Progression of Atherosclerotic Lesions in Patients With Cardiovascular Disease Can Be Controlled Naturally, But Not With Statins

V. Ivanov, MD PhD, A.Niedzwiecki PhD

A hypothesis that high cholesterol promotes the development of atherosclerotic plaques in human arteries was first proposed at the beginning of the 20th Century. It has been tested numerous times, but never convincingly proven. Although some animal species develop arterial lesions in response to dietary overload with cholesterol, these lesions are morphologically very different from human atherosclerosis. All physicians know that about half of heart attacks victims do not have high cholesterol levels. They also agree that the cholesterol-based hypothesis of heart disease does not apply in women and the elderly.

Since the 1990s and the publication of Dr. Rath’s discovery that the cause of heart disease is a long-term vitamin deficiency [2,4], research has increasingly confirmed this new concept, both through clinical studies and lab results (www.drrathresearch.org).

The cholesterol hypothesis, however, has powerful supporters in the pharmaceutical business, which exploits the hopes of millions of patients to reduce the burden of cardiovascular disease by directing their attention to the artificial lowering of their blood cholesterol levels.

Despite questionable evidence that high cholesterol in the bloodstream causes heart disease, manufacturers of cholesterol-lowering drugs have poured huge funds into scientific and clinical research. This has been coupled with the manipulation of public opinion by lobbying and aggressive marketing of this “cholesterol dogma.” The introduction of a new class of drugs called statins in the early 1990s accelerated these marketing efforts. These drugs inhibit the activity of HMG-coenzyme A reductase, a key enzyme in the cellular biosynthesis of cholesterol molecules. The introduction of these drugs has raised many concerns by physicians and researchers regarding potential side effects of this new class of medication. It is a scientific fact that inhibition of HMGCoA reductase has other metabolic consequences, including the depletion of coenzyme Q10, a critical nutrient for cellular energy production, resulting in muscle and liver damage. It can also impair the synthesis of hormones and vitamin D. Moreover, various research data indicated earlier that statins could cause cancer 6). Despite these warnings, new prescription guidelines for cholesterol drugs introduced in 2001 immediately made millions of people “cholesterol –sick” and requiring prescriptions.

Today, about 15 years after the first clinical application of statins, the health concerns regarding their use have become a reality. Serious side effects, including deaths from rhabdomyolysis (caused by the cholesterol-lowing drug Baycol/Lipobay), compelled desperate patients and their families to take legal action against the manufacturers of these drugs. This did not stop the multimillion-dollar investments in the marketing of statins. Consequently, research funds have been directed towards searching for other disease markets for statins, especially now that clinical evidence casts real doubts on the justification of statins’ use in cardiovascular problems. Here is the most recent example.

The results of a prospective clinical study on the use of standard and intensive treatment with atorvastatin (Lipitor) appeared in January 2006 in the journal Circulation published by the American Heart Association [1]. The study was funded by Pfizer GmbH Deutschland, the producer and marketer of Lipitor (atorvastatin). This multicenter, randomized, double-blind trial involved 471 patients who had more than one cardiovascular risk factor and moderate coronary atherosclerosis, estimated by electron-beam computed tomography as arterial wall calcification. Patients had been randomly assigned to a standard 10-mg-a-day or an intensive 80-mg-a-day treatment with atorvastatin for 12 months. Blood cholesterol and severity of atherosclerotic calcified lesions in coronary arteries were assessed at the beginning and at the end of statin treatment.

Statins did not curb atherosclerosis
The results of the study brought much disappointment to the sponsors and proponents of statin treatment. Despite the study’s aim to halt atherosclerosis by lowering blood cholesterol, the standard therapy did not change blood cholesterol levels after 12 months of treatment. Only with intensive treatment using an eight-fold higher dosage of atorvastatin were the blood LDL cholesterol levels brought down by 16% and total cholesterol by 9%. But this did not help halt atherosclerosis -- just the opposite. The progression of coronary calcifications in the intensive therapy group jumped up to 27% a year.

Why then are the statins still being promoted?

The approved standard atorvastatin (Lipitor) therapy did not reduce blood cholesterol levels. Only by increasing its daily dose by eight-fold could researchers lower blood cholesterol levels by 9% after a year. However, it is a well-known fact that cholesterol-reduction is possible through dietary changes and supplementation with vitamins and other essential nutrients. A cholesterol lowering effect through nutrient synergy can be even more comprehensive and includes lowering of the most atherogenic form of cholesterol, lipoprotein (a), without compromising safety [5].

Atorvastatin, on the other hand, is toxic. This is why its approved daily dose was limited by the FDA up to 10 mg a day. Still, at this dose more than a half of the patients in the Circulation study (54.5%) experienced one or more adverse effects, and serious adverse effects were recorded in every eighth participant [1]. The adverse events ranged from nausea, myalgia and gastritis to myocardial infarction, stroke and carcinoma. All this risk was taken without lowering cholesterol at all! This poses a question: Why with statin toxicity so well known was an eight-fold higher atorvastatin dose approved for this study? The logical answer is to justify increased risks of toxicity as a tradeoff for the anticipated benefit in halting the progression of heart disease. Yet it did not happen – the progression of calcification in coronary arteries was not affected. There is no future in statins.

Those following a cholesterol-heart-disease dogma may wonder why the lowering of cholesterol did not reduce the progression of coronary atherosclerosis. The logical answer is because it can’t. Elevated blood cholesterol levels are not a primary cause or even a significant driving force for the progression of atherosclerosis. Dr. Rath was right. It is “the nutrient-starving wall” that is responsible for atherosclerosis [2, 4]. Our research and other scientific evidence have proved him right. Results of our research presented to the scientific community and general public have been published in numerous scientific peer-reviewed journals. We have conducted one full-scale [3] and several pilot clinical studies [5 and www.drrathresearch.org], which have proven the beneficial effects of vitamin and essential nutrient programs in patients with different forms of cardiovascular disease. These benefits include a significant decrease in coronary calcification after one year of following the vitamin program and documented individual cases of a complete reversal of vascular deposits [3,4] – the effect that statin treatment failed to document in the Circulation study.

It is essential that this information reaches the public. How does the pharma industry communicate its message? Simply with money. A one-minute TV ad in prime time costs about $100,000.00. The cost of the study just like the one we discussed above can cost about $5,000,000.00. How many such attempts to promote statins have you seen over the last 20 years? I bet thousands. Where did the money come from? It came from the unbelievably high profit margins made on the pharmaceutical business with disease. We can overcome these deceptive practices that compromise our health only by our personal efforts. We must communicate a natural health message to the people who can benefit from it -- to family, friends, colleagues, neighbors the people we know and people we care about. For this purpose, Dr. Rath initiated his Health Alliance to unite us in our efforts to save people from heart disease and from other health problems.

References
1. Schmermund A, Achenbach S. Effect of intensive versus standard lipid-lowering treatment with atorvastatin on the progression of calcified coronary atherosclerosis over 12 months. A multicenter, randomized, double-blind trial. Circulation; 2006;113:427-437.

2. Rath M, Pauling L. Unified theory of human cardiovascular disease leading the way to the abolition of this disease as a cause for human mortality. Journal of Orthomolecular Medicine; 1992:139-143.

3. Rath M, Kalinovsky T, Niedzwiecki A. Reduction in the frequency of arrhythmic episodes in patients with paroxysmal atrial arrhythmia with a vitamin/essential nutrient supplementation program. JANA;2005:8(3):19-25.

4. Rath M. Why Animals Don’t Get Heart Attacks But People Do. Santa Clara, Ca: MR Publishing Inc. 2000.

5. Rath M, Niedzwiecki, A, eds. Cellular Health Communications. Santa Clara, CA: MR Publishing Inc; 2001.

6. Newman TB, Hulley SB. Carcinogenicity of lipid-lowering drugs. JAMA. 1996;275(1):55-60.