LONGECITY

NRH is much more potent than NR and NMN. It is bioavailable, doesn’t degrade into NAM, and generate much more NAD+.

https://www.scienced...212877819309160

Chromadex seems to hold some patents related to this.

 

https://patents.just...e/chromadex-inc

https://patents.just...patent/10183036

Both NR and NMN Have deficiencies. They both have low bioavailability, about 10% in the liver and 5% in the blood. They both degrades to NAM in the stomach and in the blood. NAM is an inhibitor in NAD+ consuming processes. So NR/NMN are not particularly effective at increasing sirtuin activities.

NAM is known to cause negative feedback loop with NAMPT.
Both NR and NMN will cause this negative feedback loop in long term use.
But NRH only increases NAM slightly probably after NAD+ was consumed.

Here is a new product I discovered at RAADfest - they claim the precursor used is not that important - but rather the cell recycling NAD+ matters more. They claim their product upregulates NAD+ recycling and increases NAD+ many more times than precursors alone.

I read that thread. They really didn’t regulate recycling.
They inhibit NAD+ consuming processes such as CD38.
You get higher levels of NAD+ when the consumption is
Blocked. What is the use of higher NAD+ if you can’t use it?
CD38 is related to immunity and the happy hormone.
The happy hormone was found to be top 2 anti aging
Ingredients in the young blood.

I read that thread. They really didn’t regulate recycling.
They inhibit NAD+ consuming processes such as CD38.
You get higher levels of NAD+ when the consumption is
Blocked. What is the use of higher NAD+ if you can’t use it?
CD38 is related to immunity and the happy hormone.
The happy hormone was found to be top 2 anti aging
Ingredients in the young blood.

"...senescent cells secrete CD38 as part of the pro-inflammatory cytokine cocktail known as the senescence-associated secretory phenotype (SASP). This mixture of pro-inflammatory signals includes CD38, and senescent cells accumulate during aging as the immune system increasingly fails to remove the problem cells. Thus, more senescent cells almost certainly means more CD38 and less NAD+ available."

https://www.leafscie.../nad-and-aging/

NAD + is destroyed by the CD38 enzyme.

"CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism."

What is bad about inhibition of CD38?
Edited by Kentavr, 09 October 2019 - 03:31 PM.

A study from April 2019 came to the same conclusion. NRH boosts NAD+. 

In summary, these findings reveal a powerful naturally occurring pharmacologic agent that can raise NAD+ levels in mammalian cells and tissues, providing an exceptional new tool to investigate how changes in NAD+ metabolism can alter cellular physiology.

 

http://www.jbc.org/c...005772.full.pdf

NRH is definitely much superior than NR/NMN even with oral consumption. NAD+ is raised 25% more than NR and probably with less NAM. More importantly NRH can get into blood stream and stay in circulation for long period time and raise NAD+ in tissues.
One possible issue is NRH is a substrate for NQO2. So it could increase NQO2 activity. NQO2 can generate significant amount of ROS and damage cells and is associated with many diseases.