Ever stand up after hours at a desk and your knees sound like a rusty hinge? Or finish a weekend run and feel like your joints mailed you a strongly worded complaint by Tuesday?

In this Deep Dive, we unpack a 2025 paper from Discovery Medicine titled “Urolithin B promotes meniscal regeneration and prevents the development of osteoarthritis in mice.” The headline is big: not just less inflammation or less pain signaling, but actual meniscus repair signals in a disease model that normally accelerates joint breakdown.

We break down what Urolithin B is, why food sources aren’t reliable for most people, and how this molecule appears to flip joint cells from destruction mode to construction mode by suppressing inflammatory cytokines and tissue-chewing enzymes (like MMP-13) while boosting cartilage-building programs (like SOX9, collagen, and VEGF). We also connect the mechanism to the real-world “why” behind delivering Urolithin B directly (as discussed in the episode).

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Article Discussed in Episode:

Urolithin B Promotes Meniscal Regeneration and Prevents the Development of Osteoarthritis in Mice

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Key Quotes From Dr. Mike:

“(Urolithin B) is tackling what many would call the holy grail of joint health… regeneration.”

“(Urolithin B) literally flipped the switch from a catabolic breakdown state to an anabolic build-up state.”

“You’re not masking a symptom, you’re trying to reboot the regenerative machinery.”

“Defend, protect, and rebuild all in one molecule." (In regards to Urolithin B)

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Key points

The big promise: regeneration — not just symptom relief.

What Urolithin B is: a gut-derived metabolite from ellagic-acid-rich foods (pomegranate, walnuts, berries).

Why diet isn’t enough for many: large portion of people may be low/non-producers due to microbiome variability.

Meniscus 101: fibrocartilage “shock absorber” between femur and tibia; when it fails, OA risk rises fast.

Current standard care problem: many options manage symptoms more than they restore tissue.

In vitro findings: Urolithin B was non-toxic and calmed IL-1β–triggered inflammatory signaling.

Stops the demolition crew: reduced destructive ECM enzymes (highlighted: MMP-13, ADAMTS enzymes).

Starts the construction crew: increased cartilage matrix building blocks (collagens, aggrecan).

Flips genetic switches: boosted transcription factors tied to cartilage formation (spotlight: SOX6/SOX9).

Supports “supply lines”: increased VEGF (angiogenesis signal), relevant given meniscus’ poor blood supply.

In vivo mouse OA model: meniscus-injury OA developed as expected in controls; EuroB-treated animals showed less erosion and better structure.

Consistent mechanism across dish → animal: inflammatory markers down, matrix destruction down, repair signals up.

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Episode timeline 

0:00–0:44 — Cold open: creaky joints, “repair the hinge” idea

0:44–1:22 — Episode mission + 2025 paper intro (Urolithin B, meniscus regeneration, OA prevention in mice)

1:34–2:17 — What Urolithin B is + “signal” framing

2:48–4:11 — Meniscus basics, OA problem, limits of symptom-based treatments

4:18–6:12 — Petri-dish phase: safety + IL-1β inflammation model + suppression of cytokines/destructive enzymes

6:18–8:13 — Rebuild signals: collagens/aggrecan, SOX6/SOX9, VEGF, proliferation markers

8:57–10:40 — Mouse OA model: structural improvements + tissue protein markers confirm mechanism

10:48–11:46 — “Triple threat” summary: anti-inflammatory, anti-catabolic, anabolic

11:49–12:55 — Why food conversion is unreliable (microbiome “lottery”) + direct-delivery rationale

12:59–14:31 — Big-picture future: “inducing repair” + closing call-to-action / wrap

-

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Most people think of health as a game of chemistry and calories. But there is a hidden layer to reality that governs how your biology functions before a single molecule ever moves: subtle energy.

In this episode, Nico Martens joins Dr. Mike to pull back the curtain on BioGeometry and vibrational physics. We explore how "The Card", which is a simple-looking tool engraved with sacred geometric symbols, can objectively alter the taste of wine and the energetic quality of a room by tapping into the "unseen" world. Nico explains why our modern environments are "energetically toxic" and how we can use the principles of BioGeometry to harmonize our homes, mitigate EMF stress, and support mitochondrial vitality at a quantum level.

Then comes the shift. We move from theory to application, discussing how these subtle forces interact with our physical structure. From clearing the "energetic memory" of hotel rooms to using geometric shapes to balance the body's internal systems, this episode provides a blueprint for tapping into the next evolution of human health.

Key Quotes From Nico Martens:

“Subtle energy are really all these energies that most of us cannot perceive with our regular senses, but that actually run this entire reality.”

“If you go down to the base level and you break it all the way down, there is no physical matter. There's only vibration.”

“Your environment is either feeding you or it's depleting you.”

“BioGeometry is the language of nature’s design system.”

“The answers to all the challenges we face in the physical world... lay in the unseen.”

Key Points:

Episode Timeline:

0:00–4:30 — The Wine Story: How Nico used "The Card" to change Dr. Mike’s wine; intro to Nico’s background.

4:31–15:40 — Nico’s Journey: From the physical world to the quantum; meeting in a creek in Tennessee.

16:40–21:15 — Defining Subtle Energy: Beyond the five senses; why Tesla was right about vibration.

21:30–35:20 — What is BioGeometry? The science of shape, the "BG3" centering quality, and nature’s design language.

35:35–45:10 — Environmental Stress: How EMFs and "dirty" energy impact mitochondrial health and the "Mitochondrial Matrix."

45:25–55:00 — Practical BioGeometry: Harmonizing your home and why your environment is either feeding or depleting you.

55:10–01:10:30 — "The Card" Deep Dive: How it works, what the symbols mean, and how to use it in daily life.

01:10:45–01:30:33 — The Unseen World: Why the next evolution of humanity lies in tapping into these subtle dimensions; closing thoughts.

Where to learn more from & about Nico Martens:

IG: @nicomartens76

Nico Martens Coaching

The Wellness Enterprise

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Deuterium depleted water: Litewater (code: DRMIKE)

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Most people think head trauma equals concussion. But there’s a silent thief that can ride along with blunt-force injury and steal something just as life-altering: vision.

In this Deep Dive, we break down traumatic optic neuropathy (TON): how shockwaves and shearing forces injure the optic nerve at a bony choke point (the optic canal), then trigger swelling, compartment-syndrome-like pressure, ischemia, and a vicious “cellular riot” that kills neighboring neurons in the days that follow. The brutal reality: traditional options like steroids, surgical decompression, or “observation” often lack strong evidence for reliably saving sight.

Then comes the twist. We review a 2025 peer-reviewed rat study (21-day follow-up) testing methylene blue (MB)immediately after optic nerve crush. MB acts like an electron “bypass road” in the mitochondrial chain, helping keep ATP online when parts of the system are damaged, while also inhibiting the trauma-driven iNOS nitric-oxide flood that creates destructive peroxynitrite. Functionally, the study shows striking preservation of retinal signaling and retinal ganglion cell function, suggesting that immediate metabolic support may blunt secondary degeneration during the “golden window” after injury.

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Article Discussed in Episode:

Neuroprotective Effect of Methylene Blue in a Rat Model of Traumatic Optic Neuropathy

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Key Quotes From Dr. Mike:

“There’s a silent thief that often rides shotgun with these head injuries… your vision.”

“The optic nerve… is basically the data cable connecting the camera of your eye to the hard drive of your brain.”

“Methylene blue… is for all intents and purposes, artificial respiration for the cell’s engine.”

“Methylene blue… can act like a temporary bypass road for the bucket brigade.”

“You support the energy, you save the structure, you save the function.”

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Key points

TON can steal vision after blunt trauma even without a direct eye puncture; the optic nerve is a vulnerable “data cable” through a tight bony tunnel (optic canal).

The most devastating loss often comes from secondary degeneration: swelling inside the canal raises pressure, chokes blood flow (ischemia), and triggers a cascading “cellular riot.”

Standard care is frustratingly limited: steroids, decompression surgery, or observation are described as controversial with limited hard evidence of superiority.

There’s a “golden window” (roughly 14–30 days) where tissue is struggling but not fully dead—yet medicine lacks reliable tools to stop the cascade.

Methylene blue is not a random supplement: it’s on the World Health Organization list and has long clinical use (e.g., methemoglobinemia).

Mechanism #1: MB acts as an electron cycler, bypassing damaged complexes to keep electron flow and ATP production going during ischemic stress.

Mechanism #2: MB inhibits iNOS, helping shut down the runaway nitric-oxide surge that forms peroxynitrite, a highly destructive oxidant.

In the rat optic nerve crush model, MB given immediately (and repeated doses over 24 hours) produced major functional preservation on ERG measures (especially inner-retina processing signals) and strong evidence of retinal ganglion cell signal preservation, aligning with better structural survival at 21 days.

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Episode timeline 

1:38–3:38 — TON explained: vision loss after trauma + why medicine feels helpless; introduce MB as the twist

4:01–5:57 — The study: 2025 rat model, what they tested and why MB fits the Energy Code framework

6:11–10:52 — Mechanism and injury cascade: optic canal choke point → swelling → ischemia → secondary degeneration + “cellular riot”

11:07–14:45 — Incidence, current options (steroids/surgery/observation), and the golden window

15:15–20:55 — Why MB: WHO essential medicine, mitochondrial bypass + iNOS/NO “poison valve” control

21:34–24:49 — Methods: optic nerve crush model, groups, dosing (2 mg/kg), timing (0–24h dosing), 21-day follow-up

25:02–31:35 — Results: ERG recovery (B-wave, OPs) + PHNR “complete preservation” of RGC function

32:04–35:17 — Stress testing (pattern ERG) + histology cell counts confirm structure matches function

35:19–38:48 — Human relevance + practicality: animal-to-human caution, but shared mechanisms; preparedness framing + close/CTA

-

Dr. Mike's #1 recommendations:

Deuterium depleted water: Litewater (code: DRMIKE)

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We all know the common saying: “the mitochondria is the powerhouse of the cell.” But this Deep Dive flips that idea on its head. Instead of a simple battery, mitochondria behave like a second genetic system with its own DNA and its own “software layer” of control.

Using a brand-new January 2026 review on mitochondrial epigenetic mechanisms in cancer by authors from University of Pisa, we explore how tumors hack mitochondrial methylation, DNA packaging, and non-coding RNAsto either floor the gas (energy production for rapid growth) or slam the brakes (metabolic dormancy for survival and metastasis). Then it gets even stranger: mitochondria can send RNA and metabolites that influence the nucleus, while the nucleus sends enzymes and RNAs back into mitochondria—creating a two-way power struggle cancer exploits.

The big takeaway: cancer isn’t only a “mutation problem.” It’s also a reprogramming problem, which opens new doors for diagnostics and therapies designed to target the mitochondrial “operating system” directly.

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Article Discussed in Episode:

Mitochondrial epigenetic mechanisms in cancer: an updated overview

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Key Quotes From Dr. Mike:

“What if the powerhouse isn’t just a battery… it’s actually more like an alien spacecraft docked inside us, running its own separate operating system.”

“Cancer is when that symbiosis turns into a power struggle.”

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Key points

The “powerhouse” metaphor is incomplete: mitochondria act like a semi-independent system with a second genome and complex regulation.

Mitochondrial DNA is small but vital (circular, bacterial-like), supporting the idea of an endosymbiotic origin.

The review focuses on epigenetics: not changing DNA letters, but changing how genes are read via methylation “switches.”

A long-running debate is framed as resolved: mitochondrial DNA can be methylated by enzymes that enter mitochondria, allowing gene silencing similar to the nucleus.

Mitochondria also regulate access to their DNA through packaging proteins (a “tape/dimmer switch” controlling expression and energy output).

Gas pedal: hypomethylation in key control regions (like the D-loop) to ramp up output for growth.

Brake: hypermethylation to suppress replication and shift toward dormancy during hostile transitions (like metastasis).

Cancer uses two strategies depending on context:

Non-coding RNAs become “regulatory managers”: sense/antisense balance can be disrupted so tumors lose “stop signals,” and restoring the “good twin” can trigger selective tumor cell death in models.

The future direction is precision oncology: using stable mitochondrial methylation/RNA signatures for screening (blood/urine signals) and designing therapies that specifically target mitochondrial epigenetic machinery.

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Episode timeline 

0:19 — Intro sting + the “powerhouse of the cell” meme setup

0:55 — Reframe: mitochondria as an “operating system” that cancer can hack

1:35 — The January 2026 review + mission: understand “mitoepigenetics”

2:13 — The “second genome”: mtDNA basics + endosymbiotic origin

3:26 — Epigenetics explained: software vs hardware; methylation as gene switches

4:40 — Debate resolved: mtDNA methylation exists; enzymes can tag/silence mtDNA

5:02 — mtDNA packaging (TFAM “tape”) + the mitochondrial “dimmer switch” idea

5:57 — Cancer’s two modes: gas vs brake strategies

6:14 — Gas pedal example: D-loop hypomethylation → increased output for growth

7:23 — Brake example: hypermethylation → reduced mitochondria + metabolic dormancy (metastasis survival)

8:40 — Drug resistance angle: methylation changes that help cells evade death triggers

9:41 — Non-coding RNAs: sense vs antisense “RNA twins” and the loss of brakes

11:26 — Viral hacking example: HPV-style mitochondrial reprogramming framing

12:30 — Therapeutic concept: reintroducing the “good twin” → selective apoptosis in models

13:25 — Circular RNAs and micro-RNAs: stable signals; cancer-type-specific roles

16:25 — Mitonuclear crosstalk: two-way signaling; mitochondria can influence nuclear epigenetics

18:55 — What this enables: diagnostics (blood/urine), mito-targeted therapies, gene-editing concepts

20:33 — Big metaphor: restoring the “peace treaty” (symbiosis) vs hacking

-

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Deuterium depleted water: Litewater (code: DRMIKE)

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In this The Energy Code Deep Dive, we start with a topic that sounds like a prank: piglets + taurine. But it turns into a surprisingly universal lesson about how gut damage happens and how recovery actually works.

We walk through research using piglets as a model for intestinal injury caused by DON (deoxynivalenol), a Fusarium mold toxin commonly found in grain contamination. DON doesn’t just irritate the gut. It collapses the mucus barrier(goblet cells and MUC2), breaks tight junction “zippers” (ZO2, occludin, claudin), and triggers apoptosis (BAX up, caspase-3 up, BCL-2 down). Underneath it all is the real root: mitochondrial failure—swollen, damaged cristae, and ATP levels dropping.

Then comes the twist: taurine doesn’t “patch the wall.” It restores the power, revives mitochondrial function (and antioxidant defenses like SOD2), and appears to reactivate the PGC-1 → NRF1/NRF2 axis—the factory-manager-and-foremen system that turns the repair program back on. The big takeaway: many “structural” problems may secretly be energy problems.

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Article Discussed in Episode:

Taurine ameliorates deoxynivalenol-induced intestinal injury in piglets: Restoration of mitochondrial function linked to the PGC1α-NRF1/2 axis

-

Key Quotes From Dr. Mike:

-

Key points

-

Episode timeline 

-

Dr. Mike's #1 recommendations:

Deuterium depleted water: Litewater (code: DRMIKE)

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Stay up-to-date on social media:

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In this Energy Code Deep Dive, we review a real-world, high-stakes study that sounds like sci-fi: using methylene blue + a specific wavelength of light to kill antibiotic-resistant bacteria. The clinical backdrop is pediatric perforated appendicitis, where bacteria can leak into the abdomen and lead to serious infections, long hospital stays, and heavy IV antibiotic use.

The paper tests photodynamic therapy (PDT): add a light-sensitive dye (methylene blue), shine 665nm light, and generate reactive oxygen species that inflict broad oxidative damage on microbes—often regardless of classic antibiotic resistance mechanisms. The results are striking for several major pathogens, with huge log reductions for E. coli and Streptococcus anginosus group, and more variable results for Pseudomonas aeruginosa.

We also keep it grounded: it’s in vitro, not yet a clinical protocol, and it didn’t test everything you’d want (biofilms, polymicrobial mixtures, anaerobes). But as a proof-of-concept, it’s a strong argument that light can be a precise medical tool—when parameters are engineered, not guessed.

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Article Discussed in Episode:

Photodynamic therapy with methylene blue effectively kills antibiotic resistant bacteria from pediatric patients with perforated appendicitis

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Key Quotes From Dr. Mike:

“Photodynamic therapy doesn’t rely on the same mechanisms as antibiotics, so it can work even when bacteria are resistant.”

“You take a dye that’s light sensitive… add it to the bacteria, then you shine a specific wavelength of light.”

“Methylene blue is the match, the light is the strike.”

“A 6-log reduction is a millionfold reduction… basically a wipeout in this kind of lab setup.”

“The key takeaway is resistance didn’t protect bacteria from this approach in most cases.”

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The study targets a big clinical problem: perforated appendicitis in kids → intra-abdominal infection risk, long hospitalization, heavy antibiotic exposure.

The intervention is photodynamic therapy (PDT): methylene blue + 665nm light → reactive oxygen species that damage bacteria.

PDT doesn’t rely on standard antibiotic mechanisms, so it can work even when bacteria are antibiotic-resistant.

Methods: bacteria isolated from peritoneal fluid samples (30 patients) and tested under 4 conditions: control, dye-only, light-only, dye+light.

Parameters matter: 665nm laser via fiber optic; low fluence rate (4 mW/cm²), total fluence 7.2 J/cm², 30 min; methylene blue 300 mcg/mL.

Most prevalent organisms included E. coli, Strep anginosus group, Bacteroides fragilis, Pseudomonas aeruginosa; polymicrobial infections were common.

Results: ~5.86–5.91 log₁₀ reductions for E. coli and Strep anginosus group (massive kill); Pseudomonas showed smaller, variable reductions (~2.23 log₁₀).

Limitations: in vitro, planktonic monocultures (not biofilms/mixed communities), anaerobes not tested in PDT setup, and parameter optimization still needed—yet the proof-of-concept is very promising for a localized surgical adjunct.

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0:19 — Intro sting + welcome back

0:32 — Topic hook: methylene blue + light vs antibiotic-resistant bacteria

1:06 — Clinical context: pediatric perforated appendicitis → infections, IV antibiotics, long stays

1:49 — PDT explained simply (dye + light → ROS; works beyond antibiotic resistance)

2:39 — Study design: 30 patient samples; isolate bacteria; 4 test conditions

3:13 — Technical parameters: 665nm laser/fiber optics; dosing details; why specs matter

3:50 — What bacteria were found; polymicrobial reality + resistance common

4:36 — Results: major kills for E. coli & Strep; Pseudomonas more variable

5:13 — Quick “log reduction” translation for normal humans

6:16 — Resistant vs susceptible strains: resistance didn’t protect (most cases)

6:54 — Big vision: localized surgical adjunct via laparoscopic illumination

7:24 — Limitations: in vitro, monocultures, no biofilms/mixed species, anaerobes not tested, optimization needed

8:19 — BioLight tie-in (light as precise tool; don’t wing it; specs matter)

9:29 — One-sentence takeaway

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In this Energy Code Deep Dive, Dr. Mike Belkowski and moderator Don Bailey break down a 2024 systematic review, “Targeting Aging With Urolithin A in Humans," that focuses on human supplementation studies, not “eat pomegranate and hope.” 

You’ll learn what Urolithin A is (and why your gut bacteria can make results wildly inconsistent), why it’s tied to “geroprotection,” and what the clinical evidence actually supports so far: dose-dependent anti-inflammatory signals, changes in mitochondrial/autophagy gene markers, and some improvements in strength/endurance — with a reality check on what didn’t move (ATP max, broad physical function, microbiome composition, body comp, cardiovascular markers in short windows).

Bottom line: promising, practical, but still early.

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Article Discussed in Episode:

Targeting aging with urolithin A in humans: A systematic review

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Key Quotes From Dr. Mike & Don:

“It’s like giving two people the same coffee beans, but one of them doesn’t own a coffee grinder!”

"It may be improving the ‘quality control and efficiency settings’ more than raw peak horsepower.“

“So it’s like tuning the car so it runs smoother; not necessarily making the top speed higher.”

"It’s not a ‘lose 20 pounds and become a triathlete’ pill.”

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Urolithin A is a gut-derived metabolite from ellagic acid foods (pomegranate, walnuts, berries), but many people don’t convert well. So food intake ≠ reliable levels.

Supplementation “skips the gut lottery” and produces higher, more consistent plasma levels than food sources.

The systematic review included 5 human studies / 250 healthy participants with 10–1000 mg/day for 28 days to 4 months.

Biggest consistent theme: dose-dependent anti-inflammatory effects (some markers improve more at 1000 mg/day over 4 months).

Mitochondria story is nuanced: it may improve gene expression signatures related to mitochondrial activity, autophagy, and fatty-acid oxidation—more “quality control” than peak power.

What it didn’t reliably do: increase maximal ATP production, consistently boost biogenesis/dynamics markers, change gut microbiota composition, or meaningfully affect body metrics/cardiovascular outcomes in short trials.

Muscle outcomes: some gains in specific strength/endurance measures (e.g., torque metrics; certain fatigue tests), but not universal (e.g., handgrip and broad function didn’t consistently improve).

Safety in these studies looked clean (no serious adverse events attributed), but the overall conclusion remains: promising—but the human aging evidence is still young and needs longer/larger trials.

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0:27 — Welcome + urolithin A is trending + episode topic

0:45 — Don’s moderator frame: “does it work / worth it?”

1:04 — Paper ID (2024 systematic review; human supplementation)

1:25 — What urolithin A is + “gut lottery”

2:02 — Why supplement (higher/consistent levels vs food)

2:24 — Why it matters: mitophagy / healthier aging angle

3:05 — What’s included (5 studies, 250 people; 10–1000 mg; 28d–4mo)

3:34 — What improved (inflammation signals, gene markers, some strength/endurance)

4:06 — What didn’t (max ATP, microbiome, broad health/body metrics)

7:02 — Dosing/PK basics (peak ~6h; half-life ~17–22h; plateau ~7d)

7:40 — Safety summary

8:06 — Practical take + “promising but early” conclusion

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Welcome to the first Energy Code Deep Dive—daily research reviews translated into real life. Dr. Mike Belkowski and co-host Don Bailey break down a brand-new (Jan 3, 2026) pilot study on transcranial photobiomodulation (tPBM) for chemobrain (cancer-related cognitive impairment).

We define what chemobrain actually feels like, why there aren’t many proven treatments, and why researchers are exploring 810nm brain-directed light + an intranasal component to support mitochondrial energy (cytochrome c oxidase/ATP), inflammation balance, blood flow, and repair signaling.

Then we walk through the real-world clinical cohort (31 women), the protocol (weekly sessions, ~20 minutes, 10+ sessions), and the eye-opening outcomes: 29/31 improved, average cognitive scores rose dramatically, and a meaningful percentage normalized. We also keep it honest—small sample, retrospective design, no control group—so you know what’s promising now and what still needs randomized trials.

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Article Discussed in Episode:

Transcranial photobiomodulation for the treatment of chemobrain: new perspectives from a pilot study

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Key Quotes From Dr. Mike:

“It’s like your brain’s running 30 browser tabs and somebody started a video call in the background.”

“Think of it like giving your brain cells a more efficient ‘charge cycle,’ not by caffeine, but by improving cellular energy production.”

“This is why device specs aren’t nerd trivia. They’re the difference between a protocol and a placebo.”

“This pilot study suggests that transcranial photobiomodulation may meaningfully improve chemobrain symptoms… but we still need larger controlled trials.”

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Chemobrain is real: attention, processing speed, verbal fluency, executive function — often lingering for years and impacting daily life.

The study reviewed a Jan 3, 2026 pilot exploring tPBM as a potential supportive treatment when proven options are limited.

Mechanism focus: light targets mitochondrial function (cytochrome c oxidase → ATP), with downstream effects on inflammation, blood flow, and repair signaling.

Cohort: 31 women, average age ~52, post-chemo cognitive impairment; cognition tracked via FACT-Cog.

Protocol: 810nm transcranial + intranasal, ~20 min/session, weekly, 10+ sessions; some also used whole-body PBM.

Why 810nm: penetration matters; modeling suggests near-optimal depth to reach cortical targets; intranasal may help access harder-to-reach regions.

Results were striking: average score improved from ~63 to ~101; 29/31 improved; ~29% normalized into typical range.

Limitations & takeaway: retrospective + no control group (can’t rule out time/placebo), but the effect size supports moving toward larger randomized trials and reinforces that parameters/device specs matter.

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00:00 – Welcome to the first Energy Code Deep Dive + Don’s role as the “question-asker”

01:30 – What is chemobrain (symptoms + what it feels like day-to-day)

04:00 – Why treatment options are limited (the “brutal part”)

05:30 – What transcranial photobiomodulation is (plain-English translation)

07:30 – Biology: cytochrome c oxidase, ATP, inflammation, blood flow, repair signaling

10:00 – Study design + who they studied (31 women, France, post-chemo, FACT-Cog)

12:30 – Real-life impacts (reading, admin work, conversations, driving, fatigue, sleep)

14:30 – Protocol details (810nm, intranasal, weekly 20 min, 10+ sessions, some whole-body)

17:00 – Why 810nm + why intranasal (penetration + access)

19:00 – Results (63 → 101, 29/31 improved, ~29% normalized, QoL changes)

21:30 – Mood/anxiety/depression findings + interpretation

23:00 – Mechanisms: chemo injury pathways vs PBM supportive pathways

25:30 – Limitations (small sample, retrospective, no control, can’t split brain vs whole-body)

27:30 – Safety notes + “what do I do with this?” (talk to clinician; parameters matter)

29:00 – One-sentence takeaway + close (“Protect your energy / mitochondria”)

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Neurodegeneration is increasingly being viewed as an upstream mitochondrial dysfunction problem and not just a symptom-management problem. 

The brain is an extreme energy consumer, so neurons are uniquely vulnerable when ATP production drops. 

Oxidative phosphorylation failure reduces cellular power and sets the stage for degeneration.

In Parkinson’s, Complex I impairment is a recurring theme → less ATP + more oxidative stress.

ROS isn’t inherently bad — it’s signaling vs “wildfire” oxidative stress when defenses get overwhelmed. 

Mitochondrial “quality control” (fission, fusion, mitophagy) is central; breakdown accelerates damage. 

Neurons depend on mitochondrial transport down long axons; transport failure can starve synapses first. 

Emerging interventions include mitochondria-targeted antioxidants, biogenesis/repair pathways, and mitochondria-relevant trials (including photobiomodulation) promising, but still evolving.

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Key Quotes From Dr. Mike

“Fission is like splitting dough into separate pizzas. Too much fission is like cutting everything into tiny crumbs.” 

“Too little fission is like refusing to separate the burnt part… it ruins the whole batch.” 

“This is the recycling program… Tag it, bag it, take it out.” 

“PGC-1 alpha is like the head contractor for building new power plants.” 

“If demand doubles, you can’t keep running on the same number of servers… you need more infrastructure.”

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Article Referenced in Episode:

Mitochondrial-based therapies for neurodegenerative diseases: a review of the current literature

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Episode Timeline

00:00 — Cold open + show intro (“The Energy Code” mission / mitochondrial matrix) 

00:45 — The “unstoppable train” problem: symptoms vs upstream causes 

02:00 — Why mitochondria matter in the brain (energy hog / “city that never sleeps”) 

04:00 — Quick definitions: Alzheimer’s vs Parkinson’s vs ALS 

05:30 — Oxidative phosphorylation explained (dam/turbine analogy) 

08:00 — Parkinson’s spotlight: Complex I disruption + downstream ROS 

10:00 — ROS with nuance: signaling vs oxidative stress + antioxidant balance 

12:30 — The quality-control trio: fission, fusion, mitophagy (pizza + recycling analogies) 

15:30 — Mitochondrial transport in neurons (train tracks: kinesin/dynein) 

17:00 — Therapy bucket #1: mitochondria-targeted antioxidants (why targeting matters) 

18:30 — “Is it being tested?” clinical trial examples across AD/PD/ALS 

20:30 — Photobiomodulation: keep it grounded (flashlight/battery analogy) 

22:30 — Biogenesis: PGC-1α + AMPK/SIRT1 + exercise mimetics 

25:00 — Frontiers: transplantation, gene therapy/CRISPR, ethics/regulation 

28:30 — Five takeaways + closing call-to-action (subscribe/review/share)

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In this episode of The Energy Code, Dr. Mike delivers a wide-ranging solo deep dive into some of the most compelling mitochondrial and longevity research published over the last several months. Moving beyond hype and “magic bullet” thinking, this episode reframes aging, energy, and resilience through the lens of systems biology — where mitochondria, immune signaling, light, stress, and the microbiome all converge.

Dr. Mike walks listeners through five recent peer-reviewed studies spanning immune rejuvenation, photobiomodulation, red light–driven lifespan extension, methylene blue–mediated neuroprotection, and microbiome-dependent longevity metabolites. Across each paper, a central theme emerges: health is not about forcing outcomes, but about restoring signaling, redox balance, and mitochondrial adaptability.

This episode highlights why fatigue is often protective, why antioxidants can backfire, how light functions as biological information, and why personalized bioenergetics — not one-size-fits-all protocols — represents the future of longevity medicine.

Longevity science has shifted from speculation to mechanism-driven biology

Immune aging is driven by mitochondrial dysfunction and cellular senescence

Red and near-infrared light act as hormetic mitochondrial stressors

Proper photobiomodulation follows a biphasic dose response

Early red light exposure can extend lifespan and healthspan in model organisms

Methylene blue supports mitochondrial redox balance and brain resilience

Fatigue is often a protective mitochondrial signal, not an energy deficit

Antioxidants can blunt beneficial mitochondrial adaptation

The gut microbiome determines urolithin A and B production

Longevity interventions are inherently n=1 and ecosystem-dependent

“Fatigue is often a protective signal — not a lack of energy.”

“Light becomes information, food becomes signaling, and molecules become tools.”

“Mitochondrial medicine isn’t the future — it’s now.”

“Longevity isn’t about magic bullets. It’s about systems biology.”

00:00 – 05:25

Introduction, 2026 vision, and expansion of Energy Code Deep Dives

05:26 – 14:18

Urolithin A & immune rejuvenation — mitochondrial metabolism and immunosenescence

14:29 – 21:57

Photobiomodulation, biphasic dosing, and mitochondrial signaling

21:57 – 26:35

Red light exposure, AMPK activation, lifespan and healthspan extension

27:01 – 30:36

Methylene blue, neuroinflammation, blood–brain barrier protection

31:06 – 34:44

Microbiome-dependent urolithin production and personalized longevity

34:45 – 38:02

Systems biology, decentralized health, and closing reflections

Nature Aging — Urolithin A & immune decline

Scientific Reports — Photobiomodulation & mitochondrial signaling

Aging and Disease — Red light–driven lifespan extension

Scientific Reports — Methylene blue & neuroprotection

Gut microbiome enzymatic mapping of urolithin production

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