Red Palm Fruit Oil

C. Artherosclerosis and Coronary Heart Disease

  • 1. Cholesterol vehicle in experimental atherosclerosis. 22. Refined, bleached, deodorized (RBD) palm oil, randomized palm oil and red palm oil

    Kritchevsky, D. et al. (2000). Cholesterol vehicle in experimental atherosclerosis. 22. Refined, bleached, deodorized (RBD) palm oil, randomized palm oil and red palm oil. Nutrition Research. 20(6):887-892

    The atherogenic effects of refined, bleached and deodorized (RBD) palm oil were compared with those of randomized RBD palm oil and red palm oil. RBD palm oil contains 41.2% palmitic acid, 2.6% at the SN2 position. In randomized palm oil, 13.6% of the palmitic acid is in the SN2 position. Randomized palm oil is significantly more atherogenic for rabbits than is RBD palm oil, supporting our earlier findings that the increasing amounts of palmitic acid in the SN2 position of a fat lead to an increased atherogenic effect. Red palm oil is the oil initially obtained from the palm fruit which contains carotenes and Vitamin E that are removed during refining. Red palm oil was significantly less atherogenic than RBD palm oil supporting the hypothesis that carotenoids and Vitamin E may protect against atherosclerosis. The oils tested had similar effects on serum and liver lipids.

  • 2. The effect of red palm olein and refined palm olein on lipids and haemostatic factors in hyperfibrinogenaemic subjects

    Scholtz et al. (2004). The effect of red palm olein and refined palm olein on lipids and haemostatic factors in hyperfibrinogenaemic subjects. Thrombosis research 113:13-25.

    Little is known about the physiological effects of red palm olein (RPO). The effects of red palm olein and palm olein (POL) compared to sunflower oil (SFO), on lipids, haemostatic factors and fibrin network characteristics in hyperfibrinogenaemic volunteers were investigated. Fifty-nine free-living, hyperfibrinogenaemic volunteers participated in this randomized, controlled, single blind parallel study. After a 4-week run-in, during which subjects received sunflower oil products, they were paired and randomly assigned to one of three intervention groups receiving products containing 25 g/day (≈12% of total energy intake) of either red palm olein, palm olein or sunflower oil for another 4 weeks. Anthropometric measurements, blood samples and dietary intakes were measured before run-in, and before and after intervention. The differences in changes in total serum cholesterol response between palm olein and red palm olein (+0.59 vs. +0.18 mmol/l; p=0.053), and between palm olein and sunflower oil (+0.59 vs. −0.003 mmol/l; p≤0.01) were significant. The low-density lipoprotein cholesterol (LDLC) response in the palm olein—and sunflower oil—groups also differed significantly (+0.42 vs. −0.11 mmol/l; p≤0.01). Tissue plasminogen activator antigen (tPAag) decreased significantly in the red palm olein group compared to the palm olein—and sunflower oil—groups. No effects were found in other haemostatic variables. Palm olein and red palm olein had no independent effect on fibrin network characteristics. In conclusion, compared to palm olein, red palm olein had less detrimental effects on the lipid profile and decreased tissue plasminogen activator antigen. Studies in larger groups are advised for confirmation of results, elucidation of mechanisms and effects of nonglyceride constituents of red palm oil (PO)

  • 3. Proposed mechanisms for red palm oil induced cardioprotection in a model of hyperlipidaemia in the rat.

    Esterhuyse JS et al. (2006). Proposed mechanisms for red palm oil induced cardioprotection in a model of hyperlipidaemia in the rat. Prostaglandins Leukotrienes and Essential Fatty Acids. 75(6):375-84.

    High-cholesterol diets alter myocardial and vascular NO-cGMP signaling and have been implicated in ischaemic/reperfusion injury. We investigated the effects of dietary red palm oil (RPO) containing fatty acids, carotonoids, tocopherols and tocotrienols on myocardial ischaemic tolerance and NO-cGMP pathway function in the rat. Wistar rats were fed a standard rat chow+/-RPO, or a standard rat chow+cholesterol+/-RPO diet. Myocardial mechanical function and NO-cGMP signaling pathway intermediates were determined before, during and after 25 min ischaemia. RPO-supplementation improved aortic output recovery and increased myocardial ischaemic cGMP concentrations. Simulated ischaemia (hypoxia) increased cardiomyocyte nitric oxide levels in the two RPO supplemented groups, but not in control non-supplemented groups. RPO supplementation also increased hypoxic nitric oxide levels in the control diet fed, but not the cholesterol fed rats. These data suggest that dietary RPO may improve myocardial ischaemic tolerance by increasing bioavailability of NO and improving NO-cGMP signaling in the heart.