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    Preventing Heart Disease

    Recently, researchers have questioned the protective effects of estrogen on cardiovascular health. Now researchers from Johns Hopkins University report that genetic factors may dictate whether estrogen will benefit your coronary arteries.

    The increase in heart disease seen in women after menopause may not be due just to decreased estrogen, but rather to a genetically orchestrated process that blocks the arteries' ability to respond to the presence of estrogen. This would explain why women with pre-existing coronary artery disease don't benefit from hormone replacement therapy.

    The blood vessels that supply the heart have estrogen receptors. If the receptors are missing or aren't functioning, it doesn't matter how much estrogen is present because the receptors and blood vessels don't know it's there.

    When the researchers compared the coronary arteries of healthy hearts to those afflicted with atherosclerosis, they found the diseased vessels had two to three times more methylated genes than the healthy heart.

    Methylation is a process that keeps a gene locked into a particular mode. Most genes have so-called switches. Methylated cells have debris on them, which gums up the switch and, as a result, shuts down the gene. When the genes shut down, the estrogen receptors can't respond.

    Estrogen has many functions, including preventing smooth muscle from overgrowth. Though many people don't think of their arteries as muscles, they do contain a muscle layer that responds to the same biochemical elements as the muscles of your stomach or uterus. Healthy arteries expand and contract.

    The current theory behind atherosclerosis is that the walls of the arteries become rough due to overgrowth of the smooth muscle layer. The rough surface then "catches" passing debris, and the arteries eventually become narrow or clogged.

    If this smooth muscle layer doesn't detect estrogen, there's no signal to stop it from overgrowth. The researchers believe that this is what happens in women with defective estrogen receptor genes. Giving these women estrogen replacement will not provide any benefit because the vessels have no way of responding to the estrogen.



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