167 replies to this topic

[Advocatus Diaboli]

Re citation in post #89, here is the authors' disclosures:

 

J.R., M.J., M.B., S.S.K. and C.C. are employees of the Nestlé Institute of Health Sciences S.A. C.B. owns stock in ChromaDex and has received a research grant and serves on the scientific advisory board of ChromaDex. C.B. is co-founder and Chief Scientific Adviser of ProHealthspan, which distributes an NR supplement. M.E.M. has received research grants and serves as a consultant for ChromaDex.

[able]

This study shows increasing NAD+ from NAMPT pathway doesn't improve muscle metabolic health. While NR studies show muscle metabolic health improved significantly. NMN showed 2 year old mice muscle turned into 3 month old in a few weeks. As suspected by many, there is a hidden benefit from NR beyond increasing NAD+.

http://m.jbc.org/con...290/3/1546.full

 

An interesting study.   It MAY be that increased NAD+ alone does not improve the metabolic health of muscle tissue.

 

But as authors note, these were young, healthy mice, so they didn't suffer from low NAD+.

 

Also, they only increased NAMPT and NAD+ in the muscle, nowhere else.

[Turnbuckle]

 

This study shows increasing NAD+ from NAMPT pathway doesn't improve muscle metabolic health. While NR studies show muscle metabolic health improved significantly. NMN showed 2 year old mice muscle turned into 3 month old in a few weeks. As suspected by many, there is a hidden benefit from NR beyond increasing NAD+.

http://m.jbc.org/con...290/3/1546.full

 

An interesting study.   It MAY be that increased NAD+ alone does not improve the metabolic health of muscle tissue.

 

But as authors note, these were young, healthy mice, so they didn't suffer from low NAD+.

 

Also, they only increased NAMPT and NAD+ in the muscle, nowhere else.

 

 

 

Looks to me that these were genetically altered mice. They weren't healthy in the normal sense.

[MikeDC]

I, NAD content of quadriceps muscle from 15-month-old mice supplied with 400 mg/kg/day NAM in the drinking water for 2 weeks.

To test whether NAD generation in mNAMPT mice is limited by NAM availability, we administered 400 mg/kg NAM in the drinking water for 1 week and examined skeletal muscle NAD levels. No further elevation of NAD was observed in mNAMPT mice under these conditions, suggesting that NAM availability does not limit NAMPT activity in muscle under standard dietary conditions


the Nampt transgene had no significant effect on the expression of genes associated with mitochondrial biogenesis (TFAM, PGC1a, mfsn2, and Sirt1), oxidative phosphorylation (CytC, Cox5b, and Ndufs8), coupling (UCP2), or substrate selection (PDK4, MCAD, and Sirt3) in quadriceps or soleus muscles (Fig. 2E).

NAM, a substrate of NAMPT, is also a non-competitive inhibitor of sirtuins and a competitive inhibitor of PARPs. Thus, one mechanism by which NAMPT overexpression might influence such enzymes is through the depletion of NAM rather than through the generation of NAD per se. Contrary to our initial expectation, we did not observe a significant depletion of NAM in quadriceps muscles of mNAMPT mice (Fig. 5A), potentially indicating that this metabolite is rapidly replenished

Sent from my iPhone

[MikeDC]

"NAM, a substrate of NAMPT, is also a non-competitive inhibitor of sirtuins and a competitive inhibitor of PARPs"

This makes NAM pro aging NOT anti aging. Maybe NAD+ difference between NAM and NR is not the main reason why the effects are significantly different. It is in the longevity gene expression and activity and DNA repair activity.

[Michael]

Ok the thread starter and moderator wants to move to a "observational" discussion so with that I stop in this topic.

 
 

The OP, Ovidus, in post #1 Question 1, asks: "Can those who have tried both and stuck with Nicotinamide + Ribose please chime in, because other than Turnbuckle I see nobody in that boat."

I've tried an earlier (not his current method) Turnbuckle protocol and the only effect I noticed was a transitory lowering of blood pressure, both systolic and diastolic, by about 15 and 10 mm, respectively (lasting about 4 hrs duration starting after about 1 hr post ingestion)

I'm currently trying HPN Niagen at 375mg/day (3x125mg) with no noticeable effects after 5 days. I will continue with whatever Turnbuckle protocol is current when my bottle of HPN Niagen is empty.

 

Two days ago I repeated OP's invitation to users of N+R to come forward. No one ventured to describe ideas or experiences. Peculiar,  since even taking just ribose gives many people a 'lift'.
Those who feel they are swayed by assertions about N+R please also read my post #3 in this thread.....

While I frankly think the idea of ignoring the absence of data on outcomes or demonstrated mechanism and proceeding on the basis of anecdote is nuts, it does seem like it would be better for those who want to have that discussion be able to have it, and  all the science on this topic would be also better served if we didn't have it scattered over so many threads.

 

If Ovidus would like, I can take all of the science-based material on a putative role for NAM + R in de novo NR synthesis and merge them into the existing "Does NR Get Broken Down into N+R or Is It Stable?" thread. I could also try to clarify the purpose of this thread by re-titling it (eg.) "Anecdotal Experience with Nicotinamide Riboside vs. Nicotinamide + Ribose." LMK.

[able]

"NAM, a substrate of NAMPT, is also a non-competitive inhibitor of sirtuins and a competitive inhibitor of PARPs"

This makes NAM pro aging NOT anti aging. Maybe NAD+ difference between NAM and NR is not the main reason why the effects are significantly different. It is in the longevity gene expression and activity and DNA repair activity.

 

 

Yes, there was evidence that NAM inhibits sirltuins IN VITRO. 

 

Unfortunately, Brenner and team constantly repeat and exaggerate that claim to validate the superiority of NR.

 

However, this study points out the flaws in that assumption, and that it raises NAD+ significantly which results in Sirtuin activation.

 

Nicotinamide is an inhibitor of SIRT1 in vitro, but can be a stimulator in cells.

 

 

Elsewhere, Dr Sinclair says that the "NAM inhibits sirtuin" thing is not really accurate, even though he would also have reason to discount NAM in favor of NMN.  That is one reason I find him to be more honest in his evaluations, compared to the NR cheerleaders.

Edited by able, 22 September 2017 - 03:46 PM.

[Harkijn]

 

"NAM, a substrate of NAMPT, is also a non-competitive inhibitor of sirtuins and a competitive inhibitor of PARPs"

This makes NAM pro aging NOT anti aging. Maybe NAD+ difference between NAM and NR is not the main reason why the effects are significantly different. It is in the longevity gene expression and activity and DNA repair activity.

 

 

Yes, there was evidence that NAM inhibits sirltuins IN VITRO. 

 

Unfortunately, Brenner and team constantly repeat and exaggerate that claim to validate the superiority of NR.

 

However, this study points out the flaws in that assumption, and that it raises NAD+ significantly which results in Sirtuin activation.

 

Nicotinamide is an inhibitor of SIRT1 in vitro, but can be a stimulator in cells.

 

 

Elsewhere, Dr Sinclair says that the "NAM inhibits sirtuin" thing is not really accurate, even though he would also have reason to discount NAM in favor of NMN.  That is one reason I find him to be more honest in his evaluations, compared to the NR cheerleaders.

 

Able, this study only concludes:

 We conclude that NAM treatment can hypothetically be stimulatory to SIRT1.

Nothing less, but also nothing more.

 

[able]

 

 

"NAM, a substrate of NAMPT, is also a non-competitive inhibitor of sirtuins and a competitive inhibitor of PARPs"

This makes NAM pro aging NOT anti aging. Maybe NAD+ difference between NAM and NR is not the main reason why the effects are significantly different. It is in the longevity gene expression and activity and DNA repair activity.

 

 

Yes, there was evidence that NAM inhibits sirltuins IN VITRO. 

 

Unfortunately, Brenner and team constantly repeat and exaggerate that claim to validate the superiority of NR.

 

However, this study points out the flaws in that assumption, and that it raises NAD+ significantly which results in Sirtuin activation.

 

Nicotinamide is an inhibitor of SIRT1 in vitro, but can be a stimulator in cells.

 

 

Elsewhere, Dr Sinclair says that the "NAM inhibits sirtuin" thing is not really accurate, even though he would also have reason to discount NAM in favor of NMN.  That is one reason I find him to be more honest in his evaluations, compared to the NR cheerleaders.

 

Able, this study only concludes:

 We conclude that NAM treatment can hypothetically be stimulatory to SIRT1.

Nothing less, but also nothing more.

 

 

 

You're right, that the conclusion in the abstract isn't firm that NAM stimulates Sirt.    

 

Read the whole review and you'll see they make a strong case that claims NAM inhibits Sirt  in vivo are misleading.

 

 

 

 

Here's a few quotes from the abstract that are stronger than the single sentence conclusion you quote :

 

"However, once administered to cells, NAM is rapidly converted to NAD+ and, therefore, the cellular concentration of NAM decreases rapidly while that of NAD+ increases. The result would be an inhibition of SIRT1 for a limited duration, followed by an increase in the activity."

 

"found that the expected inhibitory effect of NAM was either unreliable or muted in many cases"

 

"In addition, studies demonstrated NAM administration stimulates SIRT1 activity and improves the functions of cells and organs"

Edited by able, 22 September 2017 - 04:32 PM.

[MikeDC]

This paper is not a new study. It just review previous studies and proposed NAM may not be as inhibitive to Sirt1 as people expect.

Thousands of studies use NAM as Sirt1 inhibitor and got consistent results.

[able]

This paper is not a new study. It just review previous studies and proposed NAM may not be as inhibitive to Sirt1 as people expect.

Thousands of studies use NAM as Sirt1 inhibitor and got consistent results.

 

No, it clearly proposed NAM is not inhibitive, and MAY ACTIVATE Sirt1.

 

"Thousands of studies"  ????   Exaggeration doesn't prove your point.

 

One of the reasons they did the review was because the whole "NAM inhibits Sirt" is over stated and not useful science.

Edited by able, 22 September 2017 - 06:19 PM.

[stefan_001]

This paper is not a new study. It just review previous studies and proposed NAM may not be as inhibitive to Sirt1 as people expect.

Thousands of studies use NAM as Sirt1 inhibitor and got consistent results.

 

Inhibition of silencing and accelerated aging by nicotinamide, a putative negative regulator of yeast sir2 and
human SIRT1. J Biol Chem. 2002;277:45099–107. Bitterman KJ, Anderson RM, Cohen HY, Latorre-Esteves M,Sinclair DA.

 

We show that physiological concentrations of nicotinamide  noncompetitively  inhibit  both  Sir2  and SIRT1 in vitro. The degree of inhibition by nicotinamide (IC 50<50M) is equal to or better than the most effective known synthetic inhibitors of this class of proteins.

 

http://www.jbc.org/c.../47/45099.short

[able]

 

This paper is not a new study. It just review previous studies and proposed NAM may not be as inhibitive to Sirt1 as people expect.

Thousands of studies use NAM as Sirt1 inhibitor and got consistent results.

 

Inhibition of silencing and accelerated aging by nicotinamide, a putative negative regulator of yeast sir2 and
human SIRT1. J Biol Chem. 2002;277:45099–107. Bitterman KJ, Anderson RM, Cohen HY, Latorre-Esteves M,Sinclair DA.

 

We show that physiological concentrations of nicotinamide  noncompetitively  inhibit  both  Sir2  and SIRT1 in vitro. The degree of inhibition by nicotinamide (IC 50<50M) is equal to or better than the most effective known synthetic inhibitors of this class of proteins.

 

http://www.jbc.org/c.../47/45099.short

 

 

 

Yes.  IN VITRO.

 

Ignoring the stimulative effect of increased NAD+.

 

Which is the whole point of the review I posted.

[stefan_001]

 

 

This paper is not a new study. It just review previous studies and proposed NAM may not be as inhibitive to Sirt1 as people expect.

Thousands of studies use NAM as Sirt1 inhibitor and got consistent results.

 

Inhibition of silencing and accelerated aging by nicotinamide, a putative negative regulator of yeast sir2 and
human SIRT1. J Biol Chem. 2002;277:45099–107. Bitterman KJ, Anderson RM, Cohen HY, Latorre-Esteves M,Sinclair DA.

 

We show that physiological concentrations of nicotinamide  noncompetitively  inhibit  both  Sir2  and SIRT1 in vitro. The degree of inhibition by nicotinamide (IC 50<50M) is equal to or better than the most effective known synthetic inhibitors of this class of proteins.

 

http://www.jbc.org/c.../47/45099.short

 

 

 

Yes.  IN VITRO.

 

Ignoring the stimulative effect of increased NAD+.

 

Which is the whole point of the review I posted.

 

 

NAM conversion is going to be rate limited so are you sure you do the right thing by dumping in tons of NAM? In the worst case NR is nothing more than a slow release NAM but that would be enough to circumvent the peak NAD dosing and be more effective for health.

 

Edited by stefan_001, 22 September 2017 - 06:28 PM.

[able]

 

 

 

This paper is not a new study. It just review previous studies and proposed NAM may not be as inhibitive to Sirt1 as people expect.

Thousands of studies use NAM as Sirt1 inhibitor and got consistent results.

 

Inhibition of silencing and accelerated aging by nicotinamide, a putative negative regulator of yeast sir2 and
human SIRT1. J Biol Chem. 2002;277:45099–107. Bitterman KJ, Anderson RM, Cohen HY, Latorre-Esteves M,Sinclair DA.

 

We show that physiological concentrations of nicotinamide  noncompetitively  inhibit  both  Sir2  and SIRT1 in vitro. The degree of inhibition by nicotinamide (IC 50<50M) is equal to or better than the most effective known synthetic inhibitors of this class of proteins.

 

http://www.jbc.org/c.../47/45099.short

 

 

 

Yes.  IN VITRO.

 

Ignoring the stimulative effect of increased NAD+.

 

Which is the whole point of the review I posted.

 

 

NAM conversion is going to be rate limited so are you sure you do the right thing by dumping in tons of NAM? In the worst case NR is nothing more than a slow release NAM but that would be enough to circumvent the peak NAD dosing and be more effective for health.

 

 

 

Nope, not sure at all.  Just guessing really.

 

Personally, I believe NR IS much more effective than NAM.  

 

But I am guessing NAM might have some value, and might help elevate NAD+ a bit, in a more cost effective manner, than taking NR by itself.

 

If NAM truly does inhibit Sirt1 in vivo, it would be counter-productive   I just don't believe the current evidence shows that to be the case.

[MikeDC]

Search Sirt1 studies in vivo that use NAM to inhibit sirt1

[Turnbuckle]

If anyone is worried about high NAM levels they ought to avoid oral NR, as it raises NAM levels even more than NAM. See Fig. 5d in this paper.

Edited by Turnbuckle, 22 September 2017 - 08:07 PM.

[able]

I anyone is worried about high NAM levels they ought to avoid oral NR, as it raises NAM levels even more than NAM. See Fig. 5d in this paper.

 

Good point.  

 

Those worried about NAM inhibiting Sirt should avoid NR and spend the extra $$$ for NMN.  

 

I'm not that rich, but maybe some here are

[Turnbuckle]

 

I anyone is worried about high NAM levels they ought to avoid oral NR, as it raises NAM levels even more than NAM. See Fig. 5d in this paper.

 

Good point.  

 

Those worried about NAM inhibiting Sirt should avoid NR and spend the extra $$$ for NMN.  

 

I'm not that rich, but maybe some here are

 

 

Is NMN any more available than NR?

 

 

Digestion and Absorption of NAD by the Small Intestine of the Rat

 

Perfused or intact intestine rapidly hydrolyzed NMN to nicotinamide riboside, which accumulated, but was not absorbed. It was slowly cleaved by an enzyme associated with the mucosal cells to nicotinamide, which was the major if not the only labeled compound absorbed.

 

http://nadh.wiki/wp-...-of-the-Rat.pdf

 

[stefan_001]

If anyone is worried about high NAM levels they ought to avoid oral NR, as it raises NAM levels even more than NAM. See Fig. 5d in this paper.

It shows also that the corresponding NAD+ concentration is a factor 3x4 higher most of the time so not too worried about SIRT inhibition.

from the same paperr:
This is consistent with the idea that high-dose NA, though not an ideal hepatic NAD+ precursor, is effective as a cholesterol agent whereas Nam is not because high-dose Nam inhibits sirtuins1.

[MikeDC]

If NAM doesn't lower cholesterol, then doesn't have the same anti aging effect as NR. Do a trial with NAM and NR on lowering cholesterol.

[Ovidus]

...While I frankly think the idea of ignoring the absence of data on outcomes or demonstrated mechanism and proceeding on the basis of anecdote is nuts, it does seem like it would be better for those who want to have that discussion be able to have it, and  all the science on this topic would be also better served if we didn't have it scattered over so many threads.

 

If Ovidus would like, I can take all of the science-based material on a putative role for NAM + R in de novo NR synthesis and merge them into the existing "Does NR Get Broken Down into N+R or Is It Stable?" thread. I could also try to clarify the purpose of this thread by re-titling it (eg.) "Anecdotal Experience with Nicotinamide Riboside vs. Nicotinamide + Ribose." LMK.

 

 

I appreciate the very kind offer.
I personally think that it would have been better to make 2 separate threads, named:

- Studies and Facts Comparing NR vs N+R
 

- Personal Experiences with NR vs N+R

 

At no point would I advocate ignoring data and studies and biochemistry driven theoretical discussion, substituting purely anecdotal observations in their place. 
I merely think that there is a ton of indirect info we can and already did use to compare NR to N+R, yet the data is simply not conclusive no matter how hard you study it. Instead, while those discussions are running in parallel, I think we also should hear of anecdotal observations. 
Now if anyone thinks such unscientific evidence is useless, they can thus know which threads not to enter at all. However, the extremely long thread on personal experiences with NR, which is now running like almost 50 pages, proves that the overall board does not find unscientific personal experiences useless.

 

Thanks to all; I am engaged in a rigorous n=1 experiment comparing NR and N+R in more detail and will report some observations soon.

 

Ovidus

[Turnbuckle]

 

If anyone is worried about high NAM levels they ought to avoid oral NR, as it raises NAM levels even more than NAM. See Fig. 5d in this paper.

It shows also that the corresponding NAD+ concentration is a factor 3x4 higher most of the time so not too worried about SIRT inhibition.

from the same paperr:
This is consistent with the idea that high-dose NA, though not an ideal hepatic NAD+ precursor, is effective as a cholesterol agent whereas Nam is not because high-dose Nam inhibits sirtuins1.

 

 

 

Hardly. Of 7 data points, NR has a significantly higher NAD+ for just one data point. And if you look at the bar chart associated with Fig. 5b, the difference for NAD+ overall is not significant. However the difference for NAM is significant. NR produces a 50% higher level of NAM than NAM does.

Edited by Turnbuckle, 22 September 2017 - 11:12 PM.

[stefan_001]

If anyone is worried about high NAM levels they ought to avoid oral NR, as it raises NAM levels even more than NAM. See Fig. 5d in this paper.

It shows also that the corresponding NAD+ concentration is a factor 3x4 higher most of the time so not too worried about SIRT inhibition.

from the same paperr:
This is consistent with the idea that high-dose NA, though not an ideal hepatic NAD+ precursor, is effective as a cholesterol agent whereas Nam is not because high-dose Nam inhibits sirtuins1.

Hardly. Of 7 data points, NR has a significantly higher NAD+ for just one data point. And if you look at the bar chart associated with Fig. 5b, the difference for NAD+ overall is not significant. However the difference for NAM is significant. NR produces a 50% higher level of NAM than NAM does.

As you like the bar chart then you will see a NAM AUC of 6k versus a NAD+ AUC of 16k.Dont know how you read the charts but the leganda's are not the same. But I agree that the NAM supplementation shows a similar picture.

Probably we need to look at other indicators like ADPR to asses the actual NAD+ usage that goes simultanuously. NAM shows very little action there. In fact while reading the study again that's also what the authors point out:
Of the metabolites associated with NAD+-consuming activities, ADPR is the only one that must be formed from NAD+ because Nam, MeNam and the oxidized forms of MeNam could appear in liver from the gavaged Nam without conversion to NAD+.

So in the NR gavage case the graphs show in my opinion a dynamic picture where NAD+ consumption goes up simultnuously with availability. In that sense these graphs cannot be read as "absolute" NAD+ increases. Its the increase minus the increased consumption.

Edited by stefan_001, 23 September 2017 - 06:43 AM.

[Turnbuckle]

 

 

 

 

As you like the bar chart then you will see a NAM AUC of 6k versus a NAD+ AUC of 16k.Dont know how you read the charts but the leganda's are not the same. But I agree that the NAM supplementation shows a similar picture.

 

 

I am comparing the black bar with the green bar within a single plot in every case. In the case of NAD+ (the Fig. 5b bar chart), there is no significant overall difference between the NR and NAM mice. In the case of NAM (the Fig. 5d bar chart), it needs to be explained how NR produced a significantly higher rise in NAM than NAM did. That is extraordinary since the researchers also claim that NR is absorbed intact.

 

The researchers never said how much NAM they gave the mice in mg/kg. They only said--

 

We therefore designed a reverse translational experiment in which mice were administered 185 mg kg−1 of NR or the mole equivalent doses of Nam and NA by oral gavage. 

 

 

 

The molar weight of NR is 255 and the molar weight of NAM is 122, so it appears that they gave mice twice as much NR by weight than NAM, then claimed NR was twice as good. 

Edited by Turnbuckle, 23 September 2017 - 08:33 AM.

[stefan_001]

 

 

 

 

 

As you like the bar chart then you will see a NAM AUC of 6k versus a NAD+ AUC of 16k.Dont know how you read the charts but the leganda's are not the same. But I agree that the NAM supplementation shows a similar picture.

 

 

I am comparing the black bar with the green bar within a single plot in every case. In the case of NAD+ (the Fig. 5b bar chart), there is no significant overall difference between the NR and NAM mice. In the case of NAM (the Fig. 5d bar chart), it needs to be explained how NR produced a significantly higher rise in NAM than NAM did. That is extraordinary since the researchers also claim that NR is absorbed intact.

 

The researchers never said how much NAM they gave the mice in mg/kg. They only said--

 

We therefore designed a reverse translational experiment in which mice were administered 185 mg kg−1 of NR or the mole equivalent doses of Nam and NA by oral gavage. 

 

 

 

The molar weight of NR is 255 and the molar weight of NAM is 122, so it appears that they gave mice slightly more than twice as much NR by weight than NAM, then claimed that NR was twice as good based on one of seven data points in time plot of Fig. 5b, even though the overall rise of NAD+ (shown in the bar chart of the same figure) was about the same while the rise of NAM with NR was a good deal higher. If they had spelled that out in their paper, people would be taking NAM, not NR.

 

 

I am comparing the AUC bars in 5b versus 5d, they give the corresponding NAD+ and NAM rises as result of the NR and NAM gavage respectively. Like said, agree they dont solve the question.

 

Noted your comment on molar weight approach. I think the authors took a good approach. But it doesnt really matter. I think the interesting part is:

"Of the metabolites associated with NAD+-consuming activities, ADPR is the only one that must be formed from NAD+ because Nam, MeNam and the oxidized forms of MeNam could appear in liver from the gavaged Nam without conversion to NAD+"

 

So there is proof that the oral gavage with NR leads to higher NAD+ consumption but in the NAM gavage case there is no conclusive proof as the metabolic indicators that spike could be generated via other pathways. That doesnt mean NAM gavage doesnt cause increased NAD+ consumption but it points out a clear difference between the two and gives NR an extra proof point over NAM.

Also I want to repeat that the graphs show the momentary level of NAD+ which is the outcome of NAD+ creation rate minus NAD+ consumption rate. So just comparing peak levels doesnt tell the story.

 

But okay I promised to stay away here as people in this thread are able to asses their NAD+ consumption based on feelings, no need for this discussion. So have a great weekend all.

Edited by stefan_001, 23 September 2017 - 08:45 AM.

[Turnbuckle]

The bottom line is simple: They gave twice as much NR as NAM to mice, hid that fact in a throwaway line about molar equivalents, then said NR was twice as good. People don't buy products by molar equivalents, only by weight.

 

 

[Ovidus]

Turnbuckle,
Very glad you are in this thread.... Maybe you did share the specific N and R doses you took in your prior protocols or the current one even. However, I was never able to find them. Do you mind sharing some ideas (from your protocols or in broad generalities only) about dosing of N and R for those who prefer the N+R route as opposed to NR?

Thanks in advance

[Turnbuckle]

Turnbuckle,
Very glad you are in this thread.... Maybe you did share the specific N and R doses you took in your prior protocols or the current one even. However, I was never able to find them. Do you mind sharing some ideas (from your protocols or in broad generalities only) about dosing of N and R for those who prefer the N+R route as opposed to NR?

Thanks in advance

 

 

My protocol tends to get tweaked on a nightly basis as I try different things with it, but this post is close. The core is--

 

nicotinamide — 1.5g

tryptophan — 1g

ribose — 5g (recently reduced to 3g)

 

Just the nicontinamide + ribose part gives a molar equivalent of 3g of NR.

[stefan_001]

Turnbuckle,
Very glad you are in this thread.... Maybe you did share the specific N and R doses you took in your prior protocols or the current one even. However, I was never able to find them. Do you mind sharing some ideas (from your protocols or in broad generalities only) about dosing of N and R for those who prefer the N+R route as opposed to NR?

Thanks in advance

 

Indeed you should be happy Turnbuckle just ahum "proofed" that NAM by itself produces already more efficiently NAD+ than NR. So you can safe your pennies on buying ribose and just take a lot of NAM. Oh wait, I probably see this wrong again but you folks say that you should take the Ribose so it combines miraculously with NAM into NR first and then coverts to NAD+ ...but now that Turnbuckle just proofed NR is less efficient in boosting NAD+ than NAM I guess that doesnt make sense. So using this valuable reasoning of you folks my feeling tells me there is a even better protocol: deplete yourself of ribose first before taking NAM. Again now that Turnbuckle has ahum "proven" NAM is more efficient in making NAD+ than NR we need to make sure that NAM does not miraculously convert into less efficient NR and reduce the impact of straight NAM conversion....

 

I wish I would just do as I say and enjoy the weekend. Have fun here.

Edited by stefan_001, 23 September 2017 - 11:13 AM.