Dietary Flaxseed in Prevention of Hypercholesterolemic Atherosclerosis.

January 1, 1997 Human Health and Nutrition Data 0 Comments

Dietary Flaxseed in Prevention of Hypercholesterolemic Atherosclerosis.

Year: 1997
Authors: K Prasad.
Publication Name: Atherosclerosis.
Publication Details: Volume 132; Page 69.


Previous research has shown that hypercholesterolemia increases the cholesterol content of platelets, polymorphonuclear leucocytes (PMNLs) and endothelial cells. Platelet activating factor (PAF) stimulates granulocytes and the release of cytokines such as interleukin-1 (IL-1) and tumor necrosis factor (TNF). PAF, IL-1, TNF and LTB4 are known to stimulate PMNLs and monocytes to produce oxygen free radicals (OFRs) which have been implicated in the development of hypercholesterolemic atherosclerosis. Antioxidants have been reported to retard hypercholesterolemic atherosclerosis through reductions in OFRs. N-3 PUFAs have been found to suppress the production of IL-1, TNF, LTB4 and of OFRs by PMNLs and monocytes. Lignans in flaxseed are PAF-receptor antagonists and hence have anti- PAFactivity. Lignans also show antioxidant properties. Because of these findings, the author postulates in this study that flaxseed, with its high ALA and lignan content, could reduce levels of OFRs and hence prevent the development of hypercholesterolemic atherosclerosis. The effects of dietary flaxseed on a high cholesterol diet induced atherosclerosis, lipid profile and OFR-producing activity of PMNLs (PMNL-CL) were investigated in rabbits. The rabbits were divided into four groups: group 1 served as the control; Group 2 were fed a flaxseed diet (7.5 g/kg daily, orally); group 3 were fed 1% cholesterol alone; and group 4 were fed 7.5 g/kg flaxseed daily plus 1% cholesterol. Measurements of serum lipids and OFR-producing activity of PMNLs were taken after 4 and 8 weeks on the respective experimental diets. The results showed that the high cholesterol diet significantly increased serum TC levels and PMNL-CL without altering the levels of serum TGs. These changes were associated with a marked development of atherosclerosis in the aorta. The flaxseed diet reduced the development of aortic atherosclerosis by 46% and reduced the PMNL-CL without significantly lowering serum TC. In normocholesterolemic rabbits, flaxseed increased serum TC and decreased PMNL-CL without significantly affecting the serum TG. These results are inconsistent with previous observations which have shown that higher levels of flaxseed fed for longer durations reduced TC. The author concluded that dietary flaxseed supplementation is effective in reducing hypercholesterolemic atherosclerosis markedly without lowering TC. He speculates that the effectiveness of FS against hypercholesterolemic atherosclerosis may be due to suppression of enhanced production of OFRs by PMNLs in both normocholesterolemia and hypercholesterolemia. These effects may be due to both the ALA and lignan content of flaxseed. The results suggest that dietary flaxseed supplementation may prevent hypercholesterolemia-related heart attack and strokes, in part by reducing the narrowing of the lumen of coronary and cerebral arteries.

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