The Plasma NAD+ Metabolome Is Dysregulated In ‘‘Normal’’ Aging

[LeeLemonoil]

@LeeLemonoil , have you dig this topic more? Can it be, that niacinamide is indeed dangerous?
I have read some of the studies and they are concerning . But i am bad in reading studies and not sure what to think about it .

It’s not dangerous. Context is all that matters. Consuming vitaminoids of B3 is crucial to health, best from food, second best from soups but be aware of your intake.

I personally think doing something positive for the organisms NAD-Ratio and availability by substance intake is achieved better more upstream.

Taurine, Vit D, Apigenin, beta-lapachone are the 4 most impactful Supps I know for it

PARP1-inhibition. CD38-Inhibition. Lapachones effects on NQO1 Are highly interesting but maybe not yet completely safe / understood

 

[Pompadour]

@LeeLemonoil , thanks a lot for the reply! :)

 

[Mito]

NAD + Precursors: A Questionable Redundancy​

Abstract
The last decade has seen a strong proliferation of therapeutic strategies for the treatment of metabolic and age-related diseases based on increasing cellular NAD+ bioavailability. Among them, the dietary supplementation with NAD+ precursors-classically known as vitamin B3-has received most of the attention. Multiple molecules can act as NAD+ precursors through independent biosynthetic routes. Interestingly, eukaryote organisms have conserved a remarkable ability to utilize all of these different molecules, even if some of them are scarcely found in nature. Here, we discuss the possibility that the conservation of all of these biosynthetic pathways through evolution occurred because the different NAD+ precursors might serve specialized purposes.

https://mdpi-res.com/d_attachment/metabolites/metabolites-12-00630/article_deploy/metabolites-12-00630.pdf?version=1657362963

 

[LeeLemonoil]

Putting it into this thread because it’s one of few existing ones talking about senolysis.

Here is a new discovery of an in use Pharmacon able to reverse senescence in early experiments

Antagonizing the irreversible thrombomodulin-initiated proteolytic signaling alleviates age-related liver fibrosis via senescent cell killing - Cell Research

Cellular senescence is a stress-induced, stable cell cycle arrest phenotype which generates a pro-inflammatory microenvironment, leading to chronic inflammation and age-associated diseases. Determining the fundamental molecular pathways driving senescence instead of apoptosis could enable the...

www.nature.com