This week a US government advisory panel recommended that the Food and Drug Agency grant a licence to a drug called BiDiL which helps treat congestive heart failure. The decision has kicked off a huge controversy because BiDiL will be the first racially-targeted drug. BiDiL seemed proved ineffective when tested on the general population. But when given to African Americans it appeared to cut death rates from heart failure by 43 per cent. So it's being marketed as a black drug. Critics charge that the study was flawed and that NitroMed, the makers of BiDiL, are exploiting race for financial reasons - its patent for the general use of BiDiL has run out but it has won a new patent until 2020 for the use of the drug on African Americans.
The BiDiL debate gets to the heart of one of the most explosive issues in current medicine. Does race matter in medicine? Or should medicine be colourblind? The prestigious New England Journal of Medicine has argued that 'race is biologically meaningless' and that doctors should be taught about 'the dangers inherent in practicing race-based medicine.' Other disagree. The psychiatrist Sally Satel believes that in medicine 'stereotyping often works'. In her Washington drug clinic, Satel prescribes different amounts of Prozac to black and white patients because, she says, the two groups seem to metabolise antidepressants at different rates.
So who is right? As with much else in debates about race, the answer is both and neither. Different populations certainly show different patterns of disease and disorder. North Europeans, for instance, are more likely to suffer from cystic fibrosis than other groups. Tay Sachs, a fatal disease of the central nervous system, particularly affects Ashkenazi Jews. Beta blockers appear to be less effective on African Americans than on those of European descent.
Yet race is not necessarily a good guide to disease. We all know, for instance, that sickle cell anaemia is a black disease. Except that it isn't. Sickle cell is a disease of populations originating from areas with high incidence of malaria. Some of these populations are black, some are not. The sickle cell gene is found in equatorial Africa; in parts of southern Europe; in southern Turkey; parts of the Middle East; and in much of central India. Most people, however, know that African Americas suffer disproportionately from the trait. And, given popular ideas about race, most people automatically assume that what applies to black Americans also applies to all blacks and only to blacks. It is the social imagination, not the biological reality, of race that turns sickle cell into a black disease.
Genetic studies show that humans comprise a relative homogenous species and that most of our genetic variation is at individual, not group, level. Imagine that some nuclear nightmare wiped out the entire human race apart from one small population - say, the Masai tribe in East Africa. Virtually all the genetic variation that exists in the world today would still be present in that one small group. That is a dramatic way of expressing what geneticists have discovered about human differences. Around 85 per cent of human variation occurs between individuals within single populations. A further 10 per cent or so differentiates populations within a race. Only around 5 per cent of total variation distinguishes the major races. This is why many scientists reject the idea of race as meaningful.
Since most variation exists at the individual level, doctors ideally would like to map every individual's genome to be able to predict better their potential medical problems and their responses to different drugs. Such individual genotyping is currently both practically unfeasible and too costly. Therefore, doctors often resort to using surrogate indicators of an individual's risk profile - such as his or her race.
Until recently people were more likely to marry a neighbour than someone who hailed from distant lands. As a result the further apart two populations are geographically, the more distinct they are likely to be genetically. Icelanders are genetically different from Greeks, but they are genetically closer to Greeks than they are to Nigerians. The difference is tiny, but it can have a medical impact. Knowing the population whence your ancestors came can provide hints as to what genes you might be carrying. Hence race, Sally Satel suggests, is a 'poor man's clue' in medicine.
But a poor man's clue may be as reliable as an intelligence dossier from the British secret service. First, because there are no hard and fast divisions between populations. Every population runs into another and no gene is unique to one population. Cystic fibrosis may be more common among North Europeans but it is not confined to North Europeans. One of the dangers of marketing BiDiL as a black drug is that it may be given to American Americans who won't respond to it, but denied to non-blacks who would benefit.
Secondly, different genes are distributed differently among populations. The pattern of distribution of the genes for cystic fibrosis is not the same as that of sickle cell genes. Which population differences are important varies from one disease to another. Finally, many medical differences associated with race or ethnicity are likely to be the result of environmental rather than genetic differences, or to be a combination of the two. In the case of BiDiL no one knows which is more important.
What all this suggests is that the question of whether medicine should be colourblind depends on the particular problem we want to address. It is a pragmatic issue, not one rooted in scientific or political principle. Race, however, is such a contentious issue that pragmatism rarely enters the debate. On the one side, so called race-realists think that population differences are so important that all medicine should be colour-coded. On the other side, many antiracists want to ban race-based research entirely for fear of its social consequences. Both are wrong. It's time everyone calmed down and took a grown up view of the issue.