Gut bacteria play an important role in NAD production. NAD boosting effect of oral NAM (nicotinamide) NR (nicotinamide riboside) is largely dependent on gut bacteria breaking them down to nicotinic acid, and that nicotinic acid being processed via Preiss Handler pathway. Nicotinic acid highly efficient at boosting NAD in mammals.
Mice subjected to high dose ultraviolet light for about 6 months while fed a diet supplemented with 0%, 0.1%, 0.5%, or 1.0% (by dry weight of feed) of niacin showed 68%, 60%, 48%, and 28% rates of skin cancer respectively, indicating a protective effect. Elevated levels of NAD found in niacin supplemented mice. NAD modulates the function of DNA strand scission surveillance proteins p53 and poly(ADP-ribose) polymerase, two proteins critical in cellular responses to UV-induced DNA damage.
Long covid is due to changes in the metabolism of tryptophan and the lack of niacin (NAD/NADH+). Tryptophan has its metabolism altered by the lack of intestinal absorption due to internalization of ACE-2 and hypoxemia and inflammation, diverting its products to the formation of toxic Kynurenine metabolites. The longer time under hypoxemia, the less niacin and the more tryptophan will deviate to Kynurenine in an inflamed environment
Niacin involved with over 400 NAD+ dependent reactions. Essentially all cancer patients are deficient in niacin. Exposing mice to high levels of UVB radiation to induce skin cancer showed that mice on the highest doses of niacin had the lowest rate of skin cancer at 28% compared to 68% in the control group.
Peripheral blood mononuclear cells (diverse mix of highly specialized immune cells) supplemented with nicotinic acid (niacin) and then blasted by x-ray radiation showed increased NAD+ levels, improved DNA repair efficiency and enhanced genomic stability compared to control.
Patients with mitochondrial myopathy (which is associated with NAD+ deficiency) received ~1g niacin daily for 4 months. This resulting in increasing blood NAD+ levels in all patients, up to 8x, improved muscle strength, improved respiratory chain activity and reduced fatty liver.
Disruption of NAD synthesis caused a deficiency of NAD and birth defects in humans and mice. Niacin supplementation during pregnancy prevented the birth defects in mice.
Talks about how intracellular niacin depletion along leads to tryptophan depletion as the body attempts to compensate by synthesizing niacin from tryptophan. And how this imbalance impairs the immune system in HIV.
Overview of how niacin and its metabolites like NAD, NADP, NADPH play a key role in cellular signaling, apoptosis, balancing intestinal flora and gene expression. Without external supply of supply of niacin, the genome becomes unstable via the antioxidant system no longer functioning efficiently, which ultimately leads to cell death.
The GPR109A receptor and its agonists (niacin and butyrate) have anti-inflammatory actions in the skin, gut and retina. For Parkinson's disease, niacin supplementation may have 3 benefits: lower inflammation via GPR109A-related mechanisms, increase dopamine production in brain by supplying NADPH and boosting mitochondrial functions by increasing the NAD/NADH ratio.
Most "niacin" products are niacinamide. If you want the form discussed in this research, look for nicotinic acid specifically.
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