Journal Name:
J. Nutr.
Article Title:
Flaxseed Oil Supplementation Does Not Affect Plasma Lipoprotein Concentration or Particle Size in Human Subjects
Date Written:
2006
Volume:
136
Number:
0
Page:
2844
Author(s):
Harper, C.R.; Edwards, M.C.; Jacobson, T.A.
Article:
Evidence from several epidemiologic studies suggests that alpha-linolenic acid (ALA) acid may provide a substantial cardioprotective effect. The mechanism whereby ALA exerts this cardioprotective effect has not been established. Although LDL-cholesterol concentration, not the particle size, remains the primary target of therapy for the prevention of coronary heart disease (CHD), increasing research has been devoted to the study of the heterogeneity of LDL particles. Smaller diameter and denser LDL particles are known to have a greater proclivity for oxidation and an enhanced ability to penetrate the intima than larger, less dense LDL particles. Smaller, denser LDL particles are associated with an increased risk for CHD in prospective studies. HDL cholesterol particles are also heterogeneous and evidence suggests that larger diameter HDL particles may be more cardioprotective.
In this study, the effects of daily supplementation with ALA derived from flaxseed oil on concentrations of plasma LDL cholesterol, HDL cholesterol, intermediate density lipoprotein cholesterol, and lipid particle sizes was assessed. Fifty-six participants were given 3 g/d of ALA from flaxseed oil in capsules (n = 31) or olive oil containing placebo capsules (n = 25) for 26 wk. This study - the FORCE trial (Flaxseed Oil to Reduce Intermediate Cardiac Endpoints) utilized a randomized placebo-controlled study design to analyze the effect of ALA on plasma lipoprotein subfractions. The study population was predominantly African American patients with multiple chronic diseases.
Changes in plasma HDL cholesterol, LDL cholesterol, and triglyceride concentrations did not differ between the 2 groups at 26 wk. The adjusted plasma total cholesterol concentration at 26 wk was 0.45 mmol/L higher in the flaxseed oil group (5.43 ± 0.03 mmol/L) compared with the olive oil group (5.17 ± 0.07 mmol/L. ALA did not affect LDL, HDL, or IDL particle size; however, the concentrations of the large, less atherogenic LDL1 and LDL2 subfractions tended to be greater in the ALA group.
There was an unexpected increase in total cholesterol in the ALA group compared with the olive oil group at 26 wk. The increase in total cholesterol might have resulted from the increase in the less atherogenic LDL subfractions (LDL1, LDL2). There was also a trend at 26 wk for an increase in the larger, less atherogenic LDL subfractions, LDL1 (P ¼ 0.058) and LDL2 (P ¼ 0.083), in the ALA group compared with the olive oil group.
The mechanism for the ability of ALA to decrease CVD risk does not appear to be due to an alteration in lipoprotein particle size or plasma lipoprotein concentrations. The findings from the FORCE trial suggests that ALA itself may either have intrinsic cardioprotective benefits and/or the in vivo conversions of ALA to EPA or DHA, which are known cardioprotective fatty acids, are responsible for the cardiac benefit seen in observational and clinic trials with ALA. More research is needed to clarify the mechanism for the cardioprotective effects of ALA.
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