A US GOVERNMENT advisory panel recommended this week that a drug which helps to treat congestive heart failure should be granted a licence. Its decision is controversial because BiDiL will be the first racially-targeted drug. When tested on the general population it proved ineffective, but when given to African-Americans, to whom it will be marketed, it appeared to cut death rates from heart failure by 43 per cent.

The BiDiL debate gets to the heart of one of the most explosive issues in medicine. Does race matter in medicine? Or should it be colour-blind?

The New England Journal of Medicine has argued that “race is biologically meaningless” and that doctors should be taught about “the dangers inherent in practising race-based medicine.” Others 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 meta bolise antidepressants at different rates.

So who is right? As with much else in debates about race, the answer is both sides and neither. Different populations do show different patterns of disease and disorder. Northern 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 work less effectively for African-Americans than those of European descent.

Yet race is not necessarily a good guide to disease. We all think we know that sickle-cell anaemia is a black disease. Except that it is not. Sickle cell is a disease of populations originating from areas with a high incidence of malaria. Some of these populations are black, some are not. The sickle-cell gene is found in equatorial Africa, parts of southern Europe, southern Turkey, parts of the Middle East and much of central India. Most people, however, only know that African-Americans suffer disproportionately from the trait. And, given popular ideas about race, they 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 human beings comprise a relatively homogenous species and that most of our genetic variation is at individual, not group, level. Imagine that a nuclear explosion wiped out the 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. About 85 per cent of human variation occurs between individuals within local populations. A further 10 per cent or so differentiates populations within a race. Only about 5 per cent of total variation distinguishes the major races. This is why many scientists reject the idea of race.

Since most variation exists at the individual level, doctors ideally would like to map every individual’s genome to be able to predict better his potential medical problems and responses to different drugs. Such individual genotyping is currently both impracticable and too costly, so doctors often resort to using surrogate indicators of an individual’s risk profile — such as race.

Until recently people were more likely to marry a neighbour than someone who hailed from distant lands. As a result the farther 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 from which your ancestors came can provide hints as to what genes you may be carrying. Hence race, which Satel suggests, is a “poor man’s clue” in medicine.

But a poor man’s clue may be about as reliable as an intelligence dossier. First, there are no hard and fast divisions between populations. Every population runs into another and no gene is unique to one. Cystic fibrosis may be more common among northern Europeans but is not confined to them. One of the dangers of marketing BiDiL as a black drug is that it may be given to African-Americans who don’t respond to it, but denied to non-blacks who could. Secondly, different genes are distributed differently among populations. The pattern of distribution of 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 are likely to be the result of environmental rather than genetic differences, or a combination of the two. In the case of response to BiDiL, no one knows which is more important.

All this suggests 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 one side, so-called race realists think that population differences are so important that all medicine should be colour-coded. On the other, many antiracists want to ban race-based research entirely for fear of its social consequences. Both are wrong. It is time everyone calmed down and took a grown-up view of the issue.

Kenan Malik is author of Man, Beast and Zombie: What Science Can and Cannot Tell Us about Human Nature

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