Fasting HDL-cholesterol Concentrations Research Articles

Comparison of diets enriched in stearic, oleic, and palmitic acids on inflammation, immune response, cardiometabolic risk factors, and fecal bile acid concentrations in mildly hypercholesterolemic postmenopausal women—randomized crossover trial

Direct comparisons between SFAs varying in chain length, specifically palmitic acid (16:0) and stearic acid (18:0), relative to the latter's metabolic product, oleic acid (18:1), on cardiometabolic risk factors are limited. The aim of this study was to determine the relative comparability of diets enriched in palmitic acid, stearic acid, and oleic acid on inflammation and coagulation markers, T lymphocyte proliferation/ex-vivo cytokine secretion, plasma cardiometabolic risk factors, and fecal bile acid concentrations. Hypercholesterolemic postmenopausal women (n=20, mean±SD age 64±7 y, BMI 26.4±3.4 kg/m2, LDL cholesterol≥2.8 mmol/L) were provided with each of 3 diets [55% energy (%E) carbohydrate, 15%E protein, 30%E fat, with ∼50% fat contributed by palmitic acid, stearic acid, or oleic acid in each diet; 5 wk/diet phase] using a randomized crossover design with 2-wk washouts between phases. Outcome measures were assessed at the end of each phase. Fasting LDL-cholesterol and non-HDL-cholesterol concentrations were lower after the stearic acid and oleic acid diets than the palmitic acid diet (all P<0.01). Fasting HDL-cholesterol concentrations were lower after the stearic acid diet than the palmitic acid and oleic acid diets (P<0.01). The stearic acid diet resulted in lower lithocholic acid (P=0.01) and total secondary bile acid (SBA) concentrations (P=0.04) than the oleic acid diet. All other outcome measures were similar between diets. Lithocholic acid concentrations were positively correlated with fasting LDL-cholesterol concentrations (r=0.33; P=0.011). Total SBA, lithocholic acid, and deoxycholic acid concentrations were negatively correlated with fasting HDL cholesterol (r=-0.51 to -0.44; P<0.01) concentrations and positively correlated with LDL cholesterol:HDL cholesterol (r =0.37-0.54; P<0.01) ratios. Dietary stearic acid and oleic acid had similar effects on fasting LDL-cholesterol and non-HDL-cholesterol concentrations and more favorable ones than palmitic acid. Unlike oleic acid, the hypocholesterolemic effect of stearic acid may be mediated by inhibition of intestinal hydrophobic SBA synthesis. These findings add to the data suggesting there should be a reassessment of current SFA dietary guidance and Nutrient Facts panel labeling.This trial was registered at clinicaltrials.gov as NCT02145936.

Higher breakfast glycaemic load is associated with increased metabolic syndrome risk, including lower HDL-cholesterol concentrations and increased TAG concentrations, in adolescent girls.

Almost all previous studies examining the associations between glycaemic load (GL) and metabolic syndrome risk have used a daily GL value. The daily value does not distinguish between peaks of GL intake over the day, which may be more closely associated with the risk of the metabolic syndrome. The aim of the present study was to investigate the cross-sectional associations between daily and mealtime measures of GL and metabolic syndrome risk, including metabolic syndrome components, in adolescents. Adolescents participating in the 14-year follow-up of the Western Australian Pregnancy Cohort (Raine) Study completed 3 d food records and metabolic assessments. Breakfast GL, lunch GL, dinner GL and a score representing meal GL peaks over the day were determined in 516 adolescents. Logistic regression models were used to investigate whether GL variables were independent predictors of the metabolic syndrome in this population-based cohort (3.5% prevalence of the metabolic syndrome). Breakfast GL was found to be predictive of the metabolic syndrome in girls (OR 1.15, 95% CI 1.04, 1.27; P <0.01), but not in boys. Other meal GL values and daily GL were found to be not significant predictors of the metabolic syndrome. When breakfast GL was examined in relation to each of the components of the metabolic syndrome in girls, it was found to be negatively associated with fasting HDL-cholesterol concentrations (P= 0.037; β = - 0.004; 95% CI - 0.008, - 0.002) and positively associated with fasting TAG concentrations (P= 0.008; exp(β) = 1.002; 95% CI 1.001, 1.004). he results of the present study suggest that there may be an association between breakfast composition and metabolic syndrome components in adolescent girls. These findings support further investigation into including lower-GL foods as part of a healthy breakfast in adolescence, particularly for girls.

Intake of phenol-rich virgin olive oil improves the postprandial prothrombotic profile in hypercholesterolemic patients

Background: Oxidative stress associated with postprandial lipemia contributes to endothelial dysfunction, which shifts hemostasis to a more thrombogenic state.Objective: We investigated whether a high concentration of phenols in olive oil can partly reverse this phenomenon.Design: Twenty-one hypercholesterolemic volunteers received 2 breakfasts rich in olive oils with different phenolic contents (80 or 400 ppm) according to a randomized, sequential crossover design. Plasma concentrations of lipid fractions, factor VII antigen (FVIIag), activated factor VII (FVIIa), and plasminogen activator inhibitor-1 (PAI-1) activity were measured at baseline and postprandially.Results: Concentrations of FVIIa increased less (P = 0.018) and plasma PAI-1 activity decreased more (P = 0.021) 2 h after the high-phenol meal than after the low-phenol meal. FVIIa concentrations 120 min after intake of the olive oil with a high phenol content correlated positively with fasting plasma triacylglycerols (P = 0.001), area under the curve (AUC) of triacylglycerols (P = 0.001), and AUC of nonesterified fatty acids (P = 0.024) and negatively with hydroxytyrosol plasma concentrations at 60 min (P = 0.039) and fasting HDL-cholesterol concentrations (P = 0.005). PAI-1 positively correlated with homeostasis model assessment of insulin resistance (P = 0.005) and fasting triacylglycerols (P = 0.025) and inversely with adiponectin (P = 0.026). In a multivariate analysis, the AUCs of nonesterified fatty acids (R2 = 0.467; β: 0.787; SE: 0.02; P < 0.001) and adiponectin (R2 = 0.232; β: −1.594; SE: 0.629; P < 0.05) were the strongest predictors of plasma FVIIa and PAI-1, respectively.Conclusions: A virgin olive oil with a high content of phenolic compounds changes the postprandial hemostatic profile to a less thrombogenic state.

Postprandial response to a physiologic caloric load in HIV-positive patients receiving protease inhibitor–based or nonnucleoside reverse transcriptase inhibitor–based antiretroviral therapy

Features of the dyslipidemic pattern reported with the use of antiretroviral therapy predict enhanced postprandial lipemia, which is an emerging cardiovascular disease risk factor. We evaluated the postprandial response to a physiologic, meal-based challenge in HIV-positive subjects without hyperlipidemia. We measured hourly lipid, lipoprotein, glucose, and insulin concentrations during a 13-h period in 25 nonwhite patients (13 women, 12 men): 13 receiving a protease inhibitor (PI)-based regimen (6 nelfinavir and 7 indinavir) and 12 receiving a nonnucleoside reverse transcriptase inhibitor (NNRTI)-based regimen (6 efavirenz and 6 nevirapine). Mean fasting HDL-cholesterol concentrations were lower in HIV patients than in healthy subjects without HIV infection matched for age, sex, and ethnicity (z score: -0.81 +/- 0.9; P = 0.0001). Fasting triacylglycerol concentrations were not significantly different between HIV-infected patients and healthy subjects but were higher in PI-treated than in NNRTI-treated patients [median (interquartile range): 144 (110-191) and 89 (62-135) mg/dL; P = 0.007]. Average daylong triacylglycerol concentrations, but not incremental concentrations, were higher in the PI group than in the NNRTI group [205% (185-248%) and 125% (78-191%); P < 0.05]. For all HIV-positive patients, the fractional triacylglycerol increase was lower after breakfast than after lunch (20 +/- 18% and 42 +/- 40%, respectively; P < 0.04). Insulin concentrations were higher in PI-treated than in NNRTI-treated patients [22.6 (13.1-29.8) and 11.8 (7.1-19.1) microU/mL; P = 0.01] and increased in both groups in response to each meal, whereas glucose concentrations increased only after breakfast. Despite baseline differences, incremental triacylglycerol and insulin responses to a physiologic caloric load among HIV-positive patients were not significantly affected by differences in the type of antiretroviral therapy.

Postprandial response to a physiologic caloric load in HIV-positive patients receiving protease inhibitor–based or nonnucleoside reverse transcriptase inhibitor–based antiretroviral therapy

Background: Features of the dyslipidemic pattern reported with the use of antiretroviral therapy predict enhanced postprandial lipemia, which is an emerging cardiovascular disease risk factor. Objective: We evaluated the postprandial response to a physiologic, meal-based challenge in HIV-positive subjects without hyperlipidemia. Design: We measured hourly lipid, lipoprotein, glucose, and insulin concentrations during a 13-h period in 25 nonwhite patients (13 women, 12 men): 13 receiving a protease inhibitor (PI)-based regimen (6 nelfinavir and 7 indinavir) and 12 receiving a nonnucleoside reverse transcriptase inhibitor (NNRTI)-based regimen (6 efavirenz and 6 nevirapine). Results: Mean fasting HDL-cholesterol concentrations were lower in HIV patients than in healthy subjects without HIV infection matched for age, sex, and ethnicity (z score: −0.81 ± 0.9; P = 0.0001). Fasting triacylglycerol concentrations were not significantly different between HIV-infected patients and healthy subjects but were higher in PI-treated than in NNRTI-treated patients [median (interquartile range): 144 (110–191) and 89 (62–135) mg/dL; P = 0.007]. Average daylong triacylglycerol concentrations, but not incremental concentrations, were higher in the PI group than in the NNRTI group [205% (185–248%) and 125% (78–191%); P < 0.05]. For all HIV-positive patients, the fractional triacylglycerol increase was lower after breakfast than after lunch (20 ± 18% and 42 ± 40%, respectively; P < 0.04). Insulin concentrations were higher in PI-treated than in NNRTI-treated patients [22.6 (13.1–29.8) and 11.8 (7.1–19.1) μU/mL; P = 0.01] and increased in both groups in response to each meal, whereas glucose concentrations increased only after breakfast. Conclusions: Despite baseline differences, incremental triacylglycerol and insulin responses to a physiologic caloric load among HIV-positive patients were not significantly affected by differences in the type of antiretroviral therapy.

Predictors of postprandial triacylglycerol response in children: the Columbia University Biomarkers Study

Predictors of postprandial lipemia have not been explored in children. Our objective was to determine whether the postprandial triacylglycerol response is associated with low HDL-cholesterol and high fasting triacylglycerol concentrations and family history of early-onset ischemic heart disease (IHD) in children. We administered a standardized fat load (52.5 g fat/m(2)) to 60 children (mean age: 14.0 y), 20 with and 40 without a family history of early-onset IHD, and to 29 mothers, all recruited from families enrolled in the Columbia University Biomarkers Study. Plasma lipid and retinyl palmitate concentrations were measured in the fasting state and 3, 6, and 8 h after the oral fat load. In children, postprandial lipemia, as indicated by the incremental area under the triacylglycerol response curve, was associated with elevated fasting triacylglycerol concentrations (>/=1.13 mmol/L; P: < 0.01), with low fasting HDL-cholesterol concentrations (</=0.91 mmol/L; P: < 0.01), and with the combination of low HDL-cholesterol and high triacylglycerol concentrations (P: < 0.05). Family history of IHD, baseline LDL-cholesterol concentration, and apolipoprotein E genotype were not associated with the postprandial triacylglycerol or retinyl palmitate response. The mothers had fasting triacylglycerol concentrations similar to those of their children but a more prolonged response with higher triacylglycerol concentrations at 6 and 8 h (P: < 0.01 and P: < 0.05, respectively). In children, a delayed postprandial triacylglycerol response to a fat load is associated with the combination of high fasting triacylglycerol and low HDL-cholesterol concentrations. Predictors of postprandial triacylglycerol concentrations may be similar in children and adults.