Can you provide the link to the Timeline product? Thanks.
Either Amazon or Timeline. Try these:
https://www.amazon.com/ Search for Timeline Urolithin A
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ConsumerLab reports that tests done by SuppCo showed that Neurogan, CodeAge, Pure Encapsulations and Timeline contained the claimed amount.
Neurogan being the cheapest.
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I tracked down that report and yes, Neurogan did pass their testing as having the claimed amount of Urolithin A.
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I have been taking 1,000 mg/day of Urolithin-A for over two months, which is one of three periods of time required to produce different types of benefits. Two months is the target period for beginning to see measurable functional gains in muscle endurance. As someone over 70 who has experienced increasing challenges in fatigue and recovery time related to exercise over the past few years, I can report a significant improvement in both. A few years back, I did strenuous 45–60-minute mountain hikes 4-6 days a week. Gradually, these hikes became more challenging in terms of muscle soreness and especially recovery time. This past year, I have had to allow at least four and sometimes six days to elapse before I could hike again. The most interesting change I attribute to Urolithin-A is how the improvement, especially in recovery time, manifested itself. The change was almost binary. For most of the two months, I felt no effect at all. I had committed to giving the experiment a four-month run but was beginning to think I was wasting my time and money. Then, recently, I want for a hike that immediately felt like it did several years ago. The soreness was typical for the level of effort at any age but the recovery period was ~24 hours and the soreness was gone. I was eager for another hike! I do not have exact records but I estimate that it has been 15 years, maybe 20, since I felt that way. According to the research I have reviewed, this effect begins to manifest itself at around two months and plateaus at four months. I will report again at that time. I’m not going to take the time to detail the reasons I attribute these gains to Urolithin-A and not to other environmental, biochemical, or psychological effects but I am careful to rule such possibilities out to the extent possible in these contexts.
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Thanks for sharing your experience. What brand did you use?
For most of that time, I have used aeternum. I’m switching to Neorogan because they had a discount offer on Amazon and they seem to be one of the most used brands.
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Given that the improvements seem to be to a younger period and nothing beyond that, I wonder if younger people would experience meaningful benefits from Urolithin-A.
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I’m wondering the same. I think at the very least, it wont do any harm and at best, prevent any age related decline in whatever the Urolithin A is supposed to improve. The same can probably be said about a lot of interventions like GlyNAC for instance (which works in different ways).
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New Nature Aging paper of a Randomized Clinical trial of Urolithin A on aging immune systems.
Published Nov 5th 2025 but I didnt see it in this thread or w/ search.
Randomized Controlled Trial
Nat Aging 2025 Nov;5(11):2309-2322.
doi: 10.1038/s43587-025-00996-x. Epub 2025 Oct 31.
Effect of the mitophagy inducer urolithin A on age-related immune decline: a randomized, placebo-controlled trial
Discussed here: More good news on Urolithin-A - #54 by RapAdmin
It’s annoying to have two UA threads.
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Thanks! I agree, two threads is annoying. I tried to post it in the “main” thread for Urolithin-A.
This randomized, double-blind, placebo-controlled trial investigated the effects of urolithin A (UA), a mitophagy inducer, on age-related immune decline in 50 healthy middle-aged adults over a 4-week period. Participants received either 1,000 mg/day of UA or placebo, with assessments at baseline and day 28 13.
UA supplementation led to a significant expansion of peripheral naive-like, less terminally exhausted CD8+ T cells. This was accompanied by an increase in CD8+ T cell fatty acid oxidation capacity, indicating metabolic remodeling towards improved mitochondrial function 15.
Beyond CD8+ T cells, UA also increased the frequency of peripheral CD56dimCD16bright natural killer (NK) cells and nonclassical CD14loCD16hi monocytes. These immune cell populations are important for immune surveillance and inflammation regulation 7.
Mitochondrial biogenesis was augmented in CD8+ T cells of UA-treated participants, demonstrated by elevated expression of PGC-1α, the master regulator of mitochondrial biogenesis. Despite no change in mitochondrial mass or membrane potential at the 28-day timepoint, ex vivo experiments confirmed rapid mitophagy induction by UA, supporting mitochondrial quality control 7852.
UA improved immune cell function as evidenced by enhanced TNF secretion upon T cell activation and increased phagocytosis of Escherichia coli by monocytes. These functional improvements suggest a more robust immune response capability 89.
Single-cell RNA sequencing revealed that UA induced transcriptional changes across immune populations, particularly CD8+ T cells. These changes included upregulation of Wnt-associated stemness factors (TCF7, LEF1), increased IL7R expression, and downregulation of genes linked to T cell exhaustion and immune suppression. Pathways related to T cell receptor signaling, cytoskeletal remodeling, and adhesion were activated, while inhibitory GPCR–Gαs–PKA signaling was suppressed 9105253.
In NK cells and monocytes, UA induced gene expression profiles indicative of a less inflammatory, more mature state. Monocytes showed upregulation of mitochondrial genes and markers associated with anti-inflammatory M2-like polarization, along with downregulation of interferon response genes. B cells also exhibited a reduction in inflammatory gene signatures 1011.
The study concludes that short-term UA supplementation leads to phenotypical, metabolic, functional, and transcriptomic alterations that counteract features of immune aging and inflammaging.
These findings support the potential of UA as a safe and effective intervention to improve immune health during
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Thanks desertshores…I appreciate all those studies. As a long time biomedical researcher, I do put a lot more weight on in vivo studies, eg, in animals or, even, better, human clinical trials.
In vitro (eg, in glass) studies are great for helping elucidate specific mechanisms and pathways but don’t always translate to whole animal effects. I sometimes feel like you can almost show any effect in vitro with the right setup/cell system/perturbation, etc.
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I’ve been saying that for years on this site, and I’m surprised even RapAdmin cites them still. I don’t even bother reading them. The conclusion I’ve made is that it has little to no effect of telling someone this, they deeply want to still believe it.
It’s maybe because they can find anything they want that way. I prefer things that work, and I like the fact that some things do and others don’t.
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I will probably need to adjust the dose in my Max 5 Super mix as I only have 500mg per daily dose
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Amyotrophic lateral sclerosis (ALS) is a rare and devastating neurodegenerative disease characterized by the progressive degeneration of motor neurons in the brain and spinal cord, for which no cure currently exists. Previous studies have shown that abnormal mitochondrial homeostasis and defective mitophagy occur in neurodegenerative diseases, including ALS. Here, we provide evidence that PINK1-Parkin-dependent mitophagy is impaired in multiple ALS mouse models, including the SOD1G93A, TDP43A315T, and rNLS8 strains, leading to the accumulation of damaged mitochondria in affected motor neurons. These findings suggest that mitophagy may be a druggable target for ALS treatment. A classical mitophagy agonist, urolithin A (UA) was used in this study. UA-induced mitophagy antagonizes ALS pathologies in the ALS SOD1G93A transgenic C. elegans model in a pink-1 (PTEN-induced kinase 1)- and pdr-1 (Parkinson’s disease-related 1)-dependent manner. Furthermore, pharmacological activation of mitophagy by UA improves locomotor behavior, delays motor neuron degeneration and reduces neuroinflammation in ALS SOD1G93A transgenic mice. In conclusion, our results establish impaired mitophagy as a hallmark of ALS motor neuron degeneration and demonstrate that its pharmacological activation offers a neuroprotective strategy with therapeutic potential.
Animal models in worms & mice of ALS / MND (motor neuron disease) / Lou Gehrig’s disease.
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Its an obvious case of a cell failing first in the mitochondria even if the MND association said my hypothesis was premature.
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Prompt:
Are there supplements or foods that a person can take so that their body has the microbiome necessary to convert the nutrients from pomegranates into Urolithin A?
Gemini Response:
Research identifies three distinct human urolithin metabotypes (UM): UM-A (producers), UM-B (low producers/isourolithin producers), and UM-0 (non-producers). Roughly 60% of the population lacks the specific gut architecture required to convert pomegranate ellagitannins into Urolithin A (UA).
While you cannot currently buy a single “Urolithin A probiotic” pill that is widely clinically validated to colonize and convert nutrients in humans, there are emerging bacterial candidates and alternative strategies.
1. Known Bacterial Converters (The “Missing” Probiotics)
Research has identified specific strains capable of this conversion, though most are not yet available as commercial dietary supplements:
- Gordonibacter urolithinfaciens & G. pamelaeae: These are the primary species linked to the conversion of ellagic acid into urolithin intermediates. While they have been used in successful animal “synbiotic” trials to increase UA bioavailability, they are currently restricted to research use and are not found in consumer probiotics.
- Bifidobacterium pseudocatenulatum (Strain INIA P815): Identified as a rare Bifidobacterium strain capable of producing UA. While B. pseudocatenulatum is found in some advanced probiotic complexes, specific verification of the INIA P815 strain is usually absent from commercial labels.
- Enterococcus faecium (Strain FUA027) & Streptococcus thermophilus (Strain FUA329): Recent studies (2022–2024) have isolated these strains from human feces and breast milk. S. thermophilus is a common yogurt starter, but the specific FUA329 variant is what possesses the high-efficiency (82%) conversion capability.
2. Available “Proxy” Supplements
Because the primary converters are not yet “off-the-shelf” products, the industry has moved toward two practical workarounds:
| Supplement Type | Mechanism | Examples / Notes |
|---|---|---|
| Direct UA Supplementation | Bypasses the gut microbiome entirely by providing pure Urolithin A. | Mitopure (Amazentis) is the most clinically studied. Research shows it provides ~6x more UA than pomegranate juice in non-producers. |
| Prebiotic + Common Probiotics | Uses “helper” strains like Lactobacillus plantarum or Akkermansia to improve the gut environment. | Rawleigh Ultrapome pairs pomegranate extract with L. plantarum (DSM 6595), which may support the environment for native converters. |
| Akkermansia muciniphila | While not a direct UA producer, its presence is highly correlated with the UM-A (producer) phenotype. | Available via Pendulum Therapeutics. It may shift the microbiome toward a state more conducive to conversion. |
3. Knowledge Gaps and Scholarly Debates
- Colonization Persistence: A major gap in the data is whether supplementing a “converter” strain like Gordonibacter leads to permanent colonization. In mouse models, levels returned to baseline within 24–36 hours post-supplementation, suggesting a “transient probiotic” effect rather than a permanent fix for UM-0 individuals.
- The “Helper” Hypothesis: There is ongoing debate about whether conversion requires a single “super-strain” or a complex consortium of bacteria. Some data suggests that even if you have Gordonibacter, you may still need specific Lachnospiraceae (like Enterocloster bolteae) to complete the final dehydroxylation steps into UA.
4. Practical Recommendation
If your goal is guaranteed Urolithin A for longevity (mitophagy induction), the most evidence-based path for a non-producer is direct supplementation of Urolithin A rather than trying to “seed” the microbiome.
If you prefer the whole-food route, you can attempt to shift your metabotype by consistently consuming ellagitannins (pomegranates, walnuts, raspberries) alongside a high-fiber diet to support Akkermansia and Bifidobacterium populations, though success depends heavily on your baseline microbial “seed” population.
Would you like me to look into the specific dosing protocols used in clinical trials for direct Urolithin A supplementation?
Sources:
Prompt:
Are there consumer tests available to identify which of the three distinct categories people fall into, regarding human urolithin metabotypes (UM): UM-A (producers), UM-B (low producers/isourolithin producers), and UM-0 (non-producers).
Gemini Response:
There is currently only one specific consumer test commercially available that directly identifies your urolithin metabotype (UM) by measuring metabolites in your biological samples. While generic gut microbiome tests (like Viome or Zoe) can identify the presence of specific bacteria, they do not typically provide a definitive “Metabotype A, B, or 0” classification.
1. The Direct Test: “The Mitopure Challenge”
The most targeted consumer option is provided by Timeline (Amazentis), the company that manufactures Mitopure (purified Urolithin A).
- Mechanism: This is a “challenge” test. You consume a standardized amount of pomegranate juice (8 fl oz) and then collect a dried blood spot sample using a finger-prick kit.
- Result: The lab analyzes the levels of Urolithin A in your blood to determine if your microbiome successfully converted the juice’s ellagitannins.
- Stratification: This test effectively distinguishes between Producers (UM-A and UM-B) and Non-producers (UM-0).
- Source: The Mitopure Challenge
2. Indirect Testing: Gut Microbiome Sequencing
You can use high-end consumer gut sequencing services to look for the “machinery” of conversion, though you must interpret the raw data yourself or look for specific markers in their reports.
-
Key Bacterial Markers:
-
Gordonibacter urolithinfaciens and G. pamelaeae: Presence of these species is a strong indicator of UM-A or UM-B status.
-
Akkermansia muciniphila: While not the primary converter, high levels are statistically correlated with the UM-A phenotype.
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Enterocloster bolteae: Recent research (2025) identified this as a critical “secondary” converter that finishes the production of UA.
-
Relevant Services:
-
Healthpath: Explicitly mentions Urolithin A production in their literature and looks for Gordonibacter and Akkermansia ratios. Healthpath Gut Health
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Viome / Zoe: These provide “functional” scores for polyphenol metabolism, which broadly includes the ability to process ellagitannins, though they may not use the “UM-A/B/0” nomenclature.
3. Knowledge Gaps and Diagnostic Limitations
- The “UM-B” Nuance: Most consumer tests (including the Mitopure Challenge) focus on the presence or absence of Urolithin A. Distinguishing UM-A from UM-B requires detecting Isourolithin A or Urolithin B, which is typically only done in academic settings using HPLC-MS (High-Performance Liquid Chromatography-Mass Spectrometry).
- Metabotype Plasticity: Scholarly debate exists regarding whether a metabotype is permanent. Some data suggests that roughly 50% of non-producers (UM-0) can become producers after prolonged, high-dose exposure to pomegranate extract, implying the “machinery” may exist at undetectable sub-threshold levels in many people.
- Additional Data Needed: To definitively categorize a person into UM-B, a test would need to specifically report on Isourolithin A levels. Currently, no consumer-facing test explicitly breaks out these specific sub-metabolites.
Summary Table for Quick Reference
| Test Type | Brand/Method | Primary Benefit | Limitation |
|---|---|---|---|
| Metabolite Challenge | Timeline Mitopure | Confirms actual UA production in blood. | Does not distinguish UM-A vs UM-B easily. |
| Microbiome Sequencing | Healthpath | Identifies if converter bacteria are present. | Presence of bacteria doesn’t guarantee high activity. |
| Function Scoring | Viome | Gives a broad “polyphenol metabolism” score. | Lacks specificity for the Urolithin A pathway. |
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