Cholesterol is NOT the Cause for Heart Disease

We had seen more people who had so called heart attack (myocardial infarction) with normal cholesterol than with high cholesterol. Many of them had regular blood test and was told that their blood parameters essentially normal, including cholesterol however end-up with heart attack not long after.

Adopted here is the summary of the issue by Majid Ali. MD. Our approach following his “aa oxidoptahy” hypothesis yield good result more often than not consistent with his study that is about 90% at all time.

Summary of his background is as follows:

Editor, The Journal of Integrative Medicine
Formerly, Associate Professor of Pathology (adj.), College of Physicians and Surgeons of Columbia University, NY
Formerly, President of Staff and Chief Pathologist, Holy Name Hospital, Teaneck, NJ
Fellow, Royal College of Surgeons of England – Diplomate,
American Board of Anatomic and Clinical Pathology
Diplomate, American Boards of Environmental Medicine
Past President Capital University of Integrative Medicine

Original writing by Majid Ali:

The cholesterol theory has other serious shortcomings. Specifically, it fails to explain the following important issues:

1. Cholesterol is an antioxidant, albeit a weak one, and cannot be expected to cause oxidative injury that clearly initiates atherogenesis.

2. A majority of patients who develop severe IHD, including episodes of myocardial infarction, do not have elevated blood cholesterol levels.1,2,3

3. When death occurs within six to eight hours of myocardial infarction, no acute coronary thrombotic occlusions are found at autopsy in more than 75 percent of cases; however, when death occurs after 48 hours, acute thrombotic occlusion is almost always found (personal unpublished data).

4. The range of frequency of acute thrombotic coronary occlusion in survivors of out-of-the-hospital cardiac arrest extends from 36 percent as determined by angiography4 to 95 percent in autopsy studies.5

5. There is a well-recognized paradox of IHD coexisting with normal angiograms.6,7,8

6. Reduction of atherosclerotic lesions does not follow when the death rate from myocardial infarction falls.9,10,11,12

7. Lowered blood cholesterol levels in women are not associated with the reduction in the rate of acute ischemic myocardial events to the same degree as is seen among men.13

8. Lifestyle stressors,14-22 tobacco smoking,23-27 and physical inactivity28-33 are recognized independent risk factors of IHD and exert potent pro-oxidant effects. We are not aware of any valid reason to believe that the oxidative stress of all those factors is confined to oxidative modification of LDL.

9. The cholesterol theory does not explain the recognized risk factors of IHD, such as hypertension and diabetes.

10. The cholesterol theory does not explain the cardioprotective role of coenzyme Q10,34.35,36-42 nor does it explain how hyperhomocysteinemia43,44,45-59 increases risk of IHD.

11. The cholesterol theory does not explain the recognized risk factors of increased body stores of iron60,61 copper62 and mercury63,—transition metals with potent oxidizing potential.

12. The cholesterol theory does not explain the protective effects of selenium64,65,66,67 and chromium,68,69,70-73 minerals with recognized antioxidant effects.

13. The cholesterol theory does not explain the epidemiologic data showing reduced mortality from IHD in patients taking ascorbic acid74,75 and vitamin E.76,77

In the face of the above evidence, how can the proponents of the cholesterol theory persist in their enthusiasm and continue to commit enormous financial resources to cholesterol research? An explanation was provided by Ravnskov who in 1992 evaluated 22 controlled cholesterol-lowering trials and concluded, “Lowering serum cholesterol concentrations does not reduce mortality and is unlikely to prevent coronary heart disease. Claims of the opposite are based on preferential citation of supportive trials.”78 Specifically, he revealed that among the cholesterol trials published in major journals, supportive reports (n=8) were cited on average 61 times a year, while unsupportive trials (n=10) were cited eight times a year. In 14 cholesterol trials undertaken to establish a causal relationship between cholesterol changes and outcome, the data showed either an unsystematic effect or no effect at all. Ravnskov’s closing comment is especially pertinent to our discussion. It read: “Methods subject to bias, such as open trials or the use of drugs with characteristics side effects, or stratification instead of random allocation of participants, probably explain the overall 0.32% reduction recorded in non-fatal coronary heart disease.”