Studies suggest how salad may protect heart.

Carotenoids, a family of some 500 natural yellow-to-red pigments, brighten the plant world. Diets rich in at least one of these, lutein, may also brighten a person's chances of warding off heart disease, new studies indicate.

The findings stem from research linking consumption of fruits and vegetables to heart health. Since oxidation fosters artery-clogging atherosclerosis and fruits and veggies serve up a bounty of antioxidant carotenoids, these pigments made promising candidates for prevention of heart disease. When trials in people indicated that beta carotene, the most abundant carotenoid in human blood, offered no heart protection (SN: 1/27/96, p. 55), three collaborating research groups in Los Angeles turned to lutein.

This yellow agent plays a major role in coloring egg yolks, corn, and summer squash. However, the main dietary sources of lutein are dark-green veggies, such as spinach and broccoli.

Fueling interest in lutein, explains James H. Dwyer of the University of Southern California's Keck School of Medicine, were a few studies suggesting that certain cells selectively concentrate the yellow pigment. These cells include monocytes, the white blood cells that can jump start atherosclerosis.

Fatty deposits, which can evolve into atherosclerosis, can be measured as a thickening of artery walls. So, Dwyer's group and teams at the University of California, Los Angeles and Cedars Sinai Medical Center in Los Angeles looked for an effect of lutein on artery thickness. Using ultrasound, the researchers measured a carotid artery in 480 middle-age men and women at the beginning and the end of an 18-month period.

The teams also measured lutein and beta carotene in each person's blood. Beta carotene concentrations showed no link to artery thickening. But when the researchers grouped volunteers by their lutein concentrations, they found that people in the top group had almost no artery thickening over the 18 months. The measured thickening increased progressively as the team considered people in each of the four successively lower lutein-concentration groups.

To explain the finding, the researchers focused on low-density lipoproteins (LDLs) and monocytes. LDLs ferry cholesterol from blood into artery walls, and monocytes can spark atherosclerosis by oxidizing the LDLs.

The scientists incubated monocytes with pieces of the inner lining of carotid arteries that had been removed from people during vascular surgery. Artery walls pretreated with lutein attracted far fewer monocytes and sustained far less LDL oxidation than untreated walls did.

The researchers then fed large doses of lutein to mice that had been genetically engineered to develop early atherosclerosis. The animals developed atherosclerotic lesions that were only about half as large as those in the mice eating normal feed. The scientists describe their three studies in the June 19 CIRCULATION.

The new findings "are exciting and really knock [lutein] up on one's radar screen," says epidemiologist Stephen B. Kritchevsky of the University of Tennessee in Memphis. The data from cultured monocytes, mice, and people amplify each other, he says, "to make the findings a great deal more credible."

Charles H. Hennekens of the University of Miami School of Medicine agrees that the data are promising. However, he cautions, they also fall far short of proving lutein's benefits. Until those are confirmed in human dietary trials, he won't prescribe diet changes.

Acknowledging a "biological plausibility" to lutein's apparent heart benefits, Meir J. Stampfer of the Harvard School of Public Health in Boston volunteers that he's "not going to start taking lutein supplements." But he will now reexamine his group's major diet and health studies for hints of lutein benefits.