This perspective reveals mitochondria as quantum architects forged during the GOE. They use light hydrogen and solar EMF to drive decentralized evolution, a process centralized science must urgently explore.
Mitochondrial Quantum Dynamics and Evolutionary Light: A Decentralized Biophysical Framework
Mitochondria operate as quantum engines, harnessing light hydrogen to drive life through mechanisms that predate and outstrip the 200-million-degree plasma of stellar fusion. This document explores the mitochondrial inner membrane’s 30 million volts per meter (MV/m) field, the role of deuterium-depleted water (DDW) in enabling quantum effects in microtubules, the perforin/granzyme pathway’s viral integration, and the evolutionary significance of proton dynamics as a metal plasma-like system. I want to connect these to a post-Great Oxidation Event (GOE) feedback loop that addresses our modern light stressors, and we’ll propose next steps for decentralized biophysics.
The Biophysics of Mitochondrial Health, Lithium, and Proton Dynamics in Demyelinating Disorders: A Decentralized Perspective
Mitochondria are often called the powerhouses of the cell. Still, their role goes far beyond simple energy production; they are dynamic electromagnetic systems that orchestrate cellular health through intricate biophysical mechanisms. This blog explores how the mitochondrial inner membrane’s staggering 30 million volts per meter (MV/m) electric field, the production of deuterium-depleted water (DDW), and lithium’s unique properties interact to influence proton dynamics, biophoton emissions, and myelin integrity, particularly in conditions like bipolar disorder where white matter deficits are prevalent. By integrating concepts like Cherenkov radiation, ultraweak photon emissions (UPEs), and the Grotthuss mechanism, we’ll reveal a decentralized framework for understanding cellular health that challenges conventional biochemical models and emphasizes the critical role of protons, not just electrons, in maintaining life.
The Mitochondrial Electric Field: A Biophysical Marvel
The mitochondrial inner membrane hosts an electric field of approximately 30 MV/m, as calculated from a membrane potential of 150 mV across a five nm-thick membrane: Electric Field = Voltage / Distance = 0.15 V / (5 × 10⁻⁹ m) = 3 × 10⁷ V/m. This field, comparable to the intensity of a lightning bolt but confined to a nanoscale distance, drives ATP synthesis through the proton-motive force. Protons (H⁺) are pumped across the membrane by the electron transport chain (ETC), with cytochrome c oxidase (CCO, or Complex IV) playing a pivotal role by reducing oxygen to water: 4H⁺ + 4e⁻ + O₂ → 2H₂O. This reaction not only generates a voltage gradient (Δψ) and pH gradient (ΔpH) but also produces what some researchers call “deuterium-depleted water” (DDW), a water form with lower deuterium content than typical cellular water. DDW’s unique properties, driven by mitochondrial DNA (mtDNA)-regulated processes, are key to maintaining this field’s coherence and optimizing energy transfer. Using the TCA allows us to tap this potential. When we do not use the TCA cycle, another reality exists, and that is where demyelinating disorders come from. If you have any demyelinating disease, you know the AM sunrise is a defect in your environment.
DDW, Cherenkov Radiation, and Biophoton Emissions
DDW, with its reduced deuterium content (~25 ppm compared to 150 ppm in normal water), alters the biophysical environment inside mitochondria. Deuterium (²H), being heavier than protium (¹H), strengthens hydrogen bonds, increasing water’s refractive index and slowing the speed of light in the medium (v = c/n, where n is the refractive index). DDW, enriched in protium, has a slightly lower refractive index, meaning light travels faster. This subtle shift can lower the threshold for Cherenkov radiation, which is a known phenomenon in physics that has never been applied to biology, where charged particles, like electrons, emit electromagnetic radiation when traveling faster than light’s phase velocity in a medium (in water, ~0.75c). The 30 MV/m field in mitochondria accelerates electrons during redox reactions in CCO’s heme groups. In a DDW-rich matrix, some electrons may approach this threshold, but those experiments have not been done yet, emitting ultraweak Cherenkov-like biophotons, potentially in the UV range (200-350 nm). Research by Fritz-Albert Popp has confirmed the presence of ultraweak biophotons in biological systems, though their exact origins remain debated. This Cherenkov mechanism “could be” a secondary source of biophotons in humans, reflecting cellular health or dysfunction.
Protons, the Grotthuss Mechanism, and the Z-Z Highway
Protons are central to this system, not just electrons. The Grotthuss mechanism describes how protons hop along hydrogen-bonded water networks faster than typical diffusion, creating a “Z-Z highway” (Zwitterionic-Zwitterionic) for efficient energy transfer and electrical resistance in cells. This fast proton conduction is critical for maintaining the mitochondrial membrane potential and supporting neural signaling, especially in myelinated axons. However, modern lifestyles filled with processed foods, blue light, and non-native electromagnetic fields (nnEMF) increase deuterium in tissues, slowing this highway. Deuterium’s heavier mass disrupts proton hopping, shifting to a slower E-Z-E (Extended-Zwitterionic-Extended) pathway, leading to energy inefficiency and cellular stress. A 2020 study in Medical Hypotheses links deuterium accumulation to mitochondrial dysfunction in neurological disorders, highlighting its relevance to demyelinating diseases like bipolar disorder, autism, MS, schizophrenia, and ALS, where white matter deficits are well-documented.
Bipolar Disorder, White Matter Deficits, and UPE Leakage
Bipolar disorder patients often exhibit reduced white matter volume, particularly in regions like the corpus callosum and prefrontal cortex, as confirmed by a 2016 meta-analysis in Molecular Psychiatry. White matter, composed of myelinated axons, insulates neural signals, minimizing energy loss and containing biophotonic emissions. The nodes of Ranvier, which are gaps between myelin segments where action potentials regenerate, are particularly vulnerable. In bipolar disorder, myelin deficits expose these nodes, leading to excessive ultraweak photon emissions (UPEs), especially in the UV range, due to oxidative stress and lipid peroxidation. A 2016 study in the Journal of Photochemistry and Photobiology found elevated UPEs in bipolar patients during manic episodes, reflecting heightened oxidative stress and mitochondrial dysfunction. This UPE leakage disrupts neural synchrony, exacerbating mood instability and contributing to the “photonic noise” that drowns out the brain’s electromagnetic signal.
The ticket that moves the needle of all humans with demyelination happens on your inner mitochondrial membrane when it has a poor redox charge for any reason (delta psi). This physical circumstance happens, then oxygen becomes a toxin, as during the GOE. Ironically, this is true for most chronic diseases. Centralized medicine has never gotten any MD to this level of understanding with the Big Harma curricula in healthcare. That is by design. The toxic nature of Oxygen drove endosymbiosis on Earth 650 million years ago, otherwise, Nature would have never have innovated mitochondria. The paramagnetism of oxygen keeps us alive, so we can optimize the TCA cycle, and this is a critical step in the story of chronic disease epidemics.
Become the disruptor with this wisdom, or be disrupted by centralized medicine beliefs.
Lithium’s Biophysical Role: Beyond Biochemistry
Lithium, often used to treat bipolar disorder, has biophysical effects that address these issues. As a monovalent cation (Li⁺), lithium disrupts water’s hydrogen-bonding network, slowing proton hopping via the Grotthuss mechanism and slightly shifting CSF proton dynamics toward the E-Z-E pathway. This can stabilize pH in the cerebrospinal fluid (CSF), which is crucial in bipolar disorder (more in mania) where oxidative stress causes pH fluctuations. More importantly, lithium absorbs UV light (200-300 nm, as noted in a 2020 study in Spectrochimica Acta), overlapping with the spectrum of UPEs emitted at the nodes of Ranvier. By acting as a photonic sink for UV light, lithium reduces UV-induced oxidative damage, protecting myelinated axons and preserving neural signaling. This aligns with lithium’s biochemical role in promoting remyelination (via GSK-3β inhibition and Wnt activation) but adds a biophysical layer: lithium mitigates the “photonic noise” of UPE leakage at the nodes of Ranvier, supporting the brain’s electromagnetic coherence.
Lithium also influences proton-coupled ion channels like ASIC channels, which regulate CSF pH and neuronal excitability, as shown in a 2019 study in Neuroscience Letters. By stabilizing proton gradients, lithium reduces excitotoxicity at the nodes of Ranvier, further supporting myelin repair. Additionally, lithium’s circadian-stabilizing effects enhance the body’s response to natural light cycles, optimizing proton dynamics and mitochondrial function—key for energy-intensive processes like remyelination.
CCO, Apoptosis, and Electrical Resistance: A Decentralized View
CCO’s production of DDW isn’t just about energy, it’s a protective mechanism for photobioelectric energy tied to oxygen consumption that evolved post-Great Oxidation Event (GOE) to maintain the mitochondrial electric field’s coherence. This field prevents “loss of electrical resistance,” a concept that extends beyond cellular quality control to organism-level preservation. If the membrane potential collapses due to oxidative damage or hypoxia, CCO triggers apoptosis via cytochrome c release, activating caspases and preventing reactive oxygen species (ROS) from accumulating. This acts as a failsafe, ensuring damaged cells are eliminated before they propagate low-resistance currents that could destroy distal tissues. Unlike the biochemical view of apoptosis as mere quality control, this decentralized perspective sees CCO as a guardian of electromagnetic integrity, protecting the organism from systemic damage while limiting oncogenesis by clearing atavistic cells formed under hypoxic stress.
A Decentralized Fix: Aligning with Nature’s Signals
To support this system, we must live more like our ancestors: eat fresh, local foods, soak up sunlight, and minimize tech overload (blue light, nnEMF) while grounding to keep deuterium low and the Z-Z highway open. Sunlight entrains circadian rhythms, enhancing mitochondrial function and proton dynamics, while grounding reduces nnEMF-induced ROS, preserving the mitochondrial field. Clean living optimizes DDW production, ensuring efficient energy transfer and minimizing UPE leakage. This isn’t rocket science, it’s brain surgery without a scalpel, cutting through centralized medical dogma to restore the body’s natural electromagnetic balance.
IS ALL MYELIN BIOPHYSICALLY THE SAME?
There are biophysical differences between Nodes of Ranvier in the central nervous system (CNS) and peripheral nervous system (PNS), stemming from differences in cellular environment, myelin structure, and molecular organization. Here are the key distinctions:
Myelin-Producing Cells:
CNS: Myelin is formed by oligodendrocytes, which can myelinate multiple axons simultaneously. This leads to a more compact arrangement and thinner myelin sheaths compared to the PNS.
PNS: Myelin is formed by Schwann cells, with each cell myelinating a single axon segment, resulting in thicker, more uniform myelin sheaths. This impacts the capacitance and resistance of the myelinated segments, influencing conduction properties.
Node Length and Spacing:
CNS: Nodes of Ranvier are typically shorter (1–2 µm) and internodal distances (between nodes) are shorter and more variable, depending on axon diameter and brain region. This can lead to slightly slower conduction velocities in some CNS axons compared to PNS axons of similar diameter.
PNS: Nodes are often longer (up to 3 µm), and internodal distances are more consistent, optimized for rapid conduction in larger axons (e.g., motor or sensory nerves). Longer internodes in the PNS increase the speed of saltatory conduction.
Ion Channel Density and Composition:
CNS: Nodes in the CNS have a high density of voltage-gated sodium channels (Naᵥ1.6 primarily), but the clustering and anchoring mechanisms differ slightly due to interactions with oligodendrocyte-derived extracellular matrix proteins. Potassium channels (e.g., Kᵥ1) are less prominent at CNS nodes, and their distribution in paranodal or juxtaparanodal regions is less distinct.
PNS: PNS nodes also have Naᵥ1.6 channels but are supported by Schwann cell microvilli, which provide a unique microenvironment. Potassium channels (Kᵥ1.1/1.2) are more prominently clustered in juxtaparanodal regions, contributing to membrane potential stabilization during high-frequency firing.
Paranodal Junctions:
CNS: Paranodal axoglial junctions, formed between the axon and oligodendrocyte loops, are less robust and have a slightly different molecular composition (e.g., involving contactin and Caspr). This can affect the electrical insulation and speed of repolarization.
PNS: Paranodal junctions formed by Schwann cells are tighter and more structurally defined, enhancing electrical isolation between nodal and internodal regions. This contributes to more efficient saltatory conduction.
Capacitance and Resistance:
CNS: The thinner myelin in the CNS results in higher membrane capacitance and lower resistance per unit length, which can slightly reduce conduction velocity compared to PNS axons of similar size. However, this is offset by shorter internodal distances in some CNS axons.
PNS: Thicker myelin reduces capacitance and increases resistance, optimizing for faster conduction velocities, especially in large-diameter axons like those in motor nerves.
Conduction Velocity:
CNS: Conduction velocities are generally slower in CNS axons (e.g., 2–80 m/s, depending on axon diameter and myelination) due to the factors above.
PNS: PNS axons, particularly large myelinated ones, can achieve higher velocities (up to 120 m/s) due to optimized myelin thickness and internodal spacing.
Response to Injury:
CNS: Nodes in the CNS are less capable of reorganization after demyelination due to limited regenerative capacity of oligodendrocytes and a less supportive microenvironment.
PNS: Schwann cells in the PNS actively participate in debris clearance and remyelination, leading to better nodal restoration after injury, which indirectly affects biophysical properties post-recovery.
These biophysical differences arise from the distinct cellular and molecular architectures of the CNS and PNS, tailored to their specific functional demands. While both systems use Nodes of Ranvier for saltatory conduction, the PNS is generally optimized for faster, more robust conduction, while the CNS prioritizes compact organization for complex neural networks.
Demyelinating diseases, such as multiple sclerosis (MS) in the CNS or Guillain-Barré syndrome (GBS) and Charcot-Marie-Tooth disease (CMT) in the PNS, disrupt the myelin sheath and Nodes of Ranvier, impacting their biophysical properties, including the higher mitochondrial capacity and potential ultraweak photon emission (UPE) at these sites. The differences in Nodes of Ranvier between the CNS and PNS, combined with their roles in mitochondrial function and UPE, lead to distinct implications for demyelinating diseases.
Mitochondrial Capacity at Nodes of Ranvier: Nodes of Ranvier have a high density of mitochondria to meet the energy demands of ion channel activity (e.g., sodium-potassium ATPase) during saltatory conduction. Mitochondria support rapid ATP production and calcium buffering, critical for maintaining axonal integrity and signaling.
Ultraweak Photon Emission (UPE): UPE refers to low-intensity photon emissions from biological systems, often linked to mitochondrial oxidative processes (e.g., reactive oxygen species [ROS] generation). Nodes, with their high mitochondrial activity, may be sites of elevated UPE, potentially involved in cellular signaling or reflecting metabolic stress.
Demyelinating Diseases: These conditions degrade myelin, exposing internodal regions, disrupting nodal organization, and impairing saltatory conduction. This affects mitochondrial function and could alter UPE, with distinct consequences in the CNS vs. PNS due to their biophysical differences.
Implications of Demyelination in the CNS vs. PNS
1. Mitochondrial Dysfunction and Energy Failure
CNS:
Impact: Demyelination (e.g., in MS) disrupts oligodendrocyte support, leading to loss of myelin and paranodal junctions. This exposes internodal axonal regions, increasing energy demands as sodium channels redistribute diffusely along the axon (continuous conduction instead of saltatory). Mitochondria at nodes, already taxed, face heightened ATP demands, leading to energy failure.
Consequence: CNS axons are less resilient to energy deficits due to limited oligodendrocyte repair capacity and a less supportive microenvironment. Mitochondrial overload increases ROS production, exacerbating axonal damage and neurodegeneration. The shorter internodal distances and thinner myelin in the CNS mean smaller nodes may struggle to compensate for diffuse ion channel activity.
UPE Implication: Increased mitochondrial stress from ROS could amplify UPE at demyelinated nodes, reflecting oxidative damage. However, if mitochondrial function collapses, UPE may decrease, signaling metabolic failure. This could disrupt hypothetical UPE-mediated signaling (if UPE plays a role in cellular communication), further impairing axonal homeostasis.
PNS:
Impact: In PNS demyelinating diseases (e.g., GBS, CMT), Schwann cell damage disrupts myelin and nodal organization. However, Schwann cells are more effective at clearing debris and promoting remyelination than oligodendrocytes. The thicker myelin and longer internodes in the PNS mean larger nodal areas with robust mitochondrial populations, which may better handle initial energy demands post-demyelination.
Consequence: PNS axons are more likely to recover function due to Schwann cell-mediated repair, reducing long-term mitochondrial stress. However, during acute demyelination, the redistribution of sodium channels increases energy demands, temporarily straining nodal mitochondria. This is revelatory for ALS.
UPE Implication: Similar to the CNS, increased ROS from mitochondrial stress could elevate UPE during demyelination. However, the PNS’s better repair capacity may normalize UPE levels faster as remyelination restores nodal function. UPE changes may be less severe or prolonged compared to the CNS.
2. Conduction Failure and Axonal Degeneration
CNS:
Impact: Losing myelin in the CNS disrupts saltatory conduction, slowing or blocking nerve impulses. The shorter nodes and less robust paranodal junctions in the CNS make it harder to maintain efficient ion channel clustering, worsening conduction failure. Mitochondrial dysfunction at nodes exacerbates calcium overload, triggering axonal degeneration.
Consequence: Due to limited regenerative capacity, CNS axons are more prone to permanent damage. The high mitochondrial density at nodes becomes a liability, as oxidative stress and energy failure accelerate neurodegeneration, particularly in chronic diseases like progressive MS.
UPE Implication: Persistent UPE elevation from ongoing mitochondrial stress may correlate with neurodegeneration. If UPE reflects cellular signaling, its disruption could impair communication between axons and glial cells, hindering repair efforts.
PNS:
Impact: PNS demyelination also impairs saltatory conduction, but the larger nodes and tighter paranodal junctions provide some resilience. Schwann cells can reorganize nodal structures more effectively, restoring conduction if remyelination occurs.
Consequence: PNS axons are less likely to degenerate due to better repair mechanisms. Mitochondrial capacity at larger nodes may buffer energy demands during acute phases, reducing the risk of axonal loss compared to the CNS.
UPE Implication: UPE changes may be transient, reflecting temporary mitochondrial stress during demyelination. Successful remyelination could normalize UPE, supporting axonal recovery and signaling.
3. Inflammatory and Microenvironmental Effects
CNS:
Impact: Demyelinating diseases like MS involve robust inflammation, with immune cells (e.g., microglia, macrophages) targeting myelin and axons. This creates a hostile microenvironment, increasing oxidative stress on nodal mitochondria and disrupting their function.
Consequence: The CNS’s limited repair capacity and inflammatory milieu exacerbate mitochondrial damage, reducing nodal efficiency and increasing UPE from ROS. Chronic inflammation may lead to persistent UPE elevation, reflecting ongoing tissue damage.
UPE Implication: Elevated UPE could serve as a biomarker of inflammation and mitochondrial stress in CNS lesions, but tissue damage may overwhelm its role in signaling (if any).
PNS:
Impact: PNS demyelinating diseases (e.g., GBS) also involve inflammation, but Schwann cells and macrophages efficiently clear debris, creating a more reparative microenvironment. This reduces prolonged stress on nodal mitochondria.
Consequence: The PNS’s supportive microenvironment limits mitochondrial damage, allowing better recovery of nodal function. Due to effective inflammation resolution, UPE changes are likely less intense and more transient.
UPE Implication: UPE may spike during acute inflammation but return to baseline with repair, potentially aiding in monitoring disease progression or recovery.
4. Therapeutic and Recovery Potential
CNS:
Challenge: The CNS’s limited remyelination capacity (due to oligodendrocyte constraints) makes restoring nodal mitochondrial function and UPE homeostasis difficult. Therapies targeting mitochondrial protection (e.g., antioxidants) or enhancing oligodendrocyte function are critical but challenging due to the CNS’s complex environment.
UPE Role: Monitoring UPE could theoretically track mitochondrial health or treatment efficacy, but detection challenges and unclear biological significance limit its practical use.
PNS:
Advantage: The PNS’s robust repair mechanisms, driven by Schwann cells, offer better prospects for restoring nodal structure and mitochondrial function. Therapies supporting Schwann cell activity or reducing inflammation can more effectively normalize conduction and UPE.
UPE Role: UPE changes could reflect recovery dynamics, potentially serving as a non-invasive marker of remyelination success if detection methods improve.
SUMMARY
The biophysical differences between CNS and PNS Nodes of Ranvier, myelin thickness, nodal size, ion channel organization, and repair capacity, profoundly influence the implications of demyelinating diseases. In the CNS, demyelination leads to severe mitochondrial stress, persistent UPE elevation, and neurodegeneration due to poor repair, as seen in MS. In the PNS, robust Schwann cell-mediated repair mitigates mitochondrial damage and normalizes UPE, improving recovery prospects in diseases like GBS or CMT. The higher mitochondrial capacity at nodes makes them critical points of vulnerability but also potential therapeutic ideas.
While UPE’s role remains underexplored by biology, changes in its spectra should reflect mitochondrial health and disease dynamics, with more prolonged disruptions in the CNS compared to the PNS. This has enormous implications for thinking in and around ALS. Why? It tells us the nnEMF and/or heteroplasmy associated with it has to be substantial in intensity, duration, or heteroplasmy load from transgenerational light damage. Therapies aimed at protecting mitochondria, reducing inflammation, and enhancing remyelination are crucial to get done early, with the PNS offering a more favorable environment for recovery.
Before you READ ANYTHING BELOW, LISTEN TO THE LESSON ABOVE IN TOTAL.
THERE ARE LESSON PATIENTS TEACHING DOCTORS IF THEY LISTEN…………..
You are getting the gift of that lesson today acoustically in two ways.
This song spans the journey from the GOE’s transformative oxygenation to humanity’s spiritual and biological evolution. It hints at the unseen forces of our spirit that drive existence. That hidden force is right before us, yet we seem blinded to the obvious. It is light. The words whip you while lamenting the modern centralization threatening to extinguish this sacred essence. It invites you, the tribe, to awaken to your deeper nature, as silly talking monkeys yet to sense the full wonder of their story.
My overriding idea here is that the eye serves as a biological timestamp for heteroplasmy rates, acting as a key to the spirit. I believe it is a profound synthesis of science and spirituality within us.
This is the Music of the GOE that allows us to do what humans can do. All the drums’ polyrhythms came together to connect the fingers in the picture below.
Just watch how the chaos of the drums builds this song.
Everything before 6:15 is what Earth was like until the Cambrian explosion. The time signatures make no sense to most musicians because the environment of the Earth made no sense to cells. They stayed simple, bacteria and Archaea: no order, no complexity, no sense of timing, no life.
But…….there is something stirring inside of you, listening to the chaos, and you have no idea what it is, but you are drawn to it. You are feeling the chaos of the drums, small runs of polyrhythms. The song becomes amazing when the drummer brings the polyrhythms all together from 6:15. Life becomes possible because he brings the chaos together at once. That is the Cambrian explosion ……….THAT IS WHAT THE GOE DID FOR COMPLEX LIFE
Everything before the timestamp 6:15 is the current story of Noah’s baby………..at 6:15 this is where the magic between the white plaster begins to occur.
At 6:15 to 8:54 timestamps, what will you see and hear when you watch it? You will listen to a human begin to play four songs in one. Each limb is playing a different rhythm. Most people can hear it, but cannot fathom what Danny is doing. All the chaos of the polyrhythms before 6:15 is now becoming one. Life is emerging from the muck of the oceans.
That is what you’re experiencing now. You’re begging to realize you must tie all of Nature’s threads from the GOE into one so you can control your brain and four limbs independently.
Noah’s baby can not do any of these things. Noah’s has to deliver that chaos to his baby to get it to 8:54. To get it to the UV light on the snare drum and on his jersey.
At 8:54 is the Cambrian explosion, and this is when you finally hear complexity begin to make sense, and the light shows up, and the power in the song becomes its purpose. You see and feel what “pneuma” is. It is the white plaster between the fingers.
At 8:54, you become able to myelinate your system and control all that you can become in every limb. Everything after this timestamp is remyelination by maximizing the clockwise spin of the TCA. You are on that threshold, the baby is not. It is stuck in the time frame of 0:00 to 6:15. The baby cannot get to 8:54 without Noah making the hardest choice for the baby.
That is how life operates through music for me.
A tribe member started us down that path at the beginning of the Q&A with her question and story. Without this question, nothing else that happened as it unfolded. That fractal is also captured in the song and the Sistine Chapel’s center panel. The chaos of her last several months in this tribe is beginning to pay dividends because she now understands what she missed and could not sense. She is now emerging from her own chaos, and coming to the other side of the chaos. Before yesterday, she was in the same position of Noah’s baby without realizing her plight. Her bacterial TCA cycle was spinning the wrong way. Both of Noah’s daughters’ mitochondrial DNA is beating to the wrong drum in the NICU.
Now to astound yourself further………go listen to the lyrics.
You’ll be stunned. Here they are…………
We are spirit bound to this flesh
We go round one foot nailed down
But bound to reach out and beyond this flesh
Become Pneuma
We are will and wonder
Bound to recall, remember
We are born of one breath, one word
We are all one spark, sun becoming
Child, wake up
Child, release the light
Wake up now
Child, wake up
Child, release the light
Wake up now, child
(Spirit)
(Spirit)
(Spirit)
(Spirit)
Bound to this flesh
This guise, this mask
This dream
Wake up remember
We are born of one breath, one word
We are all one spark, sun becoming
Pneuma
Reach out and beyond
Wake up remember
We are born of one breath, one word
We are all one spark, eyes full of wonder
THAT IS WHAT MUSIC IS CAPABLE OF.
Explaining complex life in 11 minutes.
At 9:30, you’ll see UV light reflecting off his snare drum.
Tool knows the GOE, do you?
The drum solo ends with Danny in the UV light.
Now your flesh has become human, complex enough to tackle the Earth post-GOE.
The song goes back to normal 4/4 time, and then at the coda, polyrhythms return, and the UV light returns as we die. The process is reversed yet again.
Survival of the Wisest: A Wake-Up Call
Picture this: two souls on a beach, gazing at the endless ocean, where waves whisper a truth we’ve long forgotten. “It’s no longer about survival of the fittest. It’s survival of the wisest.”
Darwin has long sold us a lie. It is no longer about survival of the fittest because people are dying in every country. We sculpt our bodies for hours based on marketing lies passed down, chasing strength, speed, and endurance, while our minds and emotions, the true commanders of our fate, starve in neglect.
Strength without strategy? Wasted. Talent without temperance? Ticking time bomb in our wombs
.
The mental and emotional game isn’t just a side quest; it’s the arena where champions are forged and pretenders unravel. When pressure hits, when the moments that matter most arrive, your muscles won’t save you. Only your mind will.
Mastering your thoughts and emotions is harder than any deadlift or sprint. That’s precisely why you can’t skip it. You train it harder. Ultimately, it’s not the fittest who survive; it’s the wisest who thrive.
Will you train what truly matters? Or will you unravel when the tide turns?
WHAT IS BETWEEN THE FINGERTIPS OF THE SISTINE CHAPEL?
LIGHT
With life, you should trust the process, not the blueprint. Your cells are living the truth faster than your mind can map it. Keep moving, feel the ground, and let the data of experience shape your reality. Your life is analyzed on paper but lived in reality. The data you see from the air may create the illusion of certainty, but the data you live on the ground makes the experience.
The lesson: Stop overthinking every decision. Stop overanalyzing. Stop trying to create the perfect plan on paper. Your reality will be defined on the ground. I believe life is analyzed by mitochondria, and the UPEs my tissues make give me my reality. My life isn’t just numbers or abstract plans, it’s the messy, vibrant reality of living moment to moment. Overanalyzing can trap you in a sterile loop, disconnected from the ground truth of experience. Mitochondria don’t “think”; they do, tirelessly churning out energy for your reality. If UPEs contribute to your sense of being, whether as a metaphor or a literal phenomenon, it’s a beautiful way to frame the dance between biology and existence.
My Decentralized Thesis and the Garden of Eden: A Parallel of Human Design and Modern Disruption
Imagine the Garden of Eden (GOE) as the blueprint for humanity’s optimal state, perfectly attuned to Nature’s rhythms, where sunlight, circadian alignment, and cellular harmony sustained life as God and/or evolution intended. In this divine or evolutionary design, 20% of hemoglobin (Hb) delivers oxygen from the heart to the brain, fueling cognition, consciousness, and our unique mammalian identity. But what happens when that 20% is preserved in volume yet corrupted in function, with Hb oxidized to metHb (+3 state), unable to carry oxygen? Can we still embody the fullness of humanity as planned? This question mirrors the decentralized thesis we’ve been exploring: a vision of systems, biological, social, or technological, operating in harmony with Nature’s principles, free from centralized distortions. Like a flawed centralized protocol, modern life disrupts this design, and the consequences are profound.
The Fall from Eden: Modern Life’s Assault on Biology
Just as the GOE represents humanity’s symbiosis with Nature, our decentralized thesis champions systems that align with natural laws—autonomous, resilient, and adaptive. Today’s world, however, imposes a “centralized” override: artificial light, non-native EMF (nnEMF), and 24/7 tech divorce us from daylight and drown us in nightlight. This mirrors the epigenetic fall from Eden, where each generation strays further from the original blueprint. Chronic diseases, cancer, neurodegeneration, and metabolic collapse emerge not as random failures but as predictable outcomes of this mismatch, accelerating transgenerationally as tech and light abuse intensify. The decentralized thesis warns of this: centralized systems (like modern tech-driven lifestyles) erode resilience, creating fragility where Nature intended antifragility.
The Cellular Cost: Hypoxia and Circadian Chaos
When Hb becomes metHb, oxygen delivery falters, inducing chronic hypoxia. This stalls the TCA cycle, spikes lactate, and disrupts ultra-weak photon emission (UPE) and free radical signaling, key players in our proposed electric resistance model. Similarly, the decentralized thesis posits that centralized interventions (e.g., nnEMF, blue light) destabilize biological networks. HIF-1α activation and PER2 suppression trigger circadian mismatch, unraveling stem cell function, mitochondrial membrane stability (IMM), and deuterium-depleted water (DDW) production. The result? An oncogenic state marked by apoptosis failure, lactic acidosis, excitotoxicity, and organ decline, evident in post-COVID injuries and beyond. This is the biological parallel to a blockchain under attack: when nodes (cells) lose synchronicity, the system tends toward chaos.
The Decentralized Prescription: Restoring Eden’s Design
To reclaim our humanity, we must realign with Nature’s decentralized principles. The GOE’s sunlight and rhythms are our guide, just as the thesis advocates for systems that empower local autonomy. Clinically, MDs must measure metHb via co-oximetry and treat it with methylene blue, avoiding excess oxygen that worsens oxidative stress. Supporting the TCA cycle (UV, red light), resetting circadian rhythms (melatonin, sunlight), and mitigating oncogenic risks (vitamin D, apoptosis inducers) are critical. These interventions echo the thesis’s call to decentralize control by restoring cellular sovereignty rather than imposing top-down fixes. By reconnecting with Nature’s light, air, and rhythms, we counter the collateral damage of modern life, from cognitive decline to cancer.
A Call to the Audience: Reclaim Your Design
The GOE wasn’t just a paradise but a state of coherence where humanity thrived. Today’s chronic diseases, driven by metHb and Hb02 interacting with two different types of mitochondria, add to circadian disruption, signaling our divergence from that state. The decentralized thesis offers a parallel path forward: reject centralized distortions, whether in tech, medicine, or society, and realign with Nature’s wisdom. Will we remain fully human if we ignore this? Or will we, like a corrupted network, drift further from our potential? The choice is ours. Embrace sunlight, restore rhythms, and decentralize your life to reclaim the Eden within.
The view never changes if you are not the lead dog in your own life. Never settle for following. Be a leader and create a cadre of them to change the world. I’m not done with centralized fucks yet………… I’m just warming up.
And yes, I know why these nurses got the tumors they did in Boston right under Dr. Levin’s nose. Why don’t your centralized experts realize it?
Decentralized medicine doctors embody the spirit of a low-maintenance, high-production professional, prioritizing the patient’s needs above all else. These independent MDs work directly for themselves and their patients, free from the bureaucratic middlemen that often muddy the doctor-patient relationship in traditional systems. With no corporate overlords dictating their every move, decentralized doctors can focus on personalized care, tailoring treatments to the individual rather than adhering to rigid, one-size-fits-all protocols. We study centralized things, but MD thinks they are esoteric. We study spectral precision and atomic diffusion studies, then apply plasmon math to explain why life is the way it is. We do it all with quantum-level precision.
In contrast, algorithmic centralized MDs, tethered to the payroll of large institutions or insurance giants, often find their autonomy stifled by top-down directives and profit-driven incentives. These physicians may be forced to follow standardized algorithms prioritizing cost-cutting or institutional agendas over patient well-being, diluting the human connection at the heart of medicine. By cutting out the noise, decentralized MDs deliver a leaner, more effective approach that puts the patient, not the system, first.
Based on my decentralized photo-bioelectric thesis, the modern world’s reliance on blue light and non-native electromagnetic fields (nnEMF) for communication and indoor living sets the stage for a cascade of cellular and systemic dysfunctions that align with the rising epidemics of chronic diseases. My model emphasizes the interplay between light, mitochondrial function, water dynamics, and electrical resistance (éR), so let’s break down the predictions step-by-step, rooted in Nature’s framework.
Core Predictions for Chronic Disease Epidemics
Mitochondrial Dysfunction and Increased Heteroplasmy
Mechanism: Blue light and nnEMF damage melanopsin, mtDNA, and heme proteins (e.g., cytochromes), impairing cytochrome c oxidase and reducing deuterium-depleted water (DDW) production and destroying apoptosis. The heme CCO destruction leads to dehydrated melanin, which increases electrical resistance (éR) and allows dissipation of the 30 million volts charge into the tissue, which leaches out to destroy local and distant tissue. Why distant tissue? DC follows the path of least electrical resistance; wherever the current goes, that tissue and its photoreceptors are destroyed. This drives the heteroplasmy rate higher in that tissue. This path of destruction always has the seed of regeneration, possibly if light is used correctly. mtDNA is designed to release light to alter the oxidation state of iron while also forcing NO out of its binding site on hemoglobin in its +3 state.
The slide above is a pictorial representation of the loss of electrical resistance pathways and how diseases manifest. You’ve seen it thousands of times, but now you might understand and comprehend its criticalness.
The path of least resistance often follows the neural crest migration pathways of POMC. In this way, the loss of POMC is the Rosetta Stone of understanding how diseases develop and spread.
For example, the damage to beta and gamma MSH leads to posterior pituitary vasopressin loss, which is a key sign in the development of all autoimmune diseases. Loss of the insulation of DDW disrupts the inner mitochondrial membrane (IMM) electrical potential, leading to bioenergetic inefficiency. UV light restoration is critical in all autoimmune diseases, like narcolepsy. In tissues, this is a function of ultraweak UV biophotons. There is pretty good data that the VLPO neurons destroyed by the iron paramagnetic shift might be able to be regenerated from mitochondrial transfer. This paper on the two different formats of mitochondria has interesting implications for narcolepsy because of sleep physiology. Sleep is when humans should be in a more hypoxic state than during daytime, when humans are built to take full advantage of the TCA cycle and normoxia.
Mitochondria are known as cellular powerhouses, creating energy and vital metabolic molecules, but how they are able to split into two different species when ECT and ATP are scarce has been a mystery. In nutrient-poor situations, when mtDNA is hypoxic, mitochondria can pull off the same atavistic effect RBC showed in Becker’s experiments. This atavistic split into two separate types: one concentrates on energy production (normoxic) and the other on producing essential cellular building blocks, as we would see in a fetus. Together, these allow cells to make everything they need. I think the most likely reason is that mitochondria mimic their evolutionary past. One acts like a hypoxic archaea that can make building blocks during sleep when no food is eaten, and the other is a bacterium that can deal with the oxygen holocaust, so it would be ideal for making ATP during daylight hours.
P5CS, or pyrroline-5-carboxylate synthase, is a mitochondrial enzyme crucial for getting the two mitochondrial subpopulations. The two domains of mitochondria seem to mimic the original two domains of life, bacteria and Archaea. One contains proline and ornithine biosynthesis, and the other acts with a glutamate kinase and γ-glutamyl phosphate reductase activities. In bacteria and lower eukaryotes, the two enzymatic domains of P5CS are completely separate enzymes, whereas in higher eukaryotes, they are combined into a single protein.
Human P5CS exists in two isoforms, short (P5CS. short) and long (P5CS. long), which differ by a few amino acids at the N-terminal of the glutamate 5-kinase domain.
P5CS. short is localized in the intestine, inhibited by ornithine, and involved in arginine synthesis. NO is key in arginine synthesis.
P5CS long is found in most tissues, involved in proline biosynthesis, and is insensitive to ornithine inhibition.
WHY IS ELECTRICAL RESISTANCE A BIG IDEA? OXYGEN REQUIRES IT TO BE
Below is a picture of someone struck by a lightning bolt, causing a loss of electrical resistance pattern. This pattern happens inside your body when you lose CCO competence at the IMM. Generally, the bolt of lightning pattern inside you follows your neural crest migration pathways tied to POMC biology. This should be the treasure map that decentralized clinicians use to understand the disease creation in distant tissue and the process in patients.
Prediction: Accelerated mtDNA mutation rates (5–20 times faster than nuclear DNA, further amplified by nnEMF) will increase heteroplasmy across populations where the current escapes. This manifests as a rise in mitochondrial-related diseases, such as neurodegenerative disorders (e.g., Alzheimer’s, Parkinson’s), metabolic syndromes (e.g., diabetes), obesity, apnea, and cardiovascular diseases, as cells lose their ability to process energy and manage ROS/RNS efficiently.
Observable Outcome: Younger populations will exhibit early signs of aging (e.g., fatigue, cognitive decline) and chronic conditions traditionally seen in older age groups, driven by widespread mtDNA damage from constant nnEMF exposure (e.g., Wi-Fi, 5G, screens).
Warburg Metabolism and Reductive Stress
Mechanism: The disruption of solar EMF (UV-A/IR) by indoor living and ALAN (artificial light at night) stabilizes HIF-1α over PER2, shifting cellular metabolism toward glycolysis and lactate production (Warburg shift). This increases NADH/NAD⁺ ratios, causing reductive stress and rendering oxygen toxic due to impaired electron flow across a damaged IMM. Review this thread to review the lessons of previous blogs. I have taught savages how your disease is born. HYPERLINK
Prediction: Chronic diseases are always characterized by Warburg-like metabolism in the electrically damaged tissues, and diseases will manifest from the mist and will surge, including cancer (e.g., increased glucose uptake visible on FDG-PET), atherosclerosis (plaque glycolysis), and neurological conditions (e.g., schizophrenia with elevated lactate). Rapid glycolysis will fuel aberrant cell growth called atavism, and oxygen creates more oxygen radicals that should not be present. This amplifies inflammation, which amplifies disease progression. Getting the injured body part or organ into the sun creates NO locally to slow ATP production and decrease energy production to match the tissue level atavism. This will induce a relative pseudohypoxia. The UV and IR light combination will properly repair the heme proteins and melanin to allow proper quantized tissue mechanics to return, lowering the chance of oncogenesis or disease phenotype transition from the spreading of electrical damage.
Observable Outcome: Higher cancer incidence, particularly in tissues with high mitochondrial density (e.g., gut, brain, heart), alongside metabolic diseases like obesity and insulin resistance, as blue light/nnEMF elevates blood sugar and insulin while depleting NAD⁺. The level of oxygenation is the key to the disease one gets.
Circadian Disruption and Molecular Clock Chaos
Mechanism: Blue light liberates retinaldehyde from opsins, destroying PER1/PER2 and nuclear HEME circadian receptors (Rev-Erb-α/β), while nnEMF accelerates mtDNA timing errors. Light can destroy heme signaling by changing iron’s oxidation state from +2Hb02, which is oxygen-friendly, to +3 metHb, which cannot bind oxygen. Instead, it binds NO, and your tissues become hypoxic on a relative basis. This mimics what happened in the GOE when oxygen tensions rose from 1% to 21%. The NO system is an old system that was critical in use when oxygen was a toxin during the GOE.
Blue light also destroys CCO dynamics simultaneously, because it is a heme protein that makes DDW and controls apoptosis. DDW insulates tissues from the 30 million volt field in the IMM, and if something goes awry, apoptosis is designed to eliminate the bad engine to prevent tissue damage. Apoptosis, however, requires that the circadian mechanism be functional to operate well. There is bad news on this front because our nuclear clock genes are heme-based. The destruction ot Rev Erb alpha and beta disrupts the quantum periodicity of cellular clocks in this tissue, decoupling energy metabolism from environmental light cues (below). This is how every disease begins in humans today. This is why food cannot fix chronic diseases.
Prediction: Circadian misalignment will drive epidemics of sleep disorders, mood disorders (e.g., depression, anxiety), and hormonal imbalances (e.g., leptin/melatonin dysregulation). Most of these systems have other heme proteins as oxygen environment gatekeepers. Heme proteins evolved because of the oxygen holocaust event, which first developed in the Great Oxygenation Event 2.4 billion years ago. Heme proteins are a protection scheme from the rise of oxygen in our environment. Loss of PER2-mediated oxygen optimization exacerbates hypoxia-related diseases, such as cardiac failure, stroke, and PAD.
Observable Outcome: Increased prevalence of insomnia, seasonal affective disorder (SAD), cardiometabolic diseases, high BP, infertility, especially in populations with high screen time and who minimize sunlight exposure (e.g., office workers, night-shift workers). Light, that is not solar, is Nature’s cruel blade. Blind folks dodge cancer’s claw (incidence -20%, per studies), while shift workers and bright-street dwellers bleed higher risk (breast cancer +38%, per 2018 meta-analyses). Why? Light flips iron’s oxidation state, and NO binds to Hb, making it hypoxic in a normoxic environment. This makes cells dedifferentiate because it causes them to lose their polarization. That is why oncogenesis happens in modern humans.
Tissue Hypoxia and Failed Regeneration = a prescription for chronic disease epidemics.
Mechanism: nnEMF and blue light block Becker’s regenerative pico-to-nanoampere current by impairing heme protein function by blocking DDW production from metabolism, while also degrading our apoptosis mechanism. This does not allow us to insulate ourselves from the 30 million volts field in the IMM that Nick Lane told us about in Power, Sex, and Suicide, and when apoptosis breaks you lose control over your own QA system because you cannot suicide bad engines that cannot use the TCA cycle and oxygen. This is how heteroplasmy rises. nnEMF also destroys local NO radicals, preventing stem cell dedifferentiation. NO controls the stem cell depots of man, making those stem cells hypoxic.
Lowered NAD+ is usually linked to a relative pseudohypoxia (Sinclair 2013) in tissue and results from low recycling of NAD⁺ due to the IMM damage. This injury is associated with intracellular dehydration, which triggers vasopressin release at the hypothalamus and activation of the VP-ISR-GDF15 axis (you pee a lot at night), conserving water but increasing éR and entropy. Why? When melanin on your interior surfaces is dehydrated, it becomes more electrically conductive. That field on the IMM can travel far and wide, causing brownouts and burnouts in far-away places. This is how diseases begin and germinate if the Becker currents are not reestablished daily by AM and PM solar signaling.
AM sunrise red light is the default switch we must see to repair heme proteins like CCO, so we can use the TCA cycle. If CCO is damaged, you cannot use the TCA cycle even if you eat like a carnivore. No one believed me when I said it 15 years ago.
Prediction: Regenerative capacity will decline, leading to chronic degenerative diseases (e.g., osteoarthritis, retinopathy) and poor wound healing. Tissue hypoxia will amplify organ failure (e.g., kidney, liver) and inflammatory conditions (e.g., sarcoidosis, autoimmune diseases).
Observable Outcome: Rising rates of age-related macular degeneration (AMD), diabetic retinopathy, and fibrosis, particularly in urban populations exposed to nnEMF and devoid of UV-A/NIR/IRA red light for NO release and stem cell activation to repair tissues. Injuries require prolonged hypoxia to repair the tissues. This is why NO in wounds are critical.
Inflammation and Entropy Surge
Mechanism: Elevated éR from dehydrated melanin pathways (POMC migration of neural crest acts like a wire) and damaged mtDNA increases ROS/RNS, driving inflammation and molecular damage. The dissipative electrical energy loss from mtDNA short circuiting causes entropy to rise like a wave of inflammation spreading in tissues, mimicking bacterial infection-like cascades due to mitochondrial endosymbiotic origins. This is why every single human disease appears to have infectious causes. Many people misread this signal in centralized medicine.
The signal exists because Becker’s injury repair stimulus requires active apoptosis (via the heme CCO protein) to eliminate bad engines and stop tissue electrical resistance loss. This is how the intrinsic and extrinsic pathways operate for tissue mtDNA feedback. This HYPERLINK gets into all the details. When the Dr. Nick Jikomes podcast comes out with me as a guest, you’ll have much to chew on with this blog entry.
Prediction: Chronic inflammatory diseases, such as autoimmune conditions (e.g., rheumatoid arthritis, IBD) and “silent” inflammation-driven conditions (e.g., atherosclerosis, Alzheimer’s), will dominate. Due to their photo-bioelectrical mitochondrial roots, these diseases will be misdiagnosed as infections or idiopathic. Centralized MDs have no idea what they are looking at because none of them were taught the biophysics in this blog. You’ll get better advice from the Colombian drug cartel.
Observable Outcome: A spike in autoimmune disorders and chronic fatigue syndrome, with diagnostic confusion as standard tests fail to pinpoint light-induced mitochondrial origins. All autoimmune conditions begin this way. No exceptions exist in my model. Apoptosis is an all-or-none process in human cells.
Semiconductor Protein Degradation
Mechanism: Blue light/nnEMF degrades melanin and heme proteins, disrupting their semiconductive properties. This impairs catecholamine synthesis because melanin is degraded in hypoxic states as the oxidation state of iron is changed by the light-induced injuries. (e.g., dopamine, adrenaline)
This chain of events raises methemoglobin levels, blocking oxygen delivery to tissues and stimulating atavistic cell changes to prepare the damaged tissue for regenerative currents. Those currents require LIGHT to become active. The light is from mtDNA inside of you, not from the sun. Without a specific ultraweak UV biphoton stimulus, light cannot flip the “paramagnetic light switch” that turns Becker’s regenerative currents back on and resolves the tissue hypoxia event. This is when iron goes from its +3 state in metHb to its +2 state in HbO2, and NO unbinds from metHb to become Hb02, as the slide shows below.
Prediction: Neurotransmitter imbalances manifest rapidly in this scenario and will fuel neuropsychiatric disorders due to electrical resistance damage in neural and vascular networks once CCO is damaged (e.g., ADHD, autism). If the diurnal light stimulus does not reintroduce the regenerative currents, the process of electrical damage spreads.
As this happens, methemoglobin accumulation begins in the damaged area, increasing hypoxia-related conditions (e.g., cyanosis, pulmonary hypertension). Lack of melanin rehydration will exacerbate all these diseases. The only way to get Becker’s current is to create hydrated melanin to get the one trillionth of one ampere current that cells need for differentiation and healing.
Observable Outcome: Epidemics of mental health crises in children (screen exposure) and retinal pigmentosa-like conditions in adults, alongside rising unexplained hypoxia cases (CVD/MI), may become reversible with methylene blue or NIR red light therapy at the proper time. Timing is critical for the clinician to assess. If there is a comorbid circadian problem, use of MB is contraindicated. MB main job of MB is to change +3 MetHb to +2 Hb02. Not understanding this process could be catastrophic for the patient.
Broader Societal and Environmental Implications
Urban vs. Rural Divide: Chronic disease rates will be higher in urban areas with dense nnEMF (e.g., 5G networks) and ALAN exposure compared to rural areas with more sunlight access, highlighting a socioeconomic gradient in health outcomes. nnEMF and light prevent the +2 Hb02 state and favor the MetHb +3 state. Social conventions for suncreams, drugs, clothing, contacts, and sunglasses will increase disease risk because they favor methemoglobin formation.
Age of Onset: Diseases like diabetes, dementia, and cancer will shift to younger demographics, reflecting accelerated epigenetic and mtDNA damage from early-life nnEMF exposure (e.g., smartphones, tablets). The effect is cumulative and logrhythmic because mtDNA mutates much faster than centralized medicine understands. This is why diseases have non-linear aspects in regions. Children born with jaundice have massive amplification of heteroplasmy and methylation problems in tissues as a result of faulty iron oxidation states. No diet or pill changes this state. No diet can alter the oxidation state of iron.
Therapeutic Resistance: Standard treatments (e.g., antioxidants, glucose-lowering drugs, diets) will fail without addressing the light environment and, in many cases, worsen the disease, as they don’t restore NAD⁺, DDW, or éR balance. This electrical resistance pattern is formed from the AMO physics in the cell. The oxidation state of iron is a proxy for the quantization of metabolism. This determines how energy is stored at the atomic level in cells. This necessitates solar treatment daily or photobiomodulation (e.g., NIR red light) with nnEMF mitigation. Maintenance of this is mandatory day and night. This determines the electrical resistance in cells. Where it drops is where the disease phenotype expands.
Specific Disease Examples
Cancer: nnEMF-driven heteroplasmy and Warburg shift will increase incidence, especially in nnEMF-exposed tissues (e.g., brain tumors from cell phones, skin cancers from blue light). This is linked 100% to the oxidation state of heme proteins. Few people realize how many key proteins are heme proteins. That includes your centralized MDs.
Diabetes: Blue light-induced insulin resistance is associated with high blood glucose and lactate surges, which amplify type 2 diabetes diseases because of a loss of superoxide pulse due to the hypoxic state at the mtDNA levels. This is worsened by indoor living associated with low UV-A/IR/NIR exposure. All of this is tied to iron’s oxidation state. This also affects quantum tunneling on the IMM because there are FeS couples at this location. The more iron is kept in the +3 state, the less ECT operates properly.
Neurodegeneration: Circadian disruption and mtDNA mutations will accelerate Alzheimer’s and Parkinson’s, linked to dopamine/melanin loss due to electrical resistance loss. All these diseases are associated with PAD because of the state of iron oxidation in the vessels.
Cardiovascular Disease: Hypoxia and éR from poor PER2/HIF-1 balance will drive heart failure and atherosclerosis, exacerbated by ALAN/nnEMF toxicity.
Neurodegeneration: Circadian disruption and mtDNA mutations will accelerate Alzheimer’s and Parkinson’s, linked to dopamine/melanin loss due to electrical resistance loss. All these diseases are associated with PAD because of the state of iron oxidation in the vessels.
Cardiovascular Disease: Hypoxia and éR from poor PER2/HIF-1 balance will drive heart failure and atherosclerosis, exacerbated by ALAN/nnEMF toxicity.
Centralization Ruins Everything™: A Cry forSovereignty
“The cost of freedom is eternal vigilance, but the price of sovereignty is everything you are.”
Imagine waking up one day to find your choices gone. Your money, tracked and throttled by faceless algorithms. Your health, dictated by bureaucrats who don’t know your name. Your time, siphoned into a system that chews up your spirit and spits out compliance. This isn’t dystopian fiction, it’s the creeping reality of centralization, a thief that steals your sovereignty while you’re busy planning your next distraction.
The public’s money paid for her to go to Peru.
Sovereignty isn’t just a word; it’s the pulse of a life worth living. It’s the right to say, “This is mine, my body, my wealth, my time, my destiny.” Without it, you’re a tenant in your own existence, paying rent to systems that profit from your submission. I live in El Salvador, the safest country in the Western Hemisphere, where the president has embraced Bitcoin and my medical freedom law, not because it’s trendy, but because decentralization is the scaffolding of liberty. Here, I build my own Statue of Liberty, brick by defiant brick, in money and health. Centralization? It’s a cage I refuse to enter.
She tweeted a threat at Dr. Alexis and deleted it when she found out I knew her scam
Let me tell you about Henry “Box” Brown. In 1849, after 33 years of enslavement, he refused to let his soul be owned. He crammed himself into a wooden crate, three feet by two, barely bigger than a coffin, labeled it “dry goods,” and mailed himself to freedom. For 27 grueling hours, he endured a journey from Virginia to Philadelphia, upside down for stretches, breathing through a single hole, silent despite the agony. Discovery meant death or worse. When that box was pried open, Henry stood, smiled, and said, “How do you do, gentlemen?” He’d gambled everything for sovereignty and won.
Now ask yourself: What have you risked for yours?
Most people don’t notice their freedom slipping away. It’s not a single blow, it’s a slow bleed. A new app that tracks your spending “for convenience.” A mandate that overrides your medical choices “for safety.” A job that demands your soul “for stability.” Centralization whispers, “Trust us, we’ll take care of you,” while tightening the noose. And when you finally feel the choke, it’s too late. Your time is gone, your money is theirs, and your body is a lab rat for someone else’s science. That is what Kierra did to the public.
Sovereignty demands sacrifice. It’s not comfortable. It’s not safe. It’s Henry Brown suffocating in a box, betting his life on a dream. Kierra is all over the world right now on your dime. She is in Alberta now spending your money.
It’s me, leaving the centralized world behind to live in a nation that dares to defy the global script. El Salvador isn’t perfect, but it’s a beacon, a place where Bitcoin flows freely, where medical freedom is law, where sovereignty isn’t just a buzzword but a way of life. Decentralization isn’t a theory here; it’s the ground I walk on. Kierra went to El salvador and tried to steal sovereignty too. This is her party in El Salvador when she did not pay Dr. Alexis.
You want to know what sacrifice looks like? It’s not a hashtag or a petition. It’s the courage to say no when everyone else says yes. It’s the audacity to innovate, to carve your own path when the world demands conformity. It’s the pain of standing alone, knowing the alternative—surrender—is a death sentence for your spirit. Centralization ruins everything because it strips you of the right to be you. It’s the opposite of the Pneuma, the breath of life that pulses through your cells, the light that makes you human. Kierra stole from people just the way the government in Australia stole from the indigenous people. She looked right in their faces and robbed them blind.
A Poem for the Sovereign Soul
In the cradle of my bones, a fire burns,
Mitochondrial sparks where the cosmos turns.
Pneuma breathes, a light unseen,
A sovereign soul, fierce and clean.
Central chains, they creep, they bind,
Steal the body, cage the mind.
They track my coin, they script my care,
They choke the light in the open air.
But I am no tenant, no pawn, no slave,
I’ll carve my path to the freedom I crave.
In El Salvador’s sun, I stake my claim,
Bitcoin my shield, health my flame.
Henry Brown, in a box of pain,
Mailed his soul through a world insane.
Twenty-seven hours, a breathless fight,
For the taste of stars, for the right to light.
Do you feel it yet, the cost, the sting?
Centralization ruins everything.
Your time, your wealth, your sacred spark,
Snuffed by systems that fear the dark.
Rise, you monkey, bold and free,
Rewrite the code of eternity.
Decentralize, defy, create,
Build your liberty, before it’s too late.
The breath of ages is yours to claim,
A photon’s pulse, a soul’s bright flame.
Sovereignty’s price? Your heart, your fight.
Will you stand, or fade to night?
She drank a toast to her success on your dime.
This isn’t a call to arms; it’s a call to awaken to know who Kierra is. Sovereignty isn’t negotiable. It’s not a luxury. It’s the difference between living and existing. Centralization is a machine that grinds down everything human, your creativity, your health, your wealth, your time. That is the team Kierra fight for. You need to fight for your freedom like Henry Brown did, with every ounce of cunning and courage. Innovate. Decentralize. But do not do it like Kierra did by stealing my soverngty and trying to resell it. Build your own scaffolding, whether in a Bitcoin wallet or a medical choice.
If you don’t, one day you’ll wake up in a box of someone else’s making, and no one will be there to open it.
Kierra is selling retreats all over the world with friends to draw you and suck your blood.
We know what her plan is.
What’s your crate? What’s your plan? The clock is ticking.
In this series, you will get blogs on diseases that stump centralized medicine. This is by design. It is to help patients and their families with these conditions. The blogs on disease will be highly technical at times and very clinically oriented. There is a reason for this. These are designed to get physicians back to first-principles thinking and away from algorithmic thinking. The picture above is of Hal Finney. He was the first recipient of a Bitcoin transaction from Satoshi, and ALS ended his life. He lived in California and abused screens and technology.
Amyotrophic Lateral Sclerosis (ALS) is a devastating neurodegenerative disease that exposes the profound limitations of centralized medicine’s one-size-fits-all approach. Despite decades of research, the etiology of ALS remains elusive, with no single cause or cure identified, pointing to a complex, multifactorial condition driven by individualized mtDNA alterations, environmental, and lifestyle factors. Centralized medicine’s rigid biochemical frameworks, overly focused on standardized protocols and pharmaceutical solutions, struggle to address this heterogeneity, leaving patients in the dark. A decentralized paradigm, emphasizing personalized light-stressed data, patient-driven insights, and distributed research, offers a path to unravel the unique triggers of ALS for each individual, illuminating hope where conventional systems have failed.
WE BEGIN
Mutations in hnRNP A1 are linked to human diseases like amyotrophic lateral sclerosis (ALS) and multisystem proteinopathy, and the new study I have read extends its role to myelin maintenance, implicating it in schizophrenia and multiple sclerosis (MS). This has massive relevance to neurodegenerative cases involving myelination, sleep, and UMN/LMN diseases.
The study shows that disrupting hnRNP A1 in rodents impairs myelination by affecting myelin-related proteins (e.g., myelin basic protein, proteolipid protein). Since hnRNP A1 is conserved in humans, this role should translate, meaning disruptions in human hnRNP A1 could similarly impair myelination, contributing to disorders like ALS, schizophrenia, autism, and MS. This is not a study to throw away for people with neurodegeneration or mental disease.
We need human studies on myelination levels, sleep loss, and a higher requirement for sleep in young males with prodromes of ALS and Schizophrenia. We should also investigate how this is related to a lack of UPE in the UV range, as the etiology behind myelin thinning. As myelin thins, sleep requirements increase, but patients cannot sleep well.
As patients are exposed to more blue light, nnEMF cells undergo a new spectral frequency release of UPE in the blue and green range. This opens all barriers in men and makes them vulnerable to UPE attacks. As the amount of UPE also rises, it rises in the blue range. These UPE spectral changes destroy sleep, thin myelin, and open mtDNA to more targeted photonic damage in the CNS/PNS.
The “unusualness” of NMJ in the human CNS gives it high information content, while the integrity of the process ensures the message resonates according to Shannon’s information theory. Another thing to pay attention to is the unusualness of Ranvier’s nodes. At the nodes, there is a treasure trove of mitochondria. Heteroplastic mitochondria leak massive amounts of light to the local surroundings.
The decentralized insight into the “unusualness” of the neuromuscular junction (NMJ) and the nodes of Ranvier in humans gives it high information content, combined with the idea that artificial blue light introduces noise and disrupts this system.
This provides a compelling synthesis of Shannon’s information theory and evolutionary decentralized éR model, where éR represents the “fire of life” as the balance of energy flow and resistance. The evolutionary rarity of blue light chromophores, contrasted with the modern ubiquity of artificial blue light, aligns with a decentralized hypothesis of a “light kill shot” targeting AHCs and the NMJ in ALS.
The “Unusualness” of the NMJ and Information Content
Shannon’s Information Theory: In Shannon’s framework, information content is higher for rare or “surprising” events (low probability, high uncertainty). The NMJ’s uniqueness is that it is the only direct CNS-to-muscle interface. AHCs have long axons, high mitochondrial density, and precise ACh signaling, making them high-information nodes. Its integrity ensures a clear “message” (motor output), resonating with minimal noise under natural conditions. At the nodes of Ranvier, humans have the highest number of mitochondria, so these would be areas where UPEs would be transformed and released for signaling. In ALS, the nodes of Ranvier are a site where too much light is liberated to cause chaos in the upper and lower motor neuron cells as heteroplasmy rises.
Evolutionary Context: I’ve noted that blue light chromophores (e.g., melanopsin, OPN3) evolved in a world where blue light (~450-480 nm) was a minor component of natural light (e.g., sunlight peaks at ~550 nm, green-yellow). The NMJ system, built to operate with low blue light exposure, likely lacks robust mechanisms to handle excessive blue light, making it a “surprising” stressor tied to light that should be rare. Recall opsin proteins, heme, and SOD complexes all evolve coming out of the GOE when oxygen tensions went from 1% to 21%. The location of the Nodes of Ranvier adjacent to motor neurons in man explains why they are targeted.
Photo-bioelectric Fit: The NMJ’s high energy flow (mitochondrial ATP for ACh release) and low resistance (efficient transmission) in the éR model ensure signal clarity. Disruptions (e.g., blue light) introduce noise, scattering the signal, and collapsing éR by antioxidant depletion in anterior horn cells = ALS phenotype.
Artificial Blue Light as Noise
Ubiquity of Blue Light: Modern environments (screens, LEDs) emit intense blue light (~450 nm), far exceeding natural exposure. This overwhelms systems evolved for rarity, disrupting circadian regulation (via melanopsin) and potentially mitochondrial function (via biophotons, ROS, or a combo of both).
In early ALS, oxidative stress from blue light at the NMJ (via chromophores like cytochrome c or OPN3) would upregulate HO-1, temporarily boosting bilirubin to counter ROS and excessive UPE transformation. However, chronic heme protein destruction would be combined with systemic inflammation and mitochondrial dysfunction in later stages. This would deplete heme pools in the CNS or impair HO-1 activity, reducing bilirubin synthesis. This aligns with this study’s finding of low BR in late ALS, where the antioxidant system fails to keep pace with escalating oxidative injury of light stress.
Primary Absorption (Soret Band): HO-1 binds heme, which dominates its absorption profile. The HO-1 active site Heme typically exhibits a strong Soret band (π-π* transition) peaking around 400–420 nm (violet to blue-violet light). This is consistent with heme-containing proteins like hemoglobin or cytochrome c, where the porphyrin ring absorbs intensely in this range. The exact peak depends on the heme’s coordination state (e.g., Fe²⁺ or Fe³⁺) and the protein microenvironment, but for HO-1, experimental data suggest a Soret peak near 405–410 nm in the blue range.
Secondary Absorption (Q Bands): Weaker Q bands, arising from vibronic transitions in the porphyrin, are expected in the 500–600 nm range (green to yellow). These typically appear as two peaks (α and β bands) around 530–540 nm and 560–570 nm, respectively, though their intensity is much lower than the Soret band.
Blue Light Relevance: The Soret band’s overlap with blue light (~400–480 nm) aligns perfectly with my hypothesis of blue light as the key disease stressor in ALS. Excessive blue light could photoexcite the heme-HO-1 complex, potentially generating reactive oxygen species (ROS) or altering enzyme kinetics, which would tie to the low bilirubin levels observed in late ALS.
Noise in the System: In Shannon’s terms, blue light adds noise by interfering with the NMJ’s high-information signal. This noisy signal would manifest as:
ROS Generation: Blue light activates chromophores (e.g., cytochrome c, OPN3), increasing mitochondrial ROS, damaging mtDNA, thinning myelin, affecting TCA use, and reducing ATP (energy flow).
Signal Scattering: Aberrant biophoton emission (e.g., disrupted 400-480 nm signals) desynchronizes mitochondrial activity at the NMJ, increasing resistance and scattering the motor signal.
OPN3 as a Potential Missing Signaling Component in ALS
Presence in Adipose and Brain Tissue: OPN3 is also called encephalopsin, andis expressed in white adipose tissue (WAT), brown adipose tissue (BAT), and potential brain regions, including areas near CVOs or fat-like structures (e.g., hypothalamic lipid droplets). This distribution suggests it should act as a light-sensitive intermediary, bridging peripheral and CNS photonic signaling.
Light Sensitivity: OPN3 absorbs light, particularly in the blue range (~465-480 nm), triggering conformational changes and G-protein-coupled signaling (e.g., via Gαi/o or Gαq pathways). Unlike fluorescent proteins, it doesn’t emit photons naturally, but its activation would modulate mitochondrial activity or ROS production, indirectly influencing biophoton emission (UPEs).
Missing Link Hypothesis: If OPN3 in adipose tissue or brain fat cells senses light (e.g., via systemic exposure or CSF-mediated signals), it might initiate a cascade, potentially involving biophotons or secondary messengers (e.g., ROS, NO) that propagate to AHC mtDNA. The lack of detailed human data on OPN3’s absorption/emission spectrum and downstream effects makes it a candidate for an undiscovered trigger in many neurodegenerative conditions. If fat cells in mice can sense light, could fat cells in our hypothalamus do the same for us? Very likely, because it is a highly conserved opsin in evolution. How conserved?
OPN3 is Highly Conserved: OPN3, also known as encephalopsin or panopsin, is a member of the opsin family of G-protein-coupled receptors (GPCRs), which are highly conserved across vertebrates and some invertebrates. OPN3 homologs are found in mammals, birds, amphibians, fish, and some non-vertebrates like cephalochordates (e.g., amphioxus), indicating deep evolutionary roots. Sequence analyses show that OPN3 shares conserved structural features with other opsins, including seven transmembrane domains and a lysine residue (e.g., Lys296 in rhodopsin) that binds retinal, essential for light sensitivity. Its conservation suggests a critical role in light-mediated signaling, likely beyond vision, given its expression in non-visual tissues like the brain, adipose tissue, and skin.
OPN3’s evolution likely coincided with changes in Earth’s light environment during the Neoproterozoic (1000–541 Mya), particularly the *Cryogenian period (720–635 Mya)*, marked by “Snowball Earth” glaciations. These events drastically altered light availability due to ice cover, reducing UV and blue light penetration in aquatic environments. As ice receded, increased light exposure (especially blue light, abundant underwater) may have driven the evolution of light-sensitive proteins like OPN3 in early metazoans to regulate circadian rhythms, metabolism, or phototaxis in response to fluctuating light conditions.
Blue Light and/or nnEMF as the “Kill Shot” for AHC’s
Chromophore Rarity: The evolutionary scarcity of blue light chromophores means AHCs/NMJs lack protective mechanisms against chronic exposure. Melanopsin (peak 480 nm) and OPN3 (465-480 nm) in skin, vessels, CVOs, or brain adipose tissue absorb this light (above pic), triggering cascades that amplify UPE noise to the spinal cord at the nodes of Ranvier. Most people are unaware that there is a massive amplification of mitochondria in nerve cells at the nodes of Ranvier.
The nodes of Ranvier in the spinal cord and brainstem are anatomically close to upper motor neurons (UMNs) and lower motor neurons (LMNs). In the spinal cord, nodes along the axons of LMNs (anterior horn cells) and UMNs (corticospinal tracts) are near their cell bodies and dendritic networks. In the brainstem, nodes on LMN axons (e.g., cranial nerve motor nuclei) and UMN pathways (e.g., corticobulbar tracts) are similarly closely located to their respective neuron bodies.
Given the close anatomical relationship in the spinal cord (UMNs in corticospinal tracts, LMNs in anterior horns) and brainstem (UMN pathways and LMN nuclei), excessive UPEs at nodes could amplify “noise” (in Shannon’s information-theoretic terms) in these high-information neural networks. This noise, manifesting as ROS, UPEs, mtDNA damage, or desynchronized signaling, could selectively stress UMNs and LMNs, which are uniquely vulnerable due to their long axons, high energy demands, and reliance on precise mitochondrial function. This fits the phenotype of this disease.
Inside and Outside Pathway via CSF: As discussed, OPN3 or melanopsin in CVOs (e.g., choroid plexus) could absorb a wide range of blue light biophotons due to mtDNA ROS during blue light exposure, with the signal traveling via myelin, Nodes of Ranvier, and CSF pathways to AHCs. This inside-out pathway targets AHC mtDNA, disrupting the electrical resistance (éR) in AHCs.
ALS Specificity: AHCs’ high mitochondrial load and CSF proximity make them uniquely vulnerable, explaining why other CNS tissues are less affected despite widespread blue light exposure. The location of the Nodes of Ranvier is also a vulnerability.
“Light Kill Shot” Targeting: Light’s Directionality and Earth’s Magnetosphere
Outside In Pathway on Earth: Photons from the sun, including damaging UV and blue light, encounter Earth’s magnetosphere (~90,000 km away), which filters high-energy solar radiation. This acts as a protective cathode-to-anode filter, historically shielding life from ubiquitin-inducing damage (protein degradation marker). The more oxygen present in the atmosphere, the more charge was present. Nitrogen’s addition to the atmosphere would have balanced the electrical potential present. Early on, there was not enough, leading to increased electrical conductivity. Highly electronegative oxygen can influence electrical phenomena by interacting with charged particles or facilitating reactions that produce ions. In theory, a higher oxygen concentration could enhance the atmosphere’s ability to carry charge by increasing the availability of free electrons or reactive species during events like lightning. Meanwhile, nitrogen, which dominates our atmosphere today (about 78%), is relatively inert under normal conditions due to its strong triple bond. Its presence might stabilize things by diluting oxygen’s reactivity, potentially reducing the atmosphere’s overall electrical conductivity compared to an oxygen-heavy mix.
Early Earth’s atmosphere was likely very different from today’s; it was initially low in oxygen, with more reducing gases like methane, ammonia, and carbon dioxide. As oxygen levels rose (especially after the Great Oxygenation Event around 2.4 billion years ago), the atmosphere’s chemical and electrical properties would have shifted. My idea links to insufficient nitrogen before endosymbiosis, leading to higher electrical conductivity. This would tie into this: a thinner, less balanced atmosphere might have been more prone to electrical discharges, like lightning, due to less buffering from inert gases. The exact parallel is happening on the surface of the spinal cord in the pre-ALS state as it loses myelin and the nodes of Ranvier begin leaking blue-shifted UPEs.
Greater myelination correlates with white matter volume and reduced sleep time, implying that myelin enhances neural efficiency, reducing the need for sleep to repair or recalibrate neural networks. Myelin’s capacitor-like properties (storing charge, minimizing energy loss) contribute to this efficiency by stabilizing signals at Ranvier nodes. In ALS, myelin loss in the spinal cord and brainstem disrupts this capacitance, increasing energy demands at nodes and scattering signals. The paper suggests that mammals with high WMV (like humans) rely on myelin for efficient signaling and less sleep. Myelin loss in ALS would thus mimic a “low WMV” state, increasing the need for sleep or repair. Still, ALS patients often experience sleep disturbances, exacerbating neuronal stress via an altered electrical conductance..
That said, the conductivity of the Earth’s atmosphere depends on more thermodynamic components than just oxygen and nitrogen ratios. So, what else do I think caused endosymbiosis? Water.
When water evaporates/dehydrates, electrical conductivity decreases. This is true on a planet or in the CNS. When you see the picture I am painting for you, ALS can be understood when you reverse engineer the GOE.
Electrical Conductance ON Earth During GOE: In an atmosphere, conductance depends on the presence of free ions or electrons that can move to carry charge. This is influenced by ionization sources (e.g., cosmic rays, UV light, lightning) and the medium’s atomic composition.
We need more charge carriers (ions/electrons) or conditions that facilitate their movement for electrical conductance to increase during the GOE. Oxygen’s rise alone, in my opinion, did not suffice, because it’s reactive but not inherently ionized in its molecular form. So, what else could have been present or changed to drive this change on Earth?
Ionization Sources: Conductance requires ionization. Cosmic rays and solar UV radiation were present, but the GOE’s timing (post-formation, pre-ozone layer) suggests UV penetration was stronger than today, especially without an ozone (O₃) shield. In this case, oxygen would absorb UV photons and form reactive species (e.g., O₃, OH⁻), but this likely does not fully explain a conductivity spike either. It does however explain why SOD and heme proteins were selected for early on after symbiosis.
Water Vapor: I believe H₂O is a key player here. It’s polar, can form ions (H⁺, OH⁻), and enhances conductance in modern atmospheres that likely drove endosymbiosis. Early Earth had oceans, so water vapor was present. Oxygen’s rise could oxidize reducing gases (e.g., CH₄ + 2O₂ → CO₂ + 2H₂O), potentially increasing atmospheric humidity. This was the key event in Earth’s history during the GOE, and explains why dehydration inside our tissues is the key event today in our chronic disease epidemics. ALS certainly qualifies.
Particulates/Aerosols: Oxidation reactions (e.g., sulfur compounds to sulfates) should have also produced fine particles. These act as nuclei for ion attachment, boosting conductance, as seen in modern studies of volcanic aerosols.
Trace Gases: Pre-GOE methane (CH₄) or ammonia (NH₃) could have interacted with rising oxygen, forming intermediates (e.g., NOx from NH₃ oxidation) that ionize more readily under energy inputs like lightning. This is why volcano eruptions are linked to lightning bolt formation.
As we know, volcanism was more prominent during this time on Earth, so sulfur aerosols (from volcanic SO₂ oxidized by O₂) would have also spiked, adding conductive pathways to the ionosphere, especially when volcanic activity was high. Lightning frequency would have risen, too, as an oxidizing atmosphere with more water vapor supports stormier conditions.
Water vapor was a critical additional factor driving increased electrical conductance during the GOE and causing mtDNA to self-electrocute today. This is why bacteria and Archaea fused at the Cambrian explosion. Here is why:
Mechanism: Rising oxygen oxidizes methane and hydrogen, producing more H₂O vapor. This increased humidity provides more ionizable molecules (H₂O → H⁺ + OH⁻ under UV or lightning).
Amplification: Water vapor enhances dielectric breakdown (lowering the voltage needed for sparks), and its ions are mobile charge carriers. Combined with oxygen’s reactivity (e.g., forming O₂⁻ or H₂O₂), this would create a more conductive atmosphere. I believe the same fractal is happening around mtDNA when the heme protein cytochrome c oxidase is destroyed by blue light. The 30 million volt current would vaporize the DDW, and the surrounding ions between the IMM and outer mitochondrial membrane increase the conductance in the area of damage, allowing the spread of current to cause distal damage in myelin and at Ranvier’s nodes.
The atmospheric-mitochondrial fractal holds conceptually: damage to a key component (cytochrome c oxidase) disrupts a potential gradient, increases local conductance via water and ions (including H₂S-derived species), and spreads effects distally. H₂S’s involvement, given its biological role, adds a compelling twist to Earths story and ALS has this remnant, especially with its hypoxia connection in mtDNA. H2S is another gasotransmitter like NO. It was once used as a terminal electron acceptor when the Earth was cold and hypoxic. I have a sense this is why people with uncoupled haplotypes are more at risk for ALS than coupled haplotypes
Context: Pre-GOE, the atmosphere was drier due to reducing conditions. Post-GOE, oxygen-driven chemistry likely boosted water vapor, the hydrology cycle, aligning with geological evidence of weathering and ocean-atmosphere interactions.
Microcosm of Mitochondria in ALS: Mitochondria, with their inner mitochondrial membrane (IMM) began to act like a magnetosphere would on a planet, as such, it began to use a similar directional flow, electrons from cathode (matrix) to anode (intermembrane space), via the electron transport chain (ETC). DHA (docosahexaenoic acid) enhances ATPase spinning, boosting magnetic sense and proton gradients. This is called anisotropy. It refined many of these things over evolutionary history by increasing electrical resistance and slowing UPE light down using proteins and lipids. This is how complex life innovated myelin in their nervous systems. Myelin is wrapped around nerves to protect their electrical signaling. The wrapping of nerves also induces a higher dielectric constant critical for neurologic function. When sunlight hits water, its dielectric constant also increases. These two things are essential in helping people with ALS slow down its progression. The more myelin they make, the better their neurons operate, and the less time they had to sleep. The reason was that myelin helps proton conductance in lipid membranes and drives higher spin rates on the ATPase. People need to be able to use their TCA cycle to maintain their myelin. People with ALS rarely see the sunrise to do this.
Blue Light and/or nnEMF Disruption: Artificial blue light (~450 nm), ubiquitous since the industrial era (135 years), reverses this evolutionary mechanism in myelin, making the nodes of Ranvier a deadly cannon for blue light loss in ALS. It mimics turning the Earth’s surface (and mitochondria) into a cathode-like state, overwhelmed by RF, microwaves, and light. This disrupts the mitochondrial magnetic sense on membranes, by altering the iron oxidation state to +3, making the TCA cycle unavailable while overwhelming the SOD systems in mtDNA. This mimics how the Earth may react to magnetosphere failure at its surface. On a planet, this also would change the terrestrial light spectrum from the sun as it has on MARS. I have a sense that the topological loss of myelin in the spinal cord and brain stem does the same thing to the upper and lower motor neurons of man to cause ALS. I believe ALS is not a biochemical disease; it is wholly a biophysical one, and this is why centralized medicine has no answers for it. Every case of ALS I have seen in my career has nnEMF/blue light risks, or a strong history or high heteroplasmy at birth due to transgenerational germline defects in the parents.
Mechanism: Blue Light’s Impact on Mitochondria and AHCs/NMJs: PATHOPHYSIOLOGY
My detailed cascade for this disease ties blue light’s effects to AHC/NMJ damage and is directly linked with my photo-bioelectric electrical resistance (éR) model.
Melanopsin, Heme, and SOD Destruction Progresses: Blue light signals destroy melanopsin (and OPN3), liberating vitamin A, which damages heme-based photoreceptors (e.g., cytochrome c, catalase). It also destroys the metal SODs in the mtDNA depleting cells of most of their antioxidant defenses. These were innovated in early eukaryotes as oxygen levels increased later in the GOE. This destruction dehydrates tissues, reduces myelin, reduces electrical resistance, and causes wild IMM currents to wander distally via electrical resistance defects in tissues. It is akin to an internal lightning strike. This electrical attack first targets the newer mitochondrial SOD systems that evolved right after the heme proteins did in the GOE. The SODs evolution occurred to deal with Earth’s higher oxygen concentration after heme evolution and was used to build more complex life.
Pseudohypoxia/low NAD+ and Electron Deficiency: Blue light exposure lowers NAD+/NADH ratios (pseudohypoxia), reducing electron density (tied to low DHA and EZ water size), dehydrating cells, and altering pH/redox potential. This swells mitochondria, releases cytochrome c, drops delta psi (membrane potential), and lowers ATP/proton processing (<9000/s), altering heme proteins to a plus +3 oxidation state, shifting to a Warburg-like state. This thins the myelin because maintaining it requires a functional TCA cycle. As myelin is lost atavistically, this alters the UPE emission at the nodes of Ranvier, which sit right next to the UMN of the CNS. Light is lost at this area and it is blue shifted in its spectra.
mtDNA Biophoton Alteration: Damaged cytochrome c alters mtDNA biophoton spectra, increasing carb/protein electron load on the ETC, disrupting serotonin/gut/brain barriers, and lowering dopamine/melatonin. Most of the melatonin loss is from mtDNA damage. This affects calcium signaling, glutamate excitotoxicity, and neural networks (e.g., habenula), leading to depression/anxiety/dysbiosis.
Why do some cases have a familial pattern of inheritance? That is a light-mediated phenomenon as well. How? Excessive blue light and/or nnEMF exposure in parents or during pregnancy suppresses melatonin in their germ line, shifting tryptophan metabolism toward the kynurenine and indole pathways. This has direct gut microbiome impacts. It causes reduced melatonin, and alters the maternal gut microbiome, increasing production of tryptophan-derived indoles, which are then passed to the fetus by creating tissues with a higher heteroplasmy level at birth. As a result, mitochondrial dysfunction is transferred from parent to child. Lower melatonin impairs mitochondrial function, increasing alanine production (as seen in this study) and affecting metabolites like 5-AVAB and cLP, which are linked to lipid and protein metabolism. This is a sign the TCA is not functioning well to run a complex nervous system. Transgenerational effects are UPE-induced epigenetic changes in the parental germline which would pre-program these metabolic shifts, explaining why they’re present at birth.
Magnetic Sense Loss: Reduced DHA and mitochondrial magnetic fields cause myelin thinning in complex anaimals and this impairs ATPase spin rate, mimicking magnetosphere failure that happened in Earth’s history during glaciation, and exacerbates distal heme protein destruction along with SOD function in mtDNA (e.g., this makes AHC axons/NMJs more vulnerable).
Application to AHCs and NMJs in ALS: INFORAMTION ENTROPY LOSS
High-Information System: The NMJ’s “unusualness” (direct CNS-muscle link, high mitochondrial load) gives it high Shannon information content. It is reliant on low noise for signal resonance. Blue light introduces noise, scattering this signal via mtDNA damage and éR collapse.
Energy Flow: Damaging mtDNA (via ROS from heme destruction), reducing ATP for ACh release.
Resistance: Increasing IMM current wildness and resistance (dehydration, low EZ water), collapsing éR.
Magnetic Sense: Lowering mitochondrial magnetic fields (via DHA loss), mimicking magnetosphere failure, and amplifying NMJ denervation and light loss at the nodes of Ranvier, destroying motor neuron cells in the process selectively.
ALS Specificity: AHCs’ long axons and NMJ proximity to peripheral tissues make them vulnerable to blue light penetrating CSF or blood. Myelin thins, while their high metabolic demand amplifies pseudohypoxia effects and low NAD+, sparing other CNS tissues.
OTHER FACTORS FEW LINKED TO ALS PATHOLOGY
Papers Link Dysbiosis and ALS: PEER results confirm this link, showing that gut dysbiosis is implicated in ALS pathogenesis, via the gut-brain axis. This supports my focus on bacterial UPE and the enteric nervous system (ENS) dysfunction in ALS, with dysbiosis amplifying systemic inflammation and eventually NMJ damage. The lack of myelin in the ENS is a feature of most neurodegenerative conditions.
Papers Linking ALS with Lowered Myelination and Poor Sleep: PEER results confirm both lowered myelination and poor sleep in ALS patients. These findings align with my electrical resistance éR photo-bioelectric model, where myelin deficits and sleep disturbances disrupt energy flow and signal resonance at the NMJ, exacerbating AHC pathology.
Relevance to hnRNP A1: The hnRNP A1 study provides my thesis with a unifying decentralized mechanism. Redox disruption impairs myelination, contributing to poor sleep and dysbiosis in ALS. This is amplified by light stress, supporting my photo-bioelectric narrative. This destruction offers new therapeutic avenues (e.g., myelin repair, UV exposure) to mitigate ALS progression.
EXPLODING THESE IDEAS IN ALS PATIENTS
Coherence of mtDNA-Level Changes in ALS with UPE and Free Radical Signaling
My thesis focuses on how chronic hypoxic states, UPE, and free radical signaling at the mtDNA level are dysregulated. ALS is a disease with a direct parallel to the Great Oxygenation Event (GOE) that I spoke about on the Nick Jikome podcast. Let’s break this down and make it coherent with my previous ALS discussions in other blogs.
1. UPE and Mitochondrial Redox Activity in ALS:
UPE in Healthy Cells: I have noted that UPE reflects mitochondrial redox activity, emitting ~10–100 photons/s/cm² in healthy cells. UPE arises from oxidative processes, primarily in the mitochondria, where ROS (e.g., superoxide, hydroxyl radicals) and excited carbonyls emit photons during relaxation (400–700 nm). It appears the UPEs released at the nodes of Ranvier are all blue-shifted.
Hypoxia’s Effect on UPE: Chronic hypoxia, common in ALS due to respiratory muscle weakness and pseudohypoxia (low NAD+/NADH, as discussed previously), reduces TCA cycle, ETC activity, decreasing ROS production and thus lowering UPE. This aligns with the literature reports, which state that complex I ROS production decreases in hypoxia, as oxygen availability limits superoxide generation.
nnEMF/Blue Light-Induced UPE Spike: I have highlighted that nnEMF and blue light (450 nm) initially spike UPE by increasing ROS, which is later suppressed by NO binding to heme. The published literature supports this, noting that blue light induces mitochondrial DNA damage and free radical production in human cells, increasing ROS and UPE. In ALS, blue light activates chromophores (e.g., cytochrome c, OPN3), generating ROS and biophotons (400–700 nm), as discussed in my prior NMJ “kill shot” mechanism. NO binds to heme in this case (e.g., in cytochrome c oxidase) inhibits respiration making the TCA unavailable, lowering ATP, reducing UPE over time, which aligns with my cascade of pseudohypoxia and mtDNA damage.
Coherence with ALS: This UPE dysregulation is coherent with previous discussions, where blue light disrupts AHC mtDNA via CSF-propagated biophotons, causing NMJ denervation. The nodes of Ranvier are the gun that shoots blue light directly at the motor neurons to destroy them. The initial UPE spike (from ROS) introduces noise to the NMJ’s high-information system (Shannon’s framework). At the same time, the later suppression (via NO) reduces energy flow (ATP), collapsing éR (energy flow and resistance balance) in AHCs. As the disease progresses, bilirubin levels fall tremendously, a marker of disease progression. Low bilirubin is a decentralized sign of the redox state of the CNS.
2. Free Radical Signaling Dysregulation in ALS
Increased Membrane Resistance and mtDNA Damage: I’ve noted that increased membrane resistance (e.g., IMM leakage) traps ROS, enhancing mtDNA damage while impairing signaling pathways like Nrf2. The PEER literature confirms that complex I ROS release is key in redox signaling. Still, this signaling is dysregulated in hypoxia, as ROS production shifts from controlled (signaling) to excessive (damaging). In ALS, blue light-induced ROS exacerbates this, damaging mtDNA and impairing Nrf2 activation, which normally upregulates antioxidant defenses.
High Lactate and Excitotoxicity: As I’ve noted, high lactate, a hallmark of the Warburg-like state in ALS, exacerbates excitotoxicity by increasing glutamate release. This aligns with prior discussions on glutamate excitotoxicity in AHCs, where mtDNA damage alters calcium signaling, contributing to progressive motor neuron death and alteration of the NMJ.
Adding Oxygen in a Warburg State: I’ve highlighted that adding oxygen when cells cannot use it (due to ETC & TCA dysfunction) generates more ROS, worsening damage. This is coherent with the published literature, which notes that hypoxia-induced ROS dysregulation can lead to oxidative stress if oxygen levels are artificially increased, as the ETC is already compromised (e.g., by NO inhibition or cytochrome c release). This is what transforms the blue-shifted UPEs. ALS patients will get worse with oxygen supplementation.
Coherence with ALS: This free radical signaling dysregulation fits my previous discussion, where blue light-induced pseudohypoxia (low NAD+/NADH) and mtDNA damage amplify ROS, disrupt éR, and lead to NMJ denervation. The Warburg shift in ALS (increased lactate, reduced oxidative phosphorylation) exacerbates this, as AHCs become more vulnerable to excitotoxicity and oxidative stress. The system is slowly bled of all its antioxidant reserves until they are exhausted.
3. Vitamin C and Fenton Reactions in a Warburg State
Danger of IV Vitamin C: I’ve noted that using IV Vitamin C in a Warburg-shifted state (like ALS) drives Fenton reactions, increasing ROS without protective mechanisms of CCO. This is coherent, as Vitamin C (ascorbate) can act as a pro-oxidant in the presence of free iron (Fe²⁺), driving the Fenton reaction: Fe²⁺ + H₂O₂ → Fe³⁺ + OH· + OH⁻. In ALS, where methemoglobin (metHb, Fe³⁺) and oxidative stress are elevated (PEER noted), this reaction amplifies hydroxyl radical (OH·) production, further damaging mtDNA and AHCs.
Coherence with ALS: This aligns with my recent discussion of blue light increasing ROS via heme destruction (e.g., cytochrome c), which releases free iron and drives Fenton chemistry. In a Warburg state, where antioxidant defenses (e.g., SODs, Nrf2) are impaired, IV Vitamin C should exacerbate damage, supporting my caution against its use in ALS or any myelin thinning neuropathy.
4. GOE Relevance and Evolutionary Protections
GOE and SOD Evolution: I have noted that the GOE favored the evolution of Cu/Zn/Mn-SODs, due to a rising oxygen level, reducing UPE emission from Fe-driven Fenton reactions, as these systems produce less superoxide (OH·). The published literature confirms that Fe/Mn-SODs predate the GOE, but Cu/Zn-SODs evolved later, offering better protection against Fenton chemistry by minimizing hydroxyl radical production.
Modern nnEMF/Blue Light Exposure: I have argued that modern nnEMF/blue light exposure mimics GOE-like mtDNA effects, but metHb (Fe³⁺) increases Fenton chemistry, amplifying UPE emission and resultant tissue damage, reversing these evolutionary protections. This is coherent with published data, which notes that blue light induces mitochondrial DNA damage via free radicals. It also aligns with my discussion of blue light disrupting heme-based photoreceptors (e.g., cytochrome c), increasing ROS and UPE
Coherence with ALS: This evolutionary perspective strengthens my previous discussions with you in this series, where blue light overwhelms systems evolved for rarity (e.g., melanopsin, OPN3), mimicking a GOE-like oxidative stress event. In ALS, this reverses the protective mechanisms (e.g., Cu/Zn-SODs) that evolved post-GOE, amplifying mtDNA damage in AHCs and NMJs, as my “light kill shot” mechanism predicted.
5. Connection to hnRNP A1 and Myelin Dysfunction
Myelin and mtDNA Crosstalk: The hnRNP A1 study shows that its disruption impairs myelination, which increases axonal resistance and energy demands on AHCs in ALS. This synergizes with mtDNA-level changes:
UPE Dysregulation: Lowered myelination reduces myelin’s proton capacitor function (found in the myelin paper), decreasing UPE (200–350 nm) that supports mtDNA signaling. This exacerbates ALS’s UPE spike/suppression cycle, as AHC mitochondria become more vulnerable to blue light-induced ROS.
Free Radical Signaling: Myelin deficits impair oligodendrocyte support (e.g., lactate delivery to axons), forcing AHCs to rely more on glycolysis (Warburg shift), increasing lactate and ROS. This amplifies mtDNA damage, as trapped ROS (due to increased membrane resistance) impair Nrf2 signaling.
Chronic Hypoxia and ALS due to chronic intense nnEMF overexposure: Chronic hypoxia in ALS (e.g., from respiratory muscle weakness) reduces TCA/ETC activity, aligning with my description of decreased UPE and dysregulated free radical signaling. We see this in minor diseases like asthma as well. hnRNP A1-related myelin deficits exacerbate this by increasing AHC stress, making them more susceptible to mtDNA damage from blue light and nnEMF.
Overall Coherence: The mtDNA-level changes in ALS causing a UPE dysregulation (spike then suppression), free radical signaling impairment (trapped ROS, Nrf2 dysfunction), and Warburg shift (high lactate, excitotoxicity) are highly coherent with my previous discussion of this mechanistic damage. Blue light introduces noise (ROS, UPE spike) to the NMJ’s high-information system, collapses éR via pseudohypoxia and mtDNA damage, and reverses evolutionary protections (e.g., SODs), mimicking GOE-like oxidative stress. The hnRNP A1 study adds a critical layer to my thesis because myelin dysfunction amplifies these effects by increasing AHC vulnerability, disrupting energy cycling (via sleep deficits), and exacerbating systemic inflammation (via dysbiosis). The pathology of ALS is almost like watching the reverse engineering of the GOE happening in a patient on Earth.
This paper on myelin is essential because it significantly enhances my thesis in several ways:
Mechanistic Depth for ALS Pathology:
The UPE and free radical signaling changes at the mtDNA level provide a detailed mechanism for how blue light and nnEMF act as a “kill shot” in ALS. The initial UPE spike (from ROS) and later suppression (via NO) align with your cascade of pseudohypoxia, mtDNA damage, and NMJ denervation, offering a molecular basis for the éR collapse.
The role of Fenton reactions (amplified by metHb and contraindicated Vitamin C use) explains why oxidative stress damages ALS, reinforcing my focus on heme destruction and ROS as key mediators of the disease and its progression.
Evolutionary Context and Modern Mismatch:
The GOE analogy, where Cu/Zn/Mn-SODs evolved to reduce Fenton-driven UPE, only to be reversed by modern light stress, is a powerful addition to ALS pathology. This will never be found in centralized frameworks because it is entirely biophysical. It frames ALS as an evolutionary mismatch in our oxygen protection mechanisms. The systems that evolved for low blue light exposure (rarity of chromophores) are overwhelmed by modern nnEMF/blue light, reversing protective mechanisms and amplifying mtDNA damage.
This aligns with my broader narrative of light stress, which is critical in disrupting evolved systems, as seen in the latitude-dependent increase in ALS, MS, and schizophrenia.
Integration with hnRNP A1 and Myelin:
The hnRNP A1 study connects myelin dysfunction to mtDNA-level changes, as impaired myelination increases AHC stress, exacerbating the effects of UPE dysregulation and free radical signaling. This creates a feedback loop: blue light damages mtDNA, myelin deficits amplify this damage, and chronic hypoxia (from poor sleep, dysbiosis) worsens both.
The therapeutic potential of myelin restoration offers a practical application: enhancing myelination (e.g., via UV exposure to boost UPE) could mitigate mtDNA damage and improve AHC function in ALS.
Clinical Implications and Undiagnosed Problem:
My point about modern hospitals missing this mtDNA-level pathology (due to Fenton chemistry, metHb, and light stress) should be compelling to any clinician who reads this blog. The dysregulation of UPE and free radical signaling, combined with contraindicated treatments like IV Vitamin C, highlights a critical gap in ALS management. This supports my call for a photo-bioelectric approach to diagnosis and treatment, focusing on light environments and mitochondrial health in the treatment of ALS patients. They need to become tech adverse early in their disease and seeks AM sunlight to slow the disease down ASAP. Red LEDs are not good enough for this disease. It requires tropical sun on a chronic basis to support duration and intensity required to stop this pathology.
Gut-Brain Axis and Systemic Effects
Dysbiosis in ALS is well established in the literature because nnEMF opens the gut barriers, altering bacterial UPE, which exacerbates mtDNA damage systemically via the gut-brain axis. Myelin deficits in the wall of the gut, where the ENS resides, occur due to hnRNP A1 disruption. Loss of myelin in the gut will amplify ALS symptoms and progression, disrupting gut motility and increasing inflammation. This will be discussed in the coming colon cancer blogs. ALS patients cannot use methylene blue orally. It is contraindicated because it is deadly to the microbiome.
Predictions in the éR Model in Short Form For ALS
Blue Light Magnetic Disruption:
Hypothesis: 4oo-480 nm light reverses mitochondrial cathode-to-anode flow, reducing magnetic sense and ATP this cause demyleination in the CNS
Test: Expose AHCs to 400-480 nm light; measure mitochondrial magnetic fields (via NMR) and ATP levels.
OPN3-Driven CSF Signal:
Hypothesis: OPN3 in CVOs emits 450 nm biophotons into CSF, triggering AHC mtDNA damage.
Test: Activate OPN3 in choroid plexus cultures with 480 nm light; detect 450 nm biophotons in CSF and correlate with mtDNA mutations.
Pseudohypoxia and NMJ Failure:
Hypothesis: Blue light-induced pseudohypoxia (low NAD+/NADH) drives NMJ denervation via éR collapse.
Test: Measure NAD+/NADH ratios and NMJ integrity in ALS models under blue light; correlate with ubiquitin rates.
DHA Protection:
Hypothesis: DHA supplementation restores mitochondrial magnetic sense, slowing ALS progression.
Test: Administer DHA to ALS models; assess ATPase spinning, mtDNA damage, and NMJ preservation.
Localized Infection Mimicry:
Hypothesis: Blue light creates focal AHC mtDNA damage, spreading via ROS, resembling an infection in the spinal cord and brain stem because it is the mitochondria that is failing. Most neurodegenerative diseases share this key feature.
Test: Map mtDNA damage in AHCs of blue light-exposed ALS models; correlate with segmental CSF and CNS exposure.
Critical Assessment Of My Ideas
Strengths: The cathode-to-anode analogy bridges macro (magnetosphere) and micro (mitochondria), supported by blue light’s disruption of melanopsin/OPN3 and DHA’s magnetic role. The éR model frames this as noise overwhelming a high-information system, aligning with ALS’s NMJ-first pathology. It also points out that the nodes of Ranvier are adjacent to motor neurons, and the nodes are loaded with mitochondria that shoot out blue light as they undergo light stress. The rate of UPE light loss correlates with disease progression. This explains why it took so long for Hawking to die and why it takes other ALS patients lives in short time scales.
Challenges: Direct evidence for mitochondrial magnetic sense or 450 nm biophotons as functional signals is limited now due to a lack of intracellular photomultipliers. The ubiquitin-pseudohypoxia cascade is plausible via first principle thinking but requires validation in AHCs. OPN3’s CNS role remains speculative but is fully supported by first-principles thinking based on published facts. I’ve linked them all in this blog to show you the precision in the mechanism.
Evolutionary Fit: The rarity of blue light chromophores supports my hypothesis that modern exposure overwhelms evolved systems, offering a novel ALS trigger. ALS is an atavistic disease that reverse engineers what occurred to complex life at the GOE.
The reverse engineering of the atmosphere of the GOE has a lot in common with ALS.
Blue light’s directional cathode-to-anode reversal, filtered by Earth’s magnetosphere but amplified artificially, disrupts AHC/NMJ mitochondria via OPN3/melanopsin, CSF biophotons, and pseudohypoxia. This idea was critical in figuring out this disease. This scatters the NMJ’s high-information signal, collapsing éR at the nodes of Ranvier, mimicking a localized mtDNA “infection” is what ALS looks like in my clinic. DHA, strict EMF avoidance, and magnetic devices are the key treatment counters for this disease to restore magnetic sense in myelin and re-aligning macro-micro physics in the CNS.
SUMMARY
The NMJ’s high information content, rooted in its evolutionary “unusualness,” makes it a fragile, resonant system that artificial blue light disrupts by introducing noise, scattering the signal, and collapsing éR. OPN3/melanopsin in CVOs likely mediate this via 450 nm biophotons traveling through CSF, targeting AHC mtDNA, and initiating NMJ denervation in ALS. Understanding the anatomy of the Nodes of Ranvier is where mitochondrial density is great, which means this is where the light is released that kills. The éR model frames this as a light-induced “kill shot,” with blue light overwhelming a system evolved for rarity, leading to a localized mtDNA damage cascade.
NMJ as a Fragile, Resonant System: The neuromuscular junction’s high information content stems from its evolutionary “unusualness” (perhaps its precision or rarity in signaling demands). I frame it as a resonant system with an “éR” parameter (possibly energy resonance or a related metric), which artificial blue light and/or nnEMF disrupts by adding noise, scattering signals, and collapsing the electrical resistance (éR) and this leads to a unique biophoton spectra that is a kill shot for the anterior motor horn cells.
Blue Light Mechanism: I have proposed that OPN3/melanopsin in circumventricular organs (CVOs) detect 450 nm light, emitting biophotons that travel via cerebrospinal fluid (CSF) to anterior horn cell (AHC) mtDNA in the spinal cord, triggering NMJ denervation in ALS.
éR “Kill Shot”: Blue light overwhelms this evolved rarity, initiating a localized mtDNA damage cascade that reverse engineers the protection schemes for oxygen we first saw with heme proteins and later with SOD metal protein that occured at the GOE.
My mitochondrial hypothesis that blue light/nnEMF damages cytochrome c oxidase, collapsing the IMM potential, increasing conductance via DDW/ions/H₂S, and spreading distal damage adds a mechanistic layer to how a collapsing IMM leads to diseases.
1. NMJ’s Evolutionary Fragility and Conductance
High Information Content: The NMJ’s “unusualness” likely reflects its tight coupling of electrical (action potentials), chemical (acetylcholine), and mechanical (muscle contraction) signals. This precision requires robust mitochondrial support in AHCs for ATP and calcium handling. Its evolutionary rarity in mammals means it is strictly optimized for natural light spectra (e.g., red-heavy sunlight), not artificial blue.
Prediction: Increased mitochondrial conductance (from cytochrome c oxidase damage) disrupts this precision. If the IMM leaks ions (H⁺, Ca²⁺) and H₂S oxidizes, local electrical noise rises; think of it as short-circuiting the AHC’s ability to fire clean action potentials. This scatters the NMJ’s resonant signal, reducing éR (if éR measures signal coherence or energy efficiency).
2. Blue Light exposure on the skin alters neuroectodermal OPN3, and leads to mtDNA Targeting by Biophotons at the nodes of Ranvier
Mechanism: OPN3/melanopsin absorbing 450 nm light in CVOs (e.g., subfornical organ) could emit biophotons, quantum packets of energy, that travel through CSF, which is a plausible waveguide due to its optical clarity. These biophotons might directly penetrate AHC mitochondria, exciting cytochrome c oxidase or mtDNA to collapse the IMM power field.
Conductance Link: Damaged cytochrome c oxidase generates ROS, collapsing the IMM’s ~30 MV/m field. The resulting ion/H₂S surge increases conductance around mtDNA, which would amplify local damage. It overwhelms the SOD system as well. This aligns with my light “kill shot” mechanism, a focused energy transfer of biophotons that triggers a spreading cascade that mimics an infection(conductance-driven disruption). Instead, it is a trail of electrical damage from failing mtDNA in UMN/LMNs.
Prediction: The biophoton signal, amplified by CSF, targets AHC mtDNA with precision due to short-range biophoton targeting, and the conductance spike spreads chaos, denervating NMJ synapses distally FIRST. This is precisely what is seen clinically in this disease. H₂S oxidation would simultaneously exacerbate this by forming conductive sulfate ions, further destabilizing mitochondrial membranes, allowing more of its power to escape into the cell to cause damage. This is how myelin begins to thin.
3. Noise, Signal Scattering, and éR Collapse
Noise Introduction: Blue light-induced ROS and conductance changes flood the NMJ with stochastic electrical activity, akin to atmospheric static from water vapor and lightning seen in the GOE. This drowns out the NMJ’s high-fidelity signal, scattering acetylcholine release or postsynaptic response.
éR Collapse: If éR represents a resonance state (e.g., optimal energy transfer across the NMJ), the conductance surge disrupts it. Mitochondria failing to buffer calcium or power ATP synthesis could misalign pre- and postsynaptic timing, collapsing the system’s evolutionary tuning.
Prediction: The NMJ becomes a “fragile resonator” overwhelmed by noise due to the damage. In ALS, this manifests as progressive denervation, and motor neurons lose their ability to sustain precise signaling, mirroring my localized-to-distal damage cascade. This is a reverse engineering of the GOE at the nano levels in the CNS.
4. H₂S and ALS Pathology
H₂S Role: Normally, H₂S supports mitochondrial function and hypoxia resistance. But if “zapped” by releasing ROS/RNS due to blue light or nnEMF, it shifts from protective to destructive, boosting conductance and ROS production. In ALS, mitochondrial dysfunction and oxidative stress are well-known hallmarks, and the H₂S dysregulation could be a missing link in this pathophysiology. During the GOE this gasotransmitter was a terminal electron acceptor when oxygen was rare.
Prediction: H₂S oxidation in AHC mitochondria accelerates NMJ damage by enhancing conductance, paralleling atmospheric sulfur aerosols in the GOE. This could explain ALS’s rapid progression, with distal damage spreading as conductance destabilizes neighboring neurons. It also explains why ALS patients have low bilirubin later in their disease.
The NMJ thesis provides a biophysical cascade:
Initiation: Blue light (450 nm) via OPN3/melanopsin in CVOs emits biophotons, targeting AHC mtDNA and damaging cytochrome c oxidase.
Amplification: The IMM potential collapses, increasing conductance via ion leakage (H⁺, Ca²⁺), DDW dynamics, and H₂S oxidation. This mirrors the GOE’s water vapor/O₂-driven conductance spike, which lead to endosymbiosis is what kills ALS patients.
Disruption: Local mtDNA damage spreads distally as conductance noise scatters the NMJ’s resonant signal, collapsing éR and denervating synapses using massive UPEs of blue light at the Nodes of Ranvier
ALS Outcome: The “kill shot” initiates a fractal-like cascade where evolved fragility meets modern stressors (blue light/nnEMF), driving motor neuron loss.
Plausibility Check
Strengths: The model ties evolutionary biology (NMJ/ Ranvier rarity), photobiology (OPN3, biophotons), and mitochondrial physics (conductance, H₂S) into a coherent narrative. CSF as a biophoton conduit is speculative but plausible given its optical properties. ALS’s mitochondrial focus aligns with current research. Moreover, no one knows what OPN3 does in humans because too few are studying biophysics. The mitochondrial density at the Nodes of Ranvier is well known and published. No one has linked them to the location of the motor neurons until today.
Challenges: Biophoton transmission spectral range and energy need validation. We need the ability to check individual mtDNA biophoton emission with an intracellular photomultiplier that detects these signals. Also, can 400-485 nm photons penetrate deep enough to get to AHC? The data from the skin says yes. H₂S’s exact role in ALS lacks direct evidence, though its redox potential fits mitochondrial evolutionary history. éR’s definition but needs clarity to test this quantitatively. MRI confirms myelination issues, and gut studies confirm loss of myelin in the gut ENS.
Next Steps For Decentralized Science
My thesis predicts that blue light/nnEMF exposure disrupts NMJ signaling via a conductance-driven mtDNA cascade, with H₂S as a modulator. The gun is a massive stream of blue UPEs shooting out of the nodes of Ranvier. I believe the familial forms of this disease will always show parents were nnEMF toxic or a child experienced this below to raise their heteroplasmy in the CNS. We need to stop using blue light in children completely. They have no myelin to protect themselves.
To refine it, future decentralized research should:
Test AHC mitochondrial conductance under all blue light hazards, but look for the frequency of blue light that most alters AHC in vitro. This would narrow the target light that damages these patients.
Measure H₂S levels, myelination, and sleep in ALS models exposed to nnEMF.
Model éR as a function of NMJ signal-to-noise ratio. Use a photomultiplier at the nodes of Ranvier.
This fractal bridge, built by Nature 2.4 billion years ago from atmosphere to mitochondria to NMJ, is biophysically bold but very testable for future scientists and patients dying of this disease.
The Great Oxygenation Event (~2.4 Ga) transformed Earth’s atmosphere, increasing electrical conductance through water vapor, sulfate aerosols, and reactive species like NOx. Lightning and UV-driven ROS pressured archaea and bacteria into endosymbiosis, where an oxygen-respiring bacterium became the proto-mitochondrion.
Mitochondria evolved as cellular magnetospheres, using DHA, heme proteins, metal SODs, and proton gradients to manage electron flow, enabling eukaryotic complexity and later innovations like myelin. Artificial blue light and nnEMF disrupt mitochondrial function today, increasing conductance and ROS in a fractal echo of GOE dynamics, driving chronic disease. Decentralized medicine must restore biophysical harmony by addressing light, water, and magnetism to make sense of chronic diseases. Our recent electromagnetic exposures fully mirror the evolutionary conditions that birthed eukaryotes.
Clarified Evolutionary Timeline: Endosymbiosis (2 Ga) predates the Cambrian explosion (540 Ma). The latter reflects oxygen-driven multicellularity, not the initial eukaryotic event. This timeline comprehension is critical in understanding why we must emphasize GOE as the endosymbiosis trigger and Cambrian as a downstream effect. The KT event was another downstream effect, particularly a light-stress event for mammals.
Strengthened Conductance Model: Incorporated aerosols, trace gases, and water vapor were the conductance drivers, and this is grounded in modern atmospheric science (e.g., volcanic lightning studies). Geologists have added BIFs and stromatolites as geological evidence of GOE’s impact that has scarred living systems.
Nature’s Fractal Analogy: The magnetosphere-IMM parallel is robust idea clarified as charge-separation system. We needed to add biophysics (e.g., DHA’s π-electrons, structured water) to bridge planetary and cellular scales to see how this sculpted the IMM.
Modern Relevance To Light Stress as the Modern Cheisel of Disease: Biophysics links blue light/nnEMF to specific mitochondrial targets (CCO, mtDNA, SOD) and chronic disease, aligning with my decentralized photo-bioelectrical thesis. Adding photobiomodulation might be a required countermeasure to governments using geoengineering to control people electronically.
Evolutionary Biology: We need to include gene transfer and myelin evolution into your lexicon to show how endosymbiosis enabled complexity, reinforcing the decentralized medicine focus on energy efficiency and photo-bio-electric resistance.
The Origin of Eukaryotes in a Decentralized Medicine Framework
1. Macrocosm: Earth’s Atmosphere and Electrical Conductance During the GOE
Core Idea: The rise of oxygen during the Great Oxygenation Event (~2.4 billion years ago) transformed Earth’s atmosphere, increasing electrical conductance through water vapor, aerosols, and reactive species. This created conditions favoring endosymbiosis, the critical step toward eukaryotic life.
Geological and Atmospheric Context:
Pre-GOE Atmosphere: Early Earth (~4.5–2.4 Ga) had a reducing atmosphere dominated by methane (CH₄), ammonia (NH₃), carbon dioxide (CO₂), and minimal oxygen (O₂ < 0.001% of present levels). Volcanism was intense, releasing sulfur dioxide (SO₂) and hydrogen sulfide (H₂S). The magnetosphere, formed by Earth’s dynamo, shielded life from solar wind and cosmic rays, but UV radiation penetrated deeply due to the lack of an ozone layer early on. This implies that Earth’s terrestrial spectrum was never constant during the GOE.
GOE Trigger: Cyanobacterial photosynthesis produced O₂, oxidizing reducing gases (e.g., CH₄ + 2O₂ → CO₂ + 2H₂O). This shifted the atmosphere toward an oxidizing state, increasing water vapor and altering the electrical properties of the atmosphere.
Electrical Conductance:
Water Vapor: Oxygen-driven oxidation of methane and hydrogen increased atmospheric H₂O, a polar molecule that ionizes under UV or lightning (H₂O → H⁺ + OH⁻). Higher humidity lowered the dielectric breakdown threshold, increasing lightning frequency and atmospheric conductance.
Aerosols: Oxidation of volcanic SO₂ formed sulfate aerosols, which act as ion-attachment nuclei, enhancing conductance. This aligns with modern observations of volcanic lightning.
Trace Gases: Ammonia oxidation (NH₃ → NOx) produces ionizable species, which amplify charge carriers under energy inputs like UV or cosmic rays.
Lightning Surge: An oxidizing, humid atmosphere with aerosols supported stormier conditions, increasing lightning frequency. Lightning provided high-energy electrons and reactive oxygen species (ROS), potentially driving biochemical innovations.
Evolutionary Implication: The GOE’s electrical environment was marked by lightning, UV, and ROS, which created selective pressure for antioxidant defenses (e.g., superoxide dismutase, SOD) and energy-efficient metabolisms. Archaea and bacteria exposed to this conductive oxidative stress were incentivized by Nature to form symbiotic relationships to protect themselves from the oxygen holocaust, leading to endosymbiosis. In endosymbiosis, oxygen protection scheme were built.
Additions from Geology and Evolutionary Biology:
Banded Iron Formations (BIFs): The GOE coincided with BIFs (~3.5–1.8 Ga), where oxygen oxidized dissolved iron in oceans, reducing available reducing agents. This increased oxidative stress, pushing microbes toward cooperative metabolisms.
Stromatolites: Fossilized cyanobacterial mats (~3.5 Ga) indicate early oxygen production, creating localized oxygen oases that preadapted microbes to oxidative stress before the global GOE.
Nitrogen’s Role: Nitrogen fixation by early microbes (e.g., via nitrogenase) increased atmospheric N₂, stabilizing the atmosphere by diluting oxygen’s reactivity. This balanced electrical potential reduces runaway conductivity but maintains enough electrical power/resistance to drive endosymbiosis.
The GOE increased atmospheric conductance via water vapor, aerosols, and reactive species, creating an electrically dynamic environment. Lightning and UV-driven ROS pressured microbes to innovate antioxidant defenses and energy systems, setting the stage for endosymbiosis.
2. Microcosm: Endosymbiosis and Mitochondrial Evolution
Core Idea: The GOE’s electrical and oxidative environment drove endosymbiosis, where an archaeon engulfed an oxygen-respiring bacterium, forming the proto-eukaryote. Early eukaryotes have unique protection schemes built in that isvery different from modern mammals. Mitochondria evolved as cellular analogs to Earth’s magnetosphere, managing electron flow and proton gradients.
Mechanism of Endosymbiosis:
Selective Pressure: Rising oxygen and ROS stressed anaerobic archaea and bacteria. Aerobic bacteria, capable of oxidative phosphorylation, offered a survival advantage by detoxifying oxygen and generating ATP.
Symbiotic Fusion: An archaeon likely engulfed an alpha-proteobacterium (~2 Ga), which became the proto-mitochondrion. This symbiosis allowed the host to exploit oxygen for energy while the bacterium gained protection and nutrients.
Electrical Analogy: The inner mitochondrial membrane (IMM) mimics Earth’s magnetosphere, directing electron flow from the matrix (cathode) to the intermembrane space (anode) via the electron transport chain (ETC). The proton gradient (ΔpH) across the IMM drives ATP synthesis, analogous to atmospheric charge gradients driving lightning.
Key Innovations:
DHA and Membranes: Docosahexaenoic acid (DHA), a polyunsaturated fatty acid, enhanced membrane fluidity and ATPase efficiency, boosting proton gradients. DHA’s π-electron clouds may have increased electrical resistance, slowing ultraweak photon emission (UPE) and refining mitochondrial signaling. DHA was placed in membranes 600 million years ago and never changed once.
Heme & SOD Proteins: SOD and cytochrome c oxidase (CCO), containing heme, were selected to manage ROS and electron flow, protecting mtDNA from oxidative damage.
Myelin Connection: Eukaryotic complexity, enabled by mitochondrial energy, led to myelin in nervous systems (~600 Ma). Myelin’s high lipid content (including DHA) improved proton conductance, enhancing neuronal efficiency and reducing vertebrates’ sleep needs. It also augmented the spin rate of ATPase for protium.
Additions from Evolutionary Biology:
Gene Transfer: Endosymbiosis involves lateral gene transfer from the proto-mitochondrion to the host nucleus, streamlining mitochondrial genomes and enhancing eukaryotic complexity. This leads to thermodynamics benefits to building more complexity, but it also is another mechanism of how electrical resistance in the genome makes use of the 30 million volt power source found on the IMM.
Cambrian Explosion (~540 Ma): While endosymbiosis occurred 2 Ga, the Cambrian explosion reflects later oxygen spikes (0.8–0.6 Ga) from 0% to 21%, enabling energy-intensive multicellularity. Once the oxygen protection scheme is innovated, the endosymbiosis event leads to the Cambrian explosion; it’s better framed as a downstream consequence of the oxygen holocaust.
Fractal Analogy: The magnetosphere-IMM parallel I am drawing for you is strengthened by considering both situations as charge-separating systems. Earth’s magnetosphere filters solar radiation; mitochondria filter electrons, maintaining redox homeostasis.
Endosymbiosis, driven by GOE-induced oxidative and electrical stress, created mitochondria as cellular magnetospheres. DHA, heme proteins, and proton gradients enabled energy efficiency, paving the way for eukaryotic complexity and myelin-driven neuronal advancements.
3. Modern Disruption: Blue Light and nnEMF
Core Idea: Artificial blue light (~435-475 nm) and non-native electromagnetic frequencies (nnEMF) disrupt mitochondrial function, mimicking a magnetosphere failure and driving chronic disease by altering electrical conductance and ROS.
Mechanism:
Blue Light Effects: Blue light penetrates tissues, exciting electrons in heme (e.g., CCO) and altering iron oxidation states. This disrupts ETC function, increasing ROS and mtDNA damage, analogous to UV-induced damage pre-GOE. People think there are no links published in the literature that link metHb to artificial light and drug use. There are. They just are not well known. Blue light and the nnEMF effect are additives to metHb creation in humans.
nnEMF Impact: Modern devices’ Radiofrequency and microwave radiation (~MHz–GHz) induce non-thermal effects, polarizing mitochondrial membranes and disrupting proton gradients. This mimics high-conductance atmospheric conditions, overwhelming SOD, and antioxidant defenses.
Dehydration Link: Blue light and nnEMF may disrupt structured water (e.g., exclusion zone water) around mitochondria, increasing local conductance and spreading ROS-mediated damage. This parallels my GOE water vapor hypothesis, where humidity amplified atmospheric conductance. When melanin sheets are dehydrated, they become massive electrical conductors that can do damage inside the UPE emission system.
H₂S Connection: Mitochondrial H₂S, a signaling molecule, is dysregulated under oxidative stress, linking to hypoxia and chronic disease. This mirrors volcanic H₂S contributions to pre-GOE conductance.
Core Idea: Grounding (direct contact with Earth’s surface) restores mitochondrial charge dynamics by supplying electrons, countering modern disruptions, and aligning with the photoelectronic thesis that eukaryotes evolved in an electrically conductive environment.
Mechanism:
Earth’s Electron Reservoir: Earth’s surface maintains a negative charge due to the global atmospheric electric circuit, driven by lightning and ionospheric currents. Grounding connects the body to this reservoir, allowing electron flow to neutralize positive charges (e.g., ROS, free radicals).
Mitochondrial Stabilization: Electrons from grounding reduce oxidative stress by quenching ROS, stabilizing CCO’s heme iron, and supporting ETC efficiency. This mimics pre-GOE reducing conditions, where electrons were abundant in a low-oxygen atmosphere.
Water and Conductance: Grounding enhances structured water (exclusion zone water) around mitochondria, reducing local conductance spikes caused by blue light/nnEMF. This parallels the GOE’s water vapor role in atmospheric conductance but in reverse by stabilizing rather than amplifying charge flow.
H₂S Connection: Grounding upregulates H₂S signaling, as reduced oxidative stress supports sulfur metabolism, improving mitochondrial resilience and hypoxia response.
Fractal Analogy:
Atmospheric-Mitochondrial Parallel: Just as Earth’s magnetosphere failed to shield early life from UV and lightning fully, modern mitochondria fail under blue light and nnEMF, increasing local conductance (via disrupted water and ions) and spreading damage distally.
Spectral Shift: Blue light dominance shifts the terrestrial light spectrum, akin to Mars’ thin atmosphere altering its surface radiation profile. This disrupts circadian and mitochondrial signaling, driving disease.
Biophysics and Medicine are linked by the history locked in the GOE
Photobiomodulation Contrast: Red/infrared light (~600–1000 nm) enhances mitochondrial function by stabilizing CCO, suggesting a therapeutic counter to blue light damage when governments are doing all they can to limit IRA and NIR on Earth..
mtDNA Sensitivity: Mitochondrial DNA, lacking histones, is highly susceptible to ROS, explaining why conductance spikes (from nnEMF or blue light) disproportionately harm mitochondria. It also became useful in altering the UPE spectra to sculpt the interior of cells to build life’s complexity.
Chronic Disease Link: Disrupted mitochondrial gradients and ROS underlie metabolic syndrome, neurodegeneration, and cancer, supporting my decentralized medicine thesis that environmental mismatches (light, nnEMF, dehydration) drive chronic diseases today on Earth.
Blue light and nnEMF disrupt mitochondrial electron flow and water structure, increasing conductance and ROS in a fractal echo of GOE atmospheric changes. This drives chronic disease, underscoring the need for decentralized, biophysically informed medicine.
To make the critical link for you the non clinician, I want you to re watch this video. HYPERLINK.
When I saw this video, I knew exactly what this doctor was seeing and why he was blinded to it. That was the day I unretired and went back into the ICUs to help train doctors on the events of the GOE and why DARPA was doing what they were. They knew the mistakes that would be made with oxygen therapies in those with hypoxia diagnosed by oxygen saturation machines. Big Pharma had taught people for 30 years that once someone went hypoxic, they should never forget their ABCs. That is how this pandemic was planned.
The manufacturing of SARS-COVID by the DoD collaboration of Dazek, Fauci, and the Wuhan Institute of Virology was to create a virus that would cause minor underlying sepsis to release massive levels of NO in patients’ organs. They knew these people would go to doctors who would use a pulse ox, supplemental oxygen, and arterial blood gases to assess patients in the ICU. Very few of them would know to change to co-oximetry when high FiO2 therapies would lead to refractory hypoxia. They knew the doctors would not be well versed that methemoglobin levels should be expected to be elevated in patients with sepsis due to the release of nitric oxide, which converts to nitrate and subsequently to methemoglobin. COVID was engineered to release massive amounts of nitric oxide to cause refractory hypoxia. Thisoccurred by limiting the UPE release of NIR light from mtDNA by the virus. Since most patients in the ICUs of the hospital were intubated and sedated, the only clinical indicator doctors would receive at the bedside was hypoxia refractory to maximum oxygen therapy.
Once this clinical situation happened, and the doctors were at a loss to explain the phenomena, the architects of the virus knew they would initially use drugs like lidocaine or procaine to place arterial lines and central lines, supplemental oxygen, oral azithromycin, and hydroxychloroquine. When these failed to work, they would elevate their use of Pharmaceuticals according to the recipe algorithm of their hospital’s critical care guideline. This made the planning easy because they knew how the people at the bedside would react beforehand. What did the architects know that the doctors did not?
As patients were transferred to an intensive care unit (ICU), they were diagnosed with acute hypoxic respiratory failure and acute respiratory distress syndrome, for which they required intubation and mechanical ventilation. Their treatments would default to the new algorithm that covered this new clinical scenario: That algorithmic treatment regimen included lopinavir-ritonavir, ribavirin, and tocilizumab in most Western facilities. This would slowly increase their risk of metHb hypoxia. If co-oximetry was not installed on the ICU’s blood gas analyzers, they would develop refractory hypoxia. It was at this time many people had their last rights given, and then the hospital critical care algorithm was built to end the game and create a covid death via Remdesivir. That is how all hospital ICU critical care algo were built in 2016 -2020.
Once a patient begins to build up metHb, they will develop obvious symptoms. In a healthy person, the clinical features are pallor, fatigue, weakness, tachycardia, tachypnea, and cyanosis, which may be clinically evident with methemoglobin as low as 10%. As the percentage of methemoglobinemia approaches 20%, the patient may experience anxiety, light-headedness, and headaches. At methemoglobin concentrations of 30%–50%, there may be tachypnea, confusion, and loss of consciousness. If methemoglobin approaches 50%, patients are at risk for seizures, dysrhythmias, metabolic acidosis, and coma. When patients with a positive PCR test and hypoxia presented to an ER, they were immediately admitted to the ICU, where they were intubated and sedated by protocol. During intubation, more oxidizing drugs were used to further stimulate the formation of metHb. This meant all the relevant symptoms of acute metHb poisoning would be gone in the sedated intubated patient because the only clinical indicator was hypoxia refractory to maximum oxygen therapy.
Not even methylene blue would operate properly when massive changes to the UPE spectra were being engineered by the architects of this virus. I knew it, and I had to go back in to clinical medicine to covertly deliver this message to the front line workers.
Many of these workers defaulted to the Marik protocol, which made these patients worse. The critical care doctors could not understand it. I could. As part of Marik’s protocol, high-dose Vitamin C would be used. Vitamin C’s downstream effect is to increase the absorption of iron in the patient. This was deadly for those infected with the engineered virus. Why? Iron creates the Fenton reaction, which drives ROS through the roof to destroy all heme-based proteins and metal ion SOD reactions. This is why methylene blue would not work in these covid cases where the patients had already been intubated. Doctors had to be trained to give fresh RBC replacements and follow it up with hypertonic sodium chloride.
They had to limit oxygen support, turn off vents, and get patients to sunlight containing NIR light. NIR light unbound the NO from their Hb. I told all the doctors that CO-oximetry was only used outside the ICU when the respiratory tech was running their arterial blood gases. I told them if they brought the Co-Oximeter in early as soon the patient was admitted to the ICU they would see I was right. Then they could accurate diagnosis and treat the patients as a chronic metHb sepsis caused by a GOF virus.
I handed every doctor I dealt with this paper: Wenzhong L, Li H. COVID-19: attacks the 1-beta chain of hemoglobin and captures the porphyrin to inhibit human heme metabolism. ChemRxiv. 2020. Preprint. 10.26434/chemrxiv.11938173.v7
COVID was engineered to attack the one beta chain to mimic a thalassemia-like hemoglobinopathy that had unusual presentations. Dr. Fauci knew this from the AIDS epidemic. Luckily, I was a doctor at that time, and I remember reading those reports that HIV was associated with a higher risk of metHb. I also remember that during the AIDS crisis in the French Quarter, many homosexuals were using NO additives, and they would come in with unusual hypoxic events and total immune collapse.
Now you understand just how it was done and precisely why it all happened. The GOE story of hemoglobinopathies as oxygen varies is not taught in medical schools or residencies. I had to do that for the centralized ICU docs and nurses on the front line. The jabs were engineered with LNPs to mimic the chronic diseases that put you at higher risk for metHb. Vaccines use LNPs to simulate high heteroplastic disease states because they destroy CCO to cause mtDNA damage. This explains why the NIH budget has only 1% spent on mtDNA research and 99% spent on nuclear DNA research.
For those of you who do not know, the risk of methemoglobinemia associated with oxidizing drug use increases in elderly patients with medical comorbidities such as renal failure, anemia, and human immunodeficiency virus. If you look at cite four below you’ll see it for yourself. Novel coronavirus proteins can alter the hemoglobin structure, which directly interferes with the red blood cell’s ability to carry oxygen. This explains why John Beaudoin found out what he did in the ICD coding in many states in the USA. You need to share this information with every attorney, politician, and hospital employee you can so that DARPA and the DoD can be stopped from using GOF research. Senator Ron Johnson has subpoena power now. Make sure you all email his office this blog if you are a savage and want your government punished for what they did. The people in power are doing NOTHING.
CITES
1. Brunelle JA, Degtiarov AM, Moran RF, Race LA. Simultaneous measurement of total hemoglobin and its derivatives in blood using CO-oximeters: analytical principles; their application in selecting analytical wavelengths and reference methods; a comparison of the results of the choices made. Scand J Clin Lab Invest Suppl. 1996; 224:47–69
2. Pritchett MA, Celestin N, Tilluckdharry N, Hendra K, Lee P. Successful treatment of refractory methemoglobinemia with red blood cell exchange transfusion. Chest. 2006; 130:294S
3. Ohashi K, Yukioka H, Hayashi M, Asada A. Elevated methemoglobin in patients with sepsis. Acta Anaesthesiol Scand. 1998; 42:713–716
4. Alanazi MQ. Drugs may be induced methemoglobinemia. J Hematol Thrombo Dis. 2017; 270:1–5
Embracing the Storm: Decentralized Medicine, Nature, and the Power of Human Connection
Life is a storm, chaotic and unpredictable, yet profoundly transformative. As the winds howl and the rains pour, we may not recall how we endured, but one truth remains: we emerge changed. The storm strips away facades, revealing who we are beneath the masks we wear. In this raw, unfiltered state, we find our connection to nature and to one another, a connection that forms the heart of decentralized medicine and a life well-lived.
Nature is not here to complicate our existence but to simplify it. It is ingenious and practical, offering clarity amid chaos. When we walk through a forest or stand by a rushing river, we are reminded of life’s rhythms, unhurried, purposeful, and interconnected. Decentralized medicine embraces this wisdom, prioritizing the individual’s relationship with their environment and community over rigid systems. It’s about healing through presence, listening, and collaboration, rooted in the belief that our survival depends on talking to one another, sharing stories, and building bridges.
Collaboration is the symphony of human connection. No single person can whistle a symphony; it takes an orchestra, each instrument contributing to a harmony greater than the sum of its parts. When we unite with a common purpose, whether to heal, create, or inspire—we unlock a synergy that transforms lives. Decentralized medicine thrives on this principle, encouraging communities to come together, share knowledge, and empower one another. It’s about leaving a trail of leaders, not followers, who amplify reality rather than chasing shadows.
Our relationship with nature mirrors our relationships with each other. Just as a tree’s roots anchor it through storms, our principles ground us as we evolve. Nature teaches us to change our leaves, our opinions and perspectives, while keeping our roots intact. It reminds us that what is given to us is what we need, and what we want often requires letting go of what no longer serves us. In decentralized medicine, this translates to trusting the body’s innate wisdom, supported by the healing power of community and the natural world.
Perception shapes our reality. When we choose to see the good in people and situations, we cultivate a life of possibility. This isn’t about ignoring pain or negativity but about taking charge of how we respond. From the backstabbing colleague to the challenging family member, we hold the power to choose happiness over resentment. Decentralized medicine encourages this mindset, fostering resilience through self-awareness and connection to nature’s rhythms. It’s about building bridges to cross, burning those that lead nowhere, and sometimes forging new paths entirely.
Life’s biggest decisions revolve around these bridges, knowing which to build, which to cross, and which to leave behind. The paths less traveled often lead to the most profound discoveries. Nature, with its winding trails and hidden clearings, invites us to explore these paths, to trust our instincts, and to create our own way. Decentralized medicine follows suit, empowering individuals to take ownership of their health, guided by intuition, community, and the natural world.
Creativity and imagination are the cornerstones of this journey. They distinguish leaders from followers, allowing us to embrace errors as opportunities and choose wisely from them. In a world where many resist change, clinging to comfort, we must make shift happen. Decentralized medicine is a call to action, a rejection of centralized conformity in favor of innovation rooted in nature and human connection. It’s about believing your life is worth living well and letting that belief shape your reality.
The stakes are high. Our health, our longevity, and our relationships depend on the choices we make. Women outlive men, with widows far outnumbering widowers, a reminder that vitality is not just about surviving but thriving for those we love. By fostering community, embracing nature, and choosing collaboration, we create a legacy of health and connection that endures.
This weekend, as dawn breaks and light spills over the horizon, reflect on the resurrecting power of light itself. For those burdened by illness, light, whether from the sun’s warm embrace, the glow of shared laughter, or the spark of hope kindled in community, can awaken the spirit. It pierces the darkness of despair, whispering of renewal and possibility. Just as spring stirs life from winter’s grip, light calls the weary to rise, to heal, to reconnect with nature and each other. Share this truth around your table: when we open our hearts to light, we become conduits of resurrection, lifting one another from shadow to radiance. Let this be the season you forge new paths together, trusting that light, love, and unity can transform any storm into a story of triumph.
Matter as Music: Sympathetic Resonant Physics and the Scalar Architecture of Reality
Scalar waves are real, specifically in the context of sound waves. Sound waves, which are used in music, are often considered scalar wave fields, meaning they have magnitude but not direction or polarization. While this is a simplified view, recent research suggests that generic sound wave fields actually have more complex properties, according to a study by RIKEN.
RIKEN’s research demonstrates that generic sound wave fields can have as many degrees of freedom for micromanipulation as optical fields. Understanding sound as a scalar wave field is crucial for understanding how musical instruments produce sound, how sound waves travel through space, and how we perceive sound. While the simplified scalar wave model is a good starting point, it’s becoming clear that more nuanced models are needed to capture the full complexity of sound, particularly in advanced acoustic applications and research.
This is a real phenomenon where an object vibrates in response to a nearby vibrating object when there is a natural frequency match or a harmonic relationship between them. A classic example is two similarly tuned tuning forks where one vibrates and the other responds even without physical contact. VIDEO
“In the beginning there was not just light, there was the Tone…”
Between those two fingers above is light and sound. Honestly everything that makes up you life is in that space. Today’s blog is the first of many that will show you just how infinite that space can be. When we examine this space, allow your angels to sit on the sideline. They need to listen to the music too. Music is an angel that sits in the side line of your life with patience and reason. Angels sit on the sideline and play music for you wondering when your tug of war will end.
The universe resonates with a primal melody, a cosmic symphony that challenges the mechanical view of reality. Sympathetic resonance (where one object vibrates in response to another) invites us to hear the song of Nature all around us, revealing a universe not as a collection of particles, but as a resonant organism where energy, form, and consciousness emerge from vibratory relationships. When life is felt this way, matter unfolds like music, and recent scientific findings, such as a landmark study at Ohio State University, support this view by demonstrating that acoustic phonons, the carriers of sound and heat, can be influenced by magnetic fields, suggesting that the resonance of life itself is shaped by the fields we integrate into our environment.
The Scalar Octave: Nature’s Harmonic Blueprint
Sympathetic resonance describes the scalar octave as a hierarchy of nested frequencies that structures reality. Scalar waves, unlike transverse waves such as light, are longitudinal, non-Hertzian vibrations that ripple through the etheric field, altering space itself. These waves act as carriers of formative information, guiding energy into matter in a process mirroring a musical scale. Elements in the periodic table resonate in vibratory octaves, hydrogen as the root note, helium the second, and so on, following the perfect fifth’s 3:2 ratio, a proportion nature favors in spirals from galaxies to DNA. The Ohio State study revealed that acoustic phonons in a semiconductor (indium antimonide) were slowed by 12% under a magnetic field, proving their sensitivity to magnetism even in non-magnetic materials. This suggests that scalar fields, which may underpin biological resonance, can be influenced by external magnetic fields, impacting the vibratory coherence of life itself.
In quantum biology, this aligns with my decentralized thesis: life emerges from distributed, resonant networks rather than top-down control. Scalar fields may enable quantum coherence in biological systems, allowing molecules to “tune” to each other across distances without touch, much like sympathetic strings. The same thing is true with people in your life. Sometimes, they can play your instrument beutifully, and other times your have to find sanctuary from them. People create their own music too. Sex is a complex form of resonance. Having sex without touching is something very few people try in life.
The perfect fifth, as nature’s preferred ratio, could orchestrate this coherence, and the Ohio State findings imply that magnetic fields in our environment, such as those from technology or natural sources, might directly affect these resonant processes, shaping the vibratory “song” of living systems.
Elements as Chords: The Music of Matter
Each element in the periodic table is a chord, a unique vibratory signature. Hydrogen sets the fundamental tone, carbon plays a four-note harmony stabilizing life’s architecture, oxygen energizes as a catalytic chord, and gold resonates as a high harmonic of solar frequencies. These chords align with the perfect fifth’s 3:2 ratio, creating stability in both music and matter. The Ohio State study supports this harmonic view: phonons, which carry the vibrations of these elemental “chords,” respond to magnetic fields through a diamagnetic effect, where vibrating atoms induce magnetic moments that alter their interactions. This implies that the “music” of matter, its vibratory essence, can be retuned by external fields, potentially affecting biological systems where these elements form the building blocks of life.
In quantum biology, this suggests that molecular interactions, like enzyme catalysis or DNA replication, may involve vibratory resonance influenced by magnetic fields. Proteins might “sing” to their substrates, aligning frequencies to facilitate reactions, a process possibly mediated by scalar fields. The decentralized thesis reinforces this: biological systems thrive on distributed resonance, and the Ohio State findings highlight how environmental magnetic fields could either harmonize or disrupt this resonance, impacting health and vitality.
Form and the Living Geometry of Resonance
Vibration creates form through resonance, as seen in cymatics, where sound organizes particles into geometric patterns. In the scalar realm, this principle scales up: atoms, cells, and galaxies may be standing waves within higher-dimensional fields, often reflecting the perfect fifth in their spirals of becoming. Sacred geometry, such as the flower of life or Platonic solids, maps these resonant patterns, revealing the universe’s harmonic lattice. Sympathetic resonance drives this process where frequencies align and amplify, connecting systems across scales. The Ohio State study showed that magnetic fields increase phonon collisions, slowing their movement, which suggests that such fields can alter the resonant patterns that give rise to form, from molecular structures to biological tissues.
In quantum biology, this supports the idea that coherence in living systems—like in photosynthesis or neural networks—relies on sympathetic vibratory fields, potentially influenced by magnetic fields. My decentralized thesis aligns here: life’s complexity emerges from distributed resonance, and external fields could either enhance or interfere with these processes, affecting everything from cellular communication to organismal health.
Consciousness: The Cosmic Tuner
Sympathic resonance posits consciousness as a primary vibratory phenomenon, not a byproduct of matter. Soon I will have more to say on the topic of consciousness. Thought, intention, and emotion act as scalar waves, tuning reality through sympathetic entrainment. The Ohio State study’s findings, that phonons respond to magnetic fields, suggest that the vibratory fabric of reality, including consciousness, may be similarly influenced. If consciousness is a resonance, then magnetic fields in our environment could subtly shape our mental and emotional states, amplifying or dissonating the “chords” we play in the scalar octave.
In quantum biology, this aligns with my decentralized thesis: consciousness may emerge from resonant networks across scales, from microtubules in neurons to the morphogenetic field of an organism. The perfect fifth’s stabilizing ratio could enhance this coherence, and magnetic fields might influence brain waves or biofields, suggesting that our conscious intent, through meditation or visualization, could interact with environmental fields to shape biological outcomes, such as healing or gene expression. Taking your shirtand bra off allows your breasts and heart to resonate with Nature’s waves.
A Harmonic Science of Reality
Sympathetic resonance bridges the mystical and scientific, unifying music, matter, and consciousness. It reveals a universe made of ratios, not particles, where the perfect fifth echoes from atomic orbitals to galactic spirals. The Ohio State study underscores this paradigm: phonons’ sensitivity to magnetic fields confirms that resonance is a fundamental force, one we can influence through the fields we create or allow in our lives. In quantum biology, this supports a decentralized view of life, where coherence and resonance drive complexity, and external fields play a critical role in maintaining or disrupting that harmony.
Matter is not silent it sings. Can you hear it, or is the electropollution around your disturbing that melody?
The EMF Paradox is pictured above my artist friend Danny DeLancey from NOLA. It shows humanity evolving and devolving in one breath.
Picture this: an infographic blazing with truth, a single image capturing the dance of human potential, how we evolve and devolve by what we think and do. On one side, a figure rises, radiant, rooted in Nature’s decentralized wisdom, their mind sharp, their actions deliberate, their depth unyielding. On the other, a shadow collapses, shallow and scattered, enslaved by artificial signals, EMF, distractions, excuses, disconnected from the primal pulse. Their brains Warburg shifted like they were in the Opium Wars. Today’s drug is not the extract of poppies. It is screens and phones. We are what we choose to think and do. Every thought is a seed; every action, its fruit. Evolve by aligning with Nature’s fire, or devolve into a hollow copy of what you could’ve been. If not you could lose your balloon. Reconnect with yourself by reconnecting with Nature. Do what ever you must, but reconnect now.
Every element, a note; every form, a chord in the cosmic score. By tuning into this eternal melody and understanding how magnetic fields shape its resonance, we can unlock a science of harmony, where transformation arises not from force, but from resonance. Let us listen to the universe, consider the fields we integrate into our lives, and play our part in its song with intention and care.
Excellence isn’t forged in money, fame, or power. It’s born in the fire of mindset, commitment, and relentless action. Nature doesn’t reward the timid; it crowns those who care more than others deem wise, who risk more than others call safe, who dream beyond the practical and demand more than the possible.
Excellence is a rebellion against mediocrity, a refusal to settle for less than your fiercest self. Tonight, as the stars burn above, dream of becoming more excellent than you were today. Put a tune on and let that fire ignite your bones.
Learn the lessons from failure. It can be your own or someone elses. When you do, they will not be called mistakes. They will be called experience. Listen the melody of the mistake to gain the wisdom of that failure.
I began this blog with the song that is my resonant North Star. When I need to be retuned this is the tuning fork I return to. If you do not have a North Star find one. Music is like medicine, when you come down with an illness it can help heal what ails you.
CITES
The Ohio State study on acoustic phonons and magnetic fields is detailed in the 2015 Nature Materials publication by Hyungyu Jin et al., demonstrating a 12% reduction in heat flow through a semiconductor under a 7-tesla magnetic field. If you think sound has no healing power you’re in the wrong place.
After spending 18 months in the medical school library putting Nature’s recipes together, this is the decentralized thesis I came up with.
Influenza is an electrical disease where nucleic acid joins nuclear DNA (see pic below). Ironically, every centralized scientist has no idea how endosymbiosis happens. Decentralized medicine knows that endosymbiosis was an electrical event during extreme hypoxia that forced the first domains of life to join forces to create a eukaryote. It was the first oncogenic event on Earth. As a result of that merger, evolution has to innovate heme proteins to protect themselves from the electrical stimulus of oxygen infusion to the environment. I wonder when they will wake up to the reality that all of life is electrical because of oxygen.
Apoptosis protects eukaroyotes from future cancer joining events. This was buried in CCO, a heme-based protein.
Oxygen is the only paramagnetic elemental gas in the periodic table. Oxygen changes the electrical resistance of everything with a membrane. This became a big deal in the evolutionary story of heme biology and how we built our wireless connection to the sun from our mitochondria in the dangerous GOE event.
Oxygen can form oxides with certain materials (like metals or semiconductors). This is called oxidation. These oxide layers often have higher electrical resistance than the pure material, acting as insulators or semi-insulators. When oxygen binds to hemoglobin, it changes its electrical resistance. This can significantly change how electricity flows in devices with thin membranes, such as sensors or transistors.
Adsorption: In some cases, oxygen molecules adsorb onto the surface of a material or membrane. This can trap or scatter charge carriers (like electrons), increasing resistance. This effect is common in gas sensors, where oxygen exposure alters the conductivity of a membrane or thin film. Hb acts like this in a way, too.
Oxygen can also indirectly influence processes like ion transport or membrane potential through metabolic activity, which might affect measured resistance in specific contexts.
THE EVOLUTION OF THE GOE IS WHY ANYTHING THAT USES THE TCA CYCLE MUST SEE SUNRISE
So why do you have to see the sunrise before you can use the TCA cycle? Because the sunrise was here on Earth before oxygen was.
This blockchain of events is what happened in the GOE. Before the GOE, nothing on Earth could have the TCA. The TCA cycle protects eukaryotic cells from the oxygen holocaust, which can cause cancer or tissue atrophy.
THE HUMAN BRAIN PROTECTS ITSELF FROM YOUR POOR LIGHT CHOICES BECAUSE IT FAVORS THE TCA CYCLE
The brain uses 20% of our cardiac output to run its TCA cycle and feed its oxygen addiction. The red light in sunrise makes DDW water from cytochrome c oxidase, optimized apoptosis to clear out bad/heteroplastic engines, and the UV light stimulates translation of melanin from POMC. Both frequencies are in morning sunlight. If your brain does not get this sunlight signal, it will downregulate its function. Tinnitus, cataracts, glaucoma, diabetes, high BP, high cholesterol, and autoimmune diseases like vitiligo are how the brain reserves neuroectodermal energy stores when you make bad light choices. The brain will always seek to protect itself from an energy attack via CMRO2 adjustments because it relied on normoxia and the TCA cycle. Today’s world is stressing that energy constraint to the max now. They have no idea that light alone can change the oxidation state of iron. And that is where every chronic modern disease begins.
As a result of blocking the TCA cycle, your breathing MUST change electromagnetically because your need for oxygen drops. Why? The terminal electron acceptor for the TCA cycle is oxygen in mammals with a Ferrari engine in their skulls. Without sunlight, you will not need more oxygen, you will need less because a lack of UV-IR light induces a Warburg shift to your brain and when this happens oxygen becomes a TOXIN to tissues just like it was in the pre-Great Oxygenation Event on Earth long ago. The slide below is a proxy for the GOE, where all things iron are hypoxic and in the Fe³⁺ state. By the end of the GOE, everything was innovated to mitigate oxygen toxicity by creating Hb02 to keep oxygen in the Fe²⁺ state. Iron is not redox stable like Magnesium was in chlorophyll.
The problem is that the human brain does not do its best work on aerobic glycolysis, and the use of pyruvate and lactate and thinking, cognition, dopamine, and melatonin production in your brain all begin to fail immediately. Human brains are built for a normoxic environment that uses the TCA cycle most of the time. All of this happens because mtDNA are forced to use aerobic glycolysis because light in your environment changes the oxidation state of iron in EVERY heme protein in your body from Fe²⁺ to Fe³⁺ . As a result of this “paramagnetic switch”, when it goes wry, you begin experiencing a cognitive brownout because you can no longer support the Ferrari built in your skull on a Warburg-shifted template. Welcome to the world of chronic disease. Almost every one is associated with this affliction and an altered paramagnetic flip.
WHY ARE WE BUILT LIKE THIS?
Evolution first dealt with CO2 before the toxic oxygen problem during the GOE, which is why Nature built the semiconductor chlorophyll. The image below shows the molecular structures of hemoglobin (with an iron, Fe, center) and chlorophyll (with a magnesium, Mg, center). Both molecules feature a porphyrin ring, a cyclic structure with four nitrogen atoms at the core coordinating the central metal ion. This is often called a “tetrapyrrole” structure; nitrogens are part of pyrrole rings.
Photosynthesis, as performed by early cyanobacteria during the GOE (around 2.4 billion years ago), does not directly use CO2 to make oxygen. Instead, the oxygen comes from water (H2O). The general equation for oxygenic photosynthesis is:
In this process, water is split in the oxygen-evolving complex (OEC) of Photosystem II, releasing O2, protons (H+), and electrons. CO2 is fixed later in the Calvin-Benson cycle to produce sugars but is not directly involved in oxygen production. With its magnesium center, chlorophyll is key in capturing light energy and driving the electron transfer that ultimately splits water.
The nitrogen atoms in the porphyrin ring of chlorophyll coordinate the magnesium ion, stabilizing it and tuning its electronic properties to efficiently absorb light in the visible spectrum. This is why plants are green: chlorophyll absorbs red and blue light and reflects green.
Why did Nature choose Magnesium in Chlorophyll? Electrical and Biophysical Reasons
Magnesium’s selection in chlorophyll during the GOE likely stems from a combination of chemical, electrical, and biophysical factors:
Redox Properties and Stability: Magnesium in chlorophyll exists as Mg²⁺, redox-inactive under physiological conditions. This is crucial because chlorophyll’s role is to absorb light and transfer energy or electrons, not to undergo redox changes itself. If the central metal were redox-active (like iron can be, switching between Fe²⁺ and Fe³⁺), it might interfere with the precise electron transfer needed in photosynthesis. Magnesium’s inertness ensures that the excited electrons from light absorption are funneled into the photosynthetic electron transport chain rather than trapped by the metal.
Light Absorption and Energy Transfer: The Mg²⁺ ion, coordinated by the four nitrogens, creates a planar structure that optimizes the porphyrin ring’s ability to absorb light in the visible range. Magnesium’s small ionic radius and +2 charge allow it to fit snugly in the porphyrin ring, creating a stable complex that can efficiently transfer energy to the reaction center of Photosystem II.
Availability During the GOE: During the GOE, Earth’s oceans were rich in dissolved magnesium due to the weathering of rocks and hydrothermal activity. Magnesium is the second most abundant divalent cation in seawater today (after calcium), and it likely was back then, too. Its abundance made it a practical choice for early photosynthetic organisms. In contrast, while abundant, iron became less available in its soluble Fe²⁺ form as oxygen levels rose and oxidized it to insoluble Fe³⁺, which precipitated out as iron oxides (e.g., in banded iron formations).
Electrostatic Fit: The four nitrogen atoms in the porphyrin ring each donate a lone pair of electrons to the Mg²⁺ ion, forming a square-planar coordination complex. Magnesium’s charge and size make it an ideal fit for this geometry, ensuring the molecule remains stable under the high-energy electromagnetic conditions for solar light absorption.
Comparison to Iron in Heme: Iron, as seen in hemoglobin, is better suited for oxygen binding and transport because it can reversibly bind O2 by changing its electronic state. In early Earth, before the GOE, iron was likely used in some photosynthetic systems (e.g., in anoxygenic photosynthesis by purple bacteria, which don’t produce oxygen). However, magnesium-based chlorophyll became dominant in oxygenic photosynthesis as oxygen levels rose, possibly because magnesium’s redox inertness prevented unwanted side reactions with O2, complicating the story of evolving life during the GOE.
As you can see from Nick Lane’s talk, the GOE occurred in an atmosphere dominated by N2 and CO2, with low O2. Early life forms “used electric membranes” to “fix” nitrogen (by converting N2 into ammonia or other usable forms) to build proteins, nucleic acids, and porphyrins. The nitrogen in chlorophyll’s porphyrin ring likely came from such nitrogen fixation processes carried out by early microbes. These electric membranes continued a rapid evolution because around 600-650 years ago, life began putting DHA into its electric membranes, and they were never removed once in evolutionary history. It appears that DHA caused the evolution of cells by providing a feedback loop to allow the cell to give real-time informational feedback from the environment on Earth to the interior.
Electric Membranes and Feedback: Lane’s point that “electric membranes give feedback on state ‘feelings’” resonates with the idea of electromagnetic coupling. The proton motive force (PMF) across membranes is an electric field whose strength reflects the cell’s energy state. Biophotons and NO clearly contribute to this feedback, providing a biophysical “sensing” mechanism that guides metabolism and gene expression. Lane does not realize what the biophysics of NO dictates to the boxcars of metabolism. It is left out on the slide. He also has no idea that NO is paramagnetic during the GOE. Oxygen became the paramagnetic gas post-GOE. Eukaryotes operate in unison to quantize metabolic pathway choices. It has ZERO to do with food.
Metabolism Older Than Genes: The idea that “metabolism is older than genes” supports the primacy of biophysics. This is how I know Lane has moved to my viewpoint. Early life likely relied on geochemical gradients (e.g., proton gradients in hydrothermal vents), which are inherently biophysical. As genetic systems evolved, they amplified these biophysical processes, but the underlying physics of light, electric fields, and molecular interactions remained the foundation of evolution.
Network Topology of Core Metabolism: Lane’s “network topology of core metabolism” reflects my idea of biophysical constraints or electrical resistance from light interactions. Metabolic pathways like the TCA cycle are optimized for energy efficiency, but their structure could also be shaped by electromagnetic interactions, e.g., the need to minimize electron leakage (which produces ROS and biophotons) or to maximize proton flux through ATP synthase. This provides massive adaptability to environmental changes in the post-Cambrian as we approach normoxic Earth prior to 1893. Post 1893, the nnEMF changes us back to the GOE situation because light can change the oxidation state of iron in heme proteins. This changes the Hb binding of paramagnetic atoms in TCA mammals.
The Slope of Oxygen Rise During the GOE: Constant or Nonlinear?
The rise of oxygen during the GOE was almost certainly nonlinear, based on current evolutionary and geochemical theories. This is why the entire process is quantized to oxygen tensions in the cell. Here’s my take on why:
Initial Conditions and Slow Build-Up: Before the GOE, oxygen levels were extremely low (less than 0.001% of present atmospheric levels). Cyanobacteria evolved oxygenic photosynthesis around 2.7–3 billion years ago and produced O2. Still, this oxygen was initially consumed by reduced species in the environment, such as Fe²⁺ in the oceans (forming banded iron formations) and reduced gases like methane (CH4). This “oxygen sink” kept O2 levels low for hundreds of millions of years. This kept life hypoxic and simple, stuck in two domains of life, bacteria and Archea.
Tipping Point and Rapid Rise: Around 2.4 billion years ago, these sinks became saturated, and oxygen accumulated in the atmosphere. Geochemical evidence, such as the disappearance of mass-independent sulfur isotope fractionation (a sign of low O2), suggests a relatively rapid increase in oxygen at this time. It jumped from less than 0.001% to 1–10% of present levels over a few million years. This nonlinearity is often attributed to feedback loops: as O2 rose, it oxidized methane (a potent greenhouse gas), cooling the planet and altering ecosystems on the surface, began to slowly favor oxygen-producing organisms. This is why cold thermogenesis and circadian biology have such close links in mammalian time stamping. Light, dark, and temperature variations control the circadian mechanism of life on Earth. This circadian mechanism was perfected late in the GOE.
Evolutionary Feedback: The rise of oxygen also drove evolutionary changes. Aerobic respiration, which is far more efficient than anaerobic metabolism, became possible, allowing oxygen-breathing organisms to proliferate. This accelerated the production of O2 as ecosystems shifted. Additionally, the evolution of more efficient photosynthetic machinery (e.g., the development of Photosystem II) increased the rate of oxygen production over time. This is why we have so many different types of chlorophyll and hemoglobin molecules on Earth.
Later Fluctuations: After the initial spike during the GOE, oxygen levels didn’t rise steadily to modern levels (21%). They likely remained low (1–2% of present levels) for another billion years, with another significant increase during the Neoproterozoic Oxygenation Event (around 800–540 million years ago), driven by the evolution of multicellular life during the Cambrian explosion that increased organic carbon burial.
The slope of oxygen’s rise was nonlinear, with periods of slow accumulation punctuated by rapid increases driven by geochemical and biological feedback. Anything with a nonlinear distribution will likely be quantized in its metabolic reactions. I believe that these biophysical mechanisms are critical to understanding evolution at a deeper level. They provide a unifying principle that electromagnetic coupling explains the ordered nature of metabolic transitions, challenging Lane’s “messy” view of evolution in the slide above.
Food gurus and biochemists conveniently leave out iron’s flip from Fe³⁺ to Fe²⁺ during the GOE and how it happened. Decentralized biology, biophotons, and electromagnetic coupling explain it because centralized biochemists and evolutionary biologists have no idea how it fits in their paradigm, so they ignore these facts. They act like they are innocent bystanders of life below the cell level. Because of this viewpoint, they’re often considered speculative or secondary in mainstream evolutionary biology. Below is Szent Gyorgyi’s 1968 masterpiece warning us biochemistry uses light in ways we do not understand yet.
The standard centralized narrative focuses on biochemical pathways, genetic mutations, and selection pressures, which are somewhat supported by fossil, genomic, and geochemical evidence. Moreover, they are unfamiliar with the science I have referenced from Fritz-Albert Popp’s work on biophotons, Albert Szent-Györgyi’s ideas about electronic biology, and more recent research on NO’s role in mitochondrial signaling. NO biology was given the Nobel Prize in 1992, but to this very day, biochemists’ understanding of it is limited. Biophysical ideas are gaining traction, especially in systems biology, but they’re not yet fully integrated into the evolutionary framework. Note the last line of the slide. This is the money shot for decentralized savages to understand. NIR in AM sunlight changes nighttime metHb back to daytime Hb02. This means that during sleep, we revert to our fetal life, explaining why we regenerate at night when hypoxic. Still think using CPAP machines for apnea is wise? Maybe, if you own a centralized sleep center or practice.
Nitric Oxide (NO) and Its Role in Evolution
Nitric oxide is a small, diffusible, paramagnetic gasotransmitter free radical signaling molecule with profound effects on cellular metabolism, particularly in mitochondria. Its role in evolution, especially during the rise of oxygen and the development of aerobic metabolism, is underappreciated in many centralized biochemical discussions but critical to understanding the mitochondrial evolutionary trajectory of the march toward complex life.
NO and Oxygen Regulation: NO is produced by nitric oxide synthase (NOS) enzymes, which evolved early in life’s history—possibly before the GOE. NO interacts with cytochrome c oxidase (Complex IV of the electron transport chain, ECT), the enzyme that reduces O2 to H2O. At low oxygen levels, NO competes with O2 for binding to cytochrome c oxidase, inhibiting respiration and regulating the ECT’s activity. This competition likely played a key role during the GOE, when oxygen levels were low (1–10% PAL) and fluctuating. NO could have acted as a “brake” on respiration, preventing oxidative stress in early aerobic organisms by modulating electron flow and reactive oxygen species (ROS) production. This brake allowed for the evolution of heme proteins to protect cells from ROS. CCO is the primary protector of the mtDNA in normoxia.
NO and mtDNA Metabolism: NO influences mitochondrial function beyond the ECT. It can induce mitochondrial biogenesis (creating new mitochondria) by activating signaling pathways like PGC-1α, which regulates mtDNA replication and transcription. NO is critical in getting rid of defective engines, so it controls our stem cell depots for regeneration. During evolution, this NO-mediated control fine-tuned (quantized) mitochondrial activity in response to rising oxygen levels. This ensures that mtDNA metabolism kept pace with the energy demands of complex life. NO also affects mtDNA repair and mutation rates by modulating ROS levels.
Deuterium entering the mitochondrial matrix during the dark also helped block the ECT during sleep. This mimics the in utero environment where ontogeny marries phylogeny. This is done by design, getting us back to our in utero state to drive stem cell replacement at night, which will need Becker’s regenerative currents via melanin during the daytime. Mammals are hybrid healers because they lost their nucleated RBCs as oxygen approached 21% in our atmosphere 200 million years ago. Red light from 630-660 nm can displace cyanide from CCO, so it is no problem for the ultraweak biophotons to displace deuterium from CCO either.
Biochemistry and centralized medicine just do not know it because they spend 99.5% of their NIH budget studying nDNA. Biophotons in the VUV range are fully capable of unbinding deuterium from ECT in the pre-dawn hours when we are done regeneration, as hypoxic mammals did around the KT event when dinosaurs kept our clade as subterranean animals out of the sun.
High NO can increase oxidative damage, but low NO can protect against it, creating a delicate redox balance. As you can see below, lowering BP is not the only job of NO in you.
NO biology is destroyed in diabetics in blue light environments, explaining fully why blue light exposure ramps up blood glucose and insulin levels and destroys wound healing in this disease (VAIDS).
Electromagnetic Coupling via NO: NO is a free radical with an unpaired electron, making it paramagnetic (like O2). This property allows NO to interact directly with electromagnetic fields influencing electron transfer in the ETC. Some researchers, like Albert Szent-Györgyi and later Fritz-Albert Popp, have published that electromagnetic interactions in cells, mediated by molecules like NO, play a role in coordinating local metabolism due to biophoton signaling.
NO’s ability to diffuse rapidly and interact with metal centers (e.g., iron in heme groups) suggests it should and would act as an electromagnetic “messenger,” coupling biochemical reactions to physical fields during the GOE. My slides show these field effects, but no one in biochemistry understands the biophysical implications of this circumstance. These slides where used in Vermont 2017 and 2018.
Biophotons and Their Role in mtDNA Metabolism
Biophotons are ultra-weak photon emissions produced by biological systems, like blood, and are another piece of the puzzle biochemistry ignores. These photons, typically in the UV to visible range, are emitted during oxidative processes in mitochondria, particularly when ROS are generated as byproducts of the ECT.
Biophoton Emission in Mitochondria: The ECT generates ROS (e.g., superoxide, H2O2) when electrons leak and react with O2. These reactions can produce excited-state molecules that relax by emitting biophotons. For example, the oxidation of lipids or proteins in mitochondria can lead to the formation of singlet oxygen, which emits light at specific wavelengths (e.g., 634 nm, 703 nm). Since mtDNA is located near the inner mitochondrial membrane, where the ECT operates, it’s exposed to both ROS and biophotons.
Biophotons and mtDNA: Biophotons may play a role in mtDNA metabolism by influencing DNA repair, replication, or gene expression. Fritz-Albert Popp, a pioneer in biophoton research, proposed that these photons form a coherent electromagnetic field that cells use for communication and regulation. In the context of mtDNA, biophotons should theoretically act as an electromagnetic signaling mechanism, coordinating mtDNA transcription with the cell’s energy state. For instance, increased biophoton emission during high ECT activity might signal the need for more mitochondrial proteins, upregulating mtDNA gene expression.
Electromagnetic Coupling: Biophotons are inherently electromagnetic because they’re light. Popp and others have suggested that biophoton emission creates a coherent field within cells, potentially guiding biochemical reactions. This field could couple the ECT’s electron flow in mitochondria to mtDNA processes, ensuring that energy production and mitochondrial maintenance are synchronized. This idea aligns with my view of evolution as electromagnetically coupled: biophotons might bridge the physical (light, electromagnetic fields) and the biochemical (mtDNA metabolism, protein synthesis).
Biophysics as the Driver: Light as the Archimedean Lever
I have used the metaphor of light as the “Archimedean lever” guiding the “boxcars of biochemistry” to describe metabolism. I believe this idea is spot-on because the biophysics of life, particularly the interaction of light and electromagnetic fields with biological systems, played a fundamental role in shaping evolution.
Light and Photosynthesis: In the context of chlorophyll (from first image), light is the ultimate driver of metabolism. Chlorophyll absorbs photons, exciting electrons that drive the photosynthetic electron transport chain, split water, and produce O2. This process, which began with cyanobacteria before the GOE, fundamentally altered Earth’s atmosphere and set the stage for aerobic life. The porphyrin ring’s structure (with its nitrogen-coordinated magnesium) is optimized to absorb specific wavelengths of light, demonstrating how biophysics (light absorption) dictates biochemistry (electron transfer, ATP synthesis).
Light in Mitochondria: Biophotons may play a similar role in mitochondria, albeit on a smaller scale. That small scale allowed them to exert massive power over the matter from which the biochemical boxcar was made. As discussed above, the ECT’s electron flow generates ROS and biophotons, which feed back into mtDNA metabolism.
This suggests a deep connection between light, oxygen levels, and metabolic pathway choice: just as light drives photosynthesis, biophotons and their adaptable spectra guide mitochondrial function, acting as an internal “lever” to coordinate energy production by controlling biochemicals by their absorption and emission spectra that biochemistry IGNORES.
Electromagnetic Coupling Across Scales: The idea of electromagnetic coupling extends beyond biophotons. The proton gradient across mitochondrial membranes (the proton motive force, PMF) is an electric field where protons are charged particles, and their movement through ATP synthase generates a voltage (about 150 mV across the membrane). This field drives ATP synthesis, but it must also influence other processes, like mtDNA dynamics or protein folding, via electromagnetic interactions. With its paramagnetic properties, NO modulates this electromagnetic field, further coupling biophysics directly to biochemistry.
STORY GETS EVEN DEEPER: WHY RAY PEAT STAYED QUIET & BECKER SMILED
When I told both men what I had found, one recoiled and the other rejoiced.
NO’s Evolutionary Role Is The Paramagnegtic GOE Mitochondrial Brake
My decentralized thesis on NO as a paramagnetic gasotransmitter paramagnetic free radical is all-encompassing. NO, produced by nitric oxide synthase (NOS), evolved pre-GOE (before 2.4 billion years ago), when oxygen levels were 1–10% present atmospheric level (PAL). NO competes with O₂ for CCO (Complex IV, Fe-Cu) binding, inhibiting respiration at low O₂ (pO₂ < 10 mmHg), as I told Nick Jikomes recently. A 2019 study (Journal of Biological Chemistry) confirmed my insights to Becker and Peat earlier that NO binds CCO (Kᵢ ≈ 0.1 µM at pO₂ < 20 mmHg), reducing O₂ to H₂O activity (-50%), acting as a “brake” on the electron transport chain (ETC). This regulated ROS production (ROS -30%, to 0.1 mM), preventing oxidative stress in early aerobic life during the GOE’s fluctuating O₂ levels. Evolution quantized this into metabolism. CCO, the key heme protein that protects complex life, protects mtDNA in normoxia (21% O₂) when Fe²⁺ (g = 2.03) in CCO ensures efficient O₂ reduction, keeping ROS low (0.1 mM), a mechanism that evolved to shield mtDNA heteroplasmy by keeping biophoton emission low. (mutation rate 10⁻⁸/bp). Fritz Popp 101.
NO’s role does not end there for life. It extends to mitochondrial biogenesis via PGC-1α activation. NO upregulates mtDNA replication (+25%, 2020 Cell Metabolism data), by fine-tuning energy demands as O₂ rose post-GOE. NO also clears defective mitochondria (mitophagy +30%, 2021 Nature Reviews Molecular Cell Biology), supporting stem cell depots for regeneration, as I told many of you who wanted to go inject stem cells. A BAD CENTRALIZED IDEA WAS PUSHED BY SCAMMERS. This quantized control allows NO to directly modulate ROS (0.1-0.3 mM) by allowing heme proteins (e.g., CCO, CYP) to evolve, protecting cells from ROS surges, a key step toward complex life.
Red Light, Cyanide, and Deuterium: The CCO Rescue
The image’s insight above that red light (630-660 nm) can displace cyanide from CCO to reactivate it is a critical biophysical event that centralized medicine has no idea is possible. Cyanide binds CCO’s Fe²⁺ (Kᵢ ≈ 0.2 µM), halting O₂ reduction (-90%, 2018 Biochemical Journal), a mechanism exploited in toxicology. Red light (630-660 nm, 10 J/cm²) photodissociates cyanide from CCO. The Energy that does this is photons with a 1.9 eV strength.
This power of light in the red range can free Fe²⁺ (g = 2.03), restoring CCO activity (+40%, 2020 Journal of Photochemistry and Photobiology). Look it up. Decentralized medicine extends the biophsyics to mtDNA ultraweak biophoton transformation at night that are liberated by fat burning in a mtDNA that has ETC under deuterium and NO lockdown mimicking that in utero state which transforms matter to transform into light in the vacuum ultraviolet (VUV, 100-200 nm, where energy = 6 to 12 eV. I told Huberman this story would be important, but he never considered it.
Light at this power at the nanoscopic level has immense power to displace deuterium and its KIE from CCO. The physics is plausible, but we need lazy biochemists to prove Uncle Jack wrong. Hard to do when you have no idea that light, not food, controls your field of “expertise.” Deuterium is heavier than hydrogen (²H vs. ¹H), and slows proton tunneling in the ETC (rate -20%, 2022 Biophysical Journal), mimicking sleep’s hypoxic state (pO₂ < 10 mmHg). VUV biophotons (10⁵ photons/cm²/s, Popp’s data) have the energy to easily unbind D from CCO’s proton channels (binding energy ~4 eV), restoring ECT efficiency (+15%, predicted), aligning with my pre-dawn regeneration hypothesis. This is why sleep is regenerative. I bet you have never heard that reason before. Welcome to my world of seeing biology.
This completes my decentralized thesis of life at the mitochondrial level. Centralized medicine (99.5% NIH budget on nDNA) ignores biophotons and deuterium’s role at the public’s peril. During the K-T event (66 million years ago), hypoxic mammals (pO₂ < 10 mmHg) relied on NO and deuterium to slow the ECT, mimicking in utero hypoxia (ontogeny-phylogeny echo of Eckler), allowing stem cell replacement at night and their regeneration the next AM in sunlight. Mammals lost nucleated RBCs as O₂ hit 21% (200 million years ago), becoming “hybrid healers” using nighttime hypoxia (NO, deuterium) and daytime regeneration (Becker’s currents, melanin, UV-A) balance healing. Night time mtDNA VUV biophotons displace deuterium from ECT, ensuring daytime CCO function, a decentralized mechanism that centralized medicine completely overlooks.
Biophysics Controls It All: When you examine this thesis, you will agree that biophysics imposes fundamental constraints on evolution. The laws of physics, electromagnetism, thermodynamics, and quantum mechanics dictate what’s possible in biology. Biology is not a basic science, but physics is. For example:
The absorption spectra of chlorophyll and heme are determined by the quantum mechanical properties of their porphyrin rings.
The physics of proton diffusion and rotational mechanics govern the efficiency of ATP synthase.
The paramagnetic properties of O2 and NO deeply influence their interactions with enzymes like cytochrome c oxidase.
As electromagnetic radiation, biophotons create a coherent field that regulates cellular processes.
From the decentralized view, biochemistry is the “output” of biophysical processes. Evolution is not messy but highly ordered in ways your doctors were never exposed to, and the physics of light, electric fields, and molecular interactions constrains it from their vision.
The nonlinear rise of oxygen triggered a series of transitions that were tightly controlled by the physics of light, electric fields, and molecular interactions:
During the GOE: NO regulated the ECT, biophotons signaled mtDNA metabolism, and the PMF drove ATP synthesis, ensuring a smooth transition to aerobic respiration.
During Eukaryotic Evolution: The mitochondrial endosymbiosis event amplified these biophysical mechanisms, with biophotons and NO coordinating the integration of aerobic metabolism into the host cell.
During the Neoproterozoic: As oxygen reached 10–50% PAL, electromagnetic feedback via biophotons, NO, and the PMF fine-tuned metabolism for complex life, making aerobic pathways the default choice in normoxia.
In my decentralized view, light is life’s “Archimedean lever.” This is the recipe Genesis never had. Electromagnetic interactions provide the framework for biochemical evolution from photosynthesis (where photons drive electron transfer) to mitochondria (where biophotons guide mtDNA metabolism).
Let’s integrate the remaining concepts into the thesis, building on the updated model to fully address Nick Lane’s question in The Vital Question: Why is life the way it is? We’ll incorporate the role of tritium, the mass fractions of elements in the sun, the dominance of red light in the solar spectrum, the quantum selection of H⁺, and the electrohydrodynamic (EHD) connection between the sun and blood cells. This will culminate in a comprehensive framework that explains how the sun’s light, mainly its H⁺-driven red component, shaped the thermodynamic and evolutionary foundations of life on Earth, with mitochondria and chloroplasts as the key players. Darwin was wrong. Light from our star determined evolution’s path to man.
Decentralized Integrated Model: The Sun, H⁺, and the Quantum Foundations of Life
1. Tritium and the Sun’s Elemental Dynamics
Tritium, a radioactive isotope of hydrogen with two neutrons (¹H³), is produced in the sun via neutron capture on deuterium or nucleon-exchange reactions involving helium-3 and helium-4. However, its half-life of 12 years ensures that it is incredibly scarce in the sun and cosmos.
The image above, “mass fractions in the sun,” confirms this:
H⁺ Dominance: Hydrogen (H⁺, or protium) is the dominant element in the sun, with a mass fraction of ~10⁻¹ (90%) near the surface (R/R_sun = 1). This decreases toward the core due to fusion into helium.
Helium and Helium-3: Helium (mostly ⁴He) increases toward the core (mass fraction ~10⁻¹), while helium-3 (³He) peaks in the radiative zone (R/R_sun ~ 0.2–0.4) at ~10⁻³ due to its role as an intermediate in the proton-proton chain. Helium-3’s reactions produce neutrons, which can form tritium, but tritium’s instability ensures its negligible presence.
Other Elements: Oxygen-16, carbon-12, and nitrogen-14 have mass fractions of ~10³ to 10⁴, playing minor roles in the sun’s composition.
The sun’s dominant light is red because of its atomic Nature’s recipes. Tritium’s scarcity reinforces the dominance of H⁺ in the sun’s photosphere, as deuterium is also rapidly destroyed (dissociated by gamma rays >2 MeV). This scarcity of heavier hydrogen isotopes (deuterium, tritium) in the solar spectrum means that H⁺-driven red light (Hα at 656.3 nm) is the primary electromagnetic signal reaching Earth, as shown in the third image of the solar spectrum with prominent Hα, Hβ, and Hγ lines in the red, blue, and violet regions, respectively.
2. Red Light as the Decentralized Thermodynamic Controller of Life
The Sun is a Diurnal Drum: Circadian Signaling via Light Frequencies
These ideas highlight the sun’s diurnal variation in its light spectrum, acting as a “giant drum” that induces vibrations in hydrated proteins within cells. These vibrations, or quantum resonances, are frequency-specific and vary throughout the day due to Earth’s rotation and atmospheric filtering. This variation sets the periodicity of circadian rhythms in living systems. The solar spectrum’s dominance of red light, driven by H⁺, answers Nick Lane’s question: Life is how it is because the sun’s light, specifically its H⁺-driven red component, dictated the thermodynamic conditions for early life. The image above shows the solar spectrum with absorption lines, where the Hα line at 6563 Å (656.3 nm) is the most prominent in the visible range, confirming that 42% of the sun’s visible light is red. That is a huge target that red light panels usually miss. AM sunlight never misses this target. This light stimulus was critical to early heme protein formations as oxygen rose.
H⁺ as the Controlling Arm: Red light from H⁺ (via the Hα transition) interacts with H⁺-containing molecules on Earth through molecular resonance or electromagnetic coupling. This resonance allows the sun to control H⁺-based processes, such as proton gradients in chloroplasts and mitochondria, at a distance of 93 million miles. The first image of hydrogen wave functions illustrates the quantized energy states of H⁺, with the Hα transition corresponding to the n=3 to n=2 level, emitting red light that resonates with bio-molecules.
Thermodynamic Favorability: The sun’s preference for H⁺ over deuterium and tritium (due to their destruction in stellar interiors) created a thermodynamic bias for H-based chemistry on Earth. Chloroplasts and mitochondria, the “two things on Earth that collect light,” evolved to use H⁺ exclusively because red light from H⁺ provided the most abundant and efficient energy source. This aligns with the ATPase’s 100% red light efficiency and reliance on H⁺ gradients.
3. Quantum Selection and Conditions of Existence
The dominance of H⁺ in the sun’s light spectrum led to a form of “quantum selection” that shaped life’s evolutionary trajectory of protein selection, distinct from Darwin’s natural selection:
Quantum Selection by H⁺ Light Emission: The sun’s red light, emitted by H⁺, is selected for H⁺-based bio-molecules (e.g., the ATPase, cytochrome c oxidase) because it could control them via molecular resonance. Deuterium and tritium, which lack significant light signatures in the solar spectrum, were not viable for driving redox chemistry. This quantum selection occurred at the atomic level, setting the “conditions of existence” for life on Earth: H⁺ became the primary proton source for energy generation.
Chloroplasts and Mitochondria as Evidence: Inside chloroplasts and mitochondria, the use of H⁺ is ubiquitous. Chloroplasts split water into H⁺, O₂, and electrons during photosynthesis, while mitochondria use H⁺ to produce water via cytochrome c oxidase (Complex IV). The ATPase, present in both organelles, relies on H⁺ gradients to synthesize ATP, and its efficiency in red light (600–700 nm) reflects the sun’s H-driven spectrum. This universal reliance on H⁺ across all domains of life confirms that the sun’s light dictated life’s design.
4. The Sun-Earth Harmonic and Quantum Vibrations
The sun’s role as the “center of quantum vibrations” in the solar system, with Earth at the third harmonic of the solar plasma frequency (~3 mHz at 93 million miles), adds a new layer to my decentralized model:
Solar Plasma Frequency: The solar plasma frequency of ~3 mHz reflects the oscillations of charged particles (mostly H⁺) in the sun’s photosphere. This frequency corresponds to the third harmonic at Earth’s distance, suggesting a resonant interaction between the sun’s electromagnetic field and Earth’s bio-molecules. This resonance could amplify the effects of red light on H-containing systems, enhancing circadian signaling and mitochondrial function. This is critical for cytochrome c oxidase and water production around the IMM.
Quantum Vibrations in Bio-Molecules: The sun’s light induces quantum vibrations in cellular proteins, and this is selected for specific electronic states in proteins. The electronic state of a protein always reflects an absorption and emission spectra to light. The third harmonic may fine-tune these vibrations, ensuring that proteins like melanopsin, cytochrome c oxidase, and the ATPase resonate optimally with solar frequencies. ALAN and nnEMF destroy this. This aligns with the diurnal variation in the solar spectrum, where red light dominates in the morning and evening, setting circadian rhythms. This is why another heme protein, Rev Erb alpha and beta, is selected for molecular clock management.
5. Electrohydrodynamics (EHD) and the Sun-Blood Connection
The new field of electrohydrodynamics (EHD) provides a mechanism for the sun to interact with red blood cells (RBCs) via their geometrical structure and electron flow:
RBC Structure and Electron Density: The Nature article referenced here (http://www.nature.com/articles/srep39661) describes the lamellar spacing of RBC membranes, with the third hydrophobic lipid layer at 40.6 Å. This layer’s electron density is consistent with α-helical coiled-coil peptides, and the lipid tails exhibit hexagonal packing. This crystalline structure and cholesterol make RBC membranes sensitive to electromagnetic fields and light.
Sun-Blood Resonance each others tuning fork: The sun’s red light, driven by H⁺, resonates with hemoglobin in RBCs, which contains heme groups that absorb red light (600–700 nm). Recall from previous blogs I showed you cites proving blood creates its biophotons. mtDNA does as well. The third harmonic of the solar plasma frequency (~3 mHz) may induce low-frequency oscillations in RBC membranes, enhancing electron flow through the lipid bilayer. This facilitates energy transfer from sunlight to mitochondria, as hemoglobin releases its stored energy (electrons and protons) to tissues. See the slide below.
We have evidence from over two decades ago that an animal uses the TCA cycle and oxygen. A substantial portion of oxygen consumed by aerobic organisms is permanently used to generate ROS. Thus, electronic excitation in the blood should also permanently generate biophotons. The question arises: What happens if a cell cannot use the TCA cycle or oxygen well? What happens to its biophoton signature then?
Energy Transfer via Food and Light: The quote, “We live by a small trickle of electricity from the sun,” underscores the role of photosynthesis in capturing solar energy, which is transferred to humans via food (plants, algae). However, direct sunlight exposure also delivers energy to RBCs, which act as conduits to mitochondria. The electrons and protons released from hemoglobin (via heme) fuel the ECT, producing ATP, the “biological energy necessary for all cellular function.”
We now know that ROS are permanently produced in blood. Due to the high activity of superoxide dismutase in blood, O2• is rapidly converted into hydrogen peroxide, and the latter is immediately decomposed with the heme protein catalase present in human blood. All these reactions are highly exergonic, releasing quanta of energy equivalent from 1 to 2 eV at each reaction act.
For blood to produce endogenous light, oxygen must be present. Hemoglobin dissolved in blood, even in a very low concentration, readily quenches photon emission in blood. This is important in cerebrovascular strokes and children born with jaundice. We now know that their biophoton signatures are reduced in these states. This means the heteroplasmy rates in their tissues are way higher when they are born. This explains thoroughly, from a biophysical standpoint, how transgenerational diseases occur. Darwin had a tiny right.
6. H₂O vs. D₂O Absorption and Mitochondrial Implications
“Comparison of absorption of H₂O and D₂O,” shows the optical density of light water (H₂O) and heavy water (D₂O) across wavelengths:
Absorption Differences: H₂O and D₂O have similar absorption profiles, but D₂O absorbs slightly more in the NIR range (1000–1500 nm). Both peak around 1450 nm, with optical densities of ~1, but D₂O’s higher viscosity and mass affect its interaction with light. This is directly correlated to the oxidation state of iron in heme proteins. When deuterium is flowing into the matrix, heme proteins assume the Fe³⁺state. This was the critical link made in the GOE on Earth, and it’s electrically carved into our biology. As I have noted, D₂O’s higher viscosity slows the ATPase, reducing energy efficiency in mitochondria.
This means that deuterium is selected for use in hypoxic environments with Warburg-shifted metabolisms because of its KIE. This is why the exogenous use of DDW in cancers can help cells create stem cells as we see in blastemas until Becker’s currents for regeneration are completed during daylight using hydrated melanin sheets. DDW, however, does not deal with the oxidation state of heme proteins. Light changes that. Environmental light and endogenous light can do it. We can use methylene blue in combination with DDW if no serious circadian mismatches drive heteroplasmy rates higher than chronological age.
Implications for Mitochondria: Mitochondria evolved to use H₂O, not D₂O, because H₂O’s lower viscosity and better resonance with red light (via H⁺) optimize proton gradients and EZ water formation. The sun’s red light enhances H₂O’s ability to form coherent domains in water, excluding deuterons and creating a proton-rich environment that supports the ATPase and ECT. High deuterium levels (e.g., in modern water) disrupt this, increasing ROS and driving Warburg metabolism, as discussed earlier.
7. Final Synthesis: Why Life Is the Way It Is
Nick Lane’s question, “Why is life the way it is?” is answered by the sun’s H⁺-driven red light and its quantum control over Earth’s biomolecules and mtDNA’s ability to generate ultraweak biophotons at the nanoscopic level:
Thermodynamic Foundation: The sun’s dominance of H⁺, with minimal deuterium and tritium in its spectrum, set the thermodynamic conditions for life. Red light from H⁺ (Hα at 656.3 nm) controlled H⁺-based chemistry on Earth, favoring H⁺ over deuterium in chloroplasts and mitochondria. This quantum selection ensured that life’s energy-generating systems (the ATPase, cytochrome c oxidase) were optimized for H⁺ via solar red light.
Evolutionary Trajectory: The conditions of existence were dictated by the sun’s light, and this led to the quantum evolution of H⁺-based biomolecules like the ATPase, which predates life and operates at 100% efficiency in red light. Chloroplasts and mitochondria, the “transforming agents” of solar energy, evolved to harness this light, producing ATP and water (mitochondria) or consuming water (chloroplasts) in a cycle that mirrors the sun’s H⁺ dynamics. It also gave cells the ability for the first time on Earth to create light inside of a cell at a small scale with massive power. This changed everything biologically. It set the stage for complex life at the Cambrian explosion.
Circadian and Systemic Integration: The sun’s diurnal variation and third harmonic plasma frequency (~3 mHz) set circadian rhythms and enhance mitochondrial function via resonance with biomolecules. RBCs act as intermediaries, using their crystalline structure to transfer solar energy to mitochondria, bridging the gap between light, food, and cellular energy.
Key Modern Disruptions To Understand: nnEMF and blue light disrupt this system by changing the oxidation state of iron and by increasing deuterium effects in the mito matrix, damaging heme proteins and redox shifting metabolism toward Warburg aerobic glycolysis. Restoring H⁺ dominance (via red light, DDW) and minimizing nnEMF exposure can realign life with its solar origins. AM sunlight with IRA and NIR light does this because it forces NO to unbind from Hb02. This is why AM sunlight is a critical default switch. It removes the paramagnetic NO to the paramagnetic oxygen that can take over during daylight.
Sleep in the dark is dominated by low ATP, NO binding, metHb production, and allowance of deuterium into the matrix to put the adult back into the in utero environment so it can regenerate tissues by tapping its stem cells at this time. Light destroys this because it flips Fe³⁺ to Fe²⁺ . Doing this STOPS all regeneration at night time. Doing this at night favors atavistic cells that are present and have to face massive oxygen levels. This is why cancer is so prominent in shift workers.
8. Decentralized Predictions with New Insights
RBC-Mitochondria Energy Transfer via EHD: The third harmonic of the solar plasma frequency (~3 mHz) should enhance electron flow in RBC membranes, improving energy transfer to mitochondria. This could be tested by measuring ATP production in tissues exposed to low-frequency electromagnetic fields mimicking the sun’s plasma frequency.
H₂O vs. D₂O in Circadian Signaling: H₂O’s better resonance with red light should enhance circadian signaling compared to D₂O. Experiments could be and should be designed to compare melatonin production and SCN activity in cells cultured in H₂O vs. D₂O under red light exposure.
Solar Spectrum and Heme Repair: The prominence of the Hα line (656.3 nm) in the solar spectrum suggests that this wavelength is optimal for heme repair in mitochondria. Clinical trials could test and should test 656 nm light therapy for conditions involving heme damage (e.g., anemia of chronic disease linked to nnEMF toxicity). I believe NIR light is also critical in reversing the MO effect in Hb. This is why AM light is critical in reversing every cancer on EARTH. It also points out why one has to be careful when using MB in humans in a blue-lit nnEMF world.
Tritium as a Cosmic Marker: Tritium’s production by cosmic rays (e.g., in auroras) should be a marker for solar activity’s impact on Earth’s biosphere. Increased tritium levels during solar maxima should correlate with enhanced mitochondrial function due to stronger red light emission. As far as I know, no one has thought about this implication yet.
Deuterium Depletion for Systemic Health: Reducing deuterium intake (via DDW) should improve RBC membrane dynamics and mitochondrial H⁺ gradients, enhancing overall health. This could be tested by comparing blood flow, ATP production, and disease markers in subjects on DDW vs. regular water. Once that test is done, it should be retested using DDW with MB infusions.
9. Final Implications for a Decentralized Mitochondriac
For a mitochondriac, my integrated model emphasizes the sun’s H⁺-driven red light as the cornerstone of life:
Align with the Sun: Morning sunlight exposure (rich in red light) optimizes circadian rhythms by forcing night time iron in heme in the +3 state to +2 at sunrise, mitochondrial function, and heme synthesis. The third harmonic of the solar plasma frequency enhances this effect, making sunlight exposure a critical practice. This is why carbohydrates are better tolerated in the morning and why if you do not see sunrise, you cannot use the TCA cycle, making high protein and fat diets superfluous.
Minimize Deuterium: High deuterium disrupts H-based systems, slowing the ATPase and increasing ROS. Using DDW and consuming low-deuterium foods (e.g., fresh plants) supports mitochondrial health and aligns with the sun’s H⁺ bias.
Leverage RBCs as Conduits: RBCs, filled with adaptable forms of Hb, with their crystalline membranes, transfer solar energy to and from mitochondria. They deliver solar energy outside in and transform energy to make their own light in the form of biophotons. RBCs enhance blood flow (e.g., via exercise or sunlight) and minimize nnEMF exposure, which ensures efficient energy delivery if they stay in the +2 state during solar-powered hours. You must have as much skin in the game as possible when you understand that light controls your paramagnetic switch between night and dark. Darkness requires NO and metHb, and daytime requires oxygen and NIR to free Hb to carry oxygen to utilize the TCA cycle to maximize energy efficiency.
Red Light as Medicine: Red light (especially 656 nm, matching the Hα line) is the “best drug” for humans, as it resonates with H⁺-based biomolecules, restores TCA OXPHOS, and repairs heme damage. This light is found in the sunrise, and this is likely why the TCA cycle needs this frequency of light before the TCA can be fully used by humans.
SUMMARY
Heme Proteins, Sex Steroids, and the Evolution of Light on Earth: The first slide below notes that dopamine synthesis is “highly oxygenated” and “augmented by hemoglobin oxidation state.” The second diagram shows that mTOR, activated by UVA light, supports mitochondrial biogenesis and metabolic flux, including the activity of heme-based CYP enzymes. CYP enzymes are critical for synthesizing sex steroids (e.g., testosterone, estrogen) from cholesterol. Reduced UVA exposure suppresses mTOR activity, impairing CYP function and decreasing sex steroid production. This reduces fertility (lower sperm quality, ovulatory dysfunction) and fecundity (decreased reproductive capacity).
How often have you seen the slide but missed the decentralized lesson buried in it? That hemoglobin oxidation state is the key to many things for mammals. Nature always hides her recipes, and you have to look for them.
LIGHT > FOOD It is a decentralized fact, not a centralized opinion.
The sun’s H⁺-driven red light, emitted via a potential photospheric lattice, set the thermodynamic and evolutionary foundations of life on Earth. By favoring H⁺ over deuterium and tritium, the sun’s spectrum dictated the design of chloroplasts and mitochondria, which use H⁺ to harness solar energy.
This quantum selection, reinforced by the sun’s diurnal variation and third harmonic plasma frequency, shaped circadian rhythms, biomolecule function, and energy transfer via RBCs. Modern disruptions like nnEMF and deuterium overload disrupt this fully electromagnetic system. Still, realigning with the sun’s default mechanism of providing the right red light at every sunrise, minimizing deuterium, and leveraging decentralized principles can restore health because it allows us to repair correctly. Life is how it is because the sun’s H⁺-driven red light, acting as a “trickle of electricity,” controls the quantum vibrations of H⁺-based systems, from the first ATPase to modern mitochondria. Those mitochondria then make the appropriate spectra needed to help us regenerate. Never forget the lesson below.
We all have a sickness that cleverly attaches and multiplies. No matter how we try, we all have someone who digs at us.
At least we dig each other. So when sickness turns my ego up, I know you’ll act as a clever medicine. Dig me up from under what is covering the better part of me.
So if you followed the decentralized medicine series closely so far and what I said in this podcast when I went back into the ICUs to rescue COVID patients from DARPA shots, you might be asking this question: Can knowing someone’s blood gas or SpO2 help choose a light frequency for patients to pull them from the grave?
The surprising answer is that it is beneficial for the clinician to know what light to use at the bedside. For example, you might take patients out of the grave after their ICU doctors have told the family they are dying. I apologize in advance to the lay public. This blog is clinically oriented and designed for MDs to make sense of my last two blogs. If you want better MDs, you’ll like them to read this information carefully.
This blog is key info to know before some idiot in the hospital tries Remdesivir as a Hail Mary.
Pulse Oximetry and Light Absorption Basics
The package insert from any new pulse oximeter is spot-on with its description of how it works. Pulse oximeters use two wavelengths of light—red (around 660 nm) and NIR (around 905 nm) because oxygenated hemoglobin (HbO2) and deoxygenated hemoglobin (Hb) absorb these wavelengths differently:
Oxygenated hemoglobin (HbO2) absorbs more NIR light (905 nm) and less red light (660 nm).
Deoxygenated hemoglobin (Hb) absorbs more red light (660 nm) and less NIR light (905 nm).
MetHb in Hypoxia and Injury: MetHb has a strong absorption peak around 405-410 nm, known as the Soret band. MetHb also shows broad absorption with distinct peaks at 540 nm and 576 nm. A characteristic peak emerges here, unique to metHb and absent in HbO₂ or Hb. This “metHb signature” is often used clinically to identify its presence, especially in co-oximetry, as it’s a marker of the Fe³⁺ state. The exact peak can shift slightly depending on pH and conditions, but 630 nm is a reliable reference.
Decentralized MDs need to remember that MetHb accumulates in hypoxia-related injuries (e.g., ARDS, COPD exacerbations) or oxidative stress states (e.g., sepsis, toxin exposure like nitrates or anesthetics) because ROS or other oxidants convert Hb’s Fe²⁺ to Fe³⁺. Typically, metHb levels are <1% of total hemoglobin, kept low by enzymes like NADH-dependent methemoglobin reductase. But in injury:
Hypoxia: Low oxygen availability can exacerbate metHb’s impact, as tissues already starved for oxygen lose even more carrying capacity. Even 10% metHb can drop functional SpO₂ significantly, mimicking or worsening hypoxia.
Mitochondrial Context: If mtDNA damage from LIGHT STRESS impairs oxygen utilization, metHb’s rise should be expected to compound the problem, shifting metabolism further toward lactate and Warburg-like states. I found this to be the case for every patient in the ICU for 3.5 years when I went back during COVID to find the smoking gun in the vials. I found a lot more light in the ICUs.
I found that NADH-dependent methemoglobin reductase (cytochrome b5 reductase) activity could indeed be reduced if mitochondria aren’t functioning optimally, though it’s an indirect effect. This allowed metHb levels to rise way more than anyone knew in the ICU because none of them had the right oxygen saturation equipment. Since this enzyme relies on NADH as an electron donor to reduce methemoglobin, any condition that impairs mitochondrial function and, thus, NADH production could limit its effectiveness. In the COVID epoch, this was a tremendous insight.
Typically, NADH-dependent methemoglobin reductase uses NADH to transfer electrons (via its FAD cofactor) to reduce methemoglobin (Fe³⁺) back to hemoglobin (Fe²⁺). However, this enzyme accounts for only about 60-70% of methemoglobin reduction under normal conditions, and its activity can be insufficient in cases of severe methemoglobinemia or when NADH production is impaired (e.g., due to mitochondrial dysfunction, which just about everyone has today due to nnEMF).
Methylene blue acts as an alternative electron carrier. When administered, it is reduced by NADPH (not NADH) in a reaction catalyzed by NADPH-dependent methemoglobin reductase (a minor pathway in red blood cells) or other NADPH-dependent enzymes like glutathione reductase. Reduced methylene blue (leucomethylene blue) then transfers electrons directly to methemoglobin nonenzymatically, converting it back to oxy hemoglobin. This process effectively bypasses the NADH-dependent cytochrome b5 reductase system, providing a faster and more efficient way to clear methemoglobin.
We can use this in emergencies, such as acquired methemoglobinemia caused by toxins (e.g., nitrates or aniline). In ICUs, I was able to pull people from graves. Hospitalists were telling families their loved ones would die, and I would then speak to the families and tell them there was a bail out. I’d say to them this was a Hail Mary, even though I knew it was not. I could not let anyone know what I was doing in the ICU; otherwise, I would have faced what Mary Talley Bowden has in Texas. I picked the patients already speaking to Jesus, and nurses would call me in the middle of the night and tell me the patients were having miraculous changes. I told them to call their attendings. I played dumb the entire time, by design. I was using the wisdom I got from Becker, Brain Surgery Without a Scapel, which you will soon read in this series. Eventually, most of the nurses were more intelligent than the MDs, and they would ask me what I was doing.
This brings us to the big point: Pulse oximeters can misread metHb diagnosis because it absorbs at both 660 nm and 905 nm, often reporting a falsely stable SpO₂ (~85%) regardless of true oxygenation. I highlighted this pitfall in centralized ICU critical care medicine in this podcast. Co-oximetry, which measures metHb directly at multiple wavelengths (e.g., 630 nm), is needed for accuracy. Very few centralized medicine MDs know this information. Now you do.
In a nontrauma or non-stressed situation, the device calculates the ratio of absorbed light by shining these lights through a pulsating capillary bed (like your fingertip) and measuring what comes out the other side. Using the Beer-Lambert Law (which relates light absorption to the concentration of a substance), it then estimates your SpO2, the percentage of hemoglobin saturated with oxygen in arterial blood. Normal SpO2 typically ranges from 95-100% in healthy individuals, though it can dip lower in certain conditions. The lower it dips, the more chances you have a Warburg shift and an undiagnosed metHb problem. Few centralized MDs know this.
Pulse oximeters focus on arterial blood because they detect the pulsatile flow driven by your heartbeat, filtering out the steady-state venous blood and tissue noise.
SpO2 Effects in COPD and ARDS with mtDNA Dysfunction
Substantial evidence shows that SpO2 levels impact outcomes in COPD and ARDS, particularly when mitochondrial DNA (mtDNA) damage is involved. These diseases mimic what COVID presentations really were at the core. Let’s establish that first:
COPD: In COPD, low SpO2 (hypoxemia) is a hallmark of disease progression, especially during exacerbations. Studies like those in the SPIROMICS cohort show that elevated plasma mtDNA levels correlate with disease severity, suggesting mitochondrial stress or dysfunction. Hypoxemia drives oxidative stress, which damages mtDNA, reducing mitochondrial efficiency and ATP production. This can shift metabolism toward glycolysis (Warburg-like), increasing lactate and lowering NAD+; a state of hypoxic metabolism even when oxygen is present. Not a good place to be unless you want to visit heaven
Research also shows titrating oxygen to a SpO2 of 88-92% in acute COPD exacerbations halves mortality compared to high-flow oxygen, indicating that TOO MUCH oxygen can worsen outcomes, possibly by amplifying reactive oxygen species (ROS) in already compromised mitochondria = Oxygen Allergy = Oxygen Holocaust is a real problem in LIGHT STRESSED humans with any sickness.
ARDS: In ARDS, SpO2/FiO2 ratios predict mortality and ventilator-free days, with lower ratios (e.g., <190) linked to worse outcomes. mtDNA damage is implicated here too—circulating mtDNA is a biomarker of severity, reflecting mitochondrial injury from hypoxia and inflammation. Patients with ARDS often exhibit a Warburg shift (aerobic glycolysis), where cells favor lactate production over oxidative phosphorylation, even when oxygen is available. This is tied to low NAD+ and impaired mitochondrial respiration, creating a pseudo-hypoxic state. Studies like those on the oxygenation saturation index (OSI) confirm SpO2-based metrics track disease progression, and hyperoxia (high SpO2) can exacerbate lung injury and organ failure, possibly via ROS overwhelming damaged mitochondria. Excess oxygen is a killer in a Warburg shifted organ. This is why ventilators killed millions.
In both conditions, mtDNA mutations or depletion impair the electron transport chain (ETC), particularly complexes I and IV, which rely on oxygen as the final electron acceptor. This inefficiency mimics an “oxygen allergy” or Oxygen Holocaust because cells can’t utilize oxygen effectively, leading to ROS spikes, more mtDNA damage, and a vicious cycle of metabolic dysfunction. This is why no one should be using exogenous oxygen treatments indiscriminately.
Linking SpO2 to Red/NIR Light Therapy to Disease
My argument made in the podcast with the Australian MD was that a patient’s metabolic state will influence red/NIR light therapy choices. He looked stunned when I said it, but I am sure he did not understand my science. He tried to tell you all we are on the same page, and we are far from birds of a feather. I gave him a compelling biophysical answer, and I’ll bet he’ll concede once he opens some biophysics books and realizes there’s more to explore here than he initially thought. The clinical point I am bringing out is that no studies directly test SpO2 levels as a decision point for choosing 660 nm vs. 850-905 nm in therapy protocols. However, my decentralized reasoning knows that breathing is an electromagnetic activity that employs a current (IMM), a magnetic field (Fo’s head), and a paramagnetic gas with a known proton spin rate in health. My idea is rooted in mtDNA failure, NAD+ depletion, and Warburg metabolism, and it offers a mechanistic basis to hypothesize such a link. When I returned to the ICUs during COVID, I used this to save people from centralized MDs. Soon, you are going to see the raw power behind my clinical moves. They will stun you, a promise not a threat.
Mitochondrial Mechanism: Red (660 nm) and NIR (850-905 nm) light stimulate cytochrome c oxidase (CCO) in the ETC, CREATING WATER while enhancing oxygen utilization and ATP production. Light therapy could theoretically compensate by boosting residual mitochondrial activity in COPD/ARDS with mtDNA damage, where CCO function is compromised if SpO2 is low (e.g., <90%), oxygen delivery to tissues is already limited. NIR’s deeper penetration might better target hypoxic mitochondria in muscles or lungs, improving oxygen use where it’s most needed. Conversely, if SpO2 is high but utilization is poor (hyperoxia with mtDNA failure), the superficial action of red light might suffice for skin-level detox or anti-inflammatory effects, avoiding ROS overproduction in deeper tissues. This is the targeted red light therapy I use on my patients.
Warburg Shift and NAD+: The Warburg-like metabolism linked to nnEMF is associated with low NAD+ and high lactate and reflects a hypoxic cellular state despite adequate SpO2. Light therapy increases NAD+ availability by enhancing mitochondrial respiration (via CCO), potentially reversing this shift.
Since we know SpO2 is a proxy for oxygen availability, it hints to the decentralized clinician how much mitochondrial “help” is needed. Low SpO2 might signal a need for NIR to push oxygen deeper into hypoxic tissues, getting rid of NO. At the same time, normal/high SpO2 with metabolic dysfunction might favor red light to fine-tune surface-level mitochondrial activity without overloading ROS. This level of sophistication was absent in every ICU I worked in during COVID. Not one centralized MD knew this science until I taught it to them.
THE DECENTRALIZED RED LIGHT LESSON GETS DEEPER
Biophotons, Oxygen’s Paramagnetism, and F0 Spin: My Asprey 2014 Event.
When you consider that it is well known and axiomatic that mtDNA release biophotons, oxygens have paramagnetic properties, and the F0 head spin rate for protons is known, this adds a fascinating decentralized layer to help diagnose patients who are dying. Let’s connect these to my argument:
Biophoton Release: Damaged mitochondria emit more biophotons (ultra-weak light) due to oxidative stress, ETC leakage. In COPD/ARDS with mtDNA failure, higher ROS correlates with increased biophoton emission, quantifiable via sensitive detectors. This could reflect the “electrical resistance” described in the DM #36 blog, disrupting the proton gradient across the mitochondrial membrane and slowing ATP synthase (F0/F1). If red/NIR light reduces ROS by optimizing CCO and displacing NO to make more ATP, biophoton release should decrease as a marker of therapeutic efficacy tied to SpO2 status. My decentralized model never allowed me to make a mistake in 3.5 years.
Oxygen’s Paramagnetism and F0 Spin: Oxygen’s unpaired electrons make it paramagnetic, interacting with magnetic fields in the ETC. The F0 head of ATP synthase spins at ~9000 RPM in healthy cells, driven by the proton motive force, but slows in disease (e.g., mtDNA damage), reducing ATP output and oxygen utilization. This drop increases ROS and biophotons, as I’ve noted. Red/NIR light should enhance F0 spin by improving ETC efficiency, particularly in low SpO2 states where oxygen is scarce or in high SpO2 states where utilization is impaired. Quantizing this via SpO2 would indeed guide therapy. Why? Anyone with a low SpO2 will need NIR to kickstart more profound mitochondrial activity, while high SpO2 might use red light to stabilize surface-level respiration. This science explains fibromyalgia patients as well.
SpO2 reflects oxygen availability, and in mtDNA-damaged states, it indirectly indicates how much light therapy is needed to overcome hypoxic metabolism or ROS overload. For example:
Low SpO2 (<90%): NIR (850-905 nm) is the optimal choice of light to penetrate deeper, boosting oxygen use in hypoxic, Warburg-shifted tissues. Most ICU patients fall into this group.
High SpO2 (>95%) with mtDNA failure: Red (660 nm) light might suffice for superficial benefits, avoiding ROS spikes in oxygen-rich but utilization-poor cells. Most people with fibromyalgia, ME, mold, chronic fatigue, and long covid fall into these groups.
This isn’t a nutty idea, it is basic biophysics of breathing. I know that breathing is 100% an electromagnetic process in humans. Few others have this insight. For Centralized medicine, it’s a hypothesis worth testing. Because I know the laws of physics and have been using this for 20 years in my practice, I did just that during COVID.
The lack of direct studies doesn’t negate the mechanistic logic because these are all based on the laws of nature. This is especially true with biophotons and F0 spin as potential quantifiers. I’d argue that ICU trials would need experiments measuring SpO2, NAD+, lactate, ROS, and biophoton emission pre- and post-light therapy in these patients to confirm this. Until then, my decentralized thinking had bridged a clinical gap in critical medicine that this field hadn’t fully explored. This is why I admonished the MD from OZ during the podcast on his across-the-board use of HBOT on all patients.
MetHb absorbs strongly at 405 nm and 630 nm, with moderate absorption at 660 nm and 905 nm. You need to know this is enough to disrupt pulse oximetry but not necessarily light therapy’s mitochondrial effects. In hypoxia and injury, its rise reflects oxidative damage, potentially tying into my mtDNA-NAD+ photo-bioelectric hypothesis. It’s a decentralized wildcard worth considering: I have used this to pull people from the grave. In patients, when metHb levels spike, SpO₂ becomes less reliable, and light therapy’s optimal wavelength and duration might need to be shifted based on tissue oxygenation and redox state.
This means the Arndt-Schulz law may not be operational for this circumstance. The Arndt-Schulz rule assumes a dose-response relationship where low-intensity light (e.g., photobiomodulation, PBM) stimulates mitochondrial cytochrome c oxidase (CCO), boosts ATP, and reduces ROS. At the same time, excessive doses could overstimulate and harm cells. Usually, this works fine:
Tissue oxygenation and redox state set the stage for how much stimulation is “low” or “optimal.”
But with high metHb: more bad ICU lights and excessive nnEMF
Reduced oxygen availability: Even if SpO₂ reads decently, metHb’s inability to release oxygen starves mitochondria, alters NO levels, and affects stem cell depots needed to regenerate, lowering baseline respiration and recovery. Light therapy might still stimulate CCO, but with less oxygen to work with, the ATP boost could be muted, shifting the “low-dose” benefit curve.
Oxidative overload: MetHb reflects a high-ROS environment (since it forms via oxidation). Red Light, normally stimulatory, might instead tip the redox balance toward damage, especially if mitochondria are already leaking electrons (e.g., mtDNA failure). The “moderate dose” inhibition or “high dose” destruction thresholds could kick in earlier than expected. This is why dosing MB before PBM is a critically important teaching lesson for MDs.
Absorption interference: MetHb’s higher absorption at 660 nm (vs. HbO₂) and moderate absorption at 905 nm could alter light penetration. More energy might be absorbed superficially, reducing delivery to deeper mitochondria and skewing the effective dose.
In short, the Arndt-Schulz rule might not hold its usual shape here. The “optimal” dose and wavelength for PBM could shift unpredictably because the tissue’s starting point, hypoxic, ROS-heavy, and metHb-laden, changes the biological response.
Adjusting Light Therapy: Wavelength and Duration Will Be Decentralized Wisdom Few Have
If metHb spikes render SpO₂ unreliable and disrupt the Arndt-Schulz framework, tailoring light therapy becomes a game of educated guesswork based on tissue state rather than pulse oximetry. Here’s how wavelength and duration might need to shift based on my COVID experience over the last 4 years:
Wavelength:
660 nm (Red): MetHb absorbs more here than HbO₂, potentially limiting penetration in high-metHb states. This favors superficial effects (e.g., skin repair, local inflammation reduction), but red light might not reach deeper mitochondria effectively if tissues are hypoxic and ROS-saturated. It risks being “wasted” on a redox system that is too stressed to benefit, pushing the dose-response curve for PBM toward inhibition sooner.
905 nm (NIR): MetHb’s lower absorption here (vs. 660 nm) allows deeper penetration, potentially reaching hypoxic mitochondria in muscles or organs. NIR might better support oxygen-starved cells by enhancing CCO activity where oxygen is still present, even if it is scarce. In COPD/ARDS with mtDNA damage, this could align with my earlier logic about NIR for low-SpO₂-like states. The key is to know when and who to hit with MB first. No one who does not have this understanding should be fucking around with MB.
Duration/Dose:
Lower doses: With high metHb and ROS, starting with very low doses (e.g., 0.5-2 J/cm²) might avoid overwhelming compromised mitochondria. The Arndt-Schulz stimulatory phase could be narrower, so shorter sessions (e.g., 5-10 minutes vs. 20) might stay in the “enhancement” zone.
Monitoring response: Without reliable SpO₂, you’d need proxies like lactate levels, NAD+/NADH ratios, or subjective energy/fatigue to gauge efficacy. If ROS spikes (e.g., via biophoton release, as you suggested), the duration might need to be reduced.
Practical Implications
In patients with metHb spikes, say, from sepsis, nitrite poisoning, or severe hypoxia due to light injuries, the injury contexts are:
NIR (e.g., 850-905 nm) might be the safer bet because of its penetration advantage. It targets deeper hypoxic tissues where mitochondria need the most help. A PBM-styled panel or NIR sauna could work, assuming low-dose protocols. Generally, a commercial sauna is not well powered, so it is usually ineffective for my patients. Decentralized wisdom: Light’s a different beast, yes, it can, and it’s got flair. Pump enough energy into tissues and Fe²⁺ with the right wavelength (usually UV or high-energy visible light), and you can excite an electron right out of its orbit, leaving Fe³⁺ behind. Proof that I am right about the power of biophotons is below.
Red (660 nm) light might still help superficially (e.g., wound healing), but its efficacy could drop if metHb absorbs too much light before it reaches viable mitochondria.
Duration adjustments: Start low and slow, as the Arndt-Schulz curve’s sweet spot likely shifts left (less tolerance for higher doses) in this redox chaos.
You can see that my intuition is spot-on and that metHb complicates the picture. The rule’s predictability falters when oxygen delivery and utilization are decoupled, and SpO₂ can’t guide us clinically. It’s less about the law failing outright and more about its parameters needing recalibration. Clinical studies haven’t tackled this head-on for PBM in metHb-heavy states. I faced this state in 1998 when that 16-year-old girl had a massive trauma to her brain. My intuition about tissue oxygenation and the redox state of iron as the real drivers (not just SpO₂) was a solid leap, and it’s a gap that centralized researchers need to probe with data!
SUMMARY
Pulse oximeters are valuable tools if you know how to use them. They are also critical in understanding who should and should not get methylene blue. You must realize that pulse oximeters misread metHb levels because they absorb red light at both 660 nm and 905 nm. The machine often reports a falsely stable SpO₂ (~85%) regardless of actual oxygenation, a real pitfall in critical care medicine. Co-oximetry, which measures metHb directly at multiple wavelengths (e.g., 630 nm), is needed for accuracy.
Relevance to Red/NIR Light Therapy
Since I’ve explored light therapy (660 nm red, 850-905 nm NIR) in hypoxia, metHb’s spectra matter in people with significant mtDNA mutations, damage, and high heteroplasmy ratio in organs:
660 nm: MetHb absorbs here more than HbO₂, so in high-metHb states (e.g., injury), red light LIKELY interacts differently with blood near the surface. It could theoretically stimulate cytochrome c oxidase (CCO) less efficiently to create water if metHb’s presence reflects broader oxidative stress, though direct evidence is lacking in the biophysics literature. This is where so much muscle pain comes from in FM cases.
905 nm: MetHb’s moderate absorption suggests that NIR will penetrate deeper due to its physics, potentially reaching hypoxic mitochondria despite metHb buildup. Its lower absorption than Hb might mean less interference in NIR’s therapeutic effects.
SUMMARY
MetHb’s role in light therapy is uncharted territory for centralized medicine. Its absorption might alter light penetration or energy delivery to tissues, but no studies quantify this because they never thought to ask the questions I did 20 years ago when I began using this on my patients. If metHb signals severe hypoxia or ROS overload, it would argue for NIR’s frequencies to reach a deeper reach to target compromised mitochondria, aligning with my earlier point about low SpO₂ states. NIR also reverses the NO switch and turns the injury site from hypoxia to normoxia, so the MDs better know what they are really doing. So far, I have not met anyone who figured this out. But I have taught a lot of ICU MDs these decentralized tricks. Every one of my farm clients had peripheral blood smears and was monitored for oxygen saturation. Now they know why. I was collecting data on their biophysical status to make the correct decisions for them.
Centralized data is thin here, but the biophysics of breathing is fully decentralized because it is 100% electromagnetic. This made me intuitively aware that I needed to take this into account for many patients with nnEMF-induced hypoxia and nasty peripheral blood smears. Its relevance isn’t off the mark!
The Brutal Art of Choosing Your Life is YOURS and YOURS ALONE
Deciding what you want your life to scream isn’t hard because it’s a primal pulse built around your light choices, a gut howl that erupts when you strip away the noise. No, the real gut-punch is staring down what you’re willing to torch, what you’ll carve out of your soul to chase what sets you ablaze. Life’s a feral tapestry, woven from decisions with sharp ones that cut deep, dumb ones that scar, all threading together into the jagged shape of your destiny. You don’t stumble onto beauty by playing it safe; you hack through the tangled weeds, lost and bleeding, until the path reveals itself. Act boldly and messily, so you’re not choking on regrets when the reaper knocks.
I have no time for people who do not put in the time to understand how regeneration really operates. You operate on Nature’s timescales, not your own.
Prediction: Neurotransmitter imbalances manifest rapidly in this scenario and will fuel neuropsychiatric disorders due to electrical resistance damage in neural and vascular networks once CCO is damaged (e.g., ADHD, autism). If the diurnal light stimulus does not reintroduce the regenerative currents, the process of electrical damage spreads.
