I don’t know, I’m a little over my head here. I found this:
https://sci-hub.se/https://doi.org/10.1021/jf00098a011
Which says there is not a lot of ellagitannins in chestnut, though higher up in the article it talks about the percent.
I saw somewhere else where it talks about anthocyanins being the same thing? So would aronia berries work for this? I could not find a reference for ellagic acid in aronia.
The nitrosylation reaction described here was
used to analyze the chestnut tannin for ellagic acid released
by hydrolysis. Crude and purified preparations of chestnut
tannin contained 7.5% and 11.3% ellagic acid respectively
(n = 3).
10% is pretty good? Chestnut has the advantage of being cheaply available, and well studied as an animal (occasionally human) feed additive. Other things would probably work to different extents. The main ETs in chestnut might not hydrolyse completely in physiolgical conditions – I don’t see any reason why they wouldn’t release an EA molecule, but I’m really guessing there.
I think we are outstripping the easily accessible science here. We know (from a single article??) some L. plantarum cultures produce UA. We know some lactic acid bacteria hydrolyse some ellagitannins. Some, some, some. Some kind of experiment seems indicated.
Another potential high impact health longevity pathway of Urolithin A:
Aging compromises hematopoietic and immune system functions, making older adults especially susceptible to hematopoietic failure, infections and tumor development, and thus representing an important medical target for a broad range of diseases. During aging, hematopoietic stem cells (HSCs) lose their blood reconstitution capability and commit preferentially toward the myeloid lineage (myeloid bias)1,2. These processes are accompanied by an aberrant accumulation of mitochondria in HSCs3. The administration of the mitochondrial modulator urolithin A corrects mitochondrial function in HSCs and completely restores the blood reconstitution capability of ‘old’ HSCs. Moreover, urolithin A-supplemented food restores lymphoid compartments, boosts HSC function and improves the immune response against viral infection in old mice. Altogether our results demonstrate that boosting mitochondrial recycling reverts the aging phenotype in the hematopoietic and immune systems.
Hi @RapAdmin how did the test go + did the test feel reliable? If one does respond to foods via one’s gut, is the test calibrated for levels so one over time can dial in how much pomegranate, etc to consume?
Did I get that right? 299?
This Jarrow product?
Apparently 299v is a different strain ( DSM 9843 ). Maybe they both work, maybe only 299, maybe neither and my original inference from the description of the commercial product was faulty.
A non-commercial solution:
Found a DSM 6595 source.
FloraPro-LP Probiotic & Reviews | Thorne.
But it only has the probiotic, no ellagic acid, like Ultra-Pome. Ellagic acid, however, is more easily sourced, and the Thorne product is better priced.
Urolithin A is very interesting. Brian Kennedy said it extended lifespan of flies and killifish as much as rapamycin (unpublished data yet).
Urolithin A seems to be very robust in our hands so I would encourage people to think about that more in their research. We have a graduate student Stephen Raj who’s working on this and one of the things we’ve done is lifespan studies in a range of different organisms now and it works pretty robustly everywhere. It’s already been reported extend lifespan and worms. We find very significant effects in flies in both sexes for longevity. This has been repeated by Vilhelm Bohr’s lab as well. Neither of these data are published yet. We see pretty strong effects on longevity and killifish.
You’ll see on the right there that there’s lifespan extension by rapamycin and also by Urolithin A and I’m not going to show much mechanistic data on Urolithin today. but if you look at the Western blots down at the bottom what you’ll see is that Urolithin A also reduces mTOR signaling and I just want to point out that the vast majority of interventions that extend lifespan in one way or another affect mTOR signaling and so we need to keep the mTOR pathway really in the forefronts of our minds when we’re thinking about studying aging. We also see a reduction in frailty. So this is the frailty index starting at 18 months of age on the left and at two different doses of Urolithin we see a reduction in frailty. The mice maintain their weight much better on Urolithin and they also have better rota-rod treadmill performance function as well so there are a number of different healthspan parameters that are benefited by Urolithin A.
So Urolithin A reduces mTOR similarly to Rapamycin, and thus it may not make sense to take both? (Doubly true since U-A sounds expensive).
It sounds like U-A is a supplement, but I see people injecting a whole slew of peptides, so why isn’t U-A injections (to get back to “young” blood levels of U-A a thing? — also a smaller more-pure amount injected every two weeks (like the Rapamycin schedule) may be cheaper.
By the way: U-A isn’t a specific brand; I’m just too lazy to write it out over and over.
It also brings up other questions.
Should Urolithin A be taken every day or intermittently?
Could Urolithin A be used to blunt the rebound effect of Rapa?