In 2005 the American government gave its official blessing to BiDiL, a drug
used to treat congestive heart failure. The decision kicked off a huge controversy
because BiDiL was the first officially-sanctioned racially-targeted drug.
It had 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 was marketed as a black drug, transforming at a stroke
the relationship between race and medicine, and opening the way, in the words
of one medical journal, to 'a new era of race-based therapeutics'. Last year,
for instance, the pharmaceutical company Schering Plough organised a clinical
trial for a hepatitis C drug from which African Americans were controversially
excluded.
The debate about BiDiL - and the Schering Plough trial - gets to the heart
of one of the most explosive issues in current medicine. Does race matter?
Or should medicine be colourblind? Since 'race is biologically meaningless',
argued the New England Journal of Medicine so 'instruction in medical
genetics should emphasise the fallacy of race as a scientific concept and
the dangers inherent in practicing race-based medicine'. A paper in Nature
Genetics claimed that 'commonly used ethnic labels are both insufficient
and inaccurate'.
Others begged to differ. The geneticist Neil Risch suggested that 'there is
great validity in racial/ethnic self-categorisation both from the research
and public policy points of view'. In a widely reported essay in the New
York Times, psychiatrist Sally Satel admitted that 'In practicing medicine
I am not colorblind. I always take note of my patient’s race. So do
many of my colleagues'. She added that 'When it comes to practicing medicine,
stereotyping often works'.
At the Washington drug clinic where she works, Satel prescribes different
amounts of Prozac to black and white patients because 'clinical and pharmacological
research show that blacks metabolise antidepressants more slowly than Caucasians
and Asians. As a result, levels of medication can build up and make side effects
more likely'.
So, who is right? As with much else in the debate on race, the answer is both
and neither. Different populations exhibit distinct risk profiles to diseases
and disorders but the differences are not necessarily racial. According to
Sally Satel 40 per cent of African Americans metabolise anti-depressants more
slowly than do Caucasians. The majority of black Americans, in other words,
respond in the same manner as most Caucasians. Similarly with BiDiL. One of
the dangers of marketing it 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.
We know that all but a tiny proportion of genetic variation exists within
a population. Ideally, doctors would like to genetically map (or 'genotype')
every individual within a population, and hence be able to predict the medical
problems he or she may face and how each might respond to any particular drug.
Such a procedure may well become as commonplace in the future as, say, vaccinations
are today. Currently, though, individual genotyping is both practically unfeasible
and too costly. Doctors, therefore, often resort to using surrogate indicators
of an individual's risk profile - such as his or her race. Knowing the population
from which an individual’s ancestors originally came can provide clues
as to what genes that individual might be carrying. It is what Sally Satel
calls a 'poor man's clue'.
Race provides medical clues because there are clearly genetic and social differences
between population groups that have medical consequences. But it's a poor
man's clue because the way we divide up society into different groups is not
necessarily the most useful way to understand a disease or disorder - as we
saw in the first part of this essay
in the discussion of sickle cell anaemia.
When we ordinarily talk about human differences, we are often vague about
the terms we use. We may talk about races, cultures, ethnic groups, or populations.
We generally refer to whites or Europeans rather than Caucasians even though
many Caucasians are neither white nor European. On the other hand, we use
the term blacks and Africans interchangeably, even though there are many blacks
who are not African.
If we are trying to sort out the problems of life over a pint such vagueness
and confusion generally does little harm. We would expect a scientist or physician,
however, to think with greater precision. In their book Sorting Things
Out, Geoffrey Bowker and Susan Star point out that any scientific classification
must possess three properties. First, there must be 'consistent, unique classificatory
principles in operation'. So, when biologists order the living world, the
rules they use to define humans (Homo sapiens) as a species are the
same as the rules they use to define chimpanzees (Pan troglodytes)
as a species. Second, 'categories must be mutually exclusive'. A chimpanzee
cannot belong to two distinct species. And third, a classification system
must be complete and able to absorb even those entities not yet identified.
If we discover a new species we can slot it into the system we use to classify
all other known species.
Racial classifications possess none of these properties. Races are difficult
to define and there are no objective rules for deciding what constitutes a
race or to what race a person belongs. People can belong to many races at
the same time. And, finally, new races are not 'discovered' and slotted into
the existing classification system; they are 'created' by carving up the classification
system in a different way.
In the absence of a scientific classification of race, medical researchers
are forced to import the racial categories we use in everyday life. The result
is a striking contrast in many medical papers between the tightness and technical
quality of the language when the authors are discussing genes, diseases and
physiological processes and the looseness of the language about racial differences.
These problems are exacerbated by the use of self-identification as a way
of assigning of racial categories. Most medical studies allow a person to
define his or her own racial category. In the Schering Plough hepatitis C
trial, for instance, self-identified African Americans were excluded. But
those who possessed African ancestry, yet who did not identity themselves
as African American, were included. This raises important questions about
what the selection criteria for the trial could possibly tell us about the
impact of the drug on genetic differences.
In any case, much research shows that self-identity can be unstable. One study
compared data from matched birth and death certificates for infants who had
died in the first year of life. While the overwhelming majority of children
who were identified as black or white at birth were identified the same way
at death, for other populations there were significant shifts in racial identity.
Another study revealed that more than one in 10 adolescents gave a different
answer when asked to define their race at school and at home.
Many fear not just that racial categories are impossible to define, but also
that linking race and disease could entrench prejudice. 'A detectable genetic
hallmark', the bioethicist Ernst Juengst worries 'could serve as an indelible
"yellow star" marking for oppression those with indigenous ancestry.’
For instance, studies have shown that Jewish women have a higher prevalence
of a gene associated with some forms of breast cancer. This could, some fear,
turn breast cancer into a 'Jewish disease' while, at the same time, confirming
the prejudice that Jews constitute a distinct race.
There is indeed a long history of using science to 'racialise' diseases. The
designation of sickle cell anaemia as a 'black disease', for instance, was
a weapon wielded by colonial administrators in Africa and racist politicians
in the USA to brand black people as unhealthy and unclean. Until the 1980s
the US Air Force and many commercial airliners banned black pilots with sickle
cell for fear of the effects of the disease. Might not associating breast
cancer with Jewish women lead to similar problems?
Such fears have led to calls for race and ethnicity to be excluded from scientific
and medical research. One survey of medical research called for the establishment
of special committees to scrutinise all papers and decide whether their use
of racial categories is socially acceptable.
Researchers, in fact, already face a variety of restrictions in practice.
The US National Human Genome Research Institute has established a databank
of DNA polymorphisms, or gene variations, based on 450 samples from African,
Asian, European, North and South American and Native American individuals.
The samples, however, come without any information about their population
of origin or about the individual who provided it. Researchers who want to
use the database have to sign the scientific equivalent of the Official Secrets
Act. They must promise not to try to determine the race or ethnicity of the
people who contributed the DNA or even to cite papers that might have speculated
on this.
Concepts of race and the use of such concepts in medical research are, as
we have seen, unsatisfactory. Yet we should be wary of calls to ban such research.
All scientific papers are subject to peer review. But, especially when the
concept of race is so contested by scientists themselves, the idea that they
must also be scrutinised for their social consequences smacks of placing them
on an Inquisitorial Index. Who would sit on the scrutinising committee? Those
who deny the validity of race? Or those who think that the use of racial categories
is crucial for scientific and medical advances? In any case, banning scientific
research will not necessarily prevent the stigmatisation of particular social
groups. Do we really believe, for instance, that had references to sickle
cell anaemia as a black disease been banned in the first part of the twentieth
century, there would have been less discrimination against African Americans?
What really needs challenging is not research into population differences
as such, but the meaning that researchers and others often impute to such
differences. It is a fact that populations differ in their genetic profiles.
Such differences can often be important in medical research. Suppose you want
to study the impact of a new drug. It is likely that you would want to sample
genetically distinct populations, to be sure that the drug does not produce
an adverse reaction in people with particular genetic profiles. Since we cannot
sample every population in the world, researchers often use race and ethnicity
as proxies for genetic difference, as a means of creating a rough and ready
approximation of worldwide genetic diversity.
Or suppose you are looking to see if a particular condition or disease - say
breast cancer or high blood pressure - is linked to specific genes. One way
to conduct such 'association studies' is to compare the genomes of people
with and without that particular condition or disease. If the two groups are
genetically similar, then it becomes easier to spot the genetic difference
that might be responsible to producing breast cancer in one group and not
the other. Whereas in the previous example we wanted to sample as wide a range
of human variation as possible, here we want to find populations as homogenous
as possible. But human populations are rarely homogenous. So race and ethnicity,
once again, are often used as proxies, this time not for genetic difference,
but for genetic relatedness.
There is no such thing as a 'natural' or homogenous human population. Migration;
intermarriage; war and conquest; forced assimilation; the embrace of new identities;
any number of social, economic, religious, and other barriers to interaction
- these and many social other factors impact upon the character of a group
and transform its genetic profile. Yet, human groups can act as surrogates,
however imperfectly, for biological relatedness. Many of the ways in which
we customarily group people socially - by race, ethnicity, nationality, religious
affiliation, geographic locality and so on - are not arbitrary from a biological
point of view. Members of such groups often show greater biologically relatedness
than two randomly chosen individuals. Such groups have often been ghettoized
by a coercive external authority, or have chosen to self-segregate from other
groups. Many have a distinct history, perhaps deriving from a small founder
population.
Categories such as 'African American', 'people of Asian descent' and 'Ashkenazi
Jew' can be important in medical research because they are a social representation
of certain aspects of genetic variation. This is why race is a 'Poor man’s
clue' in medicine: not because races are natural divisions of humankind but
because investigating socially defined populations provides a practical means
for geneticists of dividing humans into groups that show different degrees
of biological relatedness.
In order to study human genetic diversity, scientists ironically need socially
defined categories of difference. The danger is that by using socially defined
groups for medical or other scientific research, biologists will endow differences
between such groups with greater importance than is warranted. A contingent,
pragmatic division of the world into populations useful for medical research
can all too easily turn into the argument that science has 'demonstrated'
the reality of race.
All this points to the care needed in handling racial categories in medicine.
But the fact that race is not a real biological entity does not mean that
science or medicine should necessarily be colourblind. Population differences
are important and can have medical consequences. It makes little sense from
a biological point to view to regard these differences as 'racial'. But it
also makes little sense to ignore population differences or to ban the use
of racial or ethnic categories in such research. Whether or not science and
medicine should be colourblind is a pragmatic question, not one rooted in
scientific or political principle.