Some excerpts below from an article in The Economist. I have left out all the agonizing
Last month researchers from the University of Texas and the University of Mississippi Medical Centre published a paper in the New England Journal of Medicine. They had studied three versions (or alleles, as they are known) of a gene called PCSK9. This gene helps clear the blood of low-density lipoprotein (LDL), one of the chemical packages used to transport cholesterol around the body. Raised levels of LDL are associated with heart disease. The effect of all three types of PCSK9 studied by Jonathan Cohen and his colleagues was to lower the LDL in a person's bloodstream by between 15% and 28%, and coronary heart disease by between 47% and 88%, compared with people with more common alleles of the gene.
In Dr Cohen's work, the race question proved decisive. Of the 3,363 volunteers who described themselves as "black", 0.8% carried an allele of PCSK9 called version 142X and 1.8% carried one called version 679X. Among 9,524 self-described "white" volunteers, a mere 0.02% carried version 142X and 0.04% carried version 679X. By contrast, 3.2% of white people carried the third allele under study, version 46L, while only 0.7% of black participants did. The researchers found that these relatively rare alleles correlated with low LDL, and did so in both blacks and whites, allowing them to conclude that it was the gene change that was crucial. If the team had ignored race and simply compared those who had heart disease with those who did not, and asked which alleles were linked to the risk, they would probably have missed the clinical significance of the alleles... Ignoring race altogether would be to the detriment of medical knowledge about the very people who might benefit.
In some cases, though, the difference clearly is genetic. A gene called UGT1A1 controls the metabolism of a colon-cancer drug called irinotecan. Approximately 20% of African-Americans, 15% of whites and 1% of Asians have two copies of a non-functional version of this gene called *28. Because individuals lacking functional UGT1A1 are at risk for serious complications if given the standard dose of irinotecan, genetic testing of patients before starting irinotecan therapy has become normal. Yet, while only 1% of Asians have two copies of the *28 allele, which is detected by the genetic test, 2.5% of Asians have another non-functional version called *6 which is not detected by the standard test. Indeed, it does not occur in blacks or whites. Thus, testing Asians for the *28 allele does not provide them with the same quality of care as it does for African-Americans or whites. "Identical treatment is not," as Dr Risch puts it, "equal treatment."
(For more postings from me, see EDUCATION WATCH, GREENIE WATCH, POLITICAL CORRECTNESS WATCH, GUN WATCH, SOCIALIZED MEDICINE, AUSTRALIAN POLITICS and DISSECTING LEFTISM. My Home Page. Email me (John Ray) here.)