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Dr. Mike announces upgraded BioBlue liquid formulas plus two simple new options—BioBlue Light and BioBlue Leuco Light—then breaks down two fresh urolithin A studies showing nerve-repair and immune-rejuvenation benefits via TFEB-mediated mitophagy and inflammation control.

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Dr. Mike Belkowski
What’s going on, everybody? Thanks for joining me on another episode of The Energy Code. I hope you’re having a fantastic start to November—it’s wild that we’re already in the last couple months of 2025. Quick update: as of today, at the time of this recording, we’re officially releasing our updated, upgraded formulas for the BioBlue liquid supplements. If you want all the nitty-gritty on what changed and why, check out last week’s episode where I go deep on the science behind the BioBlue methylene blue formulas.

On top of those upgrades, we’re also releasing two simple versions I think many of you will love for their minimalism: BioBlue Light and BioBlue Leuco Light. “Leuco” refers to leucomethylene blue. “Light” here means a lighter, simpler formula—just Light Water (deuterium-depleted water) plus either pharmaceutical-grade methylene blue or pharmaceutical-grade leucomethylene blue for the Leuco version. As of this recording, both Light products are available for preorder and will ship next week.

That’s it for announcements today, but expect more juicy ones next week or the week after—we have a lot dropping as we roll into the holidays. If you’re listening to this show, you’ll always hear about new releases and deep discounts first, before newsletter and social.

For today’s topic, I wanted to scan some fresh research that’s been hitting my inbox. First up: urolithin A. A paper published October 30 in International Immunopharmacology is titled: “Urolithin A promotes peripheral nerve regeneration via TFEB-mediated mitophagy and NLRP3 inflammasome suppression.”

In plain English, urolithin A is a gut-microbe–derived compound that, after peripheral nerve injury, helps the body clear damaged mitochondria and calm inflammation to support nerve repair.

Why this matters: peripheral nerve injuries are notoriously difficult to recover from. Two big bottlenecks are persistent neuroinflammation and mitochondrial dysfunction. Urolithin A, produced from dietary precursors in foods like pomegranate and walnuts, is well known for stimulating mitophagy—the selective removal of damaged mitochondria—thereby improving the ratio of healthy to dysfunctional mitochondria and boosting bioenergetics.

What the study did: researchers used a rat sciatic nerve crush model and Schwann cell cultures. They measured behavior (sciatic functional index), histology (axonal regeneration, myelination), electron microscopy for mitochondrial morphology, immunofluorescence and western blots for autophagy/mitophagy markers, and molecular docking to explore interaction with TFEB.

Key findings:
• Improved functional recovery—better sciatic functional index, less muscle atrophy, stronger axonal regeneration and remyelination.
• Increased mitophagy—more nuclear TFEB, upregulated autophagy–lysosomal genes, enhanced clearance of damaged mitochondria, and lower ROS.
• Lower inflammation—suppressed NLRP3 inflammasome activation.
• Mechanism dependent—knocking down TFEB or inhibiting autophagy wiped out the benefits; docking suggested possible direct interaction between urolithin A and TFEB.

What it means: urolithin A seems to aid nerve repair through two big levers—mitochondrial cleanup via TFEB-linked mitophagy and neuroinflammation suppression via NLRP3. This expands urolithin A’s relevance beyond energy and fitness into regenerative neurology. If you want a foundation, revisit my Aug 28 episode, “Urolithin A and B: Game Changers for Anti-Aging and Longevity.”

The second paper landed the next day (October 31)—a randomized, double-blind, placebo-controlled human trial titled: “Effect of the mitophagy inducer urolithin A on age-related immune decline.”

Why this matters: with age, we see fewer naive T cells, more exhausted T cells, and weaker responses to infections and vaccines. Mitochondrial dysfunction and impaired mitophagy are suspected drivers.

Study design: 50 healthy middle-aged adults received 1,000 mg/day urolithin A vs placebo for 4 weeks (note: many consumer products use 500 mg/day). Primary outcomes included CD3 T-cell subset shifts and immune metabolism; secondaries included cytokines (IL-6, TNF, IL-1β, IL-10), mitochondrial content, T-cell activation, monocyte bacterial uptake, and single-cell transcriptomics.

Key findings:
• Expanded naive-like, less-exhausted CD8 T cells vs placebo.
• Increased fatty acid oxidation capacity in CD8 T cells.
• Higher mitochondrial biogenesis in CD8 cells.
• More NK cells and non-classical monocytes peripherally.
• Functional gains—better T-cell activation/TNF response and improved monocyte bacterial uptake.
• scRNA-seq showed gene-expression shifts toward healthier metabolic and inflammatory states.

Takeaways and caveats: in just 4 weeks, urolithin A generated measurable rejuvenation signals in human immune profiles, supporting the idea that mitophagy enhancers can counter immunosenescence. The study was short and in healthy middle-aged adults—we still need longer-term data and broader cohorts. Mitophagy was inferred by metabolic/biogenesis markers rather than direct in-cell mitophagy assays.

Bottom line: from peripheral nerves to immune aging, urolithin A keeps showing mitochondria-centric benefits that translate to functional improvements. It remains a low-risk, high-reward option for healthspan and longevity enthusiasts, particularly alongside the lifestyle pillars—sleep, nutrition, training, light, and stress management.

Plenty more updates are coming. Stay tuned, get some sunlight when you can, and as always, light up your health.