Month: July 2024

Fact: Blue light/nnEMF dehydrates cells because they stop H2O production from the mitochondrial TCA cycle. Why is this a big deal? Neurons absorb and release water when firing information. When H2O is MIA so are neurological function/capabilities. You lose the ability to sleep and account for time in your molecular clocks when water is absent. This is why children experience time differently than adults. Less water, less sunlight, or more ALAN at night destroy the clock timing mechanism of living things. Few see this recipe in life’s blueprint

You have to remember Vitamin D is a proxy for your time machine mechanism buried inside your mitochondria.  Your job is to see Nature’s science, then understand what it means for your longevity when you are sick.  This is a huge big deal if you complied and got jabbed. Without electrification of the phospolipids in your membranes you are asking for a jab complication.

Every person has a different efficiency rate of their time machines based on how the mechanism is built to operate.  Few see that Vitamin D is just a bystander in how the process works and this is why when your Vitamin D comes back is a very complex answer.

Here is how it operates.

Did you know the molecule of “more time” (melatonin) acts to aggregate melanosomes in cells to organize them magnetically at night when light is absent?

Did you know the molecule of “more time” optimizes another time crystal in mitochondria called tryptophan in NAD+ tell mitochondria where the Earth is in relation to the sun in a calender year to “fact check” seasonal light variations?

The non visual photoreceptor system in the skin integument, like cholesterols/melanin,  concern themselves with the powerful UVB sunlight to create vitamin D as a bystander chemical that acts to electrify the membranes of mammals.  This allows for carbon fixation as the top line in the slide shows. Different domains of life use timing and genes to change where energy flows. For example, plants have their own particular route of  carbon fixation, converting inorganic carbon  in carbon dioxide into organic compounds. They use sunlight to do it. Sunlight is turned into a DC electric signal in its membranes to store energy at the electronic level.  Carbon is primarily fixed through photosynthesis, but some organisms use chemosynthesis in the absence of sunlight. Mammals do this. They use their livers to replace the sun. The fixation of carbon dioxide into the skeletal muscle glycogen in intact fasted mammals is best explained by electrification of their membranes which leads to secondary deposition of glucose in the muscle supplied primarily by the liver. We know this by isotopic labeling.

THE ELECTRIFICATION OF MAMMALIAN CELL MEMBRANES IS DONE BY SUNLIGHT.

The sun light is turned into a DC electric signal which turns on the biosynethic decision making abilities in cells.  The phtonic skin signal informs the liver and kidney what to do with cholesterol and Vitamin D from this point.  The wisdom in your body should amaze you.

Did you know the that the molecule of “more time”, melatonin,  also controls the only two programs that recycle your mitochondrial engines, autophagy & apoptosis?   Go look two pictures above. It is right there on the bottom of the slide. Without melatonin creation by mtDNA, the quality control mechanism in mt DNA manifest in your heteroplasmy rate.  That rate becomes your healthspan and your possible longevity in your life.  This is why sunlight links to longevity. That is why the slide below exists.

The efficiency of your mitochondrial “time machines” links to ROS/RNS production from mitochondrial metabolism, which in turn, controls all the magnetochemistry that controls how timing inside of cell directs the flow energy in your key metabolic pathways. Timing alone, controls the decision tree in cells that says, “should this tissue use beta-oxidation, glycolysis, gluconeogenesis, the PPP to get the job of living in this environment.

Melanin, also made from UV A,B,C light controls the levels of ROS/RNS that is coming out of the mitochondria in cells. This is a UNIQUE signal (Kruse for Dummies idea).  Melatonin, Melanin, and Vitamin D and NO all manifest from UV light’s interactions with matter in your cells.

Darkness at night, due to the absence of light, cools cells so that magnetic effects in melatonin can use second messengers in cAMP and Ca2+ to aggregate melansomes located around your mitochondria to do its magics inside of cells to tell time to control energy flows.  You can fixate carbon and nitrogen at night using the energy stored in biomolecules in your liver to run the dark program without light.

For light to have its full biological effect, photons must be absorbed by visual and non visual photoreceptors in the living body.  If one or both are missing, there is no effect. ROS/RNS creation in mitochondria and left over oxygen from metabolism begin this timing process.

Superoxide and H202 are a type of ROS made in mitochondria when we are healthy.  Melanin keeps both in check. When do we make ROS during the day?  When the sun is out.  This is when cells also make melanin.  It is also when Vitamin D has an opportunity to be made as well.

BUT WHAT IF YOUR VITAMIN D DOES NOT RESPOND TO SUNLIGHT?

WHY BEING IN THE SUN & still having a low D3 level & STILL BEING SICK TELLS ME YOU GOT A VITAMIN A/nnEMF PROBLEM?

You know Vitamin D is yoked to Vitamin A right. I’ve only said it 1000 times in blogs and podcasts. So when you live in the sun and Vitamin D does not rise here is why——-> https://lnkd.in/e6zptMZW

Non native EMF destroys your clock timing mechanism in your cells and you lose the ability to control the flow of energy in cells. Disease results and you lose time and longevity. That is the story of life in a few words.

Now that the story ion timing is complete, you can see that any kind of blue light or non-native EMF basically uncouple vitamin A from melanopsin. That released retinol from the non visual photoreceptors destroys dopamine, melatonin, melanin, and all heme based photoreceptors so that light becomes useless to cells. This is why a low Vitamin D level is possible with a tan integument or a fit looking body. It does not mean your healthy. Without proper timing longevity is impossible. There is a reason this pictured is my pinned Tweet on X.

Blue light and nnEMF becomes a nuclear weapon for all photo receptors. So you’ll be interested in this. “You may not know it, B12 is a photoreceptor in humans. B12 is another non visual photoreceptor in the liver, CNS, and circulatory system.

And guess what happens when you have melanopsin and retinol damage to B12 levels? That’s the reason why vegans have such demolished B12 level and shrinks their brains and destroys their non visual photoreceptors everywhere, including MELANIN. When melanin goes, timing inside a cell is lost. Magnetochemistry in mammals controls how energy flows. It also controls periodicity in the clock genes and makes the job of the SCN easy. When this goes awry the SCN mechanism becomes uber important to control the molecular clocks in the mitochondria of tissues.

Daylight is always associated with higher electric fields and lower magnetic fields and this correlates to mornings having higher ROS production and melanin production.  It is not always linked to Vitamin D levels because UVB light is highly variable based on your latitude and light stability.   This effect is seen in mitochondria and it helps tan your interior.

THE TIME CRYSTAL BURIED IN CYTOCHROME 1 IS MADE OF TRYPTOPHAN IS NAD+ THAT LINKS TO MELATONIN BIOLOGY

The morning AM ROS burst at cytochrome 1 (NAD+/NADH) links to the PER2 gene in the mammalian clock mechanism to begin to measure entropy in cells. These effects are rooted in the spin selected ROS partitioning between the free radicals created from metabolism, superoxide and H202, known as the radical triad/pair mechanism of quantum mechanics.

SUMMARY

Energy is trapped directly at the electronic level in cells. Energy is stored as vibrational & electronic bond energies in biochemicals (PER/HIF-1), but also in the structure of the system: its membranes, and in gradients, fields and flow patterns, compartments, organelles & cell water and tissues only gain their organization behind their QED magic. That magic is done in how time controls the flow of energy in clock genes. Just wearing sunglasses does this. This is why people who wear sunglasses burn so often. It is an issue of timing and a loss of magnetochemistry.

Clock genes and time crystalline proteins that ticked when they absorbed light in some way were used to coordinate all zip codes inside the Jacquard cards of biochemistry in cells to measure the entropy to control the overall flow of energy in metabolic pathways. Time controls the flow of energy in matter and this allows cells to extract information about where the Earth is in relation to the sun. The sun created the most powerful protein in Earth’s history (melanin) because it can harvest the entire power potential buried in the electromagnetic spectrum.  When melanin is heated up it becomes a supreme electrical conductor. When it cools it mimics what a superconductor can do with magnetic flux in light. This allows for electron- electron interactions and for electron-phonon coupling only seen in superconductors. Yes, we have superconductive proteins in us that operate with light, temperature, and precision timing.

Water was the plasma for most of Earth’s history, but nature created melanin to work with water something unique occurred.  The binary code of life that builds order from chaos begins by deciphering the code that exists between H+ and deuterium separated from water and plugged into ancient biochemical pathways to sculpt something new.

Ocular and integumentary melatonin levels both end in leptin biology.  This is why the leptin receptor sits behind the retina and infront of the hypothalamus that controls energy balance. It also explains why our subcutaneous fat sits just below the skin, and why leptin, the hormone that links to the leptin receptor in the brain visits the brain every night during the dark, in the hypothalamus to adjust the clock timing mechanism in the SCN. Few see Nature’s recipes.  Hopefully some of you can start putting the science of the blogs together like a QUILT.

Cellular disorganization is always linked to poor timing and its effects always manifests in disease creation before death manifests; Disease and death are an immutable ledger built as a consequence of how time does or does not flow in our clock timing mechanisms in cells. In this way, we always seem to get the sense that illness comes before death in most living sequences unless we are talking acute trauma. This points out why the information of the organization is as important as energy flux in a cell to maintain wellness. Timing is the MOST critical ingredient in Nature’s recipes.

When timing is off inside of a cell, the energy cost become prohibitive for a cell in a diseased person whose tissues are afflicted with defective mitochondrial DNA. This amplifies the need for precision accuracy, and when that periodicity is absent, this amplifies the creation of new mutations in the mitochondrial genome. This further lowers energy production and this further magneifies timing efficiency and forms a doom loop for the cell. The phenotype in the cell when timing is lost is the alteration of epigenetic signaling mandating for higher turnover. Mitochondria mutations speed up nuclear genome action. When the nuclear genome increases it is for one reason: To fix the atomic arrangement of atoms inside of a cell to recapture the timing mechanism required for living. The nuclear genome is designed by nature to be quite stable and quiescient.

Mitochondrial DNA is more vulnerable to alteration than nuclear DNA, for two reasons.

First, mitochondria are a major source of intracellular reactive oxygen species (ROS). Therefore mitochondrial DNA is designed to be under much stronger oxidative stress than is the nuclear DNA.

Second, mitochondria have a matrix-side negative membrane potential to carry out oxidative phosphorylation. This electric membrane potential concentrates lipophilic cations inside mitochondria up to approximately 1,000-fold.

That electric potential called redox power is created by the trsansformation of sunlight. This is how light controls metabolism. Light > Food always. It is axiomatic.

 

CITES

https://www.nih.gov/news-events/news-releases/neurons-absorb-release-water-when-firing-nih-study-suggests

https://x.com/DrJackKruse/status/1613309435073413121

https://journals.aps.org/prb/abstract/10.1103/PhysRevB.109.245132

How do eukaryotic cells make light from matter? It all begins with the fact that oxygen is the terminal electron acceptor for eukaryotes mitochindria. The oxygen molecule O2 displays some very particular features. It is a paramagnetic gas. It is the second most electronegative element in the periodic table. Because of this one should expect that O2 is a very reactive chemical compound. Counterintuitively, however, it is a quite unreactive molecule on Earth. How can I say this? . A testimony to this is the decentralized fact that we live in a planet with a 21% oxygen atmospheric content, and nevertheless life thrives and even depends on it.

The reason why O2 is so much unreactive than we expect this atom to be, in spite of its electronegativity, is the fact that in the fundamental state it assumes a triplet electronic configuration. Triplet electronic configuration occurs when the valence electrons arrange in the O2 molecule has the electronic configuration with the least energy. According to the molecular orbital theory, this arrangement has a triplet character. Triplet character occurs when the two outermost electrons in oxygen have different antibonding orbitals, but with the same spin state.

3^O2 expresses the triplet character of the ground state. This ground state has a biradical chemical character, which renders it quite unreactive to most chemical compounds. This triplet character of oxygen makes ground state O2 a paramagnetic compound, where oxygen gas tends to move to the point of strongest magnetic field. This is why oxygen is drawn to your colonies of mitochondria. Mitochondria create a magnetic field because they have electron movements along its innermitochondrial membrane while having a spinning ATPase on that same membrane. This makes all mitochondrial respiation electromagnetic at the most fundmental level.

Implications of this for cells? The cell cycle is controlled by light creation in cells.

The metabolic rate in our mitochondria drives developmental timing by controlling the cell cycle.

Having light stored at the electronic level is critical to the mystery of morphogenesis.

Back at the origin of life 3.8 billion years ago on Earth electric membranes drove CO2 fixation by converting gases from volcanoes (driven by the solar plasma) into organic chemicals to create growth in the absence of oxygen. This was the first step life took at the ocean floors.

Metabolism has always been spontaneous on Earth. Today, we believe complex life emerged from ancient autotrophic pathways fueled by volcanic gases as carbon and the sun as ultimate energy sources. Variants of these pathways remain in modern autotrophs in the deepest branches of the tree of life. In this way, the DC electric current in membranes preceded all chemistry. The energy metabolism of modern autotrophs resembles the geological interactions of H2 and CO2 gases in hydrothermal vents. Centralized science believes this points to a metabolic origin of biochemistry at the interface of the lithosphere and hydrosphere. Decentralized science believes this points to a quantum thermodynamics at the core of life because the sun drives all these processes. This step is fundamentally why light tops food in all my discussions.

Reactive oxygen species (ROS) are formed during normal metabolic processes. Mitochondrial respiration is spontaneous on Earth. Genes amplify metabolism and in this way, gene products are capable of making more or less light from how they amplify or de-amplify metabolic networks in cells.

ROS are magnetic signal created from excess oxygen in mtDNA. People forget molecular oxygen is the only paramagnetic gas on the periodic table. This makes it a unique magnetic signal used in cellular communication. All free radicals have one unpaired electron to make them magnetic sugnals. All ROS are called singlet oxygen signals that come from mtDNA actions. When electrons are added to a magnetic molecule this is called a reduction type of reaction. When singlet oxygen is reduced by the addition of electrons, the ROS magnetic signal shifts to a lower energy state and as a result emits photon.

The electronic transition of electronically excited species from the singlet or the triplet excited state to the ground state is accompanied by photon emission. This is how light is crerated by life. In this mechanism only a few photons are emitted per second per square centimeter, the photon emission is ultra-weak in nature. But it is these photons that explain how light sculpts life.

Reactive oxygen species are formed during the metabolic processes linked to life-sustaining enzyme-catalyzing reactions. They also can be formed during the response to stress reactions when any life form is exposed to biotic and abiotic stress factors from our environment. When ROS are effectively scavenged by the antioxidant defense system, the oxidative effect of ROS on biomolecules such as lipids, proteins and nucleic acids is fully prevented.

HOW IS ENDOGENOUS LIGHT CREATED?

Cells cannot product light without oxygen or ROS/RNS made in mitochondria. Mitochondria are not only time machones, they are factoried for biophotons. That is the bare minimum and is confirmed in Roeland Van Wijk book on the topic of biophotons. During the process of cellular respiration, electrons are transported through a series of mitochondrial complexes to the terminal electron acceptor, molecular oxygen (O2). In the process of cellular metabolism, the electrons released from the ETC react with O2 to produce superoxide (O−2) radicals. Mitochondrial complexes I, II, and III contribute to the maximum in redox signaling. Superoxide radicals generated at complexes I and III are released into the intermembrane space which comprises 80% of superoxide radicals generated in the mitochondria and remaining 20% are made by mitochondrial matrix.  The mitochondrial permeability transition pore in the outer membrane of the mitochondrion allows the passage of superoxide radicals into the cytoplasm where it is dismutated to hydrogen peroxide, a highly diffusible secondary messenger. This reaction is catalyzed by superoxide dismutase located in the mitochondrial matrix (MnSOD) or in the cytosol (by Cu/ZnSOD).

Furthermore, aquaporin 8 serves a channel for the release of hydrogen peroxide from the cell membranes.  There is an another major site for the generation of ROS termed as peroxisomes where superoxide and H2O2 are generated through xanthine oxidase in the peroxisomal matrix and membranes. Other sources of ROS include endogenous metabolites such as fatty acids, prostaglandins, and exogenous components including drugs, flavorings, coloring agents, antioxidants, etc. These substances are processed in the smooth endoplasmic reticulum and transformed into free radicals, especially ·OH. Macrophages and leucocytes, as a part of immune response contribute to the formation of free radicals

SO NOW YOU KNOW HOW ROS ARE MADE, HOW DO THEY TRANSFORM MATTER TO EMIT LIGHT?

However, under circumstance, when the formation of ROS exceeds the capacity of antioxidant defense system, biomolecules in cells spins are changed by magnetic forces in mitochondria. The single unpaired electron of ROS oxidizes lipids, proteins in both nuclear genome and mitochondrial nucleic acids. This interaction leads to the formation of high-energy intermediates like singlet oxygen. The decomposition of high-energy intermediates generates the electronically excited species which undergo an electronic transition from either the singlet or the triplet excited state to the singlet ground state. When there is an electronic transition of electron spin light is liberated.

When electron spin is changed, & our biomolecules are changed and the result in matter in our cells is to liberate light.

Singlet oxygen, systematically named dioxygen and dioxidene, is a gaseous chemical with the formula O=O, which is in a quantum state where all electrons are spin paired. It is kinetically unstable at ambient temperature in cells, and its rate of decay is slow.

Singlet oxygen (represented as 1ΔgO2, abbreviated as 1O2 in papers) is not a radical but represents an excited state of O2 in which the spin of one of the unpaired electrons is changed to yield two electrons with opposite spins. The terms ‘singlet oxygen’ and ‘triplet oxygen’ derive from each form’s number of electron spins. The singlet has only one possible arrangement of electron spins with a total quantum spin state of 0, while the triplet state has three possible arrangements of electron spins with a total quantum spin of 1, corresponding to three degenerate states. An excellent way to detect the presence of singlet oxygen in reactions is using steady-state or time-resolved measurements to find its characteristic phosphorescence at around 1270 nm.

When oxygen is reduced by losing an electron, singlet oxygen is created chemically. Singlet oxygen is an reactive oxygen species (ROS). The loss of the electron shifts the biomolecule to a lower energy state and as a result it emits photon. RNS works exactly the same way. This is how mitochondrion make light from matter.

The oxidation of biomolecules occurs by hydrogen abstraction by superoxide anion and hydroxyl radicals or by the cycloaddition of singlet oxygen initiate a cascade of oxidative reactions that lead to the formation of electronically excited species such as triplet excited carbonyl, excited pigments and singlet oxygen. The abstraction of hydrogen is defined by the removal of a hydrogen atom or group from a molecule by a free radical. Hydrogen/deuterium atom abstraction is often confused with deprotonation, which is the removal of a hydrogen atom (i.e., a proton) by a base in an acid-base (proton transfer) reaction.

When deuterium is abstracted out by light cells need to use more UV light to do so because you need more VUV-UVC-UVB-UVA light to abstracted the heavier isotope of hydrogen because of the extra neutron. Generally, the way oocyte selection occurs in mammals is by hydrogen abstraction. The oocytes with the lowest atomic mass are ejected first. during menarche. As time elapses, the eggs with the most deuterium and released last because more light is needed to get that job done. This drains the electronic level of its stored light.

This means the older a pregnancy becomes the more light is needed in the transgenerational process. In this way you can see now why high maternal age and transgenerational epigenetic diseases occur. It is also why more chromosomal abnormalities occur as mammals age. If the UV light is expended abstracting deuterium there is less light left at the elctronic level to drive the cell cycle past the mitosis level. This is a huge problem in infertility, cancer, and in morphogenesis (autism)

The photon emission of these electronically excited species is in the following regions of the spectrum (1) triplet excited carbonyl in the near UVA and blue–green areas (350–550 nm), (2) singlet and triplet excited pigments in the green–red (550–750 nm) and red-near IR (750–1000 nm) areas, respectively and (3) singlet oxygen in the red (634 and 703 nm) and near IR (1270 nm) areas. The understanding of the role of ROS in photon emission allows us to use the spontaneous and stress-induced ultra-weak photon emission as a non-invasive tool for monitoring of the oxidative metabolic processes and the oxidative stress reactions in biological systems in vivo, respectively.

Transcriptional regulation of proteins is done by GLUT expression by ROS in cells.

Since ROS is made from excess dissolved oxygen not used in mitochondria, when oxygen in cells decreases, ROS signaling becomes more unique because of scarcity. This should make you think about my Kruse for Dummies lecture.

Low oxygen triggers signal-transduction pathways involved in both cell death and survival. Anoxia activates proapoptotic BCL-2 proteins and caspases to initiate apoptosis. The adaptive cellular events that occur in response to hypoxia are mediated largely by the transcription factor hypoxia-inducible factor-1 (HIF-1)

During hypoxia, ROS levels increase by design and play an important role in HIF-1α stabilization. HIF-1 consists of two subunits, HIF-1α and HIF-1β. Under normoxic conditions, prolines within the oxygen-dependent degradation domains (ODDs) of HIF-1α are hydroxylated by prolyl-4-hydroxylases (PHDs; Ivan et al. 2001). This hydroxylation mechanism acts as an ubiquitination signal leading to proteasomal degradation of HIF-1α. In the absence of oxygen, HIF-1α ubiquitinylation is inhibited allowing its interaction with HIF-1β to drive transcription of various target genes, including GLUT1. This is the basis of how the Warburg shift occurs in humans.

Stimulation of cellular glucose uptake in mammalian cells is frequently observed during conditions of oxidative stress when ROS and RNS spikes. GLUT1 helps in the transport of glucose, galactose, mannose, glucosamine and ascorbic acid in mammals.

HIF-1 induces the expression of multiple antiapoptotic BCL-2 proteins to promote cell survival. Interestingly hypoxia increases production of mitochondrial reactive oxygen species (ROS), which serve as signaling molecules to activate HIF-1.

Hypoxia-inducible factors (HIFs), are major molecules that respond to hypoxia and elevated temperatures to play important roles in cancer development by participating in multiple processes. HIF1 is linked to circadian clock controls, metabolism, proliferation, and angiogenesis. The Warburg phenomenon reflects a pseudo-hypoxic state that activates HIF-1α. In addition, a product of the Warburg effect, lactate, also induces HIF-1α. However, Warburg proposed that aerobic glycolysis occurs due to a defect in mitochondria. I believe the defect occurs, first, in the circadian mechanism to affect mitochondrial metabolism. Moreover, both HIFs and mitochondrial dysfunction can lead to complex reprogramming of energy metabolism, including reduced mitochondrial oxidative metabolism, increased glucose uptake, and enhanced anaerobic glycolysis

HOW DOES HYPOXIA LINK TO ALTERED TIME STAMPING IN CELLS?

Circadian clocks are endogenous coordinators of the 24-hour rhythm of behavioral and molecular processes in living organisms. For humans, a master clock modulating circadian rhythms is located in the suprachiasmatic nucleus of the hypothalamus and is a pacemaker of the system. In mammals, the circadian clock is comprised of a set of genes, which function as activators—CLOCK and BMAL, which, similarly to HIF, are bHLH-PAS transcription factors.

HIF-1α GENE HAS A TRANSCRIPTION REGULATORY ELEMENT TO ALTER THE CIRCAIDAN CLOCK MECHANISMS. THIS IS HOW DIESESE ARE CAUSED IN THE MODERN WORLD.

Through binding to regulatory elements containing E-boxes (also present in HIF-1α gene) they activate the transcription of repressor protein period (PER) and cryptochrome (CRY). Additionally, HIF can bind to promoter regions of repressor proteins through hypoxia response elements (HRE), causing their transcrioptional upregulation leading to altered cell signaling. This is how the redox shift leads to alien light creation to lead to genetic changes we see in ALL CANCERS.

It is believed in centralized science that mitchondrial ROS oxidizes lipids, proteins and nucleic acids and thus initiate a cascade reactions that leads to the formation of electronically excited species responsible for the photon emission in near UVA, visible and near IR regions of the spectrum. I think this is a simple explanation for what is really going at the atomic level in a cell.

To make it crystal clear how bad the advice centralized medicine is giving patients you just need to review this thread in the context of what is being clearly laid out in this blog. Read this thread below in blue before going on.

https://threadreaderapp.com/thread/1754147699799040292

COVID AMPLIFIES THIS SCIENCE FOR THE SLEEPING SO THEY WAKE UP WHERE MODERN DISEASES COME FROM

TURBO CANCERS, mRNA, SV40, CIRCADIAN MISMATCH LINKS TO BIOPHOTONS

p53 is an important tumor suppressor gene, found to be mutated or absent in over 50% of all cancers studied. It functions as a sequence-specific DNA-binding transcription factor. In response to double-stranded DNA breaks, p53 is converted from a latent to an active form. This results in increased expression of p53-responsive proteins such as p21 which are required for growth arrest at the G1-to-S phase transition. It also mediates apoptosis via the increased expression of proteins such as Bax. Inactivation of p53, therefore, results in the loss of a cell cycle checkpoint control required for repair of damaged DNA and prevents apoptosis in response to severe DNA damage. In the absence of these responses, oncogenic mutations which may result in tumor progression can accumulate in nuclear DNA and this can happen quickly in people who took the mRNA jab. The damage can accumulate rapidly. From the above, it is clear that the transcriptional activation function of p53 is critical to its role as a tumor suppressor gene. Since genes amplify metabolic networks, p53 clearly clearly has a lot to do with the biophoton spectra that cells emit.

Note the history of the discovery of p53 brings us back to the story of SV40 and the polio vaccine. That is why Pfizer erased it from their plasmid map in the mRNA platform.  Simian virus 40 (SV40) large tumor antigen (T antigen) has been shown to inhibit p53-dependent transcription by preventing p53 from binding to its cognate cis element.

Why is p53 called p53?

One must know the history and the discovery of the most studied gene in human history, also known as the guardian of the genome.  Why is it considered the guardian of the genome?  Aneuploidy refers to the state of unequal chromosome copy numbers and is one of the most prominent genomic aberrations in solid tumors.  Most solid tumors are aneuploid, and p53 has been implicated as the guardian of the euploid genome.

How long did the pulse of cancer stay in human cancer data from the Cutter incident of the Polio vaccines?

Bernice Eddy found the SV40 in the Salk vaccine and told the world about it in th emid 1950s’  The NIH and FDA ruined her career over her admission and scrubbed their websites.  Most people ran from studying SV40 after this event in centralized science until the Nixon administration. What cancers in humans are linked to SV40 contamination?

In the 1970s, David Lane & Arnie Levine started studying a virus called SV40. Their interest was in a viral gene responsible for transformation, the SV40 oncogene called large T antigen.  Lane’s task was to extract the large T antigen protein from cells infected with SV40. He used electrophoresis to separate the protein molecules based on size and charge.  Whenever he ran electrophoresis to purify the large T antigen, he always found an unknown protein with a molecular weight of 53 kilodaltons. Initially, others in Lane’s lab thought it was a contaminant or a breakdown product of the large T antigen.  As reports of this protein came from other labs too, it was named p53 based on its molecular weight.

In 1979, immunological studies identified the p53 protein due to its immunoreactivity with tumor antisera, suggesting its role as a tumor-associated antigen. Everyone was convinced they had found a new oncogene. The excitement was high!  Wait a minute—did I say oncogene? p53 is actually a tumor suppressor gene! This is my favorite plot-twist of the p53 story: its mischaracterization as an oncogene.  The initial misclassification was due to the research climate of the time (1980s). Oncogenes were thought to be the key to understanding cancer, and the idea of a tumor suppressor gene was in its infancy.

As mentioned above, p53 was initially found bound to the major oncogenic protein of SV40, so it was understandable at the time to think it must be an oncogene as well. However, some experimental observations did not fit well with the idea that p53 was an oncogene.  In 1986, the first tumor suppressor gene, Retinoblastoma gene (RB1), was discovered, confirming Knudson’s Two-Hit hypothesis.  In 1989, this two-hit model was applied to p53, specifically in colorectal tumors. It fit this model, as in virtually all cases, both copies of p53 were mutated.

This conclusion was confirmed by subsequent findings that patients with inherited mutations of p53 were predisposed to diverse tumor types. Mice with engineered “knock-outs” of the p53 gene were also tumor-prone.  Today, more than 70,000 research papers are published on p53, making it the most studied human gene in history. Mutations in p53 are found in >50% of human cancers.  “It’s impossible or very difficult to get a malignant tumor without the activity of p53 being disrupted.” ~Bert Vogelstein, a legendary figure in p53 story who was the first to termed it as a tumor suppressor gene.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4855935/

SUMMARY

New centralized data does not support a role for p53 in aneuploidy surveillance in organotypic cultures. There is strong evidence indicating that the loss of p53 is associated with chromosome instability and poor prognosis in the development of several cancers. See the papers (Donehower et al., 2019; Foijer et al., 2014; Fujiwara et al., 2005; Watson and Elledge, 2017)

When p53 goes awry the majority of tumors show varied TP53 mutations based on the following papers: (Clausen et al., 1998; Muller and Vousden, 2013). Live-cell imaging of Trp53+/+ and Trp53 & mCOs showed that mitotic errors, including lagging chromosomes and multipolar mitoses, occurred frequently in cells lacking p53, consistent with several published studies (Artegiani et al., 2020; Drost et al., 2015).

The bottom line issue for me? Decentralized science must show that when p53 signaling goes awry, it corresponds to a lack of ultraweak -UV biophoton production at the mtDNA level. This is why apoptosis goes awry and this also corresponds to the following variables: Low mtDNA melatonin production, low mtDNA water production, and altered mtDNA CO2 production in most solid tumors. This results in cell cycle arrest and cells begin to migrate to other tissues that have the ability to generate the ultra weak UV biophotons to complete the cell cycle.

 

CITES

1. https://www.pnas.org/doi/full/10.1073/pnas.1431692100

2. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8208645/

3.  https://x.com/DrJackKruse/status/1804162237528998309

4. https://x.com/DrJackKruse/status/1803877114598314228