Cancer: Can often be won by diet alone. (sometimes not)

posted 300 days ago by NOT_ADMIN 300 days ago by NOT_ADMIN +100 / -1

This is how cancer grows and how to fight it.

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.
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.
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.
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.
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

Cautionary Note:
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.
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.
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.

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– NOT_ADMIN [S] 6 points 299 days ago +6 / -0

Diet alone is too myopic to really move the needle

This is false. There are plenty of cases showing exactly this.

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.

You dont know if this is a cause or an effect. Perhaps cancers starve the body of D3. Or perhaps D3 is protective lower levels lift that protection avenue.

When a cell loses energy (see below) it can become oncogenic because it enlarges.

I agree that there are avenues what may cause the cancer, I am speaking specifically on fighting cancer through starvation.

that siad i like what you posted, here is a clearer rewrite:

Cell Cycle and Volume Monitoring:

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.

G1/S 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.

Role of Na+/H+ Exchanger in Cancer:

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 Negative Charge and Cell Swelling:

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.

Connection to Mitochondria and Deuterium:

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.

Role of Albumin and Charge in Cancer:

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.

Vicious Cycle of 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.

Inflammation and pH in Cancer:

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.

Importance of Mitochondrial Function:

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 and Mitochondrial Function:

Water, containing different isotopes of hydrogen, plays a crucial role in cellular function, and the isotopic variation is linked to mitochondrial efficiency.

TLDR There is a relationship between cell volume regulation, mitochondrial function, and cancer progression. It suggests that the ability of cells to produce Deuterium-depleted water (DDW) is crucial for advancing through the cell cycle. The Na+/H+ exchanger is highlighted as a key player in cancer, influencing cell swelling and progression. The loss of net negative charge, linked to factors like sunlight exposure, is implicated in cancer cell swelling. Additionally, the importance of mitochondrial function, albumin levels, and inflammation in the context of cancer shows the complex interplay of cellular mechanisms and environmental factors in cancer development.

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