Cholesterol Does Not Cause Coronary Heart Disease

Cholesterol Does Not Cause Coronary Heart Disease, Statins Don´t Work by Lowering Lipids. The Role of Inflammation and Stress.

Paul Rosch; MD, FACP, Clinical Professor of Medicine and Psychiatry, New York Medical College, President, The American Institute of Stress, Honorary Vice President, International Stress Management Association, 124 Park Ave.Yonkers, NY 10703, USA.

1. Increased dietary fat intake does not significantly elevate cholesterol or lipid levels.

2. Elevated serum cholesterol and/or other lipids are not the cause of coronary heart disease.

3. Statins can have significant side effects that have been overlooked or deliberately suppressed. In addition to rhabdomyolysis and liver dysfunction, these include: muscle pain, weakness and fatigue and biopsy evidence of myopathy and tendinopathy in the absence of elevated CK, memory loss, global amnesia, difficulty in sleeping and concentration, erectile dysfunction, problems with temperature regulation, difficulty in managing diabetes, and peripheral neuropathy.

4. All statins have been shown to be carcinogenic in experimental animals in dosages that approximate those given to patients. Although the lag time between exposure to a carcinogen and clinical detection is often a decade or more, a disturbing increase in breast cancer has already been reported in the CARE trial as well as certain skin malignancies in the simvastatin trials. Statins could initiate and/or accelerate malignant growth by a) blocking the production of Coenzyme Q10, which has been shown to have anti-cancer effects; b) stimulating the growth of new blood vessels that malignancies require to promote their propagation; c) decreasing the cytotoxicity of natural killer cells; d) blocking the production of squalene, an intermediate cholesterol metabolite with anti-cancer activities in animal studies and currently used as adjunctive therapy in treating cancer; e) reducing the production of DHEA, which has been shown to have anticancer and immune stimulating effects in experimental studies.

5. Cardioprotective effects are seen regardless of baseline cholesterol or LDL levels or the degree to which they are reduced and are achieved far too rapidly to be due to lowering LDL. If statins worked by lowering LDL one would expect to see dose-response relationship, which has not been demonstrated in any statin trials. Cardioprotective effects are seen in the elderly where LDL or other lipids are not a risk factor for coronary heart disease and in the HPS study statin treatment also prevented ischemic stroke although high LDL is not a risk factor for stroke.

6. There is abundant evidence that reducing inflammation, thrombotic factors and endothelial
damage may explain the statin effects. For example, in the CARE, the outcome was related to the degree of inflammation but independent of any lipid response.

7. Most coronary events are not due to progressive blockage of a vessel by gradual accumulation of lipid material but to thrombosis and disruption of an asymptomatic fibrous plaque with minimal protrusion. Human atherosclerotic plaque bears little resemblance to experimental atherosclerosis in animals force-fed high-fat and high cholesterol diets, but has all the hallmarks of an inflammatory response to infection and there is considerable evidence to support such an etiology, particularly for chlamydia pneumoniae. Homocysteine, angiotensin II and a host of inflammatory agents have also been implicated.

8. Therefore, the current therapy goals of lowering LDL to arbitrary levels are not only inappropriate but also dangerous, since this will only lead to larger doses and more side effects.

Stress can contribute to the pathogenesis of coronary heart disease via a number of well documented neuroendocrine activities. With respect to inflammation, it should also be noted that CRP levels correlate best with abdominal obesity, which has been shown to be largely due to increased cortisol activities that increase adipocyte production of inflammatory cytokines. In addition to these chemical/molecular pathways there is an emerging paradigm of communication at a physical/atomic level that may help to explain other stress-related cardiovascular effects as well as the success of novel "energy treatment" effects.


http://www.thincs.org/WAPF2003.htm#Uffe