Discovery spurs debate on race-based medicine

In a finding likely to sharpen discussion about the merits of race-based medicine, an Icelandic company says it has detected a version of a gene that raises the risk of heart attack in African-Americans by more than 250 percent.

The company, DeCode Genetics, first found the variant gene among Icelanders and then looked for it in three American populations, in Philadelphia, Cleveland and Atlanta.

Among Americans of European ancestry, the variant is quite common, but it causes only a small increase in risk, about 16 percent.

The opposite is true among African-Americans. Only 6 percent of African-Americans have inherited the variant gene, but they are 3.5 times as likely to suffer a heart attack as those who carry the normal version of the gene, a team of DeCode scientists led by Dr. Anna Helgadottir reports in an article being released online by Nature Genetics.

Dr. Kari Stefansson, the company's chief executive, said he would consult with the Association of Black Cardiologists and others as to whether to test a new heart attack drug specifically in a population of black Americans.

The drug, known now as DG031, inhibits a different but closely related gene and is about to be put into Phase 3 trials, the last stage before a maker seeks the Food and Drug Administration's approval.

Last year a drug called BiDil evoked mixed reactions after it was shown to sharply reduce heart attacks among blacks. The drug, invented by Dr. Jay N. Cohn, a cardiologist at the University of Minnesota, prompted objections that race-based medicine was the wrong approach

Geneticists agree that the medically important issue is not race itself but the genes that predispose a person to disease. But it may often be useful for physicians to take race into account because the predisposing genes for many diseases follow racial patterns, being more common in one race or another.

The new variant found by DeCode Genetics is a more active version of a gene that helps govern the body's inflammatory response to infection. Called leukotriene A4 hydrolase, the gene is involved in the synthesis of leukotrienes, agents that maintain a state of inflammation.

Stefansson said he believed that the more active version of this gene might have risen to prominence in Europeans and Asians because it conferred extra protection against infectious disease.