Cholesterol, Infection and Heart
There is a general assumption that cholesterol is the prime mover in the development of coronary heart disease. There are however a few people who feel that the association between cholesterol and coronary heart disease is not a cause-effect relationship but that cholesterol is involved in a more subtle way. One of the leading components of a different approach to understanding cholesterol has been Uffe Ravnskov. There have also been proposals that coronary heart disease is due to a micro-organism. The identity of the organism has not been clearly identified but Chlamydia pneumoniae is the leading contender. It is possible that more than one organism might be involved. This is an extremely important paper in helping us understand the atherosclerotic process, the physiological role of cholesterol as LDL, the role of micro-organisms, and the importance of defective immunity in disease.
In this article, Uffe Ravnskov and his co-worker Kilmers McCully have explored in detail the link between putative micro-organisms, cholesterol and coronary heart disease, attempting to produce a pathological model of the atherosclerotic plaque. They feel that the precipitating event is a micro-organism, with cholesterol in the form of lipoproteins acting as a defensive mechanism. They present a great deal of published information concerning the beneficial functions of lipoproteins and cholesterol. For example antistreptolysin-S is part of the lipoprotein immune system, which act as an immediate defence unlike anti-bodies that require a time delay.
McCully and Ravnskov suggest that the arterial wall is damaged not via the endothelial cells, as is generally supposed, but through the vasa vasorum, the network of tiny vessels supplying blood to the walls of the arteries. The proposal is that the lipoprotein/micro-organism complex occludes the vas vasorum, and this is complicated by an inflammatory process. Veins and arteries are lined by endothelial cells, but they suggest that veins do not develop atherosclerosis because of the absence of vasa vasorum in the thin walls of the veins.
The model presented also allows incorporation of the observation that hyperhomocysteinaemia ( in those suffering from homocysteinuria) predisoses to atherosclerosis, and this is independent of cholesterol. Homocysteine binds with free amino-acids in a process called thiolation (the name derived from the presence of a free sulphydryl/sulfhydry group). When this takes place on LDL-cholesterol to an excessive degree in hypercysteinaemia, the thiolated LDL aggregates precipitate and can be taken up into foam cells, one of the major features of the atherosclerotic plaque.
The authors also point out the important suggestion that auto-antibodies against thiolated LDL may play a part in the development of a range of disease in which hyperhomocysteinaemia is found. These include lupus, rheumatoid arthritis, Behcet’s disease, inflammatory bowel disease. All have an increased susceptibility to coronary heart disease. Vasculitis is a common feature, with widespread complications.
The model is that the process starts with infection, LDL providing an immediate defence mechanism. The complex of LDL with micro-organism remnants might occlude vasa vasorum of the arteries. In the presence of normal immune competence, this products will be cleared. If immunity is impaired (
and this will include vitamin D deficiency - DSG) the the complex, especially if thiolated in hyperhomocysteinaemia, will cause damage to the wall of the artery and the vasa vasorum might rupture. If the infection is not neutralised, an unstable vulnerable plaque will result, leading to surface thrombosis and myocardial infarction.
This process can occur in arteries other than coronary arteries, and might be the mechanism of systemic arteritis/vasculitis complicating so-called auto-immune diseases. A micro-organism is the precipitating event, LDL complexes part of the defence mechanism, inflammation of the arterial wall a clinical and pathological feature, and defective immunity a necessary susceptibility factor.
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