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Niacin Clinical Studies

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Niacin is a unique class of supplement, one of the most important, here are some references:

“In the absence of an exogenous supply of niacin, there is a gradual, progressive instability of the genome, characterized by the inability of the antioxidant system to act efficiently, which ultimately leads to cell death.”

https://www.mdpi.com/1420-3049/25/15/3323

“our findings demonstrate that acting on GPR109A, niacin shows the potential to maintain energy homeostasis through multipathways, representing a potential approach to the treatment of obesity, diabetes and cardiovascular disease.”

https://faseb.onlinelibrary.wiley.com/…/fj.201801951R

“Mortality in the niacin group was 11% lower than in the placebo group (52.0 versus 58.2%; p = 0.0004). This late benefit of niacin, occurring after discontinuation of the drug, may be a result of a translation into a mortality benefit over subsequent years of the early favorable effect of niacin in decreasing nonfatal reinfarction or a result of the cholesterol-lowering effect of niacin, or both. “

https://pubmed.ncbi.nlm.nih.gov/3782631/

“oxidative stress can induce niacin/NAD+ depletion via activation of poly(ADP-ribose) polymerase (PARP), which could lead to tryptophan oxidation for compensatory de novo niacin synthesis, thereby contributing to immune tolerance and T-cell loss via tryptophan deletion and PARP-induced cell death.”

https://pubmed.ncbi.nlm.nih.gov/19857540/

“Bill acted upon Hoffer’s advice and proceeded to take 1000mg of Niacin after each of his three meals a day. Through mega-vitamin therapy, Bill’s long-lasting conditions were rapidly overcome.”

https://brainsparkhealth.com/the-forgotten-chapter-in…/

“There is an NAD ‘salvage’ pathway that can bypass KYNU and HAAO by converting dietary niacin (Vitamin B3) and other precursors into NAD 

Niacin supplementation to maternal mice prevented birth defects in the ‘null’ offspring”

https://www.nejm.org/doi/full/10.1056/NEJMoa1616361

“In conclusion, our data (1) underscore the potent role of micro-nutrient vitamin B3 as a metabolic modifier; (2) identify NAD +deficiency as a contributor to mitochondrial myopathy progres-sion; (3) point to usefulness of niacin therapy for PEO patients;”

https://pubmed.ncbi.nlm.nih.gov/32386566/

“In the present study, we investigated the impact of supplementation with nicotinic acid on resting and proliferating human mononuclear blood cells with a focus on DNA damage and repair processes. We observed that nicotinic acid supplementation increased NAD+ levels as well as DNA repair efficiency and enhanced genomic stability evaluated by micronucleus test after x-ray treatment.”

https://pubmed.ncbi.nlm.nih.gov/28216063/

“Through its involvement in over 400 NAD(P)-dependent reactions, niacin status has the potential to influence every area of metabolism. Niacin deficiency has been linked to genomic instability largely through impaired function of the poly ADP-ribose polymerase (PARP) family of enzymes. In various models, niacin deficiency has been found to cause impaired cell cycle arrest and apoptosis, delayed DNA excision repair, accumulation of single and double strand breaks, chromosomal breakage, telomere erosion and cancer development.“

https://pubmed.ncbi.nlm.nih.gov/22138132/

“In the central nervous system, vitamin B₃ has long been recognized as a key mediator of neuronal development and survival. Here, we will overview available literature data on the neuroprotective role of niacin and its derivatives, especially focusing especially on its involvement in neurodegenerative diseases (Alzheimer’s, Parkinson’s, and Huntington’s diseases), as well as in other neuropathological conditions (ischemic and traumatic injuries, headache and psychiatric disorders).”

https://pubmed.ncbi.nlm.nih.gov/30813414/

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