How Does Cancer Start?
To effectively prevent and treat cancer, a clear understanding of the origin and nature of cancer is essential. This newsletter presents a perspective on cancer that is somewhat different from the alternative and integrative practitioner’s viewpoint. It is also different from the general consensus among cancer researchers.
Mainstream oncology views cancer as build-up of genetic mutations. This is partially true but the big question is whether the genetic damage is to nuclear or mitochondrial DNA. This newsletter will explain what type of genetic damage is initially responsible for the onset of a malignant tumor or cancerous process.
The conventional approach utilizing surgery, chemotherapy and radiation does not address the root cause nor does it attempt to modify the internal environment that allows tumors to grow and proliferate. The primary object is to kill fast proliferating cells. Mainstream oncology does utilize hormonal therapies which are of value in breast and prostate cancers. Herceptin has value in HER-2 positive breast cancers. Unfortunately, mainstream oncology has limited tools to target vulnerabilities that are unique to cancer cells. Drugs that target certain genetic mutations have not been of great value.
Much has been said about cancer being the result of a failed immune system by the alternative cancer doctors featured in “The Truth About Cancer” series by Ty Bollinger. This is a patently false and scientifically unsupported idea. Cancer begins and progresses independent of the immune system. Cancer is seen in individuals with perfect immune function. 20% of cancers may be virally induced so a healthy immune system is important for cancer prevention. Cancer cells highly express CD47 which is called the “don’t eat me signal”. Cancer cells utilize many different mechanisms to evade the immune system and actually use the immune system to their advantage. Immunotherapy drugs unleash the immune system creating a systemic autoimmune storm which causes damage to organs and does not always result in much effect on the tumor mass.
Cancer, defined in the simplest terms, is mitochondrial DNA damage to stem cells. Cancer originates from stem cells or sometimes called embryonic cells. These cells exist for tissue repair or regeneration and can remain dormant for one’s entire life. Every human cell contains from 200-2,000 mitochondria except red blood cells. The primary job of the mitochondria is generating energy(ATP) for the cell. Glucose is converted to pyruvate in the cytosol. Pyruvate enters into the mitochondria where it feeds into the TCA cycle and electron transport chain generating a very high yield of ATP. Damaged mitochondrial DNA disrupts the TCA cycle and electron transport chain forcing cancer cells to up regulate glycolysis.
Mitochondrial DNA is very different from nuclear DNA. Mitochondrial DNA is circular where nuclear chromosomal DNA is linear. Mitochondria maintain multiple copies of DNA and there are not the same DNA repair mechanisms that are present in nuclear DNA. Mitochondrial DNA codes for very few genes compared to nuclear DNA and is mostly involved in regulating the TCA cycle and electron transport chain. Nuclear DNA damage is after the fact and is not the primary driver of carcinogenesis.
Stem cells possess unique characteristics that are different from regular cells. One key characteristic of stem cells is in the way they divide. Stem cells reproduce by creating an exact copy of themselves and a progenitor cell. Cancer stem cells behave exactly in this same manner. Cancer stem cells are the seed bed for tumor cell generation and for effective cancer treatment, these cancer stem cells must be eradicated or switched off.
Stem cells generate all of their energy from glycolysis even though they have intact and functional mitochondria. The high glucose metabolism of cancer cells is therefore not acquired but is already a characteristic of the stem cells from which they originated. Stem cells up-regulate UCP2 which inhibits mitochondrial ATP generation. Cancer cells also up-regulate UCP2 which limits oxidative stress that would be generated if the mitochondria were fully functional.
Inflammation is clearly related to cancer progression. The question is whether inflammation is a byproduct of the tumor environment or the cancer cells expressing inflammatory signals. Both may be true. Inflammation drives stem cell activity and tumor progression.
What appears to be going on in cancer is a process of rebuilding tissue which is what stem cells do but in a chaotic and unregulated manner. All this is happening at a high rate of growth for most cancers. Cancer cells are gobbling up nutrients to synthesize proteins and cell membranes. Growth can be slowed by limiting the pool of essential amino acids.
Cancer can theoretically begin from damage to one single stem cell. It may take 30 years or more for that single stem cell to divide many times over to become a detectible tumor. Cancer typically appears at least 7-10 years from the initiating phase according to mainstream oncologists. The actual time frame can be much longer. Tumor progression can be accelerated by dietary factors, metabolic imbalances and stress.
What causes mitochondrial DNA damage? Ionizing radiation, excess UV radiation, cosmic radiation, free radicals, excess oxidative stress, antibiotics, toxic chemicals, viruses, pesticides, herbicides, toxic bacterial byproducts and potentially various pharmaceutical drugs are the major cancer initiators. How does one protect oneself from these cancer initiators? Selenium supplementation is very important in chemo-prevention as is eating a plant-based diet of mostly organic and unprocessed foods. One should try to avoid all chemical exposures and X-rays. EMFs emitted from electronic devices have not been proven to be cancer causing but one should always use a hands free cell phone. Smart meters are not a threat to human health. Stress or emotional trauma does not cause cancer but is most certainly involved in cancer promotion.
How does this knowledge affect how cancer is treated? Effective treatments must target both tumor cells and cancer stem cells. Treatments should target key metabolic vulnerabilities of both tumor cells and cancer stem cells. Inflammation must be appropriately regulated. Understanding that mitochondrial damage is the key dysfunctional element in cancer cells and the gatekeeper of apoptosis should drive all treatments towards mitochondria as the primary target. Most of the nutraceuticals utilized within the NORI protocol are directly target the mitochondria. The idea is to damage already damaged mitochondria to trigger the release the cascade of signals that regulate apoptosis. Increasing oxidative stress (ROS) within cancer cells is the primary mechanism that the NORI protocol relies upon and some studies indicate that cancer stem cells are equally susceptible to this approach.