Urolithin A 500mg | Mitophagy Activator | PINK1/Parkin-Driven Mitochondrial Renewal for Endurance & Longevity

Urolithin A 500mg — the postbiotic molecule that triggers mitophagy, the cellular recycling program that clears damaged mitochondria so cells can build new ones. Direct supplementation, because 60–70% of human gut microbiomes cannot produce it from precursor foods. The most clinically validated mitophagy activator in human trials.

The 30-second answer

Urolithin A (UroA) is a small molecule the human gut microbiome is supposed to make from ellagitannin precursors found in pomegranates, walnuts, raspberries, and strawberries. The problem: Tomás-Barberán et al. (J Agric Food Chem, 2014; Mol Nutr Food Res, 2017) classified people into three "urolithin metabotypes" — metabotype A (produces UroA), metabotype B (produces UroA + UroB + IsoUroA), and metabotype 0 (produces nothing). Only roughly 30–40% of adults are efficient producers, and that share collapses further with age, antibiotic exposure, low-fiber diets, IBD, and dysbiosis. García-Villalba 2017 documented that elderly populations and IBD cohorts shift heavily toward metabotype 0. The other 60–70% don't get the benefit no matter how many pomegranates they eat. Direct UroA supplementation skips the gut conversion step entirely — the molecule is absorbed in the small intestine and reaches the bloodstream regardless of which bacteria you carry. Once in circulation, it activates mitophagy: the PINK1/Parkin-dependent recycling cascade that identifies broken, depolarized, low-output mitochondria and clears them so the cell can replace them with healthy ones. Mitophagy is the cellular process that fails first in muscle aging (sarcopenia), neurodegeneration, metabolic decline, and immunosenescence. Three major human trials — Andreux et al. (Nature Metabolism, 2019), Liu et al. (JAMA Network Open, 2022), and Singh et al. (Cell Reports Medicine, 2022) — established safety up to 1000mg/day, mitochondrial-gene-expression improvement at 28 days, and a measurable increase in muscle endurance after four months at 500mg/day in middle-aged adults. Our 500mg dose targets the published-efficacy range used by Liu 2022 and Singh 2022.

Why mitophagy is the missing layer in most longevity stacks

Most longevity supplements address one of three well-known cellular problems:

• Fuel — NMN, NR, CoQ10, and other NAD+ precursors give mitochondria more substrate to work with.
• Cellular cleanup — Spermidine triggers general autophagy (the cell digesting any old protein or organelle). Fisetin and Quercetin trigger senolysis (clearing entire senescent "zombie" cells).
• Antioxidant defense — Glutathione, Liposomal Vitamin C, Astaxanthin, NAC, and ALA neutralize free radicals so mitochondria don't get damaged in the first place.

None of those specifically target the population of mitochondria that are already broken — the leaky, depolarized, ATP-poor mitochondria that accumulate inside otherwise healthy cells as you age. These damaged mitochondria don't produce energy; they produce reactive oxygen species. They take up space the cell could use for working mitochondria. They lower the average performance of every tissue they live in — especially skeletal muscle, brain, heart, kidney, and immune cells, where mitochondrial density is highest.

Mitophagy is the specific cellular pathway that tags these mitochondria for destruction (via the PINK1/Parkin signaling cascade) and clears them to lysosomes for breakdown. Mitophagy declines with age — that's why old muscle has more dysfunctional mitochondria than young muscle even when the total mitochondrial counts look similar (Joseph et al., Aging Cell, 2012; Drummond et al., 2014). Urolithin A is the most studied small molecule that selectively reactivates this pathway in humans without triggering general autophagy or senolysis as side effects. Ryu et al. (Nature Medicine, 2016) demonstrated this in C. elegans, where UroA extended lifespan by ~45% through PINK1/Parkin-dependent mitophagy — one of the largest replicable lifespan extensions seen with a small molecule.

How mitophagy actually works — the PINK1/Parkin cascade in plain English

Inside every cell, mitochondria carry a small voltage gradient across their inner membrane (the "membrane potential," roughly -150mV in healthy mitochondria). When a mitochondrion gets damaged — oxidative hits, mtDNA mutations, inner-membrane lipid peroxidation, complex-I dysfunction — that voltage starts to collapse. PINK1, a kinase that normally gets imported into the mitochondrial matrix and degraded, suddenly accumulates on the outer membrane of the depolarized mitochondrion. PINK1 phosphorylates ubiquitin and recruits Parkin (an E3 ubiquitin ligase) from the cytosol. Parkin paints the damaged mitochondrion with poly-ubiquitin chains. Autophagy adapter proteins (OPTN, NDP52, p62) recognize the ubiquitin coat, recruit LC3-II-decorated phagophore membranes, and engulf the doomed mitochondrion in a double-membraned autophagosome. The autophagosome fuses with a lysosome; acid hydrolases break down the contents; recycled amino acids, lipids, and metals re-enter cellular pools. The cell then signals for biogenesis (PGC-1α, TFAM) to build replacement mitochondria — the "renewal" half of the loop. UroA's distinctive action is reactivating PINK1 stabilization and Parkin recruitment in cells where the cascade has dampened with age. Beyond PINK1/Parkin, UroA also engages BNIP3 and NIX receptor-mediated mitophagy pathways, broadening coverage across cell types where Parkin expression is low.

The microbiome problem — why most people can't make their own

The biology of urolithin production was mapped by Cerdá et al. (J Agric Food Chem, 2005), Tomás-Barberán et al. (Mol Nutr Food Res, 2017), and García-Villalba et al. (Drug Metab Dispos, 2017). The pathway is:

1. You eat pomegranate, walnuts, or berries containing ellagitannins (large polyphenols including punicalagin and pedunculagin).
2. Stomach acid and gut enzymes hydrolyze ellagitannins to ellagic acid.
3. Ellagic acid passes mostly intact to the colon (poorly absorbed in the small intestine).
4. Specific colonic bacteria — primarily Gordonibacter urolithinfaciens, Gordonibacter pamelaeae, and Ellagibacter isourolithinifaciens — perform sequential lactone-ring openings and dehydroxylations to produce UroM5 → UroM6 → UroM7 → UroC → UroA (in metabotype A) or UroA + UroB + IsoUroA (in metabotype B).
5. UroA is then absorbed across the colonic epithelium, glucuronidated by liver Phase II enzymes, and circulated as UroA-glucuronide and UroA-sulfate.

If your microbiome lacks Gordonibacter or Ellagibacter in sufficient density — metabotype 0 — the pathway stops at ellagic acid, and you produce essentially zero circulating UroA. Selma et al. (Mol Nutr Food Res, 2018) found metabotype 0 prevalence ranges from 10–40% across populations and rises with age, antibiotic use, low-polyphenol diet, and IBD. Even efficient metabotype-A converters reach plasma UroA levels of only 0.1–3.0 µM after a high-dose pomegranate beverage — below the 5–10 µM range needed to trigger meaningful mitophagy in muscle cells (Andreux 2019 PK modeling).

Direct supplementation with 500mg synthesized UroA bypasses every step of this. Andreux 2019 and Singh 2022 PK data show that 500mg oral UroA reaches plasma C-max around 0.5–1.5 µM with sustained tissue levels for 8–24 hours — sufficient to upregulate mitophagy gene expression in skeletal muscle biopsies. Liu 2022 confirmed this translates to functional muscle endurance gains. The 1000mg arm (Singh 2022) showed even larger effect sizes, but with diminishing-returns kinetics consistent with a saturable transporter.

What the human research actually shows

Urolithin A is one of the few longevity molecules where the human-trial bench is meaningful, not just rodent data extrapolated upward. The clinical evidence base, summarized at trial level:

The takeaway: human translation is solid for muscle endurance and mitochondrial-marker endpoints, with strong preclinical signal for immune resilience and neuroprotection awaiting clinical trials.

Pomegranate juice vs. ellagic acid vs. direct UroA — what actually reaches your cells

Mitopure is Amazentis's branded synthesized UroA — the same molecule used in Liu 2022 and Singh 2022. Independently produced UroA at clinical-grade purity (>98% by HPLC) delivers the same plasma exposure profile per the chemistry; the difference is brand premium, not bioavailability.

The dose curve — why we ship 500mg per capsule

• Below 250mg. Sub-PK threshold. Plasma exposure too low to consistently shift muscle-biopsy mitophagy markers (Andreux 2019).
• 250mg. Lower bound of the Andreux 2019 PK study. Produces plasma UroA exposure but inconsistent functional effects. Reasonable starter dose for cautious users; suboptimal for the published muscle endpoints.
• 500mg (this product). The Liu 2022 + Singh 2022 endurance-replicated dose. Sufficient plasma exposure to upregulate muscle mitophagy gene expression (Andreux 2019 biopsy data). The published efficacy floor for the function endpoints most users care about.
• 1000mg. Singh 2022 high-dose arm. Modestly larger effect on peak-power endpoints; comparable on endurance endpoints. Diminishing returns kinetics suggest a saturable absorption transporter. Reasonable for advanced users who don't notice change at 500mg after 8–12 weeks.
• 2000mg+. No published efficacy data. PK saturation likely; not recommended.

Our 500mg / 30-capsule format provides a one-month supply at the trial-replicated dose, with the option to double to 1000mg/day for those who want to mirror the Singh 2022 high-dose arm.

What to expect, week by week

How to stack it — three architectures

UroA is a renewal molecule. It works best layered on top of a baseline that supplies fuel and protects from new damage.

(a) Mitochondrial Renewal stack — the canonical pairing

• Pure NMN 500mg or NMN 1000mg — raises NAD+, the substrate every working mitochondrion needs.
• CoQ10 400mg — electron-transport-chain cofactor; depleted by statins and aging.
• PQQ 20mg — mitochondrial biogenesis (building new mitochondria) — pairs naturally with mitophagy (clearing old ones).
• Alpha-Lipoic Acid 600mg — mitochondrial-membrane antioxidant + glucose handling.

The logic: NMN supplies the fuel substrate, CoQ10 supports active mitochondria, PQQ builds new ones, Urolithin A clears the broken ones. ALA protects the population from oxidative damage. The full Mitochondrial Renewal collection is built around this four-layer logic.

(b) Endurance & Performance stack

• Creatine Monohydrate — phosphagen energy + sarcopenia prevention (Candow 2019).
• Taurine 1000mg — mitochondrial Ca²⁺ handling and cardiac output.
• Ca-AKG 1000mg — epigenetic age reset and TCA-cycle support.
• Omega-3 2000mg — cardiovascular efficiency + anti-inflammatory baseline.

(c) Longevity & Cellular Cleanup stack

• Spermidine 10mg — general autophagy. Spermidine cleans up old proteins; UroA cleans up old mitochondria. Different programs, complementary outputs.
• Fisetin 500mg — senolytic clearance of zombie cells. Senescent cells leak SASP factors that block mitophagy in neighbors; clearing them lets UroA work better.
• Resveratrol 600mg — SIRT1 activation; pairs with NAD+ to drive mitochondrial gene expression.
• Liquid NAD+ Berry Sticks — multi-precursor longevity drink for users wanting an all-in-one renewal layer.

(d) Brain & Cognitive resilience pairing

• Omega-3 2000mg — DHA for neuronal membrane fluidity.
• Curcumin 1000mg + BioPerine — anti-neuroinflammatory; pairs with the Tuohetaerbaike 2020 / Gong 2019 preclinical brain bench.
• Pterostilbene 100mg — SIRT1 + brain-bioavailable polyphenol stack partner.
• Ashwagandha KSM-66 — cortisol regulation; chronic-stress mitophagy suppression.

(e) Immune resilience pairing

• Vitamin D3 5000 IU + K2 — immune signaling foundation.
• Glycine 1500mg + NAC — GlyNAC pair for glutathione restoration in aging T-cells (Sekhar 2021).
• Quercetin 500mg — senolytic + immunomodulatory.

Where this sits in the catalog architecture

Urolithin A is the renewal cornerstone of the Mitochondrial Renewal layer — the only molecule in the True Health Protocol catalog with a clinically validated, mitophagy-specific mechanism. It anchors three places in the catalog:

• Mitochondrial Renewal — co-listed with NMN, NR, CoQ10, PQQ, ALA, Taurine.
• Longevity Essentials — included as one of the two "renewal" picks (alongside Spermidine) in the curated essentials shortlist.
• Foundational Health — listed as a foundational mitochondrial-aging molecule even though it's an advanced layer; reflects how central mitophagy is to multi-system aging biology.

For senolytic + mitophagy "cellular cleanup" pairing, see also the Senolytics collection.

Per-capsule ingredient panel

• Urolithin A — 500mg. Synthesized to clinical purity (>98% by HPLC). Identical molecular structure to gut-microbiome-derived UroA. Same chemical entity used in Andreux 2019, Liu 2022, and Singh 2022.
• Capsule shell. Plant-cellulose (HPMC), vegan-friendly. No gelatin. No titanium dioxide.
• Excipients. Microcrystalline cellulose (flow agent), vegetable magnesium stearate (≤1%), silicon dioxide (anti-caking). No artificial colors, no synthetic dyes, no GMOs, no soy, no gluten, no dairy.
• Bottle. UV-protective HDPE. UroA is light-sensitive — original packaging matters; transferring capsules to a clear pillbox accelerates degradation.
• Format. 30 capsules / 30-day supply at 1 capsule daily, or 15-day supply at the Singh 2022 high-dose 1000mg arm.

Daily protocol — how to take it

1. Dose. 1 capsule (500mg) once daily. The Liu 2022 / Singh 2022 trial-replicated dose.
2. With food, with fat. UroA is lipophilic; food co-administration moderately improves absorption (Andreux 2019 PK note). Pair with breakfast or lunch — the largest fat-containing meal of the day.
3. Timing relative to exercise — not critical. Mitophagy is a multi-day remodeling program, not a same-session response. Pick a meal that's most consistent.
4. Stack-coupling. Co-administer with CoQ10, Omega-3, Astaxanthin, or Vitamin D3+K2 for absorption-coupling efficiency.
5. Continuous use. The published trial bench is 28 days (Andreux) and 4 months (Liu/Singh). Conservative cycling: 12 weeks on / 4 weeks off. Continuous use beyond 4–6 months is reasonable but extrapolates from the published bench.
6. Iron-supplement separation. Take iron supplements 4 hours apart from UroA — polyphenols mildly inhibit non-heme iron absorption.
7. Storage. Keep in original UV-protective bottle. Cool, dry, out of direct sunlight. Do not transfer to clear pill organizers for long periods.

Common mistakes to avoid

• Quitting at 4 weeks. Andreux 2019 showed gene-expression shifts at 28 days, but the functional endurance gains in Liu 2022 / Singh 2022 require 12–16 weeks. UroA is a slow remodeler. Three weeks is not a fair trial.
• Expecting a stimulant effect. UroA is not caffeine. It does not produce same-day energy. Users looking for an immediate boost will be disappointed and will quit before the bench-validated window.
• Eating pomegranates instead. If you're metabotype 0 or B (60–70% of adults), no amount of pomegranate produces meaningful UroA. The molecule must be supplemented directly.
• Skipping the fuel layer. UroA clears damaged mitochondria; biogenesis builds replacements. NMN, NR, or CoQ10 supports the substrate side. Pure UroA monotherapy is weaker than the combined Mitochondrial Renewal stack.
• Light-degraded product. Transferring capsules to clear weekly pillboxes for months oxidizes the molecule. Original UV-protective bottle, full course.
• Stopping 1 day before surgery instead of 7–14 days. Polyphenols interact with platelet function and CYP450 — give a real washout window before any major procedure.
• Co-dosing with iron supplements. 4-hour separation is standard for any polyphenol + iron pairing.

Who this is for

• Adults 35+ noticing exercise recovery, walking endurance, or sustained-output stamina decline.
• Users on consistent NMN/NR/CoQ10 protocols who want the renewal layer (clearing broken mitochondria) on top of the fuel layer.
• Resistance- or endurance-trained adults who have plateaued on muscle-fatigue-resistance metrics.
• Adults with reasons to suspect they are urolithin metabotype 0 or B — antibiotic history, low-polyphenol diet, IBD/IBS, or chronic dysbiosis.
• Statin users layering UroA on CoQ10 to address statin-induced mitochondrial dysfunction (Larsen 2013).
• Older adults (60+) building immune resilience — the D'Amico 2022 T-cell mitochondrial-fitness preclinical signal extrapolates to immunosenescence biology.
• Anyone running a longevity stack who wants the most clinically validated mitophagy activator on the market.

Who this is NOT for

• Pregnant or nursing individuals — UroA has not been evaluated in this population.
• Children and adolescents under 18 — no safety bench.
• Adults on chemotherapy or active cancer therapy — mitophagy interacts with cancer-cell biology in complex ways; some tumors hijack the pathway. Discuss with oncology before starting.
• Anyone with a known severe allergy to ellagitannin-rich foods (pomegranate, walnut, raspberry) — the synthesized molecule is identical to the natural metabolite, but caution is warranted.
• Users on warfarin or apixaban without prescriber awareness — polyphenol-anticoagulant interactions are a small but real consideration.
• Anyone scheduled for major surgery within 14 days — discontinue out of caution.
• People expecting a stimulant. UroA has no caffeine-like effect; it is a slow remodeler.

Quality & sourcing

Pharmaceutical-grade synthesized Urolithin A (chemical name 3,8-dihydroxy-6H-dibenzo[b,d]pyran-6-one), third-party tested for:

• Purity. >98% by HPLC per batch — same purity standard used in the published clinical trials.
• Heavy metals. USP <232> / <233> methodology — lead, arsenic, cadmium, mercury below FDA tolerable limits.
• Residual solvents. USP <467> — no Class 1 solvents detected; Class 2 below ICH Q3C limits.
• Microbial. USP <2021> / <2022> — total aerobic count, yeast/mold, absence of pathogens.
• Stability. End-of-shelf-life testing under accelerated and ambient conditions.

Manufactured in a cGMP + ISO 9001 facility. Each batch carries a Certificate of Analysis available on request via support. Packaged in UV-protective HDPE bottles — UroA degrades under light exposure, so original packaging is part of the product, not just shipping protection.

Why not just buy it on Amazon?

• Per-batch HPLC verification. Many Amazon UroA listings publish a single COA from one batch and reuse it across the SKU's life. Our 500mg ships with batch-tied HPLC purity records, not a frozen marketing PDF.
• Catalog-architecture positioning. Urolithin A only delivers its full benefit when stacked correctly — fuel layer (NMN/NR/CoQ10) underneath, antioxidant defense layer (ALA/Glutathione) around it, senolytic clearance (Fisetin/Quercetin) periodically. The True Health Protocol catalog is designed as a coherent stack; an isolated Amazon SKU can't be.
• Fresh, light-protected stock. UroA is light-sensitive. Long warehouse residency and clear-window shipping containers degrade the molecule before it reaches you. Our fulfillment chain is short and uses UV-protective bottles end-to-end.

Safety, interactions, and timing notes

• General safety. Andreux 2019 dosed up to 1000mg/day for 28 days; Liu 2022 and Singh 2022 dosed up to 1000mg/day for 4 months — no clinically significant adverse events. UroA is among the best-tolerated longevity molecules in human-trial data.
• Anticoagulants. Pomegranate-derived polyphenols can affect CYP3A4 and may potentiate some anticoagulants. Direct UroA has a smaller theoretical interaction risk than whole-pomegranate products, but caution is warranted on warfarin or apixaban — coordinate with your prescriber.
• Cancer therapy. Mitophagy can either promote or inhibit cancer-cell survival depending on tumor type and stage. Always discuss UroA with oncology if you are in active treatment.
• Pre-surgery. Out of caution, discontinue 7–14 days before any major surgery, consistent with general antioxidant-and-polyphenol-supplement guidance.
• Pomegranate-allergy individuals. Although UroA is the metabolite (not the source food), users with documented anaphylaxis to pomegranate, walnut, or raspberry should consult an allergist before initiating.
• Iron-deficiency anemia. Polyphenols can mildly inhibit non-heme iron absorption when co-administered. Take iron supplements at a different meal, 4 hours apart.
• Long-term use. Longest published continuous use in trial is 4 months (Liu 2022, Singh 2022). Users running the molecule continuously beyond 4–6 months are extrapolating from the published bench.
• GI tolerance. Mild stomach discomfort in a small minority of users on day 1–3; nearly always resolves by day 4 with food co-administration.

FAQ

Q: Why not just eat pomegranates?
A: Because 60–70% of adults are urolithin metabotype B or 0 — their gut bacteria can't convert ellagic acid to meaningful UroA levels (Tomás-Barberán 2017, Selma 2018). Even efficient producers reach only 0.1–3 µM plasma UroA — below the mitophagy threshold suggested by Andreux 2019 PK modeling. Direct UroA supplementation bypasses the metabotype lottery entirely.

Q: How do I know if I'm a metabotype 0?
A: There is no easy at-home test — clinical metabotype determination requires a urinary urolithin profile after a polyphenol challenge dose. Practical proxies: long history of antibiotic use, low-fiber/low-polyphenol diet, IBD or IBS, advancing age, or the simple observation that pomegranate juice has never produced any noticeable energy or endurance change for you. The simplest answer: if you want UroA's mitophagy benefit, supplement directly rather than guessing your microbiome.

Q: Does Urolithin A increase NAD+?
A: Indirectly. UroA doesn't supply NAD+ precursors the way NMN or NR do, but by clearing damaged mitochondria and supporting the building of new ones, it improves the cellular machinery that uses NAD+. Pair UroA with NMN or NR for the fuel + renewal pairing.

Q: Is this the same molecule as Mitopure?
A: Yes — UroA is a single defined small molecule, identical regardless of brand. Mitopure is Amazentis's branded version that was used in the Liu 2022 and Singh 2022 trials. Independently produced UroA at clinical-grade purity (>98% HPLC) delivers the same plasma exposure profile per the chemistry. The trial data generalizes to the molecule, not the brand.

Q: How does it compare to Spermidine?
A: Different programs. Spermidine triggers general autophagy — clearing any old protein or organelle. UroA triggers mitophagy — selectively clearing damaged mitochondria via PINK1/Parkin. They're complementary, not substitutes. Many longevity protocols run both: Spermidine 10mg daily for general cellular renewal, UroA 500mg for the mitochondrial-specific layer.

Q: How does it pair with senolytics like Fisetin?
A: Strongly. Senescent cells leak SASP factors that suppress mitophagy in neighboring healthy cells. Clearing them with periodic Fisetin dosing (typical protocols: 2 days/month at 500–1000mg) creates a cleaner cellular environment for daily UroA-driven mitophagy to operate in.

Q: How long can I take it continuously?
A: The longest published continuous use is 4 months (Liu 2022, Singh 2022) without safety signals. Many users in real-world longevity protocols run UroA continuously beyond 4 months, but that exceeds the published bench. Conservative cycling: 12 weeks on / 4 weeks off, or continuous with periodic biomarker monitoring.

Q: Should I take 500mg or 1000mg?
A: Start at 500mg — that's the Liu 2022 endurance-replicated dose, and it produced significant gains over placebo on every endurance endpoint. If after 12–16 weeks you don't notice the expected change, doubling to 1000mg (the Singh 2022 high-dose arm) is reasonable. Above 1000mg there is no published efficacy data and PK saturation is likely.

Q: Can I take it with statins?
A: Yes — and this is one of the more sensible pairings. Statins deplete CoQ10 and impair mitochondrial function (Larsen 2013); UroA improves mitophagy of statin-damaged mitochondria. The standard pairing is statin + CoQ10 400mg + UroA 500mg.

Q: What about Parkinson's risk and PINK1 mutations?
A: PINK1 loss-of-function mutations cause autosomal recessive juvenile parkinsonism — these patients have impaired baseline mitophagy. UroA upregulates the PINK1/Parkin pathway in cells with normal copies of the gene; preclinical data (Tuohetaerbaike 2020) suggests benefit in dopaminergic neurons. Human trials in Parkinson's populations are pending. Discuss with neurology if you have a personal or family history of early-onset Parkinson's.

Q: Does UroA cause autophagy fatigue or compensate the wrong way?
A: No published evidence of it. Unlike systemic mTOR inhibitors (which broadly suppress protein synthesis), UroA is selective for the PINK1/Parkin and BNIP3/NIX pathways. The 4-month bench in Liu 2022 / Singh 2022 found no negative compensatory signal.

Q: Will it help with sarcopenia?
A: The clinical bench (Liu 2022, Singh 2022) is in middle-aged adults with declining muscle endurance — adjacent to but not formally diagnostic of sarcopenia. Combined with resistance training, adequate protein intake (1.2–1.6 g/kg/day), Creatine, and the broader Mitochondrial Renewal stack, UroA fits cleanly into a sarcopenia-prevention protocol.

Q: Vegan?
A: Yes. Plant-cellulose (HPMC) capsule, vegan-formula excipients, no animal-derived ingredients.

Q: Does it interact with NMN or NR?
A: No negative interaction. UroA + NMN/NR is a deliberate pairing — fuel + renewal. The combination is the backbone of the Mitochondrial Renewal collection.

Q: How is this different from a CoQ10 product?
A: Different mechanism, complementary use. CoQ10 is an electron-transport-chain cofactor — it supports mitochondria that are currently working. UroA clears mitochondria that are broken, so the cell can build new ones. Both belong in a mitochondrial-aging stack.

Q: Why is the bottle so dark / opaque?
A: UroA is light-sensitive. UV exposure degrades the molecule, so we ship in UV-protective HDPE — original packaging matters more here than for most supplements. Don't transfer to a clear weekly pillbox for extended periods.

Q: Money-back guarantee?
A: Yes — every True Health Protocol product is covered by our money-back guarantee.

Selected references

• Andreux PA 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;1:595–603.
• 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;5(1):e2144279.
• Singh A 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.
• Ryu D et al. Urolithin A induces mitophagy and prolongs lifespan in C. elegans and increases muscle function in rodents. Nature Medicine. 2016;22:879–888.
• D'Amico D et al. Impact of the natural compound urolithin A on health, disease, and aging. Trends in Molecular Medicine. 2021;27(7):687–699.
• D'Amico D et al. Urolithin A improves mitochondrial health, reduces cartilage degeneration, and alleviates pain in osteoarthritis. Aging Cell. 2022;21(8):e13662.
• Luan P et al. Urolithin A improves muscle stem cell function in aged mice via mitophagy reactivation. Cell Reports Medicine. 2021.
• Tomás-Barberán FA et al. Urolithins, the rescue of "old" metabolites to understand a "new" concept: Metabotypes as a nexus among diet, gut microbiota, and human health. Mol Nutr Food Res. 2017;61(1).
• Selma MV et al. The gut microbiota metabolism of pomegranate or walnut ellagitannins yields two urolithin-metabotypes that correlate with cardiometabolic risk biomarkers. Mol Nutr Food Res. 2018;62(9):e1701039.
• García-Villalba R et al. Metabolism of different dietary phenolic compounds by the urolithin-producing human-gut bacteria Gordonibacter urolithinfaciens and Ellagibacter isourolithinifaciens. Drug Metab Dispos. 2017;45(6):742–751.
• Cerdá B et al. Identification of urolithin A as a metabolite produced by human colon microflora from ellagic acid and related compounds. J Agric Food Chem. 2005;53(14):5571–5576.
• Tuohetaerbaike B et al. Pancreas protective effects of urolithin A on type 2 diabetic mice and its potential mechanisms. Phytomedicine. 2020.
• Gong Z et al. Urolithin A attenuates memory impairment and neuroinflammation in APP/PS1 mice. J Neuroinflammation. 2019;16(1):62.
• Joseph AM et al. The impact of aging on mitochondrial function and biogenesis pathways in skeletal muscle of sedentary high- and low-functioning elderly individuals. Aging Cell. 2012;11(5):801–809.
• Drummond MJ et al. Skeletal muscle amino acid transporter expression is increased in young and older adults following resistance exercise. J Appl Physiol. 2011;111(1):135–142.
• Larsen S et al. Simvastatin effects on skeletal muscle: relation to decreased mitochondrial function and glucose intolerance. J Am Coll Cardiol. 2013;61(1):44–53.
• Sekhar RV et al. GlyNAC supplementation improves glutathione deficiency, oxidative stress, mitochondrial dysfunction, inflammation, aging hallmarks, metabolic defects, muscle strength, cognitive decline, and body composition in older adults. J Gerontol A Biol Sci Med Sci. 2021.
• Candow DG et al. Effectiveness of creatine supplementation on aging muscle and bone: focus on falls prevention and inflammation. J Clin Med. 2019;8(4):488.

Citations of published research are provided for context and education and do not constitute endorsement of this product by the cited researchers, journals, or institutions.

Read more on the science

• Mitochondrial Health Supplements: The Renewal Layer Most Stacks Miss
• NMN, NAD+, and the Longevity Foundation
• The Protocols — True Health Protocol Methodology
• Our Science — How We Choose Molecules
• Longevity Essentials Collection
• Foundational Health Collection
• Mitochondrial Renewal Collection
• Senolytics Collection

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These statements have not been evaluated by the Food and Drug Administration. This product is not intended to diagnose, treat, cure, or prevent any disease. Consult a qualified healthcare provider before starting any supplement, especially if pregnant, nursing, taking prescription medication, undergoing cancer therapy, scheduled for surgery, or managing a chronic condition.