Niacinamide May Treat ALS (and Stroke)

haidut

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I posted a few studies in the past demonstrating that ALS is a mitochondrial/metabolic disease and as such can be treated with pro-metabolic therapies like thyroid or copper (currently in clinical trials). This new study shows that raising NAD levels with the NAD precursor nicotinamide mononucleotide (NMN) at an HED of about 30mg/kg daily for 30 days dramatically increased survival. More than 80% of the treated rodents were still alive at the point when all untreated rodents had died. The treatment also reduced the muscle wasting and strength decline in the rodents with ALS. The scientists think treatments with NMN (or niacinamide) can also serve as treatment for stroke, which Peat has mentioned before as well and is well supported by numerous studies over the last 50 years.

Btw, the chemical NMN is nothing but a fancier, more expensive NAD precursor similar to the highly marketed nicotinamide riboside (NR). Clinical, these 3 NAD precursor have been shown to be equally effective in raising NAD levels, at about the same doses. So, plain old niacinamide can do everything NMN and NR can do but at a fraction of the cost, and unlike NMN/NR niacinamide is also a SIRT antagonist which has addition benefits for diseases like cancer, estrogen opposition and increasing androgen signalling. Finally, thyroid, methylene blue and quinones like emodin and vitamin K also raise the NAD/NADH ratio.


http://www.cell.com/cell-reports/abstract/S2211-1247(17)31114-2
Researcher closes in on pathways involved in ALS disease

"...Ding and his team first observed that mice lacking the NAMPT enzyme led to progressive loss of weight, hypothermia, motor neuron degeneration, and motor function deficits. Most of these symptoms also are observed in humans with ALS. Then the team treated the mice with a product that regulates NAMPT activity. The molecule is called nicotinamide mononucleotide (NMN) and serves as a substitute for the missing enzymatic product. Mice treated with the NMN molecule exhibited enhanced motor neuron function and overall improved health. Importantly, they demonstrated that NAMPT levels were significantly reduced in the spinal cord. Their discovery indicates that NAMPT is involved in ALS pathogenesis. "What we've shown is that NAMPT is essential to neuronal function and viability," Ding said. "Remarkably, NMN improved health span, restored motor function and extended the lifespan in NAMPT-deficient mice. Based on our findings, it is an ideal candidate for further study, and the possible development of drugs in the diagnosis and treatment of ALS and stroke victims."
 

haidut

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@haidut

What are your thoughts on agmatine? Can it raise NAD levels?

Why would it raise NAD? By what mechanism?
I think it is good at lowering NO, but have not not seen it used for raising NAD.
 

dookie

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Why would it raise NAD? By what mechanism?
I think it is good at lowering NO, but have not not seen it used for raising NAD.

It just appears to have some overlapping effects with the other NAD boosters you talk about. Like it blocks NO, blocks some serotonin nerves, helps kidney function, etc. Doesn't anything which block NO indirectly boost NAD? In terms of safety, would agmatine be equally as safe as niacinamide to try?

Between the NAD "boosters", Niacinamide, Tetracyclines, Vitamin K(2), Emodin, .... (?), How would you rate them in terms of which is more powerful at restoring normalcy to the NAD ratios? (I mean, which is the most powerful in a therapeutic sense, most likely to help)
 

Brother John

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I posted a few studies in the past demonstrating that ALS is a mitochondrial/metabolic disease and as such can be treated with pro-metabolic therapies like thyroid or copper (currently in clinical trials). This new study shows that raising NAD levels with the NAD precursor nicotinamide mononucleotide (NMN) at an HED of about 30mg/kg daily for 30 days dramatically increased survival. More than 80% of the treated rodents were still alive at the point when all untreated rodents had died. The treatment also reduced the muscle wasting and strength decline in the rodents with ALS. The scientists think treatments with NMN (or niacinamide) can also serve as treatment for stroke, which Peat has mentioned before as well and is well supported by numerous studies over the last 50 years.

Btw, the chemical NMN is nothing but a fancier, more expensive NAD precursor similar to the highly marketed nicotinamide riboside (NR). Clinical, these 3 NAD precursor have been shown to be equally effective in raising NAD levels, at about the same doses. So, plain old niacinamide can do everything NMN and NR can do but at a fraction of the cost, and unlike NMN/NR

Hniacinamide is also a SIRT antagonist which has addition benefits for diseases like cancer, estrogen opposition and increasing androgen signalling. Finally, thyroid, methylene blue and quinones like emodin and vitamin K also raise the NAD/NADH ratio.



http://www.cell.com/cell-reports/abstract/S2211-1247(17)31114-2
Researcher closes in on pathways involved in ALS disease

"...Ding and his team first observed that mice lacking the NAMPT enzyme led to progressive loss of weight, hypothermia, motor neuron degeneration, and motor function deficits. Most of these symptoms also are observed in humans with ALS. Then the team treated the mice with a product that regulates NAMPT activity. The molecule is called nicotinamide mononucleotide (NMN) and serves as a substitute for the missing enzymatic product. Mice treated with the NMN molecule exhibited enhanced motor neuron function and overall improved health. Importantly, they demonstrated that NAMPT levels were significantly reduced in the spinal cord. Their discovery indicates that NAMPT is involved in ALS pathogenesis. "What we've shown is that NAMPT is essential to neuronal function and viability," Ding said. "Remarkably, NMN improved health span, restored motor function and extended the lifespan in NAMPT-deficient mice. Based on our findings, it is an ideal candidate for further study, and the possible development of drugs in the diagnosis and treatment of ALS and stroke victims."

Haidut, Thanks very very much for posting these articles. You mentioned copper in treatment of Alz.. Can you share a link on that please? I am googling it too...
Thanks,
Brother John
 

haidut

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Koveras

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Btw, the chemical NMN is nothing but a fancier, more expensive NAD precursor similar to the highly marketed nicotinamide riboside (NR). Clinical, these 3 NAD precursor have been shown to be equally effective in raising NAD levels, at about the same doses. So, plain old niacinamide can do everything NMN and NR can do but at a fraction of the cost, and unlike NMN/NR niacinamide is also a SIRT antagonist which has addition benefits for diseases like cancer, estrogen opposition and increasing androgen signalling. Finally, thyroid, methylene blue and quinones like emodin and vitamin K also raise the NAD/NADH ratio.

Some evidence for what you've been saying...

NR or NMN administered orally are converted to plan old nicotinamide in the liver before accomplishing anything

"Intravenous administration of nicotinamide riboside or mononucleotide delivered intact molecules to multiple tissues, but the same agents given orally were metabolized to nicotinamide in the liver. Thus, flux analysis can reveal tissue-specific NAD metabolism."

Quantitative Analysis of NAD Synthesis-Breakdown Fluxes
 
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