Limited impact of 2 g/day omega-3 fatty acid ethyl esters (Omacor®) on plasma lipids and inflammatory markers in patients awaiting carotid endarterectomy.

The objective of this study was to determine the effects of prescription omega-3 (n-3) fatty acid ethyl esters (Omacor®) on blood pressure, plasma lipids, and inflammatory marker concentrations in patients awaiting carotid endarterectomy. Patients awaiting carotid endarterectomy (n = 121) were randomised to Omacor® or olive oil as placebo (2 g/day) until surgery (median 21 days). Blood pressure, plasma lipids, and plasma inflammatory markers were determined. There were significant decreases in systolic and diastolic blood pressure and in plasma triglyceride, total cholesterol, low density lipoprotein-cholesterol, soluble vascular cellular adhesion molecule 1, and matrix metalloproteinase 2 concentrations, in both groups. The extent of triglyceride lowering was greater with Omacor® (25%) compared with placebo (9%). Soluble E-selectin concentration was significantly decreased in the Omacor® group but increased in the placebo group. At the end of the supplementation period there were no differences in blood pressure or in plasma lipid and inflammatory marker concentrations between the two groups. It is concluded that Omacor® given at 2 g/day for an average of 21 days to patients with advanced carotid atherosclerosis lowers triglycerides and soluble E-selectin concentrations, but has limited broad impact on the plasma lipid profile or on inflammatory markers. This may be because the duration of intervention was too short or the dose of n-3 fatty acids was too low.

Influence of very long-chain n-3 fatty acids on plasma markers of inflammation in middle-aged men.

This study investigated the effects of a moderate dose of long-chain n-3 polyunsaturated fatty acids (1.8 g eicosapentaenoic acid (EPA) plus 0.3g docosahexaenoic acid (DHA) per day) given for 8 weeks to healthy middle-aged males on cardiovascular risk factors, particularly plasma lipids and inflammatory markers. The study was double-blind and placebo-controlled. The proportion of EPA was significantly increased in plasma phosphatidylcholine (from 1.4% to 5.0% of total fatty acids; P<0.001), cholesteryl esters (from 1.2% to 4.5%; P<0.001) and triacylglycerols (from 0.3% to 1.8%; P<0.001). In contrast, the more modest increases in DHA in these lipid fractions were not significant. There was very little effect of n-3 fatty acids on the risk factors measured, apart from a reduction in plasma soluble intercellular adhesion molecule (sICAM)-1 concentration compared with placebo (P=0.05). The change in plasma sICAM-1 concentration was significantly inversely related to the change in DHA in plasma phosphatidylcholine (r=-0.675; P=0.001), but less so to the change in EPA (r=-0.406; P=0.076). Data from the present study suggest that marine oil providing 1.8 g of EPA plus 0.3g DHA/day is not sufficient to demonstrate marked effects on cardiovascular risk factors (plasma lipids and inflammatory markers) in healthy middle-aged men, although there may be a slight anti-inflammatory effect as indicated by the decrease in sICAM-1. The stronger association between changes in DHA than EPA and sICAM-1 concentrations suggest that DHA may be more anti-inflammatory than EPA. Thus, one reason why only limited effects were seen here may be that the dose of DHA provided was insufficient.