Most people believe that heart attacks are due to fatty foods that elevate blood cholesterol, which somehow clogs up the coronary arteries and eventually obstructs blood flow. As a result, we are urged to restrict fat, and if necessary, lower cholesterol with statins, which block the production of cholesterol, and/or other drugs that inhibit its absorption. But cholesterol is a large, inert molecule, and since it is difficult to see how it could infiltrate the arterial wall, it is now claimed that coronary disease is caused by LDL “bad” cholesterol. However, consider the following dozen facts:

A ten-year study involving 21 countries found that those with the highest fat consumption had the lowest mortality rates from heart disease and those with the least fat intake had the highest death rates. No dietary cholesterol lowering trial has ever resulted in a reduction of coronary disease or total mortality rates. Over thirty studies have reported that coronary heart disease patients ate less or the same amount of saturated fat as healthy controls. 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 26 patients, atherosclerosis was increased in 18 and unchanged in 8. High cholesterol does not increase risk for heart attacks in people older than 65, healthy women of any age, nor in patients with diabetes or renal failure. (Senior citizens with high cholesterols have significantly fewer infections and live longer than low cholesterol controls.) At least half of heart attack patients do not have elevated levels of cholesterol or LDL. Two recent studies found that cholesterol and LDL were lower than normal in acute myocardial infarction patients. In one of these studies in which the patients were followed for 3 years, mortalitywas highest among those with the lowest cholesterols. In familial hypercholesterolemia, there is no correlation between the very high cholesterol (1,000 or more) and LDL levels (over 250) and any increased incidence or severity of coronary disease. Lowering LDL “bad cholesterol” does not prevent heart attacks in healthy people. Clinical trials of a drug that raised HDL “good cholesterol” had to be stopped because of an increase in cardiac death rates and hypertension. Adding drugs that block absorption to a statin resulted in a greater lowering of cholesterol, triglycerides and LDL, and significantly raised HDL, but was also associated with an increase in cardiovascular deaths.

Many more examples could be cited, but contrast this with the following dozen facts demonstrating how stress contributes not only to heart attacks and coronary disease, but also cardiovascular deaths due to stroke.

Stressful life change events, Type A behavior and emotions (depression, anxiety, hostility, anger) have all been linked to higher rates of heart attacks. Stress causes spasm and constriction of the coronary arteries and increased platelet stickiness, both of which promote clot formation. Stress increases homocysteine, CRP (C-Reactive Protein) and fibrinogen, all of which are associated with increased risk for heart attack and stroke. Stress causes deep abdominal fat deposits that promote insulin resistance, Type 2 diabetes, hypertension and heart attacks. Stress can cause atrial fibrillation, a powerful risk factor for stroke. Stress causes ventricular fibrillation, the leading cause of sudden death, and can occur in teenagers with no evidence of coronary atherosclerosis. Stress causes “Broken Heart Syndrome”, particularly in women following a traumatic event. This is due to severe left ventricular contractile dysfunction that frequently mimics a massive myocardial infarction. Stress contributes to all the standard Framingham risk factors of cholesterol, smoking, and hypertension, as well as diabetes and obesity. Stress can precipitate and/or worsen congestive heart failure. Stress reduces heart rate variability, a powerful predictor of sudden death. Stress reduces resistance to infections that have increasingly been incriminated as a cause of coronary atherosclerosis. Severe stress can cause a myocardial infarction in the absence of any significant coronary disease due to direct damage from increased norepinephrine secretion at nerve endings in heart muscle.

We are all entitled to our own theories, but not our own facts. Stay tuned for subsequent blogs that will explain how this fallacious lipid hypothesis of coronary disease has been perpetuated by the cholesterol cartel of drug companies, manufacturers of low fat foods and lipid testing equipment. We will also discuss the hidden dangers of statin therapy, the role of inflammation in heart disease, why stress reduction strategies work, which one might be best for you, and related topics. Additional information on all the above can be found at www.stress.org.

Paul J. Rosch, MD, FACP

Dr. Paul J. Rosch is current Chairman of the Board 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 has served as Chair of its U.S. branch. You can follow AIS on Twitter, watch AIS videos on You Tube, become a fan of AIS on Facebook and subscribe to one or both free AIS magazines to receive the latest stress information and research from around the globe directly to your inbox.