Cardiovascular Risk Factor Reduction in First Responders Resulting From an Individualized Lifestyle and Blood Test Program: A Randomized Controlled Trial.

OBJECTIVE: We tested the hypothesis that a lifestyle program would improve risk factors linked to cardiovascular disease (CVD) in first responders. METHODS: A 1-year cluster-randomized controlled clinical trial in 10 cities. Participants were 175 first responders, with increased waist circumference and/or low levels of large (α1) high-density lipoprotein (HDL) particles. The intervention group received personalized online tools and access to telephonic coaching sessions. RESULTS: At 1 year the intervention significantly reduced body weight (P = 0.004) and waist circumference (P = 0.002), increased α1 HDL (P = 0.01), and decreased triglyceride (P = 0.005) and insulin concentrations (P = 0.03). Program adherence was associated with weight loss (P = 0.0005) and increases in α1 HDL (P = 0.03). CONCLUSIONS: In first responders, a personalized lifestyle intervention significantly improved CVD risk factors in proportion to program adherence. Changes in large HDL particles were more sensitive indicators of lifestyle changes than HDL-cholesterol measurement. CLINICAL TRIAL REGISTRATION NUMBER: ClinicalTrials.gov: NCT03322046.

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.

OBJECTIVE: 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. METHODS: Adults with obesity (n = 91) were randomized to one of four provided-food diets for 17 weeks. Diets differed in percentage energy from carbohydrate (55% or 70%) and GI (low or high) but were matched for protein, fiber, and energy. Body weight, body composition, RMR, and metabolic adaptation (measured RMR-predicted RMR) were measured during weight loss and subsequent weight stability. RESULTS: No effect of dietary carbohydrate content or GI on body weight loss or percentage of weight lost as fat mass (FM) was observed. Measured RMR was significantly lower (-226 kJ/day [95% CI: -314 to -138 kJ/day], P < 0.001) than predicted RMR following weight loss, but this difference was attenuated after 5 weeks of weight stability. Metabolic adaptation did not differ by dietary carbohydrate content or GI and was not associated with weight regain 12 months later. CONCLUSIONS: Moderate-carbohydrate and low-GI diets did not preferentially reduce FM, preserve lean mass, or attenuate metabolic adaptation during weight loss compared to high-carbohydrate and high-GI diets.

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.

The effects of low-fat, high-carbohydrate diets on plasma lipoproteins, weight loss, and heart disease risk reduction.

Although there is consensus about restriction of dietary saturated and trans fatty acids, cholesterol, and sugars, there is debate about what the optimal total fat and carbohydrate content of the diet should be for weight loss and coronary heart disease (CHD) risk reduction. The overall evidence that dietary composition plays an important role in determining caloric intake is limited. Three recent randomized trials have indicated that low-carbohydrate diets are more effective in promoting weight loss in overweight and obese subjects over 4 to 6 months, but not over 1 year. In our own randomized trial no such differences were noted, and compliance with extreme diets was limited. Moreover little attempt has been made to control for the type of carbohydrate used in the low-fat, high-carbohydrate arms of these trials. Available evidence suggests that restriction of sugars and carbohydrates having a high glycemic index would be preferable to total carbohydrate restriction, and that an increased intake of fiber and essential fats (especially omega-3 fatty acids) is also important for overall heart disease risk reduction.

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.