Niacinamide Is Androgenic And Increases Dht Effects/signaling

[charlie]

"In a recent issue of ckj, Piedrafita et al. reported that urine tryptophan and kynurenine are reduced in cardiac bypass surgery patients that develop acute kidney injury (AKI), suggesting reduced activity of the kynurenine pathway of nicotinamide (NAM) adenine dinucleotide (NAD+) synthesis from tryptophan. However, NAM supplementation aiming at repleting NAD+ did not replete kidney NAD+ and did not improve glomerular filtration or reduce histological injury in ischaemic–reperfusion kidney injury in mice. The lack of improvement of kidney injury is partially at odds with prior reports that did not study kidney NAD+, glomerular filtration or histology in NAM-treated wild-type mice with AKI. We now present an overview of research on therapy with vitamin B3 vitamers and derivate molecules {niacin, Nicotinamide [NAM; niacinamide], NAM riboside [Nicotinamide riboside (NR)], Reduced nicotinamide riboside [NRH] and NAM mononucleotide} in kidney injury, including an overview of ongoing clinical trials, and discuss the potential explanations for diverging reports on the impact of these therapeutic approaches on pre-clinical acute and chronic kidney disease."
Source: Nicotinamide and acute kidney injury

 

[charlie]

Inflammation and cellular energetics play critical roles in organ dysfunction following hemorrhagic shock. Recent studies suggest a putative role for sirtuin 1 (SIRT1) in potentiating mitochondrial function and improving organ function following hemorrhagic shock in animal models. SIRT1 is an NAD+ dependent protein deacetylase and increased availability of NAD+ has been shown to augment SIRT1 activity. As niacin is a precursor of NAD+, in this study, we tested whether niacin can improve survival following hemorrhagic shock. However niacin also mediates its biological action by binding to its receptor, hydroxyl-carboxylic acid receptor 2 (HCA2 or Gpr109a); so we examined whether the effect of niacin is mediated by binding to Gpr109a or by increasing NAD+ availability. We found that niacin administered intravenously to rats subjected to hemorrhagic injury (HI) in the absence of fluid resuscitation resulted in a significantly prolonged duration of survival. However, treatment of rats with similar doses of nicotinamide mononucleotide (NMN), a precursor to NAD+ that does not bind Gpr109a, did not extend survival following HI. The duration of survival due to niacin treatment was significantly reduced in Gpr109a−/− mice subjected to HI. These experiments demonstrated that the Gpr109a receptor-mediated pathway contributed significantly to niacin mediated salutary effect. Further studies showed improvement in markers of cellular energetics and attenuation of inflammatory response with niacin treatment. In conclusion, we report that Gpr109a-dependent signalling is important in restoring cellular energetics and immunometabolism following hemorrhagic shock. https://www.sciencedirect.com/science/article/pii/S0925443919300092

 

[Highserotonin90]

@charlie It puts me on the spot as to what is best for increasing NAD

 

[charlie]

@charlie It puts me on the spot as to what is best for increasing NAD

I think its quite clear, Niacin as Nicotinic acid is the way.

 

[Highserotonin90]

@charlie Yes, I expressed myself badly. Your quotes clarified my thoughts but Haidut's threads are all pro niacinamide...

 

[Alpha]

How is it possible that niacinamide inhibits SIRTI which is necessary to make NAD?

SIRT-2 is generally independent of NAD+ levels and mainly present in the cytoplasm of the cell. Supplementing with Nicotinic Acid will eventually increase Nicotinamide as well. Trying to raise NAD+ through Nicotinamide is inferior since it relies on a salvage pathway where methylation is the predominant metabolism. Nicotinic acid supplementation only has one pathway and that is convert to NAD+, with a rate-limiting step enzyme that is weaker than that of Nicotinamide. The reason why NA activaties SIRT-1 and not NAM is most likely NAD+ dependent through AMPK. I suspect the reason why that is, and how NAM inhibits sirtuins is because it gives the cell a false sense of high NAD+ when its not the case, thereby slowing down metabolism.

NR and NMN have shown to increase NAD+ more reliably than both.

https://www.nature.com/articles/s41392-020-00311-7

 

[Highserotonin90]

@Alfa Thank you!!!

 

[Ras]

Hoffer always advocated for nicotinic acid.

David Sinclair strikes again - Page 10 - Supplements

Page 10 of 18 - David Sinclair strikes again - posted in Supplements: Interesting article from Nutra-ingredients on nicotinamide riboside (article comes at this from a marketing perspective):Link: http://www.nutraingr...et-like-omega-3Chromadex CEO: ‘We think Niagen has a much bigger market...

www.longecity.org

 

[Digital Samurai]

Ray likes Niacinamide, not Niacin, for the record.