METHODS AND STUDY DESIGN: We searched Medline, Embase, Cochrane Central Registry of Controlled Trials and CINAHL. Clinical trials were eligible if they compared palm oil-rich diets with diets rich in MUFAs or PUFAs. We pooled results of included studies using a random effects model and assessed the quality of the evidence and certainty of conclusions using the GRADE approach.

RESULTS: Intake of palm oil intake compared to oils rich in MUFA was associated with increased levels of total cholesterol (TC) [mean difference (MD)=0.27 mmol/L; 95% CI 0.08 to 0.45], LDL-C (MD=0.20 mmol/L; 95% CI 0.02 to 0.37) and HDL-C (MD=0.06 mmol/L; 95% CI 0.02 to 0.10). Similarly, for comparison with oils rich in PUFAs, palm oil showed increased in TC (MD=0.38 mmol/L; 95% CI 0.14 to 0.62), LDL-C (MD= 0.44 mmol/L; 95% CI 0.01 to 0.88) and HDL-C (MD=0.08 mmol/L; 95% CI 0.03 to 0.13). For both comparisons, there were no significant effects on triglycerides.

METHODS: A total of 20 healthy volunteers were challenged with 3 test meals, similar in fat content (~31% en) but varying in saturated SFA content and polyunsaturated/saturated fatty acid ratios (P/S). The 3 meals were lauric + myristic acid-rich (LM), P/S 0.19; palmitic acid-rich (POL), P/S 0.31; and stearic acid-rich (STE), P/S 0.22. Blood was sampled at fasted baseline and 2, 4, 5, 6, and 8 hours. Plasma lipids (triacylglycerol [TAG]) and lipoproteins (TC, LDL-C, high density lipoprotein-cholesterol [HDL-C]) were evaluated.

RESULTS: Varying SFA in the test meal significantly impacted postprandial TAG response (p < 0.05). Plasma TAG peaked at 5 hours for STE, 4 hours for POL, and 2 hours for LM test meals. Area-under-the-curve (AUC) for plasma TAG was increased significantly after STE treatment (STE > LM by 32.2%, p = 0.003; STE > POL by 27.9%, p = 0.023) but was not significantly different between POL and LM (POL > LM by 6.0%, p > 0.05). At 2 hours, plasma HDL-C increased significantly after the LM and POL test meals compared with STE (p < 0.05). In comparison to the STE test meal, HDL-C AUC was elevated 14.0% (p = 0.005) and 7.6% (p = 0.023) by the LM and POL test meals, respectively. The TC response was also increased significantly by LM compared with both POL and STE test meals (p < 0.05).

METHOD: This is a cross-sectional study of 65 Malay obese class I and class II adults aged 20-62 years (21 male, 44 female) from sub-urban areas of Malaysia. Overnight fasting venous blood samples were obtained to determine the triglyceride level (mmol/L). Subjects were classified into either normal or elevated triglyceride level groups based on the triglyceride level (normal < 1.6 mmol/L, elevated > 1.7 mmol/L). Unhealthy lifestyle behaviors, defined as smoking status, hours per day spent on sitting passively and sitting with active motion, and the amount of saturated fat, mono-unsaturated and polyunsaturated fat from dietary intake, were measured from 24-h dietary intake and physical activity recall. We compare the variables of unhealthy lifestyle behaviors between subjects with normal and elevated triglyceride level using independent samples t-test.

RESULTS: Among 65 obese class I and II adults, 16 subjects (24.6%) were found to have elevated triglyceride levels (mean ± standard deviation of body mass index 31.89 ± 3.29 kg/m2). There are significant differences between subjects having normal and elevated triglyceride level with gender, marital status, the number of children, smoking status, weight and monounsaturated fat intake (all P-values < .05).

METHODS: This human postprandial study evaluated 3 edible fat blends with differing polyunsaturated to saturated fatty acids (P/S) ratios (POL = 0.27, AHA = 1.00, PCAN = 1.32). A cross-over design included mildly hypercholestrolemic subjects (9 men and 6 women) preconditioned on test diets fats at 31% energy for 7 days prior to the postprandial challenge on the 8th day with 50 g test fat. Plasma lipids and lipoproteins were monitored at 0, 1.5, 3.5, 5.5 and 7 hr.

METHODS: Twenty-four male, 8-week old Sprague Dawley rats with an initial weight of 160 to 200 g were randomised into three groups (n = 6 for each group): groups A (standard rat chow), B (high-fat, high-sucrose diet), and C (high-fat, high-sucrose diet + 100 mg/kg/d of glycyrrhizic acid via oral administration). The rats were treated accordingly for 4 wk. Glycaemic parameters, lipid profile, stress hormones, and adiponectin levels were measured after the treatment. Relative gene expressions of peroxisome proliferator-activated receptor α and γ, lipoprotein lipase as well as gluconeogenic enzymatic activities in different tissues were also determined.

RESULTS: Consumption of high-fat, high-sucrose diet triggered hyperglycaemia, insulin resistance, and dyslipidemia, which were effectively attenuated by supplementation with glycyrrhizic acid. Glycyrrhizic acid supplementation also effectively reduced circulating adrenaline, alleviated gluconeogenic enzymes overactivity, and promoted the upregulation of lipoprotein lipase expression in the cardiomyocytes and skeletal muscles. A high calorie diet also triggered hypoadiponectinaemia and suppression of peroxisome proliferator-activated receptor γ expression, which did not improve with glycyrrhizic acid treatment.

OBJECTIVE: To assess the association of premenopausal and postmenopausal breast cancer risk with fat and fat subtypes intake.

METHODOLOGY: This is a population based case-control study conducted in Kuala Lumpur, Malaysia from January 2006 to December 2007. Food intake pattern was collected from 382 breast cancer patients and 382 control group via an interviewer-administered food frequency questionnaire. Logistic regression was used to compute odds ratios (OR) with 95% confidence intervals (CI) and a broad range of potential confounders was included in analysis.

RESULTS: This study showed that both premenopausal and postmenopausal breast cancer risk did not increase significantly with greater intake of total fat [quartile (Q) 4 versus Q1 OR=0.76, 95% CI, 0.23-2.45 and OR=1.36, 95% CI, 0.30-3.12], saturated fat (ORQ4 to Q1=1.43, 95% CI, 0.51-3.98 and ORQ4 to Q1=1.75, 95% CI, 0.62-3.40), monounsaturated fat (ORQ4 to Q1=0.96, 95% CI, 0.34-1.72 and ORQ4 to Q1=1.74, 95% CI, 0.22-2.79), polyunsaturated fat (ORQ4 to Q1=0.64, 95% CI, 0.23-1.73 and ORQ4 to Q1=0.74, 95% CI, 0.39-1.81), n-3 polyunsaturated fat (ORQ4 to Q1=1.10, 95% CI, 0.49-2.48 and ORQ4 to Q1=0.78, 95% CI, 0.28-2.18), n-6 polyunsaturated fat (ORQ4 to Q1=0.67, 95% CI, 0.24-1.84 and ORQ4 to Q1=0.71, 95% CI, 0.29-1.04) or energy intake (ORQ4 to Q1=1.52, 95% CI, 0.68-3.38 and ORQ4 to Q1=2.21, 95% CI, 0.93-3.36).