METHOD: Secondary data from a cross-sectional survey was utilized. HRQOL was assessed for 379 HD patients using the generic Short Form 36 (SF-36) and disease-specific Kidney-Disease Quality of Life-36 (KDQOL-36). Malnutrition was indicated by malnutrition inflammation score (MIS) ≥ 5, and presence of protein-energy wasting (PEW). The individual nutritional parameters included the domains of physical status, serum biomarkers, and dietary intake. Multivariate associations were assessed using the general linear model.
RESULTS: MIS ≥ 5 was negatively associated with SF-36 scores of physical functioning (MIS
DESIGN: The Healthy Food-Environment Policy Index (Food-EPI) comprises forty-seven indicators of government policy practice. Local evidence of each indicator was compiled from government institutions and verified by related government stakeholders. The extent of implementation of the policies was rated by experts against international best practices. Rating results were used to identify and propose policy actions which were subsequently prioritised by the experts based on 'importance' and 'achievability' criteria. The policy actions with relatively higher 'achievability' and 'importance' were set as priority recommendations for government action.
SETTING: Malaysia.
SUBJECTS: Twenty-six local experts.
RESULTS: Majority (62 %) of indicators was rated 'low' implementation with no indicator rated as either 'high' or 'very little, if any' in terms of implementation. The top five recommendations were (i) restrict unhealthy food marketing in children's settings and (ii) on broadcast media; (iii) mandatory nutrition labelling for added sugars; (iv) designation of priority research areas related to obesity prevention and diet-related non-communicable diseases; and (v) introduce energy labelling on menu boards for fast-food outlets.
CONCLUSIONS: This first policy study conducted in Malaysia identified a number of gaps in implementation of key policies to promote healthy food environments, compared with international best practices. Study findings could strengthen civil society advocacies for government accountability to create a healthier food environment.
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.
RESULTS: Plasma triacylglycerol (TAG) concentrations in response to POL, AHA or PCAN meals were not significant for time x test meal interactions (P > 0.05) despite an observed trend (POL > AHA > PCAN). TAG area-under-the-curve (AUC) increased by 22.58% after POL and 7.63% after PCAN compared to AHA treatments (P > 0.05). Plasma total cholesterol (TC) response was not significant between meals (P > 0.05). Varying P/S ratios of test meals significantly altered prandial high density lipoprotein-cholesterol (HDL-C) concentrations (P AHA > PCAN). Paired comparisons was significant between POL vs PCAN (P = 0.009) but not with AHA or between AHA vs PCAN (P > 0.05). A significantly higher HDL-C AUC for POL vs AHA (P = 0.015) and PCAN (P = 0.001) was observed. HDL-C AUC increased for POL by 25.38% and 16.0% compared to PCAN and AHA respectively. Plasma low density lipoprotein-cholesterol (LDL-C) concentrations was significant (P = 0.005) between meals and significantly lowest after POL meal compared to PCAN (P = 0.004) and AHA (P > 0.05) but not between AHA vs PCAN (P > 0.05). AUC for LDL-C was not significant between diets (P > 0.05). Palmitic (C16:0), oleic (C18:1), linoleic (C18:2) and linolenic (C18:3) acids in TAGs and cholesteryl esters were significantly modulated by meal source (P
METHODS: Using 3 d of dietary records, FA intakes of 333 recruited patients were calculated using a food database built from laboratory analyses of commonly consumed Malaysian foods. Plasma triacylglycerol (TG) and erythrocyte FAs were determined by gas chromatography.
RESULTS: High dietary saturated fatty acid (SFA) and monounsaturated fatty acid (MUFA) consumption trends were observed. Patients on HD also reported low dietary ω-3 and ω-6 polyunsaturated fatty acid (PUFA) consumptions and low levels of TG and erythrocyte FAs. TG and dietary FAs were significantly associated respective to total PUFA, total ω-6 PUFA, 18:2 ω-6, total ω-3 PUFA, 18:3 ω-3, 22:6 ω-3, and trans 18:2 isomers (P < 0.05). Contrarily, only dietary total ω-3 PUFA and 22:6 ω-3 were significantly associated with erythrocyte FAs (P < 0.01). The highest tertile of fish and shellfish consumption reflected a significantly higher proportion of TG 22:6 ω-3. Dietary SFAs were directly associated with TG and erythrocyte MUFA, whereas dietary PUFAs were not.
CONCLUSION: TG and erythrocyte FAs serve as biomarkers of dietary PUFA intake in patients on HD. Elevation of circulating MUFA may be attributed to inadequate intake of PUFAs.
METHODS: Thirty human volunteers were fed complete, whole food diets during 4 wk periods, where total fat (approximately 31% daily energy, >70% from the test fats) and fatty acid composition were tightly controlled. A crossover design was used with 3 randomly-assigned diet rotations and repeated-measures analysis. One test fat rotation was based on palm olein (POL) and provided 12.0 percent of energy (%en) as palmitic acid (16:0); a second contained trans-rich partially hydrogenated soybean oil (PHSO) and provided 3.2 %en as trans fatty acids plus 6.5 %en as 16:0, while the third used an interesterified fat (IE) and provided 12.5 %en as stearic acid (18:0). After 4 wk the plasma lipoproteins, fatty acid profile, as well as fasting glucose and insulin were assessed. In addition, after 2 wk into each period an 8 h postprandial challenge was initiated in a subset of 19 subjects who consumed a meal containing 53 g of test fat.
RESULTS: After 4 wk, both PHSO and IE fats significantly elevated both the LDL/HDL ratio and fasting blood glucose, the latter almost 20% in the IE group relative to POL. Fasting 4 wk insulin was 10% lower after PHSO (p > 0.05) and 22% lower after IE (p < 0.001) compared to POL. For the postprandial study the glucose incremental area under the curve (IAUC) following the IE meal was 40% greater than after either other meal (p < 0.001), and was linked to relatively depressed insulin and C-peptide (p < 0.05).
CONCLUSION: Both PHSO and IE fats altered the metabolism of lipoproteins and glucose relative to an unmodified saturated fat when fed to humans under identical circumstances.