Effects of a vegetarian diet vs. a vegetarian diet enriched with avocado in hypercholesterolemic patients.

To determine the effects of a vegetarian diet with avocado as a source of monounsaturated fat on serum lipids, thirteen patients with phenotype II (twelve with IIa and one with IIb) dyslipidemia were included in a prospective, transversal and comparative study in which three four-week diets randomly assigned were assessed. One vegetarian diet (ALVD) was composed of 70% carbohydrates, 10% proteins and 20% lipids. Another was composed of 60% carbohydrates, 10% proteins and 30% lipids, 75% of which was supplied by avocado (AVD). A third diet was an avocado-added free diet (FDWA). Body weight, body mass index (BMI), and serum lipids (total cholesterol (TC), high (HDL) and low density lipoprotein (LDL) cholesterol and triglycerides (TG)) were evaluated. AVD produced a significant decrease in LDL. ALVD did not change TC and LDL, while FDWA increased them slightly. The three diets reduced TG levels, but only ALVD did so significantly. All three diets reduced HDL levels, particularly ALVD, which produced the greatest reduction. Low-fat, carbohydrate-rich vegetarian diets may be harmful to hypercholesterolemic patients. The avocado addition to a vegetarian diet does not correct these undesirable effects. To obtain beneficial effects on lipid profile with avocado, lower amounts of carbohydrates and polyunsaturated fatty acids are probably needed.

Effects of avocado as a source of monounsaturated fatty acids on plasma lipid levels.

To examine the effects of avocado on plasma lipid concentrations, a three-diet trial involving 16 healthy volunteers was carried out. A diet rich in monounsaturated fatty acids using avocado as their major source (30% of the total energy was consumed as fat: 75% of the total fat from the avocado), with restriction of saturated fats and less than 300 mg of cholesterol per day was evaluated. Subjects also were in a free-diet period with the addition of the same amount of avocado. Finally, volunteers received a low-saturated fat diet without avocado. The first and third diets were designed to simulate a usual diet and volunteers carried on their normal activities during the trial, only the three daily meals were eaten in our clinical unit. Diets lasted 2 weeks and they were assigned in a randomized order. In both rich-monounsaturated fat (RMF) and low-saturated fat (LSF) diets, there were similar reductions in the plasma total cholesterol and low-density lipoprotein cholesterol levels. The levels of high-density lipoprotein cholesterol significantly decreased (p < 0.05) after 2 weeks of the LSF and free monounsaturated-enriched (FME) diets. The plasma triacyglycerol levels lessened after RMF and FME diets, while LSF diet increased them. In total cholesterol and in low-lipoprotein cholesterol levels, there were statistically significant differences between the FME and the LSF diet periods. Avocado is an excellent source of monounsaturated fatty acid in diets designed to avoid hyperlipidemia without the undesirable effects of low-saturated fat diets on HDL-cholesterol and triacylglycerol concentrations.

Differences in basal nocturnal, meal-stimulated, and pentagastrin-stimulated gastric secretion values in a sample of healthy volunteers in basal conditions and under ranitidine influence.

The gastric secretion values from 16 healthy male volunteers are reported. A nasogastric tube was positioned in the gastric antrum and 10-min gastric secretion samples were obtained hourly by continuous suction. Basal nocturnal, meal-stimulated, and pentagastrin-stimulated gastric acid secretion were measured. Experimental sessions were carried out in control conditions and repeated after a 7-day treatment with placebo and ranitidine (150 mg b.i.d.) in a double-blind procedure. We found six subjects (group I) with basal nocturnal, meal-stimulated, and pentagastrin-stimulated gastric secretion values statistically lower than then rest of the group (group II). Basal nocturnal secretion mean values were 3.99 +/- 6.6 mmol/L (group I) and 59.2 +/- 22.1 mmol/L (group II) (p < 0.01). Meal-stimulated gastric acidity mean values were 33.1 + 17.3 mmol/L (group I) and 65.6 +/- 30.6 mmol/L (group II) (p < 0.05). Pentagastrin-stimulated gastric secretion mean values were 8 +/- 2 mmol/h (group I) and 19.2 +/- 2.7 mmol/h (group II) (p < 0.01). Ranitidine significantly inhibited basal nocturnal, meal-stimulated, and pentagastrin-stimulated gastric acidity values mostly in group II. These results suggest that there are two different patterns of gastric secretion in the healthy male population.