Arteriosclerosis
Atherosclerosis has usually been thought of as a chronic degenerative process that resulted from damage caused by various stressors on the interior of the arterial wall. Today more evidence is accumulating that an inflammatory component may in fact lie at the core of the plaque-forming process. For one thing, cardiovascular events like heart attack, stroke, and death are much more common in patients who also suffer from some systemic inflammatory condition like rheumatoid arthritis. Furthermore, systemic anti-inflammatory therapy does appear to reduce this risk. Also, very good research has now proven that even minor elevations of the inflammatory blood marker called CRP are predictive of excess cardiovascular events in patients without systemic inflammatory conditions. These observations allow us to better explain what we natural medicine doctors have been doing all along to help our patients, and give us an opportunity to learn how to prevent the development of arteriosclerosis. The arteriosclerosis process is very complicated. I hope that all this drug company propaganda has not lulled people into believing that as long as their cholesterol is OK, then they have nothing to worry about. I have frequently written about the various other important risk factors that are involved and can easily be measured that will help to assess cardiovascular risk. Today we take a closer look at CRP, the major marker for inflammation.

The inner lining of the blood vessels is called the endothelium. For proper circulation this single sheet of cells must be perfectly smooth. Oxidative stress (especially superoxide radicals), very high levels of blood fats, hypertension, and metabolic disorders like diabetes and insulin resistance (through glycosylation of proteins) all can damage endothelial cells. When damaged these cells produce less vessel-dilating nitric oxide  (NO…it also inhibits platelets from sticking together and white cells from adhering to the endothelium), and more inflammation -producing cyclo-oxygenase. This results in constriction of the blood vessel, and the first step in the inflammatory process which eliminates the smooth surface of the endothelium…ie, adhesion of white blood cells to the endothelial cells. It is now also well known that it is not so much the bad fats (LDL) that are a problem, but when oxidized, LDL is a very potent factor in endothelial cell dysfunction. This process sets certain biochemical processes in motion that then can be indirectly quantitated by measuring the level of CRP in the blood. In other words, arterial plaque that is unstable or inflamed will be reflected in elevated CRP levels, and will more likely be associated with heart attacks. When large groups of patients were studied it was found that levels under one are associated with very low risk for coronary arteriosclerosis, while 1 to 3 and over 3 were associated with average, and above average risk respectively. These correlations are probably more important and predictive than cholesterol levels.

Oxidative stress can be measured in a variety of ways. In arteriosclerosis patients, special methods have demonstrated increased superoxide (a damaging oxygen free radical) in the endothelium. Nitric oxide helps neutralize superoxide, but in the process, other damaging free radicals are formed, and of course the above discussion makes it clear that NO release is reduced in arteriosclerosis patients. Therefore superoxide is one reason the process gets started and keeps going. And, reduced availability of superoxide dismutase ( the internally produced superoxide radical antioxidant) in the blood, and reduced nitric oxide production from endothelial cells then allow various other unfavorable events to take place as well.

To bring this discussion to a practical level, I draw the following conclusions:

1. It’s good to know your cholesterol level, but it’s more important to know a lot of other things as well: insulin level, fibrinogen, lipoprotein (a), homocysteine, and now, of course, your CRP. If you haven’t had it tested lately, do it now.

2. Dysfunction of the endothelium caused by oxidative stress, oxidized LDL, hypertension, or glycosylation problems manifests itself through reduction in nitric oxide production and release of inflammation promoting cyclo-oxygenases.

3. Coronary disease patients should be looking for treatments that reduce oxidative stress, shore up anti-oxidant defenses, specifically increase endothelial nitric oxide secretion, reduce inflammation, and increase the availability of extra-cellular superoxide dismutase.

4. Natural medicine consultation will lead to investigation of the source of oxidative stresses, replentishment of antioxidant and other needed nutritional factors, measurement and monitoring of all relevant risk factors, and the availability of intravenous treatments that help heal the endothelium, reduce inflammation, and reduce CRP.

5. Although up to now many studies have failed to demonstrate reversal of arteriosclerotic lesions in many chelation therapy patients, chelating doctors know the treatment saves lives and prevents heart attacks and strokes. Chelation therapy does work, and it works because it stabilizes existing inflammatory plaque by eliminating free radical stress, supporting anti-oxidant function, and preventing the oxidation of LDL.  And it helps prevent progression and extension of arteriosclerosis by supporting endothelial function in collateral vessels, thus maintaining or improving total blood flow. CRP, fibrinogen, and liproprotein (a) levels do drop with chelation therapy.

6. Phosphatidyl choline is another of the intravenous therapies. This important phospholipid (contained in smaller doses in lecithin, a commonly used heart supplement) is a critical component of cell membranes. It works by stabilizing the endothelial cell membrane, maintaining NO production, and preventing distortions in the smooth interior surface of the artery wall. It also has beneficial effects on blood cholesterol and HDL.

7. As a result of recent research, we need to place even more emphasis on finding and using other therapies which support endothelial nitric oxide production, enhance extracellular SOD levels, and block the cyclo-oxygenase induced inflammatory cascade.

8. Orthodox cardiologists promote lipid lowering drugs as one way of reducing oxidized LDL damage to the endothelium, The next category of pharmaceutical they will roll out and push will be selective COX2 inhibitors that block the effect of cyclo-oxygenase and thus interfere with the inflammatory component of atherosclerosis. Natural medicine offers a better way.