There is much truth in this criticism. But sometimes you find the opposite: racial differences seem to amplify observable genetic ones. One example cited by Neil Risch, the director of the Centre for Human Genetics at the University of California, San Francisco, concerns ApoE, another gene involved in LDL metabolism. One particular allele of this gene, ApoE4, is associated with an increased risk of Alzheimer's disease.
ApoE4 is relatively common in most racial groups. About 9% of Japanese Americans have it, 14% of white Americans and 19% of black Americans. But the impact of ApoE4 differs significantly between these groups. Individuals of Japanese descent who have two copies of ApoE4 (one from each parent) have a 33-fold increased risk of contracting Alzheimer's disease compared with those who have other versions of ApoE. Those of European descent have a 15-fold increased risk. Blacks, by contrast, have a mere six-fold increase in their risk. “Whether it is due to differences in genetic background or environment, who knows? But if you ignore race, you would never know,” says Dr Risch. Moreover, if the American population was sampled for ApoE4 and Alzheimer's risk without regard for ethnicity, the risk would resemble that of whites, because their numbers would overwhelm the data from the other racial groups. As Dr Risch says, “I think these categories are useful as long as they are predictive. That doesn't prove that the difference is genetic.”
In the genes
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.”
http://www.economist.com/science/displaystory.cfm?story_id=6795348
