The lipid theory of cardiovascular disease states that atherosclerosis, lesions and inelasticity in artery walls, was caused by dietary lipids including saturated fat and cholesterol. However, the scientific evidence does not support this contention and the lipid theory of cardiovascular disease has largely been superseded by more strongly evidenced theories. In particular, recent research shows that development of the metabolic syndrome and type 2 diabetes increase the risk of cardiovascular disease significantly. Based on this observations it has been suggested that insulin resistance may be pivotal in the development of atherosclerosis, a leading cause of cardiovascular disease. One of the physiological actions of insulin is to cause vasodilation of blood vessels through a mechanism that involves the generation of nitric oxide in the endothelial lining of the blood vessels. It is believed that this vasodilatory role of insulin may result in increased blood flow to the skeletal muscle, which in turn increases nutrient uptake.
Insulin resistance may interfere with this vasodilatory role of insulin, and in turn lead to endothelial dysfunction. Endothelial dysfunction is a phenomenon that describes the inability of the endothelial wall of the arteries to dilate proportionally to the flow pressure of the blood they contain. In other words the artery walls become inelastic and are unable to accommodate higher flow rates through the muscular wall deforming in response to blood flow. Such dysfunction in the endothelium may be one of the drivers of atherosclerosis, through damage to the endothelium by increased pressure, which in turn may increase the risk of cardiovascular disease. Studies have shown that obese insulin resistant individuals and individuals with type 2 diabetes have significantly reduced blood flow rates in peripheral tissues compared to lean normoglycemic controls, but that this reduced flow is related to endothelial dysfunction and not systemic vasodilatory mechanisms1. In addition, body fat levels are associated with the same endothelium dependent impaired vasodilation.
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