UA · urolithin A · mitophagy activator
500 mg · vegan · gluten-free · 30 caps
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Urolithin-A is a natural metabolite produced by gut bacteria from ellagitannins found in pomegranates, berries, and nuts. It is the first compound shown to activate mitophagy—the selective clearance of dysfunctional mitochondria—in humans.
Urolithin-A activates mitophagy by modulating the PINK1/Parkin pathway, leading to clearance of damaged mitochondria and subsequent mitochondrial biogenesis. This "mitochondrial quality control" improves cellular energy production and reduces oxidative stress.
Adults over 65 with declining muscle function, individuals with low mitophagy capacity, those interested in mitochondrial health.
People with severe kidney disease (metabolite excretion concern), pregnant or breastfeeding women, children, individuals with inflammatory bowel disease (gut microbiome alteration).
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Click individual supplement pills above to buy each on Amazon India.
✓ Morning for mitochondrial activation throughout the day
✓ Fat-containing meal may improve absorption of this lipophilic compound
Urolithin-A activates mitophagy by modulating the PINK1/Parkin pathway, leading to clearance of damaged mitochondria and subsequent mitochondrial biogenesis.
Each bar = one cited trial. Effect varies by methodology, dose, and population.
Insomnia cohort (n≈60, PSQI scale)
PSQI score <5 = good sleep quality. Lower is better.
see study
→ Safe at all doses (500–2000 mg); altered muscle mitochondrial gene expression after 4 weeks (N=healthy elderly)
see study
→ Primary endpoints (6-min walk, max ATP) NOT significant; muscle endurance improved ~20% vs placebo (N=66, 4 months)
see study
→ Improved muscle strength and exercise performance; reduced acylcarnitines and ceramides (N=older adults)
B · Safe and bioavailable; improves muscle endurance and metabolic biomarkers; primary functional endpoints mixed; promising emerging data
A plain-English read of the literature behind this supplement. Not a clinical recommendation.
Key citations: See richResearch section. Multiple RCTs support cognitive and neuroprotective properties of Urolithin-A.
How to use Urolithin-A specifically for muscle fatigue — the right dose, timing, blood markers to track, and how to know if it is working.
A clinical evidence review of Urolithin-A — RCT data, effect sizes, evidence grade, and what the numbers mean for your specific situation.
Everything you need to know about Urolithin-A — mechanism, dose, safety, buying guide for India, and what the research actually says.
SacredBod's longer take on Urolithin-A — context the structured blocks above don't capture.
Urolithin-A is arguably the most exciting mitochondrial compound to enter human trials in the past decade. Unlike supplements that merely support existing mitochondria, UA activates mitophagy—the selective autophagic clearance of damaged mitochondria—followed by biogenesis of new, functional organelles. This “quality control” mechanism is essential for cellular health but declines with age, contributing to the accumulation of dysfunctional mitochondria that leak reactive oxygen species and impair ATP production.
The first-in-human safety data is clean. Andreux and colleagues (2019, Nature Metabolism, PMID 32694802) administered single and multiple doses of UA (500–2,000 mg) to healthy elderly volunteers in a randomized trial. UA was well-tolerated at all doses, achieved dose-dependent plasma concentrations, and after four weeks of daily supplementation at 500–1,000 mg, modulated plasma acylcarnitines and altered skeletal muscle mitochondrial gene expression in directions consistent with improved metabolic health. No serious adverse events occurred, and the compound demonstrated favorable pharmacokinetics for oral administration.
The muscle endurance trial provides the most compelling functional evidence. Liu and colleagues (2022, JAMA Network Open, PMID 35050355) randomized 66 older adults (ages 65–90) to 1,000 mg UA daily or placebo for four months. The primary endpoints—six-minute walk distance and maximal ATP production—did not differ significantly between groups. However, secondary endpoints revealed significant improvements: muscle endurance (repetitions until fatigue) increased by approximately 20% in both hand and leg muscles compared to placebo. This dissociation between maximal ATP and fatigue resistance suggests UA improves mitochondrial quality rather than maximal capacity—a nuanced but meaningful distinction for daily functioning.
The biomarker picture supports the functional data. Plasma acylcarnitines and ceramides—lipid metabolites that accumulate when mitochondria fail to oxidize fatty acids—decreased significantly in the UA group. C-reactive protein, an inflammatory marker, also declined. These changes are consistent with improved mitochondrial fatty acid oxidation and reduced metabolic stress. The honest framing: UA is safe, bioavailable, improves muscle endurance in older adults, and produces favorable metabolic biomarkers. Claims of dramatic strength gains or lifespan extension remain speculative and unsupported by current RCT evidence.
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