GREAT!. make sure it is truly all he gets. No "treats"

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.
• Low carbohydrate intake, which leads to reduced glucose availability. In response, cells may shift to alternative energy sources, including fatty acids and ketone bodies.
• 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.