- Site Disclaimer
- Why ?
- A to Z
- Cancer Main Page
- Vitamin B 3 for Alcoholism/Schizophrenia
- Niacin for Coronary Disease/Diabetes/Cancer
- Heart Disease
- DMSO/Vitamin B 12 For Chronic Fatigue Syndrome/Fibromylgia
- Chlorine Dioxide for Malaria
- DMSO/MSM for Anemia
- DMSO For Crohn’s Disease
- DMSO & Vitamin B 12 For Chronic Fatigue
- Vitamin B 12 Deficiency
- Magnesium for Diabetes
- Magnesium for Health
- Iodine for Health
- Hall of Fame
- Main Hall
- Linus Pauling/Vitamin C
- David W. Gregg Ph.D
- Dr. A. Hoffer Niacin/Vitamin B3
- Dr. Joseph Gold
- Jim Humble/Sodium Chlorite
- Rene Ciasse
- Max Gerson
- Dr. Ernst T. Krebbs/Vitamin B17 Laetrile
- Dr. Otto Warburg/Cancer Cell Metabolism
- Dr. J. Kloss/Nutrition
- Rees Evans(1919)/Divine Power/Herbs
- Dr. William F. Koch
- Harry M. Hoxsey/Formula
- Vance Ferrell/Alternative Cancer Remedies
- Dr. H.L. Newbold/Vitamin A
- Dr. P. Knekt/Vitamin E
- Dr. Walter Blumer/EDTA
- Dr. Kazuhiko Azai/Germanium-132
- Dr. William D. Kelly/Diet
- Dr. John Beard/Diet/Enzymes
- DR. Naessens/714X
- Dr. Joseph Issels/Ganzheitstherapie
- Dr. Mikkel Hindhede/Vegetarian
- Dr. Charles O. Ozias/Diet
- Dr. F. W. Forbes Ross/Potassium Iodide
- Dr. Robert Bell/Previous Injury/Diet
- Dr. John Pattison(1958)/Escharotics
- Johana Budwig/Flaxseed Oil
- Dr. D. Harman/ Antioxidants
- Dr. Coffrey & Dr. Humber/ Enzymes
- Dr. Orlando Dei Santi/Pau d’arco
- Dr. Rashida Karmali/Omega 3 Oils
- Dr. F. Sweet /Ozone
- Dr. Ross Pelton/Nutritional supplements
- Dr. Gerhard N.Schrauzer/Selenium
- Dr Tibor Hajito/Mistletoe
- Dr. Lucius Duncan Bulkley(1890)/Nutrition
- Ann Wigmore/Wheatgrass
- Main Hall
- Health Plan
- Emotional Health
- Contact Us
David W. Gregg is a retired chemist/chemical engineer and I found his pages on cancer,autism,anemia,Crohn’s disease and rheumatoid arthritis on the internet.There is a link at the bottom of the page that will take you to his “Health Notes”
In his own words;
“All of these papers are written by me, David, W. Gregg. The papers are for information only. They represent the observations, views and opinions of the author. They are NOT recommendations for treatment. For that you should see your physician. I am a retired chemist/chemical engineer and I am committed to researching the illness and issues that haunt our society. You will find my ideas on many subjects in these pages. I invite you to read them and send me your comments.”
David W. Gregg, Ph.D. 188 Calle La Montana Moraga, CA 94556 Phone/Fax (925) 284-5434
I find his research inspired and based on solid science and think if followed through can bring a revolution in the cancer field.See Below
Thank you David!!!!
As of February 2004 A Defense in Depth:
This web page presents what could be classified as an alternative-medicine, “Defense in Depth” against the progression of cancer. Two fundamentally different approaches are described, the combination of which should provide a profound defense. One invokes a nutritional approach and the other invokes the use of toxins. Each has numerous sub-options. I am not a medical doctor and am not qualified to comment on prescription drugs. Thus, they are not considered.
1) The Nutritional Approach:
The nutritional approach stimulates cancer cells to revert from anaerobic back to aerobic metabolism, causing them to revert from cancer cells back to normal cells. This process allows the cells to activate the p53 gene, which produces proteins that induce apotosis (normal programmed cell death). It involves nutrients that stimulate all three stages of aerobic metabolism, a) oxygen (oxidation potential) transport from the lungs to the cells, b) enhancing the steps of the Kreb’s cycle, and c) enhancing the Respiratory Chain. These all require a multitude of vitamins, minerals, etc. that are discussed. In most cases, enhancing oxygen transport from the lungs to the cells is probably the limiting and thus most important step and thus it will be addressed in more detail.
Oxygen Transport: Hemoglobin (Red blood cells) is the component in blood that serves as the primary transporter of oxygen from the lungs to cells. However, cancer cells cannot obtain oxygen from hemoglobin. Their anaerobic metabolism does not produce carbon dioxide, which is required to displace oxygen out of the hemoglobin. Thus, once a cancer is started it stabilizes itself in that state by obstructing the delivery of oxygen. In order to overcome this, certain nutrients (many options) can be consumed that increase oxygen carrying capacity of the blood in a way that is independent of hemoglobin and does not depend on the production of carbon dioxide to deliver oxygen (oxidative potential). The delivery of oxygen allows the cancer cells to start turning on aerobic metabolism. Once this starts, it initiates an avalanche effect. The cells start to produce carbon dioxide, which then causes the red blood cells to start to release oxygen, which stimulates more aerobic metabolism and carbon dioxide release, etc. The end result is the cancer cells receive adequate oxygen to initiate a quasi-normal, aerobic metabolism state. In this state they have enough energy to activate the p53 gene to produce the proteins that can cause apotosis. The reason cancer cells can live forever is that they can (and must) rigorously avoid apotosis. The converted cells gradually die off.
This theory makes sense to me for many reasons. It invokes sound biochemistry, is consistent with the observations I present on this web page, and clearly explains why cancer cells are destroyed why normal cells are not. In fact, normal cell health would be enhanced in the process. I suspect that most of the reported observations of various nutritional/herbal treatments resulting in recovery from cancer fall in this category even though the precise chemistry of how they work has not been identified.
When would this approach fail? I can think of one possibility. If the p53 gene has mutated (been seriously damaged) then turning on aerobic metabolism, supplying needed energy will not be sufficient to activate the p53 gene and apotosis will not take place. Unless another programmed cell death mechanism takes over, the cells will eventually return to being cancer cells. There is also a possibility that the enhanced nutrition may make the cancer cells healthier while it makes the normal cells healthier. In this situation, the toxin approach, discussed below, will have to be relied on. Thus enters the “Defense in Depth” concept.
2) The Toxin Approach:
The second approach employs the use of toxins that do kill the cancer cells by a toxic effect. There are many examples of this. However, in my analysis of the mechanism of ionic cesium (cesium chloride), combined with increased potassium (potassium chloride) intake, I was extremely surprised to discover the real mechanism by which it operates and identify how truly profound it is. I concluded the mechanism presented to date on the Internet was totally wrong and seriously obscured the true potential of this approach. My present conclusion is that it stands out from all other such toxin approaches as being almost the perfect solution.
Briefly, the cesium ions are taken into the cell via the sodium-potassium pump, substituting for potassium, and are trapped there. Not only are the cesium ions trapped, but they also block the exit of the potassium ions by blocking the potassium channel proteins in the cell walls. The accumulation of cesium and potassium ions in the cell negates the voltage potential across the cell membrane. This voltage potential is required to energize the sodium-glucose co-transport system that feeds the cell. The cell thus starves. There would also be an accumulation of ions in the cell, which will cause the cells to swell, due to osmotic pressure, and possibly burst.
This is true for all cells. Why are cancer cells impacted far faster/greater than normal cells? The sodium-potassium pump, energized by ATP, pumps two potassium ions into the cell while pumping three sodium ions out. This creates a charge imbalance that would stop the pump unless there was another path by which the sodium ions reenter. That happens via the sodium-glucose co-transport system in the cell membrane. Thus, the rate that the sodium-potassium operates is dictated by the glucose requirement of the cell. Cancer cells, which are anaerobic, require 20 times more glucose than normal cells to obtain the same amount of energy. Therefore, their sodium-potassium pumps operate 20 times faster than normal cells. Thus, they will pump cesium into their cells 20 times faster than normal cells, and will experience starvation (and bursting) 20 times faster.
Since not only are the cesium ions trapped, but also potassium ions, this will result in a serious lowering of potassium in the blood which must be compensated for, which is easy to do. If it isn’t, the lowering of the potassium level in the blood could cause death. I should mention that “Salt Substitute” available in every grocery store is potassium chloride and is a good, convenient source of potassium.
The trick is to establish a protocol where the cancer cells enter starvation and stop the treatment before the normal cells follow. Cesium eventually exits the cells, but very slowly. Thus, once the cancer cells have entered starvation, treatment can stop and the cancer cells will continue to starve for an extended period of time.
An additional feature of this approach is that the cancer cells are abruptly deprived of glucose, abruptly arresting their progression, but not necessarily resulting in an abrupt die-off. One might expect this to be more gradual than other cancer treatments. Thus there is a lower risk of experiencing severe toxic effects due to rapid cell die-off of cells common to other treatment approaches.
As broadly reported on the Internet, cesium chloride has been used successfully to treat cancer. My contribution is to discover its correct mechanism, described above. This should not only enhance its scientific credibility, but also help researchers and treatment clinics optimize its use.
Otto Warburg found that all cancer cells are anaerobic, and both of these approaches work on the anaerobic nature of cancer cells. Logically, the combination of the two should be effective for all forms of cancer. Will it be enough? Only time will tell if this dream will come true.
Cesium update as of 2/20/04: I have just had conversations with a clinic in Canada that has had considerable experience with treating cancer with cesium. They told me that they have found it to be successful in about 50% of their patients. Thus, it is not as perfect as the theory might predict. However, the patients seeking cesium therapy are generally those who have already exhausted all that current medicine has to offer and have been told there was nothing else that could be done for them. In this context, a 50% recovery rate could be viewed as quite positive. However, at this stage of experience, it is certainly not a treatment that one would choose before exploring what current medicine has to offer. Hopefully, with further development of the treatment protocol the success rate will improve, approaching the initial expectations.
Cesium update as of 5/16/04: I just received an email pointing out an important technical criticism concerning my cesium theory. It was pointed out that there is more than one glucose transport mechanism into the cells. There is the “active” sodium-glucose co-transport system that I have discussed, and there is also a concentration driven transport system depending on GLUT proteins in the cell wall that does not depend on sodium or the sodium-potassium pump. It is driven solely by the glucose concentration gradient across the cell wall. If this is the dominant transport mechanism, which is dependent on the type of cell and glucose concentrations, then my argument for the lethal mechanism of cesium starving the cancer cells no longer holds. However, the GLUT transport mechanism depends on a relatively high glucose concentration in the blood. At low glucose concentrations the active sodium co transport mechanism becomes more important. This would lead one to conclude that if the cesium treatment is going to be effective, it would be important to combine it with a diet that is low in carbohydrates.
Summary As of July 2001
Otto Warburg discovered that most if not all cancer cells are anaerobic in their metabolism. That discovery provided me with the essential lead for the theory/approach presented here, which extends this discovery in a particular way. I started with a premise, which, with extensive work, eventually evolved into a solid and useful theory. I have observed in the history of science that any particular area can wander randomly with little progress until the correct theory is identified. When it is, then, and only then, there is an explosion of progress in the field because a coordinated effort with many contributors becomes feasible. The discovery by Crick and Watson is one familiar example, but there are many more. It does not have to be complex. A double helix is not a complex concept. It just has to be the single correct theory identified in a sea of less correct ones. I can only hope that this is such a theory and will result in a dramatic improvement in the treatment of cancer. Specifically, I hope it will encourage large supplement producing/marketing companies to formulate products that will help to accomplish this goal.
The Governing Theory
Cancer cells require anaerobic metabolism to remain cancer cells. The anaerobic metabolism dictates that they are energy deficient. An anaerobic cell can derive only two ATP’s while an aerobic cell can derive 36 ATP’s from the metabolism of a glucose molecule. With insufficient energy they can no longer operate all the complex control mechanisms that exist in normal cells. Thus, they operate like primitive cells that divide and multiply in an uncontrolled manner. When they are caused to revert back to aerobic metabolism, which is feasible, they then have enough energy to operate the control mechanisms and assume characteristics of normal, non-cancer cells. This not only arrests their progression of uncontrolled division and thus growth, but if held in this state long enough, they undergo programmed cell death, a characteristic of all normal cells. In time, the cancer progression is not only arrested, but is reversed, even to the point of complete elimination.
The anaerobic metabolism is triggered by genetic damage, which is not reversible in any particular cell. However, the anaerobic metabolism is reversible without having to correct the genetic damage. It thus provides a unique focus of attack. It does not correct the genetic damage, but does safely cause the elimination of the genetically damaged cells through programmed cell death. Since it is a characteristic of most if not all cancers, the treatment should apply to most if not all cancers. Since the process of aerobic metabolism is the same for all cell types, the same specific treatment, focused on enhancing aerobic metabolism, should be effective for all types of cancer. It also has the characteristic of being safe and enhancing the health of normal cells in the process.
The basic approach is first identifying the nutrient(s) and their dose that support each step of aerobic metabolism. Then supply them all at the same time. For treatment this can require significantly enhanced doses (megadoses) of some specific nutrients for a period of time. This is not complex in concept, but it can be in practice.
The evolution of information discovery and analysis in support of the theory.
The primary impetus that stimulated me to focus on cancer and how it might be mitigated was due to a close friend being diagnosed with colon cancer. I thought I would do my best to help, starting by learning as much as I could about the disease. (2+ years later, after surgery, chemo & nutritional therapy he is presently alive and appears free of cancer.) Upon learning about Otto Warburg’s discovery that most, if not all cancer cells were anaerobic in their metabolism, a warning flag went up. My many years of experience in research said that when faced with such a profound commonality, this is where you should look for both the primary cause and the solution. After considerable thought I started with a major part of the governing theory described above, but as a premise, not a solid theory. I decided to make the assumption that it was correct and see where that led. Would it survive careful study and analysis?
Anaerobic Metabolism Stabilized in Cancer Cells: I started by looking for biochemical evidence to convince myself that Otto Warburg’s discovery of anaerobic metabolism was consistent with what is now known about the rest of the chemistry of cancer. In the process I found considerable evidence that supported Warburg’s discovery, and beyond that discovered anaerobic metabolism might be a stable, self-reinforcing state once it starts. Anaerobic metabolism, because it does not create carbon dioxide, which is required to displace oxygen out of hemoglobin, serves to prevent the delivery of oxygen to the cells. Without oxygen, they cannot revert back to aerobic metabolism. Thus, the only way they can revert back is to supply the oxygen by a mechanism that is independent of hemoglobin.
Cancer State Reversible: The next step was completed by the discovery of references in a book, “Cancer & Natural Medicine” by John Boik, reporting as many as sixteen different forms of cancer had been caused to revert back to normal cell behavior (displayed differentiation) when they were immersed in a solution of DMSO. In a previous web page on DMSO (www.krysalis.net/dmso.htm), I had already identified that most likely the primary cause of the health benefits of DMSO was caused by it forming an oxygen transport system when in equilibrium with its oxidized form, MSM. Dr. Stanley Jacob, the foremost DMSO & MSM scientist in the world, was kind enough to phone me after discovering it and congratulated me on the web page and the new insight. I thus realized that the reason the DMSO solution caused the cancer cells to turn into normal cells was because the solution was in contact with air and formed enough MSM to allow the two in equilibrium to transport oxygen to the cells, allowing them to revert to aerobic metabolism. Dr. Jacob is the author of many books on DMSO and MSM. His most recent one that summarizes his work on both DMSO and MSM is “The miracle of MSM” Jacob, et al; G. P. Putnam’s Sons, 1999.
This discovery demonstrated two major points. 1) Cancer is reversible. Cancer cells can be caused to revert back to normal cell behavior. And 2) The process by which this takes place is to cause them to change from anaerobic metabolism to aerobic metabolism. What a wonderful support for my developing theory!
Identification of Nutrient Support for Each Step of Aerobic Metabolism: I assumed that DMSO could be only a part of a solution for treating cancer. I thought it would be unrealistic to assume people could be treated with whole body doses of DMSO at levels effective for cancer without exceeding toxic limits. This would also address only one stage of aerobic metabolism. A treatment based on stimulating all stages of aerobic metabolism simultaneously was far more likely to result in a safe and successful treatment. With this premise in mind, I then proceeded to study each step of aerobic metabolism identified in biochemistry books, and identify the nutrient or nutrients that are known to assist that step. When such a nutrient was identified I then performed a literature search on Medline to see if it had been studied in relation to cancer. In every case, I discovered papers that reported the nutrient helped to mitigate cancer. This first sweep through the steps of aerobic metabolism resulted in identifying a set of nutrients that my theory said would help mitigate cancer if used together. It was a start, but certainly was not a complete list.
A First Case: I am not a medical doctor and do not treat people. However, shortly after identifying the list of helpful nutrients a close friend was diagnosed with stage-4 lung cancer. It was in both lungs and had spread to the bone. Her ribs had fractured, one clavicle was missing, and there was a tumor growing out of her back. She had lost a lot of weight and coughed continuously. When I saw her, while she was visiting her sister and elderly mother the day after the diagnosis, we all thought she was unlikely to live more than one more month. The late diagnosis was due to her doctor misdiagnosing it for several months as a pollen allergy. She knew of my efforts analyzing cancer and decided she wanted to try my proposed nutritive approach along with conventional treatments. This was in 11/99. She started immediately with the nutritive approach which included a fruit and vegetable diet supplemented with a particular comprehensive diversity of vitamins, minerals, etc. including 40 grams of vitamin C/day (neutralized with baking soda). Two weeks later she started her chemotherapy (Taxol), and by then her coughing had already subsided. Her elderly mother and sister had already started trading off staying with her on a 24-hour basis, believing she had little time left. However, much to our surprise, instead of getting worse, she got continuously better, eventually reached a point where she could live on her own. The cancer in her lungs subsided, along with the tumor in her back. She is still alive and alert at this writing, 7/01, and continues with both nutritive (with less vitamin C) and conventional treatments. Did the nutritional support contribute as an addition to the conventional treatment? When I took her in for one of her doctor’s appointments a few months ago he told us both that her case was unusual in that more than 90% of the people with her cancer history would be dead by now.
A Thousand Cases: “Vitamin C & Cancer” by Abram Hoffer MD, PhD; Quarry Press Inc.: Dr. Abram Hoffer is commonly credited with founding the alternative health movement and is the author of many books. He is credited with being the person that got Dr. Linus Pauling (double Nobel Prize winner) interested in the area resulting in his widely publicized push on Vitamin C for colds. One of his latest books “Vitamin C & Cancer”, was written in collaboration with Dr. Linus Pauling. He learned about my “First Case” from a mutual friend, Dr. Bernie Rimland, director of the Autism Research Institute in San Diego. He called me to learn more about the nutritive approach taken. He has a close family member with lung cancer and wanted to see if my thoughts could help him improve his treatment approach. (It did lead him to modify it.) During the conversation I asked if he would take a look at my web page on cancer. He did and a few days later he sent me an email with a number of comments. They not only included positive comments about the theory, but also references to several of his web pages, one of which addressed cancer. This resulted in an email exchange presented on my web page. I read his web page on cancer and his book “Vitamin C & Cancer”. This was my first awareness of his work with cancer in any detail. I knew he was active in the field but was unaware of the magnitude of his studies. I discovered he had treated thousands of cancer patients over 40+ years with remarkably successful results. In addition, his treatment approach was consistent with my theory. This is addressed in more detail in item 29. Now, instead of only one case, I had discovered thousands of cases that support the theory. Is it enough? I believe it is enough to lend it very substantial credibility.
Enhanced Anti-angiogenesis: It appears that the oxygen transport part of the treatment would not only promote aerobic metabolism but could be a powerful anti-angiogenesis treatment (preventing the formation of new blood vessels and thus prevent the growth of tumors.) See Item 35 for details.
Where from here?
In order for the theory to be successful, it has to be used to guide significant improvements in cancer treatment that carry us even beyond the impressive successes of Dr. Hoffer. As one example, based on the oxygen transport part of the theory, I would predict that megadoses of DMSO and/or MSM can be substituted for the megadoses of vitamin C employed by Dr Hoffer. It could provide an even more intense oxygen transport option with no known toxicity. Alpha Lipoic Acid (ALA) and IP6 may also be effective in that capacity. I suspect a combination of all four, vitamin C, MSM (DMSO), ALA and IP6 could end up being the most effective option.
I personally believe that the evidence is extremely convincing that this theory does present the universal cure for all forms of cancer. Could it actually be this “Golden Grail” of medicine? Only time (and use) will tell.
I am also confident the same basic treatment approach will be successful with a significant number of additional diseases, both physical and mental. It has the attractive feature of not being a case where people have to wait years for an effective treatment to finally become available. A safe and effective treatment is available now with impressive results. Continued development will start with that base and perfect it, bringing about a rapid evolution of even more effective treatments.
My original progression of discovery and analysis starting March 1999
I would like to propose/present a totally new, unified theory of cancer that identifies the single biochemical cause of all forms of cancer and its mechanism. It explains how various carcinogens, oncogenes. etc. can trigger this mechanism, and how various diets, nutritional supplements suppressor genes, etc. can prevent cancer or even cause existing cancer cells to revert back to normal cells. This understanding points to an organized direction towards curing cancer starting in the very near future. It also identifies a path for cancer research that should be far more fruitful than what has been achieved in the past.
I firmly believe that what I am going to present is fundamentally correct, but if it is found to be in error, I can only hope it will have introduced a debate/investigation that leads to an even better understanding of cancer and its treatment. For the sake of being brief enough to make this presentation readable, I will at times be making a number of assumptions without extensive background support and it will be up to the reader to decide to accept or reject them. I would be delighted to discuss/support them at a later time.
Cancer is a Degenerative Disease
Cancer is a degenerative disease in that it involves a normal cells turning into abnormal cells. I have presented/proposed a new base of understanding for the cause of degenerative diseases in my Health Note Antioxidants.
In summary, I have proposed that degenerative diseases are not caused by the conventionally accepted theory of free radical attack, but rather they are caused by the energy available to the cell dropping below the threshold that is required to maintain the essential organization of its extraordinarily numerous and complex chemical processes. At this point, the chemistry of the cell goes into disorder, and it is the disorder, not free radical attack, that causes degenerative diseases.
Cancer Cells are Anaerobic
Back in the 1920′s a cancer researcher, Otto Warburg, discovered that the metabolism of cancer cells was anaerobic, and received a Nobel Prize for this work in metabolism. He believed that all cancer cells were anaerobic, but, of course, this could never be proven absolutely since it is not economically possible to make this measurement on every case of cancer. However, the universal observation of cancer using up all nutrients, wasting the body, is a strong indication of anaerobic metabolism, which is a very inefficient use of glucose. He performed one very interesting experiment where he put human cells in a Petri dish and deprived them of oxygen. They survived, but turned cancerous. what is happening? I propose that the normal cells have a memory/capability of reverting back to a more primitive, biochemically less complex state of survival. Possibly a memory of the time when the earth had no oxygen in its atmosphere. Such primitive, single cell organisms had the property of dividing without limit (no counting mechanism “telemer” as exists in our more advanced cells). The division rate and extent was also controlled simply by the availability of nutrients. They also did not have the property of “differentiating” into specialized cells that would be required for them to participate in a coordinated way with other cells to enable a complex organism to function. Warburg believed that the deprivation of oxygen was the primary cause of cancer, but I will propose it can be more general that that. Any of many processes that can interrupt aerobic metabolism can result in cancer.
Let us first briefly outline the three major stages of energy producing metabolism. The first stage is called glycolysis. It is the anaerobic stage. It degrades glucose (from the blood) into lactic acid, or alcohol, or pyruvate. When the next two, aerobic stages of metabolism are operating, the anaerobic stage produces pyruvate exclusively which then feeds into the Krebs cycle and the following respiratory chain. The first, anaerobic step, glycolysis, produces two ATP molecules (the currency of energy in the cell) per molecule of glucose. The following two aerobic steps produce an additional 36 molecules of ATP. When the aerobic stages are not operating, the primary product is lactic acid and sometimes alcohol, but not pyruvate. It can be seen that anaerobic metabolism will result in greatly reduced energy available to the cell, and will result in a voracious appetite for glucose just to supply the small amount of energy required for its reduced state of metabolism.
The Single Cause of all forms of Cancer and the Cure
Cancer does not cause cells to turn anaerobic, but rather it is stabilized anaerobic metabolism that is the single cause (or essential requirement) that turns the normal cells that depend on aerobic metabolism into cancer cells. The proposed cure, as an alternative to protocols that focus on killing the cancer cells, is to restart aerobic metabolism, which allows the cells to revert back to being quasi-normal cells again. Genetic damage is not corrected, but if the cells are held in a normal state of aerobic metabolism, with time they will go through the normal process of programmed cell death and the cancer cells are permanently eliminated. For the proposed cure, the task is to walk through each step of aerobic metabolism, identify the nutrient that stimulates/assists it, and combine them all in a dietary/treatment protocol.
The Role of Carcinogens, Oncogenes, etc. in Causing Cancer
Anaerobic metabolism can be stabilized in a cell by blocking the aerobic metabolic sequence. This can happen anywhere beyond the glycolysis stage. There are numerous opportunities in the Krebs cycle and the respiratory chain. All the needs to occur is to remove essential enzymes essential to any step in the sequence and the entire aerobic sequence will shut down. Different carcinogens could attack any specific enzyme in the process and cancer will result. The same is true for oncogenes. They are probably genes that were essential for the production of different essential enzymes and once damaged, they no longer do their job and cancer results. The numerous opportunities for stopping the process is why there are numerous examples of carcinogens and oncogenes. They don’t have to operate everywhere, they only have to block a critical step.
This theory would also predict that the few cells of the body that are naturally anaerobic would not develop cancer. These are the red blood cells and parts of the eye; the cornea, lens and regions of the retina. They do not have mitochondria and thus depend completely on glycolysis for their energy, and that energy source is sufficient for them to remain normal. I don’t know of any cases where cancer initiates in these cells.
The Role of Diet, Nutritional Supplements, Suppressor Genes, etc. in Preventing Cancer or Converting Cancer Cells back into Normal Cells
The initial role of diet and nutritional supplements in preventing cancer is to insure the cells have sufficient energy to correct damage. In this way stabilized anaerobic metabolism never occurs. However, after cancer has occurred, there are many reports of cancer being reversed by diet and nutritional supplements. In this case, the role is to provide either an enhanced availability of oxygen or an external source of enzymes that are no longer being produced by the cell. Of course, when this is achieved, the cells are still there with the same potential problems even though they are no longer cancerous. If the external source of enzymes or enhanced oxygen transport is removed, one would expect the cells to become cancerous again, and that is the experience. The only way that a person would eventually be cured and no longer require the special diet is for the affected cells to eventually die via a normal cell death processes such as apotosis (programmed cell death). This probably occurs over time, but there is no method to measure it except for the reoccurrence of cancer after the diet/supplement regime is terminated. A test that most would not like to try.
This presentation is intended to provide only a initial brief, but sufficient presentation of the concept for the present purposes. I have reviewed it with many medical practitioners and researchers who have not only been unable to find fault with it, but have further supported it by quickly reviewing their own experience. They have also found it to be new to them. I plan to expand on it later, but I hope this presentation is sufficient to stimulate the imagination of many others, which could greatly accelerate the process.
1. DMSO (& MSM):
In my Health Note DMSO I describe how in the body DMSO forms equilibrium with MSM (the oxidized form of DMSO) and the combination becomes an oxygen transport system, enhancing aerobic metabolism. This operates at only one point, the respiratory chain (at the inner membrane of the mitochondria). John Boik, in his book “Cancer & Natural Medicine” (1996) cites a number of publications where DMSO solutions have caused fifteen different forms of cancer (in vitro) to differentiate (and thus turn into normal cells). The biochemical mechanism was not understood, however, it is fully consistent and explained by the mechanism proposed here. It also demonstrates a most essential point: It is possible to convert cancer cells back into normal cells, and it is logical to conclude that it happened by restarting aerobic metabolism.
So it works in vitro, but does it work in vivo (in living people)?
More than a year ago I was contacted by a lady who was interested in my discovery that DMSO can help Crohn’s Disease (Health note: Crohn’s Disease). During our discussion she mentioned that she had a basal carcinoma and had a date to have it removed surgically, something that she had to go through several times before. Thus, she was quite familiar with what they looked like. I told her about some of the reports of DMSO helping cancer, and she decided to try it. She told me she applied DMSO twice a day and by the time her surgery date arrived a month later the basil carcinoma had completely vanished (no surgery took place). This may be evidence of two important processes, reversal of cancer through the reestablishment of aerobic metabolism, and the eventual elimination of the cancerous cells through apoptosis. Apoptosis is programmed cell death that happens to most normal cells in a matter of 1-2 weeks or less. Even though anaerobic metabolism is the cause of the cancer, genetic damage is the cause of anaerobic metabolism. Reestablishing aerobic metabolism with DMSO could not correct the primary initiator, genetic damage. However, holding the cancer cells in a normal state long enough gives the natural process associated with healthy cells, apoptosis, time to eliminate the cancer cells. This approach kills cancer cells through making them healthy. Thus, unlike conventional chemotherapy, it makes normal cells even healthier in the process. This is addressed in more detail in later Items (below).
More recently I attended a medical conference (on alternative medicine) sponsored by the Orthomolecular Health Medicine Society in San Francisco (Feb. 26-28, 1999). One of the talks addressed DMSO. Numerous effects and benefits were described, but nothing was said about its oxygen transport characteristics or its affect on cancer. I joined a discussion group with the presenter afterwards and one lady (MD) said she had an experience where she had a melanoma on her leg and when she treated it with DMSO, it went away. She didn’t go into detail so I wasn’t able to find out how often she applied it and how long it took to go away.
My interpretation, if these reports can be trusted, is that the DMSO reversed the effect of a carbon dioxide deficiency depriving the cells of oxygen and thus stabilizing the cancer state. The DMSO-MSM complex would deliver oxygen by a mechanism that is independent of hemoglobin and thus would not be stopped by the lack of carbon dioxide. Once the cells had returned to normal they then produced enough carbon dioxide to reestablish stability in that mode. However, I would expect that the primary initiating cause may still be present and the normal state would be precarious. It also has the advantage of being able to apply a relatively high concentration of DMSO to the cancer (it is on the skin) and the DMSO has an abundant source of oxygen to transport (the surrounding air). It isn’t at all clear that this would be effective on internal cancers. The required concentration may be far higher than the body can tolerate, and the primary source of oxygen (the lungs) may not be sufficient.
This is certainly not enough experience to draw firm conclusions, but as Chairman Mao once said, “The journey of 1000 miles begins with the first step”. Any valid treatment of cancer will begin with the first case.
2. Carbon Dioxide:
Most of us are familiar with the experience of breathing very rapidly for a while and becoming dizzy. You are not becoming dizzy because of too much oxygen, but rather too little. What you have done is to exhaust too much of your carbon dioxide. Carbon dioxide is essential for displacing oxygen from your hemoglobin (red blood cells) so it can be delivered to your cells where it is needed. When the carbon dioxide concentration falls too low, oxygen is no longer displaced from the hemoglobin and thus is no longer available to your cells. At this point aerobic metabolism stops and so do you. If all is working normally, when you stop breathing, the carbon dioxide level builds back up quickly and you recover.
Now lets consider a cancer cell (with anaerobic metabolism). Anaerobic metabolism (glycolysis) derives energy by converting glucose to lactic acid (& sometimes ethyl alcohol). This process produces no carbon dioxide if lactic acid is the product and only one carbon dioxide is ethyl alcohol is the product. This is compared to six carbon dioxide molecules per molecule of glucose for aerobic metabolism. Thus, once a cell starts to turn cancerous due to some other blockage in the aerobic metabolic sequence, it will start to produce less carbon dioxide, which will further reinforce the transition to cancer (anaerobic metabolism) by reducing the availability of oxygen. In a sense, this process serves to stabilize the state of cancer.
3. An Added Insight:
The first stages of anaerobic metabolism produce pyruvate and NADH (along with two ATP’s). In the case of cancer, the next stage involves the reaction of NADH reducing pyruvate to lactic acid, liberating a little more energy and consuming the NADH. Cancer always takes this second step making lactic acid. This provides a special insight. If the final stage of aerobic metabolism was operating, the respiratory chain, (and the aerobic metabolism blockage was earlier) then the NADH would preferentially be consumed by this stage and the conversion of pyruvate to lactic acid would not occur. However, the pyruvate is converted to lactic acid and thus the respiratory chain is not operable. This further identifies a specific problem area within the total aerobic sequence, and this problem always occurs in cancer cells.
This could be explained simply by the discussion presented in the Carbon Dioxide discussion above, describing why oxygen is not being transported to the mitochondria and thus the respiratory chain. This is likely to be a major part of it, but it may not be the full explanation for all cancers. The inner membrane of the mitochondria and thus the respiratory chain could also be disabled by the lack of coenzyme Q10 (CoQ10) or the combination of vitamin B12 and folic acid as discussed in items 11 and 12 below.
We all know that the cancer danger increases significantly when the tumor becomes metastatic, spreading tumor cells to distant parts of the body, starting more tumors. If this approach of supplying missing enzymes works, it should work on all the tumors, no matter where they have spread. The spread tumors should have the same source of metabolic disorder and thus should be fixed by the same method/treatment. However, I am going to postulate a new, unrecognized hazard that could be very damaging, but could also be avoided. To do this, I am going to have to invoke some biochemical processes that have not yet been demonstrated, at least not rigorously, but I firmly believe exist. However, I hope you will still hear me out.
I believe that the process of metastasis is not unique to tumors. Rather, I believe it is a natural process that occurs with all organs (heart, liver, kidney, etc.) to some extent where their cells get released and some take up residence in other organs where they don’t belong. My primary argument is that there are too many cells in any organ for them to be perfectly contained. Thus, the body must have a mechanism for dealing with this process. If the body could not provide a remedy, our organs would gradually turn into a diversity of organs, not all in the right place. So what happens? Cells from one organ that get misplaced in another organ redifferentiate and turn themselves into the right type of cells. This redifferentiation process with cells that had already reached their final state of differentiation was once thought to be impossible. However, very recently it was reported that it can and does happen. Thus, we can now understand how the body can protect itself from natural metastasis of normal organs gradually converting each of your organs into a potpourri of organ cells.
What is the implication for cancer? Lets start with a metastasized cancer and then convert all the cancer cells back to normal cells via. the treatments proposed above. Lets say that the cancer started in the colon. Then the normalized cells would all be colon cells no matter where they have spread. What now? If we invoke redifferentiation as discussed above, these cells will then convert themselves into the type of cells of the organ they are in. However, even though they are now a different cell type, they still have the same enzyme deficiency that made them cancerous in the first place. Now let us remove the external source of enzymes. The cells will become cancerous again, but this time they will become a cancer that is characteristic of the organ they are now in. So, suddenly we not only have the original cancer form, but also all the different forms that are characteristic of the all the organs that have become host to the metastasized cells from the original cancer. Different cancers (characterized by their organ starting point) have different growth rates. Thus, this process is likely to produce a far more rapidly moving and deadly cancer.
5. A Vegetable Diet:
There are numerous reports/claims that a diet consisting almost entirely of a diversity of vegetables can cause cancer tumors to shrink or even vanish. If these reports are correct, they make sense in the context of the theory that is presented here. I am postulating anaerobic metabolism and thus cancer can be caused by the blockage of the aerobic process at any point in the Kreb’s cycle or the respiratory chain. There are numerous chemical steps that are involved in sequence and if any of them is blocked you have the potential of arresting the entire aerobic process. Each of these steps are catalyzed by specific enzymes and regulated by other enzymes. If any of these are missing, aerobic metabolism could stop.
Each vegetable has its own distribution of enzymes, some of which our bodies can incorporate sufficiently intact to help us supply our own essential enzymes. It is unlikely that one vegetable will have a distribution of enzymes that will supply all of out needs. However, a wide diversity of vegetables might. At least, the possibilities improve with the diversity of supply. This would include herbs. It is my belief that Chinese herbal medicine can be interpreted into western medicine or biochemical understanding by assuming they provide specific enzymes that are needed to remedy a particular disease that is caused by a particular enzyme deficiency. The problem, of course, is to try to identify what enzymes are missing for a particular disease state, and which vegetable or herb can provide it. This information is not available, most likely because the problem has not been clearly presented before. Since this information is not available, the safest approach is to resort to a “shotgun” approach using all vegetables in the hope that one or more will provide what is needed. I personally am comfortable with taking this approach with vegetables, but do not know enough about herbs to know when to worry about toxic effects.
I believe we need a focused research effort that identifies the enzymes that are missing in different cancers and the enzyme distribution that is provided by each vegetable or herb. Once that is in hand, treatment of cancer may become far more successful.
The primary focus that I have heard about is on maintaining a rigorous, strict vegetable diet. Fruits are avoided because they provide a ready source of sugar. Cancer cells love glucose and thus sugar, and if they can obtain that easily they will. If the sugar (glucose) is not so available, they are encouraged to go through the effort to incorporate a needed enzyme to start up the aerobic metabolism process. (This is my simplistic interpretation.)
This treatment mechanism is directed towards providing an external supply of essential enzymes that are produced internally in normal cells. As would be expected, when the external supply is terminated, by termination of the diet, one would expect the cancer to return and that is the reported experience.
6. Vitamin C:
Vitamin C has many well-known health benefits, which I won’t attempt to list here. However, there are two that should have special significance for preventing the initiation and progression of cancer.
Heavy Metal Elimination: I recently attended a paper presented at a medical conference (on alternative medicine) sponsored by the Orthomolecular Health Medicine Society in San Francisco (Feb. 26-28, 1999). The paper was focused on methods to encourage your body to excrete toxic heavy metals such as mercury, lead and cadmium. There were a number of promising treatments discussed, one of which was vitamin C. It wasn’t necessarily the most effective treatment in all cases, but it was found to be significantly effective in mobilizing such toxic metals out of the cells and causing them to be excreted in the feces. Since such toxic metals could be a root cause for genetic damage, causing anaerobic metabolism and thus cancer. Removing them from your body could help in the prevention of cancer.
Oxygen Transport: Vitamin C has often been touted as having powerful “antioxidant” properties. As explained in my Health Note Antioxidants, I interpret this to mean that it can enhance metabolism. I thus decided to look more carefully at its biochemical properties. I discovered that vitamin C can be oxidized or reduced in your body. This is not a big surprise to most. However, specifically, when it is oxidized, it gives up two hydrogen atoms forming a new internal bond between oxygen and the two hydrogen’s go into forming water. When it is reduced back again, it bonds with two hydrogen’s again, forming the original form of the vitamin C. How lets look at the oxidation reaction that takes place at the inner membrane of the mitochondria, which powers the respiratory chain of aerobic metabolism. The conventional understanding is that oxygen diffuses to this membrane and reacts with hydrogen (in the form of NADH and FADH2), picking up two hydrogen atoms per oxygen atom, to form water. It is this reaction that powers the respiratory chain to form most of the ATP that is produced in the mitochondria. Now lets look at what can happen if oxidized vitamin C diffuses up to the same membrane. It too can react with two hydrogen atoms in the same way that oxygen can, but it will form reduced vitamin C instead of water. Since this can be an exothermic reaction, it too can provide energy to power the respiratory chain in the same way that oxygen can. Thus, in effect, vitamin C can participate in the transport of oxidation potential to the mitochondria and thus help facilitate the operation of the respiratory chain, with all its anticancer implications. I believe that this oxidation transport capability might be the major explanation as to why large doses of vitamin C seem to have powerful, general health benefits. It could be giving every cell more energy to cope with a variety of health issues. Basically, the vitamin C is transported to the lungs in the blood where it is oxidized. It then is transported to the cells where it diffuses to the mitochondria and delivers its oxidation potential, powering the respiratory chain, and cycle repeats. It should be noted that there have been many reports where mega doses of vitamin C have been attributed to causing the shrinking of cancer tumors.
7. Vitamin C plus MSM:
It appears that the DMSO-MSM equilibrium can act as an oxygen transport system and vitamin C can also. What about the combination? One would expect the effects to additive. There is no reason to expect them to conflict and thus diminish the other’s contribution. As an interesting single observation, I have a friend who is a very competitive athlete. When I told him about this theory, he decided to get some MSM powder and Vitamin C powder and mix them (about equally). They are both available in our local health food stores. He said that he then put about a quarter of a teaspoon of the mixture in water and drank it in the morning. It gave him an extreme rush of energy, considerably more than either did alone.
8. Inositol Hexaphosphate (IP6):
A search on Medline yielded numerous publications that indicated that IP6 held considerable promise for treating some forms of cancer. How does it function biochemically? It has been found in the blood of birds where its function is to facilitate the release of oxygen from hemoglobin. Therefore, the treatment with IP6 would logically work to compensate for the lack of carbon dioxide in the cancer cells and promote the availability of oxygen from hemoglobin. (There is some evidence that it may also act as an oxygen transporter independent of hemoglobin.) It is most interesting to note that its effect on cancer is not to kill the cells, but rather to cause them to revert back to normal cells, as this theory would predict.
9. Synthetic Blood:
The research directed at finding effective forms of synthetic blood has included the identification of molecules that would be nontoxic and effective at transporting oxygen. If my theory is correct, all of these molecules would have potential for treating cancer although I don’t know of any attempts made to investigate the use of synthetic blood for this purpose.
10. Oxygen Transport Summary:
It appears that enhancing oxygen transport to the mitochondria of cancer cells could promote their reverting back to normal cells. This can be done either by enhancing the release of oxygen from hemoglobin, compensating for the lack of carbon dioxide (Inositol Hexaphosphate) or by providing a supplemental system of oxygen transport that does not depend on hemoglobin (DMSO-MSM system, Vitamin C, Synthetic Blood). Undoubtedly there are systems that I have not thought of, but the consequences of all such systems should be the same. They should all help to promote cancer cells to return to aerobic metabolism and thus return to being normal cells by the same basic mechanism. However, if my theory is correct, this is only part of the solution. It will work for some cancers that need the lack of carbon dioxide to stabilize their cancerous state. If the aerobic metabolism of the cell is totally blocked earlier in the aerobic metabolic sequence, providing oxygen at the end will not help. For such cancers it will be necessary to provide an external source of the missing enzymes necessary for the earlier steps. As was discussed earlier, a vegetable diet might achieve this. In such cases, a supplemental oxygen transport system in combination with a vegetable diet might be more effective than the diet alone.
There is a very reasonable concern that if one chooses to employ only one of the possible oxygen transport systems you will reach a toxic level (for the whole body) before you have adequately treated the cancer. Thought should be given to combinations (blends) of them. At first glance it would appear that their transport mechanisms would supplement each other without much interference. Thus it may be feasible to greatly enhance this mechanism with combinations while remaining below a toxic level for any one. I can only hope that those who are entitled to do cancer research will explore this.
11. Coenzyme Q10 (CoQ10):
We now move from oxygen transport to the mitochondria to the specific part of the mitochondria where it is used. Oxygen must be transported to the inner membrane of the mitochondria where the respiratory chain takes place. For this membrane to function, it is vital for it to contain the electron carrier CoQ10. In fact the CoQ10 was discovered when the treatment of isolated mitochondria with an organic solvent such as isooctane completely stopped aerobic metabolism, and when the material extracted was added back, aerobic metabolism was completely restored. In time, the essential material was identified and named CoQ10 (also called ubiquitone).
Application to cancer: If this theory is correct, one would expect the lack of CoQ10 could cause cancer, and replenishing it should cause the cancer cells to return to normal (if this was the only cause).
I would like to refer to the results presented in a paper by Lockwood K, Moesgaard S, & Folkers: “Partial and complete regression of breast cancer in patients in relation to dosage of coenzyme Q10″ (Biochem Biophys Res Commun 1994 Mar 30;199(3):1504-8 ). Pharma Nord, Vejle, Denmark. In this paper it is stated that “in a clinical protocol, 32 patients having -”high-risk”-breast cancer were treated with antioxidants, fatty acids, and 90 mg. of CoQ10. Six of the 32 patients showed partial tumor regression. In one of these 6 cases, the dosage of CoQ10 was increased to 390 mg. In one month, the tumor was no longer palpable and in another month, mammography confirmed the absence of tumor. Encouraged, another case having a verified breast tumor, after non-radical surgery and with verified residual tumor in the tumor bed was then treated with 300 mg. CoQ10. After 3 months, the patient was in excellent clinical condition and there was no residual tumor tissue.”
These results are dramatic and are fully consistent with the theory presented here, which would conclude the anaerobic metabolism causing the breast cancer was caused by a lack of CoQ10, and when it was replenished, aerobic metabolism was restarted and the cancer cells turned back into normal cells.
12. Vitamin B12 and Folic Acid:
It is well known that the combination of vitamin B12 and folic acid (both essential) are partners in the production of the heme molecule, which is essential for the production of hemoglobin. A deficiency of either will result in anemia. The combination will contribute to the production of hemoglobin and thus the transport of oxygen in the blood. It the above proposed mechanism for cancer is correct is, this mechanism alone would make one expect that the combination would be helpful in the treatment of cancer, if an oxygen release mechanism is present, such as IP6. However, the immediate focus is on the inner membrane of the mitochondria. As was discussed in 11 above, CoQ10 plays an important role. However, the inner membrane also has a series of “cytochromes” which provide the rest of the active roles. All of these cytochromes on iron incorporated in a heme molecule to function. Thus, the production of the heme molecule not only plays an essential role in oxygen transport, but also plays an essential role in the inner membrane of the mitochondria, and thus the respiratory chain. One would expect a deficiency in the production of the heme molecule would diminish aerobic metabolism from two directions, lowered oxygen transport in the hemoglobin, and reduced capability of the inner membrane of the mitochondria to carry out the respiratory chain even if the oxygen gets there.
As would be expected from the above cancer theory, a Medline search identified numerous publications that indicate an inadequate absorption of vitamin B12 or inadequate dietary folate are closely associated with increased cancer risk.
13. The Inner Membrane of the Mitochondria:
As discussed in 11 and 12 above, the respiratory chain takes place at the inner membrane of the mitochondria and carries out the process called “oxidative phosphorylation” where ADP is converted back to ATP, the energy currency of the cell. This process is discussed in essentially all books on biochemistry. The investigative work that has been done is truly beautiful, with one exception. I believe one fundamental error has been made which is present in all the books, and which has major implications. The respiratory chain operates much like a fuel cell. We manufacture fuel cells to produce electricity. They are well know for their exceptional efficiency as well as the requirement to use simple, pure reactants, such as oxygen and hydrogen and not anything so complicated as gasoline instead of hydrogen. The respiratory chain seems to have similar characteristics. The processes entering the Kreb’s cycle and the Kreb’s cycle itself proceed in a way that produces two very simple forms of hydrogen, NADH and FADH2. They are then reacted with oxygen to yield electrons in the inner membrane, which then carry out the work of oxidative phosphorylation with the help of CoQ10 and the cytochromes. However, there is one problem with the descriptions. They show the oxygen and the fuel, NADH and FADH2 in solution on the same side of the membrane. Any fuel cell engineer knows that you must keep the oxygen and the fuel (hydrogen) in solution on opposite sides of the semi-permeable membrane (the inner membrane of the mitochondria). Otherwise they will react directly in the solution, producing heat but no electrons, and thus producing no useful work. There is nothing more fundamental to the design of a fuel cell than this. To assume that nature violates this fundamental design requirement, which would greatly reduce efficiency at best, is to assume that the great designer in the sky is not as intelligent as the average fuel cell engineer. Frankly, I think She might resent that. This erroneous assumption has resulted in a number of downstream distortions in mechanisms that need correction. However, I won’t attempt to accomplish all of them. I will only address what is important to the cancer theory presented here.
I won’t reproduce the mechanism presented in the biochemical books. You can get one and read it there. I will simply state what I believe must the be correct process.
1) The fuel produced from the Kreb’s cycle, such as NADH diffuses to the inner wall of the inner membrane of the mitochondria and gives up two electrons forming NAD+ and H+, which remain in solution. 2) The electrons move through the membrane attached to CoQ10 and cytochrome molecules, doing the work required to produce ATP from ADP. 3) When the electrons (negative charges) finally reach the outer surface of the membrane they combine with two hydrogen ions (2H+) to make two hydrogen atoms (2H) attached in some way to the surface. 4) These hydrogen atoms then react with oxygen to form water (at the outer surface of the membrane). 5) It is the chemical energy of this reaction that creates the electrical potential in the membrane that allows the electrons to do the work on the CoQ10 and cytochromes needed to produce ATP from ADP. 6) The positive electric charge that is produced on the inside of the membrane due to the loss of electrons is neutralized by the diffusion of negatively charged phosphate ions across the membrane, into the matrix (along with ADP). These phosphate ions, along with the hydrogen ions that have been produced are needed to react with ADP to make ATP. The newly created ATP diffuses out of the mitochondria and is used for energy throughout the cell, creating ADP, a phosphate ion, and a hydrogen ion. The ADP and phosphate ion then pass back though the membrane, but the hydrogen ion doesn’t . It is consumed at the outer surface of the membrane to make water by the mechanism just discussed.
The importance of understanding this change in mechanism is that it shows that the oxidizing species, (O2, etc.) does not have to diffuse across this relatively impermeable inner membrane to carry out its task at the inner surface. It does it at the outer surface of the membrane. One of the added benefits is that this allows the process to be more flexible in its ability to utilize different oxidizing species. If they all had to cross this low permeability membrane to the inner surface, each would probably have to have its own specialized protein transporter embedded in the membrane. Such specialized transporters are not known to be there and would not be expected to be there if my model is correct. There are simply too many different molecules that have been found to carry oxygen potential in the blood for my model to be incorrect. Specifically, it explains why MSM and vitamin C can be effective. The oxidizing species simply have to be able to react with hydrogen to form a reduced species, delivering the energy of reaction to the oxidative phosphorylation process.
Normal cells die on a regular and planned basis, and their component molecules are metabolized and thus recycled. This planned (sometimes called programmed) cell death is called apoptosis. The life span of a particular cell can vary from a few hours to many years. However, the majority of the cells die and are replaced every few days. (“Textbook of Biochemistry with Clinical Correlations” Thomas M. Devlin, Editor, Fourth Edition, 1997) This normal process is essential for maintaining the health of the organism. One of the distinguishing features between cancer cells and normal cells is that cancer cells do not exhibit apoptosis. The live and multiply indefinitely.
How does this relate to cancer and the approach proposed here. One of the critical features distinguishing cancer cells from normal cells is that cancer cells do not undergo apoptosis. They continue to multiply unchecked, growing in number until the host is destroyed. However, if the cancer cells can be caused to revert back to normal functioning cells, the natural process of apoptosis can then proceed and the “normalized” cancer cells will gradually die. This will not be due to a chemical attack, as with chemotherapy, but rather through normalizing cell function. With luck, the remission of the cancer could take place within a matter of a few weeks. However, this depends on the cancer cells exercising their apoptosis option. If every cell chose apoptosis at the same time, we would obviously die. We want the “normalized” cancer cells to preferentially recognize their need to commit apoptosis to preserve the health of the organism. How this selection can be made to be preferential for cancer is not understood. However, there are some experimental measurements that have identified some molecules that appear to promote this. One of these is DMSO, which is discussed, in the same book referenced in Item 1 above. Others have also been identified. However, one would expect that any approach that promotes cancer cells to revert back to normal cells would result in an increase in the rate of apoptosis, and this alone could explain how some “nutrients” can induce apoptosis of cancer cells.
15. The Citric Acid (Kreb’s) Cycle:
The anaerobic stage of metabolism produces pyruvate from glucose when the aerobic metabolism sequence is operational. Pyruvate is then oxidized to acetyl-CoA, which enters the Krebs cycle (A nine step cycle). (This is also called the citric acid cycle.) The combination of pyruvate oxidation and the Krebs cycle converts one molecule of glucose into 6 carbon dioxides, 10 NADH’s, 2 FADH2′s and 4 ATP’s. The ATP molecules are then used for cellular energy. When the 10 NADH’s and the 2 FADH2′s are then fed into the respiratory chain already discussed, they are oxidized to produce an additional 34 ATP’s. It can thus be seen that the primary task of the Krebs cycle is to produce NADH and FADH2 as feed for the respiratory chain, along with the release of the carbons as carbon dioxide.
Kreb’s cycle vital to both cellular energy and primary biochemicals for biosynthesis: The Kreb’s cycle is critical not just for the production of energy (the feed of NADH and FADH2 to the respiratory chain). It also produces key biochemical feedstocks required for the further synthesis of a wide variety of biochemicals essential for cellular function. As an example, the forth step produces a-ketoglutarate. This is then used by the cell to produce at least sixteen additional essential biochemicals. The ninth step produces oxaloacetate, which the cell uses to produce an additional eight essential biochemicals. These are just some of the ones that have been identified. There are probably many others. When the Kreb’s cycle shuts down, it not only removes a vital source of energy, but it also removes a key source of biochemicals essential to a broad range of cellular function. Thus, even if the energy function was replaced (I don’t know how) the cell would still cease to function normally.
Each step of this sequence requires its own special enzymes both to catalyze the reactions as well as those that control the rate of each reaction so that they operate in a coordinated manner. If any one of the steps is blocked due to a lack of an essential enzyme, the entire sequence could shut down, stopping all of aerobic metabolism.
It is my belief that most cancers probably start with an interruption of the Kreb’s cycle, which arrests aerobic metabolism and forces the cell to revert to anaerobic metabolism. The 100 or more identified oncogenes are genes that formerly produced essential enzymes for the Kreb’s cycle, but have become damaged and no longer do so. Suppressor genes are genes that compensate in some way for the damaged genes that are now oncogenes. It is likely they produce enzymes that provide an alternative path that allows the Kreb’s cycle to continue to operate. However, it would be difficult to distinguish between a shut down caused by a direct interruption of the Kreb’s cycle or one that is caused by a shut down of the respiratory chain which in turn would shut down the Kreb’s cycle.
It has been estimated that there are as many as 100,000 genes for the entire mammalian genome. If the approximately 100 oncogenes discovered thus far represent a reasonable representation of the complete set, this would indicate that cancer is initiated/controlled by a rather small part of the complete biochemistry of the cell. Such a conclusion would be consistent with the theory of cancer presented here.
It should also be pointed out that there are two separate sets of genes in every cell. There is the set in the nucleus, derived from both the mother and the father, which is the one that we commonly think about. However, the mitochondria have there own set of genes that are derived exclusively from the mother. An oncogene that disrupts the Kreb’s cycle would have its origin in the mitochondria. An oncogene that disrupts oxygen transport would have its origin in the cell nucleus. If the origin of the oncogene was known, this would give some indication as to how it operates. There is another important difference. There is only one nucleus and thus one set of nuclear genes in a cell, but there are many mitochondria and thus sets of mitochondria genes. In fact, mitochondria can divide and thus multiply, changing the numbers in a cell in response to cellular (energy) needs. How can an oncogene in one mitochondria propagate to many mitochondria? Is it by reproduction of the mitochondria in the cell? Can you have damaged and undamaged mitochondria in the same cell and how will this affect cancer? These are some of the challenging questions I don’t have answers to.
16. Fruits, Vegetables & Herbs:
There are numerous reports that many fruits, vegetables and herbs can inhibit the onset and progression of cancer. How can this be explained within the context of the theory presented here? We have to assume that the fruits, vegetables and/or herbs contain essential cellular nutrients/biochemicals that the cancer cells can no longer produce for themselves and the consumption of the appropriate set allows them to be digested, enter the blood stream, get to the cancer cells where they are absorbed, resulting in the biochemistry of the cells returning to normal. This could happen either by the providing the missing enzymes (or coenzymes) no longer produced in the cells due to damaged genes, or by providing the end point biochemicals the missing enzymes are responsible for producing. Examples of end point biochemicals would be those that have been identified as derived from the Krebs cycle, which is not operating in the cancer cells.
One Recent Review Paper: (Craig WJ, “Phytochemicals: guardians of our health” J Am Diet Assoc 1997 Oct; 97(10 Suppl 2): S199-204) “The foods and herbs with the highest anticancer activity include garlic, soybeans, cabbage, ginger, licorice, and the umbelliferous vegetables (caraway, carrots, celery, dill, parsley). Citrus, in addition to providing an ample supply of vitamin C, folic acid, potassium, and pectin, contains a host of active phytochemicals. The phytochemicals in grains reduce the risk of cardiovascular disease and cancer.”
This should be considered a guide giving the best demonstrated effective foods and herbs, but not something that should be limiting. Other fruits, vegetables and herbs may be less effective but still helpful. This may also vary significantly between individuals. It brings to mind one lady I know who discovered that cherries, including the dried ones sold at her grocery store, greatly alleviated her arthritis. When she ate them daily, her arthritic pain went away and when she stopped, it returned in a couple of weeks. This was repeated enough to where she was convinced of the connection. I have never hear of this working for anyone else. It appears that cherries contain some specific phytochemical that addresses her individual deficiency. Thus, observe you own reactions to different variations, and trust your observations.
Garlic is a particularly interesting case because it seems to be the most effective (anticancer agent) of the vegetables or fruits, and the active ingredients have been identified. . Diallyl sulfide, a major volatile thioether present in garlic is believed to be the active ingredient most responsible for garlic’s anticancer properties. In addition, ajoene, another major compound of garlic has been shown to induce apoptosis in human leukemic cells.
Diallyl sulfide: I find it very interesting to note the similarity between diallyl sulfide and dimethylsulfide. They both consist of one sulfur with two organic molecules attached. In the case of dimethylsulfide two methyl groups (CH3) are attached, in the case of diallyl sulfide, to allyl goups (C3H5) are attached. In the health note “DMSO” it was pointed out that there is an equilibrium established between dimethylsulfide (no oxygen attached), DMSO (one oxygen attached to the sulfur) and MSM (two oxygen’s attached to the sulfur). Because of this equilibrium, this set of molecules can act as an effective oxygen transport system. Since diallyl sulfide is a very similar molecule and the same bonding sites are available on the sulfur, one would expect it to behave in a similar manner, and it seems to.
Consistent with the discussion on DMSO, this would suggest that one of the major anticancer contributions of diallyl sulfide (and thus garlic) is to enhance oxygen transport to the cancer cells.
Ajoene: Ajoene (C9H14OS3) is a major compound of garlic that has been shown to induce apoptosis in human leukemic cells (Dirsch VM et al, “Ajoene, a compound of garlic, induces apoptosis in human promyeloleukemic cells” Mol Pharmacol 1998 Mar, 53(3): 402-7). It is a linear carbon-sulfur chain containing nine carbons and three sulfurs (with two bonds each). This means that each sulfur has sufficient extra bonding sites to attach two oxygen’s. Thus, a maximum of six oxygen’s could be attached – if oxygen saturated. Thus, it too could function as an oxygen transport agent with even greater oxygen carrying capacity than DMSO or diallyl sulfide. There is some evidence that it stimulates peroxide production, which would be consistent with this interpretation.
The assumption would then be that ajoene helps the cancer cells to revert back to normal cells by enhancing oxygen transport (turning on aerobic metabolism) and once the cells become normal they go through the normal process of apoptosis.
18. Glutamine and Glucose – Cancer Foods:
As has been discussed, anaerobic metabolism primarily consumes glucose. Since it is so inefficient compared to aerobic metabolism, cancers have a voracious appetite for glucose to sustain themselves. This is why excess consumption of sugars tends to promote cancer growth. It is less well known that cancers have an equally voracious appetite for glutamine. (“Glutamine and Cancer” Wiley W. Souba M.D., Sc.D., Annals of Surgery, Vol. 218, No. 6, 715-728) Briefly, glutamine is the most important “nitrogen shuttle” in the blood. It brings the organic nitrogen to the cancer cells so they can use it to make the essential amino acids and thus proteins required to make more cancer cells. As the glutamine supply goes to zero, tumor growth goes to zero. A rich dietary source of glutamine is red meats. This is why excess consumption of red meats and other concentrated sources of protein tend to promote tumor growth. Since normal cells also require both glucose and glutamine, reducing the intake of either to zero would have an undesirable outcome. Consumption in moderation (small quantities), along with fruits and vegetables seems to be the best approach.
As was discussed in item 18, cancer tumors require glutamine to grow. So do your muscles. Body builders supplement with glutamine to help develop larger muscles. Muscles not only consume glutamine in order to grow, but in the times of insufficient dietary glutamine, muscles can serve as a source of glutamine (for the blood) and diminish is size by doing so. This is why as cancer tumors grow, there is usually a wasting away (diminishing in size) of muscle structure. As the tumor (s) extract the glutamine from the blood, the body tries to resupply it by obtaining it from the muscles (that which hasn’t been supplied by diet.)
Postulation: The tumor-glutamine-muscle degeneration connection is a reversible chemical reaction. Essentially all chemical reactions are reversible even though the degree of reversibility can vary widely. As was already discussed, the process of forming muscle tissue using glutamine from the blood, is reversible in that the muscle tissue can resupply glutamine to the blood as needed by the body. The same is most likely true for cancer tumors, even though the reversal process where the tumor wastes away by resupplying glutamine to the blood does not appear to take place as easily as for muscles. The big question is can this reverse process be made to happen for tumors and how can it be maximized? I propose that this might be achievable by exercising in a manner that promotes the building of muscle. Aerobic exercise is obviously beneficial, but body builders know full well that weight-bearing exercise is far more beneficial for building muscle. I thus propose: Exercise that builds muscle in combination with a diet that minimizes the intake of glutamine has a good chance of reversing the glutamine reaction in the tumor, causing it to degenerate to supply glutamine to the blood, thus building muscle at the expense of tumor mass. Exercising in such a manner in combination with the rest of the dietary approaches discussed in this health note should have a good chance of inhibiting the onset or progression of cancer and with luck it could even reverse its progress. However, you are attempting to force a chemical reaction to go in a direction that is less preferred. Thus, we are talking about a committed, serious exercise program. I suspect you should anticipate needing at least 2-4 hours of exercise every day. Possible even more. Mimic serious body builders.
This presents a reasonable biochemical explanation for Lance Armstrong’s dramatic recovery from cancer. Lance Armstrong is the only American ever to have won the Tour de France riding for an American team (The U.S. Postal Service Team). He won it in 1999 just two-and-a-half years after being diagnosed with advanced testicular cancer. It had spread throughout his body. He received conventional treatments, and trained intensely for racing in the Tour at the same time. He credits his commitment to an exceptionally vigorous training program to have played a key role in his recovery from cancer. The French newspaper L’Equipe called his win “the comeback of the century” and Armstrong’s response: “If you ever get a second chance in life, you have got to go all the way”.
This opens up the question as to whether some of the supplements, other than glutamine, that are used by body builders to build muscle, will enhance this tumor wasting, muscle building process. I could even envision that some of these that might risk promoting cancer growth without a coupled exercise program may become highly beneficial when, and only when combined with a muscle building program. I suspect some of them will, and I hope research will be done to evaluate this possibility.
Unfortunately, people suffering from cancer frequently have highly diminished energy. This makes this exercise option even more difficult. Thus, in reality, there may be only a limited fraction of cancer patients who will be able to explore it.
A second argument for exercise. As was pointed out in item 18, cancers have a voracious appetite for glucose due to their inefficient extraction of energy from glucose. This is an unavoidable consequence of their anaerobic metabolism. Normal aerobic cells with aerobic metabolism can obtain almost 20 times more energy from a molecule of glucose. An excess of glucose (sugar) in the diet will promote the progression of the cancer. However, aerobic (any) exercise causes the muscles to consume glucose. As the glucose is consumed during exercise its availability diminishes. This should inhibit the progression of the cancer. Exercise should also help to compensate for excess sugar in the diet (if done soon enough). Sometimes excess dietary sugar is unavoidable. During the exercise there is a competition between the cancer cells and normal cells for the glucose. As glucose levels in the blood diminish, one would expect the cancer cells to suffer the most first. Normal cells should continue to function to much lower levels due to their far more efficient use of the glucose. Conclusion: Exercise of any type should inhibit the progression of cancers.
21. Mental Exercise-Glucose:
Your brain, through mental activity, consumes considerably more than 50% of the glucose in your body, far more than any other organ or activity. Mental activity is your most efficient method for consuming glucose. Thus, to consume excess glucose I would suggest you curl up with a book that seriously challenges your brain, such as a physics or biochemistry text. If you find yourself falling asleep, this is probably due to greatly lowered glucose in your blood.
It has occurred to me that this same approach might help diabetics achieve some control of high blood sugar with reduced requirement for insulin.
22. Two Forms of Programmed Cell Death:
Programmed cell death has the characteristic of no longer needed cells committing suicide for the benefit of the whole. To be sure there may be external encouragement (catalysts) such as hormone signals from neighboring cells, but the chemical changes that lead to the demise of the cells occurs within the cells themselves. Once encouraged, they implement the rest themselves. This process of an orderly elimination of damaged or no longer needed cells is absolutely vital to survival of our bodies. I am proposing that the body has introduced redundancy into this process to better insure its success. It can take place via two quite different processes. If the primary one fails, the other can serve as a backup.
Apoptosis: Apoptosis is the commonly recognized, primary mode of programmed cell death. In this mode, the cell produces/releases enzymes within itself which proceed to dissolve the cell from within. The resulting basic nutrients reenter the blood and can be recycled.
Immune/macrophage attack/dissolution: I propose there is a second mode of programmed cell death, which at first glance appears to be an uninvited external attack by the immune system. It involves the immune system in the form of macrophages attacking, engulfing and dissolving the errant cells. This basic process is well know to happen as a mechanism for disposing not just of foreign pathogens (bacteria) but also of damaged cells. I am proposing that in some cases, there is a deliberate action by the cell to encourage the attack. Let us postulate that a cell that has experienced genetic damage can, in most cases, recognize the need for its removal and trigger programmed cell death. Apoptosis is the primary mode. However, let us suppose this mechanism fails. Then, I propose, that the cell has a second option to achieve the same result. It can deliberately display proteins on its surface that will make it look like a foreign body to the immune system and trigger an attack by macrophages. Thus, this is programmed cell death as much as apoptosis even though it depends on the immune system to complete the task.
Relevance to Cancer: With the billions of cells in the body constantly dividing and being exposed to potentially damaging chemicals, it is highly likely that millions are produced every day with the right type of genetic damage to produce cancer. However in the vast majority of these cases the cells have sufficiently functioning cell chemistry to trigger one of these forms of programmed cell death. If this is successful, the potentially cancerous cells self-destruct and the cancer never develops. For apoptosis we are depending solely on the chemistry within the cell itself. However, for the second, backup, mode we depend on the cell signaling the immune system and the immune system being able to finish the task. Because of this second system, it can be seen how a strong immune system can play a vital role in preventing these cells from progressing into the unchecked growth of cancer. I am unaware of any solid observations that apoptosis occurs to new cancer cells. This would happen quickly and would be difficult to observe. However, there are numerous reported observations of the immune system attacking and destroying cancer cells. This would support the existence of the second proposed mode of programmed cell death.
Cancer: We then have the cells that have the genetic damage for cancer and are unable to initiate either form of programmed cell death, apoptosis or immune system attack. These are the ones that develop in to unchecked cancer. The immune system is totally ineffective as a defense because the cells are not recognized as foreign cells. This explains the apparent paradox of why some cancer cells have been observed to be attacked and destroyed by the immune system while cancers that continue to develop are almost unaffected by the immune system. The first class of cells have been programmed for cell death by displaying the appropriate immune system, signaling proteins on their surfaces, and second class display no such signaling proteins.
23. Cell Aging – A Primary Cause of Genetic Damage Leading to Cancer:
All cancers start with genetic damage. All forms of genetic damage do not lead to cancer. It has been proposed above that specific genetic damage causing the cell to become anaerobic is required. What causes this damage. It has been clearly demonstrated the many toxic chemicals, called carcinogens, can cause the genetic damage that results in cancer. Some viruses have also been implicated. Recent biochemical discoveries would indicate that the process of cellular aging alone may be a primary cause. Human cells can divide approximately sixty times before they can no longer divide and die. In contrast, cancer cells have no such counting mechanism and divide indefinitely without ever dying. Normal human cells have a counting mechanism that is handled by an extension/tail on the chromosomes named a telomere. This telomere grows shorter with each division until after the last division it no longer exists and the cell dies. However, as the telomere shortens, the cells not only have fewer divisions left, but they also act like older and weaker cells. Consistent with this, as telomere grows shorter, the cell gets weaker and divisions are not so well regulated (controlled). The checking mechanism that is supposed to assure perfect divisions with no genetic alterations starts to operate imperfectly and cells with genetic damage results from an ever-increasing fraction of cell divisions. Dr. Richard Lerner and his team at the Scripps Research Institute in La Jolla compared the effects of aging on 6,000 genes and found that 61 key genes went through dramatic changes from age 9 to 90. There are checkpoint genes that assert quality control over cell division. When the checkpoint genes fail, mistakes in genes are perpetuated into the new cells and their daughter cells. Given this observation of genetic damage with age, it is reasonable to postulate that a fraction of these imperfect divisions result in genetic damage that produce cancer cells. Most of these are eliminated by the two-programmed cell death mechanism described above. However, eventually some survive, as discussed in 22 above, and develop into cancer. Thus, cellular aging alone can be a primary cause of genetic damage leading to cancer, and probably explains the onset of most cancers that occur increasingly with age.
Conclusion? Different organs in the body probably age at somewhat different rates. Once an organ reaches the age where divisions are more likely to produce cancer cells, the continued creation of new cancer cells is likely to continue, even after all existing cancer cells have been destroyed (chemotherapy or radiation) or removed (surgery). In theory this can be avoided by the removal of the entire organ (breast, prostate, etc.) if you can live without it.
Lung and Skin Cancer: I would like to propose considering a cellular aging connection between smoking and lung cancer. The smoke can damage or kill lung cells, making cellular divisions take place more rapidly, in order to provide the replacement cells. Thus, the lung cells age more rapidly. The aging then causes the cancer. This would also explain why some people can smoke while young, quit, and still get smoking related lung cancer many years later. It doesn’t make any difference when you smoke. It still ages the cells faster, and there is a memory of this in the cells for life. The same logic would apply to the exposure of skin to ultraviolet light (too much sun exposure).
24. Nutrition Prevention of Genetic Damage, its Propagation, and Cancer:
Briefly, there are a number of ways that proper nutrition (diet and dietary supplements) can prevent the onset of cancer.
Reduction of Cellular Division Rate and Thus Cellular Aging: Cells divide to provide new cells to replace old, warn out, damaged cells. To the extent that optimum nutrition can extend the useful life of existing cells, the need for their replacement slows and so does the aging/replacement process.
Reduction in Genetic Damage due to Imperfect Cellular Division: Optimum nutrition should increase the energy available to the cells and thus help the checkpoint genes do their job of assuring adequate quality control over cell division, minimizing the production of daughter cells with genetic damage due to faulty divisions.
Elimination of Genetically Damaged Cells: Optimum nutrition should help damaged cells retain enough energy to activate either form of program cell death discussed in 21 above. The cell with genetic damage that can produce cancer then has the option/energy to institute programmed cell death, eliminated the potentially cancerous cell.
Supporting Evidence: Diet and dietary supplement prevention of the onset of cancer is not a new concept. There have been a very large number of studies of diets and dietary supplements reducing cancer rates by factors as much as 50% In some cases the studies involved tracking the diet of thousands of people over tens of years, while in others it involved double-blind studies of a smaller group, taking specific dietary supplements over shorter periods of time. I won’t attempt to present a review of the studies here. The reader can do that. I am simply supporting the assertion that proper diet/nutrition can prevent the onset of cancer, which provides reasonable support for the mechanism proposed here.
25. Poor Circulation and Cancer:
If inadequate cellular nutrition can make cancer more probable, as discussed in 24, then inadequate blood circulation could contribute also. Good circulation is required to deliver adequate nutrition to the cells. There could be a number of causes for poor circulation, one of which is arteriosclerosis. Thus, one would expect arteriosclerosis could be a contributing factor to cancer. Since it usually increases with age, it correlates well with increasing cancer rates with age. In particular, it may contribute significantly to breast and prostate cancer, where circulation is low.
Lysine, Vitamin C & Argenine: It has been reported that a combination of lysine and vitamin C can reverse/prevent arteriosclerosis. Argenine is known to be a precursor to the production of NO, which can help to dilate blood vessels. It has been reported to help with heart disease. Both of these approaches would contribute to enhancing circulation and thus are promising candidates for preventing cancer.
Exercise: There is nothing more important than exercise to enhance circulation.
26. Nutrition and Chemotherapy Synergism:
It would appear that nutritional therapy should greatly enhance the effectiveness of chemotherapy in a surprising way, beyond simply enhancing general health.
To illustrate, I would like to take a specific example and then generalize. Taxol is a commonly used chemotherapy agent. It is reported to work by interfering with the transport of protein molecules along the cytoskeleton filaments in the cancer cells. This is the major transport path required for many aspects of the cell chemistry, including the ability to divide and make new cells. The interference not only stops the cancer cells from dividing but also eventually results in cell death. This can control the cancer for some time, but experience has shown that the cancer eventually “mutates” and a creates a version of the same cancer that is resistant to the Taxol. The cancer then starts to grow again and continues to progress unless another chemotherapy agent can be found to stop it again.
The mechanism that the resistant cancer cells use for defense is fascinating. It has been found that they have developed a capability to pump the Taxol out of the cell where it can do no harm.
The fact that the anaerobic cancer cells, which already lack sufficient energy to perform normal cell functions, would still have enough energy to invent and deploy this novel defense, a sophisticated Taxol pumping system, seemed inconsistent to me. After being bothered by this for a number of days, I suddenly realized how it might have happened. The cancer cells didn’t develop the Taxol pumping system. Normal, non-cancer cells did. When they became cancerous, via the ongoing, age-related, defective divisions discussed in Item 23 above, they retained this capability as they divided to form cancer cells.
It is reasonable to presume that the normal cells have developed this pumping defense because Taxol was chosen because of its ability to preferentially kill cancer cells and be far less toxic to normal cells. Why is the Taxol not so toxic to normal cells? It is reasonable to postulate it is because the normal cells quickly develop this Taxol pumping capability.
If this is true, then the key to successfully treating with Taxol is to prevent normal cells, resistant to Taxol, from undergoing faulty divisions forming Taxol resistant cancer cells. The key to accomplishing this is proper nutrition as discussed in Item 24 above. Thus, combining nutritional treatment along with treatment with Taxol should be more effective than treatment with Taxol alone. It is also possible that nutritional treatment alone would not be as effective as using it in combination with Taxol. The Taxol may kill existing cancer cells more effectively than the nutritional-programmed cell death approach. It is thus reasonable to conclude that the combination would be more effective than either used alone. However, this points out a clear need to establish the most effective protocol.
This basic theory should apply to many forms of chemotherapy where it is commonly observed that the chemotherapy ceases to be effective against the cancer with time, and a resistant variation appears. It is logical that one would expect this because chemotherapy agents are chosen because they are far more toxic to cancer cells than normal cells. This is likely to be true because the normal cells can rapidly develop a defense. It is not much of a stretch to presume that this defense, whatever it might be, could then be carried along when this normal cell undergoes a faulty division that produces a cancer cell. It is also likely that some form of pumping mechanism keeping the chemotherapy agent out of the cell is the basis of most of the defense mechanisms.
Conclusion: All forms of chemotherapy could be made more effective by combining them with nutritional therapy, using the chemotherapy agent to kill existing cancer cells and nutritional therapy to prevent new, chemotherapy resistant cancer cells from being created.
27. Oxygen Supply Inhibits Angiogenesis & Thus Tumor Growth:
It appears that oxygen supply inhibits the formation of the vascular network that that is required for tumor growth. Conversely, an oxygen deficiency promotes the production of vascular endothelial growth factor (VEGF), which plays a key role in angiogenesis (the formation of the tumor supporting vascular-blood supply-network).
This was reported in “FOCUS”, the newsletter from Harvard Medical, Dental and Public Health Schools, May 19, 2000. The article summarized work reported in the May 11, 2000 issue of Nature: “Growth Factor Expands Tumor Cell Networks” by Rakesh Jain, Gabriel Helmlinger, Mit Endo, Lynn Hlatky and Napoleone Ferrara.
Summary: Vascular endothelial growth factor (VEGF) promotes angiogenesis and thus the growth of tumors. Oxygen starvation promotes the production of VEGF and thus promotes angiogenesis. They showed that well-nourished and oxygenated cells near the edges of a tumor maintained their normal form, while the starving cells near the center began branching and forming vascular networks within a few hours. They observed a gradient of VEGF expression that was inversely correlated with, and apparently induced by, the oxygen gradient.
I believe this is exciting news because it presents an additional mechanism where promoting oxygen transport to the tumors will inhibit their growth.
28. “The Antioxidant Miracle” by Packer & Coleman (John Wiley & Sons, Inc. 1999):
This is a wonderful book which summarizes the many years of research performed by Lester Packer, Ph.D., Director of the Packer Lab., University of California at Berkeley. It presents a large amount of valuable information, far too much to attempt to summarize here. I would like to limit myself to interpreting a main thread into the context of the cancer theory presented here. His primary focus is to identify five antioxidants (and only five) that appear to form an antioxidant network, they work together. The five are Vitamin C, Vitamin E, Glutathione, Alpha Lipoic Acid and Coenzyme Q10 (CoQ10). The roles of Vitamin C and CoQ10 in the context of this theory has already been addressed (Items 6&11). However, at this point I would like to limit my comments to the mechanisms of the special synergism between Vitamin C and Vitamin E and then the special characteristics of Alpha Lipoic Acid and Coenzyme Q10 as applied to this theory. These are mechanisms I am proposing, not ones presented in the book. It would appear that this particular set of molecules work together to transport oxygen to the cells, and the mitochondria within the cells, and prepare the mitochondria to receive the oxidation potential in a way that it can be used in aerobic metabolism.
Vitamin C & Vitamin E Special Synergism: As discussed in Item 6, Vitamin C has an oxidized and reduced state in equilibrium in solution that can serve as an oxygen transport system. The same is also true of Vitamin E. Vitamin C is soluble in the aqueous phase (cell cytoplasm) an Vitamin E is soluble in the oil phase (cell membranes). In order to transport oxidation potential to the mitochondria starting at the lungs, it will be necessary to transport it across cell cytoplasm as well as cell membranes. Vitamin C and Vitamin E become partners in this process. Briefly, oxidized vitamin C diffuses up to a cell membrane and delivers it to Vitamin E in the cell membrane. The resulting oxidized Vitamin E carries it across the cell membrane and delivers it to reduced vitamin C in the cytoplasm on the other side. The newly oxidized Vitamin C then diffuses to the mitochondria and delivers the oxidation potential to the metabolic system, oxidizing food and becoming reduced in the process. The reduced Vitamin C then diffuses back to the cell membrane to become oxidized again by the oxidized Vitamin E in the membrane. And, the cycle continues. Thus, in this way, Vitamin C and Vitamin E become partners in the oxygen transport stage of aerobic metabolism. Far more Vitamin C would be needed than Vitamin E because the volume of the cytoplasm is far greater than the volume of the cell membrane. Thus megadoses of Vitamin C may be helpful while far lower doses of Vitamin E would be optimum.
This mechanism would also predict that megadoses of Vitamin C would not only assist in transporting oxygen potential from the lungs to the cells, but also would assist in the transport of oxygen potential within any given cell.
Alpha Lipoic Acid (ALA): Packer presents a multitude of benefits for ALA but I will limit myself to addressing one that applies to the cancer theory presented here which is not explained/ addressed in the book. ALA also has an oxidized and reduced state and thus can transport oxidation potential in a similar way to Vitamins C & E. However, it is unique in that it is soluble in both aqueous and oil phases. Thus, it can substitute for either or both Vitamin C and Vitamin E in the oxygen transport system. This versatility makes it an exceptionally valuable nutrient. It can substitute for deficiencies in either. This is partially supported by an experiment discussed in the book where animals made deficient in Vitamin E would not suffer from the deficiency if they were supplemented with Alpha Lipoic Acid.
Toxic Metal Elimination: Alpha Lipoic Acid promotes the synthesis of glutathione in the body. In addition to their oxygen transport capability, they both have the capability to chelate toxic heavy metals and thus assist their elimination from the body.
Coenzyme Q10 (CoQ10): The purpose of oxygen transport is to transport it to the inner membrane of the mitochondria where it can be reacted with hydrogen to make water, while using the chemical energy to produce ATP, the energy-carrying molecule in all cells. Thus, once the oxygen gets there, the membrane must be able to accept in a manner where it can be used for this process. CoQ10 is the molecule in the membrane that accepts the oxidation potential and enables it to be used in this stage of aerobic metabolism.
29. Cancer, Schizophrenia, Abram Hoffer, Linus Pauling and This Cancer Theory:
Dr. Abram Hoffer is commonly credited with being the principal founder of the alternative health movement using nutritional or orthomolecular treatment methods. During his practice, extending more than 40 years, he has treated thousands of patients primarily for cancer and schizophrenia, authoring many journal articles and books. As part of this effort he collaborated with Dr. Linus Pauling, two-time Nobel Prize winner, in his focus on utilizing vitamin C (with other nutrients) for the treatment of cancer. One unexpected result was that he discovered that very similar treatment approaches were effective for treating both cancer and schizophrenia. As will be seen, it appears that his treatment approaches are fully consistent with this cancer theory. If true, it provides a vast amount of experimental results that verify this theory and indicates it applies to serious illnesses beyond cancer.
Dr. Hoffer phoned me on 5/10/01 at the recommendation of a mutual friend, Bernie Rimland, Director of the Autism Research Institute in San Diego. Bernie had related to him a success a friend of mine had with reversing stage-four lung cancer following a nutritional treatment approach dictated by the cancer theory presented here and Dr. Hoffer has a close family member with lung cancer. During our phone conversation I first outlined the theory and he said it made sense to him. In fact he could think of a lot of published results that would support it. He also mentioned that strangely enough, he had found that schizophrenics rarely get cancer. However, he had not read this web page on cancer. I gave him the web page address and he said he would take the time to read it. We agreed to continue communication by email. The sequence of emails is as follows (with Dr. Hoffer’s permission):
Hoffer Email-1 Sent: 5/12/01 11:53 PM From: A Hoffer, email@example.com To: firstname.lastname@example.org
Dear Dr Gregg:
I have now read your proposed common cause and cure of cancer and I agree with your overall hypothesis. I knew about Warburg’s early work when I started many years ago and have followed his idea in developing the nutrients that I use which includes the ones you described with the exception of MSM and DMSO which I have not used. I do agree that it is important to maintain respiratory oxygenation and have depended on maintaining blood flow, which one can do with niacin to dilate the capillaries and with vitamin B-12 that decreases the size of the red cells and permits more efficient distribution of blood through the capillaries. Niacin also ensures proper function of the pyridine nucleotide cycle. I will look at MSM as it is very difficult to get DMSO in Canada.
I think your ideas are sound and deserve to be explored fully but I am not convinced that it is the only answer . I am sure you are not convinced as well and I do think that decreasing the ravages of excess oxidation also plays a role. What we need is a thorough examination of these ideas, which perhaps may come with the new liberation of idea in this field as the alternative complementarity ideas take hold. Thanks for letting me know about your work. I am ordering MSM immediately. MY wife is already following the rest of your program with the exception of exercise, which is very difficult for her because of severe osteoporosis which gradually crept up on her but which is not progressing any further. So far her lesion is not growing but I will not know until we have several more x ray examinations.
A. Hoffer 3 2727 Quadra Street, Victoria . B.C. Canada V8t 4E5 Fax 250 386 5828 Tele 250 386 8756,
E mail Hoffer@Islandnet.com
For information about orthomolecular treatment for schizophrenia see www.islandnet.com/~hoffer/hofferhp.htm
For more information about treatment with vitamins look up http://doctoryourself.com/hoffer_niacin.html
For information about orthomolecular treatment and heart disease see http://doctoryourself.com/hoffer_cardio.html
For information about the orthomolecular treatment of cancer see www.islandnet.com/~hoffer/homepage.htm
Vitamin B-3 and Schizophrenia , and .Vitamin C and Cancer both by A. Hoffer, Quarry Health Books, Box 1061, Kingston, Ontario, K7L 4Y5, www.quarrypress.com 1998
(Reading Dr. Hoffer’s referenced web pages is an absolute must for one to appreciate the magnitude of his accomplishments with cancer and schizophrenia.)
Thank you very much for your reply and taking the time to read my attempts to analyze cancer. I plan to read all your web pages referenced and purchase whatever of your books that are still in print. I am still puzzling over your statement that schizophrenics don’t get cancer. Could you give me a reference that I could read. I know you have a theory. I don’t want to take too much of your time, but could you briefly outline it to me again. I wonder if I can connect it to the cancer theory I have presented, or whether it involves something quite different. I would like to put some time into it and see if I can identify some useful new insights. It is a fascinating challenge.
Hoffer Email-2 Sent: 5/14/01 5:43 PM From: A Hoffer, email@example.com
To: David Gregg, firstname.lastname@example.org
The references to the relationship in the literature are few and not very convincing although they do suggest that schizophrenia do not get cancer nearly as often. A study in the mental hospital in New York showed that even the heavy smoker patients got lung cancer much less frequently. My study is based upon 6000 schizophrenics I have seen and nearly 1200 cancer patients. Ten patients had both. The ten schizophrenics all recovered on standard treatment . I have seen no deaths. They also recovered from their schizophrenia. The relationship is not as strong for first order relatives but is still very significant. I have 300 families with the index case schizophrenia and 300 families with the index cases cancer. The cancer families seldom have schizophrenia and vice versa. I use only first order relatives. The theory I am pursuing is based on the adrenochrome hypothesis, which is that schizophrenia is caused by an increased production of adrenochrome and similar oxidized derivatives of the catecholamines. A recent report by Japanese scientists showed that schizophrenics lack the gene that is responsible for helping eliminate adrenochrome. This is the first time a direct relationship has been found. An adrenochrome derivative is used in Japan as a treatment for cancer.
Adrenochrome is a potent anti mitotic. This was first found over fifty years ago. It is also hallucinogenic. For information read my book The Hallucinogens, Academic Press 1967. This book contains a petty good description of our adrenochrome hypothesis. When there is enough adrenochrome to cause schizophrenia there is too much to permit cancer. If there is not enough to cause the psychosis there is not enough to prevent cancer. I consider schizophrenia an evolutionary advance with adrenochrome as one of the main factors controlling cancer. Adrenochrome if formed from adrenaline in white cells and in heart muscle. Too much in cardiac muscle causes atrial fibrillation. I do not know what too much does in white blood cells.
Adrenochrome is irreversibly formed from adrenaline but in turn is rapidly reduced to adrenolutin. Aerobic metabolism must be involved. It is probably stored in tissues that do not divide like red blood cells , white cells. and cardiac cells.
Recently the first item of empirical evidence supporting the adrenochrome hypothesis has been presented by Harada et al. (2001). Catecholamine o-quinones (including adrenochrome) are, in part, detoxified by 5-conjugation with glutathione. This reaction is promoted by glutathione S-transferases 1 and 2 (GTM 1& 2). Harada et al. (2001) studied DNA samples from 87 schizophrenics and 176 normal controls. They found an increased frequency of deletion of this gene (frequency of the GSTM1*O allele) in the schizophrenic group (p=0.0075) and an even higher rate in the subgroup of disorganized schizophrenics (p=0.0008). They suggested that the GSTM1 gene deletion may constitute a risk factor for schizophrenia associated with an increased toxic action of catecholamine o-quinones, including possibly adrenochrome, in the brain.
Ref: Harada S, Tachikawa H, Kawanishi Y. (2001) Glutathione S-transferase M1 gene deletion may be associated with susceptibility to certain forms of schizophrenia. Biochem.Biophys.Res.Comm. 281, 267-271.
Dear Dr. Hoffer,
Thank you very much for your emails. You got me started taking a closer look at Schizophrenia, its connection to cancer, your (and Linus Pauling’s) exciting results for both, and the connection of both to my theory for cancer. I read your web pages that you referenced in your email and purchased the only two of your books carried by our local Barnes & Nobel Bookstore, “Vitamin C & Cancer” and “Dr. Hoffer’s ABC of Natural Nutrition for Children”. I also had the book “Natural Healing for Schizophrenia” by Eva Edelman (foreword by Abram Hoffer) in my library, which I finally took the time to read. It is a good start and I have not yet finished reading the books. I will attempt to get more of your books when I have finished these.
Even though I am just starting to read of your work, you have stimulated a flood of thoughts that I would like to relate. My primary problem is to keep it brief so I will present them in itemized, “bullet” form. I can expand on them later as appropriate.
I am shocked by the magnitude of work and accomplishments you have made with both Schizophrenia and Cancer and my lack of awareness of it in any detail. I knew you were highly respected for your work with applying nutrition to both, but it is the specifics that make it so profound.
It appears that it is appropriate to assign the majority of vitamin B3 discoveries to you and the vitamin C discoveries to Linus Pauling. It must have been exciting for both of you to have enjoyed the experience of collaborating.
Both sets of discoveries fit very nicely into the “umbrella” theory of anaerobic vs. aerobic metabolism I have proposed for cancer. (It also seems to apply to Schizophrenia and other degenerative diseases.) We know that all vitamins address essential roles, but why do vitamins C and B3 stand out so much above the rest as having such a broad ranging benefit to almost every illness? We know they have a multitude of biochemical uses, but what are the primary functions that make them so universally powerful?
Thinking in the context of aerobic metabolism:
Vitamin C has oxidized and reduced forms, which are in equilibrium with the distribution depending on the oxidation potential of the solution it is in. When this solution moves in the blood to the lungs it shifts towards the oxidized form and when it then moves to the cells (mitochondria) it delivers that oxidation potential, shifting towards the reduced state. In this way megadoses of vitamin C serve as an oxygen transport system supplementing hemoglobin. Increased oxygen transport allows increased aerobic metabolism resulting in increased cellular energy. The cells with more energy can do more to defend themselves and a person’s health. Since oxygen transport is so fundamentally required for aerobic metabolism, one might expect megadoses of vitamin C, enhancing oxygen transport and thus cellular energy in all cells, to have the truly broad ranging benefits that are observed.
Vitamin B3 can promote oxygen and nutrient transport by improving circulation due to dilation of blood vessels, but I do not believe this is its pivotal role that makes it so generally powerful. It is required for the production of NADH, (B3 being a precursor to the production of NADH) which is absolutely essential for the operation of almost all aspects of both the citric acid cycle as well as the respiratory chain, the two key steps in aerobic metabolism. No B3 would stop all aerobic metabolisms and low levels of B3 would restrict – set a limit on the amount of aerobic metabolism that could take place. The cells would then function only as well as the restricted availability of energy would allow. This function is as general as the need for oxygen. I believe this is the reason supplementing with megadoses of B3 exhibits broad ranging benefits similar to that of vitamin C.
It is thus obvious that vitamin C and vitamin B3, promoting key sequential stages of aerobic metabolism, should be good partners in any treatment protocol.
Why the same treatment works for both cancer and schizophrenia: Both are caused by the cells not having enough energy to operate their extremely complex biochemistry (& utilize nutrients and operate all the control mechanisms), so they can function normally as designed. I have a chart on my wall that takes a stab at outlining all the biochemical paths in a cell. To say it is extremely complex is an understatement. It involves as many as 4,000 enzymes, their products and all the interactions. This system has to operate in a well-organized, orderly way, as designed, or there is no hope. At this point you can invoke a fundamental thermodynamic argument, high degrees of order require high energy. Low energy results in disorder and high entropy. Cellular energy is the starting point for all organized cellular function. For cancer, aerobic metabolism is eliminated, dramatically restricting allowable cellular function to only what anaerobic metabolism will support, while for schizophrenia aerobic metabolism is simply reduced below the minimum amount needed for the cells to function to full capacity. For cancer it appears that the block can be in either or both the oxygen transport mechanism as well as the operation of the citric acid cycle and the respiratory chain. However, for schizophrenia the blockage appears to be dominantly in the citric acid cycle and respiratory chain.
The Adrenochrome Hypothesis: I will attempt to connect this to the aerobic metabolism theory. If the cell fluids have a high oxidation potential they are more likely to produce more adrenochrome and low oxidation potential the reverse. In the case of schizophrenia we assume the aerobic metabolism blockage is in the citric acid cycle & respiratory chain and not in the oxygen transport system. Thus, oxygen is transported to the cell from the lungs where it cannot be consumed by reaction with food (glucose) and thus stacks up — maximizing the oxidation potential in the cell fluids. This could be a contributing factor for increased adrenochrome in schizophrenics (in addition to the lack of the gene helping to eliminate adrenochrome). Thus the restricted aerobic metabolism at the citric acid stage could cause schizophrenia by two paths, reduced cellular energy and increased production of adrenochrome, a toxic causal agent. If high adrenochrome concentrations are required to have schizophrenia, it would follow that aerobic metabolism must be blocked at the citric acid cycle and not at the oxygen transport stage in order to have schizophrenia.
It makes sense that if adrenochrome is toxic/inhibiting to cancers that high concentrations would result in lower cancer rates. However, to couple to the aerobic metabolism theory, if the cancer’s anaerobic metabolism is caused primarily by a block at the oxygen transport stage and not so much a block of the citric acid cycle, the small amount of oxygen getting to the cell would be consumed, resulting in a low oxidation potential in the cell fluids and thus a low production rate of adrenochrome. With this mechanism one would expect low adenochrome levels correlated with cancer, but it would not be a factor in causing the cancer.
If this analysis is correct, and if adrenochrome is a primary causal agent for schizophrenia, one might expect that treatment of schizophrenia with megadoses of vitamin C alone would increase schizophrenia. It could only have a beneficial effect if used in conjunction with even greater amounts of vitamin B3 so that the combination increased aerobic metabolism without increasing the production of adrenochrome.
Have you observed this?
You have stated that it is your personal observation that schizophrenics have a significantly lower rate of cancer. Beyond the adrenochrome theory, could this also be because the schizophrenics you have contact with are so often supplementing with vitamins B3 and C that would mitigate both schizophrenia and cancer? I wonder if you think this is a significant factor.
I want to draw your attention to a discovery I made about five years ago, which I put on my web page and have had many reports back. It is now being used by thousands of people with dramatic results. It is more immediately powerful than anything else I have discovered and I personally have little doubt it will have equally dramatic beneficial effects for schizophrenics. I discuss it in two places on my web page: www.krysalis.net/anemia.htm and the linked web page for vitamin B12. I first dissolved vitamin B12 into DMSO and applied it to my skin (bringing it in transdermally) with striking results for me, mostly in the form of increased mental clarity (general improved mood and increased energy). I then modified the solution by adding folic acid in slightly larger amounts to the B12 solution since the two should always be used together. This seemed to have a greater benefit for me. I then got a multivitamin-multimineral gel cap, opened the gel cap and added the powdered contents to the solution. The benefits got even greater. I suspect that for schizophrenics you might want to try boosting it further with B3. Specifically I got a 2oz brown glass eyedropper bottle, added 10 — 1000mcg tablets of B12, 20 — 800mcg tablets of folic acid, the powdered contents of 2 — multivitamin-multimineral capsules and filled the bottle with 99.9% DMSO. It took a couple of days for the pills to fall apart, with periodic shaking. There is always an undissolved sludge at the bottom, which you don’t want to use. You can filter it out or simply let it settle out and use only the clear liquid above it. I then apply an eyedropper load to the outside of an arm (insensitive skin) and spread it around. It will cover the entire outside of the arm. If you are deficient, you will start to feel very good and a significantly increased mental clarity within one hour. This will last for many days. It also has a dramatic anti-depressant effect. If you try to apply this again the next day, there will not be such a dramatic effect because you are saturated with B12, etc. However, if you wait approximately a month, you will have become depleted again and the benefit will become noticeable again. I personally use it about once a month.
You might have to make a trip to the States to get some DMSO. It would be worth the trip. I get it at my local health food store. A small investment in one or two bottles will give you a several year supply. Some have also found they can order it from sources on the Internet.
One of the conditions for using this seems to be to use it only in combination with a full ranging multivitamin, multimineral supplement. One person reported a dramatic benefit that then vanished after using it for a few months. That person was not using such a diverse supplement in combination with it. Vitamins work in subtle combinations and a focus on taking one alone can deplete others. When the others get depleted the benefits of the one being taken vanish. Also, the depletion of another risks a negative effect. Taking my supplement “Sparx” along with this approach seems to avoid this problem.
WHERE FROM HERE?
I am pleased that my theory seems to be consistent with your very exciting results. It gives me personal intellectual satisfaction. However, in order for such a theory to be important it has to predict modifications that will result in improved benefits. They are obvious and you have already addressed them to some extent. You would want to add a broad multivitamin, multimineral supplement powder that is taken with a diversity of juices (providing essential diversity of phytochemicals). The purpose would be to enhance all steps of aerobic metabolism while continuing to peak on the main players, Vitamin B3 and Vitamin C. For schizophrenia you may want to peak with vitamin B3 with vitamin C being restricted to adequate amounts as a part of the “baseline” supplement formula. However, for cancer you would probably want to peak with both vitamin B3 and vitamin C added to the baseline formula. I have spent the past 5 years attempting to perfect such a baseline formula, which I have named “Sparx”. I am far more of a scientist than a businessman and saw this as more of a technical challenge than a business one. Also, it seemed to fill a void in what was available to people. My goal has been to perfect the best such formula that can be made at a very affordable price. This doesn’t just involve identifying essential components, but also involves identifying often-costly components that are promoted but do not make an important contribution. The philosophy is to rely on the juice to provide a cost-effective source of phytochemicals, which would otherwise be very costly if provided in pill form. As an engineer at heart, I had to have solid data for the benefits of each component before I would include it. Even at that, I ended up with approximately 60 components. It turned out to be the most complex formulation my manufacturer had ever made. However, I found a sole mate in him and he did his best to help in every way, including drawing from his many years of experience in the field. The first miracle was that there wasn’t any component that he could not find a source for. When I progressed to a certain point in my analysis of cancer I decided to have him produce another powder, “Aerobic Boost” to supplement Sparx for the treatment of cancer. It was designed without minerals so individuals could significantly increase the dose without risking going toxic on the minerals. I would design it with a greater emphasis on vitamin B3 now since I have learned of your work. However, it would not be advisable to add megadoses of vitamin B3 or vitamin C to this formula. Those doses should always be adjusted separately and thus independently.
You have reported that you have already used a similar product, Multijet, with a similar approach. How did that work out? I wonder how it compares with my formulation for Sparx given on my product web page www.krysalis.net I also wonder how the price compares. I would obviously be delighted to find out if Sparx or Sparx + Aerobic Boost would be effective in such a baseline supplement role. However, I don’t treat patients and thus have no means to test it. If you are interested in exploring this further please let me know.
Hoffer Email-3 Sent: 5/17/01 12:23 PM From: A Hoffer, email@example.com To: David Gregg, firstname.lastname@example.org
Dear Mr. Gregg:
I cannot take credit for all the research in which I participated. I was Director of Psychiatric Research for Saskatchewan from 1950 to 1967 and by 1960 had about 30 scientists and a budget of about one million at the University Hospital in the Province. Dr Osmond and I were the key figures of this group. All the -3 studies used in large doses came from our studies. Linus was aware of them after reading our book How To Live with Schizophrenia in about 1960 or 61. But I had nothing to do with the vitamin C studies and the credit goes entirely to Pauling who was stimulated to enter the field by Dr Irvine Stone.
Your anaerobic aerobic theory does make a lot of sense. And if one scans the literature there is ample evidence to support it. Thus, for example, schizophrenics do tend to have decreased levels of oxygenation in their frontal lobes. Circulation studies have shown than this appears to be the case. Following Karl Menninger who first stated this I have the feeling that the schizophrenic is not full awake, is in a dream like state and this would explain their hallucinations since visions and voices are not uncommon in dreams. Normally our frontal lobes call for less oxygen during sleep and more when awake but in schizophrenia there is little difference awake and asleep. Niacin may awaken them since it does increase brain circulation .
Neurons are so finally differentiated that they do not form cancers. When they become anaerobic I believe they cause Alzheimer disease/ i.e. fully differentiated cells will not form cancer even when anaerobic, they simply become quiescent. I know of one case of Alzheimer treated by chelation that recovered. I spoke to him and he had absolutely no memory of his previous condition.
I agree that the main vitamin for cancer is C with moderate amounts of B-3 while with schizophrenia it is just the opposite. In 1952 I treated a woman with beat cancer who had a mastectomy. She became infected and psychotic at the same time. I gave her 1 grams of vitamin C every hour and in 45 hours she was no longer psychotic and her ulcerated lesion began to heal. I sent her home mentally normal but had no idea that the vitamin might be helpful o her disease. She died 6 months later menially normal. But exactly where the oxidation reduction process goes wrong is open conjecture. I hope that as the adrenochrome hypothesis is resurrected scientists will enter this field and fill in the gaps that are so wide today.
I did read about your use of DMSO and B-12 in your web site and was very impressed by it. I will try it out at the first opportunity. It could be very helpful also for chronic fatigue states where injecting of B-12 has been very helpful.
Your idea why schizophrenic patients get less cancer is sound had not occurred to me before i.e. that having placed my patients on B-3 and C that this might have prevented some of them from getting cancer. It is not the only factors as I have seen many other patients on vitamins get cancer but generally they have a better prognosis when treated. It is also true that my schizophrenic population was a younger population to begin with compared to my cancer population on. The families of cancer and schizophrenic patients also showed the same pattern but it was not as clear-cut. Thanks for the suggestion.
I have not used a single multi preparation but have used a vitamin spectrum make up of single vitamins combined with the usual B-complex preparations on the market.
Sincerely, A. Hoffer
30. “Vitamin C & Cancer” by Dr. Abram Hoffer, PhD, MD, FRCPS with Dr. Linus Pauling, PhD, Nobel Laureate, Chemistry and Peace, Quarry Health Books:
This excellent book presents a summary of the outstanding work by both Dr. Hoffer and Dr. Pauling investigating the use of Vitamin C + other nutrients for the treatment of cancer. I will make no attempt to summarize it here. I would recommend it strongly for anyone attempting to learn more about the nutritional treatment/prevention of cancer. I would like to present a few of my impressions.
It would appear that essentially all the positive results presented in the book are fully consistent with the cancer theory presented here, that there is a single common cause for all cancers, anaerobic metabolism (caused by genetic damage), and a corresponding common cure, nutritionally reversing the cellular metabolism back to aerobic metabolism. The cells then become normal followed by normal programmed cell death eliminating them (along with their genetic damage). It is my opinion that the theory contributes greatly to the understanding of their profound results. To that extent it enhances credibility in both directions. It should also be possible to use it as a guide to further improve treatment.
As related to importance, I was taken by one statement (pg 27) “Most of the evidence discussed in this book relates to the effectiveness of megavitamins in the treatment of patients with advanced cancer. Our conclusion is that about 50 percent of these patients with advanced cancer can be “cured” (survival for over five years). We surmise that if the megavitamin regimen were to be started at the time of first diagnosis of cancer, as an adjunct to appropriate conventional therapy, the cancer death rate could be reduced to 25 percent of its present value, and moreover, if, in the course of time, a reasonable megavitamin regimen were to be followed regularly by every person, as a way of improving the health and decreasing the incidence of cancer and other diseases, the cancer death rate would fall to one eighth of its present value.” I was also impressed by the long list of types of cancer that were treated. The treatment approach appeared to be effective for all forms of cancer tested. This is also consistent with the theory presented here. As stated in the beginning, it should apply to all forms of cancer.
Point: (pg. 58): “In a study by V. Noto, either vitamin C or E inhibited the growth of breast carcinoma, epidermoid carcinoma, and endometrial adenocarcinoma in vitro, but when both were combined, there was a pronounced synergistic effect. Ten to 50 times lower concentrations were as effective.” This special synergism is fully consistent with the oxygen transport part of the theory presented here, addressed in more detail in Items 6 and 28. It is one specific example of how this theory can greatly help in understanding such observations.
Point: (pg. 45) One study found that increasing the daily intake of vitamin C to megadose levels did not increase the amount found in the blood in a straight line relationship. It increased to a point and then did not increase much further. This led the investigator to conclude that megadoses are of no clinical value and daily doses of 200 milligrams were sufficient. Let us assume that the blood measurements were accurate, and so are the numerous observations that megadoses of vitamin C can be very helpful (presented in this book and elsewhere). What is happening? Where is the vitamin C going (it has to be going somewhere) and why does it continue to be ever more beneficial to cancer treatment at increasing megadose levels? Is it consistent with the theory presented here? I would like to suggest an answer. Initially, at the low doses, the vitamin C concentration in the blood increased as expected with increasing dose of vitamin C. This increases oxygen transport from the lungs to the cells as already discussed (Item 6). However, what was not measured, as the vitamin C dose was increased further, the transport rate of it out of the blood into every cell in the body then accelerates in a nonlinear way with further increases in blood concentration. This second stage would involve a far larger mass of cells than the blood and would consume a far larger amount of vitamin C without a corresponding increase in concentration. At this point, the further increases in vitamin C dose would increases oxygen transport within each cell while oxygen transport in the blood is maintained at an enhanced level by the already enhanced levels of vitamin C in the blood. This cellular mechanism is described in Item 28. According to the cancer theory presented here, the resulting increase in oxygen transport within each cell would be an essential step towards further enhancing its contribution to reversing/preventing cancer.
Point: (pg 73) “We concluded that while vitamin C alone led to about 10 percent excellent responders, the addition of the other nutrients increased this to about 40 percent.” This is fully consistent with the theory presented here. According to the theory one would want to use a set of supplements that stimulate all the steps of aerobic metabolism together. That is what the additional nutrients added.
31. Three Separate Paths for NADH Synthesis Involving Niacin, Niacinamide, Vitamin B6 and Tryptophan:
According to two of my biochemistry books, “Harper’s Biochemistry” twenty fourth edition (pg 602) and “Textbook of Biochemistry”, Thomas M Devlin, editor, Third Edition (pg 560) there are three separate paths for the synthesis of NADH. One starts with niacin, another with niacinamide, and a third involves the conversion of tryptophan to NADH catalyzed by vitamin B6. There appears to be some confusion about this in Eva Edelman’s book “Natural Healing for Schizophrenia” where she shows vitamin B6 catalyzing the conversion of niacin to NADH. It does catalyze the formation of NADH, but by catalyzing the conversion of tryptophan, not niacin, to NADH.
Abram Hoffer found that megadoses of niacin or niacinamide could both be used (along with supporting nutrients) to treat schizophrenia (and cancer along with vitamin C). Carl Pfeiffer in his book “mental and Elemental Nutrients” found that megadoses of vitamin B6 (along with supporting nutrients) were very effective in treating schizophrenia. If production of NADH was the key mechanism for reversing schizophrenia, then this is what would be expected. They are two separate paths to the same goal. Bernie Rimland, of the Autism Research Institute in San Diego also found that megadoses of vitamin B6 (along with supporting nutrients) were effective in treating autism. Since the proposed mechanism, the production of NADH, was not recognized, neither Carl Pfeiffer nor Bernie Rimland tried adding a tryptophan supplement to the mega-vitamin B6 treatment. They thus were limited by the amount of tryptophan existing in the diet of the patients. I would predict that adding a significant amount of tryptophan, as a supplement to the B6 treatment would greatly enhance the results. (Are we looking at a very general cause and cure for many mental and physical problems?)
Each of these paths involves a number of steps, each requiring their own set of enzymes. If there is a block restricting the synthesis of NADH, it would be quite difficult to determine which enzymes might be missing and thus which paths are blocked. I would thus conclude that the best approach would be to enhance all three paths at the same time. This would involve supplementing with niacin, niacinamide, vitamin B6 and tryptophan at the same time (along with supporting nutrients). I could only guess as to the right distribution between these, but I would expect that by combining them, far less would be needed than the megadoses for niacin (up to 3g/day) or B6 (up to 1.2g/day) that were used by Hoffer (niacin) and Pfeiffer (vitamin B6).
32. The Megadose Application of Vitamin C and Niacin:
Dr. Hoffer, in his book “Vitamin C & Cancer” demonstrated the importance of large doses of only two vitamins, vitamin C and niacin (or niacinamide), for the treatment of cancer. Of these two, Hoffer found Vitamin C to play a greater role for treating cancer (while niacin played a greater role for treating schizophrenia). Other nutrients were added also, but more at elevated levels, not at megadose levels. I would like to make some comments about taking such large doses of these vitamins.
1. Vitamin C, Overcoming the Bowel Tolerance Limitation: Dr. Hoffer commonly prescribed 12 grams/day of vitamin C to his patients, taken in 4-gram doses three times a day. This was in combination with niacin (up to 3 grams/day) and other supplements at elevated levels but not in megadose levels. At this dose he seemed to experience more success than at lower doses. There were also some patients that increased this to 40 grams/day with what seemed to be even more success (with cancer). However, when attempting such large doses, most people experience the onset of diarrhea at considerably lower levels. Thus, as is common in the community of people advocating large doses of vitamin C, it is suggested that one take up to the “bowel tolerance level”, which is the dose rate just below that which causes the onset of diarrhea. It appeared that the bowel limitation was limiting the oral intake of vitamin C to a level that was less than optimum for the treatment of cancer, at least in some people. I decided to take a look at what was causing this diarrhea limitation and came up with a logic for both the cause and how it could be removed as a treatment limitation, while retaining oral intake.
The cause of the bowel limitation: When food leaves the stomach it enters the duodenum as an acidic chime. When the duodenum senses the acidity, it releases secretin to the blood. The secretin then stimulates the pancreas to release a bicarbonate flush into the duodenum, which neutralizes the acid and sweeps in the digestive enzymes. If this does not happen, the acidity can damage the intestine. Now lets introduce large doses of vitamin C. Vitamin C is very acidic. It increases the acid load in the stomach. Above a certain point, the volume of acid entering the duodenum exceeds the ability of the pancreas to neutralize it. The acid then starts to damage the intestine and the intestine responds with diarrhea in order to flush the acid out. Thus you have the bowel limit for vitamin C. It will vary from one individual to the next because everyone will have a somewhat different capacity for a bicarbonate flush to neutralize the acid.
The solution: The solution is very simple, neutralize the vitamin C before taking it. You can purchase the sodium salt of vitamin C (or another salt of it) but more simply you can neutralize the vitamin C yourself. I have done this many times. I simply fill a glass of water about 1/4 full and add a teaspoon full of vitamin C powder, which dissolves. If you taste the solution at this point it will be very sour (acidic). I then sprinkle in some baking soda. This results in a lot of foaming (releasing carbon dioxide) while forming the sodium salt of the vitamin C in the water phase. I taste the solution and watch the foaming as I slowly add the baking soda. When the foam stops forming, the sour taste is gone and I can hardly taste anything except a slight taste of the baking soda. The vitamin C is still there and should be just as effective for the treatment of cancer, but will no longer add to the acidity of the stomach and should no longer cause diarrhea at large doses. Thus, the vitamin C can now be added to the optimum level for the treatment of the cancer without being concerned with a bowel tolerance limitation. I have tried this on myself and found it to be quite effective for me – eliminating diarrhea. (I don’t have cancer.) Some others have found it to be effective also. However, every individual is different and it may not work for everyone.
2. Niacin, Overcoming the Niacin Flush Limitation: As Dr. Hoffer has discussed in his book; many people cannot tolerate the flush that goes with his maximum recommended dose of 3 grams/day. His remedy is niacinamide, at lower levels, which does not cause a flush. However, as I have discussed in Item 31 above, I would think it would be even better to replace it with a combination of niacin (at a much lower, flush tolerable dose), niacinamide, vitamin B6 and tryptophan. This will eliminate the flush limitation while stimulating all three paths for the formation of NADH, not just one. It should result in a more effective method of producing NADH at lower doses of each, without a serious flush limitation.
33.”Nutrition and Cancer” by Arthur B. Robinson, www.nutritionandcancer.org
Dr. Robinson presents significant evidence derived from experiments with mice and for one type of cancer, squamous cell carcinoma, which may be reasonable to generalize to more types of cancer and to cancer in humans. He concludes:
Once cancer has become established healthful diets increase its growth rate and poor diets decrease its growth rate. This is in spite of the beneficial effect that a healthful diet may have on strengthening the immune system.
The growth rate of cancer in mice varied over a 20-fold range by diet alone. Super nutrition increased the growth rate two-fold while diet restriction reduced the growth rate ten-fold.
His suggested diet is one restricted to raw fruits and vegetables alone. Such a diet has such a high water and bulk fiber content it will result in low nutritional intake and thus a low cancer growth rate. In the mouse experiments on raw fruits and vegetables the cancer slowing effect was completely lost when soy protein or other dietary improvements were added.
Experiments showed that a restricted diet slowed the growth rate of cancer, but there was no evidence of cures or remissions.
Vitamin C at ordinary doses (human equivalents of 1 to 5 grams/day) increased the growth rate of cancer while far larger doses suppressed the cancer growth rate.
As a consequence of these findings Dr. Robinson recommends what has been referred to as a “Starvation Diet” consisting exclusively of fruits and vegetables. Even though this will not eliminate the cancer, it will extend the life of the cancer patient considerably.
I find Dr. Robinson’s experiments fascinating and credible. They represent a very significant contribution that must be taken into consideration. They don’t negate my theory but they do help to set important boundaries on it.
Part of the theory that I present is in full agreement with his report. I show that cancer has a voracious requirement for glucose, because it uses it so inefficiently, and also an absolute requirement for glutamine. It makes sense that restricting both will to starve cancer cells, possibly sooner than normal cells. When an anaerobic cancer cell metabolizes one glucose molecule it produces two ATP’s. However, when a normal aerobic cell metabolizes one glucose molecule, it produces 36 ATP’s. In an environment of restricted availability of glucose, one might expect that the cancer cells would run out of energy first. I also give reference to a paper that showed that glutamine is an absolute requirement for the growth of cancer. Its richest source is meat, thus a normal diet. Its lowest source is fruits and vegetables. We both agree that a fruit & vegetable diet makes sense (being sensitive to the amount of sugar in the fruit). However, we disagree as to why. For Dr. Robertson it is primarily a matter of reduced caloric intake. The key is to starve the cancer cells to restrict their growth. My theory assumes that you do want to starve the cancer cells of glucose and glutamine, but a primary contribution of a diversity of fruits and vegetables is a rich source of phytochemicals (coenzymes, etc.). They help to make up for the essential cellular chemicals required for normal cell function that can not be synthesized by the anaerobic cancer cell, and thus helps it revert from a cancer cell to a normal cell, as part of a complete diet program involving the use of supplements.
Dr. Robinson also states that he observes a dramatic slowing of the cancer growth rate, but does not have evidence of a reversal. This is also consistent with my theory. My postulated reversal mechanism is the cancer cell becoming a normal cell and then eliminating itself by programmed cell death. This would require an intensive focus on restarting aerobic metabolism, which requires adding the right supplements, some in megadoses. One would not expect a starvation diet to achieve this. However, the feasibility of reversing cancer, using supplements is reported by Hoffer for thousands of patients. (“Vitamin C and Cancer”)
Vitamin C: Dr. Robinson reports that vitamin C in ordinary doses accelerated the growth rate of cancer. This is consistent with other reports I have encountered where it was found that tumors do consume vitamin C from the blood. These two pieces of information would indicate that cancer cells have a way of metabolizing vitamin C, enhancing growth. The evidence was convincing to me and I decided to see if I could identify the biochemical mechanism.
Instead of invoking an unknown mechanism, I though I would start by considering the biochemical sequence that produces collagen, which is known to require vitamin C. This sequence requires both vitamin C and alpha-ketoglutarate. Alpha-ketoglutarate is produced by the fourth step of the Citric Acid Cycle, along with the first molecule of NADH. The vitamin C, alpha-ketoglutarate and the molecule of NADH are required for the “side chain” that produces collagen. However, the rest of the Citric Acid Cycle is blocked at this point. Further steps produce more NADH and FADH2, both of which can be utilized only in the following Respiratory Chain. That is where, in aerobic metabolism, oxygen is reacted with the hydrogen’s on NADH and FADH2 to make water, producing enough energy to provide 33 of the 36 ATP’s. Since, for the anaerobic cancer cells, oxygen transport to the cells is blocked, the Respiratory Chain is also blocked. A blockage of the Citric Acid Cycle this point will cause a buildup of alpha-ketoglutarate. This buildup will stimulate the side reaction producing collagen, requiring and consuming vitamin C. This side reaction also allows more of the earlier, anaerobic reaction of glycolosis to take place, which provides two ATP’s of energy per glucose molecule consumed. The combination of producing collagen, a cellular building block, and a modest amount of additional energy could promote the growth of cancer. Thus one could explain how modest doses of vitamin C could promote the growth of cancer.
My theory also credits megadoses of vitamin C with greatly enhancing oxygen transport and thus turning on the Respiratory Chain. This would restart the full Citric Acid Cycle and thus all of aerobic metabolism. This would allow the cell to return to normal cell behavior. In the process it would lower the concentrations of alpha-ketoglutarate and decrease the collagen producing (and vitamin C consuming) side chain. If I stick with my theory I would expect that even though low doses of vitamin C can promote cancer, there is a dose threshold above which the oxygen transport contribution dominates. This turns on aerobic metabolism, cell normalization, and the reversal of cancer.
This is consistent with the results reported by both Hoffer and Robinson. Both find large doses of vitamin C to inhibit the growth of cancer. The difference is Robinson attributes it to a toxic effect of vitamin C, and I attribute it to turning on aerobic metabolism. Hoffer doesn’t propose an explanation in his book. Hoffer found with patients that moderate doses to have little effect on reversing cancer but high doses did. His results would indicate that the turning point is about 12g/day with larger doses being even more effective.
Alternatives to Vitamin C for Oxygen Transport: As discussed previously on this web page, DMSO, MSM, Alpha Lipoic Acid and IP6 could all be used to assist with oxygen transport. All of them are also considered to health giving in moderate doses and safe in large doses. According to my theory they could be used to substitute for megadoses of vitamin C or added to it to further enhance oxygen transport beyond what is achievable with megadoses of vitamin C alone. I suspect that some combination of all would maximize effectiveness.
Dr. Robinson also makes the point that normal levels of nutrients will enhance the growth rate of cancer even though they are known to strengthen the immune system. This is fully consistent with my discussion of programmed cell death in Item 22 above. I propose two forms of programmed cell death, apoptosis and one where the genetically damaged cells are viewed by the immune system as a foreign bodies and are attacked by the immune system. In both of these cases, cells are eliminated. However, cancer occurs only when the genetic damage does not create a cell that can be recognized by the immune system as a foreign body. Thus, one would expect the immune system to be totally ineffective at attacking this type of cell. As a result, it is the only type of cancer cell that can survive and grow. I am thus in full agreement with Dr. Robinson on this point.
Conclusion: Dr. Robinson’s results are a vital contribution to the overall picture. His results show that a moderate nutritional approach to dealing with cancer will not be effective and could accelerate the growth of cancer. Hoffer’s results indicate an aggressive treatment with megadoses of vitamin C (and niacin) is effective and is even more effective when combined with additional supplements at normal levels. This is consistent with my theory and also identifies the key blockage to aerobic metabolism in most cancers is at the oxygen transport stage. This stage must be addressed very aggressively. Once this is done, additional nutrients can then help further, but only after the problem with oxygen transport has been solved.
34. Tea and Cancer:
It was brought to my attention that green tea has been reported to have anticancer properties. In particular, I was discussing cancer with one woman and she told me that she knew of two women that had reversed their lung cancer using green tea extract. This is hardly a technical report, but it stimulated me to perform a literature search on Medline to see what had been published in the medical journals concerning tea and its effect on cancer. I found a large number of articles. One set of which touted the effectiveness of green tea (& green tea extract) preventing the onset of cancer, another with inhibiting cancer growth, and another with inducing programmed cell death (apoptosis). This was associated primarily with green tea but also black tea, and oolong tea. I won’t attempt to list the articles since anyone can call them up by doing a search on Medline using “cancer , tea” as the search words.
Can this anti-cancer effectiveness of tea be explained by the theory presented here? If my theory is correct, it should be able to accommodate their reports. To do this, I am going to postulate that the active molecular components in tea have the capacity to effectively transport oxygen. As presented in the theory, this is the dominant key step for causing the cancer cells to revert from anaerobic metabolism back to aerobic metabolism, allowing them to become normal cells again and as such go through the process of programmed cell death. This would require that the active molecules have stable oxidized are reduced states in equilibrium. As explained in the cancer theory, the equilibrium between them would allow them to transport oxygen. This would not be an unusual property. Many molecules have it, such as vitamin C.
This is consistent with and may explain why tea is a stimulant. By transporting oxygen it enhances aerobic metabolism and thus enhances cellular energy.
This could also explain why green tea has been found to have broad ranging health benefits. This property would enhance the energy and health of normal cells in general.
35. (7/10/02) Enhanced Anti-angiogenesis (for all types of cancer):
Angiogenesis is the process by which new blood vessels are formed. This is a normal, essential process for biological development. However, as related to cancer, it is also required for tumor growth. If it is properly inhibited, tumors and thus cancer growth will be arrested There is presently a large research effort developing drugs that will inhibit this process, called antiangiogenesis drugs. A recent paper published in “The Townsend Letter, June, 2002, pg. 97 describes the sequence of angiogenesis and an approach to using drugs to achieve antiangiogenesis once it has started. Upon reading this publication and studying the biochemical mechanism, I discovered an approach that appears to have been overlooked. The article focuses on attacking along the very complex biochemical sequence that takes place after the process is initiated. I was extremely impressed with the sophistication of the understanding of the complex process as well as the approaches to inhibiting it. However, it appears that simplest approach was overlooked, which was to stop the process at its primary initiating step. If this is done, then all the very complex following chemistry becomes unimportant.
The Primary Initiating Step: According to the diagram presenting the sequence of events that take place in angiogenesis, the primary initiating event is caused by a lack of oxygen. “Cells deprived of oxygen emit angiogenic signals.” The complex process of new blood vessel formation follows from there. In a way this makes sense in that one would expect a normal cell to respond in such a manner, not just tumor cells. In fact, that might be happening. Normal cells in the oxygen deficient environment of the anaerobic tumor cells may be creating the new blood vessels, not the cancer cells.
The approach presented here to cause cancer cells to revert back to aerobic metabolism and thus normal cells has three basic stages: 1) enhance oxygen transport to the cells, 2) enhance the Krebs cycle and 3) enhance the respiratory chain. When addressing the first step it would thus appear that both conversion to aerobic metabolism and antiangiogenesis would be addressed at the same time. What a fortuitous circumstance!
It would thus appear that the oxygen transport step of the approach presented here would invoke two powerful cancer-inhibiting mechanisms at the same time:
The conversion of anaerobic cancer cells into normal aerobic metabolism cells.
The promotion of anti-angiogenesis, the inhibition of the formation of new blood vessels, without which the tumor cannot grow.
Three supplement systems that provide oxygen transport have been described (proposed) above.
1) Vitamin C + Vitamin E: As discussed above, Abram Hoffer in his book “Vitamin C & Cancer” written in conjunction with Linus Pauling, found that large doses of vitamin C in conjunction with normal supplement doses of other vitamins could greatly inhibit the progression of cancer. According to my theory, the primary effect of the large doses of vitamin C is to serve as an oxygen transport molecule in the blood, substituting for hemoglobin, which cannot provide oxygen to cancer cells. I also propose that the oxygen transport properties of vitamin C are assisted by vitamin E. Vitamin C transports it in the cytoplasm (water phase) and vitamin E carries it through the cell walls (oil phase). Dr. Hoffer generally used up to 12 grams of vitamin C/day. However, up to 40 grams/day were used by some with even more success. The limitation appeared to be the onset of diarrhea. I have been told that even larger doses, 100+ grams/day (buffered) have been used intravenously with considerable success. Vitamin E has been used up to 1200 IU/day with the vitamin C.
2) MSM & DMSO: As described above, MSM is simply the oxidized state of DMSO and the two form an equilibrium in the blood that shifts towards MSM in the lungs, a more oxidizing environment, and shifts towards DMSO in the body cells, a more reducing environment. In the process oxygen is delivered to the cells. The process is continually repeated providing a continuous flow of oxygen to the cells that is independent of hemoglobin. If my theory is correct, it should have a powerful anticancer benefit in adequate doses. In a phone conversation with a local minister she told me that she knew of a number of people who had used DMSO to reverse their cancer. However, I don’t have any independent check on this. An adequate dose has not been defined. However, one might expect from the vitamin C experience that large daily doses (many grams/day) might be needed. The question of safety then arises. How large a dose can a person take safely? This is addressed in Dr. Jacob’s book “The Miracle of MSM” pg 24-25. According to Dr. Jacob, he found no toxic effects in a group of human volunteers up to an intake of one gram per kilogram of body weight per day for 30 days. This correlates to about 68 grams/day for an average 150-pound person. I would expect a similar result for DMSO.
This is in the same range as the megadoses of vitamin C used to treat cancer. Based on the theory I would expect it might be equally effective without the negative side effect of diarrhea. However, unfortunately, there is no similar large body of experimental evidence testing it for treating cancer.
For tumors on or near the skin, I would expect that applying the DMSO on the skin over the tumor would be most effective since it would maximize the dose directly on the tumor, at least initially. Also, since the goal is to increase oxygen transport, it would probably be desirable to dissolve some MSM into the DMSO. MSM is the oxidized form of DMSO and dissolving it into the DMSO would increase the immediate transport of oxygen to the tumor.
3) Alpha Lipoic Acid (ALA): Alpha lipoic acid has been studied extensively by Dr. Leser Packer and his results have been published in his book “”The Antioxidant Miracle”. He has found that ALA is an exceptionally effective antioxidant supplement. Part of the reason it is unusually effective is due to it increasing blood levels of glutathione. From my own logic and his results I have to conclude that both alpha lipoic acid and glutathione are particularly effective oxygen transport molecules. They have both an oxidized state and a reduced state, the combination of which can act as an oxygen transport system. Also, because they both have significant solubility in both oil and water. This means they both can be effective both in the cell cytoplasm and the cell walls and thus can act as a stand-alone oxygen transport supplements. I thus believe it is a particularly promising oxygen transport option. What is a safe dose? In his book, on pg. 25 he recommends 100 milligrams daily for general health. On pg. 47 he refers to an experiment where 600 milligrams/day were used successfully to help regenerate nerve fibers damaged by diabetes. No negative side effects were mentioned. I would suspect that one would have to use the upper end of this range to address cancer. However, he does not mention its use to treat cancer and I do not know of any such experiment.
Alpha Lipoic Acid has additional features.
It plays an active role in promoting the conversion of pyruvate into acetyl-CoA . This is the start of the Kreb’s cycle. It thus stimulates the Kreb’s cycle and thus aerobic metabolism by this additional mechanism.
It can chelate minerals and enhance their excretion. This is beneficial for eliminating toxic minerals, but it may also cause enhanced excretion of nutritionally important minerals. Thus, when using alpha lipoic acid I would expect it to be advisable to be taking a dietary supplement that replaces nutritionally important minerals to avoid their depletion.
4) Whey?: An article in The Townsend Letter, July, 2002, pg 108 discusses the importance of Whey as a supplement. As part of this article it is stated that “Whey is perhaps the most effective nutrient known so far for increasing glutathione levels, etc”. If this is the case and glutathione can play an important role in oxygen transport, it should also help with the treatment of cancer. I just had a phone conversation with friend of mine who has been investigating this as applied to chronic fatigue syndrome. He stated that it is true that whey can increase glutathione levels significantly. However, it has to be undenatured whey – not subjected to the heating (pasteurization) that is used to sterilize milk. The denaturing (pasteurization) process seems to destroy the ability for whey to produce glutathione. A product developed in this way is presented on the web site: www.immunotec.com Another product based on the same principal that my friend feels may be more potent is presented on the web site: www.immunepro.com
I don’t believe any of the above oxygen transport systems would be in conflict with another. Thus, I would predict that the most potent option would be some combination of all three. It would probably reduce the required dose for any one of them. I cannot predict what the doses would be, but it would appear that wide ranges of doses for each would not be toxic and thus would be safe to try.
36. (8/1/02) A Profound New Insight! -Why all Cancers are Anaerobic in Metabolism:
I have always wondered why all cancers are anaerobic in metabolism. It is almost like it is a requirement. I think I now understand the answer. It is well known that in order for tumors to grow they must form new blood vessels to supply the increased tumor size. If they can’t do this they can’t grow. This is a fundamental requirement for all cancers. If the angiogenesis theory presented in item 35 above is correct, they have to create an oxygen deficient environment to stimulate the growth of new blood vessels. The anaerobic metabolism accomplishes this. Thus, anaerobic metabolism is not just a secondary consequence of cancer, it is a requirement for cancer to grow. Cells that are not anaerobic have no means of stimulating the formation of new blood vessels and thus cannot support tumor growth. Lacking this ability they would eventually die off.
If the above logic is correct, then this is another reason why the proposed cancer treatment approach presented above should work for all forms of cancer. Specific formulations and protocols still need to be created and tested to optimize effectiveness. I can only hope that this will take place and systematic controlled studies will eventually be carried out.
Reports?: I have had many phone conversations recently with an individual in the Los Angeles area who is in contact with a group of people who have decided to try this approach to treat their cancers. He states the results have been almost unbelievably good. They start with a particularly potent multivitamin-mineral, etc. supplement and add enhanced oxygen transport relying primarily on alpha lipoic acid. So far he says that it has reversed breast, prostate, esophageal and colon cancers, in a couple of months, independent of the stage of the cancer. It seems to add support to chemotherapy and even works for those cases where chemotherapy has ceased to be effective and has been discontinued. Unfortunately I have no independent way of confirming this and it is certainly no substitute for controlled studies. However, it is all that is available at this time and I fear that such controlled studies will be funded only after the success of this approach becomes almost common knowledge.
37. (8/03) Cesium Treatment of Cancer, an Exceptionally Promising Approach:
This discussion presents an approach for treating cancer that is a total deviation from the one discussed above. It presents a special chemotherapy approach where the focus is to kill the cancer cells directly with a toxin. Upon analyzing it I felt it was sufficiently unusual and promising to warrant a presentation here.
There are numerous articles on the internet addressing the use of cesium for treating cancer. A friend brought them to my attention being convinced that there was unusual merit in this approach and requested my opinion concerning it. I thus decided to study, analyze and evaluate it with the hope that my background and way of thinking would make a positive contribution. My analysis and conclusions are presented below taking every effort to keep it as brief as possible to make it more readable and understandable, starting with the conclusions.
Cesium treatment of cancer has demonstrated considerable merit and has even greater potential.
It acts as a toxin, with its cancer selectivity depending on cancer’s anaerobic metabolism. Thus, it should be effective for all forms of cancer.
Unlike other chemotherapy drugs, it should cross the blood-brain barrier and thus be equally effective for brain tumors as for other cancers.
The proposed biochemical mechanism presented in the literature is not correct to the point of inhibiting the optimization of a treatment protocol.
In this write-up, I have identified what I believe to be the correct mechanism, which is critical for optimization of a treatment protocol, and lending scientific credibility to the approach.
Readers can do their own search on the Internet to discover and read the many publications addressing this cesium-cancer treatment approach. I will not attempt to deal with them all here. However, it is important to reference the primary paper on the internet: “The High pH Therapy for Cancer Tests on Mice and Humans” by A. Keith Brewer, Ph.D. http://www.mwt.net/~drbrewer/highpH.htm
In this paper Dr. Brewer discusses his results using cesium chloride to treat cancer. His results are truly profound and I now believe they are credible. However, I believe his explanation as to the mechanism by which it operates is not correct. Also, all the other papers seem to accept his mechanism without question, leading to some less than optimum protocols. He claims that the treatment with cesium chloride causes the pH of the cancer cells to increase (become more alkaline) to the point of killing them. This does not make sense to me for the following reasons:
Cesium is an alkaline metal and its salt, cesium chloride is fully ionized when dissolved in an aqueous solvent. Upon being dissolved, it does not change the pH of the solution. It behaves the same as other alkaline metal chlorides such as sodium and potassium chloride, which also become fully ionized when dissolved in an aqueous solvent without altering the pH. I cannot identify any credible reason why cesium chloride would alter the pH of body fluids and certainly no reason why it would do it selectively in cancer cells.
The kidneys and lungs rigorously control the overall pH of the body fluids. The kidneys control the H+ ion concentration in the blood and the lungs help regulate carbon dioxide concentration. Carbon dioxide produced in the cells by aerobic metabolism creates an acid solution in the blood and when expelled in the lungs the solution (blood) becomes more alkaline again. The combination regulates the pH of the body fluids. Individual cells do not have the capacity to alter it significantly, with the exception of macrophages, which can alter it to help oxidize pathogens, but by lowering the pH, not by raising it.
My Proposed Mechanism for Cesium Killing Cancer Cells:
Every cell depends on “Sodium-Potassium (Na-K) Pumps” embedded in the cell wall to maintain the required ionic balance/distribution across the cell wall. They pump potassium ions into the cell and sodium ions out, creating a condition where the concentration of potassium is high in the cell and low outside and the reverse is true of sodium, which is kept low in the cell and is high outside.
A disruption of this delicate ionic balance across the cell wall will kill the cell. As one example, some bacteria kill cells by drilling holes in the membrane and inserting a tube that allows free diffusion of ions in both directions. This disrupts the sodium-potassium concentration separation to the point of killing the cell.
The Na-K pumps transport three sodium ions out of the cell while transporting two potassium ions in. This imbalance is required for another vital function, the transport of glucose into the cell. Glucose is a vital fuel for most normal cells and a required fuel for cancer cells. It is transported into the cell by a system of sodium-glucose co-transport using highly specialized molecules embedded in the cell walls where the co-transport of sodium ions energizes the transport of the glucose. The transport energy is provided by two mechanisms: A large sodium concentration gradient (high outside and low inside) as well as an assisting potential gradient maintained across the cell wall. (Negative on the inside attracting the positively charged sodium ions.)
The reentry of sodium into the cell by the sodium-glucose co-transport process exactly balances the imbalance created by the Na-K pumps. I will go further to say that the activity of the Na-K pumps is greatly dictated by the cell’s requirement for glucose. This requires that a sodium imbalance be created by the Na-K pumps that then allow the co-transport of sodium and glucose into the cell to be energized.
This system requires yet another mechanism, one that allows the potassium that got pumped into the cell to diffuse back out of the cell. Otherwise potassium would accumulate in the cell and stop the process, killing the cell. This must be accomplished while maintaining the proper required high potassium concentration in the cell. It must be high, but not too high. In other words, the potassium concentration must be regulated. How is this accomplished?
To start with, the cell membrane is oil based and thus greatly obstructs the diffusion of all water-soluble ions, including potassium and sodium. If this was not the case, the sodium gradient that energizes the sodium-glucose co-transport system could not be maintained. Thus, to handle the diffusion of potassium out of the cell there is a specialized molecule (many of them) in the cell membrane that specifically attaches to potassium ions and allows them to be transported/diffuse across the membrane. This transport is not energized by ATP (like the Na-K pump) but rather is driven by diffusion, with the large potassium concentration gradient, inside to outside, being the driving force. The transport molecule in the cell wall must be highly selective to potassium and reject sodium, otherwise it would allow sodium to diffuse in and destroy the vital sodium gradient.
In such a diffusion process, the large potassium concentration inside the cell would be dissipated if there was not a mechanism to prevent it.
There are two possible mechanisms:
This might be accomplished by the cell regulating the concentration or activity of the potassium transport molecules in the membrane walls. This would require some form of active control that keeps the rate diffusing out to be exactly equal to the rate pumped in by the Na-K pump, which will be constantly changing as cell glucose requirements change.
The second mechanism, the one I prefer, operates more automatically: It is controlled by the tightly regulated potential gradient across the cell wall. The transport potential created by the concentration gradient of potassium ions across the cell wall promoting diffusion outward, is exactly balanced by the potential gradient across the cell wall promoting inward transport. This potential gradient is precisely maintained by other mechanisms, and thus would precisely regulate the high potassium concentration in the cell at the right level. It would automatically adjust to changes in the activity of thee Na-K pump.
I also propose that this potassium diffusion/concentration requirement is the controlling factor that dictates the required potential gradient across the cell wall that exists in all cells.
Introduce Cesium into the Process:
Cesium, like sodium and potassium, is a Group 1 element as listed in the periodic table. Such groups are organized according to common characteristics that cause them to have similar chemical properties. One such property is that Group 1 elements all have a single electron in their outer shell dictating that they all can have only a single positive charge in solution. The group, in order of atomic weight (AW)) is: Hydrogen (AW=1), Lithium (AW=3), Sodium (AW=11), Potassium (AW=19), Rubidium (AW=37), and Cesium (AW=55). This sequence in atomic weight plays an important role. It shows that cesium is closer to potassium than it is to sodium in characteristics, and thus is more likely to substitute for potassium than sodium in biochemical processes.
The cesium killing mechanism:
The paper by Brewer referenced above states that cesium enters the cells quickly. This would not be true if it did not have a transport mechanism. It could not diffuse across the cell membrane at a significant rate without one. Thus, it is reasonable to presume that cesium is used interchangeably with potassium (but not sodium) by the Na-K pump. It appears that the high degree of selectivity between sodium and potassium essential for the Na-K pump consists of a size barrier that does not select out Group 1 elements that are larger than potassium from substituting for potassium. This is supported by the reports that rubidium has similar effects to cesium in treating cancer. However, its selection process prevents such elements from substituting for sodium.
Once the cesium is transported into the cell, it is trapped there. The mechanisms that allow potassium to diffuse back out are not effective for cesium. The cesium ion concentration continually increases, due to continued operation of the Na-K pump. As the concentration increases it not only disrupts the delicate ionic balance, but the simple increase of total number of ions in the cell changes its osmotic pressure, causing water to diffuse in. This causes the cell to swell, eventually to its bursting point, killing it.
Update 1/04: A clearer insight into the killing mechanism:
As the cesium ions accumulate in the cell they cancel the potential gradient across the cell wall that is required to energize the sodium-glucose co-transport into the cell. This could happen quite quickly requiring only a modest concentration of cesium in the cell. Thus the cell is very quickly starved of glucose. The first thing that happens is the cell stops growing. Since the cesium exits the cell only very slowly, this effect lasts long after the cesium treatment has ceased. In time, the starved cancer cells then die off. This die off is most likely gradual, slowly releasing dead material to the body. This slow die off minimizes the chance of the toxic effects of a rapid die off, characteristic of some other cancer treatments.
This rapid arresting of the cancer growth is consistent with the common reports that once cesium treatment is initiated, the first thing that happens is all the pain goes away.
If this is all true, it would seem that treatment of cancer with cesium, to quickly arrest growth and then gradually kill the cells, is an almost perfect approach. It would be consistent with some of the amazing reports of late stage cancer being arrested in a matter of days.
Cesium Trapping Mechanisms: There are two possible mechanisms that could be responsible for the trapping of cesium:
One mechanism is the molecule that provides for the diffusion of potassium across the cell’s membrane is so selective that it does not accommodate cesium. Thus there is no way for cesium to get out. Simple diffusion across the oil-based would be far too slow.
The other mechanism is based on a concentration argument alone. If we assume that the transport molecule in the cell membrane can handle potassium and cesium equally well, The cesium ion concentration still has to rise to approximately the same concentration as the potassium ion concentration in order to have the same diffusion rate out, against the potential barrier opposing such diffusion. This would double the ion concentration in the cell. This barrier would not be so absolute as the first one mentioned above, but appears to be sufficient to kill the cell.
The preferential killing of cancer cells by cesium:
Cancer cells are anaerobic in metabolism. This has two very significant consequences for our purposes: 1) Cancer cells can obtain energy only from glucose by the process called glycolosis. They cannot obtain energy from proteins or fats, which normal cells can. 2) Cancer cells can obtain only 2 ATP’s (the currency of energy in cells) per glucose molecule via the glycolosis process. In contrast, normal cells cannot only obtain energy from proteins and fats, but also when metabolizing glucose aerobically they obtain 36 ATP’s per glucose molecule. Thus, in order for a cancer cell to obtain the same energy as a normal cell it must metabolize at least 20 times more glucose. As was discussed above, the activity of the Na-K pump is greatly determined by the sodium-glucose co-transport system, which is driven by the cell’s requirement for glucose. Thus, the Na-K pump in cancer cells will operate at a rate at least 20 times greater than normal cells. In turn, it means the cancer cells will pump in cesium at 20 times the rate of normal cells. Thus, the cesium treatment should kill cancer cells 20 times faster than normal cells.
Since it is believed that essentially all cancers are anaerobic in their metabolism, this cesium treatment approach should work for all cancers. This is truly profound.
This kill mechanism has some additional important properties:
It should take effect quite rapidly. In contrast to some other chemotherapy drugs, it does not rely on waiting for cell division to implement its kill mechanism. This is consistent with the results reported by Brewer.
In contrast with other chemotherapy agents focused on killing the cancer cells, it should cross the blood-brain barrier making it equally effective for brain tumors as for other forms of cancer.
However, if continued in a prolonged, continuous treatment protocol, the cesium concentration in the normal cells will eventually catch up with the cancer cells and kill them also.
Published Toxicity Data:
At this point I thought it would be appropriate to introduce what quantitative information is known about the toxicity of cesium chloride. I decided to also include potassium chloride and rubidium chloride for comparison. To do this I went to the book that is well known as the most credible reference in the field: “Sax’s Dangerous Properties of Industrial Materials”. The results are summarized below. Considerably more information is presented in the book and I would recommend that anyone interested in more detail read the proper sections in the book.
Sax classifies the health hazard of all three compounds, cesium chloride, potassium chloride and rubidium chloride as “Acute Toxicity”
There are two toxic classifications reported quantitatively: 1) the Lowest Published Lethal Dose (LDLo). (The lowest dose that has killed an animal.) and 2) the dose that is lethal for 50% of those receiving it (LD50). It should be noted that LDLo will always be lower than LD50. All the numbers presented are for test animals with human numbers available only for potassium chloride. They are given in weight of compound/kg of body weight. The route of introduction into the animal is also given.
Cesium Chloride: Rabbit: LDLo = 1000 mg/kg (Intravenous); Rat: LD50 = 1075 (Intravenous) to 2004 mg/kg (Oral); Mouse: LD50 = 910 mg/kg (Intravenous) to 2306 mg/kg (oral); Cat: LD50 = 640 mg/kg (Intravenous).
Potassium Chloride: Woman: LDLo=60 mg/kg (Oral); Man: LDLo = 20 mg/kg (Oral); Guinea Pig: LD50= 77 mg/kg (intravenous) to 2500 mg/kg (Oral); Rat: LD50=142 mg/kg (intravenous) to 2600 mg/kg (Oral); Mouse: LD50= 117 mg/kg (Intravenous) to 1500 mg/kg (oral).
Rubidium Chloride: Rabbit: LDLo – 100 mg/kg (Intravenous); Rat: LD50 = 4440 (Oral); Mouse: LD50 = 233 mg/kg (Intravenous) to 3800 mg/kg (Oral).
It is not clear how to quantitatively extrapolate these numbers to humans. However they can be used as the best available guide. They vary widely especially as related to the route of introduction. However, it would appear that all three compounds are very similar in their toxicity.
The only human numbers are for the LDLo for potassium chloride.
Cesium Chloride Treatment:
If we take the approach of using the lowest animal LD50 number for cesium chloride, 640 mg/kg for a cat, assume a 170-pound person (77 kg), then the LD50 for that person would be 50 grams. However, if we take the only human results, which are for potassium chloride, which are available only for LDLo, the initial onset of lethality in a fraction of the people, 20 mg/kg, this corresponds to a human LDLo of 1.5 grams. If we now assume that potassium chloride and cesium chloride have a similar LDLo’s in humans, then a dose of 1.5 grams of cesium chloride would correspond to the initial onset of lethality in the most sensitive humans.
The Biological Half-Life of Cesium =110 days (3.5 months):
How long does cesium stay in the body? This is measured as the time it takes one half of the dose to be excreted from the body, called the Biological Half-Life. The average value for the Biological Half-life of Cesium, from the International Committee on Radiation Protection (ICRP) Publication 30, is 110 days. This is not fast. It means that a series of doses taken over a month would accumulate, being additive, continually approaching closer to the LD50. It also means that in order for the dose to be reduced to 1% of the initial value, it would take 5.5 Half-Life’s or a little over 19 months.
I was unable to find the biological half-life for potassium or rubidium, but it is known that the body eliminates potassium fairly quickly. That is why there is a need to continually replace it in our diet. I would suspect its biological half-life would be far less than that of cesium. Thus recovery from an overdose of potassium would happen far faster than an overdose of cesium.
Brewer’s paper referenced above states “The toxic dose of cesium chloride is 135g. The administration of 6 grams/day therefore has no toxic effects.” He does not explain how he arrived at his toxic dose or how it might relate to a LD50, the standard way of quantifying toxicity. My conservative analysis presented above is reasonably consistent with Brewers number for the “toxic dose” – 50g LD50 vs. 135g. However, his statement that 6g/day would have no toxic effects is inconsistent for two reasons.
1) My analysis predicts that the LDLo could start as low as 1.5g total. However, this would be for only the most sensitive people, which Brewer may not have experienced.
2) He appears to be unaware that the biological half-life of cesium in the body is approximately 110 days. This would predict that daily doses would accumulate. At 6g/day, in 9 days the person would have exceeded the above projected 50g LD50 and in 23 days it would exceed Brewer’s toxic dose of 135g.
Brewer gives one case history where a lady with two hard rumor masses, 8 to 10 cm in diameter, one on her thyroid and one on her chest was given 3 to 6 months to live. She had tried chemotherapy, which was discontinued. She was taking laetrile on her own. She was given a 50g bottle of cesium chloride, was advised to take 4g/day but instead, took all of it in one week. Her tumors became soft, so she got another 50g bottle and took it the second week. By the end of that time she could not find the tumors. Two years later there was no sign of the cancer. ( I assume she discontinued taking it after the second bottle but this is not stated.) This is in the Brewer paper referenced above.
Her surviving a total dose of 100g is not inconsistent with the above lethality analysis. (It is less than Brewer’s stated 135g lethal dose.) If we assumed that the actual human LD50 was 100g, then 50%of the people would still live after such a dose. This may have been a lady that was particularly resistant to the toxic effects of cesium and thus could take a dose large enough to quickly kill her cancer cells without killing her. I found it interesting that the speed with which it appeared to kill the cancer cells is consistent with the theory I have presented. However, if the toxic projections were correct, I would expect a significant fraction of people taking such a dose would find it to be fatal.
Studies by H.E. Sartori: http://www.cancer-therapy.net/cesiumstudy.htm
In another paper I found on the internet by H.E. Sartori he describes a number of his studies. I would like to briefly summarize some of his conclusions presented in his Discussion:
The total of 50 cancer cases studied showed an impressive 50% survival rate.
It confirms the work of Messiha showing that the higher the dose the more effective it seems to be.
It should be noted, however, that cesium chloride dose regimes should not exceed 20 to 40 grams due to side effects, mainly nausea, and diarrhea.
The usual dose used in the clinic ganged from 2 to 3 grams given by mouth 3 times daily. At a later time, at which time there is no indication of cancer presence, he cesium chloride dosage was reduced to a preventative dose between 0.5 and 1 gram a day.
I was personally pleased to see him give an upper limit to the dose (20-40g), which is consistent with the lethality analysis presented above. Thus, at his dose rates, 6-9g/day, I would conclude the cesium chloride treatments lasted no more than 2-7 days, at which time there would be no detectable cancer. I would expect a rapid response but this seems a bit more rapid than even I would expect. I suspect this is not quite accurate.
His approach of giving incremental doses and watching for early negative side effects would allow him to identify those who could not tolerate larger doses before the dose level became fatal.
He also introduces the concept of a preventive dose (0.5-1.0g/day). I don’t know how he arrived at this or if it has any technical merit. The only supporting evidence may be estimated doses obtained from the environment in areas reported to have high soil cesium levels and low cancer rates.
Dead Cancer Cells:
It is common for cancer treatments to kill large amounts of cancer cells all at once. This can create a new toxic problem. The body can have considerable difficulty eliminating large amounts of dead tissue. This can be quite toxic even lethally toxic. It is a problem to watch for since the cesium therapy appears to kill cancer cells very rapidly. The cancer treatment field is well aware of this and takes precautions to avoid and deal with it.
Upon completing this analysis I came to the conclusion that cesium chloride treatment of cancer has great promise and should be the subject of well-funded, intensive study to establish an optimum protocol. In particular, there is some indication that combining with a nutritional support therapy may reduce its lethality and allow more people to tolerate the dose they need to kill their cancers. I would hope that this would be included in such a study. It will always entail a significant risk. However, I am convinced that if done properly, a protocol can be developed that will save the lives of many people.
When comparing this treatment approach to the one presented at the beginning of this web page (converting cancer cells from anaerobic to aerobic metabolism) I consider the first to be far less hazardous in terms of possible negative side effects. It is nutritional in nature while the treatment with cesium is toxic in nature, definitely vulnerable to negative side effects. If the first, nutritive approach is effective, great. However, it might fail along with the conventional cancer treatments. At this point, cesium treatment might be considered. It looks like it could be profoundly effective, at any cancer stage for those who can tolerate it. I would consider it to be a backup treatment possibility that I would want to keep available. In time, as more experience is achieved, it might shift from being a treatment of last resort to the one employed first. Only time and experience will tell.
Update 1/25/04: A communication with Rich VanKonynenburg Ph.D.:
A close and exceptionally competent friend, Dr. Rich VanKonynenburg, decided, at my request, to take a close/critical look at my Cesium theory and conclusions. A few days later he phoned me with his conclusions. Much to his surprise, he concluded that the basic thread was correct, but it could use some significant refinements/additions. 1) Cesium ions do easily substitute for potassium ions in the sodium-potassium pump, easily entering the cell. In doing so they seem to stimulate the pump to be even more active. 2) The diffusion of potassium ions out of the cell is not facilitated by a protein in the cell wall that transports it, as in some bacteria. Instead, it is facilitated by a protein in the cell wall that provides a pore, called a potassium channel, which is highly selective to potassium allowing the potassium to freely diffuse out. He also discovered that there was data that showed that this potassium channel not only blocked the exit of cesium ions, but the cesium also blocked the channel to potassium ions. Cesium is a potassium channel blocker! This is truly an extremely fortuitous situation. I asked him to email me the abstracts of some of the publications that support this (found on Medline), and he did. He sent just a few of many such abstracts and I will leave it to the readers to perform their own search to satisfy themselves. This means that once enough cesium ions are present, both cesium and potassium ions will be trapped and accumulate in the cell. Thus, far less cesium will be needed to result in the accumulation of sufficient ions in the cell to arrest the sodium-glucose co-transport system. It also explains why some of the reports on the Internet claim that it was discovered that adding potassium at the same time enhanced the cesium treatment.
My Response to Rich’s email:
Rich, Thank you so much for your critical review, discoveries and abstracts. I will read them. As you might expect I am in danger of entering an irrationally excited state, making some characteristically extreme statements. Your enhancement of the theory is truly profound. It not only verifies the expected accumulated of cesium ions in the cell, but also potassium ions at the same time. Some evidence that supports this is several reports on the Internet claim that it has been discovered that adding potassium to the cesium treatment enhances its performance. This was discovered, but not explained. Now it is explained, which not only provides important understanding, but also supports the correctness of the theory. We now have placed this cancer treatment theory on a sound technical/scientific footing. It has some critically important, fortuitous features that could not have been designed by any drug company. 1) Cancer cells need to operate the sodium-potassium pump approximately 20 times faster than normal cells. 2) Cesium readily substitutes for potassium in the sodium-potassium pump and cannot substitute for potassium in the potassium channel, preventing its exit from the cell. 3) If this wasn’t enough, it also blocks the potassium channel so the potassium ions cannot exit either. 4) The inevitable accumulation of cesium and potassium ions in the cell will cancel the potential gradient across the cell wall. In doing so, it will prevent the sodium-glucose co-transport from operating, starving the cell, with cancer cells starving far quicker than normal cells. 5) This also explains why cesium has such a long biological half-life in the body, 110 days. Once it gets into a cell it plugs the exit and can only diffuse out very slowly. Thus, once it is in the cancer cells, it will stay for an extended period, long after the treatment has ceased, another fortuitous characteristic. 6) The accumulation of the ions in the cells could also cause the cells to swell due to increased osmotic pressure and possibly burst, introducing another kill mechanism. This is truly a miraculous discovery. We can only credit another power for thinking of it first.
Upon discussing this with another friend, Dr. Frank Gojny, he pointed out that adding potassium was not only helpful for the cancer control mechanism; it was also necessary for health. Cesium treatments are known to deplete potassium levels in the blood. At that point, the light went on again. Of course! Since the cesium is blocking potassium release from the cells, it will accumulate in the cells, depleting the blood levels, even to dangerous levels. Thus, it is essential to combine potassium with cesium with sufficient potassium to maintain healthy blood levels. Again, the potassium depletion measurements validate the theory presented while giving guidance for treatment. Dr. Gojny also told me he performed an analysis that suggested that the optimum treatment time would be to spread the cesium/potassium intake over a period of approximately two weeks.
Two proposed approaches to preventing, treating and curing all forms of cancer, even in its most advanced stages, have been presented in this web page. One involves a “nutritional” approach, causing the cancer cells to revert back to normal cells. The other involves arresting and killing the cancer cells using a toxin. They are quite different in approach, each invoking different biochemical logic. This theoretical understanding is crucial not only to convince others of their credibility, but it provides an essential scientific foundation that will allow others to proceed in an orderly manner to perfect them further. I have little doubt that considerable work is still needed to identify optimum protocols for each. I hope that work will take place. However, even without further perfection, there are reports that they can be significantly effective right now for some with what is presently known and resources that are readily available. The two approaches should be mutually supportive. In the early stages of cancer taking the nutritional approach would be the safest and may be all that is needed. If it fails, then the toxin (cesium) approach can be considered. There are reports of it being effective for some even in the latest stages of cancer. I would suspect that the approaches would remain interactive in that once the cesium approach has done its job, one would still want to return to the nutritional approach for cleaning up remaining cancer cells and preventing the occurrence of new ones. Will these approaches be enough? Only time will tell.
An active clinic for cesium treatment of cancer as of 2/20/04: I have just had conversations with the Wolf Clinic in Canada (Ph: 1-800-592-9653) that has had considerable experience with addressing cancer with cesium. They sell cesium chloride and have a proposed protocol, which they will give to anyone who purchases cesium chloride from them. They told me they found it to be successful for many, but not all of those taking it. They are hesitant to claim a specific success rate, and they certainly have to be careful to avoid claiming it is a cure for cancer. Thus, it is my impression that it is not as perfect as the theory might predict. However, the patients seeking cesium therapy are generally those who have already exhausted all that current medicine has to offer and have been told there was nothing else that could be done for them. In this context, a 50% recovery rate could be viewed as quite positive. However, at this stage of experience, it is certainly not a treatment that one would choose before exploring what current medicine has to offer.
Another active cesium cancer treatment web site emailed to me 5/11/04: I received an email from “Larry” who stated that he has been working with cancer clients (using cesium chloride) for the past 2 years with “great” results. I present this as another resource for interested people to evaluate. He is located in the US.
Email: “Larry”<email@example.com> Phone: 417-546-5075
He sent his two web page addresses presenting extensive information:
I phoned him and he stated that he is not a MD and does not treat anyone. He gets feedback from “clients” and provides products. He is also quite willing to discuss details by phone. He told me that he has had approximately 1500 clients so far. They have included not only people, but also pets. He said that over time he has gradually improved his suggested protocol. His web pages, like all others, also assume that the cesium is causing a pH change, which kills the cancer. As presented above, I do not agree with this. However, he does appear to have extensive experience dealing with people who have chosen to treat themselves or their pets. I was particularly attracted to his conclusion that cesium chloride must not only be taken with an excess of potassium chloride, but also must be taken with food and additional supplements. Some feedback I have received has indicated that the cesium chloride taken orally could cause severe gastrointestinal problems. Blending/diluting with food should help to mitigate this. He could be another valuable resource for someone considering treating cancer with cesium chloride.
Three additional web sites addressing cesium referred to me by email:
A commercial source of cesium chloride for research: www.cesium-chloride.com
Potassium chloride available at grocery stores:
Potassium chloride is commonly available in the salt section at grocery stores for people sensitive to sodium chloride (table salt). It is sold under labels such as “Salt Substitute”, “No Salt”, etc. It is 100% potassium chloride approved for human consumption. There is no better form. If you want it in a liquid form, just add it to water. (If you want the cesium chloride in liquid form, just add it to water.)
38. (1/28/04) an additional insight related to the “Nutritional” treatment approach.
Early in the presentation of the nutritional treatment discussion I make the claim that the reason cancer cells never die is because they do not have enough energy to operate all the control mechanism of a normal cell, which would dictate, programmed cell death within a certain period. I would like to expand on that. I was reading the book “Medical Biochemistry”, Fourth Edition, 2002, by N.V. Bhagavan and came across the statement on pg. 250 “Mitochondria are involved in programmed cell death apoptosis”. Of course, my entire theory is that it is the shutting down of aerobic metabolism that causes cancer and it is the shutting down of mitochondria that shuts down aerobic metabolism. As I attempted to explore this further in the book I could not find where this was expanded on. Thus, I decided to try to piece it together myself. We know that the synthesis of proteins requires energy. Aerobic metabolism produces 36 of the 38 ATP’s derived from metabolizing a single glucose molecule with the anaerobic part producing only 2. Thus, a mitochondria shut down should inhibit protein synthesis. On pg. 64 the book discusses that the p53 tumor suppressor gene controls the production of a number of proteins that regulate cell growth, DNA repair and apoptosis (programmed cell death). It is known that a mutation of this gene has been linked to as many as 40% of cancers. I will take this a step further. A mutation is not required. The activity of a normal gene can be shut down by the lack of energy due to a lack of aerobic metabolism. We now come to another insight: Anaerobic metabolism shuts down apoptosis by this mechanism, allowing the cancer cells to never experience programmed cell death. Thus, we again conclude that anaerobic metabolism is required for cancer cells to survive, and thus for the disease of cancer itself.
39. (3/27/04) An Email from Chris Duffield PhD (A Cancer Researcher) Presenting Ideas as to How the Cesium Cancer Therapy Could be Enhanced.
The invention of the transistor was a great start towards producing the computers of today, but that took the cooperative efforts of many and many more inventions to arrive where we are now. Similarly, the identification of cesium chloride and its mechanism of operation on cancer is a great start but it will need the contributions of many to achieve its full potential. Consistent with this I am pleased to present the following email from Chris Duffield, with his permission.
From: Chris Duffield Subject: Cesium chloride for treating cancer Date: March 25, 2004
Hi David –
This email is a summary of some cesium chloride discussions we had by phone and email in October and November 2003. We first met by phone on Oct 19 when Rajiv Bhushan introduced us. He got me to read your cancer page, and I was very excited by your wonderful alternative cesium chloride theory. It reminded Rajiv and me of the selective tumor killing mechanism of insulin potentiation therapy (IPT), a wonderful but still little known medical procedure that was discovered and first used in 1930 by Donato Perez Garcia, in Mexico City. I have been involved with IPT since 1986, and run a large website about it at http://IPTQ.org. IPT is finally catching on; today there are about 120 IPT-trained doctors in 19 countries.
In IPT, a brief episode of insulin-induced hypoglycemia (in a fasting patient) is used to enhance delivery and effectiveness of a variety of drugs, in treatment of a wide range of diseases. Insulin is given, followed by oral and intramuscular drugs, then mild hypoglycemia develops, and finally intravenous drugs are given along with glucose to end the hypoglycemia.
In the case of cancer, the doctors have observed since the 1940s that IPT enables effective chemotherapy at about 1/10 the normal dose, with greatly reduced or eliminated side effects, and without surgery or radiation. We believe that insulin selectively targets tumor cells because they have 10 or 20 times more insulin receptors than normal cells have. Why do they have more insulin receptors? To increase glucose uptake to support their anaerobic metabolism. That’s why tumor cells show up in PET scans, by more rapidly absorbing radioactive glucose. It’s an obvious synergy with your cesium chloride story.
We think that insulin increases cell membrane permeability, and it may also enhance other active transport mechanisms (like the Na-K pumps) to increase chemotherapy drug uptake into tumor cells. Certainly insulin increases glucose uptake, which, as you have shown, also increases potassium (and cesium) uptake. We also think that insulin, by cross-reacting with other growth factor receptors, stimulates tumor cells to grow and divide, making them more susceptible to the chemo that quickly follows.
So Rajiv and I got the idea that IPT might further enhance the selectivity and effectiveness of cesium chloride in treating cancer, by further amplifying the glucose, potassium, and cesium uptake of tumor cells, and perhaps by reducing the needed dose, frequency, and side effects of cesium administration. According to your web page, tumor cells are already using glucose (and pumping in potassium and cesium) at a rate 20 or more times that of normal cells. Added insulin might boost this ratio even higher.
Hypoglycemia means low blood sugar. Insulin triggers rapid uptake of glucose into cells, thus lowering blood sugar level. Less well known is that during hypoglycemia, blood potassium also goes down, indicating that it is being pumped into the cells, too. So it is likely that the same thing would happen to cesium ions, being pumped selectively faster into tumor cells with their larger number of insulin receptors. Rajiv found the following two relevant web pages about insulin accelerating Na-K pumps:
The first page has a nice animation of the Na-K pump. So it may be worthwhile trying cesium chloride (combined with potassium chloride) as part of IPT treatments by IPT-trained physicians, along with or instead of standard chemotherapy drugs. In IPT, as typically done today, insulin, cesium/potassium, and glucose would all be given intravenously: insulin first, and cesium/potassium/glucose after hypoglycemia. A lower tech approach, perhaps more suitable than regular IPT for use in developing countries, would be closer to the way IPT was originally given. Under careful supervision by a medical professional, preferably one trained to do IPT, insulin could be administered intravenously, intramuscularly, or even subcutaneously. The patient would drink a solution of cesium chloride and potassium chloride, and while it is absorbing, wait for hypoglycemia. When hypoglycemia reaches the right level, the patient drinks a solution of sugar, preferably glucose. Alternatively, the salts could be mixed into the sugar solution and taken together at the end.
In IPT, the insulin is separated in time from the glucose and drugs, resulting in a brief episode of hypoglycemia. There may be benefits from biophysical and biochemical changes that occur during hypoglycemia. On the other hand, if the goal is just to get potassium or cesium quickly into tumor cells, this separation may not be necessary, and all the components could be mixed.
Note that some doctors have used a solution of glucose, insulin, and potassium chloride (GIK or “polarizing” solution) to revive ischemic heart tissue after heart attack, since the 1940s. First use of this mixture by Dr. Sodi Pallares in Mexico City was originally inspired, we believe, by Dr. Perez Garcia’s pioneering work there with insulin and IPT. It is now well known that this GIK mixture greatly enhances and accelerates potassium uptake into cells.
It therefore becomes obvious to suggest adding cesium chloride to the GIK mixture. A combined solution of glucose, insulin, cesium, and potassium could be injected by a physician intravenously, or perhaps even directly into tumors. We could call it GICK solution. It will take some work to find the best recipe and administration protocol.
Of course, any administration of insulin to induce hypoglycemia must always be done under the supervision of a medical professional, because uncontrolled hypoglycemia can be dangerous or deadly. The IPT doctors have found controlled and supervised hypoglycemia to be extremely safe — no patients have been reported injured or killed by IPT in 75 years.
It seems to me that use of cesium with IPT might be preferable to the current use of standard chemo drugs with IPT, because cesium has a metabolic effect, whereas some chemo drugs could cause mutations in normal cells that could lead to later cancers.
A simple at-home approach might be to drink a solution of cesium, potassium, and sugar, preferably glucose. Rajiv’s idea is to mix cesium chloride with a Gatorade drink, which already contains both potassium and glucose. Presumably the shot of sugar will stimulate the body to release a pulse of its own insulin, making the ravenous tumor cells even more ravenous. It might work better if taken in the morning after fasting overnight.
The above ideas are just speculations, and are not medical advice, recommendations, or prescriptions. I have not suggested any specific doses. Research is needed.
In our previous correspondence, I also wrote that I have doubts about the first mechanism that you proposed for cesium-caused cell death — osmotic buildup in cells, leading to their bursting. My hunch was that, since cesium chloride effects seem to have low toxicity, and sudden bursting of a lot of cancer cells would release many toxins, it is likely that tumor cells are dying from orderly apoptosis (programmed cell death) rather than bursting. After some Pub Med searching, I came up with a possible mechanism:
Perhaps cesium blocks potassium channels in mitochondria, leading to apoptosis by the direct mitochondrial route. There have been a lot of papers recently about how drugs that open the mitochondrial potassium channels can reduce or stop apoptosis. Well, cesium may do the reverse, starting or increasing apoptosis by closing or blocking mitochondrial potassium channels. Here is a recent reference that supports this idea:
Aviakosm Ekolog Med. 2002; 36(4): 50-4. [Characteristics of mitochondria and myocardium ultrastructure of rats following chronic incorporation of cesium radionuclides 137 Cs] [Article in Russian] Gritsuk AI, et al.”…. A hypothesis has been put forward according to which cesium blocks potassium channels in mitochondria and thus changes the volume and configuration of internal mitochondrial membranes, and impacts the respiratory processes. In the opinion of the authors, these changes characterize the mitochondrial phase of apoptosis….”
I have a copy of the original article, and it would be great if someone will translate it from Russian for us.
I am preparing to do some lab work to test your cesium hypothesis, and to see if insulin will enhance the effect, first in cell cultures and probably later in mice.
Thank you for discussing your ideas so openly on the web.
As you can see, you have inspired me to do the same.
Chris Duffield Ph.D. Visiting Scholar Stanford University Medical Center Web host of http://IPTQ.org and http://GetIPT.com
Cesium update as of 5/16/04: I just received an email pointing out an important technical criticism concerning my cesium theory. It was pointed out that there is more than one glucose transport mechanism into the cells. There is the “active” sodium-glucose co-transport system that I have discussed, and there is also a concentration driven transport system depending on GLUT proteins in the cell wall that does not depend on sodium or the sodium-potassium pump. It is driven solely by the glucose concentration gradient across the cell wall. If this is the dominant transport mechanism, which is dependent on the type of cell and glucose concentrations, then my argument for the lethal mechanism of cesium starving the cancer cells no longer holds. However, the GLUT transport mechanism depends on a relatively high glucose concentration in the blood. At low glucose concentrations the active sodium co transport mechanism becomes more important. This would lead one to conclude that if the cesium treatment were going to be effective, it would be important to combine it with a diet that is low in carbohydrates.
40. Update (11/22/04)
1) Mouse experiments supporting some of the key assumptions presented on this web page.
2) The apparent role of lysine and predicted role arginine.
I discovered (on the internet) a study presenting a systematic evaluation of the effect of a broad range of dietary nutrient variations on the development of cancer in mice. It is “Suppression of squamous cell carcinoma in hairless mice by dietary nutrient variation” by Arthur B. Robinson, Arnold Hunsberger and Fred C. Westall. The entire report can be found on the Internet by going to: www.ncahf.org/digest/01-01.html, scrolling to the title “Linus Pauling couldn’t face the truth” and clicking on the link “Suppression of squamous cell carcinoma in hairless mice by dietary nutrient variation.”
This is a particularly interesting study because of its magnitude (1846 mice) and the diversity of the diets tested. The primary conclusion was that good, balanced nutrition increased cancer growth rates by as much as a factor of two while severe diet restriction reduced cancer growth rates by a factor of ten. I thought it would be useful to take a close look at the data presented to see if additional useful information could be extracted in the light of the theory presented on this web page. I was surprised to discover some data that strongly supported key parts of the nutritional treatment premise/theory presented here, the significance and mechanism of which appeared to have been overlooked.
1. The role of high doses of vitamin C in oxygen transport.
The data clearly showed that low doses of vitamin C enhanced cancer growth, but at high doses its effect switched and greatly inhibited cancer growth. My premise is at low doses its effect is limited to enhancing nutrition, supporting cancer growth. However, at high doses it becomes a powerful transporter of oxygen, as discussed in this web page. The effect is to cause anaerobic cancer cells to revert to aerobic metabolism, become “normal” and exercise programmed cell death. They apparently did not recognize the oxygen transport capability of vitamin C at high doses and its potential effect on cancer. They ascribed the inhibiting effect to toxicity.
2. Synergistic effect of vitamin C and E in oxygen transport.
In another experiment they discovered a feed that contained moderately enhanced vitamin C and vitamin E had a strong inhibitory effect. They then tested each separately at the same level and found no benefit from either alone. They concluded that the benefit must have been due to something else. However, as discussed here, vitamins C and E will act as partners in the transport of oxygen potential with the vitamin C transporting it in the aqueous cell bodies and the vitamin E transporting it in the oil based membranes. This synergistic effect, explained and proposed here, was not recognized or explored further. It further supports the concept that greatly enhanced oxygen transport will inhibit cancer. It would also indicate that the high vitamin C doses that inhibited cancer could have been even more effective if combined with moderately enhanced vitamin E.
3. A number of other experiments supported the conclusion that simple enhancement of nutrition that would usually enhance general health also enhanced cancer growth rates.
They finally concluded that a strict fruit and vegetable diet had the strongest inhibitory effect. However, when they added large doses of vitamin C to the fruit and vegetable diet they found an even more inhibitory affect. The inhibitory effect went away if protein was added to the diet. It would have been interesting if they could have tested the combination of vitamins C & E with the fruit and vegetable diet. They might have done that had they recognized their synergistic effect.
The effect of lysine and arginine:
They assumed that the cancer inhibiting effect of the fruit and vegetable diet was due to it not being nutritionally balanced and was not due to any specific inhibitory effect of the fruits & vegetables. However, I noticed that they found a particularly inhibitory effect of apples and pears. They explained this as being due to their low protein content. However, I thought I would check their lysine content. Lysine is known to inhibit the herpes virus. To do this I went to www.herpes.com/Nutrition.shtml. This presents the lysine/arginine ratio for a long list of foods. Lysine inhibits herpes and arginine stimulates it. I discovered that apples and pears have the highest ratio of lysine/arginine of any fruits, and much higher than any vegetables except for beets, which has the highest of the vegetables.
The book “Cancer” by Matthias Rath
This possible lysine connection lead into another internet search where I discovered the book “Cancer” by Matthias Rath, M.D. Briefly, this scholarly book is devoted entirely to making the case for lysine inhibiting
Cancer. Dr. Rath states that in order for cancer cells to spread (metastasize) they have to penetrate the walls of blood vessels, etc. In order to do this they have to dissolve collagen. The dissolving process requires special enzymes, generated/stimulated by the cancer cells, which bond to the collagen and dissolve it. Lysine stops this process by attaching to the bonding sites preventing the enzyme attack. This is an interesting theory and is fully consistent with the mice experiments. They support each other. The special effect of apples and pears may be due to the lysine content and the lysine theory of Dr. Rath may be the correct explanation.
Dr. Rath also arrives at the conclusion that it would be best to combine lysine with vitamin C even though he does not explain clearly the role of vitamin C. I fully agree with his conclusion, giving an explanation for the role of vitamin C. The combination provides a two-pronged attack by providing an oxygen transport system with vitamin C, promoting the normalization of cancer cells, while lysine blocks the cancer spread process.
The connection to lysine inhibiting herpes viruses may be that the viruses have to stimulate the same collagen dissolving process.
A new insight?: Arginine enhances cancer growth and spread?
It is well known that lysine inhibits herpes while arginine promotes it. That is why the data presented in Diet & Nutrition is presented as a ratio of lysine to arginine. This is what is important to those suffering from herpes. Could it be that arginine does this by enhancing the collagen dissolving process? If we now extend this to cancer, it would predict that a diet rich in arginine would promote the growth and spread of cancer. Supporting evidence: When we refer back to the mouse studies, they found any benefit from a fruit and vegetable diet would be totally negated by adding protein to the diet. However, the protein they added was seeds and nuts. If we refer to the table in Diet and Nutrition, we find this source of protein is very high ( the highest) in arginine. If the above premise is true, it is no surprise that it counteracted the beneficial approaches. It would have been interesting if they added a different source of protein, such as cheese, which is very high in lysine. Perhaps they would have found that adding such protein had an inhibitory effect or at least no cancer enhancing effect. I predict it would have been a very different outcome.
This would also infer that any effective diet for inhibiting cancer would be very similar to one where a person wants to inhibit the spread of herpes. People with herpes are commonly familiar with this. That is the purpose of the table presented in Diet and Nutrition, which presents sufficient information for people to design their own diets intelligently.
One exception might be the consumption of some fruits such as blueberries, blackberries, grapes, elderberries, orange juice, etc. where they are known to have profound health benefits, but they also have a very low lysine/arginine ratio, similar to that of nuts. Even though the ratio is low, so too is the percentage of protein and thus total arginine content- unlike nuts. I would suspect that the low lysine content could be compensated for with lysine supplementation, improving the ratio. One could then still benefit from the rest of the highly beneficial phytochemicals in such fruits without stimulating cancer growth.
41. Update (12/1/04)
For years the function of the mitochondria was believed to be limited to aerobic metabolism. However, recent research has identified it as the gatekeeper of apoptosis (programmed cell death). A summary of the status of this research is presented in “Mitochondria at the Crossroads of Life and Death” by Amy Adams, published in “The Scientist”, October 11, 2004, Vol. 18, No.19, pg 25-29.
The conclusion is that mitochondria contain the proteins that are responsible for the complex sequence of biochemistry that control the onset of apoptosis (programmed cell death). This is extremely important for cancer because cancer cells do not undergo apoptosis while normal cells do. This is why cancer cells don’t die. They just continue to multiply uncontrollably. Stimulating apoptosis is the key to controlling cancer.
This is consistent with the cancer cells having anaerobic metabolism. Aerobic metabolism takes place in the mitochondria in each cell. Thus, anaerobic metabolism is the indicator that the mitochondria are shut down. One would thus conclude that functioning mitochondria are required not only aerobic metabolism, but also for programmed cell death. This is yet another piece of information that supports the primary premise presented on this web page that it is essential to turn on aerobic metabolism and thus the mitochondria to deal with cancer. The first result would be to cause the cells to revert back to the appearance of normal cells, as indicated in laboratory tests. The second would be for the mitochondria to recovery the ability to initiate programmed cell death.
It is proposed here that to do this you not only want to enhance oxygen transport to the cells (and thus the mitochondria) but you also want to provide a diversity of nutrients that support each step of aerobic metabolism which takes place in the mitochondria. This will include a large number of nutrients for steps that are known, and many that are not. Most of the well recognized vitamin and mineral supplements are known to support some steps and the demonstrated effectiveness of a diverse fruit and vegetable diet is probably due to it addressing those that are still unknown.
Suggested further enhancement of oxygen transport by breathing enriched oxygen.
The need to enhance oxygen transport to the cells by a means other than hemoglobin has been discussed. It has been suggested that large doses of vitamin C, MSM/DMSO and even alpha lipoic acid will accomplish this. These molecules circulate in the blood picking up oxygen at the lungs and transporting it to the cells. It seem reasonable to me that this step would be further enhanced by the person enhancing their oxygen intake using an oxygen bottle commonly used by many when their lungs are deficient. This would further increase the oxygen carrying capacity of these molecules.
42. Update (3/20/05)
Proposed Additional Cesium Cancer-Kill Mechanism – Stimulation of Immune System Attack?
In the prior discussion of how cesium ions accumulating in the cancer cells kill the cells, three mechanisms have been proposed:
It changes the osmotic pressure in the cells relative to the surrounding media, causing the cells to swell and burst.
It results in an opposing cesium & potassium concentration gradient that arrests the continued operation of the sodium-potassium pump, arresting the sodium-glucose co-transport system feeding glucose into the cell, thus starving the cell.
It results in an accumulation of negative ions inside the cell, canceling the potential gradient across the cell membrane, which is required to energize the sodium-glucose co-transport system, thus starving the cell. Mechanisms 1 and 2 are similar.
The proposed fourth mechanism: I would like to propose a fourth kill mechanism, which may be the most likely one, at least for some cancers.
As discussed earlier in this web page, in order for cancer cells to survive and spread, they had to have the capability to defend themselves from immune system attack. It order to do this, they had to be able to display on their surface membranes a highly specific arrangement of molecules that communicated to the immune system the erroneous perception that they were normal cells, and thus would not be subjected to attack. Mutations that resulted in otherwise cancerous cells, but without this ability, would be attacked and thus would not survive to develop into cancer, the disease. The maintenance of such a normal-cell disguise would be an ongoing sophisticated cellular process. A disruption of this process would result in an attack and destruction by the immune system. This even happens in normal cells when they are damaged. Dose the disruption caused by the buildup of cesium in the cancer cells result in a breakdown of this cancer defense mechanism and in immune system attack?
In a recent phone discussion with Larry (www.essense-of-life.com), the person previously reference who sells cesium chloride, he told me that it was common for people he had sold it to related back to him that the treatment caused their tumors to become inflamed as part of the process of shrinking. I suddenly realized that this could be a key indicator of a previously unrecognized cesium kill mechanism. Inflammation is caused by immune system attack. Thus, tumor inflammation is an indication that the immune system is attacking the tumor. Is this a major kill mechanism? This would not be a surprising result because the maintenance of the normal cell disguise, deceiving the immune system, has to be a delicate balancing act, relatively easy to disrupt.
It is possible that all four cesium cancer-kill mechanisms play a role, all at the same time. The one that plays the dominant role may be different for different cases. It might be viewed that the four different kill mechanism, all of which could operate at the same time, could be providing a certain degree if redundancy, further insuring the killing of the cancer.
43. Update (5/29/05)
Another insightful email from Rich Van Konynenburg
Hope you are doing O.K. Recently I have been doing some more digging to try to check out the mechanism for the CsCl. I want to pass on some information to you.
As you know, you suggested that one possible mechanism might be that the CsCl causes an energy crisis in the cancer cells that interferes with their ability to masquerade as normal cells to the immune system.
There are two types of cells in the immune system that are known to kill tumor cells: the natural killer (NK) cells, and the cytotoxic (or killer) T cells. The latter depend on finding non-self peptides displayed on the Class 1 MHC (major histocompatibility complex) molecules on the surfaces of cells. These are also called Class 1 HLA (human leukocyte antigen) molecules in human cells.
The NK cells, on the other hand, make their “decisions” about whether to kill cells on the basis of a combination of activator and inhibitor responses from their Class 1 HLA receptors.
Because an energy crisis would more likely result in an inability to do something that the tumor cell had been doing, I think it’s more likely that the ATP shortage would cause a loss of inhibitor Class 1 HLAs. Therefore, I think it’s the NK cells that are triggering the inflammation that Larry has heard about from his clients. I think the cancer cells are not able to maintain the Class 1 HLA molecules displaying normal peptides on the cell surface, and that’s what causes the NK cells to go after them.
I looked into how the antigen processing and presenting machinery works for the Class 1 HLA system. It turns out that it uses the cell’s normal proteasome (the complex that breaks down old proteins that have been tagged by ubiquitin) to break down cellular proteins into peptides, and then it chops them to size and hooks them onto the HLA molecules in the endoplasmic reticulum, and these then carry them to the cell surface and display them. The proteasome is an ATP-ase, and it requires quite a bit of energy to chop up the proteins. I suggest that this is where the energy crisis produced by the CsCl treatment comes into play. The proteasome can’t keep up its protein processing at a normal rate, and I suspect that this makes it impossible for the Class 1 HLA system to get the peptides it needs to keep up the masquerade. When these drop off, they reduce the inhibition of the NK cells, and they attack.
I think this story makes sense.
44. Update (6/27/05)
Over 300 Alternative Cancer Treatments: I recently discovered an unusually comprehensive web site reviewing over 300 alternative cancer treatments. Webmaster: Webster Kerr.
45. Update (7/12/05)
Cesium Interruption of Amino Acid Transport into Cells:
The transport of most amino acids into cells requires a sodium co-transport system similar to glucose but involving different molecules in the membrane that are specific to different amino acids. “Medical Biochemistry” Fourth Edition pg. 333, by N.V. Bhagavan. Thus, when the cesium disrupts the sodium co-transport of glucose, discussed above, it also disrupts the transport of amino acids into the cells. This is another mechanism that would prevent the cancer cells from making more cancer cells that is in addition to the disruption of the glucose transport.
46. Update (11/11/05)
The Cesium Puzzle:
As presented here, cesium at the right dose can kill cancer cells. However there are also reports that trace amounts of cesium in the water supply of some regions are correlated with some of the longest-lived people of the world. How could this be? Cesium is not an essential mineral and does not have any known nutritional role. I would like to suggest the answer by connecting the dots, keeping the argument as brief as possible for the sake of clarity.
Cells continually divide forming a sequence of daughter cells to replace worn out cells.
Mutations occur only during cell division.
Thus, the number of cells with mutations and the number of cells with multiple mutations gradually accumulate during life.
It takes 5-10 mutations to create a cancer cell.
The aging process itself, involving gradually reduced function of cells and thus organs, is also caused by the accumulation of mutations. (Telomere shortening is also involved, but that will be ignored for this argument to keep the concept clear.)
It is has been demonstrated that calorie restriction is by far the most powerful approach for extending life from fruit flies to mammals.
It is also been demonstrated that calorie restriction inhibits the onset and progression of cancer.
Postulated conclusion: Calorie restriction slows down the metabolism of the cells and thus slows down their division rates. This slows down the accumulation of mutations and thus delays the onset of cancer, progression of cancer and the aging process itself.
Postulated cesium conclusion: Trace amounts of cesium in the water supply of said regions, consumed over a lifetime, slowed down cell division rates in the population, resulting not only in a later onset of cancer but also slowed the overall aging process. It would essentially be a substitution for calorie restriction.
This is fully consistent with the cesium-cancer treatment mechanism presented above where cesium inhibits the uptake of glucose and amino acids by cells, slowing their metabolic rate, thus slowing their division rate.
I believe this is a very significant insight related to aging and cancer. Concerning cancer, it would indicate that treatment with relatively low doses of cesium over long periods of time should slow overall cell division rates, slowing the onset of cancer (new cancers) and its progression. Even if it doesn’t eradicate it, it will extend life. If it extends life long enough it effectively becomes a cure since all any cure does is delay the inevitable.
47. Update (1/ 06)
Hydrazine Sulfate as a Treatment for Cancer
Proposed Correct Biochemical Mechanism that Reveals its Profound Potential
The use of hydrazine sulfate to treat cancer is discussed extensively in many articles on the internet. The reports are unusually positive which drew me to try to understand its biochemical mechanism. That is the only approach I can take to convince myself as to their validity and how reproducible the results can be expected to be. Such an understanding is also essential for taking the next step, perfecting the treatment to achieve its full potential. I first concluded the conventionally accepted theory, identified in every report, was seriously flawed. Did this mean that the positive results were exaggerated? As an experiment (mental), I decided to assume that the results were valid and try to identify the correct mechanism. I believe I have done that and have concluded the treatment, properly applied, has the potential of being unusually effective. In some cases it could act as a stand-alone treatment and others as contributing to a broader treatment strategy. I suspect that the lack of understanding of its mechanism may have played a role in it becoming relatively ignored and not being perfected to its full potential.
Hydrazine sulfate was introduced in the early 1970’s and was viewed as a dramatic breakthrough in chemotherapy. It was a relatively nontoxic therapy that fights cachexia, the severe weight loss and general wasting away of the body that is commonly seen in cancer patients, one of the primary causes of death. Its effect on cancer was discovered in the 1960’s by Dr. Joseph Gold, then director of the Syracuse Cancer research Institute in Syracuse, New York. Dr. Gold proposed that it worked by blocking the liver from converting lactic acid to glucose. Cancer cells use glucose as their sole source of energy, deriving it by converting the glucose into lactic acid. The liver then converts the lactic acid back into glucose, providing a continued source of fuel for the cancer. Dr. Gold proposed that the hydrazine sulfate blocked this conversion, starving the cancer, arresting its progression.
This theory makes no sense to me. If the liver was prevented from converting the lactic acid back into glucose, blood glucose levels would decline and lactic acid would increase. There is no mechanism to slow down the cancer until the glucose level falls so low the cancer can no longer grow. This would also be associated with a toxic rise in the lactic acid. Glucose is the sole source of energy for the brain and brain function is very sensitive to glucose levels. There is no reason to believe that the cancer would cease to grow before the brain ceased to function. On top of this add the toxic effects of the increased levels of lactic acid. If the liver’s conversion of lactic acid back into glucose were arrested, one would expect as a minimum that the patient would feel quite ill, and possibly pass into a coma, similar to an insulin shock coma, which is caused by low blood glucose levels. Quite the opposite occurs. The patient feels far better and recovers his appetite. Gold’s proposed mechanism has to be seriously wrong. What is the correct mechanism?
The Proposed Correct Biochemical Mechanism
The “Glutamine Shuttle”
As presented in items 18 & 19 of this web page, cancers have a voracious appetite for glutamine. (“Glutamine and Cancer” Wiley W. Souba M.D., Sc.D., Annals of Surgery, Vol. 218, No. 6, 715-728) Briefly, glutamine is the most important “nitrogen shuttle” in the blood. It brings the organic nitrogen to all cells, including cancer cells, which use it to make additional amino acids and thus proteins required to make more cells. The paper reports measurements that show as the glutamine supply in the blood (supplying a tumor) is reduced, tumor growth rate decreases, going to zero as the glutamine supply goes to zero. Muscles also need glutamine to grow. However, muscles not only consume glutamine to grow, but in times of insufficient dietary glutamine (red meats), muscles serve as a source of glutamine (for the blood) and diminish is size by doing so. As the cancer consumes it, the muscles supply it. This, what I call, “glutamine shuttle” is responsible for cachexia, the severe weight loss and general wasting away of the body associated with cancer. (Adding red meats to the diet will reduce muscle loss while increasing tumor growth.)
Hydrazine, from Hydrazine Sulfate, Blocks the Glutamine Shuttle
Structurally Hydrazine is H2N-NH2. It is two amino groups (-NH2) bonded together. When present in amino acids, the -NH2 groups are bonded to a carbon atom in the amino acid and play a key role in forming the chain of amino acids that make up a protein. When hydrazine is reacted with a protein it breaks the bonds between amino acids and substitutes -NH2 groups for the adjacent amino acids. (“Medical Biochemistry” by N. V. Bhagavan, fourth edition, pg. 45) This feature is used as an analytical tool for separating individual amino acids from a protein chain for further analysis. As an example, consider only two amino acids, R and R’ bonded together (R-R’). When reacted with hydrazine, the bond between the two amino acids is broken and -NH2 is bonded in its place: R-R’ + H2N-NH2 = R-NH2 + R’-NH2. Once reacted with the –NH2 group, the amino acid is permanently altered so it can no longer participate in the formation of a protein. Arresting protein synthesis in a tumor will stop its growth, the Glutamine Shuttle and cachexia.
When a person consumes hydrazine sulfate it enters the blood and is widely distributed. I see two possible reaction sites, either or both of them would block the Glutamine Shuttle. It could react directly with the glutamine in the blood, deactivating it. It could also enter the cancer cell where the bonding sites of individual amino acids are being prepared for reaction with other amino acids to form proteins. Such highly reactive sites would be extremely vulnerable to reacting with the hydrazine, deactivating the formation of the protein. I suspect that the dominant blockage occurs inside the cancer cells. If the dominant mechanism was to react with the glutamine in the blood, the body might see this as a loss in glutamine and still try to replace it from muscle tissue. If this happened, tumor growth might be arrested, but the cachexia process would continue. The observation is that cachexia is arrested. This leads me to believe the dominant arresting reaction happens inside the cancer cells.
The hydrazine (hydrazine sulfate) arrests the progression of the cancer (and cachexia) but is there a mechanism that kills cancer cells? Tumor shrinkage would indicate there is. I suspect that this is caused by the accumulation of damaged protein fragments and amino acids in the cell that disrupts cell function. It could kill the cell directly or activated one of the forms of programmed cell death. If so, the treatment might be further enhanced by combining it with other treatment protocols that have programmed cell death as a strategy. This is just one suggestion. I am only one person in a world of creative people. My hope is that clarifying the mechanism will open the door for others to find innovative ways to use hydrazine sulfate, improving its protocol, or using it in combination with other treatment strategies to achieve a result that is better than what can be achieved using either alone.
Like all chemotherapy agents, hydrazine is toxic. Normal healthy cells are also going to be effected in a similar way. The cancer cells may be impacted preferentially at first, but continued use is also going to impact normal cells. Care would have to be taken using it. Reports on the internet could be used as a guide but always consult your physician.
48. Update (1/ 07)
Prostate Cancer Treatment
I received an e-mail from Jerry Nail with this information about his unusually successful approach to dealing with his prostate cancer and the detailed protocol he used to control it.
To be continued/updated as time permits.