Three months ago, after rethinking a previous series on race, genes, and intelligence, I sketched a way to think about race in the era of biology. Race is the stone age of genetics. Biologically, race is real. It’s an extension of extended family. But it’s also transitional and, in the long view, crude. Any theory of heredity that starts with observed racial patterns has to end with genetic differences that cross racial lines.
Now comes a scientific elaboration of that paradigm. In its September issue, Clinical Pharmacology & Therapeutics addresses “Pharmacoethnicity.” “Differences in response to medical products have been observed in racially and ethnically distinct subgroups of the US population,” the journal points out. In a feature commentary, a team of scientists led by Craig Venter, the human genomics pioneer, affirms this pattern and discusses examples of medically important genetic differences among ethnic populations.
Having accepted this genetic reality, Venter and his colleagues demonstrate how complicated it is. “Race/ethnicity should be considered only a makeshift solution for personalized genomics because it is too approximate,” they write. A genetic allele that affects the body’s response to codeine and antidepressants, for example, “is found in 9%, 17%, and 34% of the Ethiopian, Tanzanian, and Zimbabwean populations, respectively. Clearly, lumping together all of Africa obscures the differences between the populations.”
The same gene varies among whites. Venter’s full genome has been sequenced and published. So has the genome of legendary biologist James Watson, who got into trouble last year for expressing gloom about African intelligence. Looking at the aforementioned gene in both men, the authors point out that Watson, unlike Venter, has two copies of an allele that “is rare in the Caucasian population (3%) but prevalent in East Asian populations.” They conclude: “One’s ethnicity/race is, at best, a probabilistic guess at one’s true genetic makeup.”
In the stone age of genetics, we’ve often had to settle for racial medicine, such as BiDil, the heart-disease drug marketed to blacks. But technology and economics are beginning to carry us beyond that phase. “The costs of whole-genome sequencing and whole-genome genotyping are rapidly decreasing,” Venter and his colleagues observe. “Companies such as Navigenics, 23andMe, and deCODE will genotype 600,000 to 1,000,000 markers in an effort to offer personalized genomics; several hundred dollars covers the cost of the technology.”
As this transition becomes economically feasible, the authors suggest, it also becomes obligatory. In the case of BiDil, they note, the manufacturer “is voluntarily financing a study to investigate the genetic basis for the response to the drug.” But in general, “Once a race-based drug has been developed, there is a possibility that a drug company may terminate its research and not pursue follow-up studies into the underlying cause. This could stunt medical care with race-based medicine, rather than personalized medicine.” Accordingly, they pass along a recommendation that the Food and Drug Administration “establish regulatory requirements for the subsequent identification of biomarkers for race-based drugs.”
It’s a bold proposal. Is it practical or moral? I’d say both. If you give Watson a drug for Caucasians and he metabolizes it like an Asian, you won’t help him, and you might hurt him. You also owe him the courtesy of seeing and treating him as an individual. The most important difference between him and you is technological and economic, not hereditary: His genome has been sequenced. Now for the rest of us.
