1. Longevity in humans is linked to optimal solar exposure. The reason is simple. This protects the 7 layers of energy generation inside a cell. The more sun human gets the more diseases they can avoid and the #1 risk of most diseases is AGE. Solar exposure effectively makes you younger because it lengthens the TET mechanism inside of cells to improve the HAyflick limit in all cell lines. It is not hard to understand when your perspective is decentralized.Image
2. From an evolutionary point of view, vitamin D and melatonin appeared very early and share functions related to the defense mechanisms of the mammalian powerplant. In the current clinical setting, vitamin D is exclusively associated with phosphocalcic metabolism when it is sulfated and in its reduced state. When it is not sulfated or reduced its role in calcium control is diminished. This usually happens in winter months with mammals when they are in the cold and LDL cholesterol production is upregulated by the light stress response of the POMC gene by a lack of 380nm light. This signal is via neuropsin & ACTH in mammals. When 380 nm light is missing mTOR signaling shifts mammalian biochemistry from anabolic to catabolic. This occurs via lipid raft electrical changes mediated by cholesterol biology and proteins embedded in the mammal's membranes.Image
3. Calcium flows are critical in mitochondrial control because they are a key dopant atom in semiconductive proteins in humans. Meanwhile, melatonin has chronobiological effects and influences the sleep-wake cycle. Scientific evidence, however, has identified new actions of both molecules in different physiological and pathological settings. In centralized science, there is a belief that melatonin and Vitamin D are inversely related to solar exposure. This perspective is wrong. The decentralized idea is both are controlled by the sun because melatonin absorption spectra tell us this is the case. Melatonin's spectra are 224nm & 290nm. This light is never present at night in the environment. The spectra reflect light made internally. Centralized medicine has no idea of this concept.Image
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4. The biosynthetic pathways of vitamin D and melatonin are directly related relative to sun exposure. A deficiency of either of these molecules has been associated with the pathogenesis of cardiovascular diseases, including arterial hypertension, neurodegenerative diseases, sleep disorders, kidney diseases, cancer, psychiatric disorders, bone diseases, metabolic syndrome, and diabetes, among others. During aging, the intake and cutaneous synthesis of vitamin D, as well as the endogenous synthesis of melatonin is remarkably depleted, therefore, producing a state characterized by an increase of oxidative stress, inflammation, and mitochondrial dysfunction. Oxidation = lack of electrons = you cannot absorb solar light. Mitochondria also control the change program of mitochondria apoptosis and autophagy. Apoptosis efficiency is controlled by UV light and autophagy is controlled by IR-A lightImage
5. For example with reference to the two major diseases killing modern humans heart disease and neurodegeneration both neurohormones protect humans from both. Sunlight controls heart disease by lowering APoE, Lpa, and calcium index scores. Neurologic function is protected and extended by sunlight via POMC, VDR, RXR signaling, BDNF, and neurotrophin synthesis. Both molecules are involved in the homeostatic functioning of the mitochondria. Given the presence of specific receptors in the organelle, the antagonism of the renin-angiotensin-aldosterone system (RAAS), the decrease of reactive species of oxygen (ROS), in conjunction with modifications in autophagy and apoptosis, anti-inflammatory properties inter alia, mitochondria clearly have emerged as the final common target for melatonin and vitamin D. ROS is controlled by melanin sheets The primary purpose of these Tweets is to show the non-believers how decentralized medicine elucidates the common molecular mechanisms by which vitamin D and melatonin might share a synergistic effect in the protection of proper mitochondrial functioning.Image
6. The skin is the melaninated sheets of solar panel for the brain to give it more energy from the sun to run the Ferrari engine in our head. This has to be optimized for neurological function. Most modern human disease is linked to a break in this quantum biologic connection.Image
7. The quantum connection between the skin and brain is this. You must become aware that NON-VISUAL PHOTORECEPTION is the key to most diseases in the human heart and in the brain. What links both organs? They are both impotent without cholesterol and light stimulus. How do cholesterol, neuropsin, mTOR, melanin, and vitamins A and D link in this decentralized dance to optimize longevity? Issue one. Taking a starting is among the most ignorant thing one can do when you understand how disordered the centralized paradigm around LDL cholesterol is. Non-VISUAL photoreception controls this entire system in humans. Most of the non-visual photoreceptors are weakly covalently bound to Vitamin A and when they decouple photoreceptors are degraded = biophysical physiology fails. Let's begin. The heart response to strong light on the chest by making adenosine. Adenosign stops all aberrant calcium flows hence why it is on every crash cart for ACLS as part of the algorithm for SVY. Note how this system immediately linked the brain's SCN optical lattice clock via the PER2 gene. This gene controls the biophysics of the lipid rafts that change seasonally. How?Image
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8. BIOPHYSICS 101 OF THE SKIN related to the heart and the liver. Eating cholesterol is of zero consequence to mammals. Creating it in the liver is critical in understanding the biophysics of cholesterol non-visual photoreception. The lipid raft's ability to change in mammals occurs by seasonal light variation and collection via the non-visual photoreceptors via perception on the skin, eyes, and gut. That external light determines the reality the mammal faces. When the solar cycles change so do the lipid rafts. This photoelectric change alters biochemistry in mTOR, PPP, glycolysis, the TCA cycle, and POMC cleavage. When the lipid content changes they induce changes in the semiconductive proteins embedded in them. This changes the physiologic ability. This is why the clock mechanism in mammals is linked to light and temperature. Both signals change to the surfaces of mammals.Image
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9. This change in the skin has massive implications for the circulatory system, arteries, blood, and especially the liver. Most people do not know the deuterium content of blood and the lumen in the gut is also plastic via light and temperature signaling for two reasons. Deuterium has an extra neutron so this heavier atomic mass means more energy is needed to move it. And Deuterium has a different magnetic moment than H+ so this means it reacts differently when the electric signal in mammalian membranes changes.Image
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10. Because semiconductive proteins are embedded in the skin, what type of cholesterol and fatty acids matter to the functioning of VGCCs. Why? Because the lipid rafts are like Morse code for the Vitamin D system in the skin and Vitamin A signal in the opsin system. The rafts alter the functioning of voltage-gated channels that control the photoisomerization step of the conversion of cholesterol to 25D (OH). This chemical has to go to the kidney and/or liver for final conversion to act at target receptors in this system of the mitochondria. Sunlight increases NO and oxygen deliver to mitochondria to alter their function because sunlight controls the oxidation state of Fe and keeps it in the +3 state. This increases the sulfation of all things in the system and it makes them MORE WATER SOLUABLE. APOB and LpA drops and they cease to be an issue. It also thins the blood while lowering calcium flows in the mitochondria. Lowering calcium and raising NO both act to reduce mitochondrial power. What takes over when all this happens to create H+ and oxygen and electrons to run the system? POMC creates melanin and melanin makes all three things massively. This is why NO slows mitochondrial metabolism and lowers BP. Centralized medicine does not understand this wiring diagram in 2023. Their longevity experts are still advocating the use of statins which completely ruin the fidelity of this system. Sulfate platelets and GAGs in the vessel wall are less sticky and there is better laminar flow. This is why we have an epidemic of patients on blood thinners. No one is going outside enough. As a result, clots cause both heart and brain damage. This is why PAD is linked to both diseases. @hubermanlabImage
11. When the electric charge is altered in the skin and the membranes inside of your tissues, your tissues begin to become a net collector of the heavier isotope of hydrogen called deuterium. This occurs in the skin and your liver. Blue light/nnEMF NOT FOUND IN THE SUN CAUSES THIS ISSUES. Melanopsin is the blue light opsin of this nonvisual system. It has its highest density in the brain, arteries, and heart. All places are fed by the blood and why brain and heart diseases are always linked to PAD. This effect implies you cannot make D3 even with equatorial sun. All things centralized medicine is ignorant of.Image
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12. Centralized healthcare's ignorance of the basics of this Tweet thread has led to incalculable errors for public health. I mentioned this to @RickRubin & @hubermanlab when we spoke about Dr. Changs' belief it made 50% of what is in the textbooks obsolete. I am telling you 99.9% is hot garbage. Why? The number one opsin in mammals is MELANOPSIN and we no longer live under the sun. We live inside under LED light that destroys this non-visual photoreceptive circuit. People want to blame glucose and insulin yet, when you look at your blood you see this. Does Nature make mistakes or has centralized medicine ignored a lot of facts they should have been asking questions about? When deuterium is let into the matrix this is what redox shift all biochemical pathways the longevity experts THINK never change. This is why none of them understand mTOR and UCP-2. Those proteins embedded in the lipid rafts or connected to them by the tensegrity system change how they respond. Why does NO fall as we age? Because modern humans live under an alien light. Why do Apo proteins and LpA look like a problem to the PEter Attias of the world? Because none of his patients in NYC or San Diego live in sunlight. If they did their LDL cholesterol would be low and their HDL would be high and he would not write a new book telling everyone to take a statin because it is a GOOD plan for longevity. This message is DEAD WRONG.Image
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13. Because ideas like his are allowed to be considered expert opinion, that is why this information has been kept int he shadows by big pharma and big food. I promise you this is why all of you do not know it either. Cholesterol is another nonvisual photoreceptor of man that absorbs best in the UV range. When it is sulfated it's absorption spectra is in the 190-350nm range. When it's in its LDL it absorbs at 500-600nm (winter/blue light). For example, if you have the wrong type of cholesterol in your skin when the sun is strong you won't be able to make Vitamin D at all even at the equator. This explains why people who live indoors and work in offices all have high cholesterol. It also means they are all collecting deuterium in their systems instead of H+. Since your mito matric runs purely on H+ you might see the problem now why heart brain and PAD diseases are all linked. Cholesterol has to be sulfated and in the HDL format because those electrons are needed to absorb the 290-320 nm light. THIS IS THE REDUCED VERSION OF CHOLESTEROL mammals use in spring and summer. If your HDL is low it is because you LIVE MOSTLY IN BLUE LIGHT or nnEMF stress. REMEMBER LIGHT ONLY WORKS WITH ELECTRONS. LDL cholesterol is DEVOID of electrons and sulfur. when you have the wrong type of cholesterol in your skin, the lipid rafts change the voltage gate channel operation of proteins embedded in them to alter function to match the light. When the system is disordered, as it is in most people in California/NYC due to blue light and nnEMF, not even standing on the equator naked will raise your vitamin D level. It is Biophysics 101. Right now this is why people in California and NYC have record rates of LDL cholesterol levels, low vitamin D levels, metabolic syndrome in the liver, and higher rates of skin cancer, colon cancer, and melasma. It is fully explainable when you get how light controls mammals. Keep enjoying your tech and NYC/Cali and prep for a life filled with problems that centralized scheme will wallet biopsy with regularity.Image
14. I mentioned metabolic syndrome and liver disease. My new young protege, @MaxGulhaneMD is very concerned about fatty liver and is convinced that seed oils are behind it as most of the meat heads in carnivores seen are. Time to educate them. Image
15. There is strong class one evidence of a significant relation of 25(OH)D levels with the degree of liver dysfunction, considering that an inverse correlation of 25(OH)D levels with both Child-Pugh score and Model for End-Stage Liver Disease has been reported in the GI literature. In addition, vitamin D deficiency has been shown to increase the risk for overall mortality and infections in patients with cirrhosis. Vitamin D deficiency has been also associated with advanced stages of hepatocellular carcinoma and poor prognosis. Finally, there are studies suggesting that patients with chronic hepatitis C and normal vitamin D levels have higher virological responses to treatment. The sun is always the answer for liver disease = decentralized wisdom 101. It is not the meat diet. That solution is 4 steps below the sun.Image
16. #1 is sunlight ALWAYS. This is why Vitamin D is converted into an active neurohormone in the body. Key proxies to look at for decentralized clinicians = look at blood glucose, LDL cholesterol levels, B12, and any surface skin or colon color changes (endoscopy). If any of them are abnormal your liver is getting pounded and the melanin sheets at the organ of Zuckerkandl are being degraded. Women with melasma and men with melanosis coli you are in trouble and you are collecting deuterium in your liver to grow a fatty liver. Note the date on the paper and ask yourself why is that every time the GI guy sticks the black snake in my rectum he has never told me this if the data is 30 years old? WHY?Image
17. the organ of Zuckerlandl is a chromaffin body derived from the neural crest, loaded with melanin sheets that services the liver, intestines, stomach, pancreas, spleen, gallbladder, kidney, and adrenal medulla and is part of the melanin network that is located at the bifurcation of the aorta or at the origin of the inferior mesenteric artery. This nonvisual photoreceptive array connects with the enterochromaffin cells of the gut that contain massive stores of melanin and aromatic amino acids in the lumen of the gut and in the intestinal wall. Tryptophan is the key time crystal in the gut and the sympathetic nervous system allowing mammals to know precisely where the Earth is in relation to the sun during a revolution cycle on Earth. I wrote a blog on how that works on Patreon. Read it. This allows for the perfect planetary adaptation of the organism to change its skin and gut biology to absorb solar light PROPERLY.Image
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18. This directs the turnover of enterocytes to a 24-48 cycle designed to remove deuterium from the blood and lumen so the liver does not get fatty. This same organ of Zuckerlandl controls your adrenal medulla on the top of your kidney. The POMC gene cleavage releases ACTH. This ACTH allows for high-flux mitochondrial cholesterol trafficking in tissues where POMC is located in post-mitotic cells in adult mammals. It turns out that in the heavily melanated adrenal cortex, this is a specialized function in the mammalian clade. Chromaffin cells migrate to the area adjacent to the sympathetic ganglia with neural crest-derived POMC neurons via the somites migration plan to the adrenal medulla where they're the most abundant type of cells in mammals. The largest extra-adrenal cluster of chromaffin cells in mammals is the organ of Zuckerkandl. Sunlight expands this organ and the adrenal medulla to improve liver and kidney functioning. This is skin 25 D(OH) is converted in both organs to the active format of D3. That vitamin D3 then binds to the VDR in the matrix to slow ECT to stop the need for food to run the ATPase. The 43% of red light in the solar spectrum can spin the ATPase and the liver becomes protected from the deuterium loads. If the load gets in because of bad mammalian ideas, the enterocytes can still slough off every day to protect the liver if the SCN clock is operational because the mammal is in the sun getting UV light. The 380 nm light hitting the RPE informs mTOR to be in its catabolic or anabolic state = which controls the flow of protons into mitochondria in the liver. That is the circle of control of the liver. NOTHING is better for liver diseases than the sun.Image
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19. THE END OF THE LESSON Image
20. If you read my Patreon work on tryptophan’s role as a protein semiconductor and its seasonal role as a time crystal then understanding this post will be easy. Sunlight reduces inflammation by lowering the proton content in the cytosolic water and making sure protons stay inside the mitochondrial matrix. As a result negative charge density builds in the cytosolic regions of a cell. This high net negative charge is known as a high redox state. Persistent chronic inflammation slows the production of serotonin, steering it instead toward self-destructive quinolinic acid production.

This is thought to play a role in psychiatric symptoms associated with chronic inflammation and infections.

Without sunlight melanin is eventually degraded into quinolinic acid. This compound destroys charge density in a cell causing dielectric collapse. It mimics the effect of fluoride deposition in a cell. Sunlight exposure sets the metabolic efficiency of how the pathway operates. The image accurately represents the relative efficiency of the kynurenine pathway when solar redox is optimized.

For instance, the serotonin “branch” flows at a less efficient rate compared to the kynurenine “branch” (~98% vs ~2%). It also points out why exogenous supplementation of melatonin upsets the charge density of tissues like the retina where melanin is located. Here is the key. A lack of sunlight or melanin degradation by any cause leads to a change in how the pathway operates in neuroectoderm in humans. Chronic inflammation results from a lack of sun. It can also happen via hypoxia caused by a myriad of things such as during an infection or an autoimmune disease. Light fundamentally changes the kynurenine pathway.

The part of the pathway that normally synthesizes beneficial molecules slows to a trickle while the floodgates open for the harmful part of the pathway. Why is this?

Well, inflammation:
✅ increases the catalytic activity of enzyme IDO
Making more kynurenine and less serotonin and melatonin

AND

❌ decreases the catalytic activity of KAT
Making less kynurenine acid (protective) and more quinolinic acid (harmful) from melanin degradation. A lack of sun causes melanin degradation via hypoxia. Non native EMF via liberation of Vitamin A from the loose covalent bond is todays major cause of disruptions in this pathway. How does this happen? A lack of sun changes the catalytic efficiency of an enzyme called IDO in the pathway. This changes cytokine signaling which in turn changes the biochemistry of the pathway. Note a lack of sun or excess nnEMF is the key stimuli.
A lack of sun increases thesecytokines increase IDO activity:
✴️ IL-1b
✴️ INFg
✴️ IFNa
✴️ TNFa
✴️ IL-6
✴️ IL-12

While these cytokines decrease KAT activity:
✴️ IL-1b
✴️ INF-g
✴️ TNFa

This is how light changes disease phenotype. Hence, persistent chronic inflammation from a lack of sun or too much nnEMF slows the production of essential neurotransmitters, neurohormones, and neuroprotective substances, steering it instead toward self-destructive processes in neuroectodermal derivatives in mammals

In humans we have extra neuroectoderm to protect in our frontal lobes. That photonic switch is in the habenular nucleus. When melanin is degraded in this pathway all he’ll breaks loose in executive function. These alterations eventually lead to the disruption of limbic and paralimbic brain circuits, compromising emotional functioning. This explains how light plays the leading role in the development of psychiatric symptoms associated with altered solar redox and many mitochondrial illnesses. It’s no longer a mystery. You just need to read the literature and connect the dots to POMC biology and melanin production and degradation.Image
21. Please read the literature on BDNF. It is also increased by solar exposure and destroyed by nnEMF and build up of quinolinic acid from melanin degradation of the non visual photoreceptor system in neuroectodermal derivatives. Implications??
22. BDNF in humans is on chromosome 11.
BDNF: Brain-Derived Neurotrophic Factor
BDNF is paramount in the growth, development, and maintenance of neurons in the brain. It is linked to solar exposure via WNT signaling embryo logically. Recall that the Leptin melanocortin pathway controls fecundity and development in the human embryo.
It works to help existing neurons survive and impacts the growth and differentiation of new neurons and synapses. One can only imagine the consequences. Just think about autism for a moment and why it’s exploding since 1940 when humans began using light to communicate in tech gear.
Mutation or changes in expression could result in neurological, mood, and cognitive disorders.

It would be a terrible thing if somehow this mechanism was mutated in some way, by say, the presence of DNA plasmid contamination, that also carries an SV40 promoter, poor solar exposure, alien light, or as found in other instances, gene expression might have been acted upon by the pure presence of linear DNA plasmid pieces; don’t you think. Few are making these connections

******
There are 8 BDNF promoters. Never forget sunlight increases all of them properly.Image
23. You might want to read this paper after you read my Quantum engineering #45 blog on the link to melanin melanopsin and melatonin to autism. Why was I warning my tribe about the mRNA technology before 2020? I laid that story out to RFK Jr and Rick Rubin in 2023 Tetragrammaton podcast. Now look at this paper. I’ve known about these links for thirty years. link.springer.com/article/10.100…
24. Everything that needs to be said has already been said by me in the past (decentralized wisdom). But since too few of you were listening to me over the last 20 years (centralized fools), everything must be said again.

This is how you show centralized functional MDs they do not know shit about real decentralized health. Taking Vitamin D supplements is equivalent to going to the gym and asking a trainer to do push ups for you and you thinking youre getting the benefit from his work. Centralized psychosis is what Dr. Eric Berg shills. I teach people decentralized WISDOM and extinguish centralized ideas from medicine.

What do I sell people? Wisdom on how to maximize time. How much time can I reserve for you?

Your time and health are subject to how you value your decisions around light, water, and magnetism. That is what I am expert in teaching you. Nothing more, nothing less. I must govern you by using the lessons of the clock, and I must not allow you to governed by man's light which ruins all your clocks.

THE DECENTRALIZED TRUTH BOMB IS: Your future is created by what you do right now with my wisdom, not tomorrow. For my students, most of who have been ruined by centralization, tomorrow is often their busiest day of the week.

This is why never execute my lessons. If you give me some time to solve your problem, I will spend most of this time sharpening my thoughts before delivering you, your bounty. Don’t be fooled by life. There are only as many days in the year as you make use of. Centralized people only get a week’s value out of a year while decentralized thinkers gets a full year’s value out of a week.Image
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More from @DrJackKruse

Sep 13
Deuterium's Quantum Dual Nature: Bosons vs. Fermions

At the core is deuterium (D or ²H), an isotope of hydrogen with an extra neutron. My blog explains its particle statistics: Nucleus: A boson (spin 1, even parity), following Bose-Einstein statistics. Bosons can occupy the same quantum state, enabling phenomena like superfluidity or Bose-Einstein condensates at low temperatures.

Atom: A fermion (half-integer spin, like 1/2 or 3/2 ħ when combined with an electron), obeying Fermi-Dirac statistics and the Pauli exclusion principle. This makes deuterium atoms behave like "individualists" that can't pile up in the same state. This is why biology is racist against their use in mitochondria. The raise energy resistance.

Molecule (D₂): A boson again, due to symmetric nuclear spins in the ground state. It forms antisymmetric (para-deuterium, spin 0 or 2 ħ, even L) and symmetric (ortho-deuterium, spin 1 ħ, odd L) states.

This contrasts with ordinary hydrogen (H₂), a fermion in its para form (spin 0) and boson in ortho (spin 1), leading to different behaviors at low temperatures. Cooling deuterium near absolute zero produces pure ortho-deuterium with residual spin-2 fractions that can't be fully removed, unlike hydrogen's para form with zero angular momentum.

The takeaway: Deuterium's bosonic tendencies make cold D₂ act like a collective fluid (Bose-Einstein-like), while H₂ follows fermionic exclusion. This affects heat capacities, neutron interactions, and low-energy systems—relevant for fusion, cryogenics, and, as we'll see, biology------> All covered here. optimalklubs.com/kruse-for-dumm…
2. Biochemical Implications: Hydrogen Isotopes in Melanin and Metabolic Pathways

The diagram links this to biology, showing a pathway from acetyl-CoA (a ketone precursor) through melanin dissociation, involving clock genes, sunlight, and electromagnetic spectra. Key points:Oxygen (O₂) from NADP⁺/NADPH cycles feeds into tryptophan hydroxylation, producing intermediates like 5-hydroxytryptophan (5-HTP) and 5-hydroxytryptamine (5-HT, serotonin).

Hydrogen ions (H⁺) are central, explicitly noted as "THIS HYDROGEN CAN BE H+ or D." Protons or deuterons from the pentose phosphate pathway (PPP) influence steps like aromatic L-amino acid decarboxylase, leading to glucogenic amino acids (e.g., alanine) or neurotransmitters.

Deuterium's heavier mass (twice hydrogen's) slows kinetic reactions (kinetic isotope effect), disrupting enzyme kinetics, and the dielectric constant of the metabolic pathways altering UPE function, mitochondrial function, and water structuring in cells. The diagram implies sunlight-driven melanin creates a "plasma" for harvesting electromagnetic energy, with H/D isotopes affecting unique codes in water and biomolecules.Image
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3. Connection to deuterium's physics: In biological "condensates" (e.g., exclusion zone water around proteins), bosonic deuterium has to enable collective behaviors, like enhanced proton tunneling or spin-dependent reactions.

This fully explains why deuterium depletion (e.g., via diet) is UNDERexplored in health contexts—high deuterium foods must hinder fermionic electron flows in mitochondria, while low levels promote bosonic fluidity. This is the basis of low energy resistance and high energy resistance.

Here's how this idea flows:
Low éR = Efficiency and Flow: In healthy states, like during deep sleep or a good workout done in sunlight with proper recovery, éR is dialed down. Energy transforms smoothly, think laminar flow in a river, minimal turbulence. Your cells rebuild, adapt, and thrive. Physics analogy: It's like a superconductor with near-zero resistance, letting current (or bioenergy) zip through without loss.

High éR = Stress and Stagnation: Push too hard in a blue lit gym with nnEMF in your ears, via light stress or chronic stress of any type, poor diet, use of supplements, or disease states, and éR builds up like traffic jams in a circuit. Energy dissipates as heat, damage, or inflammation, accelerating entropy at the molecular level. This links to aging (those "hallmarks" like genomic instability) and diseases (e.g., mitochondrial disorders causing brain fog and exhaustion).

Biology tie-in: It's why exercise feels good in sunlight in moderation but wrecks you if overdone under blue light in agym it is because éR rises, signaling "back off and recover." Blue light allows deuterium to flow into the mitochondria and the KIE takes over.Image
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Read 7 tweets
Sep 10
The retina thins from the effect of man-made light and a lack of sunlight, and then your risk of Frontotemporal dementia rises. The OCT test is the best screening test for FTD. We have familial and mtDNA FTD.

The retina acts as a ‘window to the brain," and that window changes the photolithography of the retinal cells. When the light is not optimal, the retina thins and the brain degenerates. Retinal degeneration has been detectable in mutation carriers prior to the onset of cognitive symptoms, establishing retinal thinning as one of the earliest observable signs of familial (frontotemporal dementia).

nnEMF and a lack of sun lead to neural degeneration, which is primarily driven by the abnormal accumulation of misfolded proteins within neurons. Light controls the confirmation bending of proteins. The DNA code controls the AA sequence and secondary bending, but quantum processing determines tertiary and quaternary bending by UPE transformation in cells. The most common protein abnormality in FTD is the tau protein, also known as TDP-43. These protein aggregates damage and kill nerve cells, leading to brain atrophy (shrinkage) and the resulting behavioral, personality, language, and movement problems characteristic of FTD. I believe this protein also thins the retina. Light is the offender.

Blue light increases RBC turnover in the retina and changes the oxidation state of iron, and this affects the synthesis of new heme proteins in the retina and brain. Oxidative stress is a key trigger in this disease because it increases peroxide production (ROS), which alters the UPE signature of cells in the construction of the heme proteins, which changes the photolithography inside the retina and brain. Changing the photolithography = altered protein folding via the Golgi apparatus and RER. TDP-43 is a biomarker of redox imbalance in FTD-related UPEs.

The path of energy in life, based on the evidence we have as a species now, is that Optical photonics began 13.8 billion years ago. The photoelectric effect was born from the rudimentary physics present in the early universe. Photonics precedes all chemistry of all types. Functional medicine does not realize this or teach it. Molecules were and are innovated by redox chemistry, and each one has an electromagnetic barcode to program its possible states around the star it evolved in.

The TDP-43 molecule is codified by light in its absorption and emission spectra. This links it to aberrant UPE production in the central retinal pathways, as blue light increases heme turnover to alter its biophotonic signal. Look at all the places a UPE can be made from in a cell to cause this disease on the slide. You'll also see that light carries spin information that can create this disease.

Where there is a change in matter (TDP-43), there must also be a change in atomic molecular geometry in that tissue. Where normal cellular geometry ceases to exist, we will find light as the key agent of change. When both exist in simultaneity, you'd better understand Fermat's law and the photoelectric effect to understand what a disease really is. Right now, in centralized ophthalmology, none of them do. See Bruce Willis.

THE BIOPHYSICAL CODA of FTD: When Turing realized morphology in all living things had a photonic timeline in Nature, he wrote a key paper on morphogenesis. Light signaling predates biochemistry and molecular creation from redox chemistry. This paper suggested that a system of chemical substances, called morphogens, could react together as a symphony does and subsequently diffuse their electromagnetic, electrochemical, and photobiolelectric information through a tissue to sculpt it, changing its morphology without using the nuclear genome.

Turing stated in 1951 that this set of circumstances is adequate to account for the main phenomena of morphogenesis. In such a dissipative system, although the cells may originally be quite homogeneous at the embryo stage, this information upload may later develop a pattern or structure in the embryo due to the instability of the homogeneous equilibrium caused by light pollution in the parents' germ line, which is triggered by random disturbances in the tissue. Those random disturbances are UPEs. The random disturbance he hypothesized about turned out not to be random at all. UPEs are created in cells by light AMO interactions via redox chemistry that directs their own sculpting from the nuclear genome. The UPE energy transformation is driven by the mitochondrial genome, which is subject to light in the environment to create UPEs and eventually by reactive chemicals like ROS/RNS inside all cells. Any disease linked to aberrant UPEs will always present as having a spectrum of maladies. FTD has that optical signature. ncbi.nlm.nih.gov/books/NBK55928…Image
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2. The GLP-1 Drug Connection: Weight Loss at a Cost to Your Eyes and Ears

GLP-1 drugs like semaglutide (Ozempic, Wegovy) and liraglutide (Victoza) are prescribed for type 2 diabetes and weight loss, helping millions shed pounds by curbing hunger and stabilizing blood sugar. However, literature suggests that they can affect the eyes and even the inner ear (cochlea), which ties into the light biology disruptions we just discussed.

Effects on the Eyes

These drugs cause rapid weight loss, which triggers fluid shifts and reduced blood volume in the body.📷This can stress the delicate blood vessels in your retina, leading to:
Worsening diabetic retinopathy: In people with diabetes, GLP-1s can make existing eye damage worse, causing blurred vision or macular issues.

Increased risk of vision loss diseases: Studies link them to a doubled risk of neovascular age-related macular degeneration (nAMD), a leading cause of blindness.

There's also a higher chance of non-arteritic anterior ischemic optic neuropathy (NAION), where blood flow to the optic nerve drops, potentially causing sudden vision loss.

Blurred vision and other issues: Common side effects include visual impairment, which can start as early as 10 days after use. While not everyone experiences this (risks are low but real), regular eye exams are recommended for users.

How does this relate to light biology? The fluid shifts and oxidative stress from GLP-1s can amplify ROS production, disrupting UPEs and protein folding in the retina, much like exposure to bad light. This thins the retina, mimicking the early FTD signs, and could raise dementia risk indirectly through disrupted circadian rhythms.

Interestingly, while some research suggests GLP-1s might protect against general dementia by reducing inflammation, their eye effects could counteract that, especially in FTD-prone folks. My TED talk was banned because BigHarma was afraid I was going to obliterate their GLP 1 train by showing the world why they banned stopped the leptin trials early on weight loss.Image
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3. Since the ear also processes sensory info tied to your body's clock, this could feed into broader brain degeneration.

Effects on the Ears (Cochlea)The cochlea, your inner ear's hearing hub, isn't immune. GLP-1s are linked to hearing problems like hearing loss, vertigo, tinnitus (ringing), and eustachian tube dysfunction (feeling of ear fullness).

Rapid weight loss can disrupt fluid balance in the ear, similar to the eyes. Diabetes itself raises hearing loss risk via blood vessel damage, and some GLP-1s (like exendin-4 types) heighten it further. The GLP target in the ear is the stria vascularis.Image
Read 4 tweets
Sep 7
I tried to pull the veil back on the layers of the Deep State and where they are linked and why they are linked. It is a nasty story of deceit and ideological fascism where science was stolen to control modern humans with Light, drugs, and jabs.

The historical links you must know.  Why is Israel so misunderstood? Propaganda is its shield, so you can never know who is really behind it.

It is British Imperialism dressed in drag to protect its ideology of fascism, which is what a Fabian really is.

The billionaires of today are not the architects of Zionism
They’re the actors. Elon. Thiel. Gates.
They run infrastructure, but they don’t own the world.
They were groomed by systems older than corporations.
The real owners?
• BlackRock, Vanguard, BIS — own the assets
• Rockefeller, Rothschild, DuPont — own the timeline
• WEF, CFR, Chatham House, Fabians — write the script
• Think tanks + foundations — enforce ideology
Occult orders + Straussian elites — justify it all as “destiny”
This is not capitalism.
This is a technocratic theocracy—where power is hidden in algorithms, law, debt, and narrative.
They don’t fear elections.
They fear recognition.
They fear you finding out what their plan really is.
Why must we decentralize medicine?
Because it eliminates centralized Rockefeller Medicine from the World.
That is a world where drugs and jabs are used as weapons of control.
Time to wake up and do your diagnosing better today than you did in the past.

x.com/JuanGutiCA714/…
2. True Evil with assorted atrocities most often occurs when the most respectable and intelligent of people fall for it. The wise never do. They sniff out and diagnose the problem of centralization to avoid collateral damage. Be careful who packs your parachutes. Image
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3. What is modern gaslighting of the jab injured really? It is cloaked in pardons and Nobel Prizes given to the architects of the crimes. Image
Read 4 tweets
Sep 4
I started a huge Barista FIRE on the boat it appears with my Bitcoin talks with him every AM. He apparently was quite influential with the young staff and told them all they were working communist hours for communist pay, and when his manager heard it spill over to our morning conversations and how many of the krewe I am Orange pilling, they axed him. He was escorted off the book quickly in Peru, and I never knew it until this AM. Some of his barista folks confirmed it got hot quickly.

What Is the FIRE Movement, and Where Does Barista FIRE Fit In?

FIRE stands for “financial independence, retire early.” The FIRE movement puts forth the idea that becoming work-optional isn’t about reaching a certain retirement age; it’s about having enough money invested that the compound interest gains can sufficiently cover your annual expenses. Bitcoin really changes the mix for young people locked into communist like employee environments.

This is achieved by reaching what is called your FIRE number. A (very) rough calculation of FIRE number is to multiply expected annual expenses when no longer working by 25. This is the amount of retirement savings you’ll want to have ready to tap, but know that performance on investment accounts can vary widely from year to year. A traditional FIRE number is typically well north of $1 million.

There are many people who don’t actually want to stop working and enter full retirement. Instead, they want to downshift to doing more fulfilling work, or they want to be able to work part-time so that they can spend more time pursuing hobbies or passions. In jobs like medicine and cruiseship workers the math works rapidly but for different reasons. So when I explained this to Christopher he seemed to catch fire like I had poured diesel fuel on him. Never thought he'd get canned for it that fast. I guess capitalism is a bad antidote for the communist boat life.Image
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2. The Origins of the FIRE Movement

In 1998, three researchers at Trinity University published the results of a study on retirement savings.

Their projections found that, if an investor had a certain multiple of their income saved up and withdrew 4% or less of their nest egg each year, their chances of depleting their savings in a 30-year period were zero. I re-did this calculation in 2013 and added Bitcoin CAGR to the mix, and the results were more stunning. That is when I realized I could bail on centralized medicine and began teaching this method to my MD clients. Sadly, most of them crumbled because they could not fathom walking away from their jobs because of their programming. The Trinity research group was based on rates of return since the invention of the 401(k) and other tax-advantaged retirement accounts, and later became known as the "Trinity study."Image
3. The results of the Trinity study were first published in the American Association of Individual Investors Journal in 1998.

This research led to my reframe: If you could grow your nest egg large enough that the interest alone covered annual expenses and other medical expenses, most or even all of your principal would be protecting, preserving your wealth. I tweaked this big time. I realized that the decentralized mitochondrial life could bring medical expenses to zero and then I could power up my savings with the Bitcoin CAGR i could make money grow on trees for decades. IT was how I figured out that the one thing killing me, my job, could be eliminated rapidly. I got a huge settlement from a cruise incident related to a paleo meathead, and I yolo'd it into the program, and within a year, I found out this was going to be life-changing.

The Centralized Fiat Retarded Say Money Doesn’t Grow on Trees......but decentralized geniuses know it happens.

If your tree is a large enough nest egg due to the Bitcoin CAGR, it actually does. I began to realize that the traditional retirement age wasn’t dictated by age, but by whether you reach financial independence. Thus, the ORANGE FIRED MD lifestyle was born.

FIRE stands for Financial Independence, Retire Early. Over the years, however, many ORANGE FIRED MDs Savages began to break from core FIRE principles and define FIRE variations that better suit their lifestyle goals. I helped many of my tribe do just that. Membership matters in this tribe.Image
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Read 21 tweets
Aug 26
1. ANSWER: In ALAN contexts, blue light suppresses melatonin, which normally inhibits AVP and cortisol, leading to unchecked vasopressin release during "light stress." This causes a reactive hyponatremia in the posterior pituitary, activating brain osmoreceptors and RAAS, raising blood pressure and stress hormones, which fragment sleep and impair daytime recovery. They also chronically degrade the mitochondria in these neural tracts.Image
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2. Now for the dirty details.
Precise Mechanisms of Sodium Regulation in the Brain and Circulatory SystemSodium (Na+) homeostasis is tightly regulated to maintain osmotic balance, blood pressure, and neuronal function, with disruptions like hyponatremia (serum Na+ <135 mEq/L) directly impacting sleep via arousal, cognitive fog, and fragmented rest. The brain acts as the central sensor and regulator, while the circulatory system executes adjustments through hormonal and renal pathways.

Brain's Role in Sodium Sensing and Control: The hypothalamus, particularly osmoreceptor neurons in the supraoptic and paraventricular nuclei, continuously monitors plasma osmolality and Na+ levels via stretch-sensitive ion channels. When hyponatremia occurs (e.g., from ALAN-induced vasopressin overrelease diluting blood Na+), these neurons trigger arginine vasopressin (AVP, or antidiuretic hormone) secretion from the posterior pituitary.

AVP promotes renal water reabsorption via aquaporin-2 channels in the collecting ducts, conserving water but exacerbating dilutional hyponatremia if unchecked. In the brain, low Na+ also activates the subfornical organ and organum vasculosum of the lamina terminalis (circumventricular organs lacking a blood-brain barrier), which integrate signals from baroreceptors and chemoreceptors to modulate thirst and salt appetite. Chronic hyponatremia impairs neuronal excitability, leading to symptoms like headaches and insomnia, as it alters membrane potentials and synaptic transmission.

Circulatory System Integration with Hormones: In the periphery, low Na+ (hyponatremia) is sensed by renal juxtaglomerular cells, triggering renin release, initiating RAAS: renin converts angiotensinogen to angiotensin I, then II, which stimulates aldosterone from the adrenal cortex to enhance Na+ reabsorption in the distal nephron and potassium excretion. This raises blood pressure to restore volume but can cause nocturnal hypertension, disrupting sleep architecture (e.g., reduced REM). Cortisol, released from the adrenal cortex in response to stress signals (including ALAN and hyponatremia), amplifies this by promoting Na+ retention via mineralocorticoid receptors and enhancing sympathetic activity, increasing heart rate and arousal. Vasopressin interacts with cortisol and RAAS; for instance, AVP potentiates cortisol's effects on water balance, while cortisol feedback inhibits AVP in healthy states, but ALAN disrupts this, leading to unchecked stress responses. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) counterbalance by promoting natriuresis (Na+ excretion) when blood volume rises, but in hyponatremia from SIAD (syndrome of inappropriate antidiuresis), this balance fails, perpetuating low Na+ and sleep disturbances like frequent awakenings.
3. So Emily, what you should do is see the AM sunrise every AM. Drink DDW water and add high-quality salt to the water, and within 2-4 weeks, you will sleep much better. These slides support the tweets, and the last one with the D20 water spectrum really hits the mark. Image
Read 5 tweets
Aug 21
A couple of points: Not all human cells have mtDNA. See adult blood cells. This is a big deal when you consider their absorption spectra. 200-600 nm light with a sharp cut-off. Also, blood still transforms energy into UPEs. And since blood fills 20% of our CO to the CNS, this also has implications. The retina and gut increase their blood flow with light use and feeding. Feeding is a light-based phenomenon since all food webs link back to photosynthesis.

In humans, light stress does not force mitochondria to react exactly the same way as infection (no ATF4 surge, different folate handling), but there are partial overlaps in ISR activation, 1C remodeling, and mtDNA signaling.
This suggests UV light acts more as an external folate depleter for DNA protection/photorepair, while infection is an internal ATF4-orchestrated defense. If environments lack natural light controls (as in modern human life), it should exacerbate mismatches in folate biology. For deeper dives, I'd recommend reviewing the ATF4-UV papers for experimental details.

Folate as a Light-Responsive Switch: My patreon has made this point over and over again, natural folate (not folic acid) is photosensitive, degraded by UVB, and shows seasonal lows in summer (higher at low latitudes, with gender differences showing men have lower levels). This would act as a "switch" for mitochondrial/genome control, linking to melatonin/tryptophan pathways and neurotransmitter synthesis (e.g., serotonin, dopamine). In low-light/artificial blue light environments (e.g., indoors), folate stability increases unnaturally, disrupting methylation/DNA synthesis and contributing to diseases like Alzheimer's, Parkinson's, or diabetes (via melanin quenching loss and superoxide buildup). People with MTHFR and COMT defects are supersensitive to ALAN and a LACK OF SUNLIGHT. This is echoed all throughout my decentralized photo-bioelectric thesis: light refines folate via photosynthesis/food webs, but artificial setups bypass this, leading to transgenerational effects.

No Seasonal/Light Controls: absent natural light cycles (e.g., constant artificial light), retinal/CNS signaling should be expected to dysregulate—e.g., excess folic acid fortification (since 1996 in North America), which overloads 1C pathways, causing cognitive haze, sleep issues, or neural migration problems in lit environments. This photonic effect is completely missed in centralized medicine and is really missed in functional medicine, which pushes for excessive folate use with SNPs. These people need more sun and less ALAN, not drugs.

Black Swan Mitochondriac View: Melanin (from UV-absorbing aromatic amino acids) quenches mitochondrial superoxide, protecting against neurodegeneration. Blue light destroys melanin and heme proteins, amplifying risks from ALAN and a lack of sunlight which aligns perfectly with UV's mitochondrial stress but without the adaptive folate restriction seen in infection.

Now the picture is full. patreon.com/posts/decentra…
2. Why is this tweet important to the jabbed? If you follow the work of @Kevin_McKernan you'll find in his blogs many mentions of pseudouracil and jab injuries. Then you look at my blogs on jab repair, and you'll notice I recommend Tropical relocation as the best risk reduction for the compliant. WHY?

Did you know that in humans, UVR depletes folate in skin and blood, inducing S-phase arrest, affecting uracil misincorporation (frame-shift mutations), and sensitizing apoptosis in keratinocytes. This isn't "damage" but a permissive environment for seasonal phenotypic changes, e.g., increased melanin production to protect folate stores. When you understand the photorepair mechanism, you will see this is how humans can block the DoD and BigHarma death mechanism from uracil replacement induced by the jabs. @MdBreathe None of the COVID experts have this sophistication. They are still pushing detox answers when it is crystal clear that redox biology is the path for the Savage trying to stay alive and away from disease.Image
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3. Individuals with MTHFR C677T (thermolabile variant) are indeed supersensitive to light/folate fluctuations, as the mutation impairs folic acid conversion to 5-MTHF. High folic acid may select for this allele evolutionarily, acting as a "genetic time bomb" by promoting unmetabolized buildup and altering DNA/RNA biology.

People who have this SNP and took the jab have no choice but to move. If they do not, they will be taken out to Taper the Ponzi. This variant requires higher folate for stability, making carriers vulnerable in low-UVR (winter/indoor) settings, where blue light further degrades melanin (a superoxide quencher), exacerbating mitochondrial stress.Image
Read 5 tweets

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