For decades, time and money has been wasted on propagation of the cholesterol theory of cardiovascular disease. However, despite intensive propaganda campaigns the cholesterol theory of cardiovascular disease lies in tatters. And the scientific evidence is clear on the matter, despite the protestations to the contrary by proponents of the theory. There is little empirical evidence to show that high levels of dietary cholesterol, or saturated fat, are able to induce cardiovascular disease in healthy individuals. The stagnation and decline of the cholesterol theory has meant that other areas of research pertaining to cardiovascular disease have grown, and of these the role of oxidative stress is perhaps the most important and interesting. It was Denham Harman who first proposed the link between free radicals and disease in the 1950’s and since that time the scientific evidence has verified the theory with supportive data in many different diseases. Currently, studies suggest a role for free radicals in the aetiology of cardiovascular disease.
The arteries of the body are not simple tubes, but are complex reactionary systems that must respond to the pressure changes caused by the flow of blood. In particular, the muscular walls allow the arteries to widen in response to flow, and this is possible because of their muscular walls. The muscles then return the arteries to their original diameter by contracting, and this process is known as flow mediated dilation. Nitric oxide is a signal molecule in the endothelium of the arteries required for the correct dilation of arteries. Evidence suggests that oxidative stress inhibits the enzyme nitric oxide synthase and this reduces the concentration of nitric oxide in the arteries. This in turn that reduces the ability of the endothelium to relax in response to flow, raising blood pressure and leading to the development of endothelial dysfunction, a disorder characterised by an inelasticity in the artery walls. Endothelial dysfunction may initiate or contribute to the development of atherosclerosis.
The role of free radicals in the development of dysfunction in the artery walls is reasonably well understood. The idea that free radicals are able to cause damage to the endothelial lining of the arteries would suggest that antioxidants be effective at reversing endothelial dysfunction or preventing its development. A number of studies have investigated the effects of antioxidant supplements on arterial stiffness in human subjects. In one meta-analysis1, researchers assessed a number of studies that used vitamin C. E and A and β-carotene and observed effects on arterial stiffness. The results of the meta-analysis showed that antioxidant vitamin significantly reduced arterial stiffness. The benefits of antioxidant vitamin on arterial stiffness was irrespective of age the subjects and duration of intervention. As might be expected, those with a low baseline antioxidant status, as measured by plasma vitamin C levels, showed larger benefits with antioxidant vitamin therapy compared to those with a high baseline antioxidant status.
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