Study Demonstrate ChromaDex's NIAGEN® Nicotinamide Riboside Effectively Increases the Co-enzyme NAD+ and is Safe

 

- Clinical Data Presented Today at the FASEB Science Research Conference on NAD+ Metabolism and Signaling 

 

IRVINE, Calif., Aug. 12, 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, announced today that results of the first controlled human clinical study on the use of the Company's NIAGEN^®nicotinamide riboside (NR) were presented at 4^th Federation of American Societies for Experimental Biology (FASEB) Science Research Conference on NAD+ Metabolism and Signaling, currently being held in Germany.

 

Charles Brenner, PhD, a key member of the ChromaDex Scientific Advisory Board presented an oral platform talk on "How Nicotinamide Riboside Promotes Weight Loss." In addition, Dr. Brenner, Mr. Frank Jaksch, Dr. Ryan Dellinger, and their co-workers presented a poster entitled, "Dose-Dependent Elevation of the Blood NAD Metabolome by NR in Healthy Human Beings."

 

The oral presentation and poster presented data which indicate that single doses of NIAGEN^® NR can elevate the co-enzyme NAD+ in the blood by as much as 2.7-fold. In the first-in-humans clinical trial which involved dosing twelve healthy adult subjects, the group showed that blood cell NAD+ increased with single 100 mg, 300 mg and 1 gram doses of NIAGEN^® NR. Average maximal increases in blood NAD+ were approximately 30% at the 100 mg dose and approximately 50% at the higher doses. Increases in blood NAD+ tended to be sustained for longer times at higher doses.

 

These observations validate NIAGEN^® as an effective agent at elevating blood cell NAD+ metabolism in healthy human beings and are expected to support additional clinical studies that will further characterize the pharmacokinetics of NIAGEN^® and associations between elevated or depressed NAD+ metabolism with other metabolic markers, diseases and conditions.

 

Dr. Brenner commented, "The results of this study constitute a significant milestone in the translation of NR technologies as it is the first time an increase in NAD+ in humans has been demonstrated through NR supplementation. Importantly, this initial single dose study showed an increase of NAD+ across all three doses of NR. It was, in fact, somewhat surprising that a molecule as tightly regulated and abundant as NAD+ could be elevated by single doses of NR."  

 

Nobel Laureate Dr. Roger Kornberg, who chairs ChromaDex's Scientific Advisory Board, commented, "Numerous published studies have demonstrated the potential health and therapeutic benefits of NR as a precursor to NAD+. Based on encouraging findings in this single dose study, ChromaDex is planning its second human study to both further validate NR as an effective NAD+ precursor as well as to begin evaluating the therapeutic benefits of increasing NAD+."

 

NAD+ is a critically important cellular cofactor that is required for fuel utilization and function of every cell in the human body. When fuel is oxidized, NAD+ is converted to NADH for cellular energy production. The related compound NADP is converted to NADPH for synthesis of lipids and detoxification of reactive oxygen species. In 2004, then at Dartmouth College, Dr. Brenner reported NR as a previously unappreciated vitamin precursor of NAD+ in humans.

 

ChromaDex's NIAGEN® is the first and only commercially available form of NR and is supported by five patents issued and several pending, with patent rights acquired from Dartmouth College, Cornell University and Washington University.

 

In addition to functioning as a cofactor, NAD+ is required for the function of sirtuins, a family of enzymes that control gene expression, metabolism and mitochondrial functions, particularly during changing nutritional conditions. Sirtuins are key target enzymes in healthy aging, such that the search for sirtuin activators has been a major goal of academic, biotechnology and pharmaceutical research for the last decade. In 2007, Dr. Brenner reported that NR extends yeast lifespan by elevating cellular NAD and increasing sirtuin function. More recently, NR has been shown to improve the metabolism of mice on high fat diet, protect mice from noise-induced hearing loss, and protect mice from the damaging effects of mitochondrial mutations.

 

In the same presentations, Dr. Brenner reported a University of Iowa discovery of elevated nicotinic acid adenine dinucleotide (NAAD) as an unanticipated and highly sensitive biomarker of increased NAD+ metabolism. The study showed NAAD increases from non-detectable levels prior to NR supplementation, to levels that are clearly correlated with increasing levels of NAD+ with NR supplementation. A provisional patent on the discovery has been filed.

 

Maintenance of sufficient levels of NAD+ is key to cellular energy metabolism and mitochondrial function. If NAD+ levels go down or are redirected (as in cancer cells), mitochondrial function erodes, creating numerous adverse effects. For example, results of a mouse study conducted by the National Institutes of Health (NIH) in collaboration with ChromaDex published in November 2014 indicated that NR was effective at restoring NAD+ levels in mitochondria and rescuing phenotypes associated with a devastating accelerated aging disease known as Cockayne Syndrome (CS). The researchers concluded that NR showed promise as a potential therapy for the disease, as well as for other age-related neurodegenerative conditions.

 

Published research has shown that NR is perhaps the most effective precursor to boost the co-enzyme NAD+ in the cell. NAD+ is arguably the most important cellular co-factor for improvement of mitochondrial performance and energy. In recent years, NAD+ has also been shown to participate as an extracellular signaling molecule in cell-to-cell communication. NAD+ is essential in supporting healthy cellular metabolism, including the efficient conversion of blood glucose into energy. 

 

As organisms age, NAD+ levels are reported to drop, which leads to a decrease in mitochondrial health; this in turn may lead to age-related health issues. Low NAD+ levels limit the activity of a group of enzymes called sirtuins, which are believed to play key roles in longevity. NAD+ levels can be depleted by many of the stresses of life. By boosting NAD+, NR can increase mitochondrial health and induce creation of new mitochondria.

 

About the FASEB Science Research Conference on NAD+ Metabolism and Signaling:

 

A main aspect of this conference will be to foster exchange of information and technology between researchers working on the biochemical, molecular, genetic and cell biological aspects of NAD+ and related molecules. Moreover, the conference will provide a unique venue for those researchers worldwide who are interested in the basic and translational aspects of NAD metabolism and signaling. For more information about the conference, visit: http://www.faseb.org/SRC-NAD/Home.aspx.

 

About FASEB:

 

Founded in 1912, the Federation of American Societies for Experimental Biology (FASEB) was originally created by three independent scientific organizations to provide a forum in which to hold educational meetings, develop publications, and disseminate biological research results. What started as a small group of dedicated scientists has grown to be the nation's largest coalition of biomedical researchers, representing 27 scientific societies and over 125,000 researchers from around the world. FASEB is now recognized as the policy voice of biological and biomedical researchers.

 

About ChromaDex:

 

ChromaDex leverages its complementary business units to discover, acquire, develop and commercialize patented and proprietary ingredient technologies that address the dietary supplement, food, beverage, skin care and pharmaceutical markets. In addition to our ingredient technologies unit, we also have business units focused on natural product fine chemicals (known as "phytochemicals"), chemistry and analytical testing services, and product regulatory and safety consulting (known as Spherix Consulting). As a result of our relationships with leading universities and research institutions, we are able to discover and license early stage, IP-backed ingredient technologies. We then utilize our in-house chemistry, regulatory and safety consulting business units to develop commercially viable ingredients. Our ingredient portfolio is backed with clinical and scientific research, as well as extensive IP protection. Our portfolio of patented ingredient technologies includes NIAGEN^® nicotinamide riboside; pTeroPure^® pterostilbene; PURENERGY^®, a caffeine-pTeroPure^®co-crystal; ProC3G^®, a natural black rice containing cyanidin-3-glucoside; IMMULINA^™, a spirulina extract; and Suntava^® Purple Corn derived from a proprietary non-GMO purple corn hybrid which contains an extraordinarily high level of anthocyanins. To learn more about ChromaDex, please visit www.ChromaDex.com.

 

Forward-Looking Statements:

 

This release contains forward-looking statements within the meaning of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities and Exchange Act of 1934, as amended. Statements that are not a description of historical facts constitute forward-looking statements and may often, but not always, be identified by the use of such words as "expects", "anticipates", "intends", "estimates", "plans", "potential", "possible", "probable", "believes", "seeks", "may", "will", "should", "could" or the negative of such terms or other similar expressions. Actual results may differ materially from those set forth in this release due to the risks and uncertainties inherent in ChromaDex's business. More detailed information about ChromaDex and the risk factors that may affect the realization of forward-looking statements is set forth in ChromaDex's Annual Report on Form 10-K for the fiscal year ended January 3, 2015,ChromaDex's Quarter Reports on Form 10-Q and other filings submitted by ChromaDex to the SEC, copies of which may be obtained from the SEC's website at www.sec.gov. Readers are cautioned not to place undue reliance on these forward-looking statements, which speak only as of the date hereof. All forward-looking statements are qualified in their entirety by this cautionary statement andChromaDex undertakes no obligation to revise or update this release to reflect events or circumstances after the date hereof.

 

Statements in this press release have not been evaluated by the Food and Drug Administration.  Products or ingredients are not intended to diagnose, treat, cure or prevent any disease.

 

FASEB has no legal, business or other mutually beneficial relationship with ChromaDex (a sponsor) or its representative of this conference. Neither party has influenced any aspect of the program.

 

CONTACT: ChromaDex Company Contact:
Andrew Johnson
Director of Investor Relations
949-419-0288
andrewj@chromadex.com
 

ChromaDex Investor Contact:
The Del Mar Consulting Group, Inc.
Robert B. Prag, President
858-794-9500
bprag@delmarconsulting.com

 

Edited by Bryan_S, 12 August 2015 - 10:48 PM.

[albedo]

Was eagerly waiting for the results. I am happy it looks like even at 100mg there seems to be a positive effect (30%). Thank you for having posted that.

[BigLabRat]

Lycopene Pretreatment Ameliorates Acute Ethanol Induced NAD+ Depletion in Human Astroglial Cells

Received 15 February 2015; Revised 17 April 2015; Accepted 30 April 2015

Here is a study looking at Lycopene which is one of the most powerful phytochemical antioxidants. In this study they got marginal protective effects from alcohol in a very narrow dose range. I wouldn't call this study a success where I felt I could binge and save off the deleterious effects but the data and insights are well worth a read.

 

 

Well, I love wine, and I love tomatoes, so I'd take this as great news!

 

Is there any chance basil and mozzarella are involved?

 

In all seriousness, lycopene seems to have amazing properties. But I haven't seen any proposed mechanism yet...except the endless chant about antioxidants, which I think is a red herring in terms of actual benefits.

[BigLabRat]

The oral presentation and poster presented data which indicate that single doses of NIAGEN^® NR can elevate the co-enzyme NAD+ in the blood by as much as 2.7-fold. In the first-in-humans clinical trial which involved dosing twelve healthy adult subjects, the group showed that blood cell NAD+ increased with single 100 mg, 300 mg and 1 gram doses of NIAGEN^® NR. Average maximal increases in blood NAD+ were approximately 30% at the 100 mg dose and approximately 50% at the higher doses. Increases in blood NAD+ tended to be sustained for longer times at higher doses.

 

Thanks for posting this, Bryan.

 

Of course, there are still so many questions...and probably no likelihood they will get answered, given how these sorts of studies are funded. But if you or others have thoughts on this, I'd like to hear them.

 

1) Does this downregulate over time? This seems to be a study of an acute dose.

 

2) How does this compare to administration of niacin or nicotinamide?

 

3) Are blood levels of NAD+ a good indicator of beneficial effects within the cells and mitochondria?

 

4) There seems to be a steep leveling off in the response curve, but this doesn't give us much info; it would be really nice to know what happens between 100 and 1,000 mg.

 

Don't get me wrong, I'm not betting against NR: Since prices have tumbled, I'm up to 750 mg per day.
 

[Kevnzworld]

Re : the Chromadex study Bryan posted:
Unfortunately the quotes didn't elaborate on the NAD boost time frame other than to say larger doses were more effective in prolonging the increase. I'm considering breaking up my 500 mg morning dose into 250 twice a day. The difference between a 250 and 500 boost effect seems relatively small. The deterioration of the boost might be more important.
Any thoughts?

[Bryan_S]

I'm still digesting this as I'm sure everyone else is. Here is what I see as the meat and potatoes.

 

"The oral presentation and poster presented data which indicate that single doses of NIAGEN^®NR can elevate the co-enzyme NAD+ in the blood by as much as 2.7-fold. In the first-in-humans clinical trial which involved dosing twelve healthy adult subjects, the group showed that blood cell NAD+ increased with single 100 mg, 300 mg and 1 gram doses of NIAGEN^® NR. Average maximal increases in blood NAD+ were approximately 30% at the 100 mg dose and approximately 50% at the higher doses. Increases in blood NAD+ tended to be sustained for longer times at higher doses."

 

This seems to indicate 2.7 fold is the maximum measured elevation in NAD. They measured a 30% increase at 100mg and a 50% increase at 300mg and 1000mg. The half life fall off at the higher dosages helped sustain NAD levels over a longer period of time than the lower dosages.

 

That is my take away from the crumbs they've released and we also lack the metrics.

 

So how much is a "fold?" Well a fold is a doubling of something. The common "fold" expression means "100%", and it is very often misused in expressing comparisons. If something increases by 100% (that means it doubles), it increases one-fold. An increase of 180% is an increase of 1.8-fold. A 2.7-fold would indicate a 270% increase. I also have to equally assume they achieved this increase with the 300 and 1000mg dosages.

 

NAD is carefully monitored and regulated with built in feedback loops. So if 300mg and 1000mg both produced the same increase we are up against a rate limiting factor. However levels tended to be sustained at higher levels at the higher dose so the takeaway from that is fall off would be constant with the half life of the NR in circulation. The half life figures were not published and we need more data along these lines.

 

If we knew the fall off rate we might be able to calculate from an initial dose reaching peak NAD levels what timing to apply to the subsequent ingestion of NR to maintain levels. Hypothetically i.e. 250mg upon waking followed by 50mg every hour until bed time, for instance.

 

As Kevnzworld suggested for the last few months I've been doing something similar taking an initial 250mg in the morning and supplementing that with a capsule at a time thru the rest of the day. 

  

"In the same presentations, Dr. Brenner reported a University of Iowa discovery of elevated nicotinic acid adenine dinucleotide (NAAD) as an unanticipated and highly sensitive biomarker of increased NAD+ metabolism. The study showed NAAD increases from non-detectable levels prior to NR supplementation, to levels that are clearly correlated with increasing levels of NAD+ with NR supplementation. A provisional patent on the discovery has been filed." So it appears they are on to a new biomarker that's interesting.

 

We still need more data but I'd expect a publication to follow soon but even at that we will still lack long term data to form an ongoing NAD boosting strategy.

Edited by Bryan_S, 13 August 2015 - 05:46 PM.

[BigLabRat]

I'm not sure if the difference in the boost is small. (50% versus 30%. 50% is an increase of two-thirds over 30%.)

 

But you raise an interesting question: Is prolonged elevation at lower levels better, or is a higher peak followed by a decline better? Alas, we have no idea.

 

Most folks like to model of increasing blood levels of supplements round the clock, and it might or might not be the best thing with NR. I think surges as opposed to constant blood levels are less likely to result in downregulation...but we have zero info on that with NR.

 

Of course, your proposed two-dose-a-day is more like two surges in any case. So if it feels right, why not give it a try?

 

I used to take niacin in the morning and niacinamide before bed. Now I'm taking NR in the morning and niacinamide before bed. I'm trying to figure out how to work niacin back into my day. I figure three precursors and three pathways are better than one. But who knows?

[BigLabRat]

As Kevnzworld suggested for the last few months I've been doing something similar taking an initial 250mg in the morning and supplementing that with a capsule at a time thru the rest of the day. 

  

"In the same presentations, Dr. Brenner reported a University of Iowa discovery of elevated nicotinic acid adenine dinucleotide (NAAD) as an unanticipated and highly sensitive biomarker of increased NAD+ metabolism. The study showed NAAD increases from non-detectable levels prior to NR supplementation, to levels that are clearly correlated with increasing levels of NAD+ with NR supplementation. A provisional patent on the discovery has been filed." So it appears they are on to a new biomarker that's interesting.

 

 

So what's your daily NR intake, Bryan? (And do I correctly recall that you're taking niacinamide as well, or do I misremember?)

 

-----------------

 

I wonder what's up with the NaAD elevation? If I recall correctly, NaAD is the last intermediate in the conversion of niacin to NAD+. (And also the last intermediate in the body's production of NAD+ from tryptophan, which follows the same pathway.)

 

Could this mean that NR is elevating NAD+ enough that NaAD is sort of "piling up" rather than being phosphorylated to NAD+? Is there a feedback loop that is dialing down the niacin/tryptophan pathway?

 
 

[Thell]

Hot off the press Niagen Study Blurb; anyone have any info on publication of the study results?

 

The oral presentation and poster presented data which indicate that single doses of NIAGEN® NR can elevate the co-enzyme NAD+ in the blood by as much as 2.7-fold. In the first-in-humans clinical trial which involved dosing twelve healthy adult subjects, the group showed that blood cell NAD+ increased with single 100 mg, 300 mg and 1 gram doses of NIAGEN® NR. Average maximal increases in blood NAD+ were approximately 30% at the 100 mg dose and approximately 50% at the higher doses. Increases in blood NAD+ tended to be sustained for longer times at higher doses. - See more at: http://globenewswire...h.kHc5z2f9.dpuf

 

 

 

Edited by Thell, 13 August 2015 - 08:04 PM.

[Bryan_S]

 

As Kevnzworld suggested for the last few months I've been doing something similar taking an initial 250mg in the morning and supplementing that with a capsule at a time thru the rest of the day. 

  

"In the same presentations, Dr. Brenner reported a University of Iowa discovery of elevated nicotinic acid adenine dinucleotide (NAAD) as an unanticipated and highly sensitive biomarker of increased NAD+ metabolism. The study showed NAAD increases from non-detectable levels prior to NR supplementation, to levels that are clearly correlated with increasing levels of NAD+ with NR supplementation. A provisional patent on the discovery has been filed." So it appears they are on to a new biomarker that's interesting.

 

 

So what's your daily NR intake, Bryan? (And do I correctly recall that you're taking niacinamide as well, or do I misremember?)

 

-----------------

 

I wonder what's up with the NaAD elevation? If I recall correctly, NaAD is the last intermediate in the conversion of niacin to NAD+. (And also the last intermediate in the body's production of NAD+ from tryptophan, which follows the same pathway.)

 

Could this mean that NR is elevating NAD+ enough that NaAD is sort of "piling up" rather than being phosphorylated to NAD+? Is there a feedback loop that is dialing down the niacin/tryptophan pathway?

 
 

 

 

"I wonder what's up with the NaAD elevation?" Exactly what I remembered as well, which is a bit confusing in light of recent past publications.

 

My intake: I take 1000mg of NR thru the day. I take 2000mg of Niacinamide before bed.

 

I start the day with SIRT1 and SIRT3 activators in the morning with my first NR. I take Honokiol (for SIRT3) in the form of Magnolia Extract 200 mg (the cheap stuff) and Pterostilbene (for SIRT1) 50 mg twice a day. In addition I take 250mg of Grape Seed Extract also twice per day. I also take some garlic for my joints.

 

 

I started Pterostilbene for its SIRT1 activation and for its blood pressure properties. The Honokiol/Magnolia Extract which has also been recently recognized for its blood pressure reduction and up regulates SIRT3 as we previously discussed. I also incorporated the Grape Seed Extract for its blood pressure properties. I'm seeing about a 10 point reduction at the moment so nothing cumulative is going on because this is the max amount produced by any one of the 3 alone. 

 

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.

Edited by Bryan_S, 13 August 2015 - 08:27 PM.

[resveratrol_guy]

 

My intake: I take 1000mg of NR thru the day. I take 2000mg of Niacinamide before bed.

 

Based on the Chromadex study above, it sounds like you're essentially at the limits of oral NR effectiveness, not to mention that 2g of niacinamide is also very high, relative to the population at large. So I hardly think you can push NAD+ any harder, unless we entertain intraday chronic dosing, which is unknown territory with NR and liver function. Which all begs the question: have you noticed anything, apart from the prostate issue?

 

No doubt we could raise NAD+ area-under-curve even more by dosing several times per day. There might be a useful, if harrowing, health tradeoff here, if we assume that liver toxicity is somewhat easily solved with mesenchymal stem cells and liver-protective supplements, while NAD+ insufficiency and all its horrible downstream effects is otherwise essentially unsolvable. In other words, risk damaging the body's most regenerable vital organ in order to stave off chronic disease systemically. I wonder if there is evidence for the effectiveness of such a regimen, for instance, in rodents. Given that we obviously lack human data on such a strategy, is there any evidence suggesting that this turbocharging of NAD+ would be useful? (I'm thinking, for instance, of your axon micrographs above, which are night-and-day different, but no doubt occurred as a result of obscene NR concentrations relative to what we could achieve with a once-a-day NR pill.)

 

Related thread: How much is too much Nicotinamide Riboside

 

In the above thread, Bryan, you mentioned that you remembered someone taking 4 g/day. I found that thread here, which would probably interest you because the poster wrote: "I've had prostatitis for the last 15 years. It's been getting progressively worse. When I hit 2 grams per day of Niagen, my prostatitis was significantly better. I've been keeping a journal since beginning Niagen, and I keep track of how many times I urinate and what time of day. When I hit 4 grams a day of Niagen I have no urgency no tenderness, no symptoms. My trips to the bathroom has decreased significantly. No urgency at all. My prostate feels like it did when I was in my 40's."

 

Edited by resveratrol_guy, 14 August 2015 - 02:15 AM.

[Bryan_S]

 

 

My intake: I take 1000mg of NR thru the day. I take 2000mg of Niacinamide before bed.

 

Based on the Chromadex study above, it sounds like you're essentially at the limits of oral NR effectiveness, not to mention that 2g of niacinamide is also very high, relative to the population at large. So I hardly think you can push NAD+ any harder, unless we entertain intraday chronic dosing, which is unknown territory with NR and liver function. Which all begs the question: have you noticed anything, apart from the prostate issue?

 

No doubt we could raise NAD+ area-under-curve even more by dosing several times per day. There might be a useful, if harrowing, health tradeoff here, if we assume that liver toxicity is somewhat easily solved with mesenchymal stem cells and liver-protective supplements, while NAD+ insufficiency and all its horrible downstream effects is otherwise essentially unsolvable. In other words, risk damaging the body's most regenerable vital organ in order to stave off chronic disease systemically. I wonder if there is evidence for the effectiveness of such a regimen, for instance, in rodents. Given that we obviously lack human data on such a strategy, is there any evidence suggesting that this turbocharging of NAD+ would be useful? (I'm thinking, for instance, of your axon micrographs above, which are night-and-day different, but no doubt occurred as a result of obscene NR concentrations relative to what we could achieve with a once-a-day NR pill.)

 

Related thread: How much is too much Nicotinamide Riboside

 

In the above thread, Bryan, you mentioned that you remembered someone taking 4 g/day. I found that thread here, which would probably interest you because the poster wrote: "I've had prostatitis for the last 15 years. It's been getting progressively worse. When I hit 2 grams per day of Niagen, my prostatitis was significantly better. I've been keeping a journal since beginning Niagen, and I keep track of how many times I urinate and what time of day. When I hit 4 grams a day of Niagen I have no urgency no tenderness, no symptoms. My trips to the bathroom has decreased significantly. No urgency at all. My prostate feels like it did when I was in my 40's."

 

 

resveratrol_guy,

 

"Which all begs the question: have you noticed anything, apart from the prostate issue?" No this is the most recent development but at this point I'm not directly relating it to NR. Keep in mind its getting better not worse. My problems were mainly inflammatory issues and they've been mostly held at bay. My skin looks the best it has in years and some age spots have faded, all old stuff now. Its the new Normal or maybe I should say a little of the old Normal.

 

Thanks for bringing that post to my attention. I haven't studied our LongeCity posts recently to recount that kind of information your memory is impressive. I vaguely remember reading the post and personally didn't notice any change in myself at the time so I must have discounted it because I'd forgotten all about it.

 

That is interesting so there is someone else who had a similar experience and his voiding problems also diminished. So the Honokiol/Magnolia Extract may not be what worked. I concede it may have been an effect that just took longer at my lower dose. He was at 4 grams per day and got to that point of relief in 6 weeks. I've been taking this NR for a little over 1 1/2 years and just before May when I started the Honokiol my prescription for my BPH medication lapsed and it took a week to refill. I was hating life until my Doctor renewed my prescription. So I have to be a realist and consider that.

 

I know you all think I'm the one drinking hard on the NR Cool Aid, that's OK laugh but I'm also a sceptic on many levels until what ever I'm experiencing is proven right or wrong. This particular health occurrence/benefit is a long time separated from the initiation of my Nicotinamide Riboside. If it were closer I might attribute the NR to my newfound ability to void without my medication.

 

​So other than two reports from NR users with BPH we need a few more positive experiences to attribute a direct correlation. I know its a touchy subject for most of us to bebpublic about but that's the beauty of the internet, anonymity. I think there are enough of us now reading this forum today who are of the age to be suffers and if any of us are getting positive voiding benefits we should speak up. That's an invitation to speak up Guys.

 

On the other hand if I don't hear from anyone else Honokiol/Magnolia has been used for over 1,000 years as a folk medicine in Asia and my experience correlates with the new in vitro studies that are now emerging. So I'm slanting this direction at the moment as to whats working.

http://www.ncbi.nlm....les/PMC4186958/

http://www.p-interna...d_PI-14-055.pdf

I know these are scant studies and there isn't much beyond the Asian folklore about relieving BPH symptoms. There have been many more studies done on Search term "Honokiol cancer" than with BPH. Some of you guys read the LongeCity Topic New class of drugs "senolytics" extends healthspan I believe Honokiol depending on its dose is similar in its effects like senolytics but has a long Asian safety history at lower dosages.

 

I haven't read the paper on axon micrographs. My earlier mention of DRG neurons is from work by Charles Brenner Phd. When I was talking about various tissues and their preferred NAD precursors these are an important class of cells that seem to have a preference when exposed to insult.

 

" . . . the protective factor for DRG neurons appears simply to be NAD+. The evidence is as follows. Lentiviral expression of Nmnat1 protects DRG neurons from axonopathy in an active site-dependent manner (3). Overexpression of wlds or Nmnat1 prevents NAD+ and ATP decline in response to mechanical and chemical damage (89). Nam and Na also protect against axonopathy as long as Nampt or Naprt1 are concomitantly expressed in DRG neurons, whereas NR protects without engineered gene expression of a biosynthetic gene (71). Nrk2 mRNA levels following axonopathy are induced approximately 20-fold, indicating a preferential use of NR as a precursor in maintaining intracellular NAD+ levels in DRG neurons (71). Whether sufficient oral NR supplementation might protect against diabetic or chemotherapy-induced neuropathy or protect against age-associated neurodegenerative conditions remains to be determined."

 

I expect Charles Brenner Phd will eventually correlate the human clinical studies to his previous work on DRG neurons and TBI Traumatic Brain Injury and the most recent studies on experimental cerebral ischemia.

http://www.ncbi.nlm....les/PMC2677622/

 

 

I do remember a LongeCity post about a class of cells called glial cells and "NAD," cant remember who wrote that but it came to mind. Oh here it is I read this from 2 people.

http://www.longecity...jd/#entry678880

http://www.longecity...-16#entry659548

http://www.longecity...ad/#entry678524

 

 

Back to NR dosages. Looking solely at the niacinamide study data I'm keeping my total NAD precursors capped at 3 grams. Until I hear additional dosage information specifically on Nicotinamide Riboside I think its a prudent strategy. Since my doctor is keeping an eye on my liver functions I'm hoping that spreading out my dosage across the day doesn't equate to any problems. If it does I'll report it.

 

The Tolerable Upper Intake Levels of Nicotinic Acid and Nicotinamide (Niacin) URL link 

 

Also I now have a search filter set up for "Dose-Dependent Elevation of the Blood NAD Metabolome by NR in Healthy Human Beings." I will keep an eye out for this. We also have 2 other PK studies pending and haven't really been able to dissect the first one yet.

 

By the way the LongeCity HPN Group Buy starts this Saturday, August 15th.

Edited by Bryan_S, 14 August 2015 - 06:37 AM.

[albedo]

Bryan_S,

 

Sorry, a bit off topic and will move elsewhere to discuss if necessary, do you mind sharing what mediation you take for your BPH and some historic of PSA before and after NR and now the Magnolia extract? Have you ever tested your level of dihydrotestosterone (DHT)? Maybe you went also through some recording of the IPSS score?

 

I ask because I also have mild BPH as posted elsewhere. I was on tamsulosin (even up to 800mgc/d) and even if my prostate was normal, it was nevertheless slightly obstructive to the cystoscopy. To reduce the post void residual, hence trying to avoid worsening my bladder condition (or anticipating possible worse problems with kidneys) I decided to go through, successfully, a (bipolar) TURP surgery more than 2.5 years ago. I reported my experience in the link posted above. The NR potential effect is totally unexpected to me but reinforces me in continuing and possibly increase my NR dosage (now 100mg). I wonder if the magnolia extract could also be beneficial to me and will think about it (the PCa possible prevention via the pro-apoptosis action of honokiol is interesting). However for the time being I move nothing as pretty happy of my last June tests also showing, pleasantly, a lowering of PSA to 0.86.

[Bryan_S]

Bryan_S,

 

Sorry, a bit off topic and will move elsewhere to discuss if necessary, 

 

Since you have a thread already have a BPH thread I moved the conversation over there.

 

http://www.longecity...e-2#entry740308

[resveratrol_guy]

My skin looks the best it has in years and some age spots have faded, all old stuff now.

 

There are not many people who could say this and have us believe them at face value, as this is hardly a trivial observation and more often heard on cosmetics commercials, but I think we're taking you seriously here and don't regard you as an NR Coolaid drinker. To say nothing of how we might imagine this to happen (autophagy powered by NR and enabled by honokiol etc.), can you provide any further details, as in, what exactly "fade" means? Did you treat the spots directly? Measure them? (Your claim prompted me to publish some of my own age spot photos in my thread, so thanks. I'm probably going to copy aspects of your protocol as soon as I catch up on your recommended reading, so I figured it was a good time to take a baseline snapshot.)

[Bryan_S]

 

My skin looks the best it has in years and some age spots have faded, all old stuff now.

 

There are not many people who could say this and have us believe them at face value, as this is hardly a trivial observation and more often heard on cosmetics commercials, but I think we're taking you seriously here and don't regard you as an NR Coolaid drinker. To say nothing of how we might imagine this to happen (autophagy powered by NR and enabled by honokiol etc.), can you provide any further details, as in, what exactly "fade" means? Did you treat the spots directly? Measure them? (Your claim prompted me to publish some of my own age spot photos in my thread, so thanks. I'm probably going to copy aspects of your protocol as soon as I catch up on your recommended reading, so I figured it was a good time to take a baseline snapshot.)

 

 

I was a technology evangelist on the road giving broadcast equipment demonstrations for the masses for years, it likely shows. So I'm not afraid to speak up and share my mind with an audience. You come to learn if you cant laugh at yourself, then you are taking this stuff way to seriously. I also try and weigh my statements against accepted facts and I do concede I might make some errors. To be honest, recently, I'm make some "observations" and could be entirely wrong with my study connections especially with this new honokiol. So never take me to seriously, treat this as entertainment and a reason to read, think and learn. Together on these forums we'll point each other to new ideas and well discard the old ones when we have better information.

 

The skin changes you mentioned above might have been anticipated "if I'd done my research" when I started my NR supplementation. I'm a Subtype 2 Rosacea sufferer. For those of you with perfect skin my teenage years never went away and have plagued me thru adulthood. I still have the scars and broken blood vessels on my face and cheeks but the Papulopustular Rosacea has subsided and I'm now for all practical purposes a Subtype 1 which is night and day for me. Its all about your reference point and I'm pretty happy. This is not new ground Niacinamide has already paved a treatment remedy for this affliction. As far as the pigmentation spots on my hands "fading" this has already been documented again with NR's cousin Niacinamide. So the appropriate question might be which B3 works better and currently there is no data from the Nicotinamide Riboside clinical world to confirm any of this. I'm trying to being fair but we are all looking at a vastly undocumented nutrient and will find similarities with its cousins and hopefully new unique benefits will be discovered.

 

My first thought now going forward is if Niacinamide is known to produce some beneficial effect I would think Nicotinamide Riboside might do it as well or better. Time will tell.

 

 

So maybe drinking a little cool aid isn't a bad thing as long as you remain open and question what you find along the path. At times I do feel like an evangelist but preaching cellular respiration not religion.

Edited by Bryan_S, 15 August 2015 - 10:51 PM.

[Tom Andre F. (ex shinobi)]

I just seen the result of the studies done by chromadex and it makes me wonder: what if we stop the daily supplementation ? (Anti aging firewall theory is that it will go down to the original level)

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

Btw, i follow bryan on its main pathway : take care of sirt1 with pterostilbene ( and i invite you all to read my blog about it: http://www.pterostilbene.com )and increase nrf2
Nr for nad+
And im looking for a good way for sirt3 effectively.

Do you think there is also some need to also take care telomerase activation ?

[resveratrol_guy]

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.