Cancer Proposed Common Cause and Cure for All Forms of Cancer David W Gregg, PhD

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Cancer

Proposed Common Cause and Cure

for All Forms of Cancer

(and Schizophrenia?, see Item 29)

(Cesium Cancer Treatment, see Item 37)

David W. Gregg, Ph.D.

188 Calle La Montana

Moraga, CA 94556

Phone: (925) 284-5434

This Page was started March, 1999 and continually developed up to the present. I have
added new insights/information at the end as they occurr without rewriting what was
written before. This was easiest for me and also leaves a historical record of how
technical progress developed. The latest information will be at the end with the exception
of Summaries which are presented at the begining.

Send e-mail to David Gregg

at

dwgregg@krysalis.net

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This paper is for information only. It represents the observations, views and
opinions of the author, but is not a recommendation for treatment. Anyone
reading it should consult his/her physician before considering treatment.

Summary

As of February, 2004

A Defense in Depth:

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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 apoptosis (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 can
not 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 (oxidtive
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 apoptosis. The reason cancer cells can live forever is that they can (and must)
rigorously avoid apoptosis. 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 apoptosis will not take place.
Unless another programmed cell death mechanism takes over, the cells will eventually

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return to being cancer cells. There is also a possibility that the enhanced nutrition may
make the cancer cells more healthy while it makes the normal cells more healthy. 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 serously obsured the
true potential of this appraoch. 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.

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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 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
impove, 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 mecnamism 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 cotransport 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

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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.

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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 can not 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

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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

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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

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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"

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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 Kreb's 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 nomal process of programmed cell death
and the cancer cells are perminantly 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 protocal.

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 Kreb's 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

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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 apoptosis
(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.

Items

1. DMSO (& MSM):

In my Health Note

DMSO

I describe how in the body DMSO

forms an 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

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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 more healthy 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

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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 produces 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.

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4. Metastasis:

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 to. 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 to. 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

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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

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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

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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).

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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

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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

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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.

14. Apoptosis:

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 Editon, 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.

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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 Kreb's Cycle (A nine step cycle). (This is
also called the citric acid cycle.) The combination of pyruvate oxidation and the Kreb's
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 Kreb's Cycle is to produce NADH and FADH2 as feed for the respiratory chain, along
with the release of the carbon's as carbon dioxide.

Kreb's Cycle Vital to both cellular energy and primary biochemicals for
biosynthesis:
The Kreb 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
feedstock's 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 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.

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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 biochemcials the the
missing enzymes are responsible for producing. Examples of end point biochemicals
would be those that have been identified as derived from the Kreb's 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.

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17. Garlic:

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

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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.

19. Exercise-Glutamine:

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 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 explaination 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
intensly for racing in the Tour at the same time. He credits his commitment to an
exceptionally vigouous 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".

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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.

20. Exercise-Glucose:

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 diminishes, 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 diebetics achieve some control
of high blood sugar with reduced requrement 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.

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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 distruct 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.

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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 exist 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).

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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 Circulaton 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.

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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

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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 present 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.

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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
michondria 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
cyoplasm 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 beome 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 versitility
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 capabiilty 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

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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 are as follows (with
Dr. Hoffer's permission):

Hoffer Email-1

Sent: 5/12/01 11:53 PM

From: A Hoffer, hoffer@islandnet.com

To: krysalis@krysalis.net

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 Warburgs early work when I started many years ago and
have followed his idea in develping 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

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which 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 osteo porosis 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.)

My Response:

Dr. Hoffer,

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 puzzeling over your statement that schozoprenics don't get
cancer. Could you give me a reference that I could read. I know you have a theory. I don't

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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.

David Gregg

Hoffer Email-2

Sent: 5/14/01 5:43 PM

From: A Hoffer, hoffer@islandnet.com

To: David Gregg, krysalis@value.net

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 th3e 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 catechol amines. A recent report i
by Japanese scientists showed that schizophrenics lack the gene which 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
their 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 which
do not divide like red blood cells , white cells. and cardiac cells.

A. Hoffer

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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.

My Response:

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.

1. 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.

2. 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.

3.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

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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 an oxidized and reduced form, 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.

4. 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

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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.

5. 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 can not be consumed by reaction with food (glucose) and
thus stacks up &endash; 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 adreochrome 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?

6. 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 which would mitigate both schizophrenia and cancer? I wonder if you
think this is a significant factor.

7. 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:

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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 &endash;
1000mcg tablets of B12, 20 &endash; 800mcg tablets of folic acid, the powdered
contents of 2 &endash; 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"

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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 business man 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 miricle 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.

David Gregg

Hoffer Email-3

Sent: 5/17/01 12:23 PM

From: A Hoffer, hoffer@islandnet.com

To: David Gregg, krysalis@value.net

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

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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 anaeroboc 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 appear to be the case. Following Karl Menninger who first stated this I have the
feeling that the schhizophrenic 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
schiizophrenia 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 belive 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 who 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 cold 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 hey have a better prognosis when treated. It
is also true that my schiizohrenic ppulation 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 i was no 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.

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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.

1. 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 dmage), 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.

2. 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 froms of cancer tested.
This is also consistent with the theory
presented here. As stated in the begining, it should apply to all forms of cancer.

3. 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.

4. 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

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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.

5. 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 Seperate Paths for NADH Synthesis Involving Nicin,
Nicainamide, Vitamin B6 and Triptophan:

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 seperate
paths for the synthesis of NADH. One starts with niacin, another with niacinamide, and a
third involves the conversion of triptophan 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
triptophan, 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) was 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 seperate 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) was effective in treating autism. Since the proposed
mechanism, the production of NADH, was not recognized, neither Carl Pfeiffer nor

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Bernie Rimland tried adding a triptophan supplemt to the mega-vitamin B6 treatment.
They thus were limited by the amount of triptophan existing in the diet of the patients. I
would predict that adding a significant amount of triptophan 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 involve 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 triptophan 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 diarrhia at considerably
lower levels. Thus, as is common in the community of people advocaing large doses of
viamin C, it is suggested that one take up to the "bowell 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 bicarbinate 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

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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 bicarbinate 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 indivitual 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 can not tollerate 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 tollerable dose),
niacinamide, vitamin B6 and triptophan. 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, that 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.

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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

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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.

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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
affecting 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, oolong tea
and pu-erh 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

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cancer cells to revert from anaerobic metabolism back to aerobic metabolism, allowing
them to become normal cells again ang 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 Towsend 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 Pirmary 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 Kreb's 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
will invoke two powerful cancer inhibiting mechanisms at the same time:

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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 can not 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 can not 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

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tumor, at least initially. Also, since the goal is to increase oxygen transport, it would
probably be desireable 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 glutathion. From my
own logic and his results I have to conclude that both alpha lipoic acid and glutathion 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 investigaing this as applied to chrnic 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 steralize
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

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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 can not
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 Anerobic 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 accomlishes 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 stimulaing the formation of new blood vessels and thus
can not 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, esophagiel 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
warrent a presentation here.

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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

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altering the pH. I can not 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 overall pH of the body fluids is rigorously controlled by the kidneys and lungs. 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 allows 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

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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 controled 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

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(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 cotransport 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 amaizing reports of late stage cancer being
arrested in a matter of days.

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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 can not 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 can not 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 chemotheapy 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.

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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 apropriate 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 anyhone interested in
more detail read the proper sections in the book.

Sax classifies the health hazard of all three compounds, cedsium chloride, potassium
chloride and rubidium chloride as "Acute Toxicity"

There are two toxic classifications rep;orted 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).

Cesium

Chloride

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:

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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 laetril on her own. She
was given a 50g bottle of cesium chloride, was advised to take 4g/day but instead, took

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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 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 (O.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

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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 begining 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
considerred. It looks like it could be profoundly effective, at any cancer stage for those
who can tollerate 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 competant 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 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 facilited by a protein in the cell
wall that provides a pore, highly selective to potassium, that allows the potassium to
freely diffuse out, called a potassium channel. 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

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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 the 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 the cesium treatment was enhanced by
adding potassium at the same time.

My Resonse 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 characteristicly 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 can not 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 can not 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
possbly 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

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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 occurrance 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 protocal 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 succcess 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"<larry@essense-of-life.com>

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Phone: 417-546-5075

He sent his two web page addresses presenting extensive information:

http://www.essense-of-life.com/info/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 gradualy 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 refered 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 lables such as "Salt Substitute" ,
"No Salt", etc. It is 100% potassium chloide 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.

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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 anerobic part prodicing 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 metabolisn. We now come to another
insight: Anaerobic metabolism shuts down apoptosis by this mechansim, 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 Ph.D (A
Cancer Researcher) Presenting Ideas as to How the
Cesium Cancer Therapy Could be Enhanced.

The invention of the transister 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

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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:

http://arbl.cvmbs.colostate.edu/hbooks/molecules/sodium_pump.html

http://merck.praxis.md/index.asp?page=bpm_report&article_id=CPM01NP258&section=
report&ss=3

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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

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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

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Stanford University Medical Center

Webhost 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 mecnamism 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 cotransport 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.

To be continued/updated as time permits.


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