This paper explains an abnormal metabolizing or cancer cell treatment strategy. In effect, stress the cell metabolism with restricted calories (decreased carbs and glutamate) followed by specific pulse therapy to damage the increasingly vulnerable cancer cells, while normal cells are strengthened by the effects of fat metabolism product beta hydroxybutyrate that provides survival energy and rejuvenating gene expression of improved metabolic health.
This strategy is advisable for EVERYONE to reverse insulin resistance syndrome because the net result is abundant healthy and resilient cellular mitochondria.
It appears that the myriad nuclear genetic mutations are a RESULT OF and NOT THE CAUSE OF oxidative stress from anaerobic metabolism dependent cancer cells. Why are abnormal cells NOT USING mitochondrial metabolism AND becoming increasingly dependent on anaerobic fermentation (the Warburg Effect)?. METABOLICALLY DAMAGED MITOCHONDRIA!.
It is further speculated that oncogene expression such as KRAS is an epigenic change IN RESPONSE TO declining ATP production by METABOLICALLY DAMAGED MITOCHONDRIA.
I would further speculate that either or both of Sulforaphane and/or Spermidine increases the life span of yeast, worms, fruit flies and mice by 30% because of the improved cellular metabolic health in general and the number and health of cellular mitochondria. What would be even better news is if this strategy caused senescent cells to undergo apoptosis or cell death and replacement by improved and resilient stem cells. It is already proved that stem cells improve with calorie restriction and calorie restriction mimetics. The removal of senescent cells is still an open question.
The above discussion also hints at the continuum of cell health from insulin sensitive to insulin resistant. It suggests why insulin resistant type 2 diabetics have more cancer. The oxidative stress is countered by epigenic changes that express oncogenes that upregulate glycolic fermentation in the cytoplasm BECAUSE mitochondria are metabolically unhealthy.
Therefore cancer may not be exclusively caused by gene mutations but by unhealthy mitochondrial function that potentially can be recovered to health or pushed to apoptosis or natural cell death.
Press-pulse: a novel therapeutic strategy for the metabolic management of cancer
Background
A shift from respiration to fermentation is a common metabolic hallmark of cancer cells. As a result, glucose and glutamine become the prime fuels for driving the dysregulated growth of tumors. The simultaneous occurrence of “Press-Pulse” disturbances was considered the mechanism responsible for reduction of organic populations during prior evolutionary epochs. Press disturbances produce chronic stress, while pulse disturbances produce acute stress on populations. It was only when both disturbances coincide that population reduction occurred.
Methods
This general concept can be applied to the management of cancer by creating chronic metabolic stresses on tumor cell energy metabolism (press disturbance) that are coupled to a series of acute metabolic stressors that restrict glucose and glutamine availability while also stimulating cancer-specific oxidative stress (pulse disturbances). The elevation of non-fermentable ketone bodies protect normal cells from energy stress while further enhancing energy stress in tumor cells that lack the metabolic flexibility to use ketones as an efficient energy source. Mitochondrial abnormalities and genetic mutations make tumor cells vulnerable metabolic stress.
Results
The press-pulse therapeutic strategy for cancer management is illustrated with calorie restricted ketogenic diets (KD-R) used together with drugs and procedures that create both chronic and intermittent acute stress on tumor cell energy metabolism, while protecting and enhancing the energy metabolism of normal cells.
Conclusions
Optimization of dosing, timing, and scheduling of the press-pulse therapeutic strategy will facilitate the eradication of tumor cells with minimal patient toxicity. This therapeutic strategy can be used as a framework for the design of clinical trials for the non-toxic management of most cancers.
Keywords
Glucose Glutamine Mitochondria KETONE bodies Diet Warburg effect Cancer metabolism Glutaminolysis Hyperbaric oxygen
According to the paleobiologists, Arens and West, the simultaneous occurrence of “Press-Pulse” disturbances was considered the mechanism responsible for the extinction of organic populations during prior evolutionary epochs []. A “press” disturbance was considered a chronic environmental stress on all organisms in an ecological community. The press disturbance promoted extinction through habitat loss, reduced reproduction, and restriction of range and resources. Press disturbances would force a biological community into a new equilibrium where previously important species become non-viable. A press disturbance would shift the adaptive landscape to favor the fittest species while eliminating the weakest species. In contrast to the press disturbances, “pulse” disturbances were considered acute events that disrupted biological communities to produce high mortality []. Through extensive mortality in the immediate aftermath of the event, a pulse disturbance could cause extinction. However, survival of some species could occur following a pulse disturbance, as the physical and biotic environments would eventually recover to their pre-disturbance equilibria []. It was only when both the press and the pulse disturbances coincided that mass extinction of species, without recovery, was possible. We describe how a modification of the press-pulse concept can be adopted as a therapeutic strategy for the possible eradication of tumor cells. The press-pulse concept should be best considered in light of current views on the origin of cancer.
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