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Nicotinamide Riboside [Curated]

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

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#1 Bryan_S

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Posted 14 October 2015 - 06:57 PM


Nicotinamide Riboside thread moderated by the threadstarter.

 

This is still the Nicotinamide Riboside Current News and Updates thread we've all grown to know. This thread encompasses the latest articles on Nicotinamide Riboside, NAD boosting, clinical updates and emerging studies all aimed at the medical uses of the NAD precursors.

 

This thread will continue as before. This thread was started and is supported by NR users and is a tool for those in our community investigating the topic of Nicotinamide Riboside.

 

In the past we've seen some complaints as we explore and discuss some of the parallel topics and your voices have been noted. Personally I'm not totally Nicotinamide Riboside centric and comments on related current and past NAD precursor studies are welcome but lets keep the topic conversation along the lines of NAD boosting to be true to our readers. Being that we've accumulated a treasure trove of NAD medical articles and studies over the last year many visit this thread to find the latest released publications on this topic and we'll stay true to that focus.

 

If we go to far off topic on an offshoot I'm going to ask that you continue that new topic on a adjacent thread when asked so as to not dilute our primary topic. Along these lines LongeCity administrators felt I should begin to moderate this thread and here we are.

 

Please feel free to reference our earlier posts here Nicotinamide Riboside Current News and Updates

 

I've created a Channel on YouTube called NAD Repletion for content related to this thread as it becomes available.


Edited by Bryan_S, 23 October 2016 - 11:24 PM.
NAD Repletion youtube channel added

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#2 Bryan_S

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Posted 14 October 2015 - 11:54 PM

Synthesis of an oligonucleotide with a nicotinamide mononucleotide residue and its molecular recognition in DNA helices

 

http://pubs.rsc.org/...4a#!divAbstract



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#3 Bryan_S

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Posted 15 October 2015 - 12:36 AM

Can we use the epigenetic bioactivity of caloric restriction and phytochemicals to promote healthy ageing?

 

Being that the topic of Nicotinamide Riboside is directly connected to the NAD dependent sirtuin activators and this is all wrapped around epigenetic's and aging this article is a must read by those who are trying to grasp the interdependent relationship. This is an offshoot topic of NAD boosting with direct references to Nicotinamide Riboside.

 

http://www.researchg..._healthy_ageing

 

In 2011, the Centers for Disease Control and Prevention reported that half of Americans are using food supplements, intended to provide them with nutrients that they believe they consume in insufficient quantities. Dietary supplements were repeatedly said to be unnecessary if one eats a balanced diet but within the booming “silver economy”, sales of vitamins, minerals and supplements totalled nearly $23 billion in the US last year (Euro monitor International). Seventy eight “antioxidant” supplements trials including 296 707 participants were reviewed by the Cochrane Database System Review. It was concluded that beta-carotene and vitamin E supplements, instead of promoting longevity, were increasing mortality and so may high doses of vitamin A. Several nutrition interventions with or without edible phytochemicals, fasting regimens, and food supplements have now been tried to prevent the development of many different types of tumors. Most were known as antioxidants and are now repurposed because they were shown to change the epigenome. Epigenetic marks are enzymatic tags deposited on the genome which do not change the DNA sequence but change gene expression. They are reversible and epigenetic dietary interventions are thus suggested for the prevention of ageing, ageing related diseases and for breaking the vicious circle of the trans-generational epigenetic inheritance of the metabolic disorders. It is a pressing issue because more and more children are exposed to parents' obesity and are at risk of developing type 2 diabetes. Why is it relevant to propose epigenetic “Nutricures” to prevent diseases linked with ageing? To answer this question we produce this review, whose scope is to underline the importance of the nutritional contribution for a correct functioning of epigenetics. Almost all chromatin-modifying enzymes utilize co-factors, which are crucial metabolites for core metabolism pathways. Because the cellular concentrations of these metabolites fluctuate as a function of the metabolic status of the cell, the activity of most epigenetic enzymes depends on the cell metabolism and thus nutrition. Through one selected representative example, sirtuins, and their metabolic co-factor, nicotinamide, we illustrate the nutrition and epigenetic connections. Then we describe the epigenetic activities of some polyphenols. Finally we underline that with globalization there is a continuing trend changing the variety of food items that we consume. Each may have bioactive effects that may combine with additional epigenetic effects of pollutants such as pesticides. We plead likewise that because they are bioactive, “Nutricures” and food supplements should undergo better evaluation before marketing.

 

Short list of Parallel publications

http://www.ncbi.nlm....les/PMC3873820/

http://online.lieber...9/ars.2012.4600

http://www.clinicale.../content/7/1/33

 


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#4 Bryan_S

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Posted 15 October 2015 - 04:11 PM

NAD in Skin: Therapeutic Approaches for Niacin

 

http://www.researchg...ches_for_Niacin

 

Full-Text made available Oct 15, 2015

This article provides more background on the cancer fighting effects of NAD BOOSTING.

 

"Abstract: The maintenance and regulation of cellular NAD(P)(H ) content and its influence on cell function involves many metabolic pathways, some of which remain poorly understood. Niacin deficiency in humans, which leads to low NAD status, causes sun sensitivity in skin, indicative of deficiencies in responding to UV damage. Animal models of nia-cin deficiency demonstrate genomic instability and increased cancer development in sensitive tissues including skin. Cell culture models of niacin deficiency have allowed the identification of NAD-dependent signaling events critical in early skin carcinogenesis. Niacin restriction in immortalized keratinocytes leads to an increased expression and activity of NADPH oxidase resulting in an accumulation of ROS, providing a potential survival mechanism as has been shown to oc-cur in cancer cells. Niacin deficient keratinocytes are more sensitive to photodamage, as both poly(ADP-ribose) polym-erases and Sirtuins are inhibited by the unavailability of their substrate, NAD+, leading to unrepaired DNA damage upon photodamage and a subsequent increase in cell death. Furthermore, the identification of the nicotinic acid receptor in hu-man skin keratinocytes provides a further link to niacin’s role as a potential skin cancer prevention agent and suggests the nicotinic acid receptor as a potential target for skin cancer prevention agents. The new roles for niacin as a modulator of differentiation and photo-immune suppression and niacin status as a critical resistance factor for UV damaged skin cells are reviewed here." 



#5 Bryan_S

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Posted 15 October 2015 - 04:39 PM

The human NAD metabolome: Functions, metabolism and compartmentalization

 

http://www.tandfonli...38.2015.1028612

Published online: 02 Apr 2015

 

Abstract "The metabolism of NAD has emerged as a key regulator of cellular and organismal homeostasis. Being a major component of both bioenergetic and signaling pathways, the molecule is ideally suited to regulate metabolism and major cellular events. In humans, NAD is synthesized from vitamin B3 precursors, most prominently from nicotinamide, which is the degradation product of all NAD-dependent signaling reactions. The scope of NAD-mediated regulatory processes is wide including enzyme regulation, control of gene expression and health span, DNA repair, cell cycle regulation and calcium signaling. In these processes, nicotinamide is cleaved from NAD+ and the remaining ADP-ribosyl moiety used to modify proteins (deacetylation by sirtuins or ADP-ribosylation) or to generate calcium-mobilizing agents such as cyclic ADP-ribose. This review will also emphasize the role of the intermediates in the NAD metabolome, their intraand extra-cellular conversions and potential contributions to subcellular compartmentalization of NAD pools."

 

Conclusions and future perspectives "Recent research has revealed the importance of the regulatory roles of NAD. In fact, some of these pathways have already been targeted for therapeutic treatments of cancer and other diseases. While impressive progress has been made over the last years with regard to NAD-dependent signaling mechanisms, some critical issues have remained unresolved. For example, NAD-dependent signaling uses up an unexpectedly large amount of NAD. Therefore, NAD biosynthesis has to be highly active and needs to be fine-tuned to the actual demands of the cell. However, except for the identification of the principal pathways of NAD biosynthesis and the corresponding enzymes, surprisingly little is known about the mechanisms regulating NAD synthesis and how it influences signaling pathways. Moreover, cellular NAD is compartmentalized in distinct membrane-coated organelles in human cells. Yet, almost nothing is known about whether (and how) NAD enters these organelles or is produced there. In this regard more detailed insights into the interconversions of NAD metabolites will likely facilitate understanding the maintenance of individual NAD pools. It appears as an intriguing possibility that the compartmentalization might represent a means to selectively influence NAD-dependent signaling events. The tremendous medical relevance as well as the broad scientific interest in this field will promote further research into these and other exciting questions regarding NAD biology."

 



#6 Bryan_S

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Posted 16 October 2015 - 03:57 PM

OPINION Caloric restriction mimetics: towards a molecular definition

 

http://www.scribd.co...1038-2Fnrd4391#

 

Abstract | Caloric restriction, be it constant or intermittent, is reputed to have health-promoting and lifespan-extending effects. Caloric restriction mimetics (CRMs) are compounds that mimic the biochemical and functional effects of caloric restriction. In this Opinion article, we propose a unifying definition of CRMs as compounds that stimulate autophagy by favouring the deacetylation of cellular proteins. This deacetylation process can be achieved by three classes of compounds that deplete acetyl coenzyme A (AcCoA; the sole donor of acetyl groups), that inhibit acetyl transferases (a group of enzymes that acetylate lysine residues in an array of proteins) or that stimulate the activity of deacetylases and hence reverse the action of acetyl transferases. A unifying definition of CRMs will be important for the continued development of this class of therapeutic agents.



#7 Bryan_S

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Posted 16 October 2015 - 04:51 PM

SARM1 activation triggers axon degeneration locally via NAD+ destruction
 
Just as losing a limb can spare a life, parting with a damaged axon by way of Wallerian degeneration can spare a neuron. A protein called SARM1 acts as a self-destruct button and now researchers led by Jeffrey Milbrandt of Washington University Medical School in St. Louis believe they've figured out how. They report in the April 24 Science that SARM1 forms dimers that trigger the destruction of NAD+. This whole topic of Traumatic brain injury (TBI) and neuron degeneration is one which has been long associated with NAD depletion. As we all know this is but just one neurological condition where NAD+ destruction triggers the loss of a axon, there are many other conditions where the process doesn't stop here. Research along these lines has indicated that axon and neuron degeneration can be ameliorated by boosting NAD levels.  In this article the mechanics of axon degeneration are discussed. In this study Nicotinamide Riboside was used to test this hypothesis of NAD depletion and axon rescue.
 
 
Science (Impact Factor: 33.61). 04/2015; 348(6233):453-457. DOI: 10.1126/science.1258366
Received for publication 7 July 2014.
Accepted for publication 12 March 2015.
 
ABSTRACT
Axon degeneration is an intrinsic self-destruction program that underlies axon loss during injury and disease. Sterile alpha and TIR motif-containing 1 (SARM1) protein is an essential mediator of axon degeneration. We report that SARM1 initiates a local destruction program involving rapid breakdown of nicotinamide adenine dinucleotide (NAD(+)) after injury. We used an engineered protease-sensitized SARM1 to demonstrate that SARM1 activity is required after axon injury to induce axon degeneration. Dimerization of the Toll-interleukin receptor (TIR) domain of SARM1 alone was sufficient to induce locally mediated axon degeneration. Formation of the SARM1 TIR dimer triggered rapid breakdown of NAD(+), whereas SARM1-induced axon destruction could be counteracted by increased NAD(+) synthesis. SARM1-induced depletion of NAD(+) may explain the potent axon protection in Wallerian degeneration slow (Wld(s)) mutant mice.
 
axon.jpg?w=614&h=461
 
Excerpt "Together these data implicate NAD+ loss as a critical step in SARM1-mediated axon destruction. We therefore examined whether increased NAD+ synthesis could counteract the destruction program activated by sTIR dimerization. In DRG neurons, both axon degeneration and cell death initiated by sTIR dimerization were completely blocked by the expression of Nmnat1 and nicotinamide phosphoribosyltransferase (Nampt), which together synthesize NAD+ (Fig. 3A). Protection appeared to require NAD+ synthesis, because concurrent treatment with the Nampt inhibitor FK866 blocked the protection afforded by these enzymes (Fig. 3, E and F). Similarly, sTIR-induced axon degeneration and cell death were blocked by supplementation with the cell permeant NAD+ precursor nicotinamide riboside (NR)."
 
 
 
Major Pathway Identified in Nerve Cell Death Offers Hope for Therapies
 
The purine nucleosides adenosine and guanosine delay axonal degeneration in vitro.

Edited by Bryan_S, 16 October 2015 - 05:37 PM.

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#8 Bryan_S

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Posted 19 October 2015 - 12:38 AM

In a date restricted search for any "recent" publications by Leonard Guarente I found one that Google crawled 7-days ago which I hadn't seen before. I also ran a search here on longecity and could not find this study. It was . . . Published Online: December 31, 2013

 

SIRT1 and other sirtuins in metabolism

http://www.cell.com/...2760(13)00206-3


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#9 Bryan_S

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Posted 20 October 2015 - 11:33 PM

Boosting hepatic NAD+ prevents and reverses NAFLD in mice

 

http://www.nature.co...o.2015.175.html

 

NATURE REVIEWS | GASTROENTEROLOGY & HEPATOLOGY   ADVANCE ONLINE PUBLICATION Nature Reviews Gastroenterology & Hepatology advance online publication 20 October 2015;  doi:10.1038/nrgastro.2015.175; doi:10.1038/nrgastro.2015.176; doi:10.1038/nrgastro.2015.177; doi:10.1038/nrgastro.2015.178RESEARCH HIGHLIGHTSIN BRIEFNAFLD

 

Boosting hepatic NAD+ prevents and reverses NAFLD in miceFew therapies are approved for the treatment of NAFLD. Now, researchers have shown that treatment with nicotinamide riboside, a precursor for NAD+ biosynthesis, can protect mice against the development of diet-induced NAFLD by increasing hepatic NAD+ levels. The treatment also reversed the disease in mice with pre-existing NAFLD. Nicotinamide riboside activated the hepatic mitochondrial unfolded protein response, increasing fatty acid oxidation and mitochondrial complex activity. Original article Gariani, K. et al. Eliciting the mitochondrial unfolded protein response via NAD+ repletion reverses fatty liver disease. Hepatology doi:10.1002/hep.28245

 

 

On a seperate note: There could be an interesting NAFLD correlation developing here, researchers have discovered a novel protein that is released as a consequence of fatty liver and this its believed causes pre-diabetes.  http://medicalxpress...e-diabetes.html


Edited by Bryan_S, 30 October 2015 - 02:17 PM.

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#10 Bryan_S

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Posted 22 October 2015 - 05:52 PM

A Phase 3 Randomized Trial of Nicotinamide for Skin-Cancer Chemoprevention

 

In the NEW ENGLAND JOURNAL of MEDICINE October 22, 2015  Vol. 373 No. 17 issue the findings of "A Phase 3 Randomized Trial of Nicotinamide for Skin-Cancer Chemoprevention" received some new acknowledgment.

 

150513-skin-cancer-cell-yh-0317p_a4618c6

 

We've reviewed this study here on LongeCity on several occasions. Here are 2-posts.

http://www.longecity...e-6#entry727674

 

http://www.longecity...e-9#entry739280

 

Hopefully this issue of sun damage, NAD depletion and DNA repair gains some more momentum as a result. It would be interesting with all the new medical interest surrounding Nicotinamide Riboside and the associated ailments stemming from NAD depletion to see a study published looking at this same condition treated with NR.

 

 

BACKGROUND

Nonmelanoma skin cancers, such as basal-cell carcinoma and squamous-cell carcinoma, are common cancers that are caused principally by ultraviolet (UV) radiation. Nicotinamide (vitamin B3) has been shown to have protective effects against damage caused by UV radiation and to reduce the rate of new premalignant actinic keratoses.

 
METHODS

In this phase 3, double-blind, randomized, controlled trial, we randomly assigned, in a 1:1 ratio, 386 participants who had had at least two nonmelanoma skin cancers in the previous 5 years to receive 500 mg of nicotinamide twice daily or placebo for 12 months. Participants were evaluated by dermatologists at 3-month intervals for 18 months. The primary end point was the number of new nonmelanoma skin cancers (i.e., basal-cell carcinomas plus squamous-cell carcinomas) during the 12-month intervention period. Secondary end points included the number of new squamous-cell carcinomas and basal-cell carcinomas and the number of actinic keratoses during the 12-month intervention period, the number of nonmelanoma skin cancers in the 6-month postintervention period, and the safety of nicotinamide.

RESULTS

At 12 months, the rate of new nonmelanoma skin cancers was lower by 23% (95% confidence interval [CI], 4 to 38) in the nicotinamide group than in the placebo group (P=0.02). Similar differences were found between the nicotinamide group and the placebo group with respect to new basal-cell carcinomas (20% [95% CI, −6 to 39] lower rate with nicotinamide, P=0.12) and new squamous-cell carcinomas (30% [95% CI, 0 to 51] lower rate, P=0.05). The number of actinic keratoses was 11% lower in the nicotinamide group than in the placebo group at 3 months (P=0.01), 14% lower at 6 months (P<0.001), 20% lower at 9 months (P<0.001), and 13% lower at 12 months (P=0.001). No noteworthy between-group differences were found with respect to the number or types of adverse events during the 12-month intervention period, and there was no evidence of benefit after nicotinamide was discontinued.

CONCLUSIONS

Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients. (Funded by the National Health and Medical Research Council; ONTRAC Australian New Zealand Clinical Trials Registry number, ACTRN12612000625875.) https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?ACTRN=12612000625875

October 30th update:

Since this articles appearance in the NEW ENGLAND JOURNAL of MEDICINE October 22nd it has spread like a wild fire across the internet. This (NEJM) publication is beginning to turn the tide and some physicians are now beginning to recommend nicotinamide as a safe and effective means in reducing the rates of new non-melanoma skin cancers. Sadly however the American Medical Association has still not weighed in on the topic. Lets hope they eventually get onboard with this idea of B3 cancer prevention.

 

Along this logical course of NAD cancer prevention a new class of NAD dependent DNA repair enzyme's have been discovered.

http://phys.org/news...dna-enzyme.html Lets hope the medical "establishment" rallies around the evidence of what's staring them in the face.


Edited by Bryan_S, 30 October 2015 - 04:25 PM.

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#11 Bryan_S

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Posted 27 October 2015 - 05:20 PM

Protein acetylation in metabolism—metabolites and cofactors

 

Published online 27 October 2015

 

http://www.nature.co...o.2015.181.html

 

Reversible acetylation was initially described as an epigenetic mechanism regulating DNA accessibility. Since then, this process has emerged as a controller of histone and nonhistone acetylation that integrates key physiological processes such as metabolism, circadian rhythm and cell cycle, along with gene regulation in various organisms. The widespread and reversible nature of acetylation also revitalized interest in the mechanisms that regulate lysine acetyltransferases (KATs) and deacetylases (KDACs) in health and disease. Changes in protein or histone acetylation are especially relevant for many common diseases including obesity, diabetes mellitus, neurodegenerative diseases and cancer, as well as for some rare diseases such as mitochondrial diseases and lipodystrophies. In this Review, we examine the role of reversible acetylation in metabolic control and how changes in levels of metabolites or cofactors, including nicotinamide adenine dinucleotide, nicotinamide, coenzyme A, acetyl coenzyme A, zinc and butyrate and/or β-hydroxybutyrate, directly alter KAT or KDAC activity to link energy status to adaptive cellular and organismal homeostasis.

nrendo.2015.181-f5.jpg


Edited by Bryan_S, 27 October 2015 - 05:21 PM.

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#12 Bryan_S

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Posted 05 November 2015 - 07:08 AM

Fasting and refeeding differentially regulate NLRP3 inflammasome activation in human subjects

 

Javier Traba1, Miriam Kwarteng-Siaw1, Tracy C. Okoli1, Jessica Li1, Rebecca D. Huffstutler1, Amanda Bray1, Myron A. Waclawiw2, Kim Han1, Martin Pelletier3, Anthony A. Sauve4, Richard M. Siegel3, and Michael N. Sack1
First published November 3, 2015
 
I was pretty sure based on my own experience some study would soon confirm these results. "The inflammasome is responsible for activation of inflammatory processes,[2] and has been shown to induce cell pyroptosis, a process of programmed cell death distinct from apoptosis.[3]"
 
 
Excerpt To gain mechanistic insight into the role of SIRT3, genetic manipulation studies showed an essential role of SIRT3 maintenance of mitochondrial respiration and control of ROS production, underpinning its role in this nutrient-sensing inflammatory program. In parallel, a SIRT3 pharmacologic agonist, nicotinamide riboside (NR), enhanced mitochondrial function and blunted the NLRP3 inflammasome in leukocytes extracted from a group of healthy control subjects and from cells extracted in the refed state but not the fasted state from subjects enrolled in the index fasting inflammasome study.
 
In conclusion, this study shows that refeeding after a 24-hour fast increases susceptibility to inflammasome activation, in part, via refeeding-mediated activation of NF-κB signaling. Moreover, a 24-hour fast in human subjects activates SIRT3 biology, and this, in turn, appears to confer resistance to NLRP3 inflammasome activation via blunting of mitochondrial ROS levels. This inflammasome-provoking effect of refeeding after a 24-hour fast can be inhibited by SIRT3 activation using NR. These data have identified a potentially drug-modifiable SIRT3-dependent program to attenuate the NLRP3 inflammasome and suggest that this pathway may be modulated as a strategy to alleviate/attenuate NLRP3-linked inflammation.
 
METHODS. We performed a clinical study of 19 healthy volunteers. Each subject underwent a 24-hour fast and then was fed a fixed-calorie meal. Blood was drawn during the fasted and fed states and analyzed for NRLP3 inflammasome activation. We enrolled an additional group of 8 healthy volunteers to assess the effects of the sirtuin activator, nicotinamide riboside, on NLRP3 inflammasome activation.
 
RESULTS. In the fasting/refeeding study, individuals showed less NLRP3 inflammasome activation in the fasted state compared with that in refed conditions. In a human macrophage line, depletion of the mitochondrial-enriched sirtuin deacetylase SIRT3 increased NLRP3 inflammasome activation in association with excessive mitochondrial ROS production. Furthermore, genetic and pharmacologic SIRT3 activation blunted NLRP3 activity in parallel with enhanced mitochondrial function in cultured cells and in leukocytes extracted from healthy volunteers and from refed individuals but not in those collected during fasting.
 
CONCLUSIONS. Together, our data indicate that nutrient levels regulate the NLRP3 inflammasome, in part through SIRT3-mediated mitochondrial homeostatic control. Moreover, these results suggest that deacetylase-dependent inflammasome attenuation may be amenable to targeting in human disease.
 
Additional studies:
 
Professor Anthony Sauve is one of the key researchers driving the Nicotinamide Riboside studies. Here is just a small portion of what he has in the pipeline http://grantome.com/... Anthony Sauve
Here are a few of his publications. http://vivo.med.corn...ouppublications
 

Edited by Bryan_S, 05 November 2015 - 03:25 PM.

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#13 Bryan_S

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Posted 05 November 2015 - 07:13 AM

Emerging Role of Sirtuin 2 in the Regulation of Mammalian Metabolism

 

Pedro Gomes1, , , Tiago Fleming Outeiro2, 3, Cláudia Cavadas1, 4
1 CNC – Center for Neurosciences and Cell Biology, University of Coimbra, Coimbra, Portugal
2 CEDOC – Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Lisbon, Portugal
3 Department of Neurodegeneration and Restorative Research, University Medical Center Göttingen, Göttingen, Germany
4 Faculty of Pharmacy, University of Coimbra, Coimbra, Portugal
Available online 1 November 2015
 


#14 Bryan_S

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Posted 05 November 2015 - 07:23 AM

Pharmacological activation of AMPK prevents Drp1-mediated mitochondrial fission and alleviates endoplasmic reticulum stress-associated endothelial dysfunction.

 

http://www.ncbi.nlm....pubmed/26196303

 

CONCLUSION AND IMPLICATIONS:
Pharmacological activation of AMPK regulated mitochondrial morphology and ameliorated endothelial dysfunction by suppression of mitochondrial ROS-associated ER stress and subsequent TXNIP/NLRP3 inflammasome activation. These findings suggested that regulation of Drp1 phosphorylation by AMPK activation contributed to suppression of ER stress and thus presented a potential therapeutic strategy for AMPK activation in the regulation of endothelium homeostasis.

Edited by Bryan_S, 05 November 2015 - 07:24 AM.

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#15 midas

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Posted 08 November 2015 - 09:53 PM

   
Why has the Nicotinamide Riboside Current News And Updates thread been closed??? .....It is getting very difficult for some of us to follow whats actually going on with NR here these days..
 
 
ChromaDex Enters Into an Exclusive Joint Development Agreement with The Procter & Gamble Company - See more at: http://www.globenews...h.rIPeyKcH.dpuf
 


#16 bluemoon

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Posted 08 November 2015 - 10:18 PM

 

   
Why has the Nicotinamide Riboside Current News And Updates thread been closed??? .....It is getting very difficult for some of us to follow whats actually going on with NR here these days..
 
 
ChromaDex Enters Into an Exclusive Joint Development Agreement with The Procter & Gamble Company - See more at: http://www.globenews...h.rIPeyKcH.dpuf

 

 

I was going to write the same thing from Day 1. This makes no sense. I look forward to Byan_S' posts but moderated by him? huh? Weird and not helpful.



#17 Bryan_S

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Posted 08 November 2015 - 11:48 PM

Yea it was a surprise to me but I recently became a paying member and Admin felt I should be able to moderate the thread and evidently they couldn't make the first thread work. Here we are same updated content and way less views. 

 

The Procter & Gamble announcement I think is important to the long term survival of the company and the CVS announcement as well. I think greater sales volume might help bring the price down but as we can see from there financials they have a long way to go to get into the black.


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#18 midas

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Posted 09 November 2015 - 12:23 AM

 

 

The Procter & Gamble announcement I think is important to the long term survival of the company and the CVS announcement as well. I think greater sales volume might help bring the price down but as we can see from there financials they have a long way to go to get into the black.

 

I used to work for P&G and you can trust me on this........That company do not touch anything less than the best products when they buy a new brand or company worldwide......

 

"On August 1, 2014, P&G announced it was streamlining the company, dropping around 100 brands and concentrating on the remaining 80 brands, which produced 95 percent of the company's profits."..........They made $83 billion's worth of sales last year

 

........After trimming down the company the way they recently have, they wouldn't be getting into bed with Chromadex like this unless they were 100% sure that NR is the real deal.....

 


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#19 bluemoon

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Posted 09 November 2015 - 03:16 AM

Yea it was a surprise to me but I recently became a paying member and Admin felt I should be able to moderate the thread and evidently they couldn't make the first thread work. Here we are same updated content and way less views. 

 

The Procter & Gamble announcement I think is important to the long term survival of the company and the CVS announcement as well. I think greater sales volume might help bring the price down but as we can see from there financials they have a long way to go to get into the black.

 

 

There was no reason to let the other thread die so just end this one and resume the original thread. 


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#20 stefan_001

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Posted 09 November 2015 - 04:35 AM

Another interesting part on the P&G is that a "stable" NR will be developed. "Stable" so it can be processed? Or?

#21 Bryan_S

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Posted 09 November 2015 - 05:39 PM

Everyone this post was important.

 

Fasting and refeeding differentially regulate NLRP3 inflammasome activation in human subjects

 

If you can blunt NLRP3 with Nicotinamide Riboside you have a handle on the inflammatory cycle. The inflammasome is responsible for activation of inflammatory processes, need I say more.

 


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#22 Tom Andre F. (ex shinobi)

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Posted 10 November 2015 - 01:19 PM

Yea it was a surprise to me but I recently became a paying member and Admin felt I should be able to moderate the thread and evidently they couldn't make the first thread work. Here we are same updated content and way less views. 

 

The Procter & Gamble announcement I think is important to the long term survival of the company and the CVS announcement as well. I think greater sales volume might help bring the price down but as we can see from there financials they have a long way to go to get into the black.

 

the thread name "nicotinamide riboside" and the few people who complain every time we enlarge the topic (off topic) is the reason of the problem for me..


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#23 Bryan_S

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Posted 10 November 2015 - 02:31 PM

I see bluebrainboost are selling NR @ $1 per gram.  Seems like a good deal?  They offer independent lab testing on their products.  

 

Buyer beware, I've inquired about this company and as of this moment they do not appear to be reselling a verified Nicotinamide Riboside from ChromaDex. For this reason I've not mentioned them on our forums because they can not be confirmed. Last year, as a group we investigated a large number of Chinese sources, in fact today when I search for Nicotinamide Riboside News and Updates I'm overwhelmed with these Chinese advertisements. All these sources claim to have certificates of analysis (COA), paperwork. So if a Bethesda Maryland post office box at "The UPS Store" and a San Francisco California phone number gives you any sense of security be my guest. But if your going to roll the dice you are likely buying from one of these unverified Chinese sources. To date we have not identified a genuine source of NR from China. My recommendation would be to secure a sample and find a lab yourself for verification. 


Edited by Bryan_S, 10 November 2015 - 03:04 PM.

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#24 Tom Andre F. (ex shinobi)

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Posted 10 November 2015 - 02:35 PM

I second you Bryan. There is for now no way to synthesis NR without falling under the patent owned by chromadex.



 


Edited by Bryan_S, 13 November 2015 - 08:26 AM.

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#25 pleiotropic

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Posted 11 November 2015 - 10:42 AM

Yep.  Good point about not just blindly trusting them.  I'll see about testing to verify it is actually NR.

 

Either it's bunk NR (could be just niacinamide?) or someone has leaked/sold the NR-yeast biosynthesis production pipeline to another chinese lab for profit.

 

I came across the vendor after seeing them mentioned by lostfalco here on longecity for quality methylene blue.  

 


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#26 Bryan_S

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Posted 11 November 2015 - 07:26 PM

Moved from the 

Nicotinamide Riboside (NR/Niagen) personal experience thread

if NA lowers cholesterol through NAD, why Nam doesn't have the same effect...which I've wondered, too.

 

We know that Sirt3 regulates lipid metabolism and we know that Nicotinamide is inhibitory towards Sirt3

 

Now I can only point to various studies that show the various feedback loops involved. 

 

Here is a clue to what's going on that I posted back on 18 August 2015. It has to do with the Nicotinamide SIRT3 binding pocket. Its one of those inhibitory feedback mechanisms that signals our nutritional status. So as we buildup more SIRT3 thru NAD Boosting eventually nicotinamide accumulates thru the NAD salvage cycle to modulate mitochondrial activity by binding to SIRT3. 

 

So if you are looking for why NA and NR work as a treatment for Hyperlipidemia and NAM doesn't this might be why. Still I haven't seen much research directed in this direction and I would like to read more before stating this as the way things are but the research suggests this might be the active mechanism in the background. 

 

Guys we've hijacked the personal experience thread long enough. For the Tech stuff lets post those responses on http://www.longecity...boside-curated/ because we're diluting the experience thread.



#27 Asor

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Posted 12 November 2015 - 01:45 PM

Generation, Release, and Uptake of the NAD Precursor Nicotinic Acid Riboside by Human Cells*
Capsule Background: Nicotinamide riboside (NR) and nicotinic acid riboside (NAR) can serve as precursors of NAD in human cells.

Results: Human cells generate and release NR and NAR.

Conclusion: NR and NAR are authentic intermediates of human NAD metabolism.

Significance: Different cell populations might support each other's NAD pools by providing ribosides as NAD precursors.

 

Abstract

NAD is essential for cellular metabolism and has a key role in various signaling pathways in human cells. To ensure proper control of vital reactions, NAD must be permanently resynthesized. Nicotinamide and nicotinic acid as well as nicotinamide riboside (NR) and nicotinic acid riboside (NAR) are the major precursors for NAD biosynthesis in humans. In this study, we explored whether the ribosides NR and NAR can be generated in human cells. We demonstrate that purified, recombinant human cytosolic 5′-nucleotidases (5′-NTs) CN-II and CN-III, but not CN-IA, can dephosphorylate the mononucleotides nicotinamide mononucleotide and nicotinic acid mononucleotide (NAMN) and thus catalyze NR and NAR formation in vitro. Similar to their counterpart from yeast, Sdt1, the human 5′-NTs require high (millimolar) concentrations of nicotinamide mononucleotide or NAMN for efficient catalysis. Overexpression of FLAG-tagged CN-II and CN-III in HEK293 and HepG2 cells resulted in the formation and release of NAR. However, NAR accumulation in the culture medium of these cells was only detectable under conditions that led to increased NAMN production from nicotinic acid. The amount of NAR released from cells engineered for increased NAMN production was sufficient to maintain viability of surrounding cells unable to use any other NAD precursor. Moreover, we found that untransfected HeLa cells produce and release sufficient amounts of NAR and NR under normal culture conditions. Collectively, our results indicate that cytosolic 5′-NTs participate in the conversion of NAD precursors and establish NR and NAR as integral constituents of human NAD metabolism. In addition, they point to the possibility that different cell types might facilitate each other's NAD supply by providing alternative precursors.

 

http://www.jbc.org/c.../27124.abstract

 



#28 mikeinnaples

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Posted 12 November 2015 - 06:00 PM

 

Yea it was a surprise to me but I recently became a paying member and Admin felt I should be able to moderate the thread and evidently they couldn't make the first thread work. Here we are same updated content and way less views. 

 

The Procter & Gamble announcement I think is important to the long term survival of the company and the CVS announcement as well. I think greater sales volume might help bring the price down but as we can see from there financials they have a long way to go to get into the black.

 

 

There was no reason to let the other thread die so just end this one and resume the original thread. 

 

 

Agreed. This has made following the topic far worse.


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#29 Bryan_S

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Posted 16 November 2015 - 06:17 PM

ChromaDex Lead Ingredient NIAGEN® Nicotinamide Riboside Receives New Dietary Ingredient (NDI) Status From the FDA

http://investors.chr...icle&ID=2112546

 

The Federal Food, Drug, and Cosmetic Act (the FD&C Act) requires that manufacturers and distributors who wish to market dietary supplements that contain "new dietary ingredients" notify the Food and Drug Administration about these ingredients. Generally, the notification must include information that is the basis on which the manufacturer or distributor has concluded that a dietary supplement containing a new dietary ingredient will reasonably be expected to be safe under the conditions of use recommended or suggested in the labeling. (See Section 413(d) of the FD&C Act, 21 U.S.C. 350b(d)).

Frank Jaksch Jr., founder and CEO of ChromaDex, commented, “Receiving NDI status from the FDA validates the safety dossier we have compiled for NIAGEN®.  Achieving NDI status is a significant milestone given that the FDA objected approximately 88% of NDI notifications in FY 2014. NDI status opens the door for the mainstream commercialization of NIAGEN® in dietary supplements.” 



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#30 Bryan_S

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Posted 16 November 2015 - 07:06 PM

Volume: 18 Issue 11: October 26, 2015 In the "Journal of Medicinal Food" a study we touched on last May was revisited. 

http://www.longecity...e-6#entry728015

 

Nicotinamide Riboside Ameliorates Hepatic Metaflammation by Modulating NLRP3 Inflammasome in a Rodent Model of Type 2 Diabetes.

 

This reinforces the recent human study we just read:

Fasting and refeeding differentially regulate NLRP3 inflammasome activation in human subjects

http://www.longecity...ed/#entry750259

 

From these 2 studies its becoming apparent the translation of findings from animal to human subjects is proving consistent. 

 

In a parallel Niacin study The Effects of Niacin on Inflammation in Patients with Non-ST Elevated Acute Coronary Syndrome This study used a different inflammation marker called C-Reactive Protein (CRP). C-reactive protein -- or CRP -- appears to be correlated to heart disease risk. Inflammation (swelling) of the arteries has been linked to an increased risk of heart disease, heart attack, stroke, and peripheral arterial disease. While this study didn't alleviate this condition it did prove niacin therapy could lead to a significant decrease in hs-CRP levels. This finding provides evidence that niacin therapy may improve the vascular environment, and is compatible with previous studies evaluating the use of extended release niacin in patients with coronary disease. 

 

Since the B3's take different paths but suggest similar although different outcomes it would be interesting to see how Nicotinamide Riboside would fair in patients with coronary disease. Food for thought.


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

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