Hyperlipidemia is an important risk factor for cardiovascular disease and a leading cause of mortality and is often associated with obesity. Different types of fats and oils may have different effects on cardiovascular disease and obesity. This study investigated the effects of palm olein oil (PO), corn oil (CO), and camel hump fat (CHF) on plasma lipids and white adipose tissues of rats. A total of 18 male albino rats were divided equally into three groups. Each group was fed a diet containing one of these types of oils and fats for 8 weeks. The levels of total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), total triglyceride (TG), glucose, alanine aminotransferase (ALT), and aspartate aminotransferase (AST) were analyzed in blood plasma. Body mass index (BMI), body weight gain (%BWG), and the weight of adipose tissues were investigated. The results showed no significant differences between groups in TC. However, the highest level of HDL-C was observed in the CHF group, with no significant differences in the PO group and a significant decrease in the CO group. The CHF group showed a significant reduction in LDL-C, blood glucose levels, and the atherosclerosis index compared with the other groups. Furthermore, the lowest TG level was observed in the CHF group, with no significant difference compared with the CO group. The PO group showed a significant decrease in the ALT level compared with the other groups. The lowest AST level was observed in the PO group, with no significant difference compared with the CO group. A significant decrease in the percentage of total adipose tissues, namely epididymal, retroperitoneal, and perirenal cells, was observed in the CHF group. In conclusion, CHF consumption may have a positive effect on plasma lipids and obesity. Moreover, we recommend the completion of research to identify the optimal combination of vegetable oils and CHF for achieving a balance among the health indicators included in this study.

Palm oil is natural oil packed with important compounds and fatty acids ready to be exploited in lipid-based formulations and drug delivery. Palm oil and palm kernel oil contain long-chain and medium-chain triglycerides, respectively, including phytonutrients such as tocotrienol, tocopherol and carotenes. The exploitation of these compounds in a lipid-based formulation would be able to address hydrophobicity, lipophilicity, poor bioavailability and low water-solubility of many current drugs. The utilisation of palm oil as part of the drug delivery system seemed to improve the bioavailability and solubility of the drug, stabilising emulsification of formulation between emulsifier and surfactant, promoting enhanced drug permeability and performance, as well as extending the shelf-life of the drug. Despite the complexity in designing lipid-based formulations, palm oil has proven to offer dynamic behaviour in providing versatility in drug design, form and delivery. However, the knowledge and application of palm oil and its fractions in lipid-based formulation are scarce and interspersed. Therefore, this study aims to focus on the research and outcomes of using palm oil in lipid-based formulations and drug delivery systems, due to the importance of establishing its capabilities and benefits.

In the ongoing discussion on the health properties of palm oil, a study of the effect a diet supplemented with palm oil on blood and liver biochemical parameters, beta-carotene and tocochromanols content as well as antioxidant activity was undertaken. Forty Wistar rats were randomly divided into five groups, fed with a diet supplemented with plant-based frying commercial fat, palm oil, 7.5% palm oil and 2.5% concentrate from palm oil and 10% of rapeseed oil, respectively. After 21 days, blood samples and livers were collected to determine beta-carotene and tocochromanols concentrations, antioxidant activity using DPPH* radical scavenging activity and TEAC methods, insulin, glucagon, serum triacyloglycerols and cholesterol levels, glucose in blood serum and glycogen in the livers. Research has shown valuable biological properties of palm oil in terms of plasma glucose, total cholesterol, low-density lipoprotein (LDL) cholesterol, and triacylglycerol concentrations which was related to the high content of beta-carotene and tocochromanols. PRACTICAL APPLICATION: Public concern over the health properties of palm oil has been growing. Therefore, this study supplements existing knowledge in this area based on experimental rat observations. In the presented research, plasma glucose was significantly reduced and no additional growth of total or LDL cholesterol, as well as triacylglycerol concentration, was observed after consuming a palm oil-based diet. Palm oil was a good source of beta-carotene and tocochromanols, which were preferentially distributed in rats' livers. Bioavailability of vitamin E-active compounds in palm oil supplemented rats' livers was relatively high as compared to the rapeseed oil group, therefore this observation complements literature in the field of tocotrienols and tocopherols. Studies have not confirmed the harmful effect of palm oil on rats, however in depth human studies appear to be a promising direction for further research.

Palm oil consumption and its effects on serum lipid levels and cardiovascular disease in humans is still a subject of debate. Advocacy groups with varying agenda fuel the controversy. This update intends to identify evidence-based evaluations of the influence of palm oil on serum lipid profile and cardiovascular disease. Furthermore, it suggests a direction for future research. The sources of information were based on a PubMed, Google Scholar, African Journal online and Medline search using key words including: palm oil, palmitic acid, saturated fatty acids and heart disease. Published animal and human experiments on the association of palm oil and its constituents on the serum lipid profile and cardiovascular disease were also explored for relevant information. These papers are reviewed and the available evidence is discussed. Most of the information in mainstream literature is targeted at consumers and food companies with a view to discourage the consumption of palm oil. The main argument against the use of palm oil as an edible oil is the fact that it contains palmitic acid, which is a saturated fatty acid and by extrapolation should give rise to elevated total cholesterol and low-density lipoprotein cholesterol levels. However, there are many scientific studies, both in animals and humans that clearly show that palm oil consumption does not give rise to elevated serum cholesterol levels and that palm oil is not atherogenic. Apart from palmitic acid, palm oil consists of oleic and linoleic acids which are monounsaturated and polyunsaturated respectively. Palm oil also consists of vitamins A and E, which are powerful antioxidants. Palm oil has been scientifically shown to protect the heart and blood vessels from plaques and ischemic injuries. Palm oil consumed as a dietary fat as a part of a healthy balanced diet does not have incremental risk for cardiovascular disease. Little or no additional benefit will be obtained by replacing it with other oils rich in mono or polyunsaturated fatty acids.

Oleic acid has been shown to lower high blood pressure and provide cardiovascular protection. Curiosity arises as to whether super olein (SO), red palm olein (RPO) and palm olein (PO), which have high oleic acid content, are able to prevent the development of hypertension.

Four-week-old male spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats were fed 15% SO, RPO or PO supplemented diet for 15 weeks. After 15 weeks of treatment, the systolic blood pressure (SBP) of SHR treated with SO, RPO and PO were 158.4±5.0 mmHg (p<0.001), 178.9±2.7 mmHg (p<0.001) and 167.7±2.1 mmHg (p<0.001), respectively, compared with SHR controls (220.9±1.5 mmHg). Bradycardia was observed with SO and PO. In contrast, the SBP and heart rate of treated WKY rats were not different from those of WKY controls. The SO and PO significantly reduced the increased heart size and thoracic aortic media thickness observed in untreated SHR but RPO reduced only the latter. No such differences, however, were observed between the treated and untreated WKY rats. Oil Red O enface staining of thoracic-abdominal aorta did not show any lipid deposition in all treated rats. The SO and RPO significantly raised serum alkaline phosphatase levels in the SHR while body weight and renal biochemical indices were unaltered in both strains. Serum lipid profiles of treated SHR and WKY rats were unchanged, with the exception of a significant reduction in LDL-C level and total cholesterol/HDL ratio (atherogenic index) in SO and RPO treated SHR compared with untreated SHR.

The SO, RPO and PO attenuate the rise in blood pressure in SHR, accompanied by bradycardia and heart size reduction with SO and PO, and aortic media thickness reduction with SO, RPO and PO. The SO and RPO are antiatherogenic in nature by improving blood lipid profiles in SHR.

Systemic chemotherapy is the only current method of treatment that provides some chance for long-term survival in patients with advanced or metastatic cancer. γ-Tocotrienol is a natural form of vitamin E found in high concentrations in palm oil and displays potent anticancer effects, but limited absorption and transport of by the body has made it difficult to obtain and sustain therapeutic levels in the blood and target tissues. Statins are inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A (HMGCoA) reductase and are an example of a promising cancer chemotherapeutic agent whose clinical usefulness has been limited due to high-dose toxicity. Similarly, erlotinib and gefitinib are anticancer agents that inhibit the activation of individual HER/ErbB receptor subtypes, but have shown limited clinical success because of heterodimerization between different EGF receptor family members that can rescue cancer cells from agents directed against a single receptor subtype. Recent studies have investigated the anticancer effectiveness of low-dose treatment of various statins or EGF receptor inhibitors alone and in combination with γ-tocotrienol on highly malignant +SA mouse mammary epithelial cells in vitro. Combined treatment with subeffective doses of γ-tocotrienol with these other chemotherapeutic agents resulted in a synergistic inhibition of +SA cell growth and viability. These findings strongly suggest that combined treatment of γ-tocotrienol with other anticancer agents may not only provide an enhanced therapeutic response but also provide a means to avoid the toxicity, low bioavailability, or limited therapeutic action associated with high-dose monotherapy.

Individually and in combination with other oils, the tropical oils impart into manufactured foods functional properties that appeal to consumers. The use of and/or labeling in the ingredient lists give the impression that these oils are used extensively in commercially processed foods. The estimated daily intake of tropical oils by adult males is slightly more than one fourth of a tablespoon (3.8 g), 75% of which consists of saturated fatty acids. Dietary fats containing saturated fatty acids at the beta-position tend to raise plasma total and LDL-cholesterol, which, of course, contribute to atherosclerosis and coronary heart disease. Health professionals express concern that consumers who choose foods containing tropical oils unknowingly increase their intake of saturated fatty acids. The saturated fatty acid-rich tropical oils, coconut oil, hydrogenated coconut oil, and palm kernel oil, raise cholesterol levels; studies demonstrating this effect are often confounded by a developing essential fatty acid deficiency. Palm oil, an essential fatty acid-sufficient tropical oil, raises plasma cholesterol only when an excess of cholesterol is presented in the diet. The failure of palm oil to elevate blood cholesterol as predicted by the regression equations developed by Keys et al. and Hegsted et al. might be due to the dominant alpha-position location of its constituent saturated fatty acids. If so, the substitution of interesterified artificial fats for palm oil in food formulations, a recommendation of some health professionals, has the potential of raising cholesterol levels. A second rationale addresses prospective roles minor constituents of palm oil might play in health maintenance. This rationale is founded on the following observations. Dietary palm oil does not raise plasma cholesterol. Single fat studies suggests that oils richer in polyunsaturated fatty acid content tend to decrease thrombus formation. Anomalously, palm oil differs from other of the more saturated fats in tending to decrease thrombus formation. Finally, in studies comparing palm oil with other fats and oils, experimental carcinogenesis is enhanced both by vegetable oils richer in linoleic acid content and by more highly saturated animal fats. The carotenoid constituents of red palm oil are potent dietary anticarcinogens. A second group of antioxidants, the tocotrienols, are present in both palm olein and red palm oil. These vitamin E-active constituents are potent suppressors of cholesterol biosynthesis; emerging data point to their anticarcinogenic and antithrombotic activities. This review does not support claims that foods containing palm oil have no place in a prudent diet.

Several studies have reported on the effect of refined, bleached and deodorized palm oil (RBD-PO) incorporation into the diet on blood cholesterol concentrations and on the development of atherosclerosis. However, very little work has been reported on the influence of red palm oil (RPO), which is higher in carotenoid and tocopherol content than RBD-PO. Thus, we studied the influence of RPO, RBD-PO and a RBD-PO plus red palm oil extract (reconstituted RBD-PO) on plasma cholesterol concentrations and aortic accumulation vs. hamsters fed coconut oil. Forty-eight F1B Golden Syrian hamsters (Mesocricetus auratus) (BioBreeders, Watertown, MA) were group housed (three/cage) in hanging polystyrene cages with bedding in an air-conditioned facility maintained on a 12-h light/dark cycle. The hamsters were fed a chow-based hypercholesterolemic diet (HCD) containing 10% coconut oil and 0.1% cholesterol for 2 weeks at which time they were bled after an overnight fast and segregated into four groups of 12 with similar plasma cholesterol concentrations. Group 1 continued on the HCD, Group 2 was fed the HCD containing 10% RPO in place of coconut oil, Group 3 was fed the HCD containing 10% RBD-PO in place of coconut oil and Group 4 was fed the HCD with 10% reconstituted RBD-PO for an additional 10 weeks. Plasma total cholesterol (TC) and non-high-density lipoprotein-cholesterol (HDL-C) (very low- and low-density lipoprotein) concentrations were significantly lower in the hamsters fed the RPO (-42% and -48%), RBD-PO (-32% and -36%) and the reconstituted RBD-PO (-37% and -41%) compared to the coconut oil-fed hamsters. Plasma HDL-C concentrations were significantly higher by 14% and 31% in hamsters fed the RBD-PO and RPO compared to the coconut oil-fed hamsters. Plasma triglyceride (TG) concentrations were significantly lower in hamsters fed RBD-PO (-32%) and the reconstituted RBD-PO (-31%) compared to the coconut oil-fed hamsters. The plasma gamma-tocopherol concentrations were higher in the coconut oil-fed hamsters compared to the hamsters fed the RPO (60%), RBD-PO (42%) and the reconstituted RBD-PO (49%), while for plasma alpha-tocopherol concentrations, the coconut oil-fed hamsters were significantly higher than only the RPO-fed hamsters (21%). The coconut oil-fed hamsters also had significantly higher plasma lipid hydroperoxide concentrations compared to RBD-PO (112%) and the reconstituted RBD-PO (485%). The hamsters fed the coconut oil diet excreted significantly more fecal total neutral sterols and cholesterol compared to the hamsters fed the RBD-PO (158% and 167%, respectively). The coconut oil-fed hamsters had significantly higher levels of aortic total, free and esterified cholesterol compared to the hamsters fed the RPO (74%, 50% and 225%, respectively), RBD-PO (57%, 48% and 92%, respectively) and the reconstituted RBD-PO (111%, 94% and 94%, respectively). Also, aortic free/ester cholesterol ratio in the aortas of hamsters fed RPO was significantly higher than in those fed the coconut oil (124%). In conclusion, hamsters fed the three palm oil preparations had lower plasma TC and non-HDL-C and higher HDL-C concentrations while accumulating less aortic cholesterol concentrations compared to hamsters fed coconut oil.

The effects on serum lipids of palm oil (PA) used in Chinese diets were compared with those of soybean oil (SO), peanut oil (PE) and lard (LA) in normocholesterolemic subjects and with that of PE in hypercholesterolemic subjects. Normocholesterolemic subjects [120 men, 18-25 y, total cholesterol (TC) 2.8-5.0 mmol/L] were assigned to four groups to consume test diets for six consecutive weeks after a run-in period of 3 wk. About 30% of dietary energy was derived from fat, 75-80% of which came from test oils. In comparison with the entry level, the average serum TC and LDL cholesterol (LDL-C) were 6.7 and 13.1% lower, respectively, in the PA group and 22.8 and 30.7% higher, respectively, (P < 0.05) in the LA group. At the end of the test, serum TC, LDL-C and the ratio of TC/HDL cholesterol (HDL-C) in the PA group were significantly lower than those of the LA group. Hypercholesterolemic subjects (31 men, 20 women, 32-68 y, TC 5.5-7.0 mmol/L) were divided into two groups. For 6 wk, one group (15 men, 10 women) consumed the PA diet; another group (16 men, 9 women) consumed the PE diet. After a 3-wk interval, the two groups interchanged diets for another 6 wk. The test diets again contained about 30% energy from fat, 60-65% of which came from test oils. Compared with entry values, the PA diet caused significant reductions in serum TC, LDL-C and TC/HDL-C during the first 6 wk and also a significant reduction in TC/HDL-C during the second 6 wk. The PE diet had no significant influence on serum lipids in either experimental period.

The effects of dietary fat and dietary fibres on blood pressure, serum lipids and platelet aggregation in spontaneously hypertensive and Wistar-Kyoto rats have been investigated. The systolic and diastolic blood pressure values were increased with increasing amounts of dietary fat and normalized by dietary fibre supplementation. The greatest reduction in blood pressure was obtained by a combination of reduced dietary fat and supplementary dietary fibre. Addition of dietary fibre when the amount of dietary fat was high or reduction of dietary fat when the amount of dietary fibre was low gave a smaller effect. In both rat strains the decreases in systolic and diastolic blood pressure values after reducing dietary fat and/or increasing dietary fibre were about 10-15 mmHg. Serum total cholesterol and serum HDL-cholesterol concentrations were reduced by reduction of dietary fat or a combination of dietary fat reduction and dietary fibre addition. A combination of dietary fat reduction and dietary fibre addition was the most effective dietary change for reducing serum triacylglycerol concentration and platelet aggregation. The present study demonstrates that in this experimental model it is possible to reduce risk indicators of coronary heart disease significantly by changing dietary habits.

The objective of this study was to investigate the effect of psyllium husk fiber supplementation to the diets of soybean and coconut oil on serum lipids in normolipidemic humans. A 28-day study was divided into four 7-day experimental periods. Dietary periods were soybean oil (SO), soybean oil plus psyllium fiber (SO + PF), coconut oil (CO) and coconut oil plus psyllium fiber (CO + PF), and were arranged to a randomized cross over design. Ten subjects consumed controlled diet containing 30% fat calories (20% from test oils and 10% from controlled diet) and 20 g per day of psyllium during fiber supplementation periods. SO + PF diet significantly reduced serum cholesterol compared with SO diet (P < 0.001). CO + PF diet significantly reduced serum cholesterol compared with CO diet (P < 0.014). Hypocholesterolemic response was greater with SO + PF compared with CO + PF (0.36 mmol 1(-1) vs 0.31 mmol 1(-1)). Reductions in low-density lipoprotein (LDL) cholesterol and apolipoprotein (apo) B were parallel to reductions of serum cholesterol. SO diet decreased, while CO diet increased serum cholesterol, LDL cholesterol and apo B. Very-low density lipoprotein cholesterol, high-density lipoprotein cholesterol and apo A-1 were unaffected by psyllium fiber and saturation of fat. Reduction of serum cholesterol was due to reduction of LDL cholesterol. Psyllium fiber supplementation lowered serum cholesterol regardless of saturation level of dietary fat.

Substitution of palmolein (POL) for groundnut oil (GNO) doubles saturated fatty acids and decreases by half the linoleic acid (18:2n-6) content of Indian diets. The effects of this substitution on selected parameters of cardiovascular risk and membrane functions were studied in middle-aged subjects. Both metabolic (short-term) and "in-home" (long-term) studies were conducted, and the subjects were crossed over from GNO to POL or vice versa. During both studies and in both sexes, blood pressure, plasma levels of total cholesterol and triglycerides and their distributions in various lipoprotein fractions were not altered. The lower 18:2n-6 and higher 16:0 intakes were reflected in fatty acid compositions of cholesteryl esters and triglycerides. However, the plasma and platelet phospholipid fatty acid patterns did not shift toward saturation. The observation that the levels of long-chain polyunsaturated fatty acids in phospholipids were similar at the end of GNO and POL regimens indicates that 18:2n-6 furnished during POL regimen may be sufficient to maintain the levels of arachidonic acid in cell membranes. Platelet aggregation, erythrocyte membrane fluidity, and activity of Na+, K+ ATPase, a membrane-bound enzyme, were essentially similar at the end of the two oil regimens. These results indicate that POL is comparable to GNO and may not induce hypercholesterolemia in Indian subjects consuming cereal-based diets containing 30% total fat calories and low cholesterol.

In the present study the effect of replacement of dietary fat by palm oil in the normal Western diet on the in vitro release of the inflammatory cytokines tumour necrosis factor (TNF), interleukin (IL)-6 and IL-8 was examined. A maximal replacement of 700 g/kg dietary fat was achieved for thirty-eight male volunteers who consumed either a palm-oil diet or a control diet in a double-blind, cross-over study with 6-week experimental periods, and 3-week run-in and wash-out periods. At the end of both experimental periods, whole blood was stimulated in vitro with 0.02 (sub-optimal), or 10 ng lipopolysaccharide (LPS)/ml (maximal), whereafter TNF, IL-6, and IL-8 concentrations in the culture supernatant fraction were measured using specific enzyme-linked immunosorbent assays (ELISA). Mean cytokine production with sub-optimal, or maximal LPS stimulation of peripheral whole blood was similar for both the palm oil, and the control group. The relative TNF response, however, was reduced by replacement of dietary fat with palm oil. Separate analysis of the data from the first and second experimental periods strongly suggested that the residual effect of the palm-oil diet on the relative TNF response was longer than 9 weeks. Cytokine homeostasis determines the course of the inflammatory response and the progression of atherosclerosis. The effect of palm-oil consumption on the proneness of the peripheral blood cells to produce TNF may, therefore, alter the prevalence of these common diseases.

Thirty-eight male volunteers participated in a double-blind cross-over trial evaluating the effect of replacing the usual sources of saturated fat in the Dutch diet (animal fats and hydrogenated oils) by palm oil, which is virtually free of cholesterol and trans-fatty acids, on serum lipids, lipoproteins and apolipoproteins. Maximum (about 70%) replacement had no significant effect on serum total cholesterol or most lipoprotein fractions, but resulted in an 11% increase in serum high-density-lipoprotein (HDL)2-cholesterol relative to the control (P2 = 0.01). The palm-oil diet also caused an 8% decrease in low-density-lipoprotein (LDL):HDL2 + HDL3-cholesterol ratio (P2 = 0.02) as well as a 9% decrease in triacylglycerols in the low-density-lipoprotein fractions (P2 = 0.01). Palm oil consumption resulted in a 4% increase in serum apolipoprotein AI (P2 = 0.008) and a 4% decrease in apolipoprotein B (P2 = 0.01) relative to the control diet; the B:AI apolipoprotein ratio was decreased by 8% (P2 < 0.0001). These results were not significantly affected by the different lipoprotein E phenotypes of the volunteers. Although the observed differences were relatively modest, the present study, nonetheless, indicates that dietary palm oil, when replacing a major part of the normal fat content in a Dutch diet, may slightly reduce the lipoprotein- and apolipoprotein-associated cardiovascular risk profiles.