I don’t know enough about the topic to engage in an argument, but what is Mitopure but Urolithin A, possibly with other minor ingredients? It was revealed to all of us years ago that the secret sauce on the All American Burger was only Thousand Island dressing.
Is a claim of third party testing for the specific ingredient Urolithin A meaningful?
Really. I don’t know.
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LukeMV
#205
I got a massive discount from doublewood on 3 bottles of their urolithin A so I’ve been using it. It could be junk for all I know but it was too cheap not to take a flyer on it
Double Wood is one of my trusted brands until proven otherwise.
Many of their supplements have been 3rd party tested by various consumer groups.
The lowest score I have ever seen in a 3rd party test was that Double Wood only contained 95% of the claimed strength. That is good enough for me.
If anyone can find legitimate negative tests of their products, I would certainly like to know.
Double Wood makes a Urolithin A supplement but it seems to be out of stock at both Amazon and Double Wood’s sites.
“Currently unavailable.
We don’t know when or if this item will be back in stock.”
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LukeMV
#207
They usually do well on consumerlab but not always. Saffron was actually their biggest failure on there.
The thing I wonder is whether Mitopure sells a special type of Urolithin A that no one else sells which is why is so criminally expensive. So could Doublewood be selling an inferior type? That’s what I don’t know.
Yeah, on the basis of its reputation, I bought a bottle of Double Wood Urolithin A too.
A couple of months or so ago, someone here posted that he’d gone through all the Urolithin A brands on Amazon and none of them, except those using Mitopure, were third party tested. Things may have changed. My survey of four cheap brands found two that were. I’m exhausted from the four mouse clicks, but maybe someone hardier can take up the quest. How many more are there?
It’s possible that Mitopure is better. Or it may have had some kind of monopoly on supplies at that point, but no longer does. There have to be many companies capable of manufacturing Urolithin A. Maybe one or more of them saw the demand or potential demand, started making it and supplying brands that can now sell it cheaply.
LukeMV
#209
DoNotAge used to sell it but some BS law forced them to pull it a while ago. From what I understand, that brand is 3rd party tested.
It will be interesting to see how UA compares to Rapamycin. It is direction of action is the same so should in some way be synergistic. I have, however, not taken both at the same time yet. I have a Rapamycin cycle coming up in a week (I am on 21 days) so I may wait until then to take UA. It has appeared to disrupt sleep in a manner which implies autophagy.
I am doing particularly well with sleep (which was my big issue a few years ago) so I am inclined to concentrate on things that don’t disrupt it whilst I don’t have to get up early (no school for my son at the moment).
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AnUser
#211
It isn’t an mTOR inhibitor so what do you mean more precisely?
Both are intended to increase autophagy. I wonder what happens if you take UA when a high level of Rapamycin is in the body.
Ulf
#213
That thorough Gemfibrozil studyis pretty damning: some reduction in cardiovascular events, but no change in coronary mortality or all- cause mortality, and a small, non-significant increase in cancer mortality for the Gemfibrozil users.
I wonder how a well-renowned researcher like Brian Kennedy can be so enthusiastic based on great animal data, when long-term human data on Gemfribrozil is so disappointing. He believes that the anti-aging effect in animals is caused by blocking of amino-acid uptake,which in turn blocks MTor. What does this help if no effedt in humans?
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AnUser
#214
I don’t think it is possible to compare them that easily.
Ulf
#215
Could you expand on that? The two are indeed vastly different, but won’t the disappointing long-term health impact of Gemfibrozil on humans have something to say on the likelihood of an anti-aging effect on humans when the underlying data in that research is based on animals?
AnUser
#216
In the right corner of posts you can see who I am replying to, it wasn’t related to Gemfibrozil. (Icon or username)
ORRAPA
#217
Is this a mispost? The medication being referenced seems unrelated to UA.
Ulf
#218
Gemfibrozil was remarked on in the thread and I responded to that. Sorry for the confusion.
adssx
#219
Targeting aging with urolithin A in humans: A systematic review 2024
Urolithin A (UA) is a gut metabolite derived from ellagic acid. This systematic review assesses the potential geroprotective effect of UA in humans. In five studies including 250 healthy individuals, UA (10 - 1000 mg/day) for a duration ranging from 28 days to 4 months, showed a dose-dependent anti-inflammatory effect and upregulated some mitochondrial genes, markers of autophagy, and fatty acid oxidation. It did not affect mitochondrial maximal adenosine triphosphate production, biogenesis, dynamics, or gut microbiota composition. UA increased muscle strength and endurance, however, had no effect on anthropometrics, cardiovascular outcomes, and physical function. Unrelated adverse events were mild or moderate. Further research across more physiological systems and longer intervention periods is required.
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Urolithin a Alleviates Schizophrenia-Like Cognitive Impairments in Male Rats Following Maternal Separation
UA treatment exerts anti-inflammatory effects by inhibiting microglial activation and the expression of proinflammatory cytokines TNF-α, IL-6, and IL-1β. The potential mechanism involves upregulation of BDNF protein expression and activation of the ERK signaling pathway.Conclusions: This is the first preclinical evaluation of the effects of UA on cognitive function in a schizophrenia model. Our results suggest that neuroinflammation, neurogenesis, and synaptic plasticity collectively contribute to cognitive changes in schizophrenia and that UA can reverse these processes. These insights open up new avenues for developing drugs to prevent and treat schizophrenia.
UA also reduced the typically elevated in HG expression of TGF-β receptors and activation of TGF-β signal transducer Smad2. Our results indicate that in podocytes cultured in conditions mimicking diabetic milieu, UA inhibits and reverses changes underlying podocytopenia in diabetic kidneys. Hence, UA should be considered as a po-tential therapeutic agent in podocytopathies.
UA alleviated neurodegeneration and preserved visual function in SI-treated mice. Simultaneously, we observed severe proteostasis defects upon SI damage induction, including autophagosome accumulation, that were resolved in animals that received UA.
Urolithin A Targets Both PI3K/p-AKT/mTOR and p-c-RAF/MEK/p-ERK Signaling Pathways in Colorectal Cancer
Urolithin A promotes atherosclerotic plaque stability by limiting inflammation and hypercholesteremia in Apolipoprotein E–deficient mice
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adssx
#221
Interesting:
Apolipoprotein E-deficient (ApoE−/−) mice were fed a high-fat and high-cholesterol diet for 3 months to establish atherosclerosis model. Meanwhile the mice were administered UroA (50 mg·kg−1·d−1, i.g.). We showed that UroA administration significantly decreased diet-induced atherosclerotic lesions in brachiocephalic arteries, macrophage content in plaques, expression of endothelial adhesion molecules, intraplaque hemorrhage and size of necrotic core, while increased the expression of smooth muscle actin and the thickness of fibrous cap, implying features of plaque stabilization.
Thoughts on this @AnUser?
Also: does UA really increase nitric oxide production?
We demonstrated that UroA pretreatment mitigated endothelial inflammation by promoting NO production and decreasing YAP/TAZ protein expression and TEAD transcriptional activity in TNF-α-stimulated HUVECs.
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AnUser
#222
Mice model, about 90% of drug trials fail.
https://www.nature.com/articles/nrd.2016.136
Approximately 100 vaccines have been shown effective against an HIV-like virus in animal models, however, none have prevented HIV in humans.
Likewise, up to 1000 drugs have been shown effective for neuroprotection in animal models but none have been effective for humans.
…The success of the animal model in basic research can also be questioned based on the fact that, according to one report, only 0.004% of basic research papers in leading journals led to a new class of drugs.
For example, in part because the targets derived from animal models are not predictive for humans, the percentage of new drugs in development, after initial evaluation, that ultimately make it to market is somewhere in the area of 0.0002%.
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