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

Feb 5
1. Should we give the 49ers players a free lesson on what the NFL and the team will never expose on their behalf?

We need to explain why the players are getting injured at an amazing pace since 2014 and that sotry begins with the evolution of the SCN in the eye that controls the circadian clock.

The eye clock is the key to the story of their injuries.
2. Today we know that vision and hearing evolved together dating back to the PaxB gene, which is a single gene controlling eye and precursors to hearing (mechanoreceptors) in box jellyfish.

This occurred before independent Pax 2 and Pax 6 genes showed up in primates much later. There are evolutionary connections between eyes and mechanoreceptors of the inner ear to the extent that during evolution are linked to melanin generation in those sense organs.

I told you earlier in the decentralized medicine series on Patreonmelanin was the favored semiconductor of all mammals post KT event.

This story of the 49ers players fits this my thesis well because the entire team is made of mammals who are post KT evovled.

If POMC/melanin is absent for any reason in these players, at any particular body place, for any reason, including nnEMF, it appears human neuroplastiticty allows sensory cells to shift their sensory modalities to an older phylogeny experienced in evolutionary history.

Why is this a big deal for the 49ers players?
3. The SCN is controlled by ipRCGs and is a well known blue light detecotr. The melanopsin phylogeny predates even primate evolution in time.

I think this happens in modern humans because of a loss of information and energy transformation in the embryo due to a lack of POMC or POMC translation in the parents cells and their germ lines that create their child = epigenetic defect planning = childhood diseases not of genetic causes which make up the bulk of childhood disease burdens today.

This means any 49ers players future children will also carry the burden of the 2014 power plant upgrade.
Read 38 tweets
Jan 31
Here is the irony: Attia advice was wrong.

**certain body secretions in people with diabetes often contain higher levels of carbohydrates (specifically glucose, the main simple carb involved) compared to people without diabetes.**. Look it up.

This is primarily due to elevated **blood glucose** levels (hyperglycemia) in diabetes, which can cause glucose to spill over or leak into various secretions when blood levels exceed normal thresholds. Recall Attia never finished his residency. He charges 200K to see him. I’m sure many of his patients would expect him to know the basic of human secretions is based on blood sugar levels

Here's a breakdown by common secretions that have more carbs

-vaginal secretions are high in carbohydrates in diabetic women.

- **Urine** — In uncontrolled or poorly managed diabetes, urine frequently contains significantly more glucose (a condition called **glycosuria** or glucosuria). Normally, healthy kidneys reabsorb nearly all filtered glucose back into the blood, so urine has little to no detectable glucose. When blood glucose exceeds the renal threshold (typically around 160–180 mg/dL), excess glucose appears in the urine. This is a classic sign of diabetes and can be much higher than in non-diabetics (who usually have negligible amounts).

- **Saliva** — Multiple studies show that salivary glucose levels are higher in people with diabetes (both controlled and uncontrolled) compared to non-diabetics. For example, mean salivary glucose is often around 13–14 mg/dL in diabetics versus 4–5 mg/dL in healthy controls. This occurs because high blood glucose increases leakage or diffusion of glucose into salivary secretions.

- **Sweat** — Sweat glucose concentrations are generally low in everyone (often 1–2% of blood levels), but research shows a strong correlation between sweat and blood glucose. In diabetics with higher blood glucose, sweat glucose is correspondingly elevated (e.g., potentially 0.3 mmol/L or more when blood is very high, versus lower in non-diabetics). This is why sweat is being explored for non-invasive glucose monitoring devices.

- **Tears** — Some evidence suggests tear glucose can also be higher in diabetics and correlates with blood levels, though this is less commonly studied than the others.

In summary, while not all secretions are equally affected and concentrations remain much lower than in blood, **diabetics typically have more glucose (a carbohydrate) in urine, saliva, sweat, and possibly tears** when blood sugar is poorly controlled. This doesn't apply universally to every diabetic at all times (e.g., well-controlled cases may show minimal differences), but it's a well-documented pattern, especially in hyperglycemia. If this relates to a specific health concern, consulting a doctor for personalized testing is recommended.
2. This goes to show you just how uninformed Attia is on the basics. High blood sugar (hyperglycemia) can occur due to various conditions and factors outside of diabetes, potentially leading to similar effects on carbohydrate (primarily glucose) levels in body secretions like vaginal secretions, urine, saliva, sweat, and tears. Physical or emotional stress: Acute stress from illness, infection, injury, trauma, surgery, tech screen abuse, cell phone use triggers the release of hormones like cortisol and epinephrine, which raise blood sugar to provide energy for the "fight or flight" response. High-intensity workouts can cause a short-term spike in blood sugar as the body releases stored glucose for fuel, especially in non-diabetics unaccustomed to such activity. Poor sleep quality from blue light and Earpod use disrupts hormonal balance, leading to insulin resistance and elevated glucose levels. Attia is known to believe that doing 100 push ups limits nnEMF risk. Look it up. He told this to Chris Williamson on a live IG post.
3. What else did Attia miss in his answer to Epstein? Cushing's syndrome: Excess cortisol production (often from adrenal tumors or prolonged steroid use) impairs insulin function and raises blood sugar.

Polycystic ovary syndrome (PCOS): This common hormonal disorder in women causes insulin resistance, leading to chronic hyperglycemia.

Acromegaly: Overproduction of growth hormone from a pituitary tumor reduces insulin sensitivity and elevates glucose.

Other hormonal issues: Conditions like hyperthyroidism or pheochromocytoma (a tumor causing excess catecholamines) can also contribute.
Read 5 tweets
Jan 31
In my decentralized framework, this is exactly how the system is wired. The nipple-areola complex acts as a quantum-optical sensor, and the infant’s saliva is the fiber-optic cable delivering a real-time UPE (ultra-weak photon emission) status report from the child's mitochondria to the mother’s "manufacturing plant."

This isn't just convenience; it is a biophysical "handshake" that ensures the survival of the post Cambrian hardware mammals need to thrive.

1. Saliva as the "Optical Bio-Feed"

Saliva is a highly structured, mineral-rich fluid. In my thesis, it serves as the medium for optical information transfer:
The Child’s Signal: When a calf or child is sick, their internal "optical smog" increases. The VUV (Vacuum Ultraviolet) and chaotic UPEs produced by their congested Complex II are transmitted through the saliva. Congestion usually is due to reverse electron flow or deuterium.
The Mother’s Sensor: The areola is one of the most melanized and innervated tissues in the mammalian body. Melanin here doesn't just protect against the sun; it acts as a broadband transducer like an optical scanner in the grocery store. It "reads" the frequency of the biophotons in the saliva.

2. The Backflow "Optical Loop"

Research into the "infant-led" backflow confirms that when a child suckles, a vacuum is created that pulls saliva back into the mother's mammary ducts.
Information Sensing: The mother’s immune-sensing cells in the ductal walls "listen" to the ROS/RNS signatures and UPE entropy in that saliva.
The Response: If the child’s saliva "shouts" of deuterium congestion at cytochrome two because succinate is elevated  or viral "optical noise," the mother’s brain (via the SCN-hypothalamic oxytocin posterior pituitary pathway) triggers a change in milk composition. She begins to "distill" more NPD1, Iodine, and IgA antibodies into the milk to act as a "quantum reset" for the child’s mitochondria.

3. The "Rotating Mom" Phenomenon (Allomaternal Nursing)
Why do calves or elk rotate moms? In my framework, this is "Frequency Matching":
Metabolic Matching: A calf may instinctively seek a different "frequency" of milk if its own mother’s melanin-metal hardware is jammed (perhaps she spent too much time in a "dirty" environment like inside a barn under fake light).
Information Diversity: By "sampling" different mothers, the young mammal is essentially "crowd sourcing" optical coherence. They are looking for the milk with the lowest deuterium/highest DHA-D3-Iodine ratio to stabilize their own emerging Faraday cage.
Modern humans with nnEMF toxicity who cannot breast feed their children due to a lack of production should be considering what elk do when they are faced with the same problem.  This concept is foreign to humans because they do not observe nature carefully enough.

4. Milk as a "Re-Cambrian-ization" Serum

Mother's milk is the ultimate low-deuterium, high-DHA, solar-coded fuel.
Deuterium Depletion: Milk fat (cream) is naturally low in deuterium, helping the child build a "clean" 14 Angstrom tunneling gap in their developing mitochondria.
Melanocortin Programming: The act of nursing at sunrise/sunset ensures the child’s Leptin-Melanocortin pathway is synced to the mother’s, preventing the "Proterozoic regression" that leads to neolithic disease later in life.
The ranch memories you have are of a Quantum Ecosystem in action. The child’s saliva "tells" the mother's nipple exactly how the child's internal "mercury lamp" (deuterium) is burning. The mother then alters the "Optical Duty Cycle" of her milk to quench the fire.
Does this explain why formula-fed infants (drinking high-deuterium, seed-oil-heavy milk) are essentially being "pushed into the Proterozoic mud" from birth, as they lack this bidirectional optical feedback loop?  Yes, it does but few seem to care about it.

This lesson also has deep information for the diseased breast too. Men can help their women with diseased breasts by kissing their nipples religiously to transfer information to their women about how they feel for them.  This will be highly stimulatory and healing.

Cells and Stars have a lot on common.  When they fail they have mechanisms that feedback on themselves that lead to the possibility of future survival if conditions are met.  In a star when it burns through its fuel source its core gets to iron and the star begins to emit microwaves.  The microwave radiation interacts with the D shell electrons of Fe and it blows up in a super nova so the atoms it creates in this destruction can be recycled to something with more life in the cosmos.  Cells in our body use a similar idea in apoptosis, autophagy, and ferroptosis.

In my decentralized framework, the brain and breast in cancer do not operate in the same fashion regarding IDH protection because their "optical hardware" and evolutionary duty cycles are fundamentally different. Neurons are not epithelium, but breast tissue is.
While the brain relies on IDH mutations from its DHA-rich antenna to create UPEs to work and eventually help create some VUV smog from complex two back up to clean the dirty chemistry in cancer, the breast mitigates oncogenic risk through a different mechanism:

It uses the DHA-Iodine-Melanin triad.

1. The IDH Paradox: Why the Brain Needs It, But the Breast Doesn't

The brain is the ultimate "quantum sensor" that can feedback on itself and it must maintain 24/7 DHA coherence.  DHA allows for this.
The Brain (DHA Antenna): When Complex II jams, the resulting VUV emission from Deuterium threatens to shatter the DHA antenna. The IDH mutation occurs as an emergency "filter" to deplete deuterium and lower the VUV entropy.  DHA, as a PUFA explodes like the star and in its destructions NPD1 and Elovanoids along with UPEs are made which are highly anti-inflammatory.  The released UPEs feed back on IDH and mutate it in such a specific way that the brain is able to make more deuterium depleted water because of this interaction than it could before to help self sustain its survival.  This is how most low grade gliomas begin.  This process does not happen in GBM transformation due to a lack of DHA in the brain.
The Breast (The Glandular Sink): Breast tissue is not a primary "spectrometer" like the brain. Instead of a mutation-driven shunt (IDH), the breast uses Iodine as its primary "quantum ground." In the breast, the "De-Cambrian-ization" of its mitochondria is mitigated by the concentration of iodine in the Ductal-Lobular Units.
2. How the Breast Mitigates Risk: The Iodine Shield
If the brain uses the IDH mutation to "buffer" the VUV smog itsdeuterium squeeze, but the human breast uses Iodine to "quench" the fire in the cytochrome 2 Fe-S clusters that begin the disease from reverse electron flow from cytochrome 2 dysfunction.The Delta-Iodolactone Mechanism: Iodine is required to form iodo-lipids (delta-iodolactone). These act similarly to Bazan’s Elovanoids in the brain, but they are specifically tuned to inhibit the Warburg Effect in glandular tissue.
Melanin & The Nipple: The high concentration of melanin in the areola/nipple is not a "decoration." It is the Optical Port that harvests solar UV/IR to control the metal flux (Cu, Fe) in the underlying breast tissue to make sure the TCA and urea cycle are the primary pathways used to avoid cytochrome 2 congestion and Fenton reactions of Fe-S couples.
The Sink: The breast is designed as a "DHA sink" (for lactation). It mitigates VUV damage by using Melanin and Iodine to sequester the "dirty" Iron noise created from a lack of sun, nnEMF, or polarized light.  nnEMF for the breast is the stimulus that leads to ferrotoptosis destruction of the Fe-S couples and this mimics the process that happens in a star.   When Iodine is missing, the breast cannot "ground" its own self created UPE field, leading to DCIS or invasive carcinoma without the IDH "slow-burn" protection seen in the brain.
3. The Unified "De-Cambrian" Failure
Both cancers represent a Proterozoic Regression, but the "breakdown" follows the tissue's specific metal hierarchy:Brain Cancer (GBM/LGG): A failure of the DHA-VDR-IDH loop. The brain tries to mutate (IDH) to survive the VUV fire.
Breast Cancer: A failure of the Melanin-Iodine-DHA loop. Without Iodine to "buffer" the Iron D-shell electrons, the breast tissue undergoes a rapid phenotypic regression and this is how cancer begins.Image
2. Integration with Melanin and the Sun

The synthesis of both molecules is tied to the Melanin-Metal hardware:
The Sun: UVB/IR input on the skin stimulates the Leptin-Melanocortin pathway. This manages the Copper (Cu) and Manganese (Mn) levels required to build the antioxidant "Mn-SOD shield."

The Translation: Coherent UPE signals (from healthy mitochondria) then tell the cell to cleave the lipids needed for NPD1 or gamma iodolactone
.
The Result: You have a "protected" post Cambrian cell that can use oxygen via the TCA/urea cycle without producing the ionizing VUV UPEs that destroys the genome.

Bazan’s Docosanoids (Brain/Retina): These cleave from DHA to form a "Faraday cage" of 22 carbons. Their purpose is to quench the VUV (Vacuum Ultraviolet) smog emitted by deuterium in the high-density neural environment.Image
3. UPE isn't mere waste; from quantum biology, these photons (or associated fields) may mediate non-local signaling, akin to coherence in radical pairs or bystander effects.

Intensity/spectrum reflect metabolic flux:

Aerobic paths (TCA) produce more ROS/UPE than anaerobic (glycolysis); stress shifts spectra (e.g., UV-linked UPE from glycolysis/peptides). Melanin optimizes by calibrating inputs—solar photons tune metal-ROS-UPE, enabling adaptive switches via redox/epigenetic relays (e.g., NAD+/SIRT1, from the Decentralized Medicine series of blogs on Patreon).

patreon.com/DrJackKruse
Read 7 tweets
Jan 29
Plan B in El Salvador is all about the Tether gold play. This is how they want to rescue things for the surveillance state. Image
2. What is the rescue plan? Remember the famous now deleted Bessent tweet about DJT/Treasury plan to confiscate Bitcoin for the US Bitcoin Reserve? That was updated once the backlash on the tweet went out. Now it is about using Tether to centralize gold as they implode the Dollar and they will confiscate the Gold.

I've argued for 10 years that Bitcoin is a superior form of "trust-minimized" money compared to gold due to the high costs of verifying gold's authenticity.

This is the ability to own and verify an asset without relying on a third party (like a Central bank or Treasury of a government). Historically, gold's "trustless" nature was its greatest strength, but Savages now know this strength has been lost because most gold now sits in centralized vaults. This is why DJT won't let anyone audit Fort Knox. Why audit what you plan to steal?

The Cost of Validation for gold is steep so no one in the USA will want to pay that freight so now we are on the honor system for the Treasury.

Anyone who has owned gold knows that verifying that a gold bar before a sale/audit is real and pure requires specialized equipment, chemical tests, or expensive third-party audits. Because this is so difficult to do, you must have an inherit "trust" the vault or institution holding it for them. + Treasury and Bessent play. What did they do in 2025. They brought their middle man in. Tether. Go check if I am bullshitting you. Tether has bought more gold in the last 18 months than they have bought Bitcoin. Why? They are storing what the thieves in the industrial miliatry surveillence state will take down the road when the retards are sidetracked by circus maximus of some other psy-ops.

Why isn't Tether buying Bitcoin in this case? Anyone with a simple computer or smartphone can instantly verify the entire history and authenticity of their Bitcoin by running a node or using a block explorer. This "validation" is nearly free, making it more decentralized and harder to seize. Tether should be buying T bills but instead is buying Gold Reserves for the Zionist bankers to steal soon. Got it, my Savages.

Bitcoiners should know and remember their history better. This gameplan was used to before in 1933 during the Great Deperession to make it easy for governments to confiscate it.....Remember FDR's EO?

The U.S. did this already with Executive Order 6102 in 1933.

Looting and Centralization are the play. For thousands of years, physical gold was frequently stolen or seized by empires. To protect it, it was eventually moved into highly secure, centralized vaults (like those at the Federal Reserve Bank of New York or the Bank of England under control of the Treasury Head.

If the steal the gold this will tank markets including Bitcoin and then the Treasury will come in an sell gold at astronomical prices to buy Bitcoin at crashed Prices. This is how the Rockefeller and Rothschild Banks plan to do this.

If you know your history this is how the same guys did the scam during the Napoleaonic Wars. They manipulated the market with a psy-ops. In 1812 it was the Battle of Waterloo.

WAKE THE FUCK UP.

If you knew this history would would not be so gullible.Image
Read 5 tweets
Jan 29
1. New lesson today from my forum for the Savages to consider. This tweet below is the primer.
2. Question asked in last 6 weeks: Jack, My breast cancer recurrence has occured in the left auxiliary node. Currently taking Verzenio and tamoxifen. Declined ovarian suppression. Starting Dr. Makis protocol soon.

x.com/drjackkruse/st…

How can I monitor my axillary lymph nodes without using ultrasound, given your concerns about its disruption to quantum coherence in tissues? Especially since my traditional blood tumor markers (CA 15-3 and CA 27.29) have consistently tested negative?

Aside from the tests listed below, are there any additional laboratory studies you recommend prioritizing for tomorrow with Dr. G?

BUN/creatinine ratio
Vitamin D
Liver function
HsCRPImage
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3. Back round info on U/S: westonaprice.org/health-topics/…
Read 15 tweets
Jan 28
1. Today's lesson from my forum is on hyperhydrosis and dysautonimia.

QUESTION: Hi everyone,

Starting this thread to document my improvements or lack thereof, as I get closer to the Equator and further away from nnEMF.

My issue is a form of Dysautonomia driven by a small gain of function mutation in the gene encoding for Nav1.7.

The results is a persistent Na+ leak in the neurons where Nav1.7 is expressed, resulting in hyperexcitability of these neurons.

This hyperexcitability leads to the following symptoms: sympathetic overactivity, hyperhidrosis, gut hypersensitivity, more prone to visceral anxiety, bronchoconstriction, etc.

I know the decentralized medicine perspective says this is an environment problem and not a genetic problem.
But I'll only be able to confirm this once I get my environment right and get rid of these symptoms.

Best,
Alex

How can my neurons help Alex?Image
2. ANSWER:
Relationship Between Hyperhidrosis and Dysautonomia

Hyperhidrosis is frequently recognized as a specific symptom of a broader autonomic dysfunction.

In cases involving the upper neck:

1. Localized Sweating: Irritation of the sympathetic fibers around the vertebral artery often causes sweating or flushing on only one side of the face.
2. Systemic Dysautonomia: If the compression affects the brainstem's ability to regulate the whole body, you might experience more generalized symptoms like heart palpitations, temperature dysregulation, or "drop attacks" (sudden weakness).
3. Other relationships to be explored are found below

A. Vertebrobasilar Insufficiency (VBI): The bony bridge can compress or "kink" the vertebral artery, especially during head rotation. This reduces blood flow to the brainstem, which houses the primary control centers for the autonomic nervous system. This can manifest as dizziness, fainting (syncope), and nausea, all signs of dysautonomia.

B. Barré-Liéou Syndrome: This is a specific cluster of symptoms caused by irritation of the posterior cervical sympathetic chain (the nerves that control "automatic" functions like sweating and heart rate) due to cervical spine issues. Symptoms often include unilateral facial sweating, flushing, blurred vision, and ear ringing (tinnitus). Tinnitus brings the link to melanin dysfunction in the stria medullaris as I have laid out painstakingly on 7 Patreon blogs. It signifies an nnEMF etiology to the Hyperhidrosis and dysautonomia.

C. Trigemino-Autonomic Activation: When the C1 nerve or the vertebral artery is irritated by the ponticulus posticus, the signal is processed in the Trigeminocervical Complex. This can trigger a "reflex" in the autonomic system, leading to craniofacial hyperhidrosis (sweating on the face/forehead), nasal congestion, or eye-watering. This can also be stimulated by demyelination in this region by melanin POMC defects, DHA defects in the central retinal pathways, or polarization toxicity that affects the nerve complex that links these two disease. Both, hyperhidrosis and dysautonomia are located in two distinct but interconnected systems: the Central Autonomic Network (CAN) in the brainstem and the Peripheral Sympathetic Chain in the neck. Hyperhidrosis in this scenario is typically a "positive" neurological phenomenon (overactivity) caused by irritation of the Superior Cervical Sympathetic Ganglion (SCG) and the Periarterial Carotid Plexus (lots of POMC).Image
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3. ANSWER CONTINUES

The broader "dysautonomia" (dizziness, heart rate changes, nausea) stems from a defect in the Lower Brainstem, specifically the Nucleus Tractus Solitarius (NTS) and the Ventrolateral Medulla. These are the primary control centers for blood pressure and heart rate, located in the medulla oblongata of the brainstem. When these brainstem centers are deprived of oxygen-rich blood, like we see when Fe is forced into the +3 state over the +2 state, they fail to regulate the autonomic system correctly. This is why nnEMF can cause this syndrome. This results in the "mismatch" symptoms of dysautonomia, such as postural dizziness, syncope (fainting), or "drop attacks" where the legs suddenly give out.

Because these symptoms are often positional, it is highly recommended to speak with a radiologist specialist about a Digital Motion X-ray (DMX) or a CT Angiogram to see how your vertebral artery behaves when you move your neck.
Read 16 tweets

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