2255 replies to this topic

[stefan_001]

Frank Jaksch uses 500mg NR per day. Several Chromadex employees between 250 and 500mg / day. Some on ot for 3 years. Very interesting results conf call. Worth to listen

Where can we listen? Thank you

There is a transcript here: http://seekingalpha....ipt?part=single

I had to register to read it. It's an investment advice site but you can opt out of further communication by choosing judiciously.

Mike

Or go here:
http://investors.chr...&d=2&id=5220482

[Heisok]

From the earnings call at the links in previous posts:

 

"I noticed like in Life Extension’s two-a-day multiple, they just have 1 milligram of NR."

 

"The 1 milligram or the small amount that they are putting in is a multi – that is more of a multivitamin product."

 

"So multivitamins typically are not going to contain a therapeutically effective dose of everything, although 1 milligram may be a little bit short. But anyway, they were one of the first to put it in a multivitamin format and we appreciate the opportunity."

 

Why? For the label?

 

This is one of the problems I have had with LEF for a long time. I dislike paying extra for this type of addition to their products. Also they have added a significant dose of Niagen, 100 mg to one of their Resveratrol products, but in that product, they only have 500 micro-grams of Ptero.  These type of decisions on their part are part of the reason I have sought out other sources through the years, although I continue to use several of their products.

 

I have been a customer since the early 80's, and respect their cutting edge products.

 

Edited by heisoktoday, 21 March 2016 - 09:38 PM.

[midas]

 

 

 

Frank Jaksch uses 500mg NR per day. Several Chromadex employees between 250 and 500mg / day. Some on ot for 3 years. Very interesting results conf call. Worth to listen

Where can we listen? Thank you

There is a transcript here: http://seekingalpha....ipt?part=single

I had to register to read it. It's an investment advice site but you can opt out of further communication by choosing judiciously.

Mike

Or go here:
http://investors.chr...&d=2&id=5220482

 

 

Thank you for the links, especially the last one from Stefan 001 where you can just insert your name and e-mail to listen.... the interesting part starts at about 25 minutes into the podcast if you don't want to listen to the financial stuff...

 

[docmaas]

Does anyone know how Jasch takes his 500mg?  250 2x or 125 4x or 500 all at once?

 

I take 250 in the morning and 500 more MWF 30 minutes before I start my swimming which is pretty intense exercise.  

 

I'm really anxious to know how long it sticks around after consumption?  I think some here are taking it throughout the day but presumably Jasch has some better info than us so knowing how he consumes it may be of value.

 

Mike

[Bryan_S]

The 28th Annual ROTH Conference Presentation was also pretty good.

http://wsw.com/webca...cdxc/index.aspx

 

Jack hinted about a Nature publication in about 2 months featuring the human clinical study we've all wanted.

Edited by Bryan_S, 22 March 2016 - 02:52 AM.

[Bryan_S]

Enhancing NAD⁺salvage pathway reverts the toxicity of primary astrocytes expressing amyotrophic lateral sclerosis-linked mutant SOD1

 

http://www.jbc.org/c...698779.abstract

 

Increasing total and mitochondrial NAD⁺ content in ALS-astrocytes increases oxidative stress resistance and reverts their toxicity towards co-cultured motor neurons. Taken together, our results suggest that enhancing NAD⁺ salvage pathway in astrocytes could be a potential therapeutic target to prevent astrocyte-mediated motor neuron death in ALS

[Ohm]

Does anyone know how Jasch takes his 500mg?  250 2x or 125 4x or 500 all at once?

 

I take 250 in the morning and 500 more MWF 30 minutes before I start my swimming which is pretty intense exercise.  

 

I'm really anxious to know how long it sticks around after consumption?  I think some here are taking it throughout the day but presumably Jasch has some better info than us so knowing how he consumes it may be of value.

 

Mike

 

NR takes 72 hours to flush out of your system.  What I have read is that taking it upon waking is the ideal time.

 

 

We recommend taking your two Basis capsules in the morning, with or without food. Preclinical data indicates that NAD+ levels are normally circadian and show a peak during the wake cycle.  By taking Basis in the morning, you are allowing this increase in NAD+ levels from Basis to coincide with your body’s normal peak of NAD+.  Your two capsules can be taken together and there is no need to split the dose. 

 

http://www.elysiumhealth.com/help

 

 

 

I emailed Elysium Health the first month they went public and the COO responded saying that 2/3 of the Elysium founders take 125mg and the third takes 250mg a day.

 

If the CEO of Chromadex is publicly stating that he is double dosing it might just be a ruse to spur the same in customers resulting in increased profit for his company.

[Tom Andre F. (ex shinobi)]

Bryan,

 

maybe it was already discussed but do we know the role of NAD+ in senescent cells and mtDNA mutation (and the ones that already mutated..) ?

Edited by Tom Andre F. (ex shinobi), 24 March 2016 - 11:21 PM.

[Bryan_S]

Hi Tom,

 

Yes there has been some conversation along these lines, but not a lot. I haven't stopped researching this question. You won't find an expert among us, at least one who will chime in on the subject yet. Truth is there isn't a lot of research in this area. However. it appears NAD+ boosting "should" help cells remain viable longer by reenforcing cellular maintenance. There is still the inevitable Hayflick limit where cells will eventually enter into senescence, once reached I don't think anything we can do can change that or would we want to.

 

"Leonard Hayflick discovered that non-stem (i.e. non-telomerase active) cells in a dish can only divide around 60 times before the telomeres become too short to survive. The limit on a cell’s maximum lifespan with respect to its descendants is known as its “Hayflick Limit."

 

In a test tube cell division cuts off at around 60 replications. To date I haven't read any studies to investigate whether NAD+ boosting would increase the replicative life span. I take that back Brenner and yeast. So many factors contribute to healthy cell division but it stands to reason the heather the cell state is at the time of division the longer that subsequent cell line will remain viable and able to contribute.

 

I've been reading on DNA repair mechanisms and Germ cells in particular and have found some interesting theories on the energy budget required. "Two proponents for this view, Breivik and Gaudernack, have suggested that in certain situations the cost of DNA repair might exceed the cost of errors. This model predicts that genetic stability is configured for an optimal cost-benefit relationship. Natural selection is not expected to have produced the best genetic stability available in the human body, merely the best compromise of DNA repair and costs. Repair and maintenance of the vast human genome is thermodynamically expensive, and an optimal balance between DNA repair and dietary needs is likely to have originated." It appears at a very fundamental level our germ cells get the best DNA protection and our bodily tissues receive just enough repair attention to get us though the process of reproduction and raising offspring. This all ties into senescence and how long our bodily cell communities are expected to live to carry our germ cell to reproduction. It kind of makes you feel like we are just the vehicle to carry these germ cells around just to feed and protect them. All the while they get the best treatment and maintenance to preserve the integrity of the genome.

 

Some of us currently feel if a senescence cell isn't contributing to our good health its dead weight and we need to find a way to shed those zombie cells. Check out the tread on senolytics. For me right now it a little early to totally jump on this band wagon. Better more selective drugs need to be developed.

 

Last May Jun-Ichi Hayashi at the University of Tsukuba discovered the mutations we've come to believe accumulates with age is largely false. He suggests; "epigenetic regulation, may be responsible for the age-associated effects seen in the mitochondria" Remember all the talk about glycine, it appears the functionality of Mitochondria can be reinvigorated. As to damaged organelles Autophagy of our mitochondria is a safegaurd against Mitochondria that are damaged and not working. We know of disease states where this fails but there is a normal barrier in place to eliminate those nonfunctional or damaged Mitochondria. But back to the root of your question, Professor Hayashi turned the whole theory of aging on its head:

 

"This theory, the mitochondrial theory of aging, proposes that age-associated mitochondrial defects are controlled by the accumulation of mutations in the mitochondrial DNA. Abnormal mitochondrial function is one of the hallmarks of aging in many species, including humans. This is mostly due to the fact that the mitochondrion is the so-called powerhouse of the cell as it produces energy in a process called cellular respiration. Damage to the mitochondrial DNA results in changes or mutations in the DNA sequence. Accumulation of these changes is associated with a reduced lifespan and early onset of aging-related characteristics such as weight and hair loss, curvature of the spine and osteoporosis.

 

There is, however, a growing body of conflicting evidence that has raised doubts about the validity of this theory." read his labs findings. If an epigenitic reason is behind our declining Mitochondria I want to see more research to tease out a treatment.  

 

This is why I added glycine to my regiment.

Edited by Bryan_S, 25 March 2016 - 07:56 AM.

[stefan_001]

Hi Tom,

 

Yes there has been some conversation along these lines, but not a lot. I haven't stopped researching this question. You won't find an expert among us, at least one who will chime in on the subject yet. Truth is there isn't a lot of research in this area. However. it appears NAD+ boosting "should" help cells remain viable longer by reenforcing cellular maintenance. There is still the inevitable Hayflick limit where cells will eventually enter into senescence, once reached I don't think anything we can do can change that or would want to.

 

In a test tube cell division cuts off at around 50 replications. To date I haven't read any studies to investigate whether NAD+ boosting would increase the replicative life span. So many factors contribute to healthy cell division but it stands to reason the heather the cell state is at the time of division the longer that subsequent cell line will remain viable and able to contribute.

 

Some of us currently feel if a cell isn't contributing to our good health its dead weight and we need to find a way to shed those zombie cells. Check out the tread on senolytics. For me right now it a little early to totally jump on this band wagon. Better more selective drugs need to be developed.

 

Last May Jun-Ichi Hayashi at the University of Tsukuba discovered the mutation we've come to believe accumulates with age is largely false. He suggests; "epigenetic regulation, may be responsible for the age-associated effects seen in the mitochondria" Remember all the talk about glycine, it appears the functionality of Mitochondria can be reinvigorated. As to damaged organelles Autophagy of our mitochondria is a safegaurd against Mitochondria that are damaged and not working. We know of disease states where this fails but there is a normal barrier in place to eliminate those nonfunctional or damaged Mitochondria. But back to the root of your question, Professor Hayashi turned the whole theory of aging on its head:

 

"This theory, the mitochondrial theory of aging, proposes that age-associated mitochondrial defects are controlled by the accumulation of mutations in the mitochondrial DNA. Abnormal mitochondrial function is one of the hallmarks of aging in many species, including humans. This is mostly due to the fact that the mitochondrion is the so-called powerhouse of the cell as it produces energy in a process called cellular respiration. Damage to the mitochondrial DNA results in changes or mutations in the DNA sequence. Accumulation of these changes is associated with a reduced lifespan and early onset of aging-related characteristics such as weight and hair loss, curvature of the spine and osteoporosis.

 

There is, however, a growing body of conflicting evidence that has raised doubts about the validity of this theory." read his labs findings. If an epigenitic reason is behind our declining Mitochondria I want to see more research to tease out a treatment.  

 

This is why I added glycine to my regiment.

 

Glycine decline has the characteristics of another downstream effect of "something". Supplementation would then be another hack. What bothers me with Glycine supplementation is that you already get a lot of it in daily food. Here some recent metabolic profiling results:

 

Association of Plasma Small-Molecule Intermediate Metabolites With Age and Body Mass Index Across Six Diverse Study Populations.

http://www.ncbi.nlm....pubmed/26984390

 

[Bryan_S]

 

Glycine decline has the characteristics of another downstream effect of "something". Supplementation would then be another hack. What bothers me with Glycine supplementation is that you already get a lot of it in daily food. Here some recent metabolic profiling results:

 

Association of Plasma Small-Molecule Intermediate Metabolites With Age and Body Mass Index Across Six Diverse Study Populations.

http://www.ncbi.nlm....pubmed/26984390

 

 

 

I get that and we produce it internally. His study didn't address that and glycine supplementation might be a waste of money, who knows. However if there is an epigenetic reason and its production becomes faulty we need to understand this path and why giving those cells additional glycine worked.

[stefan_001]

Glycine decline has the characteristics of another downstream effect of "something". Supplementation would then be another hack. What bothers me with Glycine supplementation is that you already get a lot of it in daily food. Here some recent metabolic profiling results:
Association of Plasma Small-Molecule Intermediate Metabolites With Age and Body Mass Index Across Six Diverse Study Populations.
http://www.ncbi.nlm....pubmed/26984390

I get that and we produce it internally. His study didn't address that and glycine supplementation might be a waste of money, who knows. However if there is an epigenetic reason and its production becomes faulty we need to understand this path and why giving those cells additional glycine worked.

Yes agree with that. Okay I need to do some reading whether supplementation really can make a difference. My initial impression was that you need massive supplementation to make a difference as compared to what you already have as intake from normal food....but again didn't read that much on it. Have you noticed anything positive?

[Bryan_S]

Have you noticed anything positive?

 

 

No but would you? The NR has given me more energy overall and I only take 4 grams of Glycine. I've read the dose may be around 15-30 grams to make a difference. I'm probably not the person to ask on that note.

[docmaas]

I've been taking glycine along with NAC for the last several months 2 tsp of glycine and 3-4 g NAC morning and evening.   I did this due to reading research indicating both a deficit of glutathione in diabetics and research indicating that glycine along with NAC did raise glutathione levels.

 

However in the last few weeks I was having bouts of night sweats that I eventually traced down to the NAC so I still take the glycine though not as regularly but have stopped the NAC for the time being.  

 

I've only noticed that the glycine does help with sleep.  Other than that I haven't noticed anything but my exercise and health has been pretty good for the last year and I'm pretty sure the glycine has been a contributing factor.

 

Mike

[stefan_001]

Not about NR directly but boosting NAD+ supports sirtuin activity which is supposed to be a postive. Here however a possible contra indication for SIRT2:

 

In fact, there was a belief, based on two previous studies, that the SIRT2 enzyme might actually be a tumor suppressor, and that targeting it might promote tumor formation. That turned out not to be the case; they carried out multiple lines of experiments to demonstrate that the anti-cancer effect of TM is achieved through inhibiting SIRT2.

http://medicalxpress...ancer.html#nRlv

[stefan_001]

 

Have you noticed anything positive?

 

 

No but would you? The NR has given me more energy overall and I only take 4 grams of Glycine. I've read the dose may be around 15-30 grams to make a difference. I'm probably not the person to ask on that note.

 

 

at least some indication the body excretes Glycine more with age:

 

http://www.ncbi.nlm....pubmed/26912818

We have previously reported that salivary glycine and proline levels are increased to nearly butanoate level in elderly people.

[Ethic]

It appears at a very fundamental level our germ cells get the best DNA protection and our bodily tissues receive just enough repair attention to get us though the process of reproduction and raising offspring. This all ties into senescence and how long our bodily cell communities are expected to live to carry our germ cell to reproduction. It kind of makes you feel like we are just the vehicle to carry these germ cells around just to feed and protect them. All the while they get the best treatment and maintenance to preserve the integrity of the genome.

 

 

We're not just vehicles for those germ cells. We're moody hosts for all those little buggers in our gut as well. So, we are at least dual-purpose

[Skyguy2005]

From the earnings call at the links in previous posts:

 

"I noticed like in Life Extension’s two-a-day multiple, they just have 1 milligram of NR."

 

"The 1 milligram or the small amount that they are putting in is a multi – that is more of a multivitamin product."

 

"So multivitamins typically are not going to contain a therapeutically effective dose of everything, although 1 milligram may be a little bit short. But anyway, they were one of the first to put it in a multivitamin format and we appreciate the opportunity."

 

Why? For the label?

 

This is one of the problems I have had with LEF for a long time. I dislike paying extra for this type of addition to their products. Also they have added a significant dose of Niagen, 100 mg to one of their Resveratrol products, but in that product, they only have 500 micro-grams of Ptero.  These type of decisions on their part are part of the reason I have sought out other sources through the years, although I continue to use several of their products.

 

I have been a customer since the early 80's, and respect their cutting edge products.

 

I always found quercetin the more potent anyway, of the two (resveratrol and quercetin). 

[Skyguy2005]

I've been taking glycine along with NAC for the last several months 2 tsp of glycine and 3-4 g NAC morning and evening.   I did this due to reading research indicating both a deficit of glutathione in diabetics and research indicating that glycine along with NAC did raise glutathione levels.

 

However in the last few weeks I was having bouts of night sweats that I eventually traced down to the NAC so I still take the glycine though not as regularly but have stopped the NAC for the time being.  

 

I've only noticed that the glycine does help with sleep.  Other than that I haven't noticed anything but my exercise and health has been pretty good for the last year and I'm pretty sure the glycine has been a contributing factor.

 

Mike

 

NAC is dodgy as @#$% long term. 

Edited by Bryan_S, 27 March 2016 - 02:40 PM.
offensive language removed

[Skyguy2005]

Hi Tom,

 

Yes there has been some conversation along these lines, but not a lot. I haven't stopped researching this question. You won't find an expert among us, at least one who will chime in on the subject yet. Truth is there isn't a lot of research in this area. However. it appears NAD+ boosting "should" help cells remain viable longer by reenforcing cellular maintenance. There is still the inevitable Hayflick limit where cells will eventually enter into senescence, once reached I don't think anything we can do can change that or would we want to.

 

"Leonard Hayflick discovered that non-stem (i.e. non-telomerase active) cells in a dish can only divide around 60 times before the telomeres become too short to survive. The limit on a cell’s maximum lifespan with respect to its descendants is known as its “Hayflick Limit."

 

In a test tube cell division cuts off at around 60 replications. To date I haven't read any studies to investigate whether NAD+ boosting would increase the replicative life span. I take that back Brenner and yeast. So many factors contribute to healthy cell division but it stands to reason the heather the cell state is at the time of division the longer that subsequent cell line will remain viable and able to contribute. 

 

 

Human cells you mean? This is why stuff like Ginkgo Biloba exists, it's good, everyone knows it is, and it's on your side, no matter how impossible the battle. 

 

So don't think too much.  

Edited by Bryan_S, 27 March 2016 - 02:39 PM.
double post, repeat retracted

[stefan_001]

I havent seen this tudy posted yet. It contains a wealth of data. Going to read it when have some time.

 

Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer’s disease-relevant murine model

 

http://bmcneurol.bio...2883-015-0272-x

 

http://download.spri...b797ad781274abc

[Bryan_S]

We've posted it before but no problem. Try running the study title in the search field in the top right of this web-page if you're not sure.

 

There has been a considerable amount of research on NMN. Even if it has to be converted to NR to cross the cell membrane, if it can be stabilized and encapsulated and priced below NR we might see a product emerge. So far however there has been no such "verifiable" product. Still every NAD+ boosting study contributes to our knowledge base. However I feel since NR and NMN bypass the de novo NAD path and cut in line, I would think their study results would be almost identical if they were examined side by side. NR might win out just from a pure efficiency standpoint but NMN is going to trail in a close 2nd.

 

i.e. "no such "verifiable" product" thats changed. 

NMN β-Nicotinamide mono nucleotide buy which is exorbitantly priced and not at all competitively priced to (NR). But if you believe the hype, they say its better than (NR), so be my guest if you agree. However beware of the www.alibaba.com offers and the companies repackaging the Chinese products because independent testing is lacking.

 

Now here is an "off the wall" article that comes to us from the fringe that was just posted. AGE REGRESSION USED IN SECRET SPACE PROGRAMS CONFIRMED AS SCIENTIFICALLY FEASIBLE. Now while I don't see enough evidence to buy the ideas thrown about here, I do see where a correlation might exist in the area of repairing DNA from ionizing particle radiation while in space. These guys who put only a millimeter of aluminum between themselves and space are receiving a lot more DNA damage than we do. These guys deserve respect! Examples of ionizing radiation include gamma rays, protons, and neutrons. So I think if NASA medical scientists have been paying attention I would think the mounting NAD+ boosting evidence should have been applied if it hasn't all ready for those who expose themselves to the harshest of DNA damaging environments.  

 

Edited by Bryan_S, 12 April 2016 - 12:51 AM.
see "no such "verifiable" product" thats changed.

[Bryan_S]

2016 Mar 16. [Epub ahead of print]

http://www.ncbi.nlm....pubmed/26725653

NAD+ as the Link Between Oxidative Stress, Inflammation, Caloric Restriction, Exercise, DNA Repair, Longevity, and Health Span.

Poljsak B1, Milisav I1,2.

Author information

 

Abstract

Oxidative stress and decreased DNA damage repair in vertebrates increase with age also due to lowered cellular NAD+. NAD+ depletion may play a major role in the aging process at the cellular level by limiting (1) energy production, (2) DNA repair, and (3) genomic signaling. In this study, we hypothesize that it is not NAD+ as a cofactor in redox reactions and coenzyme in metabolic processes that has the ultimate role in aging, but rather the role of NAD+ in cellular signaling when used as substrate for sirtuins (SIRT1-7 in mammals) and PARPs [Poly(ADP-ribose) polymerases]. Both sirtuins and PARPs influence many transcription factors and can affect gene expression. As a signaling molecule, NAD+ is consumed in the reaction donating ADP-ribose and releasing nicotinamide (NAM) as a by-product. It seems that aging at the cellular level is associated with a decline of NAD+ and that NAD+ restoration can reverse phenotypes of aging by inducing cellular repair and stress resistance. Adequate intracellular NAD+ concentrations may be an important longevity assurance factor, while lowered cellular NAD+ concentration may negatively influence the life span.

 

[Bryan_S]

Assessment of Brain NAD+ in College Football Players Taking Nicotinamide Riboside vs Controls (TRMC-004)

 

https://clinicaltria...how/NCT02721537

 

Purpose:

Can nicotinamide riboside (750 mg/day for 12 weeks) affect the levels of NAD+ in the brain as measured by 31P MRS?

 

Detailed Description:

Healthy collegiate football players will take Nicotinamide Riboside (NR) or placebo twice daily for 84 days. Pre- and post-intervention evaluations include physical assessment, blood tests for safety and toxicity monitoring, blood tests for biomarkers, neurologic testing, quality of life questionnaires, and the 31P MRI exam. Healthy controls, age-matched athletes who participate in non-contact sports, will also be enrolled and will undergo the same pre-intervention evaluation, at which time their participation will be complete.

 

A nice list of human studies are coming together.

https://clinicaltria...e&Search=Search

Edited by Bryan_S, 29 March 2016 - 06:24 PM.

[Bryan_S]

Oncology Bioinformatics Unit: Research highlights | cnio.es

http://www.cnio.es/i...ion.asp?pag=457

 

"During 2014, we helped Marisol Soengas (CNIO) to demonstrate the role of RAB7 as a lineage-specific driver, and to elucidate the unique wiring of the lysosomal pathway for tumour progression in melanoma (FIGURE). We also collaborated with Nabil Djouder (CNIO) to show that restoration of NAD+ pools through a nicotinamide riboside (NR) rich diet prevents DNA damage and tumour formation in mice with liver damage and hepatocellular carcinoma (HCC), due to high expression levels of URI. With R. Guigó (CRG, Barcelona), in the context of the International Cancer Genome Consortium (ICGC), we contributed to the characterisation of new molecular and clinical subdivisions based on the expression profiles of a large cohort of chronic lymphocytic leukaemia (CLL) patients."

 

Background:

The CNIO currently houses 22 Research Groups, organised in 8 Scientific Programmes, plus 5 Clinical Research Unit(s) in the Clinical Research Programme. These scientists are supported by 18 Core Units that provide state-of-the-art facilities and technical expertise.

 

https://www.cnio.es/...y Programme.pdf

 

Excerpt

Biological concepts from our laboratory

We have proposed the following concepts :

ɗ Oncogene-induced NAD+ depletion results in DNA damage ; thus suggesting that metabolic reprogramming initiates tumourigenesis prior to genomic instability.

ɗ Nicotinamide riboside, a vitamin B3 derivative and an NAD+ booster may be used for cancer prevention and treatment.

 

Interesting to see who is adopting and using the new insights derived from Nicotinamide riboside research. However these guys aren't the only ones seeing this NAD+ boosting strategy. "Scientists Find Promising New Approach to Preventing Progression of Breast Cancer" In this study the NAD+ to NADH ratio was investigated. Professor Brunhilde H. Felding of that study from the Scripps Research Institute (TSRI) went on to write: Nicotinamide phosphoribosyltransferase can affect metastatic activity and cell adhesive functions by regulating integrins in breast cancer. So here we can see boosting NAD+ may help on the preventative side as seen from CNIO and to lessen the aggressiveness of Breast cancer by augmenting the NAD+ pool.

 

Edited by Bryan_S, 29 March 2016 - 10:00 PM.

[Heisok]

I was excited, but: "This study is not yet open for participant recruitment."

 

I thought it was a completed study. My mistake.

 

 

Assessment of Brain NAD+ in College Football Players Taking Nicotinamide Riboside vs Controls (TRMC-004)

 

https://clinicaltria...how/NCT02721537

 

Purpose:

Can nicotinamide riboside (750 mg/day for 12 weeks) affect the levels of NAD+ in the brain as measured by 31P MRS?

 

Detailed Description:

Healthy collegiate football players will take Nicotinamide Riboside (NR) or placebo twice daily for 84 days. Pre- and post-intervention evaluations include physical assessment, blood tests for safety and toxicity monitoring, blood tests for biomarkers, neurologic testing, quality of life questionnaires, and the 31P MRI exam. Healthy controls, age-matched athletes who participate in non-contact sports, will also be enrolled and will undergo the same pre-intervention evaluation, at which time their participation will be complete.

 

A nice list of human studies are coming together.

https://clinicaltria...e&Search=Search

 

 

[Bryan_S]

I'm still excited to see the University of Minnesota take this on . . . period. I've felt for awhile that athletes in contact sports should take (NR) to lessen the risk of head trauma. This study doesn't tackle that notion head on but if they can prove higher levels of NAD+ in the brain this is the first step that will open up the dialogue about using (NR) to help lesson (TBI) traumatic brain injury. So lets all hope they get the results they are seeking because there is currently no medical strategy to prevent or treat this kind of injury.

 

 

I was excited, but: "This study is not yet open for participant recruitment."

 

I thought it was a completed study. My mistake.

 

[stefan_001]

 

I'm still excited to see the University of Minnesota take this on . . . period. I've felt for awhile that athletes in contact sports should take (NR) to lessen the risk of head trauma. This study doesn't tackle that notion head on but if they can prove higher levels of NAD+ in the brain this is the first step that will open up the dialogue about using (NR) to help lesson (TBI) traumatic brain injury. So lets all hope they get the results they are seeking because there is currently no medical strategy to prevent or treat this kind of injury.

 

 

I was excited, but: "This study is not yet open for participant recruitment."

 

I thought it was a completed study. My mistake.

 

 

My father is still very active with sports (76 years) and he fell very hard on his head/face during ice speed skating and they carried him off the ice unconscious. Later in the hospital they made a headscan and triple asked his age as his brain had dealt with the fall very well. In the end they said he must have good genes....he was on NR at that point 10 months. Perhaps a coincidence but I am happy he is on the NR.

[Ethic]

 

2016 Mar 16. [Epub ahead of print]

http://www.ncbi.nlm....pubmed/26725653

NAD+ as the Link Between Oxidative Stress, Inflammation, Caloric Restriction, Exercise, DNA Repair, Longevity, and Health Span.

Poljsak B1, Milisav I1,2.

Author information

 

Abstract

Oxidative stress and decreased DNA damage repair in vertebrates increase with age also due to lowered cellular NAD+. NAD+ depletion may play a major role in the aging process at the cellular level by limiting (1) energy production, (2) DNA repair, and (3) genomic signaling. In this study, we hypothesize that it is not NAD+ as a cofactor in redox reactions and coenzyme in metabolic processes that has the ultimate role in aging, but rather the role of NAD+ in cellular signaling when used as substrate for sirtuins (SIRT1-7 in mammals) and PARPs [Poly(ADP-ribose) polymerases]. Both sirtuins and PARPs influence many transcription factors and can affect gene expression. As a signaling molecule, NAD+ is consumed in the reaction donating ADP-ribose and releasing nicotinamide (NAM) as a by-product. It seems that aging at the cellular level is associated with a decline of NAD+ and that NAD+ restoration can reverse phenotypes of aging by inducing cellular repair and stress resistance. Adequate intracellular NAD+ concentrations may be an important longevity assurance factor, while lowered cellular NAD+ concentration may negatively influence the life span.

 

 

^This paper is dope for amateurs like myself, basically a summary of NAD World. Thank you Mr. Poljsak and Mrs. Milisav, and of course you, Bryan

 

 

 

...It is not just NAD+ breakdown

reactions and biosynthetic (de novo and salvage) pathways
that are important for adequate NAD+ intracellular concentration
but also OXPHOS and PMOR systems that can
regenerate NAD+ from NADH.

 

 

All rights reserved by Mary Ann Liebert, Inc./Poljsak/Milisav

 

 

OXPHOS

PMET/PMOR System

 

Where does NQO1 fit in there?

[Heisok]

stefan, it is great to hear that your dad is OK. I take around 500 mg of N.R. myself.

 

Bryan, it is exciting, I just thought we had a breakthrough study.

 

As important as the issue of T.B.I is for sports, it is perhaps more important to protect the men and women that we put in harms way. NR could be a very inexpensive profilactic for any troops who might be at risk either in training or active service.

 

There was a study referenced in a thread a couple years ago regarding intranasal NAD+, but did not seem to gain traction.

 

"Prevention of Traumatic Brain Injury-Induced Neuron Death by Intranasal Delivery of Nicotinamide Adenine Dinucleotide

"Traumatic brain injury (TBI) is one of the most devastating injuries experienced by military personnel, as well as the general population, and can result in acute and chronic complications such as cognitive impairments. Since there are currently no effective tools for the treatment of TBI, it is of great importance to determine the mechanisms of neuronal death that characterize this insult. Several studies have indicated that TBI-induced neuronal death arises in part due to excessive activation of poly(ADP-ribose) polymerase-1 (PARP-1), which results in nicotinamide adenine dinucleotide (NAD+) depletion and subsequent energy failure. In this study, we investigated whether intranasal administration of NAD+ could reduce neuronal death after TBI. Rats were subjected to a weight-drop TBI model that induces cortical and hippocampal neuronal death. The intranasal administration of NAD+ (20 mg/kg) immediately after TBI protected neurons in CA1, CA3, and dentate gyrus of the hippocampus, but not in the cortex. In addition, delayed microglial activation normally seen after TBI was reduced by NAD+ treatment at 7 days after insult. Neuronal superoxide production and PARP-1 accumulation after TBI were not inhibited by NAD+ treatment, indicating that reactive oxygen species (ROS) production and PARP-1 activation are events that occur upstream of NAD+ depletion. This study suggests that intranasal delivery of NAD+ represents a novel, inexpensive, and non-toxic intervention for preventing TBI-induced neuronal death."
 

→ source (external link)

 

 

 

I'm still excited to see the University of Minnesota take this on . . . period. I've felt for awhile that athletes in contact sports should take (NR) to lessen the risk of head trauma. This study doesn't tackle that notion head on but if they can prove higher levels of NAD+ in the brain this is the first step that will open up the dialogue about using (NR) to help lesson (TBI) traumatic brain injury. So lets all hope they get the results they are seeking because there is currently no medical strategy to prevent or treat this kind of injury.

 

 

I was excited, but: "This study is not yet open for participant recruitment."

 

I thought it was a completed study. My mistake.

 

 

My father is still very active with sports (76 years) and he fell very hard on his head/face during ice speed skating and they carried him off the ice unconscious. Later in the hospital they made a headscan and triple asked his age as his brain had dealt with the fall very well. In the end they said he must have good genes....he was on NR at that point 10 months. Perhaps a coincidence but I am happy he is on the NR.

 

 

Edited by heisoktoday, 30 March 2016 - 12:42 AM.