Month: April 2025

After 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.

Light That Liberates Nitric Oxide Best in Humans?

If you open the centralized biochemistry book , you’ll find the following story: The liberation of NO in biological systems, particularly in humans, is often studied in the context of phototherapy or photochemical reactions involving NO donors (e.g., nitrosyl complexes or S-nitrosothiols). The wavelength of light that most effectively liberates NO depends on the specific NO-containing compound or context:

• Near-Infrared (NIR) Light (650–900 nm spectra):
  • NIR light is often cited as effective for liberating NO from certain endogenous stores, such as S-nitrosothiols or nitrosyl-heme complexes (e.g., in hemoglobin or mitochondrial cytochromes).
  • It penetrates tissues deeply due to low absorption by water and hemoglobin, making it practical for in vivo applications.
  • Studies suggest that NIR light can photolyze NO from these compounds, enhancing vasodilation and tissue oxygenation.
• Visible Light (400–650 nm spectra):
  • Blue light (400–500 nm) and green light (500–570 nm) can liberate NO from synthetic NO donors (e.g., nitroprusside or ruthenium nitrosyls) or biological complexes like nitrosylated hemoglobin.
  • These wavelengths are less penetrating than NIR but can be effective in superficial tissues or in vitro studies.
• Ultraviolet (UV) Light (300–400 nm spectra):
  • UV light is highly effective at photolyzing NO from some chemical donors (e.g., S-nitrosothiols), but it has limited use in humans due to poor tissue penetration and potential damage to DNA and proteins.

Most Effective in Humans according the biochemistry books

For practical purposes in humans, near-infrared light (around 650–850 nm) is generally considered the best for liberating NO from biological stores. This is because:

• It balances tissue penetration with photochemical efficiency.
• It aligns with the absorption spectra of some nitrosyl complexes found in blood and tissues.
• It has been explored in therapeutic contexts, such as improving blood flow or treating hypoxia.

That said, the “best” wavelength depends on the specific NO source (e.g., endogenous vs. exogenous donors) and the target tissue.

WHAT DID THE BIOCHEMISTRY BOOKS FORGET?

Fritz Popp found out that all human cells make ultraweak biophotons in the UV range. Shouldn’t this add a layer to their understanding in their books that might change their dogmatic opinion in would creation? The answer is they still do not know how to make sense of nature.

When the quantum biologist brings biophotons into the picture is does add an intriguing layer to the discussion about nitric oxide (NO), methemoglobin (metHb), and light interactions in humans. Biophotons are ultra-weak photon emissions produced by living cells and they should indeed influence how we think about NO liberation and its interplay with biological systems.

Biophotons in Human Cells

Biophotons are low-intensity light emissions (typically in the UV to near-infrared range, ~200–1000 nm) generated by oxidative processes in cells, such as mitochondrial respiration or reactions involving reactive oxygen species (ROS). These emissions are thought to play a role in cellular communication, regulation of biochemical reactions, or even redox signaling. While their exact purpose is still debated in centralized systems, but not in my system. Their very existence defines what life is all about because they suggest that human cells have an intrinsic capacity to produce light that could interact with photosensitive molecules—like those involved in NO dynamics, wound healing, and oncogenesis.

Revisiting NO and MetHb In DM #38 with Biophotons

• Biophotons as an Endogenous Light Source:
  • If human cells emit biophotons, particularly in the visible-to-NIR range (e.g., 400–850 nm), these could theoretically trigger NO release from endogenous stores like S-nitrosothiols, nitrosyl-hemoglobin, or other NO-bound complexes in or near blood vessels and tissues.
  • This mean that NO liberation isn’t solely dependent on external light (e.g., therapeutic NIR) but could be modulated by internal biophoton activity, especially in areas with high metabolic activity (e.g., muscles, brain). it turns out blood emits a steady stream of biophotons too.
• Wavelength Overlap:
  • Biophoton emissions span a broad spectrum (200-1000nm), but peaks in the 600–800 nm range (red to NIR) have been observed in some studies. This overlaps with the wavelengths I previously noted as effective for NO photolysis (650–850 nm). So, biophotons could, would, and should naturally contribute to NO release in vivo, potentially reducing metHb or regulating its levels as part of a feedback loop.
• Interaction with MetHb:
  • MetHb itself absorbs light, particularly in the 600–650 nm range (due to its ferric heme structure). If biophotons emitted nearby overlap with this absorption band, they might influence metHb’s redox state either by facilitating NO binding/dissociation or by sensitizing it to reduction back to functional hemoglobin.
  • This implies a subtle, localized mechanism where biophotons help maintain hemoglobin’s oxygen-carrying capacity under oxidative stress.
  • Nitric Oxide acts locally in human injuries, so any resultant the light stimulus for repair should be Ultraweak in nature. This means Pritz Popp’s work fits here for mammalian wound regeneration. Moreover, Popp has shown biophotons are also in the UV range So since we know that oxygen is the most critcal part of being able to make biophotons from Roeland van Wijk’s book and papers, this tells us that oxygen tensions in wound likely create specfic biophoton spectra to marry up to the tissue response. This tells me the process is entirely quantized.
  • These ideas fit perfectly with what Becker found in wound healing and regeneration in species. He told us human RBC had to de-differentiate to become a stem cell. It would make a lot of sense if the tissue hypoxia forced RBC that were HbO2 to become metHb. Why? MetHb is a hemoglobin built for an epoch were cells did not use much oxygen. This is precisely what happened during the Great Oxygenation Event on Earth. Hypoxia forms metHb in RBCs. MetHb is a more atavistic state of Hb and it is paramagnetic. This makes the RBC a new target for the photo-bioelectric current. This change inside of the RBC decreases the cystalline structure of Hb when metHb rises in an injury state. This slight change allows for de-differentiation to occur in step wise fashion. It is almost as if the cell is reversing time to go back in its evolutionary history when you observe what nature is teaching us via Becker’s experiments. It would seem to me the biophoton release from the blood would be quantized to oxygen levels in the injury to drive healing. Most wounds are hypoxic compared to the non injured state.
  • These ideas should lead the centralized biochemical paradigm to go to a complete reversal, because it refines the picture of how light can sculpt fully differentiated life. It breaks the Central Doctrine of biology that was set forth by the biochemists after DNA was discovered.

    External vs. Internal Light from our Tissues:

  • The biochemical focus has been firmly focused on external light sources (e.g., NIR therapy) as the “best” for liberating NO in humans. Biophoton creation suggest that internal light might already be doing this on a smaller more powerful scale, perhaps as part of homeostasis. Biochemists have no idea as scale shrinks the electromagnetic force gets STRONGER. They also are ignorant that the photon is the force carrier for this fundamental force. It is stronger than anything biochemist have in their tool box. This doesn’t negate the efficacy of exogenous NIR but it adds a layer of complexity, that cells are self-regulating using paramagnetic free radicals like NO, CO, H2S with metHb dynamics in RBCs for some distinct purpose that is not yet published in their text books.
    • Wavelength Specificity of Biophotons is broad: The broad spectrum of biophotons (UV-NIR = 200-1000nm) means that no single wavelength is “best” in an absolute sense. Instead, the most effective light for NO liberation could be context-dependent for the injury; external NIR for therapeutic boosts, biophotons release from mtDNA and from the blood for baseline physiological regulation.
    • Wound Creation Angle: The presence of biophotons in wounds from the blood hint at a more autonomous, light-driven cellular ecosystem than no biochemist would ever imagined. It’s almost like cells have their own “internal sun” influencing NO and metHb chemistry, which is a poetic twist on physiology. I was forced to learn all the biochemical pathways, but none of them explain how wounds are healed and regenerated. It also should make Becker and Marino smile because Jaffe and Handler and Swann work is getting ripped up by the roots by Uncle Jack like a weed. Why? Listen.
    • https://www.youtube.com/watch?v=YkBsVMjnwkA
    • The biochemists that Marino cited in the podcast above are why all of science has been blocked from Becker’s ideas. When I sat down with one such celebrated biochemist about 12 years ago, Ray Peat, he told me that biophoton intensity was only 10⁻¹⁷ to 10⁻¹⁹ W/cm², so it had no effect. Moreover, he compared it unfavorably to a 1 mW/cm² (10⁻³ W/cm²) NIR laser. That’s a 14–16 order-of-magnitude gap, which sounded damning to Peat, until you factor in scale and context that physics brings to the discussion:
      • Biochemical Bias: Peat’s reasoning leaned on macroscopic phototherapy logic = more watts, more effect. But biochemistry often overlooks how EM forces dominate at microscopic scales, where biophotons operate (e.g., nanometers to micrometers). I had a copy of Albert Szent Gyorgi’s 1968 book with me and I opened it up to a picture of a protein that showed its electronic structure. I asked Peat if he knew what Szent Gyorgi was trying to convey. He had no idea. The electronic structure means a protein has an absorbtion and emission spectra based on its amino acid sequence.
      • Photon as EM Force Carrier: Photons mediate the electromagnetic force, one of the four fundamental forces, and this force scales inversely with distance (Coulomb’s law: F ∝ 1/r²). At cellular or molecular scales (10⁻⁹ to 10⁻⁶ m), this force isn’t “weak”, it’s overwhelmingly strong compared to bulk chemical interactions. This was the moment when Peat became awfully quiet and listened to how the electronic structure of biochemicals would be controlled by endogenous biophoton signaling from the mtDNA and blood.
      • When scale shrinks light becomes like a laser.  Distance matters to photons. A biophoton emitted within a cell (e.g., from mitochondria) acts over distances of nanometers to micrometers. The EM force it carries can exert effects orders of magnitude stronger than a diffuse external laser beam penetrating centimeters of tissue. What people do not realize is that cells have the ability to use this endogenous light to reverse many things thought to be impossible because the light coming from within is exponentially strong than the light coming from outside the body. He was not expecting this turn of events. Below is an example. This implies these endogenous biophotons can also change metHb easily when the circadian biology of a cell allows for it.
      • 
      • Localized Power: A 10⁻¹⁸ W/cm² biophoton hitting a metHb molecule 10 nm away delivers energy with precision, is not diluted across a broad field. Compare that to a 10⁻³ W/cm² NIR beam scattering through skin, most of its energy is lost before reaching the target. Peat’s face was telling.
      • If biophotons are internal EM signals, their “weakness” is a misnomer due to a biochemists understanding of the power and their purpose. They’re not competing with lasers; they’re playing a different game no one sees, yet.
        • Internal Efficiency: Generated in situ (e.g., by ROS or mitochondrial activity), biophotons act where NO and metHb reside, inside cells or RBCs. No penetration barriers, no energy loss. An external NIR laser, even at higher power, wastes most of its photons before reaching the target.
        • Quantum Influence: Photons don’t just dump energy; they trigger quantized transitions inside tissues. A single biophoton with the right wavelength (UV or NIR) could flip metHb’s redox state of iron or it could liberate NO from an S-nitrosothiol, with no floodlight needed. The EM force ensures this happens with precision and strength at close range.

        Implications for NO and MetHb in Becker’s work.

        Let’s reframe the NO-metHb story with this Electro Mangetic lens:

        • NO Liberation: Biophotons, even at low intensity, could dominate NO release locally because their EM force acts directly on nitrosyl bonds (e.g., in Hb-NO or S-NO). UV biophotons (~200–400 nm) might cleave these bonds with surgical precision, far outpacing diffuse NIR therapy. This could be used to keep a cell hypoxic because of how NO blocks Hb from carrying oxygen. This is a remnant from the Great Oxygenation Event.
        • MetHb Reduction: The photo-bioelectric current I mentioned earlier stems from biophotons liberated in the injury site via EM interactions with metHb’s ferric iron. At nanoscale distances, this photon force would be quites strong to drive electron shifts (Fe³⁺ → Fe²⁺), reducing metHb to Hb more effectively than biochemical enzymes alone. This would keep the wound more hypoxic and less subject to ROS/RNS production.
        • Homeostasis: If biophotons are quantized to oxygen tension in injuries, their EM strength ensures they’re not just passive signals inside a wound but active drivers, fine-tuning NO and metHb to match cellular needs—way beyond what external light can achieve. This implies that biophotons might be critical in keeping a tissue hypoxic for a period of time by using magnetic parts of light to control the oxidation state of iron. This signal might be important in wound healing and regeneration sequencing.

        Centralized vs. Distributed Power

        My biochemical focus was “centralized” when i sat down with Peat, and he thought I was big on external light sources, like the sun, as the hero of the story. He found out quickly that was not the case. I explained to him biophoton production done by tissues injured suggested a distributed decentralized model for tissue sculpting in humans. My model showed him every cell, every RBC, is a powerhouse emitting EM force carriers, biophotons. This aligns with Becker’s amphibian-mammal split too:

        • Amphibians: Few people realizes amphibians have nucleated RBC that emit more light than mammalian blood that is enucleated. Nucleated RBCs amplify biophoton output, leveraging EM force for better regeneration stimuli. Their nucleated RBC are not great at carrying oxygen as mammalian blood is. Remember they are adapted to more hypoxic environments on Earth. This is why their RBCs are nucleated. This would make their “weaker” hemoglobin more responsive to these internal biophoton signals, sustaining metHb-driven dedifferentiation. Becker found this in his work with Salamanders. They were super regenerators. Peat’s face was white at this point.
    • Mammals: Enucleated RBCs lose this EM autonomy for regenertion, because they have to rely on biophotons released in the circulatory system and systemic biochemistry (e.g., cytochrome b5 reductase) over a more powerful localized photon power of the injured cell, favoring stability over plasticity. Mammals scar better than regenerate. Becker confirmed this in his work.Shifted Perspective by Understanding Biophysics

      This evolutionary history lesson of RBCs should flip everyone’s biochemical view: biophotons aren’t “limited” by their wattage, they’re potentially more powerful than external light from the sun is for NO and metHb dynamics in wound healing and regeneration. Their EM force, is dominant at small scales, and these factors would make them the true maestros of wound healing and homeostasis, not just a sideshow. External NIR might still have therapeutic uses, but it’s a blunt tool compared to the scalpel of internal biophotons.

    • NOW TO BECKER

      Let’s break this down:

      • Hypoxia in Wounds: Low oxygen tension (e.g., <20 mmHg in chronic wounds) stresses RBCs. HbO₂ oxidizes to metHb via ROS or NO reactions (HbO₂ + NO → metHb + NO₃⁻), This is especially true if NO production spikes from inducible NOS in inflammation due the wound.
      • Biophoton Shift: Hypoxia alters mitochondrial activity by lowering NAD+ and creating pseudohypoxia. When this occurs, it skews biophoton output. It creates a wider spectrum of light release that mimics what we see in the Domain of Bacteria and Archea. It appears that it does not enriching UV emissions because ROS excitation transitions are less prominent because oxygen is less prominent in the injury site. At the sime time ultraweak UV light decreases due to the loss of oxygen there is an expansion from 400-1000 nm light release. This fits with Popp’s work who told us about prokaryotes releasing more light than eukaryotes who are experts in using the TCA cycle and oxygen to generate massive energy from food. Van Wijk’s data on biophoton creation hints at this quantization to oxygen levels.
      • MetHb as the Injury Pivot: MetHb would act as a paramagnetic “sensor” replacing oxygen in the system as an intermediate. Interestingly, metHb absorption (e.g., ~630 nm peak) overlaps with biophoton ranges we’d expect to see in a hypoxic wound. The change in the biophoton spectra UV/blue to NIR photons can reduce it back to Hb or trigger more NO release. NO is also paramagnetic and it reduces energy production (below) to enforce hypoxia while delivering more blood to a wound that would bring more biophoton release to the wound generating a small photo-bioelectric current (as Becker’s work implied).
      • Dedifferentiation RBC Trigger: This small DC current, one trillionth of one ampere of DC, plus NO’s hyoxic signaling, would push RBCs toward a stem-like state, releasing factors (e.g., growth signals) to aid in wound healing and regeneration. Becker’s salamander studies showed dedifferentiation depended on bioelectric shifts and metHb and NO is the likely human analog, albeit less robust. Why? Amphibians and Humans do not have the same hemoglobin AMO physics.   One has a nucleated RBCs and the other does not.
      • Quantized Biophotons and Regeneration

        The decentralized idea at the cornerstone of my model is that biophoton release is “quantized to oxygen levels in the injury.” It is biophysical majesty not a biochemical reality because it suggests a feedback loop for Becker’s work that biochemistry does not have:

        • Low O₂ → More MetHb → more visible/IR Biophotons: Signals hypoxia, primes dedifferentiation, and kicks off repair. Injury and repair are linked.
        • Rising O₂ → Hb Recovery → more UV NIR Biophotons: Promotes angiogenesis (VEGF) and tissue maturation as NO vasodilation takes over. NIR restores energy production in recovery/regeneration timescale

        My model perfectly marries Becker’s photo-bioelectric currents to Popp’s biophoton coherence and van Wijk’s quantized oxygen links to tissue repair. In species with robust regeneration, this loop might be amplified due to a higher biophoton pulse, while in humans, it’s subtler because there is a huge biophysical difference Becker missed in biophoton release due to a lack if nucleated RBCs which have mitochondria. This is the reason why mammals heal but rarely regrow limbs is because mtDNA is a great source of biophotons. This also explains the phenomental regeneration of human fetus’s because they have nucleated RBCs when they are in the womb surround by amniotic fluid and fully hypoxic.

        Hemoglobin: Phylogenetic Divergence

        Hemoglobin’s structure and function have evolved significantly across vertebrates, reflecting adaptations to oxygen demands, environments, and regenerative capacity: This is why knowing your evolutionary history matters deeply to fully understand the wisdom in my decentralized thesis.

        • Amphibians (e.g., Salamanders):
          • Hemoglobin often has a simpler, less specialized structure compared to mammals. In mammals it is crystalline in structure and in amphibians it is not and does not carry oxygen as well as human hb does. In some species, it resembles ancestral globins with lower oxygen affinity (higher P₅₀), suited to aquatic or low-oxygen habitats.
          • Their RBCs are nucleated, a trait retained from early vertebrates, which allow greater metabolic flexibility, including dedifferentiation potential. This supports atavistic moves in cells during environmental changes. This makes them super adaptable to a changing landscape. This certainly was the case in the post Cambrian Earth. Remember how Huberman flubbed this on in my interview with him and Rubin? He has no idea the why humans would have so much amphibian opsin in their brains. The reason is mammals evolved from amphibians as oxygenation approached 21% and they TCA cycle replaced glycolysis.
          • MetHb formation and reduction might is less tightly regulated in amphibians, aligning with a physiology that tolerates hypoxia and supports regeneration. We see these atavisitc effects in humans in utero who are actively building out their body plans in extreme hypoxia.
          • Mammals (e.g., Humans):
            • Hemoglobin is highly specialized: It is tetrameric (α₂β₂), with cooperative oxygen binding and a lower P₅₀ (higher affinity), optimized for efficient oxygen delivery in warm-blooded, high-metabolism bodies that use the TCA cycle. Why? Mammals evovled after the Great Oxygenation Event, Cambrian explosion and the KT event when light became stable and when oxygen was plentiful in our atmosphere. Amphibians evolved much early when light was variable and oxygen was not as plentiful. Human Hb is liquid crystalline compared to amphibian Hb and this means they bind oxygen better than a salamander can.
            • Human RBCs are enucleated, which is a uniquely mammalian innovation that maximizes oxygen-carrying capacity but limits cellular adaptability (e.g., no dedifferentiation without extreme cues).
            • MetHb is actively reduced by enzymes like cytochrome b5 reductase (heme protein), reflecting a system geared toward stability in an oxygen environment that selects for TCA use rather than plasticity to regenerate your whole body.
          • Wound Healing and Regeneration: The Hemoglobin Link

            My decentralized  hypothesis finishes Becker’s life long work that oxygen tension, biophotons, and metHb dynamics drive healing and regeneration and this maps onto these differences elegantly:

            • Amphibians: Regeneration Superstars:
              • Hemoglobin Context: Lower oxygen affinity means amphibian Hb releases oxygen more readily in hypoxic wounds, amplifying local hypoxia. When you read his papers you can see the difference he noted but could not explain. This could shift RBCs toward metHb more easily, especially with ROS from the injury site.
              • Biophoton Role: Nucleated RBCs and metabolically active tissues emit a broader or but less intense biophoton spectrum because they are tuned to hypoxia. Why? mtDNA is the major SOURCE of biophotons in Nature. We now know mammalian blood also emits biophotons but the quality and character is not on par with mtDNA which can adapt its biophoton release based on oxygen tensions mtDNA senses in cells. Humans do not have any mtDNA in their RBCs, so they have lost this ability in RBCs but retain some biophoton release via neutrophils in the blood which are nucleated. The presence of mitochondrial DNA (mtDNA) angle is a game-changer, and it shifts the focus from just biochemical players like NO to the fundamental source of biophotons. This excess light mtDNA creates liberates massive amounts of NO from metHb or other stores, sustaining a prolonged “regenerative signal.”
              • Humans (Mammals): RBCs are enucleated and lack mitochondria (and thus mtDNA). This is a mammalian quirk which evolved for oxygen efficiency but it came at a cost. No mitochondria in mammalian RBCs means no internal biophoton generation in RBCs. Any biophotons in human blood come from other cells (e.g., leukocytes, endothelial cells), not RBCs themselves. The result: Human RBCs are passive oxygen carriers, not active EM signalers. MetHb form in hypoxia, but without mtDNA-driven biophotons, there’s no robust internal light to amplify regeneration signals for a sustained length of time.
              • Dedifferentiation: Robert Becker showed salamanders use bioelectric currents to dedifferentiate cells at wound sites, forming a blastema (a mass of stem-like cells). MetHb, as a primitive state, which acts as a redox chamber and photon hub (sun), to driving RBCs and other cells to revert phylogenetically, supported by their nucleated flexibility. This explains why the sun is critical in mammalian longevity. We cannot regenerate well because we have to rely on the exogenous source of light during wound healing. This fully explains the longevity benefit of man to primate because we lost our hair and made melanin with our newest semiconductor, melanin, to gain even more solar power.
              • Outcome: The amphibian system favors plasticity and this allows limbs to regrow because hypoxia, biophotons, and NO create a sustained “atavistic” environment, echoing early vertebrate development. Humans use this environment to birth their young, but they lose this effect as soon as they leave the womb and breathe.
            • Mammals: Scar Masters:
              • Hemoglobin Context: High oxygen affinity and enucleated RBCs mean mammals prioritize oxygen delivery over local release. As a result, hypoxia in human wounds is shorter-lived, and metHb is quickly reduced to Hb by enzymatic machinery, limiting its accumulation.
              • Biophoton Role: Enucleated RBCs don’t emit biophotons themselves, and mammalian tissues might produce a narrower, less UV-rich spectrum (more visible/NIR), reflecting higher oxygen baselines. This mean less NO liberation via biophotons in early hypoxia, favoring inflammation over regeneration.
              • Dedifferentiation: Mammalian RBCs lack nuclei, so dedifferentiation to a stem-like state (as Becker suggested) is rare and requires extreme conditions. MetHb would still form in hypoxia, but the bioelectric current it generates is weak and short-lived, insufficient for full blastema formation.
              • Outcome: The mammalian system leans toward stability, and scarring seals wounds fast, but regeneration is suppressed because hypoxia is short lived, as oxygen tension rise and Hb recovery outpace the “atavistic” window.

            Phylogenetic Hemoglobin and Healing Divergence

            The phylogenetic gap in hemoglobin ties directly to my quantized biophoton idea:

            • Oxygen Tension: Amphibian Hb’s lower affinity amplifies wound hypoxia, extending the metHb-biophoton-NO loop. Mammalian Hb’s high affinity shortens it, rushing tissues back to normoxia and TCA use.
            • Biophoton Spectra: Amphibians, with nucleated RBCs and less-specialized metabolism, might emit UV-rich biophotons that sustain NO-driven dedifferentiation. Mammals, with streamlined RBCs, lean toward visible/NIR emissions that support angiogenesis and closure, not regrowth.
            • Atavism: MetHb in amphibians mimics an ancestral state (e.g., early chordate globins), triggering regenerative pathways conserved from phylogeny. In mammals, metHb is a transient paramagnetic glitch, not a signal, due to evolutionary pressure favoring rapid repair over regenerative plasticity.

            Why the Difference? Hemoglobin as the semiconductor

            Evolutionarily, amphibians retained regenerative capacity because their environments (e.g., aquatic, variable O₂) favored adaptability over oxygen use, as a result, hemoglobin and RBCs stayed in a more “primitive” paramagnetic state to support this. Mammals, facing predation and thermal demands, traded regeneration for speed and efficiency and hemoglobin and RBCs evolved to lock in oxygen using the TCA cycle, not to linger in hypoxic, biophoton-driven states.

            Reptiles and Salamanders (Amphibians):

            • RBCs are nucleated and retain mitochondria with mtDNA, especially in amphibians like salamanders. Reptiles (e.g., lizards) also have nucleated RBCs with some mitochondrial activity, though it varies by species.
            • Result: Their nucleated RBCs are biophoton factories. mtDNA fuels mitochondrial ROS/RNS production, emitting a broader, more intense spectrum (UV-heavy, as Popp noted), especially under hypoxic conditions. This isn’t just about NO; it’s a full-on regenerative light show that goes on in these animals endogenously.
            • 

SUMMARY

I am hoping you have put these lessons all togther now and understand why amphibians are regeneration rockstars using primitive heme proteins. The fact that we use highly differentiated Hb is why we scar early and get cancer easily when we are not allowed to use the TCA cycle due to hypoxic signaling in cells. Today, our nnEMF environments create these signals making falling back into disease phenoptypes EASY.

This effect is amplified when we are blocked from sunlight having UV-IR light. This blocks out ability to use exogneous sunlight via melanin to augment our healing ability. This is why your modern world is creating every last chronic disease you can imagine. Awake now? We are our own Asteroid folks. This addiction to the biochemical paradigm supported by food guru ideas is a killer for humans. It has zero sophistication for the mechanism laid out in this blog and explains why billions of humans are at risk in a blue lit and nnEMF filled world.

My decentralized theory kicks the door in on the biochemical paradigm that nailed Robert O. Becker’s scientific life to a cross. Salamanders and reptiles regenerate better because their mtDNA-equipped RBCs flood wounds with biophotons, not just tweaking NO creation at the injury site. It also explains that as we turn off oxygen’s paramagnetic signal, we replace it with another paramagnetic signal in metHb production. This change drives a complete decentralized repair regeneration cascade controlled by electromagnetic signaling. This favored a broader spectrum of biophotons creation. Popp showed prokaryotes emit 5000 times more light than we eukaryotes. That fact is huge when you plug in evolutionary history I gave you here.

Mitochondria used to be bacteria so they retain this lineage of light creation via energy transformation. mtDNA-driven mitochondria emit more UV biophotons (from high-energy ROS transitions), which trigger DNA repair, protein remodeling, or cell dedifferentiation way beyond NO’s vasodilation or redox effects. Hypoxia creates the sun inside a wound of an amphibian. This hypoxia is an electromagnetic amplifier for their regeneration.

In wounds, low oxygen tensions ramps up mitochondrial ROS in these species’ RBCs, boosting biophoton output. This aligns with Roeland van Wijk’s oxygen-tension link; more photons, more regenerative signaling. It also aligns with Popps work too. Every box is checked.

My photo-bioelectric boost shows that Robert Becker’s currents in salamanders stem from this mtDNA-biophoton engine inside the blastema. Nucleated RBCs could use EM force (via photons) to polarize cells, forming blastemas. Humans, lacking RBC mitochondria, can’t polarize cells as well to sustain this. This is why depolarization in humans links to CANCEROUS human cells.

How do humans offset the inability of making biophotons to repair? Enter, melanin and sunlight exposure on their skin. Mammals need the external source of sunlight with UV-IR solar stimulus to finish the job of wound healing and guarrantee they NOT GET CANCER in an OXYGENATED ENVIRONMENT.

This is why CCO controls water production and apoptosis in mtDNA. The answer to cancer is built into our design but when we live under light that causes a chronic mtDNA hypoxia and we get no UV light, we never can tap Becker’s regenerative currents. Since Earth is heavily oxygenated today, the loss of heme proteins in mtDNA, creates the perfect storm to create cancer.

Just say NO to the ideas pushed in biochemistry that nitric oxide works the way they believe. They are beyond dead wrong. They have overfocused on NO liberation from metHb as the star of this show. They get No Quarter from me, no mea culpa. Billions have died because of their myopia. While NO matters (e.g., vasodilation, signaling), biophotons from mtDNA do way more. NO is used to keep wounds hypoxic in injury. Biochemistry still has no framework of why this is critical and why a return of NIR from mtDNA changes the oxidation state of iron to return tissues back to normoxia state where the TCA cycle can be used safely again.

• Stemness: UV biophotons directly influence gene expression via alteration of chromatin states, pushing cells toward a stem-like fate, as seen in salamander blastemas.
• Tissue Remodeling: A broader spectrum (UV to NIR) would orchestrate proteases, caspases, and growth factors (BCL-2), and ECM changes, not just rely on NO’s local biochemical effects.
• Energy Transfer: Photons are the EM force carriers and they shuttle energy and information across cells, syncing regeneration in ways mammals can’t replicate without mtDNA in RBCs. NO is also the electromagnetic signal they use to stimulate their stem cells from depots all over their body to regenerate.

Mammal vs. Amphibian/Reptile Gap Is Tied 100% to LIGHT, NOT FOOD.

• Humans: No mtDNA in RBCs = limited biophoton budget. Wound healing leans on systemic factors (e.g., macrophages, fibroblasts) with weaker, secondary biophoton input from non-RBC sources. Scarring wins over regrowth. Scarring however allows for oncogenesis if the cell remains in an atavistic state when oxygen supply comes back at the wrong time.
• Salamanders/Reptiles: mtDNA in RBCs = biophoton surplus. Wounds get a localized, intense EM signal, amplifying dedifferentiation and regeneration. Their “rockstar” status comes from this mitochondrial light advantage, not just hemoglobin or NO quirks.
• 

I think I’ve reframed Becker’s experiments perfectly using biophysics. Regeneration isn’t just about the injury hypoxia or NO liberation or the forced de-differentiation of metHb. It’s about mtDNA as the biophoton engine of creation. Salamanders and reptiles leverage this to flood wounds with light-driven EM force, dwarfing mammals’ capacity.

I hope you can visualize something larger now. There is bigger realization here why centralized medicine must be destroyed. These finishing touches to Becker’s thesis is fully decentralized and it explains oncogenesis and human development. When the injury is hypoxic and Becker’s current cannot be made, it is the perfect set up for cancer because you are feeding massive oxygenation into atavist cells. That is the cancer story.

Here is the other realization. Reading the first few lines of Genesis should now have a different meaning for you. This explains how a human child grows inside the womb. The germ line cells are kept hypoxic in an amnionitc fluid sac and that little “Salamander” stays connected to its mother’s liver by way of the umbilical cord. Many forget that during fetal life humans have fetal hemoglobin and those RBCs have mitochondria in them. Those RBC come from her liver.

That mtDNA is sculpting the child’s body plan using biophoton release from its parents germ line, just like Becker’s salamanders did. The amount of light a fetus makes supports creating a human from the germ line. This story is astounding when you realize it. It points out why our biochemical focus has blinded us from many truths and why biophysics has the answers for most of the chronic diseases now. We have built a world that simulates “an Earth” that existed before the Cambrian explosion when oxygen was rare.

What we have done to Earth with light and nnEMF is truly tragic. It is humanity’s asteroid. The injury stimulus that make is hypoxic and dehydrated making sure we run on a primative metabolic pathway that fosters atavism and then it never let us into the sun where UV and IR light awaits our body to create hydrated melanin sheets from CCO and melanin via POMC. It is stunning failure for humanity that centralized science and medicine allows.

CITES

The Body Electric, Robert O. Becker 1985

https://www.researchgate.net/publication/8465511_Biophoton_research_in_blood_reveals_its_holistic_properties

Pall, M.L. “Electromagnetic fields act via activation of voltage-gated calcium channels to produce beneficial or adverse effects.” J Cell Mol Med. 2013.

Yakymenko et al. “Oxidative mechanisms of biological activity of low-intensity radiofrequency radiation.” Electromagn Biol Med. 2016.

Leszczynski et al. “Non-thermal activation of stress pathways by mobile phone radiation in human endothelial cells.” Differentiation. 2002.