Target and Eliminate Cancer without Harm

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Conventional Therapies Cause Too Much Harm

Eliminating visible tumors is often a necessary step in treating cancer. Although conventional therapies (such as high-dose chemotherapy, radiotherapy, targeted gene therapies, and monoclonal antibodies) may be effective in shrinking tumors, they do it at the expense of damaging healthy cells and tissues resulting in a burden of harmful side effects. This damage affects the most rapidly dividing cells in the body, like the lining of the digestive tract, the hair, the cells made in the bone marrow, like red blood cells, white blood cells, and platelets, as well as the nerves in the hands and feet. All of this results in nausea, loss of appetite, ineffective digestion, constipation, diarrhea, suppressed immune system, peripheral neuropathy (tingling and loss of feeling in hands/feet), fatigue, depression, and difficulty sleeping. In addition to the extreme effect on the quality of life, metastatic spread to other organs is enhanced by various methods.

Targeting CFC Stem Cells to Prevent Metastases

One glaring disadvantage of conventional treatments is their inability to eliminate CFC (cancer) stem cells, which comprise only 0.5-1% of the cells in a tumor.  Because they are highly adaptive and metabolically flexible due to the fact that they are essential to survival, CFC stem cells are resistant to both chemotherapy and radiotherapy. Their major importance in this regard is that they are the only cell type that can form metastases in distant organs. The vast majority 90% of deaths from CFCs are caused by metastases, not the primary tumor.  What has been proven repeatedly and published in peer-reviewed studies and, hence concluded by most experts is that chemotherapy and radiotherapy are not only ineffective against cancer stem cells, but they actually enhance the ability of CFC stem cells to metastasize. Therefore, while conventional treatments may seem to work at first by eliminating the primary tumor, they greatly increase the risk of distant metastases that are the ultimate cause of death in most cases.

However, there are multiple compounds and medications proven and published in oncology journals to be effective in eliminating CFC stem cells. Therefore, the utilization of these medications is an essential aspect in not only eliminating the CFCs that currently exist in the body but also, in the prevention of CFC recurrence.

Metronomic Chemotherapy

There are still situations where the use of chemotherapy is obligatory such as life-threatening location of a tumor or a heavy tumor load. In these cases, a method of treatment known as metronomic chemotherapy can be used. Metronomic chemotherapy is the administration of low doses (10%) of chemotherapeutic agents, where there are far less unwanted effects and what’s more, there is enhancement of immune function and prevention of angiogenesis, i.e., new blood vessel growth required if a tumor is to grow.

We take this one step further and utilize a biological response modifier called insulin, which allows us to target the tumors, not the other, healthy cells. CFCs, having a greater need (19 times greater) for glucose (sugar) than healthy cells, have anywhere from 6 to 17 times more insulin receptors to pick up glucose.  The administration of insulin which would naturally be followed by the entry of sugar tricks cancer cells into engulfing the accompanying drug. This way a minimal dose of chemotherapy can be selectively targeted to cancer cells while healthy cells are spared, and the side effects minimized.

Metabolic Therapies

Other than low-dose, insulin-potentiated chemotherapy required for certain situations, the main method by which CFCs are targeted causing no harm to healthy cells is called, metabolic therapies. In order to use these therapies, a firm understanding of the biology of CFCs is required. For example, when CFCs go through their transformation from normal cells to CFCs, they downregulate (decrease) certain enzymes because they are no longer needed and upregulate (increase) other enzymes that are necessary for their new metabolic requirement of fermentation.  Furthermore, certain genes that were “silenced” (inactive) previously are now turned on and others that were active are now ‘silenced’. The result is a very different type of cell with different enzymes and different capabilities than the normal cell from which it arose.

Understanding these metabolic differences, mostly with regards to differing enzymes, one is able to put the CFCs in a position where they are required to neutralize a molecule or compound, but they lack the enzymatic capability, hence they die. The healthy cells, however, still have these enzymes for this specific purpose, hence either nothing happens to them or they receive a benefit.  Vitamin C, for example, being a reductant (antioxidant) donates one or two electrons wherever needed. So, since one of vitamin C’s primary functions is to keep iron in an active state (Fe2 ) when it encounters iron in its inactive state (Fe3) it donates the electron and one of the byproducts is the production of oxidative molecules, including hydrogen peroxide. This is the well-known Fenton Reaction required frequently to turn or slow down (modulate) the activity of the HIF-1 pathway required for wound healing or when producing neurotransmitters, like adrenaline and serotonin, etc., as well as many other reactions needed to sustain life. Since CFCs have many more receptors to pick up iron (transferrin) they need more iron than healthy cells because they are dividing so quickly, when vitamin C enters the tumor microenvironment, it does its job resulting in excess hydrogen peroxide. CFCs have very little catalase, so they are unable to neutralize the hydrogen peroxide, hence they are oxidized and killed, whereas the healthy cells use hydrogen peroxide frequently and have more than enough catalase to neutralize it. When catalase neutralizes hydrogen peroxide, the products are H2O (water) and O2 (oxygen), which are nutritive or healthy for normal non-CFC cells. Hence, good for the “good guys” and bad for the “bad guys”.  There are many other metabolic therapies, all of which take advantage of the enzymatic limitations of CFCs, such as artesunate (artemisinin), amygdalin, curcumin, quercetin, other botanicals, ozone, dichloroacetate (DCA), and more.

Strategy to Overcome the Resilience of CFCs

Since CFCs arise as an adaptive set of responses to the stress of having to function without oxygen, they are able to withstand harsh environments with much more ease than normal healthy cells. For this reason, when they are exposed to a very toxic chemical (such as chemotherapy), they learn to adapt quite readily and are said to be “resistant”, whereas the healthy cells do not have that degree of metabolic flexibility and usually fail to adapt and die. This is why the standard way of giving chemotherapy is called maximum tolerated chemotherapy, meaning that is the highest amount that can be given without killing the person. Even though the doses are highly toxic and even kill many of the CFCs, after a few doses the CFCs often learn to eliminate the toxin so quickly that they remain unharmed.  This is one of the reasons and advantages of insulin potentiated low dose chemotherapy because the CFC cannot “close” or turn off the insulin/glucose “door” since it is required for survival. Using insulin then allows more of the chemotherapy into the CFC than it can eliminate and so whereas the person was said to have developed “resistance” to a particular drug or group of drugs in a certain protocol, that same protocol will be effective in killing the CFC when used with insulin.

So, CFCs being so “clever”, it is extremely difficult to attempt to kill them with one or two methods due to their metabolic peculiarities and flexibility. This leaves us with the winning strategy of using multiple metabolic therapies at the same time. Perhaps one of them is given three times per week, another two times per week, another five times per week, and another two or three times a week, etc. Since each of these therapies requires a different enzyme that the CFC does not have and the CFC is having to expend so much energy in an attempt to protect itself on many different fronts daily, it becomes “exhausted”.

If one has also changed their internal biochemistry by following all of the suggestions for “stop making cancer” such that the body is clean, well nourished, and highly functioning producing an internal environment that is no longer suitable for the needs of CFC, which require a low oxygen, highly acidic, and inflamed milieu to survive and now, the CFCs are being exhausted daily with multiple metabolic therapies, all that remains to happen is reactivation of the immune system from the “hypnotic trance” that was induced by the CFCs. Then, not only are all CFCs and their stem cells eliminated but there is no way for them to start up again with an optimally functioning (healthy) body and an unencumbered immune system.

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References

Agrawal S., Woźniak M., Łuc M., Makuch S., Pielka E., Agrawal A., Wietrzyk J., Banach J., Gamian A., Pizon M., Ziółkowski P. Insulin enhancement of the antitumor activity of chemotherapeutic agents in colorectal cancer is linked with downregulating PIK3CA and GRB2. Scientific Reports. 2019; 9: 16647. doi: 10.1038/s41598-019-53145-x 

Chaffer C., Weinberg R. A perspective on cancer cell metastasis. Science. 2011 Mar 25;331(6024):1559-64. doi: 10.1126/science.1203543.

Huang T., Song X., Xu D., Tiek D., Goenka A., Wu B., Sastry N., Hu B., Cheng S. Stem cell programs in cancer initiation, progression, and therapy resistance. Theranostics. 2020 Jul 9;10(19):8721-8743. doi: 10.7150/thno.41648. 

Karagiannis G., Condeelis J., Oktay M. Chemotherapy-induced metastasis: Mechanisms and translational opportunities. Clinical and Experimental Metastasis. 2018 Apr; 35(4): 269–284. doi: 10.1007/s10585-017-9870-x. 

Kareva I., Waxman D., Klement G. Metronomic chemotherapy: an attractive alternative to maximum tolerated dose therapy that can activate anti-tumor immunity and minimize therapeutic resistance. Cancer Letters. 2015 Mar 28; 358(2): 100–106. doi: 10.1016/j.canlet.2014.12.039.

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