Dietary Carotenoid Lutein Reduces Atherosclerotic Lesion Formation In Mice

WASHINGTON, April 18, 1999 -- The carotenoid antioxidant lutein can significantly reduce atherosclerotic lesion formation in mice, according to a study presented today at the Federation of American Societies for Experimental Biology 1999 annual meeting.

"The area of arterial lesions in the mice that were fed chow with lutein was reduced significantly in the pilot study," reported Dr. James Dwyer, Professor of Preventive Medicine, University of Southern California. "With further research, we plan to determine whether or not the intake of foods rich in lutein slows the progression of the disease that leads to most heart attacks and strokes."

Researchers from the USC Department of Preventive Medicine and the Atherosclerosis Research Unit, University of California at Los Angeles studied the effect of inclusion of the antioxidant lutein in the diet of apolipoprotein E (apoE) null mice. Groups of apoE null mice were maintained on a diet containing zero or 0.2% (by weight) lutein for four weeks. Researchers then sectioned and examined the areas of the aortic lesions and observed that the mice on the lutein-enriched diet had significantly reduced arterial lesion area.

Mice that are "null" or deficient in apoE develop atherosclerotic lesions very rapidly in the aortic arch. Inactivation of the apoE gene in mice leads to a prominent increase in blood cholesterol and triglyceride levels and the development of premature atherosclerosis.

Studies are already under way to examine a larger group of apoE null mice. Further research is needed to determine the role that lutein may play in the prevention of atherosclerotic lesions in humans.

Lutein is found in dark leafy green vegetables like spinach and kale. Research concerning lutein has centered around its antioxidant properties. Lutein can build density of the macular pigment, and higher intake of lutein from the diet may play a role in reducing the risk of age-related macular degeneration (ARMD).

Contact: Anne B. Tramer
Selz/Seabolt Communications

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