Infections and Heart Disease
Part 1: Infections implicated in atherosclerosis
The popular belief that a fatty diet causes heart disease is untenable because the process that creates atherosclerotic plaques is not, as we are led to believe, fatty formations in the arteries themselves, but the intrusion of LDL particles into the walls of the arteries. Yet there is no obvious way in which LDL can get through the lining of artery walls (endothelium) in an otherwise healthy person because the endothelium is a barrier to LDL.[1] Let's face it; arteries wouldn't be much use if they leaked.
The only way LDL can get through the lining and into the artery wall is if that lining is damaged in some way, either by a cut, shear stress or disease. This means that anything that can damage the endothelium and/or promote the formation of a clot may have a serious impact on plaque formation, growth and rupture. What is attributed merely to cholesterol is actually a combination of damage to the endothelium followed by the formation of a clot (thrombus), which contains cholesterol, over the area to repair the damage. The endothelium then grows over the thrombus, effectively drawing it into the arterial wall — a natural inflammatory, healing process. This process, repeated, causes plaques to grow and eventually rupture, causing a blockage in an artery.
A cut or similar damage is unlikely in the coronary arteries: they are buried too deep in the body. But what about, for example, a bacterial or viral attack which damages the endothelium? This seems more likely and it is seriously considered as a likely cause. A large number of studies have reported associations between human coronary heart disease and certain persistent bacterial and viral infections.
Particularly implicated are Chlamydia pneumoniae, a bacterium that commonly causes respiratory infections, and another ubiquitous bacterium, Helicobacter pylori.[2] Other equally ubiquitous herpesviruses and cytomegalovirus are also candidates. According to Drs K Namuzaki, Assistant Professor of paediatrics, and S Chiba, Professor and Chairman, Sapporo Medical University, Japan, 'Endothelial cells are one of the main targets of the cytomegalovirus infection.'[3]
Such an effect is very likely, as atherosclerosis, the condition thought to lead to heart attacks, and sepsis, the putrefactive destruction of body tissues by bacteria, share several similarities, including immune dysfunction, increased formation of blood clots, and systemic inflammation.
In August 2007 scientists at the Atherosclerosis Research Laboratory, Texas Heart Institute in Houston, demonstrated for the first time that systemic infections themselves can trigger heart attacks.[4] To see more examples, do a search for "bacterial infection +CHD" in the PubMed online medical database
Thus by reducing the body's ability to fight infections, a 'healthy diet', based on carbohydrates, particularly sugars and fruit juices, provides several avenues which may precipitate a heart attack.
References
1. Suzanne Oparil, MD. Baylor College of Medicine, Lectures on Atherosclerosis. 2001.2. Patel P, Mendall MA, Carrington D, et al. Association of Helicobacter pylori and Chlamydia pneumoniae infections with coronary heart disease and cardiovascular risk factors. BMJ 1995; 311: 711-14
3. Namuzaki K, Chiba S. Chlamydia pneumoniae infection and coronary heart disease. BMJ 1997; 315: 1538-9.
4. Madjid M, Vela D, Khalili-Tabrizi H, et al. Systemic infections cause exaggerated local inflammation in atherosclerotic coronary arteries: clues to the triggering effect of acute infections on acute coronary syndromes. Tex Heart Inst J 2007; 34: 11-8.
