A major public health concern of affluent nations is the excessive consumption of dietary fats which are now closely linked to coronary heart disease. Against this scenario, the tropical oils and palm oil in particular, have been cast as major villains in the U.S.A., despite the fact that palm oil consumption there is negligible. The unsuspecting public may not realise that the call to avoid palm oil is nothing more than a trade ploy since in recent years palm oil has been very competitive and has gained a major share of the world's edible oils and fats market. Many also lose sight of the fact that, palm oil, like other edible oils and fats, is an important component of the diet. The allegation that palm oil consumption leads to raised blood cholesterol levels and is therefore atherogenic is without scientific foundation. Examination of the chemical and fatty acid composition of palm oil or its liquid fraction should convince most nutritionists that the oil has little cholesterol-raising potential. The rationale for these are: it is considered cholesterol free. its major saturated fatty acid, palmitic acid (16:0) has recently been shown to be neutral in its cholesterolaemic effect, particularly in situations where the LDL receptors have not been down-regulated by dietary means or through a genetic effect. palm oil contains negligible amounts (less than 1.5%) of the hypercholesterolemic saturated fatty acids, namely lauric acid (12:0) and myristic acid (14:0). it has moderately rich amounts of the hypocholesterolaemic, monounsaturated oleic acid (18:1, omega-9) and adequate amounts of linoleic acid. (18:2, omega-6). It contains minor components such as the vitamin E tocotrienols which are not only powerful antioxidants but are also natural inhibitors of cholesterol synthesis. Feeding experiments in various animal species and humans also do not support the allegation that palm oil is atherogenic. On the contrary, palm oil consumption reduces blood cholesterol in comparison with the traditional sources of saturated fats such as coconut oil, dairy and animal fats. In addition, palm oil consumption may raise HDL levels and reduce platelet aggregability. As with all nutrients, there is a need to obtain a balance of different fatty acids found in fats in edible oils and other food sources. There is no single ideal source of fat that answers to the recent American Heart Association's call to reflect a 1:1:1 ratio of saturated, monounsaturated and polyunsaturated fats in relation to the recommended dietary fat intake of 30% of calories or less.(ABSTRACT TRUNCATED AT 400 WORDS)
Atherosclerosis impairs endothelium-dependent relaxation of large conduit arteries. Because coronary resistance vessels are spared from the development of overt atherosclerosis, endothelium-dependent responses were examined in these vascular segments. Malaysian cynomolgus monkeys (n = 6) were made atherosclerotic by being fed a 0.7% cholesterol diet for 18 months. Control monkeys (n = 6) were fed a standard diet. Coronary microvessels (122-220 microns) were studied in a pressurized (20 mm Hg), no-flow state using a video-imaging apparatus. Relaxations of microvessels, preconstricted with the thromboxane analogue U46619, were determined in response to acetylcholine, bradykinin, the calcium ionophore A23187, adenosine, and sodium nitroprusside. Microvascular relaxations to bradykinin and A23187 were reduced in atherosclerotic monkeys compared with controls, whereas acetylcholine produced additional contraction in atherosclerotic monkeys. Responses of preconstricted microvessels to adenosine and sodium nitroprusside were identical in atherosclerotic and control animals. Indomethacin did not alter responses in control or atherosclerotic animals. Histologic examination revealed neither intimal thickening nor plaque formation in microvessels of this size class despite marked changes in conduit arteries. Electron microscopy showed minor alterations of endothelial cell morphology in microvessels of atherosclerotic animals. In conclusion, long-term hypercholesterolemia markedly impairs endothelium-dependent vascular relaxation in the coronary microcirculation where overt atherosclerosis does not develop. These changes in endothelial cell function may significantly alter regulation of myocardial perfusion by neurohumoral stimuli.