Dr. Jack Kruse
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DECENTRALIZED MEDICINE #39: FINISHING BECKER'S WORK
🕑 Added 2025-04-01 06:05:55 +0000 UTCLight 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.
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 electromagnetic 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 keep a cell hypoxic because NO blocks Hb from carrying oxygen. This is a remnant from the Great Oxygenation Event.
MetHb Reduction: The photo-bioelectric current I mentioned stems from biophotons liberated in the injury site via EM interactions with metHb’s ferric iron. This photon force would be quite strong enough at nanoscale distances 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. This implies that the biophoton signal would have more red light and less UV biophotons in their spectra. Nature hides some weighty recipes at the nanoscopic atomic level we do not see.
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 local NO production and biophoton creation to metHb levels to match redox 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 story's hero. He found out quickly that was not the case. I explained to him that biophoton production done by injured tissues suggested a distributed, decentralized model for tissue sculpting in humans. My model showed him that every RBC cell is a powerhouse emitting EM force carriers, biophotons. This aligns with Becker's amphibian-mammal split, too:
Amphibians: Few people realize amphibians have nucleated RBCs that emit more light than mammalian blood that is enucleated. Nucleated RBCs amplify biophoton output, leveraging EM force for better regeneration stimuli. Their nucleated RBCs are not as good 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 regeneration 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 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 makes a wider spectrum of light release, miming what we see in the domains of Bacteria and Archea. It appears that it does not enrich UV emissions because ROS excitation transitions are less prominent. After all, oxygen is less prominent at the injury site. At the same 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 biophoton creation data hints at this oxygen level quantization.
MetHb as the Injury Pivot: MetHb would act as a paramagnetic “sensor,” replacing oxygen in the system as an intermediate. Recall from my 2014 lecture where Dave Asprey escorted me to the street that oxygen is paramagnetic. 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 that 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 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 in a feedback loop.
Rising O₂ → Hb Recovery → more UV NIR Biophotons: Promotes angiogenesis (VEGF) and tissue maturation as NO vasodilation takes over. NIR restores energy production in the 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 of nucleated RBCs that have mitochondria. This is why mammals heal but rarely regrow limbs; this is because mtDNA is an excellent source of biophotons. This also explains the phenomental regeneration of human fetuses because they have nucleated RBCs when they are in the womb, surrounded 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. 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 than mammals. In mammals, it is crystalline, and in amphibians, it is not and does not carry oxygen as well as human hemoglobin 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 allows 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 on post-Cambrian Earth. Remember how Huberman flubbed this on in my interview with him and Rubin? He has no idea why humans would have so much amphibian opsin in their brains. The reason is that mammals evolved from amphibians as oxygenation approached 21%, and the TCA cycle replaced glycolysis as oxygen became a more prominent feature of Earth's environment.
MetHb formation and reduction might be less tightly regulated in amphibians by evolutionary design, aligning with a physiology that tolerates hypoxia and supports massive regeneration. We see these atavistic 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 evolved after the Great Oxygenation Event, the Cambrian explosion, and the KT event when light became stable and when oxygen was plentiful in our atmosphere. Amphibians evolved much earlier when light was variable and oxygen was less abundant. Human Hb is a liquid crystal compared to amphibian Hb, which binds oxygen better than a salamander can.
Human RBCs are enucleated, 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 easily shift RBCs toward metHb, especially with ROS from the injury site.
Biophoton Role: Nucleated RBCs and metabolically active tissues emit a broader but less intense biophoton spectrum because they are tuned to hypoxia. Why? mtDNA is the primary SOURCE of biophotons in Nature. We now know mammalian blood also emits biophotons. Still, the quality and character are not on par with mtDNA, which can adapt its biophoton release based on oxygen tensions that 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 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 mammalian quirk 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. 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 must rely on the exogenous light source during wound healing. This thoroughly explains the longevity benefit of man to primates 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 means 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, which is insufficient for complete blastema formation.
Outcome: The mammalian system leans toward stability, and scarring seals wounds fast. However, regeneration is suppressed because hypoxia is short-lived, as oxygen tension rises and Hb recovery outpaces 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 differentiation; 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. MetHb is a transient paramagnetic glitch in mammals, 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 safe, efficient oxygen handling, 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 in these animals endogenously.
SUMMARY
I hope you have put these lessons together 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 phenotypes EASY.
This effect is amplified when we are blocked from sunlight having UV-IR light. This blocks our ability to use exogenous 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 attacks 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 biophoton creation. Popp showed prokaryotes emit 5000 times more light than we eukaryotes. That fact is enormous when you plug in the 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 an amphibian's wound. This hypoxia is an electromagnetic amplifier for their regeneration.
In wounds, low oxygen tensions ramp 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's work. 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 guarantee they do 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 chronic mtDNA hypoxia and we get no UV light, we can never 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 to normoxia state where the TCA cycle can be used safely again.
Stemness: UV biophotons directly influence gene expression by altering 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, growth factors (BCL-2), and ECM changes, not just rely on NO’s local biochemical effects.
Energy Transfer: Photons are the EM force carriers that shuttle energy and information across cells, syncing regeneration in ways mammals can’t replicate without mtDNA in RBCs. NO is also the paramagnetic electromagnetic signal they use to stimulate their stem cells from depots all over their body to regenerate.
The 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 de-differentiation 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, ideally using biophysics. Regeneration isn’t just about injury hypoxia, 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 more significant now. There is a bigger realization here as to why centralized medicine must be destroyed. These finishing touches to Becker's thesis are fully decentralized, and they explain 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 germline cells are kept hypoxic in an amniotic 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 RBCs come from her liver.
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 to 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 makes it hypoxic and dehydrated makes sure we run on a primative metabolic pathway that fosters atavism, and then it never lets 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 a stunning failure for humanity that centralized science and medicine allows.
CITES
The Body Electric, Robert O. Becker 1985
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.
Comments
Dr. Gavin Nixon
Mitochondrial transfer mediates endothelial cell engraftment through mitophagy," Mitochondrial Transfer Mechanism: MSCs transfer mitochondria to endothelial cells (ECs) via tunneling nanotubes (TNTs), thin membrane structures that connect cells. This transfer occurs naturally under stress conditions, such as ischemia (low oxygen), where ECs need a bioenergetic boost to survive.
Dr. Gavin Nixon
Mitochondrial transfer mediates endothelial cell engraftment through mitophagy," published in Nature on April 30, 2024 We do have nucleated HSC in the bone marrow which we can harvest and place into injured tissues. This blog post would seem to emphasize why this therapy would be the superior way to generate a healing/regnerative response due to the presence of HSC with mitochondria. I also think these cells aside from providing signaling via bio photon release are also doing mitochondrial transplantation
