So I take Niacin 250 mg time released per the Augusta study to reduce inflammation through binding to the GPR109A researchgate.net/publicatio....
NAD+ is disrupted in PD patients "Progresses in both basic research and clinical trials of NAD+ in Parkinson's disease" 2021 pubmed.ncbi.nlm.nih.gov/339...
This study shows NAD+ normalized in these adult onset mitochondrial myopathy patients using Niacin. They were taking 750-1000 mg a day "All the subjects were supplemented with a slowly increasing dose of niacin, from 250 mg/day up to 750
or 1,000 mg/day for 4 months, and we continued the follow-up of treatment effect up to 10 months in patients" cell.com/cell-metabolism/pd...
"Niacin Restores NAD+ Concentrations in PEO Patients Niacin supplementation increased muscle NAD+ content 1.3- and 2.3-fold in patients compared with baseline after 4 and 10 months, respectively, and in the later time point NAD+ levels had reached the healthy control values (Figure 1B). In controls, muscle NAD+ content did not change, suggesting that steady-state NAD+ levels are tightly controlled in skeletal muscle (Figure 1B). Niacin supplementational so remarkably elevated whole blood NAD+concentrations both in patients (7.1-fold compared to baseline) and controls (5.7-fold) after 4 months (Figure 1C). The blood NAD+ concentrations reached an 8.2-fold increase compared to baseline after 10 months of supplementation in patients (Figure1C). The concentrations of all NAD+ metabolites increased in the blood of both patients and controls (Figures 1C–1H). Given that niacin increased the levels of muscle and blood NAM (Figures 1G and S2B) and ADP-ribose (Figure 1H), niacin was likely metabolized as NAM via salvage pathway instead of Preiss-Handler pathway, and it was effectively utilized by NAD+ consuming enzymes. The evidence indicates that niacin is a powerful NAD+ booster in humans, both healthy and diseased."
So... I'm guessing I am getting some NAD+ benefit at 250 mg of timed release Niacin. Would I get more NAD+ benefit AND still reduce inflammation at 750-1000 mg of immediate release Niacin? Something to figure out.
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IMO It is thought that vitamin B3 niacin reaches the various parts of the body evenly but this is not always the case, so higher doses are needed occasionally. On the other hand, if you increase the b3NA niacin you have to do it very gradually and increase the vitamin C and all the others in a proportionate way including minerals Ca ++ and magnesium and for a short period, let's say a few days then pause. With the high doses of b3na (more than 500mg up to 3000mg) it's the stuff of supplementation professionals I wouldn't do it if you don't know the subject, but you can learn everything. In my opinion it's the stuff of a professional athlete.
My advice is not to use the slow release forms compared to the normal form of niacina flush type at the same dose of 250 mg and get used to having a little flushing at the beginning and supplementing with all multi vitamins and minerals in low doses, eat fresh vegetables and fruit to get active after taking niacin so even in medium doses it will circulate in the body much better and evenly in all organs.
Niacin is a methyl group scavenger. It eats up methyl groups from the following :
Methionine
Choline
TMG (Betaine or Trimethylglycine)
DMG (Dimethylglycine)
Sarcosine (Methylglycine – a weak donor)
SAMe
MTHF
Methylcobalamin
DMSO
MSM
If you take any of the above supplements with niacin then you have probably not getting benefits of taking these supplements because Niacin flushing them down to the urine.
Niacin ruins DNA methylation. Niacin is specifically bad for people with MTHFR snips which I could say most of PWPd are.
To balance methylation better to use glycine .
If your methylation affected then you cannot make dopamine and you cannot get ride of it. Thousands of biochemical reactions in your body starts malfunctioning.
📍📍Methyl group:
Carbon + 3 hydrogens (CH3)
📍📍Methyl donor:
a substance that is capable of donating a methyl group to another compound. Simply because something has a ‘methyl group’ does not mean it can donate it.
Methylation:
The act of giving a methyl group to another compound altering its chemical structure thereby changing it to something else. This is a carefully orchestrated transfer from one compound to another which requires an enzymatic process.
📍📍Methylation examples:
Uracil + CH3 = Thymine
Histamine + CH3 = N-methylhistamine
Homocysteine + CH3 = Methionine
Norepinephrine + CH3 = Epinephrine
Serotonin + Vitamin B5 + CH3 = Melatonin
Guanidoacetate + CH3 = Creatine
📍📍Methyl donors:
Methionine
Choline
TMG (Betaine or Trimethylglycine)
DMG (Dimethylglycine)
Sarcosine (Methylglycine – a weak donor)
SAMe
MTHF
Methylcobalamin
DMSO
MSM
📍📍Not Methyl donors:
Caffeine
CoQ10 (any type)
Serine
Glycine (but can support methylation indirectly by increasing creatine synthesis)
Melatonin
Folinic acid
DIM (diindolemethane)
I3C (indole-3-carbinol)
📍📍Methyl conserving:
Creatine
Phosphatidylcholine
Carnitine
Melatonin
📍📍Methyl burning:
Niacin
Estrogen
Stress
Arsenic
Histamine
Lysine
Methyl blocking:
Homocysteine
Nitrous oxide
Mercury
Copper
Cadmium
Aluminum
Lead
Acetylaldehyde (from yeast and alcohol)
Hydrogen peroxide (a free radical / oxidative stress)
Nitric oxide (product of NOS enzyme)
TNF alpha (inflammation)
IL-6 (inflammation)
LPS (bacterial infections)
📍📍Methyl Trapping:
When methylfolate and methylcobalamin cannot join forces and meet together.
This is typically caused by ‘methyl blocking’ or a deficiency of one or the other (methylfolate or methylcobalamin)
This can falsely elevate serum folate and/or serum cobalamin
Methylation is as complex as quantum physics. All epigenetic alternations are controlled by methylation.
DNA methylation is an epigenetic mechanism that occurs by the addition of a methyl (CH3) group to DNA, thereby often modifying the function of the genes and affecting gene expression. ... These methyl groups project into the major groove of DNA and inhibit transcription.
Thanks Kia17. This methylation info is interesting. I won't let it prevent my trying a protocol, but good to take into account when making decisions. Good thing I take MSM too (I need to take it more often).
“Falsely” because there are elevated methylFolate and methylCobalamin in the blood but they are not functional due to various reasons including low glutathione level or because of heavy metals presence or deficiency in either one of methyfolate or methylcobalamin.
Kia -- do you mean hear that if I take niacin, it can cause high serum cobalamin? I've recently (after starting niacin) had high B1, B6 and B12 in a blood test. Can this be a result of taking niacin?
Thanks. That seems pretty low. I know the Auburn study used 250 slow release and they did not seem worried about it. Not that you should not check this out. I take 250 mg time released, but I never get my blood tested. Good luck.
In my understanding it could be. There should be a balance between B12 and B9 intake . folate (not serum folate) should be measured as well as homocysteine to see if any of these are the case.
Folate in red blood cell is much more accurate than serum folate.Folate can also be measured as the amount in the red blood cells. This test may be a better way than the plasma test to measure the amount of folate stored in the body. The amount of folate in red blood cells measures the level when the cell was made, as much as 4 months earlier.
See this link: if you haven’t done genetic testing with 23&me or AncestoryDNA, here is the best place to do that. There are lots of useful information in the website.
Niacin-mediated rejuvenation of macrophage/microglia enhances remyelination of the aging central nervous system 2020 link.springer.com/article/1...
Remyelination following CNS demyelination restores rapid signal propagation and protects axons; however, its efficiency declines with increasing age. Both intrinsic changes in the oligodendrocyte progenitor cell population and extrinsic factors in the lesion microenvironment of older subjects contribute to this decline. Microglia and monocyte-derived macrophages are critical for successful remyelination, releasing growth factors and clearing inhibitory myelin debris. Several studies have implicated delayed recruitment of macrophages/microglia into lesions as a key contributor to the decline in remyelination observed in older subjects. Here we show that the decreased expression of the scavenger receptor CD36 of aging mouse microglia and human microglia in culture underlies their reduced phagocytic activity. Overexpression of CD36 in cultured microglia rescues the deficit in phagocytosis of myelin debris. By screening for clinically approved agents that stimulate macrophages/microglia, we have found that niacin (vitamin B3) upregulates CD36 expression and enhances myelin phagocytosis by microglia in culture. This increase in myelin phagocytosis is mediated through the niacin receptor (hydroxycarboxylic acid receptor 2). Genetic fate mapping and multiphoton live imaging show that systemic treatment of 9–12-month-old demyelinated mice with therapeutically relevant doses of niacin promotes myelin debris clearance in lesions by both peripherally derived macrophages and microglia. This is accompanied by enhancement of oligodendrocyte progenitor cell numbers and by improved remyelination in the treated mice. Niacin represents a safe and translationally amenable regenerative therapy for chronic demyelinating diseases such as multiple sclerosis.
I am having a problem reconciling Kia17’s comment that “Niacin ruins DNA methylation. Niacin is specifically bad for people with MTHFR snips which I could say most of PWPd are” and “Niacin represents a safe and translationally amenable regenerative therapy for chronic demyelinating diseases” in Bolt’s recent post. I take Niacin together with Butyrex so am interested in whether Niacin’s apparent benefits are outweighed by its risks.
Doctors Best sustained release low flush Niacin 500mg with .Niaxtend - I take one per day in the evening. Butyrex 600mg x 3 in the morning from T E Neesby contains Calcium 400mg, Magnesium 240 mg and Butyric Acid 3.6g. I only started taking this combo when I read about it in Parkinsons News (UK) and I had just migrated from Agonists (Ropinirole) to a combination of that and C0-Careldopa and was having bad digestive issues. Of course `I don’t know whether this combo is responsible but all I can say is that something has returned my system to my pre-diagnosis state. My concern was because amongst the supplements recommended to me to deal with my imbalances after I spent 3 weeks at a clinic in Denver being analysed ,tested etc etc , were CoQ10 and Methylcobalamin. Butyrex and Niacin were not part of the clinic’s recommendations. So I was a trifle concerned at the likelihood that Niacin might be wiping out 2 of the supplements i had been advised to take. However my combo seems to be very beneficial to me and I have been on it for 12 months or more. I was on the clinic supplements since 2017 but I can’t pin down any tangible benefits from them - But who knows - maybe - without them I’d feel worse? (For completeness the issues Denver addressed were low B12, DHEA, Vit D, Zinc and Thiamine) and their recommended supplements included Resveratrol 100mg per day I’ve stopped that and feel no worse, D3/K2 560 mg per day - still on it but no idea if it benefits me, and a B Complex containing the B12 Methylcobalamin.The result of my high prescribed meds (Rasagiline 1mg 1 x day, Ropinirole 32 mg all in morning, and Co-Careldopa 37.5 mg 3 x per day, -all my choice) and the supplements I take, I feel good. I am a little slow and get fatigue after meals (but only up to mid after noon). I do a lot of serious work out exercise. My handwriting has improved greatly. I am told that none of my family and friends notice any abnormality and even question my diagnosis (if only!). I haven’t developed any addictions (though I think my interest in sex is increased but without the performance capability of youth! But I am nearly 74). This contrasts to my state at diagnosis - here are some examples - walking discontinuity and ungainly lack of balance - I can now stand on one leg on a semi spherical device for a minute of more - breathlessness -now I would say 80% normal - fine movement almost normal - I’m sure deterioration will come sooner or later so I just deal with the present. My biggest issue is poor sleep - I was a 4 - 5 hours a night person when working but now my sleep is shallow and short. I am getting better as I train myself into a better pattern and prepare so that the circumstances for sleep are optimum. But you don’t need to hear al this. I just thought context might assist.
Keep up the good work guys, I find the intelligent approach of this forum very stimulating, helpful and the discussion keeps me on track.
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Bilateral MR-Guided Focused Ultrasound Pallidothalamic Tractotomy for Parkinson's Disease With 1-Year Follow-Up. Published Feb 9, 2021
Encouraging results from the phase-I trial! The NADPARK study: A randomized phase I trial of nicotinamide riboside supplementation in PD
NAD+, NMN, SARM1 and neuroprotection.
