Clogged arteries block hormone effects.

Most studies of hormone-replacement therapy for postmenopausal women suggest that the treatment wards off heart disease. Last year, however, this theory suffered a blow. Among 3,000 women who already had heart disease, researchers round that the ailment progressed at the same rate in those given estrogen as in those not given the hormone-replacement therapy (SN: 10/16/99, p. 252).

A new study may help explain that finding. According to a report in the Sept. 1 CARDIOVASCULAR RESEARCH, the build-up of fatty plaques in blood vessels might muffle the gene that's responsible for making the receptors that recognize estrogen and trigger its effects in a cell. In the absence of such receptors, the tissue would, in effect, not be aware of the hormone's presence.

Tissue samples from 17 men and women with detectable buildup of fatty plaques in their coronary arteries, or atherosclerosis, showed that about 10 percent of the estrogen-receptor genes were blocked by a process called methylation, says Pascal J. Goldschmidt of Ohio State University in Columbus. In contrast, in tissue taken from the coronary arteries of 27 men and women without atherosclerosis, only about 4 percent of the estrogen-receptor genes were inactive, he says.

Further work, not yet published, shows that mimicking atherosclerosis in cell cultures increases methylation, putting more estrogen-receptor genes "out of service," Goldschmidt says. His findings suggest that compounds that activate estrogen-receptor genes might offer a novel way of treating heart disease, he adds.