"Future studies should study the effects of long-term supplementation of promising nutrients, such as butyrate and niacin, on their abilities to halt or reverse disease progression in PD. "
Niacin and Butyrate: Nutraceuticals Targeting Dysbiosis and Intestinal Permeability in Parkinson’s Disease 2020 mdpi.com/2072-6643/13/1/28/htm
10. Conclusions
Microbiome studies in Parkinson’s disease, like other conditions, suffer from methodological variation and confounding factors and, therefore, specific bacteria involved in the pathogenesis of PD are difficult to characterize. However, an overall pattern corresponding to decreases in SCFA-producing bacteria and increases in endotoxin-producing bacteria have been observed in PD subjects. Fecal microbiome transplantation (FMT) and pre- and probiotics offer potential options for restoring the microbiome to PD patients. There are no robust data to adequately support FMT efficacy on motor and/or non-motor symptoms improvement or slowing the progression of PD or which route of administration and what content/volume of FMT is optimal. Therefore, we need more rigorous and well designed clinical trials to support FMT or the use of pro- and prebiotics in selected subgroups of PD patients in the future. GPR109A, a G-protein coupled receptor found on the surface of intestinal epithelium and macrophages, closely interacts with the microbiome to permit immune tolerance or trigger an inflammatory cascade. Loss of GPR109A is associated with decreased concentration of tight junction proteins and increased intestinal permeability. In inflammatory states, butyrate acts via GPR109A to increase concentrations of tight junction proteins and improve intestinal permeability. Niacin deficiency is exacerbated in PD by dopaminergic medications. Furthermore, niacin shifts macrophage polarization from pro-inflammatory to an anti-inflammatory profile. Future studies should study the effects of long-term supplementation of promising nutrients, such as butyrate and niacin, on their abilities to halt or reverse disease progression in PD. A deeper understanding of the GPR109A pathway in modulating intestinal permeability and its interplay in the microbiome–gut–brain axis may provide therapeutic options for multiple inflammatory and other neurodegenerative conditions.
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Not at the moment. I used to take it. I take Berberine so maybe I will start rotating between berberine and butyrate. I do take Niacin. Took the 250 mg dose from the study for over a year. I have been upping that this week.
I need to research this more. I am not taking Butyrate. Maybe I should. I do take a gram of NA twice a day (which may be too much, please do your own research).
Thanks. I am planning to increase Butyrate production in the gut by consuming more fiber and resistant starch and probiotic containing clostridium butyricum.
Good idea. I already eat A LOT of pistachios EVERY morning.
"PISTACHIOS FEED YOUR BUTYRATE-PRODUCING GUT BACTERIA.
Of the short-chain fatty acids produced by the digestion of pistachio fiber, butyrate is perhaps the most important because it is responsible for providing colonic cells with approximately 70% of their energy! Put simply, without sufficient butyrate in your gut, your colonic cells may begin to digest themselves and die.
Above all other nuts, pistachios, in particular, have been found to help increase the number of butyrate-producing bacteria in the gut the most. " ayoubs.ca/blogs/news/health....
Niacin binds to GPR109a, not sure about downregulating it, but it binds to it and brings inflammation down. When I say Niacin I mean nicotinic acid. Other forms of Niacin have no effect on GPR109a (which is a major reason I don't care about the other forms).
Niacin and Butyrate: Nutraceuticals Targeting Dysbiosis and Intestinal Permeability in Parkinson’s Disease healthunlocked.com/cure-par...
We have demonstrated an up-regulation of G-protein coupled receptor A (GPR109A), a niacin receptor, in macrophages of PD subjects, suggesting an immune-regulatory role for this receptor in the pathogenesis of PD. This in vitro work and patient data substantiate an anti-inflammatory action of niacin via GPR109A in reducing the production of inflammatory cytokines through regulating phospho-NF-kB nuclear translocation. Treating neuroinflammation may open new avenues to combat motor and non-motor symptoms of PD patients by enhancing their quality of life.
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