The idea that chronic infections within arteries might cause atherosclerosis first arose when doctors observed that people with even high normal levels of c-reactive protein, a marker for inflammation, had much higher rates of coronary heart disease and stroke than those with lower levels. The natural question then arose: What infectious organism was responsible for the inflammation?
The first suggestion came in 1988 when Dr. Pekka Saikku and his co-workers reported a study of Finnish men infected during an epidemic of mild pneumonia caused by the organism Chlamydia pneumonia. They found that men who tested positive for the organism were more likely to have a heart attack than those who tested negative. Later, the Helsinki Heart Study found that patients seropositive for C. pneumonia were 2.6 times more likely to have cardiovascular disease than those who were seronegative for the organism. It is interesting to note that C. pneumonia antibodies are present in about 50 percent of the adult population, often without any clinical symptoms. Exposure to the bacteria in early childhood, combined with the difficulty of eradicating the organism from the body, permits its continued presence in the body long after initial infection or exposure.
Allan Shor, a South African investigator, first demonstrated the presence of the organism within the atherosclerotic plaque itself using electronmicrographs. This was later confirmed by Dr. Joseph Muhlestein and his co-workers when they examined the atherosclerotic crud removed from ninety patients during surgery.302 Using an immunofluorescence technique, they found that 70 percent of the specimens contained the Chlamydia organism. Similar results have been confirmed using a variety of sophisticated techniques, including electron microscopy, immunocytochemistry, direct immunofluorescence, polymerase chain reaction, and in one patient, by direct culture.
All very impressive, but the possibility still existed that it could just be an inactive coincidental organism that had nothing to do with the atherosclerotic process. In other words, C. pneumonia could simply be a free rider. Final proof depended on the ability to experimentally produce atherosclerosis in animals by infecting them with the Chlamydia organism.
Initial attempts did produce mild atherosclerotic lesions, but overall, the results were not very impressive. Dr. Muhlestein then wondered if there could be an interplay between high cholesterol levels and the infection. He repeated the experiment using rabbits, this time feeding the animals a diet high in cholesterol before infecting them with the organism. The combination produced significantly accelerated atherosclerosis. It should be noted that these animals were infected in the same way that humans would be, by entry of the bacteria into the body through the nose.
As persuasive as the evidence was, the real question remained: could eradicating the organism help prevent atherosclerosis in people? The idea was tested in sixty male patients with stable coronary heart disease. Twenty patients were used as placebos and forty were given an antibiotic known to kill Chlamydia. At the end of the study, those receiving the antibiotics had significantly fewer episodes of heart ischemia than did the controls. This study was repeated with similar results in 202 patients in Buenos Aires.
Chlamydia is a very unusual organism. Unlike conventional organisms, it can exist outside the cell in a spore-like form part of the time and then enter the cell, change form, and take over the cell's metabolism. When it is within the cell it can again change form, become inactive, and in this form effectively hide from the immune system, as well as become resistant to antibiotics. In this state it is called a persistent body.
It is for this latter reason that Chlamydia is so hard to treat. First, we do not know if antibiotics can penetrate deep enough into the plaque to kill the organism, and second, we do not know how long we should treat someone to assure that all the organisms have been killed. After all, we have to wait for the dormant organisms to reactivate before they can be killed.
Other infectious organisms are also suspect. One of the most obvious is the cytomegalovirus, a member of the herpes virus family. Many people carry this virus silently within their cells. When the immune system is impaired, the virus can activate and cause significant illness and even result in death. On some occasions, the virus can, instead of causing an acute illness with fever, chills, and muscle aches, result in a chronic infection that produces slow pathological changes in tissues, such as we see with atherosclerosis.
The strongest evidence comes from cardiac transplant patients, who frequently develop a rapidly progressive occlusion of their coronary arteries. Furthermore, patients who receive hearts from persons infected with the virus are more likely to reject the transplanted heart and to develop rapid atherosclerotic occlusion.
One study looked at patients with coronary heart disease and found that these patients were positive for the virus in 90 percent of cases, versus 60 percent in controls. Finally, chickens infected with a cancer-causing herpes virus were also found to have profound atherosclerosis throughout all their blood vessels.303
Scientists are now looking at several other organisms as possible causes of atherosclerosis. For example, the Helicobacter pylori organism is now known to be the causative organism in most cases of gastric ulcer and a particular form of stomach cancer. Another bacterium, Nanobacterium sanguineum, is smaller than many viruses, can change shape with ease, and appears to be involved in the calcification of arterial walls and heart valves. Incredibly, this bacterium can coat itself with calcium and embed itself deep within the arterial wall. In such a state, it cannot be killed by antibiotics or the immune system, and is even resistant to hydrochloric acid and formaldehyde. There is mounting evidence that it is also associated with renal stones, dental stones, plaque, and even brain calcification. Several laboratories can now test for the presence of the organism.
The bottom line is that while infection of the blood-vessel wall may not itself cause severe atherosclerosis, when combined with one or more of the other risk factors mentioned, it may greatly accelerate the process. This makes sense, because the immune attack against these organisms initiates the release of tremendous amounts of free radicals from macrophages, which in turn oxidize the LDL cholesterol. Because the infection persists for such a long period of time, the destruction is extensive. We see a similar process in the nervous system with neurodegenerative diseases.
This mechanism might also explain the effectiveness of flavonoids, vitamins, and garlic in reducing the incidence of heart attacks and strokes, and in preventing atherosclerosis in general. All of these nutraceuticals, especially vitamin C and garlic extract, have antibacterial and antiviral properties. By taking them daily, you keep your blood and tissue levels high, which kills and inhibits the growth of these viruses and bacteria over a prolonged period of time.
It has been shown that, unlike antibiotics, bacteria never become resistant to products such as garlic. In addition, not only are there far fewer side effects with natural products, they help your body in numerous other ways. For example, vitamins C and E and garlic all improve immune activity, protect against oxidation, and improve cellular function.
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