Niacinamide Reverses / Cures Duchenne Muscular Dystrophy

haidut

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It is well known even in mainstream medical circles that autoimmune conditions are characterized by greatly reduced levels of NAD. I posted a few studies in the past showing that raising NAD levels through supplementation of niacinamide can help virtually any autoimmune condition.
This study takes the research a step further and suggests that even myopatic conditions maybe be due to NAD depletion and restoring NAD levels is therapeutic for those conditions. The study focused on the Duchenne dystrophy, but the principle is generic enough to apply to other conditions such as ALS, myasthenia gravis, Huntington disease, etc. What is even more amazing is that Duchenne is considered to be a genetic disorder, and as such largely untreatable. Until now, that is :):
So much for genetics being your destiny...

NAD+ repletion improves muscle function in muscular dystrophy and counters global PARylation | Science Translational Medicine
http://medicalxpress.com/news/2016-10-vitamin-duchenne-muscular-dystrophy.html

"...Johan Auwerx's team showed that the disease leads to a second cycle of events inside the cells, a series of reactions that exacerbate the disease's damaging effects. Several processes are at work in the second cycle. First, the 'primary' inflammation overactivates a certain gene, which then consumes a large quantity of an essential component called NAD+. This causes a shortage of NAD+ within the cell. But this component acts as a fuel for the powerhouse of cells, the mitochondria, which are especially important in muscle tissue. The NAD+ deficiency therefore weakens the muscle, an effect similar to that of mitochondrial deficiency in older people. Yet the consequences are even worse than they appear. Deprived of energy, the dysfunctional mitochondria aggravate the inflammation that causes muscle loss. So much for what could have initially appeared to be just a minor side effect of the disease."

"...What if it were possible to reduce muscle inflammation - and thus muscle loss - by providing the worn-out mitochondria with fuel? That would mean administering nicotinamide riboside, the vitamin precursor of NAD+. This is the hypothesis that the researchers wanted to test after having already successfully investigated this vitamin's effect on muscle aging in their work on nutrition. They tried out their approach on animals, using C. elegans worms and mice that had been genetically modified to develop the disease. The effect was remarkable. When large doses of nicotinamide riboside were administered, the worms did not develop any of the disease's symptoms. The mice presented much lower muscular inflammation, and existing lesions were attenuated. "We have good reason to think that humans will also respond to this treatment and that we'll be able to reduce inflammation," said Auwerx, the lead author. "But we don't know to what extent. It's important to remember that we're not going after the primary cause of the disease, dystrophin deficiency." Which means it is difficult to predict the treatment's effectiveness. "Regardless, it would still be quite an accomplishment if we can prolong the patient's life by several years and increase their comfort."
 

Tarmander

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I have an auto immune and niacinamide has really stood the test of time. My regiment has changed around quite abit but I always take a little B3 each day.
 

Dante

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. First, the 'primary' inflammation overactivates a certain gene, .."
@haidut , this might sound little stupid but since methyl donors silence genes ( i know you are not a fan of methylation but it has it's place e.g the agouti mice study where prenatal nutrition destroyed the inheritance/genetics dogma kind of like what leonell strong did) so would adding a bit of methyl donors like Me-cobalmin can help in silencing this overacting gene ?
 

haidut

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@haidut , this might sound little stupid but since methyl donors silence genes ( i know you are not a fan of methylation but it has it's place e.g the agouti mice study where prenatal nutrition destroyed the inheritance/genetics dogma kind of like what leonell strong did) so would adding a bit of methyl donors like Me-cobalmin can help in silencing this overacting gene ?

How do you know that it will silence only that gene? If there was a drug that selectively delivered methyl groups only to that gene I would consider it, but there isn't AFAIK. Also, given the role of methylation in cancer and neurodegenartive conditions I would not mess with it. Methionine restriction is one of the few proven ways to extend maximum lifespan and greatly reduce risk of "aging" diseases like cancer and dementia. Niacinamide and glycine are methyl sinks, so this is probably a major reason behind their beneficial effects.
Just my 2c.
 

burtlancast

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Good news.
But Big Pharma will never allow a clinical trial for ANY vitamin to show improvement for ANY medical condition.
They will cancel the human clinical trials or rig them.

Because once a substance is officially deemed safe and effective for the treatment of a medical condition, the legislation allows doctors to use it potentially for ANY OTHER medical condition they see fit, without the opposition of any other organization being possible, unless it can prove the said utilization is detrimental to the patient.
That's we call OFF LABEL usage.Off-label use - Wikipedia

This is how once DMSO got approved for interstitial cystitis, independent cancer clinics started using it for cancer.
Or how DMSA began being used to chelate mercury once it was deemed safe for lead detoxification.
 

High_Prob

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How do you know that it will silence only that gene? If there was a drug that selectively delivered methyl groups only to that gene I would consider it, but there isn't AFAIK. Also, given the role of methylation in cancer and neurodegenartive conditions I would not mess with it. Methionine restriction is one of the few proven ways to extend maximum lifespan and greatly reduce risk of "aging" diseases like cancer and dementia. Niacinamide and glycine are methyl sinks, so this is probably a major reason behind their beneficial effects.
Just my 2c.


Haidut - Is Hydrogen Peroxide generation due to Methyl consumption something to be concerned about?

https://www.ncbi.nlm.nih.gov/pubmed/22971213
 

haidut

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Haidut - Is Hydrogen Peroxide generation due to Methyl consumption something to be concerned about?

Excessive nicotinic acid increases methyl consumption and hydrogen peroxide generation in rats. - PubMed - NCBI

The study used both niacin and niacinamide. As you can see, only niacin led to increase H2O2 generation and niacinamide did not. Moreover, the doses used were absolutely massive - the lowest dose niacin used was 500mg/kg, which would equate to about 7g for a human. The higher doses are just mind boggling and unrealistic. The niacinamide was in doses of 2,000mg/kg, which corresponds to about 30g for a human, which is insanely high, and it still did not raise H2O2 or deplete glycogen. So, in the 1g -2g doses (or lower) that seems to be the upper limit for most users on the forum niacinamide is even less likely to cause any issues.
Oh, and niacin depleted liver glycogen while niacinamide increased it. Yet another example of the different effects these two substances have. Finally, niacin caused hyperinsulinemia while niacinamide did not.
"...Nicotinic acid decreased rat liver glycogen contents in a dose-dependent manner. In contrast, nicotinamide increased liver glycogen content. High cumulative nicotinic acid exposure showed a high level of plasma insulin."
 
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TubZy

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Thanks haidut, it could also be more effective with the niacinimide + MB stack for increasing NAD.
 

sladerunner69

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Thanks haidut, it could also be more effective with the niacinimide + MB stack for increasing NAD.

Are you concerned that niacinimide will cause you to burn off your glucose to quickly? In combination with all of the other metabolic boosters you take I figure it would be all but impossible to consume enough glucose to keep your levels up.
 

Texon

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Methylation is a tricky issue, and I don't do well with methyl donors generally. For lowering homocysteine though, nothing seems to beat beet powder or daily doses of trimethylglycine for example. I absolutely cannot tolerate supplemental methyl folate, but historically I tend towards homocysteine levels of 13-16. I can intermittently tolerate methyl b12. The only thing that has helped to lower the number to 11 recently has been daily tmg powder (Jarrow in this case) of about 500 mgs/day which is pretty much the max for me. Any more than that makes me feel wired like crazy. This is a manifestation of a couple of COMT ++ snps which severely hamper breakdown of catecholamines. If anyone has a different approach, please share.
 

haidut

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Methylation is a tricky issue, and I don't do well with methyl donors generally. For lowering homocysteine though, nothing seems to beat beet powder or daily doses of trimethylglycine for example. I absolutely cannot tolerate supplemental methyl folate, but historically I tend towards homocysteine levels of 13-16. I can intermittently tolerate methyl b12. The only thing that has helped to lower the number to 11 recently has been daily tmg powder (Jarrow in this case) of about 500 mgs/day which is pretty much the max for me. Any more than that makes me feel wired like crazy. This is a manifestation of a couple of COMT ++ snps which severely hamper breakdown of catecholamines. If anyone has a different approach, please share.

Actually, high homocysteine seems to be mostly due to vitamin B6 deficiency. No need to supplement with methyl donors or folic acid and whatnot. Takign even 5mg P5P daily can bring homocysteine down by 40%+.
Pyridoxal-5'-phosphate deficiency is associated with hyperhomocysteinemia regardless of antioxidant, thiamine, riboflavin, cobalamine, and folate s... - PubMed - NCBI
Vitamin B-6 Supplementation Could Mediate Antioxidant Capacity by Reducing Plasma Homocysteine Concentration in Patients with Hepatocellular Carcin... - PubMed - NCBI
High homocysteine, low vitamin B-6, and increased oxidative stress are independently associated with the risk of chronic kidney disease. - PubMed - NCBI
 

Texon

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I've never seen p5p for this. I'll definitely try it and post results.
 

Amazoniac

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I've [..] checked the Niacin book by Hoffer, it's actually sustained-release niacin that's hepato toxic, not niacinamide.

"Sustained-, extended-, and time-release niacin are often advertised as not causing a flush at all. This claim may not be completely true; sometimes the flush is just postponed. It may be difficult to determine your optimum level with an extended-, sustained-, or time-release product. All three are also more costly. But the biggest reason to avoid sustained-release niacin is that relatively more reports of side effects stem from use of that form. 7A 2007 review by Guyton and Bays of many niacin therapy studies reveals that regular (“ immediate release,” or IR) niacin is quite safe; extended- or time-release are safe, but unnecessarily pricey, and sustained release (SR) has the most side effects. They write: Shortly after Altschul and colleagues described cholesterol lowering by niacin in 1955, sustained-release (SR) formulations were developed in an attempt to reduce flushing. However, these were quickly found to be hepatotoxic in some patients. . . . Henkin et al. 19found 8 cases of hepatitis in 15 patients using SR niacin, compared with none in 67 patients using regular niacin. Three patients who had experienced hepatitis with SR niacin were subsequently able to tolerate equal or higher doses of regular niacin. 20McKenney et al. 3directly compared IR and SR niacin in a randomized clinical trial with dosage escalation from 500 to 3,000 mg/ day over a period of 30 weeks. None of the 23 patients taking IR niacin developed hepatotoxic effects, whereas 12 of 23 patients (52%) taking SR niacin did. The increase in liver toxicity with SR niacin mainly occurred with doses 1,500 mg/ day. "

*Wrong thread. Could any divine force move this post to Niacinamide Or Just Plain Niacin?
 
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