I talked about how chemotherapy is now failing to stem the tide of rising cancer incidence in my previous piece, “Losing the War on Cancer.” I considered the causes of this situation. I talked about the natural evidence that suggests a variety of nutrient-gene interactions, rather than just an anti-oxidant effect, may be responsible for the phytonutrients in fruit and vegetables’ ability to prevent cancer. Certain phytonutrients have been shown to reduce DNA damage, enhance cell communication, enhance cell detoxification, be anti-inflammatory, boost immunity, and improve circulation, among other as of yet undefinable actions. These actions may be relevant to the phytonutrients’ ability to prevent the growth of cancer.
I firmly believe that accurately pinpointing the methods by which a normally controlled cell transforms into a “unruly” unregulated one will be the key to solving the cancer puzzle.
The cell is an incredibly intricate and subtle mechanism where every function is meticulously controlled. A typical cell only divides when it is necessary. Even when there is no requirement for division, cancer cells can divide. The cell regulators are therefore not functioning properly. Numerous attempts to distinguish between the chemical composition of a healthy cell and a malignant cell have so far failed. Only the regulators are messed up; the cellular architecture are identical. There is a problem that has to be fixed.
How does a regular cell get out of control?
The potential harm to a cell that could cause it to mutate and become aberrant has received a lot of attention in recent years. Does a virus, toxin, or free radical damage DNA and result in changes to the regulatory genes of the cell, such as those involved in typical programmed cell death? Though intriguing in theory, this hasn’t much reduced the incidence of cancer.
Some historical indicators point to a basic defect in cell metabolism that characterizes all malignancies and causes the cell to prefer the less efficient oxidative metabolism over the fermentation of glucose (using glycolysis) for energy production (which requires oxygen and generates much more energy). Szent-Gyorgyi et al. (1963); Warburg, 1930. The transition to fermentation appears to be a mechanism for enabling cell division and subsequently expansion, and it may also be the procedure that ordinarily takes place when the cell requires division. After this typical cell division, the process subsequently switches back to oxidative metabolism, which calls for a more organized cell structure and is accompanied by an associated electron flow. Therefore, it’s possible that cancer cells’ unchecked development is related to their being trapped in a fermentation process. Then, we must inquire as to what keeps them trapped in this procedure. Or what prevents the cell from returning to its typical oxidative cell metabolism, which appears to be related to cell regulation?
The Nobel Prize laureate and Hungarian-born Albert SzentGyorgyi already made these points in the 1950s and 1960s. (Dr. Albert Szent-Gyorgyi won the 1937 Nobel Prize for Physiology or Medicine for isolating and discovering vitamin C. He was the “Father of Nutritional Science” and the one who discovered vitamin P and iso-flavones. He spent the last 40 years studying the mechanisms that control cell proliferation and, by extension, the control of cancer.
Since 1930, Otto Warburg has fought for the idea that anoxia is the root cause of cancer. By subjecting heart fibroblasts in tissue culture to intermittent oxygen deprivation for extended periods of time, Goldblatt and Cameron (1953) described the first notable experimental induction of cancer by oxygen deprivation. They eventually obtained transplantable cancer cells, but not in control cultures that were maintained without oxygen deprivation. “But there is only one common cause into which all other causes of cancer blend,” says Warburg. “That reason is the irreversible injury to breathing.” I’ll show evidence later that suggests this alteration in cell respiration could not actually be permanent.
The fact that muscles hardly ever get cancer is one of the many mysteries surrounding muscles. This might be due to their extreme reliance on oxygen and oxidative metabolism or their abundance in mitochondria, the powerhouses of the cell, which create an environment where there is too much oxidative reserve for the growth of cancer.
The majority of malignancies are now widely acknowledged to be more glycolysis-dependent than normal cells. Both the ability to carry out oxidations and the systems that employ the energy of oxidation for productive work have been lost in cancer cells. Instead, energy is produced through a subpar process called wasteful fermentation. As was already mentioned, when a cell desires to divide, this may be the norm. Glucose absorption and metabolism are now confirmed to be enhanced in the majority of malignant tumors by positron emission tomography (PET) imaging. Warburg proposed (Warburg, 1930), but did not demonstrate, that this was caused by “abnormal mitochondria,” i.e., that cancer cells are compelled to adopt ineffective, non-mitochondrial methods of generating ATP (the energy unit of cells). Szent-Gyorgyi also believed that this purported “dysfunction” of the mitochondria is actually reversible. That this fermentation energy is transported to the mitotic process, where it forces cell division, was suggested by his studies. In other words, as was already mentioned, fermentation is characterized by lack of structure and a propensity for cell division, whereas efficient oxidative energy production is linked to organized cell structure. Cancer cells are simply carrying out a natural duty when they divide.
According to reports, certain non-cancerous cell lines have a stronger positive membrane potential than some human cancer cell lines, suggesting that malignancy may be associated with this (Bonnet et al, 2007). It becomes clear that this abnormal membrane potential of cancer cells is likely to be secondary to the cell being “metabolically” compromised since a significant portion of cell energy production (70% or more) is directed towards maintaining electrical integrity by supporting the ion pumps at the cell membrane.
Cancer and mitochondrial function
80% of a cell’s energy requirements are met by mitochondria, which are the site of energy synthesis in a cell. It has been found that the mitochondria of cancer cells and normal cells differ in a number of ways. Cancer may be brought on by mitochondrial abnormalities, according to some research (Woods & DuBuy, 1945). Recent research has demonstrated that mitochondria play a crucial role in apoptosis, or programmed cell death (Petit & Kroemer,1998; Zamzami et al, 1996). Less than 1% of nuclear DNA is found in the mitochondria, which may be more vulnerable to damage and mutations than nuclear DNA. It has also been proposed that the accumulation of mutations in mitochondrial DNA is a major contributing factor to aging. Different tumor cell lines differ from normal controls in the number, size, and structure of their mitochondria. Compared to mitochondria of slowly growing tumors, the mitochondria of rapidly growing tumors are often less numerous, smaller, and have fewer internal folds. There have also been changes in the inner membrane structure of tumor mitochondria (Modica-Napolitano & Singh, 2002). Cancer cells have a mitochondrial membrane potential that is around 60mV greater than control epithelial cells (Modica-Napolitano & Aprille, 1987). Unhealthy mitochondria are one of the most striking characteristics of cancer cells.
Suppression of apoptosis is necessary for the development of cancer and contributes to the disease’s resistance to treatment (programmed cell death). As was already mentioned, it is known that mitochondria regulate apoptosis.
We’ve already demonstrated that a glycolytic phenotype appears to be connected to cancer. Furthermore, it appears that a condition of apoptosis resistance is connected to the glycolytic phenotype (Plas and Thompson, 2002). Numerous oncoproteins increase the production of glycolytic enzymes, and several glycolytic enzymes are known to regulate apoptosis (Kim and Dang, 2005).
According to all the existing data, if we want to better understand cancer and discover a cure, we primarily need to focus on the mitochondria because this is where the energy abnormalities that occur in cancer may be identified.
Due to the fact that mitochondria regulate a number of crucial processes, including as calcium concentration and free radical (Reactive Oxygen Species, ROS)-redox regulation, they can have a variety of downstream consequences beyond energy production. Apoptosis resistance in many human malignancies may be explained by the crucial role mitochondria play in the process.
It has been demonstrated that cancer cells have more hyperpolarized mitochondria and have relatively less potassium channels. Reversing this metabolic-electrical remodelling could boost apoptosis and slow the spread of cancer if it is an adaptive response. By inhibiting pyruvate dehydrogenase, a crucial enzyme in the glycolytic chain, dichloroacetate (DCA), a small, orally available small molecule with good characterization, was able to switch cancer cells’ metabolism from cytoplasm-based glycolysis to mitochondria-based glucose oxidation, according to research led by Michelakis. All cancers’ potassium channel blockage was likewise reversed by DCA, but not in healthy cells. Overall, resistance to apoptosis was reversed (Bonnet et al, 2007). The metabolic cancer signature (aerobic glycolysis) is reversible rather than the result of irreparable mitochondrial damage, as suggested by the fact that DCA treatment greatly enhances glucose oxidation (which only takes place in functional mitochondria). Szent-Gyorgyi came to the same result, but Koch (1958; see below) also came to the same conclusion. Koch’s findings strongly implied that the metabolic/mitochondrial imbalance in malignancies might be reversed. In rats, DCA was found to considerably slow tumor growth without causing any negative side effects. Despite being approved as a medication to treat human mitochondrial illnesses, there are currently no rigorous clinical trials on cancer patients other from anecdotal evidence.
Dr. William Koch’s study (1958) concentrated on ways to bring the body’s oxidation system back to its original vibrancy and re-empower the body with its intrinsic capacity to recover and preserve health, not just in cases of cancer but also in a variety of other disorders.
Organized Medicine undertook a fifty-year campaign to tarnish Dr. Koch’s reputation, his clinical work, and his research, as well as the reputations of any medical professionals who ventured to support his theories or make use of his reagents. The key initiators of the illness process, according to Dr. Koch’s beliefs, are a depleted oxidation mechanism, dietary inadequacies, and environmental poisons. In his research, he found that removing an animal’s parathyroid gland caused poisonous compounds to build up in the body. Additionally, he noticed that the parathyroid-ectomized animals’ urine contained significant levels of lactic acid, indicating that the oxidation process was severely hindered by the compounds they produced. The typical tissue oxidation process had been stopped by these drugs. This proved to be a significant finding that opened the door for his initial cancer studies. He discovered that the presence of the di-carbonyl groups was a common trait among the tissues that had lasted the longest. He proposed that toxic amines from diverse metabolic, bacterial, viral, or fungal agents, including modern antibiotics, can impair these crucial processes.
via forming condensation with carbonyls. These functional carbonyls were essential for maintaining the cell’s ability to transport electrons and carry out metabolic processes, but when they were complexed by toxins, metabolic function might become irreversibly compromised. Unfortunately, Dr. Koch never received the research resources and assistance from the medical community that he requested and desired.
Even though Koch successfully treated a number of advanced cancer cases in 1919 with the help of the Wayne County Medical Society branch of the American Medical Association (AMA), the Journal of the AMA published more than 20 critical editorials and articles about Koch and his methods starting on February 12, 1921.
Dr. Szent-Gyorgyi also wrote in 1968 on the cancerostatic properties of carbonyl compounds and how they might halt cell division (Szent-Gyorgyi et al, 1967). In addition to tissue samples from many human organs, he also described these compounds in urine. According to his studies, these chemicals have the ability to prevent both cell proliferation and the maintenance of healthy oxidative metabolism in cells when present. The idea is that the body’s capacity to manufacture these compounds may diminish or become weakened, which would promote the growth of cancer.
The alleged efficiency of the Kucera cancer support regimen also raises the possibility that impaired mitochondrial function is a major factor in the emergence of cancer. A nutritional combination for mitochondrial support has been devised by Czech physician Dr. Michael Kucera, who has spent at least 20 years investigating mitochondrial medicine (Personal communication, 2009). These nutrients have been successfully used in conjunction with particular immune support nutrients to achieve exceptional results in cancer remissions. In the past ten years, this regimen has been used to treat more than 700 cancer patients. These individuals had a range of malignancies, the majority of which were non-localized, meaning they had already spread (including breast, prostate, colon and gastric cancers). Overall, remission rates of 70% at 5 years and 80–90% when chemotherapy is added to the formulations are reported. No negative effects were noticed. Contrast this to chemotherapy, which only has an effectiveness of 2% to 3% and has considerable adverse effects. I believe this to be the most efficient treatment plan now in use, and it is the one I utilize in my own practice. Even more amazing is the fact that the system is entirely oral. The primary benefit to the mitochondria must be the basic reason for this high level of efficacy.
Many of you will be more familiar with coenzyme Q10. The majority of eukaryotic cells contain this lipid-soluble material, primarily in the mitochondria. It is a member of the electron transport chain and takes part in aerobic cellular respiration, which results in the production of ATP, which serves as energy. This process generates 95 percent of the energy needed by the human body (Ernster & Dallner, 1995; Dutton et al, 2000) As a result, the liver and the heart, which have the highest energy needs, also have the highest CoQ10 concentrations (Okamato et al, 1989; Aberg et al, 1992; Shindo et al, 1994).
An observational study that discovered that people with lung, pancreas, and particularly breast cancer were more likely to have low plasma coenzyme Q10 levels than healthy controls sparked interest in coenzyme Q10 as a potential therapeutic agent for cancer (Folkers et al, 1997). Coenzyme Q10 supplementation has been linked to a few case reports and an uncontrolled trial (see below), which support the idea that it may be useful as an additional treatment for breast cancer (Hodges et al, 1999).
Although the use of CoQ10 in the treatment of heart failure is best known, two published publications in the field of medicine indicate that it has great potential in the fight against cancer. 10 cancer patients were given CoQ10 for heart failure, according to Folkers (1997). While using CoQ10 for 17 years, one of the patients, a 48-year-old man with incurable lung cancer, showed no symptoms of heart failure or malignancy.
A cancer doctor in Copenhagen, Denmark named Knud Lockwood, M.D., detailed his use of CoQ10, essential fatty acids, and antioxidant vitamins to treat 32 “high-risk” breast cancer patients in 1994. He wrote that “no patient died and all reported a sense of well-being.” These clinical outcomes are outstanding. All had lived at 24 months, when 6 deaths were anticipated. Two of the 32 patients benefited from extremely high dosages of CoQ10, and six of the patients displayed partial tumor remission. One patient, a 59-year-old woman with a family history of breast cancer, experienced a 1.5–2 cm tumor recurrence; however, one month after increasing her CoQ10 consumption to 390 mg daily, the tumor vanished. Mammography verified the lack of it. Another patient, who was 74 years old, had a tiny tumor from her right breast removed. She started taking 300 mg of CoQ10 daily instead of agreeing to have a second operation to remove further growths. A mammogram and checkup performed three months later found no signs of the tumor or metastases. According to Lockwood, who over the course of 35 years has reportedly treated 7,000 cases of breast cancer, he had “never seen a spontaneous complete regression of a 1.5-2.0 centimeter breast tumour, and has never seen a comparable regression on any conventional anti-tumor therapy” prior to using CoQ10.
Although none of the aforementioned studies were carefully designed, they nevertheless offer circumstantial support for my claim that mitochondrial metabolic dysfunction is crucial for the development of cancer and should be the focus of the fight against cancer. Indeed, I have cited data from a number of trailblazing medical professionals and researchers to demonstrate that supporting the mitochondria and/or correcting their metabolic deficiency is connected with cancer remissions. Although I am not the first to make this argument, I cannot ignore the data at hand. This, in my opinion, holds the key to solving the cancer puzzle. It’s time to stop ignoring the hints that history has provided us with!
Although the focus of this article was not anything other than the physical aspects of treatment, it would be a omission in the context of the title, “Winning the war on cancer,” to not at least mention the importance of faith and optimistic thinking in influencing the war’s outcome. This significant element has already been covered elsewhere.
|Aberg,F.et al. Archives of Biochemistry and Biophysics.1992, 295, 230-234|
|Bonnet,S; Archer, SL; Allalunis-Turner,J Haromy, A; Beaulieu,C; Thompson,R; Lee,CT;. Lopaschuk, GD; Puttagunta,; Bonnet, S; Harry, G; Hashimoto, K; Porter, CJ; Andrade, MA; Thebaud, B and Michelakis, ED. A Mitochondria-K+ Channel Axis Is Suppressed in Cancer and Its Normalization Promotes Apoptosis and Inhibits Cancer Growth. Cancer Cell, 2007, 11, 37–51.|
|Byrne, R. The Secret. 2006. Simon & Schuster Ltd Chopra, D. Quantum Healing: Exploring the Frontiers of Mind/Body medicine. Bantam books, New York, 1989|
|Dutton PL, Ohnishi T, Darrouzet E, Leonard, MA, Sharp RE, Cibney BR, Daldal F and Moser CC. 4 Coenzyme Q oxidation reduction reactions in mitochondrial electron transport (pp 65- 82) in Coenzyme Q: Molecular mechanisms in health and disease edited by Kagan VE and Quinn PJ, CRC Press (2000), Boca Rat|
|Ernster L, Dallner G: Biochemical, physiological and medical aspects of ubiquinone function. Biochim Biophys Acta 1995,1271: 195-204,|
|Folkers K, Osterborg A, Nylander M, Morita M, Mellstedt H. Activities of vitamin Q10 in animal models and a serious deficiency in patients with cancer. Biochem Biophys Res Commun. 1997;234(2):296-299.|
|Goldblatt, H; and Cameron, G. Induced Malignancy In Cells From Rat Myocardium Subjected To Intermittent Anaerobiosis During Long Propagation In Vitro. The Journal of Experimental Medicine, 1953, 97, 525-552.|
|Hegyeli, A; McLaughlin, JA; Szent-Gyorgi, A. Preparation of Retine from Human Urine. Science: 1963, 142, 1571-1572|
|Hodges S, Hertz N, Lockwood K, Lister R. CoQ10: could it have a role in cancer management? Biofactors.1999;9(2-4):365-370.|
|Kim, JW and Dang, CV. Multifaceted roles of glycolytic enzymes. Trends Biochem. Sci. 2005, 30, 142–150.|
|Koch, WF. 1958. The Survival Factor in Neoplastic and Viral Disease.|
|Lockwood, K. Biochemical and Biophysical Research Communications.1994,199, 1504-8|
|Modica-Napolitano, JS & Aprille, JR. Basis for the selective cytotoxicity of rhodamine 123. Cancer Res, 1987, 47, 4361-4365|
|Modica-Napolitano, JS & Singh, KK. Mitochondria as Targets for Detection and Treatment of Cancer. Expert Reviews in Molecular Medicine. www-ermm.cbcu.cam.ac.uk. 2002, pp1- 19|
|Okamoto, T.et al. Interna.J.Vit.Nutr.Res.1989,59,288-292|
|Petit, PX & Kroemer, G. Mitochondrial regulation of apoptosis. In Mitochondrial DNA Mutations in Aging, Disease and Cancer (Singh KK ed), pp147-165, Springer-Veerlag, Berlin 7 Plas, DR., and Thompson, CB. Cell metabolism in the regulation of programmed cell death. Trends Endocrinol. Metab, 2002, 13, 75–78.|
|Shindo, Y., Witt, E., Han, D., Epstein, W., and Packer, L., Enzymic and non-enzymic antioxidants in epidermis and dermis of human skin, Invest. Dermatol. 1994,102, 122-124.|
|Szent-Gyorgi, A. Bioelectronics and Cancer. Bioenergetics, 1973, 4, 533-562|
|Szent-Gyorgi, A; Egyud LG; McLaughlin, JA. Keto- Aldehydes and Cell Division. Science: 1967, 155, 539-541|
|Szent-Gyorgi, A; Hegyeli, A; McLaughlin, JA. Cancer Therapy: A Possible New Approach. Science: 1963, 140, 1391-1392|
|Warburg, O.1930. Metabolism of Tumours. (London: Constable).|
|Woods, MW & DuBuy, HG. Cytoplasmic diseases and cancer. Science: 1945,102, 591-593|
|Zamzami, N et al. Mitochondrial control of nuclear apoptosis. J Exp Med, 1996, 183, 1533- 1544|