This report is a compilation of 22 studies that concludes that free radical damage to tumour suppressor genes causes coronary artery disease. This mutation allows cells to proliferate out of control, resulting in benign mini tumours between the endothelium lining and the smooth muscle walls of arteries. These tumours generate microscopic tears in the endothelium, which are patched with interlacing fibrin filaments as they expand. Minerals (particularly calcium), heavy metals, macrophages, and cellular detritus are trapped in this tough scar tissue. The last smooth layer of cholesterol that coats this vascular plaque has little bearing on its progression. According to current national cholesterol standards, over 75 percent of patients hospitalised for a heart attack had cholesterol levels that indicated they were not at high risk for a cardiovascular event. As a result, there is no link between cholesterol levels in the blood and coronary artery disease.
Author (S) Details
Independent Researcher Registered with ORCID, Canada.
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