Urolithin A is a compound your gut bacteria can produce when you consume foods rich in ellagitannins: polyphenols found in pomegranates, walnuts, and certain berries. Unlike the polyphenols you eat directly, urolithin A is formed through microbial conversion in the large intestine, which means your ability to produce it depends heavily on your gut microbiome composition. Not everyone produces urolithin A efficiently, and emerging research suggests that biological sex may be one variable influencing how much your body makes and absorbs.
Interest in urolithin A has grown because of its proposed role in mitophagy: a cellular housekeeping process in which damaged or dysfunctional mitochondria are identified, removed, and replaced with healthier ones. Mitochondria are the energy-producing structures in nearly every cell, and their gradual decline is linked to age-related losses in muscle function, endurance, and overall cellular health. This article reviews what current evidence says about urolithin A with particular attention to findings relevant to women, including sex-based differences in bioavailability and production.
Key Takeaways
- Urolithin A is proposed to support mitophagy, the process by which cells remove and replace damaged mitochondria; the evidence is mostly from cells, worms and mice, and one mouse study found the benefit did not depend on mitophagy [6][7][8].
- Sex-based differences in urolithin A production from dietary precursors have been identified, meaning women and men may not make or absorb the same amounts from the same food sources [1].
- Individual gut microbiome composition determines your ‘urolithin metabotype,’ and not everyone efficiently converts dietary ellagitannins into urolithin A regardless of how much they eat [2].
- A 2022 company-funded RCT in 66 older adults, about three-quarters of them women, did not meet its primary endpoints, with muscle endurance improving only as a secondary endpoint; sex-stratified outcomes and data in younger women remain limited [3].
- Research specifically examining urolithin A in women across hormonal life stages, particularly perimenopause and postmenopause, is an important gap that current evidence does not yet fill.
How Urolithin A Works: The Mitophagy Mechanism
Mitochondria accumulate damage over time. In healthy cells, a quality-control process called mitophagy identifies and removes dysfunctional mitochondria so that newer, more efficient ones can take their place. Urolithin A appears to support this process by activating cellular signaling pathways involved in mitochondrial turnover. When mitophagy is impaired, damaged mitochondria accumulate, contributing to energy deficits in muscle and other tissues.
Research in a severe illness context illustrates what can go wrong when this process breaks down. A 2025 study found that sepsis disrupts autophagy, the broader cellular recycling process of which mitophagy is a part, and that this disruption contributed to long-term muscle and mitochondrial dysfunction. Urolithin A showed potential to address this by restoring autophagy function in that model [4]. While sepsis is an extreme scenario, the finding highlights the importance of functional mitophagy for sustained muscle health and points to a plausible mechanism through which urolithin A may support it.
Sex-Based Differences in Urolithin A Production
One of the most directly relevant findings for women is that the production and absorption of urolithin A from its dietary precursors may differ between sexes. A 2025 study using milk exosome-encapsulated ellagic acid, a precursor that gut bacteria convert into urolithin A, found measurable sex-based differences in bioavailability, urolithin production, and gut microbiota modulation [1]. Women and men in that study showed different patterns of urolithin metabolite levels, suggesting that hormonal, microbiome, or metabolic differences between sexes influence how urolithin A is synthesized and utilized.
Research note: In a small group of healthy women followed after childbirth, metabotypes A and B were each about 50% at the first visit and none were metabotype 0 [10].
This finding carries practical implications. If women produce or absorb urolithin A differently from men, then research conducted predominantly in male participants, or without sex-stratified analysis, may not accurately represent what women can expect from dietary or supplemental urolithin A. It also underscores the importance of future studies that specifically examine urolithin A outcomes in women across different life stages, including the reproductive years, perimenopause, and postmenopause.
Urolithin Metabotype: Why Not Everyone Produces Urolithin A Equally
The ability to convert dietary ellagitannins into urolithin A varies substantially between individuals, and researchers classify people into distinct ‘urolithin metabotypes’ based on which urolithin metabolites appear in their urine or plasma. Some people are efficient urolithin A producers (Metabotype A), others produce a different metabolite profile (Metabotype B or AB), and a subset produces very little urolithin regardless of diet.
A 2026 study examining jaboticaba peel and seed powder, an ellagitannin-rich food, found that both metabotype and body weight category influenced urolithin excretion patterns in adults [2]. This means two women consuming identical polyphenol-rich diets could have meaningfully different urolithin A levels. For women relying on food sources alone, this variability is worth understanding. Direct supplementation with purified urolithin A bypasses the gut conversion step and may offer more predictable levels, though dose-response data in women specifically remain limited.
Muscle Endurance and Mitochondrial Health: The Clinical Evidence
One placebo-controlled human trial tested urolithin A supplementation directly. A 2022 randomized clinical trial published in JAMA Network Open found no significant improvement versus placebo on its primary endpoints (6-minute walk distance and muscle energy production) in 66 adults aged 65 to 90, while muscle endurance, a secondary endpoint, improved [3]. Muscle endurance, a secondary endpoint, improved at 2 months, though the standard deviations were very large, and the trial was funded by Amazentis [3]. The trial included both men and women, though sex-stratified analyses were not the primary focus of the published report.
A 2024 systematic review of five human studies (250 healthy people) found some strength and endurance signals but no effect on physical function or on maximal mitochondrial energy production [9].
Muscle function matters across all life stages but takes on particular significance for women as they age. Estrogen plays a documented role in maintaining muscle mass, and its decline during menopause is associated with accelerated loss of muscle mass and function: a process called sarcopenia. Mitochondrial health is one contributing factor to skeletal muscle performance, and while urolithin A is not a treatment for menopause-related muscle changes, supporting mitochondrial turnover may be one component of healthy muscle aging. The evidence from [3] is encouraging but was conducted in adults aged 65 and older, and data on younger women remain limited.
Polyphenols and Biological Age: What the Evidence Actually Shows
A 2023 randomized controlled trial examined the effect of a polyphenol-enriched dietary intervention on biological age as assessed by DNA methylation clocks: a molecular measure of how cells are aging relative to chronological age [5]. The DIRECT PLUS trial found that the polyphenol-enriched arm showed attenuation of biological age compared to a standard Mediterranean diet group. It is important to note that this study tested a broad polyphenol dietary pattern, not urolithin A in isolation, and the results cannot be attributed to urolithin A specifically.
Urolithin A is one of several bioactive compounds produced from dietary polyphenols, and claiming it alone drives reductions in biological age would overreach what this study supports. However, the finding does reinforce the broader concept that dietary polyphenols, including precursors to urolithin A, are associated with cellular-level changes relevant to aging [5]. For women interested in long-term cellular health, a diet rich in ellagitannin-containing foods fits within a well-supported framework of healthy aging, even if urolithin A’s independent contribution to biological age remains to be established.
Practical Considerations for Women
Women who want to increase urolithin A through diet can focus on foods high in ellagitannins: pomegranates and pomegranate juice, walnuts, raspberries, strawberries, and cloudberries. However, given the wide variability in gut-mediated conversion, dietary sources alone may not reliably raise urolithin A levels for all women [2]. Supplemental urolithin A bypasses this conversion step, but most clinical trial data come from older adult populations and were not designed to capture sex differences [3].
Women who are pregnant, breastfeeding, or taking medications that affect mitochondrial function or autophagy pathways should speak with a healthcare provider before adding urolithin A to their routine. The sex-based differences identified in precursor bioavailability research [1] suggest that findings may not translate directly between the sexes, although the main older-adult trial enrolled mostly women [3]. As with any supplement, urolithin A is best viewed as a potential complement to, not a replacement for, a balanced diet, regular physical activity, and evidence-based preventive care.
🛒 Where to Buy Urolithin A
- Timeline Mitopure SoftgelsClinically studied
softgels, 500 mg/day: The clinically studied form (Amazentis); used in the human trials. - Pure Encapsulations Renual
caplique capsules, 250 mg Mitopure Urolithin A/serving (with resveratrol + CoQ10): adds resveratrol and CoQ10, a combination the published urolithin A trials did not test. - ProHealth Longevity Urolithin A
capsules, 500 mg: Longevity-focused brand, often higher dose. - Double Wood Urolithin A
capsules, 250-500 mg: Budget-friendly, widely available, COA on request.
As an Amazon Associate we earn from qualifying purchases. Prices and availability vary; verify dose and third-party testing before buying.
A Note on the Evidence
The research on urolithin A in women specifically is still in early stages: most trials have not been designed to detect sex differences, studies in women across hormonal life stages are lacking, and long-term safety data are limited. This article is for informational purposes only and does not constitute medical advice: consult a qualified healthcare provider before starting any supplement, particularly if you are pregnant, breastfeeding, managing a chronic condition, or taking medications.
Frequently Asked Questions
Does urolithin A work differently in women than in men?
Emerging evidence suggests it may. A 2025 study found sex-based differences in bioavailability, urolithin production, and gut microbiota response when women and men consumed the same ellagic acid precursor [1]. The underlying reasons (which may include hormonal differences, gut microbiome composition, or metabolic variation) are not yet fully understood, and more research comparing outcomes between sexes is needed.
Can I get enough urolithin A from food alone?
It depends on your gut microbiome. Your body does not absorb urolithin A directly from food; gut bacteria must first convert ellagitannins found in pomegranates, walnuts, and berries into urolithin A. Research shows that urolithin metabotype, your personal conversion efficiency, varies substantially between individuals and can be influenced by body weight and other factors [2]. Some people produce very little urolithin A regardless of dietary intake.
What is the strongest clinical evidence for urolithin A and muscle health?
A 2022 company-funded randomized trial in 66 older adults found no significant improvement versus placebo on its primary endpoints; muscle endurance, a secondary endpoint, improved [3]. It is one of only a few placebo-controlled human trials, and a 2024 systematic review of five human studies (250 healthy people) found no effect on physical function [9]. The trial included both sexes but was not statistically powered to detect sex-specific differences in outcomes.
Is urolithin A relevant during or after menopause?
There is no published clinical trial specifically examining urolithin A supplementation in perimenopausal or postmenopausal women as of this writing. However, urolithin A’s proposed mechanism, supporting mitophagy and mitochondrial renewal, is plausibly relevant to the muscle function changes that accompany hormonal shifts at menopause. Research on autophagy disruption and muscle health [4] reinforces why mitochondrial quality control matters in aging muscle, but menopause-specific data are an important gap.
Does urolithin A slow aging?
A 2023 RCT found that a polyphenol-enriched dietary pattern attenuated biological aging as measured by DNA methylation clocks [5]. However, that trial tested a broad range of polyphenols together, not urolithin A in isolation, so it would be inaccurate to attribute the finding to urolithin A specifically. The mitophagy mechanism is plausibly connected to cellular aging, but direct human evidence for urolithin A and biological age attenuation is not yet established.
Is urolithin A safe for women to supplement with?
The 2022 clinical trial in older adults reported no serious adverse events with urolithin A supplementation over the study period [3]. However, that trial was not designed to assess long-term safety specifically in women, and data for women who are pregnant, breastfeeding, or managing hormone-sensitive conditions are not available. Speaking with a healthcare provider before starting supplementation is the appropriate first step.
References
- Ávila-Gálvez MÁ et al. Oral Delivery of Ellagic Acid Encapsulated in Milk Exosomes: Sex-Based Differences in Bioavailability, Urolithin Production, and Gut Microbiota Modulation. Molecular nutrition & food research (2025). PMID 40351018
- Leite IB et al. The effect of jaboticaba peel and seed powder intake for three weeks on urolithin metabotype and excretion in normoweight and overweight/obese Brazilians. Food research international (Ottawa, Ont.) (2026). PMID 41794475
- Liu S et al. Effect of Urolithin A Supplementation on Muscle Endurance and Mitochondrial Health in Older Adults: A Randomized Clinical Trial. JAMA network open (2022). PMID 35050355
- Pierre A et al. Sepsis Induces Long-Term Muscle and Mitochondrial Dysfunction due to Autophagy Disruption Amenable by Urolithin A. Journal of cachexia, sarcopenia and muscle (2025). PMID 40817441
- Yaskolka Meir A et al. The effect of polyphenols on DNA methylation-assessed biological age attenuation: the DIRECT PLUS randomized controlled trial. BMC medicine (2023). PMID 37743489
- Gao Z et al. Urolithin A protects against acetaminophen-induced liver injury in mice via sustained activation of Nrf2. International journal of biological sciences (2022). PMID 35342347
- Peter M. J. Quinn et al. PINK1/PARKIN signalling in neurodegeneration and neuroinflammation. Acta Neuropathologica Communications (2020). PMID 33168089
- Ryu D et al. Urolithin A induces mitophagy and prolongs lifespan in C. elegans and increases muscle function in rodents. Nature medicine (2016). PMID 27400265
- Kuerec AH et al. Targeting aging with urolithin A in humans: A systematic review. Ageing research reviews (2024). PMID 39002645
- Adrián Cortés‐Martín et al. Urolithin Metabotypes can Anticipate the Different Restoration of the Gut Microbiota and Anthropometric Profiles during the First Year Postpartum. Nutrients (2019). PMID 31484413
These statements have not been evaluated by the Food and Drug Administration. This information is not intended to diagnose, treat, cure, or prevent any disease. Content is for informational purposes only and is not medical advice; consult a qualified healthcare provider before starting any supplement. As an Amazon Associate we earn from qualifying purchases.