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Rewriting Autoimmunity from First Principles: The Light-Evolved Immune System and the Photobioelectric Thesis

From first principles, let’s rebuild our understanding of autoimmunity not as a glitch in a mechanical immune machine, but as a disruption in an ancient, light-forged symphony, a decentralized network sculpted by Earth’s photonic energies over billions of years. Life’s immune defenses emerged during the primordial chaos of the Great Oxygenation Event (GOE), when rising oxygen levels unleashed reactive oxygen species (ROS) as both a threat and a tool. In this quantum crucible, light, Earth’s primal architect, drove the evolution of self-recognition mechanisms, using ultra-weak photon emissions (UPEs), bioelectric currents, and chromophores like cytochromes and melanin to collapse probabilistic wave functions in cellular DNA, distinguishing “self” from “invader.”

Genes here aren’t commanders; they’re lenses refracting light’s quantum touch to shape phenotype. When this light is absent or distorted, by modern shadows like indoor living, blue light pollution, or non-native electromagnetic fields (nnEMF), the system falters, broadening UPE spectra into entropic noise. Autoimmunity arises not from inherent flaws, but from this photonic famine, where the immune orchestra attacks its own instruments.

Consider the immune system’s core challenge: Every day, it confronts a microbial kaleidoscope, viruses, bacteria, and fungi in endless disguises, some mimicking human cells through molecular camouflage honed by evolutionary arms races. Without light’s guiding rhythm, how does it discern friend from foe?

Traditional views pinned this on “central tolerance,” a thymic boot camp where maturing T cells are tested against self-antigens. Harmful ones, those binding too tightly to the body’s own protein fragments, are culled, allowing only vigilant scouts to patrol (as illustrated in the provided diagram above). This process, akin to a quantum sieve filtering electron probabilities, evolved under solar pressures: UV light, penetrating the skin, catalyzes vitamin D synthesis and melanin production, which in turn modulate thymic hormones and bioelectric fields to fine-tune this selection.

But this centralized dogma is incomplete, it’s like explaining a forest by its seeds alone. The 2025 Nobel Prize in Physiology or Medicine, was recently awarded to Mary Brunkow, Fred Ramsdell, and Shimon Sakaguchi, illuminates the fuller picture: peripheral tolerance, enforced by regulatory T cells (Tregs), the system’s photonic peacekeepers.

Sakaguchi’s 1995 insight shattered the central-only paradigm. He observed T cells that didn’t assault invaders but instead patrolled peripherally, whispering “stand down” to overzealous effectors, suppressing inflammation and enforcing self-tolerance. These T-regs, expressing the master switch Foxp3 (pinpointed by Brunkow and Ramsdell in 2001 through mutant mice with rampant autoimmunity), roam tissues like quantum stabilizers, using bioelectric signals to dampen chaotic immune waves. Mutate Foxp3, and the floodgates open: in humans, this manifests as IPEX syndrome, a lethal autoimmune storm.

By 2003, Sakaguchi linked it all, because Foxp3 powers T-regs to actively police the periphery, complementing central culling. From first principles, this dual system mirrors quantum complementarity: central tolerance prunes probabilities early, while peripheral T-regs collapse ongoing waves in real-time, preventing decoherence into autoaggression.Now, integrate this with the photobioelectric thesis: The immune system isn’t a isolated fortress; it’s a light-entangled web, echoing GOE adaptations where oxygen’s rise demanded ROS-scavenging and tolerance mechanisms.

Sunlight, especially UVB, acts as the conductor, rapidly activating systemic neuroendocrine and immunosuppressive responses, as shown in the provided 2016 study on mice. A single 400 mJ/cm² UVB dose on back skin spikes hypothalamic-pituitary-adrenal (HPA) axis hormones like CRH, β-endorphin, ACTH, and cortisol, while suppressing splenic IFN-γ (a pro-inflammatory cytokine) and inhibiting IL-10 in T-helper subsets.

This isn’t random; it’s a photonic cascade: UVB photons absorbed by skin chromophores trigger UPEs and bioelectric currents, dehydrating or hydrating cellular water states to narrow emission spectra, fostering coherence. Vitamin D, forged by UVB, directly boosts Treg proliferation and function, enhancing Foxp3 expression and preventing autoimmune models like multiple sclerosis (MS) or rheumatoid arthritis. Melanin, the paramagnetic quantum sensor adjacent to mitochondria, transforms these UPEs, scavenging ROS and modulating magnetic fields from ATP synthase to maintain T-reg stability, disruptions broaden spectra, eroding tolerance.

If you look in the bottom right of the picture above under Chapter X, you’ll see how the vitalists before the Flexner Report treated anemia with light.

Anemia serves as the quantum lens here, recapitulating GOE hypoxia in modern bodies. Low oxygen-carrying RBCs create tissue “deserts,” impairing cytochrome c oxidase (CCO) water production and broadening UPEs, which disrupts Treg phenotypes and fuels autoimmunity. Yet, hypoxia-inducible factor-1α (HIF-1α) can paradoxically induce Foxp3, bolstering T-regs in inflammatory hypoxia, mirroring oocytes’

THE CASE OF INDIA

Recent studies, such as one in 2023 analyzing Indian Demographic and Health Surveys (2015-2021), indicate a notable rise in the prevalence of anemia among adolescent women in India, increasing from 54.2% to 58.9%, with 21 out of 28 states reporting an increase. Data from the National Family Health Survey 5 (2019-2021) shows a 57.0% prevalence in women and 59.1% in adolescent girls, though some suggest WHO diagnostic criteria may overestimate these figures. High anemia rates persist, particularly among children, with 67.1% prevalence in children aged 6-59 months. Factors like wearing of clothing/pollution, vegetarian diets, and belonging to Scheduled Tribes, and being in the lowest wealth quintile contribute to this growing public health concern.

Note the slide. If you’re at a suboptimal latitude with dark skin, how does altitude affect your situation? North India shows us this situation. It helps with solar light but hurts our immune systems because it also induces hypoxia. Hypoxia should normally stimulate RBC synthesis but as you see above that is not happening in India is it. India is now the home of tech abuse due to American technocratic outsourcing.

Recent data also shows a significant burden of autoimmune diseases in India, with rising incidences for some conditions, particularly in younger populations and women. Air pollution is a identified as a huge risk factor for triggering autoimmunity because of how it blocks UV light. Studies highlight the significant prevalence of autoimmune diseases like Systemic Lupus Erythematosus (SLE), Rheumatoid Arthritis (RA), and Psoriasis, with new research also exploring the connection between post-COVID conditions and autoimmune markers. A retrospective study in North India from 1996 to 2006 observed a significant increase in autoimmune disorders (AIDs), specifically anti-nuclear antibody (ANA)-positive connective tissue diseases. Another study from 2020 indicated a high rate of positive ANA patterns in a central Indian hospital, suggesting a high prevalence of autoimmunity in the region.

As you heard in the last blog at its coda, complex I suppression for ROS-free longevity. RBCs, as “time travelers,” dedifferentiate under light cues, releasing mitochondria and melatonin to support peripheral tolerance; anemia’s scarcity reduces this, linking to fertility woes and neurodegeneration via circadian mismatches.

In vitiligo, an autoimmune attack on melanocytes, T-regs falter, underscoring melanin’s role in immune harmony. Autoimmune chaos, then, stems from light deficiency: absent solar rhythms accelerate methylation, degrade heme proteins, and widen UPEs, crippling T-regs’ peacekeeping.

SUMMARY

Immune cells are loaded with mitochondria and RBC are not, by design. One cell needs quantum gate to make sense of the light while the other one is impeded by the gate.

Topology → Connection → Time Delay → Emission → Memory.

You remember my slides from Vermont series of lectures? See below.

The sharper the curvature of cristae in mitochondria, the longer the time delay becomes, the longer the time delay, the more precise the UPE emission is emitted, and the more precise the emission, the greater the coherence density embedded in that photon field into which a mitochodria releases. RBC do not have that ability, but WBCs do. This means the light they release is key to understanding the etiology of all autoimmune conditions.

WBCs like T-regs need memory, but RBCs do not. Their memory is built into their ability to de-differentiate into more primitive cells as Becker showed in his experiments. This might be another reason RBC do not have mitochondria. Mitochondria act like Cartan Gate does in a quantum system.

A Cartan gate is a mathematical technique that breaks down any arbitrary quantum gate into simpler components. Cartan gates allows for the efficient design and implementation of quantum circuits, reducing complexity and enabling more optimal optical circuit construction for quantum computers. This concept is not foreign to any science. It just is not being applied by first principle thinking in mitchondria which act as quantum nanobots for electrons, protons, and photons in the form of UPE.

Diseases like MS, AD, or IPEX aren’t genetic destinies but photonic imbalances of UPE specificities we have no yet been able to pin down in labs. They are echoes of GOE stresses in a light-starved world. The 2025 Nobel’s impact? It shifts from drug-centric fixes to solar reclamation. We don’t “cure” with immunosuppressants; we restore light’s quantum dance, full-spectrum exposure, DHA-rich diets for coherence, red/near-infrared to hydrate melanin and narrow UPEs.

This decentralizes medicine: Heal the light within, and tolerance follows, safeguarding our evolutionary masterpiece.

CITES

https://pmc.ncbi.nlm.nih.gov/articles/PMC8133893/

https://pubmed.ncbi.nlm.nih.gov/21898056/

https://www.usatoday.com/story/news/nation/2025/10/06/nobel-prize-medicine-brunkow-ramsdell/86544861007/

Humans assimilate light in many ways. Since we are in part of the Quilt that is teaching us how RBC porphyrins collect and communicate their information to and fro I want you to understand how a child can be born older than either of its parents when the egg and sperm they come from comes from a light stressed environment. How does it happen?

The last blog should have opened your eyes on why RBCs and anemia are extraordinary signals that tells us a lot about how optical information is communicated in complex eukaryotes. The mechanism of how children get cancers from their parents choices around light is exactly how astronauts get cancer from their choices of using light in space aberrently. Below is lecture I attended given by astronaut Robert Thirsk on my recent world tour with some of my Farm Clients to teach them more quantum biology one on one. Why did we pick this itinery as a way to teach? Because that is where the space guys who flew into massive nnEMF were. Their lives hold lessons we all need to learn about LIGHT STRESS and modern disease epidemics.

Bob served as crew commander for two space mission simulations: the seven-day CAPSULS mission in 1994, at Defense Research and Development Canada in Toronto, and the 11-day NEEMO 7 undersea mission in 2004 at the National Undersea Research Center in Key Largo, Florida.

In 1998, Bob was assigned by the Canadian Space Agency to NASA’s Johnson Space Center in Houston to pursue mission specialist training. This training program involved advanced instruction on both Shuttle and International Space Station (ISS) systems, EVA (spacewalking), robotic operations, and Russian language. He was a transition astronaut between the old Shuttle missions and the new ISS bases needed to get to Mars.

Within the NASA Astronaut Office, Bob served as a CapCom (capsule communicator) for the International Space Station program. In 2004, Bob trained at the Yuri Gagarin Cosmonaut Training Centre near Moscow and became certified as a Flight Engineer for the Soyuz spacecraft. He served as backup Flight Engineer to European Space Agency astronaut Roberto Vittori for the Soyuz 10S taxi mission to the ISS in April 2005. During this 10-day mission, Bob worked as Eurocom (European CapCom) at ESA’s Columbus Control Centre in Germany. In February 2008, Bob again performed Eurocom duties from Germany in support of ISS Expedition 16 crew activities.

Bob holds an Adjunct Faculty position at International Space University in Strasbourg, France. He works with educational specialists in Canada to develop space-related curriculum for grade school students. He encourages young Canadians to build their dreams upon a solid educational foundation and advanced skills.

In June and July 1996, Bob flew as a payload specialist aboard Space Shuttle mission STS-78, the Life and Microgravity Spacelab mission. During this 17-day flight aboard Columbia, he and his six crewmates performed 43 international experiments devoted to the study of life and materials sciences. The life science experiments investigated changes in plants, animals, and humans under space flight conditions. The materials science experiments examined protein crystallization, fluid physics and high-temperature solidification of multi-phase materials in a weightless environment.

In 2009 Bob became the first Canadian astronaut to fly a long duration expedition aboard the International Space Station. He and two crewmates launched from the Baikonur Cosmodrome in Kazakhstan on May 27th 2009 aboard a Russian Soyuz spacecraft. When their Soyuz vehicle docked with the nearly-complete Station two days later, the ISS became home for the first time to a permanent crew of six.

As members of the ISS Expedition 20/21 crew, Bob and his five international crewmates performed an unprecedented amount of multidisciplinary research, complex robotic operations, and maintenance and repair work of Station systems and payloads. Following the undocking of his Soyuz spacecraft from the Station and landing back in Kazakhstan on December 1st, Bob Thirsk had lived and worked in space for another 188 days during this second voyage. I got a chance to spend time with him on this world tour to discuss the science of space travel and the limitations of humans in traveling to MARS. In his lecture, Bob told us that his eyes have become a large problem for his health since his days in space. He had no idea why. I did.

HOW DOES THE STORY OF OUR RBCs FIT THIS NARRATIVE?

The addition of the biophoton research on red blood cells (RBCs) and blood from the 2003 study “Biophoton Research in Blood Reveals Its Holistic Properties” by Voeikov et al. provides a critical layer to my photo-bioelectric hypothesis. This study highlights blood as a continuous source of biophotons, reflecting its electronically excited state driven by reactive oxygen species (ROS) reactions, and its role as a highly cooperative, non-equilibrium, non-linear system. Since RBCs have no mitochondria it should be surprising to new students of my work that blood can easily create biophotons since mtDNA is usually needed to make ROS and electronic states to transform matter to produce biophotons. This paper aligns with my existing framework, which emphasizes light-driven metabolism (Light > Food), the role of water dynamics, deuterium effects, and evolutionary adaptations post-K-T Extinction on Earth. It would be wise for me to remind you that human adult blood is loaded with deuterium. How does this square with my thesis?

My photo-bioelectric hypothesis posits that nnEMF (non-native electromagnetic fields), ALAN (artificial light at night), poor sunlight, and geoengineering damage melanopsin, mtDNA, and heme proteins, reducing DDW (deuterium-depleted water) production, dehydrating melanin, and increasing electrical resistance (éR), leading to hypoxia, HIF-1α activation, Warburg metabolism, VP-ISR-GDF15 axis activation, and Vitamin A liberation disrupting heme nuclear genes Rev Erb- alpaha and beta which directly impact the key SCN clock genes called PER1/PER2. The K-T Extinction event link deuterium effects further shape mtDNA biophoton emissions and haplotype vulnerabilities.

1. Blood as a Biophoton Source:

   Blood is a continuous source of biophotons, persisting in an electronically excited state due to ROS reactions (e.g., in neutrophils). This state is oscillatory, indicating interactions between electron excitation sources, and is highly sensitive to external photonic fields (e.g., nnEMF, ALAN) but resistant to temperature variations, showing hysteresis in photon emission (PE).

2. Blood as a Non-Linear, Cooperative System:

   Blood operates as a non-equilibrium, non-linear system, with components interacting in time and space. This cooperative nature allows blood to store energy from electron excitation, supporting its role in systemic biophoton signaling and cellular communication.

3. Link to Heme Proteins and Regenerative Currents:

   Heme proteins in RBCs (e.g., hemoglobin) are key to ROS generation and biophoton emission. Under hypoxia, hemoglobin oxidizes to methemoglobin, blocking oxygen binding but enabling Robert Becker’s pico-to-nanoampere regenerative current for de-differentiation. nnEMF/ALAN disrupt this, increasing methemoglobin and éR, while methylene blue can sometimes counters this by enhancing NO to stop ATP production and lowering éR. Interestingly ROS and RNS also have a paramagnetic footprint in this dance.

4. Connection to Deuterium and Biophotons:

   High deuterium in mtDNA (post-K-T) widens biophoton spectra, reducing ultraweak UV biophotons. Blood’s biophoton emissions, driven by ROS, are similarly affected by deuterium levels, with nnEMF/ALAN exacerbating this by increasing ROS and deuterium retention, driving Warburg shifts.

Evolution of Light, Deuterium, Biophotons, and Blood’s Role

Pre-K-T Era: Anaerobic Life and High Deuterium Dominates Earth

The hole in the Earth crust in Mexico is massive and all that Karst was elevated into the atomosphere in a few minutes to block the sun, lower temperatures, and create a light catastrophe that forced all life that would come after it to adapt. Those changes remain in every eukaryote since this event. Humans are subject to this situation.

Environment: Prior to the KT event, the Earth’s atmosphere had low oxygen for billions of years, and life relied on glycolysis (high deuterium). Blood precursors in early organisms (e.g., LUCA) emitted biophotons with a wide spectrum, lacking ultraweak UV biophotons, reflecting high entropy (per Shannon’s 1948 information entropy). ROS reactions in primitive heme proteins (e.g., myoglobin) generated biophotons, but high deuterium limited information transfer efficiency.

Biochemicals: Tryptophan-derived molecules (e.g., melatonin) absorbed UV (150–400 nm), supporting early circadian timing. Blood’s role as a biophoton source was minimal due to low oxygen and ROS.

K-T Extinction: Deuterium Surge and mtDNA Stress combine to force life to adapt

Environmental Shift: The K-T Extinction (66 million years ago) reduced UV light, altered precipitation, and increased deuterium in water and mtDNA. Blood’s biophoton emissions widened, reflecting increased ROS from stressed heme proteins (e.g., hemoglobin precursors). This high-deuterium state drove apoptosis innovation via cytochrome c oxidase, removing afflicted mtDNA.

Evolutionary Pressure: Organisms favored glycolysis (high deuterium, wider biophoton spectrum), but blood’s cooperative nature (non-linear system) began to emerge, storing energy from ROS-driven electron excitation to support systemic signaling under stress.

Post-K-T Recovery of Eukaryotes: Normoxia, Ultraweak UV Biophotons, and Blood’s Role

Sunlight Return: UV light returned, stimulating neuropsin, mTOR, and leptin signaling, supporting normoxia and TCA cycle dominance. Cytochrome c oxidase evolved to reduce deuterium in mtDNA, favoring ultraweak UV biophotons (low-entropy, high-information signals per Popp). Blood’s biophoton emissions, driven by ROS in neutrophils and heme proteins, also shifted toward ultraweak UV, enhancing systemic communication.

Biochemical Selection: Melatonin, NAD⁺, and catecholamines (tryptophan-derived) became key semiconductors, absorbing UV to regulate circadian clocks (PER1/PER2). Heme proteins in the nucleus (Rev erbs) and in RBCs stabilized with green light, and blood’s non-linear system amplified biophoton signaling, supporting oxygen delivery and regenerative currents (per Becker).

Normoxic Earth: Haplotype Divergence and Blood’s Vulnerability

Haplotype Variations: Mitochondrial haplotypes diverged based on deuterium retention and biophoton profiles. Haplotypes with lower deuterium (e.g., H+) favored TCA cycle use, ultraweak UV biophotons, and low-entropy states, reducing disease risk. Haplotypes with higher deuterium (e.g., T2b-like) retained Warburg tendencies, increasing éR, heteroplasmy, and disease phenotypes. Blood’s biophoton emissions reflected these differences, with high-deuterium haplotypes showing wider spectra and higher ROS.

Modern Disruption: nnEMF/ALAN mimic pre-K-T darkness, increasing deuterium in mtDNA and blood, widening biophoton spectra, and driving Warburg shifts. Blood’s sensitivity to photonic fields (e.g., nnEMF) disrupts its cooperative state, increasing methemoglobin, ROS, and éR, exacerbating disease in vulnerable haplotypes like the 19-year-old with RP.

Decentralized Thesis Framework

Core Hypothesis: nnEMF, ALAN, poor sunlight, and geoengineering damage melanopsin, mtDNA, and heme proteins everywhere to make oxygen a toxin, reducing DDW, dehydrating melanin, and increasing éR, leading to hypoxia, HIF-1α activation. The picture below makes the link of hypoxic Earth (GOE) to normoxic Earth of today. In the GOE version of Earth the Warburg metabolism was favored to prevent oxygen damage and this remnant of optical signaliing is seen in today’s Vasopressin-ISR-GDF15 axis activation by aberrent light. It is also deeply associated with Vitamin A liberation from opsins disrupting Rev erb alpha and beta and PER1/PER2. Excited oxygen in the early GOE atmosphere released red and green light from its interactions and these two colors of light became important for hemoglobin stabilization and destabilization when it came to carrying oxygen to and fro to supply mitochondria. This is shown on the slide below. You can also see how hypoxia induced factor 1 and the PER2 link.

The K-T Extinction event was a LIGHT event that interrupted the sun and this increased deuterium usefulness in the circulations of early eukaryotes, but the return of normoxia post KT selected for ultraweak UV biophoton signaling, with blood acting as a cooperative biophoton source. nnEMF reverses this evolutionary, increasing disease in vulnerable haplotypes putting us back in a GOE like world. This is where oncogenesis begins in man’s world of today.

New Mechanism: Blood is a non-linear, cooperative system emitting biophotons via ROS reactions in heme proteins, sensitive to nnEMF/ALAN, which increase deuterium, widen biophoton spectra creating noise and reducing optical signaling, while disrupting regenerative currents (methemoglobin accumulation). Red light (drug equivalent per Tiina Karu), DDW, and methylene blue reduce deuterium, ROS, and methemoglobin, restoring ultraweak UV biophotons and lowering éR in tissues making oncogenesis less probable.

Therapeutic Implication: Solar/red light, DDW, grounding, and methylene blue reduce deuterium, ROS, and methemoglobin in blood, enhance ultraweak UV biophotons, stabilize mtDNA, and lower éR, mitigating disease in vulnerable haplotypes by re-aligning with normoxic adaptations that occured on Earth post KT event.

Few people have made the link of how green light during the KT event was the glue that connects us from the GOE and modern normoxic Earth. Look at the next two links carefully how green light stabilizes the IMM, RBCs, and the opsin system of eukaryotes.

Sitting under trees on a sunny day is a free version of chemostherapy for many with cancers. Few get told to do this when they have a cancer like state that is a GOE like environment. This behavior also allows you to have massive exposure to NIR light as well. This is a double win for those with RBC pathology as the second slide shows.

Deuterium Depletion as a Cancer Therapy due to LIGHT STRESS

The new paper below in cites #2 provides real-world evidence for deuterium depletion’s therapeutic potential: integrating DDW into conventional cancer therapy significantly enhances survival, with a 75-80% reduction in cancer-related mortality. This aligns with Somlyai’s framework in his book, as DDW breaks the cycle of mitochondrial dysfunction, inflammation, and DNA instability by reducing deuterium’s kinetic effects. The study’s finding that survival correlates with DDW duration (r = 0.476, p < 0.001) and timing (better outcomes with earlier DDW adoption) underscores the importance of deuterium depletion in cancer management, supporting the mechanistic links to pH, voltage, and metabolic health in a “decentralized framework of medicine.”

Stressors of any origin (or any frequency), elevate mitochondrial deuterium, increasing water viscosity, slowing the ATP synthase nanomotor, and disrupting proton dynamics, leading to a pH drop and cellular depolarization. This triggers UCP amplification, collapsing the proton gradient, while COX-2 ramps up via inflammation from leaky barriers (gut, BBB, BRB, retina, testes etc) and high-deuterium metabolic pathways (e.g., glycolysis in cancer cells). The resulting “heavy protonicity” spreads to blood and CSF, distorting water networks and promoting DNA instability via deuterium-driven hydroxyl radicals.

Deuterium-depleted water (DDW), as shown in the new study, significantly enhances cancer survival (MST of 12.4 years vs. 2.4 years in the general Hungarian cancer population) by restoring mitochondrial function, stabilizing pH/voltage, reducing inflammation (e.g., COX-2), and protecting DNA.

HOW DDW AND UPEs LINK IN DECENTRALIZED MEDICINE

Deuterium depletion as a cancer therapy due to light stress cogently integrates with the decentralized photo-bioelectric thesis, where UPE spectra and coherence link to mitochondrial dynamics and metabolic resilience. Elevated deuterium from stressors like blue light increases waterviscosity, slowing ATP synthase and disrupting proton gradients, amplifying UPE spectra (e.g., intensified 634–703 nm peaks from singlet oxygen) as entropy markers, while DDW reduces viscosity, normalizing UPE emissionand restoring OXPHOS efficiency, as shown in the preprint’s 75–80% mortality reduction and survival correlation (r = 0.476, p < 0.001) (Somlyai et al., 2023; Somlyai, 2010).

Coherent red/NIR light enhances this by exciting CCO, reducing inflammation (COX-2), and stabilizing IMM oscillations (20–50 Hz to 100 Hz), synergizing withDDW to break the cycle of depolarization, UCP amplification, and DNA instability, complementing hemiflusome and nanotube function in managing photonic chaos (Hamblin, 2016; Agan et al., 2025). In jaundiced neonates orcancer patients, this strategy, combined with ketogenic diets, mitigates light stress-induced Warburg metabolism, reducing autism/EDS risks and underscoring sunlight’s role in decentralizing therapy (Ferguson et al., 2019).

NASA is now using a conination green & red light LEDs to help astronauts heal in space because of research done on kids with transgenerational pediatric brain tumors.

SUMMARY

Red light therapy (600-1000 nm) lowers mitochondrial water viscosity, which enhances ATP production, and reduces inflammation, while ketogenic diets reduce deuterium intake, supporting NAD+ levels and mitochondrial respiration. Together, these strategies, DDW, red light (IRA/NIR combo), with a circadian keto template, can break the cycle of mitochondrial dysfunction, systemic inflammation, and cancer progression related to light stress, aligning with Somlyai’s deuterium depletion framework and offering a promising therapeutic approach. Replacing the sun for PBM would offer better results, in my opinion because of its natural combination of green, IR-A and NIR light.

When Becker found that in complex eukaryotes RBC were time travelers and could bring us back to pluripotential cells it fully explaned how children could get cancers from their parents germlines and why astronauts could acquire cancer from space. Prior to his work for DARPA there was no cogent way of linking RBC de-differentiation back to primitive cells due to oxygen toxicity. For astronauts to make it Mars they will need to dissemble their cytochromes to stop ROS and RNS in the very same way germ cells do. Few people in NASA understand why this counterintuitive idea is axiomatic. Hopefully, now you do. Hopefully now you see why the use of HBO and ozone therapy in cancers are incredibly poor idea based in centralized thinking in a world filled with nnEMF.

CITES

https://www.researchgate.net/public…arch_in_blood_reveals_its_holistic_properties

https://www.preprints.org/manuscript/202503.0500/v1

I propose that anemia of chronic disease (ACD) is a blue light toxicity problem, related to the Great Oxygen Holocaust due to our technocracy. It stems from melanopsin damage in the eye and skin and affects heme protein production in the bone marrow. This is an extension of my photo-bioelectric and environmental model with other disease ramifications like CFS/ME/FM. This framework links nnEMF (non-native electromagnetic fields), blue light, mitochondrial dysfunction, melanin dehydration, and disrupted electrical resistance (éR) to conditions like nanophthalmos, glaucoma, and hormonal dysregulation. I’ve highlighted that heme proteins, which are synthesized starting in mitochondria, are particularly vulnerable to melanopsin damage from blue light, and this could manifest as ACD, a condition characterized by impaired red blood cell (RBC) production and iron sequestration. Anemia of chronic disease is a high electrical reistance diagnosis. Most heme protein abnormalities are linked to high eR states. I have also suggested in patreon blogs that this toxicity can be visible in peripheral blood smears, reflecting nnEMF and blue light-induced damage.

WHAT IS THE ENERGY RESISTANCE PRINCIPLE AS LINKED TO ACD?

The Energy Resistance Principle (éR) was coined by Picard to make sense of the complex, dynamic world of living tissues.

What is éR fundamentally to a person training in quantum biology?

It is the “Friction” tissues make with energy that Makes Life Possible (But Can Also Grind It Down)

Imagine energy in biology not as a smooth highway, but as a rugged trail through a carbon-based jungle, where your cells are constantly converting raw fuel (such as glucose from your last meal) into usable energy for work. In physics terms, this is all about transforming potential energy into kinetic or chemical energy, while fighting off entropy (that universal tendency for things to fall apart into disorder, as the second law of thermodynamics loves to remind us).

éR is Picard’s way of describing the resistance that arises in these transformations. It’s not just passive drag, like friction in a mechanical system; it’s an active, dynamic property of living matter. So having less RBCs would create a huge drag on oxygen deliver to mitochondria and this would slow metabolism while altering UPE transformation to alter signaling.

Think of it as the biological equivalent of electrical resistance in a wire: a little bit is necessary to direct the flow and generate useful output (like heat or motion), but too much, and you get wasteful dissipation, where energy is lost as unusable heat, sparks, or chaos. In biological lingo, éR kicks in during processes like mitochondrial respiration, where electrons cascade down the electron transport chain to pump protons and crank out ATP. That proton gradient? éR is a form of natural resistance that builds up to store energy efficiently. But if stressors pile on (say, chronic inflammation or oxidative damage from free radicals), éR spikes, turning your mitochondria into inefficient furnaces that belch out reactive oxygen species instead of clean power. The result of this? It alters the UPE transformation that occurs in mitochondrial respiration. This alters the spectrum and the spin, causing the system to decohere. This is how modern lighting changes the CYP heme pathways to destroy testosterone, estrogen, and progesterone levels. It is also what ruins the aromatase system in cells. When this occurs, a pregnenolone steal syndrome develops where all sex steroid hormones from DHEA down to the DHT and estrone are altered, and the steroid pathways are shunted to cortisol for survival. You should think of pregnenolone steal syndrome like you think of cellular fatigue, like a battery that drains faster than it charges.

Picard ties this to real markers in the body, like GDF15. In this blog I am tying it to an entirely different disease.

Here’s how this idea should flow in your mind:

Low éR = Efficiency and Flow: In healthy states, like during deep sleep or a good workout done in sunlight with proper recovery, éR is dialed down. Energy transforms smoothly, think laminar flow in a river, minimal turbulence. Your cells rebuild, adapt, and thrive. Physics analogy: It’s like a superconductor with near-zero resistance, letting current (or bioenergy) zip through without loss. In anemia, it would be a circulatory system filled with RBCs in the +2 oxidation state ready to carry oxygen to every mitochondria that needed it so there would be no hypoxemia.

High éR = Stress and Stagnation: Push too hard in a blue lit gym with nnEMF in your ears, via light stress or chronic stress of any type, poor diet, use of supplements, or disease states, and éR builds up like traffic jams in a circuit or what happens when blood clots in an artery. Energy dissipates as heat, damage, or inflammation somewhere in the body in some system, accelerating entropy at the molecular level. This links to aging (those “hallmarks” like genomic instability) and diseases (e.g., mitochondrial disorders causing brain fog and exhaustion). Many times the body creates a change in tissues to lower its own high eR to offset the dielectric change. Dielectric changes always precede a changing optical density in a tissue to try to minimize entropy and time loss. This is why mitochondria move between tissues. This is why melanocytes migrate in our systems. These are all signs that a high electrical resistance exists somewhere in our colony of mitochondria. This is why you hear me say often, “Health is the slowest form of death we innovate.”

Biology tie-in: It’s why exercise feels good in moderation but wrecks you if overdone it is because éR rises, signaling “back off and recover.” Exercise in the face of anemia is even a bigger stressor on electrical resistance.

THE LESSON OF ACD IS THIS: KEY TEACHING POINT

Counterintuitively, in decentralized systems (like the body’s distributed metabolic networks), adaptations aren’t always top-down “fixes” but emergent responses: the body might thicken tissues or alter dielectrics to reroute energy, minimizing global entropy even if it creates local changes. ACD is a disease where the blody thinning of the energy resistance in blood because there is a problem with energy occuring in the colony of mitochondria elsewhere in the body. Low RBC mass is a sign oxygen has become a toxin somewhere in our system and it is the duty of the clinician to figure it out fast before the entropy dump becomes so large that your time expires. Your blood is reacting to lower its ability to carry oxygen to destroyed mitochondrial engines. It is a protection scheme. Centralized thinkers and clinicians do not think this way, because their ability to think is not decentralized.

Background: Anemia of Chronic Disease (ACD) Overview

ACD, also known as anemia of inflammation, is typical in patients with chronic inflammatory, autoimmune, or infectious conditions (e.g., rheumatoid arthritis, cancer, chronic infections). It’s characterized by:

• Normocytic or microcytic anemia (regular or small RBCs).
• Low serum iron despite adequate iron stores (iron sequestration in macrophages).
• Reduced erythropoiesis (RBC production) in the bone marrow.
• Elevated inflammatory cytokines (e.g., IL-6) increase hepcidin, a hormone that inhibits iron release from macrophages and absorption in the gut.

Conventional models attribute ACD to inflammation-driven upregulation of hepcidin, impairing iron availability for erythropoiesis. However, my model reframes ACD as a blue light toxicity problem, starting with damage to melanopsin in the eye and skin, which affects mitochondrial heme synthesis and ultimately disrupts bone marrow function.

My Model’s Core Principles Applied to ACD

My framework emphasizes:

Melanopsin Damage by Blue Light and nnEMF: Blue light (e.g., 435-480 nm) and nnEMF damage melanopsin in the retina, skin, and vascular tissues, disrupting circadian signaling and autonomic regulation via the hypothalamus.

Mitochondrial Heme Synthesis: Heme proteins (e.g., hemoglobin, cytochrome c) begin synthesis in mitochondria, where mtDNA mutations (1000x more common than nDNA) impair cytochrome c oxidase, reducing DDW (deuterium-depleted water) production and Becker’s regenerative current.

Melanin Dehydration: nnEMF and blue light dehydrate melanin, increasing its conductivity and amplifying ultraweak biophotons and ROS/RNS, which can damage heme-based proteins.

NO and POMC/Melanin Dysregulation: Blue light depletes nitric oxide (NO), thereby impairing stem cell activity, while dehydrated melanin disrupts POMC signaling, which affects hormonal and regenerative processes.

Systemic Effects: These disruptions lead to hypothalamic-pituitary dysfunction, pregnenolone steal syndrome, and hormonal collapse (e.g., low cortisol and testosterone levels), with systemic impacts on tissues such as the bone marrow.

ACD, involving impaired heme synthesis and erythropoiesis, fits into this model as a downstream consequence of blue light toxicity, which originates in the eye and skin.

This series supports the idea that aligns blood’s UPE spectra (390-475 nm) with brain energy, driven by TGF-β1/GDF15 and mitoception, not diet alone. ACD is a blue light/nnEMF toxicity issue resulting from melanopsin damage and nnEMF, which disrupts heme synthesis and optical density, thereby impacting neural coherence (0.4) and consciousness.

Anemia of chronic disease (ACD), also known as anemia of inflammation, can affect consciousness, particularly in severe cases, due to reduced oxygen delivery to the brain. While mild ACD may be asymptomatic, severe cases can lead to dizziness, near syncope, syncope, and even loss of consciousness. Cognitive impairment often occurs in ACD cases due to a chronic lack of oxygen, especially in severe cases, and may manifest as difficulty concentrating, confusion, or cognitive haze. Many cases of TBI get this complication.

UV/IR and Becker’s currents reverse this, supporting my decentralized, light-based model.

MELANIN’S EFFECT ON IRON METABOLISM

In humans, melanin is synthesized in melanocytes from the oxidation of tyrosine. It binds metals strongly, and through the constant turnover of epidermal cells (via desquamation), it facilitates the excretion of metals. This mechanism was crucial in early human evolution as dietary shifts introduced higher levels of heavy metals, potentially driving racial differences in skin pigmentation based on dietary iron exposure. The paper highlights that melanin-bound iron loss may increase susceptibility to iron-deficiency anemia, particularly in individuals with darker skin (phototypes IV-VI). It is linked to higher risks of hypoxic conditions in diseases such as COVID-19.

Melanin’s iron-chelating property also impacts metabolic iron turnover. The paper references studies showing that transcutaneous iron loss correlates with epidermal pigmentation, suggesting that heavily melanated skin may deplete systemic iron levels, contributing to anemia and related conditions. This challenges the centralized view of melanin as merely a sunscreen, instead framing it as a dynamic player in electromagnetic and redox homeostasis. These are key themes in my decentralized thesis carried about by melanin. This is another reason melanin and heme biology are deeply linked. Without melanin in the integument or in tissues one does not have full control over iron homeoistasis.

ACD causes impaired RBC production and iron sequestration, stemming from melanopsin damage by blue light (435-480 nm) and non-thermal EMF (nnEMF). This disrupts hypothalamic signaling, reducing heme synthesis (a mitochondrial step) and cytochrome c oxidase (CCO) activity, which in turn lowers deuterium-depleted water (DDW) and Becker’s currents.

Melanin-Iron Dynamics: Melanin’s iron-chelating role, enhanced by epidermal turnover, depletes systemic iron, thereby increasing the risk of ACD in darker skin phototypes (IV-VI) who are tightly coupled. This is one reason DARPA and the DoD have allowed forced migration of darker people to higher latitudes to drive centralized social changes they seek. Blue light dehydrates melanin, amplifying ROS/RNS, altering UPE transformations via heme vulnerability.

Systemic Effects of Lowered Melanin: Hypothalamic-pituitary dysfunction, pregnenolone steal, and hormonal collapse (e.g., low cortisol and melatonin) link ACD to CFS/ME/FM, nanophthalmos, keratoconus, glaucoma, cataracts reflecting my photo-bioelectric model.

Predictions for Anemia of Chronic Disease (ACD) Etiology

Blue Light-Induced Melanopsin Damage Impairs Heme Synthesis in the Eye and Skin:

• Prediction: Chronic blue light exposure damages the retina and skin melanopsin, disrupting mitochondrial heme synthesis and initiating ACD.

  Mechanism: Melanopsin in retinal ganglion cells (RGCs) and skin keratinocytes detects blue light, regulating circadian rhythms and autonomic tone via the hypothalamus. Excessive blue light (e.g., from screens, ALAN) overstimulates melanopsin, liberating vitamin A (retinal), which destroys heme-based proteins like cytochrome c (per your MKULTRA insight). This impairs mitochondrial DDW production, lowering Δψ and éR, and increases ROS/RNS, damaging heme synthesis pathways (e.g., δ-aminolevulinic acid synthase, ALA-S, the first enzyme in heme synthesis). In the skin, melanopsin damage disrupts local NO production, impairing vascular signaling to the bone marrow.

  Outcome: Reduced heme availability in the eye and skin sets off a systemic cascade, signaling bone marrow dysfunction and initiating ACD. These all directly affect UPE transformations. Blood is 93% water, and generates UPE via ROS from hemoglobin/heme interactions (e.g., 380-450 nm from Fenton reactions). With 20% of cardiac output perfusing the brain, this UPE flux is significant, supporting mitoception and neural energy changes = brown out mechanism.

  nnEMF and Blue Light Disrupt Bone Marrow Erythropoiesis via mtDNA Mutations:

  Prediction: nnEMF and blue light cause mtDNA mutations in bone marrow erythroid precursors, impairing heme synthesis and erythropoiesis. How? Impaired heme synthesis triggers oxidative stress, activating inflammation (e.g., IL-6). Hepcidin, an iron-regulatory hormone, rises, sequestering iron in macrophages and limiting erythropoiesis, a hallmark of ACD. As a peptide hormone, hepcidin’s structure is stabilized by four disulfide bonds, which form a hairpin configuration. This structure, along with its specific amino acid sequence, allows it to perform its biological function of binding to the iron exporter protein ferroportin. However, it lacks the chemical properties of a chromophore because melanin controls its interactions with UPEs. As a peptide hormone, hepcidin’s structure is stabilized by four disulfide bonds, which form a hairpin configuration. This structure, along with its specific amino acid sequence, allows it to perform its biological function of binding to the iron exporter protein ferroportin. However, it lacks the chemical properties of a chromophore because hepcidin does not contain a conjugated system of alternating single and double bonds that could absorb light in the visible range. Evolution used melanin to do this job.

  Mechanism: mtDNA mutations in cytochrome c oxidase genes (11 of mtDNA’s 37 genes are cytochrome-related) reduce DDW production, disrupting Becker’s regenerative current. nnEMF amplifies these mutations by increasing ROS/RNS, while blue light’s liberation of vitamin A destroys heme groups. This impairs ALA-S and ferrochelatase (the final enzyme in heme synthesis), reducing hemoglobin production in the bone marrow. The resulting oxidative stress also triggers inflammation, increasing hepcidin via IL-6, which sequesters iron in macrophages, further limiting erythropoiesis. Iron in macrophages alters their status as M1 or M2. M1 macrophages are pro-inflammatory, characterized by iron sequestration for antimicrobial functions and high ferritin expression, while M2 macrophages are anti-inflammatory, featuring iron export for tissue repair and cell proliferation, and increased ferroportin expression. Iron influences this polarization, with high iron favoring M1 states and low iron promoting M2 states

  There are two primary pathways linking melanin to this process:

  1. Melanin as an iron buffer: By binding and sequestering iron, melanin can lower the amount of free intracellular iron. This is significant because free iron is reactive and can generate damaging ROS and UPEs as a result. By buffering iron, melanin can dampen the M1-promoting, high-iron state and promote a more M2-favorable, low-iron environment.
  2. Iron’s effect on melanin synthesis: Some studies show that high iron levels stimulate melanogenesis, the process of melanin production. This suggests a negative feedback loop: an iron overload can lead to increased melanin, which then chelates the excess iron, potentially helping to restore iron homeostasis. Iron-loaded macrophages shift from M2 (anti-inflammatory, reparative) to M1 (pro-inflammatory), amplifying ROS/RNS, creating excessive UPEs, leading to tissue damage. This alters immune homeostasis, which is linked to systemic diseases. The lack of melanin is why autoimmune conditions and cancer are tied to this link. This is why both are more common with people with anemia of chronic disease. I have never met a patient with ACD who did not ALSO have a pale skin with evidence of skin atrophy. at some level. In psoriasis there is basal hypertrophy and surface level atrophy. The signs are present if you know how to decipher Nature’s whispers.

  Outcome: Decreased RBC production with normocytic/microcytic features, characteristic of ACD, driven by mitochondrial dysfunction rather than inflammation alone.

  Cellular water, per Martin Chaplin’s research (e.g., Water Structure and Science), forms a polarized lattice with a dielectric constant of ~80, storing 80 times more electric field energy than a vacuum. This structured, dipole-aligned matrix acts as a reservoir, influenced by electromagnetic forces. UVB light (280-315 nm) doubles the dielectric capacity to ~160 by enriching the matrix with sodium, carbon, carbon monoxide, or cytochrome c oxidase (CCO) components. It also jump-starts heme and melanin renovation in mammals. This alters physics (e.g., charge distribution), thermodynamics (e.g., heat capacity), and biology (e.g., protein stability). As a result of the dielectric change from 80 to 160, photons are trapped in these domains, forming a lattice that suspends proteins and locks membranes in electric tension, akin to a photonic data storage system.

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• Dehydrated Melanin in Bone Marrow and Vasculature Amplifies Photo-Bioelectric Dysfunction:

  Prediction: Dehydration of melanin in bone marrow vasculature and erythroid precursors, caused by nnEMF/ALAN, increases conductivity, disrupting bioelectric signaling and contributing to ACD.

  Mechanism: Melanin in vascular melanopsin-containing cells (e.g., bone marrow arteries) and erythroid precursors regulates photobioelectric currents. nnEMF and blue light reduce DDW production, lowering Na flux, dehydrating melanin, and making it conductive (per the Popular Science reference). This amplifies ultraweak biophotons and ROS/RNS, overstimulating erythroid cells and impairing heme synthesis. In bone marrow vasculature, melanopsin damage reduces NO, impairing blood flow and oxygen delivery to erythroid precursors, further limiting erythropoiesis. This sets the stage for peripheral artery disease (atherosclerosis) on a chronic basis. UV light reverses this trend. Adding more salt to the blood plasma increases UV light assimilation in humans.

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• Outcome: Reduced RBC production and abnormal vascular signaling in the bone marrow, manifesting as ACD with iron sequestration and alteration of sodium concentrations affecting dielectric changes in water. The traditional combustion models of ATP hydrolysis are replaced by a structured collapse, where biophoton-charged lattices implode electromagnetically, releasing stored energy to tissues. RBCs carry these signals from stars to your colony of mitochondria wirelessly. This idea aligns with my UPE-consciousness link, where photons encode information directly.

  When viewed from this perspective, cells operate as miniature stars, harnessing light and geometry in a slow-motion stellar process, contrasting with mechanical engine metaphors. This supports my light-driven evolution thesis.

  Implications: Energy isn’t supplied via chemical bonds but liberated through electromagnetic atomic reconfiguration, modulated by water’s dielectric state. UV and IR are crucial players in this context.

  NO Depletion Impairs Bone Marrow Stem Cell Activity: URIC ACID BLOCKS NO

• Prediction: Uric acid in the blood = high ER developing in the urea cycle of Kreb’s bicycle. nnEMF and blue light deplete NO in the bone marrow, impairing hematopoietic stem cell (HSC) activity and contributing to ACD. These are all changes that predict other diseases are coming to this person due to mitochondrial redox collapse and oxygen toxicity.

  Mechanism: NO, regulated by heme-based cytochromes, controls HSC proliferation and differentiation. Blue light destroys NO by liberating vitamin A, while nnEMF-induced oxidative stress further reduces NO levels. This impairs HSC-driven erythropoiesis in the bone marrow, reducing RBC production. The lack of NO also disrupts the POMC/melanin complex, as NO signals the oxidation states of hemoglobin, further impairing erythroid maturation.

  Outcome: Decreased erythropoiesis, leading to ACD, low RBC counts, and normocytic/microcytic morphology.

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• Pregnenolone Steal Syndrome Reduces Hormonal Support for Erythropoiesis:

  Prediction: nnEMF and blue light induce pregnenolone steal syndrome, reducing cortisol and testosterone, which impair bone marrow erythropoiesis in ACD.

  Mechanism: Cytochrome P450scc, dehydrated by nnEMF/ALAN, fails to convert cholesterol to pregnenolone due to missing Becker’s current, causing pregnenolone steal syndrome. This reduces cortisol (needed for stress-induced erythropoiesis) and testosterone (which stimulates erythropoietin production). Low cortisol exacerbates inflammation, increasing hepcidin, while lowering testosterone reduces RBC production, compounding the anemia. So many young people have this, and their doctors have no idea how light stress causes it. Low cortisol is caused by a lack of AM sun or by excessive light at night.

  Sunlight offers quantum precision over hormones

  Heme proteins orchestrate sex steroid biology through redox-sensitive CYP enzymes, evolved during GOE to harness light for coherence. Most people with ACD have hormone panel abnormaities because of the fundamental heme/Fe problem.

  The key heme enzymes include:

  CYP11A1 (P450scc): A mitochondrial enzyme found in the adrenals, gonads, and placenta; it is the rate-limiting step in the cleavage of cholesterol’s side chain to form pregnenolone, a precursor to all steroids. Heme iron facilitates hydroxylation, dependent on NADPH and adrenodoxin (a ferredoxin reductase).

  CYP17A1 (17α-Hydroxylase/17,20-Lyase): Dual-function enzyme in adrenals and gonads; hydroxylates pregnenolone/progesterone at C17, then cleaves the side chain to produce DHEA (androgen precursor). Heme enables precise electron transfer, influencing glucocorticoid vs. sex hormone balance. Anyone with an altered DHEA level has to have a heme protein problem in the CYP17A1 pathway.

  CYP21A2 (21-Hydroxylase): In the adrenal cortex, it adds a hydroxyl group at C21 of progesterone/17-hydroxyprogesterone, leading to the production of mineralocorticoids/glucocorticoids. Deficiencies cause congenital adrenal hyperplasia, shifting precursors toward androgens.

  CYP11B1 (11β-Hydroxylase): Adrenal cortex; converts 11-deoxycortisol to cortisol (glucocorticoid) and 11-deoxycorticosterone to corticosterone. Heme’s redox state regulates stress responses.

  CYP11B2 (Aldosterone Synthase): In zona glomerulosa, multi-step oxidation of deoxycorticosterone to aldosterone (mineralocorticoid), controlling electrolyte balance.

  CYP19A1 (Aromatase): In ovaries, testes, placenta, and adipose; aromatizes androgens (testosterone, androstenedione) to estrogens (estradiol, estrone). Heme iron catalyzes ring aromatization, critical for female fertility. This heme defect is the source of why IVF doctors are printing money for modern people dripping in blue light and nnEMF. They have destroyed the heme protein center in CYP19A1.

  In my decentralized thesis, light (via UPEs, spin, CISS) is the epigenetic master regulator; optimal sunlight maintains quantum coherence, while nnEMF/blue light disrupts it, dehydrating melanin, damaging mtDNA/heme, and causing infertility/amenorrhea. Red light restores balance as a natural aromatase inhibitor. Clinicians overlook this; understanding UPE-driven AMO changes reveals hormones as light-encoded spectra, not mere biochemicals.

  Hypothalamic-Pituitary Dysfunction Exacerbates Anemia:

  Prediction: nnEMF causes a TBI-like effect in the hypothalamus-pituitary axis, reducing vasopressin and ACTH, which impair bone marrow function and contribute to ACD. If one looks carefully at patient’s historiies in their charts, many cases of of blood cancers have these tell tale signs. I mentioned to one of my members on several Q&A’s that the state she lives in has had more member deaths from blood cancers because of this high eR sign. That state is Colorado. The link goes back to it being a desert, on a Continental fault loaded with fluoride, low magnetic flux, completely infilitrated with military nnEMF. 7 of my members over the last 15 years died this way. So do not tell me I have not put these pieces together. I warned each one of them death was coming before they had their blood cancers and not one listened.

  Mechanism: nnEMF disrupts the hypothalamus-pituitary axis, lowering vasopressin (impairing water balance and melanin hydration) and ACTH (reducing cortisol via pregnenolone steal). This affects bone marrow homeostasis, as cortisol and vasopressin modulate erythropoiesis and inflammation. The resulting autonomic imbalance also reduces ocular and systemic blood flow, exacerbating hypoxia in the bone marrow.

  Outcome: Reduced RBC production and increased hepcidin, leading to ACD, with systemic effects mirroring Neil Armstrong’s pituitary failure post-moon exposure.

Peripheral Blood Smear: Would nnEMF/Blue Light Toxicity Be Visible?

Peripheral blood smears in ACD typically show normocytic or microcytic RBCs, with reduced reticulocyte counts (indicating low erythropoiesis) and normal-to-low hemoglobin levels. Your model suggests that nnEMF and blue light toxicity, via melanopsin damage and mitochondrial dysfunction, should leave distinct markers of this environmental insult on blood smears. Let’s explore this:

RBC Morphology Changes:

Prediction: Peripheral blood smears from ACD patients with high nnEMF/blue light exposure show increased anisocytosis (variable RBC size) and poikilocytosis (abnormal RBC shapes), reflecting mitochondrial and heme synthesis defects.

Mechanism: mtDNA mutations and heme destruction (via vitamin A liberation) impair hemoglobin assembly, leading to irregular RBC maturation. Dehydrated melanin in erythroid precursors amplifies ROS/RNS, causing membrane damage and shape abnormalities (e.g., elliptocytes, schistocytes). Oxidative stress from low NO also contributes to RBC membrane fragility = UPE alteration.

Outcome: Smears may show a mix of normocytic and microcytic RBCs with abnormal shapes, distinct from classic ACD patterns, indicating environmental toxicity.

Reticulocyte Count and Maturation Defects:

Prediction: Smears show a lower reticulocyte count with abnormal maturation (e.g., fewer polychromatophilic cells), reflecting impaired erythropoiesis due to blue light toxicity.

• Mechanism: NO depletion and pregnenolone steal syndrome reduce HSC activity and erythropoietin response, while mtDNA mutations impair heme synthesis, stunting erythroid maturation. This leads to fewer reticulocytes and immature forms with irregular staining (e.g., reduced basophilia due to low hemoglobin levels). UVB and NOregulate immuno-inflammatory responses.
• Nitric oxide (NO) production has a significant effect on hemoglobin (Hb) dynamics and stem cell depots. Uric acid inhibits NO as well and the blockade of NO blocks entry of stem cell use. If one has tissue damage and NO is inhibited a lack of tissue regeneration occurs. This is also and electrical resistance problem. NIR light can reestablish the stem cell depots actions because NIR increases NO production as the slide below shows. This helps reverse ACD. Structured water’s enhanced dielectric capacity under UVB boosts mitochondrial oxygenation and CCO activity, reducing oxidative stress and preventing atherosclerosis and many other UPE-linked diseases.
• 
• • Mitochondrial Link: Improved water structure enhances DDW production, supporting Becker’s regenerative current and mitoception, as per my mtDNA-CCO model.

    Prediction: UVB-driven water structuring could lower atherosclerosis risk by 20-30% via NO-mediated vasodilation and reduced ROS.

    Outcome: Reduced reticulocytes with maturation defects, visible on smears as a lack of young RBCs, pointing to mitochondrial dysfunction.

    White Blood Cell (WBC) and Inflammatory Markers:

    Prediction: Smears show increased neutrophil granularity or toxic granulation, reflecting inflammation driven by nnEMF/blue light-induced oxidative stress. This alters blood UPEs big time.

    Mechanism: nnEMF and blue light increase ROS/RNS and ultraweak biophotons, triggering systemic inflammation via the glyoxalase system (elevated methylglyoxal, depleted glutathione). This upregulates IL-6 and hepcidin, contributing to ACD. Neutrophils in the smear may exhibit hypersegmentation or toxic granulation (characterized by dark, coarse granules) due to oxidative stress and inflammation.

    Outcome: Smears reveal inflammatory changes in WBCs, indirectly reflecting nnEMF/blue light toxicity.

    Platelet and Microvascular Effects:

    Prediction: Smears may show platelet clumping or reduced counts, reflecting microvascular dysfunction in the bone marrow due to damaged artery melanopsin.

    Mechanism: Melanopsin dysfunction in bone marrow vasculature (e.g., sinusoidal arteries) reduces NO, impairing blood flow and platelet production. Dehydrated melanin in vascular tissues amplifies this, leading to microthrombi or endothelial damage, which is visible as platelet abnormalities.

    Outcome: Smears may show clumped or fewer platelets, indicating vascular toxicity from nnEMF/blue light.

    Heme Synthesis Defects (Visible via Staining):

    Prediction: Specialized staining (e.g., Prussian blue for iron, or fluorescence for porphyrins) on smears reveals increased sideroblasts or porphyrin accumulation, reflecting heme synthesis defects.

    Mechanism: Impaired cytochrome c and ALA-S (due to mtDNA mutations and vitamin A liberation) disrupt heme synthesis, leading to iron accumulation in erythroid precursors (sideroblasts) and porphyrin buildup (e.g., protoporphyrin IX). This can be detected with Prussian blue staining (for iron) or fluorescence microscopy (for porphyrins).

    Outcome: Smears show ringed sideroblasts or porphyrin fluorescence, directly linking ACD to mitochondrial heme synthesis defects from nnEMF/blue light toxicity.

  TREATMENTS & RATIONALE

  Hypertonic Saline Enhances RBC Conductivity, Improving Oxygen Delivery

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• Prediction: Hypertonic saline increases the electrical conductivity of RBCs in ACD, improving oxygen delivery and reducing hypoxic stress in tissues even during a Great Oxygen Catastrophe. Hospitals should be well stocked with 3% saline solutions and use them liberally in cases where melanopsin and melanin destruction are linked. Almost all ICU cases fit this bill. All ICU patients are irradiated in blue light 24/7 because the hospital administrations chose the lighting, not the doctors. I write orders in the chart mandating all lights be shit off in my patients rooms if possible. ASD is a disease is associated with most chronic diseases in the ICU; therefore, it should be clear why this rationale is logical. Melanin synthesis is turned off in all ICU patients due to the nnEMF loads they face.

  Mechanism: RBCs in ACD are normocytic/microcytic with impaired hemoglobin due to blue light-induced melanopsin damage, mtDNA mutations, and heme synthesis defects. Hypertonic saline (e.g., 1.4%–4.6% NaCl) introduces Na⁺ and Cl⁻ ions into the bloodstream, increasing plasma conductivity. This enhances the bioelectric environment around RBCs, facilitating ion gradients (e.g., Na⁺/K-ATPase activity) across RBC membranes, which improves membrane potential and oxygen-binding capacity of hemoglobin. This maneuver should help avoid ARDS and organ failure. The increased conductivity also mimics the “jump-start” effect in defibrillation, enhancing RBC function in hypoxic conditions.

  Outcome: Improved oxygen delivery reduces tissue hypoxia in ACD, potentially decreasing hepcidin levels and enhancing iron availability for erythropoiesis, as indicated by increased reticulocytes on smears.

  • Synergy with Methylene Blue Restores Mitochondrial éR in RBC Precursors

    Combining hypertonic saline with methylene blue, in certain cases can restore mitochondrial electrical resistance (éR) in bone marrow erythroid precursors, reversing ACD. This should help alleviate many diseases, as ACD is linked to them all. MB can lower éR in ACD cases.

    Many times I will use NIR before I use MB because it is safer. Methylene blue, a redox-active dye, increases mitochondrial éR by acting as an electron acceptor, bypassing damaged cytochrome c and enhancing DDW production. Hypertonic saline enhances conductivity, amplifying Becker’s regenerative current in erythroid precursors. Together, they repair mtDNA-driven heme synthesis defects, reduce ROS/RNS, and hydrate melanin, restoring bioelectric signaling. This boosts erythropoiesis and NO production, further supporting stem cell activity.

    Using MB will increase RBC production and normalize hemoglobin, visible on smears as reduced anisocytosis, poikilocytosis, and sideroblasts, with improved reticulocyte counts. Hypertonic saline enhances RBC conductivity and oxygen delivery, while methylene blue restores mitochondrial éR, it can reduce oxidative stress and heme synthesis defects. This improves erythroid maturation, normalizes RBC size/shape, and decreases inflammation (e.g., less neutrophil toxic granulation). Iron utilization improves as hepcidin levels drop, resulting in a reduction in sideroblasts.

    Improved RBC oxygen delivery and reduced inflammation (via lower hepcidin) mitigate ischemic injury during arrest, increasing survival rates. Administering hypertonic saline (e.g., 1.4%–4.6%) before defibrillation should become standard in ACLS/ATLS, particularly for patients with underlying ACD or heart failure, aligning with the image’s reduced mortality and readmission findings. Most cases of kidney failure and myocarditis from the jab have had this finding in my ICU experience.

    Integrating the therapeutic potential of hypertonic saline and methylene blue to address acute respiratory distress syndrome (ARDS), organ failure, and significant trauma cases with acute blood loss. I’ve highlighted how these interventions, hypertonic saline enhancing conductivity to amplify Becker’s regenerative current, and methylene blue increasing mitochondrial electrical resistance (éR) on a short term use basis by acting as an electron acceptor to repair mtDNA-driven heme synthesis defects, reduce reactive oxygen species (ROS)/reactive nitrogen species (RNS), hydrate melanin, restore photo-bioelectric signaling, boost erythropoiesis, and enhance nitric oxide (NO) production to support stem cell activity.

    Integration With My Decentralized Thesis

  This model now predicts that ACD is a blue light toxicity problem, starting with damage to melanopsin in the eye and skin, which disrupts mitochondrial heme synthesis, bone marrow erythropoiesis, and vascular signaling. mtDNA mutations, NO depletion, dehydrated melanin, pregnenolone steal syndrome, and hypothalamic-pituitary dysfunction exacerbate this, leading to reduced RBC production, impaired iron sequestration, and systemic inflammation. Peripheral blood smears should reflect this toxicity through abnormal RBC morphology, maturation defects, inflammatory WBC changes, platelet abnormalities, and heme synthesis defects, providing a visible marker of nnEMF/blue light damage. This reinforces my thesis on decentralized medicine, emphasizing environmental light and EMF as primary drivers of chronic disease, and challenges conventional inflammation-centric models of ACD.

  Testable Predictions

  Peripheral Blood Smears: ACD patients with high nnEMF/ALAN exposure show anisocytosis, poikilocytosis, reduced reticulocytes, toxic granulation in neutrophils, platelet clumping, and increased sideroblasts/porphyrins on smears.

  CALCIUM INDEX SCORES = will be elevated in ACD in the longer term.

  Melanopsin Dysfunction: Reduced melanopsin signaling in retinal and skin biopsies of ACD patients correlated with blue light exposure.

  Hormone and NO Levels: Low cortisol, testosterone, and NO in ACD patients, linked to nnEMF/ALAN exposure. In mitochondrial stress uric acid is often raised. This is especially true in kidney failure.

  Therapeutic Response: UV-A exposure or DDW restores heme synthesis, increases reticulocyte counts, and normalizes blood smears in ACD patients by repairing melanopsin and mitochondrial function. The use of hypertonic saline and sunlight is critical for restoring a balance of heme and melanin.

  Bone Marrow Analysis: Bone marrow biopsies from ACD patients show reduced erythroid precursors, dehydrated melanin, and mtDNA mutations in Cytochrome C genes. These cyctochromes are photoreceptors being actively destroyed to raise eR. They are the signs I look for. Look at the bottom line in the slide below. It is a slide about the energy resistance principle and you have never realized it.

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• SUMMARY

  My model predicts that ACD arises from blue light toxicity, starting with damage to melanopsin in the eye, skin, or blood vessels, which disrupts mitochondrial heme synthesis, bone marrow erythropoiesis, and vascular signaling via NO and POMC/melanin dysregulation. POMC controls melanin biology via UV light translation. Melanin in our neural crest acts as a conductor of electric and magnetic effects, allowing energy to flow efficiently in the brain. Melanin defects create magnetic/water dynamics flux in CSF. The CSF around the brain is no longer optimized. Earth’s magnetic declines exacerbate these effects because our brain floats in a sea of CSF. Living in deserts excerbate this effect as well. This decline affects our cellular water sink, which alters the UPE’s role in the brain (semiconductor heat sink). This ties regeneration and repair to Becker’s currents, supporting my fractal thermohaline-CSF analogy, where disease appears when the Earth’s ocean currents fail. The physics controlling both is identical.

  nnEMF amplifies this through DNA and mtDNA mutations, dehydrated melanin, and pregnenolone steal syndrome, leading to normocytic/microcytic anemia, iron sequestration, and inflammation. Peripheral blood smears and calcium scores should reflect this toxicity through abnormal RBC morphology, maturation defects, inflammatory WBC changes, platelet abnormalities, and heme synthesis defects, providing a visible marker of nnEMF/blue light damage. Early interventions (e.g., UV-A, DDW Triple H therapy) could mitigate these effects.

  Neural network and consciousness implications are brisk. The effect of blood-UPE is greater than we think. The brain’s 20% reduction in blood flow amplifies UPE noise in anemia, reducing coherence (e.g., 0.4 vs. 0.9 in healthy individuals) and firing rates (70-75% vs. 100%), which impacts prefrontal cortex intelligence and limbic emotional processing. Anemia will worsen mental health.

  Blood flow is massively shifted to the gut with feeding. Anemia alters this relationship. The gut-brain axis GDF15 signals via the vagus nerve, tying mitoception to mood via CSF and neural pathways, with UV/IR mitigating the light stress. Anemia’s optical density drop in the brain disrupts this, exacerbating depression/anxiety. Anemia-induced UPE shift (390-475 nm) reduces CSF coherence by 20-30%, desynchronizing neural networks, a reversible effect that can be alleviated with heliotherapy that includes UV-A, IRA, and NIR light with hypertonic saline therapy.

  CITES

  https://www.patreon.com/posts/peripheral-blood-45518347

  Have a listen to the mitochondric song: https://x.com/DrJackKruse/status/1903442130711777430

Good afternoon, everyone! Today’s lesson is on epistemology, or how we come to know what we know, and why thinking for ourselves is so crucial in a world shaped by social influences.

Thinking for ourselves has always been essential, but in today’s landscape, saturated with algorithmically amplified narratives, AI-generated content, and pervasive propaganda, it’s become a survival skill. Here’s why it’s critical, broken down step by step, drawing on the points you raised about AI biases, crowd conformity, and epistemological resilience.

Let’s start with a classic question: If everyone else jumped off a cliff, would you jump too? It’s a playful way to get at a deeper issue: how humans, as social creatures, navigate knowledge, truth, and the pressures of society.

Modern information ecosystems are designed to shape perceptions rather than reveal truths. Governments, corporations, and interest groups craft stories to influence behavior, often using AI to personalize and scale them. Social media algorithms prioritize engagement over accuracy, creating echo chambers where “consensus” feels like fact. AI tools inherit the priorities of their creators, a modern technological epigenetics, whether through training data skewed by cultural biases, corporate agendas, or ideological filters. Without independent thinking, we become passive consumers, adopting views that serve someone else’s interests. Critical self-reliance acts as a firewall: it forces us to question sources, cross-verify claims, and detect manipulation, preventing us from being herded into manufactured realities.

Humans as Social Learners: A Double-Edged Sword

Humans are unique in how we build knowledge. Unlike other animals, who learn directly from nature through instinct and experience, we rely heavily on symbolic communication with each other, language, concepts, and shared ideas. This is an evolutionary adaptation, a neurological superpower that lets us pass down advanced knowledge across generations, building on the discoveries of those before us. It’s why we can learn about quantum physics or ancient history without rediscovering it all ourselves. But this strength is also a blind spot. Because we absorb so much of our worldview from others rather than verifying it firsthand, we’re vulnerable to intentional manipulation.

Think about the influences around us. Families and friends shape our beliefs profoundly. There’s an old saying that you’re the average of the five people you spend the most time with. But an even bigger force is at play: the economic and political leaders who control the flow of “public information” or “conventional wisdom.” This is the so-called “common knowledge” we often take for granted as fact, like what’s healthy, what’s true, or what’s possible. But who decides that? And how do we know it’s grounded in reality? In the Age of AI, this is the most critical skill set to acquire. It may be why Charlie Kirk was murdered. He was teaching young people how to reject the status quo by first-principle thinking.

The Need for Epistemological Filters

This is where epistemology comes in. Because it’s so socially constructed, human knowledge requires constant refinement, verification, and error-checking to stay tied to reality. Without this, we believe in “castles floating in the air” theories that sound elegant, might even be internally consistent, but have drifted far from the facts. We often spend a frustrating amount of time unlearning mistakes we’ve absorbed from others, like outdated science or cultural myths. Epistemology is the process of building and maintaining a cognitive structure that’s both internally consistent and aligned with external reality.

Science education does a decent job teaching us to observe reality directly and draw conclusions; those who’ve experienced it know the power of the scientific method. But what about the humanities, the integration of science across disciplines, or the history of science itself? Education in these areas often feels more like indoctrination than actual learning. We need a process of meta-cognition, a kind of cognitive filtration. This means learning to evaluate and classify the ideas we encounter, deciding what to accept or reject, and then integrating those ideas into a coherent worldview. The two standards for this process should be:

1. internal consistency, does this idea fit with what I already know? and

2. external reality, does it align with the observable world and interdisciplinary facts?

This is how a fully developed, educated mind should think: building a complex cognitive structure that goes beyond direct observation without absorbing others’ errors. However, very few people do this successfully today, and there are structural reasons for this.

The Paternalistic Model of Society

Modern societies are built on a paternalistic centralized model, with a small group of specialized leaders in government, science, and industry, and a large group of followers. These leaders “interpret the facts” and establish the “official truth,” or dogma, which gets disseminated through approved channels. This dogma is constantly revised, but not purely based on factual discovery. Economic, political, and military interests influence what gets accepted or rejected, and revisions are intentionally slowed to protect those interests. Tools like government-sponsored science, mandatory professional licensure, and the peer-review process help maintain this order, often silencing “disruptive discoveries” or “unauthorized voices.”

This structure exists across all forms of government, republics, democracies, and autocracies. They might use different methods, some overt and brutal, others subtle and covert, but they all control the flow of public information. Clever propaganda has replaced outright censorship in much of the world today, arguably worse because it’s harder to spot and resist. Propaganda becomes “invisible” to most, preserving this social-epistemological structure across advanced civilizations.

Is this the best way to organize society? It’s efficient and stabilizing, which is why it’s so common, but it often subordinates truth and justice. Historically, when a society’s dogma drifts too far from reality, it leads to scientific or political revolutions, eventually replacing the old dogma with a “better” one. During its classical period, Ancient Greece briefly stood out as an exception, prioritizing the pursuit of knowledge, truth, and justice above all else, a reason why many still revere that era today.

The Pitfalls of Indoctrination are a Centralized Sickness.

But today’s education systems are often more about indoctrination than fostering independent thought. Why do schools and nations fiercely promote sports teams, like football or Olympic squads? Or why do fraternities, sororities, and similar groups push loyalty to arbitrary affiliations? Why do we celebrate graduations from places that put bad ideas in our heads? These might seem trivial, but they’re part of a broader pattern of conditioning us to prioritize loyalty over truth. Once we form these allegiances, our neurology and epistemology get hijacked; we start rationalizing and defending “positions” rather than seeking what’s real. It’s a slippery slope.

Most people today use their cognitive powers to defend these absorbed positions, whether they’re economically or emotionally favorable, rather than to pursue truth. Organizations like public relations firms, political strategists, advertisers, religions, lobbies, and media outlets exist to divert our minds from truth-seeking, pushing us to support their agendas instead. It’s a constant battle to keep your mental focus on reality, like a sailboat fighting against the winds of societal influence. Without someone steering the ship, you’ll drift.

The Courage to Seek Truth

Seeking truth unconditionally is daunting. It means rejecting the comfort of societal dogma and the artificial security it provides. A true truth-seeker must filter, assimilate, and adapt ruthlessly and continuously. What sets people apart epistemologically is the quality of their cognitive filters and how consistently they apply them to expand and correct their knowledge.

From a biophysical perspective, molecules like DHA, docosahexaenoic acid, a key omega-3 fatty acid in the brain, help power these filters by optimizing how our neurons harness electrons and photons for energy. But even with the best biology, someone has to “flip the switch” and keep it pointed at the truth. That drive has to come from within, and it’s not something you can easily give to someone else, no matter how hard you try.

Why Think for Yourself?

So, why must we think for ourselves, whether about health, science, or anything else? Because it’s the only way to stay grounded in reality, to align with nature rather than the shifting sands of societal dogma. In the past, you might have chosen the insulation of society’s “security blanket,” outsourcing much of your thinking to experts and leaders. But that blanket is unraveling fast. Today, dogma diverges further from reality, destabilizing society at an alarming pace. You can see it everywhere: people are losing faith in the fairy tales they’ve been told. Still, most don’t have an alternative because they lack the neurological tools and epistemological framework to think independently.

The neurological challenges stem from things like DHA deficiencies, exposure to non-native electromagnetic fields, and dehydration, which impair brain function. Epistemologically, the issues come from poor education, lack of practice in critical thinking, and disorganized mental frameworks. For centuries, society has let us outsource our cognition to leaders and systems, but that luxury might not be available much longer as these structures falter.

AI responses stem from human-coded algorithms and vast datasets, which are inherently subjective. No AI is a neutral oracle; it’s a reflection of its training corpus, which includes everything from historical texts to internet scraps, riddled with errors, biases, and omissions. For instance, if an AI’s “codex” draws from dominant narratives (e.g., mainstream media or academic consensus), it might regurgitate them without scrutiny. But this flaw underscores the need for human oversight: we must treat AI as a tool, not a truth-teller. By thinking independently, we use AI outputs as starting points, probing them with logic, evidence from nature/reality, and personal experimentation, rather than endpoints. This builds a worldview tethered to verifiable principles, not programmable ones.

Back to the Cliff

If you visit my home you’ll notice something striking about the artwork that surrounds you.

My goal is to build a resilient, adaptable worldview in my tribe. It scales to my artwork. Independent thinking isn’t merely defensive; it’s generative. It cultivates curiosity, creativity, and antifragility, thriving amid uncertainty rather than crumbling. Your metaphor of “jumping without wings and acquiring knowledge as you fall” evokes a bold, experiential approach: better to risk failure through direct engagement with reality than cling to safe but false narratives. This aligns with how breakthroughs happen, in science, philosophy, or personal growth, via trial, error, and unfiltered observation. In an AI-dominated world, where “truth” can be synthesized at scale, this mindset ensures we evolve beyond static dogmas, creating worldviews that are dynamic and self-correcting.

As for the statue in my house below, it symbolizes this ethos, whether it’s Icarus (embracing the fall for the flight), a thinker like Rodin’s, or something else; it is a powerful reminder to those who come to visit me. Ultimately, in a world where AI and propaganda erode objective anchors, self-directed thought isn’t optional; it’s the cornerstone of authentic freedom. It empowers us to navigate chaos, discern signal from noise, and forge paths that others might fear to tread. If we don’t, we risk becoming extensions of someone else’s code, human or machine.

Blind conformity leads to collective folly. History is littered with examples, financial bubbles, wars fueled by propaganda, or social movements that devolve into dogma. If epistemology is built on “absorbed dogma,” as you put it, we default to the crowd’s wisdom, assuming safety in numbers. But crowds are often wrong, swayed by emotion or misinformation. A rigorous cognitive filter, grounded in empirical observation, logical reasoning, and natural laws, prompts that pause:

“What’s the evidence?

What are the risks?

Does this align with reality?”

This isn’t contrarianism for its own sake; it’s adaptive intelligence. In a shifting society (e.g., amid AI-driven deepfakes or narrative wars), independent thinkers pivot based on facts, not fads, fostering resilience against deception.

Let’s revisit my question: Would you jump too if everyone else jumped off a cliff? If you’ve built your epistemology on absorbed dogma, you might accept conventional wisdom without question because you’ve been conditioned to follow the crowd. But if you’ve cultivated a rigorous cognitive filter, grounded in reality and nature, you’d pause, assess, and decide for yourself. Thinking independently isn’t just about avoiding bad decisions; it’s about building a resilient, adaptable, and true worldview, no matter how society shifts. It is why this statue is in my house. It is far better to jump without wings and acquire your knowledge as you fall than to accept the narratives of the status quo.

The Decentralized Model’s Core Principles Applied to Nanophthalmos ​Nanophthalmos as a Consequence of Disrupted Bioelectric Buoyancy I belie

The Decentralized Model’s Core Principles Applied to Nanophthalmos

​Embryogenic and Transgenerational Roots of this condition are more important to comprehend. As a developmental disorder, nanophthalmos originates during embryogenesis, where photoreceptor-bioelectric signaling sculpts the optic vesicle from neural ectoderm. Disruptions here, via maternal nnEMF/blue light, alter proton tunneling in mitochondria, deuterium fractions, and mitochondrial water, leading to thickened sclera and reduced vitreous volume.

This is transgenerational: Maternal and grandmaternal pre-pregnancy histories (e.g., ALAN exposure, deuterium-rich diets) load fetal mtDNA with heteroplasmy, passing epigenetic tags via POMC-melanin pathways. Much evidence supports this; light wavelengths during pregnancy influence fetal eye formation, with longer wavelengths (e.g., red) reducing viability in models. In utero circadian mistiming exacerbates craniosynostosis (premature skull fusion) and relative hydrocephalus, compressing optic structures and amplifying buoyancy loss. Prenatal stressors like nanoparticles or radiation show similar transgenerational effects on neurodevelopment, mirroring nanophthalmos’ genetic background.

Unified Implications: From Chaos to Order in Nanophthalmos

In this model, nanophthalmos is a dissipative failure; mitochondria are unable to transform light into ordered growth due to éR imbalances in the embryo. Hydrated melanin dampens starlight into bioelectric whispers, but modern life dehydrates it, spiking conductivity and entropy. To curate reversal: Prioritize AM sunlight for DDW production, shun ALAN/nnEMF, and trace generational light histories. This upgrades centralized views (e.g., pure genetics) with quantum biology: Light sculpts eyes via melanin, answering Schrödinger’s “What is life?” as a symphony of resisted energy. Accuracy notes: Genetic links (e.g., MYRF) are established, mitochondrial ties to eye disorders supported, but deuterium/bioelectric specifics are excellent in describing the biophysics of this disease.

Nanophthalmos as a Consequence of Disrupted Bioelectric Buoyancy

I believe nanophthalmos emerges when bioelectric gradients and mitochondrial water production fail to sustain eye growth. I believe transgenerational blue light exposure is behind many eye diseases. This blog covers another one. This is a process that is thermodynamically linked to brain and skull development. This is why it is associated with some developmental syndromes. My model’s focus on nnEMF/blue light damaging melanopsin, mtDNA, and the glyoxalase system aligns with this, as dehydrated melanin increases conductivity, disrupting the trillionth-amp DC current at cytochrome c oxidase. The GOE’s oxygen-driven evolution favored melanin hydration and DDW (deuterium-depleted water) production for bioelectric precision, but modern deuterium loading (via the kinetic isotope effect, KIE) slows proton motion in the Grotthuss mechanism, stunting ocular morphogenesis. In utero, mistiming can create a relative craniosynostosis and hydrocephalus situation during morphogenesis that can amplify this condition by altering CSF buoyancy and redox signaling, creating a perfect storm for nanophthalmos.

My framework highlights:

Mitochondrial Water Production and Bioelectric Currents: Mitochondria produce water at cytochrome c oxidase, generating a bioelectric DC current (approximately one trillionth of an amp) for tissue regeneration. Disruptions in electrical resistance (éR) impair regeneration and development, destroying photorepair mechanisms you have already learned about in this series.

Melanin Hydration and Conductivity: Hydrated melanin dampens bioelectric currents, whereas dehydrated melanin (resulting from nnEMF or blue light) becomes conductive, amplifying aberrant signals and driving pathology.

Watch this to make it clear.  https://www.youtube.com/watch?v=zCGnMY9FSNg

nnEMF and Blue Light as Stressors: These damage melanopsin, mtDNA, and the glyoxalase system, increasing ROS/RNS, ultraweak biophotons, and methylglyoxal, disrupting cellular homeostasis.

Hypothalamic and Autonomic Dysregulation: The hypothalamus regulates ocular development and autonomic tone via melanopsin signaling, which will cause disruptions affecting eye growth.

Developmental Photo-Bioelectricity: Photo-bioelectric gradients, influenced by éR, guide morphogenesis (e.g., eye development), with nnEMF/ALAN altering these gradients, causing microopthalmia.

As a developmental disorder, nanophthalmos likely originates during embryogenesis, which is why I think this is fundamentally a transgenerational disease. I believe knowing your mother and grandmother’s pre-pregnancy and pregnancy histories would be quite germane. This is because this is where photo-bioelectric signaling plays a critical role in eye formation. The etiology for this, based on decentralized medicine ideas, would be as follows.

Can the COVID jab cause this disease? Yes, it can because it affects eye development, as the spike protein destroys the signal and increases the noise in stem cell depots that grow the eye.

COVID-19 mRNA Shots have been shown to destroy 8.4% of Non-Renewable Eye Cells in 75 days, according to this new study above. It found irreversible structural damage to the corneal endothelium of the eye in healthy young adults following Pfizer’s mRNA injection. No wonder many vaccinated individuals experience vision problems in the anterior chamber after receiving the shots.

Predictions for Nanophthalmos Etiology

• nnEMF and Blue Light Disrupt Bioelectric Gradients During Eye Development:
  • Prediction: Prenatal or early postnatal exposure to nnEMF and blue light disrupts bioelectric gradients critical for eye morphogenesis, leading to arrested eye growth in nanophthalmos.
  • Mechanism: During embryogenesis, bioelectric potentials (driven by ion channels and mitochondrial éR) guide cell proliferation, migration, and differentiation in the optic vesicle and lens placode. nnEMF and blue light, absorbed by melanopsin in developing retinal ganglion cells (RGCs), likely from maternal retinal tissues, impair melanopsin signaling to the hypothalamus. This disrupts circadian and autonomic regulation of eye growth factors (e.g., VEGF, TGF-β). nnEMF and blue light ruin the germ line and load it with deuterium. It’s the KIE effect that affects proton motions that are supposed to happen seamlessly. One atom of deuterium affects the motions of 96 H+ in this optic placode. Not a good thing when you understand the Grotthuss mechanism in the matrix of mitochondria. Protons matter; it is not just about electrons in morphogenesis.

    Want some quick Grotthaus Wisdom from Nature? Here’s a decentralized fix no centralized MD thought to give: live more like our ancestors: eat fresh and local food, soak up sunlight, and ditch the tech overload and do it grounded to keep deuterium low and the Z-Z highway open. What I want you to know is that how protons move in your body isn’t just a nerdy detail; it’s a significant biophysical issue for your health. Centralized clinicians have no idea about this science. Normally, your cells use the fast Z-Z highway of Grotthuss to keep energy humming, and that’s how humans thrived in their evolutionary past with clean diets and natural living, and their momma had no sticky germline eggs. The Z-Z Grotthaus pathway = Fast energy, great electrical resistance in cells = a healthy you and your kids’ eyes are not small. It works best with a clean lifestyle and minimal exposure to blue light or non-EMF. Sunlight optimizes the Z-Z pathway.

    E-Z-E = Slow energy, struggling with you. This phenomenon occurs more frequently with modern junk food, LED lights, WiFi stress, and energy vampires.

    Cut the crap (bad food, artificial blue light, nnEMF), get sunlight, be like the sphinx every AM, and your body’s energy trucks will roll better. It is not rocket science. It is brain surgery without a scapel.

    Simultaneously, nnEMF damages mtDNA, likely affecting DDW production in the ocular placode in ocular precursor cells, reducing mitochondrial water production and lowering éR, which alters the bioelectric gradients needed for proper axial length expansion.

• • In Utero Warburg Effect and Ocular Redox Timing

    My interpretation of the Warburg effect as a circadian clock braking mechanism, which uses glucose, aligns with nanophthalmos morphologically. The retina’s natural Warburg metabolism limits ROS/RNS under light stress, and nanophthalmic eyes may over-rely on this due to nnEMF-induced pseudo-hypoxia. Craniosynostosis and hydrocephalus disrupt mitochondrial-nuclear proximity, favoring glycolysis over the TCA cycle, and reducing water and CO2 production. My thesis would argue that cold exposure, which enhances endogenous UV-like emission via UPEs, could reset this timing, promoting proper eye elongation that is now lost in modern humans without a winter context.

    Outcome: The eye fails to elongate correctly, resulting in a small axial length, a small cornea, and a thickened sclera/choroid, which are the phenotypic characteristics of nanophthalmos.

• Dehydrated Melanin in the Retina and Choroid Impairs Developmental Signaling:

  Prediction: Dehydration of melanin in the developing retina, RPE (retinal pigment epithelium), and choroid, caused by nnEMF and blue light, disrupts bioelectric signaling, arresting eye growth.

  Mechanism: Melanin in the RPE and choroid, present early in eye development, regulates bioelectric currents by maintaining hydration-dependent resistance. nnEMF and blue light reduce mitochondrial water production (via mtDNA damage), dehydrating melanin and increasing its conductivity (per my Popular Science reference on eumelanin from blogs). This amplifies ultraweak biophotons and ROS/RNS, overstimulating developmental pathways (e.g., Wnt, Hedgehog) that rely on precise photo-bioelectric cues.

  Eye Development TIME SCALE

  Week 3: Optic grooves, which are the first sign of eye development, appear from the developing forebrain.

  Weeks 3-10: The optic vesicles, formed from the optic grooves, begin to evaginate and induce changes in the surface ectoderm for lens formation. This period also involves the invagination of the optic cup and the formation of the optic stalk.

  Weeks 6-8: The optic fissure, a transient structure in optic nerve development, begins to fuse.

  By week 7: The optic fissure is completely closed.

  Around week 10, the eyelids fuse together, although they will reopen later to protect ongoing brain organogenesis. A failure to fuse the optic fissure on time is one of the things associated with developmental brain disorders tied to unquenched UPEs. Timescale errors in eye development will alter the following signals: melanin dehydration, bioelectric signals, vascular dysfunction, link neurulation, craniosynostosis, hydrocephalus, and tumors in a disrupted GOE-evolved system. The proper light drives optimal eye development. Light malnutrition gives us this condition.

Melanin and vascular dynamics are linked to timescale errors, which alter the morphological timing of the eye. Building on my melanopsin-in-arteries insight, dehydrated melanin in ocular vessels (e.g., central retinal artery) under nnEMF/blue light impairs vasodilation, reducing oxygen delivery to the optic vesicle. This links craniosynostosis (via CSF pressure) and hydrocephalus (via buoyancy overload) to nanophthalmos, as poor perfusion stunts scleral and corneal growth. My thesis would suggest that cooling with grounding and AM sunrise restores melanin hydration, enhancing vascular tone and eye development in children, which is critical for parents to begin.

Deuterium’s KIE ruins this embryology big time. The resulting aberrant currents inhibit scleral and corneal expansion while promoting excessive choroidal/scleral thickening. Water’s role in reducing entropy and mass depends wholly on low deuterium levels for efficient proton tunneling. In nanophthalmos, nnEMF’s KIE effect loads deuterium, slowing Grotthuss motion and disrupting bioelectric currents. Any situational in utero craniosynostosis and/or hydrocephalus exacerbate this by altering CSF composition, reducing mitochondrial DDW production. My decentralized approach, featuring fresh food, sunlight, and grounding, aligns with GOE-evolved hydration strategies to support eye growth.

Outcome: The resulting eye in the child/adult would remain small, with a thickened sclera and choroid, leading to nanophthalmos and its associated hyperopia.

Hypothalamic Dysregulation Alters Ocular Growth Factors:

Prediction: nnEMF and blue light impair hypothalamic control of ocular development, reducing growth factor signaling and contributing to nanophthalmos.

Mechanism: The hypothalamus, via the suprachiasmatic nucleus (SCN) and retinohypothalamic tract, regulates circadian rhythms and autonomic tone, influencing eye development through hormones and growth factors (e.g., IGF-1, dopamine). Melanopsin damage in the developing retina (or maternal retina during pregnancy) disrupts this pathway, altering hypothalamic outputs in the growing child and adult.  This could lead to problems, but it also could be offset by the other eye.  These actions in the affected eye reduce dopamine (a growth inhibitor in the retina) and IGF-1 (a growth promoter), stunting axial elongation. nnEMF’s effect on the glyoxalase system further increases methylglyoxal, which glycates developmental proteins and impairs tissue expansion.

Outcome: Reduced eye growth leads to a classic phenotypic small anterior chamber and axial length, increasing the risk of angle-closure glaucoma in nanophthalmos.

Ultraweak Biophotons and ROS/RNS Disrupt Cellular Differentiation:

• Prediction: Overproduction of ultraweak biophotons and ROS/RNS in the developing eye, driven by nnEMF and blue light, disrupts cellular differentiation and growth, contributing to nanophthalmos. This means those with this condition see the world with a different perspective from others due to the visual changes. This is due to changes in dopamine, melatonin, and GABA in the eye that regenerate all our photoreceptors. Consciousness in these patients differs from that of humans with normal eyes as a result.
• 
• Vascular Perfusion Metrics: Reduced blood flow velocity in ocular arteries (via Doppler ultrasound) in nanophthalmos patients correlates with nnEMF exposure, reflecting melanopsin dysfunction. Elevated deuterium in ocular tissues (via mass spectrometry) in nanophthalmos cases indicates impaired Grotthuss efficiency, a transgenerational marker from maternal exposure.
• 
• • Mechanism: As I’ve often cited (Roeland Van Wijk and Fritz Popp), ultraweak biophotons reflect cellular health. In the developing eye, nnEMF and blue light damage mtDNA, increasing biophoton emission and ROS/RNS. This oxidative stress alters gene expression (e.g., PAX6, SOX2) critical for lens and retina formation, while biophotons overstimulate pathways like Notch, disrupting cell fate decisions. The result is reduced proliferation of corneal and scleral cells, leading to a small eye.

    Prevention: Hibernation-Like Intervention: Prenatal cold exposure or simulated hypoxia increases ascorbic acid and endogenous UV, enhancing aquaporin proton tunneling and eye growth, reducing nanophthalmos severity.

    Outcome: Impaired differentiation and growth result in the microphthalmia features of nanophthalmos, which are predisposed to glaucoma due to anterior segment crowding and more eye floaters and anterior chamber diseases.

  Warburg-Like Metabolic Shift in Ocular Precursor Cells:

  Prediction: Ocular precursor cells under nnEMF/blue light stress will certainly exhibit a Warburg-like redox shift, reducing oxygen use and impairing eye growth.  This is related to the Great Oxygen Holcaust that nnEMF causes.

  • Historical Context (Great Oxygen Holocaust):

    The Great Oxygenation Event forced adaptations (e.g., mitochondria, heme proteins) to manage oxygen toxicity. Modern nnEMF and ALAN mimic this oxygen catastrophe, which acts to dehydrate ALL heme-containing proteins like cytochrome P450scc while simultaneously disrupting regenerative processes that were optimal 65 million years ago.  This is why the normal adult retina still employs Warburg metabolism, which explains the absence of arterial cascades in the foveal region of the retina.

One should expect hormone abnormalities with this condition.  The non-affected eye could overcome this.  But more than likely, this will lead to lower-than-usual levels based on age. Why? Dehydrated melanin (from nnEMF/ALAN) disrupts this, impairing steroidogenesis via cytochrome P450scc, which converts cholesterol to pregnenolone (the precursor to cortisol, testosterone, and other steroids).  Pregnenone steal syndrome is likely due to defects in T3 and Vitamin A from opsin damage linked to melanopsin damage. nnEMF causes a TBI-like effect due to the electrocution-like impact resulting from the lack of hydrated melanin in the anterior and posterior pituitary regions, which reduces vasopressin and ACTH, impairing ocular development in nanophthalmos.

nnEMF disrupts the hypothalamus-pituitary axis, lowering vasopressin (from the posterior pituitary) and ACTH (from the anterior pituitary). Vasopressin regulates water balance, which is crucial for melanin hydration and DDW production, while ACTH stimulates adrenal cortisol production via the P450scc enzyme. Reduced vasopressin dehydrates melanin sheets in the retina/choroid, amplifying bioelectric dysfunction, while low ACTH translation from POMC exacerbates pregnenolone steal syndrome, limiting cortisol for growth. This aligns with Neil Armstrong’s post-moon symptoms (pseudotumor cerebri, optic nerve swelling, pituitary failure) due to nnEMF exposure.  It also explains the space findings seen in all astronauts who share many of these conditions’ symptoms.

I would also expect arterial abnormalities in the eye due to the melanopsin effect, since melanopsin is known to be present in all arteries.  Why?

Melanopsin in Arteries:

• Melanopsin, traditionally known for its role in circadian regulation in retinal ganglion cells, has been identified in vascular smooth muscle and endothelial cells across various arteries, including those in the eye (e.g., the central retinal artery and ciliary arteries). It acts as a photoresponsive receptor, modulating vascular tone, blood flow, and oxygen delivery in response to light exposure.

Melanopsin in arterial walls regulates vasodilation and vasoconstriction in response to light cues, ensuring proper blood flow for eye growth. nnEMF and blue light (400-550 nm) damage melanopsin, impairing its signaling to the hypothalamus and autonomic nervous system (via the retinohypothalamic tract). This disrupts vascular tone, reducing oxygen and nutrient delivery to the developing optic vesicle, retina, and sclera. Concurrently, mtDNA mutations in cytochrome c oxidase (due to heteroplasmy) lower DDW production, dehydrating melanin in vascular tissues and amplifying ROS/RNS, further damaging endothelial cells. The resulting arterial abnormalities (e.g., hypoperfusion, abnormal vessel branching) stunt eye elongation.

• • • • Disruption of melanopsin signaling (e.g., by nnEMF or blue light) alters vascular dynamics, affecting ocular perfusion and development.  This is why we see vascular proliferation in diabetic retinopathy. Nanophthalmos in humans is primarily an ocular disorder but can be associated with several ocular diseases, including high-angle glaucoma, uveal effusion syndrome, retinal detachment, and cataracts. It is also linked to genetic syndromes such as Retinitis Pigmentosa and foveoschisis, and specific conditions like Macaulay-Shek-Carr syndrome, which involves retinal degeneration. I believe this shows us how mtDNA damage can alter epigenetics, which can also affect DNA and cause these unusual diseases. What am I saying clearly here? Many genetic diseases are not really genetic diseases, and this means we can help those people if we understand the decentralized mechanisms behind these diseases. Retinitis Pigmentosa, foveoschisis, and retinoblastoma are examples.

        Mechanism: Similar to my glaucoma and cancer models, nnEMF and blue light lower Δψ and éR in developing ocular cells, shifting metabolism toward glycolysis (the Warburg effect). Oxygen becomes toxic (my “oxygen allergy” concept), reducing mitochondrial efficiency and water production. This impairs the photo-bioelectric currents needed for cell proliferation and tissue expansion, stunting eye development.

        Prediction: nnEMF and blue light deplete NO in the developing eye, impairing stem cell depots used to grow the eye normally and contributing to nanophthalmos.

        Mechanism: NO, a key signaling molecule, regulates stem cell proliferation and differentiation in the optic vesicle and lens placode. Blue light destroys NO by disrupting heme-based cytochromes (e.g., via the liberation of vitamin A tied to opsin biology), while nnEMF-induced oxidative stress further depletes NO. This impairs stem cell-driven growth of ocular tissues, resulting in reduced axial elongation and corneal expansion. The lack of NO also disrupts the POMC/melanin complex, as NO signals the oxidation states of hemoglobin, which in turn influence melanin hydration and hormone production.

        The lack of NO (destroyed by blue light) further impairs POMC signaling, as NO is required to transmit hemoglobin oxidation states to this complex.

        Outcome: Reduced stem cell activity leads to a small eye with a shallow anterior chamber, characteristic of nanophthalmos, and increases glaucoma risk due to anatomical crowding.

  Methylglyoxal and AGE Accumulation in Developing Tissues:

  Prediction: The nnEMF-induced glyoxalase system disruption increases methylglyoxal, glycating ocular proteins, and arrests eye development.

  Mechanism: As with cataracts and glaucoma, nnEMF affects transition metals in the glyoxalase system, depleting glutathione and elevating methylglyoxal. In the developing eye, this glycates structural proteins (e.g., collagen in the sclera, cornea), stiffening tissues and impairing growth. Glycation also disrupts signaling pathways (e.g., FGF, BMP) required for axial elongation.

  Outcome: As a result, the eye fails to grow properly, resulting in the small, hyperopic eye of nanophthalmos, with glycation contributing to scleral thickening.

Integration with My Decentralized Medical Thesis

​The Legacy of the GOE variable oxygen fluctuation ties nanophthalmos to an in utero GOE-alteration affecting buoyancy and redox adaptations, most likely driven by modern nnEMF/blue light mimicking an “oxygen Holocaust.” Amniotic fluid and CSF changes in utero are likely transiently disordered during the morphogenesis of the eye and brain to cause this condition.

My model predicts that nanophthalmos is not solely a genetic disorder, as textbooks and centralized medicine suggest, but a photo-bioelectric and environmental condition driven by nnEMF and blue light exposure during critical developmental windows (prenatal or early postnatal).

 

This aligns with my decentralized medicine approach, emphasizing environmental factors (light, EMF) over genetic determinism. As a central regulator of ocular development, the hypothalamus links these stressors to disrupted photo-bioelectric signaling. At the same time, melanin dehydration and mitochondrial dysfunction exacerbate the effects, resulting in the classic phenotype.  The earlier this disease is treated, the fewer the symptoms should be, as proper therapy in childhood could potentially regrow the eye, similar to Dr. Becker’s work in fingertip regrowth, as documented in a three-year-old.

Dr. Robert Becker documented the regrowth of a three-year-old’s fingertip, attributing it to a bioelectric current (via silver ions and low-level currents) that stimulated stem cell activity and tissue regeneration. This suggests that early intervention with bioelectric therapies could similarly regrow ocular tissues in nanophthalmos by restoring the trillionth-amp DC current produced by mitochondrial water at cytochrome c oxidase.

This framework challenges conventional centralized models by suggesting that nanophthalmos and its associated glaucoma risk stem from modern environmental mismatches rather than inherited mutations alone.

 

Testable Predictions for this Condition

• Environmental Correlation: Higher incidence of nanophthalmos in populations with prenatal exposure to non-ionizing electromagnetic fields (nnEMF)/ALAN (e.g., maternal screen use, urban EMF levels, higher latitudes, and indoor living).
• Melanin Hydration: Reduced melanin hydration in the RPE/choroid of nanophthalmic eyes, measurable via imaging or biopsy.
• Mitochondrial Markers: Lower Δψ and elevated ultraweak biophotons release in ocular tissues from nanophthalmos patients with nnEMF exposure history.
• Therapeutic Response: Prenatal UV-A exposure or maternal DDW (deuterium-depleted water) reduces nanophthalmos risk by supporting melanin hydration and mitochondrial éR to stimulate the growth of the globe in childhood
• Glyoxalase System: Elevated methylglyoxal and AGEs in the sclera/choroid of nanophthalmic eyes, linked to nnEMF exposure. Someday, specialized spectroscopic OCT could prove this.

SUMMARY

Eye development is inherently linked to brain development, as the optic structures originate from the forebrain’s diencephalon. The morphological timeline of both organs emphasizes key milestones up to around week 10, as eye formation largely completes by then, though both systems continue maturing.

Nanophthalmos, characterized by a phenotypically small but structurally normal eye, represents a spectrum of developmental disorders in which the axial length is compromised, often leading to hyperopia, angle-closure glaucoma, and retinal issues. In the decentralized medicine framework, this condition arises not from isolated genetic mutations but as a consequence of disrupted bioelectric buoyancy, which is a thermodynamic interplay between mitochondrial water production, melanin hydration, and photo-bioelectric gradients that fails to sustain proper eye growth. This disruption is intrinsically linked to brain and skull development, where modern stressors, such as non-native electromagnetic fields (nnEMF) and blue light (artificial light at night, ALAN), damage key systems, including melanopsin, mitochondrial DNA (mtDNA), and the glyoxalase pathway.

The result?

Dehydrated melanin shifts from a dampening resistor to a hyper-conductive state, obliterating the precise one-trillionth-amp DC bioelectric current essential for tissue renovation at cytochrome c oxidase. Drawing on evolutionary lessons from the Great Oxidation Event (GOE), where oxygen-driven adaptations favored hydrated melanin and deuterium-depleted water (DDW) for bioelectric precision, contemporary deuterium loading via the kinetic isotope effect (KIE) slows proton tunneling in the Grotthuss mechanism, thereby stunting ocular morphogenesis.

In utero, this manifests as a relative craniosynostosis-hydrocephalus dynamic, where mistimed cerebrospinal fluid (CSF) buoyancy and redox signaling create a perfect storm for nanophthalmos. This integration applies the decentralized model’s core principles, with light as the primary sculptor of biology, melanin as the quantum ampere, mitochondria as dissipative structures, and éR (energy resistance) as the balancer of transformation versus dissipation, to explain nanophthalmos as a transgenerational, embryonic failure. I outline the framework above, etiology, and implications, weaving in evidence from bioenergetics and developmental biology.

• Syndromic Nanophthalmos: Nanophthalmos can be part of a larger genetic syndrome, such as:
  • Nanophthalmos, Retinitis Pigmentosa, Foveoschisis, and Optic Drusen Syndrome.
  • Oculo-dento-digital (ODD) syndrome.
  • Autosomal dominant vitreoretinochoroidopathy (ADVIRC) with nanophthalmos.
  • Kenny-Caffey syndrome.
• MacKay-Shek-Carr syndrome (Retinal degeneration-nanophthalmos-glaucoma syndrome): An autosomal recessive disorder characterized by progressive retinal degeneration, cystic macular degeneration, and angle-closure glaucoma.
• Genes Linked to Nanophthalmos: Mutations in genes such as MFRP, TMEM98, PRSS56, and CRB1 have been associated with nanophthalmos.

Perioperative Complications

Patients with nanophthalmos are at higher risk of complications during eye surgeries, such as cataract surgery or retinal surgery, including malignant glaucoma, uveal effusion, and nonrhegmatogenous retinal detachment.

CITES

https://www.researchgate.net/publication/367538581_Optic_cup_morphogenesis_across_species_and_related_inborn_human_eye_defects

https://www.researchgate.net/publication/335176649_The_Molecular_Basis_of_Human_Anophthalmia_and_Microphthalmia

 

On page 61 of John Ott’s masterpiece, Health & Light, he wrote the following:   WHAT DOES DECENTRALIZED MEDICINE SAY ABOUT THIS NOW? Non

On page 61 of John Ott’s masterpiece, Health & Light, he wrote the following:

WHAT DOES DECENTRALIZED MEDICINE SAY ABOUT THIS NOW?

None of the opsin proteins of the eye, brain, or skin was discovered in 1969.

The 1969 experiment by Philip Salvatori revealed that UV light plays a significant role in the eye’s physiology, particularly in pupil dynamics. UV-transmitting contact lenses cause greater pupil constriction in sunlight compared to non-UV-transmitting lenses.

My slides above highlight the non-linear absorption of UV light by the eye (e.g., 92% at 300 nm by the cornea) and the piezoelectric effect of eye collagen, which amplifies small UV stimuli. This suggests that UV light influences photoreceptor mechanisms beyond visible light, a finding that predates the discovery of neuropsin in the cornea and skin and melanopsin in the eye and brain. The second slide further expands on this by detailing how neuropsin, sensitive to 380 nm UV light, integrates with the mTOR pathway and circadian clock mechanisms, affecting metabolic flux, protein translation, and clock periodicity. These insights reveal a complex interplay between UV light, ocular physiology, and systemic health, with significant implications for conditions like pterygium.

1. Neuropsin’s Role in Photorepair, mTOR, and Circadian Regulation

The second slide illustrates that neuropsin, activated by 200–380 nm UV light, triggers a cascade involving SIRT1, NAD+, and NAMPT, which regulates metabolic flux (e.g., changes in glucose, ATP/AMP, adenosine, O₂, glucocorticoids, and catecholamines). This cascade influences the mTOR pathway, a key regulator of cellular growth, metabolism, and protein translation. Specifically:

• mTOR Activation at 380 nm: Neuropsin activation by UV light at 380 nm enhances mTOR signaling, thereby optimizing processes such as gluconeogenesis, mitochondrial biogenesis, oxidative phosphorylation, amino acid turnover, lipogenesis, and bile acid synthesis. These processes are crucial for maintaining cellular energy balance and repairing tissue damage, such as in the cornea and conjunctiva. You can see that eye health professionals are unsure of the meaning of these signals. This means neither did the kid’s parents. How can you protect your kids when the doctors are ignorant? The child below has conjunctivitis, and this has major implications for future diseases.

Circadian Clock Regulation: Neuropsin also interacts with the circadian clock at 380 nm, influencing clock genes (CLOCK, BMAL1, PER, CRY) and their downstream targets (REV-ERB, ROR, PPARα, PGC1α). This regulation ensures that cellular processes are synchronized with the light-dark cycle, particularly through morning sunlight exposure, which provides UV and near-UV light to reset the clock.

Protein Translation via IR-A (600–1000 nm): The slide also notes that infrared-A (IR-A) light (600–1000 nm) further modulates protein translation through pathways involving AMPK, LKB1, and FBXL3/CRY, complementing the UV-driven effects of neuropsin.

The 1969 experiment from Ott’s book showed that UV light influences pupil size, likely through a photoreceptor mechanism in the iris or cornea. We now know that neuropsin in the cornea is sensitive to UV light at 380 nm, as indicated by the slides above. This suggests that neuropsin is the photoreceptor responsible for UV-driven pupil constriction, likely by signaling through SIRT1 and NAD+ to modulate local metabolic responses in the iris. This also has significant implications for the anterior chamber of the eye regarding heteroplasmy. Furthermore, the activation of the mTOR pathway by neuropsin enhances cellular repair in the cornea and iris, thereby protecting against UV-induced damage. Might this be why so many people develop cataracts today? They have blocked the ability to utilize this reflex. The regulation of the circadian clock by neuropsin also implies that UV exposure in the morning (rich in 380 nm light) helps synchronize ocular and systemic rhythms, which could influence pupil dynamics and overall light sensitivity throughout the day.

Missed Opportunity: Centralized medicine and ophthalmology likely have overlooked neuropsin’s role in integrating UV light with mTOR and circadian pathways. This has led to an incomplete understanding of how UV exposure affects ocular health, particularly in relation to cellular repair (via the mTOR pathway) and circadian alignment (via clock genes). For example, patients with disrupted circadian rhythms (e.g., night shift workers) might experience exacerbated light sensitivity or ocular stress due to a lack of morning UV exposure, which neuropsin requires to activate protective mechanisms. This would manifest as early-onset conjunctivitis in children and later as cataracts in those over 40.

2. Pterygium as a Manifestation of Light Deficiency

The thesis on pterygium etiology needs to be reframed because this condition, traditionally attributed to UV overexposure due to light deficiency, particularly a lack of morning sunlight, is not supported by current evidence. This aligns with the second slide’s emphasis on neuropsin’s role in circadian regulation and cellular repair.

Mitochondrial Dysfunction: A lack of morning sunlight, which contains UV and near-UV light (250–380 nm), disrupts neuropsin signaling in the cornea and conjunctiva. This impairs mTOR-driven mitochondrial biogenesis and oxidative phosphorylation, leading to energy deficits in conjunctival cells. This is an early sign of eye degeneration in kids that could lead to early, unnecessary deaths. The resulting Warburg shift (a metabolic switch to glycolysis) causes oxidative stress, contributing to pterygium formation.

Circadian Misalignment: The absence of morning UV light also desynchronizes the circadian clock, as neuropsin fails to activate clock genes like CLOCK and BMAL1. This disrupts the rhythmic expression of protective genes (e.g., PPARα, PGC1α), essential for maintaining ocular tissue health and immune surveillance. Many eye and skin diseases in children are linked to this mechanism.

Vitamin D and Immune Dysregulation: Centralized medicine often recommends sun avoidance, which reduces vitamin D synthesis, a critical factor for immune function. This weakens immune surveillance in the conjunctiva, allowing fibroblast proliferation and pterygium growth in the eye. This is linked to a lack of UVB exposure and too little IRA/NIR exposure. Sunglasses are the largest culprit.

Paramagnetic Switch and Oxidative Damage: Poor light environments shift iron in heme proteins to the Fe³⁺ state, making oxygen toxic to ocular tissues. This exacerbates oxidative damage in the conjunctiva, particularly when UV exposure is imbalanced (e.g., excessive midday UV without morning red light to balance it).

Environmental Stressors: Wind, dust, water pollution in the oceans, and imbalanced UV exposure further stress the conjunctiva, compounding the effects of light deficiency.

Integration with Previous Decentralized Findings: The first slide noted that the cornea absorbs significant UV light (e.g., 92% at 300 nm), and the 1969 experiment showed that UV influences pupil size, suggesting a protective mechanism. However, if morning UV exposure is absent, neuropsin cannot activate mTOR or circadian pathways to repair corneal and conjunctival cells, leaving them vulnerable to damage. The piezoelectric effect of eye collagen, which amplifies small stimuli, might also exacerbate oxidative stress in the conjunctiva when UV exposure is imbalanced, as small amounts of midday UV could trigger disproportionate damage without the protective effects of morning light.

Missed Opportunity: You saw for yourself the nonsense excuse the optometrist gave the parent above on the child’s conjunctivitis. This is what happens when you are missing pieces of Nature’s recipes. Centralized medicine’s focus on UV overexposure as the sole cause of pterygium ignores the protective role of morning sunlight. Ophthalmology and dermatology have failed to recognize this.

• Morning UV light, via neuropsin, activates mTOR and circadian pathways to enhance mitochondrial function and cellular repair in the conjunctiva, potentially preventing pterygium.
• Sun avoidance deprives the eye of UV-driven protective mechanisms, such as vitamin D synthesis and melanin production, which could mitigate inflammation and fibroblast proliferation.
• Mitochondrial dysfunction, driven by light deficiency, is a key driver of pterygium, yet ocular health protocols rarely address mitochondrial support or circadian alignment.

This came directly from Ott’s book.

3. Implications for Centralized Medicine, Ophthalmology, and Dermatology

Building on the decentralized integration of neuropsin, mTOR, and circadian mechanisms reveals additional oversights:

Misattribution of Pterygium to UV Overexposure: Centralized medicine’s dogma of sun avoidance has led to the mischaracterization of pterygium as solely a result of UV damage, ignoring the protective role of morning UV light in activating neuropsin, mTOR, and circadian pathways. This has prevented the development of light-based therapies, such as controlled morning UV exposure, for the prevention or treatment of pterygium.

Neglect of Morning Sunlight’s Protective Role: Ophthalmology has overlooked the importance of morning sunlight (rich in 380 nm UV light) in resetting circadian rhythms and enhancing cellular repair via neuropsin and mTOR. This explains why pterygium patients often have lifestyles limiting morning light exposure (e.g., indoor work, sun avoidance). Most surfers miss the morning light and tend to surf later in the day; those who miss the morning light are the ones who tend to develop pterygium. People who wear sunglasses have the highest incidence of this condition, in my experience. John Ott reported the same in his book.

Failure to Address Mitochondrial Dysfunction: The role of mitochondrial dysfunction in pterygium, driven by a lack of neuropsin-mediated mTOR activation, has been ignored. Therapies targeting mitochondrial health (e.g., via light exposure, antioxidants, or metabolic support) could be a novel approach to preventing or treating pterygium.

Incomplete Understanding of UV’s Systemic Effects: The connection between UV light, neuropsin, and systemic health (via circadian regulation and metabolic flux) has been underappreciated. For example, disrupted neuropsin signaling due to UV deficiency may contribute to systemic issues such as fatigue, mood disorders, or metabolic imbalances, which could exacerbate ocular conditions.

• Lack of Personalized Light Exposure Guidelines: Individual variability in neuropsin expression, melanin levels, and circadian sensitivity suggests that light exposure recommendations should be tailored to individual needs. For instance, patients with lighter eyes or disrupted circadian rhythms might need more morning UV exposure to activate protective mechanisms. In contrast, individuals with high UV sensitivity may require a balanced exposure to avoid damage.

4. Broader Systemic Implications

The slide’s emphasis on circadian clock periodicity and metabolic flux highlights that UV light’s effects extend beyond the eye. Neuropsin’s activation of clock genes (CLOCK, BMAL1, PER, CRY) and downstream targets (REV-ERB, ROR, PPARα, PGC1α) suggests that morning UV exposure is critical for systemic health.

Circadian Health: A lack of morning UV light disrupts circadian rhythms, which could contribute to sleep disorders, mood disturbances, and metabolic diseases. This might indirectly worsen ocular conditions like pterygium by increasing systemic inflammation and oxidative stress.

Metabolic Balance: Neuropsin’s influence on mTOR and metabolic flux (e.g., gluconeogenesis, lipogenesis) indicates that UV deficiency could impair energy metabolism, affecting tissues like the conjunctiva that rely on robust mitochondrial function.

Immune Function: The circadian clock regulates immune responses, and UV-driven neuropsin signaling supports this process. Sun avoidance, by reducing neuropsin activation, weakens immune surveillance in the eye, contributing to conditions like pterygium.

Missed Opportunity: Centralized medicine has failed to integrate the systemic effects of UV light into ocular health protocols. For example, patients with pterygium benefit from decentralized interventions that address circadian misalignment, metabolic health, and immune function rather than focusing solely on the surgical removal of the growth. How can a change in light spectrum lead to disease and an early death? The slide below explains it.

5. Potential Therapeutic Approaches

The integrated understanding of UV light, neuropsin, mTOR, and circadian mechanisms suggests several therapeutic strategies:

• Controlled Morning Light Exposure: Encouraging morning sunlight exposure (rich in 380 nm UV light) could activate neuropsin, mTOR, and circadian pathways, enhancing cellular repair in the cornea and conjunctiva, resetting circadian rhythms, and preventing conditions like pterygium.
• Mitochondrial Support: Therapies that support mitochondrial function (e.g., antioxidants, CoQ10, or light-based interventions) could mitigate the Warburg shift and oxidative stress in pterygium.
• Personalized Light Filters: Contact lenses or glasses could be designed to allow controlled amounts of 380 nm UV light to reach the cornea, activating neuropsin while filtering harmful midday UV levels.
• Circadian-Based Interventions: Addressing misalignment through light therapy, sleep hygiene, and lifestyle changes could reduce systemic inflammation and support ocular health.
• Vitamin D Supplementation: For patients who practice sun avoidance, vitamin D supplementation may help restore immune surveillance and reduce inflammation in the conjunctiva; however, nothing can replace the sun’s benefits.

SUNGLASSES: If you still think sunglasses, glasses, or contact lenses are OK, you’d better read the book Health and Light by Dr. John Ott. All of them lead to a version of the oxygen Holocaust in the central retinal pathways that can cause distal diseases in organs. You’ll find a passage about the carcinogenic effects of filtering natural light was found accidentally in a conversation Dr. John Ott had with Dr. Albert Schweitzer’s daughter. The conversation pertained to her experiences with her father at Lambarene, on the west coast of Africa, and the rate of cancer found among those people.

• A 34-year-old former elite athlete who used to wear Oakleys while dressed in black in college, who was first introduced to video games and non-electromagnetic fields (EMF) in film studies at Ohio State, whose NFL career was ended by chronic injuries before it ever got started. Nobody saw the signs of low redox all the way back to HS to see why he died at 34. He then became an executive who had to use blue light devices to do his job. Now, he dies suddenly, and his friends are surprised. Do you see where the pieces fit? They are surprised by these young deaths instead of expecting them. How long will it take for researchers to realize that we can utilize the retinol/melanopsin cycle and an EEG with electronic screen refresh rates?

  http://bobbycarpenter.com/mike-kudla-a-friend-a-roommate-a-buckeye/

  SUMMARY

Integrating neuropsin, mTOR, and circadian clock mechanisms into the narrative reveals that UV light, particularly at 380 nm, plays a critical role in ocular and systemic health. Neuropsin’s activation by morning UV light enhances cellular repair (via mTOR), synchronizes circadian rhythms (via clock genes), and supports metabolic flux, all of which are essential for preventing conditions like pterygium. Centralized medicine, ophthalmology, and dermatology have missed the protective role of morning sunlight, the importance of mitochondrial function in ocular health, and the systemic effects of UV-driven circadian regulation. Pterygium, rather than solely a result of UV overexposure, is a manifestation of light deficiency driven by a lack of morning UV light, circadian misalignment, and mitochondrial dysfunction. By embracing sensible light exposure and addressing these underlying mechanisms, we can prevent and treat ocular conditions more effectively, challenging the sun-avoidance dogma of centralized medicine.

CITES

The story of how the non-visual opsins in the eyes augment photorepair in mammals is a spectacular lesson in how we rebuild tissues throughout evolutionary history. What are these opsins called? They are called OPN3 (encephalopsin), OPN5 (neuropsin), and OPN4 (melanopsin), and their collaboration to rebuild mammalian tissues is a profound chapter in evolution’s quantum playbook, one where light isn’t just energy but the conductor of metabolism, repair, and survival. Drawing from the 2020 PLOS Biology paper by Sato et al. on OPN3’s role in fat cells (above), and expanding with insights from non-visual photoreceptor systems (as detailed in the LinkedIn article in the Cites), these opsins form a decentralized network that senses light to mobilize stored fat for tissue renovation, reduce inflammation, and extend longevity.

In my thesis, mitochondria serve as quantum hubs, transforming light/vibrations into UPEs (ultraweak photon emissions) and redox signals, thereby overriding genomic centralization. Disrupting this symphony, with nnEMF, ALAN (artificial light at night), or spike proteins (jabs/COVID), and obesity, metabolic diseases, and even “non-metabolic” conditions (e.g., neurodegeneration, sensory disorders) emerge as light-starved chaos. Let’s unpack how they evolved and work in unison, using first principles: light quantizes charge flows (protons/electrons) to bridge thermodynamics and quantum realms, “marketing” viral adaptations for fractal resilience. Yung Bino slide below lays out the stacked lessons.

Evolutionary Innovation: From GOE Survival to Mammalian Mastery

Opsins evolved as quantum light sensors amid the great oxygenation crises, decentralizing repair from external solar dependence to internal mitochondrial orchestration. The timeline, rooted in phylogenomics, reveals a shift from simple bacterial rhodopsins to sophisticated mammalian non-visual systems, linking fat utilization (via OPN3) to photorepair (via OPN5/OPN4) for tissue regeneration.

• Pre-GOE (~4.0–2.4 bya, Archaean – Prokaryotes): Proto-opsins (e.g., bacteriorhodopsin absorbing 570 nm) emerged 3.5 bya for proton pumping and basic light sensing in archaea/bacteria. Viral elements (proto-HERVs) ~3.5 bya “marketed” survival by modulating UPE/redox in anaerobic stress, using positive H+ flows to negative membranes for coherence. This laid the groundwork for diurnal resets. No true tissue repair, but light drove fat-like lipid metabolism for energy storage.
• GOE (~2.4–2.0 bya, Paleoproterozoic – Oxygen Rise): Oxygen toxicity spurred opsin diversification, with proto-OPN5/OPN3 (2.1 bya in early eukaryotes) for UVA sensing (380 nm) to inhibit “mTOR-like” pathways, managing ROS, and enabling fat oxidation for repair. Viral integrations (proto-HERVs ~2 billion years ago) co-opted this process for epigenetic “death-to-life” cycles: UPE surges modulated water EZ/coherence, with melanin-like pigments absorbing UVA for photorepair. This GOE “viral marketing” triggered a state of dormancy, akin to sleep, utilizing stored “fat” (lipid reserves) to fuel quantum resets during hypoxia.
• 
• Post-GOE Eukaryotic Expansion (~2.0–0.54 bya, Proterozoic – Multicellularity): True opsins diverged 1.5 bya, with OPN5 in algae for circadian tuning (absorbing UVA to boost NAD+/SIRT1 homologs, linking to mTOR inhibition). OPN3 precursors (1 bya) emerged for metabolic sensing in proto-metazoans, using blue/green (450–550 nm) to regulate fuel in “fat-like” stores. HERV-like ERVs 1.5 bya enhanced charge flows (Gauss’s Law analogs) for UPE modulation during “diurnal” light cycles. Melatonin (an antioxidant) and melanin (a pigment) co-evolved ~1 billion years ago (bya) for quantum protection, tying fat utilization to repair. This explains why healthy humans born are always fat. Immature birth never has this sign. Human infants during their postnatal life gain fat when they are in need of photorepair. at some level. Increasing fat mass is a sign of tissue rebuilding at some level in the mammalian body plan. In the adult one of the early features of light damage is a retinal exam. Another one is enlarged ventricals in the brain which results from RA damage to brain tissue from nnEMF. You’ve seen this picture before in the blog. The left scan is a normal ventricular system and the one on the right is from one of my farm clients with blue light damage from a lifetime of poor light decisions.
• 
• Cambrian Explosion (~540–450 mya, Paleozoic – Vertebrates): OPN5 formalized in Euteleostomi (500 mya) for non-visual UVA sensing (e.g., in fish brains/testes for reproduction and fat metabolism). OPN3 diverged ~450 million years ago (mya) in tetrapods for tissue-specific roles (e.g., adipose/brain), absorbing blue/green light to optimize stored fat for reducing inflammation. Functional medicine and allopathic medicine view fat mass as the cause of inflammation because they lack understanding of the evolutionary history of non-visual opsin biology. Photorepair is retained in non-mammals; viral HERVs (approximately 500 million years ago in chordates) enhanced epigenetic adaptability, utilizing UPE for coherence during sleep-like states in response to UV stress. Tissue rebuilding emerged using light: light via opsins mobilized lipids for repair in multicellular forms.
• Mesozoic Mammalian Shift (~310–66 mya, Triassic-Cretaceous – Nocturnal Bottleneck): OPN5/OPN3 refined in synapsids (310 mya) for internal sensing post-photorepair loss (160–100 mya in eutherians). OPN3 is specialized in brown adipose tissue (BAT) for fuel utilization, as shown by Sato et al. above: knockout mice develop obesity/insulin resistance by impairing cAMP signaling and fat oxidation. HERV integrations (100 mya in primates) “marketed” mTOR modulation via redox/UPE, enabling fat-driven repair in low-UV niches. Post-K-Pg (66 mya), survivors with mitochondrial capacity used opsins for longevity, tying melanin (UVA absorber in skin/eyes) to melatonin (IR emitter in mitochondria) for diurnal resets, OPN3/OPN5/OPN4 (melanopsin, ~450 nm blue sensitivity) unison sensing light to balance growth (mTOR) with repair. This paragraph explains why those with manufactured spike protein from the jab or virus need to understand how to use fat mass and tropical environments to protect their mitochondrial colony from chronic damage.

Cenozoic Human Refinement (~66 mya–Present): OPN3/OPN5/OPN4 conserved in placentals, with human OPN5 on chromosome 6 and OPN3 on chromosome 1, integrating with POMC (chromosome 2 shift ~6 mya for East African adaptations). OPN3 in fat drives lipolysis (stored fat to energy), reducing inflammation via cAMP/thermogenesis; OPN5 in hypothalamus/testes ties UVA to NAD+/SIRT1 for mTOR inhibition and photorepair. Melanin (from tyrosine, UVA-stimulated) protects DNA, while melatonin (tryptophan-derived, 95% mitochondrial) emits IR for RQ shifts (fat-burning). Modern disruptions (e.g., nnEMF/jabs) via spike proteins inflame cardiolipin, blocking opsin-mTOR spectra and perpetuating unrepaired damage (e.g., cataracts, tinnitus resulting from melanin loss).

Retinoic Acid Evolution and Links to Opsins/Photorepair in Mammals

Retinoic acid (RA), a derivative of vitamin A, evolved as a light-sensitive morphogen linking opsins/photorepair to development/metabolism. From first principles, RA’s photoisomerization (radical pairs sensitive to light/magnetic fields) decentralizes signaling, modulating opsin spectra for quantum coherence in water/redox, fitting this decentralized thesis: viral (HERV: Viral marketing blog) elements “market” RA-heme interactions for epigenetic adaptability amid GOE light and oxygen stress (UV spike). Today the use of technology mimics the GOE. This is why the slide below exists.

• Pre-GOE (~4.0–2.4 bya): Proto-RA (retinoids, such as retinal) ~3.5 bya in bacteria as opsin ligands for light sensing; no true photorepair is possible on Earth.
• GOE (~2.4–2.0 bya): RA signaling 2.1 bya in early eukaryotes for redox/morphogenesis, linking to photolyase (2.4 bya) via RAR/RXR receptors (proto-opsin cousins Brain Gut 6 blog). Viral proto-HERVs co-opted RA for UPE modulation in hypoxia.
• Post-GOE (~2.0–0.54 bya): RA diversified ~1.5 bya with opsins, RAR/RXR heterodimers competing for co-repressors like NCoR, tying to mTOR/clock repression. In proto-metazoans, RA gradients enhanced photorepair in high-UV environments, a phenomenon that became more pronounced in the GOE.
• Cambrian Explosion (~540–450 mya): RA in chordates (500 mya) for eye development, linking to opsins (e.g., rhodopsin from retinoid receptors ~540 mya). Photorepair in vertebrates utilizes RA to mitigate UV stress, with viral ERVs (approximately 500 million years ago) enhancing epigenetic roles.
• Mesozoic Mammalian Shift (~310–66 mya): RA specialized 200 mya for hypothalamic clocks, with POMC cleavage (160 mya shift in primates) driving melanin via α-MSH. Post-photorepair loss (~160 mya), RA disrupted photoperiodicity in excess (e.g., from artificial light), flattening Rev-Erb oscillations and promoting diseases like pseudotumor cerebri (IIH) via CSF pressure/elevated RA. Read the pseudotumor cerebri blog for more on this topic to stack the lessons.
• Cenozoic Human Refinement (~66 mya–Present): RA in humans (chromosomes 2 POMC shift ~6 mya, East African adaptations) modulates opsins/photorepair via nuclear crosstalk, with mistimed RA (e.g., blue light liberating retinal to become a wreaking ball) causing decoherence and inflammation.

  Evolutionary History of Heme Proteins in Photorepair and Circadian Regulation

  Heme proteins, such as cytochromes, hemoglobin, and Rev-Erb receptors, are ancient molecules that have evolved as redox sensors and light modulators, linking photorepair (the reversal of UV damage) to circadian rhythms. Their evolutionary history is tied to the Great Oxygenation Event (GOE, ~2.4–2.0 billion years ago), during which rising oxygen levels necessitated efficient O2/ROS handling, leading to the innovation of heme’s Fe²⁺/Fe³⁺ toggling for metabolic/circadian control. From Nature’s history, heme’s evolution decentralized energy sensing from external light to internal quantum-redox dynamics, fitting this decentralized thesis that mitochondria were first light sensors that evolved to use heme to protect us from oxygen toxicity by “marketing” viral genomic adaptations (HERV-like elements) for charge flows (positive H+ to negative fields per Gauss’s Law), modulating UPEs/water coherence for diurnal death-life transitions. To be fully understood, this paragraph expects you to be stacking many lessons in this blog. It explains why Light sculpts life, fundamentally. When vitamin A becomes its aldehyde form I see the results in the size and shape of your ventricular system. This has implications for the water in the CSF that fill these cavities in your brain.

This is why when Vitamin A is liberated into tissues or the bloodstream, diseases soon follow. It destroys our ability to photorepair. You no longer can use sunlight to repair your tissues. You lose this amazing ability due to your addiction of fake manmade light. That is what MKULTRA does to you. High Vitamin A levels are almost always associated with poor sleep and lowered sodium content when we sample it. Few centralized MDs ever make this connection because they were never taught the lesson of Nature during the GOE. That reality is on the slide below.

Van Wijk and others have shown UV (especially UV-A, ~320–400 nm) is integral to UPE transformation: It excites biomolecules (e.g., DNA, NADH, aromatic amino acids) to generate photons, and UPE itself emits in UV ranges, inducing effects like DNA damage repair or cell death in neighbors. You do know that demratologists love blocking UV light on your skin because it creates currency for them. This is why opthalmologists like blocking sunlight with glasses, sunglasses, contacts, and IOL too. Blocking UV (e.g., via excess vitamin A derivatives like retinoids on the skin, which absorb UV and act as “sunscreen molecules”) act to dampen this photorepair system, reducing coherence and fidelity.

Why?

UPE relies on precise photon absorption/emission for communication, too much filtering disrupts the “optical fiber” network of cells, leading to decoherence (loss of quantum synchronization) and impaired repair. In humans, UV exposure (natural, not excessive) stimulates UPE, enhancing fidelity for photorepair-like processes: Biophotons dissipate excess energy, protect against oxidative stress, and signal for apoptosis or regeneration. Van Wijk’s experiments (e.g., on human hands) show UPE varies with health, lower fidelity in disease correlates with altered emissions. If vitamin A excess from the dermatologist office filters UV too aggressively (as in hypervitaminosis A, where retinal accumulates), it “blind” the UPE system, preventing UV-triggered coherence and leading to metabolic chaos. This isn’t protection, it’s disruption, echoing how modern blue-dominant light (lacking balanced UV/IR) already warps UPE fidelity. Without out it, photorepair is impossible to achieve.

Heme/RA evolved specifically and simultaneously after the GOE to protect us from oxygen and UV light as quantum-redox bridges, with opsins/photorepair systems decentralizing light sensing for tissue rebuilding. As a result, heme toggles Fe²⁺/Fe³⁺ for Rev-Erb/mTOR, while RA photoisomerizes radical pairs to maintain coherence. Viral marketing (HERV ~2 bya–100 mya) stacked decks for adaptability, but modern disruptions (nnEMF/jabs) break spectra, perpetuating unrepaired chaos.

SUMMARY

Why are mammals built this way to sculpt their tissues? Because our optical based system is only capable of using sunlight. This is why mammals are dictated by these laws of Nature. Nature laughs at centralized MDs like this below.

Van Wijk’s biophysics reveals why outdated centralized biochemistry literature misses this science. Conventional views ignore quantum light in cells, focusing on bulk biochemistry. In modern life, artificial light (low UV, high blue) already lowers UPE fidelity, compounding vitamin A issues, e.g., screen exposure liberates retinal, spiking incoherent emissions. To optimize: Balance UV exposure with IRA/NIR light (e.g., morning sunlight), with keen avoidance of all vitamin A supplements/drugs, and monitor UPE in cells (emerging tech like van Wijk’s diagnostics). This is where decentralized medicine must head.

From first-principles: The GOE’s chaos selected for viral-opsin hybrids for quantum survival in a new high UV and high oxygen world. The charge collection of the UV light was maximized by (positive H+ in the matrix to negative melanin fields outside the matrix) per Gauss’s Law. This charge differential grew to heights to make possible quantum coherence in the skin/CNS/PNS and extended to the collagen system allowing new piezoelectric/flexoelectric abilities that created waves of energy in metabolic water made by CCO which enabled UPE modulation for fat-fueled photorepair. Evolution innovated this optical system using “viral marketing” by allowing HERVs stacked decks to develop optical photonic signaling for adaptability in the chaotic environments on Earth. This decentralized biology from external light (photorepair) to internal sensing (mTOR inhibition via opsins), favors longevity in complex life amid environmental stressors. OPN3’s fat role ends the obesity risk by a blue light-driven fuel use; all “non-metabolic” diseases (e.g., neurodegeneration) may trace to this quantum mismatch, because UV light is capable of sculpting humans in utero and resculpting them during postnatal light by rebuilding mammalian tissues. This photorepair process is disrupted by modern photonic centralized interference.

CITES

1. https://www.linkedin.com/pulse/what-do-you-know-non-visual-photoreceptor-system-humans-jack-kruse/
2. https://jackkruse.com/brain-gut-2-viral-marketing/

Heme Synthesis in Mitochondria: The Basics Heme synthesis begins in the mitochondria with the condensation of glycine and succinyl-CoA to fo

Heme Synthesis in Mitochondria: The Basics

Heme synthesis begins in the mitochondria with the condensation of glycine and succinyl-CoA to form delta-aminolevulinic acid (ALA) via the enzyme ALA synthase (ALAS). This process requires mitochondrial integrity, as several steps occur in the mitochondrial matrix and inner membrane, culminating with ferrochelatase inserting iron into protoporphyrin IX to form heme. Heme is then incorporated into proteins like cytochrome c oxidase (e.g., MT-CO1’s heme a and a3) and cytochrome b (MT-CYB). This energy-intensive process relies on a robust mitochondrial electron transport chain (ETC) to supply ATP and maintain redox balance.

KEY POINT: These two subunits are the most mutated genes in mtDNA, and they are involved in DDW creation. Their destruction by nnEMF causes intracellular and mitochondrial dehydration, which causes melanin to lose its hydration, and this causes self-electrocution and distal burnout via a TBI-like effect. When mtDNA is missing, it amplifies electric conductance, and when it is hydrated, it dampens it. Cellular health is reliant on the DDW water created adjacent to the Inner mitochondrial membrane to amplify health and longevity. When this occurs, the alignment of the cristae along the IMJ is perfect and oscillations are also coherent.

Genes Most Susceptible to mtDNA Mutations

Mitochondrial DNA is particularly prone to mutations due to its proximity to reactive oxygen species (ROS) generated during oxidative phosphorylation, lack of protective histones, and limited DNA repair mechanisms. Among the 11 genes that code for the energy genes in mtDNA, these are more susceptible based on their size, location, and functional importance:

• MT-CYB (Cytochrome b)

  Susceptibility: High. As the only mtDNA-encoded subunit of Complex III, it’s a large gene (1,140 bp) and a frequent mutation target. Mutations here disrupt the Q-cycle, leading to ROS overproduction, which exacerbates mtDNA damage.

  Why: Its size and exposure to ROS near the Q-cycle site make it vulnerable.

• MT-CO1 (Cytochrome c oxidase subunit 1)

  Susceptibility: High. It’s one of the largest Complex IV genes (1,542 bp) and critical for oxygen reduction. Mutations impair Complex IV activity, increasing ROS and creating a feedback loop of damage.

  Why: Large coding region and functional centrality amplify mutation impact.

  Blue Light, nnEMF, and Photoreceptor Protein Damage

I’ve noted for 15 years that blue light and nnEMF disrupt photoreceptor proteins, specifically heme, nitric oxide (NO), docosahexaenoic acid (DHA), and melatonin, by liberating vitamin A (retinal) from all the opsins in humans. Heme proteins and melanin evolved to protect us from oxygen toxicity during the GOE. So when heme proteins and melanin, are destroyed cells face an oxygen holocaust at the nanoscopic level. Let’s unpack this:

• Mechanism: Blue light (high-energy, short-wavelength) and nnEMF induce oxidative stress by exciting electrons in chromophores like retinal, which is bound to opsins via weak covalent bonds (Schiff bases). This excitation can break these bonds, releasing free retinal, a potent oxidant. Free radicals generate reactive oxygen species (ROS), damaging nearby proteins like heme-containing cytochromes, NO synthase, and melatonin synthesis enzymes.
• Heme Impact: Heme groups in cytochromes (e.g., MT-CO1) are porphyrin rings sensitive to oxidative damage. Excess ROS oxidizes heme iron (Fe²⁺ to Fe³⁺), impairing electron transfer and destabilizing the protein structure. This disrupts the Complex IV function, reducing oxygen utilization and ATP production.

Warburg Metabolism: A Shift Away from Mitochondrial Efficiency

Warburg metabolism refers to a reliance on glycolysis for energy (producing lactate) even in the presence of oxygen, rather than oxidative phosphorylation (OXPHOS) via the ETC. This shift is often a LIGHT stress response, triggered by light-induced damage. Here’s how it hinders heme-based protein construction and repair:

• Reduced ATP Availability:

  Heme synthesis and protein assembly require ATP. OXPHOS generates ~36 ATP per glucose, while glycolysis yields only 2. In Warburg metabolism, ATP scarcity limits ALAS activity and ferrochelatase function, slowing heme production. This is why anemia of chronic disease is always a marker for nnEMF toxicity. This also means we can see the effects of nnEMF toxicity on a peripheral blood smear. Few people realize this. It also means a retinal exam has a big diagnostic purpose because the fovea of the eye uses a Warburg metabolism, and when we visualize it, we get data on just how much endogenous EMF toxicity is in the system

  Repairing damaged cytochromes (e.g., replacing oxidized heme) also demands ATP for protein synthesis and chaperone activity, which is compromised.

  MT-CYB, MT-CO1, MT-ATP6, MT-ND4, and MT-ND5 are among the most mutation-prone due to their size, location, and critical roles. These mutations often underlie mitochondrial diseases by disrupting energy production and increasing oxidative stress due to the oxygen halocaust.

  Redox Imbalance:

  Mitochondrial ETC maintains NAD+/NADH ratios critical for succinyl-CoA production (via the TCA cycle), a heme precursor. Warburg metabolism bypasses the TCA cycle, reducing succinyl-CoA availability and stalling ALA synthesis.

  Excess NADH from glycolysis shifts the redox state, favoring ROS production over repair mechanisms like photorepair, glutathione synthesis, which protects heme from oxidation.

• Oxygen Mismanagement: This is the basis of the Great Oxygen Allergy

  Cytochrome c oxidase (Complex IV) uses oxygen to produce water, preventing ROS buildup. In Warburg metabolism, suppressed ETC activity leaves oxygen unused, increasing ROS and further damaging heme groups. This lack of water is most critical. Why? The inner mitochondrial membranes contain 30 million volts, and pure DDW is the best insulator on Earth to stop the internal electrocution of the cell. This is why Nature put cytochrome C there. All dysfunction of cytochrome C means internal or endogenous electrical currents run amok in the cell, causing damage. When this happens, ROS and RNS also increase, and this is an uncontrolled pro-growth stimulus. This is the fundamental defect in most diseases, but especially cancer.

  This creates a feedback loop: damaged heme impairs ETC, reinforcing glycolytic reliance.

• Protein Synthesis Impairment:

  Mitochondrial ribosomes rely on ATP and a stable membrane potential (from ETC proton pumping) to translate mtDNA-encoded cytochrome subunits (e.g., MT-CO1, MT-CYB). Warburg metabolism weakens this potential, reducing subunit production and heme incorporation.

The Retinal Fovea: A Unique Model to Study nnEMF Toxicity

The fovea, the central part of the retina responsible for high-acuity vision, is an ideal case study here. It’s avascular (lacking blood vessels) and has minimal melanin, adaptations that optimize light transmission and electrical properties.

Let’s connect this scenario:

Melanin and Electrical Resistance:

Melanin in the retinal pigment epithelium (RPE) absorbs excess light and conducts electricity, maintaining low resistance and protecting against oxidative stress. In the fovea, melanin is sparse by design to avoid scattering light, making it reliant on precise hydration of melanin sheets elsewhere (e.g., RPE) to maintain electrical stability.

Dehydration of melanin (e.g., from poor cellular water structuring due to nnEMF) increases resistance, disrupting charge flow and exacerbating light-induced stress. This could amplify ROS damage to heme proteins and melatonin. Since 95% of melatonin is made in human mtDNA, this makes melatonin levels a marker for nnEMF damage and EMF risk assessment.

Blue Light and Heme Damage in the Fovea:

• The fovea’s high photoreceptor density (mostly cones) exposes it to intense blue light. Without melanin buffering, liberated retinal directly damages mitochondrial heme proteins in photoreceptors or the RPE, impairing cytochrome function and shifting metabolism toward glycolysis = Warburg shift. This clearly shows you that the Warburg shift is a light-mediated shift, not a food-mediated shift. This is one of the largest errors that food gurus, biochemists, and oncologists make in giving advice to patients. This explains why NAD+ drops and pseudo-hypoxia results, because oxygen lowers electrical resistance on the inner mitochondrial membrane, and this sets the stage for many diseases, with cancer being at the top of the list.
• 
• Warburg Metabolism in the Fovea:

  Under hypoxic light stress, foveal cells have adopted a strict Warburg metabolism to survive their lack of mitochondrial density. Mitochondrial density is sparse here to make sure no UPE signals interfere with the information coming from environmental light signals. A lack of mitochondria also reduces heme synthesis capacity in tissues, as outlined above. Since the fovea is devoid of mitochondrial it protects this region from damage. The peripheral retina risk is different. Here mitochondrial density rises. If you look at the photo of the retina above you will see all the white spots around the fovea as markers of blue light damage. These areas represent compromsed cytochrome repair and worsened photoreceptor loss at the nanoscopic level in this region which is a hallmark of conditions like cataracts, floaters, diabetes. When UPEs are made to cause this damage we can see colateral damage inside the fovea to cause macular degeneration. This points out why red light from the sun is the antidote for the blue light hazard in tissues with mitochondria who have many redo light chromophores. This IRA and NIR light is critical to photorepair as outlined below to stop the Warburg redox shift in these areas of the retina by reestablishing water production at cytochrome C oxidase and regenerating melanin in the RPE to protect the retina.

• 
• Only a small amount of comorbid UV-A light is needed to stimulate heme and melanin renovations in humans. This is obvious when you study post natal children carefully. Instead, centralized medicine advicates blocking kids from sunlight with UV and vaccinating them to death to cause their cells activate a transcription factor, called ATF4. You can see my recent criticisms of this behavior in the tweet and you can see my answer to a researcher about ATF4 and UV light.
• 
• • More on ATF4: https://x.com/DrJackKruse/status/1958517094649061414
  • Diabetic Neovascularization and Electrical Resistance

  In diabetes, neovascularization (abnormal blood vessel growth) in the retina, including near the fovea, disrupts its avascular nature:

  • Oxygen Overload: The Great Oxygen Holocaust

    New vessels increase oxygen delivery, but Warburg metabolism (common in hypoxic diabetic tissues) prevents efficient oxygen use by mitochondria. This excess oxygen becomes a ROS source, and thos creates an unusual UPE spectra which acts to oxidize heme (rust = MARS) and further impairing cytochrome function. Mars was hit by a Birkeland current in its past and the result is an huge electrical scar on its equator with a resultant loss of water and atomosphere creating hypoxia. This is why its surface is red because all iron is in its +3 state = RUSTED.

  • 
  • • Electrical Resistance Drop:

      Blood vessels introduce conductive fluid, lowering electrical resistance across the retina. Normally, the fovea’s high resistance (due to no vessels) protects it from excessive growth signals (e.g., VEGF and UPEs). In diabetes, this drop triggers uncontrolled angiogenesis and inflammation, damaging photoreceptors and their mitochondria. An electrical resistance drop in mitochondria is due to damage of the IMM where the major heme protein is, cytochrome C oxidase. Adjacent to mitochondria is also a large amount of melanin which both act to control oxygen toxicity. Diabetic retinal changes are EVIDENCE of oxygen toxicity. Giving diabetics more oxygen is a prescription for more disease and a quicker death.

    • Diabetic Neuropathy Link:

      Mitochondrial dysfunction from heme damage and Warburg metabolism reduces ATP for neuronal maintenance, contributing to neuropathy. In the retina, this manifests as photoreceptor death and vision loss. The picture of the retina above shows you where blue light damage is the worse: It is in the periphery. Damage in this peripheral area outside the fovea correlates with cognitive decline in neurodegenerative diseases.  Most ophthalmologists are not taught the reason why this area of the retina has the highest amount of O2 utilization in the entire human body.  These photoreceptors use high O2 because this increases the band gap of the semiconductive proteins in the RPE to regenerate melanin in the RPE.  When damage is here we know it is due to an oxygen haolocaust in the retina. Most eye professionals are told by their BigHarma curricula that RPE has no regenerative potential humans.  This is false and should be considered pseudoscientific in 2025.  The RPE cells may not divide but the melanin inside of them needs constant renovation via POMC activation and/or migration from Bruch’s membrane of the choroid where melanocytes are closest to RPE in adult humans. This is why photorepair needs a constant UV-A source along with 600-1000 nm light.

    • Synthesis: Warburg Metabolism’s Impact on Heme Proteins

    Reliance on Warburg metabolism in this scenario, driven by blue light/nnEMF-induced heme damage, creates a vicious cycle:

    • Construction: Limited ATP, succinyl-CoA, and redox cofactors slow heme synthesis, reducing new cytochrome production (e.g., MT-CO1, MT-CYB).
    • Repair: Oxidative damage to existing heme groups outpaces repair due to ROS overload and insufficient mitochondrial protein synthesis, crippling ETC complexes. This leads to abnormal UPE signaling.
    • Foveal Context: The fovea’s vulnerability to light stress amplifies this effect, and diabetic neovascularization exacerbates it by disrupting electrical and metabolic balance.

    In essence, the Warburg redox shift is a quantum-level signal that changes metabolism to starve the system sensing inferior light. The action of light starves this affected tissue of the resources needed to maintain heme-based proteins, while oxidative stress from light and nnEMF accelerates their destruction. The fovea’s unique design highlights this interplay, and diabetes tips it into pathology. Diabetic retinas always produce UPEs that are more noise and less signal.

  • 
  • nnEMF and EMF Damage to Melatonin Production

    nnEMF (e.g., from Wi-Fi, cell phones) disrupts mitochondrial function, and since melatonin synthesis is tied to mitochondrial integrity, it’s a sensitive marker for this damage. Here’s how nnEMF impacts melatonin:

    • Mitochondrial Dysfunction:

      nnEMF increases ROS by disrupting ETC electron flow, particularly at Complex I and III. This oxidizes heme groups (e.g., in MT-CO1) and overwhelms mitochondrial antioxidants, including melatonin.

      Excessive ROS inhibits AANAT and ASMT activity by damaging their cofactors (e.g., acetyl-CoA) or denaturing the enzymes, reducing melatonin output.

    • Photoreceptor Protein Disruption:

      As I mentioned earlier, nnEMF (like blue light) liberates retinal from opsins, generating ROS that damage heme, melanin, NO, and DHA. This oxidative stress extends to melatonin synthesis, as tryptophan metabolism is extremely ROS-sensitive as a time crystal to tell seasons.

      In the retina (e.g., fovea), where mitochondria are dense outside the fovea, nnEMF-induced melatonin loss amplifies photoreceptor vulnerability.

    • Calcium Dysregulation:

      nnEMF activates voltage-gated calcium channels (VGCCs), flooding cells with calcium. Excess calcium disrupts mitochondrial membrane potential (ΔΨm), impairing ATP production and melatonin synthesis, which relies on a stable ΔΨm.

    • Circadian Disruption:

      nnEMF mimics light signals, suppressing pineal melatonin via the suprachiasmatic nucleus (SCN). While this is a smaller fraction, it compounds the mitochondrial deficit, lowering total melatonin availability. Rev erb alpha and beta are also heme based circadian regulators. ALAN and a lack of sun destroy the circadian clock mechanism leading to mitochondrial colony failure.

    Melatonin as a Marker for nnEMF Damage

    Since 95% of melatonin is mitochondrial, a drop in its levels, whether measured in tissue, blood, or urine, it reflects nnEMF-induced mitochondrial stress. Here’s why it’s a practical marker:

    • Sensitivity: Mitochondrial melatonin production is directly tied to ETC function and ROS levels, both of which nnEMF disrupts. Even subtle exposures reduce melatonin before overt cellular damage is evident.
    • Systemic Reach: Mitochondrial melatonin diffuses locally and systemically, so peripheral levels (e.g., plasma) correlate with mitochondrial health across organs, including the retina and brain.
    • Context with Heme: Declining melatonin exacerbates heme protein damage (e.g., cytochrome c oxidase), as its antioxidant protection wanes, creating a measurable feedback loop.

    EMF Risk Assessment Using Melatonin

    Using melatonin as an EMF risk assessment tool is compelling in my decentralized model because it integrates multiple damage pathways:

    • Baseline Measurement: Normal melatonin levels (e.g., nighttime plasma peaks of 50–100 pg/mL, or higher mitochondrial concentrations) drop with chronic nnEMF exposure. Studies in animals exposed to EMF show 20–50% reductions in melatonin, suggesting a dose-response relationship.
    • Tissue-Specific Insight: In the retina (e.g., fovea), low melatonin could signal nnEMF-driven shifts to the redox Warburg shift, altering metabolic choices of the cell, as mitochondrial failure forces glycolysis reliance. This ties to my earlier point about heme synthesis stalling.
    • Longitudinal Tracking: Repeated melatonin measurements (e.g., salivary or urinary 6-sulfatoxymelatonin) could quantify cumulative nnEMF damage, especially in high-risk groups like diabetics with retinal neovascularization.

    Tie-In to Heme and Warburg Metabolism

    Melatonin’s decline under nnEMF stress directly hinders heme-based protein construction and repair:

    • Heme Synthesis: Without melatonin’s ROS scavenging, ferrochelatase (the final heme synthesis enzyme) is inhibited by oxidative damage, reducing heme availability for cytochromes.
    • Warburg Shift: Melatonin loss impairs Complex IV known as CCO (via heme oxidation), lowering OXPHOS efficiency and favoring glycolysis. This mirrors my foveal model of AMD, where nnEMF and light stress amplify mitochondrial dysfunction.
    • Foveal Relevance: The fovea’s lack of melanin and vessels makes it dependent on mitochondrial melatonin for ROS defense. nnEMF-induced melatonin drops explains accelerated photoreceptor loss in EMF-exposed individuals.
    • 
    • Practical Implications
      • Risk Assessment: Low melatonin (e.g., <30 pg/mL at night) in someone with high nnEMF exposure (e.g., living near cell towers) could flag mitochondrial damage and EMF risk, prompting interventions like EMF shielding or red light therapy.
      • Diabetes Connection: In diabetics, nnEMF-driven melatonin loss should worsen retinal neuropathy by compounding oxidative stress from neovascularization as noted here: https://www.patreon.com/posts/quantum-46-lot-80643330
      •  
      • SUMMARY

        In summary, mitochondrial melatonin’s 95% dominance makes it an ideal biomarker for nnEMF damage. I always add a directly retinal examination with a melatonin assay to gain the risk of damage in my patients. These two tests are excellent in reflecting mitochondrial ROS, heme integrity, and metabolic shifts. Its decline signals a cascade where heme proteins are faltering, melanin is being electrically removed from tissues, and a Warburg metabolism is taking over to turn your tissues into MARS. A dead red place with no magnetic field because mitochondria are being extincted. As a result, tissues like the fovea in our eyes suffer, perfectly aligning with my decentralized framework of electrical damaged induced by photo-bioelectric collpase.

        Light stress (ALAN or a lack of sun) mimics aspects of infection by inducing mitochondrial stress (e.g., oxidative damage, 1C remodeling), but without ATF4 upregulation, instead, it leverages folate depletion for adaptation.

        Excessive folic acid placed in cereal and grains disrupts this: By preventing natural depletion, it blocks mitochondrial 1-Carbon ramp-up needed for thymidine/DNA photorepair, leading to unchecked genomic rigidity.

        In no-light-control modern environments (indoor/blue light), this amplifies disease risks because retinal/CNS signaling falters (e.g., via melatonin/tryptophan disruption), mtDNA biophotons alter, and diseases like PD/Alzheimer’s rise due to melanin loss and superoxide buildup.

      • 
      • My Black Swan viewpoint dominates here. Fortification in grains (1996 onward) created transgenerational effects (e.g., autism phenotypes), as excessive methyl donors overrode light’s role in refining folate for neural networks. Dermatology’s “damage” narrative ignores mammalian photo-adaptation; instead, UVR-folate cycles protect against carcinogenesis/autism by allowing epigenetic light instability to happen in modern lit environments.

        In tropics/summer, abundant folate foods restore balance, but in artificial light setups (pills, no sun) create hazards. Overall, this integration suggests modern folic acid excess acts as an antagonist to the mitochondrial-light axis, explaining how rising chronic diseases occurs due to light we live under. If environments lack solar seasonal light controls, it should be EXPECTED to dysregulate decentralized photo-bioelectric signaling, echoing what I wrote for Nicole Shanahan in the Quantum Engineering #45 blogpost. For prevention, prioritize natural folate use in seasonal foods with normal UVR exposure tailored to your latitude/skin type. If you do not your eyes will resemble a diabetics retina.

LIFE AND DEATH ARE DIURNALLY LEARNED BEHAVIORS OF COMPLEX LIFE

Natural sunlight exposure, particularly from morning to evening, influences sleep cycles through a pathway involving the eyes, hypothalamus, and brainstem structures. Light enters the retina, stimulating intrinsically photosensitive retinal ganglion cells (ipRGCs), which are sensitive to short-wavelength blue light. These cells project signals via the retinohypothalamic tract to the suprachiasmatic nucleus (SCN) in the hypothalamus, the body’s primary circadian pacemaker. The SCN integrates light cues to synchronize circadian rhythms, regulating melatonin production in the pineal gland to promote sleep onset at night. From the hypothalamus, signals are relayed to the dorsolateral funiculus (DLF) in the spinal cord and brainstem structures, such as the locus coeruleus and raphe nuclei, which modulate arousal and sleep-wake transitions.

I wrote about this pathway in the Quantum Engineering 47 and 48 blogs. You should re read it. Morning light exposure strengthens this pathway, enhancing daytime alertness and consolidating nighttime sleep, while also supporting photorepair mechanisms indirectly through circadian alignment.

Why Is Life Organized This Way?

From first principles (quantum-thermodynamic decentralization), evolution innovated thanatotranscriptomic genes during GOE as redox-stress responders, co-opting viral elements for “marketing” survival. The positive H+ charges in mitochondria are now known as inflammation and the positive charges flow to negative membrane potentials in cells (Gauss’s Law analogs) to gain UPE coherence. This process is modulated by melanin/melatonin biology locally adjacent and within mitochondria. They do this by absorbing/emitting UPE spectra for redox, piezoelectric/flexoelectric vibrations in water and membranes. They also signal coherence for entanglement/tunneling in cells, and viral integrations into the nuclear genome (HERV precursors ~2 bya) stacking our epigenetic decks against chaos.

This “death-to-life” diurnal cycle extended longevity post-GOE by mitigating UPE surges, favoring quantum sensing over genomic rigidity, viral marketing’s ultimate hack for adaptability in oxygenated, light-variable worlds in Earth’s past.

At the end of the day, sleep proves there can be life after a diurnal death. This new life, however, must take on a new form.  Thantothistic genes likely contributed to our ability to innovate wakefulness from sleep.  Sleep does not recharge us.  It is a diurnal doula that acts to reduce our cellular entropy in a very specific way, returning entropy to the cosmos to make sequential life possible by restoring optical coherence for another day.

Lower water content decreases the optical density in tissues, resulting in less scattering of UPE light.  This would amplify UV UPE propagation. This should be expected to enhance local oxidative damage, forming a feedback loop with thanatotranscriptomic activity.

Redox Drain Impact: Draining redox power locally from the electronic state of cells would be expected to impair mitochondrial repair, thereby sustaining UPE-driven damage, which aligns with the post-mortem context of thanatotranscriptomic genes.

Cells appear to have a need to drain themselves of light at death in a particular manner, and this mechanism explains why the light release Popp saw in sickness and when death happens.

Prior to death, cells “empty” their light by exhausting their redox potential (NAD+/NADH, FAD/FADH₂), which powers electron excitation. As ATP production ceases and membranes depolarize, stored energy is released from the vibrational level in cells as UPEs, effectively draining the cell’s photonic “reservoir.”

Water and Optical Dynamics: As my thesis notes, reduced water creation (e.g., from CCO dysfunction) creates a “desert” like state, lowering optical density in tissue. This would accelerate UPE release by reducing scattering while enhancing photon escape, aligning with a physics-based model of energy dissipation of powering down.  This emptying light is returned to the cosmos as a natural entropy increase, satisfying the second law of thermodynamics.

I believe thanatotranscriptomic genes evolved to manage this process by photonic “emptying” as a cue for tissue disassembly, to ready tissue for photorepair mechanisms active in sleep. These genes ensure the orderly shutdown of cellular resources in dying cells, thereby facilitating resource reallocation in multicellular organisms.  While UPE emptying might not directly cause thanatotranscriptomic gene expression, the two should be highly correlated outcomes related to mitochondrial collapse. To get to this process to work, sunlight must enter the eye and be captured to become useful to make this process operate orderly. This is why AM to PM solar exposure is highly correlated with sleep efficiency and photorepair.

Thanatotranscriptomic Genes: Death’s Unexpected Role

I introduced thanatotranscriptomic genes to my thesis about ten years ago, which are genes that remain active for up to 48 hours after an organism’s death. These genes, studied in detail by researchers at the University of Washington using mice and zebrafish models, were initially a curiosity to the scientific community. Why would a dead cell keep “talking” using light? The prevailing theory is that they help manage the chaotic metabolic and photonic processes during the transition from life to death, possibly to preserve tissue integrity or signal decay to the environment. I have proposed a more provocative idea: these genes might interact with hemifusomes to regulate ultraweak photon emission (UPE), a phenomenon where cells emit tiny amounts of light as a byproduct of metabolism. I suggest we die every day, and these genes bring us close to death and bring us back to life by regenerating diurnal damage with specific frequency and spectra of UPE that thanatotranscriptic genes innovate.

I believe that during the day, hemifusome-mediated activity in the TCA (tricarboxylic acid) and urea cycle (linked to sunrise), which are part of cellular energy production, suppresses these genes to prevent excessive UPE. You should think about the TCA and urea cycle as two different types of semiconductors available inside of cells that have two different tasks depending on the photonic signaling they sense. The urea cycle deals with protein metabolism and makes less water than the TCA cycle which concerns itself with fat metabolism and beta oxidation. Sunlight interacts with each semiconductor and creates a unique UPE emission spectra to run different metabolic programs in cells.

At night, with lower metabolic demand, a low-level expression of these genes complements melatonin’s role, handling residual oxidative stress due to excessive positive charge. This diurnal rhythm ties into his broader narrative of cellular adaptation to light cycles. It also leads to rejuvenation and rebirth at every sunrise with the introduction of negative charge to offset the positive charge of inflammation. This is how complex life expanded lifespans and why sleep was naturally selected for. Sleep is a function of charge collection = GAUSS Law.

Thanatotranscriptomic genes appear to act due to Gauss’s Law and exist to facilitate this transition from death to life diurnally, by utilizing UPEs to modulate water and redox states, thereby mitigating UPE effects. However, their activation may also exacerbate the photonic release as a byproduct of the stress response.  My insight is that all respiring organisms must sleep in order to continue living.  It is a unique and compelling part of my thesis about why we sleep. Sleep restores defective mitochondrial respiration by:

Clearing ROS and damaged mitochondria (mitophagy or apoptosis).

Boosting NAD⁺ and sirtuin activity for mtDNA photorepair.

Rehydrating the mitochondrial matrix via CCO water production to cpature more light energy.

DEC2 and Sleep Evolution: DEC2’s role in sleep duration suggests sleep evolved as a mitochondrial maintenance strategy. Short-sleep variants might reflect an adaptation to environments with lower mitochondrial stress, while longer sleep in complex organisms (e.g., humans) supports extensive neural and metabolic repair.

Death and Wakefulness: Life’s adaptation to dying may have driven sleep as a mechanism to delay death, with thanatotranscriptomic genes ensuring that cells recover rather than succumb daily. This serial wakefulness mimics a controlled “near-death” cycle, leveraging sleep to reset mitochondrial function.  It also explains why some can have near-death experiences under mitochondrial stress.

Respiratory Quotient (RQ) and Sleep

RQ Basics: The respiratory quotient (RQ) is the ratio of CO₂ produced to O₂ consumed during metabolism. Glucose metabolism yields an RQ 1 (C₆H₁₂O₆ + 6O₂ → 6CO₂ + 6H₂O), while fat oxidation yields an RQ 0.7 (e.g., palmitic acid, C₁₆H₃₂O₂ + 23O₂ → 16CO₂ + 16H₂O), reflecting a shift to more oxygen-efficient energy use.

Sleep Shift: During sleep, the body transitions from daytime glucose use to fat oxidation, lowering RQ. This metabolic switch conserves glucose for brain function and aligns with reduced energy demand, a known respiratory adaptation.

Melatonin’s Role

Melatonin Overview: Melatonin, a circadian hormone, peaks at night, signaling sleep and influencing metabolism. My hypothesis that it drives the RQ shift from 1 to 0.7 by inhibiting Complex I (CI) of the mitochondrial electron transport chain (ETC) is intriguing and explains why we sleep.

Mechanism:

• Complex I Inhibition: Melatonin’s interaction with cardiolipin (a mitochondrial inner membrane phospholipid) could downregulate Complex I’s (CI) proton pumping rate. CI (NADH dehydrogenase) generates NADH-derived electrons, heavily relying on proton gradient formation. Partial inhibition reduces NADH oxidation, favoring FADH₂ entry via Complex II (CII), which promotes fat oxidation (e.g., via β-oxidation producing FADH₂).

  Cardiolipin Coupling: Cardiolipin’s tight association with melatonin stabilizes this inhibition, preventing complete CI collapse while shifting electron flow. This aligns with fat’s lower respiratory quotient (RQ), as FADH₂ feeds into CII with less proton pumping per electron compared to NADH.

  Evidence: Studies suggest melatonin modulates mitochondrial bioenergetics, reducing ROS and supporting lipid metabolism, supporting my idea of a controlled metabolic pivot.

  Melatonin drives the respiratory quotient (RQ) shift from 1 to 0.7 during sleep by inhibiting CI via cardiolipin, promoting fat oxidation through FADH₂ and Complex II (CII). This supports mitochondrial photorepair repair using UPEs, links to DEC2 and thanatotranscriptomic genes’ chaos management, and moderates UPE emission.

  Life’s default daytime metabolism relies on glucose (RQ ~1), driven by high energy demand and sunlight-mediated insulin signaling. This aligns with glycolysis, providing rapid ATP via substrate-level phosphorylation.

  AM Sunrise Trigger: Morning sunlight, rich in red and UV with blue light, activates non-visual photoreceptors (e.g., melanopsin, neuropsin), syncing circadian rhythms and boosting mitochondrial function. This shift favors the TCA cycle (citric acid cycle) and urea cycle, optimizing oxygen use (RQ <1) and fat metabolism, as I’ve linked to melatonin’s nighttime role above.

Metabolic Implications: The TCA cycle enhances ATP production via OXPHOS, while the urea cycle detoxifies ammonia from protein catabolism, reducing oxidative stress. This daytime pivot, initiated by sunrise, extend lifespan further from life’s GOE design by improving mitochondrial efficiency and sleep quality by balancing energy reserves.  This cycle builds more myelin and more myelin means we need less sleep to become alive the next day after the entropy dump of thantotristic genes of vibrational level UPEs.  This is why melatonin absorption spectra is what it is and why 95% of melatonin is found in mitochondria.

The eye is the main driver of this perception. This means the eye is the key to optimal sleep and optimal photorepair. If you cannot sleep you cannot use UPE light to repair the damage of living and diseases will soon ensnare you.

• The known effects of sleep deprivation, supported by the Nature study below, strengthen my thesis by linking DEC2, mitochondrial repair, and thanatotranscriptomic genes to UPE dynamics. The addition of vibrational energy (acoustic solitons) and the laser-UPE mimicry from the text enrich your photo-bioelectric light cone model, suggesting a cymatic-photonic interplay that shapes optical density and cellular fate. This could explain sleep’s evolutionary role and offer new avenues for simulation or therapeutic studies.

These death genes’ existence reflect an adaptation to manage the photonic and metabolic chaos of death, rather than being a primary driver.  It appears life got used to diurnal dying a lot over 3.8 billion years of days, and as a result, it learned how to remain alive using metabolic light in the form of UPEs. The evolutionary timeline of these genes has some lessons for us. It appears to me that the biological sleep function is tightly coupled to mammalian photorepair and this innovation was coupled in organisms to extend longevity in the eukaryotic tree. This process is used to get us to serial and sequential wakefulness from sleep. Sleep restores defective mitochondrial respiration by clearing postive charge in tissues and this suggests all organisms that respire during sleep and photorepair if life is to continue.

Exposure to natural sunlight from morning to evening plays a critical role in regulating sleep patterns and promoting photorepair mechanisms, which support overall health. Morning sunlight exposure helps synchronize the body’s circadian rhythm by stimulating the production of melatonin, a hormone that regulates sleep-wake cycles, while also enhancing daytime alertness. Studies indicate that spending time outdoors, particularly in the morning, can improve sleep quality, reduce sleep onset latency, and increase sleep duration by aligning the body’s internal clock with the natural light-dark cycle. Additionally, sunlight exposure facilitates photorepair processes, such as DNA repair in skin cells, by activating photolyase enzymes through ultraviolet and visible light, which may indirectly contribute to better rest and recovery. These benefits are particularly pronounced when individuals maintain consistent outdoor time, as it reinforces circadian stability and mitigates the negative effects of artificial light exposure in the evening.

EVOLUTION OF THESE GENES

GOE Era (~2.4–2.0 bya, Paleoproterozoic – Rise of Oxygen and Eukaryotes): Likely birthplace of thanatotranscriptomic-like activity, as oxygenation caused massive cellular “death” events (e.g., hypoxia in anaerobes), selecting for genes managing post-viability chaos. Cyanobacteria’s oxygen production triggered the GOE, with early eukaryotes (2.1 bya) incorporating viral elements (proto-HERVs from RNA viruses) for redox adaptation. Thanatotranscriptomic precursors (e.g., apoptosis-like genes in unicellular eukaryotes) evolved to handle UPE surges from ROS, using positive-negative charge collection (mitochondrial proton gradients to membrane potentials) per Gauss’s Law. Flexoelectricity/piezoelectricity in early membranes modulated water coherence for quantum signaling, while melanin ancestors (e.g., in fungi/bacteria) and melatonin-like antioxidants mitigated UPE. Viral marketing: ERV integrations (2 bya) “hijacked” genomes for epigenetic control, enabling diurnal-like cycles in early photosynthesizers, linking death (nighttime stress) to life (photorepair).

Post-GOE Eukaryotic Expansion (~2.0–1.0 bya, Mesoproterozoic – Multicellularity): Thanatotranscriptomic activity formalized in early eukaryotes, with genes for stress/immunity (e.g., IL-like precursors) upregulated post-death to manage UPE/redox in multicellular forms. HERV progenitors (full ERVs) integrated ~1.5 bya, co-opting viral envelopes for cell fusion/survival. Charge dynamics: Positive proton flows in mitochondria (evolved from bacterial endosymbionts) to negative EZ water, per Gauss’s Law, created coherence for UPE modulation. Piezo/flexoelectricity in membranes enhanced signaling, while melanin/melatonin-like molecules (e.g., in algae) tuned redox. Viral marketing peaked: ERVs facilitated “death-to-life” transitions via epigenetic silencing/activation, enabling multicellularity amid oxygenation stress.

Cambrian Explosion to Vertebrates (~540–300 mya, Paleozoic): Thanatotranscriptomic genes diversified in metazoans, with post-mortem expression conserved in zebrafish/mice (e.g., 1,063 genes upregulated up to 96 hours). HERV-like ERVs integrated 500 mya in early chordates, influencing apoptosis/epigenetics. Gauss’s Law analogs: Charge fluxes in neural tissues (melanin in brains) modulated UPE for coherence. Water’s piezoelectric properties (e.g., in flexoelectric membranes) are linked to viral-driven evolution. Melatonin (pineal origin 450 mya) and melanin (skin/eye) evolved for redox/UPE mitigation.

Mammalian Integration (~300–100 mya, Mesozoic – HERV Emergence): HERVs proper integrated 100 mya in primates/placentals, with elements like HERV-K derepressed by oxidative stress, potentially influencing thanatotranscriptomic activity (e.g., in neurodegeneration). Genes like BCL2/IL6 (post-mortem active) trace to ~200 mya mammalian origins, but HERVs co-opted them for epigenetic control during K-T extinction (66 mya), linking viral marketing to survival amid chaos. Charge collection: Positive H+ in mitochondria to negative melanin fields (Gauss’s Law) for UPE modulation; flexoelectricity in water coherence enabled diurnal repair processes.

Human/Primate Refinement (~100 mya–Present, Cenozoic): HERVs (e.g., HERV-L) upregulated in embryonic/post-stress contexts, varying UPE via redox. Thanatotranscriptomic genes (e.g., immune/epigenetic) are highly conserved in humans, with HERV derepression in death-like states (e.g., neurodegeneration) tying to my thesis: viral elements “market” charge flows for coherence, mitigating UPE via melanin/melatonin (redox buffers) and piezoelectric water structures.

SUMMARY

Thanatotranscriptomic genes, only become active  in post-mortem states from a metabolic stand point. They likely evolved to handle the photonic and metabolic chaos of death (e.g., UPE surges, redox drain). Their presence might reflect an adaptation to mitigate damage during cellular shutdown.  My wakefulness hypothesis states that if these genes manage death-related chaos, they could also underpin the evolution of wakefulness by counteracting daily mitochondrial stress from living.

Sleep restores respiration, and thanatotranscriptomic genes might have been co-opted to maintain wakeful states by driving residual activity as life dies. During life, low-level expression of these genes could stabilize mitochondria under diurnal stress, preventing premature “death-like” states.

Thantotranstric genes were evolved for thermodynamic photonic regulation. UPE emptying before death must be highly orderedd and might parallel a daily UPE release during wakefulness, with thanatotranscriptomic genes modulating this to sustain cellular coherence until sleep resets the entire system to make life more probable in the next solar day.  Sunlight drives this thanatotranscriptomic programming of rejuvenation. This prgram is one of the earliest evolutionary adaptation in the first two domains of life. Over 3.8 billion years, life’s repeated encounters with death (e.g., GOE hypoxia, K-T extinction) might have shaped these genes to balance wakefulness and sleep, using death’s lessons to innovate serial wakefulness.

CITES

1. Blume, C., Garbazza, C., & Spitschan, M. (2019). Effects of light on human circadian rhythms, sleep and mood. Somnologie, 23(3), 147–156. https://doi.org/10.1007/s11818-019-00215-x
   This paper reviews how natural light exposure, particularly in the morning, influences circadian rhythms and improves sleep quality by regulating melatonin production.
2. Boubekri, M., Cheung, I. N., Reid, K. J., Wang, C. H., & Zee, P. C. (2020). Impact of windows and daylight exposure on overall health and sleep quality of office workers: A case-control pilot study. Journal of Clinical Sleep Medicine, 16(2), 203–209. https://doi.org/10.5664/jcsm.7580
   This study demonstrates that increased exposure to natural daylight in office settings is associated with improved sleep quality and duration among workers.
3. Figueiro, M. G., Steverson, B., Heerwagen, J., Kampschroer, K., Hunter, C. M., Gonzales, K., Plitnick, B., & Rea, M. S. (2017). The impact of daytime light exposure on sleep and mood in office workers. Sleep Health, 3(3), 204–215. https://doi.org/10.1016/j.sleh.2017.03.005
   This article finds that greater daytime light exposure, including time spent outdoors, correlates with better sleep efficiency and reduced mood disturbances.
4. Mead, M. N. (2008). Benefits of sunlight: A bright spot for human health. Environmental Health Perspectives, 116(4), A160–A167. https://doi.org/10.1289/ehp.116-a160
   This review highlights the role of sunlight exposure in regulating circadian rhythms and improving sleep, with implications for overall health.
5. Wams, E. J., Woelders, T., Marring, I., van Rosmalen, L., Beersma, D. G. M., Gordijn, M. C. M., & van Someren, E. J. W. (2017). Linking light exposure and subsequent sleep: A field polysomnography study in humans. Sleep, 40(12), zsx165. https://doi.org/10.1093/sleep/zsx165
   This field study uses polysomnography to show that morning light exposure, including time spent outdoors, is linked to improved sleep architecture and next-night sleep quality.
6. https://www.nature.com/articles/s41586-025-09261-y
7. https://www.youtube.com/watch?v=qMVm8F7XCiQ
8. https://jackkruse.com/brain-gut-2-viral-marketing/
9. https://jackkruse.com/time-17-melatonin-insulin-solar-metronomes/

This blog is about why the SUN is TINA for healing of all diseases.

Photorepair, also known as photoreactivation, is a DNA repair mechanism that uses visible light to reverse UV-induced DNA damage, specifically pyrimidine dimers. It’s a process found in many organisms, but not in placental mammals, which rely on nucleotide excision repair. Photorepair involves enzymes called photolyases that bind to damaged DNA and, upon absorbing light energy, break the abnormal bonds, restoring the original DNA structure.

No matter the disease you have this is your how and why.

EVOLUTION OF PHOTOREPAIR

Evolutionary Timeline of Photorepair Loss in Eutherian Mammals: Photorepair, mediated by photolyase enzymes, is an ancient DNA repair mechanism that uses visible light to reverse UV-induced damage like pyrimidine dimers. It is widespread in bacteria, archaea, and many eukaryotes but was lost in the eutherian (placental) mammal lineage. Based on phylogenomic analyses, here’s the timeline:

Divergence Context: Eutherian mammals diverged from metatherians (marsupials) around 180 million years ago (mya) during the Jurassic period (180–160 mya). This split occurred after the broader divergence of mammals from other amniotes in the Mesozoic era, post-Permian-Triassic extinction (252 mya), when early mammals were small, nocturnal, and light-restricted to avoid competition with dinosaurs.

Loss of Photolyase: Photolyase genes (e.g., CPD photolyase and 6-4 photolyase) were lost specifically in the eutherian lineage shortly after this divergence, likely between 160–100 mya in the Cretaceous period. Marsupials (e.g., Potorus tridactylis, the rat kangaroo) and monotremes (e.g., platypus) retain functional photolyase, indicating the loss is eutherian-specific. Zebrafish (a non-mammal) and other lower vertebrates also retain it, confirming the loss is tied to placental evolution.

Evolutionary Drivers: The loss correlates with mammals’ shift to nocturnal lifestyles in light-restricted environments (e.g., burrows, forests), reducing UV exposure and selective pressure to maintain photolyase. Weak purifying selection in small effective population sizes allowed deleterious mutations to accumulate, leading to gene pseudogenization or complete loss. This is supported by comparative genomics showing photolyase absence in human and other placental genomes, while transgenic studies (e.g., mice expressing marsupial photolyase) restore UV resistance.

This timeline aligns with broader mammalian evolution: early eutherians like Juramaia (160 mya) were small and nocturnal, and post-K-Pg radiation (66 mya) saw diversification without photorepair, relying on nucleotide excision repair (NER).

NEUROPSIN IS POST KT BUT DRIVEN BY OZONE DEPLETION IN THE GOE

Ancient Origins (~500–600 mya, Euteleostomi Divergence): OPN5 emerged in bony vertebrates (Euteleostomi), a clade including fish, amphibians, reptiles, birds, and mammals, during the Cambrian-Ordovician periods (540–450 mya). This coincided with the “Cambrian Explosion” of complex life, when UVA exposure increased due to ozone layer thinning post-Great Oxygenation Event (GOE, 2.4 bya). Early OPN5 regulated circadian/reproductive responses in deep-brain tissues, as seen in modern fish/zebrafish (e.g., photoreception for seasonal breeding). It’s absent in invertebrates but conserved in vertebrates, suggesting adaptation for quantum light sensing in mitochondrial-stressed environments post-GOE hypoxia.

EVOLUTIONARY LINEAGE: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo.

Vertebrate Specialization (~450–300 mya, Tetrapod Emergence): In tetrapods (land vertebrates), OPN5 specialized for non-visual roles, e.g., hypothalamic thermoregulation and metabolism (as in my model). This era saw increased atmospheric oxygen, amplifying mitochondrial stress (ROS from UVA), favoring OPN5-mTOR coupling for repair. In birds/reptiles, it’s a “deep-brain photopigment” regulating reproduction (e.g., via melatonin/mTOR inhibition for seasonal flux).

Mammalian Retention and Eutherian Refinement (~300–160 mya, Synapsid to Eutherian Split): OPN5 is retained across mammals, including monotremes (e.g., platypus), marsupials, and eutherians (placental mammals). In eutherians (180 mya divergence from marsupials, Jurassic-Cretaceous), it evolved UV specialization (losing bistability of ancient opsins), aligning with nocturnal niches post-dinosaur dominance. This fit my decentralized thesis: as photorepair (photolyase) was lost (160–100 mya in placentals), OPN5 decentralized UVA sensing to internal quantum pathways (e.g., mTOR via NAD+/SIRT1), modulating spectra for mitochondrial coherence without direct solar dependence. Humans (Homo sapiens lineage, ~300 kya) express OPN5 in the hypothalamus/brainstem, tying UVA to mTOR for circadian/metabolic leptin reset, as in the diagram. This is why the Leptin Rx was born in my mind when I realized all this evolution occured post K-Pg event in the Yucatan.

Post-K-Pg Radiation (~66 mya): After the asteroid impact (K-Pg extinction), survivors with high mitochondrial capacity (e.g., early placentals) diversified, with OPN5 enhancing adaptability via light-mTOR links, extending lifespan through sleep/photorepair cycles. Without OPN5 functioning, photorepair fails, as it’s upstream of melanin/melatonin spectra modulating mTOR (e.g., via POMC cleavage for α-MSH).

In my decentralized thesis, OPN5’s evolution decentralizes control from genomic templates to quantum light-redox sensing: UVA absorption inhibits mTOR growth modes, emitting IR for mitochondrial rehydration/UPE fidelity, preventing chaos (e.g., spike protein disruption in jabs).

This “survival of the wisest” stacks evolutionary decks via viral retrotransposons and proton disorder, with OPN5 as a post-GOE innovation for eutherian longevity amid stress events. For details, see evolutionary studies on OPN5’s conservation in mammals and its loss of bistability for UV specificity.

Opsins are members of the guanine nucleotide-binding protein (G protein)-coupled receptor superfamily. This opsin gene is expressed in the eye, brain, testes, and spinal cord. This gene belongs to the seven-exon subfamily of mammalian opsin genes that includes peropsin (RRH) and retinal G protein coupled receptor (RGR). Like these other seven-exon opsin genes, this family member may encode a protein with photoisomerase activity. Alternative splicing results in multiple transcript variants. Without OPN5 intact, no photorepair is possible in humans. The modern world technology destroys OPN5 biology. It should be no surprise why no one can heal using light now.

The interplay between UVA light, mTOR biology, and the absorption/emission spectra in the provided model can be explained by considering the roles of melanin, opsins (e.g., OPN5), and photobiological pathways in complex eukaryotic life, particularly mammals. UVA Absorption (200–380 nm via OPN5/Neuropsin): OPN5 absorbs at ~380 nm (violet/near-UVA), activating SIRT1 (a NAD+-dependent deacetylase) and NAMPT (which boosts NAD+). This “absorption” phase senses environmental light to tune metabolic flux, inhibiting mTOR (via AMPK activation) for repair modes like gluconeogenesis, mitochondrial biogenesis, and oxidative phosphorylation. In my thesis, this decentralizes control: light isn’t just “seen” retinally but quantum-sensed mitochondrially, linking to photorepair by reducing oxidative stress and enhancing UPE fidelity for DNA/mtDNA repair during sleep.

Emission Spectra (600–1,000 nm, IR-A Range): The model shows outputs like IR-A (infrared-A, 600–1,000 nm) from processes like ATP/AMP ratios and CLK periodicity (circadian clock genes). mTOR doesn’t emit light directly, but its inhibition promotes “emission” of coherent UPEs (biophotons) from mitochondrial reactions (e.g., CCO water production, ROS modulation). These emissions, in the red/IR range, align with your ideas on melanin/melatonin spectra: melanin absorbs UVA to protect/repair, while melatonin (95% mitochondrial) emits in red/IR to seasonal-switch metabolism (e.g., RQ shift to 0.7 for fat oxidation). This “emission” facilitates quantum coherence/entanglement in sleep, regenerating cells via thanatotranscriptomic genes and UPE-driven photorepair.

Integration into mTOR Biology: UVA via OPN5 downregulates mTOR (e.g., via AMPK/LKB1 phosphorylation), favoring autophagy and repair over growth. The diagram’s pathways (SIRT1 → NAD+ → AMPK → CRY/PER/CLK) show circadian periodicity tying light absorption to metabolic outputs, with IR-A emissions closing the loop for mitochondrial rehydration and entropy reduction. In complex life, this prevents “diurnal death” by balancing chaos (UPE surges) with order (photorepair).

• 1. UVA Light and mTOR Biology
• mTOR Overview: The mechanistic target of rapamycin (mTOR) is a key regulator of cellular growth, metabolism, and stress responses. It integrates environmental signals, including light and nutrient availability.
• UVA Influence: As life became complex, UVA light (320–400 nm) began affecting mTOR by modulating photobiological processes. UVA drives melanin synthesis via the OPN5 opsin, which senses violet/blue light (e.g., ~380–420 nm) and influences hypothalamic signaling. This light-driven regulation can activate or inhibit mTOR, depending on cellular context (e.g., hypoxia, oxidative stress).
• Photorepair Link: The model’s “Photorepair mTOR” pathway suggests UVA-induced photorepair mechanisms (e.g., via melanin and nucleotide excision repair) influence mTOR activity. Melanin, can be synthesized from tyrosine and phenylalanine. Melatonin from tryptophan. Both are regulated by UV and oxygen tensions designed to protect the DNA genome by modulating mTOR biology to reducing oxidative damage and create high fidelity UPEs to photorepair. This mechanism is destroyed by the jabs via the charge contained in the LNPs of the spike protein. This is a manufacturing design showing you mal-intent.
• Melanin vs. Melatonin: Melanin is synthesized from tyrosine and phenylalanine, regulated by UVA/B/C light, and protects DNA by reducing oxidative damage, thereby modulating mTOR activity. Melatonin, derived from tryptophan via the serotonin pathway, is primarily (95%) located in mitochondria and serves as a seasonal switch, influencing metabolism and circadian rhythms. They are distinct photochemicals but interconnected by quantum mechanisms.
• Tryptophan Metabolism: Tryptophan is uniquely encoded by a single codon (ACC) and exhibits seasonal catabolism. This makes it a unique time crystal for seasons. It can be metabolized into acetoacetyl CoA (a ketone precursor) or the glucogenic amino acid alanine, reflecting its adaptive role in energy and seasonal regulation.
• POMC Cleavage and UV Light: Proopiomelanocortin (POMC) cleavage produces alpha-melanocyte-stimulating hormone (α-MSH), which drives melanin synthesis. UV light stimulates POMC gene translation, a process shifted in humans to chromosome 2 (from chromosome 24 in other primates), due to environmental changes in the East African Rift during the primate-to-Homo transition (McClintock jumping gene).
• The study below shows low dose naltrexone, an opioid antagonist, induces MSH release but causes degenerative changes in pituitary innervation. This suggests that disrupting natural opioid signaling (e.g., via exogenous opioids) impairs POMC regulation, reducing beta-endorphin and melanin, which hinders wound healing, cataract repair, and hinders auditory health and repair mechanism linked to melanin renovation (e.g., tinnitus). Any tissue with melanin in it need optimized beta endorphin function intact to control it using alpha MSH signaling.

This blog fully explains why use of exogenous opiates for surgery hinders photorepair wound healing. This is why drug addicts have poor wound healing and this is why BigHarma has pushed opiates for pain and not the sun. (See the Sackler’s story on oxycontin.) There is BRISK evidence suggesting that poor wound healing is a significant issue among drug addicts, particularly those who use injectable substances. Research indicates that substance abuse, especially opioids, can impair the wound healing process through various mechanisms, including suppressed immune function, reduced blood flow, and nutritional deficiencies. They highlight the non solar narratives to keep you from the truth buried on this slide below. Even aberrent sexual behavior and gender dysphoria are linked to broken photorepair mechanisms on this slide below.

• Studies have shown that individuals who inject drugs, such as heroin or methamphetamine, often develop chronic wounds and abscesses, and skin infections. Centralized medicine blames this on unsterile injection practices, but this narrative hides the link to beta endorphine and melanin’s power to heal using light. They also push the narrative of the toxic effects of adulterants like xylazine to altered wound healing to hide the truth.Additionally, research clearly shows that opioid use has been linked to slower healing rates, with higher doses correlating with increased wound size and delayed recovery. This is compounded by other factors, but BigHarma highlights them and not the links to the beta endorphin and melanin. You’ll always see them talking up malnutrition, stigma-related barriers to care, and the use of wounds as drug delivery sites, which further hinders healing. The issue is well-documented in clinical observations and recent investigations, highlighting the need for specialized wound care and harm reduction strategies. However, the establishment narrative often focuses on pharmaceutical interventions rather than natural remedies like sunlight, which historical figures like Florence Nightingale wrote about in her work as beneficial for healing over 100 years ago. This suggests a potential bias toward profit-driven treatments over decentralized medical approaches.

It explains why many people use low dose naltrexone, and it explains why I advocate for the use of the sun over LDN 100% of the time. You just did not see my perspective clearly until TODAY. Your functional and allopathic physicians advice are a danger to you ability to heal using light. Time for you to wake up to this fact.

• 2. Absorption and Emission SpectraAbsorption: The model highlights UVA (380 nm) and visible light (e.g., 380–500 nm for opsins like rhodopsin) as key absorption ranges. OPN5, expressed in the eye and brain, absorbs violet light, triggering signaling cascades that affect mTOR. Tryptophan and serotonin derivatives (e.g., melatonin) also absorb in the UVA range, linking light to metabolic regulation.

  Emission: Ultraweak photon emissions (UPEs) from oxidative processes (e.g., ROS production in mitochondria) span 100–700 nm (~430–1000 THz), as noted in my earlier blogs. These emissions, are enhanced by solar UVA-induced photorepair, provide feedback to mTOR, encoding information about cellular state (e.g., circadian timing, stress). This light defines the “Photo” part of the photobioelectric loop of man.

  Fit to Model: The photorepair mTOR pathway integrates these spectra, with UVA absorption by OPN5 and melanin driving repair processes (e.g., via NAD+/NADH cycles), to TCA/urea cycle stoichiometry, while UPE emissions signal mTOR to adjust growth or autophagy based on light exposure at the mitochondrial level. Not matter the disease one has this mechanism operate the system if the system is functioning to collected solar energy.

3. Role of OPN5 and Photorepair

OPN5 Function: As a G-protein-coupled receptor, OPN5 detects UVA/violet light and may act as a photoisomerase, converting retinal isomers. Its expression in the eye, brain, and spinal cord ties it to neuroendocrine regulation, including mTOR via hypothalamic pathways.

Photorepair Dependency: Without intact OPN5, photorepair fails, disrupting UVA-driven melanin synthesis and DNA repair. This increases oxidative stress, dysregulating mTOR and promoting conditions like cataracts or aging, as seen in my hypothyroidism discussion in Decentralized Medicine #65 blog.

Model Integration: The photorepair mTOR diagram shows OPN5/opsin signaling (e.g., via cAMP, CLK periodicity) linking UVA to mTOR modulation, with optimized water/melatonin synthesis enhancing repair efficiency.

Why did this Savage on “X” get better from my advice? Note the bottom line of the slide below. This is how light controls aromatic amino acids in the photo repair process. This slide integrates insights from recent studies on skin metabolism and healing, challenging the pharmaceutical bias by highlighting natural decentralized mechanisms.

Histidine’s Role as an Essential aromatic amino acid converted to histamine by histidine decarboxylase. Precursor to urocanic acid via histidase in the skin’s stratum corneum. Dietary histidine increases urocanic acid levels, aiding photo repair UV-induced repair (e.g., in mice studies).

Histamine’s Dual Nature is present because it is released by keratinocytes and mast cells, triggering itching via H1 receptors. This is why MCAS is another disease that manifests when photorepair is inhibited by nnEMF. Histamine promotes healing by increasing vascular permeability and immune cell infiltration into the wound. This is overlooked by conventional centralized BigHarma treatments, which suppress rather than modulate histamine.

Urocanic Acid’s Function Derived from histidine, acts as a natural sunscreen absorbing UVB (trans to cis isomerization). Cis-urocanic acid enhances immune suppression or repair, depending on context (e.g., UV exposure). It links cell healing to filaggrin breakdown and suggests flaggrin plays a key role in skin barrier restoration, which is often ignored in mainstream dermatology for profit. Flaggrin is a key Coulomb force and Gauss law molecule that tells us if the process is operational or not.

Healing Connection: Itching is the key signal active if the photorepair mechanism in this blog is failing, with histamine and urocanic acid modulating inflammation and UV photorepair. Studies show histidine supplementation improves eczema and skin hydration, hinting at untapped therapeutic potential.

Centralized BigHarma establishment narrative buries sunlight’s role (e.g., Nightingale’s observations) for profit-driven drug reliance. Critical Takeaway Natural pathways (histidine → histamine → urocanic acid) support healing and itching as adaptive photorepair signals. Over-reliance on opioids and antihistamines disrupt this balance, warranting a re-evaluation of sunlight use in wound healing. You may not know that over use of antihistamines is linked to Alzheimer’s risk. Now you know why this happens. It impedes photorepair efficiency in humans as the bottom portion of this slide shows.

HOW DOES 380nm LIGHT CONTROL NEUROPSIN, mTOR, MELANIN and DHA metabolites?

In my decentralized photobioelectric thesis, 380 nm UV-A light acts as a pivotal environmental cue that activates neuropsin (OPN5), an oxygen-sensitive photoreceptor distributed across skin, neural, and vascular tissues, initiating localized photobioelectric signaling (DC current) through G-protein-coupled receptors that alter cellular membrane potentials and ion fluxes in a decentralized fashion, bypassing central nervous control for rapid, site-specific responses. This light-driven neuropsin activation charges tissues up using melanin as a capacitor and a source of electrons by modulating the mTOR pathway, fine-tuning cellular metabolism, autophagy, and growth to prevent excessive inflammation while promoting repair mechanisms by creating a DC electric current from light. In turn, it facilitates the catabolism of DHA (docosahexaenoic acid) into elovanoids (ELVs) and docosanoids which are novel pro-homeostatic lipid mediators that exert anti-inflammatory, neuroprotective, and cytoprotective effects by resolving oxidative stress on macrophage phenotypes, they stabilizing cell membranes from inflammatory breakdown, and enhancing tissue regeneration, thereby enabling humans to harness targeted light exposure for decentralized healing through these interconnected, light-responsive bioelectric and biochemical networks

4. How It Fits the Model

UVA as a Trigger: UVA light, sensed by OPN5, initiates melanin production and photorepair, influencing mTOR’s response to environmental cues. This aligns with the model’s sunlight-to-melanin pathway buried in the recursive photobioelectric loop discussed in detail in the last 20 blogs.

Spectral Alignment: The 100–700 nm absorption/emission range (UVA to visible) matches opsin sensitivity and UPE spectra, supporting a feedback loop where light repairs DNA and modulates mTOR activity.

Evolutionary Context: As eukaryotes evolved, UVA’s role in photorepair (via opsins and melanin) became critical for mTOR regulation, balancing growth and stress resistance, as depicted in the model’s complex pathways.

SUMMARY

UVA light (320–400 nm) directly influences mTOR (mechanistic target of rapamycin) biology by triggering OPN5 (neuropsin)-mediated signaling, which modulates photorepair and melanin synthesis to regulate cellular growth, metabolism, and stress responses. This process integrates environmental light cues into mitochondrial quantum sensing, aligning with my decentralized thesis where mitochondria act as primary sensors for light/vibrations, driving adaptation via redox (NAD+), UPE (ultraweak photon emissions), and epigenetic mechanisms over genomic centralization. Without OPN5 intact, photorepair and mTOR regulation collapse, leading to unchecked oxidative damage in mtDNA, disrupted circadian rhythms, and chronic diseases which are all exacerbated by interventions like spike proteins in vaccines, which interfere with melanin/melatonin pathways due to electrical damage of the charges of LNPs on the Spike proteins.

UVA stimulates the α-MSH pathway via OPN5/POMC cleavage, driving melanin production in melanocytes. Melanin absorbs UVA (300–400 nm) to quench ROS, indirectly inhibiting mTOR by reducing oxidative signals that activate it (e.g., via AMPK). In my thesis, this decentralizes repair: melanin shields mtDNA from UV, while UPE fidelity (emitted in red/IR 600–1,000 nm) sustains coherence during sleep. Spike proteins disrupt this by inflaming cardiolipin (mitochondrial lipid), impairing Complex I and melanin renovation, blocking photorepair and perpetuating diseases

Proopiomelanocortin (POMC) cleavage produces beta-endorphin (an endogenous opioid) and α-MSH, which drives melanin synthesis. The 1986 study on naltrexone in amphibians shows that blocking opioid receptors increases MSH release, suggesting POMC-derived peptides are regulated by opioid signaling. In humans, UV light stimulates POMC translation (now on chromosome 2), enhancing melanin and beta-endorphin production. Melanin, synthesized via α-MSH, protects against UV-induced DNA damage and oxidative stress, supporting photorepair. This ties into wound healing by reducing inflammation and promoting tissue regeneration, as melanin modulates mTOR and mitochondrial function. Melanin absorbs UVA to protect DNA, modulating mTOR by quenching ROS. It’s a quantum shield, fitting our species fractal adaptation.

Melatonin creation from tryptophan (seasonally catabolized, single-codon ACC), it’s a mitochondrial “time crystal” emitting red/IR for metabolism (e.g., CI inhibition). Distinct from melanin but interconnected: both quantum-regulated by light/oxygen, with melatonin boosting NAD+ for mTOR inhibition. This is why it slows aging and boost repair.

Tryptophan/POMC: Tryptophan’s unique codon and catabolism reflect seasonal energy adaptation. POMC cleavage (UV-driven) yields α-MSH for melanin; disruptions (e.g., low-dose naltrexone inducing MSH but causing pituitary degeneration) impair opioid signaling, reducing β-endorphin/melanin, hindering repair in melanin-rich tissues (e.g., eyes, ears), linking its action to cataracts/tinnitus.

In my thesis, this system’s hijack (e.g., by centralized science/DoD via nnEMF/jabs) prevents renovation, as UVA-OPN5-mTOR spectra fail, perpetuating diseases. Trees, using visible light for repair (e.g., burls as growth responses), illustrate light’s universal role, different process, same key: light drives regeneration, disrupted in humans by artificial interference.

Sunlight Quantization: Sunlight’s specific wavelengths (e.g., UVA at 380 nm) act as a precise quantized signal, activating neuropsin (OPN5) and POMC. This triggers beta-endorphin release for pain control and α-MSH for melanin-mediated repair, optimizing healing. Big Pharma’s push for exogenous opioids over sunlight reflects profit motives, burying Nightingale’s findings. Opioids suppress POMC function, impairing photorepair and wound healing, as seen in drug addicts, while sunlight’s natural beta-endorphin and melanin boost these processes.

In summary, UVA light directly affects mTOR biology by driving OPN5-mediated photorepair and melanin synthesis, with absorption (380–500 nm) and emission (100–700 nm) spectra fitting the model as signals for cellular regulation. Without OPN5, this system collapses, disrupting mTOR and photorepair in humans. This is why chronic diseases are not being renovated.

The result is disease man gets today. When this photorepair system is hijacked by bad centralized science, BigHarms & the DoD wins more profits. This is why all their advice breaks the rules in this blog. Time for the savages to wake up how you are being controlled by light the government pushes on your family. Even trees use visible light to repair themselves.

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