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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Mar 12

https://x.com/DrJackKruse/status/2032072467666088001

You are A MORON. THIS PAPER IS DEVASTING. You do not seem to be able to read the literature nor decipher the implications.

Here is how this data likely fits into and strengthens my arguments in CPC #79 & 80:

1. Moving Beyond "Sarcopenic Obesity"
Standard critiques of GLP-1s focus on the ratio of fat-to-muscle loss. Mythesis can now argue that the problem isn't just the quantity of muscle lost during the weight loss phase, but a fundamental degradation of the quality and regenerative capacity of the remaining tissue. This is a loss of longevity due to Rockefeller time inflation. I’ve successfully moved the goalposts from a simple "muscle loss" argument to a
"regenerative failure" model, which is much harder for critics to dismiss as just a side effect of dieting. My term "drug time inflation" is a powerful way to describe the trade-off. While Ozempic might "buy" time by reducing cardiometabolic risk, the Blau data suggests it "spends" it by functionally aging the muscle’s repair system. What is the most important muscle in humans? The Heart. Damaging it will kill humans sooner. Never forget this effect will be minimized in mice because they are nocturnal and do not have the mitochondrial capacity in their hearts that humans do. I'd expect the fact to be magnified in humans.

2. The Mitochondrial Density Gap
The human heart is the most mitochondrial-dense organ in the body, requiring constant ATP for rhythmic contraction. Unlike mice, which have a much higher heart rate but lower overall mitochondrial "reserve" due to their size and nocturnal metabolic patterns, humans rely on PGE2-mediated repair to maintain cardiac density over decades.

My Argument: If Ozempic blocks PGE2 signaling via the Gerozyme pathway, the human heart cannot "rescue" damaged mitochondria. In humans, this doesn't just lead to "weakness"; it leads to cardiac remodeling and diastolic dysfunction.

3. Nocturnal vs. Diurnal Disconnect
Mice are nocturnal, meaning their repair cycles (melatonin/autophagy) happen during the day in a state of rest. Humans are diurnal.

The Problem: GLP-1 drugs have long half-lives (roughly 7 days for semaglutide). This means the "signal" never turns off. In humans, this persistent signaling may interfere with the circadian rhythm of mitochondrial repair in the heart, an effect that is minimized in short-lived, nocturnal mice who don't have to maintain cardiac tissue for 80+ years.

4. Magnification of Effect
I think my thesis is likely correct that the effect will be magnified in humans. In mice, the study showed an 8% recovery in strength, a catastrophic failure. In a human heart, an 8% recovery rate after minor cellular stress or sub-clinical ischemia is essentially a death sentence or a fast-track to heart failure with preserved ejection fraction (HFpEF).

5. Heteroplasmy in the Myocardium
Because the heart is post-mitotic (the cells don't divide often), it is uniquely susceptible to the heteroplasmy that I mentioned earlier. If the "repair signal" (PGE2) is degraded by the Gerozyme, and the GLP-1 drug is preventing stem cell activation, the human heart is forced to run on "broken engines" (damaged mitochondria) without the ability to replace them.

Summary From My Thesis: I can now argue based on the Blau data that the "Ozempic face" (loss of facial fat/collagen) is just a visual precursor to "Ozempic heart," a state where the most vital muscle in the body is losing its regenerative capacity and accumulating mitochondrial mutations (heteroplasmy) faster than it can repair them. I bet this will get this will get this pre print retracted and this will never be in PEER reviewed literature.

6. Identifying a Specific Biological Mechanism
The study suggests that semaglutide doesn't just "cause" muscle loss via weight loss; it appears to interact with the 15-PGDH (Gerozyme) pathway.

The Problem: Ozempic alone seems to suppress muscle stem cell function (down to 20% in mice), effectively "locking" the repair mechanism. When you realize in humans BCL11A is tied to regeneration and also sits on Chromosome 2 in humans with the glucagon gene. This is a high-level genetic catch from my thesis. I'm pointing to a "hot spot" on Chromosome 2 (2p15-p16) where the Glucagon gene (GCG), the precursor to GLP-1, resides near BCL11A.

The Link: BCL11A is famous for the "fetal-to-adult" hemoglobin switch, but recent research also ties it to regenerative capacity and cell fate.

My Thesis Fit: If GLP-1 drugs over-stimulate pathways linked to this region, they might inadvertently trigger a "switch" that favors immediate metabolic stability over long-term regenerative "fetal-like" plasticity. This supports my idea of a fundamental "locking" of repair and dying early from these drugs.

The Result: This leads to a failure in regeneration and strength recovery (dropping to 8% in the study), suggesting that users might not just be "thinner," but biologically "older" in terms of muscle resilience due to increased heteroplasmy. I said this in my thesis and now I have proof of it.

7. The "Gerozyme" Link
By linking GLP-1s to the 15-PGDH enzyme, my thesis can bridge metabolic health with longevity science. If 15-PGDH degrades PGE2 (the repair signal), then GLP-1 drugs "inadvertently accelerate" a marker of aging in muscle tissue. Human studies have shown that 15-PGDH activity is elevated in aged cardiac tissue, leading to a localized drop in PGE2. Human Relevance: Microarray data from human biopsies shows that 15-PGDH expression increases significantly with age in cardiovascular tissues. The GLP-1 Interaction: If GLP-1 drugs further suppress the "repair signal" (PGE2) while this enzyme is already high, it creates a "perfect storm" for cardiac cell failure. In mice, inhibiting this enzyme reversed diastolic dysfunction and reduced Troponin I (a marker of heart damage). Without this "fix," the damage this is why I anticipate in humans the process is deadly. Fits with the Rockefeller eugenics plan (COVID jab).

My point about the human heart's mitochondrial density is the "smoking gun for the death sentence these drugs are delivering to people today."
Mitochondrial "Lock-out": 15-PGDH inhibition has been shown to restore mitochondrial morphology, turning "large, distended, vacuous" aged mitochondria into "round, compact, healthy" ones.
The Human Penalty: Because humans have higher mitochondrial capacity requirements, the failure to repair these organelles (due to the GLP-1/Gerozyme interaction) will lead to accelerated heteroplasmy in the heart much faster than in the short-lived mouse. The known already published research indicates that 15-PGDH promotes cardiac fibrosis (scarring) via TGF-β1 signaling.

My Thesis Fit: You can argue that the "weight loss" seen on GLP-1s hides a "stiffening" of the heart. While the patient looks "fit" due to the scale, their myocardium is accumulating fibrotic tissue because the PGE2 "anti-fibrotic" shield has been compromised. This means anyone on these drugs needs to have invasive caridac testing to see how the drug has already damaged their hearts. Sounds a lot like the COVID jab if you ask me (myocarditis risk).

Comparison: Mouse vs. Human Cardiac Impact slide below.

Dr. Williams is a danger to patients. The public should be aware he cannot read well, and not comprehend the implications of recent research.

https://x.com/DrJackKruse/status/2032072467666088001

2. A Path to "GLP-1 Plus" Protocols
The most provocative part of this data for my thesis is the "Rescue" effect. By blocking the Gerozyme, the researchers restored muscle mass to 80% and regeneration to 95%. This suggests that the future of GLP-1 therapy might not be a drug, It should be UV-A-NIR light with occasional cold therapy, in a combination therapy approach designed to protect the "regenerative engine" of the body.

SUMMARY

By lowering their function to 20%, the drug essentially creates a "debt" of repair capacity that may only become visible after an injury or as the user ages further. this means doctors will be blinded to this as it happens. So we should expect more sudden heart attacks in humans who use them. My intuition about increased heteroplasmy (the presence of mutated mitochondrial DNA alongside healthy DNA) fits the "Gerozyme" model perfectly. The Mechanism: The Blau Lab found that 15-PGDH degrades PGE2, which is critical for mitochondrial health.
The Proof: When PGE2 is low, mitochondria struggle. This "mitochondrial stress" is a known driver of heteroplasmy. If Ozempic exacerbates this by not addressing the Gerozyme rise, the "thinness" achieved is indeed "biologically older" because the cellular power plants are degrading.
The "GLP-1 Plus" Protocol Rx is: Light & Cold = Leptin Rx.
I’ve pivoted from a pharmaceutical fix to a biophysical one. This aligns with the "Hallmarks of Aging" approach:

UV-A/NIR Light: Near-Infrared (NIR) light is known to stimulate cytochrome c oxidase in mitochondria, potentially mimicking the "rescue" effect of PGE2 by boosting ATP and reducing the ROS (reactive oxygen species) that Gerozymes thrive on.

Cold Therapy: This triggers hormetic stress, which can improve insulin sensitivity and mitochondrial biogenesis via the AMPK/SIRT1 pathway—the same pathway GLP-1s use, but without the stem cell "lockout".
Now you know why they buried the synthetic leptin trials. Now you know why they banned my TED talk on this topic.

3. It seems from the decentralized perspective that Big Harma technology and Big Tech's use of light has reversed engineered and stolen from mammalian biophysics and our cosmological upbringing of ozone filtered light, and hence this has led to a modern devolution and atavism in society.

That should be a profound realization for the public whose brain still operates to think, that moves the conversation from biology into archeo-physics. What I'm describing in my thesis is the Technological Mimicry Trap: the idea that modern "innovation" is actually a simplified, "dead" imitation of the complex, living quantum-coherent systems already perfected by Archean evolution. By reverse-engineering these biological "vows" into silicon, steel, & LED light we create a world that is fundamentally atavistic, designed to drag the highly evolved, coherent human biology back toward a state of disordered, into a world of high-entropy chaos where drugs can be sold to soothe your ills.

1. The Parasitic Nature of Technology
Technology often "steals" a biophysical principle but strips cells of its Isotopic Filter for deuterium and masses and removes Chiral Spin Selectivity of melanin.

The Grid vs. The Vagus: The AC power grid is a "stolen" version of the nervous system’s oscillatory signaling that occured during the Electric Wars by JP Morgan. However, while the Vagus Nerve operates on coherent, p-mode oscillations tuned to the Earth's Schumann resonance, the 60Hz grid is a "heavy" frequency that vibrates at a scale that shatters the IMJ geometry by letting deuterium rush in to destroy the matrix.

The Processor vs. The Mitochondria: A computer chip uses electron flow across junctions, but it lacks the CISS effect linked to melanin. It doesn't care about spin; it only cares about charge. Melanin cares about BOTH. This "crude" movement of electrons generates heat (entropy) which is why computer centers need AC/water cooling, whereas the IMJ's spin-polarized transport generates light (information) and not much heat.

2. Devolution Through "Externalization"
When we externalize a biological function into a gadget, we cause the biological "organ" to atrophy, leading to biological devolution/atavism:

GLP-1 as Externalized Vagal Tone: Using a drug to force satiety is a "stolen" version of the VN-NTS feedback loop. By using an external chemical "wrench" to slow the stomach, the body’s internal deuterium-dumping mechanisms (the exocrine and autonomic circuits) go dormant.

The Atavistic Result: We lose the ability to sense our own isotopic load (deuterium interoception). As a result, we become "biological zombies,"physically present but quantum-topologically disconnected from the fabric of Nature.

3. The Reversal of the "Geometric Vow"
The "Geometric Vow" of the IMJ is a commitment to negentropy (increasing order). Technology, by its current design, enforces a 51% attack on the Vow:

Deuterium Accumulation: Our technological environment (nnEMF, processed foods, blue light) actively prevents the body from "dumping" deuterium.

The Atavistic Shift: This forces the cell into the M1/Cell Danger Response (CDR). The M1 phenotype is a "throwback" to a more primitive, anaerobic, "survival-only" state of existence (Warburg shift). This is the definition of atavism, the return to an ancestral, less-refined biological state in evolutionary history. Your life is lived backward in time but your anatomy is that of the latest versions of mammals. This is the ultimate thermodynamic mismatch.

4. Sovereignty as "Anti-Tech" Biophysics
If technology is "stolen" biophysics, then true health is a reclamation of the original code based in the mammalian blueprint.

The Solar-Terrestrial Interface: Instead of using an external "bio-hack" or drug, sovereignty comes from honoring the Sunrise/Melanin/Cold trinity. These are the original "technologies" that defend the IMJ against the heavy-neutron interference of deuterium from the unfettered electromagnetic spectrum in the Archean world which is now being built by the modern technological world.

Blockchain of Quantum Events: I've mentioned biology as a TIME blockchain. In this sense, the "consensus mechanism" of your health is the coherence of your Vagus Nerve. Every time you align with the natural light-dark cycle, you "mine" a coherent block and time controls the flow of energy in cells well.

Every time you rely on a "stolen" technological proxy (like a GLP-1 agonist), you allow a "fork" in your biological code that leads toward devolution via atavism. You lose time. Loss of time is an inflationary event for longevity. This is why GLP 1 drugs will shorten your life.

I am effectively arguing that we are living in a biophysical plagiarism. We have built a world that mimics our form but destroys our essence.

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@DrJackKruse

Mar 12

Elliot needs to brush up on the embryology of the face.
It is intimately linked to NCC which follow melanopsins lead into the cells that become the the mid face and jaws and they develop based on brain growth. I'm not surprised that a food guru has no clue how melanin from NCC drives this process. LOL.

Elliot seems to be ignorant that NCCs are the progenitors of both melanocytes and much of the craniofacial mesenchyme (e.g., maxilla, mandible via ectomesenchyme), tha tbecome the HUMAN FACE.

This shared origin explains evolutionary yoking of facial shape and pigmentation, as variations in NCC genes (e.g., Pax3/7) affect both melanin density and craniofacial morphology. Sorry to tell you Elliot, but it appears you are dumbass for not knowing how melanin is directly related to your double jaw surgery.

Low maternal UV/IR exposure is a known risk factor reducing melanin synthesis, increasing NCC vulnerability to apoptosis via chaotic UPE (ultra-weak photon emission), as NCCs are sensitive to oxidative stress in the embryo's face. Disruptions in NCC migration/differentiation lead to hypoplasia; e.g., in Waardenburg syndrome, and today it is well known by all except Elliot, that melanin defects correlates with craniofacial anomalies.

pmc.ncbi.nlm.nih.gov/articles/PMC43…

If the "mass" of NCC does not arrive to the correct sites in the embryo, the geometry of the face is never correct and leads to post natal deformities and associated risks.

The DC Current: In optimal health, the embryo generates a bioelectric field which forms primitive version of the Melanin-Water battery created by NNC and CCO function in mitochondria. This field acts as a "GPS" (Galvanotaxis) for NCCs to migrate into the somites and arches that form facial structures.

The Hypoplasia: If this current is weak (due to low maternal redox or nnEMF interference), the NCCs "stall" or "get lost in migration patterns of the embryo." This leads to Maxillary and Mandibular Hypoplasia (receded jaws), which can be the structural root of the Sleep Apnea. The "Mass" simply never arrives at the "Scene of face."

In the decentralized framework, Craniofacial Dysmorphology is a failure of Topological Embryogenesis due to altered DC electric currents that ultimate come from melanin via neural crest cells that have to migrate into the embryonic facial structures to complete its growth. The lack of neural crest cell (NCC) migration is the result of a "cold" or "dark" Bioelectric Field that fails to provide the DC current necessary to guide these cells to their destination.

The NCC "Galvanotaxis" Failure Neural crest cells are the "Exploratory Stem Cells" of the vertebrate body. They migrate from the neural tube to form the Maxilla and Mandible by following a voltage gradient.

The palate/jaw act as a mechanical resonator for brain growth, with receded mandible shrinking the airway, triggering Piezo1 sensors in the brainstem for a "bunker" response in sleep apnea. Bone's piezoelectricity generates DC currents during chewing to hydrate the "vascular pecten" via CCO that is needed to hydrate melanin for the DC current to be optimized in the picoampere range per Becker's work for bone growth.

The palate and jaw influence airway patency; mandibular hypoplasia in PRS or craniosynostosis causes glossoptosis and OSA via mechanical strain.

Piezo1, a mechanosensitive channel, is expressed in the brainstem and responds to stretch/shear stress, potentially linking airway obstruction to respiratory control disruptions in OSA. Bone is piezoelectric, generating DC currents under mechanical load (embryonic movement of tongue or chewing), which stimulates osteogenesis and vascular hydration of NCC derivative via CCO (cytochrome c oxidase) in mitochondria. Low NCC mass from defective maternal/paternal redox in their germlines reduce this "charge," impairing brain vascular support leading to aberrent craniofacial growth. Very embarrassing for you Elliot to be undressed a decade later wearing a T shirt that you never explored.

2. The interplay of NCC (melanin), the VDR and CCO on the IMM regulates mtDNA-driven melatonin production, which is critical for hormonal signaling and bone growth. Embryonic hypoxia disrupts CCO activity, CCO activity changes the DC current from melanin in NCC's and CCO is also capable of reducing melatonin and altering UPE transformation in embryogenesis, thus, damaging mtDNA via ROS, leading to altered developmental patterns in craniosynostosis (suture fusion), scoliosis(vertebral asymmetry), and malocclusions (maxillary/mandibular growth defects). Melanin and Melatonin links these conditions by modulating osteoblast activity and hormonal pathways (e.g., estrogen, IGF-1), while UPE and bioelectric currents (per Becker) provide biophysical signaling mechanisms that coordinate NCC and mesodermal development. VDR dysfunction amplifies these effects by impairing mitochondrial function and calcium signaling, particularly in NCC-derived tissues (maxilla, mandible, sutures) and mesodermal tissues (vertebrae).

Ultra-Weak Photon Emission (UPE):
UPEs, are generated by CCO activity and ROS in the IMM, and serve as a biophysical signaling mechanism, coordinating cellular differentiation and tissue morphogenesis. Reduced UPE due to impaired CCO (e.g., from hypoxia or VDR dysfunction) disrupt:
Suture patency, leading to craniosynostosis.
Vertebral symmetry, contributing to scoliosis.
NCC migration, causing maxillary/mandibular growth defects and malocclusions.
Melatonin, as an antioxidant created by ELF-UV light emission, reduces excessive ROS, helps create Vitamin D and stimulates the VDR on the IMM to affect electron tunneling, which can stabilize UPE signaling. Mitochondrial melatonin deficiency and altered DC currents from the hydration status of CCO on melanin will lead to erratic UPE patterns, disrupting developmental signaling in NCCs and mesodermal cells.....So Elliot you remain a dumbass for a decade now. I hope your oral surgeon is better informed so you do not get a nerve injury from this henious surgery. LOL

3. The "Mitochondriac" Conclusion: You cannot fix a "Proterozoic Face" with a dental appliance or a double jaw surgery, alone. You must restore the Picoampere Current by re-hydrating the Melanin via the Sunrise/Grounding/CT triad to reduce the risk of OSU in the adult. That is the evidence Elliot. You remain a clueless food guru.

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@DrJackKruse

Mar 11

https://x.com/DrJackKruse/status/2031717801803534791

Sleep apnea is the brain protecting itself from nnEMF and blue light. Oxygen is toxin to people with sleep apnea, and it also has a U shaped curve based on GOE evolution, hence why modern humans have it so commonly today since nnEMF mimics dehydration and hypoxia in our environment.
What did the blogs say about exogenous oxygen? Oxygen is quantized to the stoichiometry of the TCA/urea cycle. What if you Kreb's bicycle is dysfunctional because you never see the sunrise?

https://x.com/DrJackKruse/status/2031717801803534791

https://x.com/DrJackKruse/status/2031397014009675916

2. What happens to melanin when pseudohypoxia occurs due to nnEMF = Melanin dehydrates and become massively conductive in cells = Archean legacy = causes damage too all evolution built from the GOE onwards. No one sees it until they do.

https://x.com/DrJackKruse/status/2031397014009675916

3. Sleep apnea is the brain protecting itself from nnEMF and blue light. Oxygen is toxin to people with sleep apnea, and it also has a U shaped curve based on GOE evolution, hence why modern humans have it so commonly today since nnEMF mimics dehydration and hypoxia in our environment.

What happens to melanin when pseudohypoxia occurs due to nnEMF = Melanin dehydrates and become massively conductive in cells = Archean legacy = causes damage too all evolution built from the GOE onwards. No one sees it until they do.
Sleep Apnea is not a respiratory failure, but a Topological Defense Mechanism. The brain induces apnea to limit oxygen entry because, in a decoherent system, oxygen is the "match" that ignites the sPLA2-IIA Supernova to destroy organs.

If your nnEMF/Blue light environment mimics deuterium-induced dehydration, your Inner Mitochondrial Junctions (IMJs) collapse. You lose the CISS (Chiral Induced Spin Selectivity) needed to spin-match oxygen. In this "M1" state, incoming oxygen cannot be reduced cleanly to metabolic water. Instead, it creates a "flood" of Superoxide. The brain senses this oxidative "fire" and stops breathing (Apnea) to prevent the total destruction of the neural mitochondria.
x.com/DrJackKruse/st…

My blogs and my thesis align on apnea being a "Proterozoic" survival strategy. Oxygen is a powerful paramagnetic radical. During the Great Oxidation Event (GOE), life had to evolve the Melanin-Metal shield and D-shell transition metals to "gate" oxygen.

Sleep Apnea is the body's attempt to regress to a Proterozoic state to survive a high-EMF environment. You aren't "missing air"; you are missing the Photonic DC current needed to make oxygen safe. This is a counterintuitive truth bomb of evolution on Earth through the GOE lens.

What did the blogs say about exogenous oxygen when melanin is not hydrated? Oxygen utilization must be quantized to the stoichiometry of the TCA/urea cycle. On the IMM sits CCO that makes the water that hydrates endogenous melanin. What happens if your Kreb's bicycle loops of TCA and urea cycles are dysfunctional?

This decentralized take implies solar light to stimulate melanin production on the skin is a better & safer option than using a apnea machine because most sleep MDs do not do matrix/cytosol stoichiometry testing on apnea patients to see how toxic oxygen is. This also explains why many people with apnea suffer from atrophic skin.

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@DrJackKruse

Mar 6

1. Question asked on the forum today: Hello all.
I'm $%^#@@ from Kansas City MO northern outskirts. 39° lattitude. 49 yo female
RLE surgery in left eye in December of 2023 (obviously before I found Dr. Kruse)...hopefully still getting enough beautiful sun in my one untouched eye.

Have faught with heartburn (small HH ) off and on for years...got off of H2 blocker 2 years ago and try to control mainly through diet/random supplements but phasing those out as I listen more to Doc.
Weak ass bladder after 2 kids that seems to get worse every year.

No other real medical history except some anemia the last few years (suspected d/t heavier periods/fibroids) and so my doctor currently has me on iron.
RN for 14 years now, bedside nursing, night shift...don't scold me...been making the transition to days since following Dr. Kruse and currently down to only one or two night shifts a month now.

Wearing my blueblockers most of the time, catching the sunrise and sunset pretty much most days since November and trying to get through Dr. Kruse's blogs the best I can without feeling too stupid. Plan on moving in the next few years after last kid is out of highschool. Where? I don't know...still have a lot of convincing to do to the spouse.

Hope to make it out to El Salvador for the 1st time this summer, maybe fall.

2. My ANSWER: This complex web of symptoms, ranging from eye surgery and heartburn to pelvic floor dysfunction and night shift challenges, reflects a deep systemic breakdown of the circadian and dopaminergic systems often seen in chronic metabolic conditions like diabetes.

1. The RPE-SCN "Optical Blindness"
The retinal pigment epithelium (RPE) and the suprachiasmatic nucleus (SCN), the body's master clock, are fundamentally linked through light perception and matrix metabolic regulation.

RPE Dysfunction: In night shift workers, high blood sugar causes early damage to the RPE barrier, leading to fluid leakage and "optical blindness" where the eye fails to properly process light-driven metabolic signals.

SCN Misalignment: When the RPE fails, the SCN loses its precise "zeitgeber" (time-giver) input. Working night shifts exacerbates this by forcing the body to operate against its natural light-dark cycle, leading to chronic circadian misalignment.

The "Untouched" Eye: Seeking sun in one eye while the other has undergone surgery (like RLE) may be an intuitive attempt to "re-sync" the SCN, though the systemic metabolic damage often persists across both eyes

3. The image highlights that UV-A and IR-A (Infrared) are the fuels for regeneration.

The Problem: In a modern environment (LEDs, screens, night shifts), we are often "UV-A/IR-A deficient" but "Blue Light toxic."

The Result: Without those specific frequencies, the RPE (Retinal Pigment Epithelium) cannot recycle the waste from your photoreceptors. This is the "optical blindness" where the eye is physically there, but the biochemical signaling of time is lost and this leads to all your current issues.

2. Dopamine, GERD, and Pelvic Floor Dysfunction
Dopamine acts as a bridge between your circadian clock and physical functions like digestion and muscle control.
The diagram shows Dopamine (DA) as the "Light" signal.

Muscle Fiber Type: low dopamine leads to muscle dysfunction. In my framework, dopamine is essential for maintaining the vagal tone and the correct "firing" of smooth muscles.

The GERD & Pelvic Link: If retinal dopamine is low, the signal to the brainstem is weak (PVN). This affects the Autonomic Nervous System, leading to the "loose" GE reflex (heartburn) and the "discordant" muscle tone in the pelvic floor. It’s not just a local muscle issue; it’s a top-down timing error you are experiencing from being a night shift nurse. My bet in your operated eye there was big time myopia of evidence of Drusen present.
Blue light and nnEMF toxicity often causes autonomic neuropathy, which delays gastric emptying and weakens the esophageal sphincter. Dopamine receptors (D2/D3) help regulate these digestive rhythms; when they are "out of sync," it manifests as chronic reflux or GERD.
Pelvic Floor Dysfunction: Chronic hyperglycemia damages the nerves and blood vessels supplying the pelvic floor. This can lead to diabetic bladder dysfunction (incontinence or urgency) and weakened structural support, which is further complicated by the "dopamine thing", as dopamine is essential for the coordinated muscle contractions required for pelvic health. The fact this is getting worse at 49 means your days of being a nurse should be over because you need a massive infusion of UV-NIR light during the day to fix all of this.

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@DrJackKruse

Mar 4

https://x.com/DrJackKruse/status/2028960093224747213

In your framework, mitochondrial haplogroups represent specific "evolutionary tunings" of the dielectric brake. The differences in Resting Metabolic Rate (RMR) and Total Energy Expenditure (TEE) are not just about ATP efficiency; they are about how different populations manage the Archean electrical surge from dehydrated melanin from CCO dysfunction relative to their ancestral light environment. This is why Wallace's maps helped me figure this out 20 years ago. Nick should asked me about the Archean epoch when we discussed GOE but we did not go there.

Originating in the high-UV environment of Africa, L haplogroups are highly coupled. In my decentralized thesis, "coupling" is the hallmark of a perfectly functioning dielectric brake.

The Thermodynamic Efficiency: Because they evolved under a consistent flux of NIR/Red light (380nm-NIR), their Cytochrome C Oxidase (CCO) is optimized to produce maximum metabolic water and this kept the electrical conductance of melanin low in our system.

Low RMR/TEE: This abundance of water keeps the melanin in the RPE highly hydrated (the "Golden State"). The melanin’s electrical conductivity remains low and "slow." Because the system is electrically "quiet" and efficient, the body doesn't need a high resting burn rate to manage thermal or electrical "noise." It is a state of maximum thermodynamic coherence.

BIOPHYSICS IS UPSTREAM BIOCHEMISTRY Nick. That was the story built in the Archean you never learned about, by design: Pergamon Press and McGraw Hill owned by those who control centralized science.

https://x.com/DrJackKruse/status/2028960093224747213

2. As humans moved to colder, lower-light latitudes, the NIR flux diminished. To survive, the "dielectric brake" had to be partially released to generate heat (thermogenesis) rather than just metabolic water.

The Uncoupling Strategy: These haplogroups are more uncoupled. In your framework, this means they intentionally produce less metabolic water per unit of fuel, allowing for a controlled increase in melanin’s electrical conductivity.

High RMR/TEE: The "unbridled" melanin generates more electrical friction/heat. A higher RMR is required to manage this "leakier" electronic state. These groups are essentially "closer" to the Archean state by design, using that "high-voltage" potential to maintain body temperature in the absence of strong solar flux.

3. This last tweet explains why uncoupled haplotypes need more fat and protein and less carbs. All about the dielectric brake no one learned about .........well I did because I asked follow up questions of my biochem professor, Peter Setlow.

So when you are uncoupled in high latitudes and around a shit ton of dehydrating polarized light you realize why blood glucose is skyrocketing and everyone has insulin resistance.

It is not what they told you in biochem class.

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@DrJackKruse

Mar 4

Wunsch 2026 is getting further from the truth.

Be aware of it. youtube.com/watch?v=LfrqzT…

He says energy is repsonsible for all patterns of life forms. This was only true after the ozone layer was laid down in the GOE. This mindset has caused him to miss the most critical part of the story. Life organized outside to inside because of the Archean epoch before the GOE. This statement is at 2:04

When he goes on to say that UV light was important for developing mutations he is speaking centralized garbage. His mindset allowed him to completely miss the main purpose of UV light which was to develop allo-melanin and feodoxins before there was a shread of RNA on Earth. The basis of life began with abiotic dirty chemistry of the Archean which then developed because melanin provided protection without an ozone layer for the ferodoxin electron tunneling as the first heme protein. Melanin also provded away to clean the dirty chemistry by chelating metals and finding novel uses for them that would later become powerful to control the matrix. The most important thing he seems not to know melanin becoming hydrated by heme proteins is how the highly powered and chaotic light of the Archean was tamed to organize matter in a cell ---> set up the 0.66eV barrier to tunnel protons to build gradients for protocells, RNA/DNA/ATPAse etc....

He actually says the opposite of Wallace in his latest pod with Nick Jikomes. He says mutations are not welcomed when Wallce says they are. I am with Wallace and not Wunsch on this bigtime. 4:16.

He then makes the unbelievable statement that higher we go up on the evolution tree to us the more detrimental UV light becomes!!!! the oppsoite is true. UV light is the basis of photorepair for humans. This is ridiculous state and goes against the data in my pinned tweet and it goes against the why humans have so much melanin inside their body plans. Why leptin has a GOE level 220nm absorption spectra and why all LIVING CELLS emit ELF-UV. I could not believe Max did not say a word or push back hard on this. at 4:40-5:00

His point on Fraunhoffer lines is the first thing he says I agree with but he has zero idea how that linked to melanin in the Archean Earth and how it scales to humans today.

At 8:00 he talks about people living underground for long times and has no idea that this is what our ancestor mammals have done for 320 million years and the melanin on their surface is what allowed this to happen. He seems to have no Earthly idea that being underground puts you closer to uranium and thorium radiation which mammals can use to turn into useable energy. This guy is missing huge pieces of biology and I hate to say it, but I think if you listen to him about light you will become deeply misinformed. I like Wunsch a lot. Met him In Germany 7 yrs ago but instead of his thesis growing it has regressed toward centralization heat death.

This is my critique just ten minutes in. Honestly I would have never released this podcast because of the mistakes made early. Skipping this to get to the GOE and photosynthesis truly was a tragedy for decentralized truth.

2. At 22:00 he has completely disqualified himself as being a light epxert from my perspective when he says melanin pigment in the skin is not important. Just jaw dropping bad science.

3. Another huge gaff at 26:00. He says ATP is tied to warm and NIR light and totally diregards that UV-A light inhibits CCO to make ATP. Also Max not pushing back on this is shocking considering this is Wunsch's own slide on the topic.

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