Urolithin A: Mitochondrial Recycling and Muscle in Older Adults

Table of Contents

1. From Food to Urolithin A
2. Why People Differ: Metabotypes
3. Mitophagy in Plain Words
4. Trials in Older and Middle-Aged Adults
5. Trials in Athletes
6. Heart, Blood Vessel and Immune Trials
7. What the Pooled Review Found
8. Who Paid for the Trials
9. Safety Data and Kidney Stones
10. Fermentation: Laboratory Work Only
11. What Is Not Known
12. Key Research Papers
13. Connections
14. Featured Videos

From Food to Urolithin A

The chain runs from a large plant molecule to a small one made by bacteria. Ellagitannins in pomegranate, berries and walnuts release ellagic acid in the gut, and colon bacteria then trim ellagic acid step by step into urolithins. The walnut gut microbiome page follows those steps and the walnut feeding trials in detail, and the pomegranate punicalagin page covers the main pomegranate tannin.

The bacteria were hard to pin down. A 2014 paper reported that the bacteria behind this conversion were still unknown, then described a new species isolated from healthy human stool, Gordonibacter urolithinfaciens, which metabolizes ellagic acid to urolithins. It grows only without oxygen. A later report also names Enterocloster among the bacteria that mediate the conversion.

Thirteen urolithins and their linked forms had been described by 2022, found depending on the type in urine, blood, stool, breast milk and prostate, colon and breast tissue. After absorption the body attaches other chemical groups to urolithin A. In a kidney stone report, the glucuronidated and sulfated forms ran about 100-fold and 10-fold higher in blood and urine than the free molecule. This matters for reading laboratory work, because a 2022 review from the group that first described urolithins in humans says that cell studies still lack realistic molecular forms and concentrations, "making some reported urolithin activities questionable."

Why People Differ: Metabotypes

People fall into three groups according to what their gut bacteria produce. These groups are called urolithin metabotypes. A 2014 summary of human feeding trials gave these ranges:

• Metabotype A produced only urolithin A forms: 25–80% of volunteers, depending on the trial.
• Metabotype B also produced isourolithin A and/or urolithin B: 10–50%.
• Metabotype 0 had none of these urolithins detected: 5–25%.

The wide ranges are a finding in themselves, since they show how much the answer changed from one trial group to the next. That summary described the groups as independent of age, sex and body weight. A later study of 839 people aged 5 to 90 reached a different conclusion about age, reporting aging as the main factor that determines the gut bacteria involved. The two papers come from overlapping authors.

A direct test with a real food came from a supplement-maker study of 100 participants, randomized to a glass of pomegranate juice or a food product containing 500 mg of urolithin A:

• Only 12% had detectable urolithin A at the start.
• After the juice, about 40% converted the precursors into a significant amount of urolithin A.
• Producers had higher gut bacterial diversity and a higher ratio of Firmicutes to Bacteroides.
• The 500 mg product gave more than 6-fold the exposure of the juice (p < 0.0001).

That 6-fold gap is one reason the supplement trials do not translate directly to eating fruit or nuts. The trials below gave 500 to 1,000 mg a day directly, which bypasses the gut bacteria altogether.

Metabotype may also shape what a food does. In overweight and obese adults with mildly abnormal blood fats given a pomegranate extract, falls in stool bile acids and in coprostanol, a bacterial breakdown product of cholesterol, tracked with urolithin levels, mainly urolithin A in stool, and the shift was strongest in metabotype B. The authors suggest urolithin A as a direct driver of these effects, although its abstract reports no heart outcomes.

Whether gut bacteria can be shifted is under early study. In a trial of 32 healthy adults, a daily capsule combining 24 probiotic strains with 400 mg of pomegranate extract was compared with placebo for 91 days. By day 91, all participants on the capsule could convert polyphenols to urolithin A, against 44.4% on placebo (p < 0.01), and the paper reports a 49-fold increase in urinary urolithin A production. The paper itself states that probiotics alone do not raise urolithin A in healthy adults. Two of its authors work for the capsule's maker and two more advise it. No muscle or aging outcome was among its listed end points.

Mitophagy in Plain Words

Mitochondria are the small structures inside cells that turn food and oxygen into usable energy. They wear out. Mitophagy is the process by which a cell marks a damaged mitochondrion, wraps it and breaks it down so its parts can be reused. It is a specific form of the wider cell clean-up called autophagy. A 2025 review describes urolithin A as acting mainly on mitophagy, through a signalling route involving two proteins, PTEN induced kinase 1 (PINK1) and Parkin, while spermidine acts more broadly on autophagy.

The idea rests on a 2016 animal paper. In the roundworm Caenorhabditis elegans, urolithin A prevented the build-up of faulty mitochondria with age and extended lifespan. In two mouse models of age-related muscle decline, and in young rats, it improved exercise capacity. Those are results in worms and rodents. Several of that paper's authors later worked on the human trials below, and the supplement's maker is among its author affiliations.

Measuring this in people is harder than in worms. The human trials mostly report indirect signs: fats in the blood called acylcarnitines, which rise when mitochondria burn fuel poorly; activity of mitochondrial genes in muscle; and levels of mitophagy-linked proteins in muscle samples. These are signs that something changed in the cell, and they are a separate question from whether a person walks further or stays stronger, which is where the results below become mixed.

One modelling study adds a caution. A 2023 computer model of how urolithin A moves through the human body, checked against data from human intervention studies, predicted that the concentrations which cause either harm or benefit in cell experiments are unlikely to be reached in the body by supplementation. The authors say this supports its safety and also "challenge[s] the potential for readily achieving beneficial effects by postbiotic supplementation." It is a prediction and does not settle what the trials measured.

Trials in Older and Middle-Aged Adults

These three trials are the core of the claim, and the two muscle trials both missed the main measures they set out to test.

First human trial, 2019: safety and blood and muscle markers

Healthy, sedentary older people received urolithin A as a single dose or as repeated doses for 4 weeks. The primary outcome was safety, reported as a favorable profile. At 500 mg and 1,000 mg a day, urolithin A reached the blood and changed plasma acylcarnitines and the activity of mitochondrial genes in muscle. Its abstract reports safety and markers, not strength or walking.

Older adults in Seattle, 2022: main measures missed, endurance improved

This double-blind trial randomized 66 people aged 65 to 90 to 1,000 mg a day or placebo for 4 months (33 in each group; mean age 71.7; 75.8% women; all White). It had two primary end points, and neither improved significantly against placebo:

• 6-minute walk distance: up 60.8 m on urolithin A and 42.5 m on placebo, a gap that was not statistically significant, with both groups improving.
• Peak energy production in muscle: maximal adenosine triphosphate (ATP), the cell's energy currency, measured by magnetic resonance. In the hand it changed by 0.07 mM/s on urolithin A and 0.06 on placebo. In the leg it changed by −0.03 and +0.03. This measure of mitochondrial output did not differ from placebo.

The secondary measures did better. The number of muscle contractions before fatigue rose significantly at 2 months against placebo, by 95.3 versus 11.6 in a hand muscle and 41.4 versus 5.7 in a leg muscle, although the spread between people was wide (standard deviations of 115.5 and 147.4 in the hand). Several acylcarnitines, ceramides and C-reactive protein, a blood marker of inflammation, fell at 4 months (C-reactive protein 2.14 to 2.07 on urolithin A, 2.17 to 2.65 on placebo). Adverse events did not differ between groups. The authors state that "future work is needed to confirm this finding."

Middle-aged adults, 2022: main measure missed, strength improved

This placebo-controlled trial gave two doses (500 mg and 1,000 mg, according to the 2026 pooled review) for 4 months. The primary end point, peak power output, did not improve significantly. Muscle strength improved by about 12%. The authors describe clinically meaningful improvements in peak oxygen consumption and the 6-minute walk, a judgement by the authors of the paper. Acylcarnitines and C-reactive protein fell significantly, and proteins linked to mitophagy and mitochondrial metabolism rose in muscle samples. The title of the paper reports the favorable results; the missed primary end point is stated in its abstract.

Trials in Athletes

Three small trials tested urolithin A in young and trained people, a very different group from older adults. Results in athletes cannot be carried across to people losing muscle with age.

• Distance runners, 2025. Forty-two competitive men took 1,000 mg a day or placebo for 4 weeks at an altitude camp. In a subset of 22, 3,000 m time-trial performance did not improve significantly in either group. Aerobic capacity showed no significant difference between groups over time (p = 0.138), though it rose 5.4% on urolithin A and 3.6% on placebo. Perceived effort (p = 0.02) and a blood marker of muscle damage, creatine kinase (p < 0.0001), were lower after the time trial. In muscle samples from 20 runners, markers of mitophagy did not rise significantly and mitochondrial function did not change, while inflammatory protein pathways were lower. The authors conclude it "did not further enhance performance."
• Resistance-trained men, 2024. Twenty men took 1 g a day or placebo for 8 weeks. One-repetition maximum did not differ significantly from placebo (bench press 3.50 kg, p = 0.462; squat 2.55 kg, p = 0.710). Isometric force (43.50 Nm, p = 0.048) and repetitions to failure (2.00, p = 0.011) did. C-reactive protein was 0.79 mg/L lower than placebo (p = 0.032), although within the urolithin A group it rose by 0.71 mg/L from baseline (p = 0.001). The antioxidant enzyme superoxide dismutase fell compared with placebo (4.32 U/mL, p = 0.041), which the authors read as lower oxidative stress. This trial reported no conflict of interest.
• Academy soccer players, 2025. A single-blinded pilot gave 20 males with a mean age of 17.5 years 1,000 mg a day or placebo for 6 weeks of preseason training. A running endurance test improved by 239 m over placebo (95% confidence interval 20 to 454 m, p = 0.048) and jump height by 3.33 cm (p = 0.020). Sprint speed, jump power and saliva antioxidant measures showed no group difference. The authors note that their confidence limits were broad. One author reported travel reimbursement from a supplement company for presenting these data, and the authors state the company had no role in the study.

Heart, Blood Vessel and Immune Trials

• Heart failure, 2024: null. In a crossover trial, 10 patients with heart failure with reduced ejection fraction took 500 mg twice a day or placebo for two 4-week periods, separated by a 2-week washout. Heart ultrasound measures did not change, nor did pro-B-type natriuretic peptide (pro-BNP, a blood marker of heart strain), glucose or C-reactive protein. High-density lipoprotein (HDL) cholesterol rose by 6.46 mg/dL against placebo (p = 0.026), while other blood fats did not change. The authors state that their results "do not support any positive effect" on these heart failure measures. They call for higher doses and longer trials.
• Blood vessels in obesity, 2026: null on the main measure. Fifty adults aged 40 to 64 with a body mass index of 30 or more took 1,000 mg a day or placebo for 4 weeks, and 7 were lost to follow-up. The primary measure, flow-mediated dilation of the arm artery, did not differ significantly (0.3% on placebo, 1.3% on urolithin A), and neither did the other measures of blood vessel lining function. Blood-flow responses in the brain during tasks were greater on urolithin A, while task performance itself did not change. The authors call the brain finding one that "warrants further investigation." This trial reported no conflicts of interest.
• Immune cells, 2025: main measures met, blood cells only. Fifty healthy middle-aged adults took 1,000 mg a day or placebo for 4 weeks. The share of naive-like CD8 T cells, immune cells that are less worn down, rose by 0.50 percentage points over placebo (95% confidence interval 0.16 to 0.83, p = 0.0437), and their capacity to burn fat for fuel rose by 14.72 percentage points (6.46 to 22.99, p = 0.0061). Some other immune cells and functions also shifted. This trial measured cells in blood samples, and its abstract reports no infections, vaccine responses or illness. An author correction was published in 2026.

What the Pooled Review Found

A 2026 systematic review and meta-analysis searched four databases through December 2025 and found five randomized trials of urolithin A with muscle outcomes, 236 people in total. Only one outcome could be pooled at all, the 6-minute walk, and it rested on two trials:

• The pooled difference was +17.03 m (95% confidence interval −5.33 to 39.40 m; p = 0.135), which the authors call directionally favorable but statistically inconclusive.
• The certainty of that evidence was rated low.
• Strength, endurance, aerobic capacity and blood or mitochondrial markers differed too much between trials to pool. The authors report them as "exploratory signals rather than reproducible effects."

Their conclusion is that larger, longer and more standardized trials are required "before firm clinical recommendations can be made." The authors reported no commercial or financial conflict. A separate 2026 narrative review likewise describes the human evidence as preliminary, concentrated in muscle function, exercise, selected markers and short- to medium-term safety.

Who Paid for the Trials

Much of the work on purified urolithin A comes from one source: the company that sells the supplement. The papers state this in their disclosures.

• Maker named as sponsor or funder: the juice-versus-supplement study, the middle-aged adults trial, the distance runners trial and the immune cell trial, each with company employees among the authors.
• Maker's staff or founder among the authors: the first human trial, the Seattle older adults trial and the rat safety study.
• No such tie reported: the resistance-trained men, heart failure and blood vessel trials. The blood vessel and heart failure trials were null on their main measures, and the resistance trial was mixed. The soccer trial reported only the travel reimbursement described above.

Maker funding does not make a result false, and supplement trials are often paid for this way. It is a reason independent replication matters, and the pooled review notes that the existing trials are small, short and differ widely. Even in the maker-funded trials, the published abstracts state the missed main measures.

Safety Data and Kidney Stones

Trials and animal testing

In the trials, short-term use has looked well tolerated. The first human trial reported a favorable safety profile, the Seattle trial found no statistical difference in adverse events over 4 months, and the blood vessel and soccer trials also describe it as well tolerated. These are small groups followed for weeks to months.

The formal toxicology work was done in rats. Laboratory tests found no genotoxicity, meaning no DNA damage, and 28-day and 90-day feeding studies found no changes in blood tests or target organs. The highest dose tested was 5% of the diet, or 3,451 mg per kilogram of body weight a day in males and 3,826 mg in females, and it caused no observed harm. Staff of the maker were among the authors. The 2023 modelling paper notes that a few studies raise possible adverse effects at high doses in laboratory settings, including genotoxicity and estrogen-like effects, and predicts such concentrations are unlikely to be reached in the body.

The first human urolithin A kidney stones

A 2026 report describes a finding the trials could not have shown. From 2024, a US stone analysis laboratory began receiving urinary stones containing a compound missing from its reference library. Chemical analysis identified it as urolithin A. The report's details:

• Stones from 8 patients aged 59 to 87 contained urolithin A, at 5% to 80% of the stone. Seven of the 8 were women.
• Every stone also contained calcium oxalate or calcium phosphate. The authors say it remains unclear whether urolithin A starts a stone or joins one already forming.
• Six patients gave a diet history. All 6 ate walnuts daily or nearly daily, often in smoothies, and some also ate blueberries, strawberries or almonds.
• None of those 6 was taking a urolithin A supplement. The stones arose with food alone.
• The free molecule was the form found in the stones. The authors suggest these patients may combine bacteria that make urolithin A with poor attachment of the other chemical groups, leaving more of the poorly soluble free form in urine. That is a hypothesis, not a finding.

The authors also recall that urolithin A was first described in 1964 as the main component of "clover stones" in Australian sheep, which died of kidney failure from blockage. They write that supplement trials have run up to 4 months and reported only one urinary stone event, with no stone composition given, and that they anticipate cases may emerge as supplement use grows, given the higher exposure it produces. That last point is their expectation, as no supplement-linked stone had been reported in this series.

This is a case series with no comparison group, so it cannot say how often this happens or whether walnuts caused the stones. Most urinary stones are made of other materials, such as calcium oxalate, calcium phosphate, uric acid or struvite; see Kidney Stones for the general picture. These findings matter most for people with a history of stones, about whom the trial abstracts read for this page report nothing. Decisions about supplements for anyone with a medical condition belong with a clinician.

Gaps in the safety record

The trial reports read for this page give no safety data on pregnancy, breastfeeding, kidney disease, young children or use with medicines. Case reports of pomegranate juice and warfarin, covered on the Ellagic Acid page, concern the juice and not urolithin A.

Fermentation: Laboratory Work Only

Because urolithin A is made by bacteria, researchers have asked whether food fermentation can make it before the food is eaten. The work so far is in the laboratory:

• Strawberry juice fermented with a Limosilactobacillus fermentum strain reached 10.27 µM of urolithin A.
• Three Lactobacillus plantarum strains produced 15.90 to 32.01 µM, and pomegranate juice extracts fermented with them extended lifespan in worms by 26% to 46%, again a worm result.
• A Streptococcus thermophilus strain, the species used as a yogurt starter, converted ellagic acid to 7.38 µM of urolithin A at an 82% conversion rate. This strain came from human breast milk and was tested in culture, not in yogurt.

No human trial of a urolithin A fermented food turned up in the search for this page, and no study was found that measured urolithin A in natto, miso, tempeh, ordinary yogurt or other everyday fermented foods. These strains are specially screened ones, so these results do not show that common fermented foods contain it.

What Is Not Known

• Whether it changes anything people care about over years. The trial abstracts read here report no falls, fractures, disability or loss of independence. The trials ran from 4 weeks to 4 months.
• Whether the main results can be repeated. Both muscle trials in non-athletes missed their primary end points, and the secondary findings are called exploratory by the pooled review.
• Whether mitophagy is the mechanism in people. Muscle protein and gene changes were reported in the first human and middle-aged trials. In the runners, markers of mitophagy did not rise significantly and mitochondrial function did not change. In the Seattle trial, maximal adenosine triphosphate production did not improve.
• Whether food does the same thing. In the juice comparison, the purified product gave more than 6-fold the exposure of pomegranate juice. Trials giving food to producers and non-producers with muscle outcomes were not found.
• Who the results apply to. The Seattle participants were all White and mostly women, and the athlete trials were men. People with frailty or diagnosed muscle loss were not the focus of the trial abstracts read here.
• How common urolithin A stones are, and whether long-term supplement use changes that risk.
• What metabotype means for health, and whether a non-producer gains anything by becoming one. The evidence so far is correlations and one short trial funded by a capsule maker.
• What level of independent evidence exists. Most positive muscle results come from maker-funded work, and independent trials are few and small.

Key Research Papers

1. Andreux PA, Blanco-Bose W, Ryu D, et al. The mitophagy activator urolithin A is safe and induces a molecular signature of improved mitochondrial and cellular health in humans. Nature Metabolism. 2019;1(6):595-603. PubMed PMID: 32694802
2. Liu S, D'Amico D, Shankland E, et al. Effect of Urolithin A Supplementation on Muscle Endurance and Mitochondrial Health in Older Adults: A Randomized Clinical Trial. JAMA Network Open. 2022;5(1):e2144279. PubMed PMID: 35050355
3. Singh A, D'Amico D, Andreux PA, et al. Urolithin A improves muscle strength, exercise performance, and biomarkers of mitochondrial health in a randomized trial in middle-aged adults. Cell Reports Medicine. 2022;3(5):100633. PubMed PMID: 35584623
4. Singh A, D'Amico D, Andreux PA, et al. Direct supplementation with Urolithin A overcomes limitations of dietary exposure and gut microbiome variability in healthy adults to achieve consistent levels across the population. European Journal of Clinical Nutrition. 2022;76(2):297-308. PubMed PMID: 34117375
5. Dao T, Nguyen TT, Gariani K, et al. Effects of Urolithin A supplementation on muscle health outcomes in humans from randomized controlled trials. Frontiers in Nutrition. 2026;13:1834344. PubMed PMID: 42559151
6. Whitfield J, McKay AKA, Tee N, et al. Evaluating the Impact of Urolithin A Supplementation on Running Performance, Recovery, and Mitochondrial Biomarkers in Highly Trained Male Distance Runners. Sports Medicine. 2025;55(12):3183-3200. PubMed PMID: 40839339
7. Zhao H, Zhu H, Yun H, et al. Assessment of Urolithin A effects on muscle endurance, strength, inflammation, oxidative stress, and protein metabolism in male athletes with resistance training: an 8-week randomized, double-blind, placebo-controlled study. Journal of the International Society of Sports Nutrition. 2024;21(1):2419388. PubMed PMID: 39487653
8. Monsalve Acevedo A, Sanctuary C, Aitken RJ, et al. Effects of Urolithin A supplementation on performance and antioxidant status in academy soccer players during preseason: a pilot randomised controlled trial. Frontiers in Nutrition. 2025;12:1674446. PubMed PMID: 41245402
9. Jamialahmadi T, Hasanpour M, Vakilian F, et al. Evaluation of Urolithin A Efficacy in Heart Failure Patients with Reduced Ejection Fraction: A Randomized, Double-blind, Crossover, Placebo-controlled Clinical Trial. Reviews on Recent Clinical Trials. 2024;19(3):221-228. PubMed PMID: 38415449
10. da Costa Pinaffi-Langley AC, Gulej R, Kaposzta Z, et al. Urolithin A and Endothelial and Cerebrovascular Function in Middle-Aged Adults With Obesity: A Randomized Clinical Trial. JAMA Network Open. 2026;9(10):e2638047. PubMed PMID: 42853569
11. Denk D, Singh A, Kasler HG, et al. Effect of the mitophagy inducer urolithin A on age-related immune decline: a randomized, placebo-controlled trial. Nature Aging. 2025;5(11):2309-2322. PubMed PMID: 41174221
12. Denk D, Singh A, Kasler HG, et al. Author Correction: Effect of the mitophagy inducer urolithin A on age-related immune decline: a randomized, placebo-controlled trial. Nature Aging. 2026;6(2):463. PubMed PMID: 41491872
13. Best SL, Gruzdys V, White M, et al. First Reported Human Cases of Urolithin A Renal Calculi. Kidney International Reports. 2026;11(6):106515. PubMed PMID: 42058113
14. Heilman J, Andreux P, Tran N, et al. Safety assessment of Urolithin A, a metabolite produced by the human gut microbiota upon dietary intake of plant derived ellagitannins and ellagic acid. Food and Chemical Toxicology. 2017;108(Pt A):289-297. PubMed PMID: 28757461
15. Aichinger G, Stevanoska M, Beekmann K, et al. Physiologically-Based Pharmacokinetic Modeling of the Postbiotic Supplement Urolithin A Predicts its Bioavailability Is Orders of Magnitude Lower than Concentrations that Induce Toxicity, but also Neuroprotective Effects. Molecular Nutrition & Food Research. 2023;67(15):e2300009. PubMed PMID: 37195009
16. Ryu D, Mouchiroud L, Andreux PA, et al. Urolithin A induces mitophagy and prolongs lifespan in C. elegans and increases muscle function in rodents. Nature Medicine. 2016;22(8):879-88. PubMed PMID: 27400265
17. Borsky P, Holmannova D, Soukup O, et al. Distinct roles of urolithin A and spermidine in mitophagy and autophagy: implications for dietary supplementation. Nutrition Research Reviews. 2025;39:e8. PubMed PMID: 41404767
18. Yang Z, Guo C, Deng Z, et al. Health Benefits and Molecular Mechanisms of Urolithin A: From a Gut Microbiota-Derived Metabolite to Translational Applications. Food Science & Nutrition. 2026;14(7):e72167. PubMed PMID: 42502809
19. Tomás-Barberán FA, García-Villalba R, González-Sarrías A, et al. Ellagic acid metabolism by human gut microbiota: consistent observation of three urolithin phenotypes in intervention trials, independent of food source, age, and health status. Journal of Agricultural and Food Chemistry. 2014;62(28):6535-8. PubMed PMID: 24976365
20. Cortés-Martín A, García-Villalba R, González-Sarrías A, et al. The gut microbiota urolithin metabotypes revisited: the human metabolism of ellagic acid is mainly determined by aging. Food & Function. 2018;9(8):4100-4106. PubMed PMID: 30004553
21. Cortés-Martín A, Iglesias-Aguirre CE, Marín A, et al. Urolithin A production drives the effects of pomegranate on the gut microbial metabolism of bile acids and cholesterol in mild dyslipidaemic overweight and obese individuals. Food & Function. 2024;15(5):2422-2432. PubMed PMID: 38329279
22. García-Villalba R, Giménez-Bastida JA, Cortés-Martín A, et al. Urolithins: a Comprehensive Update on their Metabolism, Bioactivity, and Associated Gut Microbiota. Molecular Nutrition & Food Research. 2022;66(21):e2101019. PubMed PMID: 35118817
23. Selma MV, Tomás-Barberán FA, Beltrán D, et al. Gordonibacter urolithinfaciens sp. nov., a urolithin-producing bacterium isolated from the human gut. International Journal of Systematic and Evolutionary Microbiology. 2014;64(Pt 7):2346-2352. PubMed PMID: 24744017
24. Napier BA, Allegretti JR, Feuerstadt P, et al. Multi-Species Synbiotic Supplementation Enhances Gut Microbial Diversity, Increases Urolithin A and Butyrate Production, and Reduces Inflammation in Healthy Adults: A Randomized, Placebo-Controlled Trial. Nutrients. 2025;17(17):2734. PubMed PMID: 40944126
25. Wu Q, Ma W, Liu S, et al. Urolithin A-producing Limosilactobacillus fermentum FUA033 fermentation significantly improves the sensory and antioxidant properties of strawberry juice. Food Chemistry: X. 2025;29:102805. PubMed PMID: 40726490
26. Zhang M, Cui S, Mao B, et al. Urolithin A Produced by Novel Microbial Fermentation Possesses Anti-aging Effects by Improving Mitophagy and Reducing Reactive Oxygen Species in Caenorhabditis elegans. Journal of Agricultural and Food Chemistry. 2023;71(16):6348-6357. PubMed PMID: 37040550
27. Liu Q, Liu S, Ye Q, et al. A Novel Streptococcus thermophilus FUA329 Isolated from Human Breast Milk Capable of Producing Urolithin A from Ellagic Acid. Foods. 2022;11(20):3280. PubMed PMID: 37431038

PubMed Topic Searches

1. PubMed: Urolithin A randomized trials
2. PubMed: Urolithin metabotypes
3. PubMed: Urolithin A, mitophagy and muscle
4. PubMed: Urolithin and kidney stones

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Connections

• Other Polyphenols — the parent category
• Ellagic Acid — the compound urolithin A is made from
• Walnuts: Gut Microbiome and Urolithins — the walnut feeding trials
• Pomegranate Punicalagins and Antioxidants — the main pomegranate ellagitannin
• Mitochondrial Health and Oxidative Stress — the wider mitochondria research
• Spermidine for Autophagy Induction — the broader cell clean-up pathway
• Creatine for Aging and Sarcopenia — another muscle-aging evidence base
• Mitochondria: How Your Cells Make Energy — an interactive animation
• Kidney Stones — how stones form and what they contain

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