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- 171
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I was wondering if anyone has taken niacin at relatively high doses (1500mg/day) in the form of either instant release Niacin or modified release (Niaspan)?
I am not insterested in Niacinamide or Nicotinamide which is commonly taken as part of the methylation/mitochondrial augmentation protocols as this does not reduce neuroinflammation in animal models.
Niacin acts as an agonist at the Hydroxycarboxylic acid receptor 2 - interestingly as does butyrate.
https://www.ncbi.nlm.nih.gov/pubmed/18778774
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885546/
Therefore these may have some potential in the treatment neuroinflammation. Also having recently been diagnosed with cranio cervical instability, atlantoaxial instability and found to have a small posterior fossa, I do think there seems a possibility of brain stem compression mediating dysautonomia causing neuronal hypo perfusion, subsequent hypoxia and therefore microglial activation.
HIF1 modulation has always appeared a target of interest to me and could be a key mediator of systemic metabolic perturbations, neuroinflammation etc. However, excessive inhibition of such could induce necrosis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762339/
I am not insterested in Niacinamide or Nicotinamide which is commonly taken as part of the methylation/mitochondrial augmentation protocols as this does not reduce neuroinflammation in animal models.
Niacin acts as an agonist at the Hydroxycarboxylic acid receptor 2 - interestingly as does butyrate.
https://www.ncbi.nlm.nih.gov/pubmed/18778774
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2885546/
Therefore these may have some potential in the treatment neuroinflammation. Also having recently been diagnosed with cranio cervical instability, atlantoaxial instability and found to have a small posterior fossa, I do think there seems a possibility of brain stem compression mediating dysautonomia causing neuronal hypo perfusion, subsequent hypoxia and therefore microglial activation.
HIF1 modulation has always appeared a target of interest to me and could be a key mediator of systemic metabolic perturbations, neuroinflammation etc. However, excessive inhibition of such could induce necrosis
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762339/