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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Oct 11, 2025 • 13 tweets • 12 min read • Read on X

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What do you know about the Stiles-Crawford effect in a healthy eye? What if I told you this effect is how we sharpen central vision and narrow the periphery of the retina from too much blue light. Would you believe it? Did you know melanopsin has a specific topographic map on a healthy retina? A lesson no has taught you is incoming.

2. All opsins are topologic insulators. You might want to read that threadroll above now to understand topology well.

Topology changes in a cell = geometry change of cristae = UPE change from mitochondria = the optical signal changes in the same tissue altering physiology.

So what happens if you sustain mitochondrial damage in your retina's colony of mitochondria to the Stiles Crawford effect?

What are the implications?

3. The Stiles–Crawford effect (SCE) is the human eye's phenomenon of reduced light sensitivity when light enters the pupil from its periphery compared to the pupil's center. This effect is due to the optical properties of photoreceptors, which act as waveguides and are aligned to channel light towards the fovea, the central point of vision. The SCE makes vision less sensitive to light entering the periphery, thus reducing glare and improving visual clarity. It also keeps a lid on the amount of blue light the periphery the retina gets.

This sharpens vision, makes myopia, glaucoma, cataracts, hyperopia, and AMD almost impossible to get. Makes one resistant to mental illness too. Makes one impervious to diabetic transformations. Makes neurodegeneration rare.

You feeling me yet?

4. Since blue light destroys all photoreceptors what happens to the optics of the eye to the brain?

Mammalian photoreceptors aggregate numerous mitochondria, organelles chiefly for energy production, in the ellipsoid region immediately adjacent to the light-sensitive outer segment to support the high metabolic demands of phototransduction. However, these complex, lipid-rich organelles are also poised to affect light direction, polarization, and passage into the outer segment of the photoreceptor.

Did you know mitochondria in cone photoreceptors act as microlenses to enhance photon delivery and confer directional sensitivity to light? What if I told you that altering the passage of light through the eye is the first step in changing the size of the ventricles of your brain would believe that? Is this how people develop Normal Pressure hydrocephalus?

Is this why people with concussion get immediate photosensitivity as part of the TBI? Yep

5. No one in centralized medicine is making these connections because the labs studying UPEs are looking at bioelectricity instead of UPE transformation and topologic changes happening the eye.

these tightly packed mitochondria “focus” light for entry into the outer segment and that mitochondrial remodeling affects such light concentration. This “microlens”-like feature of cone mitochondria delivers light with an angular dependence that determines retinal photoreceptor damage. That damage then is propagated via electric resistance changes to the rest of the connectome via current flow.

Why are kids becoming more crazy than at any time in human history? This post explains it in detail.

Stack the lessons.

6. In primates and human cells, mitochondria form a reticular network surrounding the nucleus. However, cone photoreceptors of the retina in humans have an abundance of tightly packed mitochondria, which are arranged into an elongated bundle as seen below.

This bundle occupies the ellipsoid, the distal portion of the cone inner segment (IS), immediately proximal to the light-sensitive outer segment (OS).

7. Why has centralized opthalmology failed you?

Generally, they have assumed that such a high density of mitochondria at this unusual location is optimally situated to supply ample adenosine triphosphate (ATP) to support phototransduction in the cone OS because that is what is in the BigHarma medical school curriculum.

They never pushed back on BigHarma education because the evidence for 50 years has shown that photoreceptors ALWAYS rely more on glycolysis than mitochondrial oxidative phosphorylation for their energy needs. In fact the retina uses more Warburg emtabolism than any other organ per volume in humans.

This is another reason why biochemist Seigfried beliefs that Warburg metabolism is pathologic. If he was right every humans should have cancerous retinas. We don't. The reason we use it is because this part of the retina does not get much oxygen from the RBCs.

So this means, there must be another reason that mitochondrial cones receptors in our retina operates this peculiar way, no?

Is this why the RPE is loaded with melanin? Is it an fire wall for this design?

8. The more likely reason is topology and polarization effects. This situation explains why our retina's are built backward. It allows the mitochondria to act as a posterior lens in the eye to improve the signal in light and reduce the noise. This helps craft the perfect UPE signal as an output.

9. The decentralized explanation for this precise arrangement of cone mitochondria lies in their role in shaping the path of light as it passes toward the Outer segment of cones.

The vertebrate retina has an inverted structure with many neural layers through which light must pass before successful detection by the photoreceptor OS.

Thus, there placed substantial evolutionary pressure upon the retina to facilitate light delivery to the OS for detection. This is why you always hear me rail against PhDs touting their data in nocturnal animals and thinking it links to humans.

They say it because they do not understand every tweet in this thread. They are ignorant of evolution, light, and how all the pieces fit together.

For instance, in nocturnal mammals, the compact arrangement of chromatin in rod photoreceptor nuclei is believed to minimize light scatter.

CITE

Solovei, M. Kreysing, C. Lanctôt, S. Kösem, L. Peichl, T. Cremer, J. Guck, B. Joffe, Nuclear architecture of rod photoreceptor cells adapts to vision in mammalian evolution. Cell 137, 356–368 (2009).

In addition, Müller glia, support cells that axially span the retina from its inner surface to the base of the photoreceptor IS, have been shown to have optical fiber–like light guidance properties. I told people this in my Vermont 2018 talk and showed them a cover of a journal that showed this relationship. Note the dates on the cites below.

CITES

1. K. Franze, J. Grosche, S. N. Skatchkov, S. Schinkinger, C. Foja, D. Schild, O. Uckermann, K. Travis, A. Reichenbach, J. Guck, Müller cells are living optical fibers in the vertebrate retina. Proc. Natl. Acad. Sci. U.S.A. 104, 8287–8292 (2007).

2.S. Agte, S. Junek, S. Matthias, E. Ulbricht, I. Erdmann, A. Wurm, D. Schild, J. A. Käs, A. Reichenbach, Müller glial cell-provided cellular light guidance through the vital guinea-pig retina. Biophys. J. 101, 2611–2619 (2011).

3. A. M. Labin, S. K. Safuri, E. N. Ribak, I. Perlman, Müller cells separate between wavelengths to improve day vision with minimal effect upon night vision. Nat. Commun. 5, 4319 (2014).

This is not a new idea. It was ignored by centralized opthalmology at your peril.

The photoreceptor inner segmentconstitutes the last structure that light must pass through before reaching the OS. There, the SHAPE of photoreceptors and their elevated average refractive index have been recognized for their similarity to the design of miniature dielectric antennas. SHAPE and SIZE = topology effect folks. 2016 they gave a Nobel for it.

You starting to see what they all missed?

10. Where is my Vermont 2018 talk to fact check me?

patreon.com/posts/nourish-…

11. What else did they miss? The UPE story. patreon.com/c/DrJackKruse

12. Here is the Muller Cell paper. pnas.org/doi/10.1073/pn…

The picture of the Muller cells is on the cover of Proceedings of the National Academy of Sciences (PNAS) featured on June 12, 2007, issue of the journal.
The cover illustration by Andreas H. Reichenbach accompanies a study in the issue that found Muller cells act as living optical fibers, guiding light through the vertebrate retina to the photoreceptors. The artwork showing Muller cells as fiber optic cables

The cover shows stylized Muller cells functioning as a high-tech fiber optic plate, a striking visual metaphor for the biological discovery.

The featured article, "Müller cells are living optical fibers in the vertebrate retina," demonstrated that these glial cells, which span the entire thickness of the retina, act as waveguides. This mechanism efficiently transports light to the light-sensitive rods and cones, minimizing scattering and distortion.

The context: This discovery helped explain how the vertebrate eye's "inverted" retinal structure, where light must pass through several layers of cells before reaching photoreceptors, is optimized to prevent image degradation.

13. When these things are all jacked up this is how eye disease like keratoconus, AMD, and cataracts occur. Centralized Opthalmology has no answers for these conditions. patreon.com/posts/decentra…

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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Feb 5

https://x.com/DrJackKruse/status/2019454199256207483

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.

https://x.com/DrJackKruse/status/2019454199256207483

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

☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Jan 31

https://x.com/DrJackKruse/status/2017638218741780967

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.

https://x.com/DrJackKruse/status/2017638218741780967

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.

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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Jan 31

https://x.com/DrJackKruse/status/2016990657450299837

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.

https://x.com/DrJackKruse/status/2016990657450299837

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.

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

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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Jan 29

https://twitter.com/GhostOfStoneyX2/status/2016730195701489736

Plan B in El Salvador is all about the Tether gold play. This is how they want to rescue things for the surveillance state.

https://twitter.com/GhostOfStoneyX2/status/2016730195701489736

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.

https://x.com/DrJackKruse/status/2016961157823688910

3. Learn the lesson.

https://x.com/DrJackKruse/status/2016961157823688910

Read 5 tweets

☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Jan 29

https://twitter.com/DrJackKruse/status/2013641720785686687

1. New lesson today from my forum for the Savages to consider. This tweet below is the primer.

https://twitter.com/DrJackKruse/status/2013641720785686687

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
HsCRP

3. Back round info on U/S: westonaprice.org/health-topics/…

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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

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?

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).

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.

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