For the past four decades we have been taught that cholesterol was the cause of atherosclerosis and increased cardiovascular risk.
For several generations of physicians this much maligned substance has been considered public health enemy number one. Now we find that this was nonsense and physicians are finally awakening to the new reality that cholesterol is not the cause of atherosclerosis.This new paradigm is all but indigestible for doctors. Four decades of false premise is not easy to overcome. I was an ardent disciple of the anti-cholesterol crusade. I must have written ten thousand prescriptions for whatever cholesterol buster was in vogue and lectured thousands of patients, friends and even my family or the evils of eggs, whole milk and butter This bowing to a false God was not only wrong, it all but stopped forward thinking in cardiovascular research.
The emotional burden of having been proven wrong for all these years is extraordinarily difficult for doctors now to accept (myself included.) Many still cling desperately to bits and pieces of the collapsing façade of cholesterol causation as if seeking to somehow escape the truth, but they cannot escape, only delay confrontation with frustrated and increasingly skeptical patients.
That inflammation is real cause of cardiovascular disease; we now know to be likely. It appears to be endothelial inflammation from numerous causes that trigger the atherosclerotic process. Cholesterol is but an innocent bystander important only in those special cases of genetically predetermined familial hypercholesterolemia.
For most of us, cholesterol is the most important and valuable biochemical in our body. Our brains are substantially filled with cholesterol and only in the last few years have we learned how important it is to cognitive function. Kilmer McCully was one of the first to scorn cholesterol causation. It was this man who identified homocysteine as a major contributor to endothelial inflammation and arthrosclerosis. By his own estimate some 40% of heart attack and strokes are associated with elevated homocysteine levels due to inherited or otherwise acquired defects in vitamins B6, B12 and folic acid availability. He postulated the others were likely due to such factors as omega 6 excess, Trans fats, smoking, inherited coagulation defects and inherited platelet abnormalities.
Recently it has been discovered that another trigger is probably involved, one that may be far more significant than previously suspected - that of infections in the mouth in the form of periodontal disease, gingivitis and apical abscesses. Even when one is without symptoms, significant oral infection can be present. This is true also for a CRP test - it can fool you.On 1 March 2007 the NEJM published an article by Tonetti MS and others titled Treatment of Periodontitis and Endothelial Function. One hundred twenty patients were randomly assigned to community based or intensive periodontal care and tested on days 1, 7, 30, 60 and 180 for tests of markers of inflammation, coagulation and endothelial activation. Predictably, these markers were elevated in the first 24 hours after intensive periodontal treatment but the same tests over the next six months were substantially improved in this group reflecting not only improvement in periodontal disease but substantial improvement in endothelial function.
The bacterial flora of the human mouth includes hundreds of potentially very serious pathogens held in check by other less harmful bacteria. Oral disease upsets this balance, exposing the endothelial lining of our blood vessels to toxins as well as actual bacteria. That this can be an important contributor to endothelial inflammation and artheromatous change should come as no surprise. Actually we have known this for years and today's rediscovery is really not new. Those with oral infections, beware.
Duane Graveline MD MPH
Former USAF Flight Surgeon
Former NASA Astronaut
Retired Family Doctor