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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.

• CITES
• Allaw, F., Zakhour, J., & Kanj, S. S. (2023). Community-acquired skin and soft-tissue infections in people who inject drugs. Journal of Infection and Public Health.
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• Dahlman, D., Håkansson, A., Kral, A. H., Wenger, L., Ball, E. L., & Novak, S. P. (2017). Behavioral characteristics and injection practices associated with skin and soft tissue infections among people who inject drugs: A community-based observational study. Substance Abuse, 38(1), 105-112. https://doi.org/10.1080/08897077.2016.1263592
• Di Trana, A., Berardinelli, D., Montanari, E., et al. (2022). Molecular insights and clinical outcomes of drugs of abuse: Adulteration: New trends and new psychoactive substances. International Journal of Molecular Sciences, 23(23), 14619.
• Friedman, J., Montero, F., Bourgois, P., Wahbi, R., Dye, D., Goodman-Meza, D., & Shover, C. (2022). Xylazine spreads across the US: A growing component of the increasingly synthetic and polysubstance overdose crisis. Drug and Alcohol Dependence, 233, 109380.
• Harris, M., Brathwaite, R., Scott, J., Gilchrist, G., Ciccarone, D., Hope, V., & McGowan, C. R. (2018). Comparing injecting and sexual risk behaviours of migrant and non-migrant people who inject drugs and attend syringe exchange programmes in the UK. Addiction, 113(10), 1790-1801. https://doi.org/10.1111/add.14257
• Jawa, R., Ismail, S., Shang, M., et al. (2024). Drug use practices and wound care experiences in the age of xylazine adulteration. Drug and Alcohol Dependence, 263, 112390.
• Malayala, S. V., et al. (2022). Xylazine-Associated Wounds and Related Health Concerns Among People Who Use Drugs: Reports From Front-Line Health Workers in 7 US States. Substance Use and Addiction Journal, 45(2), 222-231.
• Roose, R. J., Hayashi, A. S., & Cunningham, C. O. (2009). Self-management of injection-related wounds among injecting drug users. Journal of Addictive Diseases, 28(1), 74-80.
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• Zagorski, C. M., Hosey, R. A., Moraff, C., et al. (2023). Reducing the harms of xylazine: Clinical approaches, research deficits, and public health context. Harm Reduction Journal, 20(1), 141.

The best cataract avoidance strategy is to stop breaking Nature’s laws around light.

Cataracts, the leading cause of blindness globally (WHO, 2023), not only cause vision loss but also disrupt systemic light-driven processes (e.g., hypothalamic regulation, circadian rhythms). They lead to mitochondrial stress and organ damage (e.g., liver, kidney) due to oxidative imbalance, altered UPE function, and altered mTOR activity. Perception of reality changes as light fails to modulate the distal neural networks in the brain, increasing mental fog, altered consciousness, or misaligned decision-making.

For an audience concerned about cataracts, the information provided highlights a complex interplay between light exposure, melanin, and metabolic processes in the eye. Recent research, such as the August 2025 Nature Communications article, demonstrates that melanin-like nanofibers offer exceptional electromagnetic interference shielding, outperforming lab-made shields. This suggests melanin, naturally produced in the skin and eyes (RPE), serves as a critical defense against non-native electromagnetic fields (nnEMF), which are implicated in cataract formation.

HOW ARE CATARACTS FOUND?

The severity of cataract formation, is primarily assessed using a Snellen visual acuity test. This of course assumes no other ocular disease is present. What really causes the opacification of the lens. The story that follows explains in detail why decentralized medicine > than centralized medicine when it comes to this eye disease.

nnEMF drives high blood glucose and insulin, which causes a hazy lens caused by the brain trying to protect itself. This is the same way tinnitus tries to protect us from acoustic brain damage by putting a melanin sheet between the environment and our acoustic tracts in the brain. No one sees the targets I see in how nnEMF causes these diseases.

The glyoxalase system is a set of enzymes detoxifying methylglyoxal and the other reactive aldehydes produced as a normal part of metabolism. This system has been studied in bacteria and eukaryotes and is linked to human cataract formation.
The glycation of lens proteins essentially drives cataract formation in the eye. The glycation of lens proteins is primarily driven by methylglyoxal. In direct contradiction to much of the low-carbohydrate literature, glycation is not all driven by dietary carbohydrates. It is driven by light. This is why the next slide exists and why it is true.

The 1981 PubMed riboflavin study (https://pubmed.ncbi.nlm.nih.gov/7234715/) links B vitamin deficiencies, which are cofactors in mitochondrial function, leads to redox imbalances in the anterior and posterior eye chambers, contributing to lens opacification. Excessive nnEMF exposure, including blue light and microwaves, disrupts this balance, driving high blood glucose and insulin levels. This metabolic stress leads to glycation of lens proteins, primarily via methylglyoxal, a reactive aldehyde detoxified by the glyoxalase system. Methylglyoxal, is derived from glucose, ketones, or proteins, binds heavy atoms to proteins, impairing semiconduction and causing lens opacity, which are key steps in cataract development.

nnEMF drives opacification of the lens because this enzyme operates with transition metals susceptible to nnEMF in the microwave range. This is why in Dr. Becker’s book, “The Electric Body”, ophthalmologist Savitz found increased cataract formation in people who were exposed to RF/microwaves at their jobs in the 1960s for DARPA. That covers everyone reading this blog today. These cases are easily found with a minimum of research to support Savitz’s work. DARPA destroyed his career because he reported this Becker.

Environments and jobs loaded with this type of nnEMF ruins the heat sink in the eye and distal organs which alters semiconductive current which alter UPEs. When the heat sink is ruined it affects the optics in the lens, eye, and visual tracks. Methylglyoxal is quantitatively the most important source of advanced glycation end products in the body that are linked to the UPE problem. It is not diet that does it.⠀Few people seem to know that, too. The Decentralized Medicine #35 blog on Patreon lays the etiology out for you. But you must read it to gain the wisdom of Nature.

Methylglyoxal can be derived from glucose, or it can be derived from ketones, or it can be derived from protein. So, diet CANNOT be not the driver of this condition; ALAN and a lack of TINA is. The other evidence of proof comes from retinal spacialists themselves. 20 years ago I asked them why does vitrectomy hasten cataract formation if you think the sun causes them? I got a lot of blank stares from them. I explained to them that vitrectomy increases oxygen levels in the eye, which increases ROS and causes more UPEs to be made which damages the anterior and posterior chamber’s redox power. This is the key cause why oxidative damage to the proteins in the lens leading to cataracts. None of them made the link that blue light and nnEMF also raise ROS. I did not expect them to know about Popp and van Wijk’s work on UPEs but they even were ignorant of the basics. This is why they continue to blame diet and sunlight for cataracts. They are a danger to the public health.

This paper below should illuminate how nnEMF destroys glutathione levels via the glyoxalase system. Once you dehydrate melanin sheets of the nerves that innervate the cornea and orbit, you will likely get a cataract. If you are unlucky, you can wind up with a lot worse in your brain due to the electrical scaring. The brain is acting to block blue light from causing this electrical scarring and that is why the lens opacifies. Methylglyoxal causes heavy atoms to bind to proteins they are not supposed to, this ruins semiconduction in the eye and you get an opacified shade on your eye. https://pubs.acs.org/doi/abs/10.1021/jacs.0c01329

Light that comes through the eye programs the hypothalamus. So it stands to reason this evidence that aberrent light would be the leading cause of cataracts, but centralized medicine will produce papers and miss this point, yet, the conclusion of the paper say this: “Conclusions: Our study provides strong evidence that hypothyroidism is a causal determinant of ARC risk”

Lets review what I have taught you alredy in decentralized medicine on this topic.

In a 2025 April blog on hypothyroidism I told you: People with hypothyroidism of any cause will experients sunburning in the sun in a few minutes due to a lack of melanin, melatonin, and Vitamin D. This is due to a lack of Coulomb charge in the skin which alters Gauss law and you cannot collect enough net negative charge in your skin. Well the same thing happens in your lens and this is why it opacifies and ruins your vision. Let’s review why this happens?

Thyrotropic-releasing hormone (TRH) released from neurons in the paraventricular nucleus of the hypothalamus (autonomic center of the brain) is stimulated directly by the hormone, LEPTIN via the leptin-melanocortin pathways.

MASSIVE BLOG POINT: Leptin normally increases melanocortin (α-MSH) and it is required for TRH expression! This means people with hypothyroidism cannot make POMC or melanin well!! This means their longevity will be cut. This is why hypothyroidism is a gateway disease to many others and leads to an earlier demise. Cataracts are one of those gateway diseases. Those with hypothyroidism need massive solar exposure to change their outcomes. This also implies that hypothyroid patients should have worse outcomes from melanin-related diseases, and they DO!

This makes their skin pale, their lens opacify, and these people will also seem to burn more and not know why. Many will develop autoimmune conditions in the skin and gut and their docs will remain impotent to know why. Many will tell you they are allergic to the sun. I just laugh at these comments. When you know better you do better.”

What else did I say in this blog? “TRH serves as a neurotransmitter or neuromodulator outside the hypothalamus. TRH is a general stimulant and induces hyperthermia on intracerebroventricular injection, suggesting a role in central thermoregulation.”

Hyperthermia = heat and heat decreases your heat sink in all things derived from your brain. Your retina is one of those things. When the heat sink is destroyed cataracts become more probable outcome for patients. I also want to remind you that light dark, and temperature control your circadian mechanism. So any form of heat stress is linked to cataract formation. This is called stacking the lessons in the blogs to explain new diseases to you. I mentioned this to several members in the August 2025 Q&A. If you do not stack the lessons you will never learn how the system robs you of time.

Heat intolerance and heat shocks link to many diseases because the lack of water in the heat sink directly alters the UPEs emission spectra you are now learning about. This is why the circadian clock mechanism is linked to the heat shock proteins. Go look at the Quilt document and you’ll notice I talk about them in it.

HIF-1 and HSP90 Interaction

HSP90 is a molecular chaperone that stabilizes client proteins, including HIF-1α, and plays a role in circadian regulation. The interaction between HIF-1 and HSP90 is well-documented in the literature but it is not well known in opthalmology circles.

Stabilization of HIF-1α: Under normoxic conditions, HIF-1α is hydroxylated by prolyl hydroxylases (PHDs) and targeted for degradation via the von Hippel-Lindau (VHL) pathway. HSP90 binds to HIF-1α, preventing its degradation and promoting its stability, even in normoxia. This allows HIF-1α to accumulate and translocate to the nucleus, where it dimerizes with HIF-1β to activate target genes that increase oxygenation and affect TCA metabolism. (e.g., VEGF, EPO).

HSP90 Inhibition: Inhibitors of HSP90 (e.g., geldanamycin) destabilize HIF-1α, reducing its activity. This demonstrates that HSP90 is uber critical for HIF-1 function, particularly in hypoxic or light stressed conditions we see in cataracts.

Circadian Connection: HSP90 also interacts with circadian proteins, including PER2 and CLOCK. It stabilizes these proteins, ensuring proper circadian clock function. For example, HSP90 modulates the nuclear translocation of CLOCK/BMAL1 complexes, which drive PER2 expression. Since HIF-1α and PER2 both rely on HSP90, this chaperone may serve as a molecular hub linking hypoxia and circadian pathways. Why is this big? All these circadian genes are need for PHOTOREPAIR OF CATARACTS. See the picture below for that review. What does this all imply? If your circadian cycle is jacked up, you will NEVER heal your cataracts. This is why eye docs are not taught this biology by the curriculum paid for by BigHarma and intraocular lens companies. They want to sell you drops, potions, and IoL that will make your mtDNA worse so you become a life long patients for other diseases. You clearly have no idea how the centralized Ponzi scheme is built if you are not following this story well enough. How bad are the centralized ideas?

The implications are VAST. Changes in light input through the eye are designed to predict epigenetic programming. What happens when a cataract is between the sun and your DNA, based on my decentralized thesis? Blocked sunlight disrupts histone modifications and DNA methylation, contributing to diseases like cataracts, diabetes, and neurodegeneration, rather than being solely genome-driven. This idea challenges the Darwin-Watson-Crick genomic focus, emphasizing epigenetics (the “junk DNA” or silent genome) is the true regulator of identity and health.

• Circadian and Heat Shock Connections to CATARACTS

Light, dark, and temperature regulate the circadian clock. Hypothyroidism’s impact on melatonin and TRH disrupts this rhythm, exacerbating heat stress and lens damage. Heat intolerance and shocks alter ultraweak photon emissions (UPEs), are linked to circadian and HSP regulation (as noted in the Quilt document). HSPs, stabilizing proteins under stress, tie directly into cataract formation when heat sinks fail in the organs where the disease exists.

Hypothyroidism reduces the lens’s protective mechanisms (melanin, melatonin, vitamin D), impairing its ability to dissipate heat and light. This, combined with TRH-mediated hyperthermia and circadian misalignment, “stacks” stressors that opacify the lens, leading to cataracts. The study conclusion aligns with my thoughts, but its methodology was set up by BigHarma who paid for it so that it would misses the light-heat-cataract nexus I am emphasizing to you in this blog. Wake up. They are lying to you.

MITOCHONDRIA REDOX DAMAGE OPACIFIES YOUR LENS

Blue light at night, disrupts the circadian clock, increasing appetite, insulin resistance, and diabetes risk, which further exacerbate lens haze. Dr. Becker’s work, including “The Electric Body” and “Cross Currents,” supports this, noting that heat exposure from nnEMF or blue light ruins the eye’s heat sink (water and melanin-based), linking dry eye syndrome and cataracts.

Dryness, worsened by screen use and reduced hydration, amplifies this effect via Carnot’s theorem, reducing semiconductive efficiency. The best strategy to avoid cataracts is to minimize nnEMF exposure (e.g., reducing blue light at night) and support natural defenses like melanin and glutathione levels. Artificial light at night (ALAN) emerges as a key driver, not just diet, highlighting the need to respect natural light cycles. This multifaceted approach, protecting against nnEMF, optimizing hydration, and maintaining mitochondrial health, offers a proactive defense against cataract formation.

What are the details to this biophysical approach to lens opacification?

THE DESTRUCTION OF THE HEAT SINK OF THE EYE BY BLUE LIGHT and nnEMF

Dry eye syndrome is a common condition in the modern world, with prevalence varying based on screen abuse, climate, ethnicity, lifestyle, and cultural factors. Dry is is related to blue screen technology and as the eye dries, Carnot’s theorem kicks in and the heat sink for semiconduction decreases and this is why dry eye and cataracts are linked. The passage below from the consciousness blogs show you how blue light exposure, poor sleep, and cataracts can begin. The path to getting a cataract is many. There is not one way. Becker showed in Cross Currents that heat exposure alone, from any cause, can lead to cataract formation. He also talked about the work of Dr. Savitz in this disease. Excessive chronic blue light exposure causes dry eye by disrupting hydration signals and vitamin A metabolism. Reduced water production at CCO alters the heat sink (per semiconduction principles below) leading to heat buildup. Heat exposure, as noted by Becker, contributes directly to cataract formation.

What are the neurological loops that control making the eyes wet?

The neurological loops controlling tear production (keeping the eyes wet) involve a complex interplay of the autonomic nervous system, sensory feedback, and central nervous system regulation. Anyone of these pathways can be disrupted to lower tearing to lead to a cataract. Here’s a concise overview of these pathways.

1. Lacrimal Functional Unit: Tear production is regulated by the lacrimal gland, accessory glands, and the ocular surface, coordinated via neural pathways.
2. Parasympathetic Pathway:

   Trigeminal Nerve (CN V): Sensory nerves in the cornea and conjunctiva detect dryness or irritation, sending signals via the ophthalmic branch to the brainstem. This is the nerve of the first pharyngeal arch.

   Facial Nerve (CN VII): The superior salivatory nucleus in the pons receives these signals and activates the pterygopalatine ganglion. Postganglionic parasympathetic fibers then stimulate the lacrimal gland to produce reflex tears. This is the second pharyngeal arch innervation.

3. Sympathetic Pathway:

   The superior cervical ganglion provides sympathetic innervation to the lacrimal gland, modulating basal tear secretion. This is less dominant but helps maintain baseline moisture. This is commonly disrupted in most cases. This pathway also cause dry mouth and lowers parotid salivary flow. This is why many cataract suffers have dry eye and dry mouth and poor dentition.
   

   Cataract patients all have mitochondrial inefficiencies. In yesteryear this was blammed on old age, but today nnEMF makes us old when we are young. Patients with low mitochondrial redox frequently experience dry eye and dry mouth, which is linked to autonomic dysfunction, systemic conditions, or medication use. The Nature Communications study of 2025 suggests that sympathetic overactivity in the SCG can suppress lacrimal gland secretion, contributing to aqueous-deficient dry eye, a common complaint in mitochondrial low redox populations.

4. Similarly, sympathetic modulation of salivary glands can reduce saliva production, exacerbating xerostomia. Cataracts are often associated with low reodx states like aging, and mitochondrial inefficiencies are more likely to have comorbidities like diabetes, hypertension, or autoimmune diseases (e.g., Sjögren’s syndrome), which can disrupt autonomic innervation. For example, diabetes can cause autonomic neuropathy, affecting both sympathetic and parasympathetic pathways, leading to reduced tear and saliva production. This is why diabetics commonly get cataracts. Diabetes is a blue light toxic disease.

   Medications used to manage these conditions, such as beta-blockers or diuretics, are also known to cause xerostomia and dry eye as side effects. This implies they do not treat the proper etiology of the disease, because they do not reverse the dry eye or xerostomia effects. Furthermore, cataract surgery itself can exacerbate dry eye by damaging corneal sensory nerves, reducing reflex tear secretion, and amplifying reliance on basal tear production, which is already be compromised by sympathetic dysregulation. Poor dentition in cataract patients may be a downstream effect of chronic dry mouth, as reduced salivary flow increases susceptibility to caries and periodontal disease. While no single study directly links SCG dysfunction to cataracts, dry eye, dry mouth, and poor dentition, the shared autonomic pathways and systemic factors (aging, medications, comorbidities) provide the quantum biological connection as seen in the picture above.

5. Central Regulation:

   The hypothalamus and limbic system integrate emotional triggers (e.g., crying) and stress responses, influencing tear production via the autonomic nervous system.

   The brainstem (pons and medulla) coordinates reflex tearing in response to environmental stimuli (e.g., wind, , sunlight, and blue light exposure).

6. Feedback Loop:

   Dryness or blue light-induced disruption affects hydration signals and vitamin A metabolism) reduces sensory input to the trigeminal nerve, dampening the reflex arc. This can lead to decreased tear production, aligning with my heat sink hypothesis. My thesis was the basis of all these predictions in 2010.

   

WISDOM OF NATURE: A STORY OF BIOPHYSICS

We are all beautiful broken mosaics, pieces of light, love, history, and stars, glued together with quantum magic, music, and words. Do you know where your pieces fit? The glass blower can take shattered glass and apply heat and time to breathe new life into the mosaics, creating an even better version of what existed before. To repair cataracts, you need to understand how the photorepair mechanism in mammals works. This was spoken about in the Quantum Engineering series. This slide is a gentle reminder to re read those blogs.

BIOPHYSICS LESSON OF CATARACTS IS A GOE STORY

How much do you know about the decentralized hybrid theory of the Great Oxygen Holocaust in human history? Here is a quick rundown. I know why he got tinnitus, do you? https://threadreaderapp.com/thread/1898906739673563628.html

Modern modeled = a slow evolving zombie apocalypse designed by DARPA. That is how it feels from within when you’re 135 years into the 6th extinction. We like to think we are all smarter than the T-Rexes were, but when you realize we are silly talking monkeys “addicted to our version of the asteroid,” we have no idea what is coming as they did not. I teach Black Swan mitochondriacs how to think to see what few do. Thinking changes your perspective. Many realities are hidden behind a wall of perception. The cause of this extinction is hidden, yet the effect is visible to all mankind.

FIRST PRINCIPLE THINKING ON MY FARM PATIENTS FOR CATARACTS

Considering that we know the innervation of the cornea and orbit as first principle ideas, we should be able to link the lack of melanin to a specific place in the brain to see where nnEMF is causing melanin destruction and mtDNA mutation for water production. For example, we know the human cornea and orbit receive innervation primarily from the ophthalamic branch of the trigeminal nerve (CN V1), with its branches, including the nasociliary nerve and long ciliary nerves, providing sensory innervation to the cornea, and the oculomotor (CN III), trochlear (CN IV), and abducens (CN VI) nerves controlling the extraocular muscles within the orbit. What place in the brain would include where these neural networks connect?

Innervation of the Cornea and Orbit: Neural Pathways

1. Sensory Innervation (Trigeminal Nerve, CN V1):

The cornea is one of the most densely innervated tissues in the body, receiving sensory innervation primarily from the ophthalmic branch of the trigeminal nerve (CN V1).

Nasociliary Nerve: A branch of CN V1, it gives rise to the long ciliary nerves, which innervate the cornea, iris, and ciliary body, carrying sensory (pain, temperature, and mechanical) and sympathetic fibers.

• Pathway to the Brain:

  Sensory fibers from the cornea travel through the long ciliary nerves to the nasociliary and ophthalmic nerve (CN V1).

  These fibers enter the brainstem at the pons level via the trigeminal nerve root.

  They synapse in the trigeminal sensory nucleus, a complex structure spanning the brainstem:

  Spinal trigeminal nucleus (caudal part, extending into the medulla and upper cervical spinal cord): Primarily processes pain and temperature sensations from the cornea.

  Principal sensory nucleus (in the pons): Processes touch and pressure sensations.

  Second-order neurons from the trigeminal sensory nucleus cross the midline and ascend via the trigeminal lemniscus to the thalamus’s ventral posteromedial nucleus (VPM).

  From the VPM, third-order neurons project to the primary somatosensory cortex (S1) in the postcentral gyrus (Brodmann areas 3, 1, 2) for conscious perception of corneal sensation.

  Associated Areas: The trigeminal system also projects to the insula and anterior cingulate cortex for emotional and autonomic responses to corneal pain (e.g., tearing, blinking). Many cataract sufferers also have comorbid ADHD and OCD. Now you know why.

2. Motor Innervation (CN III, CN IV, CN VI):

The extraocular muscles within the orbit are controlled by:

Oculomotor nerve (CN III): Innervates the superior, medial, and inferior rectus muscles, inferior oblique, and levator palpebrae superioris (for eye movement and eyelid elevation).

Trochlear nerve (CN IV): Innervates the superior oblique muscle.

Abducens nerve (CN VI): Innervates the lateral rectus muscle.

Pathway to the Brain:

CN III (Oculomotor):

Originates from the oculomotor nucleus in the midbrain (at the level of the superior colliculus), which controls voluntary eye movements.

• This also includes the Edinger-Westphal nucleus (midbrain), which is responsible for the parasympathetic innervation of the pupil (via the ciliary ganglion).

  Receives input from the superior colliculus (for reflexive eye movements), frontal eye fields (FEF) (Brodmann area 8, for voluntary saccades), and pretectal area (for pupil reflexes).

  CN IV (Trochlear):

  Originates from the trochlear nucleus in the midbrain (at the level of the inferior colliculus).

  Receives similar cortical and subcortical inputs as CN III for coordinated eye movement.

  CN VI (Abducens):

  Originates from the abducens nucleus in the pons.

  Coordinates with the oculomotor nucleus via the medial longitudinal fasciculus (MLF) for conjugate eye movements (e.g., horizontal gaze).

  Receives input from the paramedian pontine reticular formation (PPRF) (for horizontal saccades) and the superior colliculus.

  Higher-Level Control:

  The frontal cortex’s frontal eye fields (FEF) and supplementary eye fields (SEF) plan voluntary eye movements.

  The parietal eye fields (PEF) in the posterior parietal cortex (e.g., lateral intraparietal area, LIP) integrate sensory and motor information for spatial attention and eye movement.

  The cerebellum (especially the flocculus and vermis) fine-tunes eye movements and coordinates with the brainstem nuclei.

3. Autonomic Innervation (Sympathetic and Parasympathetic): 

Sympathetic: The long ciliary nerves (via CN V1) carry sympathetic fibers from the superior cervical ganglion to the dilator pupillae muscle (pupil dilation).

Parasympathetic: The oculomotor nerve (CN III) carries parasympathetic fibers from the Edinger-Westphal nucleus to the ciliary ganglion, innervating the sphincter pupillae (pupil constriction) and ciliary muscle (accommodation).

These autonomic pathways connect to the hypothalamus (for circadian regulation) and pretectal area (for light reflexes).

Where Do These Neural Networks Converge in the Brain?

The innervation of the cornea and orbit involves sensory, motor, and autonomic pathways, which converge in several key brain regions:

Brainstem:

Trigeminal Sensory Nucleus (Pons and Medulla): The first relay for corneal sensory input (pain, touch) via CN V1.

Oculomotor, Trochlear, and Abducens Nuclei (Midbrain and Pons): These control the motor of extraocular muscles, coordinated via the MLF.

Reticular Formation (PPRF): Coordinates conjugate eye movements with input from higher centers. Blue light here is why people with cataracts struggle with sleep. If you have a sleep issue and cataract I know how deep your electrical scar goes in you compared to a newer cataract.

Thalamus: The Sensory Processing behemoth of humans

Ventral Posteromedial Nucleus (VPM): This relays sensory information from the trigeminal system to the neocortex. The less myelin present here from blue light damage the more likley you are to sneeze with bright light exposures.

Lateral Geniculate Nucleus (LGN): Though primarily visual, it integrates with eye movement and pupil control pathways via the pretectal area. This is where many transgeneration causes of eye motions come from via the germline. You heard about these in the August 2025 Q&A when we mentioned amblyopia and nystagmus. Re Listen to it with this blog in mind to see what you missed.

Cortex:

Primary Somatosensory Cortex (S1): Processes corneal sensation (pain, touch).

Frontal Eye Fields (FEF) and Supplementary Eye Fields (SEF): Plan voluntary eye movements. This is why many people have amblyopia and are more prone to seizures from light.

Posterior Parietal Cortex (PPC): Integrates sensory and motor data for spatial awareness and eye movement. This is why so many cataract suffers need Waze and google maps. Their electrical scar in their brain extends here from their cataract defect.

Insula and Anterior Cingulate Cortex: Handle emotional and autonomic responses to corneal stimuli. Many people with cataracts are highly emotional. When the electrical scar is here I look at brain MRIs to see if there is a white matter volume deficit present.

Hypothalamus and Pretectal Area:

Hypothalamus: Regulates autonomic responses (e.g., pupil dilation) and circadian rhythms, influencing melanin production via melanopsin signaling.

Pretectal Area: Mediates pupil light reflexes, connecting to the Edinger-Westphal nucleus.

Cerebellum:

Fine-tunes eye movements and integrates sensory-motor feedback, mainly via the flocculus and vermis. Many people with posterior cataracts get bouts of nystagamus and this is why it can happen. Many people also develop balance problems with cataracts. This is why it happens. This tells the decentralized clinician just how widespread the blue light induced electrical scar is on the neocortex. This directly impacts how long a photorepiar reversal should take.

Linking Lack of Melanin to a Specific Brain Region

​The decentralized MD focus should be melanin and its neural crest migratory path.  Why?  Melanin’s role in bioelectric signaling suggests that a lack of melanin in the cornea and orbit might disrupt these neural networks, particularly at points where melanin-containing cells (e.g., melanocytes) or melanin-dependent bioelectric processes are critical. NCC migration is the motherboard of the cell and explains to us the extent of the electrical resistance in the brain from blue light and nnEMF abuses. Let’s explore this:

Melanin in the Cornea and Orbit:

The cornea itself lacks melanin, but the surrounding structures (e.g., iris, ciliary body) contain melanocytes. The retina (closely related to the orbit) is rich in melanin (e.g., retinal pigment epithelium, RPE). The optic nerve and its projections also involve melanin-containing cells.

As I’ve noted in many blogs, melanin in these areas acts as a photo-bioelectric charge regulator, dampening currents when hydrated and becoming conductive when dehydrated (per my slides and the Popular Science article on eumelanin’s conductivity).

The Impact of endogenous Melanin Deficits in Humans:

Lack of endogenous melanin = destroyed endogenous heat sink = alien UPEs

A lack of melanin (or dehydrated, conductive melanin due to nnEMF/ALAN) in the iris, ciliary body, or retina could disrupt local bioelectric signaling, affecting the trigeminal sensory fibers (CN V1) and autonomic innervation (via CN III). This leads to aberrant signals (e.g., pain, photophobia) or impaired pupil responses, contributing to cataracts or other dysfunctions. This is why TBI patients have photophobia and never show up on imaging. It also explains why concussion patients are at a higher risk to develop cataracts in the future.

In the orbit, extraocular muscles and their innervation (CN III, IV, VI) rely on precise bioelectric coordination. Disrupted melanin in nearby structures (e.g., optic nerve sheath) would alter these signals, affecting eye movement or gaze stability. This is why TBI patients get double vision. Cataracts and TBI share etiology. They both cause organic brain damage.

Central Brain Region Most Affected:

The hypothalamus stands out as a critical convergence point where a lack of melanin has a profound impact:

Melanopsin Connection: The hypothalamus, particularly the suprachiasmatic nucleus (SCN), receives input from melanopsin-containing retinal ganglion cells (via the retinohypothalamic tract). Melanopsin, a light-sensitive pigment, regulates circadian rhythms and pupil responses. A lack of melanin in the retina or iris (due to dehydration or degradation) should impair melanopsin signaling, disrupting hypothalamic control of autonomic functions (e.g., pupil dilation, tear production) and circadian alignment. This is why dry eyes are always linked to cataract formation.

Autonomic Dysregulation: The hypothalamus integrates autonomic inputs from the orbit (via CN III’s parasympathetic fibers and sympathetic pathways). Disrupted bioelectric signaling due to melanin deficits might lead to autonomic imbalance, exacerbating conditions like cataracts & tinnitus (via methylglyoxal accumulation) via downstream effects on auditory pathways in the medial geniculate nucleus).

Photo-bioelectric disruption: My decentralized model emphasizes that dehydrated melanin increases conductivity, amplifying aberrant currents to lead to distal electrical scarring and loss of myelin and MT function. In the hypothalamus, this would disrupt the bioelectric environment, affecting its role in regulating the trigeminal-autonomic reflex (e.g., tearing, blinking in response to corneal irritation) and circadian-driven melanin production. It can also cause memory loss. All of these are seen in TBI patients and most cataract patients.

Secondary Impact: Brainstem and Thalamus:

The trigeminal sensory nucleus in the brainstem might also be affected, as it processes corneal sensory input. If melanin deficits in the cornea/orbit lead to aberrant bioelectric signals (e.g., due to nnEMF-induced dehydration), the trigeminal nucleus might overcompensate, contributing to pain or reflex issues.  Trigeminal neuralgia could be a photo-bioelectric problem, too.  So might intraocular opthalmoplegia which is most often linked to MS. Internuclear ophthalmoplegia (INO) is a disorder of eye movements caused by a lesion in an area of the brain called the medial longitudinal fasciculus (MLF). The most common causes of INO are multiple sclerosis and brainstem infarction. Both of these diseases are also photo-bio-electric diseases associated with demyelination and loss of white matter volumes. In the eyes, OCT studies help predict future risks.

The thalamus (VPM) can misinterpret these signals as a sensory relay, leading to altered perception or chronic conditions (e.g., photophobia, linked to cataracts). TBI patients should wake up about now. I think I just explained symptoms that centralized experts do not. In my worldview, cataracts are brain TBI caused by blue light and nnEMF at chronic levels. The severity of the opacity of the lens links directly to mitochondrial CCO function and VDR on the IMM to protect the mitochondria from stray electrical currents from migrating in the brain. The more UV and IR is subtracted from your life, the worse the opacification will be and the more damage in the brain their will be.

KEY LESSON IN THIS BLOG: Many people do not realize the outer retina has a massive density of mitochondria in the eye and this is why cataracts are so common in our modern world.

Tying these lesson back to My Photo-Bioelectric Framework

​My decentralized medicine thesis links nnEMF and ALAN to melanin dehydration, mitochondrial dysfunction, and bioelectric disruption. In the context of the cornea and orbit:

Melanin Dehydration in the Hypothalamus: The hypothalamus, via its role in melanopsin signaling and autonomic control, is a likely central target. A lack of melanin (or its functional degradation) in the retina/iris could impair light-dependent hypothalamic functions, disrupting circadian rhythms and autonomic responses, which in turn exacerbate corneal/orbital pathology (e.g., cataracts via methylglyoxal).

I believe glaucoma is also an nnEMF blue light disease. Why?

My Glaucoma Prediction: Chronic exposure to nnEMF (microwave range) and blue light (e.g., from LED screens) damages melanopsin in retinal ganglion cells (RGCs) and mtDNA in the retinal pigment epithelium (RPE) and optic nerve head. In glaucoma cases patients always show evidence of light damage. They are missing melatonin = lack of UV and IR light. They have low vitamin D levels = lack of UVB exposure and presence of CCO dehydration, and a serious lack of NO = lack of UV and IR light = higher BPs, higher eye pressures, evidence of photoreceptor damage on eye exam.

Mechanism: Blue light, absorbed by melanopsin, disrupts the retinohypothalamic tract, altering hypothalamic regulation of circadian rhythms and autonomic tone in the eye. nnEMF, affecting transition metals in the glyoxalase system, depletes glutathione, melanin, and melatonin. These all degrade and lead to abnormal UPE fpormation and this light destroys internal tissue optics. This increasing methylglyoxal and advanced glycation end products (AGEs) in the trabecular meshwork in the lens, canal of Schlem, and optic nerve. This impairs mitochondrial water production, lowering Δψ and electrical resistance in retinal cells. This is how glaucoma, cataracts, and retinal damage all begin. It is not hard to see when you see it from 100,000 feet with the explanation in front of your eyes.

Outcome: Reduced photo-bioelectric in the anterior and posterio chamber signaling leads to RGC apoptosis and optic nerve degeneration, all hallmarks of glaucoma, independent of IOP in normal-tension glaucoma cases. They also lead to lens opacification.

Bioelectric Consequences: Dehydrated melanin in the orbit increases conductivity, potentially sending aberrant signals through CN V1 to the trigeminal nucleus and hypothalamus. This amplifies ROS/RNS and ultraweak biophoton transformation from the excessive bioelectric currents in the eye (per the work of Roeland Van Wijk and Fritz Popp references), further driving pathology in the central retinal pathways proximally and distally in neural structures and circulatory structures. This is how we get opthalmic aneurysms too.

Tinnitus Connection: The hypothalamus also influences the auditory system indirectly via autonomic pathways (e.g., trigeminal-autonomic interactions). Disrupted melanin in the orbit might contributes to tinnitus (as in Dr. Poland’s case) by altering photo-bioelectric signals that reach the brainstem and auditory cortex. Never forget spike protein is a mitochondrial toxin that mimics blue light and nnEMF damage.

SUMMARY

Cataracts’ cause a creeping blindness that disrupts light’s quantum role, damaging organs and perception via altered UPEs and epigenetics, not just vision. Light’s power depends on absolute darkness at night, and its blockage shifts human evolution toward disease unless addressed with wisdom and unconventional approaches. Modern centralized science’s irony, is that astrophysicists study stellar light without ever linking it to cellular evolution. This defect in methodology underscores the need to prioritize light-driven epigenetics over genomic dogma. Nothing in the literature is trustworthy because of this disconnect.

The real issue isn’t too much sunlight, it’s the wrong kind of light, at the wrong time, without the full-spectrum solar balance nature intended. You must get more sun, not less when your lenses are opacified. There are many pathways to cataract formation but excessive blue light and nnEMF exposure is by far the number one cause in the modern world.

The neural networks of the cornea and orbit converge in several brain regions. Still, the hypothalamus is the most likely central hub where a lack of melanin would have a significant impact in cataract formation, given its role in melanopsin signaling, autonomic regulation, and circadian control.

When you have a cataract, you have sustained a light injury to the hypothalamus. A cataract, therefore, should be thought of as a TBI, made chronically by low intensity nnEMF exposure of the eyes.  This mimics an electric scar on the lens. The pathology all begins with vasopressin release from the light injury.  Quantum Engineering #23 explains why this is the case. Please review it. Therefore, the decentralized clinicians should employ antagonists of the vassopressin signal.  That would be sunlight with more red diurnally than expected because this light makes more DDW water from mitochondria.

This water is not as conductive to the exposed 30 million volt charge of the mtDNA exposed where melanin degradation has occurred. A melanin deficit in the cornea/orbit (or its functional dehydration due to nnEMF/ALAN) should be expected to disrupt hypothalamic functions, leading to autonomic and bioelectric imbalances that exacerbate conditions like cataracts, photophobia, or even tinnitus.

Many other conditions of the hypothalamus should be expected in these patients. Consideration for those with obesity (choroid/arcuate nucleus), Hashimotos (Ant pituitary), anorexia, ASD (thalamus), ADHD (habenular nucleus), altered perceptions of reality, poor first principle thinking, or gender dysphoria. The trigeminal sensory nucleus and thalamus are secondary regions where these effects might manifest as altered sensory processing disorders because their perception of reality is altered. This makes change hard for them to accept and perform.

This blog should make you understand why I have rejected competition (Darwin’s “survival of the fittest”) for cooperation (Survival of the Wisest) and creativity aligns with epigenetic adaptability. Wisdom, gained through learning and error, decodes the “rainbow” in non-coding DNA and non-verbal communication in biology. Ignoring the centralized noise (genomic or verbal) so we can focus on the improbable (e.g., light’s evolutionary role) because when we do, this reveals nature’s secrets, as stars’ light evolves the entire universe. Cataract formation stops that process in you.

CITES

Are all buried in the substance of the blog. Review them all.

Why are eye diseases in California exploding?

The hospital data has it.  CMS data reflects it. The evidence is everywhere.  Why?  The cornea of the eye touches the environment and this is where its oxygen, Vitamin D and water come from from the actions of CCO on th eIMM.  How does it all fit?

Being above the age of 55 is a primary risk factor for age-related macular degeneration.  This means the longer you inhabit a a toxic environment the higher chance you get an eye disease.  You never get told this in the centralized doctors office.

In California, eye diseases like glaucoma, age-related macular degeneration (AMD), diabetic retinopathy, and cataracts are prevalent, with varying incidences and prevalence across different regions and demographics.Glaucoma affects a significant portion of the Medicare population, and its severity varies, with older individuals, Black individuals, and those with higher comorbidity scores being at higher risk. Chronic eye diseases like glaucoma, AMD, diabetic retinopathy, and cataracts also show varying prevalence across different Service Planning Areas (SPAs) in Los Angeles County, highlighting potential disparities related to residential location due to nnEMF risks.  nnEMF risks from all causes raise the risk of eye disease.

We know melanin protects from nnEMF radiation.  This implies that all the black and brown people in California should fare well there.  Do they?

• Ethnicity: California has one of the most diverse populations in America. In 2023, the U.S. Census Bureau found that 40.3% of Californians are Latino, 34.7% are Caucasian, 16.8% are Asian American or Pacific Islander, 6.5% are African American, and 1.7% are Native American or Alaska Natives.
• As reported by the American Academy of Ophthalmology and other publications, certain ethnicities, such as Latinos, Asian Americans, and African Americans, have A MUCH HIGHER risk of developing glaucoma. With these ethnicities making up nearly two-thirds of the California population, the risk for glaucoma in California is vast. Why does this congruence exist?

Glaucoma:

• A study of the 2019 California Medicare population found that 3.8% of beneficiaries had any glaucoma, with 2.9% having primary open-angle glaucoma (POAG), and 0.2% having secondary open-angle glaucoma (SOAG) and angle closure glaucoma (ACG).
• Moderate to severe glaucoma was reported in 31.0% of those with any glaucoma, and 24.4% of those with ACG were reported as severe, according to the American Journal of Ophthalmology.
• Older individuals (85+), females, Black individuals, and those with higher comorbidity scores were found to be at HIGHER risk of having glaucoma.  This explains to why California is toxic to humans.  The nnEMF is destroying their biology.

Other Chronic Eye Diseases in Los Angeles County:

• A study in Los Angeles County found that 14.11% of Medicare beneficiaries had any eye disease, including glaucoma, AMD, diabetic retinopathy, and cataracts.
• The prevalence of these diseases varied across different Service Planning Areas (SPAs), with some areas having significantly HIGHER rates than others.  Why would anyone live there knowing these FACTS?
• For example, residents in SPA 5 had significantly higher odds of having any eye disease compared to residents in SPA 3.

Other Relevant Information:

• Episcleritis and scleritis have higher specific incidence and prevalence rates in Northern California where latitude and pollution exist.
• Uveitis also has incidence and prevalence rates in Northern California, with higher rates in older age groups and in women.
• Dry eye syndrome is a common condition in California, with prevalence varying based on screen abuse, climate, ethnicity, lifestyle, and cultural factors.
• Visual impairment and severe visual impairment increase with age, and prevalence rates are higher in Black and Hispanic populations compared to whites. These people have more melanin, yet they are destroyed faster?  Might it be that their dark skin prevents them from making enough Vitamin D in their skin and blood to protect their IMM from CCO damage via water production?  When CCO is damaged oxygen become a toxin.  That is the story of the entire decentralized medicine series.  Are you stringing any of these lesson together?

Factors Influencing Eye Health:

• Age, sex, race, and socioeconomic factors can influence the risk and prevalence of eye diseases.  More money leads to more tech abuse.
• Access to healthcare, including rural and underserved areas, is also a key factor in California.  Shows you centralized care is impotent in helping anyone with this problem because nnEMF is the driver.
• Social determinants of health, such as social vulnerability, can also play a role in eye health outcomes. The nnEMF flying over the heads of Californians in poor areas is coming from the rich areas and it affects the entire socio economic strata health metrics.
• Eye Care Trends in California 2025 -Jan 9, 2024 — A recent study was conducted by Investigative Ophthalmology & Visual Science (IOVS) to examine the association between …
• Prevalence of Glaucoma, POAG Associated With Age, Race in …Nov 2, 2023 — Medicare beneficiaries in California who were aged 65 years and older were included in this study; individuals with Par…AJMC
• Prevalence and Severity of Glaucoma in the California …Of 5,856,491 beneficiaries in the 2019 California Medicare population, there were 220,662 (3.8%) with any glaucoma, 171,988 (2.9%) American Journal of Ophthalmology

  READ THE LINKS TO ALL TO SEE WHAT THE DATA REPORT.

NOW READ MY IDEAS BELOW ABOUT WHY IT IS HAPPENING.

• Time without health is a nightmareThe Photobiological Recursive Loop: A First-Principles Breakdown of how the environment destroys your patients.

  My photo-bioelectric  recursive loop is a self-reinforcing cycle where UPEs act as quantum signals, linking mitochondria, myelin, MTs, and circadian rhythms. Let’s build this theory from the ground up:

  UPE Generation in Mitochondria:

  Fundamental Mechanism: Mitochondria, the cell’s powerhouses, produce ATP via oxidative phosphorylation (OXPHOS). During the TCA cycle, pyruvate is oxidized to generate NADH (redox potential -0.32 V vs. SHE), which donates electrons to the electron transport chain (ETC). This creates a proton gradient across the inner mitochondrial membrane (IMM), with a potential (Δψ) of 150–180 mV, driving ATP synthesis.

  Quantum Signal: Reactive oxygen species (ROS), a byproduct of ETC activity, can emit UPEs when excited. For example, superoxide (O₂⁻) can form singlet oxygen (¹O₂), which emits UV light (3–6 eV, 200–400 nm) upon relaxation. Cytochrome c oxidase (CCO), with an absorption peak at 400 nm, absorbs UVA light, enhancing electron transfer, potentially via quantum tunneling (probability ~e^(-βr), where β is the tunneling barrier and r is distance).

  Tweet 4: https://x.com/DrJackKruse/status/1613299267703308289

  Claim: “The non-linear optical effect in cells is directly tied to the production of DDW water via CCO around the mitochondrial membranes. Mitochondria are the key source of UPE in cells. UPEs are a type of biophoton released in the UV range that acts like a quantum cell phone to signal in the body.” The two slides lay this case out with precision.

• Evaluation:Scientific Plausibility: Mitochondria do produce UPEs during OXPHOS, primarily from reactive oxygen species (ROS) or excited chromophores (e.g., heme, flavins), with emissions in the UV-Vis range. These biophotons can act as photonic signals, although their role in cellular communication remains poorly understood in mainstream centralized science. It is well established in the biophysics literature. DDW water’s proximity to mitochondrial membranes enhances local optical properties because the physics of light and water show an altered refractive index.Quantum Relevance: UPEs, as “quantum cell phones,” align with my model, where UV biophotons drive MT reorganization and quantum coherence, via wavefunction collapse, as per the Orch-OR model of Hameroff.

  Relevance to Model: UPEs from mitochondria are central to the recursive loop, linking mitochondrial function (via mtDNA UPEs) to MT dynamics and centrosome activity.

  Tweet 7: https://x.com/DrJackKruse/status/1613300571741487104

  Claim: “The mitochondrial matrix is filled with DDW water transformed by metabolism by the actions of CCO.  The VDR is the brake mechanism to stop electrical damage from occuring in tissues when CCO is defective for any reason because a disruptions in CCO makes oxygen a toxin and this brings the patient colony of mitochondria back to the GOE inside them self.  This creates massive AMO physics damage inside destroying melanin, melatonin, and Vitamin D leading to massive disease manufacturing in the modern world.

  This is the key to how UPEs are made because the matrix is where the TCA cycle spins, made to capture electrons to make ROS and RNS species that can lead to UPEs when they are excited by UV light in the mitochondria.”is well known, through spectrographic analysis, that water and other dipole molecules are able to be entrained to exogenous oscillatory patterns by rearranging their cluster patterns. Light and free radicals are capable of doing this. The cluster rearrangements then resonate with the entraining frequency of light.

• Sunlight creates electric fields that not only allow electrons to delocalize, but sunlight can free up hydrogen protons to move.When they move they activate the semiconductive molecules in cells to action or inaction.  Electrical fields Water, being dipolar, can be partly aligned by an electric field

  The electric field may be found at surfaces. Electric fields break hydrogen bonds giving less cyclic hydrogen bonded clustering and raising the hydrating abilityof the water. Water production is stochastically related to whether oxygen is a toxin or not for my patients. Less water means, even small amount of oxygen can cause diseases and kill them. So this implies intracelluar hypoxia really signals a patient is experiencing an oxygen halocaust inside of them and this destroys, melatonin, melanin, and the VDR mechanism.

• Taking an exogenous substrate will never repair the deficits of having excited electrons creating these substrates. The reason is simple. Feedback loops use the substrates they create as their interactive controller of the cycle. Loss of this control causes the cycle to uncouple and heat is thermalized to the local environment and quantum coherence is lost as water loses its coherent domains. As coherence is lost in cell water, redox power drops exponentially. There are physical manifestations of this in the matrix of size and shape change of the mitochondria, along with spacing out of the cytochrome proteins that tunnel electrons from food.Scientific Plausibility: The mitochondrial matrix contains structured water due to its high protein and lipid content. The TCA cycle generates electrons for the electron transport chain (ETC), producing reactive oxygen species (ROS) and reactive nitrogen species (RNS), which can emit ultraweak photon excitations (UPEs) when excited. UV light in mitochondria (e.g., from endogenous UPEs or external sources) can excite these species, although chromophores like the VDR facilitate UV penetration into the matrix. The Vitamin D receptor (VDR) can be found on the mitochondrial membrane, not just in the nucleus.

  This localization is essential for VDR’s role in regulating mitochondrial function and cell health, particularly in proliferating cells. It protects them from a chronic endosymbiosis we know as cancer. Now you know why Nature put the VDR on your inner mitochondrial membrane during the GOE. It was an “electron and proton brake” to protect itself from burning up electrically on the IMM during the GOE. When you patient is in a geopathic stress zone, it makes oxygen a toxin and they are effectively back in the GOE in the modern world.  This is where all diseases begin.  Putting the VDR on the IMM was became Nature’s best chemotherapy for all disease innoculation.  The mitoception loop of VDR protection for CCO allowed complex life to compund time to live.  Time with out health was hell on Earth.  That was the lesson of the GOE.  Complex eukaryotic life solved this problem to build out the 32 phylla over night.

• What happened in California the last 5 years?Why were jab injuries concentrated there in the compliant group?

  They pushed the jabs on everyone including kids.  It is required for school.  This is why parents must homeschool.  Think of jab status and the vaccine schedule like the Sahara desert.  This is where life goes to die slowly. This is why life is sparse in these environments. Most of Southern Cali is a desert.

  Without the VDR brake operational on the IMM, organ damage can also occur more easily, because CCO gets electrically fried.   This is why eye diseases are spiking in this state. It is also why the kidney was the most damaged organ due to the LNP of the jabs.  The heart was second and the brain thrid because of their protection mechanism.  https://www.sciencedirect.com/science/article/pii/S2213231724000387

  QUANTUM MECHANICAL DETAILS OF THIS GEOPATHIC STRESS REGION

  Southern California’s high nnEMF environment (e.g., dense cell tower networks and the Van Allen belt issue) all should be expected to contribute to human Vitamin D levels because the rules for Vitamin D synthesis are highly constrained by Nature’s requirements. They are unusual. Think Shannon’s theorem.

  The UV index (UVI) measures total UV intensity but doesn’t guarantee UVB quality or coherence for 7-DHC conversion. Factors like atmospheric scattering, pollution, dehydration, or ozone can alter the UVB spectrum, reducing the proportion of effective wavelengths (~295–300 nm). The Quantum coherence of UVB photons is critical for efficient photolysis, but environmental EMF by itself isn’t likely to significantly disrupt this at the molecular level.

  But it is the combination of effects that occur in this location to destroy what Nature requires to make Vitamin D from cholesterol and this is the big deal that people in California refuse to see. They all can tan, but they cannot make Vitamin D well. This tells you their is a precision error that has compounded in this region. The rules for UVA tanning are not a stringent via nature as the rules for making Vitamin D. As a consequence, practical factors like cloud cover, altitude, sunscreen, tattoo’s and sunglass use and latitude HAVE magnified effects in disturbing the quantum rules for conversion. This is why people in SoCal are more likely to be affected UVB quality and quantum yield.

• This is why transgenerational issues between mom and child are so much more common in California because this quantum information is transfered via oxidative stress signaling in ROS/RNS and manifests in altered UPE creation and this leads to immune dysregulation. This is why eye diseases are more common in California then say in Florida, where the population is the OLDEST in the country. OLDEST should imply more eye diseases if you realize what I said about AMD above. But the reality of living in California explains why it is so dangerous to eyes.Orange County’s Context: Orange County, a tech-heavy urban area in Southern California, has high nnEMF (e.g., dense cell tower networks), heavily tattoo’d humans, atmospheric pollution (smog, ozone), and potential geomagnetic influences, and jab requirements, which disrupt the quantum coherence required for 7-dehydrocholesterol (7-DHC) to previtamin D3 conversion, contributing to low 25(OH)D levels despite retaining their tanning ability.

  Autism as a Covariable: High autism rates in Orange County are directly linked to vitamin D deficiency, nnEMF-induced oxidative stress, and immune dysregulation, which also exacerbate skin diseases like atopy, eczema, roascea, psoriasis, and many other transgenerational effects in neuroectrodermal tissues that abut the environment of California.

  Glaucoma as a Covariable: According to the Centers for Disease Control and Prevention (CDC), about three million Americans have glaucoma, and a large portion of that population comes from California​​ even though more elederly live in Florida.

  Quantum Constraints on Vitamin D Synthesis: The 7-DHC photolysis is a precise, UVB-dependent reaction (~295–300 nm) requiring quantum coherence, likened to Shannon’s theorem. Environmental “noise” (nnEMF, smog, etc.) in Orange County reduces quantum yield, explaining poor vitamin D synthesis.

  Coulomb Force and Gauss’s Law: Skin’s insulating properties amplify electrostatic fields (∇·E = ρ/ε₀), influencing melanin, melatonin, and vitamin D synthesis. nnEMF disrupts these charge dynamics on the surface of the eye and skin, contributing to disease.

  Transgenerational Eczema is another Covariable: Maternal nnEMF exposure and low vitamin D in Orange County may drive epigenetic changes, increasing eczema and autism risk in offspring.

  ICD-10 Code W90.0: The new CMS code for radiofrequency exposure supports nnEMF’s health impacts, relevant to vitamin D deficiency, eczema, and autism. It is most commonly used in California.

• Vitamin D Synthesis in Orange CountyQuantum Requirements: The 7-DHC to previtamin D3 conversion requires UVB photons (~295–300 nm) to excite pi electrons, triggering a conrotatory ring-opening per Woodward-Hoffmann rules. This process demands quantum coherence, and it is akin to Shannon’s theorem, where high-fidelity energy transfer is disrupted by environmental “noise.” Coherent water domains, produced by mitochondrial cytochrome c oxidase (CCO), are critical for stabilizing 7-DHC during photolysis. nnEMF may impair CCO activity, reducing hydration and quantum yield. These factors are bigtime affected by the Californication experience.

• Orange County stands out for another pardoxical reason. It has a Mediterranean climate, characterized by warm, dry summers and cool, wet winters, according to the California Native Plant Society. Many of the neighboring counties, are deserts, yet they do not have the disease burden rate that Orange County does. This magnifies the tech abuse risk. Orange County’s coastal location and mountainous terrain create a milder climate and should foster lower autism, Vitamin D risk, yet it does not.Orange County has notably high autism spectrum disorder (ASD) rates, with new prevalence data estimates around 1 in 24 children (updated in 2025 from CDC, 2021), with higher in affluent areas due more tech abuse. More tech = more CCO dehydration and if you add a few jabs to this situation you can see clearly why ASD is spiking there. all jabs are mitochondrial toxins which destroy the CCO and VDR loop buried in the core of my decentralized photobioelectric thesis. Studies now link low maternal or neonatal 25(OH)D to increased ASD risk, particularly in regions with environmental stressors.

  The data backs up my ideas in the thesis.

  A 2019 Stockholm Youth Cohort study found neonatal 25(OH)D <25 nmol/L associated with 1.33 times higher ASD odds (95% CI: 1.02–1.75) compared to ≥50 nmol/L. A 2015 Swedish sibling study reported lower neonatal 25(OH)D in ASD cases (M = 24.0 nM) vs. siblings (M = 31.9 nM, p = 0.013), independent of season.

  In Orange County, low maternal 25(OH)D (due to nnEMF, smog, and lifestyle) impairs humans fetal neurodevelopment because centralized MDs ignore all these factors and never piece together how precise these mechanism are so even small environmental factors lead to outside risks in offspring, increasing ASD risk. nnEMF-induced oxidative stress could exacerbate this by disrupting mitochondrial function and immune regulation.

  Southern California is a super entropy environment for modern human fragility. Trust me, there are other zipcodes who also now fit this geopathic definition. The Role of Entropy is being “a soil” that furnishes future growth. That growth maybe in pathological states. This state maybe necessary to create new antifragile humans. Be sure they won’t resemble modern humans.

  Wisdom should be seen as an anti-entropic force, organizing experience into coherent, actionable insights despite reality’s tendency toward disorder. Yet, paradoxically, wisdom also embraces entropy by accepting impermanence because truths evolve, and what’s wise today may not be tomorrow. This dynamic tension is what makes wisdom creation mimic the scientific method. AI can never replace what the human mind can.

  Orange County’s high nnEMF (cell towers), abundance of screen and tech abuse, smog, ozone, and lifestyle factors (sunscreen, tattoos humans, sunglasses) and the altered Van Allen Belts above all act to disrupt the quantum coherence required for 7-DHC to previtamin D3 conversion, causing low 25(OH)D despite tanning.

  This occurs even as UVA tanning is less sensitive than UVB-driven synthesis. nnEMF impairs mitochondrial CCO and hydration, reducing quantum yield, while Coulomb forces (∇·E = ρ/ε₀) amplify charge disruptions in skin, affecting melanin, melatonin, and VDR function. High autism rates in Orange County covary with low vitamin D and nnEMF-induced oxidative stress, driving immune dysregulation and neurodevelopmental issues. Maternal nnEMF and low 25(OH)D cause epigenetic changes (e.g., IL-4 methylation), increasing eczema and ASD risk in children, more prevalent in Orange County than Florida due to greater environmental “noise”.  Autism and eye diseases are telling us a story that centralized healthcare ignores. It is not just autism speaking loudly.

  According to the CDC, roughly three million people in California have diabetes, that’s nearly 8% of its total population. Another 14.8% have been notified of prediabetes. California’s high prevalence of diabetes is a significant risk factor for diabetic retinopathy. Diabetic retinopathy is another leading cause of blindness in adults, but does anyone believe it can be prevented or slowed down with Casey Means glucose monitors and regular eye exams based on the slide below?

• MORE PROOF HOW BAD CALIFORNIA IS COOKED?California’s regulatory landscape for eye care can be as complex as a multifocal lens to hide this information from the public. Understanding state guidelines for optometrists, ophthalmologists, and emerging eye care technologies like telemedicine and AI-powered diagnostics is crucial for staying ahead of the curve if you are ignorant enought to continue to live there.

Ask yourself why California passed The Telehealth Eye Care Act? Was it for the public benefit, or was it for the government benefit to dumb them down and control them further and make sure corrupt politicians stay in power? The Telehealth Eye Care Act sets the stage for wide scale use of augmented reality (AR) headsets to be used for remote eye examinations, and virtual reality (VR) programs are available for visual rehabilitation and therapy for conditions like amblyopia and age-related macular degeneration. Do you think this is healthy?

• Even corporate California giant APPLE is bailing on this technology, but California politicians are doubling down.The MANDATED use of AR and VR for eye exams reminds me of the MANDATED use of the vaccine schedule.

Artificial Inteeligence algorithms are being trained in Californai to analyze retinal scans and detect eye diseases like glaucoma, diabetic retinopathy, and AMD, with the establishment tellin you about the potential for earlier and more accurate diagnoses. They never tell you about the dystopia risks and why California has so many eye diseases they should not. Regulations haven’t caught up to the dangers of AI, so questions remain about the validation, bias, and data privacy implications of these algorithms. Both the FDA and California regulatory bodies are actively working against the public health on many guidelines for AI-powered medical devices, including those specific to eye care. Be aware of this.

If California was so safe why is this code used so commonly there? ICD-10 code W90.0 validates RF’s health impacts. For me, reducing nnEMF, terrestrial and non terrestrial, optimizing UVB exposure, using AM sunlight to renovate CCO and midday sun to renovate the VDR on the IMM while improving skin light mechanics to create optimal blood level vitamin D3 after the liver and kidney can can convert to 1,25 states. This process requires QUANTUM precision and California creates quantum noise at every level. This is why so many who live here have the sense they must use antioxidants can mitigate eczema and ASD risk. Savages should understand clearly why living in a modern Chernobyl environment is not a wise choice because they understand the implications of Woodward-Hoffmann rules and the narrow band spectrum of UVB imply for humans.

Nature gives too fucks what you think about this situation too. You have to follow her rules, not your wants needs, or desires. If you do not, be ready to pay her toll in disease.

• One of readers posted this in a comment on another blog and I updated it for this one. The top of the HEALTH pyramid is not material. It is the Quantum Field. The Quantum Vacuum. Silence. The Zero Point.The foundation of this pyramid is Action.

  Movement.

  Without action, philosophy is meaningless.

  The layer from top down should be arranged like this:

  •    FIELD

  •    CONSCIOUSNESS

  •    RHYTHM

  •    FRACTAL

  •    SYSTEM SUN

  •     Atomospheric gases

  •    METABOLISM

  •    FOOD

  •    COMMUNITY

  •    BODY

  •    ACTION

  And here’s the important part: When a person falls into total chaos, when nothing works, when there’s no intention, no clarity, no movement

  the problem is not in metabolism or food. The problem is higher up.

  In that moment, one must return to the very top: Silence everything. Be alone.

  Tune into the Field.

  Reconnect with Self and the Field.

  Without that, nothing else can stand.

  The pyramid is a fractal.

  If something doesn’t work on a lower layer, you look at the layer above.

  But if nothing works, you go all the way to the top.

  Silence first.

  Action last.

  In between: everything in rhythm.

  MDs are trained to push actions.

  Most centralized actions are superfluous.

  Remember that.

  Reconnect your sick patient with Nature first.

  Redox before detox.

  Fix CCO and water production

  Restore the solar VDR break to control oxygen endogenously

  Disease will melt away

  SUN = TINA

  You are now a decentralized Savage MD.

  Join me in spreading this missing information.

• CITEShttps://iovs.arvojournals.org/article.aspx?articleid=2788017

WHY ARE EYE DISEASES MORE COMMON TODAY? 

 

The neurosensory retina is a layered tissue that lines the back of the eye, communicating with the brain via the optic nerve. Blood is supplied to the neurosensory retina by retinal blood vessels originating from the central retinal artery. Transport across retinal blood vessels is limited by endothelial tight junctions, which constitute the inner blood–retinal barrier. Allan Frey’s work with DARPA in the 1960s demonstrates that non-thermal electromagnetic fields (nnEMF) open this barrier and make the eye more susceptible to damage when present in our local environment.

We forget that the optic nerve is comprised of ganglion cell axons, the “output neurons” of the retina. The retina is composed of three layers of cell bodies and two plexiform layers of synapses, which are clearly defined on histological sections. The innermost layer is the ganglion cell layer. The inner nuclear layer, featuring the cell bodies of bipolar, amacrine, and horizontal cells, is sandwiched by an internal plexiform layer and ganglion cell layer on one side, and outer plexiform layer and outer nuclear layer on the other. The outer nuclear layer contains the cell bodies of most photoreceptors, including the rods and cones. A third class of photoreceptor, intrinsically photoreceptive ganglion cells (melanopsin blue light detectors), is situated in the ganglion cell layer. All photoreceptors depend on a vitamin A-derived chromophore to detect light and adequate dopamine and melatonin levels to regenerate them in sunlight. The chromophore associated with light-transducing proteins, opsins, undergoes photoisomerization during light transduction. Expended and spent melanopsin or neuropsin chromophores and their associated retinal then enter the visual cycle, a sequence of reactions that facilitates regeneration and re-association with opsins for further transduction.  If regeneration pathways are blocked, the free Vitamin A (retinal)becomes a wrecking ball for the human retina.

THEY ARE BLINDING US WITH BLUE WHILE STOPPING UV-IR REGENERATION Rx.

Carnot’s theorem, formulated by Sadi Carnot in 1824, establishes the maximum efficiency of a heat engine, defined as the ratio of the temperature difference between the heat source (e.g., the engine’s interior) and the cold sink (e.g., the surroundings) to the absolute temperature of the heat source. In biological terms, as you’ve suggested, mitochondria can be viewed as “hydrogen heat engines” that produce ATP (energy) by maintaining a proton gradient across their inner membrane, effectively creating a temperature and electrochemical gradient. Cooling can tan your interior and your exterior and centralized science ignores it.

Application to Mitochondria: In retinal cells, which have high metabolic demands due to constant phototransduction, mitochondria generate heat and energy. According to Carnot’s principle, the efficiency of these mitochondrial “engines” increases with a greater temperature differential between the mitochondrial matrix (heat source) and the cellular environment (cold sink). Cold thermogenesis, which involves exposing the eye to cold, enhances this gradient by lowering the external temperature, forcing mitochondria to work harder and produce more heat, thereby improving efficiency and resilience.

Impact on Eye Health: Under indoor conditions with stable temperatures (e.g., thermostat-controlled environments), this gradient diminishes, leading to mitochondrial atrophy. This reduces the retina’s ability to repair damage from blue light hazard, where reactive oxygen species (ROS) from all-trans-retinal accumulation overwhelm cellular defenses. My chronic point about “chronic widespread mitochondrial colony failure” due to lack of seasonal variation aligns here, because without cold stress, mitochondrial efficiency drops, exacerbating retinal degeneration.

Haplotypes and Susceptibility to Blue Light Hazard

Haplotypes, which are specific combinations of genetic variants inherited together, can influence mitochondrial function, melanin biology, and photoreceptor health, potentially making certain populations more vulnerable to blue light damage.

Mitochondrial Haplogroups: Human mitochondrial DNA (mtDNA) is organized into haplogroups (e.g., H, U, J, T), which vary by geographic origin and affect metabolic efficiency. For instance:

Haplogroup H (common in Europe) is associated with higher basal metabolic rates but may be less adaptable to oxidative stress, potentially increasing susceptibility to blue light-induced ROS in the retina.

• Haplogroup J (prevalent in the Near East and Caucasus) shows enhanced thermogenic capacity and cold tolerance, possibly offering better mitochondrial resilience against blue light damage.

  Studies (e.g., Mitochondrion, 2015) suggest that haplogroups with lower electron transport chain efficiency (e.g., some African haplogroups like L0) might accumulate more ROS under blue light stress, heightening retinal risk. Their skin and RPE also have more melanin, so they need much higher amounts of sunlight to tap into their regeneration programs. This is why African Americans have such high rates of cataracts, diabetes, and retinal diseases when they move to America, where the technocracy destroys their retinal biology.

Melanin and Photoprotection: Haplotypes also influence melanin production via POMC and MC1R gene variants. Lighter-skinned individuals (e.g., those with haplogroup H) have less melanin in the retinal pigment epithelium (RPE), which reduces photoprotection against blue light. Darker-skinned individuals (e.g., haplogroup L) with higher melanin levels are more resistant, as melanin scavenges ROS and conducts bioelectric signals (per Becker’s work). This increases the signal-to-noise ratio.

Heat Production Link: Mitochondria in haplotypes with lower thermogenic capacity (e.g., due to indoor living) struggle to maintain the Carnot-efficient temperature gradient, amplifying damage from blue light. Cold thermogenesis selectively benefits haplotypes with adaptable mitochondria (e.g., J or U), enhancing repair pathways, such as those involving Müller glia, while less adaptable haplotypes (e.g., H) remain vulnerable to a lack of repair. Cellular retinaldehyde-binding protein (CRALBP) supports production of 11-cis-retinaldehyde and its delivery to photoreceptors. It is found in the retinal pigment epithelium (RPE) and Müller glia (MG). Recent data reveal a dominant role for RPE-CRALBP in supporting rod and cone function, highlighting the importance of the RPE for cone regeneration. Unlike rods, cones have a unique requirement for rapid pigment regeneration to maintain their function in bright light and enable quick recovery after exposure to light.

• Carnot efficiency, derived from the Carnot cycle in thermodynamics, describes the maximum efficiency of a heat engine converting thermal energy into work, dependent on the temperature gradient between a hot source and a cold sink. In biological systems, mitochondria maintain a temperature gradient across membranes to optimize ATP production via oxidative phosphorylation (OxPhos). For Müller glia (retinal support cells) and the RPE (the pigmented layer that supports photoreceptors), a Carnot-efficient gradient enhances energy transduction, supports repair and regeneration, and maintains metabolic homeostasis. This gradient is disrupted by indoor living, which flattens thermal differences, atrophying mitochondrial colonies.

  Why Eye Diseases Are More Common Today: Haplotypic and Thermodynamic Perspective

  Blue Light Hazard and Mitochondrial Strain: Chronic ALAN liberates all-trans-retinal, generating ROS that tax mitochondrial defenses. Haplotypes with inefficient heat production (due to indoor warmth) and lower ROS scavenging (e.g., lighter melanin) are more susceptible to heat stress. The lack of UV/IR from sunlight, which boosts POMC and melanin regeneration, compounds this, as does nnEMF opening the blood-retinal barrier (Frey’s DARPA findings).

  Carnot’s Efficiency Loss: Since indoor living flattens the temperature gradient, atrophying mitochondrial colonies in modern humans, haplotypes less adapted to this (e.g., those without cold-tolerance variants) experience greater energy deficits. This will impair retinal repair. Cold thermogenesis restores this gradient, but its efficacy varies by haplotype; individuals with thermogenic haplogroups may thrive, while others may lag behind. Heat production is tied to the Carnot Efficiency and directly alters the UPEs in the system (the thermodynamic limit of energy conversion). This varies by haplogroup and environmental context. This can change the noise in the system.

  Thermogenic Capacity: Haplogroups like J, with cold-tolerance adaptations (e.g., UCP1 upregulation), maintain a temperature gradient via uncoupling, dissipating excess energy as heat. This supports Müller glia repair pathways under blue light stress, reducing ROS damage.

  Indoor Living Impact: Modern indoor environments flatten this gradient, causing mitochondrial colonies to atrophy. Haplogroups without thermogenic variants (e.g., H) struggle to compensate, impairing energy supply to the retina. The Kowald and Kirkwood (2018) paper’s mtDNA deletion model suggests this stress could drive clonal expansion, worsening retinal decline.

• Cold Thermogenesis Benefit: Exposing mitochondria to cold restores the gradient, enhancing repair in adaptable haplogroups (e.g., J, U). Less adaptable haplogroups (e.g., H) show limited response, highlighting haplotype-specific resilience.

  Blue light’s disruption of this gradient, by overexciting ETC and increasing ROS, further taxes non-thermogenic haplotypes, linking indoor living to retinal atrophy.

  Regeneration Blockade: Sunlight’s UV/IR, absent indoors, drives Becker’s photo-bioelectric regeneration via DC currents and POMC. Haplotypes with robust melanin responses (e.g., L) regenerate better, while those with atrophied mitochondria (e.g., H under ALAN) face stalled repair, explaining rising disease prevalence and incidence.

  Haplogroups influence melanin production via proopiomelanocortin (POMC) and melanocortin 1 receptor (MC1R) variants, affecting photoprotection:

  Lighter Skin (e.g., Haplogroup H): Lower melanin in the RPE, driven by MC1R variants favoring lighter skin, reduces ROS scavenging and bioelectric conduction (Becker’s work). This heightens blue light damage, as melanin normally absorbs UV/visible light and emits ultraweak photon emissions (UPE) to signal repair.

  Darker Skin (e.g., Haplogroup L): Higher melanin levels enhance photoprotection, neutralizing ROS and conducting bioelectric signals. However, in low-sunlight environments (e.g., northern U.S.), this advantage wanes, as melanin synthesis requires exposure to UV radiation. Migration disrupts this balance, explaining higher disease prevalence in African Americans as latitude rises despite innate resilience.

  The decentralized thesis aligns here: melanin acts as an electromagnetic buffer, and its decline in mismatched environments (e.g., indoor technocracy) disrupts cellular coherence, increasing anterior chamber and retinal vulnerability.

• Why Eye Diseases Are More Common Today: The Technocratic Perspective

The increase in eye diseases, such as age-related macular degeneration (AMD), cataracts, and diabetic retinopathy, correlates with modern environmental and lifestyle shifts. Here’s a breakdown based on my research and related science:

• Shift to Artificial Light and Indoor Living:

• Most people now spend over 90% of their time indoors, exposed to artificial light (e.g., LEDs, screens) rather than sunlight. As our spectroscopes show, this light is dim and unbalanced compared to the sun’s full spectrum, which includes UV and infrared (IR) components essential for retinal health.

  Artificial light at night (ALAN), rich in blue light (400-500 nm), disrupts the visual cycle. The chromophore all-trans-retinal, liberated from opsins during photoisomerization, accumulates when the retinal pigment epithelium (RPE) is overwhelmed, leading to oxidative stress and photoreceptor damage. This aligns with my “wrecking ball” metaphor for liberated vitamin A from the retina.

  Blue light’s high energy penetrates the retina, exciting ETC complexes and generating ROS. Haplogroup-specific responses amplify disease risk:

  Haplogroup H: Lower oxidative stress resilience and reduced melanin lead to increased ROS accumulation, heightening the risk of cataracts and age-related macular degeneration (AMD), especially indoors.

  Haplogroup L0: Higher baseline ROS from ETC inefficiency, compounded by low sunlight in America, drives cataracts, diabetes (via mitochondrial dysfunction in pancreatic cells), and retinal diseases. The technocracy’s blue light dominance disrupts L0’s sunlight-dependent regeneration, explaining elevated rates in African Americans.

  Haplogroup J: Thermogenic adaptability mitigates ROS, offering protection, but indoor living still poses a risk if sunlight exposure is insufficient.

  The decentralized thesis suggests that blue light’s electromagnetic interference disrupts retinal coherence, a vulnerability that is magnified by haplotype-specific traits. Michael Rosbash’s 2017 Nobel Prize-winning insight, that the lack of sunlight during the day is worse than the artificial light at night, clearly supports my damaged retinal view, but he overlooks Becker’s work on regeneration. For me, the paper is important, but it misses a lot of quantum biology. Sunlight’s UV and IR are absent indoors, halting regeneration pathways that rely on POMC, melanin, and bioelectric signals (as per Becker’s work), thereby exacerbating damage.

• Evolutionary Context: Haplogroups evolved with environmental niches, H for Europe’s moderate climate, J for cold regions, L0 for high-sun tropics. Migration to mismatched environments (e.g., African Americans in the U.S.) unbalances these adaptations, increasing disease susceptibility as sunlight and melanin levels diverge from optimal.

  Practical Solutions

  Sunlight Exposure: 30–60 minutes of morning UV/infrared light boosts melanin synthesis and mitochondrial function, reducing ROS in all haplogroups. L0 benefits most with higher doses.

  Blue Light Mitigation: Blue-blocking glasses or reduced screen time minimize ETC stress, especially for H and L0.

  Cold Thermogenesis: Enhances mitochondrial gradient for J and U, supporting retinal repair, though less effective for H.

  Melanin Support: Diets rich in tyrosine and copper (e.g., nuts, seafood) enhance POMC/MC1R activity, boosting photoprotection. When one integrates how melanin, iron, and blue light fit into this decentralized thesis, you have to leverage insights from this paper in the Biomedical Journal of Scientific & Technical Research

  The paper (https://biomedres.us/pdfs/BJSTR.MS.ID.008142.pdf) explores their roles in evolutionary adaptation, electromagnetic coherence, and disease. The paper reframes melanin’s evolutionary role from photoprotection to a metal-chelating agent, particularly for iron, facilitating the excretion of heavy metals via epidermal turnover in humans. This aligns with my decentralized thesis by positioning melanin as a dynamic electromagnetic black box regulator in eukaryotes.

  Melanin was an Evolutionary Driver: Dietary shifts in early humans introduced excess iron, driving melanin synthesis in melanocytes to bind and excrete it through desquamation. This explains racial pigmentation differences, with darker skin (phototypes IV-VI) evolving in high-iron environments, which supports the view that melanin acts as a calibrator of environmental inputs.

  Iron Homeostasis: Melanin-bound iron loss through skin turnover depletes systemic iron, increasing the risk of anemia in heavily melanated individuals, as noted in the paper. This challenges the centralized “sunscreen” model, framing melanin as a redox and electromagnetic stabilizer in humans

  Quantum Interface: Melanin’s lattice absorbs all light frequencies and chelates iron without reflection, converting electromagnetic energy into bioelectric signals, consistent with my black body analogy.

  The thesis highlights blue light’s role in shifting iron to Fe²⁺, generating nitric oxide (NO) and localized hypoxia, while the paper adds melanin’s amplifying quantum effect:

  Photoexcitation: Blue light (380–450 nm) excites melanin, triggering a one-electron transfer that produces ROS (superoxide, hydrogen peroxide). Iron-saturated eumelanin enhances this, broadening near-infrared absorption and intensifying oxidative stress, disrupting cellular redox fields. This alters UPE signaling.

  Retinal Impact: In the RPE, melanin binds iron to mitigate ROS, but blue light’s interaction with this complex increases UPE and oxidative damage. This aligns with my mitoception thesis, where UPE signals mitochondrial stress (e.g., via GDF15), contributing to eye diseases.

  ECS Disruption: Blue light’s oxidative assault stresses the ECS (Di Meo et al., 2025), impairing electromagnetic stability and amplifying mitochondrial dysfunction, a key theme in this framework. This would also alter UPEs in the ECS system.

  Blood-Retinal Barrier Disruption by nnEMF:

  Allan Frey’s 1960s DARPA research demonstrated that non-native electromagnetic fields (nnEMF) from technologies (e.g., microwaves, Wi-Fi) can open the blood-retinal barrier by affecting endothelial tight junctions. This increased permeability allows toxins and inflammatory molecules to reach the retina, heightening susceptibility to damage from ALAN and free retinal.

  This mechanism is less emphasized in centralized ophthalmology, which focuses on genetic or aging factors; however, it supports my claim of environmental exacerbation due to changes in the ionosphere’s conductance, which are radically inducing eye pathology. The establishment’s centralized narratives clearly downplay nnEMF’s role due to industry interests, a point worth questioning because their incentives are driving chronic eye disease epidemics.

• Evolutionary Context: Haplogroups evolved with environmental niches, H for Europe’s moderate climate, J for cold regions, L0 for high-sun tropics. Migration to mismatched environments (e.g., African Americans in the U.S.) unbalances these adaptations, increasing disease susceptibility as sunlight and melanin levels diverge from optimal.

  Practical Solutions

  Sunlight Exposure: 30–60 minutes of morning UV/infrared light boosts melanin synthesis and mitochondrial function, reducing ROS in all haplogroups. L0 benefits most with higher doses.

  Blue Light Mitigation: Blue-blocking glasses or reduced screen time minimize ETC stress, especially for H and L0.

  Cold Thermogenesis: Enhances mitochondrial gradient for J and U, supporting retinal repair, though less effective for H.

  Melanin Support: Diets rich in tyrosine and copper (e.g., nuts, seafood) enhance POMC/MC1R activity, boosting photoprotection. When one integrates how melanin, iron, and blue light fit into this decentralized thesis, you have to leverage insights from this paper in the Biomedical Journal of Scientific & Technical Research

  The paper (https://biomedres.us/pdfs/BJSTR.MS.ID.008142.pdf) explores their roles in evolutionary adaptation, electromagnetic coherence, and disease. The paper reframes melanin’s evolutionary role from photoprotection to a metal-chelating agent, particularly for iron, facilitating the excretion of heavy metals via epidermal turnover in humans. This aligns with my decentralized thesis by positioning melanin as a dynamic electromagnetic black box regulator in eukaryotes.

  Melanin was an Evolutionary Driver: Dietary shifts in early humans introduced excess iron, driving melanin synthesis in melanocytes to bind and excrete it through desquamation. This explains racial pigmentation differences, with darker skin (phototypes IV-VI) evolving in high-iron environments, which supports the view that melanin acts as a calibrator of environmental inputs.

  Iron Homeostasis: Melanin-bound iron loss through skin turnover depletes systemic iron, increasing the risk of anemia in heavily melanated individuals, as noted in the paper. This challenges the centralized “sunscreen” model, framing melanin as a redox and electromagnetic stabilizer in humans

  Quantum Interface: Melanin’s lattice absorbs all light frequencies and chelates iron without reflection, converting electromagnetic energy into bioelectric signals, consistent with my black body analogy.

  The thesis highlights blue light’s role in shifting iron to Fe²⁺, generating nitric oxide (NO) and localized hypoxia, while the paper adds melanin’s amplifying quantum effect:

  Photoexcitation: Blue light (380–450 nm) excites melanin, triggering a one-electron transfer that produces ROS (superoxide, hydrogen peroxide). Iron-saturated eumelanin enhances this, broadening near-infrared absorption and intensifying oxidative stress, disrupting cellular redox fields. This alters UPE signaling.

  Retinal Impact: In the RPE, melanin binds iron to mitigate ROS, but blue light’s interaction with this complex increases UPE and oxidative damage. This aligns with my mitoception thesis, where UPE signals mitochondrial stress (e.g., via GDF15), contributing to eye diseases.

  ECS Disruption: Blue light’s oxidative assault stresses the ECS (Di Meo et al., 2025), impairing electromagnetic stability and amplifying mitochondrial dysfunction, a key theme in this framework. This would also alter UPEs in the ECS system.

  Blood-Retinal Barrier Disruption by nnEMF:

  Allan Frey’s 1960s DARPA research demonstrated that non-native electromagnetic fields (nnEMF) from technologies (e.g., microwaves, Wi-Fi) can open the blood-retinal barrier by affecting endothelial tight junctions. This increased permeability allows toxins and inflammatory molecules to reach the retina, heightening susceptibility to damage from ALAN and free retinal.

  This mechanism is less emphasized in centralized ophthalmology, which focuses on genetic or aging factors; however, it supports my claim of environmental exacerbation due to changes in the ionosphere’s conductance, which are radically inducing eye pathology. The establishment’s centralized narratives clearly downplay nnEMF’s role due to industry interests, a point worth questioning because their incentives are driving chronic eye disease epidemics.

• Integration of these ideas into the Decentralized Thesis

  Light as Primacy: Melanin’s light absorption and iron chelation convert environmental photons into bioelectric currents, regulating mitochondrial coherence. Blue light, however, disrupts this, shifting iron oxidation states while generating ROS, which my thesis identifies as a root cause of systemic imbalance.

  Electromagnetic Coherence: Melanin and iron form a quantum interface, modulating EMF interactions. Blue light’s interference with this system, via ROS and UPE, destabilizes cellular fields, necessitating ECS-mediated repair.

  Evolutionary Context: Following the Post-GOE period, melanin’s iron-binding capacity evolved to manage oxidative stress resulting from increased oxygen levels, integrating with mitoception and the leptin-melanocortin pathway.

  Regeneration Blockade:

  The visual cycle, which regenerates 11-cis-retinal from all-trans-retinal, depends on sunlight’s UV and IR to stimulate POMC and melanin production. POMC-derived peptides (e.g., α-MSH) enhance melanin’s photoprotective and regenerative roles, while Becker’s bioelectricity research suggests UV/IR-induced DC currents are needed to activate retinal repair (e.g., Müller glia = eye stem cells need NO). Glaucoma is also related to these effects of a lack of UV-IR on eye pressure gradients.

• Indoor living blocks these pathways, as you argue, preventing regeneration. The atrophy of mitochondria, our “hydrogen heat engines”, due to lack of seasonal temperature variation (e.g., cold thermogenesis) further impairs energy for repair, aligning with Carnot’s efficiency principle: greater temperature gradients enhance engine performance.

  Tech Addiction and Neurochemical Disruption

  My “zombie” analogy reflects how screen addiction, driven by blue light’s temporary dopamine boost, disrupts melatonin and GABA signaling (slide below). This circadian misalignment, compounded by indoor confinement, reduces retinal health and systemic resilience.

  Casinos and tech companies exploit this, designing blue-rich environments to sustain engagement, given dopamine’s role in the brain as a reward.

• Mitochondrial Failure and Thermodynamic Loss

  Mitochondria in retinal cells, with high oxygen demand, are vulnerable to blue light-induced ROS, as noted in recent studies on AMD. My Carnot efficiency argument suggests that hotter engines (mitochondria) run more efficiently, which implies that cold thermogenesis boosts mitochondrial function by increasing the temperature gradient, thereby countering atrophy from thermostat-controlled indoor life.

  This thermodynamic perspective is unconventional in medicine but aligns with Becker’s bioelectric findings and my call to reconnect with nature’s frequencies.

The Centralized narrative often attributes rising eye disease prevalence to aging, genetics, and lifestyle factors like diabetes, overlooking environmental drivers like ALAN, nnEMF, and sunlight deficiency. The destruction of heme, along with all our other photoreceptors, explains fully why modern chronic disease epidemics are present.

The synergy of melanin, iron, and blue light defies reductive biochemical models, embodying a Camus-esque revolt. This thesis empowers individuals to reclaim coherence by aligning with natural light and EMF, countering the technocracy’s disruptive influence. Melanin’s iron-chelating role is amplified by the oxidative effects of blue light, allowing for a perfect integration into this decentralized thesis as a quantum interface regulating electromagnetic coherence. Evolving post-GOE, it supports mitoception via UPE and GDF15, with blue light disrupting this balance in diseases such as AMD and mental health disorders. Restoring natural light and minimizing disruptors restores this system, aligning with my vision of biological agency.

HOW DID THIS HAPPEN?

F1-ATPase explains how this all happened. Here are the basics explaining how uncoupled haplotypes evolved due to variable EMFs as latitude and longitude changed: F1-ATPase is a rotary molecular motor within mitochondria that synthesizes ATP by harnessing the proton motive force across the mitochondrial membrane. Protons flow through the enzyme’s F0 subunit, driving the F1 subunit’s rotation (the “spin rate”) to catalyze ATP production from ADP and inorganic phosphate.

The cited paper in Figure 1 above models F1-ATPase’s dynamics, showing it’s highly reversible: it can synthesize ATP when rotating forward (hydrolysis-driven) or hydrolyze ATP when forced backward. However, under high external torque, caused by stressors such as oxidative damage due to excessive oxygen, insufficient sunlight, or a lack of melanin resulting from environmental changes, a metabolic imbalance occurs. This enzyme undergoes “mechanical slip,” where rotation occurs without effective ATP production, resulting in the dissipation of energy as heat. This is precisely how uncoupled haplotypes were innovated as humans left their tropical habitats to conquer colder climates.

The “mechanical slip” is a state in which the enzyme rotates without effectively producing ATP, instead dissipating energy as heat. This inefficiency, noted in the paper as reducing free energy transduction by 40–80% below optimal, reflects a breakdown in chemomechanical coupling under nnEMF light stress. Light stress leads to an increase in deuterium concentration, causing a mechanical shift in the ATPase. LIGHT > FOOD

Environmental Stressors and Torque on F1-ATPase

As humans migrated out of the tropics (~200,000 years ago), they encountered varying EMFs, latitudes, and longitudes, altering sunlight exposure, oxygen levels, and melanin production. These changes acted as external torques on F1-ATPase:

Sunlight Reduction: Tropical regions receive abundant UV and infrared light, which optimizes mitochondrial function through photobiomodulation (e.g., enhancing cytochrome c oxidase activity). At higher latitudes, reduced sunlight, especially UV, disrupted this, lowering ATP efficiency and increasing ROS, a stressor that torques F1-ATPase.

Oxygen Variability: Colder climates often have higher oxygen partial pressures, which enhances ROS production during OxPhos. Excessive oxygen, as a stressor, should force F1-ATPase into reverse or slip modes, dissipating energy.

Melanin Decline: In the tropics, high melanin levels protected against UV and stabilized redox balance, supporting F1-ATPase efficiency. As humans moved to northern latitudes with less UV, melanin production decreased (e.g., lighter skin evolved), reducing antioxidant capacity and exacerbating oxidative stress, further torquing the enzyme to slip more.

Sleep Mechanics and eye diseases: GDF15 signals mitochondrial stress (mitoception), which causes a rise with electron surplus, prompting sleep as a mitoceptive response. Melanin’s UPE release, shared with GDF15, reinforces this photonic feedback loop in humans. My thesis posits that cellular health depends on “field stability” in tissues. An electron surplus disrupts this, and sleep is driven by UPEs and melanin’s photonic feedback, restoring it. Melanin’s UPE emission, tied to ROS and iron, signals this surplus, linking this signal to mitoception. The GOE enabled OxPhos and UPEs to manifest, thereby driving the electromagnetic origins of sleep. Leptin’s 220 nm absorption, tied to endogenous light transformation, evolved to regulate this surplus, integrating with the leptin-melanocortin pathway. Red light’s role in mito-dR supports my light-centric view, countering the disruptive effects of blue light (e.g., ROS from melanin-iron complexes). This aligns with the retina’s glycolysis adaptation under photonic stress. (seen below)

This environmental shift created a metabolic imbalance, where the spin rate of F1-ATPase struggled to match energy demands, leading to mechanical slip and heat dissipation rather than ATP synthesis.

The innovation of uncoupled haplotypes involved mtDNA mutations affecting F1-ATPase or UCP expression:

Mutation Selection: Random mtDNA deletions or point mutations, as modeled in the cited paper, should disrupt F1-ATPase’s coupling efficiency, favoring slip under torque. Over generations, these variants were selected in cold climates where heat generation was prioritized over ATP maximization.

UCP Upregulation: UCPs (e.g., UCP1 in brown fat) evolved to uncouple OxPhos, dissipating PMF as heat. The torque-induced slip phenotype prefigured this out, with natural selection amplifying UCP expression in uncoupled haplotypes. Natural selection rendered melatonin’s function less important for overall energy balance and expanded the leptin-melanocortin pathway because it was more accurate. Today, melatonin production in the mtDNA is the only remnant of its GOE importance.

Geographic Divergence: Haplogroups (e.g., H in Europe, M in Asia) reflect these adaptations, with northern populations exhibiting higher uncoupling efficiency (e.g., via UCP1 polymorphisms) to counteract low sunlight and cold temperatures. The paradox of haplotype vulnerability, a strength in one environment that becomes a weakness in another, mirrors a dead man walking who seeks Bitcoin. My decentralized approach rebels against the technocracy’s indoor, blue-light-dominated paradigm, advocating light and coherence to reclaim retinal health. This aligns with Sartre’s concept of freedom: individuals can choose to align their environment to mitigate haplotype-specific risks.

SUMMARY

Mitochondrial haplogroups (H, J, L0) influence metabolic efficiency, melanin production, and photoreceptor health, modulating blue light vulnerability. H and L0 face higher risks due to oxidative stress and melanin mismatch in indoor settings, while J’s thermogenic resilience offers protection.

The technocracy’s disruption of sunlight and temperature gradients exacerbates this, driving diseases like cataracts and AMD. Restoring natural light and thermogenesis can mitigate these effects, empowering haplotype-specific resilience.

I challenge this narrative by linking these to industrial and technological agendas (e.g., DARPA’s nnEMF research, tech addiction), suggesting a deliberate blinding and regeneration suppression. While evidence supports ALAN’s role in AMD and nnEMF’s barrier effects, the regeneration claims (e.g., UV/IR, Becker’s work) are less mainstream, though emerging research on melanin’s protective role and optogenetic repair lends credence to explaining the modern disease epidemics linked to the eye.

Eye diseases are more common today due to chronic exposure to ALAN and nnEMF, which damage the retina and open the blood-retinal barrier, combined with the loss of sunlight’s UV and IR, which halt regeneration via POMC, melanin, and bioelectric pathways. Mitochondrial atrophy from indoor life further compounds this, as per Carnot’s efficiency principle. Reconnecting with nature, through sunlight and cold thermogenesis, will restore these processes, countering the degenerative effects of artificial frequencies and tech addiction.

Sleep in humans is triggered by an electron surplus, creating charge density, and acts as a cellular sweep to restore electromagnetic coherence, which is signaled by adenosine and modulated by UCP4, red light, and sesB. This aligns with my decentralized thesis, connecting to melanin’s UPE, mitoception’s GDF15, and the primacy of light in most diseases.

CITES

https://www.frontiersin.org/journals/aging-neuroscience/articles/10.3389/fnagi.2024.1509434/full

https://www.linkedin.com/pulse/blinding-us-while-stopping-our-regeneration-jack-kruse-6jsze

https://pmc.ncbi.nlm.nih.gov/articles/PMC9339908/

The Hidden Risks of LASIK Surgery: How Light, the Opsin System, and Central Retinal Pathways Shape Your Mind, Mood, and Destiny

LASIK SURGERY BLOWS OUT THE INSIDER WORLD OF YOUR MIND.

I strongly recommend you watch the first ten seconds of the video above………..then proceed.

Introduction: A Decentralized Thesis on Light-Driven Biology
Today, nearly everything such as the excimer lasers used in LASIK surgery is manufactured in China. But courage? That’s made in your mitochondrial DNA (mtDNA), a biological forge that transforms light into the fuel of life. My decentralized medical thesis, rooted in light-driven biology, quantum coherence, and circadian synchronization, reveals how sunlight shapes our blood, mitochondrial DNA (mtDNA), and frontal lobes to foster courage, a trait closely tied to executive functions such as decision-making and fear regulation. But what happens when a surgeon’s laser, an artificial sun, disrupts this delicate dance of light in your eye? The consequences ripple far beyond vision correction, impacting your mood, pain, and even the risk of suicide, as the tragic outcomes of LASIK patients reveal. Let’s explore why.

The Quantum Dance of Light in Your Eye: More Than a Camera
The cornea isn’t just a lens; it’s a quantum gateway where light shapes your perception of the outside world by altering the biology inside your eye. Neuropsin, a UV-A light detector, is located in the cornea, while melanopsin, a key regulator of the circadian rhythm, lies just behind it in the retina. These opsins, along with the central retinal pathways, form a semiconducting circuit that processes light to regulate your body’s master clock, the suprachiasmatic nucleus (SCN). This clock doesn’t just tell time; it orchestrates the melatonin, dopamine, and proopiomelanocortin (POMC) systems, which break down into hormones such as β-endorphin, ACTH, and α-MSH. These chemicals govern mood, pain, energy, and even your drive to thrive.

Sunlight, with its full spectrum of UV-A, IR-A, and NIR wavelengths, is Nature’s recipe for this system. It regenerates photoreceptors, stabilizes mitochondrial function, and keeps your circadian rhythm in sync. However, an excimer laser, used in LASIK to reshape the cornea, emits monochromatic ultraviolet light (typically 193 nm). It’s not the sun. It lacks the broad spectrum needed to maintain the quantum coherence of your eye’s signaling pathways. Worse, surgeons often don’t even know neuropsin and melanopsin are there, right in the path of their laser.

The Fallout of LASIK: Disrupting the Opsin and POMC Systems
When a laser cuts into the cornea, it doesn’t just alter refraction; it disrupts the light alphabet your eye uses to communicate with your brain. Here’s how:

Opsin System Damage: Neuropsin and melanopsin are photoreceptors sensitive to UV-A and blue light (around 380-484 nm). LASIK’s laser can damage these opsins, impairing their ability to detect natural light cues. This disrupts the SCN’s rhythm, reducing melatonin production, a hormone rebuilt by daytime UV-A light. Low melatonin levels result in poor sleep, increased oxidative stress, and a cascade of hormonal imbalances. Dopamine, which relies on light-driven signals, also drops, leading to apathy, depression, and a dulled sense of motivation.

POMC System Dysregulation: POMC, a 241-amino-acid precursor, is cleaved into hormones such as β-endorphin (which mediates pain relief and mood regulation), α-MSH (involved in melanin production and neuroprotection), and ACTH (involved in the stress response). These hormones are light-dependent and are synthesized in the retina and pituitary via the central retinal pathways. LASIK’s disruption of melanopsin signaling reduces POMC cleavage, lowering β-endorphin levels (linked to pain and depression) and α-MSH (which protects against ischemia and reperfusion injury). As my slide show, this can lead to “CLIP = etiology of diabetes,” where POMC dysregulation contributes to metabolic chaos.

Central Retinal Pathways and Mitochondrial Chaos: The central retinal pathways, a semiconducting circuit, rely on mitochondrial health to process light signals. Mitochondria in retinal pigment epithelial cells (RPE) utilize UV-A and IR-A to regenerate photoreceptors and maintain DHA (docosahexaenoic acid) levels, which are crucial for retinal health. LASIK’s artificial light introduces “noise” (per Shannon’s information theory), spiking reactive oxygen species (ROS), and damaging mtDNA. This disrupts ATP production, impairing the retina’s ability to signal the brain, which can manifest as nighttime halos, accommodation defects, and even retinal degenerative diseases.

The Tragic Outcomes: Mood, Depression, Pain, and Suicide
The Daily Mail article from May 2025 highlights an alarming trend: LASIK patients, including a police officer, have taken their own lives post-surgery. Why? The answer lies in the interconnected photonic systems LASIK disrupts in the central retinal pathways and the brain:

Mood and Depression: Reduced melatonin and dopamine from melanopsin dysfunction lead to poor sleep and low motivation. Dopamine, tied to reward and executive function, is critical for courage, a frontal lobe specialty. When dopamine levels decline, apathy sets in, widening the Dunning-Kruger effect: patients become less aware of their own decline, accepting superficial trends without questioning them.

Pain: β-endorphin, a POMC derivative, is a natural analgesic. Its reduction post-LASIK increases pain sensitivity, compounding emotional distress. Chronic pain, paired with poor sleep, is a known risk factor for depression and suicidal ideation.

Suicide Risk: The retina and pituitary, both downstream of the SCN, regulate hormones like ACTH and α-MSH. When LASIK disrupts this light-driven axis, the pituitary struggles, leading to fatigue, hormonal imbalances, and a sense of disconnection, for some, this culminates in a profound loss of hope, tragically evident in the suicides reported.

Man-Made Light vs. The Sun: A Losing Battle

An excimer laser in the hands of an eye doctor is like giving a serial killer a universal hotel room key. It’s a tool of precision, but it’s blind to the quantum signaling pathways it disrupts. The sun, with its full spectrum, regenerates photoreceptors and supports mitochondrial health, as Kruse’s slides emphasize: “UV-A and IR-A regenerate all photoreceptors.” AM light, rich in UV-A and IR-A, rebuilds melatonin and dopamine, tuning your SCN to Nature’s rhythm. LASIK’s laser, however, is a monochromatic 193 nm beam, far from the sun’s 200-800 nm biophotonic symphony. It destroys photoreceptors by freeing vitamin A, contributing to conditions like AMD (age-related macular degeneration), which is now “explosive.” Getting Lasik surgery is akin to speeding up the death of chronic diseases in a few months from blue light because the acute intensity of the laser mimics decades of light abuse.

The Courage to Choose Nature Over Vanity
Courage, rooted in mtDNA’s energy transformation, is the fuel that enables us to thrive. LASIK, often driven by vanity, robs you of this fuel by altering the light your eye clock receives. It’s a gamble with your mind, not just your vision. The centralized medical system, focused on the cornea’s “camera” function, ignores the eye’s role as a circadian metronome. This superficial approach, planning LASIK at its most “commercial” level, creates an alien sun that corrupts your natural thoughts, as I wrote in 2017: “Light, alien man-made light, let in by a laser beam is a modern theme leading to man’s inability to communicate with man.”

A Call to Action: Let the Sun Rewire You
You’re not broken; you’re biologically starved for sunlight. The cornea’s shape is molded by the light you feed it, a life in the shadows of artificial blue light (from screens, LEDs) leads to misshapen corneas and blurred vision. LASIK might seem like a quick fix, but it’s a Faustian bargain. Instead, embrace Nature’s decentralized thesis: step outside, let UV-A and IR-A regenerate your photoreceptors, and retune your photoreceptors in front of your SCN that project to your frontal lobes.

Avoid the massive photoelectric scar that a laser in your eye can leave in your frontal lobes, as the picture below shows. Sunrise, with its red light, meets the water in your eyes to alter magnetic free radicals in mitochondria, resetting your internal clock. Small, daily actions such as 10 minutes of morning sunlight improve you by 1% a day, as I wrote earlier.

LASIK LIGHT IS NOT EQUIVALENT TO SUNLIGHT AND YOUR EYE IS BUILT FOR SUNLIGHT

The human eye was designed by Mother Nature to capture the quality and character of sunlight at the microscopic level. Why? The sun’s power is distributed over a vast area on the macroscopic level. This is precisely the opposite of what the refractive surgeon’s laser light is. He is using light that your mtDNA makes at the nanoscopic level, and this can create massive electrical scars distal to its application.

The line width of the surgeon’s laser light is very narrow compared to the sun. Here is what I mean by that. Imagine you have a device that measures the wavelength of incoming light. Then if you were to measure the wavelength of the sun the an actual device would say that it is not a single number but the wavelength is in a range between X and Y. While this would also be true if you measure the wavelength of a laser, the difference between Y and X would be very very small compared to that of the sun.

Hence, narrow line width.

The surgeon’s laser uses light that is coherent, meaning it has = specific frequency and power.

The light coming out a laser will be of same wavelength and of same phase.

Both of these are essential for most quantum experiments and precision cutting in eye surgery. But that precision comes with significant time risk because centralized medicine has no earthly idea about the eye, SCN, brain, and photo-bioelectric blueprint. It is not taught in medical school or residency. Their laser light is highly powered and significantly more focused, capable of causing electrical damage. Most eye lasers use a lens and focus the power to a small point. This allows for greater control over the use of power. This clinical situation should remind you of the warnings I gave Scott Zimmerman and Sabine Hazan in the two podcasts I did with Dr. Alexis Cowan. I was trying to draw their attention to Harold Morowitz’s principle, the flow of energy through a system acts to organize that system via AMO principles in cells. This was time-stamped into many of Mae Wan Ho’s papers, but I doubt any eye surgeon has read any of them. His ideas help forge my decentralized framework in exploring how light, as the force carrier of the electromagnetic force, drives biological organization at the nanoscale. It also explains how laser light applied to our surfaces mimics a nuclear blast distally in the brain.

IMPLICATIONS OF MISSING THE BASIC PHYSICS OF LIGHT AT THE EYE DOCTOR?

RAPID DEATH BECOMES A REAL POSSIBILITY

The application of the laser in the anterior chamber causes a massive fireball on the cornea, and then the shockwave hits the rest of the eye. As the shock continues along the central retinal pathways, the heat blast hits the brain’s circuitry and causes massive complete dehydration and destruction of the IMM of trillions of mitochondria. It mimics what happens to LA with a surface-level nuclear explosion.

HYPERBOLE, OR DO I UNDERSTAND PHYSICS OF LIGHT BETTER THAN THEY DO?

Centralized Biology Centralized biology’s focus is on the procedural ability to reshape the cornea. They fail to realize the eye is designed as a light antenna for MACROSCOPIC defocused light with a visible spectrum. It is not intended for laser light that mtDNA and RBCs can make. Their macroscopic focus overlooks the nanoscale potency of laser light to transform the tissues distal to the laser rapidly. This rapid death effect is driven by the electromagnetic force’s concentration at small scales, which fully aligns with Morowitz’s principle of energy-driven organization. Macroscopic blue light and non-native electromagnetic fields (nnEMF) from technology disrupt these processes on a more chronic basis by oxidizing heme proteins (e.g., Fe²⁺ to Fe³⁺), destroying Fe-S couples in the IMM and its ability to make DDW water, while generating ROS, and altering proton tunneling in Z-Z pathways, injuring distal tissues contributing to chronic diseases (e.g., neurodegenerative disorders, diabetes).

Getting LASIK surgery is speeding up the process in 13 minutes, and this is why you can die in days, weeks, and months. It is akin to plugging in your 1920 wired home into one of China’s new nuclear power plants and thinking you’re safe. It is just like a nuclear blast to the brain.

The laws of physics determine this effect, not Uncle Jack’s opinion.

The inverse square law states that the intensity of light decreases with the square of the distance from the source: where I is intensity and r is distance.

An eye laser and the sun are fundamentally different, like an arc welder using his torch in seawater versus forging steel in a controlled furnace. In arc welding, the welder meticulously controls voltage (typically 20–40 V), amperage (50–300 A), and shielding gas (e.g., argon) to maintain a stable arc and produce a clean weld. Any deviation, wrong settings, a contaminated electrode, or moisture in the environment disrupts the arc, leading to defects like oxidation, porosity, or cracks that weaken the weld.

The welder relies on real-time feedback, such as the arc’s light and sound, to adjust parameters and ensure precision. Similarly, the sun provides a broad-spectrum, biologically tuned light (0.89–3.94 eV) that gently shapes the eye’s quantum signaling pathways, supporting opsins like neuropsin and melanopsin with coherent, low-energy photons. In contrast, a LASIK excimer laser (193 nm, 6.41 eV) is akin to arc welding in seawater, an unstable and chaotic environment.

The inverse square law (above) shows that light intensity increases dramatically as distance as (r )shrinks. At nanoscale (10⁻⁹ m), atto (10⁻¹⁸ m), and femto (10⁻¹⁵ s) scales, light’s near-field effects dominate, and its interaction with matter becomes more particle-like (photons). This amplifies the energy density. LASIK lasers create light with 6.41 eV photon energy. The chart below show you how powerful that number really is as scale shrinks.

The laser delivers high-energy photons at the nanoscale, creating massive energy fluctuations in the cornea and beyond, with no biological feedback to guide its impact. This disrupts the eye’s delicate photoreceptors and central retinal pathways, spiking reactive oxygen species (ROS) and damaging mitochondrial DNA (mtDNA), much like how seawater would corrode a weld. The downstream effects, altered dopamine, melatonin, and POMC signaling, can lead to mood disorders, chronic pain, and even suicide, as seen in LASIK patients. The sun heals with precision; a laser in the eye burns with reckless abandon.

The Nature Communications study (2015) showed us that cristae alignment is tightly light-regulated in its relation to OPA1. This photonic linkage determines mitochondrial respiratory efficiency in the eye, and it carries implications for health and disease. When you add laser light to this system, you demolish cristae alignment in nanoseconds.

THE EVOLUTIONARY LESSON I HAVE TAUGHT YOU: REMINDER

Picture your mitochondria as ancient forges, stoked by the fiery dawn of the Great Oxygenation Event (GOE) 2.4 billion years ago, when oxygen and UV light quantized metabolism into a celestial rhythm. The TCA and urea cycles are like a cosmic metronome, keeping time across eons. At the heart of this forge stand two photo-bioelectric titans: the Vitamin D receptor (VDR) and cytochrome c oxidase (CCO). Sunlight, a celestial painter, deftly brushes UV, IRA, and NIR across your inner mitochondrial membrane, activating VDR through sulfated Vitamin D3, a molecule your skin crafts in UV’s radiant embrace. VDR, a vigilant sentinel, restrains mitochondrial respiration, thereby slashing reactive oxygen species (ROS) and reactive nitrogen species (RNS), as studies reveal that silencing VDR unleashes a ROS tempest. CCO, our light-hungry alchemist, absorbs these wavelengths, fine-tuning electron transport to keep mitochondrial DNA (mtDNA) as stable as a galactic orbit. Together, they echo the GOE’s legacy, utilizing the sun’s visible light spectrum to mitigate environmental chaos and shield cells from entropy’s relentless tide, a decentralized masterpiece that centralized biochemistry cannot comprehend.

AM sunlight acts as a photonic trigger, modulating the light cone’s optical density of the chambers of the eye via TCA-driven water production and UPE coherence. This added a diurnal photonic rhythm to life in the GOE and is critical in my thesis. Enhancing AM light exposure (e.g., UV-mimicking therapies) could amplify TCA/urea benefits, complementing DDW and PBM to extend life and improve sleep. Over 3.8 billion years, sunrise’s role in TCA/urea activation might have evolved with sleep to optimize energy and repair, with thanatotranscriptomic genes adapting to this cycle. Lasik destroys that rapidly and this activates thanatotranscriptomic genes aberrently. Normally these genes are only turned on by environmental chaos. LASIK defines light chaos for the eye.

How does this system work and fit together? AM sunrise shifts daytime metabolism from glucose (RQ ~1) to TCA/urea cycle dominance. This normally extends life by reducing oxidative stress and improving sleep by optimizing mitochondrial repair. This integrates with melatonin’s CI inhibition, DEC2 regulation in cells. This is the normal stoichiometry life used in the first two domains of life to order light and dark by mandating sleep occur to fix the damage of the day on the IMM and inside the cell. The thanatotranscriptomic genes’ evolved in the first two domains of life to be chaos managers of light stress. 3.8 – 1 billion years ago melatonin was the most important part of this mechanism. These ideas have enriched my photo-bioelectric light cone model because it adds the key diurnal photonic-vibrational dynamic that explains why the eye and brain worked in unison during evolution to innovate sleep. It was done to handle evolving light and oxygen stress life experienced for long time scales in the GOE.

My comprehension of visualizing the evidence of the precision stoichiometry built into the photo-bioelectric circuitry of human systems allows me to understand how lasik kills rapidly. Placing a laser in front of this delicate GOE masterpiece of engineering produces massive voltage and amperage variations in SECONDS in the eye and everything connected to it distally. It is like a nuclear explosion in the anterior chamber, and the sound blast destroys the city of circuits distally connected to it in the brain. This is why the first ten seconds of the video above are critical. The video is not hyperbole when a refractive surgeon uses lasers on your anterior eye.

This example I am giving you also fully explains why the centralized scientific communities fail to recognize how LASIK can KILL like a nuclear bomb does. They do not understand that light gets more potent as the scale shrinks. They cannot explain why people can die rapidly by their own hand due to perception change caused by alteration of the AMO arrangement in your eyes from laser light.

LASIK: Is a Prescription for Ruin with a Nuclear Fallout

In a healthcare system warped by profit-driven incentives, patients are lured by voices that dismiss the sun’s healing power, prescribing instead a cascade of interventions that drain wallets and slash lifespans, misdiagnoses, costing the U.S. billions annually.

Centralized ophthalmology has never put the story of light and the eye together. Neuropsin, melanopsin, and melatonin are the initial protection schemes for the eye. The next guardian is the Vitamin D receptor (VDR), placed in what seems like an unusual spot on the IMM. This is nature’s mitochondrial guardian activated by the visible spectrum in sunlight. When doctors introduce lasers into this system, they are adding nuclear-level light stress to the eye’s photobiological circuits with a massive effect. They completely overlook the VDR inactivation step, and this is why rapid disease creation becomes more probable than not. They have unleashed massive, uncontrolled cataplerosis at the Krebs cycle, driving mtDNA damage, rampant biosynthesis, and systemic decline.

This isn’t just a financial blunder by the patient, it’s a devastating subtraction from your longevity bank account, as the absence of sunlight’s protective brake is over come by the laser light to (via VDR and sulfated Vitamin D) accelerates diseases that centralized medicine fails to diagnose or treat, costing you decades of healthspan in a world where laser and blue light are used indiscriminately by “light experts” who are medical arsonists.

Laser damage and blue light toxicity can be explained by first-principles thinking, and this is a poignant critique. It aligns seamlessly with my photobioelectric thesis. The stoichiometry of mtDNA-driven processes, integrating light, water, and magnetism through the surfaces of the skin, eyes, and brain. Visible low-powered sunlight creates a precise “arc weld” for health, once the light is processed and transformed by our blood, mtDNA, and DNA to sculpt our tissues.

Carefully look AT THE ELECTRON VOLTAGE OF BOTH LIGHTS ABOVE

Are they the same?

6.41 eV does not equal 0.89 – 3.94 eV, does it?

Remember that the 3.94 eV is at the macroscopic level. Is the 6.41 eV delivered the same way? Nope. It is at the nanoscale. What happens to light at the nano, atto, and femtoscales?

What does the physics of the inverse square law say about light as scale shrinks? What has my thesis said about the power of ultraweak UPEs? Calling them “weak” is a failure in understanding how light power changes as scale varies.

No, it’s not. Sunlight’s macroscopic delivery supports broad biological harmony, while the LASIK laser’s nanoscale delivery is a localized, high-energy intervention. This difference in scale fundamentally alters how the light interacts with biological systems, especially at the quantum level.

The mitochondrial weld requires precise “settings” (light, DDW, oxygen). The surgeon’s laser destroys this stiociometry in seconds in the eye. This creates a tsunami of destruction distally in the brain. Low-powered blue light taken out of its sister colors causes blue light toxicity because of the photonic precision with which the system was designed. It is akin to a welder using the wrong electrode, causing defects (altered consciousness, mental disease) in the weld seam (health). When this balance is disrupted by modern stressors like an excimer laser, that type of light becomes capable of altering consciousness, impairing cognitive clarity, creating acute massive emotional changes, and the misunderstanding of how light changes its power as scale, blinds researchers to the quantum underpinnings of the damage this iatrogenic procedure can cause.

CLOCKS WORK BY LIGHT AND TEMPERATURE

I bet you did not know temperature effects also get stronger as the scale decreases. 6.41 eV photonic power = 150 degrees C. Recall that circadian biology operate by light and dark and temperature variations. That lesson goes all the way back to the Cold Thermogenesis 4-6 blogs. Read them again.

Temperature at Macroscopic Scales:

At larger scales (e.g., the whole anterior chamber, ~250 µL of aqueous humor), temperature is relatively stable due to thermal diffusion and convection. The cornea’s baseline temperature is ~34°C (slightly cooler than body temperature, 37°C, due to exposure), and the aqueous humor helps maintain thermal homeostasis.

• Sunlight’s diffuse exposure (0.89–3.94 eV) causes negligible temperature changes in the eye, as its energy is distributed over a large area and absorbed gradually by photoreceptors and chromophores.Temperature at Nanoscale: Localized Spikes:

  At the nanoscale, where the LASIK laser interacts with the cornea, temperature behaves differently due to the confinement of energy and limited thermal diffusion:

  Energy Confinement: The LASIK laser delivers 1.256 mJ per pulse (as calculated earlier) over a tiny area (~0.00785 cm²) and volume (1.9625 × 10⁻⁷ cm³). This concentrated energy causes a rapid, localized temperature spike at the ablation site, estimated to be 100–150°C for a duration of nanoseconds (see previous answer).

  Reduced Thermal Diffusion: At nanoscale distances and femtosecond-to-nanosecond timescales, heat dissipation is hindered. The thermal diffusion length ( L ) is given by:

• 
• 
• • Biological Implications in the Anterior Chamber: WITH SUNLIGHTThe anterior chamber is a small, enclosed space (~3 mm deep, 12 mm diameter). A localized temperature spike of 100–150°C at the cornea-laser interface, even for a brief duration of nanoseconds, can create a shockwave and microcavitation in the aqueous humor, as the rapid vaporization of tissue forms a plasma plume. This can mechanically stress nearby structures, such as the iris and lens. The same effects can occur during cataract surgery when a laser is used.

    The SCN, located posterior to the anterior chamber, isn’t directly heated but is affected by the disruption of light signaling. The temperature spike damages neuropsin in the cornea, impairing UV-A detection and desynchronizing the suprachiasmatic nucleus (SCN). This cascades to the leptin-melanocortin pathways (reduced POMC cleavage, lower β-endorphin, and α-MSH) and the habenular nucleus (dopamine suppression, increased depression risk).

  Temperature and Circadian Biology: Scale Effects of LASER LIGHT

  Macroscopic Temperature: The SCN responds to gradual temperature changes (e.g., diurnal cycles of 1–2°C) to entrain circadian rhythms. A stable temperature in the anterior chamber supports this process by maintaining the flow of aqueous humor and promoting corneal metabolism.

  Nanoscale Temperature Spikes: The LASIK laser’s 100–150°C spike, though brief, disrupts the anterior chamber’s homeostasis massively. It damages all the photoreceptors anterior to the SCN and the SCN itself and spikes ROS in corneal mitochondria, sending aberrant light signals to the SCN. This desynchronization affects the leptin-melanocortin system (metabolic chaos, pain) and habenular nucleus (mood disorders), aligning with the LASIK suicide outcomes I’ve highlighted in this blog. Decentralized medicine understands what it cannot. So, when you sign their consent form for lasik or cataract surgery, are you really informed of the real risks?

  HOW IS SEE LASIK FROM THE CIRCADIAN PERSPECTIVE:

  Watch 5:35 to 8:00 HYPERLINK

  This theoretical temperature scale below underscores the disruptive potential of the LASIK laser’s high-energy photons on the cornea’s quantum signaling pathways, as your thesis highlights. It’s a stark contrast to sunlight’s biologically tuned interaction

• STILL THINK COMPARING LASIK TO A NUCLEAR BLAST IS HYPERBOLE?I think it is the best descriptor I can imagine.

SUMMARY

See the World as It Could Be when light and temperature from light are being delivered at a small scale, not as it should be, to understand disease.

The miracle of your mind is seeing the world as it isn’t, imagining possibilities beyond the present. But LASIK traps you in a RAPID, destructive cycle of repetitive, dopamine-starved thinking, blocking untapped potential. It can unravel your life in a matter of months.

Think of your body as a city that runs on sunlight, with tiny light sparks (UPEs) keeping everything in sync, like a conductor for an orchestra. Sunlight sets your body’s clock by hitting special proteins in your eyes (like neuropsin, melanopsin, CCO, and water) that love the combo of UV, blue light, and IR light found in the sun, telling your cells when to burn fat (beta-oxidation) and make energy. Tiny helpers in your cells, IMM, called NAD+ and NADH, catch sunlight’s energy and glow a bit, passing it to other proteins (flavins) to keep your energy factory (mitochondria) humming. This system received a significant boost billions of years ago (GOE) when Earth’s atmosphere became more oxygen-rich, allowing cells to utilize light and oxygen to produce these sparks and specialized water for enhanced cooperation.

Vitamin D, made from sunlight in your skin, also plays a role. It’s built without nitrogen (unlike most proteins), so it can catch the right kind of sunlight (UVB) without messing up to act as a brake. It is a protection system to protect the ATPase from short-circuiting. The strip of blue glow inside the sun’s small sliver of light helps your body’s clock, too. But modern life, with screen light and Wi-Fi, throws this off; it’s like a loud noise drowning out the conductor, making your cells confused and sick. An excimer laser is a nuclear explosion in this system. There is no protection from this blast of light.

The decentralized dance of light, opsins, and mtDNA is your path to courage, clarity, and resilience. So, do you have the courage to avoid modern refractive surgery and let the sun heal you safely? Share this truth: post a sunrise selfie with #SolarRewire, challenge friends to 10 minutes daily in Nature, and spread the message that sunlight is life’s conductor. Your journey to a vibrant, electrified self starts now. #NatureIsTheCure, not refractive surgery.

CITES

1. https://www.dailymail.co.uk/health/article-14741503/lasik-eye-surgery-patients-police-officer-suicide-ryan-kingerski.html

2. The Laws of Physics tied to QFT