Not only are individual nutrients capable of modifying cardiovascular risk factors and augmenting endothelial function, they also have the capacity to exert beneficial athero-protective effects at various stages of the development and progression of atherosclerotic plaque. Modulation of endothelial function is, therefore, the likely mechanism through which medical nutrition therapy, either those targeting diet responsive risk factors or the systemic pro-inflammatory and pro-oxidative state of individuals with atherosclerosis, have been shown to delay the onset and progression of atherosclerosis. Its onset has been deemed a sentinel event in the progression to atherosclerosis. Endothelial dysfunction may be precipitated by genetic factors, such as hypercoagulability and blood group, and it has been proposed as the mechanism linking cardiovascular risk factors to established disease. Endothelial dysfunction is a state of impairment of these regulatory functions, characterised by an impaired endothelium dependent vasodilatory response to changes in flow or stimuli and a systemic pro-inflammatory and pro-oxidative state. It is a dynamic organ that plays a key role in vascular homeostasis and systemic well-being. The vascular endothelium is a single, monolayer of cells acting as a barrier between blood and a pro-thrombotic vessel wall.
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