One hundred years ago many researchers considered atherosclerosis as an infectious disease. It was known that people who died from an infection were more atherosclerotic if they had been infected a long time before death than if they had acquired the infection a few days before. (4)

The following statement by two American pathologists, Oskar Klotz and M. F. Manning is typical for the general view at that time: There is every indication that the production of tissue in the intima (the innermost layer of the arterial wall) is the result of a direct irritation of that tissue by the presence of infection or toxins. (5)

Today more than one hundred reviews about this issue have been published in medical journals. However, almost all authors think that the infections are secondary; that the microorganisms locate to atherosclerotic tissue because here they are able to multiply without being disturbed by our immune system.

What most researchers also accept is that the starting point of an occluding thrombus is a soft bubble lying just beneath the inner surface of the artery wall. It is called a vulnerable plaque, discovered by Danish pathologist Erling Falk. He examined the hearts of patients who had died because of an acute myocardial infarction and noted that the occluding thrombus almost always was situated close to a ruptured bubble. (6)

Now to the crucial questions. What is causing the inflammation and how is the vulnerable plaque created?

According to the present view the first step is what researchers call activation of the arterial endothelium, the thin cell layer that covers the inside of all vessels. There are many factors that are said to activate or irritate the endothelium, for instance the toxic chemicals present in tobacco smoke, too little vitamins or copper in our food, and too much iron or homocysteine in our blood.

Homocysteine is an amino acid normally present in minute amounts. If its concentration is too high the risk of cardiovascular disease increases. Children born with an extremely high level of homocysteine due to an inborn error of metabolism rapidly become atherosclerotic and may die before the age of ten from a stroke or a heart attack.

Some researchers think that microbes circulating in the blood may attack the endothelium, in particular if it has been damaged by toxic factors, but the prevailing idea is that high LDL cholesterol is the main culprit.

When the endothelium is activated, a condition named endothelial dysfunction, it is said to allow LDL-cholesterol to pass through the endothelial cells and enter the intima, the innermost layer of the arterial wall.

That LDL-cholesterol enters the intima when it is activated is also a hypothesis. It is a necessary assumption to explain why so much cholesterol is found in the arterial wall, because normally cholesterol is not able to enter an endothelial cell or any other cell for that matter. The activated endothelium is also said to attract a type of white blood cells named monocytes and invite them to enter the interior of the arterial wall.

When LDL-cholesterol has passed through the endothelial cells, they are said to be attacked by cells in the intima resulting in a change of their structure; LDL becomes oxidized. It is this process which is considered as the cause of inflammation. After having been oxidized, the monocytes (now converted to macrophages) take up the oxidized LDL-cholesterol.

I have not yet found anyone who has been able to tell me why LDL molecules become oxidized, just because they enter the arterial wall, but this is the official explanation which is necessary to explain the next step.



The Real Cause of Heart Disease? Part 2



Dr. Uffe Ravnskov MD

Author of "The Cholesterol Myths" and "Fat and Cholesterol are Good for You"

Creator and spokesman of THINCS, "The International Network of Cholesterol Skeptics" www.thincs.org



Sources

1. Ravnskov U, McCully KM. Ann Clin Lab Sci 2009;39:3-16.

A short version in Swedish is available in Medicinsk Access 2009;2:15-8.

2. Ott SJ and others. Circulation 2006;113:929-37.

3. Melnick JL and others. Lancet 1983;2:644-7.

4. Pampou Syu and others. Virchows Arch 436, 539-52, 2000.

5. Shi Y and othhers. Pathol Int 2002;52:31-9.

6. Wiesel J. Zeitschr Heilkunde 1906;27:262-94.

September 2011