Am J Phys Heart Circ Physiol, 2011, Volume Dec 301; Issue 6: Pages H2220 - 2226.

The alpha-linolenic acid content of flaxseed can prevent the atherogenic effects of dietary trans fat.

Bassett, CM. McCullough, RS. Edel, AL. Patenaude, A. LaVallee, RK. Pierce, GN.

Key Findings:

In this research, both milled flaxseed and ALA reduced atherosclerotic plaque development induced by trans fatty acids. Flaxseed fractions (oil, fiber, and lignan) resulted in  lipid-lowering effects in the presence of cholesterol compared with control diets in the presence of two atherogenic agents. The findings are significant as, because it is difficult to eliminate cardio-toxic trans fats in foods, adding flaxseed to the diet may be an effective strategy to offset the effects of trans fats.

ABSTRACT:

Dietary intake of industrially hydrogenated trans fatty acids (TFA) has been associated with coronary heart disease. Dietary flaxseed can inhibit atherosclerosis induced by dietary cholesterol. The aim of this study was to determine whether supplementing the diet with flaxseed could protect against atherosclerosis induced by a diet enriched in TFA. Low-density lipoprotein receptor-deficient (LDLr(-/-)) mice were fed 1 of 14 experimental diets for 14 wk containing one of two fat sources [regular (pork/soy) or trans fat] at two concentrations (4 or 8%) and supplemented with or without dietary cholesterol (2%), whole ground flaxseed, or one of the components of flaxseed [alpha-linolenic acid (ALA), defatted fiber, or lignan]. Adding flaxseed to the diet partially mitigated the rise in circulating cholesterol levels induced by the cholesterol-enriched diet. Atherosclerosis was stimulated by TFA and/or cholesterol. Including milled flaxseed to an atherogenic diet significantly reduced atherosclerosis compared with the groups that consumed cholesterol and/or TFA. ALA was the only component within flaxseed that could inhibit the atherogenic action of cholesterol and/or TFA on its own. Dietary flaxseed protects against atherosclerotic development induced by TFA and cholesterol feeding through its content of ALA. (Authors Abstract)

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