Understanding the Link Between Inflammation and Atherosclerosis

‘Cardiovascular disease: Inflammation drives atherosclerosis—and may also help limit it’, is the title of the press release issued by Ludwig Maximilian University of Munich (LMU), which aims to instill confidence. The study by LMU researchers, published in the journal Circulation, uses mice to investigate the influence of inflammatory processes in blood vessels on cholesterol deposition. In doing so, the large team of authors draws on the repeatedly stated theory that atherosclerotic plaques form because immune system cells (macrophages) attach themselves to the vessel wall to absorb fats and cellular debris, but in the process accumulate themselves and partially transform into so-called foam cells, thereby further driving local inflammation.

What this theory cannot explain is why the deposition of blood lipids in the vessel walls occurs in just a few specific areas of the arterial circulatory system (namely, almost exclusively in the region of the heart), while plaques are practically nonexistent in the venous system. The authors write that the immune system is involved in this process. That is not incorrect. However, it can obviously be ruled out as a causal factor. The inflammatory lesions are a consequence of the atherosclerotic process.

According to their theory, the LMU researchers see a small RNA molecule (miR-147)—which is produced by macrophages (phagocytes) that are still intact and is thought to regulate their activity—as a potential therapeutic target. Their goal is to reactivate the macrophages that have been converted into (inactive) foam cells, thereby promoting the removal of stored blood lipids and cellular debris. The researchers are well aware that this approach does not address the actual cause of atherosclerotic deposits. They are satisfied with the prospect of slowing down atherosclerosis.

Nearly forty years ago, Dr. Matthias Rath and Dr. Linus Pauling pointed out the link between the development of atherosclerosis and the compromised integrity of connective tissue, which is responsible for the stability and elasticity of blood vessels. They identified a chronic deficiency of the required micronutrients—primarily vitamin C and the amino acid lysine (both essential for humans)—as the key factor in the inadequate repair of connective tissue, which is primarily composed of collagen. Scurvy is known as an extreme case of acute vitamin deficiency. It is now considered largely eradicated. The situation is entirely different with the epidemic occurrence of atherosclerosis: it develops with a persistent undersupply of these micronutrients and can thus be regarded as an early form of scurvy. The rupture of blood vessels that have become unstable is prevented over the long term by the deposition of blood lipids, particularly lipoprotein(a). At the latest since 2015, when definitive proof of this concept regarding the formation of atherosclerotic plaques through compensatory repair with Lp(a) was established, the cholesterol hypothesis—upheld for decades—must be considered obsolete. The fact that it is still being championed, contrary to scientific logic, can be explained by the exorbitant profit prospects of unscrupulous pharmaceutical manufacturers, who, at the expense of the health of millions of heart patients.

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