In the ibuprofen group, the mean increase from baseline after 3 weeks of treatment was significant in the average supine diastolic blood pressure (6.4 mm Hg; 95% confidence interval [CI], 1.05 to 11.75; p = 0.0239); supine mean arterial pressure (6.6 mm Hg; 95% CI, 1.25 to 11.95; p = 0.0205); and sitting mean arterial pressure (5.8 mm Hg; 95% CI, 1.57 to 10.04; p = 0.0123). The mean increase in blood pressure variables in the ibuprofen group was significantly different compared with the mean increase in the variables in the placebo group after 3 weeks of treatment: supine systolic blood pressure (7.1 mm Hg compared with -4.5 mm Hg; 95% CI for the difference in means, 2.5 to 20.6; p = 0.0133); supine diastolic pressure (6.4 mm Hg compared with 0.0; 95% CI for difference in means, 0.87 to 12.4; p = 0.0250); supine mean arterial pressure (6.6 mm Hg compared with -1.5; 95% CI for difference in means, 2.0 to 14.2; p = 0.0110); sitting systolic pressure (6.8 mm Hg compared with -3.7; 95% CI for difference in means, 2.0 to 19.0; p = 0.0169); sitting diastolic pressure (5.3 mm Hg compared with -1.1; 95% CI for difference in means, 0.76 to 12.1; p = 0.0273); and sitting mean arterial pressure (5.8 mm Hg compared with -2.0; 95% CI for difference in means, 1.5 to 14.1; p = 0.0169).(ABSTRACT TRUNCATED AT 400 WORDS)
Although the hypotriglyceridemic effect of large doses of n-3 fatty acids (n-3 FAs) is well established, the effects of prolonged use of very low doses on lipids, lipoproteins, and apolipoproteins have not been clearly defined. This investigation compares the relative effects of very low, clinically practical doses of n-3 FAs on lipids, lipoproteins, and apolipoproteins in hypertriglyceridemic subjects. Ten subjects received 2.2 g n-3 FAs/d (group 1), seven received 1.1 g n-3 FAs/d (group 2), and eight received olive oil (group 3, placebo control) for 20-wk treatment period. In group 1, both low-density-lipoprotein cholesterol (LDL-C) and LDL-apolipoprotein B concentrations increased significantly from baseline values (28% and 23%, respectively; p less than 0.05) after treatment. Compared with the placebo group, the increase in LDL apolipoprotein B in both fish oil groups was statistically and clinically significant (p less than 0.05). Only minor changes in plasma triglyceride concentrations occurred. The data suggest that very low doses of n-3 FAs may cause potentially adverse increases in LDL-C and LDL-apolipoprotein B concentrations.
Animal studies and a single human epidemiological study have suggested that chlorine in drinking water may raise the level of blood cholesterol. The purpose of this study was to determine whether a 4-week exposure to drinking water chlorine (1.5 L per day) at a concentration of 20 ppm (ppm = mg/L) under controlled conditions would alter circulating parameters of lipid metabolism in healthy humans. Thirty men and thirty women each completed an 8-week protocol during which diet (600 mg cholesterol per day, 40% calories as fat) and other factors known to affect lipid metabolism were controlled. For the first 4 weeks of the protocol, all subjects consumed distilled water. For the second 4 weeks, half of the subjects were assigned randomly to drink 1.5 L per day of chlorinated water (20 ppm), while the others continued drinking distilled water. Four blood samples were collected from each subject at the end of each 4-week study period. Compared to the control group, those subjects given chlorine showed no significant changes in total plasma cholesterol, triglycerides, HDL-cholesterol, LDL-cholesterol, or apolipoproteins A1, A2, or B. There was a trend toward low serum thyroxine and triiodothyronine levels in men given chlorine, though thyroid-stimulating hormone levels were unchanged. This trend, if real, was not clinically significant. Thus, short-term exposure to chlorinated drinking water at 20 ppm appears to have no significant impact on parameters of lipid or thyroid metabolism in healthy humans.
The potentially beneficial blood pressure (BP)-lowering effects of marine omega-3 polyunsaturated fatty acids (omega-3-PUFAs) remain controversial. The objective of this qualitative and quantitative (meta-analysis) analysis was to evaluate the results of all available randomized controlled trials that studied the effect of omega-3-PUFAs on BP response. A comprehensive search of the English literature from 1970 to 1988 disclosed only six randomized controlled investigations out of 22 published reports. Four of these were evaluable and therefore eligible for this analysis. Of these, only one evaluated hypertensive subjects. In two trials, there were statistically significant reductions in BP; the one reporting an investigation of hypertensive subjects showed the greatest reduction. Using established methodologic criteria, the quality of each report was evaluated by independent observers. Following this appraisal, the outcomes of each investigation were reanalyzed and pooled using a meta-analysis. There was no statistically significant difference between the omega-3-PUFA groups and the control groups, possibly because of failure to include hypertensive subjects in all but one trial. Despite the positive effects in two studies, little scientifically valid evidence is available to demonstrate a significant BP-lowering effect of omega-3-PUFAs. Areas needing more attention in future research are identified and methods to improve study designs are suggested.
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