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

Photo
* * * * - 16 votes

Nicotinamide Riboside [Curated]

nicotinamide riboside nicotinamide nad boosting charles brenner david sinclair leonard guarente niagen niacinamide nicotinamide mononucleotide

  • This topic is locked This topic is locked
2262 replies to this topic
last few days remaining!! ❶ AgeMeter fundraiser ❷ regimen prize competition

#1591 Bryan_S

  • Topic Starter
  • Member
  • 1,154 posts
  • 363
  • Location:Orlando

Posted 27 November 2016 - 12:31 AM

And we wonder why people don't like these rants against one another. This is a forum to share and discuss research surrounding NAD repletion. I don't require you to discuss nicotinamide riboside exclusively because it is just one facet of interrelated topics surrounding NAD boosting. But I do require that all members be civil with one another. The way I see the whole picture is that with each study our understanding of aging changes in some way. Lets take for instance the Mitochondrial Theory of Aging. There are researchers challenging the status quo like Professor Hayash.

 

Now we can't keep digging into the record to see if someone was right or not each time the story changes a few degrees. The story of senescence, CD38, PARP, the slow drift of our epigenome are all weighing into the story of aging and all it takes is a small insight to change everything. Any timelines we put forward are useless. All it takes is a paper like this one from Northwestern University and the whole field could take another direction. This paper ties reproductive maturity with epigenetic changes leading to old age.

 

So that being said I don't see NAD repletion as the end story either. Many of our assumptions will inevitably be challenged, some reaffirmed some trashed as these metabolic studies move from animal to human trials. At one point I also had a difference of opinion with Michael and there have been a couple of dozen papers between then and now and to argue a point based on the understanding of that particular day that we've seen redefined since seems a waste of time. So lets all turn off the biased marketing claims from the sidelines, focus on the current research and forget about what someone opinionated yesterday, especially since the pace of change is going to get more rapid.


Edited by Bryan_S, 27 November 2016 - 12:37 AM.

  • Agree x 3

#1592 Michael

  • Advisor, Moderator
  • 961 posts
  • 1,344
  • Location:Location Location

Posted 27 November 2016 - 12:36 AM

I'd certainly acknowledge that some of the questions and objections I raised in my QOTM post almost exactly a year ago have been addressed in subsequent research. As Midas points out, there's now evidence that NMN can work after oral administration, and the same study reported finding elevated NMN in plasma following oral gavage. A previous study found that "Perfused or intact intestine rapidly hydrolyzed NMN to nicotinamide riboside, which accumulated, but was not absorbed. It was slowly cleaved by an enzyme associated with the mucosal cells to nicotinamide, which was the major if not the only labeled compound absorbed." I assume this is why all of Imai's and Sinclair's studies prior to this new one delivered NMN via injection, which is a lot more troublesome than orally in water or feed: Imai seems to be hinting at just that when he writes, "In our previous study, we showed that a bolus intraperitoneal administration of NMN (500 mg/kg body weight) increased tissue NMN and NAD+ levels within 15 min in the liver, pancreas, and white adipose tissue (WAT) in regular chow-fed wild-type mice (Yoshino et al., 2011). To make long-term NMN administration possible, we decided to test lower doses, which could potentially be translatable to humans, and add it to drinking water."

 

Charles Brenner has recently reported that NR elevates NMN levels in several tissues after oral absorption, and in the process substantially changed our understanding of the metabolism of NAD precursors; he had cited NMN's hydrolysis in the intestine per the earlier study in outlining the proposed route of uptake of NAD precursors from the diet in a review several years back. One way to reconcile these findings is of course that NMN is indeed hydrolyzed to NR in the intestine, but that NR is then taken up and elevates NMN in the blood, though I don't know what explains the finding of non-absorption even of NR in the earlier study.

 

Similarly, several studies have also now reported nicotinamide riboside to elevates NAD in muscle, most importantly Zhang, Auwerx (2016), et. al. discussed above.


Edited by Michael, 27 November 2016 - 12:41 AM.

  • Good Point x 3
  • like x 2

sponsored ad

  • Advert
To book this BIOSCIENCE ad spot and support Longecity (this will replace the google ad above) - click HERE.

#1593 Bryan_S

  • Topic Starter
  • Member
  • 1,154 posts
  • 363
  • Location:Orlando

Posted 27 November 2016 - 12:50 AM

Michael don't be chased away because all researched opinions are welcomed here. In all honesty I was one of your original critics and may have set the tone here, for that I'm sorry. We are all just trying to take this research in and make sense of it and the rate at which these papers are being published is escalating. So as we sift thru these papers we're hoping to attract some reasoned commentary, so stick around and join the conversation.  :)


  • Agree x 4
  • Cheerful x 2

#1594 bluemoon

  • Registered User
  • 446 posts
  • 24
  • Location:south side
  • NO

Posted 27 November 2016 - 01:58 AM

 

 

(b) The full quote is, "it hasn't been, since 1950, that we've made much change at the far end" (emphasis added). Median LS of course still incorporates ongoing progress in lowering deaths childhood mortality, and "premature" mortality in midlife.

 

 

 

See? I didn't chase Micheal away. What's wrong prophets? I didn't create a safe place for Michael? He isn't 11 years old, right? 

 

Michael, you were simply wrong about what you said then as life expectancy over 65 had increased about 6 or 7 years since 1950 independent of childhood longevity.

 

You also said in your presentation that if a person is 50 today (58 in 2016) than only a third of you are 'going to make it' and added "A lot of you are going to make it as far as 150 years and still cough out - but that ain't bad! But you know what, we don't have a cure today... (so worse odds).

 

You were telling the audience that many of those who "won't make it" (to escape velocity) will live until the year 2108 (!) as if you knew what longevity science would look like in the 22nd century to say nothing of 2070 or 2030. That is the point I rolled my eyes and thought you can't have a science background. But as you wrote, you studied biology for 3 years, so I take that back.

 

As for cheer leading, I clearly stated that is very important. What I wrote: "Rae is a cheerleader, and we need those." I also consider Aubrey de Grey a cheerleader, and a great one for longevity. 

 

Prophets has been full of it - twice. First, I have never gone off topic considering I responded to bold statements that were previously made. Second, I have never attacked a person. To me, saying Michael didn't have any science background seemed obvious from that presentation but I admit I was wrong.

 

以上です。


  • Off-Topic x 5
  • dislike x 3
  • Agree x 2
  • Pointless, Timewasting x 1

#1595 Iporuru

  • Registered User
  • 91 posts
  • 108
  • Location:Europe

Posted 27 November 2016 - 09:31 AM

http://www.ebiomedic...0524-2/fulltext

 

Article Outline

 

    1. Introduction

    2. Ageing as a Clinical Indication

    3. Repurposing Drugs to Combat Ageing

        3.1. Rapamycin and mTOR Inhibition

        3.2. TAMEing Ageing With Metformin

        3.3. Second Generation Repurposed Anti-ageing Compounds?

    4. New Compounds Specifically Developed to Target Ageing

        4.1. NAD+ Supplementation

        4.2. Senolytics

    5. Biomarkers for Detecting Drug Efficacy Against Ageing

    6. Conclusions

    7. Outstanding Questions


  • Informative x 6
  • like x 1

#1596 Mike C

  • Registered User
  • 75 posts
  • 13

Posted 27 November 2016 - 11:33 PM

WRT MIchael Rae I have been following his posts for 20 years and the attackers have come and gone over the years on the CRsociety as well as this site and Michael just keeps on plugging away. He is not one to be the least bit intimidated by this so I would not get to concerned about it. IAC, his input is certainly one I pay close attention to for the very reasons Sthira has pointed to in his post. Thanks Sthira!
  • Off-Topic x 2
  • Informative x 2
  • Needs references x 1
  • Good Point x 1
  • Agree x 1
  • Pointless, Timewasting x 1

sponsored ad

  • Advert
To book this BIOSCIENCE ad spot and support Longecity (this will replace the google ad above) - click HERE.

#1597 Thell

  • Registered User
  • 54 posts
  • 14
  • Location:Arkansas
  • NO

Posted 28 November 2016 - 06:02 PM

Recent NMN discussion on this thread made me wonder a little bit more about the specifics of NMNAT. While studying I ran across this...

 

NMNAT1 inhibits axon degeneration via blockade of SARM1-mediated NAD+ depletion (October 13, 2016)

Abstract

Overexpression of the NAD+ biosynthetic enzyme NMNAT1 leads to preservation of injured axons. While increased NAD+ or decreased NMN levels are thought to be critical to this process, the mechanism(s) of this axon protection remain obscure. Using steady-state and flux analysis of NAD+ metabolites in healthy and injured mouse dorsal root ganglion axons, we find that rather than altering NAD+ synthesis, NMNAT1 instead blocks the injury-induced, SARM1-dependent NAD+ consumption that is central to axon degeneration.

 

Excerpt

 

...Surprisingly, we find that neither NAD+loss nor NMN accumulation trigger axon degeneration. Instead, both NMNAT1 and NMN deamidase prevent axon degeneration via blocking the injury-induced NAD+ consumption that occurs following activation of the axodestructive molecule SARM1.


→ source (external link)

 

 


  • Informative x 2

#1598 albedo

  • Registered User
  • 1,017 posts
  • 311
  • Location:Europe
  • NO

Posted 30 November 2016 - 09:19 AM

Metabolic control of muscle and muscle stem cell function

http://memento.epfl....le-stem-cell-2/



#1599 Bryan_S

  • Topic Starter
  • Member
  • 1,154 posts
  • 363
  • Location:Orlando

Posted 02 December 2016 - 06:49 PM

Reductive carboxylation is a major metabolic pathway in the retinal pigment epithelium
 
'NAD+ declines with age (47, 51), and supplementation with NAD precursors can delay aging, liver disease, and vascular dysfunction (52–54). NAD+ precursors, such as nicotinamide riboside, can be used safely in humans (55, 56). In the absence of animal models for AMD, our findings highlight the need for clinical trials that evaluate NAD+ precursors for their ability to prevent and treat AMD."
 
Significance
In the vertebrate eye, a monolayer of cells, called the retinal pigment epithelium (RPE), is between the choroidal blood supply and the retina. The RPE provides metabolic support for the retina, including delivery of glucose and other nutrients. Here, we show that reductive carboxylation of α-ketoglutarate, a type of metabolism that supports growth and survival of cancer cells, is a prominent feature of RPE cells. We show that extreme oxidative stress can overwhelm the reductive carboxylation pathway. However, we also found that the RPE can be protected from extreme oxidative stress by supplementation with an NAD+ precursor or α-ketoglutarate.
 
Abstract
The retinal pigment epithelium (RPE) is a monolayer of pigmented cells that requires an active metabolism to maintain outer retinal homeostasis and compensate for oxidative stress. Using 13C metabolic flux analysis in human RPE cells, we found that RPE has an exceptionally high capacity for reductive carboxylation, a metabolic pathway that has recently garnered significant interest because of its role in cancer cell survival. The capacity for reductive carboxylation in RPE exceeds that of all other cells tested, including retina, neural tissue, glial cells, and a cancer cell line. Loss of reductive carboxylation disrupts redox balance and increases RPE sensitivity to oxidative damage, suggesting that deficiencies of reductive carboxylation may contribute to RPE cell death. Supporting reductive carboxylation by supplementation with an NAD+ precursor or its substrate α-ketoglutarate or treatment with a poly(ADP ribose) polymerase inhibitor protects reductive carboxylation and RPE viability from excessive oxidative stress. The ability of these treatments to rescue RPE could be the basis for an effective strategy to treat blinding diseases caused by RPE dysfunction.
 

  • Informative x 2

#1600 midas

  • Registered User
  • 348 posts
  • 69
  • Location:Manchester....UK
  • NO

Posted 07 December 2016 - 12:12 PM

I pointed this out a week or two ago......Keep in mind that the majority of cancers in later life and NAD declines with age. So, if NAD was such a big deal when it comes to cancer wouldn't that mean we were more susceptible to cancers when our NAD pool was full rather than when its running low.


  • Good Point x 3
  • Disagree x 2
  • like x 1
  • Informative x 1

#1601 Daniel Cooper

  • Member
  • 289 posts
  • 17
  • Location:USA

Posted 07 December 2016 - 02:56 PM

So at this point the summary seems to be that higher NAD+ levels are unlikely to cause you to develop cancer and in fact my offer some protection against the formation of cancerous cells, but once you actually get cancer higher NAD+ levels may cause come cancers to become more aggressive (e.g. glioblastoma) but may have the opposite effect on others (e.g. breast cancer).

 

If so, it this makes determining what to do with regards to NR supplementation very murky indeed.  None of us has a crystal ball to see what types of cancer we will ultimately develop.  I have suspended my NR supplementation for other reasons but have intended to restart it in a few months.  Now I'm not so sure.  This would seem to merit more study and some caution.  I can certainly say that if I had relatives that developed glioblastoma I would be very reluctant to supplement with NR at this time, but even that position has it's difficulty as glioblastoma is not currently thought to be strongly tied to heredity.

 

 



#1602 Daniel Cooper

  • Member
  • 289 posts
  • 17
  • Location:USA

Posted 07 December 2016 - 03:26 PM

So let's take the assumption I made above, i.e. that increased levels of NAD+ don't generally cause cancer, but they can fuel some cancers once they develop, glioblastoma in particular.

 

That assumption would probably lead you predict that children (which have higher NAD+ levels) which develop glioblastoma would have a worse prognosis than those that develop glioblastoma at middle age or later.

 

However, that doesn't seem to be the case.  

 

Long-term outcomes in children with glioblastoma     https://www.ncbi.nlm...pubmed/20672935

 

Of course, we're trying to look a single variable here in isolation, which we can't do.  Perhaps a child's immune system is a bit more successful at fighting glioblastoma than someone in middle age.  Or it could be one of any numbers of other differences in a child versus an adult that overcome to some extent the tendency for higher levels of NAD+ to fuel glioblastoma.

 

 

 

 


  • like x 1

#1603 Harkijn

  • Registered User
  • 271 posts
  • 66
  • Location:Amsterdam
  • NO

Posted 07 December 2016 - 04:20 PM

Valid points Midas and Daniel, though I am not totally reassured yet. Meanwhile I am happy that this press release just reached me.

 

 https://www.elysiumh...l-press-release


  • like x 3

#1604 Daniel Cooper

  • Member
  • 289 posts
  • 17
  • Location:USA

Posted 07 December 2016 - 04:31 PM

Valid points Midas and Daniel, though I am not totally reassured yet. Meanwhile I am happy that this press release just reached me.

 

 https://www.elysiumh...l-press-release

 

 

Oh believe me, I am by no means reassured.  In fact I have to be careful in my evaluation of this given how badly I don't want this to be a problem with NR.  At this point all I see is murkiness, and the study on glioblastoma in children vs adults is by no means any sort of definitive answer.  It's really only an indication of how inadequate our knowledge is on NR vs. cancer promotion.

 

 

What we really need is a mouse model for glioblastoma (does one exist?) and then feed a control and study group NR and see what happens.

 

 


Edited by Daniel Cooper, 07 December 2016 - 04:35 PM.

  • Well Written x 1
  • Good Point x 1

#1605 Thell

  • Registered User
  • 54 posts
  • 14
  • Location:Arkansas
  • NO

Posted 07 December 2016 - 04:42 PM

Valid points Midas and Daniel, though I am not totally reassured yet. Meanwhile I am happy that this press release just reached me.

 

 https://www.elysiumh...l-press-release

 

We've been waiting to hear some results information (let alone the study publication) so this is indeed a happy occasion.

 

A quote to those involved in the 'max' NAD+ level discussion a few pages back...

 

 

The study, which was placebo-controlled, randomized, and double-blinded, evaluated the safety and efficacy of BASIS™ [nicotinamide riboside (NR) and pterostilbene] in 120 healthy participants ages 60-80 over an eight-week period. Participants received either the recommended dose (250 mg NR and 50 mg pterostilbene), double the recommended dose or a placebo daily for the eight-week trial.

The study found that participants experienced no serious adverse events and confirmed that BASIS™ is safe for daily use as determined by standard safety measures. The study also showed that in participants taking the recommended dose of BASIS, ™ NAD+ levels increased from baseline in whole blood by an average of 40% at four weeks and maintained that increase for the duration of the trial. Participants taking double the recommended daily dose saw their NAD+ levels increase approximately 90% at four weeks, and a significantly higher level of NAD+ (compared to the recommended dose of BASIS™) was maintained for the duration of the trial. This first-in-humans study demonstrates clearly that BASIS™ can increase NAD+ levels in the blood safely and sustainably. Confirming that BASIS™ is an effective NAD+ precursor in humans is a vital first step to elucidating how BASIS™ supports human health.

 

Can't wait to read the study!


Edited by Thell, 07 December 2016 - 04:43 PM.

  • Informative x 2

#1606 bluemoon

  • Registered User
  • 446 posts
  • 24
  • Location:south side
  • NO

Posted 07 December 2016 - 05:10 PM

 

Can't wait to read the study!

 

 

But how long for the wait? Late next year, right?



#1607 Anthony_Loera

  • Lifetime Member
  • 3,114 posts
  • 695
  • Location:Miami Florida

Posted 07 December 2016 - 05:28 PM

 

Valid points Midas and Daniel, though I am not totally reassured yet. Meanwhile I am happy that this press release just reached me.

 

 https://www.elysiumh...l-press-release

 

We've been waiting to hear some results information (let alone the study publication) so this is indeed a happy occasion.

 

A quote to those involved in the 'max' NAD+ level discussion a few pages back...

 

 

The study, which was placebo-controlled, randomized, and double-blinded, evaluated the safety and efficacy of BASIS™ [nicotinamide riboside (NR) and pterostilbene] in 120 healthy participants ages 60-80 over an eight-week period. Participants received either the recommended dose (250 mg NR and 50 mg pterostilbene), double the recommended dose or a placebo daily for the eight-week trial.

The study found that participants experienced no serious adverse events and confirmed that BASIS™ is safe for daily use as determined by standard safety measures. The study also showed that in participants taking the recommended dose of BASIS, ™ NAD+ levels increased from baseline in whole blood by an average of 40% at four weeks and maintained that increase for the duration of the trial. Participants taking double the recommended daily dose saw their NAD+ levels increase approximately 90% at four weeks, and a significantly higher level of NAD+ (compared to the recommended dose of BASIS™) was maintained for the duration of the trial. This first-in-humans study demonstrates clearly that BASIS™ can increase NAD+ levels in the blood safely and sustainably. Confirming that BASIS™ is an effective NAD+ precursor in humans is a vital first step to elucidating how BASIS™ supports human health.

 

Can't wait to read the study!

 

 

Well this is some good news Thell,

 

Thanks for sharing.

A


  • Pointless, Timewasting x 1

#1608 bluemoon

  • Registered User
  • 446 posts
  • 24
  • Location:south side
  • NO

Posted 07 December 2016 - 05:40 PM

Ten years ago David Sinclair said that he thought there would be a pharmaceutical drug that would cost about $3 a day that would boost surtuins and lower the risk of some major diseases. If one takes the double dosage of Elysium Basis at 500 mg of NR and 100 mg of pterostiline for the 90% boost of NAD+, that is about what it costs with a subscription: $3.33 a day. 


Edited by bluemoon, 07 December 2016 - 05:43 PM.


#1609 Thell

  • Registered User
  • 54 posts
  • 14
  • Location:Arkansas
  • NO

Posted 07 December 2016 - 09:59 PM

Pathway linked to slower aging also fuels brain cancer

http://medicalxpress...ging-fuels.html

 

We don't know what this study will reveal since it doesn't seem to be listed anywhere on pnas.org even though the 'press statement' states it was published Dec. 5 in Proceedings of the National Academy of Sciences. The primary author's lab publications list indicates it will be named 'NAMPT controls tumor growth and therapy responsiveness in glioblastoma'.

 

Also, keep in mind that NAMPT is not needed for conversion of NR to NAD+. To me, the interesting aspect of the various studies done regarding NAMPT and cancer/tumors is we know that the vast majority of cancer is recorded in the elderly and NAMPT is shown to decrease with age and yet the correlation seems to indicate the presence of over expression of NAMPT. I'd like to know what leads to an over expression of NAMPT where it should be reduced rather than seeing multiple studies saying that things (PARP, SIRT, COX, CD38, etc...) that prolong cell life also support cancer growth. There's a non-repaired mutation in there somewhere!

 

Given that last statement I find it encouraging to see that Paul Modrich joined the Elysium Health scientific advisory board, as noted in that earlier press release today. He won a 2015 Nobel Prize in Chemistry for work showing how cells monitor and signal for repairing incorrect replications of DNA. Perhaps he is in it for the money but I think not. I think it may be believed that a properly functioning NAD cycle will help keep mutations down.


  • Disagree x 1
  • Agree x 1

#1610 Bryan_S

  • Topic Starter
  • Member
  • 1,154 posts
  • 363
  • Location:Orlando

Posted 07 December 2016 - 10:06 PM

Valid points Midas and Daniel, though I am not totally reassured yet. Meanwhile I am happy that this press release just reached me.

 

 https://www.elysiumh...l-press-release

 

I just pass this stuff on. I think its better to have NAD levels at more youthful levels for the prevention of cancers but should one develop consult your oncologist.

 

========================================================

 

ELYSIUM HEALTH™ RAISES $20 MILLION IN SERIES B FINANCING LED BY GENERAL CATALYST, ANNOUNCES TOPLINE CLINICAL TRIAL RESULTS FOR ITS FIRST PRODUCT BASIS™, AND WELCOMES LEADING SCIENTISTS AND PHYSICIANS TO ITS SCIENTIFIC ADVISORY BOARD

 
The human clinical trial, evaluating safety and efficacy of BASIS™,met its primary and secondary endpoints
 
NEW YORK (December 6, 2016) – Elysium Health, Inc. ™, a provider of scientifically-sound dietary supplements, today announced it has raised $20 million in Series B financing led by General Catalyst and joined by Breyer Capital, Morningside Ventures and Sound Ventures. Existing investors include Jim Manzi, chairman, Thermo Fisher Scientific Inc. and former chairman, president and CEO of Lotus Development Corp.; biotech venture capitalist Robert Nelsen; and entrepreneur Matthew Mullenweg.
 
The funding will enable Elysium to expand its operations to support the rapid growth of its customer base, as well as initiate additional human clinical trials to evaluate the safety and efficacy of new products it plans to add to its offerings. In addition, the funds will support Elysium’s mission to be a leader in the study of NAD+ and sirtuins within the context of human aging.
 
“Since launching Elysium two years ago, we have worked tirelessly to create entirely new ways to make scientific breakthroughs accessible and actionable for people who want to take a proactive role in supporting their health,” said Eric Marcotulli, CEO and co-founder of Elysium. “Our first product BASIS™ is designed to optimize cellular health and is based on expansive research. We look forward to working with our financial partners and scientific advisory board to further develop our product pipeline to continue to bring meaningful health products to market.”
 
“Elysium is an innovative company, with an amazing executive team and scientific advisory board, committed to reframing the way we think about our health,” said David Fialkow, managing director, General Catalyst. “We are thrilled to invest in Eric and his team to help expand and enhance the scientifically-sound products they intend to bring to the market in the future.”
 
Elysium Announces Topline Clinical Trial Results
Elysium also announced today that its first human clinical trial designed to evaluate the safety and efficacy of its first product, BASIS™, met its primary and secondary endpoints. The study, which was placebo-controlled, randomized, and double-blinded, evaluated the safety and efficacy of BASIS™ [nicotinamide riboside (NR) and pterostilbene] in 120 healthy participants ages 60-80 over an eight-week period. Participants received either the recommended dose (250 mg NR and 50 mg pterostilbene), double the recommended dose or a placebo daily for the eight-week trial.
 
The study found that participants experienced no serious adverse events and confirmed that BASIS™ is safe for daily use as determined by standard safety measures. The study also showed that in participants taking the recommended dose of BASIS, ™ NAD+ levels increased from baseline in whole blood by an average of 40% at four weeks and maintained that increase for the duration of the trial. Participants taking double the recommended daily dose saw their NAD+ levels increase approximately 90% at four weeks, and a significantly higher level of NAD+ (compared to the recommended dose of BASIS™) was maintained for the duration of the trial. This first-in-humans study demonstrates clearly that BASIS™ can increase NAD+ levels in the blood safely and sustainably. Confirming that BASIS™ is an effective NAD+ precursor in humans is a vital first step to elucidating how BASIS™ supports human health.
 
“As we age, NAD+ levels in our cells decline. The trial results, which are the first of their kind, indicate that BASIS™ increases NAD+ levels in a sustained way. And since NAD+ is involved in hundreds of critical cellular processes, it is a vitally important component to optimizing our cellular health as we get older,” said Dr. Lenny Guarente, chief scientific officer and co-founder of Elysium who also serves as the director of the Glenn Laboratory for the Science of Aging at Massachusetts Institute of Technology. “We plan to submit the full results of the trial to a peer-reviewed scientific journal.”
 
Elysium Adds Three World-Renowned Scientists and Physicians to Its Scientific Advisory Board
To support Elysium’s mission of researching, validating and distributing scientifically-sound health products, it established an unprecedented Scientific Advisory Board composed of more than two dozen of the world’s leading scientists and clinicians. This scientific board works with the Elysium team to accelerate the exchange of ideas and research findings, evaluate data and help ensure a high level of scientific rigor and transparency in the development of Elysium’s products.
 
Elysium is honored to welcome to its Scientific Advisory Board:
 
George M. Church, the Robert Winthrop Professor of Genetics at Harvard Medical School and Professor of Health Sciences and Technology at Harvard and MIT.
Richard Granstein, M.D., Chairman of Dermatology Weill Cornell Medical College.
Paul L. Modrich, James B. Duke Professor of Biochemistry at Duke University and recipient of the Nobel Prize in Chemistry in 2015.
About BASIS™
BASIS™ is a daily product that supports metabolic health. The proprietary formulation of nicotinamide riboside and pterostilbene is designed to increase levels of the coenzyme NAD+ and to support a class of proteins called sirtuins. NAD+ and sirtuins work together in vital cellular processes including energy production. BASIS™ is available to consumers exclusively through the Elysium Health™ website (www.elysiumhealth.com). The cost for BASIS™ is $60 for a 30-day supply or $50 per month on a subscription plan.
About Elysium Health™
Elysium Health’s™ mission is to solve the biggest challenges in health with science, to help people live healthier, longer lives. Working directly with the world’s leading scientists and clinicians, Elysium Health™ translates advances in science and technology into effective, scientifically-sound products that help people manage their health in an actionable way.
 
###
 
Media Contacts:
Victoria E. Davis
Cell: 410-279-3049
Victoria@elysiumhealth.com
 
Pia Chatterjee
Cell: 510-384-0845
Pia@elysiumhealth.com

  • Good Point x 2
  • Informative x 1
  • like x 1

#1611 Bryan_S

  • Topic Starter
  • Member
  • 1,154 posts
  • 363
  • Location:Orlando

Posted 07 December 2016 - 10:17 PM

Replicatively senescent human fibroblasts reveal a distinct intracellular metabolic profile with alterations in NAD+ and nicotinamide metabolism

 

http://www.nature.co...es/srep38489#f4

 

Conclusions

Although the metabolic profile of established PEsen cells is superficially complex there are two conclusions that are consistent with a large amount of the data. Firstly, PEsen cells appear to activate the same mechanisms that delay the initiation of senescence; a shift from oxidative phosphorylation towards glycolysis and the pentose phosphate pathway to reduce the production of ROS23 and an upregulation of pathways involved in redox homeostasis to ameliorate the effects of hydrogen peroxide. Secondly, other alterations such as the maintenance of NAD+ and nicotinamide levels, nucleotide catabolism, membrane breakdown and alterations in creatine metabolism could be interpreted as a strategy the senescent cells adopt to promote cell survival and generate energy and the building blocks for cell growth in the absence of functional mitochondria and oxidative phosphorylation. Our results also suggest caution in the use of supplements such as nicotinamide and antioxidants, as whilst there is evidence that these compounds may delay cellular senescence and age-related diseases, they are unlikely to eliminate existing PEsen cells and may actually aid their survival. Lastly, senescent cells are known to be generally resistant to apoptosis1 and recently targeting apoptotic pathways has achieved some success in selectively eliminating senescent cells and producing ‘senolytic drugs’14,53. Therefore, some of the senescence-specific pro-survival alterations in the metabolic pathways described here may also serve as targets for the future development of such drugs.

  • Informative x 2

#1612 albedo

  • Registered User
  • 1,017 posts
  • 311
  • Location:Europe
  • NO

Posted 07 December 2016 - 10:28 PM

Nicotinamide riboside has also an entry in the Geroprotectors.org curated data base and probably additional inputs will be done in future, to keep an eye on. Geroprotectors.org is "...a manually curated online database that provides instant access to all of the above. An up-to-date, rapidly explorable system that catalogues and summarizes over 200 geroprotective compounds and links them to over 250 studies that support (or refute) their effects in model organisms, Geroprotectors is for the entrant or expert in the field alike..." (1).  Type "nicotinamide riboside" in the search engine.

 

(1) Moskalev A, Chernyagina E, De magalhães JP, et al. Geroprotectors.org: a new, structured and curated database of current therapeutic interventions in aging and age-related disease. Aging (Albany NY). 2015;7(9):616-28.

 


  • Informative x 1

#1613 bluemoon

  • Registered User
  • 446 posts
  • 24
  • Location:south side
  • NO

Posted 07 December 2016 - 10:35 PM

I just checked and saw Chromadex's stock price is still at a three-year low of $2.34 after the Elysium press release. Interesting. Maybe the Elysium press release wasn't surprising and not that important compared to the next efficacy results coming.

 

Jun  7  $5.49

July 7  $3.81

Aug 7  $4.04 

Sep 7  $2.94

Oct 7   $2.45

Dec 7  $2.34


  • Informative x 2
  • Off-Topic x 1

#1614 Oakman

  • Member
  • 312 posts
  • 132
  • Location:CO

Posted 08 December 2016 - 04:31 AM

I just checked and saw Chromadex's stock price is still at a three-year low of $2.34 after the Elysium press release. Interesting. Maybe the Elysium press release wasn't surprising and not that important compared to the next efficacy results coming.

 

Jun  7  $5.49

July 7  $3.81

Aug 7  $4.04 

Sep 7  $2.94

Oct 7   $2.45

Dec 7  $2.34

 

The market is suspicious of pharma companies' success rate, and rightly so. I would venture 1 out of 1000 investors would have heard of Chromadex. Plus, for those that do, their sales went down last quarter1. Not much to go on for the average investor, and way too small for most institutions to have significant holdings2.  Press releases are not given much heed. 

 

1) "For the three months ended October 1, 2016 (“Q3 2016”), ChromaDex reported net sales of $5.0 million, a decrease of 20% as compared to $6.3 million for the three months ended October 3, 2015 (“Q3 2015”)."

 

https://globenewswir...al-Results.html

 

2) http://www.nasdaq.co...tional-holdings


  • Informative x 2
  • Off-Topic x 1

#1615 bluemoon

  • Registered User
  • 446 posts
  • 24
  • Location:south side
  • NO

Posted 08 December 2016 - 05:50 AM

But then you could say the same thing about Chromadex crashing in June after the short-sell report. Apparently there are investors paying attention even if volume is usually low. 

 

I would have guessed a bump up but there are of course many factors involving the price.The fun starts if NMN can be sold at competitive prices to NR or if a pharmaceutical starts to sell a drug by 2018 or 2019 as David Sinclair thought in 2013 that would compete with NR.

 

  


  • Off-Topic x 2

#1616 Thell

  • Registered User
  • 54 posts
  • 14
  • Location:Arkansas
  • NO

Posted 08 December 2016 - 08:56 PM

 

Dietary proanthocyanidins boost hepatic NAD+ metabolism and SIRT1 expression and activity in a dose-dependent manner in healthy rats

http://www.nature.co...es/srep24977#f3

 

rReceived 21 October 2015

Accepted: 08 April 2016
Published online: 22 April 2016
 
Abstract
 
"Proanthocyanidins (PACs) have been reported to modulate multiple targets by simultaneously controlling many pivotal metabolic pathways in the liver. However, the precise mechanism of PAC action on the regulation of the genes that control hepatic metabolism remains to be clarified. Accordingly, we used a metabolomic approach combining both nuclear magnetic resonance and mass spectrometry analysis to evaluate the changes induced by different doses of grape-seed PACs in the liver of healthy rats. Here, we report that PACs significantly increased the hepatic nicotinamide adenine dinucleotide (NAD+) content in a dose-dependent manner by specifically modulating the hepatic concentrations of the major NAD+ precursors as well as the mRNA levels of the genes that encode the enzymes involved in the cellular metabolism of NAD+. Notably, Sirtuin 1 (Sirt1) gene expression was also significantly up-regulated in a dose-response pattern. The increase in both the NAD+ availability and Sirt1 mRNA levels, in turn, resulted in the hepatic activation of SIRT1, which was significantly associated with improved protection against hepatic triglyceride accumulation. Our data clearly indicates that PAC consumption could be a valid tool to enhance hepatic SIRT1 activity through the modulation of NAD+ levels."
 
So Proanthocyanidins might be another route to increasing NAD+.

 

 

It looks like there is now a discussion thread for a grape seed extract product whose extract was used in this study. I'm not sure if it will be an 'open' discussion on the merits and efficacy or a 'sales' thread but I know that I'm definitely interested in another pathway. :-D


  • Informative x 2

#1617 bluemoon

  • Registered User
  • 446 posts
  • 24
  • Location:south side
  • NO

Posted 09 December 2016 - 05:11 PM

I've been curious about Elysium's trial compared to Chromadex's trial. Elysium limited the age of participants from 60 to 80 years old while Chromadex's 12 participants were not, right? 

 

250 mg of NR with 50 mg of pterostilbine increased NAD+ in blood by 40%. Chromadex showed 100 mg of NR alone increased NAD+ by 30%.  If both studies used the same ages then it would be reasonable for someone to take just 125 mg of NR (what I take) and no pterostilbine for $0.75 a day to get nearly the same boost as taking Elysium's Basis 250 mg of NR with 50 mg of pterostilbine for $1.70 a day. Yet, the age group isn't the same so...

 

I've wondered ever since Guarente told reporters what he was taking, Basis, along with 250 mg of resveratrol and 2500 IU of vitamin D, if he was taking a double dose of Basis or the dose that his company recommends. To get the 90% increase in NAD+ at $3.30 a day is well beyond what most will pay among those who are willing to try NR in the first place unless the results come back are a health home run, which I doubt - but maybe. 

  


Edited by bluemoon, 09 December 2016 - 05:16 PM.

  • Enjoying the show x 1

#1618 Oakman

  • Member
  • 312 posts
  • 132
  • Location:CO

Posted 09 December 2016 - 05:54 PM

I've been curious about Elysium's trial compared to Chromadex's trial. Elysium limited the age of participants from 60 to 80 years old while Chromadex's 12 participants were not, right? 

 

250 mg of NR with 50 mg of pterostilbine increased NAD+ in blood by 40%. Chromadex showed 100 mg of NR alone increased NAD+ by 30%.  If both studies used the same ages then it would be reasonable for someone to take just 125 mg of NR (what I take) and no pterostilbine for $0.75 a day to get nearly the same boost as taking Elysium's Basis 250 mg of NR with 50 mg of pterostilbine for $1.70 a day. Yet, the age group isn't the same so...

 

I've wondered ever since Guarente told reporters what he was taking, Basis, along with 250 mg of resveratrol and 2500 IU of vitamin D, if he was taking a double dose of Basis or the dose that his company recommends. To get the 90% increase in NAD+ at $3.30 a day is well beyond what most will pay among those who are willing to try NR in the first place unless the results come back are a health home run, which I doubt - but maybe. 

 

It is a bit of a problem to try to equalize these different studies to get a consistent picture. As far as cost, right now I take 375mg Niagen w/150mhg Pterostilbene in the morning, then 125mg Niagen in the evening for $1.83/day. You just need to dig a bit for deals, it's still not cheap, but gets more reasonable. 

 

Lower cost gives greater flexibility for adjusting dosing to see what happens. As we're all N=1 studies, as no one really knows (yet) what's most effective at any age...we're all longevity explorers. As always, many more studies are needed, esp. segregated as to age group, IMHO



#1619 mrkosh1

  • Registered User
  • 199 posts
  • 139

Posted 09 December 2016 - 06:06 PM

If we want to go into maximum NAD+ boosting, I think a supplement that was a combination of NR, R-ALA, and ALCAR would give basis a run for its money. When my financial situation improves, this is the stack I want to try. Although it may be irrational, I trust R-ALA and ALCAR more so than anything like resveratrol.



sponsored ad

  • Advert
To book this BIOSCIENCE ad spot and support Longecity (this will replace the google ad above) - click HERE.

#1620 Oakman

  • Member
  • 312 posts
  • 132
  • Location:CO

Posted 09 December 2016 - 06:52 PM

If we want to go into maximum NAD+ boosting, I think a supplement that was a combination of NR, R-ALA, and ALCAR would give basis a run for its money. When my financial situation improves, this is the stack I want to try. Although it may be irrational, I trust R-ALA and ALCAR more so than anything like resveratrol.

 

If it helps you mrkosh1, with what I mentioned above, I take also (among others):

 

500 mg ALCAR, 150 mg R-ALA, 500 mg trans-Resveratrol

 

Unsure what my NAD+ levels are or if they've changed, trusting they've gone up :)  . What I can say is that in the week since I upped my dose of NR to 500 mg from 375mg (not changing anything else), I'm absolutely stronger at the gym, wake up earlier and feel more refreshed. Also, I feel the resveratrol is helping a lot since starting it.  It's all good together, and I strongly feel that these compounds are synergistic together.


Edited by Oakman, 09 December 2016 - 06:53 PM.

  • Agree x 1





Also tagged with one or more of these keywords: nicotinamide riboside, nicotinamide, nad boosting, charles brenner, david sinclair, leonard guarente, niagen, niacinamide, nicotinamide mononucleotide

3 user(s) are reading this topic

0 members, 2 guests, 0 anonymous users


    Bing (1)

Topic Led By