Ben Mason
3-2-2012
Race and Ethnicity: Soc 341
The Biology of Race
Before World War II the sociology classes of America taught the youth of America how to
recognize race, that race represented separate biological entities; separate subspecies of human
beings, and that some were inherently better than others. Today they teach us that race is no
more than a social construct; that race is not to be thought of as a biological phenomenon, and
has no more meaning than that which is endowed upon it by our society. Given the inconsistency
of our nation’s educational institutions thus far it is not unreasonable to call these ideas into
question. Is there any biological basis for race? And if there is, what is it? In this essay I will
explore the idea of race as a biological phenomenon, briefly observing the history of race as a
biological concept, examine the contemporary science of biological anthropology, and ultimately
attempt to evaluate the validity of the concept of race as biology.
Evolution is a word with unfortunate stigma attached to it. Common misconceptions about the
process of evolution include such ideas as evolution being the process of a lower form of life
ascending to some higher form, or the idea that evolution acts with some deliberate purpose, or
in some purposeful direction. It is these lines of thinking that have led to misconceptions such as
Caucasians constituting a higher form of life than Africans, and drawing up evolutionary
timelines to show the evolution of the African Negro from monkeys, and the subsequent
evolution of the Caucasian from the African Negro, placing Africans in the middle as some
intermediary step between modern humans and monkeys, that people of African descent are
psychologically inferior to Caucasians and constitute a threat to “racial purity,” that if African
genes were to infiltrate into the Caucasian genome it would be erasing forward progress, and
finally perverting the history of human evolution to support such a hypothesis. The vulgarity of
these ideas, and the genocide committed during World War II has led to such a powerful
backlash that today’s sociology literature tends to argue that race is primarily a social construct,
has little to no grounding in biology, and has no more meaning than that which is endowed upon
it by society. The words “eugenics” and “human evolution” have been largely skunked and both
words now conjure associations of racism and bigotry.
It is important to recognize that as human evolution was taking place in Europe, Asia, and the
Americas, human evolution had not halted in Africa. Human evolution has been taking place for
populations currently in Africa just as long as it has for populations outside of Africa, and while
one can reasonably make scientific arguments for races being different physiologically due to
things like regional differences in diet and climate, unless there has somehow been selective
pressure unique to Africa that favors stupidity, or selection for intelligence unique to the rest of
the world that has not existed in Africa, there is little reason to suspect that genetic drift alone
has lead any one lineage of human beings to be psychologically superior to any other. “Evolution
produces a tree, not a ladder — and we are all just one of many twigs on the tree” (Caldwell et
al.).
Just how dissimilar are different races? The debate over the degree of distinction between
different races of human beings is an old one, dating back to when the nations of Europe began
using concepts of racial superiority and inferiority as a justification for imperialism. Charles
Darwin addressed the subject of human races in his Paper “The Descent of Man”: “Whenever it
can be shown, or rendered probable, that the forms in question have remained distinct for a long
period, this becomes an argument of much weight in favour of treating them as species” (The
Descent of Man, And Selection in Relation to Sex, Darwin 1871, p.114). The idea that being
“distinct for a long period” is important in order to be able to classify different races as
subspecies of human beings has manifested itself in the debate on human evolutionary history in
the different models that have been used to map human divergence. There seems to have been a
concerted attempt to maintain models that show different races of human beings as being
“distinct for a long period”. One of the problems with human evolutionary science up until very
recent years is that it has been largely dominated by white males, which has had the consequence
of heavily biasing the science. Within recent human evolution, there are four competing models:
The first is the “Candelabra” model, and is closely linked with a history of racial supremacy and
bigotry. It holds that current populations of humans constitute monophyletic groups with a
history dating back a million years or more. This model was shot down with genomic data, and a
similar model representing an attempt to save the Candelabra model, called the “multiregional”
model, holds basically the same ideas as the Candelabra model with the concession that there
was interbreeding between the three major populations of humans. Professor Douglass Taylor,
chair of the biology department at the University of Virginia said in a lecture that in reading the
literature “there is definitely a sort of white male thing with trying to hold on to this model. (…)
A lot of the hanging on to Europeans as a distinct lineage was a little bit of racial pride”. To the
dismay of those that would like to believe that their race is a separate and distinct subspecies
from other races, the model that is currently held to be correct is the “African Replacement
Model”, which contends that the bulk of human evolution has occurred within Africa, and that in
relatively recent history a subset of the African population came out of Africa and spread around
the globe. The most important difference between the African Replacement Model and the other
two is that the other two models contend that the evolutionary divergence of humans took place
millions of years ago, while the African replacement model posits that the split took place within
about 200 thousand years ago (the “split” here being homo sapiens from H. hiedelbergensis, not
the split between different races of human beings). Evidence for the first two theories being
incorrect lies in the patterns of genetic diversity observable in human races today. The
Candelabra and multiregional models predict that the three major lineages of human beings
would be roughly equivalent in terms of genetic diversity, while the African Replacement model
would predict that within Africa there should be a lot of genetic diversity, and that peoples
outside of Africa should be subsets of that diversity. This is indeed what we see. The alleles
possessed by Europeans and the alleles possessed by Asians are a subset of those found within
Africa. An analysis of microsatellite markers in the human genome confirms this vividly. The
bar graphs below show, for the people of particular geographic regions, the frequencies of the
various alleles (numbered 4-15) at a short tandem-repeat locus on chromosome 12.
So, different races are certainly not different subspecies of human beings. But then why do we
look so different? If there is so little biological difference between us, why is it so easy to tell at a
mere glance by external physical characteristics that a person is most likely of African, European,
or Asian descent? “If we are all so recently ‘out of Africa,’ why don't we all look like Africans?”
(Science Daily 1998). The explanation that I propose is that the amount of dissimilarity in the
external morphological phenotype of individuals is disproportionate to the amount of
dissimilarity among physiological and psychological characteristics, and that this is due to
differing degrees of “stabilizing selection” that depend on the relative importance of the
characteristic in question. As opposed to destabilizing selection, stabilizing selection is the effect
of selective pressure that acts to prevent change in allele frequencies of a given trait. A
commonly cited example of stabilizing selection is the gene that codes for the hemoglobin
molecule in red blood cells. Due to its medical importance, the hemoglobin molecule in red
blood cells has been studied extensively and its structure is very well understood. Hendrickson
and Love (1971) analyzed in detail the structure of the hemoglobin molecule of the sea lamprey,
and classified its amino acid sites into four groups: surface, exposed, buried, and heme pocket.
They examined the sequence similarities and differences between the lamprey hemoglobin
molecule and the human hemoglobin molecule, and assuming that the divergence of lampreys
and humans occurred 500 million years ago, calculated the evolutionary rates of amino acid
substitutions for the four classes of amino acids they came up with. The rates for the surface
region of the molecule and the heme pocket are as follows:
Region
Hemoglobin alpha
Hemoglobin beta
1.35
2.73
Surface
0.165
0.236
Heme Pocket
“Population Genetics, Molecular Evolution, and the Neutral Theory” (Kimura 1994, p.601).
The above data indicates that evolutionary rates for amino acids making up the surface of the
hemoglobin molecule are almost ten times that of the rates of amino acids making up the heme
pocket part of the hemoglobin molecule. What does this data mean, and how does it relate to
populations of humans? The hemoglobin molecule is an oxygen-carrying protein found in the red
blood cells of all vertebrates and some invertebrates. Its purpose is to pick up the oxygen we
breathe in from our lungs, and carry it through our bloodstream to the rest of our body, and our
lives depend on it functioning properly. The surface of the molecule serves relatively little
purpose, and if a mutation should occur in one of the codons encoding a surface amino acid of a
person’s hemoglobin molecule, there’s a pretty good chance that that person will be perfectly
fine and exhibit a normal phenotype. The heme pocket of the hemoglobin molecule is the part of
the molecule that carries the oxygen; it’s the business part of the molecule. If a person is unlucky
enough to have a mutation occur in a codon encoding one of the amino acids constituting the
heme pocket of their hemoglobin molecule, there is a good chance that they will not be a viable
fetus, and die before they are even born, or as soon as their fetal hemoglobin is replaced with
adult hemoglobin. This is why you see such relatively low rates of evolution for the amino acids
making up the heme pocket as opposed to the surface of the hemoglobin molecule. The takeaway message from this data is that in general, if something is important, it experiences a
relatively slow rate of evolution. If something is unimportant, it experiences a relatively rapid
rate of evolution. This concept has important implications not just in evolution of small-scale
molecular phenotype, but large-scale organismal phenotype as well. It means that when
populations diverge and experience periods of geographical isolation, the evolution that takes
place as a result of genetic drift acts on unimportant parts of an organism much faster than
important parts, and as a result relatively unimportant parts like external morphological
phenotype are liable to change much more rapidly than important parts like our internal
physiology and psychological characteristics. If a mutation should occur that affects an
individual’s brain physiology, there is a good chance that person will never see the light of day.
But in the majority of cases, external characteristics like the shape your face or the texture of
your hair have relatively little impact on odds of survival. As a matter of fact, people’s external
appearances could not possibly be a poorer indicator of genetic distance: “The largest genetic
distance between any two continents is between Africa and Oceania at 0.2470%. Based on
physical appearance this may be counterintuitive, since Indigenous Australians and New
Guineans resemble Africans with dark skin and sometimes frizzy hair. This large figure for
genetic distance reflects the relatively long isolation of Australia and New Guinea since the end
of the last glacial maximum when the continent was further isolated from mainland Asia due to
rising sea levels” (“Race and Genetics” 2012). Mutations in alleles affecting external
morphological phenotype are much more likely to arise and spread to fixation in a population
than mutations affecting physiological or psychological traits. In other words, we are much less
different than we look.
That said, if the races of human beings diverged about 70,000 years ago (Science Daily, 1998), if
we pick a generational gap of about 25 years, that allows for the passage of 2800 or so
generations. Is that enough time for divergent evolution of human beings to occur? Yes. When
populations of organisms are isolated for hundreds of generations, effects of genetic drift and
selective pressures can and will change allele frequencies in those populations. This is true of all
organisms, and human beings are no exception. Our best current estimate for the age of our
species is 170,000 years (Evolutionary Analysis, Freeman & Scott, 2007). If the major lineages
of humans diverged 70,000 years ago, that means we’ve been apart for approximately 40% of
our history. During this time several factors have acted to hasten, as well as to hamper the
divergent evolution of human beings.
One factor that can act to hasten or hamper the divergent evolution of individual populations of
humans is their degree of isolation from other populations. Interbreeding has historically taken
place between most if not all geographically isolated populations of humans. Interbreeding acts
to introduce alleles from one population into another, sometimes rescuing alleles that would
otherwise have disappeared from the population, and at other times introducing new alleles that
had never existed in the population before. Interbreeding acts to erase dissimilarities between
extant populations of humans, and hamper divergent evolution. However some argue that gene
flow between populations of human beings has been relatively slow. Professor Henry
Harpending, author of a study on human genetics from the University of Utah, Salt Lake City,
US, said: "The dogma has been these [differences] are cultural fluctuations, but almost any
temperament trait you look at is under strong genetic influences.” “Genes are evolving fast in
Europe, Asia and Africa, but almost all of these are unique to their continent of origin," he
added. "We are getting less alike, not merging into a single, mixed humanity" (Lever, 2007).
Another Factor that can act to hasten or hamper the divergent evolution of a species is effective
population size. In general, evolution due to genetic drift occurs at the same rate in large
populations as in small populations. This is because even though the odds of any one given allele
spreading to fixation in a large population is quite low in large populations when compared to
smaller ones, the rate of introduction of new alleles is proportionately higher in a large
population due to increased chances for mutation. However, due to the decreased chance of new
alleles spreading to fixation, large population size acts to hamper the effects of selection on
evolution, and as a consequence evolution proceeds more slowly in larger populations. In small
populations, the rate of introduction of new alleles via mutation is decreased, and the odds of any
one given allele spreading to fixation are increased. “Gene frequencies in small, isolated
populations do not reflect those of the larger founding population from which they were derived
because of two factors, founder effect and random genetic drift. Founder effect occurs when the
population grew from a few founding individuals. A few individuals cannot represent all of the
genomes of the founding population” (University of Illinois). Small population size has the effect
of decreasing overall genetic diversity through genetic drift, as well as facilitating rapid
evolution via selection. In extreme cases this is referred to as the “bottleneck” effect. Population
bottlenecks occur when a population’s size is reduced for at least one generation. “Because
genetic drift acts more quickly to reduce genetic variation in small populations, undergoing a
bottleneck can reduce a population’s genetic variation by a lot, even if the bottleneck doesn’t last
for very many generations” (Caldwell et al.). As the genomic data presented in this paper
indicates, there appears to have been a significant reduction of genetic diversity in populations
outside of Africa. It is likely that this has to do with a genetic bottleneck experienced by humans,
which is likely to have coincided with the second major migration of human beings out of
Africa. Geneticists have argued for a long time that there has been a bottleneck in recent human
history, but for a long time no one offered any explanation as to the causes of the crash and
recovery. One hypothesis offered by anthropologist Stanley Ambrose of the University of
Illinois, proposes that “A volcanic winter reduced populations to ‘levels low enough for
evolutionary changes, which occur much faster in small populations, to produce rapid population
differentiation.’” If, as he believes, the eruption of Mount Toba in Sumatra caused the bottleneck
in the global population of humans, “then modern human races may have diverged abruptly, only
70,000 years ago” (ScienceDaily, 1998). Ambrose linked geneticists’ research to the research of
volcanologists which shows that the super-eruption of Toba on the island of Sumatra caused a
volcanic winter, and an “instant ice age” (ScienceDaily, 2009) that lasted for six years and
significantly altered global climate for the next 1,000 years. “Those six years of ‘relentless
volcanic winter’ led to substantial lowering of global temperatures, drought and famine, and to a
global human population crash during which, if geneticists are correct, no more than 15,000 to
40,000 people survived. (…) We assumed that humans differentiated gradually because ancestral
populations were large and stable, but genetic research now demonstrates that changes in
population size were sometimes dramatic. The new model resolves the paradox of the recent
African origin model: If we are all so recently ‘out of Africa,’ why don’t we all look like
Africans?” “’When our African recent ancestors passed through the prism of Toba’s volcanic
winter, a rainbow of differences appeared.’ Ambrose said.” (ScienceDaily, 1998).
Population bottlenecks are able to speed up evolution because of the effects of selective pressure.
While the effects of genetic drift act at the same rate on large populations as small populations,
reducing overall population size can still dramatically affect that rate of evolution due to changes
in allele frequency that are driven by selective pressures. It is still important to understand that
most evolution occurs via the effects of genetic drift, and is largely arbitrary. If any evolution has
some semblance of directionality to it, it is that which occurs via selective pressure. One
commonly cited example of this is variation in skin color. That there are few dark-skinned
individuals among northern-European populations and few light-skinned individuals among
African populations is likely a result of “purifying”, or “positive” selection. Purifying selection is
selection that acts to drive one allele in a population to fixation, eliminating others. The relative
lack of variation in skin color among populations is likely due to selective pressure promoting
the spread of alleles for dark pigment in regions where large quantities of sunlight are liable to
cause skin cancer, and promoting the spread of alleles for lighter pigment in regions where a lack
of sunlight is liable to result in vitamin D deficiency, which is associated with Rickets
(weakening of the bones) as well as cancer. Modern techniques that scan the human genome for
genes that have been subject to selection reveals evidence of positive selection in major lineages
of human beings. One such technique, the “sliding window” technique, measures the number of
SNPs (single nucleotide polymorphisms [places in the gene where a nucleotide is different]) in a
large sample of individuals from different populations. Below is an example of a gene
(C21orf34) that shows evidence for positive selection in different populations of humans.
Evidence for selection in a region containing part of the gene C21orf34. (A) Haplotype plots in a
500-kb region on chromosome 21 surrounding the locus. Each row represents a haplotype, and
each column a SNP. Rows are colored the same if and only if the underlying sequence is
identical (some low-frequency SNPs are excluded). For full details on the generation of these
plots, see Conrad et al. (2006). (B) Heterozygosity in the same region. Lines show heterozygosity
calculated in a sliding window of three SNPs across the region in different populations. Black
arrows at the top of the plot represent the positions of SNPs with FST > 0.6 (i.e., in the 0.01% tail
of worldwide FST). (C). A pie chart of the worldwide distribution of a SNP that tags the red
haplotype in A (rs2823850). (Red) The derived allele frequency; (blue) the ancestral allele
frequency.
“Signals of recent positive selection in a worldwide sample of human populations” (Pickrel et al.
2009)
The above data begs the question: What does C21orf34 code for? We don’t know. The function
of C21orf34 is as of yet unknown to geneticists. Whatever the gene codes for, statistics suggest
that it has experienced positive selective pressure in populations outside of Africa. The takeaway message from this data is that differences in allele frequency in human populations are due
to selective pressure in addition to genetic drift.
What is the utility of data like this? Information on the roughly 6.3% of human genetic variation
that distinguishes different races does not have a lot of useful applications. A recent topic of
controversy in biological anthropology is the Human Diversity Genome Project. One goal of the
project is to counteract the “Eurocentric bias” (Wakeham 2008, p.197) of the Human Genome
Project, compiling a more complete and representative database on the human genome. In
addition to furthering anthropological history the program has a more practical goal as well;
differences in physiology can also affect how people of different ethnic backgrounds metabolize
certain drugs. This is most likely due to regional differences in diet. “The risk of angioedema
(swelling) with blood pressure lowering drugs is three times greater in black patients than nonblack patients” (Science Daily 2006). “There is wide inter-individual variability in the
pharmacokinetics, pharmacodynamics and tolerance of anticancer drugs. Recent evidence
suggests that there is even greater variability between individuals of different ethnicity (…) some
of these variants result in altered enzyme function (…) Emerging evidence indicates that toxicity
from certain anticancer treatments is much greater in Asian patients than Caucasians in breast
and lung cancers. Understanding the causes of ethnic differences in cytotoxic metabolism may
promote improved understanding of inter-individual differences in the pharmacokinetics and
tolerance of cytotoxic drugs leading to improved and more individualized prescribing” (Phan et
al.). “Ethnicity is an important demographic variable contributing to interindividual variability in
drug metabolism and response” (Xie et al.). In 2010 the first drug approved only for use by
people of specific ethnic backgrounds was patented. (Douglass Taylor 2011). There are many
diseases that have a higher rate of incidence among people of specific ethnic backgrounds.
Certain African populations are known to have a genetic predisposition to sickle-cell anemia,
certain northern European populations to have a genetic predisposition to type II diabetes, and
Ashkenazi Jews to have a genetic predisposition to Tay-Sachs disease. One of the goals of the
HGDP is to “help lead to the identification of genetic factors in some human diseases and
eventually to ways to treat or prevent those diseases” (Morrison Institute 2011). This program
has received a lot of criticism, critics warning that the potential dangers presented by the HGDP
outweigh the few benefits. One fear is the possibility that “governments armed with genetic data
linked to individual racial groups might deny human rights based on this genetic data” (“Human
Genome Diversity Project” 2012). There is even fear among some of the potential that “HGDP
research data and techniques could make it easier for those so inclined to design new biological
weapons against specific populations” (Foster 1999).
At this point I have discussed in this paper the unequal distribution of genetic variation in the
human species, the effects of stabilizing selection, degree of isolation, effective population size,
and purifying selection on the external phenotypic expression of populations, as well as possible
applications of racial data in medicine. All of this data, however, only applies to ancestry, and
really only applies to the term race insofar as the definition of race overlaps with ancestry. The
process of “racialization” is one example of creating a race based on social criterion rather than
ancestry. Defining race as anything other than ancestry tends to destroy its objective value and its
usefulness altogether. “For purposes of medical testing we do not want to know whether a person
is “Hispanic” but rather whether that person’s family came from a Caribbean country such as
Cuba, that had a large influx of West African slaves, or one in which there was a great deal of
intermixture with native American tribes as in Chile and Mexico, or one in which there was only
a negligible population of non-Europeans” (Lewontin 2006). In this respect, “white” is only
useful insofar as it refers to European ancestry, and “black” is even less useful because even
when referring to recent African ancestry, the diversity within Africa is much greater than that
within Europe, and there are comparatively few genetic traits that can be said to be common
among the majority of Africans. Indeed the breadth of the spectrum of ways in which the term
race has come to be used, and which of those usages hold precedence over others, and how the
different usages of the term vary globally, is far beyond the scope of this paper.
Central in the debate on the biology of race are the arguments of Richard Lewontin and his
critics. In 1972 Richard Lewontin demonstrated that 85% of human genetic variation was to be
found within a single continental population, and only 6.3% serves to differentiate races.
Lewontin’s argument led a number of authors publishing in the 1990s and 2000s to follow his
verdict that race is a biologically meaningless concept. In 2003 A.W.F. Edwards argued in his
paper “Human Genetic Diversity: Lewontin’s Fallacy” that the conclusion that racial groups
cannot be genetically distinguished from each other is incorrect, asserting that “when multiple
alleles are taken into account genetic differences do tend to cluster in geographic patterns
roughly corresponding to the groups commonly defined as races.” Edwards contended that even
if the probability of misclassifying an individual based on a single genetic marker is as high as
30% (as Lewontin had reported), the probability of misclassification becomes close to zero if
enough genetic markers are studied simultaneously.
(“Race and Genetics” 2012 [originally from gnxp.com])
“Edwards saw Lewontin’s argument as being based mostly in a political stance that denies the
existence of biological difference in order to argue for social equality” (“Race and Genetics”
2012).
Much of the controversy over the issue of race has centered on the debate between the social
constructionist paradigm vs. the biological paradigm. This is a false dilemma, and the two
paradigms are not mutually exclusive, rather they represent two different definitions of the same
word, both being correct and the only real issue of contention being the degree to which each
paradigm is important in different contexts. The tendency to impose such a false dilemma likely
stems from a desire to circumvent complexity and simplify the issue. The definition of race as it
has come to be used is broad and vague. The only thing all of the various definitions of race
share in common is their illusory nature. Socially constructed conceptions of race forge
meaningless classifications and assert meaning where there was none, and even when viewed as
an objective categorization system based on ancestry and genetic data, race is but a small beast
that casts an enormous shadow. Even so, A.W.F. Edwards hit the nail on the head when he
accused Lewontin of downplaying the genetic differences between races for the political purpose
of promoting social equality. Contemporary sociology literature also downplays the biological
significance of race to such an extent that most students of the discipline come under the false
impression that the biological aspect of race is negligible and race is not biologically
distinguishable on a genetic level.
One might be tempted to make the paternalistic argument that this misconception is actually for
the best; as ignorance of the minute biological distinctions between people of different racial
groups does no harm. It is certainly true that teaching that there are concrete and measurable
biological distinctions between different human races but failing to impart an understanding of
what these distinctions are not is an invitation to hatred and bigotry. It is human nature to think
of oneself as special. This tendency carries over to groups, and whenever you create recognizable
groups of people, the perception of your own group as superior to other groups is a natural
product of human nature. Modern society’s social taboos have succeeded in hiding racism from
plain sight, but I believe that the sort of ubiquitous, sub-surface racism that persists in the United
States today is not helped by the way students in elementary through college level courses are
taught that different races are genetically identical, and to believe otherwise is to be a racist; any
bright young boy or girl who takes a course in biology or even just develops a very basic
understanding of genetics is liable to see through the farce in short order. Such individuals are in
danger of reaching the conclusion that racist ideologies have practical and scientific merit.
Without an understanding of what evolution is and how it works, many people arrive at
erroneous conclusions regarding the nature of race. I believe that we cannot combat prejudice
and bigotry by downplaying the biology of race and sweeping diversity under the rug. The
question of whether or not people will ever be capable of recognizing that they are different
without clinging to notions of superiority and inferiority is just as much beyond the scope of this
paper as any sort of comprehensive definition of the term “race,” but one cannot effectively fight
ignorance with more ignorance.
Works Cited
"Ancient 'Volcanic Winter' Tied To Rapid Genetic Divergence In Humans." ScienceDaily.
ScienceDaily, 08 Sept. 1998. Web. 26 Feb. 2012.
<http://www.sciencedaily.com/releases/1998/09/980908074159.htm>.
Caldwell, Roy et al. "Misconceptions about Evolution." Understanding Evolution. The National
Science Foundation. Web. 27 Feb. 2012.
<http://evolution.berkeley.edu/evolibrary/misconceptions_faq.php>.
Caldwell, Roy et al. "Bottlenecks and Founder Effects." Evolution 101:. University of California
Museum of Paleontology and the National Center for Science Education. Web. 27 Feb.
2012. <http://evolution.berkeley.edu/evosite/evo101/IIID3Bottlenecks.shtml>.
Darwin, Charles. The Descent of Man And Selection in Relation to Sex. 1st ed. Vol. 1. London:
John Murray, 1871. The Complete Works of Charles Darwin Online. 14 Feb. 2011. Web.
26 Feb. 2012. <http://darwinonline.org.uk/content/frameset?itemID=F937.1&viewtype=text&pageseq=214>.
Foster, Meika. "THE HUMAN GENOME DIVERSITY PROJECT AND THE PATENTING OF LIFE:
INDIGENOUS PEOPLES CRY OUT." Foster, Meika --- "The Human Genome Diversity
Project and the Patenting of Life: Indigenous People Cry Out" [1999] CanterLawRw 7;
(1999) 7 343. University of Canterbury, 1999. Web. 02 Mar. 2012.
<http://www.nzlii.org/nz/journals/CanterLawRw/1999/7.html>.
Freeman, Scott, and Jon C. Herron. Evolutionary Analysis. 4th ed. New York, NY: Pearson
Custom, 2007. Print.
"Human Genome Diversity Project." Wikipedia. Wikimedia Foundation, 26 Feb. 2012. Web. 02
Mar. 2012. <http://en.wikipedia.org/wiki/Human_Genome_Diversity_Project>.
Kimura, Motoo. Population Genetics, Molecular Evolution, and the Neutral Theory: Selected
Papers. Chicago: University of Chicago, 1994. Print.
Lever, Anna-Marie. "Human Evolution Is 'speeding Up'" BBC News. BBC, 12 Nov. 2007. Web. 27
Feb. 2012. <http://news.bbc.co.uk/2/hi/7132794.stm>.
Lewontin, R. C. "Confusions About Human Races." Welcome. SSRC, 07 June 2006. Web. 01 Mar.
2012. <http://raceandgenomics.ssrc.org/Lewontin/>.
Morrison Institute. "Morrison Institute for Population and Resource Studies." Human Genome
Diversity Project Frequently Asked Questions. Stanford University, 10 Mar. 2011. Web.
02 Mar. 2012. <http://hsblogs.stanford.edu/morrison/2011/03/10/human-genomediversity-project-frequently-asked-questions/>.
Phan Et Al. "Expert Opinion on Drug Metabolism & Toxicology." Ethnic Differences in Drug
Metabolism and Toxicity from Chemotherapy, , Informa Healthcare. Informa Healthcare,
Mar. 2009. Web. 02 Mar. 2012.
<http://informahealthcare.com/doi/abs/10.1517/17425250902800153>.
Pickrel Et Al. "Signals of Recent Positive Selection in a Worldwide Sample of Human
Populations." Genome Research. CSH Press, 2009. Web. 26 Feb. 2012.
<http://genome.cshlp.org/content/19/5/826.full>.
"Race and Genetics." Wikipedia. Wikimedia Foundation, 03 Jan. 2012. Web. 01 Mar. 2012.
<http://en.wikipedia.org/wiki/Race_and_genetics>.
"Some Ethnic Groups More Susceptible To Adverse Drug Reactions." ScienceDaily. ScienceDaily,
06 May 2006. Web. 02 Mar. 2012.
<http://www.sciencedaily.com/releases/2006/05/060506103939.htm>.
"Supervolcano Eruption -- In Sumatra -- Deforested India 73,000 Years Ago." ScienceDaily.
ScienceDaily, 23 Nov. 2009. Web. 27 Feb. 2012.
<http://www.sciencedaily.com/releases/2009/11/091123142739.htm>.
Taylor, Douglas. Lecture: “Human Evolution.” Gilmer Hall Auditorium, Charlottesville. 29 April.
2011.
Tissot, Robert. "HUMAN GENETICS." Human Genetics. University of Illinois. Web. 27 Feb. 2012.
<http://www.uic.edu/classes/bms/bms655/lesson13.html>.
Wakeham, Pauline. Taxidermic Signs: Reconstructing Aboriginality. Minneapolis: University of
Minnesota, 2008. Print.
Xie Et Al. "Supplemental Content." National Center for Biotechnology Information. U.S. National
Library of Medicine, 2001. Web. 02 Mar. 2012.
<http://www.ncbi.nlm.nih.gov/pubmed/11264478>.