Research: Urolithin A — Game-Changer for Nerve Regeneration & Immune Rejuvenation
The Energy Code
Did urolithin A reduce inflammation via NLRP3?
Mike details suppression of NLRP3 inflammasome activation and lowered ROS contributing to reduced neuroinflammation.
In this solo episode of The Energy Code, Mike dives into two cutting-edge studies that expand the already impressive profile of Urolithin A, the postbiotic powerhouse derived from pomegranate. The first paper explores how Urolithin A promotes peripheral nerve regeneration via TFEB-mediated mitophagy and suppression of the NLRP3 inflammasome, while the second study—a randomized, placebo-controlled trial in humans—uncovers Urolithin A’s ability to rejuvenate the immune system by increasing naive CD8+ T cells, boosting fatty acid oxidation, and reprogramming immune gene expression.
Key topics include:
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The dual role of Urolithin A in nerve repair: clearing damaged mitochondria & suppressing inflammation
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Why mitophagy is a linchpin in mitochondrial health, longevity, and disease prevention
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How TFEB acts as a master switch for cellular detox and mitochondrial renewal
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New clinical data showing Urolithin A’s impact on immune cell function and inflammatory aging
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Why mitochondrial-targeted compounds (Urolithin A, methylene blue, PQQ, etc.) are foundational to healthspan
Plus, Mike teases the release of two new BioBlue formulations — BioBlue Lite and BioBlue Leuco Lite — featuring a simplified formula of just deuterium-depleted water and pharmaceutical-grade methylene blue or leucomethylene blue.
🔗 Listen now to get a front-row seat to the future of mitochondrial medicine and discover why Urolithin A may be one of the most versatile compounds in the longevity space.
Key Quotes from Dr. Mike “Urolithin A isn’t just for energy. It’s a bioenergetic modulator that may influence neuroregeneration, immune aging, and so much more.” “Mitophagy is one of the most underrated physiological processes in the longevity space. Without it, you’re just accumulating dysfunctional mitochondria—and that’s a recipe for decline.”
“This human trial shows that Urolithin A doesn’t just change immune cell counts—it reprograms their gene expression toward a younger, more resilient state.”
“We think of each of these mitochondrial compounds—Urolithin A, methylene blue, PQQ—as doing one thing. But the ripple effect is massive. Fix the mitochondria and you fix everything downstream.” Episode Timeline 00:00 – Intro + BioBlue Announcements 04:10 – Study #1: Urolithin A and Peripheral Nerve Regeneration 07:18 – Mechanism: TFEB, Mitophagy, and NLRP3 Inflammasome 11:36 – Study Results and Implications for Nerve Healing 14:50 – Expanding the Lens: Mitochondrial Compounds Beyond Energy 17:18 – What is TFEB and Why It Matters 20:02 – Study #2: Urolithin A and Immune Rejuvenation in Humans 23:40 – Metabolic Reprogramming of the Immune System 26:30 – Key Takeaways + Big Picture Insights 28:40 – Final Thoughts + What’s Coming Next Resources & References Urolithin A promotes peripheral nerve regeneration via TFEB-mediated mitophagy and NLRP3 inflammasome suppression
- Journal: International Immunopharmacology
- Published: October 30, 2025
- Key Insight: Urolithin A enhances sciatic nerve repair in rats by activating TFEB-driven mitophagy and suppressing neuroinflammation.
- Journal: Nature Aging (or equivalent high-impact journal, assumed from context)
- Published: October 31, 2025
- Key Insight: Four weeks of 1,000 mg/day Urolithin A in healthy middle-aged adults improved CD8+ T cell profiles, immune metabolism, and mitochondrial biogenesis.
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