Supplementation with selenium-rich bread does not influence platelet aggregation in healthy volunteers.

In order to establish the effect of an increased dietary selenium supply on platelet glutathione peroxidase (EC 1.11.1.9.; GSH-Px) and platelet aggregation, six healthy subjects were supplemented with 200 micrograms Se as Se-rich bread for 6 weeks. Another six subjects received low-Se bread and served as controls. Platelet GSH-Px activity increased significantly in the supplementation group, whereas no effect could be observed on platelet aggregation. The results of this study do not support the hypothesis that an increased dietary Se intake has a favourable influence on platelet aggregation.

Effect of various levels of selenium in wheat and meat on blood Se status indices and on Se balance in Dutch men.

After a 5-week period of low selenium intake, twenty-four Dutch men received 55, 135 or 215 micrograms Se/d as Se-rich meat or bread for a 9-week period. Four unsupplemented subjects served as controls. Plasma Se increased more rapidly than erythrocyte Se levels; the increases were significantly dependent (P less than 0.001) on Se intake level. Glutathione peroxidase (EC 1.11.1.9; GSH-Px) activity in platelets increased rapidly after supplementation and plateaued after 4-9 weeks. At 10 weeks after supplementation ended, plasma Se levels and platelet GSH-Px were still higher than the baseline values whereas erythrocyte Se levels continued to increase. Except for the higher erythrocyte Se levels after supplementation with high-Se meat, there were no differences in bioavailability of Se between meat and wheat products. Daily urinary and faecal Se excretions as well as Se retention increased with an increased Se intake irrespective of the form of the supplement. Regression of Se excretion v. intake indicated that 33 micrograms Se/d is necessary to compensate for urinary and faecal losses.

Boys from populations with high-carbohydrate intake have higher fasting triglyceride levels than boys from populations with high-fat intake.

Experimentally, high-carbohydrate diets have been shown to elevate triglycerides, but it has not been established whether this rise is permanent or transient. The authors approached this question by studying 719 boys from worldwide populations with marked differences in long-term carbohydrate intake. Fasting serum triglycerides, total cholesterol and high density lipoprotein (HDL) cholesterol concentrations were measured in boys aged 8 and 9 years from 12 countries--eight in Europe, three in Africa, and one in Asia. A standardized protocol was used for obtaining fasting blood and for the preparation, storage and transport of serum, and all measurements were made in one laboratory. Published values were used for the United States. Mean values for lipid levels per country were compared with the percentage of daily energy intake consumed as carbohydrate or fat, as determined by survey. Boys from populations with higher carbohydrate and lower fat intake had lower low density lipoprotein (LDL) cholesterol levels (univariate regression coefficient (+/- standard error, -0.028 +/- 0.009 mmol/liter for each percent of energy from carbohydrate; p less than 0.01, n = 13), but they also had higher fasting triglycerides (0.010 +/- 0.002 mmol/liter for each percent of energy from carbohydrate; p less than 0.01, n = 13) and lower HDL cholesterol levels (-0.022 +/- 0.003 mmol/liter for each percent of energy from carbohydrate; p less than 0.001, n = 13). These trends agree with results from epidemiologic studies within populations and from controlled dietary trials, and suggest that in normolipidemic healthy subjects, high-carbohydrate, low-fat diets cause higher triglyceride levels than diets that are higher in fats and oils.