Medicine, anti-realism, and ideology

Variation in medical genetics does not show that race is biologically real
Advanced draft of: https://doi.org/10.1515/sats-2020-2003

Black Community Survival Conference, March 30th, 1972 (USA)

https://exhibits.stanford.edu/fitch/browse/black-panther-party-oakland-california-1968-1972
Medicine, anti-realism, and ideology: variation in medical
genetics does not show that race is biologically real

Abstract

Lee McIntyre’s Respecting Truth chronicles contemporary challenges regarding the relationship
between evidence, belief formation, and ideology. Discussion in his book focuses on the
‘politicization of knowledge’ and the purportedly growing public (and sometimes academic)
tendency to choose to believe what is determined by prior ideological commitments rather than
what is determined by evidence-based reasoning. In considering these issues, McIntyre posits that
the claim “race is a myth” is founded on a political ideology rather than on support from scientific
evidence. He contrasts this view with the argument that racially correlated biomedical outcomes
for self-identified racial groups suggest that biological races are real. I explore how McIntyre’s
framing of the claim “race is a myth” as fundamentally ideological results in him failing to engage
with the arguments and evidence many constructionists and biological anti-realists put forward in
support of their views. I also show how the biomedical evidence he thinks supports biological
realism is unconvincing.

1. Overview: medicine, genetics, race, and the project of Respecting Truth

In a few pages, Lee McIntyre (2015) in his Respecting Truth gives an appraisal of the current
debate about race in which he concludes that those who hold that ‘race is a myth’ have fallen prey
to a politically correct ideology. McIntyre is not alone in this claim: it has also been made by a
minority of thinkers in the mainstream debate (e.g., Sesardić 2010; Shiao et al. 2012). Although
McIntyre does not engage with this literature in depth, he summarises a view that considers the
evidence of population differences from physical anthropology, genetics, medicine, and related
biological sciences as proof of the existence of races. In this paper I show why his conclusions
based on this literature are premature and rest on a series of misconceptions about what it is that
anti-realists about biological race argue in respect to what kinds of views current scientific
evidence supports.

Part of what is at stake in this debate is the direction in which policy may take on the basis of what
we believe about races. There are non-trivial consequences to our metaphysical positions that can
inform what interventions we think are appropriate in, for instance, clinical settings (Spencer 2019;
Yudell et al. 2016) and in social, political, and interpersonal relations including those of personal
identity and reparative justice (Msimang 2019, 23–24). It is for these and other reasons that it is
important for us to get our metaphysics of race correct. As difficult of a task as this may be, I
believe McIntyre’s comment is a useful foil for exploring the relationship the metaphysics of race
has to questions in medical genetics and racial classification more broadly construed.

I take particular issue with McIntyre’s case for self-identified races being biological
classifications. I argue that the examples of health disparities from medical genetics and the
biological differences between individuals that McIntyre uses in his argument do not show that
races are biologically real. On the contrary, I show how his examples undermine the kind of

1
biological realism he is in favour of. There may be other ways to formulate biological realism
about race, but his view that self-identified racial groups are biological classifications does not
succeed as it is misguided about the relationship between race and biology.

The current wave of biological realism about race has been inspired by advances in population
genetics and interpretations thereof (see Spencer 2015; Foster 2009). In particular, advances in
human molecular biology have given new life to the question of whether there are biological races
in humans (e.g., Shiao et al. 2012) even if the geneticists making these findings have cautioned
against racial readings of their data (e.g., Rosenberg et al. 2005, 668). This race debate depends on
a number of taxonomical issues which determine the extent to which data on population
stratification can be used to support claims about particular populations being grouped one way or
another (Edwards 2003) and whether those population groups can constitute ‘races’ by any
ordinary biological standards (Baker et al. 2017; Winther 2014; Templeton 2013).

A subset of the more general attempt to formulate a biological theory of race is the attempt to infer
races from differences between people(s) found in the biomedical sciences (e.g., Adler 2009; Risch
et al. 2002). In these views it is generally assumed that biological regularities and patterns among
demographic groups in clinical outcomes reflect genetic differences between those demographics
as populations that differ from each other in biologically notable ways (Burchard et al. 2003; Risch
et al. 2002). These presumed genetic differences are meant to explain some of the observed clinical
outcomes we see, such as disease susceptibility, disease burden or incidence, and drug efficacy in
particular population groups. There is presently a lively debate in this regard (cf. Spencer 2018;
Yudell et al. 2016; Hardimon 2013; Kahn 2013).

Although it is now considered to be beyond reasonable doubt that the efficacy of some drugs differs
across racial (and ethnic) groups, it is not always clear that this is because of biological differences
between those groups. Drug metabolism, for instance, is affected by numerous factors apart from
underlying genetic differences between individuals and groups. To understand drug action in the
human body, we need to “consider human biochemistry and physiology, but also the effects of
age, smoking, legal and illegal drug usage, gender, diet, environment, disease and finally genetic
variation” (Coleman 2010, 159). This means that the detection of individual or group differences
does not necessarily imply an individual- or group-specific genetic difference is at its base.

Nevertheless, subpopulations of particular race groups do sometimes exhibit some genetic

differences that relate to clinical outcomes (e.g., Nazha et al. 2017). One risk profile that could be
argued to stereotypically face a particular race group because of a biological trait are particular
kinds of skin cancer (Jablonski 2012a). It is by now mundane to point out facts such as people of
paler skin are more susceptible to particular kinds of skin damage from UV rays that can affect
them disproportionately in causing sunburn and thereby increasing their risk of developing certain
kinds of skin cancer (Jablonski 2012a). Skin colour is a biological trait, and one that is interesting
to biology and medicine given the differential outcomes it may have on health and reproductive
success (Jablonski 2012b). Skin colour has been an evolutionarily significant trait as evidenced by
its development through purifying selection (Jablonski 2012c). But are such facts enough to
ground a biological formulation of race, especially when the distribution of this trait is clinal? Can
these (and other) populations which are clearly interesting to medical genetics be considered to be
indications of natural taxonomic divisions? Although my response here will not be comprehensive,

2
it is this form of question that this paper addresses through considering the examples from medical
genetics that McIntyre uses as evidence for the purported reality of biological races.

I begin by reconstructing his view of the debate in §2 and outline why he argues that the claim that
“race is a myth” is mistaken. In §3, I review evidence against McIntyre’s argument that suggests
that contemporary biomedical science supports biological racial realism by rebutting each of his
reasons (that I present in §2). I close in §4 by summarizing the central points of my response.

2. Race ‘respecting truth’: outlining McIntyre’s case for why race is not a myth

In Chapter Four of Respecting Truth, McIntyre lays out his reasons for believing that whether race
is biological remains, at the very least, an open question. He explains why we should be sceptical
of the claim ‘race is a myth’ by presenting evidence that suggests race may be biologically real.

The ‘race myth’, as he describes it, is the idea that there is no such thing as race. He does not make
a distinction between the thought that race in general is a myth (e.g., the racial scepticism of Appiah
1996 and Zack 1995 or the anti-realism of Blum 2010 developed along similar lines in Hochman
2017) or if it is only race as a biological classification that is ‘a myth’ (e.g., Smedley & Smedley
2005 or Fujimura et al. 2014). McIntyre only discusses biological realism and not social realism
about race. In this way, McIntyre does not make an explicit connection between his own position
and the mainstream metaphysical debate about race.

In the mainstream metaphysical debate about race, five positions dominate the discussion: naïve
racial naturalism, scepticism, comprehensive anti-realism, population naturalism, and
constructionism (see the row labelled “General Categories” in Figure 1). Scepticism and its
consequent racial eliminativism argued for by Appiah (1996) and Zack (2002) posit that “talk of
races is no better than talk of witches or ghosts, and in order to achieve racial justice we should
stop participating in [the] fiction [of racial terminological use] that underwrites racism” (Haslanger
2012, 299). Comprehensive anti-realists like Blum (2010) and Hochman (2017) are more radical
than the sceptics and argue that ‘race talk’ is never legitimate as there are only racialised
individuals and groups (Msimang 2019). Population naturalists argue that races have a biological
basis but that races are not necessarily what people generally think they are (e.g., Andreasen 2007;
Spencer 2017a,b). Population naturalists argue that races are some particular biologically real
population-level grouping of humans (Spencer 2017a,b). Some population naturalists hold that
their classifications are a “natural division [that] is socially and politically important for the
purposes of achieving racial justice… by enabling us to address racially divergent medical needs”
(Haslanger 2012, 299–300; see Spencer 2019 and Hardimon 2013). Constructionism is the view
that races are socially real (Mallon 2018). A common normative accompaniment to this
metaphysical claim is that “racial justice requires us to recognize the mechanisms [and the
histories] of racial formation so that we can undo their damage” (Haslanger 2012, 299).
Constructionism as it applies to race in this literature is naturalistic—its claims should not
contradict empirical evidence in the biological sciences (Hochman 2013; Haslanger 2012; Mallon
2007). Naïve racial naturalism is one or another idealisation of modern theories of race, often also
associated with racialism. It is the position that common sense races are biologically real and often
that those races are essentialist biological groupings. In its formulation as racialism, it is the view

3
 that “we could divide human beings into a small number of groups, called ‘races,’ in such a way
that the members of these groups shared certain fundamental, heritable, physical, moral,
intellectual, and cultural characteristics with one another that they did not share with members of
any other race” (Appiah 1996, 54). Racialism and modern theories of race are false and are most
commonly discussed as foils through which contemporary concepts of race are introduced.

Philosophical framework Naturalism

Basic positions Realism Anti-realism

General categories Population

naturalism
Social
constructionism
Naïve racial
naturalism Racial skepticism
Comprehensive
anti-realism

Cladistic race Conferralist races Racialism Referential Interactive

Specific positions (etc.) (etc.) (etc.)
eliminativism constructionism
about *RIGs
(etc.)

Figure 1: A flow diagram showing the main metaphysical positions in the contemporary naturalistic debate
about race. *’RIGs’ are “racialized individuals and groups”.

Despite constructionism’s ostensibly naturalistic positioning in the contemporary debate, McIntyre

construes constructionism as anti-naturalistic. This is borne out in his arguing that constructionists’
and anti-realists’ claim that race is a (biological) myth is ideological rather than evidence-based
and scientific. Anti-naturalist social constructionism argues that facts are socially constructed in a
global sense, meaning that all claims about knowledge are relative to the social context in which
those claims are made (Mallon 2013; cf. Boghossian 2006). McIntyre argues that social
constructionists about race can only hold that race is a myth if they take the facts of human
biological diversity to be constructed or for constructionists to ignore them and actively discourage
their serious consideration (McIntyre 2015, 120–121). To illustrate the point, he rhetorically states:

…“we share 98.4% of our genes with chimpanzees [but] few would argue that makes us nearly
identical to them.” We share approximately 85 percent of our genes with mice and 60 percent with
the fruit fly… But does this mean that the concept of “species” too is a cultural creation? We may
only be 1 percent different from one another, but shouldn’t science study that 1 percent? (McIntyre
2015, 120–121)

The suggestion here is that the ‘1% difference’ between human beings is a significant biological
difference, and one which is only by a small degree further than the distance between humans and

4
chimpanzees. 1 McIntyre alludes that there may be significant population-level racial differences
in the assortment of that ‘1% difference’. He supports this argument by pointing to racial
differences in responses to medication, health disparities in diabetes, hypertension, and sickle cell
anaemia among other medical conditions (McIntyre 2015, 122–124).

On one hand, McIntyre is developing a notion of race in which folk or common sense racial
concepts such as ‘self-identified African American’ (viz., US black) 2 or ‘self-identified white’
have biological purchase in their correlation with health outcomes (McIntyre 2015, 122). These
are seen to be confirmations of geographical folk races as valid biological classifications (McIntyre
2015, 122–124). McIntyre argues, for instance, that the efficacy of BiDil (a medication that treats
heart failure) on self-identified African Americans (and its purported non-efficacy on other self-
identified racial groups) suggests that African Americans may constitute a biological race
(McIntyre 2015, 123). 3

On the other hand, McIntyre develops a notion of race determined by genetic ancestry indexed by
assumed geographic ancestry (McIntyre 2015, 123). For this idea of race, McIntyre uses the same
evidence of differential biomedical health outcomes between people of presumably different
geographical ancestries to also imply that these groups are significantly genetically different. It is
well-established that ancestry is a crucial biomedical codeterminant of clinical outcomes (Rotimi
& Jorde 2010), and thus an important variable in biomedical settings. One such example McIntyre
gives is that African Americans, who are presumably mostly of African ancestry, have a higher
chance of having sickle cell anaemia because of their genetic ancestry (McIntyre 2015, 123). The
higher prevalence of sickle cell anaemia in African American populations is argued to show that
races such as ‘African American’ (US blacks) have a biological basis in genetics because of these
correlations (McIntyre 2015, 123). 4 Discussing Adler (2009) who reported “nine clinical trials that
were studying diseases or treatments in groups that were defined by race”, McIntyre argues that
racial groups are biologically valid classifications because the manifest differences in health and
clinical outcomes suggest fundamental genetic differences between these groups (McIntyre 2015,
123).

In light of this evidence, McIntyre suggests that race is a valid biological category and that the
denial of biological race is due to an ideological disregard of the scientific evidence for the position
(McIntyre 2015, 117–125). He compares constructionism and biological anti-realism about race
to forms of science denial such as climate change denial and ‘Intelligent Design’ evolution denial.
Couching this criticism in the context of American politics, he claims that in the same way “many
on the right do not believe in the truth of evolution by natural selection or in human-caused global
warming,” it is the case that on “the left, there is widespread acceptance of the idea that race is a
biological myth” (McIntyre 2015, 85).

McIntyre serves a harsh indictment to those who argue that biological races are a myth, specifically
to anti-realists about biological races. I argue below that this indictment is unfounded as it does
not apply to the reasons mainstream biological anti-realists and social constructionists give for

1
See §3–2–3 for commentary on this point.
2
‘African American’ is not a race but a demographic that is part of a race.
3
See §3–2–1 for commentary on this point.
4
See §3–2–2 for commentary on this point.

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their positions. In the following section, I will be arguing that McIntyre’s view of anti-realism
about biological race can only be maintained by mischaracterising the naturalistic debate about
race. I show (1) that anti-realism about biological race, inclusive of social constructionism, is not
maintained through an ignorance or disregard of scientific evidence but is rather continuous with
such evidence, and (2) that McIntyre’s formulation of ‘biomedical race’ is confused and fails to
establish a coherent theory of biological race.

3. There is good reason to believe that race is a (biological) myth: rebutting McIntyre

3–1. McIntyre mischaracterizes the positions he argues for and against

McIntyre notes that the direction of the race debate is dependent on what it is that is being referred
to by the use of the term ‘race’ (McIntyre 2015, 118). In a sense, this is true: the semantic question
of what race is to refer to determines much of what the argument is about (Mallon 2006; cf.
Hochman 2019). However, the semantic question is to a large extent a matter of convention or an
‘representational tradition’ about the use of a term (see Haslanger 2019). Once a convention is
established or a representational tradition decided on, it is an empirical question whether or not the
convention refers to anything.

The term ‘race’ has a varied history of use, and it is a term that displays a great deal of ambiguity
in the biological literature (Templeton 1999). Race as a biological concept in modern and
contemporary usage, however, has usually been construed as a taxonomically significant
classification (Hochman 2013; Templeton 2013). 5 In biology, there exists established conventions
as to how much genetic variation must exist between populations within a species for any one
population to be considered a subspecies; human variation does not meet this standard (Templeton
1999; Templeton 2013). Therefore, contemporary biological realists have to rely on other possible
below-species classifications for their demarcation of races (e.g., those reviewed by Andreasen
2007 and Spencer 2017a,b).

This is a basic point of departure for biological anti-realists from biological realists. Findings such
as Templeton’s are meant to show that race is not a taxonomic classification (Templeton 1999;
Templeton 2013). The biologically anti-realist tradition which uses this form of argument based
on scientific evidence is often traced back to early studies on variance in blood type by race (see
Lewontin 1972; Brown & Amelagos 2001) and more recent studies directly addressing the
question of human genetic variation especially in biomedical and clinical contexts (e.g., Goodman
2000; Smedley & Smedley 2005; Maglo et al. 2016). These and other studies by geneticists
conclude that race is not an objective biological category and does not feature in human biological
taxonomy (e.g., Baker et al. 2017; Winder & Winder 2014). Earlier studies conducted in fields
such as physical anthropology are another starting point for constructionism (or even scepticism
and comprehensive anti-realism) for reasons such as the clinal variation of different traits used to
delineate races being non-concordant and the use of any one particular trait to define race being
arbitrary—as would be the boundaries made between such races (e.g., Livingstone 1962; Sauer
1992; cf. Edwards 2003; Sesardić 2013 and Hochman 2013).

5
Some contemporary thinkers have argued for weaker versions of biological realism. See Kitcher (1999), Pigliucci &
Kaplan (2003), Hardimon (2017), and Spencer (2017b).

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McIntyre purports to be criticizing this constructionism and biological anti-realism, but his
criticisms are distinct to how he describes his target. Naturalistic biological anti-realism and
constructionism are distinct from anti-naturalistic views in that they do not accommodate “more
radical anti-scientific and anti-realist theses” (Mallon 2013). Naturalistic constructionism in
particular is not the claim that genetic diversity and health disparities are ‘socially constructed’
non-objective facts; its claim is that, given all the facts of human genetic diversity, including health
disparities (whatever their causes may be), there is no reason to believe that race is a biological
category (see Baker et al. 2017; Maglo et al. 2016; Fujimura et al. 2014; Fofana 2013). McIntyre
confounds his criticism of anti-naturalists’ anti-realism with naturalistic forms of anti-realism
whose traditions are continuous with the findings of the biological sciences. This is surprising
given that McIntyre explicitly refers to the work of anti-realist biologists such as Templeton (1999)
and Lewontin (1972) in his anti-naturalistic conception of constructionism and anti-realism.

Discussing this biologically anti-realist tradition—from Lewontin to Templeton—McIntyre refers

to a study which argues that even though the genetic variation observed between human
populations does not reach the values used to delineate subspecies, human genetic variation is
highly structured (cf. Edwards 2003). From this he attempts to support the view that common sense
racial categories have a biological basis (McIntyre 2015, 122). This argument contrasts with
biological anti-realism.

Rather than an ideological dispute, this is a genuine academic dispute still raging on today (e.g.,
Glasgow et al. 2019). Nevertheless, McIntyre holds it to be sustained by an anti-scientific ideology
that persists in wishing away biological race as a myth (McIntyre 2015, 116–119). Despite the
political and ideological commitments he attributes only to authors arguing against biological
realism about race, McIntyre does not make a compelling argument for why we should believe
that the basis for this disagreement against biological conceptions of race rests on an undue
influence of politics and “liberal ideology” (McIntyre 2015, 116) rather than on the interpretation
of the facts under dispute (cf. McIntyre 2015, 118–119).

Of course, findings in the study of race can and do get used in the social sphere to support particular
ideologies or social policies (e.g., Galton 1869; Pearson 1919 [1902]; Herrnstein & Murry 1994),
and it is many researchers’ explicit purpose in doing research on race to leverage their research to
achieve some particular social or political goal that has some ideological alignment (Norton et al.
2019; Fofana 2013; Williams & Eberhardt 2008; Haslanger 2000; Gould 1996). In this endeavour,
it is possible that researchers could show bias towards some particular conclusions and betray their
wishes that some facts were one way or another (see Edwards 2003 for a short discussion).
However, for such researchers to be taken seriously in the academic sphere, they would still have
to substantiate their positions by presenting evidence for their claims, and by putting forward well-
reasoned supporting arguments for those claims. The standards of a discipline are not changed or
challenged by a single individual’s wishes or biases; rather, the standards of a discipline operate
on institutional standards against which any claim in its domain must compete (Lakatos 1978).

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This means that despite any researchers’ personal biases and preferences, there remain standards
that their claims must meet to be considered. 6

Andreasen, responding to Gannett (2004), points out that the claim to her having bias for her
version of biological realism for ideological reasons would “need to [be] demonstrate[d]
empirically” (Andreasen 2007, 476; original emphasis). McIntyre’s claim that the rejection of
biological formulations of race is due to ideological bias and is not supported by evidence is also
a claim that would need to be demonstrated empirically. The fact that both opposing views have
been said to be put forward purely for the purpose of the confirmation of prior ideological
commitments is telling: accusations of ideological motives for the formulation of race (or any
hypothesis, in fact) does not settle the question. Taking seriously the accusations of bias on either
side does not necessarily get us any closer to finding the ‘truth’ of the matter.

Discussing Herrnstein and Murry’s controversial The Bell Curve (Herrnstein & Murry 1994),
McIntyre notes that “the book was initially attacked even by scientists for its political implications”
(McIntyre 2015, 120). This seemed to him “a deplorable intrusion of ideology into science”
because “if the work was flawed” nothing would “make shorter work of it than to reveal its
scientific shortcomings” (McIntyre 2015, 120). This is a moot point. For the purposes of this
discussion, I will leave aside overtly political or normative critiques of McIntyre’s work and focus
on the scientific shortcomings of his treatment of race.

3–2. Confusions about BiDil, disease, and genetics

In the previous section, I outlined how McIntyre mischaracterises the debate about biological racial
realism, particularly the constructionist and anti-realist objections against it in the mainstream
philosophical debate. There are three fundamental contentions against McIntyre’s position
regarding scientific evidence that I explore in this section. These are:

(1) That there is no evidence that BiDil’s efficacy is race-specific both because (a) the genetic
or ancestral backgrounds of self-identified African-Americans are so diverse, and because
(b) no clinical trial has been undertaken that demonstrates the race-specific efficacy of
BiDil;
(2) That the most well-established scientific theories about the distribution of sickle
haemoglobin (HbS) explain why the prevalence of sickle cell anaemia has been highest in
parts of Africa – and, consequently, the differential frequencies in African Americans and
US whites – and why it would nevertheless be incorrect to think of sickle cell anaemia as
a racial condition or disease;
(3) That statistical statements about human biological diversity do not tell us anything about
the apportionment of that diversity between groups. Arguments about biologically realist
racial classification depend on how diversity is apportioned between populations and not
merely on there being diversity among individuals.

6
Notoriously, institutional prejudices or biases are more difficult to guard against—especially for the individual
researcher working within that institutional environment. See Lakatos (1978) on this point in general and see Gould
(1996) and Jackson & Weidman (2004) who specifically discuss the point regarding the history of racial thought,
eugenics, and racism.

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I present arguments for these three points which undermine McIntyre’s particular proposal for
biological race as illustrations of how the metaphysical debate can turn on empirical findings and
their interpretation, among other considerations, rather than on an undue influence of ideology on
the academic debate.

3–2–1. There is no evidence that BiDil’s efficacy is ‘race-specific’ despite FDA indication

McIntyre makes the claim that “despite the absurd statement that ‘racially based medical
differences just do not exist,’ we now have concrete evidence that this view is wrong” (McIntyre
2015, 112). Expanding on this view and presenting support for the case of biological racial realism,
he says that it “is surely not cultural construction, but a fact of biology, that BiDil relieved
hypertension in those who self-identify as African American, but not other ethnic groups”
(McIntyre 2015, 112).

The claim that “BiDil relieved hypertension in those who self-identify as African American, but
not other ethnic groups” (McIntyre 2015, 112) is founded on interpretations of three clinical trials
used by the FDA to indicate the use of BiDil specifically for African Americans (see Kahn 2013).

The African-American Heart Failure Trial (A-HeFT) upon which BiDil’s approval was ultimately
decided (Temple & Stockbridge 2007) 7 was very successful, reducing “mortality by 43% and death
or first hospitalization for heart failure (HF) by 37%” (Anand et al. 2014, 759). Only self-identified
African Americans were enrolled into the A-HeFT clinical trial. This is because the V-HeFT
clinical trials—V-HeFT I which began in 1980 and was completed in 1985 (Cohn et al. 1986) and
V-HeFT II which started in 1986 and ended follow-ups in 1991 (Cohn et al. 1991)—were taken to
suggest that a supposedly pharmacologically equivalent treatment was effective on African
Americans ostensibly. 8 Thus, the A-HeFT clinical trials undertaken from 2001–2004 using BiDil
were taken to be a confirmation of the hypothesis drawn from the V-HeFT trials from a decade
earlier. The A-HeFT studies demonstrated decisively that BiDil has benefits for African
Americans. The reason for suggesting that this finding is not generalisable to other racial groups
relies on claims to differential outcomes in heart disease pathology and its treatment between races
(Lindhorst et al. 2007; cf. Gillum et al. 2012). What these experiments have demonstrated is the
efficacy of the treatment in at least one of these races—namely, African Americans 9 (Temple &
Stockbridge 2007).

A fundamental issue with the claim of the race-specific efficacy of BiDil is that both the V-HeFT
I and II clinical trials did not test or control for race. The claims made for racial differences were
derived through post-hoc analyses of the clinical trial data undertaken years after the clinical trials

7
This publication expresses the official position of the FDA on its reasons for approving BiDil with an indication for
use by African Americans.
8
The FDA later announced that the treatments from the V-HeFT trials and BiDil are not bioequivalent, undermining
and somewhat contradicting their own justification for the evidential support behind the race-based indication of BiDil
and the rationale for embarking on the A-HeFT trial whose design led to the approval of BiDil indicated for use by
one race (Kahn 2007, 215).
9
For the sake of argument, let us take for granted that ‘African American’ can be considered a race rather than an
ethnicity. Let us put to one side that African Americans are generally considered ‘black’ in respect to their race.

9
had taken place. By the time these analyses of the data were made, heart failure statistics across
racial demographics had shifted significantly (Kahn 2013, 77–78). It was through “retrospective
analysis of V-HeFT I and II [that] … an association between race and drug response” was
suggested (Cole et al. 2011, 2415) on the basis of outdated data (Kahn 2013, 79–80). Cole and
colleagues explain:

In V-HeFT I, blacks had a survival benefit from H-ISDN (hazard ratio, 0.53; 95% confidence
interval, 0.29 to 0.98), whereas whites did not (hazard ratio, 0.88; 95% confidence interval, 0.63 to
1.24). Results from V-HeFT II revealed that although whites had a better survival with enalapril
compared with H-ISDN (31% versus 39%; P_0.02), there was no difference with either therapy in
blacks (37% versus 36%; P_0.96). With no placebo arm in V-HeFT II, it cannot be determined
whether the equivalence of the 2 drugs [assumed to be bioequivalent to BiDil] in blacks was due to
a better response to H-ISDN or a worse response to enalapril. It should be noted, however, that
these data are limited by the wide confidence intervals around the effect estimates, and that the
study was not powered to assess noninferiority among blacks. In addition, these were secondary
analyses of observations within clinical trials not designed to address this issue specifically. Hence,
these results may merely represent a chance finding (Cole et al. 2011, 2415; emphasis mine).

The clinical trials and the experimental data produced from them were not designed to show that
BiDil is in any way more efficacious in African Americans than it is in other racial demographic.
To prove the claim of efficacy in only African Americans, the relevant clinical trial would have
needed to have been conducted. It is argued that this was not done because it was too expensive to
run such a clinical trial (e.g., Temple & Stockbridge 2007). This also means that it was too
expensive for the makers of BiDil to prove the claim of the race-specific efficacy of BiDil
scientifically. BiDil, nevertheless, met FDA administrative standards for their claim (Kahn 2013).
Given the suggestive results of the V-HeFT I & II clinical trials—results that may have been
coincidence due to a lack of controls for
establishing such a reading of the data (Cole
et al. 2011, 2415)—there was enough
evidence for the FDA to justify allowing the
A-HeFT trial to commence, and,
subsequently, to approve the use of the drug
BiDil for the demographic group in which it
was tested and demonstrated to be successful
in. That group was self-identified African
Americans (Temple & Stockbridge 2007).
Scientifically, though, there is no concrete
evidence that BiDil’s efficacy is race-
specific because this claim has not been
tested or demonstrated experimentally
Figure 2: This is a frequency histogram showing the according to ordinary scientific standards
percentage of African ancestry in a population in the US (Cole et al. 2011; Kahn 2013).
in “Self-Reported Race and Genetic Admixture” by Sinha
and colleagues (Sinha et al. 2006). The data suggests
Furthermore, since self-identified race is not
that self-identified race can be reasonably accurate
the same as genetic ancestry, we find that
although there are cases where self-identification maps
there are populations which BiDil could be
onto the wrong genetic profile from the one that would
efficacious in despite self-identified race
be assumed given a person’s self-identification.

10
even if the reason for its efficacy is genetic. This raises the question of whether self-identified race
is the correct dimension for the indication of efficacy in the first place and whether race is a
biological factor in its efficacy at all (Kahn 2013).

An assumption of its indication to African Americans is that self-identified race is a proxy for the
relevant genetic profile in which BiDil is efficacious (see Temple and Stockbridge 2007). But the
genetic profiles of African Americans are diverse and US whites can overlap with these profiles.
Individuals meant to be of different races could have profiles which are practically
indistinguishable from one another. This can have the result of cross-classifying self-identified
race with the incorrect genetic ancestry (e.g., see Figure 2). This could mean that BiDil may not
be efficacious on some self-identified African Americans and may be efficacious for some self-
identified US whites. We cannot merely assume the efficacy of BiDil is due to biological
differences and that those differences are distributed along racial lines (self-identified or
otherwise). This is an assumption there is not enough evidence to support (Brody & Hunt 2006;
Maglo et al. 2016). In fact, adding further suspicion to the race-specific efficacy hypothesis of
BiDil, clinicians and researchers from the V-HeFT and A-HeFT trials (and the company that
funded it) have claimed on record that BiDil may be efficacious in other self-identified racial
groups as well (Kahn 2013, 100–103). While “the efficacy of the hydralazine/isosorbide dinitrate
combination [the bioequivalent of BiDil] in blacks is clearly established given the results of the
A-HeFT trial, the lack of efficacy in whites is not” (Bibbins-Domingo & Fernandez 2007, 214).
The claim that BiDil is more effective in African Americans than it is in US whites because of
their belonging to different (biological) races has not been demonstrated empirically and there is
no scientific reason to believe that the efficacy of BiDil is race-specific (Cole et al. 2011; Brody
& Hunt 2006). BiDil cannot be used as evidence for the existence of biological races.

3–2–2. Sickle cell anaemia is not racial: global evidence

McIntyre claims that the prevalence of a disease or a particular trait can be a proxy for a biological
race. He suggests that these patterns in disease occur due to inherent biological differences between
races. He says that “it is well known that certain diseases such as sickle cell anaemia and
thalassemia have different rates of racial susceptibility” and asks “Shall we call this something
other than race?” in light of the fact that these “disease patterns are nonetheless real” (McIntyre
2015, 112; emphasis mine).

The claim reflected here is that being of a particular race makes you more or less ‘susceptible’ to
particular diseases. In this part of McIntyre’s argument, the notion of race is of self-identified race
that is meant to be a proxy for medically relevant genetic ancestry (McIntyre 2015, 112–123). The
example of sickle cell anaemia is meant to support the view that self-identified races have a
biological foundation in the shared genetic ancestry of those races. I will shortly explain why this
is not so.

Individuals have sickle cell anaemia due to having particular genetic traits—i.e., a mutation of the
human hemoglobin (Hb) gene known as sickle hemoglobin (HbS). HbS and its different mutations
are more prevalent in African Americans than in US whites (Piel et al. 2010). This is due to the
general correlation of ancestral origins of individuals that self-identify as US whites and those who

11
identify as African Americans. These identities are associated with patterns of European migration
and displacement through the colonialisation and enslavement of ostensibly Africans (Piel et al.
2010). The underlying biological patterns may not be surprising since genetic studies have shown
that there is a reasonable correlation between self-identified race and genetic ancestry in America
(Sinha et al. 2006; cf. Spencer 2018).

Today, there are five main haplotypical variants of the HbS mutation. These are the “Benin,
Cameroon, CAR [Central African Republic], Senegal, and Arab-India” haplotypes which “are
often called ‘classical haplotypes’, while less common haplotypes are usually termed ‘atypical
haplotypes’” (Piel & Williams 2016, 29). Knowledge of their distribution is limited although it is
known that they are found in varying prevalence in populations in Africa, the Mediterranean, the
Middle East, and India (Piel & Williams 2016, 27–28). These and other derivative HbS mutations
appear in different rates in populations in the USA (Piel et al. 2010; Piel & Williams 2016).

These HbS mutations have varying clinical consequences in different populations (Piel & Williams
2016, 31) and the prevalence of these mutations in populations around the world correlate with the
prevalence of malaria in their ‘founder populations’ (Piel et al. 2010; compare Figure 3 and Figure
4). These would be either three distinct populations in Africa and one in the Middle East or India,
or a single more evolutionarily distant population in Africa (Piel & Williams 2016). 10

What does this mean for McIntyre’s argument that the prevalence of genetic diseases like sickle
cell can be the basis for biologically realist racial classifications? What does this mean if we take
his suggestion that self-identified race can be our guide? It means that ancestry is the key to
dividing up populations into races. But the origins and distribution of sickle cell anaemia do not
match up with self-identified race groups. This undermines McIntyre’s thought that disease
prevalence can indicate racial differences where those racial differences are also supposed to be
genetic and correlate with self-identified racial groups like ‘African American’ or ‘US white’.
McIntyre’s reasoning is erroneous on the grounds that the racial categories themselves are not
biological despite some correlations of self-identified race with some limited set of clinical
outcomes and its limited relationship with some individuals’ biological ancestry in particular
circumscribed circumstances.

On a global level, cross-classification between racial groups would occur if race were to be
delineated by disease prevalence—be it sickle cell anaemia, hypertension, or numerous other
conditions and diseases. There is heterogeneity of risk within, between, and across racial groups
that makes racial classification on the basis of differences in disease prevalence confused (see
Goodman 2000; Valles 2012; Maglo et al. 2016). On one interpretation, accepting ‘sickle cell race’
would mean that McIntyre may have to allow populations from India, Saudi Arabia, the
Mediterranean, and Africa to be considered a race separate from US whites, for example, because
of the differences in HbS distribution. Another interpretation could be that each classical (or even
atypical) HbS mutation is what would delineate a race, meaning that there would be (at least) three
different HbS races in Africa and (at least) one HbS race established in India and the Middle East.

10
Visit The Malaria Atlas Project for data, visualisations, and reports about contemporary trends since the year 2000:
https://malariaatlas.org/

12
 Figure 3: HbS frequency from Piel et al. (2013) Global epidemiology of sickle haemoglobin in neonates:
a contemporary geostatistical model-based map and population estimates, p. 144.

Figure 4: Historical map of global malaria endemicity around 1900 as in Dalrymple et al. (2015, 2).

Neither of these options support the view that the prevalence of sickle cell in different demographic
groups indicates biological group belonging that also corresponds to self-identified race. The case
of sickle cell anaemia does not support what McIntyre mobilized it for: the distribution of this
disease is not evidence of biological racial realism especially for self-identified races. This despite
the different rates of distribution of sickle cell in various self-identified race groups in the US.
Sickle cell anaemia makes nonsense out of a biological racial realism rooted in its prevalence in
different population groups, but this insight applies more generally to correlations between racial
groups and clinical outcomes (see Valles 2012; Maglo et al. 2016).

13
3–2–3. The existence of biological races depends on the differential apportionment of genetic
diversity

McIntyre asks: “We may only be 1 percent different from one another, but shouldn’t science study
that 1 percent?” (McIntyre 2015, 120–121). He suggests that what he says is a 1% difference in
genes between humans is a significant biological difference—one which is only by a small degree
further than the distance between humans and chimpanzees. McIntyre’s presentation of this
statistic is misleading about the meaning of biological differences. 11

McIntyre uses this statistic to imply that the small difference between people in their DNA is a
significant difference that justifies study analogous to how we study small genetic differences
between species. This difference between humans is, indeed, worthy of study and has already
advanced our knowledge in human biology with consequences in areas such as personalised
medicine (see Vogenberg et al. 2010) and human behavioural genetics (e.g., Chamorro-Premuzic
et al. 2011). However, citing this statistic in the context of support of biological race is misleading;
this difference refers to individual allelic differences and does not make comment on population
structure and diversity between such populations (let alone differences arising from gene deletions
or insertions between species). It is only if genetic diversity is distributed in particular patterns
across populations that it is possible to delineate populations as candidates for racial classification
(cf. Edwards 2003). McIntyre bringing attention to the fact that there is diversity among humans
does not help his case because it in no way shows that the distribution of that diversity follows any
pattern we could justifiably call racial – a fortiori, it does not show how self-identified races match
up with these patterns or how they could be biologically real.

It is not clear how the fact that there is biological diversity among humans is meant to support the
idea of biological races in McIntyre’s account, especially biological races that are to generally
correspond to self-identified racial identity. These are, in essence, distinct racial concepts that
would require explication on how they are related if they have any such relationship at all. There
have been more recent attempts at making such formulations by other authors (e.g., Spencer 2019
and Hardimon 2017) although these are not always considered to be successful (e.g., see Jeffers
2019, 178–183 and Hochman 2014 or Hochman 2016).

4. Conclusion

In this paper, I have outlined McIntyre’s view that there is reason to believe that biological races
are real as purportedly evidenced by biomedical facts and clinical outcomes. McIntyre argues that
it is the ideology of left-wing politics that has scientists, philosophers, and the general public
adhere to the idea that biological race is a myth and/or that race is a social construct. His claim is
that such constructionists and anti-realists disregard science as a consequence of their prior
ideological commitments formulated in their liberal politics. It is his view that contemporary
evidence strongly suggests that biological races are real.

11
Initially, it was thought that humans are 99.9% similar to one another but subsequent investigation shows that this
could range from about 99.0 to about 99.9%. Levy and colleagues (2007) present this finding of ≈ 99.5%.

14
My purpose in this paper has been twofold. Firstly, it has been to show that the academic race
debate is not unduly influenced by politics, contra McIntyre. Mainstream constructionist and anti-
realist positions are formulated in agreement with contemporary scientific evidence. The first part
of the paper reinforced the point that in the mainstream debate there is a basic consensus on what
the scientific facts pertaining to racial classification are and that each contemporary metaphysical
position in the mainstream debate accommodates these facts in their theories of race or denials of
race. Secondly, my purpose has been to interrogate McIntyre’s own offering of a biomedical
classificatory scheme of human race. I focused on how the three examples he provides for thinking
biomedical facts support biological racial realism—i.e., the case of BiDil, sickle cell anaemia, and
general human biological diversity—and showed that they do not support his biological racial
realism. I reviewed the reasons why BiDil’s efficacy is not seen to be race-specific. Based on the
evidence of the geographical distribution of sickle cell anaemia, I showed how the geographical
groupings it makes contradict the self-identified race groups McIntyre uses the example of sickle
cell to support. Finally, I argued that the fact that there are biological differences between people
does not tell us how those differences are distributed among populations or what the structure of
this distribution within or between population groups is. The purpose of this second argument is
to show that additional arguments are needed for us to accept some set of biological differences as
constituting a racial difference or that biological races are real. Rather than arguing whether there
really are biomedical races or whether constructionism or anti-realism is right, the purpose of this
paper is to show that McIntyre’s line of argument for biological realism is not convincing.

Although somewhat sympathetic to McIntyre’s project and view that a respect for truth would
mean that evidence-based reasoning must out-weigh politics and ideology, I have argued that he
has not shown that the contemporary race debate is one that has been unduly influenced by political
and ideological commitments. I have made this point by presenting scientific evidence that
undermines McIntyre’s view and have outlined some of the philosophical reasons for why the
claim that race is a myth—particularly the claim that biological races are not real—is a rational
response to the scientific evidence we have regarding race.

References
Adler, Jerry. 2009. “What’s Race Got to Do with It?” Newsweek 12 153.2: 16.
Anand, Inder S., Sithu Win, Thomas S. Rector, Jay N. Cohn, and Anne L. Taylor. 2014. “Effect
of Fixed-Dose Combination of Isosorbide Dinitrate and Hydralazine on All
Hospitalizations and on 30-Day Readmission Rates in Patients with Heart Failure:
Results from the African-American Heart Failure Trial.” Circulation, Heart Failure 7.5:
759–765.
Andreasen, Robin O. 2007. “Biological Conceptions of Race.” In: M. Matthen, M. and C.
Stephens, eds., Philosophy Of Biology (The Netherlands, Elsevier), 455–481.
Appiah, Kwame A. 1996. “Race, Culture, Identity: Misunderstood Connections.” In: K.A.
Appiah and A. Guttmann, eds., Color Conscious: The Political Morality Of Race
(Princeton, NJ, Princeton University Press), 30–105.
Baker, Jennifer L., Charles N. Rotimi, and Daniel Shriner. 2017. “Human Ancestry Correlates
with Language and Reveals that Race Is Not an Objective Genomic Classifier.” Scientific
Reports 7: 1572.

15
Bibbins-Domingo, Kirsten, and Alicia Fernandez. 2007. “BiDil for Heart Failure in Black
Patients.” Annals of Internal Medicine 147.3: 214-215.
Blum, Lawrence. 2010. “Racialized Groups: The Sociohistorical Consensus.” The Monist 93.2:
298–320.
Boghossian, Paul. 2006. Fear of Knowledge: Against Relativism and Social Constructionism.
New York, NY, Oxford University Press.
Brody, H. and Hunt, L.M. 2006. “BiDil: Assessing a Race-Based Pharmaceutical.” Annals of
Family Medicine 4: 556–560.
Brown, Ryan A., and George J. Armelagos. 2001. “Apportionment of Racial Diversity: A
Review.” Evolutionary Anthropology 10: 34–40.
Burchard, Esteban González, Elad Ziv, Natasha Coyle, Scarlett Lin Gomez, Hua Tang, Andrew
J. Karter, Joanna L. Mountain, Eliseo J. Pérez-Stable, Dean Sheppard, and Neil Risch.
2003. “The Importance of Race and Ethnic Background in Biomedical Research and
Clinical Practice.” The New England Journal of Medicine 348.12: 1170–1175.
Chamorro‐Premuzic, Tomas, Sophie Von Stumm, and Adrian Furnham.2011. The Wiley-
Blackwell Handbook of Individual Differences. Edited by T. Chamorro-Premuzic, S. Von
Stumm and F, Furnham. West Sussex, Wiley-Blackwell.
Cohn, Jay N., Donald G. Archibald, Susan Ziesche, Joseph A. Franciosa, W. Eugene Harston,
Felix E. Tristani, W. Bruce Dunkman et al. 1986. “Effect of Vasodilator Therapy on
Mortality in Chronic Congestive Heart Failure”. New England Journal of Medicine 314:
1547–1552.
Cohn, Jay N., Gary Johnson, Susan Ziesche, Frederick Cobb, Gary Francis, Felix Tristani,
Raphael Smith et al. 1991. “A Comparison of Enalapril with Hydralazine–Isosorbide
Dinitrate in the Treatment of Chronic Congestive Heart Failure.” New England Journal
of Medicine 325: 303–310.
Coleman, Michael D. 2010. Human Drug Metabolism: An Introduction, 2nd ed. West Sussex,
John Wiley & Sons.
Dalrymple, Ursula, Mappin, Bonnie, and Gething, Peter W. 2015. “Malaria mapping:
understanding the global endemicity of falciparum and vivax malaria.” BMC Medicine 13
(1): 1–8.
Cole, Robert T., Kalogeropoulos, Andreas P., Georgiopoulou, Vasiliki V., Gheorghiade, Mihai,
Quyyumi, Arshed, Yancy, Clyde, & Butler, Javed. (2011). “Hydralazine and Isosorbide
Dinitrate in Heart Failure. Circulation 123 (21): 2414–2422.
Dalrymple, Ursula, Mappin, Bonnie, and Gething, Peter W. 2015. Malaria mapping: understanding
the global endemicity of falciparum and vivax malaria. BMC Medicine 13 (1): 1–8.
Edwards, Anthony W.F. 2003. “Human Genetic Diversity: Lewontin’s Fallacy.” Bioessays 25:
798–801.
Fofana, Mariam O. 2013. “The Spectre of Race in American Medicine.” Medical Humanities 39:
137-141.
Foster, Morris W. 2009. Looking for race in all the wrong places: analyzing the lack of
productivity in the ongoing debate about race and genetics. Human Genetics 126: 355–
362.
Fujimura, Joan H., Deborah A. Bolnick, Ramya Rajagopalan, Jay S. Kaufman, Richard C.
Lewontin, Troy Duster, Pilar Ossorio, and Jonathan Marks. 2014. “Clines without
Classes: How to Make Sense of Human Variation.” Sociological Theory 32.3: 208–227.

16
Galton, Francis. 1869. Hereditary Genius: An Inquiry into Its Laws and Consequences. London,
Macmillan & Co.
Gannett, Lisa. 2004. “The Biological Reification of Race.” British Journal for the Philosophy of
Science 55: 323–345.
Gillum, Richard F., Alem Mehari, Bryan Curry, and Thomas O. Obisesan. 2012. “Racial and
Geographic Variation in Coronary Heart Disease Mortality Trends.” BMC Public Health
6.12: 410.
Glasgow, Joshua, Haslanger, Sally, Jeffers, Chike, and Spencer, Quayshawn. 2019. What is
race? Four philosophical views. Oxford: Oxford University Press.
Goodman, Alan H. 2000. “Why Genes Don’t Count (for Racial Differences in Health).”
American Journal of Public Health 90.11: 1699–1702.
Gould, Steven J. 1996. The mismeasurement of man. New York & London: WW Norton &
Company, Second Edition.
Hardimon, Michael O. 2013. “Race Concepts in Medicine.” Journal of Medicine and Philosophy
38: 6–31.
———. 2017. Rethinking Race – The Case for Deflationary Realism. US, Harvard University
Press.
Haslanger, Sally. 2000. Gender and Race: (What) Are They? (What) Do We Want Them to Be?
Noûs 34: 31–55.
———. 2012. “A Social Constructionist Analysis of Race.’ In: Resisting Reality: Social
Construction and Social Critique (New York: Oxford University Press), 298–310.
———. 2019. Tracing the socio-political reality of race. In Glasgow, Joshua, Haslanger, Sally,
Jeffers, Chike, and Spencer, Quayshawn (eds) What is race? Four philosophical views.
Oxford: Oxford University Press, 4–37.
Herrnstein, Richard J., and Charles Murray. 1994. The Bell Curve: Intelligence and Class
Structure in American Life. US, Free Press.
Hochman, Adam. 2013. “Against the New Racial Naturalism.” The Journal Of Philosophy 110:
331–351.
———. 2014. “Unnaturalised racial naturalism.” Studies in History and Philosophy of
Biological and Biomedical Sciences 46: 79–87.
———. 2016. “Race: deflate or pop?” Studies in History and Philosophy of Biological and
Biomedical Sciences 57, 60–68.
———. 2017. “Replacing Race: Interactive Constructionism about Racialized Groups.” Ergo, an
Open Access Journal of Philosophy 4.3: 61–92.
———. 2019 (online first). “Race and reference.” Biology & Philosophy 34(32).
Jablonski, Nina G. 2012a. Living Color: The Biological and Social Meaning of Skin Color. US,
University of California Press.
———. 2012b. “The Evolution of Human Skin Colouration and Its Relevance to Health in the
Modern World.” Journal of the Royal College of Physicians of Edinburgh 42: 58–63.
———. 2012c. “Human Skin Pigmentation as an Example of Adaptive Evolution.” Proceedings
of the American Philosophical Society 156.1: 45–57.
Jackson, John P., and Nadine M. Weidman. 2004. Race, Racism, and Science: Social Impact and
Interaction. Santa Barbara, ABC-CLIO.
James, Michael. 2016. Race. The Stanford Encyclopedia of Philosophy, Spring 2016 edition.
E.N. Zalta, ed. http://plato.stanford.edu/archives/spr2016/entries/race/ (Accessed 17 April
2016).

17
Jeffers, Chike. 2019. “Jeffer’s reply to Glasgow, Haslanger, and Spencer”. In Glasgow, J.,
Haslanger, S., Jeffers, C., and Spencer, Q. (eds) What is race? Four philosophical views.
Oxford: Oxford University Press, 176–202.
Kahn, Jonathan D. 2007. “BiDil for Heart Failure in Black Patients.” Annals of Internal
Medicine 147: 215.
———. 2013. Race in a Bottle: The Story of BiDil and Racialized Medicine in a Post-Genomic
Age. US, Columbia University Press.
Kitcher, Philip. 1999. “Race, Ethnicity, Biology, Culture.” In: L. Harris, ed., Racism (Amherst,
NY, Prometheus Books), 87–117.
Lakatos, Imre. 1978. The Methodology of Scientific Research Programmes. Philosophical
Papers, Vol I. Cambridge, Cambridge University Press.
Levy, Samuel, Granger Sutton, Pauline C. Ng, Lars Feuk, Aaron L. Halpern, Brian P. Walenz,
Nelson Axelrod et al. 2007. “The Diploid Genome Sequence of an Individual Human.”
Plos Biology 5.10 E254: 2113–2144.
Lewontin, Richard C. 1972. “The Apportionment of Human Diversity.” In: T. Dobzhansky,
M.K. Hecht, and W.C. Steer, eds., Evolutionary Biology 6 (New York, NY, Appleton
Century Crofts), 381–98.
Lindhorst, Jane, Nicole Alexander, Juliet Blignaut, and Brian Rayner. 2007. “Differences in
Hypertension between Blacks and Whites: An Overview.” Cardiovascular Journal of
Africa 18.4: 241–247.
Livingstone, Frank B., and Theodosius Dobzhansky. 1962. “On the Non-Existence of Human
Races.” Current Antropology 3.3: 279–281.
Maglo, Koffi N., Tesfaye B. Mersha, and Lisa J. Martin. 2016. “Population Genomics and the
Statistical Values of Race: An Interdisciplinary Perspective on the Biological
Classification of Human Populations and Implications for Clinical Genetic
Epidemiological Research.” Frontiers in Genetics 7.22: 1–13.
Mollon, Ron. 2006. “Race: Normative, Not Metaphysical or Semantic.” Ethics 116: 525–551.
———. 2007. “A Field Guide to Social Construction.” Philosophy Compass 2.1: 93–108.
———. 2013. “Naturalistic Approaches to Social Construction.” Stanford Encyclopedia of
Philosophy, Winter 2014 edition, E.N. Zalta, ed.
http://plato.stanford.edu/archives/win2014/entries/social-construction-naturalistic/
(Accessed 15 August 2016).
———. 2018. “Constructing Race: Racialization, Causal Effects, or Both?” Philosophical
Studies 175.5: 1039–1056.
McIntyre, Lee. 2015. “Respecting Truth: Willful Ignorance in the Internet Age.” Oxon.
Routledge.
Msimang, Phila M. 2019. “Racializing races: The Racialized Groups of Interactive
Constructionism Do Not Undermine Social Theories of Race.” Ergo, an Open Access
Journal of Philosophy 6.1: 1–30.
Nazha, Aziz, Karam Al-Issa, B. Przychodzen, Nour Abuhadra, Cassandra Hirsch, J.P.
Maciejewski, and Mikkael A. Sekeres. 2017. Differences in genomic patterns and clinical
outcomes between African-American and White patients with myelodysplastic
syndromes. Blood Cancer Journal 7.9: e602.
Norton, Heather L., Ellen E. Quillen, Abigail W. Bigham, Laurel N. Pearson, and Holly
Dunsworth. 2019 (online first). Human races are not like dog breeds: refuting a racist
analogy.” Evolution: Education and Outreach 12 (17), 1–20.

18
Pearson, Karl. 1919. The Function of Science in the Modern State, 2nd ed. Cambridge,
Cambridge University Press.
Piel, Frédéric B., and Thomas N. Williams. 2016. “Sickle Cell Anemia: History and
Epidemiology.” In: F.F. Costa and N. Conran, eds., Sickle Cell Anemia (The Nethelands,
Springer), 23–47.
Piel, Frédéric B., Anand P. Patil, Rosalind E. Howes, Oscar A. Nyangiri, Peter W. Gething,
Thomas N. Williams, David J. Weatherall, and Simon I. Hay. 2010. “Global Distribution
of the Sickle Cell Gene and Geographical Confirmation of the Malaria Hypothesis.”
Nature Communications 1.104: 1–7.
Pigliucci, Massimo, and Jonathan Kaplan. 2003. “On the Concept of Biological Race and Its
Applicability to Humans.” Philosophy of Science 70.5: 1161–1172. Risch, Neil, Esteban
Burchard, Elad Ziv, and Hua Tang. 2002. “Categorization of Humans in Biomedical
Research: Genes, Race and Disease.” Genome Biology 3: 1–12.
Rosenberg, Noah A, Saurabh Mahajan, Sohini Ramachandran, Chengfeng Zhao, Jonathan K
Pritchard, and Marcus W Feldman. 2005. Clines, clusters, and the effect of study design
on the inference of human population structure. PLoS Genetics 1: 661–671.
Rotimi, Charles N., and Lynn B. Jorde. 2010. “Ancestry and Disease in the Age of Genomic
Medicine.” New England Journal of Medicine 363: 1551–1558.
Sauer, Norman. 1992. Forensic anthropology and the concept of race: if races don’t exist, why
are forensic anthropologists so good at identifying them? Social Science and Medicine
34.2: 107–111.
Sesardić, N. 2010. Race: A social destruction of a biological concept. Biology and Philosophy
25: 143–162.
———. 2013. Confusions about race: a new installment. Studies in History and Philosophy of
Biological and Biomedical Sciences 44, 287–293.
Shiao, Jiannbin L., Bode, Thomas, Beyer, Amber, and Selvig, Daniel. (2012). The genomic
challenge to the social construction of race. Sociological Theory 30, 67–88.
Smedley, Audrey, and Brian D. Smedley. 2005. “Race As Biology Is Fiction, Race As Social
Problem Is Real.” The American Psychologist 60.1: 16–26.
Spencer, Quayshawn. 2015. Philosophy of race meets population genetics. Studies in History and
Philosophy of Biological and Biomedical Sciences 52: 46–55.
———. 2017a. “Racial Realism I: Are Biological Races Real?” Philosophy Compass
13.E12468: 1–13.
———. 2017b. “Racial Realism II: Are Folk Races Real?” Philosophy Compass 13.E12467: 1–
16.
———. 2018. “A Racial Classification for Medical Genetics.” Philosophical Studies 175: 1013–
1037.
———. 2019. “How to be a biological racial realist”. In Glasgow, J., Haslanger, S., Jeffers, C.,
and Spencer, Q. (eds) What is race? Four philosophical views. Oxford: Oxford University
Press, 73–110.
Temple, Robert, and Norman L. Stockbridge. 2007. “BiDil for Heart Failure in Black Patients:
The U.S. Food and Drug Administration Perspective.” Annals of Internal Medicine
146.1: 57–62.
Templeton, Alan R. 1999. “Human Races: A Genetic and Evolutionary Perspective.” American
Anthropologist 100.3: 632–650.

19
———. 2013. “Biological Races in Humans.” Studies in History and Philosophy of Science Part
C: Studies in History and Philosophy of Biological and Biomedical Sciences 44.3: 262–
271.
Valles, Sean A. (2012). Heterogeneity of risk within racial groups, a challenge for public health
programs. Preventive Medicine 55 (5), 405–408.
Vogenberg, F. Randy, Carol Isaacson Barash, and Michael Pursel. 2010. “Personalized
Medicine. Part 1: Evolution and Development into Theranostics.” Pharmacy and
Therapeutics 35.10: 560–562, 565–567, 576.
Williams, Melissa J., and Jennifer L. Eberhardt. 2008. “Biological Conceptions of Race and the
Motivation to Cross Racial Boundaries.” Journal of Personality and Social Psychology
94.6: 1033–1047.
Winder, Isabelle C., and Nick P. Winder. 2014. Reticulate evolution and the human past: an
anthropological perspective. Annals of Human Biology 41.4: 300–311.
Winther, Rasmus G. 2014. The Genetic Reification of “Race”?: A Tale of Two Mathematical
Models. Critical Philosophy of Race 2.2: 204–223.
Yudell, Michael, Dorothy Roberts, Rob DeSalle, and Sarah Tishkoff. 2016. “Taking Race Out of
Human Genetics.” Science 351.6273: 564–565.
Zack, Naomi. 1995. Race and Mixed Race. US, Temple University Press.
———. 2003. Philosophy of Science and Race. US, Routledge.

20