METHODOLOGY: The patients were 487 non-diabetic Malay women who had an uncomplicated antenatal course and delivered healthy singleton babies at term. Cord blood and maternal post-partum venous blood samples were taken for assay of serum cholesterol and triglyceride concentrations using standard enzymatic methods.
RESULTS: Maternal total serum cholesterol concentrations (mean +/- SD; 7.5 +/- 2.5 mmol/L) were higher than in other reported series (range of published means 5.2-6.5 mmol/L) with a correspondingly low high-density lipoprotein (HDL): total cholesterol ratio. The mean cord blood total serum cholesterol (1.7 +/- 1.0 mmol/L) was consistent with previously reported population means (1.5-1.9 mmol/L) but there was a relatively high low-density lipoprotein (LDL)-cholesterol and depressed HDL: cholesterol ratio. Significant correlations between maternal and neonatal serum total (P = 0.038) and especially HDL-cholesterol (P < 0.001) were observed. Maternal and cord blood serum triglyceride levels were comparable to those in other series.
CONCLUSIONS: These cross-sectional data provide evidence that abnormal serum cholesterol profiles are found in pregnant Malay women and their neonates which may have implications for the prevalence of macrovascular disease in the Malay population.
METHODS: Using a randomised double-blind crossover design, 21 (men = 6, women = 15) T2D subjects consumed test meals (3.65 MJ) consisting of a high fat muffin (containing 50 g test fats provided as PO, IPO or HOS) and a milkshake. Postprandial changes in gut hormones, glucose homeostasis, satiety, lipid and inflammatory parameters after meals were analysed. Some of the solid fractions of the IPO were removed and thus the fatty acid composition of the PO and IPO was not entirely equal (PO vs IPO: palmitate 39.8 vs 38.7; oleate 43.6 vs 45.1). PO, IPO and HOS contained 9.7, 38.9 and 0.2 g/100 g total fatty acids of palmitic acid at the sn-2 position, respectively. At 37 °C, IPO contained 4.2% SFC whereas PO and HOS were completely melted.
RESULTS: Our novel observation shows that the incremental area under curve (iAUC) 0-6 h of plasma GIP concentration was on average 16% lower following IPO meal compared with PO and HOS (P
METHODS: We studied 125 287 participants from 18 countries in North America, South America, Europe, Africa, and Asia in the Prospective Urban Rural Epidemiology (PURE) study. Habitual food intake was measured with validated food frequency questionnaires. We assessed the associations between nutrients (total fats, saturated fatty acids, monounsaturated fatty acids, polyunsaturated fatty acids, carbohydrates, protein, and dietary cholesterol) and cardiovascular disease risk markers using multilevel modelling. The effect of isocaloric replacement of saturated fatty acids with other fats and carbohydrates was determined overall and by levels of intakes by use of nutrient density models. We did simulation modelling in which we assumed that the effects of saturated fatty acids on cardiovascular disease events was solely related to their association through an individual risk marker, and then compared these simulated risk marker-based estimates with directly observed associations of saturated fatty acids with cardiovascular disease events.
FINDINGS: Participants were enrolled into the study from Jan 1, 2003, to March 31, 2013. Intake of total fat and each type of fat was associated with higher concentrations of total cholesterol and LDL cholesterol, but also with higher HDL cholesterol and apolipoprotein A1 (ApoA1), and lower triglycerides, ratio of total cholesterol to HDL cholesterol, ratio of triglycerides to HDL cholesterol, and ratio of apolipoprotein B (ApoB) to ApoA1 (all ptrend<0·0001). Higher carbohydrate intake was associated with lower total cholesterol, LDL cholesterol, and ApoB, but also with lower HDL cholesterol and ApoA1, and higher triglycerides, ratio of total cholesterol to HDL cholesterol, ratio of triglycerides to HDL cholesterol, and ApoB-to-ApoA1 ratio (all ptrend<0·0001, apart from ApoB [ptrend=0·0014]). Higher intakes of total fat, saturated fatty acids, and carbohydrates were associated with higher blood pressure, whereas higher protein intake was associated with lower blood pressure. Replacement of saturated fatty acids with carbohydrates was associated with the most adverse effects on lipids, whereas replacement of saturated fatty acids with unsaturated fats improved some risk markers (LDL cholesterol and blood pressure), but seemed to worsen others (HDL cholesterol and triglycerides). The observed associations between saturated fatty acids and cardiovascular disease events were approximated by the simulated associations mediated through the effects on the ApoB-to-ApoA1 ratio, but not with other lipid markers including LDL cholesterol.
INTERPRETATION: Our data are at odds with current recommendations to reduce total fat and saturated fats. Reducing saturated fatty acid intake and replacing it with carbohydrate has an adverse effect on blood lipids. Substituting saturated fatty acids with unsaturated fats might improve some risk markers, but might worsen others. Simulations suggest that ApoB-to-ApoA1 ratio probably provides the best overall indication of the effect of saturated fatty acids on cardiovascular disease risk among the markers tested. Focusing on a single lipid marker such as LDL cholesterol alone does not capture the net clinical effects of nutrients on cardiovascular risk.
FUNDING: Full funding sources listed at the end of the paper (see Acknowledgments).
METHODS: Data of 328 eligible housewives who participated in the MyBFF@Home study was used. Intervention group of 169 subjects were provided with an intervention package which includes physical activity (brisk walking, dumbbell exercise, physical activity diary, group exercise) and 159 subjects in control group received various health seminars. Physical activity level was assessed using short-International Physical Activity Questionnaire. The physical activity level was then re-categorized into 4 categories (active intervention, inactive intervention, active control and inactive control). Physical activity, blood glucose and lipid profile were measured at baseline, 3rd month and 6th month of the study. General Linear Model was used to determine the effect of physical activity on glucose and lipid profile.
RESULTS: At the 6th month, there were 99 subjects in the intervention and 79 control group who had complete data for physical activity. There was no difference on the effect of physical activity on the glucose level and lipid profile except for the Triglycerides level. Both intervention and control groups showed reduction of physical activity level over time.
CONCLUSION: The effect of physical activity on blood glucose and lipid profile could not be demonstrated possibly due to physical activity in both intervention and control groups showed decreasing trend over time.