The root of cardiovascular disease almost always starts with endothelial dysfunction. The endothelia are the cells that line the blood vessels and are constantly exposed to the numerous toxins, waste products and metabolites that are present in the blood stream – components that are simply a fact of life, and more so, modern life. Chronic exposure to these blood-borne metabolites can inflame the endothelia. Inflammation of the endothelia is almost always the true starting point of CVD. Importantly, several longitudinal studies have demonstrated that there is a marked degree of individuality to the resilience of the endothelia – some of us are born with that admirable Teflon-coating to our blood vessels, others among us, less so.
The presence of inflammatory blood-borne metabolites is strongly associated with not only environmental exposures, lifestyle, nutrition and medical choices, but also genetic predispositions. Several well-studied and documented gene pathways are intimately involved in the unique capacity an individual has to detoxify and remove blood-borne metabolites. Simply stated, the innate detox capacity from one person to the next can vary widely.
When the vascular endothelium is chronically exposed to blood-borne toxins/metabolites, cellular changes associated with inflammation occur. Systems such as methylation must then be initiated to reduce this inflammation. If endothelial methylation is suboptimal, the inflammation to the lining of the blood vessels continues unchecked, paving the way for chronic vascular inflammation and eventually vascular dysfunction.
Chronic vascular inflammation initiates a cascade of events that includes the release of lipids from the liver and the transportation of these lipids to the vascular endothelia.
The final series of events that culminate in the formation of vascular plaque and more acute symptoms of CVD include the oxidation of the deposited lipids and the initiation of localized calcification.
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