The following is from http://www.neoeugenics.com/
Race and Medicine, by Matt Nuenke
As the Human Genome Project progressed over the last decade, many on
the Left felt the heat of renewed interest in racial differences—they
could not be so easily dismissed once we could look inside the genetic
code. As a result they have renewed their efforts to deny that racial
differences exist in any form other than simply the color of one's
skin or the shape of one's lips. However, the denial of racial
differences has been based on the specious premise that race is
defined by distinct boundaries—a premise that no one but a scientific
illiterate could entertain.
As Jon Entine wrote in "Why Race Matters in Sports" on his website:
"In truth, while technically correct, such assertions are
scientifically meaningless and provide absolutely no support for the
popular myth that 'race has no biological reality.' There is zero
genetic difference between a wolf and a cocker spaniel. If one really
believes that such genetic similarity means that there is no
hard-wired functional difference between a wolf and a hand-licking
spaniel, then I invite that person to adopt a wolf as a house pet for
the children. Such differences are grounded in gene sequences and
proteins and are activated by obscure environmental triggers. All the
training in the world is not likely to turn an Inuit Eskimo,
programmed to be short and stout, into a NBA center or an American
(black or white) into a great marathoner: nature sets limits." (Also
see Entine, 2000)
Anyone familiar with the principles of evolution must recognize that
racial differences come about simply because different people evolved
under different ecologies—both physical and social environments. When
this occurs, we must expect differences in the average number of gene
expressions (allele frequencies) between any two population groups.
These differences include average expressions in behavior,
intelligence, and medical responses to treatment, as well as physical
differences.
As Arthur Jensen describes it (Jensen, 1998), when it comes to
studying differences between races there are lumpers and splitters.
That is, there are no clear racial boundaries. Splitters could
theoretically divide the human species into individual races down to
identical twins. Lumpers tend to define races into much larger groups
like Blacks, Whites and Asians. Cavalli-Sforza divides all humans into
separate population groups (races) that "were in the area of study in
A.D. 1492" before the great migrations. That is, wherever he could
find a group of people today that could trace their ancestry to a
people who lived in 1492, they are defined as a race for the purposes
of studying genetic differences. He excludes "Samaritans, Jews,
Gypsies, and several others" because they are landless people and need
"special study." (Cavalli-Sforza, 1994)
Still, the Left has held rigidly to the notion that racial differences
do not exist, but now they face a new challenge from medicine. Racial
genetic differences are now being used to better understand how to
treat people for illness, especially giving different medicines to
different races—because they have different genes "on average." This
is exactly the same assertion made to account for differences in
wealth and income between races—because they have different genes "on
average" that causes differences in life's outcomes—like intelligence
and conscientiousness. Now, if medical treatment leads to the
ineluctable conclusion that racial differences are real, the radical
egalitarian agenda of the Left no longer has the charge of "scientific
racism" to hurl at genetic studies.
The journal SCIENCE, put out by the American Association for the
Advancement of Science, has summarized the dilemma quite nicely in an
article written by Constance Holden entitled "Race and Medicine," in
the October 24, 2003 issue. The AAAS has been a left leaning
organization; its past presidents included the radical Marxist Stephen
J. Gould and the (duped) cultural anthropologist Margaret Mead. It
treads on the racial difference issues very gently. So it comes with
some surprise that they have begun to address the quandary of facing
up to racial differences in the drive to help heal the sick.
Holden writes, "Mention race and medicine in a group of scientists,
and you are likely to provoke a range of heated opinions on whether it
is useful, or even ethical, to consider how people of different
ancestry respond to disease and treatments. No one disputes that some
diseases strike disproportionately in some racial or ethnic
groups—thalassemia in people whose ancestors came from the
Mediterranean area, sickle cell anemia in people of African origins,
for example. Less clear-cut than these single gene disorders but the
subject of increasing research—is the medical significance of a host
of more subtle gene variants that appear in differing frequencies in
various populations and that seem to influence a multitude of
conditions. So far, few candidate genes have been spotted, and the
evidence is largely circumstantial. Some scientists dismiss the data
as too preliminary, or the differences as insignificant. They worry
that emphasizing biological differences in how people of different
racial and ethnic groups respond to disease and treatments could
unfairly stigmatize some patients and lead to inferior health care.
Yet many scientists see exploration of differences among ancestral
groups as a way to learn more about complex diseases and ultimately
improve treatment for some groups of patients."
Notice how the Left yet again tries to claim that understanding racial
differences in medical care needs will "lead to inferior health care."
The problem is, they never explain why or how this could come about.
We at least need some prospective scenario as to how being able to
better treat people, will lead to just the reverse! Again, they are
attempting to put the genetic genie back in the bottle so that they
can continue to use racism as a tribal weapon against all Whites and
especially White males. We are the ones who would be responsible of
course for making sure that the oppressed would get "inferior health
care." That's right; the same White males who have invented effective
medicines against AIDS, and have also contributed millions if not
billions of dollars to help fight the disease that primarily inflicts
"oppressed peoples."
The article also explains that yes, it would be nice if we could just
take an individual's genes, assess their particular genome, and leave
race out of it. But that procedure will not be available for decades.
For now, race serves as a beneficial proxy for genetic patterns that
respond differently to treatments. Different races have different
patterns of gene frequencies, and race serves as the best first guess
how a patient will respond to differing treatments. This is the same
as using age or gender when treating patients—humans vary on multiple
levels and over time.
Holden addresses Richard Lewontin's old canard, "The chief argument
against the notion that biological race can be medically meaningful is
that there are far more genetic differences among individuals than
there are between different ancestral groups. Neil Risch of Stanford
University says that comparison is misleading, however. He and others
argue that if 30% of one population can't metabolize a certain drug,
compared with 10% of another population, the between-group variability
is low because most people in both groups lack this metabolism
polymorphism. Nonetheless, this variation is significant when it comes
to estimating the probability of response to treatment, he says.
Geneticist David Goldstein of University College in London agrees: 'If
you say on average the difference between West Africans and Europeans
is slight, that does not rule out a great many variants that influence
how people respond to drugs.'"
"Joel Buxbaum, who studies the molecular basis of disease at Scripps
Research Institute in La Jolla, California, is persuaded as well. 'A
call to ignore [race] in diagnosis and treatment is a call to ignore
biology,' he says. 'Research in the last 35 years has uncovered
significant differences among racial and ethnic groups in their rate
of drug metabolism, in clinical responses to drugs, and in drug side
effects.'"
"The most definitive evidence is on different levels of certain
drug-metabolizing enzymes found in whites, blacks, and Asians. Some of
these differences are quite dramatic; for example, Genaissance
Pharmaceuticals in New Haven, Connecticut, has found a mutation of a
major metabolism-controlling enzyme that occurs in 30% to 40% of
Asians and less than 5% of members of other groups. Such findings help
explain what many doctors have long observed—that many people of East
Asian ancestry need smaller than average doses of a variety of heart,
pain, and psychotropic drugs."
If different races can vary so much in response to health due to their
different ecological history, we would expect differences in other
areas as well including intelligence, behavior, ethnocentrism,
stature, etc. There are no constraints on genetic variation in
averages between racial groups, and that is exactly what Jensenists
have proposed to explain racial and gender differences in intelligence
and other cognitive characteristics; it is the default hypothesis
because it is biologically the most likely—whether breeds of dogs or
human races—differences are to be expected.
Even the government is getting involved; "Increasing awareness of
possible genetic contributions to ethnic differences is reflected in a
recommendation issued last January by the U.S. Food and Drug
Administration (FDA). Calling for more scrutiny of subpopulations, FDA
wants drug testers to use racial divisions specified by the Census
Bureau 'to ensure consistency in evaluating potential differences in
drug response.'"
Note however how naïve the FDA is about "racial divisions." The Census
Bureau does not use race alone in counting heads, they also use
ethnicity/language. Maybe, with a renewed interest in racial
differences we can start to look at races in a more rational way. As
it now stands, the Census Bureau's racial/ethnic classification system
is without a scientific foundation, and will not lend itself to what
the FDA is calling for: Hispanics for example are not a racial
category; Semites are now lumped in with Caucasians; and East Asians
and South Asians are lumped together as Asians, even though they are
genetically quite different. To use racial differences, along with
racial mixing, they must for the first time address race
scientifically and not politically as has been done in the past.
Companies are also pursuing teasing apart racial differences for
profit. Holden notes, "Genaissance, set up 6 years ago to develop and
market genetic data. 'Our company was founded on the principle that
human genetic variation is critical to drug response,' says Claiborne
Stephens, vice president for genetics. The obvious way to make a first
cut at that variation, he notes, is to look at how evolution parceled
out different versions of various genes according to the environments
in which early human populations evolved."
One thing the article failed to mention is that we can now determine a
person's race, or racial admixture in the cases of mixed race people,
to help profile the best treatment. For example, Blacks in the United
States are a mixture of Whites (mostly) and West Africans. To find out
what racial group an individual should fit into, it would help to
determine the correct racial make-up of the person. No doubt computers
along with new gene chips that show genetic markers will advance what
we know about racial differences. But at least for now, it looks as
though the Left is stuck with quite a conundrum—denying racial
differences will also lead to denying people the best health care
available. The complete article in SCIENCE follows:
-----
Race and Medicine by Constance Holden
SCIENCE 24 OCTOBER 2003, pgs. 594-6.
Mention race and medicine in a group of scientists, and you are likely
to provoke a range of heated opinions on whether it is useful, or even
ethical, to consider how people of different ancestry respond to
disease and treatments. No one disputes that some diseases strike
disproportionately in some racial or ethnic groups - thalassemia in
people whose ancestors came from the Mediterranean area, sickle cell
anemia in people of African origins, for example. Less clear-cut than
these single gene disorders but the subject of increasing research -
is the medical significance of a host of more subtle gene variants
that appear in differing frequencies in various populations and that
seem to influence a multitude of conditions.
So far, few candidate genes have been spotted, and the evidence is
largely circumstantial. Some scientists dismiss the data as too
preliminary, or the differences as insignificant. They worry that
emphasizing biological differences in how people of different racial
and ethnic groups respond to disease and treatments could unfairly
stigmatize some patients and lead to inferior health care. Yet many
scientists see exploration of differences among ancestral groups as a
way to learn more about complex diseases and ultimately improve
treatment for some groups of patients.
Already, drug companies are hunting for genetic reasons behind
commonly observed medical differences between groups. Scientists are
doing retrospective genetic analyses of data from drug trials. And 18
months ago a company called NitroMed launched a trial of a heart drug
directed at compensating for what is believed to be a nitric oxide
(NO) deficiency in many African Americans.
Everyone's ultimate dream is to have evidence on individual genotypes
to guide medicine, a development that would make racial identity
biologically irrelevant. But that is decades away. Meanwhile, some
scientists maintain that race can serve as a useful, if crude,
indicator in sorting out why people experience diseases and their
treatments - differently and in finding new targets for drugs.
The argument
The chief argument against the notion that biological race can be
medically meaningful is that there are far more genetic differences
among individuals than there are between different ancestral groups.
Neil Risch of Stanford University says that comparison is misleading,
however. He and others argue that if 30% of one population can't
metabolize a certain drug, compared with 10% of another population,
the between-group variability is low because most people in both
groups lack this metabolism polymorphism. Nonetheless, this variation
is significant when it comes to estimating the probability of response
to treatment, he says. Geneticist David Goldstein of University
College in London agrees: "If you say on average the difference
between West Africans and Europeans is slight, that does not rule out
a great many variants that influence how people respond to drugs."
Joel Buxbaum, who studies the molecular basis of disease at Scripps
Research Institute in La Jolla, California, is persuaded as well. "A
call to ignore [race] in diagnosis and treatment is a call to ignore
biology," he says. "Research in the last 35 years has uncovered
significant differences among racial and ethnic groups in their rate
of drug metabolism, in clinical responses to drugs, and in drug side
effects."
The most definitive evidence is on different levels of certain
drug-metabolizing enzymes found in whites, blacks, and Asians. Some of
these differences are quite dramatic; for example, Genaissance
Pharmaceuticals in New Haven, Connecticut, has found a mutation of a
major metabolism-controlling enzyme that occurs in 30% to 40% of
Asians and less than 5% of members of other groups. Such findings help
explain what many doctors have long observed - that many people of
East Asian ancestry need smaller than average doses of a variety of
heart, pain, and psychotropic drugs.
Less well documented - and more controversial is emerging evidence on
different patterns of cardiovascular disease among various
populations. Researchers are looking for biological roots not only of
the well-known differences between blacks and whites, but also of
another, much less
publicized pattern of heart disease that disproportionately affects
Asian Indians. Although neither of these groups seems more disease
prone in its ancestral environment, modern diets and life styles -
particularly increased consumption of salt and fat, smoking, and
inactivity hit them hard. Even when investigators try to control for
environmental factors that could explain group differences, says
cardiologist Clyde Yancy of the University of Texas Southwestern
Medical Center in Dallas, "you can still see excess expression of
disease." Yancy and others see this as strong evidence for something
genetic at work. But teasing it apart from other risk factors is
proving daunting.
African-American risks
Blacks don't have more heart attacks than whites, but in the United
States they die sooner from cardiovascular problems - both heart
failure and strokes, says Yancy. They also have 10 times the rate of
kidney failure, three times the incidence of cardiac hypertrophy, and
more than twice the rate of diabetes, a destroyer of blood vessels.
High blood pressure, which afflicts almost one-third of the U.S. black
population, is the engine that, in large part, drives these related
conditions. It leads to excess stress on organs, which respond with
hypertrophy, or abnormal cell growth. Intertwined with the problem is
a shortage of nitric oxide and, in many cases, excess salt sensitivity
that in turn leads to fluid retention. Heart failure in blacks often
occurs from damage to the left ventricle, which is responsible for
sending freshly oxygenated blood through the body. Indeed, according
to Yancy, in blacks, heart failure "may be a different disease with
less favorable outcomes" than in whites.
Scientists are looking for genes that would explain these patterns, in
particular for genes related to hypertension. Because NO, the chemical
responsible for keeping blood vessels fit and toned, is important in
the action of ACE (angiotensin-converting enzyme) inhibitors, genes
for NO synthesis, the enzyme most important for vascular NO
production, are prime candidates. Dennis McNamara of the University of
Pittsburgh Medical Center says the prevalence of certain versions of
these genes is "much different in blacks and whites." The variant that
ACE inhibitors work best with is found in 60% of whites but only 30%
of blacks, he says.
Also blood pressure-related is the gene for transforming growth factor
- beta (TGF-beta). A group led by Phyllis August at Weill Medical
College of Cornell University in New York City reported in 2000 that
TGF-beta1 is overexpressed in black patients with end-stage renal
disease or severe hypertension and more so than in white patients with
the same diseases. This looks like a promising genetic candidate for
hypertension, the authors say, because TGF-beta1 regulates substances
that act both as vasoconstrictors and as growth factors for vascular
cells.
In addition to genes involved in high blood pressure, researchers have
found a significant difference between blacks and whites in genes that
manipulate the response of the sympathetic nervous system to hormones
like adrenaline. Stephen Liggett and colleagues at the University of
Cincinnati reported last fall that possessing a combination of two
particular versions of alpha and beta adrenergic receptors raised
heart failure risk for blacks 10-fold. The high-risk version of the
alpha-receptor occurs almost exclusively in people of African origin
and is present in about 40% of U.S. blacks, says Liggett. The
researchers believe that depressed receptor function leads to excess
release of norepinephrine, which is bad for the heart. The study is
relevant for the use of beta-blockers, which inhibit the effects of
adrenaline on beta receptors and which may be less effective in black
heart patients. Liggett's team reported in the September issue of
Nature Medicine that the high-risk beta receptor, which is also more
common in blacks, raises the risk of heart failure in both mice and
people and forebodes a poor response to beta-blockers.
Drug trials
Clinical trials have not been particularly helpful in illuminating
such differences, says McNamara, because usually at least 80% of
participants are white, and the pooling of data often obscures any
racial differences.
That is why many researchers are particularly excited about the first
clinical trial of a heart failure treatment that exclusively targets
African Americans. It was launched in March 2001 by NitroMed, a
company in Bedford, Massachusetts, to test a drug that may be uniquely
beneficial to heart patients with NO deficiencies. The
first-of-its-kind trial, called A-HeFT (for African-American Heart
Failure Trial), is testing a drug called BiDil that was originally
developed in the 1980s. BiDil combines vasodilators with an NO source
and antioxidant properties to help potentiate treatment by ACE
inhibitors. All patients in the trial will get standard medication;
half will also get BiDil. Scientists believe that the trial, which has
been endorsed by an array of groups, including the Association of
Black Cardiologists Inc., should produce some definitive data on the
role of so-called NO subsensitivity in heart disease. McNamara, who
calls the trial "very unique and very important," says he and
colleagues will do a genetic substudy, looking at a number of
candidate markers for correlations with treatment response.
Researchers are also combing through data from earlier big heart
trials. To get a fix on the nature of the suspected racial difference
in response to beta-blockers, Buxbaum and colleagues are looking at
data from BEST (the Beta-Blocker Evaluation of Survival Trial), which
tested a nonselective beta-blocker called Bucindilol. In 2700 people
with congestive heart failure, black patients as well as sicker ones
generally failed to benefit from the drug. So the scientists are
genotyping the 600 black patients to see if they can spot a genetic
marker that will serve as a better indicator than race for whether the
drug is likely to work. The results will be put in a DNA bank
available for other investigators.
Although these studies are important, says Yancy, there is still no
substitute for getting data from really big populations, not only to
find vulnerability genes but to sort out what's "normal" - that is,
genetic patterns (in any race or ancestral group) that do not
predispose to heart disease. He has high hopes for another initiative,
called UNITE-HF, led by the University of North Carolina with support
from the drug company AstraZeneca, a U.K.-based company with U.S.
headquarters in Wilmington, Delaware. UNITE-HF is collecting blood
samples from the country's "stroke and heart attack belt" in the
southern and southeastern United States. So far investigators have
samples from some 800 ambulatory heart patients, both black and white,
which they will analyze for the prevalence of suspect genes.
Indian hearts
The other population with a big heart disease problem is South Asian
Indians. "Until 50 years ago it was hardly ever heard that Indians had
high heart attack risk," says cardiologist Prakash Deedwania of the
University of California, San Francisco, Fresno, School of Medicine.
But as more Indians are becoming westernized, many now have heart
attacks as early as their mid-30s, and, he says, "the risk is
enormously high all over the world." A major risk factor is diabetes,
which, according to figures collected by F. P Cappuccio of St.
George's Hospital Medical School in London, is roughly four times as
prevalent among Indians (in urban India and abroad) as in Londoners.
Indians also tend to have high levels of triglycerides and low levels
of HDL, the "good" cholesterol. One evolutionary explanation is the
"thrifty gene hypothesis": Over the millennia people in India endured
cyclical famines; those who fared best were those who could conserve
energy in abdominal fat. Now, for those exposed to plenty, this
ability has turned into a disadvantage.
Some preliminary evidence for a genetic connection is emerging.
Michael Miller, director of the Center for Preventive Cardiology at
the University of Maryland Medical Center, says his group has found a
high prevalence of an alteration in the apolipoprotein C3 gene, which
regulates triglyceride metabolism, in Indians living in the United
States. The researchers found this polymorphism by taking blood
samples from 99 attendees at an Indian festival in Northern Virginia,
as they describe in the January 2001 American Journal of Cardiology.
This alteration is also associated with low HDL levels, says Miller,
and possibly also insulin resistance. The group is now looking to see
if people in India show the same pattern.
Investigators in New Delhi have already reported from a genetic
analysis of 139 healthy males in Northern India that almost one-third
carried a related variation in the apolipoprotein gene, a rare
mutation in Caucasians. Furthermore, it was twice as frequent among
those with elevated triglycerides - a risk factor for coronary artery
disease.
More clues on how genetic variation could translate into different
responses to medication should come from a new 6-week clinical trial,
sponsored by AstraZeneca. It will compare Crestor (rosuvastatin), a
new cholesterol-lowering drug that won government approval in August,
with an older one (atorvastatin) in South Asian Americans. Deedwania
says it will be the largest prospective trial ever done on Indians,
with some 800 subjects from 150 centers around the country. Miller
says Crestor may be better for Indians because it does a little better
job at raising HDL.
Many Indian doctors believe that the Indian vulnerability to heart
disease is striking enough to justify more preventive vigilance.
Cardiologist Enas Enas, director of the Coronary Artery Disease in
Indians Foundation in Lisle, Illinois, has stated that the goals of
treatment for high blood pressure and obesity should be at least 10%
lower, and cholesterol 20% lower, for Asian Indians than the goals
recommended for Caucasians.
Era of transition
Increasing awareness of possible genetic contributions to ethnic
differences is reflected in a recommendation issued last January by
the U.S. Food and Drug Administration (FDA). Calling for more scrutiny
of subpopulations, FDA wants drug testers to use racial divisions
specified by the Census Bureau "to ensure consistency in evaluating
potential differences in drug response."
Drug-makers are already on the lookout for genetic subgroups that
could divulge new targets for therapeutic drugs. "I think we all
believe there's a lot of potential there," says Gary Palmer, a Pfizer
vice president in New York. Pfizer is particularly interested in
hypertension-related genes in blacks and diabetes-related genes that
could account for the high rates of the disease in both Asian Indians
and Native Americans. AstraZeneca is also looking for population
differences in drug response in its clinical trials. Spokesperson Gary
Bruell says that if the company found that a drug has a "profound
effect" on a particular group, it would label and promote it
accordingly. "If a population doesn't benefit, that could end up on
the label too," he adds.
Companies will probably be getting more help from outfits like
Genaissance, set up 6 years ago to develop and market genetic data.
"Our company was founded on the principle that human genetic variation
is critical to drug response," says Claiborne Stephens, vice president
for genetics. The obvious way to make a first cut at that variation,
he notes, is to look at how evolution parceled out different versions
of various genes according to the environments in which early human
populations evolved.
One of its projects is a detailed data repository of more than 7000
genes from 93 whites, blacks, and Asians, including information on the
origins of their parents and grandparents, which companies can use as
a reference in clinical trials. This is enough to give "a reasonable
idea of what the gene frequencies are" in those groups, says Stephens
(see chart).
Although everyone agrees that data are still preliminary, there's been
enough talk to get people concerned over how these findings could
affect medical care. For example, Richard Cooper, a cardiologist at
Loyola University Medical Center in Chicago, worries that any new
information on race differences will lead to inferior care for
non-whites. He says that so far, the best data on biological race
differences are only "mixed," and even where differences do exist they
are never great enough to justify any race-based generalizations in
the absence of genetic tests. He says there's no evidence that risk
factors don't operate the same way for all groups. BiDil developer Jay
Cohn of the University of Minnesota, Twin Cities, agrees that the best
treatment is the same for any race. But he wouldn't have a problem
with, say, prescribing a drug that will boost NO in a black heart
patient. If a doctor knows that a trait is "more common in one
population than another," that could be enough to "consider modifying
one's treatment strategy," he says.
Although scientists hope that the advent of genomic medicine will
obviate the need to grapple with race issues, Goldstein warns that the
day of individually tailored treatments may be far away. Even after
relevant genes are identified, it will be a chore to sort out what all
the alleles do, he says. And so far, only a handful of such genes have
been identified. "Pharmacogenetic studies are in their absolute
infancy," he says. So "the big question is the interim strategy: how
to use ancestry now."
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