Infective agents cause Plaque formation

Below is on the immediate cause of cardiovascular disease (CVD). Science progresses upon asking the right question. In this case “Why is among aboriginal peoples is CVD virtually unknown, until they switch to the western diet which is high in sugar??? The answer is fructose, which is one-half of the disaccharide sucrose (table sugar). We have gone from about 10 pounds of sugar all sources to over 150 pounds per year. Fructose which is a net 15 times more reactive than glucose damages the liver to cause insulin resistance. High insulin and the subsequent fatty liver cause the conditions associated with the western diet that includes a long list of age related conditions, not just CVD, all of which but cancer are very rare among the elderly aborigines on their traditional diet. This damages causes endothelial dysfunctions (the cells which line the artery walls and keep pathogens out of the interior of the arteries). Thus, we have the answer to why we get what wild animals including men do not get. The fix is to cleanse the liver through fasting, then gradually over years the body will heal itself.

A century ago the cause of arteriosclerosis was generally considered to originate from "direct irritation of [arterial] tissue by infection or toxins." Bacteria and viruses were considered as the main cause of atherosclerosis, because of increased plaques in patients dying of typhoid fever and other infections.

Sir William Osler, the Canadian pathologist and physician who became the Regius Professor of Medicine at Oxford and a leading physician of his time, described the vulnerable plaque as a pustule. More recently, much evidence has been reported to support the role of infections in vascular disease. In particular, cardiovascular mortality increases during influenza epidemics. A third of patients with acute myocardial infarction or stroke have had an infectious disease immediately before onset. Bacteriemia and periodontal infections are associated with an increased risk of cardiovascular disease. Serological markers of infection are elevated in patients with cardiovascular disease. And coronary arteries of children are found to be narrowed in children who died of infectious diseases. Beginning in 1939 and in the next decade, investigators discovered that lipoproteins function as a nonspecific immune system that is capable of inactivating a wide variety of bacteria, viruses, protozoans and their toxins. Lipoproteins form complexes with these organisms that render them inactive, and macrophages in the tissues are capable of phagocytosis of these complexes, leading to formation of foam cells that destroy these organisms. Homocysteine participates in the aggregation of lipoproteins by reacting with the protein to form cross-linkages, leading to aggregation, spontaneous precipitation and phagocytosis by macrophages to form foam cells. Thus in persons with elevated homocysteine levels, there is an increased ability of lipoproteins to form aggregates, leading to foam cell formation from macrophages by phagocytosis. Dr Kilmer McCully at http://www.spacedoc.com/ https://spacedoc.com/articles/kilmer-mccully-vulnerable-plaques-pt1-of-2
https://spacedoc.com/articles/kilmer_mccully_vulnerable_plaques_2

Also worth reading is https://spacedoc.com/articles/uffe-ravnskov-the-real-cause-of-heart-disease-3

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