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Sublingual NMN neurotoxic risk?

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#1 stefan_001

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Posted 08 April 2019 - 10:05 AM


Probably not a popular topic here, but perhaps too much NMN in circulation has negative side effects?

 

https://medicine.uio...europathic-pain

 

Brenner’s labs’ latest result—a collaboration with Dr. Richard Goodman’s group at Oregon Health Sciences University—was interesting for two reasons. First, they gained insight into what disturbance in the NAD pathway makes a neuron degenerate. Second, they found an unexpected drug combination that could prove to be more powerful than NR for neuroprotection. In short, they found that two compounds related to NR have opposite effects on a damaged neuron. NMN (NR with a phosphate added to it) is neurotoxic while NAR (NR with an oxygen in place of an amino group) is neuroprotective. By combining a drug that blocks NMN formation with NAR, they can get the NR pathway to make NAD and protect the neuron without making the neurotoxic compound NMN. Dr. Brenner’s group understand these pathways pretty well and are confident to be able to evaluate the drug potential of this combination in relatively short order.


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#2 stefan_001

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Posted 08 April 2019 - 03:41 PM

Folks when you disagree or flag misinformed feel free to shed a light on the topic. Sublingual = NMN into circulation and hence the researchers findings seem relevant:

 

"they found that two compounds related to NR have opposite effects on a damaged neuron. NMN (NR with a phosphate added to it) is neurotoxic while NAR (NR with an oxygen in place of an amino group) is neuroprotective"


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#3 ceridwen

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Posted 08 April 2019 - 04:26 PM

Is NAD also neurotoxic?

#4 able

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Posted 08 April 2019 - 05:31 PM

Is this the study that you reference but neglect to link to?  It  shows that in chemotherapy damaged cells that cannot process  NMN to NAD+, the buildup of NMN can be neurotoxic.

 

That is  not NMN in the bloodstream, but  INSIDE the CELLS.  

 

 

As you know, there is zero debate that once inside a cell, ANY NR MUST CONVERT TO NMN BEFORE BECOMING NAD+.

 

So, please explain how an NR supplement would have any different effect?

 

 

 

 

 


Edited by able, 08 April 2019 - 05:31 PM.

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#5 stefan_001

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Posted 08 April 2019 - 06:34 PM

Is this the study that you reference but neglect to link to?  It  shows that in chemotherapy damaged cells that cannot process  NMN to NAD+, the buildup of NMN can be neurotoxic.

 

That is  not NMN in the bloodstream, but  INSIDE the CELLS.  

 

 

As you know, there is zero debate that once inside a cell, ANY NR MUST CONVERT TO NMN BEFORE BECOMING NAD+.

 

So, please explain how an NR supplement would have any different effect?

 

Well you probably recall something called Slc12a8, the famous direct into the cell NMN transporter? Or are you now saying its insignificant and all NMN first is converted to NR outside the cell? I would see that Slc12a8 path as more force feeding than the NRK path.
 


Edited by stefan_001, 08 April 2019 - 06:37 PM.

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#6 LawrenceW

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Posted 08 April 2019 - 07:38 PM

Is this the study that you reference but neglect to link to?  It  shows that in chemotherapy damaged cells that cannot process  NMN to NAD+, the buildup of NMN can be neurotoxic.

 

 

 

I completely agree with Stefan.  If you have chemotherapy damaged cells, then it is probably not a good idea to take NMN or NR.

 

If you do not find yourself in that unfortunate medical circumstance, then the study provides no reason to discontinue your current NMN routine.


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#7 able

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Posted 08 April 2019 - 09:04 PM

Stefan is trying to imply that there is some risk from NMN that doesn't apply to NR, which is absurd.

 

The study found that the last step conversion from NMN to NAD+ was impaired. 

 

If some NMN supplements build up inside of cells and cause neurotoxicity, NR incur the same risk.

 

After all, NR  MUST convert to NMN inside the cell before NAD+.

 

 

 


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#8 stefan_001

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Posted 08 April 2019 - 09:30 PM

Stefan is trying to imply that there is some risk from NMN that doesn't apply to NR, which is absurd.

 

The study found that the last step conversion from NMN to NAD+ was impaired. 

 

If some NMN supplements build up inside of cells and cause neurotoxicity, NR incur the same risk.

 

After all, NR  MUST convert to NMN inside the cell before NAD+.

 

No it is not the same with NR. Actually the study says that when NAD+ in the cell is low then high levels of NMN cause axon degeneration. Sublingual use of NMN and the Slc12a8 transporter can cause a spike in NMN levels in cells, its a faster pathway than NR. So for example in the very early morning when NAD+ levels are low it could be a risk. IV NMN even more and definitely during disease.
 


Edited by stefan_001, 08 April 2019 - 09:31 PM.

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#9 LawrenceW

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Posted 08 April 2019 - 10:33 PM

Very interesting in how the story has changed.  For years the NR shills were subjecting us to "no NMN gets into the cells".  Now it has changed to too much NMN is getting into the cells too quickly. 

 

 


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#10 able

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Posted 08 April 2019 - 10:44 PM

Very interesting in how the story has changed.  For years the NR shills were subjecting us to "no NMN gets into the cells".  Now it has changed to too much NMN is getting into the cells too quickly. 

 

 

Eh, to be fair, he hasn't decided if he thinks maybe there is too much NMN entering the cells, or, it is too fast.



#11 LawrenceW

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Posted 08 April 2019 - 11:29 PM

Eh, to be fair, he hasn't decided if he thinks maybe there is too much NMN entering the cells, or, it is too fast.

 

Eh, to be fair "Sublingual use of NMN and the Slc12a8 transporter can cause a spike in NMN levels in cells, its a faster pathway than NR." 

 

"spike" sounds like too much

 

"faster" sounds like too fast.

 

Either way, it is a huge change from no NMN getting into the cells.


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#12 Fredrik

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Posted 09 April 2019 - 01:20 AM

Here is the paper referred to in the original post:

 

Abstract

Axon degeneration, a hallmark of chemotherapy-induced peripheral neuropathy (CIPN), is thought to be caused by a loss of the essential metabolite nicotinamide adenine dinucleotide (NAD+) via the prodegenerative protein SARM1.

 

Some studies challenge this notion, however, and suggest that an aberrant increase in a direct precursor of NAD+, nicotinamide mononucleotide (NMN), rather than loss of NAD+, is responsible.

 

In support of this idea, blocking NMN accumulation in neurons by expressing a bacterial NMN deamidase protected axons from degeneration. We hypothesized that protection could similarly be achieved by reducing NMN production pharmacologically. To achieve this, we took advantage of an alternative pathway for NAD+ generation that goes through the intermediate nicotinic acid mononucleotide (NAMN), rather than NMN.

 

We discovered that nicotinic acid riboside (NAR), a precursor of NAMN, administered in combination with FK866, an inhibitor of the enzyme nicotinamide phosphoribosyltransferase that produces NMN, protected dorsal root ganglion (DRG) axons against vincristineinduced degeneration as well as NMN deamidase."

 

From Discussion

"Taken together, our results largely support the idea that NMN promotes axon degeneration. Depressing levels of NMN confers axon protection even in the face of lower NAD+ levels"

 

https://www.pnas.org...392115.full.pdf

 

 

 

 

 

 



#13 Phoebus

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Posted 09 April 2019 - 02:06 AM

I completely agree with Stefan.  If you have chemotherapy damaged cells, then it is probably not a good idea to take NMN or NR.

 

If you do not find yourself in that unfortunate medical circumstance, then the study provides no reason to discontinue your current NMN routine.

 

 

that is a fair point 

 

However there could be many circumstances that create a similar effect of chemo damage to cells 

 

In other words what exactly is the chemo doing to the cell that causes NMN to be toxic to it? And furthermore are there other things that could duplicate that?

 

Really seems like NAD+ powder sublingual is the way to go to simply eliminate all these problems that realistically we just don't have the data to solve right now.  


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#14 Fredrik

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Posted 09 April 2019 - 12:41 PM

that is a fair point 

 

However there could be many circumstances that create a similar effect of chemo damage to cells 

 

In other words what exactly is the chemo doing to the cell that causes NMN to be toxic to it? And furthermore are there other things that could duplicate that?

 

Really seems like NAD+ powder sublingual is the way to go to simply eliminate all these problems that realistically we just don't have the data to solve right now.  

 

Why would sublingual NAD+ be "the way to go"? What human data is there on sublingual NAD+ powder do you mean? 



#15 Phoebus

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Posted 09 April 2019 - 01:57 PM

Why would sublingual NAD+ be "the way to go"? What human data is there on sublingual NAD+ powder do you mean? 

 

None! AT least none that I know of. Which is the whole issue, there is so little data about all of this we are all just stumbling in the dark. 

 

My experience with NAD+ sublingual with enhanced dermal penetration methods has been excellent so far. Of course that is N=1, subjective, etc. 

 

All I'm saying is that delivering NAD+ direct to the bloodstream will sidestep all of these issues regarding "this is the best NAD precursor! NO, this one is better and that other one is terrible and will do terrible things to you!"

 

Why mess around with precursors if you can just get NAD? 


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#16 Fredrik

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Posted 09 April 2019 - 03:33 PM

None! AT least none that I know of. Which is the whole issue, there is so little data about all of this we are all just stumbling in the dark. 

 

My experience with NAD+ sublingual with enhanced dermal penetration methods has been excellent so far. Of course that is N=1, subjective, etc. 

 

All I'm saying is that delivering NAD+ direct to the bloodstream will sidestep all of these issues regarding "this is the best NAD precursor! NO, this one is better and that other one is terrible and will do terrible things to you!"

 

Why mess around with precursors if you can just get NAD? 

 

Why mess around with NAD when you can give the body precursors?

 

I feel more comfortable letting my body decide in WHAT cells, WHEN and HOW much NAD to produce by ensuring enough precursors are there when needed.
 
Not by flooding the system with ready made NAD and completely sidestepping all the enzymatic limitations, negative feedback mechanisms, and other cellular gatekeepers that evolution probably set up to be there for a reason.

Edited by Fredrik, 09 April 2019 - 03:34 PM.

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#17 Fredrik

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Posted 09 April 2019 - 06:04 PM

So it is "ill informed" to lean toward trying orally available precursors with human safety data vs chomping down some unregulated untested NAD-powder with zero proof of efficacy or oral bioavailability? Lol.

 

The FDA did not allow NAD to be used by compounding pharmacies because of the lack of efficacy data and inherent problems with stability.

 

On the other hand there are readily available prescription drugs and non-prescription NAD-precursors with GRAS status such as nicotinic acid, niacinamide, nicotinamide riboside, acipimox and l-tryptophan (the human safety data of NMN is yet to be published but will be this year, according to David A Sinclair). 


Edited by Fredrik, 09 April 2019 - 06:20 PM.

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#18 ceridwen

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Posted 09 April 2019 - 06:43 PM

These sort of things seem to have given me shoulder tendonitis. I didn't even know it was possible to get tendonitis there. It's called an impediment and I had a local anaesthetic and a cortisol shot in my shoulder this morning. I had been taking a lot of sublingual NAD. Trying for 8 tabs a day. Obviously too much for me. Any advice as to what I should do now as far as NAD is concerned?
Should I stop taking NAD?

#19 able

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Posted 09 April 2019 - 07:01 PM

 

 

The FDA did not allow NAD to be used by compounding pharmacies because of the lack of efficacy data and inherent problems with stability.

 

 

How are compounding pharmacies regulated by the FDA?

 

I thought products that exist in nature, like NR,NMN, NAD are allowed to be freely sold.  

 

Do they have more regulation for such products than everyone else?


 

 inherent problems with stability.

 

 

Do you mean, degradation when taken as capsules?   Other than stomach acid environment, I thought it was inherently more stable than NMN or NR, which is why ABN can sell it in liquid form, but NMN and NR can not.


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#20 Fredrik

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Posted 09 April 2019 - 08:23 PM

No. I meant unstable under storage conditions. According to the FDA, there is no pharmacokinetic data on oral NAD in humans. NAD seems to be legal to compound by pharmacies but not recommended in FDAs review of compounded NAD as an answer to a request to use it to treat MS-related fatigue.

 

ABN wants to sell products and I would not trust them as a source of any information regarding NAD-precursors without verifying that data from other sources. When Alive By Nature were allowed to sell NR they were over the moon for this molecule. When they were dropped by Chromadex (only LEF and Thorne can sell Niagen under their brands) then NMN and NAD were the best things ever.

 

This is the FDAs decision from 31 march 2017, page 16 of 330:

 

"We have balanced the criteria described in section II above to evaluate NAD for the 503A Bulks List. After considering the information currently available, a balancing of the criteria weighs against NAD being placed on that list based on the following:

 

1. NAD is well characterized physically and chemically. However, it is susceptible to substantial degradation when exposed to light, moisture, alkaline pH, or standard room temperatures. Unless multiple compensatory measures to improve its stability are implemented, NAD will likely be unstable when compounded in a capsule, the proposed dosage form.

 

2. Nonclinical data found in the literature are inadequate to characterize the potential toxicity profile for NAD, particularly for use in a chronic disease such as MS. Similarly, we did not find sufficient clinical data about NAD to evaluate whether it is safe for use in compounded drug products.

 

3. We found no published information regarding the clinical evaluation of the use of NAD supplementation in the treatment of MS-related fatigue or MS. Therefore, we have insufficient information on the efficacy of NAD to support the nominated use.

 

4. Information is insufficient to determine the length or extent of historical use of NAD in compounded drug products. Based on internet searches, NAD appears to be available as a compounded product in both topical and intravenous forms. Based on the information the Agency has considered, as described above, a balancing of the four evaluation criteria weighs against NAD being added to the 503A Bulks List.

 

https://www.fda.gov/...e/ucm553368.pdf


Edited by Fredrik, 09 April 2019 - 08:42 PM.

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#21 Phoebus

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Posted 09 April 2019 - 08:45 PM

But what is their basis for claiming "it is susceptible to substantial degradation when exposed to light, moisture, alkaline pH, or standard room temperatures"?

 

Like its just a claim hanging there, where is the reference? Just because someone at the FDA claims something does not mean its accurate. 

 

EDIT:

 

okay now I see, they conflated NAD+ and NADH and are treating them as the same molecule. There really is no data on how stable NAD+ itself is, only NADH 

 

From this data here the worst thing that happens to your NAD+ powder is that it converts to nicotinamide mononucleotide (NMN) and adenosine monophosphate (AMP) 

 

 

NADH is extremely reactive and can oxidize very rapidly when exposed to air. Degradation also happens very quickly upon exposure to light and heat (Wu et al. 1986). At 41°C, the half-life of NADH in pure water is 400 minutes at pH 6 and 5.5 minutes at pH 4. It is easily oxidized to generate hydrogen peroxide and nicotinamide adenine dinucleotide (NAD),2 which can then be further degraded into nicotinamide mononucleotide (NMN) and adenosine monophosphate (AMP) (Benofsky et al. 1982). According to Sigma-Aldrich product information,3 the solid form of NADH should be stored at -20 °C, protected from air and light, and desiccated. Aqueous solutions of NADH are even more unstable than the solid form of NADH. Acidic and basic conditions can accelerate the degradation.

 


Edited by Phoebus, 09 April 2019 - 08:50 PM.


#22 able

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Posted 09 April 2019 - 09:16 PM

It sounds like someone was trying to get it approved for use in treating  MS. 

 

FDA was concerned it might degrade by x% when sitting on a shelf for x months.  So a patient might get a product that is partially degraded to NMN.

 

Which is a problem when buying from a pharmacy and taking in place of a prescription drug, but not much of  a concern when taking a supplement.  


Edited by able, 09 April 2019 - 09:28 PM.

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#23 Fredrik

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Posted 09 April 2019 - 10:03 PM


 

 

okay now I see, they conflated NAD+ and NADH and are treating them as the same molecule. There really is no data on how stable NAD+ itself is, only NADH 

 

From this data here the worst thing that happens to your NAD+ powder is that it converts to nicotinamide mononucleotide (NMN) and adenosine monophosphate (AMP) 

 

 

 

What do you mean? They don´t treat them as the same molecule. They review both NAD (page 15) and NADH (page 31) separately and rejects both as compounded ingredients on their recommended list. 


Edited by Fredrik, 09 April 2019 - 10:03 PM.


#24 Phoebus

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Posted 09 April 2019 - 10:39 PM

 

 

What do you mean? They don´t treat them as the same molecule. They review both NAD (page 15) and NADH (page 31) separately and rejects both as compounded ingredients on their recommended list. 

 

 

okay my bad, I'm reading thru it and looking at the references now. 



#25 Michael

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Posted 12 April 2019 - 03:07 PM

Sometimes, I think discussion forums must induce memory impairment in most people.

 

We've discussed this before, in scientific detail and far less silliness.



#26 stefan_001

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Posted 12 April 2019 - 05:26 PM

Sometimes, I think discussion forums must induce memory impairment in most people.

 

We've discussed this before, in scientific detail and far less silliness.

 

Any views on the tittle on the thread "sublingual NMN neurotoxic risk"  dont think it has been discussed?
 


Edited by stefan_001, 12 April 2019 - 05:30 PM.

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#27 able

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Posted 12 April 2019 - 07:21 PM

Any views on the tittle on the thread "sublingual NMN neurotoxic risk"  dont think it has been discussed?
 

 

You agree that if there is any risk from exogenous NAD+ precursors to increase neurotoxicity in chemo patients, NR would have the exact same risk as NMN?

 

So your only reason for starting this thread was to imagine that the increased effectiveness of sublingual delivery  (of NMN AND NR) might increase this theoretical neurotoxic risk in chemo patients?



#28 stefan_001

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Posted 12 April 2019 - 08:56 PM

You agree that if there is any risk from exogenous NAD+ precursors to increase neurotoxicity in chemo patients, NR would have the exact same risk as NMN?

 

So your only reason for starting this thread was to imagine that the increased effectiveness of sublingual delivery  (of NMN AND NR) might increase this theoretical neurotoxic risk in chemo patients?

 

No the study says that an accumulation of NMN in cells while NAD+ is low is neurotoxic. In chemo that comes from the treatment. However spiking NMN in the bloodstream, in my view, could lead to the same result in particular when the NAD+ is low during the circadian cycle. Whether that is a possibility in real remains open. Fact is a lot of people here state they use NMN sublingual and that the pure powders dissappear super fast from under the tongue.

 

If you believe there is no NMN transporter then yes NR and NMN should be similar but well you, Lawrence and others have claimed and at least one study has shown NMN enters the cells directly.

 

Are you now saying that contrary to other posts that using NMN can have at best the same effect as using NR because it has to convert to NR?

 

And even if that is the case would you agree that using NMN sublingual may cause a neurotoxic reaction?

 

 

 

 


Edited by stefan_001, 12 April 2019 - 09:16 PM.

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#29 able

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Posted 12 April 2019 - 10:01 PM

No the study says that an accumulation of NMN in cells while NAD+ is low is neurotoxic. In chemo that comes from the treatment. However spiking NMN in the bloodstream, in my view, could lead to the same result in particular when the NAD+ is low during the circadian cycle. Whether that is a possibility in real remains open. Fact is a lot of people here state they use NMN sublingual and that the pure powders dissappear super fast from under the tongue.

 

If you believe there is no NMN transporter then yes NR and NMN should be similar but well you, Lawrence and others have claimed and at least one study has shown NMN enters the cells directly.

 

Are you now saying that contrary to other posts that using NMN can have at best the same effect as using NR because it has to convert to NR?

 

And even if that is the case would you agree that using NMN sublingual may cause a neurotoxic reaction?

 

Wow - you really dont understand?

 

A roadblock to the last step conversion to NAD+ which results in a buildup of NMN inside a cell would not be any different if the origional source was NMN or NR.  

 

NR MUST go thru NMN before NAD+

 

Trying to imply that NMN could be more risky than NR because of this is ridiculous.

 

The route it takes before entering a cell has zero impact on what happens to the molecule once inside a cell.

 

The pathway, slc12a8, sublingual NMN, or NMN/NR/NAM from the liver, does not change what happens once the molecule is inside a cell.

 
 

 

As for Slc12a8 - I do believe Dr Sinclairs peer reviewed research which very clearly prove SOME NMN may use the SLC12a8 to enter cells in the small intestine to increase NAD+ there, totally bypassing NR.

 

I dont think there is any indication at all if that is a significant or trivial amount of NMN.  

 

But that applies to NMN capsules, so bringing that into your argument about sublingual NMN is 100% irrelevant, which  is why ignored it earlier.

 

 

NMN or NR would follow the same exact pathway inside a cell.


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#30 stefan_001

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Posted 12 April 2019 - 10:24 PM

@able your comment about route is nonsense, ofcourse that has an influence. The NRK expression in a cell varies and it has been shown to be more stronger expressed for cells that need it and is as such a regulated path to transport NR into the cell where it get converted to NMN unless there is a rate limiting factor inside the cell. No NRK expression means no matter how much NR you pop it will not enter the cell.

 

NMN with the direct transporter skips a few conversion steps and is therefore more able to spike NMN inside the cell.

 

I dont think sinclair has investigated the expression of SLC12a8 in all the various cell types or has investigated how expression varies based on needs. The SLCs are common transporters of cell needs so their expression may be driven by other factors which are not in sync by NAD+ needs. For sure this is more relevant to sublingual than oral capsules. You bring NMN directly into the bloodstream and with the SLCs it get straight into the cell which may lead to the neurotoxic reaction if at the same time NAD+ is low.

 

You are always so defensive of NMN, makes one wonder.

 

 

 

 


Edited by stefan_001, 12 April 2019 - 10:30 PM.

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