The mitophagy activator urolithin A is safe and induces a molecular signature of improved mitochondrial and cellular health in humans.
Level 3 - non-randomized controlled study
First-in-human intervention study without randomization or control details specified in abstract
PubMed 32694802 · doi:10.1038/s42255-019-0073-4
What was done
First-in-human clinical trial administering urolithin A (UA) either as a single dose or as multiple doses over a 4-week period (including 500 mg and 1,000 mg doses) to healthy, sedentary elderly individuals. The primary outcome was safety; secondary outcomes were plasma bioavailability, plasma acylcarnitines, and skeletal muscle mitochondrial gene expression.
What was found
UA demonstrated a favourable safety profile and was bioavailable in plasma at all doses tested. A 4-week treatment at 500 mg and 1,000 mg modulated plasma acylcarnitines and skeletal muscle mitochondrial gene expression. The abstract does not provide exact numerical values, effect sizes, or statistical confidence intervals.
Why it matters
Provides initial human evidence that oral urolithin A is bioavailable, tolerated, and induces molecular signatures associated with mitochondrial health in older adults, translating earlier animal findings.
Limits
The abstract does not disclose sample size, blinding, or control group details. The duration was short (4 weeks), and outcomes were limited to molecular biomarkers rather than functional muscle strength or clinical endpoints.
Cited by
- supports Human muscle biopsy studies confirm that oral urolithin A activates mitophagy.
- supports Randomized controlled trials in humans demonstrate that urolithin A stimulates mitophagy in blood cells and skeletal muscle biopsy samples.