You see what Dr. Grimm sees in this paper, but what do I see in this paper?

This answers, definitively the question I posed to Huberman on the Tetragrammaton podcast, that the KT event drove internalization of melanin in eutherian mammals but not so much in birds. Perioxisomes burn fat and release UPEs. See the slide below in #7 and 18. That is the real story here. Light sculpted many changes with a rejection of chromophores in eutherians mammals and push for endothermy that lead to optimaization of the leptin melanocortin pathways.

Expanded Biophoton Sources: Explosion Post K-T

My list of 20 intracellular biophoton sources (e.g., NADH/NADPH, ROS, mitochondrial chain, melanin) shows an "explosion" post K-T, driven by adaptations like mitochondrial/peroxisomal amplification and melanocortin internalization.

This Fits ideally into my photobiolelectric thesis. Post K-T event we had a surge of changes that lead to more UPE creation: Reduced external UV forced internal UPE reliance, with sources like peroxisomal oxidation adding to mitochondrial ROS.

This ties to leptin-melanocortin (e.g., melanin in pigment cells emitting UPEs), myelin (membrane potential changes triggering UPEs), and quantum endothermy (IR as biophotons structuring water). The list expands our UPE narrative: post K-T, mammals/birds amplified endogenous light for signaling, reducing entropy via Shannon's theorem, enabling complex behaviors and longevity (e.g., human fur loss for more UV-to-UPE conversion). I see targets that others do not even know are there.Image
2. What were the only two animals that made is past the 5th extinction? Therapod dinosaurs became birds and eutherian mammals became humans.

Differences as Adaptations:

Birds' higher temperature/metabolic rate suits flight, while mammals' BAT-focused NST (with peroxisome augmentation) emphasized grounded endurance underground.

The unappreciated metric, quantum-tuned endothermy, directly affected endogenous water chemistry in cells, as IR from both mitochondria/peroxisomes structures cytoplasmic water, enhancing coherence for UPE signaling. This was a critical step in evolutionary history of the mammals post KT.Image
3. What was the key in eutherian mammals? Innovating a placenta from HERV retrotransposons to build a placenta that had nuclear weapon capability to build complex life because the placenta are the major way eutherians make UPEs. That should raise the question in your mind, what drove placenta; growth in eutherians? My Brain Gut series covered that 15 years ago.
4. After my Factor X webinar which discussed the KT event, people learned that the currency of survival for all eutherian mammals was a new biologic strategy to speed up DNA expression to adapt more quickly to the environment. UPEs are how they accomplished this task.

The reasons eutherian mammals survived is because they use a placenta to birth their young. There is now strong evidence from molecular biology that the genes that coded for the evolution of the placenta were heavily selected for after the K-T event.

How do we know this?

The first mammals were rather old in an evolutionary scale, about 210 x 10 to the 6th years before the present time (YBP). These early mammals (such as multituberculates) were small, furry, egg-laying, monotreme-like insect predators. They were present prior to the advent of the dinosaurs, but became extinct about 35 x 10 to the 6th YBP.

We know nothing about their molecular genomes, but what we do know, is that two other mammalian lines developed from them directly, the marsupials and the eutharian placentals. Humans are in the later class.

How do we know placenta were heavily selected by a post K-T world? Well, the marsupials are only found in the southern hemisphere with the few exceptions. This fits perfectly with how Factor X occurred 66 million years ago as well as I laid out in my Webinar. Moreover, the placental mammals were far more successful because they radiated over 2000 genera, to about only 140 genera in the marsupial clade.

Most of the surviving species left on the land of this planet is due to that formative moment in evolution. This is a big step in knowing who we really are and how we are built. Factor X (KT Event) is huge history story one must know for any mammal that evolved after it to explain why biology is what it is.

How does viral marketing, CT, Factor X, and CT-6 all come together for Homo’s solution?

Here is the most important fact in all of mammalian evolution in my opinion that is not talked about enough. With these placental mammals, we see clear and compelling patterns of acquisition of genetic parasitic elements in their genomes, mainly in the context of retroviruses like LINES, SINES, and ERVS.

After K-T the best source of food was located in the deep polar seas with its huge collection of marine life and cauldron of viral particles as we covered in Brain Gut 2. The predominate macronutrient in the sea is seafood/microalgae.

This means that all the animals left on our planet at some point after the K-T event would of had their food supply mostly tied to the ocean as some point.

It was also bitter cold for many years after a sudden global event like K-T impact. This induced PPAR and mitochondria adaptation of quantum endothermy.

What would life do in this case like this? It would have to evolve to that environment rapidly and that is precisely what happened to our deepest ancestors by using viral marketing as laid out in Brain Gut 2.

That program is wired into the neural structures of every surviving animal left on the planet. This was my thought process when I was thinking about finding the Ancient Pathway in the mammalian brain I laid out in CT-6 blog post. I think it is no coincidence that eutherian mammals 66 million years ago and modern man 13,000 years ago had to navigate the same freezing environment and survive. Clearly, this ancient program was wired into the mammalian nervous system for a deep evolutionary reason.

Let us now fast forward to 2.6 million years ago where our recent ancestors come from, the transitional apes. I have already showed you in Parts 1-3 of the Brain gut series that primates and humans use massive amounts of these transposable genetic elements to create new genes to adapt quickly by using UPEs as their fuel source to complete the task.

Evolution uses a fractal design where form always meets function, of course, and we did the very same thing again in our speciation as life did after the K-T event.Image
5. There is now an abundance of evidence that during embryogenesis and organogenesis, the development of the human placenta is supported by histotrophic nutrition secreted from endometrial glands rather than maternal blood. This means that circadian clock mismanagent of the uterus is one of the keys in creating transgenerational epigenetic diseases. See the slide. These secretions provide a plentiful supply of glucose, lipids, glycoproteins and growth factors that stimulate rapid proliferation and differentiation of the villous trophoblast.

I have already showed you in Parts 1-3 of the Brain gut series that primates and humans use massive amounts of these transposable genetic elements to create new genes to adapt quickly by using UPEs as their fuel source to complete the task of editting out ill fitting nuclear DNA damage to create a new life. The placenta is the ultimate organ in the photorepair process. Evolution uses a fractal design where form always meets function, of course, and we did the very same thing again in our speciation as life did after the K-T event with the eutherian placenta leading the way. Light has always sculpted life this way. UPEs are the light that completes that task.Image
6. Just how important is keeping the lining of the uterus clean from circadian damage or from spike protein infiltration? It determines more about your kid than your DNA does because it makes the UPEs that sculpt the nuclear genes that comprimise your kid.

The human placenta is unique in many ways. It is the first and the largest fetal organ to develop and during early pregnancy performs the functions of diverse organ systems while these differentiate and mature in utero. Furthermore, the placenta undergoes major changes in its own structure and function during gestation while providing constant support for the growing fetus.
Immunologically, it is interposed between two genetically related, but different, individuals, the only situation in mammals where this is tolerated.Image
7. Recent advances in fields as diverse as molecular phylogenetics, genomic imprinting and medical imaging have revolutionized our understanding of the evolution and physiology of the organ, challenging many dogmas held since the nineteenth and twentieth centuries.

At the same time, it has become apparent that the influence of the placenta extends beyond the embryonic/fetal period, and that its functions lay the foundation for life-long health of both the offspring and mother.

Thus, aberrant placentation not only has immediate consequences for the outcome of a pregnancy, but also predisposes the offspring to metabolic, cardiovascular and neuropsychiatric disorders and certain cancers in adult life due to structural and epigenetic changes in organ systems. These findings have demonstrated that abnormal placentation has its pathophysiological roots in the earliest stages of development from the time of implantation onwards, and possibly, as recent evidence suggests, even in the preparation of the uterus preconceptionally. THAT IS HOW POWERFUL THE UPE LIGHT OF THE PLACENTA IS.Image
8. What else do we need to build a human brain when the placenta is optimized?

a. Iodine from the marine chain

b. Iron for heme protein construction to product us from an oxygen halocaust

c. A placenta that is capable of creating a massive fat furnace to fuel to release STAR like UPEs that has the perfect mix of 03 DHA to 06 EPA to make the initial neural framework manifest inside the cranium.

d. Lots of oxygen to complete the desaturation converting shorter chain to long chain PUFA’s: DHA requires 6 O2 molecules. This is why previous to the Cambrian explosion we have no ‘big brained’ animals in the fossil record. We had no oxygen to fuel a brain’s growth. When O2 showed up life exploded.

e. Efficient mitochondria carry out the oxidative metabolism and lots of them in the brain.

f. Phospholipids and the special chemistry of lipids in aqueous milieu (brain and spinal cord sit in a bag of CSF fluid) to create more unique UPE spectra to build things never seen in evolutionary history before.

g. Cell membranes respond to diet, temperature and to pressure changes epigenetically. Since humans are homeothermic, our neural lipid epigenetic variables are diet and environment dependent. These features allow biochemistry to specifically affect the acyl groups on our lipid layers in the brain for optimal cell signaling.

You might be a great biochemist or organic chemist but if you do not know neural biochemistry you might not be aware of just how much you do not know.

Proteins receptors are inserted in these special lipids to signal cells chemically and electrically. This means lipid rafts in the CNS of man have to contain unique proteins have to be multidimensional in configuration and must thermodynamically matched to the lipids in our membranes. DHA is that “magic lipid” that does all of these functions and it is why it has not been replaced one time in the evolution of brains since the Cambrian explosion. You don’t find that information in fossils or in bones on the land.Image
Image
Image
Image
9. It has long been known that the placenta is different from other human organs. In one to two per cent of pregnancies, some placental cells have a different number of chromosomes to cells in the fetus which is normally considered a genetic flaw in centralized biology that could be fatal to the fetus, but with which the placenta often functions reasonably normally.

Despite the placenta genetic robustness, problems with the placenta are a major cause of harm to the mother and unborn child, such as growth restriction or even stillbirths. My theory, a photobioleelctric theory of life makes sense of all these pardox to make sense.

Consider the 2021 study where they completed a first high-resolution survey of the genomic architecture of the human placenta. Scientists at the Wellcome Sanger Institute and the University of Cambridge conducted whole genome sequencing of 86 biopsies and 106 microdissections from 42 placentas**, with samples taken from different areas of each organ.

The team discovered that each one of these biopsies was a genetically distinct ‘clonal expansion’ which means a cell population descended from a single common ancestor. This finding indicates a clear parallel between the formation of the human placenta and the development of a cancer. This is exactly what my thesis has laid out on Patreon. Patreon.com/DrJackKruse

Analysis also identified specific patterns of mutation that are commonly found in childhood cancers, such as neuroblastoma and rhabdomyosarcoma, with an even higher number of these mutations in the placenta than in the cancers themselves. This peels back how these cancers form via transgenerational epigenetic defects in mom and dad.
10. This thread teaches you an in depth lesson on how the leptin melanocortin pathways evolved from our integuments to our interiors.

Chromatophores, common in pre-K-T reptiles and early mammals, were energetically expensive in a low-UV world post asteroid impact.

Eutherians streamlined to melanocytes, conserving energy for thermogenesis and prioritizing survival over spectacle. This aligned with post-K-T food shifts to marine sources (seafood/algae rich in DHA, iodine, BCAAs), where viral particles in seas provided genetic material for rapid innovation, and the HERV genes build organs like the placenta and hemiflusome to fat burn to create massive UPEs light used to sculpt new eutherians rapidly echoing the "viral marketing" from my Brain Gut series of blogs.

jackkruse.com/brain-gut-3-lo…

• • •

Missing some Tweet in this thread? You can try to force a refresh
 

Keep Current with ☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆 Profile picture

Stay in touch and get notified when new unrolls are available from this author!

Read all threads

This Thread may be Removed Anytime!

PDF

Twitter may remove this content at anytime! Save it as PDF for later use!

Try unrolling a thread yourself!

how to unroll video
  1. Follow @ThreadReaderApp to mention us!

  2. From a Twitter thread mention us with a keyword "unroll"
@threadreaderapp unroll

Practice here first or read more on our help page!

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
Image
Image
Image
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
Image
Image
Image
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

Did Thread Reader help you today?

Support us! We are indie developers!


This site is made by just two indie developers on a laptop doing marketing, support and development! Read more about the story.

Become a Premium Member ($3/month or $30/year) and get exclusive features!

Become Premium

Don't want to be a Premium member but still want to support us?

Make a small donation by buying us coffee ($5) or help with server cost ($10)

Donate via Paypal

Or Donate anonymously using crypto!

Ethereum

0xfe58350B80634f60Fa6Dc149a72b4DFbc17D341E copy

Bitcoin

3ATGMxNzCUFzxpMCHL5sWSt4DVtS8UqXpi copy

Thank you for your support!

Follow Us!

:(