Three of the four documents on this page are considerable evidence of the internal struggle going on within the Board of Directors of ACAM. I am sure that most of the doctors who are members do not know about this issue. The Board of Directors of ACAM, our alternative medical friends, have been deliberately withholding information the value of oral EDTA from their membership. I had to face this reality back in March 1999 when I changed my position on the value of oral EDTA and actually added EDTA to my famous Life Glow formula. Now it is time for the whole world to learn that the people they had thought of as their friendly chelation doctor, at least at the top of that organization, has been deliberately suppressing valuable information about how to treat heart disease! Even though I never tried to do it, there are many companies who sell vitamins and who pay for a booth at the quarterly meetings of ACAM. These vitamin companies attempt to market their products to doctors. Some of those vitamin companies have been offering "oral chelation" formulas for sale at the ACAM meetings. However, one particular company, called Longevity Plus, was turned down for a booth because this company was going to have Dr. Garry F. Gordon as its "consultant" at the booth -- to explain to his fellow-chelation doctors what the values were of oral EDTA. ACAM decided it was not willing to have that happen and refused this vitamin company permission to sell its oral chelation formula at that meeting. This appears to be illegal commercial discrimination to me, and it appeared the same way to the company -- Longevity Plus. So, the lady in charge simply sent a lengthy letter to the Board of Directors of ACAM. Click here to read that letter -- fascinating! When that letter was made public on the internet, there was an even greater shocker -- click here to read a letter from Dr. Garry F. Gordon to the Board of Directors of ACAM, letting them know that their policy of deliberate suppression of factual evidence about oral EDTA will only harm their own organization. This is the letter with references to a very large number of scientific studies about the value of oral EDTA. I had never seen these studies until a friend suggested I look at them, on Dr. Gordon's web site. That was when I announced my change of position on "oral EDTA." There is a second medical association, called GLACAM whose members offer intravenous chelation therapy. GLACM - Great Lakes Association of Clinical Medicine,
Inc. The GLACAM group has invited Dr. Gordon to present information about oral EDTA to one of their upcoming conferences. They are NOT falling behind the times. They even had me, Karl Loren, as one of their speakers some years ago. Next, the whole world of cardiology is falling apart now that no less than the President of the American Heart Association has asserted that more than 50% of bypass surgeries are failures. Click here to read that story. |
814 N. Beeline Hwy.#I
Phone, 520/474-3684 fax, 520/474-1297
Alexandra Van Cleve
President
April 1, 1999
American College for Advancement in Medicine
23121 Verdugo Drive #204
Laguna Hills, CA 92653
Re: ACAM Ban on Oral Chelation
Attn: Nancy Morgan – Operations Manager
Dear Ms. Morgan:
Thank you for your call reminding us of your unanswered fax. I am in receipt of that March 22 fax which stated that "ACAM by policy does not support the use of oral chelation products. Consequently, we are unable to approve your application to exhibit in Orlando unless you will agree not to market "Beyond Chelation" and to eliminate promotional literature on it and related oral chelation products."
Previously ACAM has attempted to deny me the right to the support at my booth of my consultant, Dr. Garry Gordon, President of Gordon Research Institute. Believing that ACAM already had enough legal problems to contend with, I did not bring my attorney into that obviously harassing and possibly illegal action, but instead I went ahead and paid separate registration fees for him as you requested, although he was there primarily to assist me in the exhibit area. I will not continue to do this, and he must receive an exhibitor badge as any other consultant for an exhibitor would.
Now ACAM has chosen to become involved in what I can only perceive to be illegal restraint of trade, discrimination, and the withholding of vital information from its membership.
It is truly sad that with such a great need for physicians wanting to leave the AMA and needing some RESPONSIBLE organization with which to affiliate that your leadership has not learned to be more thoughtful about what it stands for and puts in writing, especially after the recent FTC experience and its possible far reaching consequences!
As a co-founder of ACAM, Dr Gordon has until now been attempting to support the organization by directing all health professionals interested in longevity medicine to the ACAM courses, even though ACAM’s leadership fails to openly recognize him for his documented efforts in helping create this obviously immensely successful new specialty. I have no doubt that enlightened leadership could make ACAM the LARGEST alternative medical organization in the anti-aging field for years to come. Such an organization would welcome new, state of the art products, and not fear them.
My attorney and I can only perceive that your current demand regarding oral chelation products relates either to Dr Janson’s unthinking comments (sent to the entire board of ACAM by e-mail on February 10th 1999) OR to the inability of ACAM competitors to compete with the overall unmatched value provided in Beyond Chelation.
The product, Beyond Chelation, is in fact not simply an oral chelator, but a TOTAL cardiovascular multi-vitamin, mineral, essential fatty acid, herbal, homeopathic, amino acid formula with therapeutic quantities of over 60 well documented cardiovascular nutrients, all routinely prescribed by ACAM physicians.
It’s inclusion of EDTA may readily be attributed to its well documented efficacy in helping to prevent the oxidative breakdown of nutrients in the formula itself --the same function it normally has when added to our food supply -- here it is stabilizing the ingredients of the formula.) However, Dr. Gordon feels that it has additional uses about which ACAM has some disagreement.
These nutrients, costing over $100 were they purchased separately, are sold at a "show special" price of $20. There is NOTHING that comes even close to this amount of nutrients, with or without EDTA, for this price at your conferences! Either way, your intended actions cannot be allowed to go unchallenged for the sake of your membership. Nevertheless, I am willing to drop this matter if you rescind your letter immediately and rethink your clearly outmoded and indefensible "policy" against oral chelators and oral chelation.
Beyond Chelation’s warm and immediate acceptance by many leading ACAM physicians is one of the major reasons I have priced this product so low. In fact, many of your members are my primary market and yet you are attempting to deny me access to my customers. If we need to take this matter to court, it will be interesting to see what comes out regarding ACAM’s motives on this ban, especially when the court learns of ACAM’s long term pattern of attempting to suppress knowledge to its members regarding all oral chelation products (including the FDA approved status of oral EDTA) in favor of IV chelation. Fortunately, my consultant Dr Gordon has extensive records on all this.
I further suspect that this entire subject will be of interest to the CME accreditation board who until now have been lead to believe that ACAM presents a BALANCED VIEW as part of their mandate for providing approved continuing medical EDUCATION!
If ACAM truly wanted to provide balanced continuing medical education to its membership, would they not have accepted Dr Gordon’s offer of February, 1999, to present over 30 years of his knowledge on the subject of keeping his patients alive without relying solely on IV chelation? Wouldn’t Dr. Gordon’s offer to debate with Dr. Janson about the efficacy of oral chelation have been accepted? Such suppression of this potentially life-saving information is untenable.
With all the research that’s surfaced about the ongoing hazard of elevated lead in children, the significantly elevated average lead levels in humans today, and lead’s documented adverse effect on health and IQ, it seems incongruous that ACAM now chooses to hold the position that EDTA is dangerous or not effective if taken orally but safe to take intravenously in large dosages.
The way in which you worded your letter about "ACAM policy" incites me to ask you to supply the WRITTEN policy about which you refer regarding the (non-) use of oral chelation products. Naturally, if we are forced to meet in court, my attorney will obtain all such information relevant to this subject in the act of discovery anyway. Thus, if you do not drop this new policy, in order to minimize your damages to my business and save time, please supply me with copies of any written materials including internal memoranda or memos or correspondence as well as copies of ALL transcripts of all relevant board discussions on the topic of ACAM’s policy on oral chelation products and the DATES that this "policy" was adopted.
There is no fault with an organization establishing policies and patterns conducive to its best interests, however when those "best interests" are not "best" for doctors treating patients or when they are discriminatory, those policies must be called into question. As a case in point, has anyone else been notified in writing to date regarding this policy? Or has any other company been denied the right to have their nutritional products exhibited because they were deemed "oral chelation products"?
Has ACAM given this same written warning to every exhibitor at its shows? For years, many of them have had what can be demonstrated in court to be oral chelators in their product line and on their price list. To be free of any discrimination charges, ACAM must show that it has and is willing to apply this new "policy" evenly across the board! This will mean that the majority of attending exhibitors will have to generate new product literature and price lists just for ACAM shows in a very short period of time!
To be absolutely certain that I do not somehow violate your order, by selling any garlic, amino acids, Vitamin C, or other potential oral chelator, (since there are textbooks showing well established stability constants for so many compounds, which apparently could come under ACAM’s ban on ORAL CHELATING agents), I request that you supply me in writing the definition of oral chelators which are banned from products that are sold at your conference.
If ACAM had treated my company, Dr. Garry Gordon, and its members in an open, honest manner, I would respect your wishes and display only those products, which would be in keeping with the organization’s goals. Unfortunately, the manner in which the organization has veered from its early noble purposes has lost my respect. Thus, rather than succumb to your discrimination, I prefer to fight for my rights as a businessperson and for the rights of the medical practitioner members who is expected (by his patients) to know the truth about all forms of chelation therapy and who needs to know Truth. I have been advised that it is easier to establish the dollar value of my damages based on my historical sales increases following prior conferences to delay any necessary legal action until well after May 9 1999.
I plan to display and market any of my products in Orlando that get through your new litmus test, one of which is Wobenzym. Wobenzym has already spent approximately $50 million on research making it probably the most extensively documented nutrient supplement in your entire Exhibit area. Its parent company, Mucos, of Germany, has already begun additional FDA approved studies this year (on Osteoarthritis and Multiple Myeloma) estimated to cost approximately $5 million. My company is their official representative for the professional market. I trust Dr Gordon and I would not be evicted over their product for it carries valuable and important information for your attendees with regards to the oral treatment of vascular disease.
A major research breakthrough was recently announced by Valentin Fuster, MD PhD., cardiologist from Mt Sinai in NYC, President of the American Heart Association, which demonstrates that heart attacks are strongly related to thrombosis and inflammation. My product, Wobenzym, is the widest selling non-aspirin anti-inflammatory in Europe, used by over 100 million Europeans. Mucos and my company feel strongly that your Physicians’ need to know that Wobenzym is a SAFE well documented, anti-inflammatory without the 20,000+ annual deaths associated with the use of NSAIDs and without the side-effects of aspirin. Besides being a safe anti-inflammatory, Wobenzym simultaneously provides anti-thrombotic, antiviral, fibrinogen lowering, anti-arthritic and probable anti-aging benefits (decreasing TGFB1, auto-antibodies, immune complexes, adhesion molecules etc).
Dr. Gordon believes that although the recent scientific breakthrough regarding vulnerable plaque as the primary cause of vascular related death makes the use of IV EDTA as a primary or single therapy for the prevention of heart attack or stroke less cost-effective, there is still tremendous need for it in longevity medicine. Further, he hopes that as other new, more cost effective approaches become available for the prevention of heart attack and stroke, that ACAM can adapt to this information, just as the vascular surgeons will have to adapt. If not, it will be simply a question of time until another organization will usurp ACAM’s position in the field of alternative medicine.
Further, Dr Gordon thinks this dramatic breakthrough regarding VULNERABLE PLAQUE is vitally important information for your members to learn about, because it clearly establishes the need for DAILY, LONG TERM, SAFE anti-thrombotic and anti-inflammatory protection if they are going to prevent heart attacks. This is exactly why, as my consultant, he has lead me to represent Wobenzyme for the professional market AND to provide at the LOWEST possible COST, the most comprehensive cardiovascular nutritional support formula in existence today, Beyond Chelation. Could it be this low cost that is causing my product to be discriminated against by ACAM? (Please check www.gordonresearch.com for the products ingredients and their well-documented benefits). The combination of these 2 products addresses most of the old as well as the NEWLY defined risk factors leading to heart attack or stroke.
According to Dr Gordon, this new research strongly suggests that most heart attacks that happen in patients before, during or after their IV chelation directly relate to these inflammatory and thrombotic factors, which CLEARLY IV chelation therapy does not adequately address in the months and years after the IV therapy is finished! Again, this information should be brought ACAM physicians, many of whom will see the need to provide such long term preventive therapy for their patients. That is why affordability seemed so important in my bringing these products out and why chelation physicians need to be informed about its existence.
Dr Gordon has been keenly interested in Dr Fusters’ work ever since it first appeared in the special 31 page supplement on Coronary Artery Disease published by Lancet and he has continually attempted to bring ACAM’s attention to this vital information.
It might appear that with Dr. Fusters’ appointment as the President of the American Heart Association, that perhaps Dr Gordon’s judgment regarding the need for SAFE affordable oral long-term anti-thrombotic and anti-inflammatory, anti-oxidant therapy will appear meritorious to whoever is deciding what to do regarding my Beyond Chelation product which, I repeat, in NOT simply an oral chelation issue.
Nothing in Beyond Chelation was ever intended to replace the appropriate use of IV EDTA! This is an effort to recognize new scientific developments and attempt to make this information benefit mankind without the usual 15-year delay seen in standard medicine that so commonly finds new information threatening to their status quo.
As you may be aware, EDTA is on the GRAS list, and is in many foods, because it ties up the transition metals and thus helps diminish the oxidative breakdown of vitamin C and other antioxidants. You also must know that the average person already is receiving an estimated intake of 15 mg to as high as 50 mg of EDTA in their DIET, and that it is in every Lavender tube used for blood tests because of its widely recognized anti-coagulant activity, even if only 4-8 % of our products’ EDTA is absorbed. Beyond Chelation contains MANY useful nutritional compounds and does not rely on EDTA or any Chelating effects for its well-documented benefits.
I look forward to receiving ACAM’s definition of those Chelating ingredients that are outside the bounds of acceptable, non-chelating nutritional products. Maybe the name "Beyond Chelation" is the problem. If so, I am willing to change it, but it seemed that something like "After Chelation" was not a fair name. Because there are now so many proven cardiovascular risk factors that EDTA cannot address, it seems misleading to call the product After Chelation. IV Chelation does what it can, and these products do what they can -- but only through molecular medicine, doing all the tests that we recommend, can the doctor know for certain what is the BEST and most cost-effective combination of therapies for the patient.
Since ACAM claims to be a non-profit professional educational organization, I wonder where independent experts would draw the line regarding intentional suppression of vital information to the ACAM members.
We are talking about patients lives here, not how many doctors will join ACAM to make some money selling IV chelation for heart disease, when clearly IV EDTA is not the most correct or cost effective therapy for many major cardiovascular risk factors including Homocysteine, high fibrinogen, and chronic inflammation. (C-reactive protein is now a required test for competent cardiologists!) I hope that your organization doesn’t become like those traditionally organizations from whose tight restrictive dogmas your forefathers rebelled which called you into being.
I am aware of several companies exhibiting at ACAM that have sold ORAL EDTA containing products some of them for more than 10 years. Unfortunately they are now simply way under powered and badly over priced compared to Beyond Chelation. If they are allowed to continue selling while I am not, my case will be easily won.
You should also advise all exhibitors of your new rules so that none of them try to sell any oral chelators including GARLIC, Chlorella, Alginates, or Vitamin C, or any of the sulfhydryl containing amino acids such as cysteine or methionine containing products, as that will also be discriminatory and unfair to my company. Please also make sure there are NO references to DMPS, DMSA, Penicillamine, or oral EDTA at any of the compounding pharmacists exhibits, as that again would be discriminating against my company. Will your new policy against oral chelators also require that you inform your speakers not to mention any of these oral chelators from the podium?
I hope that because of your educational omissions, your members will not one day be sued for FRAUD for suggesting to patients there is no other safe way to remove heavy metals from the body without using their intravenous therapy --- particularly if they make the mistake of suggesting oral EDTA is fraud, thus ignoring the up to 10 fold increase in urine lead excretion that is published that helped lead to the FDA’s approval of oral EDTA! Do the ACAM members really have to be protected from this dangerous knowledge about oral chelators, the omission of which may place them in professional jeopardy?
Well, I have aired my thoughts. Step one has been completed. I truly hope that the members of your board will stand up for the truth as they may come to know it from this letter and Dr Gordon’s website, where they can read the Newsweek review of Dr Fuster’s work that says the problem in heart attacks and stroke is in the BLOODSTREAM, not the blood vessel! This should make it obvious that something needs to be done long-term, (and probably orally, to be cost-effective) if this war against sudden death from heart attack and stroke is to ever be won.
I hope that the fire that I feel now will kindle a change in ACAM’s paranoid policy regarding anything that may have some oral Chelating activity as a PART of its mechanism of action before the chance for peaceful change has expired. I hope that this letter will bring forth positive ramifications rather than court costs. I hope for ACAM’s continuance in the future as it still has potential that could surpass most of your dreams --- IF it can stand for truth, progress, and the goals for which it was originally established.
I expect a response to this letter in the very near future.
Alexandra Van Cleve
President
AVC:cdu
CC: ACAM Board of Directors
Dr. Garry F. Gordon
Other Potentially ConcernedIndividuals
The following appeared in Newsweek
Last year the American Heart Association reported the good news that the
death rate from heart attack, stroke and other cardiovascular diseases had
dropped 20 percent in the past decade-thanks to advances in research and
remarkable progress in the treatment and prevention of these diseases. Despite
this progress, heart attacks remain the number-one killer of Americans, strokes
the number-three killer. The World Health Organization predicts heart disease
will be the leading cause of death and disability worldwide by the year 2020. Gene Therapy Last year, Dr. Jeffrey Isner and his team at St. Elizabeth's Medical Center
in Boston used gene therapy to grow new blood vessels in the legs of nine
patients to bypass those obstructed by atherosclerosis. The scientists have
since treated 20 more patients, with good results. Even more exciting, they used
this technique to treat 14 men who suffer severe chest pains, called angina,
because the blood vessels feeding their heart are choked due to plaque
obstructions caused by atherosclerosis. All but one experienced a dramatic
decrease in chest pain and required less angina medication. Many have been able
to resume activities, such as swimming, that were impossible before treatment. In this experimental treatment, the researchers surgically inject copies of a
special gene into the patient's heart muscle at the site of the blocked vessel.
The gene "instructs" the heart cells to make a protein called vascular
endothelial growth factor (VEGF). This protein makes new blood vessels grow to
bypass the blockage. Researchers in Germany are using a protein produced by genetic engineering to
grow new blood vessels in the heart. Dr. B. Schumacher and colleagues at the
Fulda Medical Center are injecting a growth factor called FGF-I into the heart
muscle near the blocked coronary artery. In a study involving 20 patients, the
researchers saw evidence that new blood capillaries (tiny, thin-walled blood
vessels) had grown and were delivering more blood to the heart within four days
of treatment. As a result, the patients' hearts grew stronger and were able to
pump more blood to the body. All 20 patients were alive three years after
treatment. At the present time, in a number of institutions in the United States
and Europe, various forms of VEGF and FGF are being delivered via catheter
directly into the coronary arteries without requiring any surgical intervention.
The results of this simple delivery approach will be available within one year. Up to half of all coronary artery bypass surgeries fail. In these surgeries,
portions of veins are surgically inserted to bypass clogged blood vessels to the
heart. Gene therapy shows promise of reducing this failure rate. Drs. Victor
Dzau and Michael Mann at Brigham and Women's Hospital in Boston have developed a
gene therapy technique that may prevent the growth of new cells lining the
inside of these grafted blood vessels. The new cell growth is a fertile ground
for the growth of the plaque obstructions that characterize atherosclerosis. Thus far, the Boston researchers have investigated the gene therapy approach
in preventing the growth of new cells in vessels grafted to bypass obstructed
vessels in the legs of patients. Their next step is to evaluate this approach to
reduce the failure rate of coronary bypass surgeries. Their gene therapy
approach involves soaking the blood vessel prior to grafting with a short
segment of DNA that blocks the genetic machinery needed to form the new cells.
Not all plaques are equal. The most dangerous ones are soft and consist
largely of a pool of cholesterol covered by a thin fibrous cap. The stress of
blood flow can tear the caps and cause a blood clot. These plaques are often
inflamed and the inflammation can further weaken the thin cap. However, the
harder, more stable, calcium-rich plaques can also trigger a stroke or heart
attack by blocking the flow of blood so much that blood pools behind it.
Stagnant blood is more likely to clot. New medical imaging techniques for finding vulnerable plaques-those prone to
rupture and orm a dangerous blood clot-may soon be available. Patients who have
been diagnosed as having vulnerable plaques are treated to reduce the changes
that blood clots can form, if indeed their plaques rupture. My colleagues and I at the Mount Sinai Medical Center found that strokes can
be triggered by soft plaques in the aorta, the main artery in the chest. It was
already known that strokes can result when the carotid arteries-the blood
vessels in the neck that transport blood to the brain-become so large that they
vibrate in the turbulent blood flow. When the turbulence and vibrations become
severe enough, a tear in the artery can occur. That tear can launch a blood clot
to the brain. Our own research has shown that magnetic resonance imaging (MRI)-a diagnostic
technique that can create detailed images of the body without surgery-can
painlessly distinguish the most vulnerable plaques in the aorta. MRI allows us
to see not just the size but also the composition of the plaques. We may soon be
able to do the same for arteries that supply the heart. The great challenge for
looking at coronary arteries with MRI has been to freeze the motion of the
beating heart. We have developed techniques that for the first time have allowed
us to see coronary artery plaques with MRI. Researchers elsewhere are testing other imaging techniques for detecting
vulnerable plaques. For example, Dr. James E. Muller at the University of
Kentucky in Lexington is testing an infrared (heat-seeking) sensing device on
the end of a catheter for analyzing the chemical composition of plaques. The
method is a variant of a technique that NASA scientists used to analyze rocks on
Mars. Understanding Genes, Physical
Exercise and Diet Another common genetically influenced condition that determines how well
individuals respond to a lower-fat diet is called "LDL subclass pattern
B." About one in three adult men and one in five to six postmenopausal
women have this trait. LDL in the blood of people with this trait is transported in small, dense
particles. These people also have elevated blood levels of triglycerides-fats in
the blood that come from food. They also have lower levels of the protective
cholesterol called high-density lipoprotein (HDL), which helps the body get rid
of LDL cholesterol. People with LDL subclass pattern B are at higher risk for
developing diabetes and heart disease. However, patients with pattern B respond
much better to low-fat diets than do patients who have the larger, less dense
LDL particles (pattern A trait). Researchers at the Stanford University School of Medicine recently showed
that a low-fat, low-cholesterol diet failed to lower LDL cholesterol levels in
some men and women with high-risk LDL levels unless they also engaged in regular
aerobic exercise. This finding highlights the importance of combining physical
activity with a low-fat diet in the treatment of elevated LDL cholesterol
levels. Recent animal and human studies have identified genes-called the obesity
genes and the diabetes genes-that are helping us understand the causes of and
possible treatments for obesity. Leptin, a by-product created by one of the
obesity genes, is a hormone that regulates food intake and body weight. A
diabetes gene codes for the protein that forms cell receptors for leptin.
Defects in the production of either protein may lead to a tendency toward weight
gain and obesity. These findings show that obesity-which is a major risk factor for heart
disease, diabetes and other illnesses-often results from an inherited condition
rather than from the patient's lack of willpower. Further research may lead to
effective treatments for preventing and treating obesity. How Low to Go An analysis of recent studies suggests that people who have heart disease
should work with their physician to lower their LDL level to 100 mg/dl. Reducing
it any further will not offer increased protection against heart attacks. Future
studies, however, may show that lower LDL levels might provide increased
benefits for some groups of people. The Role of Inflammation During the inflammatory process, a substance-C-reactive protein-is produced
in the blood. By measuring blood levels of C-reactive protein, researchers now
have an important tool for studying the role of inflammation in heart attacks
and strokes, since the amount of inflammation can be measured by the C-reactive
protein. A study this year by Dr. Paul M. Ridker and colleagues at Brigham and Women's
Hospital showed that measuring C-reactive protein levels can help predict the
risk of heart attack in postmenopausal women. Last year, the researchers showed
that C-reactive protein was an excellent way to gauge the heart attack risk in a
group of middle-aged men. Inflammation can limit the effectiveness of clot-busting drug therapy, which
is the first line of treatment for patients suffering a heart attack. Dr. Agha
W. Haider at Boston's Massachusetts Veterans Research Center and colleagues at
Hammersmith Hospital in London showed that heart attack patients with high
levels of C-reactive protein respond more slowly to treatment with clot-busting
drugs called thrombolytics. The longer that blood flow to the heart muscle is cut off, the greater the
damage to the heart. This study suggests that anti-inflammatory drugs may
improve the effectiveness of anticlotting treatment in patients with high levels
of C-reactive protein. Lives can be saved by Studies done in our laboratory, and in other laboratories, have shown that
high cholesterol levels can cause an inflammatory response in the circulating
blood. People who smoke cigarettes have elevated levels of C-reactive protein.
Having increased inflammation in their blood may one of the reasons smokers are
at a much higher risk of death from heart disease and stroke than nonsmokers.
One the most remarkable findings reported at the American Heart Association's
Scientific Sessions last year was from a University of Minnesota study of nearly
13,000 men in Europe, Japan and the United States. The study followed the men
for 25 years and found that those who smoked fewer than 10 cigarettes a day had
a 30 percent higher risk of death from heart disease or lung cancer than
nonsmokers. Those who smoked 10 or more cigarettes a day had a whopping 80
percent higher incidence of death from these diseases. This is one of the most
convincing studies to date measuring the deadly effects of tobacco. Education Saves Lives The REACT study compared two communities, one of which had been exposed to an
educational campaign about how to identify the first signs of a heart attack.
Although the study was designed to compare the time it took for heart attack
victims to seek emergency care, the researchers found little difference in the
response time between the two communities. It did find that people in the
educated community were much more likely to seek lifesaving care when they had a
heart attack than people in communities with a lower degree of education. This
study shows that teaching people about heart attacks can save lives.™ Dr. Fuster is director of the Cardiovascular Institute at Mount Sinai School
of Medicine, New York, N.Y., and president of the American Heart Association.
by Valentin Fuster, M.D., Ph.D.
Researchers gained insights in 1998 into a powerful new weapon against heart
disease. They are using gene therapy to promote the growth of new blood vessels
to bypass diseased ones in a process called angiogenesis. They have also
evaluated gene therapy as a way to reduce the failure rate of cardiac bypass
surgeries. The results are exciting.
Gene therapy to
grow new blood vessels in the heart. [Courtesy Dr. Jonathan Marmur,
Mount Sinai School of Medicine].
Identifying Vulnerable Plaques
The coronary arteries (blood vessels feeding the heart) of most people develop
some fatty deposits known as plaques. Plaques become a major concern when they
grow large enough to obstruct blood flow to the heart, brain or other organs, or
become fragile and prone to rupture. Plaques that rupture form blood clots that
can break off and clog a vessel that feeds the heart or brain, resulting in a
heart attack or stroke. Over the last few years, we have learned much about how
plaques cause blood clots.
Figure 1 (left):
Magnetic resonance coronary images obtained without any dye injection,
shows a blockage (arrow) in the left coronary artery. Figure 2 (right):
Magnetic resonance images of the aorta which is the main artery that
carries blood from the heart to the body. The high resolution images of
the top portion of the aorta, reveal the makeup of the plaque (arrow)
such as cholesterol deposits, calcium, and blood clots or thrombus (T).
[Courtesy Dr. Zahi A. Fayad, Mount Sinai School of Medicine].
We have begun to unravel the mystery of why some people with
elevated blood cholesterol levels seem to be helped by eating a low-fat diet,
while others do not. For many, the differences appear to be inherited. About one
in seven people in the United States have a gene that makes a variant of the
protein apolioprotein E (apoE), which is a "ferry service" for
transporting fat through the bloodstream. Individuals with this protein tend to
have elevated levels of low-density lipoprotein (LDL, or the "bad
cholesterol") and are at increased risk of developing heart disease. Those
with this gene variant respond well when they consume a low-fat diet. However,
people who have the "normal" gene variant, called apoE3, show much
less reduction in LDL levels when they adhere to a low-fat diet.
Researchers
at the Stanford University School of Medicine recently showed the importance of
combining physical activity with a low-fat diet in the treatment of elevated LDL
cholesterol levels.
There is no longer any question about the health benefits of lowering high
levels of LDL cholesterol through diet, exercise or drug therapy. But how low is
low enough? Can LDL cholesterol be lowered too much?
Evidence accumulated over the past year suggests that inflammation in the
circulating blood may play an important role in triggering heart attacks and
strokes by activating blood-clotting mechanisms, which in turn can slow down or
stop blood flow. Inflammation is the body's natural response to injury and blood
clotting is often part of that response.
educating the public about
the need to seek prompt
emergency care at the
first signs of a heart attack.
Another study conducted at the University of Minnesota showed that lives can be
saved by educating the public about the need to seek prompt emergency care at
the first signs of a heart attack.
Garry F. Gordon., M.D, D.O.,M.D.(H.)
901 Anasazi Road, Payson, Arizona 85541-5858
520-472-9086 Fax 520-474-1297
October 3, 1997
Dr. Terry Chappell
President ACAM
Bluffton, Ohio
Dear Terry,
Thank you for your FAX of 10/1/97. I appreciate the time and thought that went into your response.
In your FAX you stated that in the stack of documents you reviewed on oral EDTA there was very little evidence that it impacts vascular disease, improves clotting, or reduces iron or heavy metal stores already in the body. You admit that such actions could result in reduced free radicals. I am supplying you with articles that clearly document the strong binding capacity of EDTA to copper and iron (Exhibit 1). This is cited as the primary reason that 90 million pounds of this substance are utilized annually, much of it as a food additive.
I am also sending a reference from the Annals of Internal Medicine, Vol. 47, 1957, "Editorial: Chelation," (Exhibit 2) which states on page1037 the well known ascending order of some of the metals of biological interest that are chelated by EDTA. Furthermore, this article states that there are reports showing an effect of EDTA prolonging prothrombin time, citing Am. J. Clin. Path 24: 39, 1954; and J.Lab & Clin Med 42: 550, 1953; and furthermore I enclose "A Comparative Study of the Use of Ferric Chelate in Iron Deficiency Anaemia," C.F. Herridge, British Medical Journal, V. 2, P. 140, July 19, 1958 (Exhibit 1). This last article reports that lowering of the prothrombin activity was found in half of the group, though it was not thought to be of clinical importance at that time.
I personally believe that generally the anti-clotting effect is far more subtle, and probably more of a synergistic influence with other anti-clotting, anti-platelet substances such as garlic, ginkgo, polysaccharides, EPA.
I am also supplying you with 6 references regarding the benefits from oral EDTA, all documenting a lowering of cholesterol. There is one article showing an increase in cholesterol levels but this was only in RATS. (Exhibit 3.) I think the preponderance of favorable evidence regarding cholesterol lowering in humans from ingestion of oral EDTA is clear.
Although the evidence regarding removal of copper was limited to 3 out of 6 cases in Wilson’s Disease and although oral EDTA was not always beneficial in iron overload, the evidence that oral EDTA inhibits the absorption of iron and copper seems overwhelming. Even that beneficial and probably life-extending activity may not be as important as the potential for continuous, economical, and convenient presence of EDTA in body fluids binding copper and iron so tightly that they are largely unavailable for biological activities including catalyzing free radical reactions.
I am enclosing 11 abstracts and 17 portions of published articles regarding the influence EDTA has on iron bioavailability (Exhibit 1), including
"The effect of various ligands on the absorption, distribution, and excretion of iron following oral administration." W. Forth, et al, Arch. Exptl. Pathol. Pharmakol. 252(3), 242-57 (1965) (Ger.) In the presence of EDTA, diminished iron retention appeared to be due to a marked increase in excretion. Furthermore, EDTA-bound iron is poorly utilized by the erythropoietic system.
"Food iron absorption in man; the effect of EDTA on absorption of dietary non-heme iron." Amer. J. of Clin. Nut. 1976: 29(6), 614-620. This study reports a decrease of absorption of non-heme iron of 72% when EDTA is present at a 2:1 molar ratio.
"Effect of orally administered EDTA on iron absorption in man." P. S. Davis et al. Australis Ann. Med. 16(1), 70-4. 1967. EDTA significantly reduces iron absorption when present in a ratio of 10:1 or more.
"The Enhancement of Iron Excretion in Iron-Storage Diseases," W.G. Figueroa. Metal-Binding in Medicine, M.J. Seven, M.D., ed., J.B. Lippincot, Ch. 17 (1960). This study claims that oral EDTA does not increase output of iron in the urine.
"The Effect of the Prolonged Intake of EDTA on the Utilization of Calcium & Iron by the Rat." B.A. Larsen, Can. J. Biochem. Physiol. Vol. 38 (1960) p. 813-817. This author states that EDTA ingestion causes less iron to be absorbed, and more of what is absorbed to be excreted.
"Effect of pH and chelating agents on iron binding by dietary fiber: implications for iron availability." M.J. Leigh, Am J Clinical Nutrition 38: Aug 1983, p 202-213. This article states that all iron research must take into account the level of ascorbic acid. The key end result may be assumed to be due to the great stability of the iron/EDTA complex at all pH levels.
"A comparison of the effect of Fe-3-Specific EDTA on urinary iron excretion in a patient with hemochromatosis." F. Gilbert McMahon, Journal of Lab and Clinical Med., p. 600, October 1956. This reports a two-fold increase in urinary iron excretion from intravenous administration.
"Design of chelates for therapeutic objectives." Martin Rubin, Fed Proc 20(Suppl.10; Pt.2):149-157. Sept 1961, states that EDTA is able to hold iron in the presence of even a specific iron-binding protein (siderophilin) of the plasma. Dr. Rubin states that iron, presented to the cell in the form of an EDTA chelate, is unavailable for incorporation into hemoglobin. This strongly suggests that it is not available to catalyze free radical pathology!
I believe that your concern that oral EDTA might chelate out normal minerals through the GI tract has been more than adequately answered by the 21 abstracts and/or portions of published articles I am submitting that show in fact oral EDTA appears to treat malabsorption problems, and that EDTA is apparently absorbed as the complexes of several minerals (Exhibit 2). In fact there are two rat studies (Exhibit 2) that indicate increased deposition of calcium and phosphorus in the bones following oral EDTA administration. (See Abstracts No. CA55:5762e, Vozar; CA54:25290h, Vozar, both included.) EDTA has been able to virtually substitute for zinc in zinc-deficient animals, and has been shown to enhance the absorption of heparin, Vit. B12, and increase the blood levels of antibiotics in chickens by 100%. Special salts of iron EDTA are being considered for worldwide application because of these well documented studies on EDTA, which is commonly used as a feed additive for animals and thus has been studied extensively.
I agree with you that the effective dose of EDTA in products ought to be at least 500 mg, preferably 800 or more. Researchers calculate the average human is already ingesting 15 to 50 mg in their standard diet.
Your comment that "There is evidence that lead workers taking oral EDTA can reduce the amount absorbed into the body" clearly indicates that ACAM failed to provide you with any of the 88 abstracts and portions of 27 published articles that I am supplying to you at this time (Exhibit 4), which is but a fraction of what Mr. Scharffenberg has collected. These references come from mainstream medicine, and have documented without exception an increase of excretion of lead with oral EDTA of from 3 to 30 times. Virtually every one of these articles describes significant lead lowering benefits from the oral ingestion of EDTA.
There may be some relative contraindications to the use of oral EDTA in the case of an acutely lead poisoned person unless the intestinal tract is emptied with something like an enema, as per the review article "Lead Poisoning, Review of the literature and report on 45 cases." R.K. Byers, Children’s Hosp., Boston, Harvard Med. School, Pediatrics 23: 585-603 March 1959. It apparently enhances lead absorption from the gut so it would seem rather obvious that good medicine requires that, whenever possible, you first remove patients from all known sources of lead for maximum effectiveness.
The issue regarding the absorption of lead from the intestinal tract has been studied in some depth. "Effects of calcium sodium ethylenediamin-etetra-acetate on the kinetics of distribution and excretion of lead in the rat," N. Castel-lino and S. Aloj, Brit.J. Indust. Med., 1965, 22, 172, reviewed this issue and concluded that oral administration of calcium EDTA caused a great increase of urinary lead excretion without modifying its intestinal absorption. They reported that approximately 18% of orally ingested lead was absorbed by rats whether they were treated with EDTA or not.
The main problem that led to the loss of favor of oral EDTA around 1960 was the AMA’s strong concern regarding the potential for abuse by industrial physicians who would use the tablets instead of improving the working conditions. Now that it is well documented that all of us provably have adverse health effects because of the levels found in everyone today, and since there is no safe level and these adverse effects have been documented at every measurable level, the widespread employment of nontoxic and inexpensive therapies for removing lead must take on greater importance. Oral EDTA must be evaluated versus penicillamine and DMSA, both of which are far more expensive and clearly more toxic.
Since the dangers of low level lead toxicity are supposedly known by all ACAM members, then they should also know how to facilitate removal of lead with the use of natural therapies including Vit. C., garlic, zinc, and calcium. Oral EDTA is a vitally important additional method of increasing lead removal from the body. These natural adjunctive deleading therapies provide significant protection to patients because, for example, by aggressively administering zinc, any potential for zinc deficiency associated with oral EDTA therapy is entirely avoided. These recommendations, therefore, should help to mitigate any of the criticisms ever leveled at oral EDTA, such as the fear of mutagenesis if zinc is allowed to become deficient. Just as we chose to point out where the early researchers with intravenous EDTA had erred, and we were able to overcome their errors successfully through such cautions as mineral replacement.
I have indicated to you that if ACAM chooses to persist in pretending
that there is inadequate documentation regarding the benefits from the oral ingestion of EDTA after you have reviewed the extensive materials I am supplying you here, after it was in the PDR for 20 years, approved years ago by FDA for lead poisoning, and has been used widely throughout the world, that I will find it necessary to resign.
I believe there is legitimate confusion regarding the therapeutic potential of oral EDTA in vascular disease, which I can agree is not yet solidly established. However, it would seem likely that if we look at stability constants, EDTA certainly prevents excess iron absorption and, depending on other factors such as pH, etc., it is really chelating iron out of the body as the literature indicates. The published stability constants clearly indicate that oral EDTA would decrease the circulating levels of free iron and copper because they are now bound to EDTA and not therefore biologically available to catalyze free radical reactions. While these actions may be considered by some to be theoretical, the removal of lead from the oral ingestion of EDTA cannot be considered as anything other than established FACT!
In order for ACAM to again meet our ethical responsibilities to the public
and to our members, I believe they need to openly state that oral EDTA effectively lowers lead levels in humans. Members may want to review the literature for themselves to learn why it is so commonly added to our food, and what researchers believe is its mechanism of action in preserving foods. Once this is understood it will become clear that since it is extremely cheap and safe when taking adequate mineral replacement, the benefit-risk ratio of including it with other known metal chelator/anti-platelet substances such as garlic makes total sense.
Further, I believe it is unethical and irresponsible to fail to advise our physician members about the effectiveness of oral EDTA with a clear statement from the academy, or at least from our scientific committee. Without that action I fear that many members will continue to tell patients that oral EDTA supplements are a waste of time, thereby dangerously misinforming patients since all studies clearly show the dangers of gradually accumulating levels of toxic metals such as lead and cadmium in tissues, especially in the brain (particularly the pituitary gland) with aging, and oral EDTA clearly can help to prevent and possibly even reverse this problem.
You may recall that ACAM gave medical researcher Richard Scharffenberg a very short time, (less than 3 months!) and an entirely inadequate budget to begin to research the oral EDTA issue. ACAM’s decision not to permit him to complete the task did not endear the academy to Mr. Scharffenberg; but as I have remained friends with him I still get some updates. Presently, an outside party has commissioned Scharffenberg to do the job that I asked ACAM to pursue. Since his work product belongs to someone else, I am not able to supply ACAM with more than a fraction of what has been located by Mr. Scharffenberg. ACAM can certainly get all of these published articles from someone else, and I again urge ACAM to get its own complete file on EDTA.
I fear that our EDTA "war" is not over, even when we settle with the FTC. For example, the Federal Health Office in Germany published the article "Implications of Heavy Metal Toxicity Related to EDTA Exposure" (H.H. Dieter, Toxicological and Environmental Chemistry, Vol 27, pp. 91-95, 1990). (Exhibit 5.) This article sounded the alarm that EDTA is building up in all surface waters at an alarming rate. And although there is extensive documentation regarding its usefulness and safety, there is new research regarding nephrotoxicity from accumulated cadmium after chronic low-level exposure of an EDTA/cadmium complex that forms in surface water and potentially may accumulate in renal tubular cells. The German health office has published more on this subject, emphasizing their concerns in subsequent medical literature.
I am sending you an article regarding cadmium toxicity documenting that this theoretical danger can be avoided when the dose of EDTA is higher than the amount of cadmium. (See "Effects of Chelation Agents on Oral Uptake and Renal Deposition and Excretion of Cadmium," Brigitta Engstrom, National Institute of Environmental Medicine, Stockholm, Environmental Health Perspectives, Vol. 54, pp. 219-232, l984.) (Exhibit 6.) The Engstrom article clearly shows increased body elimination and decreased acute toxicity. Note: It is only very low intakes of EDTA in combination with cadmium that produce this theoretical risk.
I believe that the current FTC problem would be better handled if ACAM really had a well organized, complete file of the world’s chelation literature; meaning you get every reference from every reference, and you even get things translated as needed. Also please remember, Martin Rubin still has in his possession scientific information regarding EDTA from ACAM that is not available anywhere else.
I am giving you some references from my slide outline, which I have shown around the world (Exhibit 7). I can’t understand how anyone questioning the effectiveness of oral EDTA in lead toxicity who then fully reviews these references can deny this useful application of oral EDTA to the public. I see such denial as no different from mainstream physicians who, because of their vested self-interest, choose to dismiss anything we publish re EDTA and vascular disease.
I have copied all of one article just to give you some flavor of the type of references contained in all of them. (Morgan, South Med J., Vol 68, No.8.)
(See Ref. Nos. 10,12, 13, Brit J Ind. Med and Arch of Indust. Health.) All of these references need to be obtained in order to do a comprehensive search of the literature.
I am sending you 7 articles regarding the influence of various diseases on the absorption of EDTA (Exhibit 8). The proven increased intestinal absorption of chromium EDTA with various diseases makes the oral route all the more effective in sicker patients who are PROVEN to absorb a higher percentage of EDTA (probably up to the 18% level published elsewhere).
For years, a common method of taking 3 gm of oral calcium EDTA was in grapefruit juice. Current interest in the drug interactions with grapefruit juice are still inconclusive as to how all of these effects are generated, so it is possible that there was some hidden benefit from this approach to oral EDTA administration.
Ward Dean, MD, has been actively studying oral EDTA and wrote about it in the August and Sept. 1997 issues of Nutrition News (Exhibit 9). In April 1997 I gave an interview to Life Enhancement News where I stated that the mechanism of action of oral EDTA will NEVER replace intravenous EDTA; it merely complements it. Additionally I’m enclosing a copy of my article "Oral chelation with EDTA," from the 1986 issue of the Journal of Holistic Medicine, Vo. 8 Nos. 1 & 2. (Exhibit 10.)
The incomplete copies of oral EDTA-related literature described herein that I am sending you under separate cover represent a mere fraction of the resource references that I have, which is a small portion of the more than 400 articles regarding oral EDTA that Richard Scharffenberg has gone on to collect.
With my own extensive clinical experience as Medical Director of the largest alternative medicine clinic in California, and as Medical Director of Mineralab where I routinely dealt with an international clientele and saw first hand the effectiveness of oral EDTA combined with other natural chelators such as garlic in heavy metal cases, supported by the VOLUME of papers I have reviewed regarding its effectiveness in lead toxicity, it is clear to me that it is urgent for ACAM to set aside any political and economic fears it may have and provide this important information to its members.
If ACAM decides to inform their membership that there is such substantial evidence that the benefit-risk ratio of using oral calcium disodium EDTA in cases of low level lead exposure is virtually beyond question, I believe our member physicians will be motivated to further study the entire issue of oral calcium EDTA. There are so many other potential benefits that they need to become aware of.
For instance, it appears that by binding free copper and iron there may be significant improvement with some of the newer markers of free-radical damage, such as provided by Genox Labs in Baltimore (Exhibit 11), (from Richard Cutler, Ph.D. who did 18 years research with Natl. Institutes of Aging and is a recognized expert on aging; who in his introduction to the use of his tests clearly advocates the use of food additives that bind copper and/or iron).
If ACAM members are denied this kind of information because some members fear a loss of revenue it would be a big mistake, because the fact is that this information properly applied would increase their revenue because their patients live longer, so they keep coming back.
I have sent you many articles regarding the use of EDTA in food (Exhibit 12), and how it not only enhances the uptake of several essential nutrients from vitamin B12, heparin and essential minerals, but also has a synergistic effect with certain nutrients such as polysaccharides (which I have studied intensively since I worked with Lester Morrison, M.D., who spent more than $10 million developing a synergistic formula based initially on tracheal cartilage rings, later going to other sources of polysaccharides, which he documented, would reverse arteriosclerosis and protect from myocardial infarction etc.) When we added EDTA to his formula, the effective dose required to prevent blood clotting in the standard Chandler loop test employed in his research was substantially reduced. My knowledge of this research combined with the incredibly low mortality rate I experienced in my practice has made me extremely optimistic regarding the benefits of what I consider to be a total oral chelation approach, which finally involved the use of more than 70 different synergistically combined nutrients. (AMNI-OC PAK) Morrison’s formula alone showed a better than 70% reduction in second heart attack rate. (Morrison, Lester M., M.D., and Schjeide, O. Arne, Ph.D. Coronary Heart Disease and the Mucopolysaccharides (Glyco-saminoglycans). (1974) Charles C. Thomas, Publisher. 2600 S. First Street, Springfield, Illinois 62717. ISBN 0-398-02903-2. Morrison, Lester M., M.D., and Schjeide, Ole A. Ph.D. Arteriosclerosis. Prevention, Treatment, and Regression. (1984) Charles C. Thomas, Publisher. 2600 S. First Street, Springfield, Illinois 62717. ISBN 0-398-04919-X. Morrison, Lester M., M.D., with Nugent, Nancy. Dr. Morrison’s Heart-Saver Program. (1982) St. Martin’s Press, 175 Fifth Avenue, New York, N.Y. 10010. ISBN 0-312-21481-2.)
It seems unlikely to me that since EDTA has been documented
to be an effective food preservative that prevents oxidative damage
to food by free metals, and has FDA approval to be added to our diet
at levels of 25-800 mg, that ACAM could effectively argue that its physician members shouldn’t be fully informed regarding every potential use of this molecule that our organization has championed all these years.
Interestingly, since we became aware of the negative articles in the literature regarding the use of EDTA for vascular disease, we were able to overcome these objections through our careful review of all the relevant literature. There are strong similarities to the story regarding the effectiveness of oral EDTA in heavy metal toxicity.
In the final analysis, there are so many publications supporting the effectiveness of oral EDTA alone in treating lead toxicity, that for ACAM not to support this is WORSE than mainstream medicine ignoring our claims of effectiveness with intravenous chelation, because supposedly our members believe they are experts in the use of EDTA.
It is unfortunate that ACAM has ignored my advice to have ALL published articles at its fingertips as well as someone who knows the subject inside and out so we can better defend it, our organization, and its members, when we predictably are attacked.
If our academy believes that EDTA is nontoxic enough to inject intra-venously into our patients, then they must believe that it is virtually nontoxic. The fact that it prevents the copper catalyzed oxidation of Vit. C should make ACAM interested in seeing that all of our patients get this remarkably inexpensive compound included in our oral supplement programs. (See H.L. Aamoth et al, Annals, N. Y. Acad. of Sci., V. 88, 1960.) (Exhibit 12.)
Included in the literature I am sending you is documentation (7 articles, Exhibit 8)) that the sicker the patient, the more likely the leaky bowel will supply even greater absorption of the oral EDTA. The proven ability of EDTA to chelate with metals such as copper and iron so they are completely inactivated and cannot react as metal ions, holds some interesting prospects for future life extension research; leading experts in aging research continue to believe that these metals catalyze free radicals, to our great detriment.
In any event, without proven harm, it is baffling how ACAM can fail to support something that lowers the levels of toxic metals while enhancing the uptake of essential nutrients, while CLEARLY enhancing Vit. C antioxidant properties.
In 1959 F. Bersworth and Martin Rubin got a patent for the prophylactic use of Ca EDTA, to be blended with food products, to PREVENT metal poisoning. Today, with our food supply so challenged, this idea appears quite rational. We know that EDTA protects against many toxic metals including nickel, cadmium (as long as dose is high enough), vanadium (which some research links to diabetes), cobalt, iron, and copper overload. EDTA has also been shown to help lower the body burden of internally deposited fission products (U.S. Atomic Energy Commission) . In fact, a rat study showed significant protection against the toxicity of cisplatin.
I have included substantial documentation (15 articles, Exhibit 13) regarding long term safety which, after careful review, cannot be considered a significant issue. (See "The Metabolism of EDTA, Food and Cosmetic Toxicology." British Industrial Biological Research, "Safety evaluation studies of calcium EDTA." Bernard L. Oser et al, Food and Drug Research Labs. Toxicol. Appl. Pharmacol. 5, 142-162, 1963. Also, Toxicological Profile, Current Use, and Regulatory Issues on EDTA compounds for assessing use of Sodium Iron EDTA for food fortification; Paul Whittaker et al, Center for food safety, FDA, Washington D.C. Regulatory Toxicology and Pharmacology 18, 419-427 (1993))
The complex issue regarding iron balance is covered in Fd. Cosmet. Toxicol. Vol 2 pp. 741-750. Pergamon Press (1964) which shows that iron absorption is apparently only decreased when positive iron balance exists.
It is interesting that many experts in anti-aging are convinced that lowering the levels of iron in our bodies should increase life span; and the studies I have included show that oral EDTA prevents absorption of iron (UNLESS you are deficient).
It is also interesting that although ACAM is well aware of how I feel about oral EDTA, I am never invited to address the membership to let them make up their own minds. I have never even been invited to sit on a Hot Seat Panel!
With the documentation I am supplying you herewith, I insist that it is unprofessional conduct for any ACAM physician who is supposed to know all about the adverse health effects associated with increased levels of lead, to tell ANYONE that taking oral EDTA is like throwing money down the drain, or any words to that effect. Any statement that would cause a patient to stop talking a garlic/EDTA chelation product in this day and age of known virtually universal heavy metal toxicity affecting the health of every one of us, has to constitute unprofessional conduct. I sincerely believe such statements are doing irreparable harm if the patient listens and stops receiving the protection.
Even if the physician chooses not to believe in the effectiveness of EDTA, refusal to accept the extensively documented benefits of garlic, not only as a heavy metal chelator but also for its documented protection against organic toxins including food dyes etc. and its known anti-platelet and anti-cancer and cholesterol-lowering activities, would seem to be a wanton disregard of their patient’s best interests.
I am sending you just a few pages from Scharffenberg’s printout of more than 400 references as Exhibit No. 14. This should make it clear how inadequate ACAM’s submission to you of oral EDTA articles was.
Exhibit 15 discusses benefits from EDTA in epilepsy, porphyria, and psoriasis. There are many additional and interesting references like this that ACAM members should finally have information about.
Thank you for your attention and reviewing this lengthy document. I know that you will personally see that this request is honored. Thank you again for your FAX explaining that the issue regarding oral EDTA may be beginning to adversely affecting my professional standing.
Sincerely,
Garry F. Gordon
EXHIBIT LIST
Exhibit No. Description
1 Iron and EDTA
2 Enhanced absorption of useful nutrients and detoxification of heavy metals including vanadium and fissionable materials
3 Benefits of oral EDTA on cholesterol metabolism
4 115 references showing positive benefits with oral EDTA in lead toxicity
5 H.H. Dieter. German Federal Health Office concerns re EDTA accumulating in the environment
6 Oral EDTA removed by cadmium as long as molar ratio achieved, i.e., adequate dosage
7 Dr. Gordon’s slide presentation re lead removal with oral EDTA
8 Enhanced intestinal absorption of essential nutrients including Vit. B12, zinc, cobalt, heparin, and synergy with polysaccharides
9 Ward Dean article in Nutrition News, Vol. 11 No. 9, Sept. 1997
10 Garry Gordon interview in Life Enhancement Magazine, No. 32, April 1997, "Chelation with EDTA…"
11 Genox Laboratory literature (Dir., Richard Cutler, Ph.D.) suggesting benefits in their free radical marker tests with food additives that combine with iron and/or copper
12 Articles re usefulness of EDTA in the food supply to prevent food spoilage and protect ascorbic acid from oxidation
13 Research articles re safety of EDTA
14 Small portion of more than 400 references regarding oral EDTA organized by Richard Scharffenberg
15 Miscellaneous uses of EDTA
Gordon Research Institute
901 Anasazi Road, Payson, AZ 85541-5858
Phone, 520/472-9086 Fax, 520/474-1297
E-mail, dr
Garry F. Gordon, President
Oral Chelation debated:
Dear ACAM Board of Directors, Friends, and Colleagues:
An ACAM member, Dr. William S. Eidelman, became interested in several comments I had put on the Gordon Research.com website while it was still under construction. As the information was interesting to him, he commented favorably on it to me and also decided that Dr. Michael Janson should be made aware of it.
I believe that Dr. Janson responded to the information in a hurried manner, making statements about my interest in oral chelation which need to be put in proper context. I initially had put most of this information together for Dr. Terry Chappell in 1997. I believed that ACAM should make its members fully informed regarding the published research that exists showing the benefits of oral EDTA, including significantly increased excretion of lead in children.
After all, oral EDTA was a drug approved by the FDA for many years and can still be found by looking at older PDR books.
I had asked ACAM to make the entire package that I turned over to Dr. Terry Chappell available to the ACAM membership for a fee, however my request was refused. I am now in the process of putting copies of these published articles on my website so they can be reviewed by all interested parties. I believe that since commercial interests will attempt to exploit our years of efforts with EDTA, either by overstating its benefits or by making improper formulations, every ACAM health professional should be fully informed regarding what oral EDTA can and can not do.
With this objective in mind (and to try to set the record straight about oral EDTA), I have taken the liberty of attaching a copy of my original letter to Dr. Chappell along with a revised version which will be easier for the public to reference and digest. The information on EDTA now appearing on my website consists of this edited version of that 1997 letter. (If you are unable to open the Windows attachment holding these documents, please Email me and I will see that you receive them by another means.)
I believe that it is essential to the integrity of ACAM that its members do not mislead their patients regarding oral chelation by claiming that it has NO potential benefits. New information regarding vulnerable plaque should cause every ACAM doctor to review and perhaps revise their approach for the long term prevention of heart attacks and strokes to include anti-inflammatory, anti-thrombotic, anti-oxidant, and other specific targeted activities that IV chelation alone clearly can NOT accomplish in the months and years following treatment.
Even the single article published in JAMA on February 3rd citing a 55% decrease in heart attacks with just the single use of an effective antibiotic in a three year period should illustrate the enormous changes made in our understanding of vascular disease and motivate us to continually reevaluate the entire chelation issue, focusing on the real goal: keeping our patients alive.
For the following four reasons, am I now formally requesting the opportunity to debate Dr. Janson at the next ACAM conference on the subject of Oral EDTA:
1.) Because I consider it important for these new discoveries to be presented to the ACAM membership;
2.) Because I have been studying oral chelation intensively for many years and have a wealth of information to present and draw from;
3.) Because I believe our members MUST be fully informed about any cost-effective ORAL approach (whether it be to lower their patients’ total body burdens of heavy metals or to increase the effectiveness of a cardiovascular support program);
4.) And because Dr. Janson and I appear to have a significant difference of opinion regarding the use, or even the safety, of ORAL EDTA.
Such a debate would allow the ACAM membership to hear the pros and cons of oral EDTA supplementation, increase membership interest and attendance, and have a win-win result for both ACAM and its members.
On a different train of thought, I had suggested to Dr. Janson that InCALM have a combined meeting with ACAM in the fall. To date I have not heard from Dr. Janson whether there is enough interest on the part of ACAM for me to attempt to finalize the arrangements with the InCALM membership.
In conclusion, I eagerly await your comments about my website, your decision about my proposed debate with Dr. Janson, and about the possibility of a joint InCALM-ACAM meeting in the fall.
Sincerely,
Garry F. Gordon, M.D.
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