Dr. Jack Kruse
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DECENTRALIZED MEDICINE #40: METHYLENE BLUE USE AND TURBOCANCER RISKS
🕑 Added 2025-04-02 13:20:58 +0000 UTCAfter the last blog on Becker's work and wound healing, a question should have arisen in your brain. Methylene blue is the treatment for methemoglobinemia in humans. So, if metHb is a signal used in regeneration, is MB use safe for all?
Most cancer cells also show the depolarized signal, undergoing atavistic changes like those in wound healing. This implies that wounds create a stimulus for hypoxia, and this stimulus immediately changes the biophysics of heme proteins in us. Evolution teaches us this is what happened in the Cambrian Explosion.
It turns out that injuries do stimulate the creation of metHb from HbO2. MetHb stimulates the depolarization of cells, which uses this signal to dedifferentiate and prepare for wound healing. What happens if this quantized process is ruined by modern light stress or modern mitohacking beliefs?
What happens if someone uses MB but gets no sun, no sunrise, and no UV and IR together? What might go wrong? Without the sunrise, you cannot use the TCA cycle, and the Earth is still loaded with 21% oxygen. This seems to be a situation that selects for cells to react atavisitically. Said another way, this is how modern humans get cancer MOST OFTEN. Without AM sunrise, you are selecting for your cells to default to a Warburg metabolism.
What happens if the pico or nano current Becker discovered that is made in combo by CCO creating DDW using SUNRISE and the following UV light to translate melanin from POMC to make hydrated melanin sheets is never reestablished? What happens if there is a co-morbid condition of improper circadian regulation? Wouldn't this mean we get early revascularization into a hypoxic wound bed with no or low production of Becker's regenerative current?
This implies that our cells never get the signal for regeneration, but they remain Warburg shifted. Then, we add a massive infusion of oxygen from vascular regrowth. In this case, what would you predict is the fate of these atavistic cells?
This may be the key defect in oncogenesis that centralized medicine misses because its methodology focuses on biochemistry and not biophysical changes over time in injuries.
These questions weave together a profound hypothesis that bridges wound healing, regeneration, cancer biology, and biophysics in a way that challenges conventional biochemical paradigms.
I am suggesting that the atavistic changes seen in wound healing, namely hypoxia, normal methemoglobin (MetHb) accumulation, and cellular depolarization, mirror cancer’s Warburg-shifted, dedifferentiated state, driven by bioelectric signals like those Becker harnessed with pico/nano-scale DC currents. Hydrated melanin sheets and circadian rhythms must mediate these signals to get regeneration. What happens if they fail to resolve it correctly? Instead, rapid revascularization floods the tissue with oxygen when its mitochondria cannot handle the influx. This blocks all the restoring regenerative cues Becker found. What happens to these atavistic cells?
Setting the Stage: Atavism in Wounds and Cancer
Wound Healing: In a hypoxic wound, MetHb-rich RBCs and local cells experience depolarization (loss of membrane potential), a signal we’ve linked to dedifferentiation into stem-like states under Becker’s currents. This atavistic shift augmented by NO is reverting our tissues to a primitive, glycolytic (Warburg-like) metabolism, which enables regeneration ONLY if guided by photo-bioelectric cues, such as those from hydrated melanin sheets producing pico/nano currents in a circadian pattern (CCO heme mechanism also controls apoptosis!)
Cancer Parallel: Cancer cells also depolarize, shift to glycolysis (Warburg effect), and dedifferentiate, resembling embryonic or stem-like states. This atavism is often framed as an evolutionary throwback, where cells revert to a proliferative, survival-focused mode under stress (e.g., hypoxia). This was critical in our evolutionary history when oxygen was a toxin before mitochondria were innovated. Unlike wound regeneration, cancer lacks the coordinated resolution to rebuild functional tissue via Becker's mechanism. The main reason is that the injury could have knocked out ENOUGH DDW production, and/or there is not enough melanin in the injury site, while the stressor destroys the heme-based nuclear circadian genes Rev erb A and B (slide below bottom).
It might even mean melanin is missing because there is no IV light to create the dampened regenerative currents. Carefully look at the slide title. Fully differentiated RBCs are porphyrins, light sensors for UV and IR light. This slide is from Vermont 2017. Is metHb the same type of optical light sensor in an injury? It is not, and Nature did this by design. NO also controls our stem cell depots. They must be kept hypoxic as well. This is why NO is the key player here.
MetHb in an injury is a key driver of RBC dedifferentiation, which Becker found in his experiments on amphibians, reptiles, and humans. This occurred via ROS, redox signaling, or low oxygen-favoring glycolysis = Warburg redox is favored when RBC are incapable of using oxygen = which is what metHb is. Wound repair requires our RBC to enter its past Oxygen Holocaust to regenerate. I bet you did not see that coming on your bingo card.
Nitric oxide (NO) plays a significant role in human interaction with methemoglobin (metHb). Methemoglobin is a form of hemoglobin in which the iron in the heme group is in the ferric (Fe³⁺) state rather than the ferrous (Fe²⁺) state, rendering it unable to bind oxygen effectively.
NO is liberated in injury in response to hypoxia. However, excessive NO (e.g., from exogenous sources or in pathological states) can paradoxically contribute to metHb formation by reacting with oxyhemoglobin (HbO₂), producing metHb and nitrate (NO₃⁻). We saw this in the AIDS epidemic.
This scenario posits a wound where this bioelectric guidance fails for some reason: the pico/nano currents from melanin sheets (disrupted, perhaps by circadian dysregulation) don’t reestablish, and revascularization abruptly oxygenates the hypoxic, MetHb-driven, depolarized bed without Becker’s regenerative signal. Let’s predict the outcome using first-principle thinking.
Key Factors in the Scenario
Initial State: Hypoxia and MetHb accumulation depolarize cells (RBCs, fibroblasts, etc.), triggering dedifferentiation. The Warburg shift (glycolysis dominance) supports this plastic, atavistic state, poised for regeneration if the photo-bioelectric cues align. This tells you that because metHb is the key stimulus for injury and the regeneration loop, clinicians might need to make you think twice about using methylene blue in every case, right? It also turns out the presence of metHb alters the Anders-Schultz law for PBM use. I bet you did not see that coming either.
Failed Bioelectric Signal: Hydrated melanin sheets, which might naturally generate Becker's pico/nano currents (e.g., via water splitting or proton gradients, as melanin research suggests), don’t reset in a circadian rhythm mismatch. This means that Becker’s regenerative currents should also be absent when this clinical state is present, so the depolarized state persists in cells without direction from the photo-bioelectric current that is missing in action. Big Problem. This is really where cancer comes from, folks. If you read Becker's book carefully, you will see that he had a huge problem with Andy Bassett regarding using exogenous DC currents to stimulate bone. Becker was right to be cautious, but the DC electric current will not cause cancer. MB use, in this scenario, might.
Revascularization: Blood vessels regrow rapidly in mammals (VEGF), flooding the tissue with oxygen early and shifting the onjur site from hypoxic to normoxia. Adding exogenous oxygen through ozone, CPAP, or HBOT is also dangerous. MetHb reduces to HbO₂ under the power of NIR light, as the slide shows. This allows them to flip aerobic metabolism back on. However, if the cells at the injury site remain in the Warburg-shifted state, depolarized due to the missing Becker current, these cells are missing the regenerative photo-bioelectric “off switch.” New oxygen rushing in causes massive growth of atavistic cells. This is called CANCER.
Predicted Fate of Atavistic Cells
Without the pico/nano current to guide regeneration and with a sudden oxygenation event at the injury site, these dedifferentiated, Warburg-shifted cells face a critical juncture. Here’s their progression:
Persistent Dedifferentiation:
Bioelectric Stasis: Depolarization, usually a transient signal for plasticity, becomes chronic without circadian current restoration in the tissue daily. I told you that AM sunrise was critical in avoiding cancer. In regeneration, bioelectric gradients (e.g., -50 mV in stem states vs. -70 mV in differentiated cells) resolve to direct tissue patterning. They don’t have that electrical resistance patterning, leaving cells in a stem-like, hyper-proliferative limbo. ROS and RNS drive them to divide. The more oxygen you give this tissue, the worse the disease you get. That is a turbo cancer.
If you go back and have a listen here, you'll see I gave this foolish centralized MD this warning you are getting in this blog. https://rumble.com/v6qrm46-graham-and-john-interview-dr-jack-kruse-with-a-panel-discussion.html
Warburg Lock-In: Despite oxygen influx, the glycolytic shift persists because the injury remains, namely blue light or nnEMF exposure, a hallmark of cancer. Studies show cancer cells maintain glycolysis even in normoxia (aerobic glycolysis), suggesting metabolic inertia or epigenetic reprogramming (e.g., HIF-1α upregulation) could keep these wound cells “stuck” in this mode. This makes them risky cells until they are removed. Typically, apoptosis would remove them, but CCO, the heme protein defective in heteroplastic mitochondria, cannot do this. This makes these cells time bombs until the light environment is altered to rebuild the regenerative process Becker discovered.
Uncontrolled Proliferation:
Oxygen Paradox: The sudden oxygen surge, paired with lingering ROS from MetHb or inflammation, would damage DNA or mitochondria, amplifying the atavistic state. In cancer, this “oxygen shock” mimics the Cambrian explosion atmosphere, except the change is rapid and dramatic in modern humans. After hypoxia often drives mutations or clonal expansion. How? People forget what is in Roeland van Wijk's books. Cells need oxygen to create biophotons. ROS creates massive amounts of biophotons when cells are at this atavistic state while oxygenating. In this state, huge amounts of ROS/RNS and biophoton release would all co-occur. This would drive a massive pro-growth signal in the affected tissue. Wound cells from any cause, already dedifferentiated, might respond similarly, proliferating without proper differentiation cues. Why? Apoptosis has an extrinsic pathway that this scenario can co-opt. This is why Popp found that in humans with disease, massive biophoton release happens, which is quite different from the healthy state.
Loss of Patterning: Becker’s currents likely mimic embryonic bioelectric fields that spatially organize regeneration (e.g., limb regrowth in amphibians). Without them, these cells lack positional identity, potentially forming disorganized masses akin to tumorigenesis rather than functional tissue. Ya' feeling what Uncle Jack is telling you now?
Oncogenic Transformation:
Cancer-Like Fate: These atavistic cells are chronically depolarized, glycolytic, and proliferative, and they mirror cancer stem cells. If revascularization sustains them without resolving their state (e.g., via apoptosis or differentiation), they could acquire hallmarks of malignancy: self-sufficiency, evasion of growth suppressors, and eventually genomic instability from oxidative stress. This certainly looks like what cancer is, doesn't it?
Tipping Point: The lack of a photo-bioelectric “reset” (e.g., repolarization via melanin currents) prevents normal wound resolution (scarring or regeneration), while oxygen fuels unchecked growth. Over time, stochastic mutations in CCO or the nDNA's p53 or Ras pathways could lock in a cancerous phenotype in a tissue once the injury stimulus's intensity or duration meets the phenotype's conditions. This is why altering your environment matters BIGTIME in oncogenesis. This is why AM sunrise and PM sunset are not to be missed EVER if you have any cancer. Truthfully, it is axiomatic in any disease where the clinician expects a Warburg shift due to light stress. This is also why one has to be careful when using MB in these patients.
Predicted Outcome From These Decentralized Medical Ideas
In this scenario, the atavistic cells don’t regenerate into functional tissue (e.g., bone, per Becker) or heal conventionally (e.g., scar). Instead, they persist as a Warburg-shifted, depolarized population that, with revascularization’s oxygen boost, transitions into a pre-cancerous or fully oncogenic state. The wound bed becomes a “tumorigenic niche”—a disorganized, proliferative mass lacking the bioelectric coordination needed for regeneration. Over time, this could evolve into a carcinoma or sarcoma, depending on the cell types involved (e.g., dedifferentiated RBCs, fibroblasts, or epithelial cells).
Why Centralized Medicine Misses This
My intuition is spot-on that mainstream oncology’s biochemical focus, targeting pathways like VEGF, EGFR, or glycolysis while overlooking biophysical the timing dynamics:
Bioelectric Oversight: Cancer research rarely measures membrane potential or circadian bioelectric rhythms, yet depolarization is a consistent feature of malignancy. Wound healing studies similarly ignore these signals, assuming revascularization alone resolves hypoxia.
Time Dimension: Biochemical snapshots (e.g., gene expression at one point) miss the temporal evolution of biophysical states, which evolve from hypoxia with a depolarization bioelectric signal to a failed repolarization state critical in the regeneration feedback loop Becker discovered. This is critical to my decentralized model for medicine.
Melanin and Circadian Link: Hydrated melanin’s role in generating currents (explored in bioelectronics but not medicine) and its circadian regulation (tied to light and water dynamics) are considered fringe topics, yet they ARE the missing “conductor” orchestrating regeneration vs. oncogenesis. Understanding the heme proteins and CCO is critical in managing cancers.
SUMMARY
This suggests the key defect in cancer initiation: disrupted photo-bioelectric signaling during injury repair. If wounds naturally induce atavism (dedifferentiation) but lack the circadian pico/nano currents to resolve it, perhaps due to modern disruptions like light pollution, poor sleep, melanin dysfunction, or any chronic infection or trauma that starts the cascade. Then, revascularization onset might “feed” these cells into a pre-malignancy state rather than a well-differentiated state required for regeneration. Centralized medicine’s focus on downstream biochemistry (e.g., oncogenes) misses this upstream biophysical trigger, treating symptoms rather than the root cause.
Testable Decentralized Medicine Predictions
Model: Create a hypoxic wound in mice, disrupt circadian melanin currents (e.g., via constant light or melanin inhibitors), allow revascularization, and track cell fate (stem markers, proliferation, tumor formation).
Metrics: Measure depolarization (via voltage-sensitive dyes), MetHb levels, Warburg shift (lactate production), and oncogenic markers (e.g., Ki67, p53) over time.
Outcome: We expect a higher tumor incidence without bioelectric restoration vs. regeneration with applied Becker-like currents.
This could redefine cancer as a “regeneration gone rogue” due to photo-bioelectric failure—a paradigm shift worth pondering as all these people who complied with jabs sit with trillions of Warburg shift cells everywhere in their bodies. The LNPs of these jabs damage the CCO mechanism. Before patients can use MB, they must rebuild their solar callus and be in intense UV, NIR, and IRA light. LED light panels do not offer this recipe up. This is why I warned you that the sun cannot be replaced in any cancer case. Misusing MB and exogenous oxygen with PBM might get you killed.
Does this resonate with you? Is it time to view oncogenesis as a timing and signaling defect tied to light and dark cycles? I told you I was warming up.
Comments
Gabriel
Every time I read one of your articles, it’s like witnessing a master puzzle-solver in action. You’re constructing an entirely new perspective, piece by piece, using nothing but pure, unfiltered wisdom. Brilliant!
Susan Spence
Shit, no wonder my heart rate is up!!
