This is how cancer grows and how to fight it.
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Aerobic Glycolysis (Warburg Effect): In normal cells, glucose is metabolized through a process called aerobic respiration, which involves glycolysis followed by the citric acid cycle and oxidative phosphorylation in the mitochondria. However, cancer cells tend to favor glycolysis even in the presence of oxygen, leading to the production of lactate as a byproduct. This allows cancer cells to generate energy rapidly, support their high proliferation rates, and adapt to the microenvironment of tumors.
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Lactate Fermentation: In addition to aerobic glycolysis, cancer cells may also rely on lactate fermentation. This involves the conversion of pyruvate, a product of glycolysis, into lactate. This process helps regenerate the cofactor NAD+ (nicotinamide adenine dinucleotide), which is required for glycolysis to continue. Lactate fermentation can occur under both aerobic and anaerobic conditions, contributing to the metabolic flexibility of cancer cells.
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Oxidative Phosphorylation (OXPHOS): Some cancers rely on oxidative phosphorylation for energy production rather than aerobic glycolysis. This is more typical in certain tumor types and can involve efficient utilization of mitochondrial function.
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Glutamine Metabolism: Glutamine is an amino acid that cancer cells can use as an alternative substrate for energy production and as a source of carbon and nitrogen for biomass synthesis. Some cancer cells exhibit high dependence on glutamine metabolism.
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Fatty Acid Oxidation (FAO): In addition to glycolysis, cancer cells may enhance fatty acid oxidation to meet their energy needs. This is particularly relevant in certain cancers where lipid metabolism is upregulated. This could be a problem for ketogenic diet solutions as it increase Fatty Acid availability in the body. This is why a meat based diet which is higher in proteins and lower in fats than typical keto diet is recommended.
- SOLUTION: A carnivore ketogenic diet + Fasting, which involves low carbohydrate intake and increased consumption of fats, can hinder aerobic glycolysis in cancer cells.
- The rationale behind this lies in the reduced availability of glucose, a primary substrate for glycolysis. Secondarily, it induces Glycogen Depletion. the body will shift its energy metabolism away from glucose utilization toward the breakdown of glycogen and fatty acids.
- As glucose levels decrease, the rate of glycolysis and, consequently, lactate fermentation may decrease.
- Some studies suggest that a ketogenic diet may influence mitochondrial function, potentially affecting oxidative phosphorylation.
- Fasting has been associated with an increase in the utilization of glutamine by certain tissues, including the liver and immune cells. This adaptation may provide an additional energy source during periods of nutrient scarcity.
- Switching to Keto and fasting may cause mitochondrial Stress: Increased reliance on oxidative metabolism might place stress on mitochondria, potentially leading to the induction of apoptosis (programmed cell death) in cancer cells with mitochondrial dysfunction
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Cautionary Note:
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Enhanced Fatty Acid Availability: A ketogenic diet increases circulating fatty acids, which could potentially provide more substrate for FAO, and this may support the growth of certain cancers that thrive on fatty acid metabolism.
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Ketone Body Utilization: Some cancer cells may adapt to utilize ketone bodies as an energy source, potentially sustaining their growth even under conditions of reduced glucose availability.
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It is important to lookup and learn what type of cancer you or your loved one has, and what mechanisms your cancer uses for growth.
Diet alone is too myopic to really move the needle. The Biophysics of how light interacts with biology is the key orchestrator of how biochemistry works or goes awry.
EVERY paper that looks at Vitamin D3 levels links it to cancer risk and low melatonin levels. This alone tells the curious mind that the solar exposure and light/dark cycles in one's environment are the critical factors.
When a cell loses energy (see below) it can become oncogenic because it enlarges. To get into the nitty gritty, here is the real reason why the Warburg shift is observed in oncogenesis:
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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's ability or inability to make Deuterium-depleted water (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 (protium isotope, in cotrast to the heavy hydrogen isotope deuterium) 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.
Non structured water from extra cellular fluid (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 zone of water (EZ). Note that SUNLIGHT in the Ultraviolet (UV) and Infrared (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 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 DDW water makes the ideal liquid crystalline EZ to get the perfect viscosity to run the ATPase spin rates with the 42% IR from sunlight. Any increase of deuterium in the wrong place 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.
that siad i like what you posted, here is a clearer rewrite:
Cells constantly monitor their volume through water networks. The ability to produce Deuterium-depleted water (DDW) in the mitochondrial matrix is crucial for cell progression through the cell cycle. If a cell fails to reach the desired volume, it may be unable to progress to the next phase, particularly at the G1/S transition checkpoint.
At the G1/S checkpoint, inadequate volume can lead to cell arrest at an intermediate stage. The cell may either enter the G0 step, becoming a dormant non-cycling cell, or undergo programmed cell death (apoptosis) if recognized as non-viable.
Cancer cells up-regulate sodium/hydrogen exchangers (Na+/H+ exchangers) to seek light hydrogen from pathways other than the TCA matrix source. Na+/H+ exchangers transport sodium into the cell, causing water to passively follow. Cancer cells swell due to the influx of water, which is linked to the loss of net negative charge from a reduction in the exclusion zone of water.
Loss of the net negative charge, influenced by sunlight exposure, leads to changes in the surface area charge of the cell. Cancer cells swell as they progress through the cell cycle, reaching a critical volume that triggers cell division.
Mitochondria play a role in the production of Deuterium-depleted water, crucial for maintaining the ideal conditions for cellular processes. An increase in deuterium in the wrong place is associated with lowered ATPase spin rates, leading to pseudohypoxia observed in cancers.
Decreased albumin levels, produced in the liver, lead to reduced oncotic pressure, causing water leakage and swelling in cancer patients. Hypoalbuminemia and hyponatremia are independent risk factors for death from cancer.
The progression of cancer leads to a loss of net negative charge throughout the body. Decreased albumin in the bloodstream causes water and sodium to leak out, contributing to cancer cell swelling and progression.
Cancer is associated with inflammation, and the text suggests that inflammation involves high pH. Deuterium in tissues can lead to increased temperature due to the added mass requiring more energy input from mitochondria.
Exercise is mentioned as beneficial for cancer patients with decent mitochondrial function as it helps control cell volumes by increasing charge in cell membranes.
Water, containing different isotopes of hydrogen, plays a crucial role in cellular function, and the isotopic variation is linked to mitochondrial efficiency.
Simple refutation: if your assertion is correct, then there must be higher cancer incidence where people live under less sunlight overall. Eskimos did not have cancer until their diet changed to "white man's food." Nordic people don't have higher cancer rates than anyone else in first world countries. People in the lowest parts of South America also do not vary in cancer rates.
Your independent facts may be valid but your narrative assembly is illogical and unsupported by evidence. Perhaps sift through the data freshly, and recategorize causal factors versus symptoms? Take into account real life observations of recovered patients, other deficiencies perhaps like D3 or B17 (that last one is a deep rabbit hole).