New strategy to augment cancer prevention and treatment suggested by research showing that cancer is a metabolic disease and is reduced by restoring optimum mitochondrial metabolism.
This article notes that cancer turns off the enzyme that ultimately converts glucose into fuel for mitochondria.
By depriving the mitochondria of fuel, ROS is reduced.
ROS radical oxygen species kills cancer cells primed for apoptosis.
Blocking or reducing that enzyme directly or indirectly by fasting/ nutrient deprivation results in increased levels of ROS which drives cancer cell death that can be augmented with cancer treatments.
The Warburg Effect is glucose burning without mitochondrial help. This allows glucose imaging molecules to show cancer like metabolism on PET scans as highly metabolic cells that light up.
It also suggests that increasing mitochondrial metabolism would increase ROS and cancer cell death. For example the Ketogenic diet.
If, however, the ketogenic diet is "running hot" with meaningless noise or H2O2 the UPR unfolding protein response dissipates the ROS produced.
How to run hot with signaling ROS that drives cancer cell death apoptosis without activating the unfolded protein response UFP meant to protect the mitochondria and ER endoplasmic reticulum from harming the non resilient cell?
Clean up noise, ROS, that are unimportant to signaling. (Hydrogen Rich Water)
Block the UPS with mitochondrial/ER specific antioxidant function. (Wheat germ/Spermidine)(sulforaphane)
Add ketones as fuel to produce " important ROS signaling" that kill cancer cells. (Fasting) (modified fasting diet per Valter Longo) (medium chain triglyceride or coconut oil supplements that are metabolized into ketones by the liver- bulletproof coffee)
Breaking Mitochondrial Fasting for Cancer Treatment: Old Wine in New Bottles
Many malignant cells exhibit the Warburg effect, first described by Otto Warburg in 1924 (1). Since then, this phenomenon has been well documented and characterized by augmented aerobic glucose uptake, glycolytic shift, decreased utilization of pyruvate by mitochondria, and increased lactate production, all of which are mainly controlled by hypoxia-induced factor 1 alpha (HIF-1α) and Myc overexpression in neoplastic cells (1). HIF-1α and Myc attenuate mitochondrial function by activating pyruvate dehydrogenase kinases (PDKs), which phosphorylate and inactivate the pyruvate dehydrogenase complex (PDC). Hence, inhibiting the PDKs can shuttle more pyruvate into mitochondrial oxidative phosphorylation and away from lactate synthesis, resulting in oxidative stress, triggering apoptosis, and augmentating host immuno-surveillance, ultimately leading to diminished tumor proliferation (2). Additionally, the Warburg effect leads to increased lactate in cellular and extracellular compartments....
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