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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Sep 13

Deuterium's Quantum Dual Nature: Bosons vs. Fermions

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

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

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

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

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

2. Biochemical Implications: Hydrogen Isotopes in Melanin and Metabolic Pathways

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

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

Deuterium's heavier mass (twice hydrogen's) slows kinetic reactions (kinetic isotope effect), disrupting enzyme kinetics, and the dielectric constant of the metabolic pathways altering UPE function, mitochondrial function, and water structuring in cells. The diagram implies sunlight-driven melanin creates a "plasma" for harvesting electromagnetic energy, with H/D isotopes affecting unique codes in water and biomolecules.

3. Connection to deuterium's physics: In biological "condensates" (e.g., exclusion zone water around proteins), bosonic deuterium has to enable collective behaviors, like enhanced proton tunneling or spin-dependent reactions.

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

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

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

Biology tie-in: It's why exercise feels good in sunlight in moderation but wrecks you if overdone under blue light in agym it is because éR rises, signaling "back off and recover." Blue light allows deuterium to flow into the mitochondria and the KIE takes over.

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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Sep 10

The retina thins from the effect of man-made light and a lack of sunlight, and then your risk of Frontotemporal dementia rises. The OCT test is the best screening test for FTD. We have familial and mtDNA FTD.

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

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

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

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

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

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

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

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

2. The GLP-1 Drug Connection: Weight Loss at a Cost to Your Eyes and Ears

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

Effects on the Eyes

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

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

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

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

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

Interestingly, while some research suggests GLP-1s might protect against general dementia by reducing inflammation, their eye effects could counteract that, especially in FTD-prone folks. My TED talk was banned because BigHarma was afraid I was going to obliterate their GLP 1 train by showing the world why they banned stopped the leptin trials early on weight loss.

3. Since the ear also processes sensory info tied to your body's clock, this could feed into broader brain degeneration.

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

Rapid weight loss can disrupt fluid balance in the ear, similar to the eyes. Diabetes itself raises hearing loss risk via blood vessel damage, and some GLP-1s (like exendin-4 types) heighten it further. The GLP target in the ear is the stria vascularis.

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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Sep 7

I tried to pull the veil back on the layers of the Deep State and where they are linked and why they are linked. It is a nasty story of deceit and ideological fascism where science was stolen to control modern humans with Light, drugs, and jabs.

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

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

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

x.com/JuanGutiCA714/…

2. True Evil with assorted atrocities most often occurs when the most respectable and intelligent of people fall for it. The wise never do. They sniff out and diagnose the problem of centralization to avoid collateral damage. Be careful who packs your parachutes.

3. What is modern gaslighting of the jab injured really? It is cloaked in pardons and Nobel Prizes given to the architects of the crimes.

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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Sep 4

I started a huge Barista FIRE on the boat it appears with my Bitcoin talks with him every AM. He apparently was quite influential with the young staff and told them all they were working communist hours for communist pay, and when his manager heard it spill over to our morning conversations and how many of the krewe I am Orange pilling, they axed him. He was escorted off the book quickly in Peru, and I never knew it until this AM. Some of his barista folks confirmed it got hot quickly.

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

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

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

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

2. The Origins of the FIRE Movement

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

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

3. The results of the Trinity study were first published in the American Association of Individual Investors Journal in 1998.

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

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

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

FIRE stands for Financial Independence, Retire Early. Over the years, however, many ORANGE FIRED MDs Savages began to break from core FIRE principles and define FIRE variations that better suit their lifestyle goals. I helped many of my tribe do just that. Membership matters in this tribe.

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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Aug 26

1. ANSWER: In ALAN contexts, blue light suppresses melatonin, which normally inhibits AVP and cortisol, leading to unchecked vasopressin release during "light stress." This causes a reactive hyponatremia in the posterior pituitary, activating brain osmoreceptors and RAAS, raising blood pressure and stress hormones, which fragment sleep and impair daytime recovery. They also chronically degrade the mitochondria in these neural tracts.

2. Now for the dirty details.
Precise Mechanisms of Sodium Regulation in the Brain and Circulatory SystemSodium (Na+) homeostasis is tightly regulated to maintain osmotic balance, blood pressure, and neuronal function, with disruptions like hyponatremia (serum Na+ <135 mEq/L) directly impacting sleep via arousal, cognitive fog, and fragmented rest. The brain acts as the central sensor and regulator, while the circulatory system executes adjustments through hormonal and renal pathways.

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

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

Circulatory System Integration with Hormones: In the periphery, low Na+ (hyponatremia) is sensed by renal juxtaglomerular cells, triggering renin release, initiating RAAS: renin converts angiotensinogen to angiotensin I, then II, which stimulates aldosterone from the adrenal cortex to enhance Na+ reabsorption in the distal nephron and potassium excretion. This raises blood pressure to restore volume but can cause nocturnal hypertension, disrupting sleep architecture (e.g., reduced REM). Cortisol, released from the adrenal cortex in response to stress signals (including ALAN and hyponatremia), amplifies this by promoting Na+ retention via mineralocorticoid receptors and enhancing sympathetic activity, increasing heart rate and arousal. Vasopressin interacts with cortisol and RAAS; for instance, AVP potentiates cortisol's effects on water balance, while cortisol feedback inhibits AVP in healthy states, but ALAN disrupts this, leading to unchecked stress responses. Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) counterbalance by promoting natriuresis (Na+ excretion) when blood volume rises, but in hyponatremia from SIAD (syndrome of inappropriate antidiuresis), this balance fails, perpetuating low Na+ and sleep disturbances like frequent awakenings.

3. So Emily, what you should do is see the AM sunrise every AM. Drink DDW water and add high-quality salt to the water, and within 2-4 weeks, you will sleep much better. These slides support the tweets, and the last one with the D20 water spectrum really hits the mark.

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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

@DrJackKruse

Aug 21

A couple of points: Not all human cells have mtDNA. See adult blood cells. This is a big deal when you consider their absorption spectra. 200-600 nm light with a sharp cut-off. Also, blood still transforms energy into UPEs. And since blood fills 20% of our CO to the CNS, this also has implications. The retina and gut increase their blood flow with light use and feeding. Feeding is a light-based phenomenon since all food webs link back to photosynthesis.

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

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

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

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

Now the picture is full. patreon.com/posts/decentra…

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

Did you know that in humans, UVR depletes folate in skin and blood, inducing S-phase arrest, affecting uracil misincorporation (frame-shift mutations), and sensitizing apoptosis in keratinocytes. This isn't "damage" but a permissive environment for seasonal phenotypic changes, e.g., increased melanin production to protect folate stores. When you understand the photorepair mechanism, you will see this is how humans can block the DoD and BigHarma death mechanism from uracil replacement induced by the jabs. @MdBreathe None of the COVID experts have this sophistication. They are still pushing detox answers when it is crystal clear that redox biology is the path for the Savage trying to stay alive and away from disease.

3. Individuals with MTHFR C677T (thermolabile variant) are indeed supersensitive to light/folate fluctuations, as the mutation impairs folic acid conversion to 5-MTHF. High folic acid may select for this allele evolutionarily, acting as a "genetic time bomb" by promoting unmetabolized buildup and altering DNA/RNA biology.

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

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☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆

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