Kill Cancer Cells The life and death of cancer cells

PROPOSED COMMON CAUSE AND CURE FOR ALL FORMS OF CANCER: ITEMS 33-39 (SECTION 4)

Prepared for educational use by David W. Gregg, PhD.
Used with permission.

These web pages are for information only. They represent the observations, views and opinions of the author, and are not a recommendation for treatment. Anyone reading it should consult his/her physician before considering treatment.




Items 33-39 (Section 4)


33."Nutrition and Cancer" by Arthur B. Robinson, www.nutritionandcancer.org
34. Tea and Cancer
35. (7/10/02) Enhanced Anti-angiogenesis (for all types of cancer)
36. (8/1/02) A Profound New Insight! Why all Cancers are Anerobic in Metabolism
37. (8/03) Cesium Treatment of Cancer, an Exceptionally Promising Approach
37. – Update 1/04: A clearer insight into the killing mechanism
37. – Update 1/25/04: A communication with Rich VanKonynenburg Ph.D.
38. (1/28/04) An additional insight related to the "Nutritional" treatment approach
39. (3/27/04) An Email from Chris Duffield Ph.D (A Cancer Researcher) Presenting Ideas as to How the Cesium Cancer Therapy Could be Enhanced



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:

1. 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.

2. 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.

3. 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.

4. Experiments showed that a restricted diet slowed the growth rate of cancer, but there was no evidence of cures or remissions.

5. 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.

My Response/Comments
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.

1. 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.

2. 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")

3. 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.

4. 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.

5. 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:

1. The conversion of anaerobic cancer cells into normal aerobic metabolism cells.

2. 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: http://www.wellwisdom.com/all-immune-enhancing-products

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.

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.

General Background

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

Technical Background:
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
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:

1. The total of 50 cancer cases studied showed an impressive 50% survival rate.

2. It confirms the work of Messiha showing that the higher the dose the more effective it seems to be.

3. 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.

4. 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.

Conclusion
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.

Summary
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"
Phone: 1-800-760-4947

He sent his two web page addresses presenting extensive information:
http://www.essense-of-life.com/moreinfo/healthtopics/A-203/about+cesium.htm
http://www.essense-of-life.com/info/petphtherapy.htm

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:
http://www.advancedhealthplan.com/2cesiumchlorideforcancer2.html
http://www.ithyroid.com/cesium.htm
www.cancer-coverup.com/story/dosage.html

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.com. 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:

Article 1: The Na+-K+,ATPase (Sodium Pump)
Article 2: Site no longer available

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.

Sincerely,
Chris
---------------------------------
Chris Duffield Ph.D.
Visiting Scholar
Stanford University Medical Center

Web host of http://IPTQ.com 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.





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