Key Findings:
Plaque formation in the arteries can lead to a heart attack and in the brain to a stroke. This research is very significant as it demonstrates that flaxseed supplementation accelerated the regression of atherosclerotic plaques in a rabbit model. The investigators found high levels of omega 3 fatty acids in the animal’s aorta which may have led to reductions in inflammation – an important variable in atherosclerotic plaque regression. Additionally, the flaxseed lignin secoisolariciresinol diglucoside are antioxidants and can reduce the onset of oxidized lipids that can stimulate atherosclerosis. Lignans too show powerful anti-inflammatory effects.
ABSTRACT:
Dietary flaxseed can retard the progression of atherosclerotic plaques. However, it remains unclear whether these antiatherogenic effects extend to plaque regression. In the present study, the therapeutic potential of dietary flaxseed on atherosclerotic plaque regression and vascular contractile function was evaluated using a novel rabbit model. Rabbits were randomly assigned to receive either a regular diet for 12 wk (group I) or a 1% cholesterol-supplemented diet for 4 wk followed by a regular diet for 8 wk (group II). The remaining experimental animals were treated as in group II but were fed for an additional 14 wk with either a regular diet (group III) or a 10% flaxseed-supplemented diet (group IV). Animals in group II showed clear evidence of plaque growth stabilization. Their vessels also exhibited significantly lower norepinephrine-induced contraction and an impaired relaxation response to acetylcholine compared with animals in group I. Dietary flaxseed supplementation resulted in a significant ≈40% reduction in plaque formation (P = 0.033). Animals in both groups II and III displayed improved contraction and endothelium-dependent vessel relaxation. Dietary flaxseed is a valuable strategy to accelerate the regression of atherosclerotic plaques; however, flaxseed intervention did not demonstrate a clear beneficial effect on the vessel contractile response and endothelium-dependent vasorelaxation.
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