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The Role Of Chelation of  Zinc in Cancer Treatment -- Simplified by Karl Loren

This page is linked from a page showing a hypothesis originated to me by one Fred Greenwood.  It was brand new to me, and far more complex in its terminology than my vocabulary or training would comprehend.  But, I saw a glimmer of truth in his material and have featured it HERE.  But, that material IS complex, and I announced on that page that I would seek to explain his concepts in language more comfortable for the average reader. That is this page.

I, Karl Loren, have started my research and writing about cancer, before receiving Greenwood's material.  I started with an initial hypothesis -- that cancer (as well as heart diseases and generally all degenerative diseases) are caused by free radical activity.  (I also have a "higher level" hypothesis on the cause of cancer and have included these as "musings" below.)

I had believed that cancer, unlike heart disease, involved an uncontrolled reproduction of cells.  I understood that the ONLY difference between a cancer cell and a normal cell was in this reproduction rate.  I discovered that I was wrong -- that I had an incomplete view of cancer cells.

As part of this research I discovered that it is not only the increased rate of growth that indicates cancer, but also an alteration of the cell itself, in ways other than the rate of growth. That information is described HERE.

That material is part of the general consensus (shared reality) of so-called cancer experts.  Here is an excerpt:

What causes cancer?

Cancer occurs when the DNA present in a gene is altered in such a way that the gene can no longer instruct the cell in which it resides to produce a certain protein in the normal manner. Such an alteration can take place when a gene is exposed to radiation or particular drugs or chemicals, or when some as yet unexplained internal signal occurs. These factors can cause the DNA within a gene to break and recombine incorrectly or to mutate. Once one of these changes has taken place, certain genes may be transformed into oncogenes, while other genes (cancer-suppressing genes called anti-oncogenes) may be inactivated.

If a gene has become an oncogene, the cell in which it is located may begin to produce unusually large amounts of one of its normal proteins or to manufacture an altered form of that protein. If an anti-oncogene has been rendered inactive, the cell containing it can no longer produce a normal protein whose function is to suppress cancer. In rare cases, an aberrant protein is manufactured when a cancer virus enters a cell and introduces an oncogene. Once any of these deviations in protein production has occurred, the cell alters its size, shape, surface characteristics and behavior. Thus, it becomes a cancer cell that is distinguishable from a normal cell.

How does cancer progress within the body?

Every cancer starts with a single cell that has been released from the growth restraints placed on all normal cells. Because the changes that have taken place within the cancer cell have been directed by the cell's DNA (the molecular basis of heredity), they are passed on to each of the daughter cells arising from the original cancer cell. Eventually, a family of abnormal cells is formed. Except in the case of leukemia, these cells form a mass, or tumor.

The cells of the tumor then push outward from their boundaries, infiltrating surrounding normal tissues. Small clumps of cells may then dislodge from the tumor and migrate to distant sites, often by invading the circulatory system of the blood or lymph. After traveling to a new organ, the cancer cells burrow out of the blood or lymph vessels and invade the surrounding tissues. There they continue to multiply, forming secondary tumors. This process of spreading to a distant site is called metastasis. Eventually, either local invasion or metastasis disrupts the body's normal functions and often leads to death.  (source)

From this material I realized that my view of cancer may have been too limited.  It appears that there is MORE than simply damage to the DNA relating to reproductive rates which causes cancer.  I accept the above text as accurate. There you find  the reference to the alteration by free radicals of the DNA ALSO means that the cell can no longer "produce certain protein," etc.

If that hypothesis is to be true, I would then want to explain Fred Greenwood's theory as being in alignment with this "free radical origin of cancer."  In other words, Mr. Greenwood's hypothesis may well include an important role for free radicals, but it was not apparent to me at first reading.  So, if my hypothesis AND his are both correct, then there must be some method of demonstrating that alignment.  That is this page.

Let the research begin.

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To repeat, my earlier understanding was that the free radical is small, but large enough to affect the DNA molecule.  The DNA controls the method and rate of reproduction of the cell in which it resides.  If a free radical, in some random fashion, hits and damages even one electron amongst the large number within the DNA, there might be a genetic mutation -- a cancer started.

Science has addressed just this issue in many places.  That is, the issue of the role of free radicals in the origin of cancer and other diseases.

Evidence is accumulating that most of the degenerative diseases that afflict humanity have their origin in deleterious free radical reactions.

These diseases include atherosclerosis, cancer, inflammatory joint disease, asthma, diabetes, senile dementia and degenerative eye disease.  (source)

Dr. Denham Harman, of course, is the "father" of the free radical theory of disease.  I have many pages about him and his work amongst these pages.  CLICK HERE for an interview with him, done in 1998.  Here is an excerpt from that interview with the Life Extension group:

Denham Harman: I was essentially talking to myself for about 10 years. The biologists at that time knew very little chemistry, certainly nothing about free radical chemistry, but it was vice versa with the chemists. The first life span study was presented as an abstract at the American Federation of Clinical Research. I think it was in 1956 or 1957 in Carmel, Calif. There was gradual interest. Then in the mid 1960s it started to increase further, and when the SOD business [the discovery of superoxide dismutase, a natural enzyme that destroys superoxide free radicals in the body] came out in 1969, it took off.

We gradually accumulated a lot of data in the mid-1960s that showed, yes, we increased the average life expectancy, which is what I expected to see. But I did not see such an increase that I could really be sure, in terms of maximum life span. On that basis, the question came up, is the failure to increase maximum life span because the theory is wrong or because it should be modified? I kind of concluded it should be modified, and I wrote a small paper that was published in the April issue of The Journal of the American Geriatrics Society in 1972. The title was, "The Biologic Clock: The Mitochondria?" I followed it up subsequently with a paper in 1983, I think, which was published in AGE, called "The Free Radical Theory of Aging: the Consequences of Mitochondrial Aging."

There is a great deal of work going on today in that area, but at that time, I didn't know a lot about mitochondria, per se. But it didn't take much imagination to figure that your DNA or your membranes could be subject to free radical attack. So basically, the paper suggested that free radicals generated by the mitochondria would kill us, so to speak.

At any rate, right now, I think what's important, aside from the past history, is that there's a growing consensus that aging changes are induced by free radical reactions, largely initiated by the mitochondria, and that the rate of damage to the mitochondria determines our life span. I think that's the essence. People still disagree with it. But the point is that people have been going in so many different directions that a lot of people could not be brought to bear on one subject. I think that is changing now.

Life Extension Interviewer: Certainly, the free radical theory has inspired more research than any other concept in aging, there's no question about that. There are more data related to that theory than on any other subject in aging. Most facts are consistent with the theory.

DH: Well, I think you have to actually accept that at some point in time you establish a fact, and maybe we're reaching that point now. Probably, we're past that point, or past the point when something which is called a theory becomes a fact and you just take it as such.  (source)

Here is another typical comment about free radicals.  This includes reference to the multiplying effect of metals on free radical activity.

A wide variety of oxygen free radicals and other reactive oxygen species can be formed in the human body and in food systems.

Transition metal ions accelerate free-radical damage. (source)

Here is another

Most human cancers may be considered `spontaneous' in nature as no evident specific inducing agent is usually identified. Development of cancer is linked to a number of genetic alterations caused by both endogenous and exogenous factors (1). These alterations are continuously selected for improved proliferation according to a Darwinian process. This phenomenon is fortunately very long and development of frank malignancies may take decades. The very slow selection of the spontaneous cancer phenotype has always been a major hindrance to cancer research. The development of new strategies to counteract the phenomenon may take advantage of simpler and more convenient systems that mimic the in vivo process.

Most primary animal cells exhibit a limited lifespan in culture and eventually undergo senescence, during which time the cells cease to proliferate with resultant cell death (2). With varying frequency, especially dependent on the species of origin, a few cells survive the senescence crisis and acquire unlimited proliferative potential. At the same time, measurable in months, they also spontaneously become neoplastic, displaying an increasing capacity to grow in soft agar and induce tumors in nude mice. A number of comprehensive reviews on in vitro spontaneous transformation have been produced (3–8) and for a detailed description of the phenomenon we refer to them. Transformation of cultured rodent fibroblasts has been used until recently to assess the carcinogenic properties of various drugs and metabolites (9,10), but exploitation of this phenomenon to investigate new strategies to prevent or reverse the spontaneous cancer phenotype has declined. This is somewhat surprising given the important achievements that have been made in understanding the molecular changes that underlie spontaneous in vitro transformation and the parallels between this phenomenon and human carcinogenesis. We here propose making use of spontaneous in vitro transformation to investigate the possible protecting role of accelerated DNA base excision repair (BER), the main pathway that repairs endogenous damage in mammalian cells.(source)

With these and other scientific reference I have felt comfortable in claiming that the free radical is generally responsible for cancer.  Thus, when I read a study that shows that IV Chelation reduces cancer 90% from what would normally occur, I am not surprised.  After all, IV Chelation removes metals.  Contrary to some opinion, IV Chelation does NOT directly remove blockage within the arteries.

My concept of HOW chelation works has been developed over many years, presented in literally thousands of page on my many web sites.  The chelating substances (whether oral or IV) remove the metals. I have always realized that I didn't know HOW this metal removal took place.  I knew only THAT it did.  Fred's material suggests a mechanism by which chelation "works."  It is not different my earlier view, but it is a further insight into the process.  I am delighted to gain this understanding.

The reduction in these metals brings about a reduction in free radical activity. The reduced number and activity of free radicals in the body bring about a reduction in arterial blockage, and, not to my surprise, a reduction also in cancer. The Swiss study was a shot across the bow of the ignorant medical profession -- they have been deliberately looking the other way, ignoring the truth of free radical pathology for heart disease AND cancer.

That Swiss study has been "lying around" for many years, but now, on my pages, it will start to get some real exposure and perhaps the world of cardiology will wake up?

So, we start now to examine the data presented HERE by Fred Greenwood.

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There is one very important word that must be well-understood:

matrix metalloproteinases  or "MMP"

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One-third of all proteins are "metalloproteins", chemical combinations of protein atoms (carbon, nitrogen, oxygen, hydrogen, sulfur) with ions of metals such as iron, calcium, copper, and zinc.

The hemoglobin, for example, that carries oxygen in the bloodstream, is an iron-containing metalloprotein.

The metal ions in metalloproteins are critical to the protein's function, structure, or stability. In fact, numerous essential biological functions require metal ions, and most of these metal ion functions involve metalloproteins. Thus, metalloproteins make life on Earth possible and the ability to understand and ultimately control the binding and activity of protein metal sites is of great biological and medical importance.

Over the next five years, this Program aims to overcome current problems relating metalloprotein structure and function. Our major focus is to establish a direct experimental correlation between structural design parameters and metalloprotein properties by using an accurate database of protein metal sites, explicit evaluation of possible states, projects that separate general and framework-specific effects, and efficient computational searches in the vast combinatorial landscape of the metal site environment.

The ultimate goal of our research is to achieve a comprehensive understanding and the successful design of metalloproteins.   (Source)

The Scripps Research Institute is the largest, private, non-profit research organization in the U.S. It has attained recognition as a center of excellence in a highly focused branch of research, the nexus of the structure of biological molecules and their cellular functions with chemical synthesis.

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Recent advances in our understanding of the molecular mechanisms of pancreatic cancer progression are resulting in novel approaches to therapy. The matrix metalloproteinases (MMPs) have emerged as promising new targets for therapeutic intervention strategies. More than 20 MMPs have been identified, which can be subcategorized according to preferential substrate.  (source)

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The word "metalloproteinase" can be understood in its components.  The term "metalloprotein" is described above. 

When you add "-ase" onto the end of protein, as a suffix,  you are then describing a Biochemistry term, forming the name of an enzyme (amylase).

The word "amylase," for instance is a Biochemistry term for an enzyme that converts starch and glycogen into simple sugars. [amyl + -ase]

So, metalloproteinase means a type of enzyme related to a form of protein that has a metallic component.

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Proteins can accelerate the numerous chemical reactions that occur in our bodies. They accomplish this by acting as biological catalysts or enzymes which are present by the thousands in our cells.

Definition:  Recall that a catalyst is something that accelerates a reaction without actually being consumed by the reaction. An ordinary catalyst acts by lowering the activation energy of a particular reaction pathway The role of an enzyme or series of enzymes, while similar in terms of lowering the activation or transition state energy, is far more efficient and specific. 

Examples:  Have you ever put household hydrogen peroxide on a cut or scrape? It bubbles and fizzes, doesn’t it. If you apply it to undamaged skin you will also notice the absence of this effervescence. Hydrogen peroxide naturally decomposes over time to produce water and molecular oxygen according to the reaction:

2H₂O_{2 à} 2H₂O + O₂

When we apply it on a cut, it bubbles because our blood contains catalase, a protein enzyme that accelerates the above reaction. The hydrogen peroxide is useful on the wound for two reasons: the fizzing of the oxygen bubbles helps to mechanically clean the wound and the hydrogen peroxide destroys the cell membranes of any bacteria present, partly due to the fact that the bacterium do not contain this enzyme, catalase.  (source)

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The word "matrix" means, casually, a network of some sort, as opposed to some single item.  Most components of the body are fixed in some position.  You could say that they are fixed in a "matrix."

Years ago I wrote about "how bones grow."  The bone is made up of a "matrix," which I likened to a fishnet, into which fastened particles, including calcium.  Here it is from THIS PAGE.

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There IS fishnet involved. Rather than there being a separate glue, let’s just figure that the fishnet has two unique characteristics.

The fishnet, itself, is sticky. You don’t have to coat it with glue to make it sticky.

And, second, the fishnet is alive!

The rocks are NOT alive, but the fishnet IS alive. That means that the fishnet part of this combination can grow. Rocks don’t grow!

Now you are getting the picture.

Our bones are a combination of living fishnet with non-living rocks. The rocks are mostly calcium, but there are a few other minerals involved.

The fishnet?

Ah, there is where people’s attention should go when they want to understand bones! Rocks are not hard to swallow, but fishnet is not easy to grow!

The fishnet has a more elegant name when it comes to science. Let’s call the fishnet a matrix.

Matrix

Now you are getting there.

Matrix is described in a standard encyclopedia as

connective tissue, supportive tissue widely distributed in the body. Consisting mainly of substances certain cells secrete, it contains relatively few cells. The connective tissue that forms tendons and ligaments is mainly collagen—white, inelastic protein fibers. Cartilage, vital to the skeletal system of vertebrates, is fibrous collagen in a gel; it is firm but flexible. Connective tissue found under the skin and supporting most organs contains collagen and other fibers as well. Bone connective tissue is made up largely of collagen fibers and calcium salt crystals; its structure is strong and rigid. Blood and lymph have a fluid connective tissue matrix. [Matrix]

Now, you can begin to see that the health of our bones depends at least as much on the health of the matrix as it does the rocks which stick to it.

In biology, many a phenomenon are not understood exclusively through Scientific logic, as that fails.  The simplest example is "Those who eat more are not always FAT,  and those who eat less are not always THIN. 

 "Matrix" is OK to compare with a "Fishnet" - for easy understanding.  If one link is broken in a fishnet, it can still function as a leaking fishnet, and will function "only" as a fishnet while fishing.  

 But in Bio-matrix if one link is broken,  the entire "functional behavior" changes radically.  This is where the same logic cannot be extended.    (Dr. Ayyangar)

In fact, the big myth in all the talk you hear about "calcium" is that such talk doesn’t put the emphasis where it belongs.

Most people don’t suffer from a shortage of "calcium," but rather from two related shortages.

They suffer from the lack of a healthy matrix in which the calcium can be embedded

or

They suffer from the lack of the right type of calcium which CAN be embedded on a healthy matrix.

So, to understand bone strength, you need to understand the matrix and the types of calcium which will embed readily on that matrix.  (Source)

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Here is a more technical clue to "matrix" as used in the phrase "matrix metalloproteinase:"

     Soft connective tissue has generally been shown to consist of collagen fibrils embedded in a gel-like matrix. The collagen fibrils are complex structures which are assembled from tropocollagen sub-units, and which function primarily as supporting elements. These fibrils are surrounded by an extrafibrillar matrix, the macromolecular components of which are mainly proteoglycans.  (Source)

Another, more technical description of "matrix" is here:

Connective tissues are responsible for the form and shape of the animal body and, in addition, provide protection for vital organs and facilitate locomotion.

The term connective tissue is also applied in a more restricted sense to structures such as dermis, tendons, fascia, bone, cartilage, and the capsules of the joint.

All cells, however, make contacts with surrounding structures that involve connective tissues as components of the extracellular matrix. The matrix possesses chemical, physical, and mechanical properties uniquely suited to the function of tissues and organs of which the cells are a part.

The extracellular matrix may be rigid (e.g., bone), elastic (e.g., blood vessel walls), compressible (e.g., cartilage), or liquid (e.g., synovial fluid). Most connective tissue matrices derive these properties by virtue of the content of fibrillar proteins, nonfibrillar macromolecules, and low molecular weight proteins and electrolytes.  (source)

So you can now envision an enzyme fixed in some sort of matrix. The enzyme can't easily move around. The particular type of enzyme being presented here is related to a metal-containing protein.

The several sections above are intended simply to show what the definition of "matrix metalloproteinase" is.

This phrase is usually abbreviated as MMP.

I'll restate it to say that it stands for an enzyme related to a protein, where the protein has a metal as part of it. This enzyme exists in a matrix within the body.

They would have zinc in them.

There is a representation of zinc on the left.  It normally has 30 electrons to balance the 30 positively charged particles in the center.  Note that zinc has two electrons in the outer ring.  It is relatively easy for zinc to lose one of these electrons, turning that atom into a free radical form of zinc.

The word "ion" simply means a molecule, atom, etc., with "some" charge -- either plus or minus.

The word "cation" means the charge is plus.

The word "anion" means the charge is minus.

Zinc has 30 electrons in the shells, with two in the outer shell.  It is NOT an ion because the nucleus has 30 positively charged particle balancing the 30 negatively charged electrons.  No charge there. 

If the two outside electrons are moved away, it becomes Zinc 2+, an ion, and a cation, and has 28 electrons in the shells.  It is not a free radical because it has no unpaired electron.

 (leaving aside the concept of one unpaired electron in one shell and another unpaired electron in a different shell -- I believe that "cures" itself when the atom "settles" back to a normal energy level ??)

 If (I don't know if it can) the Zinc loses ONE electron instead of two, it is Zinc 1+, it is a cation, and it is a free radical. 

Hydrogen is inherently a free radical because it has only one electron.  It is not an ion as long as it has that one electron in its orbital because there is only one positively charged particle in the nucleus.

 I believe you can take away that electron, causing this to be H 1+.  ( I don't know, but assume that it is not a free radical because there is no unpaired electron.)

 Normal hydrogen could, instead, gain one electron and become H 1-  and is no longer a free radical.  This is referred to as "minus Hydrogen."

 I sell this stuff and have a technical page on it here:

 http://www.chelationtherapyonline.com/technical/p20.htm

As a free radical of zinc, or possibly also an ionic form of zinc, when it is within one of these MMPs?  It starts to degrade the matrix and leads to cancer. That is the source of cancer in virtually all cases.

Chelation removes ONLY the free radical form of zinc (or the ionic form), thus eliminating this as a source of cancer.  This would be called an "ionic matrix metalloproteinase" component, or an "free radical matrix metalloproteinase" component.  The term in actual use is "active MMP."

Thus, it is active MMPs that cause cancer.  It does this by allowing something called angiogenisis.  Once a cancer starts, it is very tiny.  It gets its blood supply from the surrounding area of blood capillaries.  But, as the cancer mass grows in size the inner parts cannot get blood from those surrounding capillaries, and the cancer mass must start to develop its own internal blood supply.

This process is called angiogenesis. 

Active MMPs allow this angiogenesis to take place.

If you can somehow change the proportion of bad MMPs to good MMPs, this angiogenesis will stop, or never start.

Thus, the prevention of cancer and the cure of cancer would be to reduce the number of active (bad) MMPs.

The miracle here is that chelation removes ONLY the MMPs containing one of the non-normal forms of zinc.  (This calls, also, for a more sophisticated view of "chelation" as a process.)

This is the wonder of chelation in preventing and curing cancer.

Here is one of the activities of the degraded matrix:

Degradation of extracellular matrix is crucial for malignant tumour growth, invasion, metastasis and angiogenesis.

Matrix metalloproteinases (MMPs) are a family of zinc-dependent neutral endopeptidases collectively capable of degrading essentially all matrix components. Elevated levels of distinct MMPs can be detected in tumour tissue or serum of patients with advanced cancer and their role as prognostic indicators in cancer is studied.

In addition, therapeutic intervention of tumour growth and invasion based on inhibition of MMP activity is under intensive investigation and several MMP inhibitors are in clinical trials in cancer.  (source)

and here:

The matrix metalloproteinases (MMPs) are a family of at least fifteen secreted and membrane-bound zinc-endopeptidases.

Collectively, these enzymes can degrade all of the components of the extracellular matrix, including fibrallar and non-fibrallar collagens, fibronectin, laminin and basement membrane glycoproteins.

MMPs are thought to be essential for the diverse invasive processes of angiogenesis and tumor metastasis. Numerous studies have shown that there is a close association between expression of various members of the MMP family by tumors and their proliferative and invasive behavior and metastatic potential.

In some of human cancers a positive correlation has also been demonstrated between the intensity of new blood vessel growth (angiogenesis) and the likelihood of developing metastases.

Thus, control of MMP activity in these two different contexts has generated considerable interest as a possible therapeutic target.

The tissue inhibitors of metalloproteinases (TIMPs) are naturally occurring proteins that specifically inhibit matrix metalloproteinases, thus maintaining balance between matrix destruction and formation. An imbalance between MMPs and the associated TIMPs may play a significant role in the invasive phenotype of malignant tumors.  (source)

Here is the final powerful point.  Chelation of the zinc prevents degradation of a matrix, and thus prevents cancer from growing.

The molecular mechanisms by which tumor cells metastasize to bone are likely to involve invasion, cell adhesion to bone, and the release of soluble mediators from tumor cells that stimulate osteoclast-mediated bone resorption.

 

Bisphosphonates (BPs) are powerful inhibitors of the osteoclast activity and are, therefore, used in the treatment of patients with osteolytic metastases. However, an added beneficial effect of BPs may be direct antitumor activity.

 

We previously reported that BPs inhibit breast and prostate carcinoma cell adhesion to bone (Boissier et al., Cancer Res., 57: 3890-3894, 1997).

 

Here, we provided evidence that BP pretreatment of breast and prostate carcinoma cells inhibited tumor cell invasion in a dose-dependent manner.

 

The order of potency for four BPs in inhibiting tumor cell invasion was:

 

zoledronate > ibandronate > NE-10244 (active pyridinium analogue of risedronate) > clodronate.

 

In addition, NE-58051 (the inactive pyridylpropylidene analogue of risedronate) had no inhibitory effect, whereas NE-10790 (a phosphonocarboxylate analogue of risedronate in which one of the phosphonate groups is substituted by a carboxyl group) inhibited tumor cell invasion to an extent similar to that observed with NE-10244, indicating that the inhibitory activity of BPs on tumor cells involved the R2 chain of the molecule.

 

BPs did not induce apoptosis in tumor cells, nor did they inhibit tumor cell migration at concentrations that did inhibit tumor cell invasion. However, although BPs did not interfere with the production of matrix metalloproteinases (MMPs) by tumor cells, they inhibited their proteolytic activity. The inhibitory effect of BPs on MMP activity was completely reversed in the presence of an excess of zinc.

 

In addition, NE-10790 did not inhibit MMP activity, suggesting that phosphonate groups of BPs are responsible for the chelation of zinc and the subsequent inhibition of MMP activity.

 

In conclusion, our results provide evidence for a direct cellular effect of BPs in preventing tumor cell invasion and an inhibitory effect of BPs on the proteolytic activity of MMPs through zinc chelation. These results suggest, therefore, that BPs may be useful agents for the prophylactic treatment of patients with cancers that are known to preferentially metastasize to bone.  (source)
 

In contrast to the above approach to cancer, billions of dollars in research are currently being spent on what might seem to be the same thing.

However, this research will never pay off if the end result is a validation of chelation therapy.  There is no money in that result.

I think that does it.  This page is extremely technical, but it is a forthright extrapolation of the material referenced by Fred Greenwood (HERE) and further verified with my own extensive and independent search for various words and issues.

Removing zinc 2+   is the key to inhibiting the action or degrading the matrix that then allows cancer to pass the stage where it can grow from internal resources alone.  Cancers all grow, initially, from their own use of blood from the outer extracellular environment.  Once they pass a critical size, mass, they must develop an INTERNAL network of capillaries, etc., to supply blood.  This is angiogenesis.  This net work cannot be created unless the existing matrix (network) has been degraded.  If you remove the unwanted zinc from these substances, the extracellular matrix is NOT degraded and the cancer clumps are unable to develop their own internal supply of blood.

Thus, oral chelation removes only CERTAIN forms of zinc.  It is not "curing" cancer.  But, the removal of that zinc means that the cancer does not grow, cannot spread.

This is the modern miracle, so far never revealed anywhere, except because of the research done by Fred Greenwood.

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I, Karl Loren, am now satisfied, independent of anything referenced by Fred Greenwood, that there is such a thing as "matrix metalloproteinase" and that it is one of the hottest items in research for preventing and treating cancer.  I see scientific studies that indicate how removal of zinc can prevent cancer.

I don't need to know much more about this to know that it is "hot."  Here is a quote that is exciting:

By definition, a phase 1 clinical trial is designed to simply examine the toxicity of a given drug. Beginning in February 1997, Vitaxin was given once a week for 6 weeks to 15 patients with late-stage cancer in a dose-escalation study. No side effects or toxic reactions were observed. However, surprisingly, 9 of the patients had either disease stabilization or clinical benefit. One patient who responded early to the treatment was allowed to continue treatment and has been taking the drug for more than 18 months. This patient has experienced steady shrinkage of tumor and no side effects. Although these results are preliminary and anecdotal, a phase 2 trial will begin soon to actually measure the potential clinical benefits of this drug.  (Source)

Here is a quote from the manufacturer of Vitaxin:

Significant medical attention has been paid to anti-angiogenesis products and their ability to slow or stop the growth of tumors and the surrounding vasculature. Once a solid tumor reaches a certain size and mass, it can no longer grow or spread without the help of blood vasculature. To accomplish this, tumors release specific growth factors which cause angiogenesis, or the growth of new blood vessels from existing vessels toward and into the tumor. During angiogenesis, proteins called integrins are expressed on the surface of these new vessels, which enable the integrins to adhere to the surrounding tissue, allowing them to continue their extension toward and into the tumor. Vitaxin has been shown to bind and block alpha-v beta-3, an integrin which is specifically found on these newly sprouting blood vessels, and to stop the growth of these vessels through an apoptotic (programmed cell death) signaling mechanism. This inhibition of new blood vessel formation has been shown to block the growth and spread of solid tumors in various animal models.  (source)

Is this big business?  Or no!  Yes it is.  For a mere $4,100 you can buy the report, sometime in the next couple years, about this stuff.  The drug industry is abuzz with the news about "matrix metalloproteinase" and how it can prevent and cure cancer.  The terrible problem is that they haven't found a DRUG which can do the simple job that the artificial amino acid, EDTA, can do.  It happens that my oral chelation formula, on the market almost 20 years, the most well known formula of its type, can and does do exactly what the drug companies are looking for. 

Drugs KILL.  What is needed here is NOT some substance that kills, but a substance, such as EDTA, Cysteine and N-Acetyl lCystein that can remove unwanted forms of zinc from the core of the material being talked about here. The revolution in cancer treatment has arrived and no one knew it was here.  The paid guys are busily looking amongst the drugs, where patents are available, because that is where they are paid to look.  They will get no pay for "finding" that a non-patentable substance, already on the market for many years, will do the job.  This will be one of the nails in the coffin of the industrial medical/drug complex.

So, Fred Greenwood has presented me with a tantalizing tidbit -- still needing further study and explanation, but one thing is certain.  A fair number of billions of dollars are now dedicated to doing this same study -- and none of them want to find out that EDTA or Cysteine can do it!

Wouldn't that be interesting?

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Now, let me look at the references Fred suggested about ZINC. That is a key here.  Fred is suggesting that chelation can remove certain forms of zinc and that somehow the removal of that zinc from some substance in the body is the remedy for cancer.

I am confident that my formula will remove zinc.  But, let's check on this.

One of his references says this:

 EDTA also binds strongly to other metals. Thus, following intravenous infusion of CaNa2EDTA in healthy subjects the urinary excretion of calcium, copper, iron, magnesium and zinc were assessed. CaNa2EDTA significantly increased the urinary excretion of all metals except magnesium with greatest increases for iron (x 3.8 above baseline) and zinc (x 22).  (Source)

It turns out that zinc, itself, has different forms.  There is "regular" zinc, then there is zinc which has some sort of extra charge -- often called Zn2+ .  This means Zinc with a valence of two.  The whole subject of valences, as well as free radicals, is covered in my "Ultimate Primer on Free Radicals" located HERE.

So, let's see why that might be useful.

Although the exact mechanism by which zinc shortens common colds may never be determined, the Zn²⁺ ion has multiple, biochemical effects in vitro, almost certainly acting synergistically in common cold therapy. According to Charles A. Pasternak of the St. George's Hospital Medical School at the University of London, hydrated Zn²⁺ ion at 6 to more than 60 times normal zinc serum concentration has multiple beneficial effects, increasing as extracellular Zn²⁺ ion concentration increases.(1) 

. . . .

Elevated extracellular Zn²⁺ ion is beneficial and elevated intracellular zinc is cytotoxic, although recently some authors have suggested that slightly elevated extracellular zinc is cytotoxic. In some cells, rounding and refractile changes occur at about 0.1 mMol Zn²⁺ ion and at much lower concentrations for most lipophilic and strongly chelated zinc complexes. These observations were interpreted as cytotoxicity and suggested a low 1:2 or 1:4 antirhinoviral therapeutic index for zinc.

Researchers highly familiar with the unique appearance of cell plasma membranes after the astringent action of Zn²⁺ ions, place the index at 10 to 100 times higher; as extracellular Zn²⁺ ion is a newly recognized host defense according to Pasternak.(1) Hydrated Zn²⁺ ions protect cell plasma membranes against damage induced by cytotoxic agents of environmental origin long enough for other defense mechanisms to be brought into play. Up to 1 mMol, Zn²⁺ ions protect cell plasma membranes in vitro.(1) (source)

The word cytotoxic means something which will kill cancer cells.

Here is where the excitement begins:

Degradation of extracellular matrix is crucial for malignant tumour growth, invasion, metastasis and angiogenesis.

Matrix metalloproteinases (MMPs) are a family of zinc-dependent neutral endopeptidases collectively capable of degrading essentially all matrix components. Elevated levels of distinct MMPs can be detected in tumour tissue or serum of patients with advanced cancer and their role as prognostic indicators in cancer is studied.

In addition, therapeutic intervention of tumour growth and invasion based on inhibition of MMP activity is under intensive investigation and several MMP inhibitors are in clinical trials in cancer. (source)

I'll let this be for now and for here.  I await the review of these pages by others to find whatever error thay can!

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Karl Loren Musings!

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