Saturated Fat and Cholesterol Do Not Cause Coronary Heart Disease

dr_paul_rosch_131By Paul J. Rosch, M.D., M.A., F.A.C.P.

It's not difficult to understand why most people, including physicians, are convinced that high blood cholesterol is the major cause of heart disease and that elevated cholesterol is due to eating saturated fats.

It's easy to visualize how fatty foods raise blood cholesterol, which, despite being a large inert molecule, somehow precipitates out to infiltrate the inner lining of the coronary arteries, where it forms fatty atheromatous plaques.

These plaques slow the flow of blood and eventually completely obstruct it to cause the death of myocardial tissue. This sequence of events was similar to the gradual buildup of lime and rust in pipes, and the terms coronary occlusion, myocardial infarction and heart attack are still often used as synonyms.

What is hard to believe is that there is no evidence much less proof to support this entrenched lipid theory of coronary atherosclerosis. In point of fact, it has been completely refuted by numerous scientific studies. Consider the following half dozen examples:

1. Almost two-dozen studies have reported that coronary heart disease patients ate less or the same amount of saturated fat as healthy controls. The huge World Health Organization project MONICA (Monitoring of Trends and Determinants in Cardiovascular Disease) that collected data from 21 countries for over 10 years failed to find any correlation between heart attacks and fat consumption or cholesterol.

Every single country with the lowest fat consumption had the highest mortality rates from heart disease and those with the most fat consumption had the lowest. The French consumed three times as much saturated fat compared to Azerbaijan but had one-eighth the rate of heart disease. The heart disease death rate in Finland was three times greater than in Switzerland, even though the Swiss ate twice as much fat.

2. No dietary cholesterol lowering trial has ever shown a reduction in lowering coronary disease or total mortality. In the "Prudent Diet" study of 49 to 59 year-old men, one group substituted margarine for butter, cold cereal for eggs, and chicken and fish for beef. Controls ate eggs for breakfast and meat three times a day.

After ten years, cholesterol levels averaged 30 points lower in the first group, but they had eight deaths from heart disease compared to none for the meat eaters. Ancel Keys also fed middle-aged men a very high cholesterol diet but found that their cholesterol levels were no different than a control group who consumed less than half as much.

Two decades later, he finally admitted "There's no connection whatsoever between cholesterol in food and cholesterol in blood. And we've known that all along. Cholesterol in the diet doesn't matter at all unless you happen to be a chicken or a rabbit."

3. In the Framingham study, which was responsible for establishing cholesterol, hypertension and cigarette smoking as the three major risk factors for coronary heart disease, a 26-year follow-up report found that 50% of cases occurred in people with below average cholesterol. There was a direct association between falling cholesterol levels over the first 14 years of the study and increased mortality rates over the following 18 years.

For men above the age of 47, those with low cholesterol had greater mortality rates than those with high cholesterol. Subjects whose cholesterol had decreased spontaneously over 30 years were also at greater risk of dying from heart disease than those whose cholesterol had increased. In addition, the more saturated fat and the more cholesterol people ate, the lower their serum cholesterol was. Those who ate the most saturated fats weighed the least.

4. No association between cholesterol levels and the severity or extent of atherosclerosis has ever been found in postmortem studies of the general population. No clinical or imaging study has found any relation between the degree of cholesterol lowering and improvement.

In one angiography study, in which blood cholesterol had been reduced by more than 25% in 24 patients, atherosclerosis was increased in 18 and unchanged in eight. Cholesterol rose in 12 other patients but only 4 showed an increase in atherosclerosis.  A Mayo Clinic study similarly found that in all patients whose cholesterols had decreased by more than 60, there was a significant increase in coronary atherosclerosis.

5. High cholesterol does not increase risk for heart attacks or other coronary events in people older than 65, women of any age, as well as patients with diabetes or renal failure. Senior citizens with high cholesterols have significantly fewer infections and live longer than low cholesterol controls. In familial hypercholesterolemia, there is no association between the very high cholesterol and LDL levels and a corresponding increased incidence or prevalence of coronary disease.

6. The huge and lengthy MRFIT study (Multiple Risk Factor Intervention Trial) was designed to prove the links between diet, cholesterol, and other Framingham risk factors with heart disease. Cholesterol consumption was cut by 42 percent, and saturated fat consumption by 28 percent and on long-term follow-up, those adhering to this dietary fat restriction had slightly lower coronary heart disease death rates.

However, this benefit was far outweighed by significantly increased total mortality rates, especially from hemorrhagic stroke, cancer, suicide, accidents and violence. The risk of dying from a cerebral hemorrhage was 500% greater in those with low cholesterol compared to those with high levels. In most other studies, the incidence of stroke was higher in those who ate less saturated fat.

Excerpted, with permission, from: Health and Stress, The Newsletter of The American Institute of Stress. (

Paul J. Rosch, M.D., M.A., F.A.C.P.
Former President of The American Institute of Stress,
Clinical Professor of Medicine and Psychiatry at New York Medical College,
Honorary Vice President of the International Stress Management Association and Chairman of its U.S. branch.

Updated November 2016


Since this article was first written in September 2010, additional evidence has accumulated to support the assertion that heart attacks are not due to elevated cholesterol or LDL, and that these are merely risk markers because of a statistical association rather than risk factors that have a causal relationship.

In addition, the important role of stress has been increasingly confirmed.
Abundant updated support for both of these claims can be found in numerous chapters in a recent book that I edited entitled Fat and Cholesterol Don't Cause Heart Attacks And Statins Are Not The Solution, especially:

Monteiro C. "Stress as a cause of atherosclerosis" – (The Acidity Theory)
Kendrick M. "Cardiovascular disease is primarily due to blood clotting" – (discussion of the effects of stress on clotting and nitric oxide by the author of The Cholesterol Con)
Okuyama H. Langsjoen PS et al. "Industrial Control of Guidelines for Lipid Nutrition" – (update of previous article by this group showing that lowering cholesterol with statins stimulates atherosclerosis and heart failure)
Harcombe Z. "How Dietary Guidelines, Bad Science, Politics And Profit Have  Contributed To The Current Epidemic of Obesity and Incidence of Heart –Disease" – (incontrovertible proof that there was never any scientific basis for recommendations to sharply restrict dietary fat)
de Lorgeril M, Rabaeus M. "Critical Review Of Recent Drug Company Sponsored Trials About Statin Efficacy And Safety" – (one of several chapters  explaining how drug company sponsored trials hype efficacy and minimize or ignore adverse side effects)
Graveline D, Rosch PJ. "Why Reported Statin Side Effects Are Just The Tip Of A Titanic Iceberg"

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Cholesterol is Not the Culprit
The Statin Damage Crisis
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