Race - and medical response
- From: Earl <neptune@xxxxxx>
- Date: 14 Apr 2006 09:49:13 GMT
A nearly totally taboo issue.
Races are different -- you dare not mention it even if the
result is death from failure to give the best medical treatment.
http://www.economist.com/science/displaystory.cfm?story_id=67953
48
***********
Not a black and white question
Apr 12th 2006
From The Economist print edition
Medical research is starting to take account of people's race
LAST month researchers from the University of Texas and the
University of Mississippi Medical Centre published a paper in
the New England Journal of Medicine. They had studied three
versions (or alleles, as they are known) of a gene called PCSK9.
This gene helps clear the blood of low-density lipoprotein
(LDL), one of the chemical packages used to transport
cholesterol around the body. Raised levels of LDL are associated
with heart disease. The effect of all three types of PCSK9
studied by Jonathan Cohen and his colleagues was to lower the
LDL in a person's bloodstream by between 15% and 28%, and
coronary heart disease by between 47% and 88%, compared with
people with more common alleles of the gene.
Such studies happen all the time and are normally unremarkable.
But this was part of a growing trend to study individuals from
different racial groups and to analyse the data separately for
each group. The researchers asked the people who took part in
the study which race they thought they belonged to and this
extra information allowed them to uncover more detail about the
risk that PCSK9 poses to everyone.
Yet race and biology are uncomfortable bedfellows. Any
suggestion of systematic biological differences between groups
of people from different parts of the world?beyond the
superficially obvious ones of skin colour and anatomy?is almost
certain to raise hackles. There are good reasons for this. The
eugenics movement of the late 19th century soon turned racist
and that sorry story culminated with the doctrine of racial
hygiene and the death camps of Nazi Germany. Yet decades ago,
Luca Luigi Cavalli-Sforza of Stanford University showed that the
frequencies of different alleles of genes for several blood and
immune-system proteins vary geographically. It is now starting
to be accepted that these sorts of variation can matter for
health. If so, searching for genetic variations in different
racial groups is not only acceptable, but also obligatory.
In Dr Cohen's work, the race question proved decisive. Of the
3,363 volunteers who described themselves as ?black?, 0.8%
carried an allele of PCSK9 called version 142X and 1.8% carried
one called version 679X. Among 9,524 self-described ?white?
volunteers, a mere 0.02% carried version 142X and 0.04% carried
version 679X. By contrast, 3.2% of white people carried the
third allele under study, version 46L, while only 0.7% of black
participants did. The researchers found that these relatively
rare alleles correlated with low LDL, and did so in both blacks
and whites, allowing them to conclude that it was the gene
change that was crucial. If the team had ignored race and simply
compared those who had heart disease with those who did not, and
asked which alleles were linked to the risk, they would probably
have missed the clinical significance of the alleles. This is
because they would have appeared so infrequently?in less than
0.3% of the whole study population for version 142X?that their
effects would have been swamped. That is even truer for less
populous racial groups; indeed, the smaller the group, the less
likely researchers are to find important but rare alleles unless
they can break the population down. Ignoring race altogether
would be to the detriment of medical knowledge about the very
people who might benefit.
It is this?the question of who gains?which is allowing the
otherwise taboo subject of racial genetics to be broached. If it
is minority groups (or, at least, groups that are minorities in
America, where most of this work is being done) who are likely
to reap the rewards, then the objections are likely to be muted.
But they have certainly not gone away.
Race to the finish
For example, according to Richard Cooper, a professor of
medicine at Loyola University in Chicago, talking about black
people having a gene that predisposes them to some disorder or
another ?feeds a social process? that is deeply negative. As he
observes, black Americans suffer more from high blood pressure
than white Americans. ?We don't know why, but everyone says it
is genetic. But if you look around the world, by far the highest
hypertension rates are in Poland, Finland and Russia. Much
higher than black Americans. The average difference in blood
pressure between blacks and whites is about 4mm of mercury, the
difference between whites in the US and Russia is about 20mm. No
one has ever said that these white people are genetically
predisposed to hypertension: it must be their diet. But when
they talk about blacks, it has to be genetics. That, in a
nutshell, is the whole problem with this whole way of thinking.?
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.?
On the other hand, focusing too closely on race may not be the
right answer either, as the tale of a drug called BiDil
illustrates. The drug was originally tested some 20 years ago
for its ability to reduce heart failure in high-risk patients.
Overall, it had limited effect. In recent years, however,
researchers noticed that the few blacks in the study tended to
have a better response than the majority white population did.
Thus, Nitromed, the company that now owns the drug, designed a
clinical trial that compared BiDil plus standard therapies to
standard therapies alone, but only in African-American patients.
The drug worked, reducing deaths from heart attacks by 43%, and
the Food and Drug Administration approved BiDil for use in black
Americans, making it the first racially-targeted drug. The flaw,
as critics point out, is that the drug was not tested in other
racial groups, so there is no strong evidence that it worked
better in black Americans than in any other group?nor is there
any reason, genetic or environmental, why it should.
This sort of work raises another question, with its own set of
sensitivities: how, scientifically, do you define someone's
race? In studies such as Dr Cohen's this question is fudged,
because people defined themselves. That is a reasonable starting
point. But America's population is descended mainly from
immigrants and those ancestors have been meeting and mating for
centuries. Few native-born Americans trace all of their
ancestors back to the same part of the world, so how closely are
genes affecting disease linked to genes affecting racial self-
identification?
Perhaps the last word should go to Francis Collins, who led
America's contribution to the Human Genome Project, and thus
helped to open the debate. ?The downside of using race, whether
in research or in the practice of medicine,? he says, ?is that
we are reifying it as if it has more biological significance
than it deserves. Race is an imperfect surrogate for the
causative information we seek. To the extent that we continue to
use it, we are suggesting to the rest of the world that it is
very reliable and that racial categories have more biological
meaning than they do. We may even appear to suggest something
that I know is not true: that there are bright lines between
populations and that races are biologically distinct.?
Eventually, the technology developed to carry out the Human
Genome Project, and the science it has made possible, will make
the whole question redundant. It will be possible to look at the
genes of each person as an individual. But until that time race,
used sceptically, does have value. And unlike previous attempts
at racial science, this one could actually do people some good.
***********
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