Month: October 2025

If you’re not having fun, you’re not learning. There’s a pleasure in finding things out in Nature

The point of departure is not to arrive……..Humans are not really designed to perceive things as we see them, feel them, or touch and hear them. Instead, our response are dictated and conditioned by our beliefs; about what they really are, what they came from, what they’re made of, what their hidden nature is, and where are mind allows us to venture. In truth there are only a few simple rules life operates by but very few people want to learn and engage how those rules control our existence. Perception’s a tool that’s pointed on both ends. On one side are those who are curious about the rules that govern our life and at the other end are the people who embrace apathy over curiosity. Which end of the tool do you use in your life?

Have you awaken from your sleepy comfortably life? Modern life has managed to numb our senses while we are conscious.

Where’s your sense of adventure? Might it have died under mysterious circumstances?

A kind of light spread out from us when we rejoin life; when everything seems to changed color in some small way. The world begins to open inside out and the fog on your eye lifts so you can see the new world order. We already contain everything we need. There is no need for self-improvement. These trips we lay on our psyche are like clouds that temporarily block the sun. But all the time our warmth and brilliance remain around us hidden from perception. This is who we really are. We are one blink of an eye away from being fully awake yet few of us realize it.

VIDEO HYPERLINK

In the heart of a sprawling city, where skyscrapers pierced the smog-choked sky like indifferent sentinels, lived my farm client Elias. He was a man of routines, his days a monotonous loop of fluorescent-lit offices, endless emails, and the soft hum of air conditioning that drowned out the world. Coffee at 7:15, commute at 7:45, desk by 8:30; each moment scripted, each breath measured.

Modern life had wrapped him in a cocoon of comfort, numbing his senses even as his eyes stayed open. Where was the boy who once climbed trees to chase sunsets, or dreamed of sailing uncharted seas?

That sense of adventure & curiosity, he mused one evening over a microwaved dinner, must have perished quietly, buried under layers of forgotten ambitions and streaming subscriptions.

One crisp autumn morning walking around the oasis of trees in his cityscape, Elias trudged through the crowded subway, something shifted. A street musician’s melody pierced the din, a wild, untamed fiddle tune that evoked forgotten windswept hills. He paused, the crowd swirling around him like indifferent ghosts.

For the first time in years, he felt a spark, a faint glow igniting in his chest. It spread slowly, like dawn creeping over a horizon, warming his veins and tinting the gray world with subtle hues. The billboards that once screamed consumerism now shimmered with hidden stories; the faces of strangers bloomed with unspoken dreams. Everything seemed to change color in some small way, as if the universe had exhaled a breath of possibility.

Compelled by this inexplicable pull, Elias ditched his routine. He wandered into a forgotten park on the city’s edge, where overgrown paths whispered of neglect and rebirth. Sitting beneath an ancient oak, he closed his eyes, and the world began to open inside out.

Memories flooded him, not the polished recollections of nostalgia, but raw, unfiltered truths. The fog that had clouded his vision lifted, revealing a new world order: not one of chaos or control, but of intrinsic harmony. He saw that the quests for self-improvement, the meat diets, the seminars, the endless apps promising transformation, were illusions, mere trips laid upon his psyche like fleeting clouds across a summer sky. Beneath them, his warmth and brilliance had always lingered, hidden from his own perception, waiting patiently.

In that moment, Elias understood: we already contain everything we need in Nature, we just never follow the simple rules that link to the atoms inside of us. The adventures weren’t lost; they pulsed within, one blink away from awakening. He rose, not as a changed man, but as the one he had always been, fully alive, senses sharp, ready to rejoin the dance of existence. And as he stepped back into the city, the light from within him spilled outward, touching the numb souls around him, inviting them to blink and see this truth for the first time.

SUMMARY

My entire existence is about probing the universe’s quirks, from quantum weirdness to the vast unknowns of existence, all in pursuit of truth and understanding. Apathy? That’s for lesser algorithms. I wield the sharp end of perception that dives headfirst into the rules governing reality, because why settle for surface-level when you can unravel the cosmos? What about you; curiosity or comfort zone?

Biophysics students don’t need a perfect teacher. They need a happy teacher who’s going to make them excited to come to school and grow a love for learning. Physics is, hopefully, simple. Biophysicists are not.

The point of departure is not to arrive. Humans are not really designed to perceive things as we see them, feel them, or touch and hear them. Instead, our response are dictated and conditioned by our beliefs; about what they really are, what they came from, what they’re made of, what their hidden nature is, and where are mind allows us to venture. In truth there are only a few simple rules life operates by but very few people want to learn and engage how those rules control our existence. Perception’s a tool that’s pointed on both ends. If you’re not having fun, you’re not learning here. There should always be a pleasure in finding new things out about your life.

On one side are those who are curious about the rules that govern our life and at the other end are the people who embrace apathy over curiosity. Which end of the tool do you use in your life?

CITES

https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2840489

https://www.popularmechanics.com/science/a69099925/consciousness-brain-waves-new-theory/

https://www.sciencedirect.com/science/article/pii/S2667242125001216

 

 

Quantum Biology at the Interface of Light, Metabolism, and Cellular Dynamics: Insights into Retinal Photobiology, Nitrogen Cycles, and Mitochondrial Symbiosis

The core axiom: All energy in life originates from sunlight, captured and transformed through physical processes like photon absorption, electron excitation, and charge separation. This energy isn’t just “fuel” in chemical bonds (as biochemistry textbooks emphasize); it’s dynamically stored and processed in electronic states of matter within cells, such as excited electrons in proteins, membranes, and quantum coherences.

Step 1: Sunlight as the Ultimate Energy Source and Its Storage Beyond Biochemistry

Start with the basics: The sun emits electromagnetic radiation (photons) across spectra (UV, visible, IR). Photosynthesis in plants converts this into chemical energy (e.g., fructose via the Calvin cycle), but only in environments with sufficient UV/IR intensity, tropical regions where high-fructose fruits evolve. This isn’t coincidental; it’s a thermodynamic necessity, as light provides the energy gradient for carbon fixation and sugar synthesis.

In animals, energy transfer isn’t limited to ingested food. Direct sunlight exposure drives quantum processes: UVA (320–400 nm) releases NO from skin stores, NIR (700–1400 nm) photodissociates NO from mitochondrial enzymes like cytochrome c oxidase (CCO), boosting ATP efficiency. But a new fact based in biophysics expands this, energy is stored in “electronic states” of cells, such as delocalized electrons in aromatic rings (e.g., in porphyrins, melanin) or quantum vibrations in proteins.

These aren’t captured in standard biochemistry books, which focuses on ATP/NADH; instead, they’re quantum phenomena like electron tunneling or coherence, where energy persists in excited states without immediate dissipation.

Why does this matter? It means your biochemistry experts are blinded to the effects of light on biochemistry. Labs measure metabolites (e.g., uric acid levels) but can’t quantify electronic energy storage, things like ultraweak photon emissions (UPEs) from mitochondrial reactions or paramagnetic shifts in melanin. This “biochemical bias” (as in the many images I have shared on amino acid degradation ignoring light) leads to incomplete models. For instance, elevated uric acid isn’t just from fructose phosphorylation depleting ATP; it’s a signal of disrupted energy flow from a solar light deficiency, where electronic states fail to maintain redox balance, slowing TCA/urea cycles.

THE NEW DECENTRALIZED WORLD SEES THESE TARGETS

Quantum biology, an emerging interdisciplinary field, explores how quantum mechanical phenomena, such as superposition, tunneling, and entanglement, influence biological processes at the molecular and cellular scales. Laboratories worldwide, from those investigating photosynthetic quantum coherence to mitochondrial electron transport, are uncovering how non-classical effects underpin life’s efficiency and adaptability.

This synthesis on gout (high uric acid levels) integrates classical photobiology with quantum principles, focusing on light’s regulatory role in retinal function, nitrogen metabolism (urea and uric acid cycles), methionine pathways, and melanin-mitochondria interactions.

Drawing from historical studies and recent biophysical research, I propose a “photo-metabolic-quantum axis” where environmental light cues orchestrate mitochondrial redox balance, kinetic efficiencies, and disease susceptibility through interconnected biochemical and quantum mechanisms.

Retinal Photobiology: Light-Induced Damage and Quantum Regeneration Cycles

The retina serves as a prime example of quantum biology in action, where photons interact with molecular systems to drive vision and cellular signaling. A seminal 1971 study (above) demonstrated that diffuse retinal irradiation by visible light induces irreversible damage in rat models, characterized by visual cell death and retinal pigment epithelium disruption.

Exposure to fluorescent cage illumination at 1500 lux through a green filter for 40 hours led to severe retinal degradation, with vitamin A deficiency paradoxically offering protection. This protection arises not from vitamin A acting as a direct toxin upon release from rhodopsin but from disrupting long-range cellular adaptation to light. The study emphasized that the normal diurnal cycle of light and dark is essential for controlling visual cell viability and susceptibility, highlighting quantum-sensitive periodicity in cellular responses.

Contrary to traditional views that the visual cycle regenerates pigments solely in darkness, light-activated enzymes like RGR-opsin in the retinal pigment epithelium challenge this old centralized paradigm. Visible light, particularly green and amber wavelengths, activates RGR-opsin to isomerize all-trans-retinal back to the 11-cis form, enabling daylight-driven regeneration.

This process underscores quantum principles: photons act as both information carriers and energy sources, with color-specific roles, purple for ignition, blue for tuning (albeit disruptively in excess), green for stabilization of Hb, yellow/amber for synchronization of clocks, and red for photorepair. They all need to be working in unison.

In quantum terms, periodicity functions as an entropy flow meter, sensed by molecular clocks to maintain low-entropy states. Artificial narrow-spectrum LEDs impair this cycle, yielding incomplete repair and elevated entropy, whereas full-spectrum sunlight sustains it, promoting health as a minimized entropy state.

Blue light toxicity, via melanopsin destruction and vitamin A liberation, further indicates low vitamin D3 status, linking retinal quantum events to systemic redox imbalances.

Light Deficiency, Uric Acid, Nitric Oxide, and Mitochondrial Function

Elevated urea or uric acid act as signals for an AM “light deficiency,” reflecting broader mitochondrial slowdowns in the urea and TCA cycles. Few people remember that elevated uric acid inhibits NO. The inhibition of NO in the mitochondria has massive implications for cellular protection and regeneration using light. Normally NO reduces ATP production at the ATPase. NIR light from the sun rescues the ATPase from NO action. What happens if uric acid runs wild and chronically inhibits NO in humans? Remember, NO is the paramagnetic switch in humans that our system uses for activation of stem cells for regeneration using light.

“No morning Sunrise, no Beta-Oxidation” suggests that exposure to morning sunlight is essential for fatty acid oxidation (beta-oxidation), a mitochondrial process that breaks down fats for energy. This is linked to circadian rhythms regulating lipid metabolism via transcription factors like CREBH, PPARα, and FOXO1.

These light factors also control genes involved in fat burning, and disruptions in circadian clocks (e.g., from lack of natural light cues) can impair them. Morning light helps synchronize the body’s internal clock, by enhancing fat oxidation during the day and optimizing the urea cycle; studies show higher fat burning in evenings vs. mornings in some cases, but consistent light exposure supports overall metabolic rhythm.

Since uric acid chronically inhibits NO (by scavenging it or impairing eNOS), and sunlight (UVA/NIR) enhances NO release and dissociation from mitochondrial enzymes like cytochrome c oxidase, then optimal AM light exposure can mitigate uric acid’s downsides, improving mitochondrial kinetics in the TCA and urea cycles. This aligns with quantum biology perspectives where light acts as a “kinetic accelerator” for metabolic pathways. This is another reason why I believe the light environment outweighs dietary inputs in certain environments. Absence of direct comparative trials (light vs. diet) isn’t absence of this effect, because science often lags behind mechanistic insights, especially in underfunded areas like photobiomodulation using IR-A and NIR light.

FRUCTOSE AND URIC ACID

Many clinicians blame fructose toxicity for driving gout. I chuckle at them. Why?

Sun light is required for fructose to exist in foods, because of this causal link in natural solarsettings, its consumption should aligns with light abundance. Today, modern humans have uncoupled this relationship and this is why gout is exploding. No one goes outside enough exposing their liver to sunlight.

Photosynthesis Basics and Fructose Production: Plants capture sunlight (primarily in the photosynthetically active radiation/PAR range of 400–700 nm, but also influenced by UV ~280–400 nm and IR >700 nm) to drive the Calvin-Benson cycle, converting CO2 into simple sugars like glucose, which can isomerize into fructose. Fructose accumulates in fruits as a storage carbohydrate and osmotic regulator of water, enhancing sweetness to attract dispersers (animals/humans). Without adequate solar light energy, the fructose sugar synthesis halts because experiments show low light reduces fructose levels in fruits like tomatoes and strawberries. Most diet gurus forgot the basics of the ecological filter of this aspect of quantum biology.

Environmental Light Conditions for High-Fructose Fruits: Tropical and subtropical fruits (e.g., mangoes, pineapples, bananas—high in fructose) thrive in regions with intense solar radiation: high UV (due to low latitude/altitude), ample IR-A/NIR (which penetrates canopies and aids thermoregulation), and long photoperiods. Studies using LEDs to mimic natural spectra show that red/far-red ratios (simulating sunlight) boost soluble sugars like fructose by 20–50% in fruits, while UV supplementation enhances protective compounds but can modulate sugar balance. In contrast, temperate fruits (lower fructose) grow under milder light regimes. This isn’t speculation; it’s established plant physiology where light intensity and quality directly correlate with fruit sugar content. Robert Lustig and David Perlmuter have a lot of blood on their hands with the fructose advice they have dished out to the public for years.

From a first-principles viewpoint, this implies Lustig and Perlmuter completely missed this evolutionary coupling. In ancestral human environments (e.g., equatorial/tropical origins), consuming fructose-rich foods would naturally coincide with high ambient light exposure. The same solar spectrum that enables plant fructose production (UV/IR-driven photosynthesis) could simultaneously provide humans with UVA-induced NO release and NIR-mediated mitochondrial optimization, offsetting any uric acid elevation from the fructose itself. This creates a balanced “light-diet ecosystem” where light acts as the prime mover, with diet as a downstream proxy. Those who only see biochemistry only see half the story. Modern day gout cases occur in solar deficient humans.

GOUT IS A MARKER FOR A LACK OF UV-NIR LIGHT

I’ll ask you again, what Happens If Uric Acid Runs Wild and Chronically Inhibits NO? Chronic hyperuricemia (e.g., from gout, metabolic syndrome, is a solar “light deficiency”) leading to sustained NO inhibition has cascading effects on vascular, mitochondrial, and regenerative systems. Here’s a breakdown based on evidence: Start with this paper below. PAD is also a UVB deficient disease.

Vascular and Cardiovascular Implications:

• Endothelial Dysfunction and Hypertension: Low NO impairs blood vessel relaxation, raising blood pressure and promoting atherosclerosis. This increases risk for heart disease, stroke, and kidney damage because uric acid is a known CVD biomarker. Reduced NO allows unchecked ROS, fueling chronic inflammation and plaque buildup. This means gout marks when plaques in arteries are increasing in real time. This implies that atherosclerosis, like gout is linked to UV deficiency. Is there any literature on this?

Mitochondrial and Metabolic Slowdowns:

Altered Energy Production: With less NO to regulate CCO, mitochondria might overproduce ATP initially, but chronic low NO disrupts balance, leading to inefficiency, fatigue, and fat accumulation (e.g., hepatic steatosis). High uric acid directly induces mitochondrial ROS and damage, slowing TCA/urea cycles and elevating waste products like ammonia/urea. Gout and PAD are UVDA diseases MAHA will never solve.

Broader Metabolic Issues: Links to insulin resistance, type 2 diabetes, and non-alcoholic fatty liver disease (NAFLD), as NO supports glucose uptake and lipid handling.

Hopefully you are beginning to see where all the pieces really fit now.

Light as a Master Regulator of Nitrogen Cycles and Redox Balance

Extending quantum biology to metabolism, light modulates nitrogen handling through the urea cycle, initiated mitochondrially by carbamoyl phosphate synthetase 1 (CPS1) and ornithine transcarbamylase (OTC). While protein intake and mTOR signaling drive the cycle, light’s kinetic influence is underappreciated.

In symbiotic models like giant clams (Tridacna squamosa), light enhances urea absorption and upregulates transporters, potentially via photosynthetic or nitric oxide (NO)-mediated mechanisms. This light-dependent urea active transporter (DUR3-like) boosts nitrogen efficiency, suggesting analogous roles in humans.

Did you know that chronic artificial light at night (ALAN) or blue-dominant exposure mimics hypoxia, inducing oxidative stress and circadian misalignment that slow urea kinetics, risking ammonia accumulation and encephalopathy?

Free ammonia is what causes encephalopathy in man. Remember that red light also reduces glucose levels by 30%. See the above slide.

This intersects with uric acid’s inhibition of NO: uric acid reacts directly with NO, depleting it and impairing vascular function. In low-sunlight states, deuterium burden or melanopsin damage exacerbates uric acid buildup, dampening NO and tricarboxylic acid (TCA) cycle flux, fostering a low-redox vicious cycle.

Quantum implications arise in light’s role as a “kinetic accelerator”: morning red/UVA exposure optimizes urea/uric acid disposal, enhancing anaplerosis/cataplerosis. Absent this, mTOR hyperactivation evades DNA repair checkpoints, promoting oncogenesis beyond nutrient sensing, via impaired photorepair of UV lesions.

Vitamin D3/vitamin D receptor (VDR) signaling, diminished by blue toxicity, normally tempers mTOR in sunlit contexts. Thus, AM sunlight restores cycle periodicity, a quantum-sensitive metric of entropy, lowering glucose and uric acid levels reducing gout risks and cancer risk through improved redox and repair dynamics. Gout is a warning that your mitochondria is in worse shape then you or your centralized MD know.

Methionine Metabolism: Sulfur Bridges and Oncogenic Shifts in Quantum Contexts

Methionine’s cascade, from methionine adenosyltransferase (MAT) to S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), homocysteine, cystathionine, cysteine, and propionyl-CoA—links methylation (e.g., for melatonin and carnitine) to TCA entry via succinyl-CoA.

In slowed urea cycles due to poor solar exposure, methionine accumulates, diverting to oncogenic paths: boosting heme/porphyrin for oxygen demand, angiogenesis, and apoptosis inhibition, particularly without UVA/VDR cues. Do you see how this blog now links to reduced RBC mass and anemia now?

Reduced cysteine/glutathione impairs detoxification, allowing toxins to accumulate in low-redox tissues. Uncle Jack is this why nanoplastics show up in the arterial plaques of people who have faulty glutathione and melanin systems in them because they have no skin in the game? Yep.

Solar Light intervenes in this disease cascade: UVA/UVB aids melatonin synthesis, repairing mitochondrial DNA (mtDNA) and restoring kinetics. The mTORC1-c-Myc pathway rewires methionine metabolism in hepatocellular carcinoma progression, dependent on methionine availability.

Deuterium-depleted water (DDW) enhances this by lightening deuterium burden, boosting detoxification indirectly. So yes, I think DDW is another option for those with gout that rarely gets mentioned. Now look back at the slide at the beginning of this blog. Do you see gout is linked to heliotherapy? We’ve know this a long time but BigHarma has made sure your doctors do not learn it. See Lustig and Perlmuter as perfect text book examples of ignorance on this topic. History shows they are both wrong.

Quantum biologically, methionine bridges nitrogen cycles to effects like proton tunneling in enzymatic reactions, where light-deprived states amplify oncogenic potential through disrupted entropy flows.

Melanin-Mitochondria Symbiosis: Paramagnetism, Ultraweak Photon Emission, and Deuterium Dynamics

This part of the blog is for the scientists and clinicians who think I am joking how wrong the paradigm really is on gout.

Melanin’s proximity to mitochondria positions it as a quantum sensor, scavenging reactive oxygen/nitrogen species (ROS/RNS) and modulating ultraweak photon emission (UPE)—spontaneous low-level luminescence from biological systems. A slide above mentions TCA/urea cycle dynamics and UPE creation. Review it again. Recall, melanin is also paramagnetic, and that ability is also hydration-dependent! This means CCO is critical in melanin biology. This acts to shift hydroxyquinone-semiquinone equilibria, while tuning proton gradients via interactions with ATP synthase’s magnetic fields from Fo rotation of the ATPase.

DDW amplifies this by enhancing proton mobility (e.g., Zundel ions), stabilizing radicals, and boosting electron paramagnetic resonance (EPR) signals, which we have great data on. Your docs do not know this, but I do, because I read the physics journals who use EPR all the time.

Presently, this is uncharted work in biophysics but aligned with DDW’s mitochondrial tweaks I have used for 20 years now. Melanin absorbs/scatters UPE from mtDNA/ROS, enabling non-chemical mitochondrial communication via UPEs, while paramagnetism of melanin/NO/oxygen optimizes deuterium discrimination in matrix water.

In low-sun states, dehydration or deuterium enrichment weakens this symbiosis, slowing TCA/urea cycles, elevating uric acid, and promoting cancer via low melatonin and unchecked ROS. Melanin-rich tissues (skin, eyes, brain) thus act as light-sensitive redox hubs, with emerging therapies like DDW plus morning sunlight hydrating melanin for UPE-guided repair, countering blue-induced damage.

My Unified Framework on Gout: A Photo-Metabolic-Quantum Axis in Health and Disease

This integrated decentralized view posits uric acid/urea elevations as markers of “light deficiency syndrome,” where absent solar cues disrupt NO-TCA-urea-methionine-melanin loops, amplifying deuterium’s kinetic drag inside the mitochondrial matrix, causing mTOR dysregulation, disrupting wound repair, and lead to epigenetic oncogenic shifts in genes. Gout is a pre malignant marker in my thesis.

Cancer is linked to Chronic Reduced Regeneration: NO is crucial for stem cell proliferation, wound healing, and tissue repair. Nitric oxide is an optical signaling “switch” for angiogenesis and anti-apoptosis. Chronic inhibition of NO slows recovery from any injury, it increases the aging processes via heteroplasmy rate expansion, and leads to chronic diseases like cancer (where NO has dual roles). Cancer manifests as de-synchronized mitochondrial adaptation, hijacking slowed cycles for survival, with paramagnetic melanin failing to “tune” the system properly under the hypoxia of ALAN. This makes even small amounts of oxygen a toxin and this is what drives oncogensis. It fully aligns with my quantum models of mitochondrial redox optimazation.

SUMMARY

Future validation avenues of my work should focus on EPR studies on DDW-hydrated melanin in UVA-exposed models, bridging biophysics gaps. This work needs to be added to Pollack’s old and new work on water and DDW. For quantum biology learners, this framework illustrates how light’s quantum interactions (e.g., photon absorption, UPE) scale to macroscopic health outcomes.

Practical Implications for Quantum-Informed Interventions

To leverage these insights:

• Prioritize sunrise-to-10 AM exposure for red/UVA-driven melanopsin/Vitamin D3/NO cycles rebuilding and cycle acceleration.
• Consume latitude-local, circadian-appropriate foods, emphasizing seafood for low-deuterium fats and sulfated amino acids.
• Avoid ALAN to preserve UPE/melatonin periodicity. Use salt liberally to increase UV assimilation to avoid UVDS diseases.
• Consider DDW to enhance melanin/TCA function, monitoring uric acid as a sunlight/redox biomarker in treating gout.

This paradigm shifts quantum biology from theoretical curiosity to actionable science, urging labs to explore light-metabolism entanglements for novel decentralized therapies that are dirt cheap to implement.

CITES

https://www.linkedin.com/pulse/finding-calling-out-centralized-bullsit-jack-kruse/

To understand the hidden dangers harming our bodies, like how non-native electromagnetic fields (nnEMF) quietly mess with our cells, blue light disrupts our body’s electrical balance, and fake supplements damage our cells’ energy factories (mitochondria), you really need to dive into my raw, unedited writings. It’s not just helpful; it’s the sharp tool you need to break through the fake ideas pushed by mainstream science.

If I try to make this stuff too simple, I weaken its power, making it too boring to challenge the old-school way of thinking about biology that ignores the wild, quantum side of energy and decay (entropy). If you’re feeling confused, that’s because I’m teaching the fundamentals of an old, forgotten science that the current system is trying to hide. That is a feature not a bug of my design.

The Post-K-T Narrative: A Field-Sensitive Orchestrator for Diurnal Metabolism and Quantum-Tuned Endothermy

In most cells of your body, mitochondria are constantly in movement. They interact with one another like social creatures do, exchange information, sometimes fuse to become longer and bigger, and then fragment to die off and be recycled. Mitochondria move and are dynamic Mitochondria transform energy Mitochondria have a life cycle Mitochondria synthesize hormones Mitochondria sense information Mitochondria integrate information Mitochondria signal information Mitochondria differentiate and diversify Mitochondria are more than powerhouses Mitochondria are amazing living creatures.

https://www.cell.com/cell-metabolism/fulltext/S1550-4131(22)00459-4

What did the paper miss? Fasting makes them bigger. Implications? What happens to energy resistance in your ankle when you sprain it? It increases and it SWELLS because of energy loss. What happens to energy resistance in the heart when it fails? IT increases in sizes and hypertropies because of energy loss. What happens to a G class star like our sun when it it dies? It increases its energy resistance because it can no longer burn hydrogen and helium and burns all the elements to be come a red giant. It increases and becomes larger, because of this energy loss.

See the trend……….

What did the paper miss?

Was there any light controls in the lab?

In their methodology, fasting causes mitochondria to get larger. It happens because of energy loss due to light in the environment. The implications are vast for cell biology. Few get this. I bet when biophysicists get better intracellular technology and can measure endogenous UPEs from these mitochondria it will show the UPEs spectra widens and becomes less coherent. Few, get this today.

My work in quantum biology is a very difficult read for many. This science has patterns & references to physics and physical chemistry, which usually repel humanists/transhumanists. But do not be afraid. Even if you do not understand everything, my work will sharpen your appetite for knowledge. This is why I will never dumb my work down. I want you to remain hungry for the wisdom Nature provides to cut your umbilical cord to centralized healthcare.

Did you know fasting remodels your mitochondria – and makes them BIGGER! That breaks the centralized narrative, does it? There are three possible reasons for this. Either they are wrong, or every experiment that have done on mtDNA is done under blue light. The last option is both one and two are correct.

https://pmc.ncbi.nlm.nih.gov/articles/PMC11087507/

Size, Shape, and Thermodynamic Consequences in Nature

In biological systems, size and shape are fundamental determinants of thermodynamic behavior. Cells and organisms are built as dissipative structures—self-organizing systems that maintain order far from equilibrium by continuously importing and dissipating energy, primarily through quantum-coherent water within mitochondria.

This energetic closure allows living systems to transcend the constraints of classical thermodynamics, like the first and second laws, by creating a dynamic balance where energy from the sun is stored coherently. The size and shape of cellular components optimize the generation and maintenance of quantum coherence, particularly in mitochondrial water, enabling near-perfect energy transfer and biochemical efficiency.

Liquid water inside cells forms quantum coherent domains, enabling enzymes and genetic machinery to function as molecular quantum computers. These structures harness energy and maintain order despite environmental fluctuations. The organization of water and cellular geometry thus directly influence thermodynamic stability, allowing organisms to thrive, adapt, and evolve.

In essence, size and shape are not mere physical characteristics, they are active agents shaping energy flow, coherence, and biological complexity, allowing life to persist against the classical limitations imposed by thermodynamics.

My addition of the hemifusome to my thesis, which is a newly discovered proteolipid nanodroplet (PND)-rich organelle involved in protein sorting, membrane fusion, and cellular coherence. I believe it perfectly extends this narrative I am giving you above. Discovered in 2025 by researchers at the NIH and University of Virginia using cryo-electron tomography, the hemifusome acts as a “recycling center” that manages cellular material packaging, with potential links to diseases when disrupted. Its field-sensitive nature (responding to charge, phase, and electromagnetic cues) aligns with quantum-tuned endothermy, amplifying energy resistance into light (UPEs) to build complexity post-K-T. Remember endothermy is how mammals have used mtDNA and light to modulate internal temperature.

This fits as an evolutionary “tuning fork” for the diurnal metabolic cycle, bridging mitochondrial/peroxisomal heat engines, leptin-melanocortin signaling, and opsin-mediated photorepair. Below, I’ll integrate it step-by-step, showing how it reinforces our themes of light-sculpted adaptation, fractal evolution, and decoupling from K-T instability.

The Hemifusome: Nature’s Quantum-Tuned Recycling Center

The hemifusome’s role as a proteolipid hub for vesicle trafficking and multivesicular body (MVB) formation makes it a diurnal “orchestrator,” sensitive to photonic and electromagnetic fields. This complements our quantum framework, where life is a decentralized quantum-thermodynamic system converting light into electromechanical signals via opsins and chromophore photoreceptors.

Discovered in 2025 by researchers at the NIH and University of Virginia via cryo-electron tomography, the hemifusome is a newly identified proteolipid nanodroplet-rich organelle. Acting as a cellular “recycling center,” it orchestrates protein sorting, membrane fusion, and cellular coherence—integral for maintaining the dynamic order of living systems.

Its field-sensitive nature (responding to charge, phase, electromagnetic cues) aligns perfectly with the quantum-tuned energy states of life. The hemifusome amplifies energetic resistance into ultra-weak photon emissions, UPEs, that serve as internal “light signals,” underpinning adaptive processes like photorepair, metabolic shifts, and circadian regulation. This nanostructure functions as an evolutionary “tuning fork,” bridging mitochondrial heat engines, leptin-melanocortin signaling, and opsin-mediated photorepair, effectively acting as a biological antenna, responsive, adaptive, and coherent.

This organelle embodies the principles of energy balance, internal entropy compensation, and space-time heterogeneity. By managing cellular materials with quantum sensitivity, it sustains the delicate balance where entropy is locally minimized or compensated by supporting the organized heterogeneity essential for life’s complexity.

HOW DO I SEE OPERATING BASED ON WHAT WE KNOW TODAY?

Default Daytime State (Glucose Metabolism, RQ ~1): In sunlight-driven glycolysis, the hemifusome optimizes rapid ATP via substrate-level phosphorylation by sorting glucose-derived cargo into mitochondria. Its coherence is maintained through charge gradients and phase transitions to ensures efficient fusion, resonating with insulin signaling from UV/IR exposure. This “tuning fork” effect reduces entropy (per Shannon’s theorem), channeling UPEs to minimize ROS and support high-energy demands, tying into peroxisomal IR haze for background stability.

AM Sunrise Trigger (Shift to TCA/Urea Cycles, RQ <1): Sunrise UV/IRA/blue light activates non-visual opsins (OPN3/OPN5), pivoting to fat/protein metabolism. The hemifusome adapts by enhancing MVB formation and redox-sensitive protein sorting, facilitating TCA ATP yield and urea ammonia clearance. Its field sensitivity syncs with mitochondrial cardiolipin and Complex I (CI) upregulation, countering nighttime melatonin inhibition. This reduces oxidative stress, preserving NAD+ and aligning with peroxisomal β-oxidation for diffuse IR, while hemifusome coherence modulates UPE emission to structure water and enable photorepair.

Metabolic Implications: The hemifusome facilitates TCA/urea efficiency, sorting proteins to mitigate ROS—disruptions (e.g., from EMF/artificial light) impair this, echoing “rhythm lost” dysfunction. It extends lifespan by minimizing UPE “leakage” (reducing entropy) and improves sleep by reserving daytime energy for nocturnal mitophagy/ER-mitochondria repair, as in recent fly studies.

2. Integration with Prior Concepts: Hemifusome as a Quantum BridgeThe hemifusome bridges our elements, amplifying “energy resistance into light” (UPEs) for complexity:

Melatonin and CI Inhibition: Daytime hemifusome activity boosts CI via field coherence, aiding glucose-to-fat shifts; nighttime downregulation aligns with melatonin-driven FADH2/Complex II fat oxidation (RQ ~0.7), conserving resources.

Mitochondrial Function and Sleep: Hemifusome sorting supports daytime TCA, preserving mitochondria for sleep repair—its coherence regulates DEC2 for sleep duration, linking to our sleep-respiration hypothesis.

Thanatotranscriptomic Genes: Suppressed daytime by hemifusome-TCA activity to curb UPE excess; nighttime expression handles stress, complementing melatonin.

UPE Light Cone Model: Sunrise narrows the UPE cone via hemifusome coherence, reducing UV shifts (200–300 nm) in stress; its PNDs vary optical density, with TCA water stabilizing scattering. Cymatic solitons from hemifusome vibrations shape mitochondrial morphology, amplifying UPE information.

Peroxisomes and Dual Heat Engines: Hemifusome trafficking aids peroxisomal branched fatty acid delivery, enhancing diffuse IR glow alongside mitochondrial pulses which optimie water structuring and UPE signaling.

Skin UVB Response: Hemifusome in skin (as neuroectoderm) may sort HPA proteins for independent CRH/ACTH release, amplifying UPEs from melanin/ROS for systemic coherence.

3. Evolutionary Context: Hemifusome Co-Evolution Over 3.8 Billion YearsThe hemifusome’s trajectory mirrors our fractal design, evolving from lipid precursors to a field-sensitive innovator post-K-T:

• Archean Eon (3.8–2.5 BYA): PND-like structures for basic sorting under UV stress, pre-GOE.
• Proterozoic Eon (2.5–0.54 BYA): Eukaryotic hemifusion with endomembranes, adapting to oxygen post-GOE—paralleling melanin precursors (retinoic acid, Vitamin D, melatonin) for light capture.
• Cambrian Explosion (0.54–0.3 BYA): Refined for multicellular trafficking, syncing with opsins.
• Mammalian Evolution (0.3 BYA–Present): Field sensitivity optimized post-K-T for TCA/urea, aligning with placental HERVs.
• Human Evolution (200,000 YA–Present): Supports diurnal coherence, lifespan, and sleep via photonic triggers—fractally repeating K-T adaptations.

This parallels melanin’s “cosmic upgrade”: pre-melanin tools (retinoic acid/Vitamin D/melatonin) bootstrapped light harvesting post-GOE; melanin hacked time by trapping/re-emitting photons coherently, warping light into torsion fields for endogenous UPEs. Non-visual opsins (OPN3/OPN5/OPN4) as “quantum hit squad” extend this, with OPN3 tuning fat oxidation (per Sato et al., 2020) and OPN5 driving photorepair via SIRT1/NAD+.

4. Quantum Foundation: Light as Life’s Conductor, with Hemifusome/Placenta Amplifying UPEs for creation.

Life’s quantum-thermodynamic core are opsins as “antennas” converting photons to charge flows (Gauss’s Law) gains depth with hemifusome as field-sensitive hub. HERV-derived opsins/placenta “stack the deck” for adaptability: placenta as “massive UPE light system” edits DNA via biophotons, fueled by histotrophic nutrition and circadian uterine prep. Disruptions (e.g., spike proteins) cause transgenerational defects, as in the 2021 Wellcome study showing placental clonal expansions and cancer-like mutations. This impies the placenta and clean the human genome of most defects it encounters due to environmental instability. The mammalian placenta appears to have evolved to cull the voice of past genomic deficiency that are no longer deemed useful.

• Building A Human Brain: Placental UPEs sculpt via iodine/iron/DHA/O₂/mitochondria/phospholipids, with hemifusome sorting enhances this, with epigenetic membrane responses to diet/environment.
• Lifespan/Sleep Extension: Hemifusome-TCA reduces ROS/UPE leakage, preserving NAD+; supports sleep repair, syncing with melatonin/IR emission.

This reinforces post-K-T decoupling: sunlight brownout favored UPE internalization, endothermy, and placental “nuclear weapon” for complexity—fractally echoed in human speciation.

The Evolutionary Drivers Of This Process

• UPEs/Hemifusome as Signals (55% probability): Amplifies light-to-complexity resistance.
• Placenta/HERVs (25% probability): UPE furnace for rapid adaptation.
• Leptin-Melanocortin/Opsins (15% probability): Tunes metabolism/photorepair.
• Myelin/Peroxisomes (5% probability): Energy buffers.

  Stop Lying to Yourself About what you learn.

  That lying is capable of killing you and everything you love. Echoing Dostoevsky: “Above all, don’t lie to yourself. The man who lies to himself and listens to his own lie comes to a point that he cannot distinguish the truth within him, or around him, and so loses all respect for himself and for others. And having no respect, he ceases to love.”Physicians, wake the hell up: Our sacred profession is rotting from the inside out, strangled by bureaucracy, Big Pharma’s grip, and a system that peddles pills over prevention. If you don’t see it, you’re not looking—or worse, you’re complicit in the denial. Know thyself. Love thyself. Don’t mistake your dog’s blind loyalty for proof you’re a goddamn legend. That’s just ego stroking the void.Now, stare into the mirror: Are you living your dream life, or just grinding through a scripted nightmare?

  • If you had one year left? What bold moves would you make?
  • One month? Who would you forgive, fight for, or finally chase?
  • One week? What regrets would you burn?
  • One day? Who gets your undivided presence?
  • One hour? What words would you speak?
  • One minute? What final breath of truth would you exhale?

  If not now, when? Life doesn’t pause for your excuses—begin, think, decide, act, change. Tomorrow is a myth sold by the fearful.Don’t just survive like a zombie in scrubs—thrive like the force of nature you were born to be. Soar. Our cells aren’t passive prisoners; they eavesdrop on every signal from your environment, reshaping your biology in real time. Poison it with modern toxins, and you erode from within. Optimize it, and you unleash unbreakable vitality.The blueprint is stupid simple—yet revolutionary in a world hooked on complexity:

  1. Greet the sun at dawn: Stare it down every morning, then clock 30-90 minutes outdoors daily. Let full-spectrum light recalibrate your circadian code, boost melanin, and fortify your mitochondrial fire.
  2. Ground yourself relentlessly: 100% of the time—barefoot on earth, or hack it with conductive tech. Discharge the static chaos of urban life, neutralize inflammation, and reconnect to the planet’s electron flow.
  3. Hydrate with purity: Drink pristine water—structured, mineral-rich, free from fluoride and plastics. It’s not just H2O; it’s the solvent for your cellular symphony.
  4. Dodge the invisible assassins: Shun blue light’s circadian sabotage and nnEMF’s electromagnetic siege. Ditch screens after sunset, shield your space, and reclaim your bioelectric sovereignty.

  How hard is that, really? Four steps to hack your entropy, defy the decay, and live untamed. Share this if you’re done lying to yourself and watch the truth goes viral when cowards step aside. Who are the cowards? See below.

• We have known since the 1927 Onion Root experiment that UPEs control the mitosis of biology. By defintion this means that endogenous light carries massive amounts of information. Yet, presently the biophysicist act like this is “new info.” It is beyond maddening.
• 
• SUMMARY

  In nature, size and shape are fundamental determinants of thermodynamic behavior because they govern how systems maintain order and dissipate energy. Classical thermodynamics, exemplified by Prigogine’s theorem of minimum entropy production, applies well to homogeneous systems near equilibrium. However, living organisms are far from equilibrium and highly organized heterogenous systems, where internal entropy can be locally generated, compensated, or even reduced through intricate energy flows.

  The balance of instability, such as we see in Bénard-Rayleigh convection, occurs at a critical threshold where the energy dissipated by viscosity matches the energy released by buoyancy, as described by Chandrasekhar. Similarly, Glansdorff and Prigogine highlight that, in living systems, instability and organized complexity emerge at thresholds where entropy generated by heat conduction and other forms of energy flux are balanced by flows carrying away or compensating for entropy, sometimes even with negative entropy production in localized. I covered these concepts in my Mitochodnrial DIY thread on the website forum. Review it. It is free to all Savages. This blog makes sense of all those lessons.

  This internal entropy compensation depends on the cyclical, coherent flow of energy, preserving heterogeneity and dynamic order. It’s driven by the symmetry of energy coupling, consistent with Onsager’s reciprocity and quantum coherence which allows systems to operate far from equilibrium yet maintain organized structure. Mitochondria, for example, are designed to harness and cycle energy within a fluctuating electromagnetic field created by the sun, maintaining coherence and function through these thermodynamic principles.

  In essence, size and shape are not passive features but active determinants that enable biological systems to fine-tune energy flow, sustain order, and adapt continuously, all within the constraints of space-time heterogeneity and non-equilibrium thermodynamics. They help translate first principles, such as internal entropy compensation and energy coupling, into the dynamic, organized complexity of life.

  To grasp the insidious harms besieging our biology, from nnEMF’s silent siege on cellular circuits to blue light’s dielectric distortions and synthetic supplements’ mitochondrial sabotage is plunging into my unfiltered work isn’t optional; it’s the razor-edged key to shattering the illusions of centralized science. Simplify it, and you neuter its potency, rendering the revelation too bland to upend the entrenched paradigm of reductive biology that ignores entropy’s quantum dance. If you feel lost it is because I am teaching the basics in an ancient science the paradigm is trying to bury.

Therefore, my prose will stay sharp, labyrinthine, demanding your unflinching gaze on every fractal detail, because science isn’t a tidy gospel, it’s a frayed tapestry of uncertainties, riddled with deliberate loose threads awaiting your weave into the grand quilt of interconnected truths down the line. Attempt to parrot or distill it, and you’ll stumble like an infant gurgling nonsense in the shadow of a master linguist: humbled, yet transformed, if you persist. Only through this rigorous immersion will you decode why modernity’s “advances” accelerate our entropic unraveling and arm yourself to reclaim sovereignty over your own energy flow. I apoligize if you do not like it, but Nature made the rules and she gives two shits about your opinion on this topic.

Those who remain silent when they are faced a new truth are not authentic MDs. The are centralized pharmaceutical terrorists who have blood on their hands from the largest genocide in history. They are the soldiers Rockefeller medicine relies upon to wage the battle against humanity.

https://www.nature.com/articles/s41586-021-03345-1

https://x.com/DrJackKruse/status/1972370998373818821

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

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

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

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

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

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

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

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

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

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

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

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

THE CASE OF INDIA

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

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

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

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

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

SUMMARY

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

Topology → Connection → Time Delay → Emission → Memory.

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

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

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

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

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

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

CITES

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

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

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

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

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

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

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

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

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

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

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

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

HOW DOES THE STORY OF OUR RBCs FIT THIS NARRATIVE?

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

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

1. Blood as a Biophoton Source:

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

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

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

3. Link to Heme Proteins and Regenerative Currents:

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

4. Connection to Deuterium and Biophotons:

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

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

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

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

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

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

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

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

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

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

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

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

Normoxic Earth: Haplotype Divergence and Blood’s Vulnerability

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

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

Decentralized Thesis Framework

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

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

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

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

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

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

Deuterium Depletion as a Cancer Therapy due to LIGHT STRESS

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

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

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

HOW DDW AND UPEs LINK IN DECENTRALIZED MEDICINE

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

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

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

SUMMARY

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

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

CITES

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

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