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Juli 9, 2014

diam2suka: terap1 khela$1 @ aterosklerosis … kah (090714)

Filed under: Medicine — bumi2009fans @ 2:04 pm

What is chelation therapy?

Chelation therapy is a chemical process in which a synthetic solution—EDTA (ethylenediaminetetraacetic acid)—is injected into the bloodstream to remove heavy metals and/or minerals from the body. Chelation means “to grab” or “to bind.” When EDTA is injected into the veins, it “grabs” heavy metals and minerals such as lead, mercury, copper, iron, arsenic, aluminum, and calcium and removes them from the body. Except as a treatment for lead poisoning, chelation therapy is controversial and unproved.

Chelation therapy is performed on an outpatient basis.

What is chelation therapy used for?

Chelation is a very effective way to treat heavy-metal poisoning. The U.S. Food and Drug Administration (FDA) has approved prescription chelation therapy for the treatment of lead poisoning. Injected EDTA binds with the harmful metal and both are then eliminated from the body through the kidneys.

Some health professionals have also used chelation therapy to treat atherosclerosis and/or coronary artery disease, although there is not enough scientific evidence to prove that this treatment is effective. Some people believe that EDTA binds with calcium deposits (the part of plaque that obstructs the flow of blood to the heart) in the arteries, and then EDTA “cleans out” the calcium deposits from the arteries, reducing the risk of heart problems. Research results have been inconsistent.

Some health professionals also suspect that EDTA may act as an antioxidant by removing metals that combine with LDL cholesterol, which can damage arteries. The theory is that when you remove metals that flow freely through arteries (such as copper or calcium), you may slow down diseases such as atherosclerosis. Research has not proved this theory. Some experts believe that EDTA could remove calcium from healthy bones, muscles, and other tissues, as well as from diseased arteries.

Many people report less pain from chronic inflammatory diseases such as arthritis, lupus, and scleroderma after chelation therapy. The theory is that EDTA acts as an antioxidant, which protects the body from inflammation and protects blood vessels. Again, this idea has not been proved by scientific research.
Is chelation therapy safe?

Children, pregnant women, and people who have heart or kidney failure should not have chelation therapy at any dose.

Many years ago, chelation therapy was given in high doses and may have been linked to kidney damage, irregular heartbeats, and other serious consequences. Even when this treatment is given in

low doses, some negative effects may occur, including high blood pressure, headache, rash, low blood sugar, and/or thrombophlebitis.

EDTA may remove vital minerals from the body along with the toxic metals. Vitamins and minerals are added to the EDTA solution to help keep them at an optimal level in the body to maintain health.

Always tell your doctor if you are using an alternative therapy or if you are thinking about combining an alternative therapy with your conventional medical treatment. It may not be safe to forgo your conventional medical treatment and rely only on an alternative therapy.

If EDTA Chelation Therapy is so Good, Why Is It Not More Widely Accepted?

1 Votes / Pilihlah

Written by James P. Carter, MD, DrPH

When he wrote this original article Dr. Carter was Professor and Head, Nutrition Section, Tulane University School of Public Health and Tropical Medicine, New Orleans, Louisiana.

Reprinted from the Journal of Advancement in Medicine, Volume 2, Numbers 1/2, Spring/Summer 1989, pages 213-226.

ABSTRACT: A summary of the medical politics, turf struggles between medical specialties and factions in the health care professions, and the medical economics of EDTA chelation therapy is described in detail to answer the question, “If EDTA chelation therapy is so good, why is it not more widely accepted?”

Most people, including physicians, are not aware of the medical politics, legal machinations and economic sanctions that covertly control the practice of medicine in the United States. A physician who introduces an innovative and nontraditional type of therapy often becomes the target of those forces. That is especially true if a new therapy, like EDTA chelation: 1) involves a major shift in the scientific paradigm; 2) if acceptance of the new therapy somehow implies that currently used medical practices are inappropriate; or 3) if the new therapy threatens the financial well being of a politically powerful and well established branch of the medical profession. Quite the opposite occurred with the immediate and widespread acceptance of bypass surgery and balloon angioplasty, which quickly brought wealth and fame to surgeons, cardiologists, large teams of health care professionals, and the hospital industry.

When a radical new therapy like chelation is first introduced, physicians who do not utilize that therapy feel threatened, both professionally and financially. Their professional integrity is threatened by obsolescence of their scientific knowledge and they lose patients who seek out the new therapy. They forget that if their established treatments were really successful, and without major disadvantages, patients would not look to another type of treatment.

As with EDTA chelation therapy, major pressures are brought to bear on the “deviant” physician to coerce him back into the accepted mold. He is ostracized by his peers; he comes under professional attack for “lack of ethics;” his medical and mental competence are questioned; he is accused of “exploiting” his patients for personal gain; and epithets of “quack” and “charlatan” are hurled his way. Ad hominum attacks are common, in the absence of more cogent and scientific criticisms.

Well known historical examples of that phenomenon occurred with the introduction of the germ theory of disease. That simple concept took 50 years for complete acceptance by the medical profession.

Lister was viciously attacked when he proposed that wound infections were not inevitable after surgery if aseptic techniques were used. Semmelweis was likewise dealt with when he urged doctors to wash their hands before delivering babies to prevent maternal deaths from puerperal sepsis. Lister’s recommendations were not accepted by mainstream medicine for many decades, and Semmelwels was persecuted to his death by medical colleagues, who were incensed by the notion that they themselves transmitted disease from patient to patient on their unwashed hands. Has human nature changed since that time?

The history of medicine is replete with examples of medical “heretics” who were eventually credited with major advances. They were often not recognized for their achievements until after death. Paracelsus, for example, is exalted as one of the great pioneers in medicine, but he was the original “quack” in his own time. Paracelsus introduced the use of mercury to treat syphilis. There was no other cure for syphilis at the time, although, as with many treatments today, the lethal dose of mercury was close to the therapeutic dose. Paracelsus was viciously attacked by his medical peers and derisively called a “quack” (short for “quacksalber,” the old German word for mercury).

Inertia in science and medicine is a powerful force and is reinforced by major economic and legal forces in the United States. Many industries and special interest groups that are politically and economically powerful would be hurt financially if chelation therapy were to become more widely accepted. Those same industries have a major influence in our society at all levels. Grants for university and medical school research often stem from those same sources. They spend heavily to lobby for laws, regulations and government funded medical research to favor their own interests and to suppress competition. It is difficult to obtain NIH research funds in the face of opposition from powerful lobbies when that research goes against those special interests.

Those same special interests have a major influence on lay and professional exposure through the news media. Advertising revenues are essential to the survival of medical journals, newspapers, magazines, television and radio. Even with freedom of the press, the media cannot survive without advertising revenues. There often exists an understandable reluctance to bite the hand that feeds them. It is difficult to educate the public and the medical profession about new developments without media cooperation. Medical schools also cannot afford to offend their corporate sources of research funds.

The welfare of the American public is often pushed aside by the industrial quest for profits and pressures to suppress competition. Every industry wants a monopoly, if that can be achieved. Mainstream medicine has come very close to that goal.

Scientific arrogance is commonplace. Physicians consider themselves to be experts in their own field. If a majority of physicians do not endorse a new therapy, they collectively rely on public recognition of their own “expertise” to discount a new concept that they themselves have not yet embraced. They forget that all great advances in medicine began with a small minority. Their thinking tends to follow along these lines: “If I’m the expert and I don’t use this new therapy and if my many colleagues and peers are experts and they don’t believe in the new therapy, then we must be right and that small group of physicians who believe differently must be wrong. We’re the experts.”

The most frequent criticism leveled by critics of non-traditional and alternative medical therapies is that new treatments are “unproven” because randomized, double-blind, controlled studies have not yet been done to prove effectiveness. Those criticisms ignore the fact that most medical procedures routinely performed in the practice of medicine are also unproven using those same criteria.

The Office of Technology Assessment, a branch of the United States Congress, with the help of an advisory board of eminent university faculty, has published a report with the conclusion that, ” . . . only 10 to 20 percent of all procedures currently used in medical practice have been shown to be efficacious by controlled trial.” Therefore, 80% to 90% of medical procedures routinely performed are unproven.(1) That report further points out that research which purports to prove effectiveness of the remaining 10% to 20% of medical procedures is largely flawed, and ” . . many of the other procedures may not be efficacious.” The most frequent reason for not accepting the value of EDTA chelation therapy reflects a flagrant double standard.

A complete program of chelation therapy involves dietary changes, away from highly refined and processed foods. The use of nonprescription nutritional supplements is emphasized, more than expensive and highly profitable drugs, patented and marketed by the pharmaceutical industry. Chelation therapy is performed in doctors’ offices, without the need for hospitals, surgeons, cardiologists and the large team of health professionals who profit greatly in dollars and reputation from the $6 billion per year bypass surgery and balloon angioplasty industry.

For obvious reasons, double-blind studies have never been done to prove or disprove clinical benefits from bypass surgery or balloon angioplasty. The effectiveness of EDTA chelation therapy has been clinically proven to the same extent as bypass surgery and angioplasty, or more so, as established in data from the clinical studies published in the TEXTBOOK OF EDTA CHELATION THERAPY.

Recent reports conclude that from 44% to 85% of coronary artery bypass surgery is routinely performed on patients who do not meet the criteria for benefit, even using standards derived from non-blinded studies.(2-9) The media consistently makes light of such flagrant abuses of surgery, while widely publicizing any hint of “quackery” associated with chelation. The American Medical Association, in its official journal (JAMA), admits that at least 44% of all coronary artery bypass surgery is done for inappropriate reasons.(9)

When a therapy is widely accepted by the medical profession, no scientific proof of effectiveness is required, and anecdotal evidence is accepted as valid. If an alternative therapy is contested by those physicians, however, they attack by demanding that the therapy in question be subjected to very expensive and time-consuming double-blinded, placebo controlled trials costing tens of millions of dollars to meet FDA requirements. Medicare regulations also exclude the need for scientific proof for treatments that are utilized by a majority of physicians. The federal government thereby adds support to this double standard.

In the case of EDTA, those demands ignore the fact that it would normally cost many millions of dollars for double-blind studies to prove effectiveness, and public funding for medical research cannot be obtained without political support. Without patent protection, pharmaceutical manufacturers will likewise not fund that research. The cost and time required for research of that scope is also beyond the resources of the clinicians in private practice who utilize chelation therapy. EDTA chelation therapy has therefore been an “orphan” without a source of financial support for research.

Despite those drawbacks, even in the face of a severe and unjust double standard imposed by opponents, research money has been successfully obtained from private foundations and from patients and physicians who believe in this treatment. Patients have been accepted into double-blind studies, beginning in mid-1988 [those studies were not completed for political reasons].

Deprived of reimbursement by medical insurance, patients have thus far paid for EDTA chelation therapy entirely from their own pockets. If Medicare refuses to pay for a therapy, most other insurance companies follow suit. It costs far more to fight those unjust policies in court than to pay for the treatment.

Historical examples of similar campaigns to control the practice of medicine, in favor of organized medicine and other special interests, against the public interest, are easy to find. As many innovative physicians have discovered, one of the quickest ways to become the target of opposing forces is to utilize nutritional or other nontoxic and noninvasive treatments for cancer.

On August 3, 1953, Charles W. Tobey Jr., son of the late Senator Charles Tobey, Chairman of the Senate Interstate and Foreign Commerce Committee, entered into the Congressional Record a report of an investigation by Benedict F. Fitzgerald Jr., Special Counsel to the Committee on Interstate and Foreign Commerce. Fitzgerald’s investigation was directed at an alleged conspiracy to suppress what, in the 1950s, would have been considered alternative methods of treating cancer. His findings could equally have been applied to other innovative and nontraditional methods of treating any disease.

Fitzgerald criticized those who supported the party line of the American Medical Association (AMA), and who applied themselves to efforts to hinder, suppress, and restrict the free use of new therapies. Those therapies included medicines that were supported by evidence of success from clinical records, case histories, pathological reports, and x-ray and other photographic proof, together with living testimony of former cancer victims. Fitzgerald concluded that a conspiracy existed, and that public and private funds had been “thrown round like confetti at a country fair” to shut down clinics, hospitals and research laboratories which did not conform to the AMA’s viewpoint.

Investigation tactics used against emerging and nontraditional medical therapies show a consistent pattern of: 1) arrogance; 2) a sense of mission and of knowing what is best and right for other people; 3) depriving citizens of their constitutionally protected rights to freedom of choice; and, 4) acceptance of the concept that the end justifies the means. Opponents of nontraditional therapies have viewed as legitimate activities: disinformation, smear campaigns, harassment, instituting IRS tax audits, encouraging patients to sue physicians, entrapment, illegal wiretaps, and possibly even break-ins. These tactics have been used against physicians for nothing more serious than administering intravenous EDTA chelation therapy.

When evidence, real or fabricated, is uncovered which is unfavorable to the targeted physician, a representative of the opposition will contact the state board of medical examiners, asking for an official investigation and prosecution. Pressures are brought on the physician to cease and desist his aberrant practices or lose his license to practice medicine.

Investigations and proceedings of licensing boards are often confidential and not available, even to the physician under investigation. By definition, it is difficult for an outsider to learn all of the specifics of such covert tactics, although a good approximation of how these things work has gradually emerged over the years.

The power structure of organized medicine may be visualized as a pyramid, with the sides composed of different physician specialty associations, each with its own special interests to protect. The result may be collectively called “organized medicine.” The apex of the pyramid represents the governing boards and officers of those groups, while the base represents the broad general membership. Local and state chapters centralize the power and influence from the base upward to the national level. This pyramidal structure in medical politics forms the basis for a conspiracy that operates in coalition with other groups to benefit the individuals who compose the core of the pyramid. Although the composite organizations draw authority to sanction their collective actions from individual members, those members are often unaware of the larger structure within which power brokers and medical politicians operate.

By representing almost every practicing physician and specialty group in the country, this coalition has enormous influence in the affairs of our nation. That is especially true when an alliance is formed between organized medicine, the pharmaceutical industry and food processing corporations. The food industry profits greatly from sales of margarine [trans fats], unsaturated fats, fake eggs, and other refined and fractionated foods with the endorsement of physicians.

The AMA and other segments of organized medicine are second only to the National Rifle Association in political campaign contributions to senators and congressmen at the national level. They give more than any other special interest groups in the country. Through political influence, bought and paid for, the policies of public institutions and federal and state agencies can be influenced by this group, including medical schools and universities, HHS [DHEW], PHS, FDA, FTC, NIH, state medical licensing boards, etc. When a physician is selected for censure by organized medicine, the FDA, FBI, IRS, postal inspectors, district attorneys, Antifraud Division of Medicare and other agencies with quasi-police powers are quick to join the fray. This has occurred to physicians who have had the courage to offer EDTA chelation therapy to their patients.

An average of approximately 60% of all state medical licensing boards’ time is spent confronting, rehabilitating or defrocking physicians who are impaired or otherwise incompetent. Most of those are chemically dependent on alcohol and drugs. Increasingly, addicted physicians are being successfully rehabilitated, with the help of medical societies and recovered physicians. That function is truly in the best interests of both the medical profession and the consumer.

The remaining 40% of state medical licensing boards’ time is, on the average, spent “witch-hunting,” in the manner described above, in an effort to control the practice of medicine. The result is to force conformance with majority practices and to protect the medical profession against financial competition from “maverick” physicians who are bold enough to espouse innovative practices ahead of their peers. Restraint of trade and government support of a medical monopoly is the bottom line.

All too often, academic physicians on medical school faculties and research scientists allow themselves to be influenced by propaganda and disinformation, instead of obtaining the true facts and relying on their own analytical abilities and scientific methodology to determine the truth. The overwhelming majority of physicians in clinical practice appear to be totally unaware that a conspiracy exists and that covert activities are routinely taking place to protect their monopoly and to prevent competition.

The AMA Coordinating Conference on Health Information (CCHI) was formed in 1964, as an offshoot of the AMA’s Committee on Quackery.(10) All responsible citizens, by definition, must be opposed to quackery. The main difference between the AMA Committee on Quackery and the newly formed CCHI was that the CCHI was a totally secret and covert organization which functioned in coalition in a network with other, similar groups. The CCHI operates in partnership with the National Council on Health Fraud with regional chapters in many states. The director of each regional chapter must swear to an oath of secrecy. National and regional chapters of the Council on Health Fraud stay in communication with individual members of each state’s board of medical licensing examiners. The CCHI operates through this secretive network, without access from public scrutiny. There are no checks and balances.

Both the CCHI and the National Council on Health Fraud purport to be scientific and authoritative sources of information. A significant portion of their activities, however, have nothing to do with real quackery, but are rather a means to coerce practitioners of medicine to adhere to practices approved by medical politicians. The end result is to preserve certain monopolistic and economic advantages enjoyed by organized medicine.

An important reason that research into the use of EDTA in the treatment of atherosclerosis and its complications stopped after 1960, until the mid 1980s, was because of an active and vicious campaign of misinformation and unjust harassment of physicians who used EDTA in their practices. Scientific researchers who showed an interest were also discouraged and harassed.

Practicing physicians who used EDTA have been summoned to appear before state boards of medical examiners to answer complaints. Charges were often contrived and rarely documented by careful investigation. The Federation of State Boards of Medical Examiners is associated with the CCHI network. State boards of medical examiners are legally constituted bodies that have ultimate authority to revoke a physician’s license to practice medicine. Medical licensing boards in at least six states have attempted to mandate a blanket prohibition against chelation therapy within their states. Fortunately, the courts have been quick to nullify most such arbitrary rulings.

EDTA was already on the market as a legitimate pharmaceutical agent to treat lead toxicity, digitalis toxicity and acute hypercalcemia. EDTA is legally available for physician use, and it is quite legal for any licensed physician to utilize a drug for any purpose which, in that physician’s judgment, is best for his patient. The only restriction is that pharmaceutical companies [and compounding pharmacies] that manufacture EDTA cannot make advertising and marketing claims of effectiveness in the treatment of atherosclerosis, in the absence of FDA approval for that indication.

The patent on EDTA expired many years ago. It is now a generic drug. Any drug company can manufacture and sell EDTA. There is no longer any patent protection to allow recovery of research, development and licensing costs. It customarily costs a drug company tens of millions of dollars for research and paperwork to satisfy FDA requirements for the addition of a new therapeutic claim to the package insert of an established drug such as EDTA. No company will spend the money without the ability to recover those costs in the marketplace. This lack of FDA approval for atherosclerosis is commonly used against physicians by opponents of chelation, although it has always been a fully accepted and common practice for doctors to use medicines for diseases not yet approved for marketing claims by the FDA. This is another blatant example of double standard.

A communication from Dr. John Parks Trowbridge, a physician using chelation therapy in Texas, dated August 1986, illustrates very succinctly the difficulties physicians have encountered when they offer chelation therapy to their patients. The following illustrates how the system of repression often works:

“In the last 90 days, at least 3 chelating physicians have been hauled before the Texas licensing board—1 lost license, 2 threatened. We’ve been put ‘on notice,’ through one who was threatened, that they were going to ‘get’ each of us, one by one.”

Such legal harassment can bankrupt a doctor in order to pay the legal fees to defend himself against ongoing attacks by legally constituted agencies. Due process is a constitutional right but can be very expensive. The state pays its attorneys and legal costs with public funds. An unjustly accused physician must defend himself at his own expense. That is the basis for a tactic used by state licensing boards to keep up the pressure until a targeted doctor can no longer afford to pay for his defense. At that point, more than one highly competent and ethical physician has submitted to injustice and agreed to stop using EDTA chelation therapy in his practice, accepting probation and censure, just to end the mounting legal expenses and other stresses of harassment.

The original motivation to discredit EDTA as a treatment for atherosclerosis may have stemmed from ignorance of its benefit and arrogance in the belief that EDTA was dangerous treatment and that it did not work. The motivation may have once been to weed out fraud and quackery. With the development of enormously profitable coronary artery bypass surgery and angioplasty, however, not to mention peripheral and carotid artery surgery, it is obvious that many influential groups in organized medicine and the hospital industry would suffer greatly if EDTA chelation therapy, administered in physicians’ offices at approximately 10% of the cost, became widely accepted. That now seems to be the most significant reason for ongoing attempts to suppress the practice and clinical investigation of EDTA chelation therapy. What other explanation could there be in the face of the large body of clinical and scientific data in support of EDTA chelation therapy?

In recent years, mainstream medical journals have refused to publish the results of research supporting EDTA chelation therapy for atherosclerosis, while at the same time publishing many frivolous letters to the editor and editorial comments criticizing chelation therapy [as well as flawed studies deceptively alleging to disprove benefit]. This ongoing editorial bias and censorship have largely prevented ready access by interested clinicians and, researchers to favorable clinical data. Most literature searches begin and end with the Index Medicus or its electronic counterpart, the MEDLINE computer database. Recent studies of chelation therapy have been published in less widely circulated journals, many of which are not included in the Index Medicus.

Most physicians and medical students are not aware that only 10% of the world’s total biomedical literature [in all languages] can be found in those databases.(11) If a physician becomes interested enough to do a computer search of EDTA chelation therapy for treatment of atherosclerosis, he will find a plethora of negative editorial comment and propaganda, but no negative data to support that criticism. Most clinical data to support the effectiveness of EDTA in treatment of atherosclerosis has appeared in journals that are not listed in easily accessible references. [The most pertinent of that data is summarized on this website and republished in A TEXTBOOK ON EDTA CHELATION THERAPY.]

The first randomized, double-blind, controlled study of EDTA chelation therapy for treatment of atherosclerosis was conducted by Professor Doctor Schettler, et al, in the clinics of the University Hospital in Heidelberg, West Germany, while Dr. Schettler was Chairman of the Department of Internal Medicine and President of the International Atherosclerosis Research Association. That study was funded by Thiemann Pharmaceutical Company, manufacturers of the platelet inhibitor, bencyclan, marketed as Fludilat®. Fludilat® is widely prescribed in Europe to treat atherosclerosis. EDTA chelation therapy was compared with bencyclan.

It is unknown why a pharmaceutical company would fund a study of a generic drug for which the patent had expired. It is possible that Thiemann believed AMA propaganda stating that EDTA was ineffective. Why else would Thiemann put EDTA up against their own Fludilatl®?

Thiemann did take precautions, however. When the grant was awarded, Thiemann reserved the right, in its written contract with Schettler, to edit any published reports of the study. Thiemann reserved the right to interpret the final data for publication and to do the statistical analysis themselves. All recorded data from the study were to be the property of Thiemann. It was agreed that all data would be given to Thiemann at the end of the study. Such a contract seems to eliminate the possibility of an unbiased report, and it eliminates free access to the original data by other investigators.

A total of approximately 48 patients were treated, 24 in the Fludilat® group and 24 in the EDTA group. Disodium EDTA was administered in a dose of 2.5 gms in 500 ml 1/2N Saline. Treatments were given five days each week for a total of four weeks. Each patient received 20 infusions. Only patients with peripheral vascular disease who could not walk 200 meters without pain of claudication were included in the study. Pain-free walking distance was measured before, during and after therapy on a treadmill, at 3.5 km/hr with a 10% uphill gradient.

The measured results showed a 250% increase in distance walked before onset of claudication pain in the EDTA-treated group after four weeks of therapy. By comparison, there was only a 60% increase in the bencyclan group. Bencyclan, however, is a drug proven to be of benefit in this disease and is widely prescribed in Europe for that indication.

There were four patients in the EDTA group who experienced more than a 1,000-meter increase in their pain-free walking distance at the end of only 30 days treatment. Highly favorable data from those four patients mysteriously disappeared when the final results were made public. Thiemann, of course, had a legal right under terms of their contract to edit the final results and to interpret the data in any way that suited them. Their final report contained data that reduced observed benefit from EDTA by 72%, from 250% increase to only 70%. The fact that data from the best EDTA responders were altered would not have been known if scientists from Heidelberg with intimate knowledge of the study had not been shocked by what they considered unethical and dishonest scientific conduct. Raw data from the study were personally delivered to an official of ACAM for an independent interpretation.

The fact that a highly placed representative of American organized medicine went to Heidelberg and met with Dr. Schettler while the study was in progress may or may not be significant.

The study was reported at the Seventh Atherosclerosis Congress in Melbourne, Australia, 1985. An attachment to the abstract of that presentation, available at the meeting, contained a graphic plot of pain-free walking distance extending out to three months after the end of therapy. By that time, even using the modified data made public, the increase in pain-free walking distance in the EDTA-treated patients had increased to 430% of the baseline, while bencyclan-treated patients averaged less than half that much with no significant improvement after therapy was stopped at 30 days. Nothing in the text of the abstract described that graphically depicted observation, despite its great clinical significance in proving the effectiveness of EDTA chelation therapy. The report analyzed data only to the end of 30 days, when the bencyclan and EDTA groups had responded equally. It is well known that full benefit from EDTA is often delayed for up to three months after therapy. (12,13)

When deleted data from the EDTA subjects with maximum relief of symptoms is considered, average walking distance increased by more than 400% three months following EDTA chelation therapy.

The data reported in Australia show only a 70% average increase in pain-free walking distance in the EDTA-treated group (instead of the 250% increase at 30 days indicated by the raw data) and was compared with a 76% average increase in the group treated with bencyclan. Even that amount of improvement is significant. It is rare for placebo effect alone to exceed 33%.

The only patient death was in the bencyclan group. No serious side effects were observed from EDTA. The reportedly negative results of this study received widespread coverage in the news media, but the data were never published in a peer-reviewed journal. Furthermore, the press release stated that “EDTA was no better than a placebo,” without mentioning that the “placebo” in this case was Thiemann Pharmaceutical’s very own Fludilat®, a proven effective drug.

By way of comparison, in the study which resulted in U. S. FDA approval of pentoxifylline (Trental®), for the treatment of claudication, walking distance before pain of claudication increased by only an average 25% over baseline with treatment. Nonetheless, that small amount of improvement was considered statistically significant and Trental® was approved for marketing by the FDA. EDTA was more than twice as effective, even using the publicly announced results of the Heidelberg study.

The intensity of the attitudes and the arrogance that has lead to a conspiracy of this enormity will ultimately be responsible for its exposure and eventual downfall. It might be argued by some that such a strategy was justified as a means of eliminating widespread quackery. But who is to decide what is quackery, and who is to give a self appointed group of physicians with vested interests in competing therapies the right to assume that they alone know what constitutes quackery and what is in the public’s best interest?

With 800,000 people per year dying in the United States alone from atherosclerosis and its complications, despite the best of high-technology hospital and surgical care that is available, it is imperative that the public be given the option to receive EDTA chelation therapy. It would be senseless and even criminal for medical insurance companies to continue to deny payment for a therapy which has the potential to greatly reduce long-term medical expenditures by reducing the need for far more expensive hospitalization, surgery or angioplasty. Savings to medical insurance companies with resulting reduction in insurance premiums could be great.

A physician signatory to the Constitution of the United States of America, Dr. Benjamin Rush, wrote:

“The Constitution of the Republic should make special provisions for medical freedom as well as religious freedom. To restrict the art of healing to one class of men and deny equal privileges to others will constitute the Bastille of medical science. All such laws are un-American and despotic.”

The chiropractic profession was the first to feel the sting of the CCHI. On August 28, 1987, Federal District Judge Susan Getzendanner ruled that the AMA led an effort to destroy the chiropractic profession by engaging in “systematic, long-term wrong-doing with the long-term intent to destroy a licensed profession.” That was also the ruling in an anti-trust lawsuit filed in 1976.

The “conspiracy” described in this chapter cannot be dismissed and called paranoid or a figment of someone’s imagination. Chiropractic physicians were not the only target. With ample funding from membership dues, enormous real estate holdings, and advertising revenues from their many publications, supplemented by contributions to the Council(s) on Health Fraud by the pharmaceutical industry, food processing companies, and others, the AMA and organized medicine has led efforts to discredit EDTA chelation therapy and nearly every other therapy that is less invasive, less toxic, nutritionally oriented or more natural, when such treatments have competed directly with mainstream physicians for patients and health care dollars.

It is hoped that this information, together with results of research now underway, will eventually cause the medical profession and victims of atherosclerosis to become more open-minded and receptive to the benefits of EDTA chelation therapy.

References:

Assessing the Efficacy and Safety of Medical Technologies. Washington, DC, Congress of the United States, Office of Technology Assessment, Publication No. 052003-00593-0. Government Printing Office, Washington, DC, 20402, 1978.
Preston TA: Marketing an operation: Coronary artery bypass surgery. J Holistic Med 1985;7(1):8-15.
Luchi RJ, Scott SM, Deupree RH, et al: Comparison of medical and surgical treatment for unstable angina pectoris. N Engl J Med 1987;316(16):977-984.
Cass Principal Investigators and Their Associates: Coronary artery surgery study (CASS): A randomized trial of coronary artery bypass surgery. Circulation 1983; 68(5):951-960.
Cass Principal Investigators and Their Associates: Myocardial infarction and mortality in the coronary artery surgery study (CASS) randomized trial. N Engl J Med 1984;310(12):750-758.
Glagov S, Weisenberg E, Zarins CK, et al: Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 1987;316(22):1371-1375.
Paulin S: Assessing the severity of coronary lesions with angiography. N Engl J Med 1987;316(22):1405-1407.
Cashin LW, Sanmarco ME, Nessim SA, Blankenhorn DH: Accelerated progression of atherosclerosis in coronary vessels with minimal lesions that are bypassed. N Engl J Med 1984;311(13):824-828.
Winslow CM, Kosecoff JB, Chassin M, et al: The appropriateness of performing coronary artery bypass surgery. JAMA 1988;260:505-509.
Lisa PJ: The Great Medical Monopoly Wars, International Institute of Natural Health Sciences, Inc., Huntington Beach, California, 1986.
Cranton EM: Limitations of the Index Medicus and Medline computer program. J Holistic Med 1982;4(2):103-104.
Diehm C, Wilhelm C, Poeschl J. Effects of EDTA-Chelation Therapy in Patients with Peripheral Vascular Fisease–A Double-Blind Study. An unpublished study performed by the Department of Internal Medicine, University of Heidelberg, Heidelberg, Germany in 1985. Presented as a paper before the International Symposium of Atherosclerosis, Melbourne, Australia, October 14, 1985.
Diehm C. Zeit Deutsch Herzstiftung. Vol 10, July 1986

Breakthroughs in Atherosclerosis Treatment
New research may lead to new drugs for heart disease.

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By Katherine Kam
WebMD the Magazine – Feature
Reviewed by Brunilda Nazario, MD

In the battle against atherosclerosis, the stakes remain high. Scientists have made exciting medical advances, but the disease persists as a leading cause of illness and death in the United States. This year alone, atherosclerosis will contribute to about 1.2 million heart attacks among Americans.

“While we have very good therapies and tests to identify the disease and predict the risk, none of them is perfect,” says Stephen Nicholls, MBBS (bachelor of medicine/surgery), PhD, clinical director of The Cleveland Clinic Center for Cardiovascular Diagnostics and Prevention. “We need better tools and better therapies to have a greater effect on preventing heart disease.” Scientists are striving continually to improve their understanding of how atherosclerosis develops as well as the role of risk factors. Researchers hope that, as a result, new therapies will emerge.

Atherosclerosis involves inflammation and buildup of fatty plaques, or atheromas, within vessel walls, which eventually lead to the hardening and narrowing of the arteries. When an atheroma ruptures, a blood clot can form to trigger a heart attack or stroke.

Because development of atherosclerosis in the body is a complex process, researchers are laboring on many fronts to find new ways to understand and treat this serious disease.

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New drugs for heart disease

Statin drugs, first on the market in 1987, offered a breakthrough in atherosclerosis by working to lower LDL “bad” cholesterol and raise HDL “good” cholesterol. Scientists are now testing other potential therapies — for example, novel ways to increase levels of protective HDL or new drugs that target the inflammation in artery walls.

One area of intense interest: boosting HDL cholesterol’s role as an ally against heart disease, Nicholls says. However, the failure and increased mortality rates of one HDL-raising trial drug, torcetrapib, in 2006 highlights the challenges of discovering the right therapy. “It has raised concerns that maybe it’s not raising the right kinds of HDL,” Nicholls says. While doctors agree all forms of LDL are bad, “HDL is a much more complicated story,” he says. HDL is called the “good cholesterol,” but in truth, HDL particles vary in size and composition, and “we don’t know if all forms of HDL are good,” Nicholls says.
Anti-inflammatories for the heart

Still, researchers are cautiously hopeful because other experiments continue to show promise, he adds, including one in which researchers infused HDL preparations into people who had the disease and found that atherosclerosis regressed in artery walls in as little as four or five weeks. “I think that there’s clear evidence that if you directly give HDL, it’s a good thing,” Nicholls says. “But the complexity of HDL is that it may be that not all forms of HDL are protective. For that reason, it’s going to be about finding the right therapy that raises the right kind of HDL and has the best chance at reducing cardiac risk.”

The role of HDL-cholesterol in preventing atherosclerotic disease

Philip Barter*

+ Author Affiliations

The Heart Research Institute, 145 Missenden Road, Camperdown, Sydney 2050, Australia

*Corresponding author. Tel: +61 2 95503560; fax: +61 2 95503302. E-mail address: p.barter@hri.org.au

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Abstract

The cholesterol required by peripheral tissues, including vascular cells, is provided both by new synthesis in the cells and by a delivery from low-density lipoproteins (LDLs). When the level of LDLs is high, they accumulate in the artery wall where they are oxidized and taken up by foam cells in a process that leads to the development and progression of atherosclerosis. High-density lipoproteins (HDLs) oppose atherosclerosis directly, by removing cholesterol from foam cells, by inhibiting the oxidation of LDLs, and by limiting the inflammatory processes that underlie atherosclerosis. HDLs also have antithrombotic properties. Thus, HDL-cholesterol interrupts the process of atherogenesis at several key stages.
Key words

HDL-cholesterol
Atherosclerosis
Inflammation
Cardiovascular risk
Dyslipidaemia

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Introduction

Cardiovascular disease remains the world’s leading cause of death, with age-standardized annual cardiovascular death rates ranging from about 60/100 000 in Japan to 700–800/100 000 in Russia and the former Soviet Republics.1 Preventing atherosclerosis holds the key to reduce the burden of cardiovascular disease, and a detailed understanding of the pathophysiology of atherosclerotic disease will facilitate the design of innovative therapeutic strategies for the management of dyslipidaemia and the prevention of morbid cardiovascular events.

The relative contributions of individual lipoproteins to overall cardiovascular risk have been intensively studied over the last several decades. The role of LDLs in causing atherosclerosis is well known. It is also well known that HDLs protect against the disease. For example, as long ago as 1976, the Framingham study showed that depressed levels of HDL-cholesterol were significantly and independently associated with an increased risk of coronary death,2 a finding confirmed by further analyses based on longer follow-up.3,4 Further, cohort studies have strengthened the association between low HDL-cholesterol and adverse coronary5 and cerebrovascular6 outcomes. Recent studies have shown that low HDL-cholesterol is common in the insulin-resistant states, such as the metabolic syndrome and type 2 diabetes, and may account for a substantial portion of the excess cardiovascular disease observed in patients with these conditions.7

It is important to understand the complex and multifactorial ways in which HDLs protect the vasculature. This review provides an overview of plasma lipoproteins and atherosclerosis with particular reference to the role of HDLs.
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Overview of lipid metabolism
Normal metabolism

The liver secretes very low-density lipoproteins (VLDLs) that are rich in triglyceride and relatively poor in cholesterol (Figure 1). The endothelial enzyme, lipoprotein lipase, converts much of the triglycerides in VLDLs to free fatty acids, which are used by peripheral tissues as an energy source. As a result, the VLDL particle is converted first to an intermediate-density lipoprotein and then to an LDL particle. LDLs (the main cholesterol carrier in blood) are cholesterol-rich and triglyceride-poor when compared with VLDLs. LDLs deliver cholesterol to peripheral tissues, where it contributes to the synthesis and maintenance of cell membranes.
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Figure 1 Overview of lipoprotein metabolism with special reference to the role of HDL-cholesterol. FC, free (unesterified) cholesterol; CE, cholesterol ester; TG, triglyceride; FFA, free fatty acids; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; LPL, lipoprotein lipase. Reproduced with permission from Barter PJ, Brewer HB Jr, Chapman MJ et al.11

Most extrahepatic cells (with the exception of those synthesizing steroid hormones) are unable to metabolize cholesterol, which would therefore accumulate if supply exceeded demand. HDLs are the principal means by which excess cholesterol is removed from extrahepatic cells. The major apolipoprotein (apo) of HDLs, apoA-I, is secreted from the liver in a lipid-poor form. Once in plasma, it rapidly acquires lipids to be converted into an HDL particle via several mechanisms. The initial reaction is with a membrane transporter termed the ATP binding cassette transporter A-1 (ABCA1).8 This mediates the transfer of phospholipids and some unesterified cholesterol from the peripheral cell to generate a nascent, disc-shaped HDL particle. This HDL disc then acquires further unesterified cholesterol from other plasma lipoproteins and from cell membranes. ApoA-I-mediated activation of the enzyme, lecithin cholesterol acyltransferase (LCAT), results in the esterification of the free cholesterol to form a spheroidal HDL particle containing a core of cholesterol ester.9 In addition, apoA-I-containing particles may fuse with apo-A-II-containing particles to form spherical HDLs containing both apolipoproteins.

HDL particles dispose of their load of cholesterol either by returning it directly to the liver via the scavenger receptor SR-B1 for excretion in bile or for recycling,10 or by indirectly transferring it to the VLDL/LDL fraction in a process mediated by cholesteryl ester transfer protein (CETP). The cholesterol transferred to other lipoproteins by CETP may then be delivered to the tissues (including the liver) by the LDL-receptor. This CETP-mediated transfer of cholesterol from HDLs to the VLDL/LDL fraction may be pro-atherogenic by delivering cholesterol from the protective HDLs to the pro-atherogenic VLDL/LDL particles. The effects of pharmacologic inhibition of CETP are currently under clinical investigation,11 although treatments based on this mechanism will not be available for several years.

The complexity of these interactions renders HDL particles highly heterogeneous in their shape, size, and surface charge. Most of the HDL particles in the circulation are spherical in shape and have a surface charge producing alpha migration.
Insulin resistance and atherosclerosis

Lipolysis in fat cells is normally effectively suppressed by insulin in the fed state. In insulin-resistant individuals, lipolysis persists despite post-prandial increases in circulating insulin concentrations, leading to an increased release of free fatty acids. A proportion of these free fatty acids is transported to the liver, where they promote an increased synthesis of triglycerides, an increased production of the triglyceride-rich VLDLs, and an increase in the secretion of these particles into the plasma. The increased pool of VLDLs provides a larger pool of acceptors of the cholesterol transferred from both HDLs and LDLs into VLDLs. This transfer is accompanied by a reciprocal transfer of triglyceride into LDLs and HDLs, which therefore become enriched in triglyceride. Hydrolysis of the triglyceride in LDLs and HDLs by hepatic lipase reduces their particle size and generates small, dense LDLs and small, dense HDLs. Small, dense LDLs are especially prone to oxidation and thus more likely to be taken up by macrophages in the artery wall, leading to further progression of the atherosclerotic plaque.
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Pathophysiology of atherogenesis

Atherosclerosis is an inflammatory disorder that may be initiated by several factors. One of the most important factor is LDLs. LDLs enter the artery wall from plasma. They may also return to the plasma. However, if the plasma level of LDLs exceeds a threshold, they enter the artery faster than they can be removed and thus accumulate. When they accumulate, they become modified, including being oxidized. The modified LDLs then stimulate endothelial cells to express a protein, monocyte chemotactic protein-1 (MCP-1), that attracts monocytes from the blood into the artery wall. The modified LDLs also promote the differentiation of monocytes into macrophages. Macrophages, in turn, express scavenger receptors to take up the modified LDLs, resulting in the formation of lipid-filled foam cells, the hallmark cells of atherosclerosis. Macrophages express a range of cytokines, including tumour necrosis factor-alpha (TNF-α) and interleukin-1, both of which activate endothelial cells to express the adhesion molecules, E-selectin, VCAM-1, and ICAM-1. These adhesion proteins bind plasma monocytes to the endothelium where they are then attracted into the artery wall by MCP-1. Thus, the entry of LDLs into the artery wall begins a cycle that both commences atherosclerosis but also leads to its progression. Figure 2 shows the role of LDLs in these early stages of atherosclerosis. It also shows the points at which HDLs oppose this process (described subsequently).
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Figure 2 Principal steps in early atherogenesis. Stages opposed by HDL-cholesterol are shown in white text on a black background. Reproduced with permission from Barter PJ, Nicholls S, Rye KA et al. Antiinflammatory properties of HDL. Circ Res 2004;95:764–772.
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Anti-atherogenic properties of HDL-cholesterol

Removal of excess lipids from the vascular wall by HDL-cholesterol is a key anti-atherogenic mechanism of HDL-cholesterol, as described earlier. However, atherogenesis is more than a straightforward over-supply of cholesterol to vascular cells, and several other important mechanisms are involved. These are shown schematically in Figure 2, and the involvement of HDLs in inhibiting these processes is described as follows.
Inhibition of monocyte adhesion

Endogenous,12 purified,13,14 or reconstituted HDLs,15,16 or HDL-associated lysosphingolipids (sphingosylphosphorylcholine or lysosulfatide),17 have been shown to inhibit the expression of E-selectin or other adhesion molecules by vascular endothelial cells exposed to cytokines. The results of one of these studies,15 in which human vascular endothelial cells were exposed to TNFα in the presence and absence of a reconstituted HDLs, are shown in Figure 3. The TNFα-induced increase in the expression of both E-selectin and VCAM-1 was powerfully inhibited by exposure to HDLs.
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Figure 3 Inhibition of TNFα-induced expression of the endothelial adhesion molecules, VCAM-1, and E-selectin by a reconstituted form of HDL-cholesterol. Drawn from data presented by Clay MA, Pyle DH, Rye KA et al.15

This reduced expression of adhesion molecules has also been shown to result in decreased binding of inflammatory cells, which is consistent with functional inhibition of atherosclerosis.16 Further, supportive evidence for these anti-atherogenic mechanisms of HDLs is available from clinical studies, in which increased levels of adhesion molecules correlated with low HDL-cholesterol levels.18–20 Interruption of a signalling pathway involving generation of sphingosine-1-phosphate by sphingosine kinase has been proposed as a mechanism for the beneficial effects of HDL-cholesterol on the expression of adhesion molecules.21 Sphingosine-1-phosphate is involved in mediating endothelial activation and adhesion molecule expression in response to certain cytokines.

C-reactive protein is a marker of systemic inflammation but may also play a more direct role in mediating inflammation during atherogenesis. The influence of both native human HDL and a reconstituted apoA-I-containing version on C-reactive protein-induced expression of adhesion molecules was evaluated in cultured human vascular endothelial cells in vitro.22 Physiological concentrations of native HDLs and low concentrations of the reconstituted HDLs effectively abolished the increased expression of E-selectin, ICAM-1, and VCAM-1 (Figure 4). These effects appeared to arise via a novel mechanism distinct from those previously described, by which HDLs inhibit the expression of adhesion molecules by cytokines.
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Figure 4 Native human HDL-cholesterol and apoA-I-containing reconstituted HDL-cholesterol inhibit the increase in E-selectin expression induced by C-reactive protein. Per cent inhibitions were calculated from mean levels of expression of E-selectin before and after exposure to HDL-cholesterol and/or C-reactive protein (mean expression after stimulation by C-reactive protein=100%). Drawn from data presented by Wadham C, Albanese N, Roberts J et al.22
Inhibition of LDL-cholesterol oxidation and MCP-1 expression

Oxidized LDLs are a potent inducer of MCP-1 expression within the developing atherosclerotic plaque. HDLs contain an enzyme, paraoxonase, which is believed to confer protection against oxidation of LDL-cholesterol in the artery wall. HDLs with and without paraoxonase were incubated with an endothelial cell line in the presence of LDL-cholesterol.23 The paraoxonase-containing HDLs significantly protected LDL-cholesterol from oxidation and inhibited expression of MCP-1, whereas the paraoxonase-deficient species were without effect on either parameter.

Co-cultures of human arterial endothelial cells with smooth muscle cells provide a useful model for evaluating the effects of HDL-cholesterol on monocyte recruitment. One study, involving incubation of such a co-culture with lipoproteins and human serum, showed that LDL-cholesterol induced a marked increase in the expression of MCP-1, and a seven-fold increase in the rate of migration of monocytes into the sub-endothelial space of the co-culture.24 Addition of purified human HDLs to the LDLs reduced the rate of monocyte infiltration by ∼90%.

Similarly, potentially beneficial effects of HDL-cholesterol have been demonstrated in human subjects. A study in women evaluated the relationships between the plasma lipid profile and expression of the CCR2 receptor, which mediates the binding of monocytes to the MCP-1 receptor.25 In women with low LDL-cholesterol, variations in HDL levels had little effect on CCR2 expression. However, in a subset of patients with high LDL-cholesterol, low HDL-cholesterol was significantly associated with increased CCR2 expression (Figure 5). There was a significant inverse correlation between HDL-cholesterol levels and CCR2 expression in women with high LDL-cholesterol (r=−0.62, P=0.028). Treatment of women who had isolated low cholesterol with oestrogen improved both the LDL-cholesterol/HDL-cholesterol ratio and approximately halved CCR2 expression.
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Figure 5 Relationship between levels of HDL-cholesterol and expression of the CCR2 receptor, which recognizes the MCP-1, in women with low and high LDL-cholesterol. *Significantly different from other groups (P<0.05, Mann–Whitney U test). Drawn from data presented by Han KH, Han KO, Green SR et al.25
Antithrombotic properties of HDL-cholesterol

The final event in the evolution of a myocardial infarction or stroke is the generation of an occlusive intra-arterial thrombus. Thus, agents that reduce the coagulability of the blood, either through improved fibrinolysis or through reduced platelet aggregation, may prevent or delay a cardiovascular event. The fibrinolytic capacity of the blood is determined by the balance of activities of tissue plasminogen activator, which normally removes intravascular fibrin and its endogenous inhibitor, plasminogen activator inhibitor-1 (PAI-1). Elevated PAI-1 is often part of the cluster of metabolic risk factors associated with the metabolic syndrome, as is low HDL-cholesterol. It is perhaps not surprising, therefore, that low HDL-cholesterol has been shown to correlate with elevated PAI-1 in humans.26

A further observational study in 60 hypercholesterolaemic men showed that both levels of fibrinogen and an index of platelet aggregability were significantly associated with reduced levels of the anti-atherogenic HDL sub-fraction-2 (HDL2).27 Moreover, platelet aggregability was significantly associated with low HDL2 on multivariate analysis. A study in 132 men without history of cardiovascular disease confirmed the relationship between HDL2-cholesterol concentration and fibrinogen levels.28 The level of HDL2-cholesterol, but not that of total HDL-cholesterol or HDL3-cholesterol, was significantly lower in men with the highest quartile of fibrinogen compared with the other three quartiles. Triglycerides and VLDL-cholesterol were also significantly associated with fibrinogen levels.
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Conclusions

Mounting clinical and experimental evidence shows that HDLs exert multiple anti-atherogenic and anti-thrombotic effects that together are consistent with a marked reduction in the risk of a morbid cardiovascular event. Indeed, the epidemiological, clinical, and experimental evidence supporting an anti-atherogenic role for HDL-cholesterol is now overwhelming. These findings support the use of therapeutic strategies to counter the common finding of low HDL-cholesterol in patients with dyslipidaemia.
5 Ways to Raise Your HDL Cholesterol

Some diet and lifestyle changes help boost HDL cholesterol levels:

Get active. Physical activity can boost your HDL level. Get at least 30 minutes a day of moderate activity, most days of the week.
Lose extra weight. If you’re overweight, losing extra pounds can help raise your HDL levels, as well as cut your LDL (“bad”) cholesterol levels.
Choose better fats. The healthier choices are monounsaturated and polyunsaturated fats. You’ll find these in plants, nuts, and fish like salmon or tuna. And, like everything you eat, keep your portion sizes small. Fats pack a lot of calories in small amounts.
Alcohol in moderation. Drinking moderate amounts of alcohol is linked to higher HDL levels. If you don’t drink now, check with your doctor before you start, since alcohol has some risks not related to cholesterol.
Stop smoking. Kicking the cigarette habit can raise your HDL level.

The Importance of Vitamin D for Normalizing Your Cholesterol Levels

April 14, 2014 |

By Dr. Mercola

The video above is a nice confirmation from the traditional media of the importance of vitamin D. However, they still get it wrong by stating that you can get the vitamin D you need from foods. Appropriate sun exposure can easily provide over 20,000 units per day, while food rarely provides over 400 units.

Back in 2011, I published a series of interviews with Dr. Stephanie Seneff, a senior MIT research scientist who, more recently, rocked the world with her discovery of glyphosate’s mechanism of harm.

Three years ago, however, she was one of the first to point out the links between cholesterol and vitamin D, presenting a hypothesis that made me even more convinced that raising your vitamin D levels through sun exposure may be far more critical than previously thought.

Now, research published in the journal Menopause1, 2 appears to offer support for Dr. Seneff’s theories on the cholesterol-vitamin D link. But first, a quick review of cholesterol, and why your body actually needs it.

What Is Cholesterol, and Why Do You Need It?

That’s right, you do need cholesterol. This soft, waxy substance is found not only in your bloodstream but also in every cell in your body, where it helps to produce cell membranes, hormones, vitamin D, and bile acids that help you digest fat.

Cholesterol also helps in the formation of your memories and is vital for neurological function. Your liver makes about three-quarters or more of your body’s cholesterol, and according to conventional medicine, there are two types:

  1. High-density lipoprotein or HDL: This is the “good” cholesterol that helps keep cholesterol away from your arteries and remove any excess from arterial plaque, which may help to prevent heart disease.
  2. Low-density lipoprotein or LDL: This “bad” cholesterol circulates in your blood and, according to conventional thinking, may build up in your arteries, forming plaque that makes your arteries narrow and less flexible (a condition called atherosclerosis). If a clot forms in one of these narrowed arteries leading to your heart or brain, a heart attack or stroke may result.

Also making up your total cholesterol count are:

  • Triglycerides: Elevated levels of this dangerous fat have been linked to heart disease and diabetes. Triglyceride levels are known to rise from eating too many grains and sugars, being physically inactive, smoking cigarettes, drinking alcohol excessively, and being overweight or obese.
  • Lipoprotein (a) or Lp(a): Lp(a) is a substance that is made up of an LDL “bad cholesterol” part plus a protein (apoprotein a). Elevated Lp(a) levels are a very strong risk factor for heart disease. This has been well established, yet very few physicians check for it in their patients. (Lp(a) also was not assessed in the featured study.)

Study Finds Vitamin D + Calcium Supplementation Improves Lipid Profiles

The featured study sought to evaluate whether increased serum 25-hydroxyvitamin D3 (25OHD3) concentrations are associated with improved lipid profiles in postmenopausal women.

The study had over one million people so it was a big deal. The test group received a daily dose of 1,000 mg of elemental calcium along with 400 IUs of vitamin D3. Please note that this dose of vitamin D is ridiculously low and will not provide help for most people. The control group received a placebo.

Blood levels of vitamin D, fasting plasma triglycerides, HDL, and LDL cholesterol levels were assessed at the beginning and end of the trial. After two years, women who received the vitamin D and calcium supplements had a 38 percent increased mean vitamin D level compared to the placebo group.

They also had a 4.46-mg/dL mean decrease in LDL. Furthermore, higher vitamin D concentrations were associated with higher HDL combined with lower LDL and triglyceride levels. According to the authors:

“These results support the hypothesis that higher concentrations of 25OHD3, in response to [calcium/vitamin D3] supplementation, are associated with improved LDL cholesterol.”

After discussing the link between vitamin D and cholesterol with Dr. Seneff, I became convinced that raising your vitamin D levels through sun exposure may have far greater benefits than taking a supplement. I’ve even warned that vitamin D supplementation might not achieve optimal health results, the reason for which I’ll discuss in just a moment.

Remember that this study used a virtually insignificant dose of vitamin D that will not increase levels to optimum in anyone. Yet despite this nearly homeopathic dose, it still led to small, yet noticeable, improvements in lipid profile (i.e. increased HDL, in combination with reduced LDL and triglycerides).

Imagine what they would have found had they given doses 10 to 20 times higher that we know will put people into optimum ranges? In my view, this strengthens the hypothesis that naturally-acquired vitamin D, created by your skin in response to UV exposure, would likely have an even greater effect, and here’s why.

Cardiovascular Disease—A Compensatory Mechanism for Cholesterol Sulfate Deficiency?

Through her research, Dr. Seneff has developed a theory in which the mechanism we call “cardiovascular disease” (of which arterial plaque is a hallmark) is actually your body’s way to compensate for not having enough cholesterol sulfate. To understand how this works, you have to understand the interrelated workings of cholesterol, sulfur, and vitamin D from sun exposure.

Cholesterol sulfate is produced in large amounts in your skin when it is exposed to sunshine. When you are deficient in cholesterol sulfate from lack of sun exposure, your body employs another mechanism to increase it, as it is essential for optimal heart and brain function. It does this by taking damaged LDL and turning it into plaque.

Within the plaque, your blood platelets separate out the beneficial HDL cholesterol, and through a process involving homocysteine as a source of sulfate, the platelets go on to produce the cholesterol sulfate your heart and brain needs. However, this plaque also causes the unfortunate side effect of increasing your risk of cardiovascular disease. So how do you get out of this detrimental cycle?

Dr. Seneff believes that high serum cholesterol and low serum cholesterol sulfate go hand-in-hand, and that the ideal way to bring down your LDL (so-called “bad” cholesterol, which is associated with cardiovascular disease) is to get appropriate amounts of sunlight exposure on your skin. She explains:

“In this way, your skin will produce cholesterol sulfate, which will then flow freely through the blood—not packaged up inside LDL—and therefore your liver doesn’t have to make so much LDL. So the LDL goes down. In fact… there is a complete inverse relationship between sunlight and cardiovascular disease – the more sunlight, the less cardiovascular disease.”

What this also means is that when you artificially lower your cholesterol with a statin drug, which effectively reduces the bioavailability of cholesterol to that plaque but doesn’t address the root problem, your body is not able to create the cholesterol sulfate your heart needs anymore, and as a result you end up with acute heart failure.

Heart Disease Is the Number One Killer Worldwide

According to the World Health Organization (WHO), heart disease was the leading cause of death, globally, in 2011 and 2012. Even children are becoming increasingly at risk.3, 4 Recent research suggests as many as one-third of children have or are at risk for high cholesterol, which conventional medicine views as a risk factor for heart disease.

Bear in mind that, contrary to the conventional ideology, your total cholesterol level—which includes HDL, LDL, triglycerides, and Lp(a)—is just about worthless in determining your risk for heart disease, unless it is above 300. Still, high total cholesterol can in some instances indicate a problem, provided it’s your LDL and triglycerides that are elevated and you have a low HDL. I have seen a number of people with total cholesterol levels over 250 who actually were at low heart disease risk due to their high HDL levels. Conversely, I have seen even more who had cholesterol levels under 200 that were at a very high risk of heart disease based on the following additional tests:

  • HDL/Cholesterol ratio. This is a very potent heart disease risk factor. Just divide your HDL level by your cholesterol. That ratio should ideally be above 24 percent
  • Triglyceride/HDL ratio. Here, you divide your triglyceride level by your HDL. This ratio should ideally be below 2

That said, these are still simply guidelines, and there’s a lot more that goes into your risk of heart disease than any one of these numbers. In fact, it was only after word got out that total cholesterol is a poor predictor of heart disease that HDL and LDL cholesterol were brought into the picture. They give you a closer idea of what’s going on, but they still do not show you everything. Additional risk factors for heart disease include:

  • Your fasting insulin level: Any meal or snack high in carbohydrates like fructose and refined grains generates a rapid rise in blood glucose and then insulin to compensate for the rise in blood sugar. The insulin released from eating too many carbs promotes fat accumulation and makes it more difficult for your body to shed excess weight. Excess fat, particularly around your belly, is one of the major contributors to heart disease
  • Your fasting blood sugar level: Studies have shown that people with a fasting blood sugar level of 100-125 mg/dl had a nearly 300 percent increase higher risk of having coronary heart disease than people with a level below 79 mg/dl
  • Your iron level: Iron can be a very potent cause of oxidative stress, so if you have excess iron levels you can damage your blood vessels and increase your risk of heart disease. Ideally, you should monitor your ferritin levels and make sure they are not much above 80 ng/ml. The simplest way to lower them if they are elevated is to donate your blood. If that is not possible, you can have a therapeutic phlebotomy and that will effectively eliminate the excess iron from your body

Beware of Treating Elevated Cholesterol in Childhood with Drugs

Getting back to the study in question,5 a research team at Texas Children’s Hospital examined the medical records of more than 12,000 children between the ages of nine and 11, and found that 30 percent of them were at risk of elevated cholesterol levels. Elevated LDL and triglyceride levels were found to be more common among boys. Not surprisingly, obesity and lifestyle were deemed to be significant factors.

Universal cholesterol screening guidelines6 were issued in 2011, which strongly recommend all children be screened between the ages of nine and 11, and again between 17 and 21. The authors of the featured study say they hope their findings will give added weight to these guidelines. However, there are serious concerns that universal screening will simply place children on cholesterol-lowering medications, which do absolutely nothing to address the underlying problem… As reported by Eurekalert:7

“‘There is concern by some in the medical community that children will be started on medication unnecessarily,’ [lead investigator, Dr. Thomas] Seery said, emphasizing that adopting a healthy diet and engaging in routine physical activity are first-line therapies for children with abnormal cholesterol levels.

He adds that cholesterol-lowering medications are typically needed in one to two percent of children with dyslipidemia, primarily in those with very high cholesterol resulting from a genetic lipoprotein disorder. Genetic lipoprotein disorders, such as familial hypercholesterolemia, result in very high cholesterol levels that can be detected in childhood but are felt to be underdiagnosed, he said. ‘Kids need to have their cholesterol panel checked at some point during this timeframe [9 to 11 years old],’ Seery said. ‘In doing so, it presents the perfect opportunity for clinicians and parents to discuss the importance of healthy lifestyle choices on cardiovascular health.'”

To Save Our Kids, We Must Address Their Lifestyle

It is indisputable that childhood obesity is placing an increasing number of people at risk of an early death. I address this topic in my book Generation XL. If the childhood obesity epidemic is not reversed, we will, for the first time in history, see children living shorter lives than their parents! Clearly, something must be done about escalating childhood obesity and “adult” diseases showing up in our children. But placing kids on statins8 is certainly NOT the answer. The cause of the problem is unhealthy lifestyle choices—and drugs do nothing to address this. On the contrary, statins have been linked to a wide range of devastating side effects, including but not limited to:

Muscle problems and muscle damage (including the heart muscle) Neurological problems, including memory loss and Lou Gehrig’s disease Nerve damage
Liver enzyme derangement Kidney failure Elevated blood glucose
Tendon problems Anemia Sexual dysfunction

 

Recent research,9, 10 which followed subjects for 25 years, suggests there’s a very important relationship between your heart health and your brain function, and that this relationship starts much earlier in life than previously thought. The study links late-teen to early adulthood blood pressure, blood sugar, and cholesterol levels with mental acuity in your mid-life years:

  • People with higher blood pressure and/or higher blood glucose early in life scored lower on all tests devised to assess memory and learning, brain aging, and decision processing speed
  • People with higher cholesterol early in life scored lower on the learning and memory tests

Now, when you consider the negative effects statins have on your heart muscle, combined with their detrimental neurological impact and their tendency to elevate blood glucose, it would seem like these drugs might actually significantly speed up the onset of dementia when given to young children, thereby doing more damage than simply living with health risk factors such as high blood pressure, blood sugar, and cholesterol.

Vitamin D Also Plays a Role in Alzheimer’s Prevention

Your brain function, as your heart health, is also dependent on both appropriate amounts of cholesterol and healthy vitamin D levels — a fact that again ties heart and brain health together. A recent article in the Daily Herald,11 written by Dr. Patrick B. Massey, MD, Ph.D., medical director for complementary and alternative medicine at Alexian Brothers Hospital Network, discusses the importance of vitamin D for the prevention of Alzheimer’s disease.

“‘Not by coincidence, vitamin D deficiency exists in 70-90 percent of patients diagnosed with Alzheimer’s disease,’ he writes. ‘Medical studies have demonstrated that increased vitamin D levels either through sun exposure or supplementation improves cognitive function in the elderly. These positive results have been seen in those diagnosed with Alzheimer’s disease as well as those who do not have this illness.

The benefits of vitamin D supplementation may appear in four weeks resulting in enhanced processing speed as well as cognitive abilities. Indeed, one recent medical trial demonstrated that taking vitamin D and the Alzheimer’s medication memantine resulted in better outcomes than either memantine or vitamin D alone. Vitamin D supplementation is a simple and effective way of treating and preventing Alzheimer’s disease and may be the best option at this time.'”

As you can see, vitamin D and cholesterol are integral players in both heart disease and Alzheimer’s disease, and that while statins can dramatically reduce your cholesterol, these drugs tend to have a detrimental effect on both your heart and brain. According to Dr. Seneff, insufficient fat and cholesterol in your brain play a critical role in the disease process, and she makes a compelling case for how statin drugs promote the disease. For more in-depth information about this, please refer to Dr. Seneff’s MIT paper, “APOE-4: The Clue to Why Low Fat Diet and Statins May Cause Alzheimer’s.”12

Tying It All Together

All in all, Dr. Seneff’s research makes a very compelling case for getting appropriate sun exposure in order to normalize your cholesterol levels, thereby promoting both heart and brain health. While you can take oral vitamin D pills, there is virtually no doubt in my mind that future research (likely 20-30 years from now) will show that increasing your vitamin D levels through sensible sun exposure or a safe tanning bed is far superior to swallowing vitamin D. To summarize Dr. Seneff’s research into layman’s terms the two inter-related disease processes described earlier would look something like this:

Lack of sun exposure → cholesterol sulfate deficiency → plaque formation (to produce cholesterol sulfate that protects your heart) → cardiovascular disease (which places you at greater risk for decreased brain function)

 

Furthermore, Dr. Seneff and many others also stress the importance of reducing your refined sugar and processed fructose consumption to prevent heart disease. While not specifically addressed in this article, as I chose to focus on cholesterol and vitamin D, fructose consumption also significantly contributes to cardiovascular disease in the following manner:

High fructose consumption → over-taxed liver → impaired cholesterol formation → cholesterol deficiency → plaque formation to compensate for cholesterol sulfate deficiency → cardiovascular disease

 

The reversal of these disease processes would then look like this:

Appropriate sun exposure + low-sugar diet = optimal cholesterol production in your liver + optimal cholesterol sulfate production in your skin → healthy cholesterol levels and absence of arterial plaque

 

Naturally, while sun exposure and a low-sugar diet are important, if not critical, for optimizing your heart health, there are many other lifestyle factors that can make or break your cardiovascular health. For more suggestions on how to optimize your cholesterol levels without drugs, please see my previous article, “Statin Nation: The Great Cholesterol Cover-Up.”

How Vitamin D Performance Testing Can Help Optimize Your Health

 

A robust and growing body of research clearly shows that vitamin D is absolutely critical for good health and disease prevention. Vitamin D affects your DNA through vitamin D receptors (VDRs), which bind to specific locations of the human genome. Scientists have identified nearly 3,000 genes that are influenced by vitamin D levels, and vitamin D receptors have been found throughout the human body.

Is it any wonder then that no matter what disease or condition is investigated, vitamin D appears to play a crucial role? This is why I am so excited about the D*Action Project by GrassrootsHealth. It is showing how you can take action today on known science with a consensus of experts without waiting for institutional lethargy. It has shown how by combining the science of measurement (of vitamin D levels) with the personal choice of taking action and, the value of education about individual measures that one can truly be in charge of their own health.

In order to spread this health movement to more communities, the project needs your involvement. This was an ongoing campaign during the month of February, and will become an annual event.

To participate, simply purchase the D*Action Measurement Kit and follow the registration instructions included. (Please note that 100 percent of the proceeds from the kits go to fund the research project. I do not charge a single dime as a distributor of the test kits.)

As a participant, you agree to test your vitamin D levels twice a year during a five-year study, and share your health status to demonstrate the public health impact of this nutrient. There is a $65 fee every six months for your sponsorship of this research project, which includes a test kit to be used at home, and electronic reports on your ongoing progress. You will get a follow up email every six months reminding you “it’s time for your next test and health survey.”

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