2255 replies to this topic

[Nate-2004]

For those of us who did not watch the video as a whole: in a short aside Dr. Brenner stresses the importance of  eating whole foods in order to keep NR  body levels up. Pretty obvious perhaps but important info for the many people who seem to be averse to eating vegetables :-)

 

That would be me, I seriously hate spinach, kale, broccoli, etc. Hopefully I'm fine without that.

[Andey]

Are there any consensus on NR dosage ? 

Looks like Chareles Brenner was surprised about 1 g dosing amongst Longecity members )

[Bryan_S]

Nicotinamide riboside (NR) plays a critical role in the most efficient path to cellular energy production

 

http://investors.chr...icle&ID=2214976

 

This is from the second paper Brenner was associated with from author Carles Cantó.

Nestlé Institute of Health Sciences (NIHS), Lausanne CH-1015, Switzerland

School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne (EPFL), Lausanne CH-1015, Switzerland

 

http://www.nature.co...les/ncomms13103

 

 

[stefan_001]

Charles Brenner, PhD discusses Nicotinamide Riboside

 

Charles Brenner, PhD - University of Iowa Carver College of Medicine speaks with the Nicotinamide Riboside [Curated] user group at LongeCity.org October 15th, 2016 following his Nature Communications article, "Nicotinamide riboside is uniquely and orally bioavailable in mice and humans." Dr. Brenner answers questions about NAD supplementation and the history of the B3 discoveries and metabolism. He speaks off the cuff to a somewhat advanced audience level.

 

 

Great discussion, thanks Brian for setting this up and investing your time. I especially like the parts about NRK and the secondary wave of metabolism benefits with NR

Edited by stefan_001, 25 October 2016 - 03:18 AM.

[Bryan_S]

We just got our first review on the LongeCity Dr. Brenner Interview http://www.timelessl...ide-user-group/

Thanks for the bump on timelesslifemag.com and I assume you're a LongeCity member so say hello to our community because we've been collaborators on this topic.

Edited by Bryan_S, 25 October 2016 - 07:49 AM.

[bluemoon]

1) The summary linked above states that Brenner takes NR twice a day but if you listen carefully, he does not say that. He only says if you want to increase your night time NAD levels then you would want to also take it in the evening. He says he takes NR without food but adds he is about to eat when he takes it.

 

2) The final point on that list is that Brenner implies supplementing with NMN has no benefit. David Sinclair has said he would be "very tempted" to take NR except that he is taking another NAD precursor molecule. It seems like NMN would be a likely candidate.

 

 

[Bryan_S]

1) The summary linked above states that Brenner takes NR twice a day but if you listen carefully, he does not say that. He only says if you want to increase your night time NAD levels then you would want to also take it in the evening. He says he takes NR without food but adds he is about to eat when he takes it.

 

2) The final point on that list is that Brenner implies supplementing with NMN has no benefit. David Sinclair has said he would be "very tempted" to take NR except that he is taking another NAD precursor molecule. It seems like NMN would be a likely candidate.

 

He never said NMN had no benefit, the general thrust of what he said is the benefits we see in NMN are the same in NR because NMN becomes NR at the cell membrane. The cell membrane is the great equalizer and not just for NMN but all NAD forms as well. So any implied advantages to taking NMN over NR have been leveled by their latest findings and any benefits generated by NMN research are 100% applicable to NR. So the appropriate point he made was NMN has "no real advantage" over NR and NR is the most direct path.

 

I think the cost of NMN was enough of a barrier anyway. Other than the Japanese source there wasn't any other trusted source. The thing to keep in mind is if there is a perceived market in something there will be counterfeit products offered. Nicotinamide Mononucleotide is no different and there are those who would pray on that interest.

 

I expect the search for a specific NMN transporter to continue as he suggested.

[Thell]

 

1) The summary linked above states that Brenner takes NR twice a day but if you listen carefully, he does not say that. He only says if you want to increase your night time NAD levels then you would want to also take it in the evening. He says he takes NR without food but adds he is about to eat when he takes it.

 

2) The final point on that list is that Brenner implies supplementing with NMN has no benefit. David Sinclair has said he would be "very tempted" to take NR except that he is taking another NAD precursor molecule. It seems like NMN would be a likely candidate.

 

He never said NMN had no benefit, the general thrust of what he said is the benefits we see in NMN are the same in NR because NMN becomes NR at the cell membrane. The cell membrane is the great equalizer and not just for NMN but all NAD forms as well. So any implied advantages to taking NMN over NR have been leveled by their latest findings and any benefits generated by NMN research are 100% applicable to NR. So the appropriate point he made was NMN has "no real advantage" over NR and NR is the most direct path.

 

I think the cost of NMN was enough of a barrier anyway. Other than the Japanese source there wasn't any other trusted source. The thing to keep in mind is if there is a perceived market in something there will be counterfeit products offered. Nicotinamide Mononucleotide is no different and there are those who would pray on that interest.

 

I expect the search for a specific NMN transporter to continue as he suggested.

 

 

The summary is incorrect in stating that Brenner takes NR twice a day. He says,

 

 

 

5:53

boost my day and night time he i would

5:57

split a daily dose into um you know I'm

6:00

first thing in the morning dose and and

6:03

a an evening dose but I wouldn't I don't

6:06

see any point in in splitting it more

6:10

than two times per day that isn't making

6:11

sense

 

Edited by Thell, 25 October 2016 - 07:21 PM.

[Bryan_S]

Tissue-specific regulation of sirtuin and nicotinamide adenine dinucleotide biosynthetic pathways identified in C57Bl/6 mice in response to high-fat feeding

http://www.jnutbio.c...0360-6/abstract

[Bryan_S]

PPARγ-coactivator-1α gene transfer reduces neuronal loss and amyloid-β generation by reducing β-secretase

in an Alzheimer’s disease model

http://www.pnas.org/.../12292.full.pdf

 

AD decreased Aβ generation and increased nonamyloidogenic sAPPα levels (7, 8). Additionally, we showed that PGC-1α me- diates this effect by reducing β-APP cleaving enzyme (BACE1) gene transcription via a PPARγ-dependent mechanism (7). Conversely, crossing Tg2576 with mice deficient in PGC-1α or silencing PGC-1α using siRNA transfection in neuronal cells, led to increased Aβ levels (7–9). Pharmacological stimulation of PGC-1α synthesis with nicotinamide riboside, the precursor of NAD+, resulted in reduced Aβ levels and attenuated cognitive deterioration in Tg2576 mice (9). Furthermore, treatment with resveratrol, another PGC-1α activator, increased the activity of the Aβ-degrading enzyme neprilysin and reduced amyloid plaques (10). Nevertheless, these drugs may promote these beneficial ef- fects by acting on molecules other than PGC-1α, and an additional independent approach to investigate these specific functions of PGC-1α in AD was therefore considered relevant. We hypothe- sized that gene therapy with PGC-1α delivered in the brain could be neuroprotective because of its effect on the transcription of genes involved in Aβ generation, energy and glucose metabolism, and oxidative stress.

[stefan_001]

 

PPARγ-coactivator-1α gene transfer reduces neuronal loss and amyloid-β generation by reducing β-secretase

in an Alzheimer’s disease model

http://www.pnas.org/.../12292.full.pdf

 

AD decreased Aβ generation and increased nonamyloidogenic sAPPα levels (7, 8). Additionally, we showed that PGC-1α me- diates this effect by reducing β-APP cleaving enzyme (BACE1) gene transcription via a PPARγ-dependent mechanism (7). Conversely, crossing Tg2576 with mice deficient in PGC-1α or silencing PGC-1α using siRNA transfection in neuronal cells, led to increased Aβ levels (7–9). Pharmacological stimulation of PGC-1α synthesis with nicotinamide riboside, the precursor of NAD+, resulted in reduced Aβ levels and attenuated cognitive deterioration in Tg2576 mice (9). Furthermore, treatment with resveratrol, another PGC-1α activator, increased the activity of the Aβ-degrading enzyme neprilysin and reduced amyloid plaques (10). Nevertheless, these drugs may promote these beneficial ef- fects by acting on molecules other than PGC-1α, and an additional independent approach to investigate these specific functions of PGC-1α in AD was therefore considered relevant. We hypothe- sized that gene therapy with PGC-1α delivered in the brain could be neuroprotective because of its effect on the transcription of genes involved in Aβ generation, energy and glucose metabolism, and oxidative stress.

 

 

The article above appears to refer to this study:

http://www.timelessl...s-mouse-models/

 

Similar indications have been observed with NMN:
http://www.timelessl...eimers-disease/

[Thell]

Funny that was posted today as yesterday I was re-reading the 2011 review paper Cellular and molecular effects of sirtuins in health and disease. In the section ORGAN-SPECIFIC FUNCTIONS OF SIRTUINS we find

 

 

SIRT1 is widely expressed in the brain [113]. SIRT1 is shown to protect neurons expressing mutant SOD1, a model of ALS (amyotrophic lateral sclerosis) [48]. In a mouse model of AD, SIRT1 protects neurons and reduces the Aβ levels [48,114,115]. AD mice develop Aβ plaques in the brain at 3–5 months after birth. AD mice crossed with SIRT1 transgenic mice show a marked reduction of plaques in the brain, while AD mice with inactivated brain SIRT1 increase Aβ plaques and all die between 3 and 5 months [115]. The sequential cleavage of APP (amyloid precursor protein) by the β and γ secretases produces Aβ, and this process is inhibited by an alternate cleavage of APP by the α and γ secretases. SIRT1 increases the α secretase levels by deacetylating and activating retinoic acid receptor β [115] and by reducing the expression level of ROCK1 (Rho-associated kinase 1), a downstream serine/threonine kinase of Rho [114].

 

Being that we now have a reliable supplement (so far as we know) for making massive amounts of NAD available I was looking into how to maximize what is done with it. My focus was on neuron regeneration and Aβ cleanup. One thing that really stood out to me was the how the SVZ works and the possibility to stimulate production and cell survival rates. With NR as the STAC, curcumin for the BBB as a vaso and tight junction regulator and intranasal insulin to directly influence the olfactory bulb when everything is primed. Just a thought...

 

I'm thinking daily for 1 month; 375mg Niagen upon waking then either 1 metacurcumin ~6.5 hours later or 1 curqfen 7 hours later followed by 1 spray of intranasal insulin at ~7.5 hours and 12 minutes KK mediatation at 8.5 hours with fasting from dinner the night before until at least 9.5 hours after waking.

 

[Bryan_S]

 

 

PPARγ-coactivator-1α gene transfer reduces neuronal loss and amyloid-β generation by reducing β-secretase

in an Alzheimer’s disease model

http://www.pnas.org/.../12292.full.pdf

 

AD decreased Aβ generation and increased nonamyloidogenic sAPPα levels (7, 8). Additionally, we showed that PGC-1α me- diates this effect by reducing β-APP cleaving enzyme (BACE1) gene transcription via a PPARγ-dependent mechanism (7). Conversely, crossing Tg2576 with mice deficient in PGC-1α or silencing PGC-1α using siRNA transfection in neuronal cells, led to increased Aβ levels (7–9). Pharmacological stimulation of PGC-1α synthesis with nicotinamide riboside, the precursor of NAD+, resulted in reduced Aβ levels and attenuated cognitive deterioration in Tg2576 mice (9). Furthermore, treatment with resveratrol, another PGC-1α activator, increased the activity of the Aβ-degrading enzyme neprilysin and reduced amyloid plaques (10). Nevertheless, these drugs may promote these beneficial ef- fects by acting on molecules other than PGC-1α, and an additional independent approach to investigate these specific functions of PGC-1α in AD was therefore considered relevant. We hypothe- sized that gene therapy with PGC-1α delivered in the brain could be neuroprotective because of its effect on the transcription of genes involved in Aβ generation, energy and glucose metabolism, and oxidative stress.

 

 

The article above appears to refer to this study:

http://www.timelessl...s-mouse-models/

 

Similar indications have been observed with NMN:
http://www.timelessl...eimers-disease/

 

 

 

Lets compare to see if they are the same or if they intersect with a any researchers?

 

Neurobiol Aging. 2013 Jun;34(6):1581-8. doi: 10.1016/j.neurobiolaging.2012.12.005. Epub 2013 Jan 9.

Nicotinamide riboside restores cognition through an upregulation of proliferator-activated receptor-γ coactivator 1α regulated β-secretase 1 degradation and mitochondrial gene expression in Alzheimer's mouse models.

Gong B1, Pan Y, Vempati P, Zhao W, Knable L, Ho L, Wang J, Sastre M, Ono K, Sauve AA, Pasinetti GM.

Author information

1Department of Neurology, Center of Excellence for Novel Approaches to Neurotherapeutics, Mount Sinai School of Medicine, New York, NY, USA.

 

 

PPARγ-coactivator-1α gene transfer reduces neuronal loss and amyloid-β generation by reducing β-secretase

in an Alzheimer’s disease model

Loukia Katsouria, Yau M. Lima, Katrin Blondratha, Ioanna Eleftheriadoub, Laura Lombarderoa, Amy M. Bircha,

Nazanin Mirzaeia, Elaine E. Irvinec, Nicholas D. Mazarakisb,1, and Magdalena Sastrea,1

aDivision of Brain Sciences, Imperial College London, London W12 0NN, United Kingdom; bGene Therapy, Division of Brain Sciences, Imperial College London, London W12 0NN, United Kingdom; and cInstitute for Clinical Sciences, Medical Research Council Clinical Sciences Centre, London W12 0NN, United Kingdom

Edited by Gregory A Petsko, Weill Cornell Medical College, New York, NY, and approved August 23, 2016 (received for review April 18, 2016)

 

The papers share one not so obvious commonality Cornell. Anthony A. Sauve is the Associate Professor of Pharmacology from Weill Cornell Medical College in the first paper. He has been a fervent Nicotinamide Riboside researcher. The 2nd paper from the UK was edited by Gregory A Petsko also of Weill Cornell Medical College. So there is an intersection but the list of researchers looks different. Its possible they collaborated.

 

The article from timelesslifemag.com wasn't associated with David Sinclair to the best of my knowledge.

 

Nicotinamide mononucleotide protects against β-amyloid oligomer-induced cognitive impairment and neuronal death.

Wang X1, Hu X2, Yang Y2, Takata T3, Sakurai T4.

Author information

1Department of Gerontology and Geriatrics, The First Affiliated Hospital of China Medical University, Shenyang, China. Electronic address: wxiaon9981@yahoo.co.jp.

2Department of Gerontology and Geriatrics, The First Affiliated Hospital of China Medical University, Shenyang, China.

3Saiseikai Nakatsu Hospital, Osaka, Japan.

4National Center for Geriatrics and Gerontology, Japan.

 

My take away is we have multiple Labs confirming similar data which is great news. Now that the pathway of NMN has been shown to intersect with NR at NRK1 (sometimes called NMRK1) anything NMN was shown to yield can also be attributed to NR. One of the benefits of the Charles Brenner/Carles Cantó paper is hopefully a large amount of research duplication and grant spending can be avoided.

 

We will see how this all shakes out because as the "Charles Brenner, PhD discusses Nicotinamide Riboside" interview suggested at 21:43, there is still another team searching for a dedicated nicotinamide mononucleotide pathway. 

[mrkosh1]

Good interview Bryan.

 

The most interesting information revealed was that not only do all cells have a transport mechanism to bring in NR, but that cells under stress activate a secondary transport mechanism as well. This could make NR much more effective against disease conditions, because the cells under stress could be the ones taking in the most NR. Also, the fact that the consumption of NAD+ may be going up even if elevated levels are not detected.

 

I know the interview was time limited, but I wish that more questions would have been asked. The following would be my list of questions.

 

1) Do you think that the lag time of several hours before the peak of NAD+ after NR administration could be partially due to the rapid initial consumption of NAD by SIRT1-6 and other cellular processes?

 

2) Do you think that there is a maximum level of NAD+, obtainable by supplementation of NR at typical dosages, beyond which no health benefits will occur? Rephrased, if there was no limit to the amount of NAD+ that could accumulate before the conversion to NAAD began, what would be the point of severely diminishing returns?

 

3) Since NR is water soluble, what does he think about I.V. transfusions of NR into the bloodstream of humans after heart attacks, strokes, or other severe events that would create an immediate demand for additional NAD+?

 

4) I've read mixed data about the ability of NR to penetrate the blood brain barrier. Does he think the evidence is solid that oral NR consumption boosts NAD+ in brain cells?

 

5) PGC-1a is a gene that activates many others that can start a chain reaction that increases the copies of sirtulins, increases the levels of NAD+, and even boost telomerase. Two supplements that have proven ability to boost PGC-1a are R-alpha lipoic acid and acetyl-l-carnitine. Combined, they are able to produce the same effects at much lower dosages. Since NR has also proven to boost PGC-1a, what does he think about testing NR along with R-ALA and ALC?

 

6) Related to the above question, many of us would like to optimize the anti-aging effects of NR to the greatest extent possible. Other than combining NR with other supplements, what options does he see as plausible?

[bluemoon]

I read that in addition to the U of Minnesota/Mayo Clinic NR trial for traumatic brain injury/concussion patients (I thought around 2,000 mg) I read that maybe the same researchers are planning a trial of stroke victims at also around 2000 mg.

 

Does anyone know if the University  of Washington NR trial with congestive heart failure patients has started?  

 

Also to Bryan or anyone else, what was Brenner saying about heart cells toward the end? I got the gist of it but not sure of the details.  He didn't flat out say NR is good for the heart, right? 

[mrkosh1]

It would be nice to find out if 2000mg of NR actually boosts peak NAD+ beyond that of lower doses that are more typical.

 

In addition, even if NAD+ is boosted to a higher peak at 2000mg, it would be nice to know if this would also produce higher peak SIRT expression. We don't know if after a certain level of NR administration of NAD+ and SIRTS reach a maximum as excess NAD+ is converted to NAAD.

[bluemoon]

Thank you for the link.

[Bryan_S]

I read that in addition to the U of Minnesota/Mayo Clinic NR trial for traumatic brain injury/concussion patients (I thought around 2,000 mg) I read that maybe the same researchers are planning a trial of stroke victims at also around 2000 mg.

 

Does anyone know if the University  of Washington NR trial with congestive heart failure patients has started?  

 

Also to Bryan or anyone else, what was Brenner saying about heart cells toward the end? I got the gist of it but not sure of the details.  He didn't flat out say NR is good for the heart, right? 

 

U of M guys will get 750 mg/day for 12 weeks or three capsules, twice per day for 84 days.  They are already well into this trial. https://clinicaltria...riboside&rank=6

 

One trial with the University of Washington National Heart, Lung, and Blood Institute (NHLBI) with Kevin O'Brien has been completed. We are waiting for results.

https://clinicaltria...riboside&rank=1

 

He touched on the heart 3 times I believe. Mostly he was describing NRK2 in the context of gene expression. "For some reason" many researchers are looking into why this enzyme, which is used to convert NR to NAD is expressed exponentially during times of stress and injury in muscle, cardiac and nerve tissue. The heart is one area he touched on.

 

If you give me the time code I can give you an idea of what exactly he was trying to embrace. I'm correcting the Closed Captioning in a few select areas, what is the timecode number?

 

Charles Brenner, PhD discusses Nicotinamide Riboside Back to the point. "He didn't flat out say NR is good for the heart, right?" Many are asking why this tissue would express NRK2 at these times of stress. So its a question with an implied unproven answer since we know what the cell uses NRK2 for . . . only animal research will prove or disprove this hypothesis. This question can never be tested in humans. We can't sacrifice a human heart. What you're seeing is the scientific process. I pushed this question down three avenues to lay the ground work for his answer. In this case the gene expression mapping is telling us NRK2 is being produced and the researchers are asking why, and also asking where would the Nicotinamide Riboside would come from? Talk about bleeding edge, this is where Nicotinamide Riboside research is suggesting heart patients "might" be helped.

 

So I think the takeaway is follow the chemistry and it will show you the way. Here is a general search on NR and ischemia. What's been proven is other NAD precursors have already worked at saving tissue. Now that we know all larger NAD molecules have to be broken down to enter the cell, even the NMN molecule is broken down at the cell membrane to NR. So NR is the common denominator. We might be able to throw the most efficient precursor at a failing heart and get even better results than whats been shown on other more complex and smaller precursors. Its a hypothesis with strong supporting evidence.

Edited by Bryan_S, 27 October 2016 - 08:06 AM.

[warner]

He touched on the heart 3 times I believe. Mostly he was describing NRK2 in the context of gene expression. "For some reason" many are looking into why this enzyme which is used to convert NR to NAD is expressed exponentially during times of stress and injury. The heart is one such tissue.

As I recall, he didn't seem to know exactly why NRK2 levels rose in such situations, but speculated that,

 

- NR is very difficult to measure, so perhaps there's more of it around than we think with injury/stress

- damaged cells may release NR (leading to segway about getting it from whole foods)

- higher NRK2 may be attempt to use whatever little NR is available, since takes less energy to convert to NAD+

Edited by warner, 27 October 2016 - 07:59 AM.

[Bryan_S]

 

He touched on the heart 3 times I believe. Mostly he was describing NRK2 in the context of gene expression. "For some reason" many are looking into why this enzyme which is used to convert NR to NAD is expressed exponentially during times of stress and injury. The heart is one such tissue.

As I recall, he didn't seem to know exactly why NRK2 levels rose in such situations, but speculated that,

 

- NR is very difficult to measure, so perhaps there's more of it around than we think with injury/stress

- damaged cells may release NR (leading to segway about getting it from whole foods)

- higher NRK2 may be attempt to use whatever little NR is available, since takes less energy to convert to NAD+

 

 

Exactly its a hypothesis with sound supporting evidence surrounded by another dozen questions. Its also the idea thats driving the U of M study on football players . . . that is the expression of NMRK2 in damaged nerve tissue. No one has come out and said it but Its a study to see if NR could be a useful tool in mitigating football concussions and Traumatic Brain Injury. 

Edited by Bryan_S, 27 October 2016 - 08:19 AM.

[Freebytes]

Hi Nate, thanks for the reply but this site generally does not accept anecdotal evidence or am I mistaken.

 

This site does not accept anecdotal evidence as fact, but hearing the viewpoints of people is certainly beneficial.  I accept negative anecdotes more quickly than positive ones, though.  If 10 people say, "This is working great," and two say, "This made me throw up!" I am going to believe the ones throwing up.  The subjective nature of the anecdotal evidence leads to the assumption that it is not to be regarded, and it is certainly something of which to be wary since the placebo effect is very strong, but that is not to say we should not discuss our own experiences.  There are people in this forum doing things that have never been studies.  There are people taking doses of medicines that some may not even consider to be medicine, e.g. cancer drugs, megadosing, and fish tank cleaners!?  There are not always studies to back up claims so we must look at the results of brave people willing to experiment.

 

It should never be weighted as heavily as actual experiments, but there are many 'studies' that are full of errors as well.  No one should accept research unless it is repeatable, non-biased, and properly controlled.

[Supierce]

Hi Nate, thanks for the reply but this site generally does not accept anecdotal evidence or am I mistaken.

 
This site does not accept anecdotal evidence as fact, but hearing the viewpoints of people is certainly beneficial.  I accept negative anecdotes more quickly than positive ones, though.  If 10 people say, "This is working great," and two say, "This made me throw up!" I am going to believe the ones throwing up.  The subjective nature of the anecdotal evidence leads to the assumption that it is not to be regarded, and it is certainly something of which to be wary since the placebo effect is very strong, but that is not to say we should not discuss our own experiences.  There are people in this forum doing things that have never been studies.  There are people taking doses of medicines that some may not even consider to be medicine, e.g. cancer drugs, megadosing, and fish tank cleaners!?  There are not always studies to back up claims so we must look at the results of brave people willing to experiment.
 
It should never be weighted as heavily as actual experiments, but there are many 'studies' that are full of errors as well.  No one should accept research unless it is repeatable, non-biased, and properly controlled.

Which is why there's a "Nicotinamide Riboside Personal Experience" topic.

Edited by Supierce, 27 October 2016 - 02:44 PM.

[warner]

 

Hi Nate, thanks for the reply but this site generally does not accept anecdotal evidence or am I mistaken.

 

This site does not accept anecdotal evidence as fact, but hearing the viewpoints of people is certainly beneficial.  I accept negative anecdotes more quickly than positive ones, though...

Another thing to consider is that the best scientific models/theories must be able to explain personal experience (or what's the point of the model?).  The explanation of an anomalous experience might be trivial, such as placebo effect, wishful thinking, etc., but it is ultimately just as important to understand such experiences as it is to develop a well-supported theory/model via controlled studies.  Our understanding of the world remains incomplete without understanding personal experiences that appear to contradict our best models.  So I never discount personal experience, especially my own, or from those who appear to be trustworthy observers - the best model must ultimately explain such experience.

 

For example, I'm inclined to believe everything that Bryan says on this forum with respect to his NR experience (that is, the experience itself, if not his interpretation of it).  And if a study appeared supporting a theory that was in conflict with Bryan's experience, then I'd be inclined to think that the theory is incomplete (perhaps Bryan has a peculiar genetic makeup, etc.).  So that's a simple case where personal experience would trump a well-run study's results, in the sense that the study's conclusions are incomplete and misleading, whereas Bryan's experience may be undeniable.

 

That's not to say that the study would be more or less valuable than Bryan's experience - happy to have both sets of data to work with.  Just that figuring out the nature of reality is not as simple as just doing a bunch of controlled experiments.  Rather, it takes putting everything you know, including personal experience and controlled studies, into a coherent theory.

[samstersam]

 

 

3) Since NR is water soluble, what does he think about I.V. transfusions of NR into the bloodstream of humans after heart attacks, strokes, or other severe events that would create an immediate demand for additional NAD+?

 

 

 

I made a post in another subforum of telemores (which I think is a mistake) but I linked an article about NAD+ therapy in the UK where they are charging people 500 for an injection based NAD booster.

 

http://www.longecity...ns/#entry793481

 

Can you inject Nicotinamide Riboside IV and achieve the same or better effects?

[Bryan_S]

 

 

 

3) Since NR is water soluble, what does he think about I.V. transfusions of NR into the bloodstream of humans after heart attacks, strokes, or other severe events that would create an immediate demand for additional NAD+?

 

 

 

I made a post in another subforum of telemores (which I think is a mistake) but I linked an article about NAD+ therapy in the UK where they are charging people 500 for an injection based NAD booster.

 

http://www.longecity...ns/#entry793481

 

Can you inject Nicotinamide Riboside IV and achieve the same or better effects?

 

 

I think you touched on why P&G is so interested in the IP to produce an aqueous version of NR.

http://investors.chr...icle&ID=2107715

[Bryan_S]

The first human clinical study for NMN has started in Japan

http://www.nature.co...es/npjamd201621

 

Its an open editorial

 

Here is the clinical announcement

https://upload.umin....ptno=R000024575

Edited by Bryan_S, 27 October 2016 - 06:24 PM.

[Female Scientist]

I don't comment much, but I just want to take this opportunity to thank Bryan and the rest of the smart people here for bringing us this fascinating and important material. It is a very exciting time for these discoveries, and I am so grateful for the chance to learn about it on the cutting edge via this forum. THANK YOU! I will continue to enjoy reading my LongeCity updates every morning (immediately after taking my first NR of the day, natch). 

[Kirito]

New article on NMN.

 

http://www.independe...s-a7383411.html

 

Completely fails to mention NR, but NMN being naturally occurring in broccoli, cucumber, and cabbage is new to me.

[mrkosh1]

The more I read the more likely it seems that NR could be more effective for a host of physical ailments than current prescription drugs.

 

Since NR is already found in food is this enough to guarantee that even if a company made a pharmaceutical out of NR that they could not ban over the counter NR supplements?

[bluemoon]

 

He touched on the heart 3 times I believe. Mostly he was describing NRK2 in the context of gene expression. "For some reason" many researchers are looking into why this enzyme, which is used to convert NR to NAD is expressed exponentially during times of stress and injury in muscle, cardiac and nerve tissue. The heart is one area he touched on.

 

If you give me the time code I can give you an idea of what exactly he was trying to embrace. I'm correcting the Closed Captioning in a few select areas, what is the timecode number?

 

Charles Brenner, PhD discusses Nicotinamide Riboside Back to the point. "He didn't flat out say NR is good for the heart, right?" Many are asking why this tissue would express NRK2 at these times of stress. So its a question with an implied unproven answer since we know what the cell uses NRK2 for . . . only animal research will prove or disprove this hypothesis.  

 

 

I was referring to the discussion at the end starting at around 39:00 but going back realize he also discussed the heart ten minutes earlier. 

 

Brenner said that NR was the least stressful way for the heart to get NAD+ (I think) but wasn't clear to me if NR helped the heart. Anyway, great interview!

Edited by bluemoon, 27 October 2016 - 08:14 PM.