Low-and High-Dose Plant and Marine (n-3) Fatty Acids Do Not Affect Plasma Inflammatory Markers in Adults with Metabolic Syndrome

January 1, 2011 Human Health and Nutrition Data 0 Comments

Low-and High-Dose Plant and Marine (n-3) Fatty Acids Do Not Affect Plasma Inflammatory Markers in Adults with Metabolic Syndrome

Year: 2011
Authors: Dewell, A. Marvasti, F.F. Harris, W.S. Tsao, P. Gardner, C.D.
Publication Name: Journal of Nutrition
Publication Details: doi: 10.3945/jn.111.142240


Chronic inflammation is considered to play a role in the development of cardiovascular disease. (n-3) Fatty acids (FA) have been reported to have antiinflammatory effects, but there is a lack of consensus in this area, particularly in regard to optimal source(s) and dose(s). This study aimed to determine the effects of high and low doses of (n-3) FA from plant and marine sources on plasma inflammatory marker concentrations. One-hundred adults with metabolic syndrome were randomly assigned to a low or high dose of plant- (2.2 or 6.6 g/d alpha-linolenic acid) or marine- (1.2 or 3.6 g/d EPA and DHA) derived (n-3) FA or placebo for 8 wk, using a parallel arm design (n = 20/arm). Fasting blood samples collected at 0, 4, and 8 wk were analyzed for concentrations of monocyte chemotactic protein-1 (MCP-1), IL-6, and soluble intercellular adhesion molecule-1 (sICAM-1) and for cardiovascular risk factors. Baseline concentrations across all 5 groups combined were (mean +/- SD) 103 +/- 32 ng/L for MCP-1, 1.06 +/- 0.56 ng/L for IL-6, and 0.197 +/- 0.041 ng/L for sICAM-1. There were no significant differences in 8-wk changes in plasma inflammatory marker concentrations among the 5 groups. Plasma TG and blood pressure decreased significantly more and the LDL cholesterol concentration increased more in the high-dose fish oil group compared to the 8-wk changes in some of the other 4 groups (P < 0.04). In conclusion, no beneficial effects were detected for any of the 3 inflammatory markers investigated in  response to (n-3) FA in adults with metabolic syndrome regardless of dose or source. (Author's abstract)
Chronic inflammation plays a major role in the development of atherosclerosis and CVD. Potential anti-inflammatory roles of 3 common dietary (n-3) FA: ALA, EPA, and DHA have been recognized as one of the numerous mechanisms by which (n-3) FA may reduce the risk of CVD. A number of clinical trials have investigated the effects of  higher doses of (n-3) FA ( >1 g/d EPA and/or DHA) and have had mixed results. The majority of clinical trials have used marine sources of (n-3) FA (EPA and DHA from capsules or fish), whereas few have examined plant sources (ALA from flax oil). There is a lack of consensus regarding the optimal source(s) and dose(s) for reducing and preventing inflammation.  In this study, the effects of flaxseed oil (plant) and fish oil, in two different doses (low vs. high) on three markers of inflammation in adults with metabolic syndrome, in particular blood concentrations of selected markers of inflammation (MCP-1, IL-6, and sICAM-1). The results showed no significant changes in any of the 3 inflammatory markers investigated regardless of dose or source of (n-3) FA supplementation. LDL-cholesterol concentrations were increased and TG concentrations and blood pressure levels were reduced by fish oil consumption. These results are not consistent when compared with more rigorous and recent investigations which reported reductions in  different concentrations of inflammatory biomarkers for both ALA as well as  EPA+ DHA.  Baseline concentrations of inflammatory markers may be important in eliciting detectable effects. No effects on inflammatory marker concentrations have been noted overall when baseline levels are low. The specific markers of inflammation selected as study outcomes are also an important variable of these study designs.  It is possible that an intervention study of several weeks or months is not of sufficient duration to alter inflammatory processes.  The trial had several limitations including enrolling some participants that had relatively low concentrations of inflammatory markers to begin with. A second limitation is that the 3 inflammatory markers investigated in this trial may not have been the most suitable to capture the effects of (n-3) FA. The authors speculate that the potential health benefits of (n-3) FA may be mediated by a mechanism that has an insignificant effect on specific markers of inflammation
such as the prevention of fatal arrhythmias. Further research is warranted to better elucidate the mechanism of action and ideal consumption of (n-3) FA for potential health benefits. (Editor's comments)

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