2255 replies to this topic

[Bryan_S]

Now that we know NR is life prolonging (in mice), we need basic longevity testing including equimolar NR, NaR, NMN, NaMN, Nam, Niacin, and possibly NAD+, NaAD+ administration to sort out some candidates and to better understand the exact mechanisms. Because as stefan said, labs still use NMN due to the 2013 paper.

 

There is NMN <-> NaMN and/or NR <-> NaR conversion in the liver, see Figure 1B+1E in the last Brenner/ChromaDex paper (NAD+/NaAD+ ratio is about 1:10, same for these ones?), but maybe that's old news.

 

And then there is Nam. As far as I remember Bryan saw improvements from both Nam and NR. I'd be glad to read more experiences from people who used (high-dose) Nam and now NR. When seeing some results, I think there is still a chance for it.
 

 

I've discontinued the NAM. I've upped the SIRT activators and felt I was fighting my investment. The NAM did give me skin improvements, but having dialed that back and eliminated it I'm still happy with the NR alone. The only real difference is I sustain the NR levels by breaking up the dosage thru the day. Still taking 1000mg following this half-life chart.

 

 

 

Hoping the next bit of data we get will help us refine these charts.

[Nate-2004]

The NAM did give me skin improvements...

 

How so? I'm guessing NR wouldn't have any effect on skin or collagen regrowth or any kind of rejuvenation. I think that's what most people want and it disappears so fast. I look at pictures just 12 years back and it's incredible what aging did to me. My eyes don't look the same shape, my mouth can't even make the same shape anymore. It's like I'm not even the same person. So weird. You look at pictures of Harrison Ford from the first Star Wars and then new pictures from the most recent Star Wars and it's like, wow... Imagine if that weren't a problem.

[Ethic]

The clinical trial (n=12) in your last post is showing that a single 1000 mg dose can sustain NAD+ levels consistently high for about 20 hours, for details see the n=1 experiment.

 

 

 

The only real difference is I sustain the NR levels by breaking up the dosage thru the day. Still taking 1000mg following this half-life chart.

 

Hoping the next bit of data we get will help us refine these charts.

 

 

 

[Smedvick]

I’ve read every post on this topic with great interest, and I even understood some of it. However I seem to be missing something key in the conversations about translating the dose given to mice to that of humans.  If we know that doses of 300mg – 1g result in a 50% increase in NAD+ in humans, do we know what percentage of NAD+ increase was observed in the mice given 400mg/Kg/day?  I’m currently taking 500mg/day and it seems that knowing the NAD+ percent increase in the mice would be helpful in my guestimation of the proper dose.

Edited by Smedvick, 06 May 2016 - 09:30 PM.

[stefan_001]

I’ve read every post on this topic with great interest, and I even understood some of it. However I seem to be missing something key in the conversations about translating the dose given to mice to that of humans.  If we know that doses of 300mg – 1g result in a 50% increase in NAD+ in humans, do we know what percentage of NAD+ increase was observed in the mice given 400mg/Kg/day?  I’m currently taking 500mg/day and it seems that knowing the NAD+ percent increase in the mice would be helpful in my guestimation of the proper dose.

 

That's a good question and I am pretty sure, like you, that the answer is not in the posts. I recall seeing it somewhere and that it doubles the concentration in young mice and almost triples it in old mice (not in absolute terms but relative). But the effect in mice might be also reached at a lower dose. The researchers simply didn't test for that. My guess is they went with feeding on the high end to make sure they would see effect.

[Bryan_S]

Ethic,

 

The chart I posted only represents the half-life of (NR) and what the effect of subsequent dosing "might" look like following the first application. Its an attempt to graph the predictable fall off and elimination from the blood. I expect they will publish better data, so we can produce better charts.

 

If the relative raise in NAD can only produce, "approximately 30% at the 100 mg dose and approximately 50% at the higher doses" that suggests the 300 mg and 1 gram doses yielded relatively the same peak NAD rise. . . correct?

 

They have not released enough information for us to thoroughly pick that press release apart, "yet," but we will get there.

 

They did suggest the higher dose maintained NAD levels longer but in reality we are still confronted with the slow and gradual elimination of the absorbed (NR) thru the kidneys, so we can assume dosing to excess will be flushed down the drain. That was the real purpose of my chart, so we could avoid waste and maintain the maximum useful blood levels, since a time-released version is not available.

 

Looking at the Human n=1 experiment "Peak NAD+ was at 8.1 hrs and was temporally coincident with peak Nam and N-methyl-4-pyridone-5-carboxamide (Me4PY), a nonsalvageable waste product."

The 7-day chart also suggests the NAD levels rose higher with continued use thru hour 167.6." I found these results very encouraging and expected tons of replies.

 

So we need more information in order to combined the NAD rise with the expected (NR) excretion thru its half-life.

 

Still at day-7 it was interesting to see a higher NAD peak than at the end of the first day. Keep in mind however they didn't publish the graph between hours 23.8 and 167.6, so we don't know if a plateau was reached sooner or if the experiment continued, would levels have risen further?

 

 

The clinical trial (n=12) in your last post is showing that a single 1000 mg dose can sustain NAD+ levels consistently high for about 20 hours, for details see the n=1 experiment.

 

 

 

The only real difference is I sustain the NR levels by breaking up the dosage thru the day. Still taking 1000mg following this half-life chart.

 

Hoping the next bit of data we get will help us refine these charts.

 

 

 

Edited by Bryan_S, 07 May 2016 - 07:13 PM.

[Nate-2004]

 

Now that we know NR is life prolonging (in mice), we need basic longevity testing including equimolar NR, NaR, NMN, NaMN, Nam, Niacin, and possibly NAD+, NaAD+ administration to sort out some candidates and to better understand the exact mechanisms. Because as stefan said, labs still use NMN due to the 2013 paper.

 

There is NMN <-> NaMN and/or NR <-> NaR conversion in the liver, see Figure 1B+1E in the last Brenner/ChromaDex paper (NAD+/NaAD+ ratio is about 1:10, same for these ones?), but maybe that's old news.

 

And then there is Nam. As far as I remember Bryan saw improvements from both Nam and NR. I'd be glad to read more experiences from people who used (high-dose) Nam and now NR. When seeing some results, I think there is still a chance for it.
 

 

I've discontinued the NAM. I've upped the SIRT activators and felt I was fighting my investment. The NAM did give me skin improvements, but having dialed that back and eliminated it I'm still happy with the NR alone. The only real difference is I sustain the NR levels by breaking up the dosage thru the day. Still taking 1000mg following this half-life chart.

 

 

 

Hoping the next bit of data we get will help us refine these charts.

 

 

Wouldn't it be better to time the NR intake somehow with taking the Resveratrol or other SIRT1 or SIRT3 activators rather than try to keep NAD high throughout the entire day?

 

Like how long are Sirtuins activated and to what degree, when taking 500mg of Resveratrol or Pterostilbene or other substances?  How soon? Where? Is it in the same places where NAD is boosted so that these Sirtuins use it?

Edited by Nate-2004, 07 May 2016 - 07:21 PM.

[Bryan_S]

Wouldn't it be better to time the NR intake somehow with taking the Resveratrol or other SIRT1 or SIRT3 activators rather than try to keep NAD high throughout the entire day?

 

Like how long are Sirtuins activated and to what degree, when taking 500mg of Resveratrol or Pterostilbene or other substances?  How soon? Where? Is it in the same places where NAD is boosted so that these Sirtuins use it?

 

 

Some of us do, I start and end the day with my SIRT1 & SIRT3 activators. As far as the NAD I just want sustained levels and I don't want to be flushing the excess so I break it up thru the day. Nate maybe you can dig up the time related Sirtuin info you seek. I haven't found enough data yet for me to chart any of that but I'm sure there is something out there.

[stefan_001]

Looking at the Human n=1 experiment "Peak NAD+ was at 8.1 hrs and was temporally coincident with peak Nam and N-methyl-4-pyridone-5-carboxamide (Me4PY), a nonsalvageable waste product."

The 7-day chart also suggests the NAD levels rose higher with continued use thru hour 167.6." I found these results very encouraging and expected tons of replies.

 

 

 

Hey Brian, the poster was a great find, thanks for uploading it. I thought the levels were same ballpark beginning to end, nevertheless that is positive but not surprising. I think we all have the experience that the effect stays.

 

Overall I found the material really weak. I am sure Chromadex has much more data. Seriously the CEO claims he is on it for years as well as several other employees and all they present is a n=1 data poster? My best guess, they are / were negotiating and as part of that have an agreement of low profile.

 

 

Edited by stefan_001, 07 May 2016 - 08:37 PM.

[Ethic]

Ah okay, that makes sense I somehow overlooked the chart title...but AFAIR we still don't know if we have to produce a high peak or maintain a steady level of NR itself for its signaling benefits, right?

 

 

 

Ethic,

 

The chart I posted only represents the half-life of (NR) and what the effect of subsequent dosing "might" look like following the first application. Its an attempt to graph the predictable fall off and elimination from the blood. I expect they will publish better data, so we can produce better charts.

 

 

[Ohm]

Elysium Basis (NR+Pterostilbene product from Leonard Guarente) website states,

 

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.  Many customers tell us that making it a central part of their morning routine works best, especially because some say they experience a slight rise in energy after intake and don’t want that to interfere with sleep.   The most important thing to remember is to take Basis daily for best results, as cellular health optimizes over time. We recommend leaving your Basis jar on your kitchen counter or on your desk at work so it can become a habit to take it every day.

 

http://www.elysiumhealth.com/help

 

I know that the three founders of Elysium take either a lone 125mg or 250mg dose per day, and Gaurente is one of the experts on this stuff (he mentored David Sinclair at MIT).  I would be wary of individuals/companies pushing a "more is better!" approach unless there is very clear data behind that position.

[sthira]

Has anyone who is regularly taking NR checked for elevated homocysteine? When I take niacin, for example, I get significant rises, which appears to be in my genetics.

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

[Bryan_S]

My guess is we are talking about single dose results and the 7-day results. To-date there has been 3 completed human studies and 4 more are recruiting. I've searched for the 56-year old for 7 consecutive days and the poster is the only reference to this study data. Just that one mention has me asking how many elderly subjects and what were the comparative results between them?

 

Here is a short blurb about the poster. It was presented at 4th Federation of American Societies for Experimental Biology (FASEB) Science Research Conference on NAD+ Metabolism and Signaling, held in Germany last year.

 

I'm not sure all the studies are being filed with the clinical research trials website. One study not listed will be with the University of Colorado Boulder. 

 

I agree there are deals in the background and it looks like only select morsels of information are being publicly released.

 

Hey Brian, the poster was a great find, thanks for uploading it. I thought the levels were same ballpark beginning to end, nevertheless that is positive but not surprising. I think we all have the experience that the effect stays.

 

Overall I found the material really weak. I am sure Chromadex has much more data. Seriously the CEO claims he is on it for years as well as several other employees and all they present is a n=1 data poster? My best guess, they are / were negotiating and as part of that have an agreement of low profile.

 

 

Edited by Bryan_S, 08 May 2016 - 05:47 PM.

[bluemoon]

 

 

 

"Wouldn't it be better to time the NR intake somehow with taking the Resveratrol or other SIRT1 or SIRT3 activators rather than try to keep NAD high throughout the entire day?

 

Like how long are Sirtuins activated and to what degree, when taking 500mg of Resveratrol or Pterostilbene or other substances?  How soon? Where? Is it in the same places where NAD is boosted so that these Sirtuins use it?"

 

 

Guarante said last spring that he was taking 250 mg of resveratrol along with Basis, which I assumed was the suggested 250 mg of NR with 50 mg of Pterostilbebe. I'm curious why he takes Resveratrol as well as Pterostilbene. 

[Nate-2004]

 

Wouldn't it be better to time the NR intake somehow with taking the Resveratrol or other SIRT1 or SIRT3 activators rather than try to keep NAD high throughout the entire day?

 

Like how long are Sirtuins activated and to what degree, when taking 500mg of Resveratrol or Pterostilbene or other substances?  How soon? Where? Is it in the same places where NAD is boosted so that these Sirtuins use it?

 

 

Some of us do, I start and end the day with my SIRT1 & SIRT3 activators. As far as the NAD I just want sustained levels and I don't want to be flushing the excess so I break it up thru the day. Nate maybe you can dig up the time related Sirtuin info you seek. I haven't found enough data yet for me to chart any of that but I'm sure there is something out there.

 

 

I did find this: http://www.pteropure...ptero/resv.html

 

So at best it's around 4 hrs or so with the pterostilbene, that doesn't mean however that sirtuins don't remain active for a longer period of time which is what I'm trying to find out. I'm still searching but not coming up with any info on this. I'm probably not using the right terms.

[Bryan_S]

Ethic,

 

Signaling benefits? You mean as far as nuclear or circadian rhythms. As far as NAD levels they begin to rise just before we wake up and decline before sleep. So it makes sense to re-enforce those rhythms rather than work against them.

 

The Time of Metabolism: NAD , SIRT1, and the Circadian Clock

"In this context, it is the chromatin landscape that most likely functions as molecular substrate of where to “write” or “erase” specific marks by posttranslational modifications of DNA and/or histones (Borrelli et al. 2008). Thus, we hypothesize that the chromatin remodel- ers (“writers” and “erasers” of posttranslational modifica- tions) specifically implicated in circadian control of the genome play a central role in translating changes in cellu- lar metabolism into epigenetic regulation."

 

Circadian clock is key to firing up cell's furnace

"Mitochondria regulate the supply of energy to cells when we are at rest, with no glucose available from food. In a study of mice, the researchers found that the circadian clock supplies the match to light the furnace and on the match tip is a critical compound called NAD+. It combines with an enzyme in mitochondria called Sirtuin 3, which acts as the flint, to light the furnace. When the clock in an animal isn't working, the animal can't metabolize stored energy and the process doesn't ignite."

 

"We have established the chain of events that couples the clock's control switch with the machinery of the mitochondria," said Bass, who also is a member of the department of neurobiology at the Weinberg College of Arts and Sciences. "We now have identified an additional link in the supply chain that provides energy to the cell at different phases of our daily sleep-wake cycle. These findings establish a key role for the NAD+ biosynthetic cycle in this process."

 

So there is some data on this, mostly on mice but these are conserved feedback systems and we share the same machinery. As I said; "it makes sense to re-enforce those rhythms rather than work against them."

 

This is where Nate can start his research being that this is where his questions are arising.

 

We also have to fall back on the comments of Leonard P. Guarente of MIT. He said; "sirtuins have an absolute requirement for NAD+ for their activities." 

 

What does he know? He was the father of the ideas we are kicking around.

Small-Molecule Allosteric Activators of Sirtuins

 

 

Ah okay, that makes sense I somehow overlooked the chart title...but AFAIR we still don't know if we have to produce a high peak or maintain a steady level of NR itself for its signaling benefits, right?

 

Edited by Bryan_S, 09 May 2016 - 06:17 PM.

[bluemoon]

Does anyone know when ChromaDex's patent for the manufacturing process for NR expires?

[Smedvick]

Does anyone know when ChromaDex's patent for the manufacturing process for NR expires?

 

It looks like they only license the rights from Dartmouth who holds the patent.  

 

I can't seem to make external links work.  Sorry. 

Edited by Smedvick, 10 May 2016 - 03:53 PM.

[HappyPaul]

 

Does anyone know when ChromaDex's patent for the manufacturing process for NR expires?

 

It looks like they only license the rights from Dartmouth who holds the patent.  

 

I can't seem to make external links work.  Sorry. 

 

http://investors.chr...icle&ID=1936672

 

Not all the data but an explanation. 

[Yajerman]

 

Does anyone know when ChromaDex's patent for the manufacturing process for NR expires?

 

It looks like they only license the rights from Dartmouth who holds the patent.  

 

I can't seem to make external links work.  Sorry. 

 

 

I found some additional information:

 

"Although the financial terms of the deal were not disclosed, Dartmouth College splits licensing revenue down the middle with inventors, once it has recovered its costs. Of Dartmouth College’s share, 40 percent is distributed between the inventor’s department and laboratory."

Edited by Yajerman, 10 May 2016 - 05:45 PM.

[Nate-2004]

 

Ethic,

 

Signaling benefits? You mean as far as nuclear or circadian rhythms. As far as NAD levels they begin to rise just before we wake up and decline before sleep. So it makes sense to re-enforce those rhythms rather than work against them.

 

The Time of Metabolism: NAD , SIRT1, and the Circadian Clock

"In this context, it is the chromatin landscape that most likely functions as molecular substrate of where to “write” or “erase” specific marks by posttranslational modifications of DNA and/or histones (Borrelli et al. 2008). Thus, we hypothesize that the chromatin remodel- ers (“writers” and “erasers” of posttranslational modifica- tions) specifically implicated in circadian control of the genome play a central role in translating changes in cellu- lar metabolism into epigenetic regulation."

 

Circadian clock is key to firing up cell's furnace

"Mitochondria regulate the supply of energy to cells when we are at rest, with no glucose available from food. In a study of mice, the researchers found that the circadian clock supplies the match to light the furnace and on the match tip is a critical compound called NAD+. It combines with an enzyme in mitochondria called Sirtuin 3, which acts as the flint, to light the furnace. When the clock in an animal isn't working, the animal can't metabolize stored energy and the process doesn't ignite."

 

"We have established the chain of events that couples the clock's control switch with the machinery of the mitochondria," said Bass, who also is a member of the department of neurobiology at the Weinberg College of Arts and Sciences. "We now have identified an additional link in the supply chain that provides energy to the cell at different phases of our daily sleep-wake cycle. These findings establish a key role for the NAD+ biosynthetic cycle in this process."

 

So there is some data on this, mostly on mice but these are conserved feedback systems and we share the same machinery. As I said; "it makes sense to re-enforce those rhythms rather than work against them."

 

This is where Nate can start his research being that this is where his questions are arising.

 

We also have to fall back on the comments of Leonard P. Guarente of MIT. He said; "sirtuins have an absolute requirement for NAD+ for their activities." 

 

What does he know? He was the father of the ideas we are kicking around.

Small-Molecule Allosteric Activators of Sirtuins

 

 

I looked through a bunch of those links on Google and what you linked above. I don't see a lot of answers to this question: "When sirtuins are activated by CR or by other newly discovered means (resveratrol, pterostilbene, honokiol, etc), how long do they stay active?" Is it as long as they have NAD to "feed" on or is it based on a clock or the half life or continuation (CR) of whatever activated it?

 

Also from what I understand the availability of NAD+ itself can activate sirtuins? (Assuming Sirt1?)

 

Also, side topic on NAD+, there's a quote here by Aubrey de Grey from Ending Aging (2008), what do you make of it?

 

NAD+ is required for a wide range of cellular functions unrelated to energy production—and each time these functions utilize NAD+, they not only reduce the pool of available NAD+ , they also convert it to yet more NADH, further upsetting the cell's metabolic balance. In fact, some researchers believe that many of the complications of diabetes are caused by an excess of NADH and a lack of NAD+ , leading to disruption of these various metabolic processes (although the imbalance of NAD+ and NADH in diabetics has different causes than the loss of OXPHOS capacity).

 

Also is it understood *why* NAD+ levels drop after a certain age yet?  I realize this seems to just be one key to the puzzle of aging, with telomeres and limited cell divisions and damage to mitochondrial DNA and the need for constant repair. I'm assuming something gets damaged and lost at some point so NAD levels begin to drop and this is just a symptom that starts contributing further to some runaway process.

Edited by Nate-2004, 10 May 2016 - 06:00 PM.

[bluemoon]

 

 

http://investors.chr...icle&ID=1936672

 

Not all the data but an explanation. 

 

 

Thanks for the link. Maybe it isn't so easy to find when the patent was filed by Dartmouth. That might not affect the price for NR much if pharmaceuticals enter the fray but then again those pills might have a somewhat different market than those potentially interested in taking NR. 

[Bryan_S]

“Nicotinamide Riboside: Investigating Novel Therapy for Heart Failure” – Presented by Division of Cardiology Grand Rounds

 

WHEN: May 13, 2016 @ 7:30 am – 8:30 am

WHERE: Health Sciences Building

Room D-209

COST: Free

 HEALTH SCIENCES BULLETIN

Sophia Airhart, MD

Cardiology Fellow

 

University of Washington

 

https://depts.washin...nstance_id=2637

 

OK guys who's going? Take notes and post them here! No I'm not kidding. These guys are doing a ton of NR study.

 

Check out all these papers! They just keep turing out eye opening (NR) papers. One of us needs to attend some of these seminars and report back.

Edited by Bryan_S, 12 May 2016 - 12:22 AM.

[Bryan_S]

Congratulations, Dr. Tian!

Rong Tian, MD, PhD, Professor, Anesthesiology & Pain Medicine, South Lake Union, received $2.7 million (total cost over 4 years) from the NHLBI to test novel strategies for targeting fatty acid oxidation in hearts with pathological hypertrophy. She has also received $3.1 million (total cost over 4 years) from the NHLBI to study glucose and amino acid metabolism in cardiac stress responses. The NHLBI and Office of Dietary Supplement has awarded her $478,000 (total cost over 2 years) to perform the first in human safety and tolerability study of nicotinamide riboside in heart failure. Amgen has recently awarded her $87,000 (total cost for 1 year) to study cardiac metabolism in heart failure with preserved systolic function.

 

 

• Department of Anesthesiology & Pain Medicine
• University of Washington, Box 356540
  1959 NE Pacific Street, BB-1469
  Seattle, WA 98195-6540

[Nate-2004]

Now can the alternatives fix the gradual decline of NAD which seems to be tied to the gradual reduction of NAMPT which recycles the residual nicotinamide after the elections have been depleted from the NAD? What causes this decline? My hunch (opinion) is it's being downregulated somewhere in the epigenome and this is where the fix likely hides. So I agree NR supplementation isn't a fix for this problem but by the same token can these alternatives produce as much or more NAD to maintain NAD's downstream functions that are dependent on having an adequate pool to function properly?

 

Is there a forum or thread discussing theories as to what causes the decline in NAD? It's a question that I think is pretty important. Internet searches on NAD decline merely reveal that it does, but no information or theories on why it does and that's pretty sad. I wonder if any scientists are doing the research on this to determine why. If it's epigenetic and/or related to some kind of damage or mutated DNA then that makes sense I suppose, but then again that's pretty consistent considering that same exact mutation happens with everyone... which leads me to believe it can't be that, or isn't just that.

[stefan_001]

 

Now can the alternatives fix the gradual decline of NAD which seems to be tied to the gradual reduction of NAMPT which recycles the residual nicotinamide after the elections have been depleted from the NAD? What causes this decline? My hunch (opinion) is it's being downregulated somewhere in the epigenome and this is where the fix likely hides. So I agree NR supplementation isn't a fix for this problem but by the same token can these alternatives produce as much or more NAD to maintain NAD's downstream functions that are dependent on having an adequate pool to function properly?

 

Is there a forum or thread discussing theories as to what causes the decline in NAD? It's a question that I think is pretty important. Internet searches on NAD decline merely reveal that it does, but no information or theories on why it does and that's pretty sad. I wonder if any scientists are doing the research on this to determine why. If it's epigenetic and/or related to some kind of damage or mutated DNA then that makes sense I suppose, but then again that's pretty consistent considering that same exact mutation happens with everyone... which leads me to believe it can't be that, or isn't just that.

 

 

Likely there is no single cause. My view is that its epigenetics. The human body is never really in balance, was never build to be in balance. So the methylation patterns continue to shift while we grow and onwards. And even if the cells are pretty robust machines eventually they start to malfunction due to the continuous changes, they are just dumb chemical machines with an operating range. I think NR is pretty cool hack to push back the system in a better working range and perhaps this push back changes some of the epigenetics as well. Personally I am more interested in what other areas need a push also to come closer to a "youthful" methylation state.

Edited by stefan_001, 14 May 2016 - 07:52 PM.

[Nate-2004]

Likely there is no single cause. My view is that its epigenetics. The human body is never really in balance, was never build to be in balance. So the methylation patterns continue to shift while we grow and onwards. And even if the cells are pretty robust machines eventually they start to malfunction due to the continuous changes, they are just dumb chemical machines with an operating range. I think NR is pretty cool hack to push back the system in a better working range and perhaps this push back changes some of the epigenetics as well. Personally I am more interested in what other areas need a push also to come closer to a "youthful" methylation state.

 

I agree, but I'm also a fan of aiming for root causes. I mean, whatever can take people like Brendan Frasier and rejuvenate him back to his look and state of health on the left lol. Aging is such a tragedy.

 

[Anthony_Loera]

SENS have weighed in on NR supplementation with their own analysis of the mouse research on NMN (Posted 23rd November 2015):

 

http://sens.org/rese...ng-mitochondria

 

From the article:

The studies showing benefits of NR supplementation in mouse models of disease have used doses of 400-500 milligrams of NR per kilogram of mouse body weight. Even after adjusting for the different metabolic rates of mice and humans, an approximate equivalent adult dose would range from 2000 to 4000 milligrams of NR per day. Commercially-available NR supplements contain between 75 and 125 mg NR per capsule, at a cost of roughly 0.6-0.8 cents per milligram of NR; to experiment with even the lower end of the human-equivalent dosage range would thus involve swallowing 18-30 NR pills a day, at a cost of $400-550 a month.

 

Oh... and is this thread a big advertisement for Chromadex? Because to me it certainly sounds like it.

 

A

[Tom Andre F. (ex shinobi)]

 

SENS have weighed in on NR supplementation with their own analysis of the mouse research on NMN (Posted 23rd November 2015):

 

http://sens.org/rese...ng-mitochondria

 

From the article:

The studies showing benefits of NR supplementation in mouse models of disease have used doses of 400-500 milligrams of NR per kilogram of mouse body weight. Even after adjusting for the different metabolic rates of mice and humans, an approximate equivalent adult dose would range from 2000 to 4000 milligrams of NR per day. Commercially-available NR supplements contain between 75 and 125 mg NR per capsule, at a cost of roughly 0.6-0.8 cents per milligram of NR; to experiment with even the lower end of the human-equivalent dosage range would thus involve swallowing 18-30 NR pills a day, at a cost of $400-550 a month.

 

Oh... and is this thread a big advertisement for Chromadex? Because to me it certainly sounds like it.

 

A

 

 

.... says the fat guy who sells TA65 (the best crap / scam ever) at 500$ per bottle :D

 

[super-human]

Question, since NR was not used in the mouse studies and the molecular weight of NMN is less than 500 mol why not create a NMN patch instead of ingesting pills of the potentially very less effective pre-cursor?

 

 

Edited by super-human, 14 May 2016 - 10:52 PM.