2255 replies to this topic

[Tom Andre F. (ex shinobi)]

Yes exactly, the NAD+ ase make it release Nam that will in turn shut down SIRT. But we cant do anything against it, only solution is to keep your NAD+/NADH level very positive as its the case in young mamals. this will also control your weight and you will avoid for instance the adipose white tissue Nicotinamide N-methyltransferase (NNMT) rich that does the following: http://www.ncbi.nlm....pubmed/18996527 These data support the concept that adipose tissue NNMT contributes to the increased plasma homocysteine levels in patients treated with NA.

 

according to this paper in nature: http://www.nature.co...bs/nm.3882.html :

"Nicotinamide N-methyltransferase (Nnmt) methylates nicotinamide, a form of vitamin B3, to produce N¹-methylnicotinamide (MNAM)." but note that Nnmt in liver seems to have different effect than the one in white adipose tissue

 

NR will release also directly Nam using a certain pathway. When I say all B3s it include also NR of course, since it even if it was not directly tested for homocysteine, its Nam metabolite will for sure:

 

http://www.ncbi.nlm....pubmed/23768418

 

Nicotinamide (Nam) supplementation increased the plasma levels of nicotinamide, N1-methylnicotinamide and choline and decreased the levels of betaine, which is associated with a decrease in global hepatic DNA methylation and uracil content in DNA. Nicotinamide had gene-specific effects on the methylation of CpG sites within the promoters and the expression of hepatic genes tested that are responsible for methyl transfer reactions (nicotinamide N-methyltransferase and DNA methyltransferase 1), for homocysteine metabolism (betaine-homocysteine S-methyltransferase, methionine synthase and cystathionine β-synthase) and for oxidative defence (catalase and tumour protein p53). It is concluded that nicotinamide-induced oxidative tissue injury, insulin resistance and disturbed methyl metabolism can lead to epigenetic changes. The present study suggests that long-term high nicotinamide intake (e.g. induced by niacin fortification) may be a risk factor for methylation- and insulin resistance-related metabolic abnormalities.

 

EDIT: oh and when I say "it's not that easy" its because here as you can see we do not target one specific tissue such as muscle using intramuscular injection. We speak about a precursor taken orally that involve much more pathway and has to target different tissue and face with Nampt leakage for instance. But same concern will happen if you use NMN orally

Edited by Tom Andre F. (ex shinobi), 28 June 2016 - 08:39 PM.

[Nate-2004]

Yes exactly, the NAD+ ase make it release Nam that will in turn shut down SIRT. But we cant do anything against it, only solution is to keep your NAD+/NADH level very positive as its the case in young mamals. this will also control your weight and you will avoid for instance the adipose white tissue Nicotinamide N-methyltransferase (NNMT) rich that does the following: http://www.ncbi.nlm....pubmed/18996527 These data support the concept that adipose tissue NNMT contributes to the increased plasma homocysteine levels in patients treated with NA.

 

This is all very informative.

 

My question here is this:

 

You say that keeping NAD+ levels high will keep sirtuins activated and that will also control weight and reduce white adipose tissue rich with NNMT.  Does that mean that if one is not exercising and staying at their ideal weight through calorie restriction or at least maintenance levels, they will be at risk for increased homocysteine levels especially if taking Na or NR?  

 

So in other words, am I safe from increased homocysteine levels if I stay at my ideal weight while taking Na/NR?  I exercise at least four times a week for at least 30 minutes with variety and I try my best not to eat too much. I've maintained a relatively ideal weight for 3 years now. Is that safe enough? Should I go to the doctor now after 2 months of NR to have my homocysteine levels checked?

 

According to Wikipedia:

 

In healthy, non-overweight humans, white adipose tissue composes as much as 20% of the body weight in men and 25% of the body weight in women. Its cells contain a single large fat droplet, which forces the nucleus to be squeezed into a thin rim at the periphery. They have receptors for insulin, sexual hormones,norepinephrine, and glucocorticoids.

 

Edited by Nate-2004, 28 June 2016 - 09:26 PM.

[Tom Andre F. (ex shinobi)]

Nate, I think you should read my post #59 in beta-lapachone thread: http://www.longecity...e-2#entry778471

 

NAD/NADH ratio control ATP production, and then control the energy expendure, and your full metabolism, the rate you burn calorie etc. About adipose white and brown, what you would like is more brown instead of the white since brown fat is the one present in young and low in old people. In some forum some speculated that missing brown fat in scalp bring to hairloss, but I never looked deep enough into that.

 

Have a good weight, especially avoiding belly fat (the one linked to cortisol and aging most often) is always a good thing and indeed seems a way to reduce homocysteine nicotinamide induced. But NNMT doesnt play same role in all tissue, for instance in liver. So im not sure about the full mechanism

 

vitamin B6 and B12 are best way to control homocysteine. Betaine (that also seems to play a role in liver), MSM are also mentioned as good for homocysteine.

 

 

[ta5]

...and now my last bet : rosmarinic acid (I have a data published in a japanese study showing it is a REAL and maybe most potent AGE breaker known to date. It will not for sure break glucosepane since they used a ribose instead of a glucose for the reaction but still impressive + data showing good for inflammation http://www.ncbi.nlm....pubmed/16604092 and Im on a vegetarian diet and lactose/ casein free diet

result is hard to say since im still young (30yo) but still 0% white hair, full head of hair, skin without wrinkles and no health problem. My goal is stop aging as much as possible

 

Tom,
Where you get your rosmarinic acid? How much do you take? (Sorry, kind of off topic.) 

[Bryan_S]

Have y'all taken into account the homocysteine levels raise by NA? 'Cuz I suffered it in my own skin, I had one blood test showing 12 for homocysteine and after 3 months and having added too my diet, B12, B6, folic acid , taurine and NAC to lower my homocysteine levels and found myself with 16..... So , I sat and I looked at what I had added apart from all that, yep Niacin 500 mg in the morning with breakfast

http://www.ncbi.nlm....pubmed/11895163

As we all know . High homocysteine means faster shorten of the telomeres , and accelerating the telomeres fraying is no bueno IMHO

 

Sorry to hear that, I don't think this is an issue for Tom since he's only taking 50mg per day of Niacin (Na). I've read Niacin (Na) can produce a balancing act on how much methylation is needed. I'm not sure if that's part of what happened to you. Here was some discussion, I can't speak to this point myself. Overmethylation and Undermethylation: Case Study I know we have some Niacin Pro's lurking that can speak to this and it was a topic here on LongeCity and the homocysteine symptoms appear common enough.

 

I haven't found any clear NAD+ charts with Niacin vs dose, guess someone will have to visit that in a future study. However I did find a chart depicting therapeutic dosages and lipid responce with a time released version, which we know can be problematic. Niaspan wikipedia "A prescription extended release niacin, Niaspan, has a film coating that delays release of the niacin, resulting in an absorption over a period of 8–12 hours"

 

This is a coating method I think that would be advantages for Nicotinamide Riboside users.

 

Edited by Bryan_S, 29 June 2016 - 08:04 AM.
LongeCity link added

[Bryan_S]

 

Steve H,

 

I have to ask have you read the latest papers on NAD+ Repletion and what happened to senescent cells?  Restoring stem cells — all you need is NAD+

 

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

 

Senolytics has been a topic of great interest to many of us here. Especially from the standpoint of the inflammation senescent cells contribute. However now that results have been seen in improving their metabolism with NAD+ (reference above) this whole engrained idea of the Hayflick limit may have been pushed a few cell divisions further down the line (reference above). This make's some of us question if killing off our senescent cells might be premature if they can be restored to a functional status. (reference above) It appears once NAD+ levels are restored even what we thought was a hopeless situation now appears to be reversible enabling us to rejuvenate stem cells and extend lifespan in mice.

 

I mention this because as your group writes their mission statement some of the game pieces are being re-thought. Project Summary Senolytics Phase 1 Our humble group isn't on the forefront of chasing these leads down and picking the research projects but it appears the landscape is changing rapidly and with it the targets with the most beneficial information to uncover like this CD38 we spoke of.      

 

 

I have read them yes and in my view simply replacing NAD is not a magic bullet and anyone who suggests it is has a simplistic view of the forces involved here. Senolytics addresses the probable root cause of NAD decline which is inflamation and increase of the NF-KB pathway which in turn leads to rising CD38, there is no point addressing CD38 if you are not fixing the rising NF-KB regulating CD38 at the top of the chain. Whilst I have no doubt restoration of NAD levels and NAD ratio is good (the Sinclair data shows it) it isnt the full story and I am focused on getting to the root of the problem which Sinclair himself suggests is chronic inflammation. What may be going on in these experiments is the increased NAD levels are allowing the cells to overcome the deleterous effects of CD38 to a certain point by chanigng the NAD/NADH ratio, thus we see the cells are able to proliferate for longer and indeed are functionally younger. If so it still does not address the root of the problem which is inflammation and the NF-KB pathway which includes CD38.

Now a therapy that addresses the CD38 levels ideally from its source NF-KB should hypothetically help the body restore its own production of NAD by reducing the CD38 on hand to destroy NAD, Senolytics is one possible way to achieve that as the data shows that NF-KB and CD38 are reduced by their action. This is something we can easily demonstrate in our Senolytic program simply testing the NAD/NADH ratio and how if it changes plus NF-KB and CD38 levels and changes post Senolytic treatment.If we are VERY lucky the levels will return to normal simply by removing CD38 but that would need to be demonstrated.
 

Another target is NQO1 which regulates the NAD=NADH ratio.

 

I highly recommend Anti-Aging firewalls NAD 5 part series here for those of you who have not read it:
 

http://www.anti-agin...he-nad-world-2/

 

 

Steve H,

 

​Thanks for the response, I just wanted your perspective now that there seems we have a glimmer of hope that senescent cells can be rescued in some instances. Maybe the initial step is to eliminate them and going forward extend the longevity of those that might later turn senescent. In the end we have a finite number of stem cells as defined by the Hayflick limit and if we can clean up the neighborhood "so to speak" we can reduce the stress placed upon the remaining stem cells.

 

I think we agree there is no magic bullet and we are simply forestalling the inevitable unless we address the inflammation issue. I also agree CD38 is a symptom of an upstream issue.

 

I wish you luck in demonstrating this with your Senolytic program. I think the growing awareness in places like LongeCity will help draw the support towards your program and others like this.

[Bryan_S]

Quercetin & Apegenin slow down the escalating NAD+ consumption by CD38 as we age

 

June 29, 2016

 

 

Timeless life magazine also picked up on the CD38 topic and boiled it down. http://www.timelessl...cd38-as-we-age/

Edited by Bryan_S, 29 June 2016 - 11:38 PM.

[mrkosh1]

Can someone test Rosmaric acid to see if it can break glucosepane?

 

It is already a more effect crosslink breaker than ALT-711 according to this paper.

 

http://www.toukastre...015/GS15-26.pdf

 

[Tom Andre F. (ex shinobi)]

 

...and now my last bet : rosmarinic acid (I have a data published in a japanese study showing it is a REAL and maybe most potent AGE breaker known to date. It will not for sure break glucosepane since they used a ribose instead of a glucose for the reaction but still impressive + data showing good for inflammation http://www.ncbi.nlm....pubmed/16604092 and Im on a vegetarian diet and lactose/ casein free diet

result is hard to say since im still young (30yo) but still 0% white hair, full head of hair, skin without wrinkles and no health problem. My goal is stop aging as much as possible

 

Tom,
Where you get your rosmarinic acid? How much do you take? (Sorry, kind of off topic.) 

 

 

I ordered mine from swanson

 

Can someone test Rosmaric acid to see if it can break glucosepane?

 

It is already a more effect crosslink breaker than ALT-711 according to this paper.

 

http://www.toukastre...015/GS15-26.pdf

 

Yes this is the study I have too. It was conduced by a french company and published first in the japanese paper.

 

They then performed vivo test in human to see if it changed the wrinkles profile in 93 women, average 57yo for 1 month

 

they even used the elasticity test Cutomètre® wich is a reliable method and got a +17% increase for elasticity of the skin. Rest of  the parameter performed even better

 

However, in the vitro study you can see they used a ribose instead of a glucose, means, we dont know if it break glucosepane with this study. They guy admited that it is unlikely it will break glucosepane "even if we dont know". Glucosepane problem is the bond is too strong you can break it without damaging around. Thats why we still today look for a good candidate

[mikeinnaples]

 

 

Have y'all taken into account the homocysteine levels raise by NA? 'Cuz I suffered it in my own skin, I had one blood test showing 12 for homocysteine and after 3 months and having added too my diet, B12, B6, folic acid , taurine and NAC to lower my homocysteine levels and found myself with 16..... So , I sat and I looked at what I had added apart from all that, yep Niacin 500 mg in the morning with breakfast

http://www.ncbi.nlm....pubmed/11895163

As we all know . High homocysteine means faster shorten of the telomeres , and accelerating the telomeres fraying is no bueno IMHO

 

This is disconcerting. In reading all these arguments between Tom, Stefan and Bryan I concluded that Na was just as useful in some ways as NR and so I figured why not take them together. I didn't know that Na raised homocysteine levels though, that's not good at all for aging. Does NR raise homocysteine? What can be done to counter this effect? Anything?

 

What is so "dangerous and irresponsible" about my posts lately? Just asking questions, jeez.

 

Also Tom seems to be suggesting that NR inhibits Sirtuins? I was under the impression that the exact opposite is the case.

 

 

The homocysteine issue was picked apart in another long running thread on this board. Personally, I have kept mine in check with sublingual methyl-b12 and TMG
 

Apparently it is easier for people to flag posts as needing references that making the effort to use the forum search tool. sad

 

 

Edited by mikeinnaples, 30 June 2016 - 01:27 PM.

[Bryan_S]

NAMPT-mediated NAD+ homeostasis in skeletal muscle: Implications for healthy aging

David W Frederick, University of Pennsylvania Dissertation

http://search.proque...view/1795570200

http://repository.up...ns/AAI10120633/

 

"Abstract

Mammalian skeletal muscle is a highly dynamic organ capable of structural and metabolic remodeling in response to exercise demands, nutrient supply, and environmental insults. Muscle also plays a central role in the maintenance of whole-body energy balance, capable of both storing and oxidizing carbohydrate and lipid fuels. The course of natural aging leads to a gradual decline in the mass, strength, and oxidative capacity of skeletal muscle, which increases the susceptibility of the elderly to frailty and metabolic diseases, such as Type II Diabetes. Ectopic muscle lipids can also exacerbate the metabolic complications of obesity, prompting interest in new means of combating this effect by stimulating aerobic muscle metabolism. Several lines of evidence have converged on the fundamental electron-shuttling metabolite, nicotinamide adenine dinucleotide (NAD), as a co-factor and signaling intermediate uniquely positioned to modulate whole-body energy balance through transcriptional and post-translational mechanisms. Though it has long been known that NAD supports essential metabolic pathways in muscle, attempts to stimulate oxidative metabolism by systemically increasing intracellular NAD concentration have been unable to resolve the specific contribution, if any, of skeletal muscle to the resulting phenotypes. Furthermore, the observation that muscle NAD content tends to decline with age has never been demonstrated to have functional consequences. I have addressed these questions experimentally by generating transgenic mice with altered muscle expression of nicotinamide phosphoribosyltransferase (Nampt), the rate-limiting enzyme in the mammalian NAD salvage biosynthetic pathway. Despite effectively increasing the muscle NAD pool, Nampt expression alone is not sufficient to stimulate mitochondrial function in young mice and provides no protection from diet-induced obesity. However, aging these mice for 24 months revealed partial preservation of youthful exercise capacity through primarily non-transcriptional mechanisms. Specific deletion of Nampt in adult mice elucidated a critical threshold of NAD required to maintain the exercise performance, as well as the mass and strength of muscle, by directly supporting aerobic ATP synthesis. Importantly, these parameters can be rapidly and uniformly restored by administration of the NAD precursor, nicotinamide riboside. These studies indicate that loss of NAD homeostasis is a reversible cause of skeletal muscle dysfunction with wide- ranging therapeutic implications."

[ROBST3R]

Quercetin & Apegenin slow down the escalating NAD+ consumption by CD38 as we age

June 29, 2016



Timeless life magazine also picked up on the CD38 topic and boiled it down. http://www.timelessl...cd38-as-we-age/

Looks promising Bryan.

Do you plan to take supplements like quercetin and apegenin?

[Yajerman]

ChromaDex Vindicated By Retraction And Apology From Author Of Misleading And Factually Inaccurate Article *

Thursday 06/30/2016 06:30 AM ET - Dow Jones News.

 

http://finance.yahoo...-103000769.html

 

Now back to our regular program.

Edited by Yajerman, 30 June 2016 - 05:41 PM.

[bluemoon]

ChromaDex Vindicated By Retraction And Apology From Author Of Misleading And Factually Inaccurate Article *

Thursday 06/30/2016 06:30 AM ET - Dow Jones News.

 

http://finance.yahoo...-103000769.html

 

Now back to our regular program.

 

I don't think it is that simple. Here is the text, and I underlined the last sentence:

 

 Bleecker Street Research is removing its article on Barry Honig, ChromaDex, and Pershing Gold. After further research we believe that the statements were not supported and the premise of the article was allegedly factually inaccurate. Bleecker Street would like to apologize to ChromaDex, Pershing Gold, and Barry Honig for an allegedly misleading article and to immediately set the record straight for our readers who should not rely on certain aspects upon the withdrawn article or statements of the author therein. To our readers: In the future we will document everything even more carefully.”

 

This makes me think there will be a more detailed statement coming from Bleecker Street Research in coming months. 

Edited by bluemoon, 30 June 2016 - 06:50 PM.

[tunt01]

 

I don't think it is that simple. Here is the text, and I underlined the last sentence:

 

 Bleecker Street Research is removing its article on Barry Honig, ChromaDex, and Pershing Gold. After further research we believe that the statements were not supported and the premise of the article was allegedly factually inaccurate. Bleecker Street would like to apologize to ChromaDex, Pershing Gold, and Barry Honig for an allegedly misleading article and to immediately set the record straight for our readers who should not rely on certain aspects upon the withdrawn article or statements of the author therein. To our readers: In the future we will document everything even more carefully.”

 

This makes me think there will be a more detailed statement coming from Bleecker Street Research in coming months. 

 

 

I've read the Bleecker report several times and gone through most of Chromadex's recent filings.  In my opinion (IMO), Bleecker and Chris Drose better have good lawyers.  If I were Chris Drose, I would never publish about Chromadex again, because what he's already written is false (as explained by the company) in at least one area.  I've probably trained a a couple hundred CFAs, CPAs, financial analysts, MBA students, private equity executives, etc.  I have no idea what this guy (Bleecker/Drose) is thinking when he writes this crap.  It's so amateurish and nonsensical to anyone who even has a basic, sophomore understanding of accounting.

Edited by prophets, 01 July 2016 - 12:12 AM.

[Bryan_S]

 

Quercetin & Apegenin slow down the escalating NAD+ consumption by CD38 as we age

June 29, 2016

Timeless life magazine also picked up on the CD38 topic and boiled it down. http://www.timelessl...cd38-as-we-age/

Looks promising Bryan.

Do you plan to take supplements like quercetin and apegenin?

 

 

I've been following the Senolytics quercetin connection. I'm in a wait and see mode because I've already had some experience with quercetin. I'm one of those who suffered severe headaches while taking it and didn't feel so well. No, for now I'll report what I can dig up and I'll let this science develop till it looks more user friendly. 

 

As far as the ChromaDex stock shorting incident master minded by Chris Drose at Bleecker Street Research I wonder what his financial take was? I think this should be made public to lend awareness to the abuses perpetrated by thugs like him upon the public. Look at all the class action lawsuits this one person generated against ChromaDex. I know at some point these cases will be consolidated but who foots that bill and court costs? "The investor" Drose and his buddies stripped the company of some 42% by slandering its primary corporate investors and board members and if you were a stockholder that money came out of your pocket into his. I sure hope they'll be held responsible but have seen misinformation like this used countless times to strip investor assets and no one ever pays or goes to jail. Its just flat out wrong. 

ChromaDex Vindicated by Retraction and Apology

Edited by Bryan_S, 01 July 2016 - 05:47 AM.

[Nate-2004]

 

 

Quercetin & Apegenin slow down the escalating NAD+ consumption by CD38 as we age

June 29, 2016

Timeless life magazine also picked up on the CD38 topic and boiled it down. http://www.timelessl...cd38-as-we-age/

Looks promising Bryan.

Do you plan to take supplements like quercetin and apegenin?

 

 

I've been following the Senolytics quercetin connection. I'm in a wait and see mode because I've already had some experience with quercetin. I'm one of those who suffered severe headaches while taking it and didn't feel so well. No, for now I'll report what I can dig up and I'll let this science develop till it looks more user friendly. 

 

Bryan I see Quercetin available on amazon and it's with Bromelain, which in a cursory search is apparently for making it more bioavailable. How well does bromelain work to make it bioavailable and was this the kind you took? Why do you think it gave you a headache?

[Bryan_S]

I've been following the Senolytics quercetin connection. I'm in a wait and see mode because I've already had some experience with quercetin. I'm one of those who suffered severe headaches while taking it and didn't feel so well. No, for now I'll report what I can dig up and I'll let this science develop till it looks more user friendly. 

Bryan I see Quercetin available on amazon and it's with Bromelain, which in a cursory search is apparently for making it more bioavailable. How well does bromelain work to make it bioavailable and was this the kind you took? Why do you think it gave you a headache?

 

Forgive me for not recommending this path yet. Browse the LongeCity board link above and see whats going on in general. Some are already experimenting but I think its a bit premature. As far as why I felt ill, if it was working, killing senescent cells that could be one reason but in researching its side effects what I experienced appears documented. But it could have been a host of reasons.

 

For now I'm concentrating on the inflammation and NAD Repletion side and letting others blaze this path until we know more.

[Steve H]

Bryan I am glad you spotted the Quercetin and CD38 connection I was going to cite that today. A number of Senolytic studies reduce SASP significantly which improves healthspan, we know that SASP contains our friend CD38 in increasing amounts (Campisi et al) along with other chemockines and cytokines eg, IL6, TGF-b, TNF-a and other NF-KB associated signals. So for me I find the NAD and inflammation connection compelling and combined with the Sinclair data the connection becomes even more obvious. 

So I have recommended we monitor NAD, NAD/NADH ratio, CD38 and NF-KB as additional metrics in our research program. I suspect Aubrey is correct and if we reduce CD38 levels by removing SASP we might see the NAD levels "bounce" back up as the CD38 is not destroying it. 

http://www.ncbi.nlm....pubmed/27304511
http://diabetes.diab...ntent/62/4/1084

Ultimately Quercetin, ABT737, Venetoclax and so on give us useful insights into aging and indeed could reveal the link between NAD/NADH and inflammation and clearly show us how a large part of aging occurs. Of course these drugs are not a full on therapeutic answer as they all exhibit "selectiveness" on cell types effected. However the good news is companies like Osiin Biotechnology and Unity are developing drugs and therapies that have much wider mutli cell application, this will allow us to systemically treat inflammation and potentially restore NAD system wide. The closest we have come to seeing this in practice is the Barker studies which used a genetic trigger to kill P16 cells system wide, the results were impressive. 

http://www.nature.co...ature10600.html
http://www.ncbi.nlm....pubmed/26840489

 

Edited by Steve H, 01 July 2016 - 07:38 AM.

[bluemoon]

As far as I can tell, there are still two class action shareholder law suits going forward against ChromaDex as well as presumably an investigation by the SEC. Have all of those been dropped?

[stefan_001]

As far as I can tell, there are still two class action shareholder law suits going forward against ChromaDex as well as presumably an investigation by the SEC. Have all of those been dropped?

 

I dont think they will push these through. All of this is driven by an ability to gain financially. None of these law offices or bleeker street will continue unless they see more gain opportunity.

[bluemoon]

 

As far as I can tell, there are still two class action shareholder law suits going forward against ChromaDex as well as presumably an investigation by the SEC. Have all of those been dropped?

 

I dont think they will push these through. All of this is driven by an ability to gain financially. None of these law offices or bleeker street will continue unless they see more gain opportunity.

 

 

There is nothing at all wrong by gaining financially by showing a  company has cooked the books and bet that many investors will sell. Obviously, I don't mean making things up about a company. 

 

From what I can tell, there are now at least six law firms that say they are investigating ChromaDex on behalf of shareholders. Some of those six may not follow through, but I bet some will. It isn't clear to me that ChromaDex is in the clear at this point, and I don't think we will know for a few weeks. (Never invested and had no plans to)

[HappyPaul]

As far as I can tell, there are still two class action shareholder law suits going forward against ChromaDex as well as presumably an investigation by the SEC. Have all of those been dropped?

This will be my last OT stock response post (I hope)  Some firms announced they were investigating suits I believe.  My guess is they will just fade away as the report was pulled as factually inaccurate.  I am not very concerned about ChromaDex being sued over this but welcome to the real world ChromaDex and out of the penny stocks. 

 

Chromadex did and perhaps does have some issues which opened them up to this sort of action, being attacked by short sellers.  They admit having spent something like $40k in the past on a firm and one of their board members (now gone) was being charged by the SEC in a matter not related to Chromadex.  Another board member has been involved in several companies with this now resigned and charged board member and I know I don't like what I saw.  Chromadex did a horrible job responding, it took far too long and their new board member resigned when this came down which looks bad.  I am sold on NR but a company needs good management.  Perhaps this will ultimately be a positive as it happened fairly early, got some dirty laundry out there to be cleaned up and may engender better management from here on out but this showed they are out of their league management wise dealing with issues like this which were somewhat their own making from having a board member who is being charged.   I had been invested in Chromadex for at least 18 months.  I sold everything when I read the report as there was enough there to make me concerned.   I did my research and bought back in last Friday.  I was fortunate to catch it all live as it was happening, if I hadn't I would have just ridden it all rather than bailed.  I know that last night in after hours trading they were 4.24.  Pre reverse stock split that works out to $1.41 which is about what they were before they were up listed to Nasdaq.  

 

Sold on NR which I have been taking through Basis.  Sold on the future of NR understanding the risks that the patent for production will expire someday and that another, better cheaper compound that may raise NAD may be found etc...   

Edited by HappyPaul, 01 July 2016 - 12:42 PM.

[tunt01]

 

 

There is nothing at all wrong by gaining financially by showing a  company has cooked the books and bet that many investors will sell. Obviously, I don't mean making things up about a company. 

 

From what I can tell, there are now at least six law firms that say they are investigating ChromaDex on behalf of shareholders. Some of those six may not follow through, but I bet some will. It isn't clear to me that ChromaDex is in the clear at this point, and I don't think we will know for a few weeks. (Never invested and had no plans to)

 

 

Except Chris Drose/Bleecker didn't show this and by all appearances, he manufactured an outright lie claiming the largest distributor of Chromadex products was controlled by insiders.  His entire write-up was laden with innuendo and hysteria.  Just his proclamation at the outset that "new unsealed court documents" reveal this massive Honig conspiracy, but those documents have been up on the web for almost 2 years.  And he leads the readers along in this winding tawdry tale with numerous "guilt by association" examples, most of which are in fact true, but totally inappropriate comparisons and delusional conjecture.  

 

Putting those "opinions" aside for a moment (as it is perfectly legal for anyone to come up with idiotic theories/opinions), it's how he closes with these remarks about the largest distributor of Chromadex products being controlled by insiders and that the profit would not have occurred, if not for this nefarious behavior of selling to related parties.  It's just flatly not true.  Period.  It's outright, boldfaced lie.  He's not engaging in conjecture at this point, he's making a direct claim that is tantamount to fraud.  It's amazing to me anyone would have the gall to write something like this, and it's all probably done for money.

 

IMO, the guy is a liar, plain and simple.  He's probably fronting for some hedge funds who bought puts in front of the publication and killed the stock to toy with some poor retail investors who don't understand this write-up.  It's disgusting really.  I find it to be truly and completely disgusting.  The guy is a disgusting human being.

 

IMO, the guy should be investigated by the SEC and/or US Attorneys and hopefully disbarred from the markets for a period of time.

 

IMO, the class action lawsuits should be aimed at Drose/Bleecker -- not the company.

 

 

This obviously assumes my analysis of the facts/situation is correct, which may or may not be the case.  And nothing I've written here should be construed as a stock recommendation or anything thereabouts. 

 

Edited by prophets, 02 July 2016 - 01:29 AM.

[Bryan_S]

I wrote 2 pages about this Bleecker Street Research stock scam and after finishing it I don't see the point in posting it. I hope they are investigated and dealt with. Lets get back into the research portion of this thread.  

[bluemoon]

  Lets get back into the research portion of this thread.  

 

Speaking of the research side, Chromadex's CEO said during the late winter stockholder's meeting that was on a podcast that a major science journal would be publishing some Chromadex human results very soon. It has been 3 or 4 months, and I haven't seen anything. Does anyone know if such a study was in fact published?

[Bryan_S]

The Metabolic Impact on Histone Acetylation and Transcription in Ageing 

http://www.cell.com/...0004(16)30040-8

Jun 6, 2016

"Loss of cellular homeostasis during aging results in altered tissue functions and leads to a general decline in fitness and, ultimately, death. As animals age, the control of gene expression, which is orchestrated by multiple epigenetic factors, degenerates. In parallel, metabolic activity and mitochondrial protein acetylation levels also change. These two hallmarks of aging are effectively linked through the accumulating evidence that histone acetylation patterns are susceptible to alterations in key metabolites such as acetyl-CoA and NAD+, allowing chromatin to function as a sensor of cellular metabolism. In this review we discuss experimental data supporting these connections and provide a context for the possible medical and physiological relevance."

 

​Another article suggesting NAD Repletion.

Edited by Bryan_S, 02 July 2016 - 03:29 PM.

[Bryan_S]

 

  Lets get back into the research portion of this thread.  

 

Speaking of the research side, Chromadex's CEO said during the late winter stockholder's meeting that was on a podcast that a major science journal would be publishing some Chromadex human results very soon. It has been 3 or 4 months, and I haven't seen anything. Does anyone know if such a study was in fact published?

 

 

There have been some amazing (NR) articles in Cell.com, Nature.com and Science.org just not the one I thought was implied. I was expecting one of Brenner's students to be publishing something related to this poster presentation. The submission process as we've seen can be a lengthy one. I've begun to check various University's dissertation library's in hope of glimpsing early abstracts. This is how I turned up Nicotinamde Riboside Delivery Generates NAD+ Reserves to Protect Vascular Cells Against Oxidative Damage and 

NAMPT-mediated NAD+ homeostasis in skeletal muscle: Implications for healthy aging. I also contacted Dr. Jonas Treebak at the University of Copenhagen where there are ongoing Human Trials in hopes of learning if one of his students had submitted anything. He wouldn't suggest anything was in the pipeline. So I'm afraid my efforts have been in vain and we just have to wait for the natural publication process. 

[bluemoon]

First, I was curious if anyone else remembers what the CEO of ChromaDex said in late winter with respect to Chromadex results being published in a major journal "soon" or "this spring".i can't remember the exact wording except we could expect it, but nothing as far as I can tell, so far. I completely understand the publishing process can be quite lengthy, but he seemed sure it would be out by now.

 

I was also excited about the Science article on NR but when my scientist friend read the full article, he was less impressed. This isn't his area of expertise, but he follows NAD+ fairly closely (not as closely as many of you!)  and has been taking NADH for 2 years (I told him I wasn't  so sure that works) as well as branch amino acids - he likes those. Unfortunately, at the time he didn't fully explain why the Science article wasn't so important and maybe he was wrong about that.

 

I'm curious what people think about the difference between publications about resveratrol and publications on NR.  My understanding is that to do one well is too expensive for one company to undertake apart from the small "poster" study ChromaDex did. 

 

   

Edited by bluemoon, 02 July 2016 - 10:15 PM.

[Bryan_S]

First, I was curious if anyone else remembers what the CEO of ChromaDex said in late winter with respect to Chromadex results being published in a major journal "soon" or "this spring".i can't remember the exact wording except we could expect it, but nothing as far as I can tell, so far. I completely understand the publishing process can be quite lengthy, but he seemed sure it would be out by now.

 

I was also excited about the Science article on NR but when my scientist friend read the full article, he was less impressed. This isn't his area of expertise, but he follows NAD+ fairly closely (not as closely as many of you!)  and has been taking NADH for 2 years (I told him I wasn't  so sure that works) as well as branch amino acids - he likes those. Unfortunately, at the time he didn't fully explain why the Science article wasn't so important and maybe he was wrong about that.

 

I'm curious what people think about the difference between publications about resveratrol and publications on NR.  My understanding is that to do one well is too expensive for one company to undertake apart from the small "poster" study ChromaDex did. 

 

I remember that, its what I've been searching for. Either it was stockholder conference call or one of the podcasts.

 

Well the NADH market has contested the results on numerous studies and the word is its broken down upon ingestion. Now I at least thought NAD and NADH had similar fates and if taken Orally you would at least get the benefit of the cleaved (NAM), however the linked study above even disputed that. "In fact, incubation of NADH at acidic pH to mimic the stomach resulted in rapid conversion of NADH to an unknown compound. Better understanding of the fate of oral NADH is needed for its therapeutic and supplemental use."

 

"I'm curious what people think about the difference between publications about resveratrol and publications on NR" Whats the question again? Resveratrol studies abound however David Sinclair and Leonard Guarente discovered the SIRT activators did little to raise NAD of themselves. They consume NAD to do their jobs and Raising NAD levels with a precursor helped Resveratrol activate sirtuin-1. (it was in one of Leonard Guarente's videos) Now on the other hand Nicotinamide Riboside raised SIRT1 & SIRT3 without Resveratrol, so I'm less impressed with Resveratrol. Also to be honest I take Pterostilbene which is claimed to be more bioactive than Resveratrol but I'm considering dropping that from my regiment. 

Edited by Bryan_S, 03 July 2016 - 03:12 AM.