☣️ Pleb Kruse = BTC foundationalist in exile 🟩🔆 Profile picture
I am a neurosurgeon on a mission to create health from disease by decentralized thinking & BTC! Bitcoin pleb decade club in exile https://t.co/W4I1WtqhJY
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Oct 18 19 tweets 15 min read
1. The terms anaplerosis and cataplerosis describe reciprocal and correlative reactions involved in the function of the TCA/urea cycle. The enzymatic steps in these processes have long been known, but the overall concept of a linkage between anaplerosis and cataplerosis should be underscored because the balance between these two processes controls the entry and exit of TCA cycle anions.

Anaplerotic and cataplerotic reactions are involved in the ultimate disposal of all metabolic intermediates. The metabolic role of anaplerosis and cataplerosis in amino acid metabolism varies with the light environment, specific organs and is dependent on the nutritional/metabolic status of the individual.

If the AM sunrise is seen by the eye, skin, and sensed by the gut via the skin clocks, during feeding, the intestine is an important site of catabolism of enterally derived amino acids, whereas in the starved state amino acid catabolism occurs primarily in the kidney, liver, and muscle. The light environment is critical in how anaplerosis and cataplerosis operate in people.

Every tissue differs in how it uses anaplerosis and cataplerosis.This implies the regulation of anaplerosis and cataplerosis is very dependant on deuterium kinetics in the matrix from normal or abnormal metabolic and physiologic states.

Methionine: Propionyl-CoA forms as a catabolite of methionine, threonine, and the branched-chain amino acids. β-Oxidation of fatty acids with an odd number of carbon atoms yields propionyl-CoA. The oxidation of the side chain of cholesterol also yields propionyl-CoA. Thus, propionyl-CoA is derived from the catabolism of lipids and proteins.Propionyl-CoA is converted to succinyl-CoA, which is oxidized or converted to glucose by way of oxaloacetate and pyruvate. Succinyl-CoA may also form δ-aminolevulinate, a precursor of porphyrin biosynthesis.

This is critical in oncogenesis because cancer cells need brisk ECT which means that cancer cells can use methionine to usurp oxygen using methionine to increases both angiogenesis and hemoglobin production to make sure that oxygen delivery is brisk and apoptosis stays inhibited PROVIDED VDR/D3 and/or UVA are absent to slow ECT flow.

NO is used to slow ATPase as a braking mechanism when oxygen is a toxin. This is a remnant from our GOE evolution before heme proteins and melanin were innovated to protect us as a firewall from oxygen. NO is liberated by UVA light and NIR.

Update your biochemical models because they are all broken.Image 2. Anaplerosis and Cataplerosis: They are Light-Dependent Gatekeepers of TCA/Urea Cycle Dynamics and Metabolic Fate

From first principles, metabolism is fundamentally an energy and information flow process, governed by thermodynamic gradients where sunlight provides the primary low-entropy input to drive organization and efficiency.

The tricarboxylic acid (TCA) cycle, also known as the Krebs or citric acid cycle, serves as life's central hub for oxidizing nutrients to generate ATP, but it doesn't operate in isolation.

Anaplerosis (replenishment of TCA intermediates like oxaloacetate or succinyl-CoA) and cataplerosis (removal of these intermediates for biosynthesis or disposal) act as reciprocal OPTICAL valves, ensuring the cycle's continuity while adapting to cellular demandsImage
Oct 15 5 tweets 5 min read
There is only one kind of shock worse than the totally unexpected outcome: the expected for which one has refused to prepare. This is the new jouney for those who complied with tyranny and joined the experimental group the last 5 years.

The expected always happens and this can be a problem too. Sometimes the most scenic roads in life are the detours you didn't mean to take. This is true for the control group.

The results of traveling the road less traveled surprises us. So, would you really like to know your future?

If your answer is yes, think again. Not knowing is the greatest life motivator for thriving for those of us who rejected compliance.
So enjoy, endure, survive each moment as it comes to you in its proper sequence -- a surprise. Embrace the chaos and the suck for a change, but never comply with tyranny.Image 2. People who complain they have no time or wish they could control how they spend their time to do what they should are stuck in a low dopamine state because of the light they live under. Few of them are aware of the implications.

Here is how it works: Know how to get the most results in the least amount of time. That’s the ultimate aim of productivity skills. Savages know we all have the same amount of time in a day so when somebody tells you they do not have time to do something they have a made choice with their time to do something else. In the age of information, ignorance of the wisdom of reality and nature is a choice.Image
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Oct 15 4 tweets 4 min read
He said, "the same command becomes a metabolic loan the body can’t repay."

This is why evolution put the VDR recpetor on the IMM. When you have UV and IRA/NIR you can repay the loan. This means the SUN is TINA. Why? It slows the charge on the IMM.

It should not make sense why I do use affliate codes for red lights.

They are a half truth to those with electrical resistance problems in the IMM.

You always need purple and red to pay the loan back. Purple and red together renovate the poor engines to restore the default state.Image 2. The U.S. has the highest first-day infant mortality out of industrialized world About 11,300 newborns die within 24 hours of their birth in the U.S. each year, 50 percent more first-day deaths than all other industrialized countries combined.
This is that awkward moment when the statistics confirm that the experts are wrong about something, and the children are dying because of it.
The problem in the U.S. is that many of the babies born here are premature.

cbsnews.com/news/us-has-hi…

What are the reasons that babies are born prematurely?
Risk Factors for Premature Birth are all correlated with artificial light melanopsin damage. Can you imagine that?
Many risk factors can be reduced or eliminated altogether. Talk to your doctor or midwife about your individual risk factors and what you can do to diminish them.

Risk factors include:

Prior premature birth.
jaundice requiring blue light therapy
Multiple pregnancies.
Uterine or cervical problems.
Chronic high blood pressure.
Diabetes.
Smoking.
Jab compliance.
Age.
Lack of UV exposure prenatally.
Poor nutrition due to missing DHA.
Untreated infection.Image
Oct 14 8 tweets 5 min read
1. How will the transhumanist technologists use AI in the future?

I often think of how compliant we have become. Anytime you use Google or have an iPhone or any phone for that matter, you have to ‘agree to the terms’, every Apple update there is something new to comply with.  This is a problem of how they suck you into the matrix.  Your land line phones never did this.  

The transhumanist tech companies know the addicted will comply and agree to any terms to suit their addiction to technology and don’t bother to read anything they want you to bend the knee for. The trade off for entertainment for the soul has been around for a long time. But the manner in which these transhumanist are capturing people should be unsettling to anyone who can think.

x.com/DrJackKruse/st… 2. Wireless radiation is being used to surveil people without their knowledge or consent, even if they aren’t wearing a “smart” device or holding a cellphone, according to the authors of a new study.

The study authors engineering faculty members with the Institute for Systems and Computer Engineering, Technology and Science at the University of Porto, Portugal posted their report Jan. 24, 2025 on the Cornell University open-access research website, arXiv.

The study showcases hardware the authors designed that leveraged ambient wireless radiofrequency (RF) radiation to detect and render a visual image of human activity such as waving a hand or a person’s breathing rate with over 90% accuracy.

Their design involved a thin programmable surface a Reconfigurable Intelligent Surface (RIS) that communicates with computers and artificial intelligence (AI).
Oct 11 13 tweets 12 min read
What do you know about the Stiles-Crawford effect in a healthy eye? What if I told you this effect is how we sharpen central vision and narrow the periphery of the retina from too much blue light. Would you believe it? Did you know melanopsin has a specific topographic map on a healthy retina? A lesson no has taught you is incoming.Image
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2. All opsins are topologic insulators. You might want to read that threadroll above now to understand topology well.

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

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

What are the implications?Image
Oct 10 17 tweets 21 min read
Another new podcast from me with Smuggling Hope. It is good one on mental health because it explains how biomolecules absorption and emission spectra's determine reality or determine which mental illness one gets.

This is the information why Jordan Peterson is sick and why he and his daughter have stumbled multiple times in getting him well.
ivoox.com/.../exposing-t…...
Biophotons are ultra-weak light emissions produced by living organisms, thought to arise from metabolic processes like oxidative reactions in mitochondria. Centralized scientists and AI bots hypothesized them to play a role in cellular communication, potentially influencing gene expression or signaling pathways. FIAF, also known as angiopoietin-like protein 4 (ANGPTL4), is a protein produced by tissues like fat and the gut, and it’s a key player in lipid metabolism and microbiome construction. Neither understand how UPEs control FIAF. If the UPE is coherent then FIAF inhibits lipoprotein lipase, affecting how fats are stored or broken down, and its expression ramps up during fasting. The microbiome, meanwhile, is the community of gut microbes that can shift in response to diet, fasting, or host metabolism, influencing energy balance and health. If the UPEs in mitochondria is not coherent, the UPE changes and mental illness becomes more probable. You cannot burn fat so it changes neural signaling.

Centralized scientists and technocrats who build AI systems will say no direct study says “biophotons control FIAF to affect the microbiome,” but we can hypothesize based on related mechanisms. This is patently false. Why?

FIAF has known absorption and emission spectra to light frequencies. Because of that, a study is superfluous because each chemical in the world has an optical fingerprint. Just because a scientist has not published the work is immaterial to this BASIC biophysical fact in spectroscopy. This was what I brought Ray Peat over ten years ago, and he was impotent enough to answer my critiques of his work. This podcast covers these details.Image 2. Is nerve pain caused by a Lyrica deficiency?
Is Lyme disease linked to a lack of doxycycline?
Is depression due to Prozac deficiency.
Are heart attacks are due to Lipitor deficiency.
Is obesity due to Ozempic deficiency.
Are Headaches due to Tylenol deficiency?
Is Bipolar disorder due to lithium deficiency?
Any questions?
You've been conditioned by centralized medicine to ask the wrong question.
You have a solar deficiency combined with a nnEMF toxicity problem.

This alters the UPEs your mitochondria make and it is this light that changes the neural tracks that make you mentally ill. This is why your Bipolar Disorder exists. The defect is not in you; it is in your environment.Image
Oct 9 16 tweets 16 min read
When matter experiences this topologic change do you know it become capable of emitting photons? In biology we call this UPEs. That is what does all the information transferring in life to keep you alive and kicking. Image 2. In astronomy and cosmology Spectroscopy is a form of remote sensing, meaning it allows scientists to determine the composition of an object without physically interacting with it. This is how we examine remote atoms in deep space.

How do we know what other worlds are made of? Planets we’ve never touched, stars we’ll never reach? By reading their light. Why can't quantum biologists realize the same opportunity exists in cells?Image
Oct 8 7 tweets 6 min read
Cutaneous antimicrobial effects of sunlight on cholesterol conversion to Vitamin D components are today's PSA boys and girls.

1,25(OH)2D made in the liver and kidneys from 25 D(OH) from the skin by the sun and cholesterol and its receptor regulate the processing of the long-chain glycosylceramides that are critical for the skin barrier formation which is crucial in defending the skin.

Do you know how the heme protein enzymes CYP control this process?

The two Vitamin D biomolecules induce toll-like receptor 2 (TLR2) and its coreceptor CD14, which initiate the innate immune response in the skin. Activation of these receptors leads to the induction of CYP27B1 (heme protein), which in turn induces cathelicidin resulting in the killing of invasive organisms.
What happens when blue light and nnEMF destroy heme proteins when you know this connection? Innate immunity is destroyed. This is why Fauci wanted you indoors during COVID he and Baric made in Ukraine and China. ncbi.nlm.nih.gov/pmc/articles/P…Image 2. See how the heme photoreceptors are blown away? Image
Oct 8 5 tweets 6 min read
Fire your centralized doctor by hiring nature for your reversal! Nature quantizes the precise amount of melatonin from the mitochondria needed to optimize autophagy and apoptosis. 95% of melatonin is made in human mitochondria. It is not your pineal or your gut. Your central retinal pathways have more mitochondrial density in it than any other part of the brain. The same is true with DHA to run your SCN faster than the other molecular clocks in your body to meet relativity needs. Want more info on exogenous melatonin? Use Yandex search with my name and mitohack #722. Your welcome in advance.Image 2. Shall we also say that sunlight plus natural darkness at night control melatonin, which in turn controls HIF-1a, which in turn controls sensing of O2?

Guess what happens to your mitochondria when oxygen tensions change? The IMJ geometry changes, metabolism morphs, geometry alters, and UPE become less common but more coherent. Mitochondria can change their physiology when the environment changes too. This is a remnant of the GOE when we had chronic hypoxia. this is why we innovated HIF1 and linked it to the PER clock genes.

Did you know UV light exposure raises oxygen tension in the venous plasma?

Guess what that all implies?

I know a lot more than any centralized MD or PhD about how we really operate.

ncbi.nlm.nih.gov/pubmed/20449875

Yes, light shapes life by sculpting your colony of mitochondria to make coherent UPEs to build longevity.Image
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Oct 6 5 tweets 5 min read
If you have a T1D child you have a light problem. That light problem has manifested in your germ line.

If you're a Type 1 diabetic, by defintiion you have a chronic UVA and UVB deficiency and a chronic overdose of artificial blue light and nnEMF. It is also axiomatic.

Look at the chart below. T1D is almost nonexistent near the equator

This isn't a coincidence. Diabetes is a LIGHT story not a food one. pubmed.ncbi.nlm.nih.gov/18548227/Image 2. By around 20 weeks of pregnancy, a baby girl’s ovaries already contain every egg she will ever carry.
Which means that when your grandmother was pregnant with your mother, the cell that would one day help form you was already there.

Three generations, held in one body.
This isn’t folklore. It’s embryology.

Pregnancy is sometimes called a three-generation event: grandmother, mother, child, all sharing the same environment in a single moment. Scientists call it multigenerational exposure. I call transgeneration biology.Image
Oct 5 9 tweets 9 min read
1. Today's lesson is an ass kicker. It begins with one of my long term members asking a question on my website forum.

CITE
A. forum.jackkruse.com/threads/climat…Image 2. All one needs to know about the climate scam in one slide. Humans are the penultimate primate. We need more CO2 so plants make more 02 in our environment. Coupled oscillators, are C02 and 02 for the clade of silly talking monkeys.

The text in my slide below claims a "40-year hoax" and "CO₂ famine," arguing we need CO₂ at 1,200 ppm to avoid calamity, with humans as "penultimate primates" benefiting from more CO₂ for plant growth and thus more O₂.

This echoes decentralized climate views held by me: Earth has been in a relative CO₂ "famine" for millennia compared to geological highs, and rising CO₂ (now ~420 ppm as of 2025) has driven global greening, increased crop yields, and reduced famine risks.

For example, India's shift from famine-prone in the 1960s to agricultural exporter is partly attributed to CO₂ fertilization alongside green revolution tech. Some argue past low CO₂ contributed to events like the Carboniferous rainforest collapse or even the Permian extinction via "phytoplankton blackout."

Every single thing the government is behind is a bullshit story to enslave silly talking monkeys.Image
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Oct 1 5 tweets 5 min read
So why have I been traveling to the highest points on Earth and visiting many deserts along my path? A new blog covering it.

SPACE & EARTH ARE ENTANGLED AND LEAD YOU TO THE DISEASES Astronauts get. All Chronic diseases of man have the same etiology but few see it.

This blog starts at the magneto-heliosphere for the lesson and then I introduce you to an astronaut who has experienced this nnEMF in his own life so you can learn about your disease from his experience.

Learn the real ticket that moves the needle. If you want to know why your kid has childhood diseases and cancers I guarrantee you after this master class in quantum biology you'll know why.

We are the product of stardust that has burned us using oxygen. It light is the anvil which forged me which gave the will to make me formibile for my misfits because I will not break under force. All living things are electric and magnetic and they use the electromagnetic radiation of the sun and the earths magnetic field to create life. Man made radiation disrupts the natural order of atoms in our cells. The electromagnetic signals that come from the organization of these cells in mtDNA creates our health span or chronic diseases epidemics. This is plants and animals.

Humans are diurnal animals who need sunlight and darkness after sunset to function. This makes them fully decentralized. They cannot be optimal with too much of either. Indoor living, sun avoidance, constant exposure to artificial lights and man made electromagnetic radiation = a shifted metabolism from light that leads to all chronic diseases. Optimizing melatonin, dopamine, and melatonin (sunlight/darkness) and solar derived vitamin D, melanin, and NO is how you avoid chronic disease.

patreon.com/posts/decentra… 2. You don’t need more time.
You need more clarity in how you approach learning

Ask yourself 3 questions every morning:

1. What really matters most right now?
2. Who needs to hear from me today?
3. Am I living in alignment with what I say I value?

These 3 questions cut through the noise to get you to the signal of things that matter - at work, at home, in life.Image
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Sep 29 5 tweets 4 min read
If you think the Federal government is working for you you are an idiot. First they banned light bulbs that could help reduce oncogenesis. A peer-reviewed study showed that 734 nm near-infrared (NIR) can do this. Then the DOD, Fauci and Baric made a virus and jab designed to give you cancer. Then DARPA is supporting Gates research to block the sun at rhe same time they are inflating you money away as M2 rises. Every part of the government is involved in TIME THEFT.

Thomas Jefferson told us about clowns like this and in his time he told people to shoot the King over things way worse than what Americans are being force fed.Image
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2. ^^^^^that was my second to last slide in the latest talk. This was another from the slide deck. Image
Sep 28 11 tweets 8 min read
What did the paper miss? Fasting makes them bigger.

Implications?

What happens to energy resistance in your ankle when you sprain it? It increases and it SWELLS because of energy loss.

What happens to energy resistance in the heart when it fails? IT increases in sizes and hypertropies because of energy loss.

What happens to a G class star like our sun when it it dies? It increases its energy resistance because it can no longer burn hydrogen and helium and burns all the elements to be come a red giant. It increases and becomes larger, because of this energy loss.

See the trend..........

What did the paper miss? Fasting causes mitochondria to get larger..........

It happens because of energy loss. The implications are vast for cell biology. Few.

I bet when @msahsorin gets better technology and can measure endogenous UPEs from these mitochondria it will show the UPEs spectra widens and becomes less coherent. Few.

@MitoPsychoBio 2. What happens in cells when UPEs output changes. Let us just look at one system to get a small picture of what light is capable of in information transfer? @msahsorin Image
Sep 24 10 tweets 12 min read
These guys dying are just like the autism story is being sold by RFK Jr to give people breathing room. None of this is the truth. Everyone wants to blame one thing but it is a combination effect that assaults their colony of mitochondria slowly reducing the delta psi to cause electrical resistance in our semiconductive circuits to rise. This destroys the heat sink of metabolic water and directly alters information transfer in UPEs. It is obvious why this happens in decentralized medicine. It is shocking to the morons in centralized healthcare.Image
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2. Number one cornerstone risk that raises energy resistance most is blue light and nnEMF that destroys the endogenous photolitholithograpghy biology needs to main entropy in the cell. Today biophysicists keep shitting the bed on what UPEs are. They are information qubits we use to stay healthy and alive and how they are controlled is the story of decentralized biology. Anyone who does not get this idea should be IGNORED.

“Previous studies showed that the plasma of a healthy individual contains up to 50,000 times more mitochondrial DNA than nuclear DNA,” said Dr. Alain Thierry, a researcher at the Montpellier Cancer Research Institute.

Biophysicists keep saying they do not know.........
Why do I know what it means? Because I understand what Shannon taught us about information. The uniqueness is the signal, not the noise.Image
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Sep 23 4 tweets 5 min read
In 2019, I said I expected viral epidemics breakout in certain zip codes more significantly because viral infections react to the environment that is suboptimal. I also reminded my readers that these viral infections will cause rapid significant mitochondrial damage which in turn will liberate Vitamin A from opsins in cells and this puts downward pressure on endogenous production of Vitamin D. Then in September 2020, I said one thing is clear.........those who got C19 all had low levels of Vitamin D and immunodeficiency at some level that impacted their care and outcomes. This will affect their mitochondrial delta psi and lead to many other complications. I spoke about all those links here in this blog work. patreon.com/posts/22117599

TODAY IN 2025 I AM TELLING YOU IF YOU TOOK THE JAB AND HAVE A HIGH SPIKE PROTEIN ARRAY, YOU NEED TO MAXIMIZE THE VITAMIN D AND A cycles in your body and then the more controversial idea. If you are woman, even if you have infertility you should continue to try to become pregnant because there is a change the placenta from the pregnancy will retain the ability to clear a lot of the genetic damage from the jabs and limit intercalation. Let me be clear, the pregnancy will help you, it may not help the child so think about this before action.

The human placenta acts like plasmapharesis for DNA RNA and mtDNA damage. Few centralized MDs know this. My tribe does.

Recently 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 link between genetic aberrations in the placenta and birth outcomes has been established in the literature by this study but few MDs read outside their expertise, further studies using larger sample sizes could help to uncover the causes of complications and diseases that arise during pregnancy.

This study confirms for the first time in the PEER literature that the placenta is organized differently to every other human organ, and in fact resembles a patchwork of tumors collected from the circulatory system of Mother and fetus. The rates and patterns of genetic mutations were also incredibly high compared to other healthy human tissues.

The human placenta is akin to the ‘wild west’ of the human genome, completely different in its structure from any other healthy human tissue. It helps to protect humans from flaws in our genetic code, but equally there remains a high burden of disease associated with the placenta. This is why the DOD engineered spike protein to affect the uterus and hinder pregnancy creation. These findings now provide a rationale for my tribe for studying the association between genetic aberrations in the placenta and birth outcomes at the high resolution we deployed and at massive scale by the jab. I have been telling jabbed members who still bleed they should seek continuous pregnancy to rid their bodies of the genetic defects these bioweapons bring to people. No one knows how effective this information is but I guarrantee you no one is getting this information but my FARM members.

I encourage you to read the paper before deciding what to do. No one can legislate your sexual activity so having sex to get pregnant to save your life or improve it will not be interrupted by the state as yet.

The paper was fascinating because it allowed us to observe how such serious genetic flaws like a chromosomal copy number error could be ironed out by the baby tissues, but not by the placenta. the placenta seemed to be built to absorb all the genetic mistakes. I want to remind all my female savages that this is a way to lower heteroplasmy rate in your germ line eggs too. These errors would have been present in the fertilized egg. The paper showed us that derivative cell populations, and most importantly those that went on to form the child, had the correct number of copies of chromosome 10, whereas parts of the placenta failed to make this correction and it COLLECTED THE DEFECTS LIKE A FILTER. The placenta also provided a clue that the baby had inherited both copies of the chromosome from one parent, which can itself be associated with problems. Share this info with female savages who complied with tyranny.Image
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2. Publication:

Tim H. H. Coorens, Thomas R. W. Oliver and Rashesh Sanghvi et al. (2021). Inherent mosaicism and extensive mutation of human placentas. Nature. DOI: 10.1038/s41586-021-03345-1

doi.org/10.1038/s41586…
Sep 22 10 tweets 7 min read
How many savages know that use of tylenol cause destruction of endogenous glutathione recycling?

Few. ROOM silent as I spoke. It's a true story........

It was Decemeber 2010 and a my team of anesthesia people asked me to sit in on a continuing education class in the surgery department on one my surgery days.

I realized in 1 minute this was a BigHarma circle jerk.

The primary brand name for intravenous (IV) acetaminophen in the United States is Ofirmev. The medication is used to treat mild to moderate pain, fever, and moderate to severe pain in combination with opioid analgesics. They wanted my opinion on if I was OK using this as part of the anesthesia alogrithm for post op pain management in brain and spine cases and because I did most of the neurosurgery volume in the hospital in 2010 they wanted me to make the call. They knew I knew a lot of pain, POMc, and tylenol, because I had banned the use of this drug from all my patients in 2002.

I listened to the drug reps and reviewed what they brought me. First question I asked the reps what did they think about the 1998 actions of the UK on this drug.

Dead silence in the conference room filled with free BigHarma merch and food. 5 reps to cover the entire anestheisa and surgery dept. At the time, the anesthesia and general surgery depts were filled with employed MDs who worked for the hospital system. No one in the neurosurgery or orthopod dept were employed. At this time I noted the COO of the hospital was sitting in the back of the room.

I told the room filled with MDs and CRNAs that I banned the use of this drug after the 1998 UK black box warning. The published stories of the UK action was that typical UK pack size became restricted. In 1998, the UK limited the pack sizes of paracetamol available over-the-counter to reduce cases of intentional self-poisoning. If you could self poison yourself with an OTC medicine I said I need to find out why that happens.

ROOM silent as I spoke because they knew about how I fact check everything.Image
Sep 20 10 tweets 11 min read
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
Sep 18 7 tweets 6 min read
Photoreceptors are useless without retinal, which is produced in the eye. When retinal is liberated oxygen becomes a toxin and Fe is a wrecking ball.
phys.org/news/2018-08-c…

nnEMF activates VGCCs, flooding cells with Ca²⁺ and ROS/RNS, damaging mtDNA and heme proteins (cytochromes, CYP11A1, CYP19A1). Blue light liberates retinal, impairing melanopsin and dehydrating melanin, lowering éR and DDW production. This stalls StAR (STARD1)-mediated cholesterol import via TOM/TIMM/VDAC2, blocking pregnenolone synthesis.

Dehydrated melanin disrupts microtubule dynamics and protein synthesis, exacerbating "pregnenolone steal" toward cortisol, depleting sex steroids. The retina, as a "window to the brain," thins under suboptimal light causung blindness, degenerating brain tissue (e.g., frontotemporal dementia precursors). nnEMF/lack of sun alters AMO in skin/eye, changing central retinal pathways. Oxidative stress increases peroxide (ROS) levels, altering UPE signatures and heme construction, and is linked to hormone-related disorders by disordered UPE transformation in the CYP enzyme system.

In humans, iron is a double-edged sword, especially in the brain. It’s essential for energy production in mitochondria and for synthesizing neurotransmitters like dopamine, which governs movement and reward. Iron accumulates naturally in the brain as we age, particularly in regions like the basal ganglia, globus pallidus, and substantia nigra. These areas, rich in gray matter, hold two to four times more iron than white matter, where myelin insulates nerve fibers.

But when iron accumulates excessively, trouble brews. In neurodegenerative diseases such as Parkinson’s, Alzheimer’s, and Friedreich’s ataxia, iron overload in neurons triggers oxidative stress, resulting in the production of reactive oxygen species (ROS) that damage lipids, proteins, and DNA. This process, known as ferroptosis, is particularly devastating in the retina, where photoreceptors and intrinsically photosensitive retinal ganglion cells (ipRGCs) are particularly vulnerable.

These cells, which detect light to regulate our circadian rhythms, rely on iron-containing proteins and melanin, a pigment that chelates iron to protect against oxidative damage. When this balance falters, ferroptosis destroys neurons, disrupting circadian signaling and contributing to diseases such as Parkinson’s, where the loss of dopamine-producing neurons in the substantia nigra is linked to iron overload and reactive oxygen species (ROS).

Why does iron accumulate in sick or dying neurons? The answer echoes the stars. Just as a star amasses iron in its core as it runs out of energy, neurons hoard iron when their energy production falters, often due to mitochondrial dysfunction. In both cases, iron signals a system on the brink, teetering between stability and collapse. 2. 95% of melatonin is made from mitochondria. So what happens when mitochondria are damaged from blu elight toxicity? You get high blood glucose and insulin and flatlined cortisol.

What happens when you knock out melatonin receptors via melanopsin dysfunction from the liberation of Vitamin A? You get insulin resistance and set the stage for many mitochondrial diseases like diabetes and cancer.
Do you know what I'm talking about? Light shapes life. How is it shaping yours? The link below should open your mind.
onlinelibrary.wiley.com/doi/full/10.10…Image
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Sep 13 7 tweets 7 min read
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.Image
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Sep 10 4 tweets 7 min read
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…Image
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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.Image
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