If anyone wants Timeline and has American Express platinum, I just received an email that you’ll get $30 back from a $150 purchase.
I love the gummies, so I think I’ll get them with the thinking that I’m paying extra for candy …
I’d still like to spend less, but I’m not just sure on sourcing. Neurogan, which passed testing, no longer offers UA at all.
“Quercetin inhibits CYP3A4—the main enzyme metabolizing rapamycin—so taking them together could meaningfully boost rapamycin blood levels.”
How does this compare with drinking Grapefruit juice for those who try to maximize their Rapamycin consumption? Why drink Grapefruit juice with it’s unknown potency when Quercitin could do the job in a quantifiable dosage?
Rob Tuck’s AI deep dive above says quercetin’s effect on rapamycin absorption isn’t always the same: “The in vitro CYP3A4 inhibition is genuine but the potency estimates are all over the map depending on system and marker substrate …”
And I believe, for any real effect, it’s referring to high dosage, which is hard to accomplish due to quercetin’s low bioavailability. For a more thorough understanding, you may want to read the whole response. The AI knows all and tells all.
True, grapefruit or grapefruit juice won’t be exactly the same every time either, but unless you’re trying to measure precisely, it’ll probably get the job done.
Hi Beth, I bought some neurogan pro+ urolithin A on 27 August 2026 from iHerb. It’s out of stock now but says it’s available in September?
it’s cost 120 USD / 100grams to source from a reputable supplier in China, I just not sure whether we should take UA but ITP aging program is currently testing UA on mices, the results would come out maybe in a few years hopefully…
I am thinking just to purchase some imeglimin from India instead, imeglimin seems way more promising than UA.
There was also another trial in middle-aged adults published in Cell Reports Medicine that reported improvements in muscle strength, exercise performance and mitochondrial biomarkers. PMID 35584623.
The main caveat is that Amazentis, the company behind Mitopure, has been involved in much of the research, so I’d still keep that in mind when interpreting the results.
Mitopure also isn’t the only option anymore. I’ve been looking at Welzo Ultra Purity MitoRenew as another Urolithin A option, especially in the UK. Personally I’d compare products based on the actual Urolithin A dose, purity/testing and cost rather than assuming Mitopure is automatically better just because it’s the branded ingredient.
The mitophagy angle is probably the most interesting part for me, but I’d still describe Urolithin A as promising rather than proven as a longevity intervention.
This post was flagged by the community and is temporarily hidden.
Is this a joke? If so there’s a joke thread on this site where this eyeroller belongs.
In case this is posted as “information”, it’s on the level of urban legends of the kind “buying leather pants turned me gay”.
C’mon, this is clearly lazy trolling the hot button preoccupation with transgender controversies. How do you know this is a troll fabrication? Here:
Before he started urolithin last year, Ted was basically a normal boy, you know got good grades,
OK, someone who is shaken and traumatized by what happened to their boy and wants to warn others would not write in a leisurely style mentioning his good grades 
… dead giveaway. It’s a style that just does not fit the emergency circumstance. That’s not how real people write about real tragedies.
Do people really have such poor BS detectors that they can’t spot lazy trolling from a mile away? This is an especially egregious example playing on the current hot button transgender hysteria of the moment for maximum engagement and all written with lurid and way, way, excessive and irrelevant details. Maybe if you’re a sheltered granny in the midwest with little exposure to the world of internet trolls you might fall for this, but c’mon.
People, tune up your BS detectors, or get one to begin with because if you fall for this one, you ain’t got one. Sheesh, SMH.
I just had a flashback to 8th grade when I was sent to the principal’s office for cutting up in class. Mr. Haynes gave me a good telling to. I got an F in the class.
Back on topic (
). I continue to recognize benefits from ~1,000 mg/day of UA. It is by no means a miracle drug but it has clearly given me more functional lower body muscle function. I’m hesitant to offer what could be a misleading marker but it is accurate to say that they feel they way I recall their feeling several years ago. It is not inexpensive but the return is worth it.
Is anybody feeling benefits with 500 mg / day or is there a threshold closer to 1000? How did the 1000 mg/day dose get established?
Urolithin A exhibits a dose-response effect on inflammation, with some RCTs showing that 1000 mg reduces CRP, whereas 500 mg does not.
I’ve taken 1000 and 500… off brand and brand. I don’t feel either one.
Claude Fable told me this:
What the trial shows — Singh 2022, Cell Reports Medicine, Timeline-funded, 88 people, 4 months. Human trial (randomized).
• Strength: hamstring peak torque rose at both 500 mg (p = 0.027 vs placebo) and 1,000 mg (p = 0.029). Roughly 12% and 10% — the two doses are the same on this outcome.
• Endurance: 6-minute walk distance, author-confirmed figures: 500 mg arm −0.74 m, 1,000 mg arm +33 m, placebo −0.52 m. Only 1000 moved. But the pooled result across trials was +17 m and not significant (p = 0.135), low-certainty by GRADE. Meta-analysis.
• Aerobic capacity: peak VO2 rose within the 1000 mg group (p < 0.01), but against placebo only p = 0.058 — just missed.
• Anything else: hand-grip trended up at 1000 only (p = 0.08). Not significant.
I have looked extensively at the literature and personally spent some bucks on urolithin A supplements. Asked all of my paid AIs about it.
Ignore the YouTube gurus:
The consensus is MEH.
Save your money for some better drugs and supplements. Adding urolithin A just increases the number and price of your supplement list.
I have bulk powder and capsules. partly because it is easier, I have been alternating 1,000 mg and 500 mg/day. I do not have any hard metrics but based on my year or so taking it and inadvertently falling off for a couple of months due to a scam product, I would recommend that a first time person try 1,000/per day for at least four months (minimum time for full effect) and then see if you can hold that line with 500 mg.
Another consideration is that you may be too young to see too much benefit. There is some reason to think the benefits accrue mostly to muscles over 65-70. It could also be that some muscles are too old or too far structurally transformed to realize benefit. I believe its effects are complex, that it does not benefit everyone. A deep AI dive, separating mechanistic from functional empirics will suggest significant potential benefit.
Thanks Rob for your comments. Curious what type of testing you were able to do (and where) to confirm your bulk powder is clean and Urolithin A? Do you put it in capsules or sprinkle it on your cheerios 
I’m buying the Toniiq stuff but it is still pretty expensive given that a single dose is 6 capsules. Not sure how long I’ll take this stuff, seems there is not a lot of evidence that it is doing much but I like the idea of targeting CNS mitophagy. I don’t feel any different with 500 / day but I’ll bump it to 1000 to see if I sense anything.
I’m using Aeternum bulk powder and Toniq. The Aeternum is comparatively economical in the 100 gram bulk powder form. They have a lab certificate of purity and potency but of course that doesn’t mean the 100 grams I purchased is unadulterated. When the Toniq is gone, I think I will continue with the Aeternum power. The company seems to have a good reputation.
You have no doubt studied the several stages of transformation associated with UA supplementation and their time lines totaling 4-6 months. They align well with my personal experience. I don’t think I could observe any effects for the first two months and since I was engaged in exercise of various kinds and intensities over the period it would be difficult to fully isolate the impact of UA. It wasn’t until I was no longer getting 500-1,000 mg/day that I noticed an unmistakable regression in how my lower body muscles felt and seemed to perform during intense exercise. This benefit could be idiosyncratic. If you look carefully within the findings, ignoring means and p-values, you see a high degree of variation in, suggesting that individual underlying metabolic differences may play a role in whether UA is beneficial.
Two effects, however, are consistent across every adult age bracket: the UA biomarker signature (acylcarnitines down, hsCRP down, muscle mitophagy/OXPHOS proteins up) and, strangely primary-endpoint misses. As I said, the functional hits are almost always secondary or within-group endpoints.
If I were advising someone whether it was worth a minimum four month investment, I would base is on a frank assessment of lower body muscle function. If these muscles are behaving more-or-less according to expectations and as they have in the past, it may not be worth the time and expense.
@RobTuck thanks for the share, I’ll now feel confident to return to Aeternum. I was taking their pills and then switched to Timeline gummies (only during a huge sale and I justified the cost because they are enjoyable sweet treat that I wouldn’t have thought was too much for a month of chocolates (oh, the brain gymnastics I do to justify expenditures!!!)
You are welcome @Beth @59vw (a '59, Wow!). Report back as soon as you have something. I think many of us are on one side or other of the fence on UA, especially those of us who are older. On the other hand, it is possible that further research will demonstrate that it slows decline and is therefore useful for a younger audience.
One issue I would like to see investigated more is whether it has any impact on the gradual replacement of the general category of Type II muscles with a one of the more narrow function Type I muscle fibers – a normal progression in aging and having ties to sarcopenia.
Urolithin A, a postbiotic metabolite derived from dietary ellagitannins, significantly alleviates heart failure with preserved ejection fraction in a mammalian model. The compound restores diastolic cardiac function and reduces tissue fibrosis by activating AMPK, inhibiting mTOR, and enhancing mitophagy, while simultaneously remodeling the gut microbiome to lower circulating lipotoxic ceramides.
Heart failure with preserved ejection fraction accounts for approximately half of all heart failure cases globally and currently lacks effective mechanism based cellular therapies. The pathology is heavily driven by systemic metabolic comorbidities such as obesity and hypertension, which converge to cause profound myocardial remodeling, fibrosis, and mitochondrial dysfunction. Researchers investigated Urolithin A to determine if this gut microbiome derived compound could reverse established cardiac pathology.
The study utilized a two hit mouse model combining a high fat diet with a nitric oxide synthase inhibitor to accurately replicate the systemic metabolic stress seen in human patients. Following disease establishment, Urolithin A administration successfully restored diastolic relaxation and reduced cardiac hypertrophy. Notably, the intervention produced these structural cardiac benefits without altering the subjects total body weight, fat mass, or daily food intake.
At the molecular level, the compound activated the AMPK signaling pathway and inhibited mTOR, effectively reestablishing PINK1 and Parkin mediated mitophagy. This clearance of damaged mitochondria preserved cellular architecture and restored oxygen consumption rates. Furthermore, researchers utilized shotgun metagenomic sequencing and lipidomics to discover a secondary systemic mechanism. Urolithin A actively remodeled the gut microbiome, suppressing specific bacterial populations responsible for de novo ceramide biosynthesis. This resulted in a marked reduction of circulating lipotoxic ceramides. This dual action of direct myocardial mitochondrial quality control and systemic microbiome modulation provides a clear mechanistic rationale for evaluating Urolithin A as a targeted therapy for age related cardiac dysfunction.
Translating these findings to human healthspan optimization reveals practical applications for maintaining cardiovascular longevity and aerobic capacity. Urolithin A demonstrates a measurable ability to reduce structural cardiac stiffness and preserve mitochondrial spare respiratory capacity under extreme metabolic stress. For individuals actively tracking their VO2 max and performing regular high intensity interval training, maintaining this baseline mitochondrial flexibility is mandatory for optimal cellular energy output and recovery speed.
The data illustrates significant real world effect sizes. Urolithin A reduced pathological cardiac perimysial fibrosis by 50 percent compared to the untreated disease state. Furthermore, the reduction of systemic ceramides via gut microbiome remodeling presents a powerful secondary longevity benefit. Lowering circulating lipotoxic lipids directly supports the maintenance of clean vascular endothelium and aligns perfectly with aggressive targets for apolipoprotein B and high sensitivity C-reactive protein. The intervention also reduced lung congestion markers by 45 percent, fully returning them to baseline control levels. This strongly suggests Urolithin A operates as a potent systemic geroprotector capable of modifying both localized tissue quality and circulating inflammatory lipid profiles.
Instead of relying solely on statistical significance, the magnitude of the physiological improvements demonstrates the practical strength of the intervention.
Diastolic Function (E/A ratio): The ratio worsened to approximately 5.5 in the disease group but improved to 4.0 with treatment, yielding an absolute improvement of 1.5 units and a relative functional recovery of 27 percent.
Cardiac Fibrosis: Perimysial ECM accumulation increased from a baseline of 5 percent to 18 percent under stress. Treatment reduced this to 9 percent, generating a relative risk reduction of 50 percent for fibrotic tissue accumulation.
Pulmonary Congestion: The lung wet to dry weight ratio increased to a pathological score of 10. Treatment reduced this parameter to 5.5, a 45 percent relative reduction that completely normalized congestion back to control levels