Dietary Fat and Cholesterol Dilemma: Acute Vascular Events

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Abstract
Several studies have shown that elevated serum low-density lipoprotein cholesterol (LDL-C), with sedentary habits, is the driving force for development of subclinical atherosclerosis, and hardening of the arteries. Oxidized lipids, including fatty acids, and cholesterol, play a key role in the pathogenesis of atherosclerosis. Based on the results of earlier epidemiological studies, professional societies, funding agencies, and regulatory agencies, developed dietary guidelines to limit the intake of trans-fats, saturated fats, and cholesterol-rich foods such as eggs. Some experts feel, that this approach and aggressive implementation of such guidelines to some extent, is responsible for the rapid increase, in the incidence of obesity and type-2 diabetes. The reason for this kind of thinking is related, to the promotion of low-fat-high-carbohydrate diets in these recommendations. In recent years, there seems to be some shift in the thinking of experts. Currently, some of the restrictions have been relaxed, and modifications in the guidelines, and guidance statements, seem to be imminent. Having said that, we would like to inform the readers, to be cautious about what they read in the print, because contrary to the conclusions derived from such diet-heart studies, the data on blood cholesterol still shows, a key role for these lipids and their oxidized products, in the development of atherosclerosis, endothelial dysfunction, and acute vascular events. Recent studies have shown that LDL-C is an independent risk, for the development of subclinical atherosclerosis, and hardening of the arteries in middle-aged, asymptomatic adults. Aggressive lowering of LDL-C, seems to be associated with better outcome, in several clinical studies. Furthermore, in individuals on statin prophylaxis, addition of an antinflammatory agent as complementary therapy, seems of offer better protection against CVD-events, suggesting a potential role for inflammation in the progress of the disease. The debate about the diet-heart is an age-old phenomenon, a complex topic, and it is too early to draw final conclusions. Furthermore, arterial thrombosis is a complex phenomenon, initiated and promoted by several cardiometabolic risks, and cluster of risks, and the story of thrombosis is not fully revealed as yet.
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