The weight of evidence does not support the traditional cholesterol theory of cardiovascular disease. Instead, as molecular biology techniques improve, research is accumulating to suggest that a general poor quality diets lead to systemic inflammation and oxidative stress, and that this causes the physiological changes that lead to cardiovascular disease. For example, recent evidence suggests that inhibition of endothelial flow mediated dilation (FMD), caused by disruption to nitric oxide (NO) formation, is a contributory factor in the development of cardiovascular disease. Vascular endothelial dysfunction is associated with many of the traditional risk factors for cardiovascular disease including age, diabetes, smoking, dyslipidaemia and hypertension. Hyperglycaemia, at levels below clinical diagnosis for diabetes are known to inhibit normal flow mediated dilation in arteries. The mechanism by which this occurs could be through an increase in lipid peroxidation and decrease in NO bioavailability through hyperglycaemic induced oxidative stress.
One group of researchers1, investigated the effects of postprandial hyperglycaemia on the endothelial function of healthy men using a randomised cross-over trial. Following an overnight fast, 75 grams of glucose or fructose were ingested by the subjects and the brachial artery flow mediated dilation was assessed at intervals during the 3 hour postprandial period. At baseline there was no difference between the glucose or fructose groups, but flow mediated dilation decreased after the glucose ingestion, suggesting that the effect was related to insulin. When compared to fructose, ingestion of glucose caused a greater increase in plasma malonaldehyde, a decrease in arginine, an increase the asymmetric dimethylaginine (ADMA) to arginine ratio, suggesting that lipid peroxidation and NO synthesis had been affected. An inverse association between area under the curve for FMD and malonahdehyde suggested lipid peroxidation had suppressed NO production.
Acute ingestion of 75g of glucose (the amount ingested during an oral glucose tolerance test) may therefore suppress endothelial function in healthy men via lipid peroxidation. Increasing the ADMA:arginine ratio may imply that NO formation has been disrupted. The lack of change in inflammatory makers during this study suggest that these changes are independent of inflammation. That these changes are caused by insulin, is supported by continued FMD following fructose ingestion, and by maximum FMD suppression corresponding to peak glucose levels. Chronic postprandial hyperglycaemia is associated with oxidative stress, and this oxidative stress could cause inhibition of FMD and lead to the formation of vascular endothelial dysfunction. This may ultimately lead to the development of cardiovascular disease. Diets high in refined carbohydrates, and low in fibre, that induce high postprandial increase in glycaemia may therefore increase the risk of developing cardiovascular disease.
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