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Background: Several lines of evidence suggest that supplementation of diet with omega-3 polyunsaturated fatty acids ([omega]-3 PUFA), commonly referred to as fish oils, may reduce blood pressure (BP). However, most clinical trials of [omega]-3 PUFA supplementation have been of insufficient size to detect relevant BP changes. Methods: We conducted a meta-analysis of 17 controlled clinical trials of [omega]-3 PUFA supplementation. To estimate an overall effect of [omega]-3 PUFA supplementation on BP, we calculated the net BP change in each trial (BP [DELTA] in [omega]-3 PUFA group minus BP [DELTA] in control group), which was then weighted according to the inverse of the variance. Results: In the 11 trials that enrolled normotensive individuals (n=728), [omega]-3 PUFA supplementation led to significant reductions of systolic BP (SBP) and diastolic BP (DBP) in two and one trials, respectively. In the six studies that enrolled untreated hypertensives (n=291), significant reductions of SBP and DBP were present in two and four trials, respectively. Weighted, pooled estimates of SBP and DBP change (mm Hg) with 95% confidence intervals were - 1. 0 (-2.0 to 0.0) and -0.5 (-1.2 to +0.2) in the trials of normotensives, and -5.5 (-8.1 to - 2.9) and -3.5 (-5.0 to - 2.1) in the trials of untreated hypertensives. In 13 of 17 studies, trial duration was less than 3 months. Doses of [omega]-3 PUFA tended to be high (average dose >3 g/d in 11 trials). The magnitude of BP reduction was greatest at high BP but was not significantly associated with dose of [omega]-3 PUFA. Side effects, most commonly eructation and a fishy taste, occurred more frequently in [omega]-3 PUFA participants than in control participants (28% vs 13%, P

Background: Low serum levels of [Beta]-carotene have been associated with increased risk of cancer and cardiovascular disease. However, in clinical trials, supplementation of the diet with [Beta]-carotene either had no benefit or caused harm. This pattern of findings raises the possibility that confounding by other factors might explain the association between serum [Beta]-carotene level and disease risk. Methods: We used data from 14470 current smokers, ex-smokers, and never smokers aged 18 years or older who participated in the Third National Health and Nutrition Examination Survey to assess the relationship between serum [Beta]-carotene and markers of inflammation (C-reactive protein and white blood cell count). Results: After adjustment for [Beta]-carotene intake and other factors, geometric mean levels of serum [Beta]-carotene for individuals with undetectable ([is less than] 0.22 mg/dL), mildly elevated (0.22-0.99 mg/dL), and clinically elevated ([is greater than or equal to] 1.0 mg/dL) C-reactive protein levels were 18.0, 115.1, and 13.6 [micro]g/dL, respectively, in never smokers; 18.1, 15.7, and 13.9 [micro]g/dL in ex-smokers; and 11.3, 10.2, and 9.4 [micro]g/dL in current smokers (P [is less than] .001 for all). In corresponding analyses, white blood cell count was also inversely related to serum [Beta]-carotene concentration (P [is less than] .05 for all). Conclusions: The strong and inverse association of serum [Beta]-carotene level with C-reactive protein level and white blood cell count suggests that the relationship between serum [Beta]-carotene concentration and disease risk might be confounded by inflammation. More broadly, for [Beta]-carotene and likely other nutrients, it seems unwise to interpret biomarker data as prima facie evidence of dietary intake without a more complete understanding of the physiologic processes that affect nutrient levels. Arch Intern Med. 2001;161:1903-1908