Joi A. Gleason

Dietary Fructose and Glucose Differentially Affect Lipid and Glucose Homeostasis

Absorbed glucose and fructose differ in that glucose largely escapes first-pass removal by the liver, whereas fructose does not, resulting in different metabolic effects of these 2 monosaccharides. In short-term controlled feeding studies, dietary fructose significantly increases postprandial triglyceride (TG) levels and has little effect on serum glucose concentrations, whereas dietary glucose has the opposite effects. When dietary glucose and fructose have been directly compared at approximately 20-25% of energy over a 4- to 6-wk period, dietary fructose caused significant increases in fasting TG and LDL cholesterol concentrations, whereas dietary glucose did not, but dietary glucose did increase serum glucose and insulin concentrations in the postprandial state whereas dietary fructose did not. When fructose at 30-60 g ( approximately 4-12% of energy) was added to the diet in the free-living state, there were no significant effects on lipid or glucose biomarkers. Sucrose and high-fructose corn syrup (HFCS) contain approximately equal amounts of fructose and glucose and no metabolic differences between them have been noted. Controlled feeding studies at more physiologic dietary intakes of fructose and glucose need to be conducted. In our view, to decrease the current high prevalence of obesity, dyslipidemia, insulin resistance, and diabetes, the focus should be on restricting the intake of excess energy, sucrose, HFCS, and animal and trans fats and increasing exercise and the intake of vegetables, vegetable oils, fish, fruit, whole grains, and fiber.

Effects of Atorvastatin on Fasting and Postprandial Lipoprotein Subclasses in Coronary Heart Disease Patients Versus Control Subjects

The effects of atorvastatin at 20, 40, and 80 mg/day on plasma lipoprotein subclasses were examined in a randomized, placebo-controlled fashion over 24 weeks in 103 patients in the fasting state who had coronary heart disease (CHD) with low-density lipoprotein (LDL) cholesterol levels >130 mg/dl. The effects of placebo and atorvastatin 40 mg/day were examined in 88 subjects with CHD in the fasting state and 4 hours after a meal rich in saturated fat and cholesterol. These findings were compared with results in 88 age- and gender-matched control subjects. Treatment at the 20, 40, and 80 mg/day dose levels resulted in LDL cholesterol reductions of 38%, 46%, and 52% (all p <0.0001), triglyceride reductions of 22%, 26%, and 30% (all p <0.0001), and high-density lipoprotein (HDL) cholesterol increases of 6%, 5%, and 3%, respectively (all p <0.05 at the 20- and 40-mg doses). The lowest total cholesterol/HDL cholesterol ratio was observed with the 80 mg/day dose of atorvastatin (p <0.0001 vs placebo). Remnant-like particle (RLP) cholesterol decreased 33%, 34%, and 32%, respectively (all p <0.0001). Lipoprotein(a) [Lp(a)] cholesterol decreased 9%, 16%, and 21% (all p <0.0001), although Lp(a) mass increased 9%, 8%, and 10%, respectively (all p <0.01). In the fed state, atorvastatin 40 mg/day normalized direct LDL cholesterol (29% below controls), triglycerides (8% above controls), and RLP cholesterol (10% below controls), with similar reductions in the fasting state. At this same dose level, atorvastatin treatment resulted in 39%, 35%, and 59% decreases in fasting triglyceride in large, medium, and small very LDLs, as well as 45%, 33%, and 47% reductions in cholesterol in large, medium, and small LDL, respectively, as assessed by nuclear magnetic resonance (all significant, p <0.05), normalizing these particles versus controls (77 cases vs 77 controls). Moreover, cholesterol in large HDL was increased 37% (p <0.001) by this treatment. Our data indicate that atorvastatin treatment normalizes levels of all classes of triglyceride-rich lipoproteins and LDL in both the fasting and fed states in patients with CHD compared with control subjects.

Cardiovascular Risk Reduction and Dietary Compliance with a Home-Delivered Diet and Lifestyle Modification Program

Lack of adherence to diet contributes to ineffective dietary responsiveness and elevated cardiovascular risk factors in coronary heart disease (CHD) patients. Our purpose was to determine if home-delivered, heart-healthy meals and snacks, combined with telephone diet education, would be efficacious in improving dietary compliance, quality of life, and cardiovascular risk factors (primarily low-density lipoprotein [LDL] cholesterol and body weight) in CHD patients. Participants were 35 free-living subjects (21 men, 14 postmenopausal women) with a mean age of 62 (ranging from 40 to 79 years) in an 8-week diet intervention. A registered dietitian provided diet education over the telephone and weekly menus averaging 67% carbohydrate, 16% protein, 17% fat, 4% saturated fat, 5% monounsaturated fat, 128 mg cholesterol, and 25 g fiber. Lipid profiles, anthropometric measures, food records, and quality of diet, and life questionnaires were obtained at baseline, week 4, and week 8. Mean compliance-defined as percentage of prepared food energy consumed divided by percentage of prepared food energy provided-was 91% at 4 weeks and 88% at 8 weeks. After 8 weeks, significant reductions in weight (-3.7 kg), waist circumference (-2.0 in), hip circumference (-1.3 in), body mass index (-1.21 kg/m2), total cholesterol (-0.17 mmol/dL, -7.0 mg/dL), and LDL cholesterol (-0.19 mmol/dL, -7.5 mg/dL) (P<.05) were achieved without significant changes in high-density lipoprotein cholesterol (0.00 mmol/dL, 0.0 mg/dL) or triglycerides (+0.06 mmol/dL, +2.5 mg/dL). Significant improvements in quality of life and quality of diet (P < .05) were also demonstrated. This program could be a useful additive component to traditional medical nutrition therapy to improve dietary adherence.

Effects of eicosapentaenoic acid and docosahexaenoic acid on cardiovascular disease risk factors: a randomized clinical trial

BACKGROUND Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), the primary omega-3 fatty acids in fish oil, have been shown to reduce cardiovascular disease (CVD) risk. OBJECTIVE This study aimed to examine the independent effects of EPA and DHA on lipid and apolipoprotein levels, as well as on inflammatory biomarkers of CVD risk, using doses often used in the general population. DESIGN A blinded, randomized 6-week trial was performed in 121 healthy, normolipidemic subjects who received olive oil placebo 6g/d, EPA 600mg/d, EPA 1800mg/d, or DHA 600mg/d. The EPA was derived from genetically modified yeast. RESULTS The subjects tolerated the supplements well with no safety issues; and the expected treatment-specific increases in plasma EPA and DHA levels were observed. Compared to placebo, the DHA group had significant decreases in postprandial triglyceride (TG) concentrations (-20%, -52.2mg/dL, P=0.03), significant increases in fasting and postprandial low-density lipoprotein cholesterol (LDL-C) (+18.4%, 17.1mg/dL, P=0.001), with no significant changes in inflammatory biomarkers. No significant effects were observed in the EPA 600mg/d group. The high-dose EPA group had significant decreases in lipoprotein-associated phospholipase A2 concentrations (Lp-PLA2) (-14.1%, -21.4ng/mL, P=0.003). CONCLUSIONS The beneficial effects of EPA 1800mg/d on CVD risk reduction may relate in part to the lowering of Lp-PLA2 without adversely affecting LDL-C. In contrast, DHA decreased postprandial TG, but raised LDL-C. Our observations indicate that these dietary fatty acids have divergent effects on cardiovascular risk markers.

Effects of carbohydrate quantity and glycemic index on resting metabolic rate and body composition during weight loss.

To examine the effects of diets varying in carbohydrate and glycemic index (GI) on changes in body composition, resting metabolic rate (RMR), and metabolic adaptation during and after weight loss.