BEFORE YOU WATCH THE VIDEO READ THE BLOG FIRST………….THEN GO BACK AND WATCH IT.
Throughout the history of oncology research, in both the conventional and alternative cancer research realms, there has been a cause and effect relationship that has been largely ignored. The ability of a cell to divide, whether it be a malignant or non-malignant cell, is highly dependent on cell volume, as well as membrane potential. The collagen tensegrity system is piezo and flexoelectric and releases and absorbs light from the sun diurnally, and this is why cell volume and cancer are related; so when you lose energy and charge in a cell, the cell, mitochondria and nuclear membrane all enlarges. The temporal sequence of the enlargement is what differs. Mitochondrial morphology is one of the earliest changes because of changes in how electrons and protons are used in the matrix.
This is why I call the sun the vaccine for cancer on Earth, and why EVERY paper that looks at Vitamin D3 levels links it to cancer risk and low melatonin levels. If you watch the Vermont 2017 video, then you will see why AM light keeps you far from the cancer state. The volume change is quantized to light frequency and charge of the cells in question. This biggest key is the deuterium fractionation in the cell over all. Where this fraction occurs is also huge.
So when a cell loses energy it can become oncogenic because it enlarges. Our body uses obesity as its defense mechanism in this case. Before it destroys the mitochondria it expands our fatness in the SQ region to store protons and CO2 for later use in TCA cycle, DNA/RNA and in our mitochondrial matrix. Your mitochondria are worthless if there is no light H+ in its matrix. This is the key metric to understanding the bio-physics of the cancer state. The H+ has to be able to make the kind of water than can tunnel out of the matrix to make water and fit into the proton channel in the ATPase. The saved fat in that SQ space is in the protium state and deuterium depleted. This is why animal fat is an excellent source for other animals to eat with a mitochondrial disease. Animal fats are around 110 ppm while DHA family of PUFA’s is the lowest at 101-105 ppm. The reason DHA is so depleted is because seafaring algae and plankton fats have the best deuterium fractionations below 110 ppm.
What about neuro-degeneration? Same story. When an organism is exposed to too much of the wrong frequencies of light, or too little of the right light, electrons build up in the transfer chain in mitochondria. If oxygen is around in this living system when the poor light is present, this buildup can lead to a harmfully reactive oxygen state. If nitrogen is around it can increase RNS. The cancer state is different because it is always associated with an oxygen poor state. So let us put this together. Size is related to charge (redox) and energy state in a cell because of photon frequency controls size and shape. That is the key idea to get. So when the brain expands due to energy loss, CSF water decreases, and your water battery drops at a macroscopic level. This is associated with a drop in DHA or the quality of protons in your DHA in your brain because your ubiquitination rates are increased by nnEMF exposure ( in the case blue light over nnEMF) but likely both are at play. This implies you need a “zip code” change to regain the light frequencies that control this system in this case. Adjuvants are ketosis, carotid cooling, and AM sunrise experiences chronically is needed to radically affect proton spin (H+), CO2 and O2 in your brain’s mitochondria.
http://jackkruse.com/tensegrity-2-cortisol/
Cells that are cycling (dividing), progress through the following phases: G1 (Gap 1) – this is the phase where the cell is preparing for the next phase, which is the S phase, or DNA Synthesis phase. Once DNA synthesis is complete, the cell enters the G2 phase (G 2), where it prepares to enter the final phase, called the M phase, or mitosis. During mitosis, the cell divides into 2 cells. The cell volume is at its smallest at G1, and gradually increases its volume until it reaches its largest volume in the M phase. This should be intuitive, because the cell must become large enough to divide and then support two cells.
Throughout the cell cycle, the cell is constantly monitoring the volume by way of water networks. these networks are directly tied to the mitochondrial matrix ability or inability to make DDW. If the cell does not reach the desired volumes, the cell will be unable to progress to the next phase of the cell cycle.
There is a G1/S transition “checkpoint,” which commonly causes the cell to arrest at this intermediate stage, if adequate volume is not reached. When a cell is arrested due to inadequate volume, there are two possible ensuing events: either the cell will leave the cycle and enter G0 step, and become a dormant, non-cycling cell, or the cell will be recognized as non-viable, and undergo mitochondrial-induced programmed cell death (apoptosis).
It will also increase eNOS to increase albumin in our plasma and the Na /H+ transporter in cell membranes. Cancer cells up-regulate sodium/hydrogen exchangers (Na+/H+ exchangers) because they are looking for light hydrogen in other pathways than the TCA matrix source. This means the cancer state is intimately tied to the inability to generate light hydrogen from the TCA intermediates.
The Na+/H+ exchanger is a membrane-bound protein that transports 1 molecule of Na+ into the cell while effluxing 1 molecule of H+. Water passively follows Na+ (modern belief). Because cancer cells over-express the Na+/H+ exchanger, the cells rapidly pump sodium into their cells.
Water (non structured from the ECF) passively follows the sodium, causing the cancer cells to swell. The oncology folks believes this happens because of the Na/H+ transporter, but it is really due to the loss of the net negative charge from a reduction in the amount of exclusion of water (EZ). Recall that sunlight in the UV and IR range build the largest EZ and the size of the EZ directly effects the Coulomb charge. That Coulomb charge is a synonym for your redox potential in the cell.
Biologic researchers fail to realize that charge is also a quantized property in nature. All cancer cell lines are known to have a lower membrane potential. What they don’t realize is that the membrane potential is lowered because of the lack of EZ production from water in the mtrix of mitochondria by proton recycling in two key steps. A loss of charge can occur from the ECF fraction of water (F- and Br- dielectric blockade), but in healthy mitochondria this is a very small amount. This is why heteroplasmy matters deeply to a mitochondriac. If your mitochondria are in decent shape you will never recycle protons from the ECF. This is why the water you drink in a low heteroplasmy state is not a huge factor. When heteroplasmy rises because of aging or disease then it is a massive factor. The reason will become clear soon.
The result of the loss of net negative charge changes the surface area charge and by the laws of physics the cell MUST get larger. The cell continues to swell as it progresses through the cell cycle, until it reaches the critical volume, at which it divides because cell volume is the stimulus to cell division. So it should be clear that the Na+/H+ exchanger plays a critical role in cancer cell swelling. It is the loss of light and charge of the EZ that causes a cell to swell in cancer states and this is why cancer proliferates and leads to Warburg shifts in mitochondria. When this occurs you can bet the cell is filled with deuterium. The mitochondrial matrix makes deuterium depleted water normally. This type of water makes the ideal liquid crystalline EZ to get the perfect viscosity to run the ATPase spin rates with the 42% of sunlight. Any increase of deuterium ruins this crystalline aspect and this lowers the ATPase spin rate and this is what causes the pseudohypoxia associated with all cancers.
As a result, cellular charge changes in all membranes and cancer manifests because the charge in the blood plasma is what stimulate the liver to make less protein (albumin) and the liver begins to focus on glucose metabolism and the oxidative branch of the PPP to rid the body of deuterium in 5 and 6 carbon sugars that make up every cell membrane in your body and all RNA and DNA.
Albumin is the main carrier protein, produced in the liver, which exerts the large majority of oncotic pressure in the blood stream. Oncotic pressure is a form of osmotic pressure that pulls water from the ECF into the circulatory system. As cancer patients progress in their disease, and become malnourished, their albumin levels fall. They are also usually dehydrated. As their albumin levels fall, the oncotic pressure falls, and water will start to leak out of the bloodstream, causing swelling in the extremities and soft tissue.
Hypoalbuminemia (low albumin levels) is an independent risk factor for death from cancer. Many people do not know this and clinicians have no clue about the links back to protons. Albumin is also a large negatively charged particle that attracts the positively charged sodium (Na+) ion. So as albumin falls, both water and sodium will leave the bloodstream. Low albumin levels, allowing sodium to leave the blood vessels, will cause hyponatremia (low sodium levels).
Hyponatremia is also an independent risk factor for death from cancer too. Low salt labs values are sure sign of high heteroplasmy rate and poor mitochondrial energy. This is why why salt addition might be a great little hack for those who live in a blue light nnEMF toxic world. As a matter of fact, hyponatremia has been shown to be an independent risk factor for death of all causes.
CIRCLING THE DRAIN:
The Vicious Cycle of Cancer: As the cancer patient progresses through their disease, net negative charge is lost everywhere in the body. In nature, all things made of any mass tend to have balanced charges in order to exist.
What happens when the main albumin decreases in the bloodstream. Water and sodium will then passively leak out of the vessels, into the extra-cellular space. Cancer cells, through their over-expression of the Na+/H+ exchangers, will pull the Na+ into their cells, allowing water to passively follow, resulting in cancer cell swelling.
Cancer cell swelling alters the volume relationships inside cells and this allows the cancer cell to progress through the cell cycle, ultimately causing cell division. The ever-increasing tumor burden will cause the patient to deteriorate, and their albumin production will fall. The cycle continues……This is also why exercise helps some cancer patients with decent mitochondria in other tissues. Exercise controls cell volumes by increasing charge in cell membranes to control cell volume.
Why is cancer associated with inflammation? Isn’t inflammation a high pH? yes, and pH is a hydrogen log scale. When our H+ fractionation is more deuterium what happens in tissues? Temperature rises. Why is that the case? Is it because of deuterium? Yes. The added mass of the deuterium requires more energy input from mitochondria to offset the excess neutron mass. Recall that that neutron alters bonding strenght. If the bonds are too strong you need more energy to break them to move things in the TCA cycle in the matrix. Can we see this happening to patients on MRI scans? Yes, we can if we know what to look for. Food cannot salvage a cancer state but food that is deuterium depleted is adjuvant just like chemotherapy acts.
Remember, without food you can live without food for 30 days because of the fat mass under your skin, but you cannot live without water for 7 days. 75% of our body is water that has two version of hydrogen’s in it that vary because of how well mitochondria work. Those two isotopes are H+ and deuterium. People do not realize that neutrons also have a nuclear spin number and neutrons are scattered by light due to their nuclear spin, which causes incoherent scattering!!!!
This means that tissues with a lot of neutrons will have different imaging characteristics than those without neutrons. Coherent elastic scattering gives important information about structure of anatomy while incoherent inelastic gives us information about the internal dynamics inside a cell (bio-chemistry details).
Inelastic scattering experiments in biology are rare up to this point, but this will be a critical part of biology’s future, because of the effect of deuterium on diagnosis using light. INS studies are complementary to IR or Raman spectroscopy too. In the coming age of quantum cancer therpaies this will become critical for physicians to understand.
Today, clinicians do not realize the type of water molecules strongly affect protein fluctuations and protein structure fluctuates thermally. Warmer tissues have more deuterium and are associated with NRF2 activation and cancer states. When thermal changes are present proteins mis-fold in cells. This is how protein mis-folding occurs in cells because of random nnEMF in all neurodegenerative cases.
INS experiments have taught is that hydration with H+ suppresses the harmonic motions of protein in both time and space. Deuterated water alters these harmonics and changes the bio-physics locally around proteins.
This can create a signal for protein replacement by increasing ubiquitin marking. Normally proteins hydration shells should be deuterium free. This water cannot have deuterium for cell physiology and mitochondrial physiology to work optimally. This means getting your water deuterium depleted is way more important than getting the food right when you have cancer. The metabolic machinations of the hydrogen movements in TCA intermediates, glycerol, glycogen, ribose, and glucose is the real job of metabolic pathways in mitochondria because of changes in inelastic scattering. In fact, that is their primary importance to the mitochondriac.
That is the macroscopic view of cancer generation. What does it look like at the small quantum scale?
How would you expect nature build a cell to respond? Might there be a mechanism tied to excessive ELF-UV release tearing through a plasma to some how regenerate us? Why did Popp find all cancer lines release massive amount of light from their cells? Why are mitochondria at this time all running on glucose? Did you know that when high energy photons are traveling through hot and sparse plasma (just like the interstellar medium or deuterium loaded water) they normally get redshifted without scattering light. Did you know that? Mother Nature did…….because she operates by charge and frequency at all times. Even when someone has cancer there is bail outs to help reverse the process because all of Nature is quantized. She knew that red shifted ELF-UV light could be a bail out to increase the red activation of water. This only works if the water is deuterium depleted!!!!!
We make our DDW in mitochondrial matrix. This means the first step in any reversal should be to focus in on proton recycling. When we have too much deuterium inside of us when we are leaking massive light back to the environment in any cancer state. Why?
Fumerase and isocitrate de-hydrogenase control the spin of the TCA.
Most biochemists also don’t seem to know how water is added to TCA intermediates to get into RNA and DNA. Nor do they know about the effects of red and NIR light on nitric oxide (NO) at cytochrome c oxidase or the ATPase spin rate in helping to drive the ECT and the TCA forward either. Few realize the spin rate is quantized to the amount of oxygen a mitochondria needs in this process. The addition of UV-A light makes the forward progress more likely too. This is why cytochrome 1 (NADH/NAD+) is a flurophore chromophore. It absorbs light best from foods and blood sources at 340nm. Fumerase’s main function is to add water to TCA intermediates aconitase and citrate synthetase. The TCA cycle procede foward in do this when UV and IR light and a large EZ is present from the matrix. The tCA cycle occurs in the mitochondrial matrix exclusively.
The hydrogen isotope type is the catalytic controller for succinate and fumarate in the TCA. Nature requires that it must be made of light hydrogen if the cycle is to move forward to reduce oxygen. When it moves the other way, bad things called diseases manifest.
The TCA cycle normally consumes two water molecules per turn in mammals. The first step is by aconitase and the second by the enzyme called fumerase. The second step is the key for the mitochondriac.
This proton is the key for NADPH synthesis for RNA and DNA base creation and for cell membrane creation (DHA) which drives the epigenetic programming that is possible with incident light. Carbohydrates do not have as much hydrogen as saturated fats, so if a diet has more carbs in it, it is more likely to allow a backward flow in the TCA when two conditions are met according to the bio-physics. One, if the light environment changes from the solar spectrum, or there is too much deuterium present in the matrix or the cell.
Saturated fat has the highest amount of hydrogen in them and they are highly depleted of deuterium (110ppm). Kenneth Mellanby was an ornithologist who showed in 1942 that 100 grams of fat makes 110 grams of water for our hydrogen furnace in the matrix when he studied desert animals in 1942.
Mellanby studied desert snakes and noted that they had to have massive lungs and fat stores to make enough water so they did not have to drink water in these environments. This adaptation is why snakes, camels, and desert birds do not have to drink water in the desert to survive. Their mitochondria makes all the water they need if they consume fats from their prey or diet. Camels figured out how to do using fats in plants. This is why the camel humps are 100% fat. Plant fats are around 101-110 ppm.
If you add an good oxygen source to this fat you can make a ton of water in your matrix because of the mechanism Mellanby uncovered in desert animals. This also points out why humans can benefit from hyperbaric oxygen therapy when they have mitochondrial disease, poor lungs, or are obese with sleep apnea. In humans deuterium usually winds up in the liver and cannot escape because of the ATPase channel size. We can see this fat on CT and MRI. To get rid of visceral and subcutaneous fat with defective mitochondrial you can use an exogenous oxygen boost (cold/UV light) to stimulate the burning of fat to make mitochondrial water. Cold stimulates urination and we can eliminate excess deuterium this way as well.
UV light is know stimulator of the oxygen cycle in the atmosphere from ozone and this atmospheric reaction can stimulate venous O2 in animals in the desert. The desert scape normally has a ton of UV light. This is also why snakes light direct sun exposure. It not only raises their temperature, but its main effect is to help oxygenate their body like a hyperbaric machine does on humans.
Mellanby found the enlarged lungs could help desert animals make matrix water from the fat they consumed. It turns out desert snakes have larger lungs and live in high UV environments. This is why light frequencies, altitude, and proton recycling are fundamental bio-physical mechanisms that drive bio-chemical pathways in mitochondria. Note, it is not the bio-chemistry that controls forward flow in the TCA cycle. It is light frequencies and the resultaant charges that do!!!!
This is why diabetics, folks with sleep apnea, and the obese have low superoxide burst. They do not have enough oxygen capacity in their lungs or their hemoglobin to burn their excessive fat loaded with deuterium when they are not in direct solar light. The situation get worse in fake light. If they are in artificial light the oxygen tensions go even lower and pseudohypoxia and low NAD+ result. If these things go low, long enough enough, oncogenesis results.
Nothing stimulates pseudohypoxia like blue light. To make the point clear why biochemistry is a secondary effect to light reactions consider the following. What is the key difference between two rats, one who is alive and the other which is dead?? The dead rat and a live one both have the same bio-chemicals in their bodies, but the key difference in both is how light energy and protons are able to act in both. The biochemical pathways are identical and it that points out why just understanding the bio-chem is immaterial to a clinician.
NITTY GRITTTY:
The hydrogen at cytochrome 1 in the NADH/NAD+ couple is carried all the way to cytochrome 4 to make matrix water. So the NAD+/H connection is the key reaction in the TCA cycle in mitochondria. The hydrogen’s are taken from the metabolites of the TCA intermediates in health. The most interesting step of the TCA cycle is that not all carbons spots are oxidized in the turns of the cycle and water is consumed by these steps while oxygen is being reduced. Mammals use water for reductive synthesis very differently than desert animals.
In fact, when mammals cannot use water in this way, cancer is much more likely because the TCA cycle flow reverses, ROS changes, and the cell leaks ELF-UV light. Moreover, the cell has to rely on a hydrogen supply from other sources. It’s only choice is from foods and water that makes up the ECF space.
Mutations of fumerase is a classic example in renal cell cancers. Fumerase (Szent Gyorgi) main function is to add water to TCA intermediates. Hydrogen type is the catalytic controller for succinate and fumarate in the TCA and it must be made of light hydrogen. The cycle consumes two water molecules per turn in mammals. The first by aconitase and the second by fumerase. The second step is the key is the key for CANCER. Why?
This proton is the key for NADPH synthesis for RNA/DNA synthesis and cell membrane turnover (DHA). Cells become unable to use TCA intermediates when fumerase or isocitrate dehydrogenase have enzyme defects (deuterium stops flow because bonding energy is too high compared to H+) The matrix must limit dueterium in them to recycle hydrogen fast enough to turn the TCA forward to reduce oxygen. This make heteroplasmy a quantum problem tied to sticky enymes. You don’t need a gene defect to cause cancer. This is why we are not solving cancer. We have no idea that a gene defect is uneeccasry because we seem to have forgot that all enzymes work via proton tunneling!!! If the protons are deuterium they work a lot more slowly because they have increased bond strenght. This means to break the bond a cell needs more energy added to overcome the isotope effect in the TCA. This is why cancer cells emit more ELF-UV light. They are trying to overcome the bonding strength and rid the matrix of deuterium.
The fractionation of deuterium affects the circular flow or energy flux of the TCA cycle because of the excessive kinetic isotope effect. This tells us the direction of flow in the TCA cycle is associated with wellness or illness in the mitochondrial matrix.
The weight of hydrogen in NADH is also a big key in understanding how the kinetic actions in the ATPase pumps work with the movements of hydrogen in TCA intermediates. This explains fully why Warburg found what he did.
The more deuterium cells have in the matrix and NADH, the more altered energy production is in the matrix and the less brisk is proton recycling. this occurs simultaneously at one time. Cells cannot recycle mitochondrial matrix water, and when this occurs and they must use other areas to get a source of light hydrogen.
When hydrogen recycling is broken in the matrix, TCA intermediates increase slowly over decades, as the cycle slows further with time, pyruvate cannot get into the mitochondria and no substrates can be oxidized in mitochondria at ALL. This is what really happens in a Warburg shift at a quantum level.
QUANTUM CLINICAL PICTURE OF CANCER
What also happens simultaneously in the cytosol is the key to cancer: the cells NADPH pool begins to have its deuterium levels rise. This is really bad news for RNA/DNA bases that are made by the PPP that use NADPH as its main reducing bio-molecule (EMF4).
The desaturates enzymes (fumerase and isocitrate dehydrogenase) inside of mitochondria are the main deuterium depleters in mammalian matrix. When they fail, volumes change in mitochondria, heavy water gets trapped in the matrix, and heteroplasmy manifests as size increases in the mitochondria.
We often will see fat in the liver, and that fat is loaded with deuterium of we use MRI to see it. Tissue energy production drops like a rock, and this means oxygen levels must also drop as a consequence. This is why pseudohypoxia and low NAD+ levels were found in Sinclair’s 2013 paper.
Why does ketosis help in any heteroplastic state? 90% of Acetyl Co-A comes from fats in the TCA cycle. We know this because of data we have from stable isotope studies that prove it. It’s been shown that ketogenic diets can deplete the TCA intermediates down to 110ppm IF WE CAN USE THEM IN DEFECTIVE MITOCHONDRIA. Not all cancer patients can. This is why ketosis is an adjuvant and not a cure for all cancers.
Different TCA metabolites build up inside the mitochondrial matrix and those metabolites are associated with different cancers because bonding energies change in many biochemical pathways as a collateral effect. This is not a gene issue……it is a deuterium issue. Where deuterium winds up acts as sticky glue in bio-chemical pathways and this tells us how proton dysfunction leads to energy loss and oncogenesis. Protons must be recycled in mitochondrial matrix to reverse a cancer state. They are massively important as the initial steps of oncogenesis before the nuclear genome is turned on, to allow the NADPH pool to exert its deleterious effects on RNA and DNA.
The goal of mitochondria is to have a low deuterium content so that NADPH creates DNA with way more hydrogen in it than deuterium. The amount of oxygen in a cell is stochastically linked to where hydrogen recycling comes from in a cell. So when oxygen tensions are proper in tissues, ROS will remain stable, and hydrogen will be pulled into the NADPH pool from the mitochondrial TCA intermediates. The Ferrari will purr.
CANCER AND METHYLATION IS ALSO A DEUTERIUM STORY
The TCA intermediates have a base fractionation rate of 120 ppm of deuterium which is fine for RNA/DNA stability. What happens when deuterium gets in RNA and DNA? They become sticky because of the increased bonding energies of deuterium. The methyl groups become impossible to move epigenetically using light frequencies in a cell. This is why cells increase ELF-UV light release in cancer. They are adding energy to the bonds to BREAK THEM!!!! (FUNCTIONAL MED FAIL)
When deuterium enters the methyl groups on RNA and DNA it alters methylation kinetics because of the kinetic isotope effect of deuterium, The presence of deuterium in nucleic acids affect DNA methyltransferase enzymes and the repair enzymes for DNA. Its presence also increase aneuploidy because chromosomes cannot pull apart as they should due to the amount of deuterium in the 3’ and 5’ positions that increased bonding strength. Aneuploidy is always associated with cancer.
This means the next step in oncogenesis is deuteration of RNA/DNA. This happens before methylation defects. So how does deuterium get into DNA? When oxygen drops, cells stop using protons from TCA intermediates for their hydrogen source. Cells also stop using TCA for hydrogen harvesting when they have to use the serine oxidation glycine cleavage system. The serine glycine cleavage system is a back up system for H+ harvesting. It is made up of an H-protein, a protein that carries the amino-methyl intermediate and then hydrogen through the prosthetic lipoyl moiety, and a L-protein, a common lipo-amide dehydrogenase like lignoceric acid. Lignoceric acid is a fatty acid that makes up the lipid rafts of all eukaryotic cell membranes including the nuclear membrane. It controls the size and shape of the the nuclear membranes!!!! And here we are back to the link to size and thermodynamics.
When cells can no longer harvest H+ from the matrix they default to free water in a cell which is made up from the ECF and carbohydrate metabolism to get water. Both places have a much higher deuterium content than the matrix. The third fail safe to gain hydrogen is via the pentose phosphate pathway (PPP: EMF4 blog) because of its link to sugar metabolism.
This one is the fastest go to for heteroplastic mitochondria because the hydrogen source is deep, but it has the highest amount of deuterium in a cell. In fact, the anticancer drug Gleevac blocks this pathway to cure some blood cancers. Note I SAID CURE. If you fix the hydrogen problem cancer is curable.
Gleevac blocks the ability of a cell to harness bad hydrogen from the oxidative branches of the PPP and then the last bailout is water we drink. If we are wise we make sure our water is always deuterium depleted below the 120ppm if possible. It is not possible in all locations. This is why Australia and New Zealand really have a cancer problem and why I’ve been adamant about drinking better water there. Now you know why 100%!!!!
So why is the Warburg shift associated with glucose? Is glucose really bad or is it really a deuterium story? Cells have to default to glucose when a cell cannot get its light hydrogen from the beta oxidation of fats due to a defective matrix filled with deuterium. All a cell has left to use is glycolysis, the PPP, and SOGC pathways or ECF water. In a cancer state it is the ONLY source for light hydrogen to fix the issue.
All four fail safes are loaded with deuterium compared to the matrix. The mammalian matrix runs at 110-120ppm. This explains why DDW works in cancers because it adds in DDW water via the oxidative branches of the PPP to offset the loss of hydrogen harvesting in the matrix. Eating fats can make the matrix situation worse when you understand all these details. It shows you why I am a stickler for details now.
Deuterium’s isotope effect causes DNA to be a heavy sticky mess because the deuterium content increases bonding energies. Deuterium will not let go of enzymes to do their job in the matrix!!!! This means we lose the ability to recycle DDW water!!
It also means that all cell membranes are going to be loaded with deuterium too. They become quite sticky as a result. This affects the lipid rafts where DHA controls the lipid cytosocial architecture in how they operate with incident light frequencies. Why? NADPH is also the main reducing element in making cell membrane fats!!!!!
The deuterium content ruins optical signaling with ELF-UV because deuterium massive increases bonding energies anywhere it is located in a CELL!!!!! So you might begin to see why this proton thing is a BIG DEAL!
It also explains why cancer states are associated with more ELF-UV light release when our deuterium fractions are up. The cell knows it needs more light power to overcome the bonding strength of deuterium in the cell membranes. Deuterium also make chromatin sticky and it blocks normal functioning of unwinding DNA for coding and protein translation. It ruins everything a cell needs to do in running through the cell cycle. This is why tje growth switch stays ON and why cancer manifests.
WHAT ABOUT THE NUCLEUS?????
Nuclear lipid microdomains (NLMs) are critically different in cancer and normal cells. Cerebrosides are the common name for a group of glycosphingolipids called monoglycosylceramides which are important components in animal muscle, nerve cell membranes, and the eukaryotic nuclear membrane. Monogalactosylceramide is the largest single component of the myelin sheath of nerves (think MS now). Deuterium is the main cause of sticky AQA 4 gates in neurons and this is why myelination is broken. You cannot make myelin when deuterium is sticking all the pathway enzymes together. Sphingomyelin is a cerebroside and make up the largest FA in myelin and nerves. When both have a ton of deuterium in them disease result where the deuterium is.
Lignoceric acid is another FA that is in many cerebrosides in the nuclear membrane. In fact, lignoceric acid makes lignocerate which maintains aneuploidy and makes 30% of the structural lipids of the nuclear membrane and controls the size and shape of the nucleus.
Research has shown that NLMs lose saturated very-long-chain fatty acid (FA; C24:0) called sphingomyelin series of FA’s in cancer cells and become enriched in long-chain FA (C16:0) sphingomyelin series of FA’s. These lipids all need to be deuterium depleted to work properly photo-electrically.
Chromatin relies on the nuclear membrane lipid raft for proper photo-electric operation. Lipid microdomains are localized in the inner nuclear membrane and are considered the main lipid platforms for active chromatin anchoring in humans. Lignoceric acid and DHA are fatty acids in these locations which are critical in these lipid rafts. DHA is a depelted marine PUFA that controls how these rafts are built.
The amount of deuterium in these membranes is also linked to the mitochondrial matrix proton recycling network. It turns out DDW has been shown to result in deuterium depleted lignoceric acid in the nuclear membrane in cancer too. This change has been associated with a decrease in size of the nuclear membrane. This decrease in size is a thermodynamic
changes that explains to us why DDW improves matrix proton recycling via the oxidative branch of the PPP and ECF water. When this occurs, by itself, guess what the research has shown? Tumorigenicity of tumors DROPS dramatically. Still think cancer is a genetic disease or a mitochondrial one?
Stimuli such as surgery, deuterium fractionation, vitamin D3 status, DNA duplication, RNA synthesis, or glucocorticoid drugs influence their gene expression because of the amount or lack of deuterium in the receptors that control the down stream effects.
WHAT ABOUT METHYLATION?
Here is proof positive your function docs don’t get it.
Methylation defects can go both ways and cause cancer research. So if deuterium increases the bond strength of methyl groups you can easily see how this epigenetic program links it to cancer. Cancer-associated DNA hypomethylation is as prevalent as cancer-linked hypermethylation, but these two types of epigenetic abnormalities usually seem to affect different DNA sequences. If your methyl groups have deuterium in different spots (CH4) it will effect how tumor genes and suppressors can or cannot function. It has nothing to do with the gene more often then not.
Much more of the human genome is generally subject to undermethylation rather than overmethylation in cancer. Genomic hypermethylation in cancer has been observed most often in CpG (cytosine is made by the PPP) islands in gene regions.
In contrast, very frequent hypomethylation is seen in both highly and moderately repeated DNA sequences in cancer, including heterochromatic DNA repeats, dispersed retrotransposons, and endogenous retroviral elements. Also, unique sequences, including transcription control sequences, are often subject to cancer-associated undermethylation.
The high frequency of cancer-linked DNA hypomethylation, the nature of the affected sequences, and the absence of associations with DNA hypermethylation are consistent with an independent role for DNA under-methylation in cancer formation or tumor progression. Increased karyotypic instability and activation of tumor-promoting genes by cis or trans effects, that might include altered heterochromatin-euchromatin interactions, may be important consequences of DNA hypomethylation which favor oncogenesis. All of them are ruined by deuterium increased binding capabilities.
So why is blue light associated with cancer and deuterium fractionation?
Yes blue light is everyone’s big issue. Why? Blue light has less energy in its photons than UV light does. It cannot separate deuterium from TCA intermediates as well due to the lack of power. It also turns out NADH is a fluorophore molecule in cytochrome one that best absorbs 340nm light. What is the light detector of NADH? FADH2 in cytochrome two. What are all flavins responsive to in mammals? blue light frequencies. Riboflavin is the base of all flavins and it acts like a cryptochrome. Guess what it is really bad news? All cryptochromes that control circadian biology are run by flavin proteins in them. So this is how blue light ruins your cytochromes. This also allows more deuterium in the NADPH pool for RNA/DNA synthesis via the PPP for creation of the nuclear bases. The bases need the correct amount of light hydrogen in them to run our epigenetic programs. Remember in photosynthesis water is consumed and not made. D20 in water consumed in plant foods like carbohydrates by photosynthesis means more sunlight exposure is required to break the bonds deuterium forms inside of cells. The kinetic isotope effect of deuterium cause it to form STRONGER bonds not weaker ones. Blue light is incapable of breaking those bonds so it allows more deuterium to remain in NADPH, cell water, and in our cell membranes. So deuterium acts like an optical switch for this reason. Cells appear to want less deuterium to run mitochondrial metabolism smoothly with good flux. We know that Blue light also releases cytochrome C in position 4 to cause mitochondrial swelling. It also destroys DHA levels and melatonin in cell membranes lowering your ability to load sulfated cholesterol with electrons. The hydrogen atoms in NADPH is needed to recycle cell membranes to so deuterium can affect this replacement cycle as well if there is too much deuterium present there. It turns out with normal oxygenation levels, then and only then, NADPH proton recycling goes through the mitochondrial matrix and this is a cells anticancer move. Pseudohypoxia cause more deuterium in the NADPH pool. Blue light hazards also LOWERS your melatonin levels in your brain’s mitochondrion which raised heteroplasmy rates and allows more deuterium inside the mitochondria. It also makes your gut microbiome more simplified because it destroy the anoxic environment it needs to communicate with cytochrome one. Remember your mitochondria used to be a bacteria and it is designed to communicate with cytochrome 1 via the NADH and NAD+ levels. So when cytochrome 1 is broken and it is in most blue light toxic people. (insert Mr. Moore) you get increased blue light toxicity. Nothing matter when you live in a microwaved blue lighted world. This is why Mr. Moore and many others using ketosis are failing………..and you need to understand why he is. I am just the dude with the flashlight showing you why they might be dead wrong.
That is the basics of cancer bio-physics.
Is there another switch in this story that links the entire mechanism to nnEMF? Yes. Calcium. Alterations in calcium ionic resonance is why nnEMF from blue light, RF, and microwaves cause cancer. How you ask?
There is a growing consensus that the various forms of cell death (necrosis, apoptosis and autophagy) are not separated by strict boundaries, but rather share molecular effectors and signaling routes. Among the latter, a clear role is played by calcium (Ca2+), the ubiquitous second messenger involved in the control of a broad variety of physiological events. Fine tuning of intracellular Ca2+ homeostasis by anti- and pro-apoptotic proteins shapes the Ca2+ signal to which mitochondria and other cellular effectors are exposed, and hence the efficiency of various cell death inducers. Calcium controls all the voltage gates on the surfaces of cells. This means it is the switch that controls charge on the surface of a cell. It also means this where voltage drop leads to cell volume expansion. When this occurs system wide in a human changes are immediately produced in the blood plasma and this is what simples the microbiome using light frequencies to build up fat mass to protect the human stem cell line. This is why the obesity paradox exists and it is why obesity seems to be linked with most cancers.
Sunlight is a tyrosine kinase inhibitor and a natural calcium channel blocker. This…….this is why SUNLIGHT is cancer’s ideal vaccine because it raises our charge by exciting electrons and making a larger EZ to increase the net negative charge; hence, this is why D3 levels and a low albumen level are linked to oncogenic risk. The ability to harvest the information and energy in the subatomic particles in our tissues and water eventually decays back to ground state. If you do not have the ability in your cells, plasma, or tissues to capture the red shifted energy you lose it to the environment and entropy rises all tissues and their mitochondria swell and this = high heteroplasmy.
Your tissues has a time window to capture this energy and altering your environment is the SMARTEST move you need to make in this time window. This is why the circadian mechanism exists and is primordial. Circadian cycles are linked to the red shifting of light release in our hot plasma of our cells loaded with heteroplastic mitochondria. That is why red giants are the longest lived stars and why those with the longest healthy longevity are sun worshippers.
That is the basic bio-physics of cancer risk.
Still afraid of the sun? Still think genes are the cause of cancer??
BECOME A MITOCHONDRIAC!!!!!
CITES
Tensegrity 2 blog post by Jack Kruse MD
https://www.cellsignal.com/contents/science-protein-kinases/protein-kinases-interactive-human-kinome/kinases-human-kinome
“Redshift of photons penetrating a hot plasma” Ari Brynjolfsson https://arxiv.org/abs/astro-ph/0401420
https://www.medicalnewstoday.com/articles/319390.php
https://www.ncbi.nlm.nih.gov/pubmed/11797936
https://www.ncbi.nlm.nih.gov/pubmed/18815148?dopt=Abstract
https://www.popsci.com/science/article/2011-01/chinese-invent-new-method-producing-healthier-light-water
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2844952/
http://www.cell.com/cell-metabolism/fulltext/S1550-4131(17)30567-3
http://pubmedcentralcanada.ca/pmcc/articles/PMC4571297/pdf/2418.pdf
https://www.nature.com/articles/1205651