RACISM, NOT RACE

Racism, Not Race

A N S W E R S TO F R E Q U E N T LY A S K E D Q U E S T I O N S

Joseph L. Graves Jr. and

Alan H. Goodman

Columbia University Press

New York
 Columbia University Press
Publishers Since 1893
New York Chichester, West Sussex
cup.columbia.edu

Copyright © 2022 Joseph L. Graves Jr. and Alan H. Goodman

All rights reserved

Library of Congress Cataloging–in–Publication Data

Names: Graves, Joseph L., 1955– author. | Goodman, Alan H., author.
Title: Racism, not race : answers to frequently asked questions /
Joseph L. Graves Jr. and Alan H. Goodman.
Description: New York : Columbia University Press, [2022] |
Includes bibliographical references and index.
Identifiers: LCCN 2021014721 (print) | LCCN 2021014722 (ebook) |
ISBN 9780231200660 (hardback ; alk. paper) | ISBN 9780231553735 (ebook)
Subjects: LCSH: Racism. | Race.
Classification: LCC HT1521 .G678 2022 (print) | LCC HT1521 (ebook) |
DDC 305.8—dc23
LC record available at https://lccn.loc.gov/2021014721
LC ebook record available at https://lccn.loc.gov/2021014722

Columbia University Press books are printed on permanent and durable acid-free paper.

Printed in the United States of America

Cover design: Milenda Nan Ok Lee

For those whose shoulders we stand upon, especially Kazutoshi Mayeda,
Beverly Rathcke, and John Vandermeer (JLG); and George J. Armelagos,
Franz Boas, and Frederick Douglass (AHG), mentors, professors, and
intellectual ancestors who helped us see farther.
 CONTENTS

L I ST O F QU E ST IO N S IX

P R E FAC E XV

Introduction
What Are Race, Racism, and Human Variation? 1

Chapter One
How Did Race Become Biological? 21

Chapter Two
Everything You Wanted to Know About Genetics and Race 42

Chapter Three
Everything You Wanted to Know About Racism 59

Chapter Four
Why Do Races Differ in Disease Incidence? 82

Chapter Five
Life History, Aging, and Mortality 102
 viii
CONTENTS

Chapter Six
Athletics, Bodies, and Abilities 113

Chapter Seven
Intelligence, Brains, and Behaviors 134

Chapter Eight
Driving While Black and Other Deadly Realities of
Institutional and Systemic Racism 158

Chapter Nine
DNA and Ancestry Testing 179

Chapter Ten
Race Names and “Race Mixing” 197

Chapter Eleven
A World Without Racism? 221

Conclusions 237

NOTES  

INDEX 
 QUESTIONS

Introduction
What is race? 3
Race is real and not real? Huh? 3
How many races are there? 6
What do geneticists mean by the structure of human variation? 7
How does human variation come about? 13
If race isn’t biological, how do you explain the differences we see? 15
What is a social construction? 16
What is racism? 18

Chapter 1
Did the ancient Egyptians, Greeks, and Romans have a concept of race? 23
What changed in Spain in 1492? 25
What led to the idea of biological race? 27
Did slavery make race necessary, or did race make slavery acceptable? 30
How could European colonists justify enslavement and the decimation
of native peoples? 31
How did eighteenth- and nineteenth-century scientists turn a folk idea
of race into a scientific concept? Why did these scientists do that? 32
Did the end of slavery change ideas about race? 37
In the twentieth century, were Jews, Italians, and Irish thought to be
separate races? 39
 x
QUESTIONS

Although cultural ideas about the number and types of races change, why
does the fundamental concept—that humans are divisible by discrete
biological groups—persist? 40

Chapter 2
What is the human genome, and how did we come to read it? 43
How much do humans vary genetically from one another and by
population? 45
How do scientists evaluate genetic differences among groups
of individuals? 45
How does the total and apportioned human variation compare with the
variation among Gorillas and other mammals? 46
What explains human genetic differences? 48
Are human genetic differences clustered into geographic areas, or do we
continuously vary, like a weather report of temperatures? 51
Why do some genetic traits correlate with each other, whereas most traits
are independent (not correlated) with other traits? 54
Is there one human species? Can we define subunits within our species?
If so, what do we call them? 56
Why is it that you can almost always tell a Nigerian from a Norwegian, yet
a Nigerian and a Norwegian do not genetically differ that much? 57
Do our social categories of race map onto “biological units”? That is, how
close are our social definitions and ideas about race to some sort of
biological group? 57

Chapter 3
What are the differences among the terms “bigotry,” “bias,” “prejudice,”
“xenophobia,” “ethnocentrism,” and “racism”? How are they defined and
connected? 60
Are there different forms of racism? 63
When did racism begin? 66
What are explicit and implicit biases? 69
Am I a racist if I . . . ? 71
Is there such a thing as kind racism? 72
Is using the “N word” racist? Is it racist if I am white? Is it racist
if I am Black? 73
Is anti-Semitism a form of racism? 73
 xi
QUESTIONS

Is Islamophobia racism? 76
People keep talking about “reverse discrimination,” but what is it? 76
Can anyone be a racist? Can a person with little access to power be
racist? 77
Is white supremacy on the rise, and if so, what’s going on? 78
What is white fragility? 79
What are the differences and similarities between race and caste? 79
What is institutional racism? How do we know that it still exists? 80

Chapter 4
My doctor’s office intake form asks for my age, sex, and race. Why does it
ask for my race? 83
When doctors, epidemiologists, and other medical scientists say that race is
a risk factor, what do they mean? 85
Are there race-specific diseases? 87
Does blood differ by race? Can I donate to or receive a blood transfusion
or an organ from a person of another race? 89
Are certain medicines more effective depending on your race? Should a pill
be color-blind? 92
In the United States, races differ in the rates of the most complex diseases,
such as diabetes, high blood pressure, congestive heart failure, and
cancer. What explains these differences if the genetic differences are so
minimal? 94
Why are results from a bone density test race-specific? 98

Chapter 5
Why do Blacks seem to age slower than whites?
(And is that true?) 104
Why are there more Black than white babies with low birth weight? 107
Does life expectancy vary by race? 110
If races are not biological, why are there such persistent differences in
health among races? 111

Chapter 6
Do races differ in their athletic ability? 114
Are Finns the world’s best athletes? 117
Do Africans run faster and jump higher than Europeans and Asians? 119
 xii
QUESTIONS

Why are there so many African American basketball players and Latin
American baseball players? 123
Are Europeans stronger than Africans and Asians? 126
Are Asians more flexible than Africans and Europeans? 129
Do Africans have thicker bones, extra muscles, or extra tendons? 131

Chapter 7
What is intelligence? 134
Do races differ in their cognitive abilities and intelligence? 135
Is there a genetic basis for intelligence? 136
Do genes associated with intelligence differ among races? 139
Does musical ability differ by race? 143
Do races differ in personality? 144
Do genes associated with personality differ among races? 147
Do genes associated with mental illness differ among races? 148
Do races differ in criminal behavior and violence? 152

Chapter 8
Driving while Black, or, why do African American men get pulled over by
the police more often than others? 160
Why is there a racial difference in incarceration rates? 162
Why is there a racial difference in educational attainment? 167
Does perceived race affect employment opportunities? 171
What is environmental racism? 172
Is there a racial dimension to climate change? 174
Why is there a racial difference in family wealth? 175

Chapter 9
What is ancestry? 179
If race isn’t genetic, how come my DNA test results are telling me my
ancestry? 181
How is ancestry determined by DNA? Are genetic ancestry and race the
same thing? 182
Are some ancestry-testing services better than others? 184
How is ancient DNA (DNA obtained from archaeological and fossil
materials) changing our understanding of human evolution? 187
How can morphology and DNA be used in forensics? 193
 xiii
QUESTIONS

Chapter 10
Why does the United States collect census data by race? 198
Are racial classifications the same in different countries? 200
What is the “one-drop rule”? 202
What do I call persons with African, Latin American, and Asian
ancestry? 203
What will society call my children? 205
Will my children be healthy and good-looking if I reproduce with someone
outside my race? 208
Why do some people say that interracial children are better looking? 210
What does “Caucasian” mean? 211
Are “Jews” a race? What about people of Italian and Irish descent? 213
Am I white? 215
What is white supremacy? 216
What is white nationalism? 217

Chapter 11
How does one become antiracist? 223
Isn’t focusing on race making it even more real? 224
When will we know we have reached racial equality? How do we get to
racial equality? What is postracial? 225
Intersectionality: how does antiracism fit with the fight against other forms
of oppression and social injustice? 235
 PREFACE

In the spring of 2019, when America was on the brink of a racial crisis, we
first discussed collaboratively writing this book. Much has changed and
stayed the same in the last two years. COVID-19 became a global pandemic
in March 2020; we fought about the best ways to “dampen the curve”; as we
write, vaccines are being distributed, and yet, a full year later, we continue to
suffer through the biggest health crisis in a century. Black and brown individ-
uals have disproportionately been infected with and died from COVID-19,
yet another example of racial inequalities that are everywhere and linked to
racism, not biological race.
On May 25, 2020, as we began writing, a white police officer, Derek
Chauvin, casually kept his knee on the neck of a Black man, George Floyd,
for 9 minutes and 29 seconds. Floyd, who had been pleading for his life, was
killed. Among his last words: “please man!” and “Momma!, I’m through.”
Other officers watched without showing emotion. Protests of police violence
against Black men and women spontaneously emerged in thousands of cit-
ies throughout the United States and around the world. Signs proclaiming
“Black Lives Matter”—as if that were a radical idea—adorned lawns.
We also suffered through the presidency of Donald Trump, who was
finally voted out of office on November 3, 2020. He was kicked off Facebook
and Twitter because of his stream of hate filled lies. Yet the racism he brought
to the surface is still with us. The COVID-19 pandemic finally might be slow-
ing, but it, too, exposed existing racial inequalities. Derek Chauvin has been
 xvi
P R E FA C E

convicted of murder. Conspiracy theories intersected with beliefs by the so-

called neo-Nazi (though we are not sure what is neo about them) and white
nationalists, leading to the storming of the U.S. Capitol on January 6, 2021,
with Confederate flags and chants to kill members of Congress and the vice
president. Much has changed, but racism remains.
American society has never been without the idea of race and the reality
of racism, which are linked and part of the founding and foundation of the
United States. In 2016, President Barack Obama hosted a national conversa-
tion on race. His aim had been to transform our understanding of race from
“charged” to “smarter and deeper.” And yet, even with all this talk about
understanding race and combating racism, we never got close to his hope
for smarter and deeper. We never even got to thinking about race as not a
thing but, rather, an idea we made real about humans and their differences.
As a presidential candidate, Trump gained the support of racists and
white supremacists with his railings against Mexicans and Muslims. Close to
a majority of voters approved and elected him later that year. Over the years
of his presidency, Trump and his administration set an example of intoler-
ance that has brought into public view racial hatred and quite possibly has
deepened racial divisions. The FBI reports that hate crimes, of which the
majority are motivated by racism, reached an all-time high in 2018, the last
year for which the agency has complete data.
Witness the tragedy in Charlottesville, Virginia, in August 2017. Thou-
sands of self-proclaimed white nationalists descended on the city to “unite
the right.” Their purpose, they claimed, was to protest the removal of a public
statue of Confederate General Robert E. Lee, but what they did was spew
racist hate. They chanted, torches in hand, “The Jews will not replace us.”
Heather Heyer was murdered when white nationalist James Alex Fields Jr.
drove his car through a crowd of counter-protesters. Then, on October 27,
2018, another white supremacist planned and carried out the killing of eleven
Jews at the Tree of Life synagogue in Pittsburgh. Robert Bowers, the alleged
shooter, had targeted Jews because he believed they were aiding immigra-
tion. Hate crimes against Jews in the United States reached an all-time high
in 2019.
In September 2019, a woman in Atlanta had the “N” word scrawled on
her receipt after dining in a Mexican restaurant. Later that same month,
two white University of Arizona students brutally assaulted a Black stu-
dent. White supremacist massacres are on the rise, including the horrific
mass shootings like the ones at two mosques in Christchurch, New Zealand,
 xvii
P R E FA C E

during Friday prayer on March 15, 2019, and another targeting Mexicans at a
Walmart in El Paso on August 3, 2019.
If 2019 wasn’t bad enough, the horrible killings of nonwhites (specifically
Blacks) intensified in 2020. Months before the murder of George Floyd in
Minneapolis, Ahmaud Arbery was brutally killed by vigilantes in Georgia
while out for a jog, and Breonna Taylor was shot and killed by police in Ken-
tucky as they executed a no-knock warrant on her apartment, apparently in
search of a former boyfriend. Jacob Blake was shot in the back seven times
by a police officer responding to a domestic violence call in Wisconsin on
August 23, 2020.
Meanwhile, less attention-grabbing racial inequalities persist, as repre-
sented in infant mortality and deaths from chronic diseases. Black infants
die at twice the rate of white infants. Hispanic families have less than a tenth
of the wealth of white families. Race is undeniably important from the cradle
to the grave and pretty much every age in between. But what, exactly, is this
powerful idea called race? Even at the height of this crisis, the vast majority
of Americans are left without factual and clear answers to this most funda-
mental of questions. Many even get anxious about using the right name to
designate members of a particular race. Is it Native American or American
Indian? Is it African American or Black?
We get stuck on names and drive into a sort of superficial racial conversa-
tion gridlock. Fewer follow President Obama’s hope and focus on the under-
lying question of what is race and its connections to racism. As individuals
and as a society, we seem to be dazed and confused when it comes to race.
The confusion is deep but also something we can solve if we ask the right
questions and get clear answers.
Most people who are fighting against racism are doing so with their meta-
phorical hands tied behind their backs because they are not clear about what
race is and what it is not. They might know about the history of slavery and
other forms of racism, but they are limited in their knowledge of the history
of the idea of race. Most important, many do not know that the science of
human genetic variation shows with certainty that there are no biological
races. Without this knowledge, it is difficult to confront biases that are based
on biological and genetic myths about race. Knowledge about what race is
and is not is a necessary tool to pull out racism at its roots.
So, how do we win the centuries-long fight against racism and for racial
justice? First, we need to ask the right fundamental questions about race.
Most people, including socially progressive ones, think race is real, and
 xviii
P R E FA C E

they are obviously right. Race is real. But how is race real? Critically, race
is not real in the way most of us have come to think of it: as natural,
fixed, and based on biological differences. Beverly Tatum, psychologist
and former president of Spelman College, says this view of race is akin
to ideological smog that we all breathe every day of our lives. Violent
racists breathe this polluted air. We all do. It is time to stop polluting and
clean it up.
For centuries, it was assumed that the idea of race was founded on bio-
logical differences. But that idea is as wrong as continuing to believe that
the earth is flat or the sun revolves around the earth. Disentangling the idea
of race from the tangible reality of biological variation allows us to see how
this idea of race fuels racism. And it allows us to see that institutions and
everyday racism, not minuscule biological differences among races, explains
the glaring inequalities in infant mortality, life expectancy, and other critical
aspects of life. Understanding what is and is not race can eliminate racial
smog at the source.

It may surprise most readers to hear that, like the overwhelming scientific
consensus on climate change, scientists and anthropologists have for decades
had a clear consensus about what race is and what it’s not. Although the idea
that biological races exist among humans has been completely dispelled, this
advancement in understanding and its implications have somehow failed to
influence the way most individuals think of race. Among other causes, this
lack of public understanding can be linked to the vested interests of a society
that is structured on racism, the inability of some scientists to craft a clear
and appealing antiracism narrative, the conservative nature of science, the
inability of scientists to let go of the dominant paradigm of human races, and
the failure of society to support broad scientific literacy.
Despite the advancement of scientific understanding concerning the rela-
tionship of human genetic variation to conceptions of race, the United States
(and many other countries) seems to be backsliding toward greater racial
misunderstandings and intolerance. Thus, in this work, we hope to impart
three important lessons:

1. Racism created the idea of race.

2. The idea of race has real effects. It gives cover to racism.
3. Human genetic variation is real (and quite wonderful) and is absolutely not the
same as race.
 xix
P R E FA C E

It’s crucial for all of us to know what race is not. Race is not based on biol-
ogy and genetics. Race is not “in the genes,” and it is not the same as human
variation. Racial differences in opportunity and outcomes cannot be blamed
on genetics.
Unpacking this myth of a link between socially defined races and genetic
variation requires an understanding of the relationship among social classi-
fication, evolution, and how human genetic variation is globally distributed.
Our goal in this book is to clearly show what the powerful idea of race is,
how it intimately connects to racism, and how it has been falsely linked to
biological variation. Once these lessons are understood, we can dispel many
myths about race associated with, for example, health, athletic ability, and
intelligence, and present a path for living in a more just and equitable world.
Because contemporary myths about race have their roots in the concept’s
history, we will help readers to add context to what race is and what it is not
by stepping into the fascinating history of the idea of race, one akin to an
emperor with no clothes (which, incidentally, is the title of Joe’s first book on
this topic). We then bring our discussion up to the present and look ahead to
a more equitable and just future. We recognize that this is no small feat. But
in small portions it is easy—and liberating—to understand.
Between the two of us, we’ve taught and written on race, racism, and
human genetic variation for almost a century. Here we provide concise and
accessible answers to the questions about race and racism that routinely
come up during our conversations with students, educators, policy makers,
friends, family, and the public.
This book is for people who want to work toward human equity and those
who are nervous about saying the wrong thing. In many cases, the two groups
overlap. We hope to encourage readers to have deeper and factually correct
conversations concerning race, racism, and human variation. As we discuss
in the following pages, this is a conversation that we dare not get wrong.
Throughout the book, readers will encounter different schemes for defining
socially designated racial groups. For example, the U.S. Bureau of the Census
uses terms such as white, Black or African American, American Indian or
Alaska Natives, Asian, and Native Hawaiian or Pacific Islander (see chapter 10).
These terms might be familiar to most people but can also be misleading.
Some schemes of racial definition use colors (black, brown, red, white, yel-
low), whereas others utilize variants of nineteenth-century anthropological
and fake science categories (Caucasian, Mongoloid, Negroid). Whenever
possible we adhere to the principle of parallelism when we describe socially
 xx
P R E FA C E

defined racial groups. So, if we say Black, all other groups discussed in that
section will be described in the color scheme system. In addition, because
we cite examples from primary disciplines (anthropological, biomedical,
genomic, historical, and sociological research), material from those cita-
tions will use the terms employed by those authors. Throughout this work
we provide readers with examples that illustrate the limitations of all of these
schemes when they are used to describe human biological variation. Finally,
the confusion arising from the various schemes and names and numbers of
races is also further evidence that there are no biological races. Furthermore,
it is proof of the chameleon-like nature of race, which changes its appearance
to fit the needs of those with political power.
Finally, we use technical language because a good many of the terms carry
an important precision. Whenever possible, we define the terms so that they
are clear to the reader. As well, a number of online glossaries are available,
including the National Human Genome Research Institute’s Talking Glos-
sary of Genetic Terms (https://www.genome.gov/genetics-glossary), Ameri-
can Anthropological Association’s public education project on race (https://
understandingrace.org/Glossary), PBS’s Evolution Glossary (https://www
.pbs.org/wgbh/evolution/library/glossary/index.html), and the Dictionary
of Anthropology (http://www.anthrobase.com/Dic/eng/).

ABOUT THE AUTHORS

This is the first time that Joe and Alan have written together. We took the
leap because of our mutual goal of increasing public understanding about
what race is and is not and how race interrelates with racism and does not
explain human variation. Our personal stories, positions, and training are
mutually complementary. Alan approached Joe with the idea for a question-
and-answer book. Joe had already been considering such a format.
We have lived thousands of miles apart and have led very separate and
distinct lives, but we came to share deep concerns and commitments. Each
of us grew up in the 1960s and came into our chosen academic fields in the
1970s and ,80s. Different paths led us to our present positions as senior aca-
demics and scientists. We have always shared a commitment to science and
social justice.
Alan’s parents lived valiant lives. They were working-class Jews who
strived to live decently. Alan’s dad was a refrigeration mechanic who loved
ideas and hated bigotry, and although he surely faced it, he never talked
 xxi
P R E FA C E

about anti-Semitism. His mother was silent until near her final days about
her own mother’s life, including how she escaped to the United States after
being brutally tortured, part of a routine Russian pogrom.
Alan, a couple years older than Joe, grew up in Quincy, Massachusetts, a
suburb of Boston. In the 1960s, shipbuilding was the main industry there.
Quincy was composed mainly of Irish and Italian families. Alan’s dad was a
World War II veteran and came home to marry, start a family (of five chil-
dren), and train to become a refrigeration mechanic and a member of the
pipefitter’s union. Growing up, Alan was well aware of his duality as a work-
ing-class kid, along with most of his friends, and a Jewish kid, unlike his
Catholic friends. Alan became much more aware of the salience of his white
skin privilege when he went to college.
Joe lived racism. His mother and father survived Jim Crow in Virginia.
His father landed on Utah Beach in 1944, participated in the battles to lib-
erate France and the low countries, and was in the Arden Forest during
the Battle of the Bulge. He helped to build a bridge across the Rhine and
was decorated three times. Still, when he came home to America, jobs and
other opportunities were denied him due to his race. Joe’s mother was “the
help,” and after she cleaned the homes of wealthy women during the day, she
worked in a plastics factory at night. Joe’s background made him an unlikely
candidate for becoming a scholar in evolutionary biology.
Joe is an evolutionary biologist (the first African American to earn a PhD
in this field). His primary research concerns the genetic basis of adapta-
tion. His research training was “pre-adapted” to understanding the nature
of biological variation within species. This phenomenon is the basis of all
biological conceptions of race. Thus, it was easy for him to see the utter
lack of concordance between social characterizations of race and the actual
distribution of biological variation within our species. As an African Ameri-
can, Joe has lived experience as a racially subordinated person in the United
States. This has informed his understanding of both the conceptual basis and
actual practice of racism.
Alan is a biological anthropologist with a deep interest in both the history
of racial science and the details of the science. His perspective is that one can
critically evaluate racial science on two intersecting levels: in context and on
its own terms.
At the contextual level, one can evaluate the reasons a study might have been
written and its assumptions. If one is taking time to measure the size of skull dif-
ferences among races or testing a drug on different races, then one assumes that
 xxii
P R E FA C E

this question is important and that there is an assumption that race is a mean-
ingful biological category. One can also ask, “What does this study do for us?”
At the scientific level, one takes the study at face value, assumes that the
assumptions are justified, and then evaluates the study purely as a piece of
science. Questions one might ask include whether the methods are sound
and if the conclusions follow from the results.
Alan learned about the myths of race as an undergraduate and early in
graduate school. Back in the early 1970s, he assumed that the destructive idea
of race—an idea used against Jews and Black and brown peoples—would go
away. Don’t flawed explanations, like phlogiston and the homunculus, go on
the scrap heap of dead scientific ideas when proven wrong? But he did not
realize the power that race held. And so he began to study race science in
the early 1990s.

ACKNOWLEDGMENTS

Any book is a project of both solitary efforts and a network of supporters. We

would like first to acknowledge those who have helped envision this book
and bring it to press. Beth Vessel and Callie Deitrick found this book a sup-
portive home during the pandemic with Columbia University Press. That
was no small feat! Fiona Marks, Hampshire College undergraduate, helped
with references and proofreading. Eric Schwartz, editorial director, and his
staff at Columbia University Press have been thoroughly responsive and have
greatly improved the accessibility of the book.
Joe would like to acknowledge his students from his evolution, genetics,
and anthropology courses. Their questions helped clarify his thinking. Joe
dedicates this book to those whose shoulders he has stood upon, especially
Beverly Rathcke (1945–2011), who taught him how to be critical of received
scientific knowledge; John Vandermeer, who taught him that biology could
be a social weapon; and Kazutoshi Mayeda (1928–2008), who pushed him to
better understand human genetics.
Alan also wishes to acknowledge the colleagues who have been in front of
and beside him in his efforts to teach a nonracial approach to human varia-
tion and the compatibility of good science and social justice. These include,
but are certainly not limited to, Michael Blakey, Joseph Jones, and Yolanda
Moses and the many colleagues who worked with him on the AAA public
education project on race (understandingrace.org).
 xxiii
P R E FA C E

Alan also wishes to express his thanks to those who helped him think in
creative ways about how to express scientific information and ideas while
working together on the PBS documentary Race: The Power of an Illusion
and the AAA traveling exhibit on race and, most recently, the RaceGen list
server. These include Robert Garfield, Joanne Jones-Rizzi, Larry Adelman,
Llew Smith, and Christine Sommers. Many other colleagues have supported
him throughout his efforts to educate people about race, racism, and human
variation, including Clarence Gravlee, Ricardo Santos, Faye Harrison, Leith
Mullings, Audrey Smedley, Agustin Fuentes, Ken Kidd, Brooke Thomas,
Ann Mourning, Lynn Morgan, Thomas Leatherman, Troy Duster, Char-
maine Royal, Alondra Nelson, Nancy Krieger, Deborah Bolnick, Jonathan
Kahn, Evelynn Hammonds, and Jon Marks. George Armelagos taught him
that science could be fun, fulfilling, and relevant.
Alan also wishes to acknowledge his parents, whose humility and bravery
taught him more than they will ever know. It has been a pleasure for Alan
to write this book with Joe Graves. He is humbled and honored. This book
would absolutely not be possible without the love and support of Alan’s wife
and daughter, Chaia Heller and Ruby Heller-Goodman.
RACISM, NOT RACE
 Introduction

WHAT ARE RACE, RACISM, AND

HUMAN VARIATION?

A few years ago, a student of African descent came into Joe’s office worried
that she had scleroderma, a chronic connective tissue disease that is gen-
erally thought to be part of the family of autoimmune rheumatic diseases.
She sounded confused and told Joe that her doctor would not diagnose her
disease as such. She recalls her doctor saying something about “Black people
not getting scleroderma.”
Marta, a fifty-something-year-old colleague of Alan’s, has Native Ameri-
can, European, and African ancestry. Like two-thirds of the people in the
world and all other mammals, she is lactose intolerant because she does not
produce sufficient lactase, the enzyme that digests lactose. Thus, she avoids
consuming dairy products. Because of her restricted diet, Marta feared that
her calcium intake was low and that it might put her at risk for osteoporosis.
She raised her concerns with her primary care physician and asked if he
would order her a bone density test. Her doctor responded that she didn’t
need one because she is Black, and Blacks do not get osteoporosis.
Despite their intensive medical training, these two doctors made a com-
mon error. They made judgments about their patients’ race based on their
“looking Black.” Black, that vaguely defined group, is culturally real and vis-
ible in our society and to the medical profession. “Black” or “African Ameri-
can” is what we call the members of a group who were not long ago referred
to by other terms, such as “Negro.” And who is Black, or of any other race,
has always been poorly defined. But that Black is socially salient, an indexed
group, is certain. Medical textbooks are chock full of statements about
 2
INTRODUCTION

different rates of disease by race: Black is a “risk group.” Even the thoroughly
outdated “negroid race” is still a medical search term.
Regarding scleroderma, a pamphlet from the Scleroderma Foundation
proclaims that “race and ethnicity may influence the risk of getting sclero-
derma,” and the website Sclero.org states, “Factors that may incline a person
to develop scleroderma include race, ethnicity, and geography.” Regarding
osteoporosis, echoing lots of medical textbooks, the popular website WebMD
states, “Research shows that Caucasian and Asian women are more likely to
develop osteoporosis than women of other ethnic backgrounds. Hip frac-
tures are also twice as likely to happen in Caucasian women as in African-
American women.”
So, as Alan’s friend and Joe’s student looked Black to their doctors, the
physicians decided to not offer a diagnosis and not treat the women because
they thought that the risk of disease was diminished because the patients
were Black. These two medical care errors take us from social classifications
of race—specifically, “Black” in these cases—to genetic differences among
individuals—what we will refer to later as the amazingly interesting global
structure of human genetic variation—and its significance for disease risk.
These physicians’ faulty assumption that human genetic variation is pat-
terned along socially defined race or color lines is deeply embedded in how
nearly everyone, including the vast majority of doctors, think about race. We
see similar slippages in the day-to-day events and decisions made in hospi-
tals, schools, banks, courts, and other institutions. A system of ideas that
links race and human genetic variation underlies the fraught interactions
we witness every day. This is a huge scientific error, because social classifica-
tions of race change over time and place. They are unstable. And all known
social classifications fail to map onto genetic variation. This easy conflation
of social race with genetic variation is the most consequential error of how
we have thought and continue to think about race.
In this introductory chapter, we do an initial unraveling of the problem-
atic connections between the social categorization of race and the realities of
human genetic variation. We explore how the mythic idea of biological race
within our species continues to give ideological cover to racism. So, what
better way to start than with the big three questions we encounter in the
classes we teach, in the presentations we give, and in our own lives:

What is race?
What is human genetic variation?
What is racism?
 3
INTRODUCTION

We will also discuss how these concepts have been falsely connected and
how they should be connected.

WHAT IS RACE?

Here is our short definition: race is a worldview and social classification that
divides humans into groups based on their appearance and assumed ances-
try, and that has been used to establish social hierarchies. Our definition is
that of social race. Race is a social classification based on assumptions about
ancestry and appearance. Socially defined races are unstable categories in
that definitions, names, and color lines change. Nonetheless, social race is
very real, as exemplified by differences in wealth and health.
Many still think that the way we classify race in humans is fundamentally
biological. However, that race, what we call biological race, does not exist in
our species. It is a long-standing myth that provides cover for racism. But
race is real as a social category.

RACE IS REAL AND NOT REAL? HUH?

Nearly everyone is confused about what race is and what it isn’t. Parents,
pollsters, principals, and politicians are confused. People of all skin colors,
ethnicities, classes, and religions are confused. If you are, too, you’re not
alone.
Part of the problem comes from the fact that what everyone, including
scientists, thinks race is has changed over time. Moreover, we have never
had a clear and broadly accepted definition or even known what should be
part of the definition.
A first dip into history. Carl Linnaeus (1707–1778) was one of the first in
a long line of scientists to try to define and classify races. He was a Swed-
ish naturalist who lived in Uppsala, just north of Stockholm, and is consid-
ered the father of modern taxonomy, the science of classification. Linnaeus
invented the modern binomial nomenclature that separated all living things
into species and genus, and then lumped species and genus into broader
categories. For example, we now agree that we are all part of the genus and
species Homo sapiens and are part of the order Primates, along with chim-
panzees, gorillas, orangutans, monkeys, and prosimians.
Linnaeus traveled at the beginning of his career but mostly relied on oth-
ers to send him descriptions of plants and animals (and better yet, samples
when possible). Linnaeus believed that he was put on earth to classify God’s
 4
INTRODUCTION

creations and took as his modest motto, Deus creavit, Linnaeus disposuit
(“God created and Linnaeus organized”). His creation of the binomial sys-
tem of classification was quickly and widely regarded as a great scientific
advance. Philosopher-naturalist Jean-Jacques Rousseau said, “I know of no
man greater on Earth.”
Linnaeus wrote a number of editions of Systema Naturae (Systems of
Nature). His first, published in 1735, and his tenth, released in 1758, expanded
his thoughts on the taxonomy of humans. He called humans Homo sapiens,
as we still do, and divided us into varieties based on the information he
received from travelers. He included categories of monstrous and wild men
that later could not be confirmed as human. He also included four continen-
tal and scientific-sounding varieties of human: Europaeus, Asiaticus, Africa-
nus, and Americanus. Linnaeus described them all by color, temperament,
and governance. For example, Europeaus was white, clever, and ruled by law,
and Americanus was red, free, and ruled by custom.
These ideas about each variety morphed into what eighteenth-century
naturalists came to think of as subspecies and races. That idea is based on
two underlying notions: stability of type and hierarchy. These notions of sta-
bility and hierarchy continue to undergird racist ideologies today and are
elements of the pervasive racial smog that we all breathe.
Working within the Platonic system of imagining that all things, living
or inanimate, have distinct attributes, Linnaeus and other naturalists con-
sidered each race as similar to other things, each with its own essences and
specific traits. The idea of race was founded on the notion of an unchanging
earth created by God, so that what is now has always been.
The aspect of hierarchy is traced to the doctrine of a great chain of being,
which began with the Greeks and was later adopted by Christians. All crea-
tures were arranged in order of their relative closeness to God. Linnaeus’s
job was simply to describe and put these things in order. God created, and
Linnaeus classified.
Importantly, the idea of race is interwoven with colonization and slavery.
Vilifying reports about newly encountered peoples from colonizers and sla-
vers often made their way into Linnaeus’s classification. And his classifica-
tion looped back and lent scientific support for slavery and colonization.
Having bent science to their side, the aristocrats of Europe adopted a view of
slavery and colonization as just and inevitable. Africans were seen as inher-
ently incapable of governing themselves, and Native Americans were not
God’s children. That formulation of race was invented and quickly accepted
 5
INTRODUCTION

because it provided a scientific cover for colonization, plundering, and slav-

ery. The institutional racism of slavery and colonization gave vitality to the
essentialist biological race concept. More briefly: racism made race.
Of course, in the end, the science of putting humans into discrete races
failed because humans cannot be divided into convenient color categories
or biological races (see chapter 3 for details). But that critical fact has done
little to derail the essentialist view of human variation that still fuels viru-
lent racists and unfortunately is still the primary way in which most people
understand race and human biological variation. It was behind the enslave-
ment of fifteen million Africans. It was behind the murder of six million
Jews in Europe. It was behind the murder of eleven individuals, including
a Holocaust survivor, at the Tree of Life Synagogue in Pittsburgh in 2018;
the Christchurch mosque murders of fifty-one people in March 2019; the
murder of twenty-two people, mostly Mexican Americans, at a Walmart in
El Paso in August 2019; and the violent storming of the U.S. Capitol on Janu-
ary 6, 2021.
These views of race as biological, innate, and hierarchical are not limited
to eighteenth-century plantation owners, Nazis, and twenty-first-century
white supremacists. Most people believe that something innately genetic
makes each race unique. Indeed, a recent survey of more than sixteen hun-
dred Americans demonstrated that the vast majority of individuals felt that
race was both a social category and based on biological attributes.
Thus, nearly six decades after the passage of the Civil Rights Act of 1964,
views continue that align with eighteenth-century pre-Darwinian and myth-
ical thoughts that racial differences are natural and that some races are supe-
rior to others. Laws can change suddenly, as with the Civil Rights Act, but it
takes much longer to change worldviews, especially those that support the
status quo.
In a democratic society, changing laws is a long and complex process.
Serious struggle ended slavery and led to the passage of the Civil Rights Act
a century later. Yet, as hard as it is to change laws, it is even harder to change
how citizens think and what we all believe in. And beliefs are difficult to
change when they come with deep investments. Indeed, the growing polar-
ization we are observing in American society is associated with the fact that
people hold to different systems of what they believe to be the truth.
So, race as a worldview and social classification divides humans into
groups based on assumptions about their appearance and ancestry. It came
about as a justification for colonization, appropriation of land and goods,
 6
INTRODUCTION

and enslavement. Before scientists got involved, race began as a folk idea
about differences between and fears of the “other.” Racial thinking was likely
to be a form of ethnocentrism, the belief that one’s society and culture is
superior to those of others.
What’s unique about race is that scientists made race real through their
pseudoscientific studies purporting to show that races were biological units
and that differences between races were immutably based on biological dis-
tinctions. This process of trying to make something seem real by constant
use—especially when supported by those with authority, such as scientists—
is called reification. Biological race, even though it is fiction, became rei-
fied. It came to be seen as unquestionable and real. Biological races are a
myth. Throw them on the scrap heap of dead scientific ideas. But social race
lives on.

HOW MANY RACES ARE THERE?

If by “race” we mean clear and logical divisions in the human species based
on evolved genetic differences, then there are no races. Human beings are
simply not divisible into unambiguous biological races. Why this is true is
explained in chapters 3 and 9.
If, on the other hand, we see race as a social classification, then the answer
to “How many races are there?” is, “It depends.” It depends on one’s goals.
For example, the number of races in the Brazilian census is different from
the name and number of races in the U.S. census. This is due to different
histories and different configurations of social and political importance of
the race concept in each country. Moreover, the number of races and how
we refer to them also changes over time. For example, in the U.S. Census of
1790, only five categories were enumerated: Indians, free white males, free
white females, all other free persons, and slaves. In the 1850 census, the race
categories were Indian, white, black, and mulatto. What’s most striking at
the time when slavery was being challenged is the addition of “mulatto”—a
person of both white and black parentage. In 2000, the following catego-
ries were recognized: white, Negro or black, Japanese, Chinese, Filipino,
Korean, Vietnamese, American Indian, Asian Indian, Hawaiian, Guama-
nian, Samoan, Eskimo, Aleut, and Other (specify).
In Brazil, efforts have been made to track individuals by skin color, and
this reflects the fact that admixture (reproduction between people of differ-
ent geographic ancestries) has been much greater in that country than in
 7
INTRODUCTION

the United States. Brazilian categories today include brancos (white), pre-
tos (black), and pardos (mixed or multicultural) and are designed to cap-
ture degrees of mixing among Europeans, Africans, and indigenous South
Americans.
The U.S. census and the Brazilian census are but two examples highlight-
ing the fact that official racial classifications are unstable. They bend to meet
the needs of those in power. In addition, racial terms in common use are
even more fluid. The assumed definitions of the categories also change. The
criteria for inclusion of an individual in a race is both fluid and ill-defined.
This is particularly problematic in scientific studies, in which reliability, the
ability of different researchers and the same researcher to classify individuals
in the same way over time, is paramount. Without reliability, race science is
a version of junk in, junk out.
Witness the racial category of European or white. In 1939, Carleton Coon,
distinguished professor of anthropology at Harvard, wrote in The Races of
Europe that there were eighteen or so European racial types. He mapped
out and described the biological characteristics of groups such as Lappish,
Nordic, Dinaric, Alpine, Baltic, Upper Paleolithic Survivors in Ireland,
Long-Faced Mediterraneans, Armenoids, and Jews. After the horrors of the
Holocaust, many of the groups that were not fully considered to be white
by American Anglo-Saxons began to be more fully accepted as white. Yale
historian Mathew Frye Jacobson refers to these groups as whites of a differ-
ent color.
Race is a flexible classification because the salience of social categories
changes over time and place and with different needs. In other words, race
is a chameleon; it changes to fit different social and political environments.
That makes sense for a social concept. However, this instability of racial clas-
sification makes it impossible to generalize. That flexibility is also not accept-
able for a scientific classification, as all classifications depend on consistency
of reliability classification. Finally, social races do not map onto any sort of
genetic divisions.

WHAT DO GENETICISTS MEAN BY THE STRUCTURE

OF HUMAN VARIATION?

A key question, maybe the key question, is whether the concept of race
describes or explains biological differences within our species. To get to that
question, here we will take a first step into the world of science and come to
 8
INTRODUCTION

understand what scientists mean by the term “structure of human variation”

and then how variation comes about.
People are unique. To understand the reality of biological variation, all
you have to do is look at the people around you in a room or on a street. No
two individuals look the same. Even genetically identical twins have subtle
differences that parents discover and use to tell them apart. Indeed, we have
learned that identical twins differ in non-nucleotide-based genetic variation
(epigenetics). These epigenetic differences can lead to sometimes large dif-
ferences in traits, such as twins’ predisposition to and severity of disease.
A recent example is shown by identical twins who developed dramatically
different levels of illness when infected by COVID-19.
Humans are a highly visually aware species, and we home in on the
incredible variety of observable appearances in skin tone; hair length and
style; nose, eye, mouth, and ear shapes; height and body shapes; and even
how a person stands and moves. There are also many differences that require
special instruments to uncover, such as blood pressure and blood type, along
with a host of other physiological, metabolic, and genetic traits. Evolutionary
geneticists study how variations change over time, and population geneti-
cists study how variations are patterned or structured within individuals and
among individuals and groups.
By “structure of human variation” we mean two interrelated things. The
first is the pattern of variation among traits within individuals. For example,
height and weight are strongly related, or correlated, whereas height and
blood types are not. The second meaning refers to the pattern of differences
and similarities among humans at three levels: among individuals within a
group, among groups, and among purported races. One issue we encounter
is that what is meant by group—or, biologically speaking, a population—and
especially by race, is not consistently defined. As noted earlier, groups and
especially races are poorly reproduced. A group, for example, could be an
ethnicity or a country. We know from the previous discussion that these
groups and populations are socially defined and that the criteria for who is
in and out change through time. Definitions and group memberships are
unstable.
That caveat aside, the structure of variation is, in a sense, about levels of
variation: within an individual, among individuals within a group, among
groups, and among purported races and across the globe. A key test of the
salience of race is the amount of variation that exists among socially defined
races. As we will illustrate, it is shockingly small.
 9
INTRODUCTION

There is another distinction we want to introduce before moving on:

genotype versus phenotype. A phenotype is a fancy word for any observable
trait or characteristic. This includes visible and easily measurable traits, such
as height, and also more complex characteristics, like personality and musi-
cal ability. Are you a dog person? Do you like games? Are your eyes glazing
over? These are all phenotypes.
Some phenotypes are strongly determined by development and aspects of
the environment, and others are fundamentally due to the genes you were
born with. And the vast majority are a complex mix of genotypes, environ-
ments, and interactions of genotypes and environments.
Genotype refers to the composition of your deoxyribonucleic acid
(DNA). You’ve probably heard that our genomes are composed of DNA, a
long molecule that has the shape of a double helix. DNA itself is a string of
nifty chemicals called nucleotides that point inward and are held together by
strong hydrophilic (water-loving) forces. The four nucleotides of DNA are
adenine, thymine, cytosine, and guanine, abbreviated to A, T, C, and G. The
A’s and T’s are always paired, and the C’s and G’s are always together.
The full human genome contains about 3.3 billion nucleotide letters. Some
of the genome codes for amino acids: a sequence of three nucleotides in a
row (triplets) corresponds to one of the twenty-three naturally occurring
amino acids. The amino acids are assembled into proteins. Some proteins
make crucial structures such as collagen, and others are enzymes and cata-
lysts that promote vital biochemical reactions that keep us going. Proteins
are absolutely critical to life and thus so are the amino acids that make up the
sequential structure of proteins and so are the nucleotides that code for the
amino acids. But of course, life is also more than nucleotides, amino acids
and proteins.
Let’s briefly consider height as an illustration of the structure of a phe-
notypic variation. Height varies among individuals within a group, and
the average height differs slightly among groups and has varied over time.
These are all measurable facts. We do not know much about height variation
among socially defined races, because the groups and individuals in each
socially defined race change. For example, in America, “Black” is culturally
defined as anyone with detectable African ancestry; in Puerto Rico, the term
denotes anyone who has no European ancestry; and in Britain, it can include
anyone who isn’t a European.
Individual height is highly heritable (an estimated 80 percent deter-
mined by genes). More than 180 genetic loci have been found to have
 10
INTRODUCTION

significant effects, and thousands more are known to have some effect
on height. At a more complex level, height is influenced by environmen-
tal factors such as early life nutrition and pollution. While we do not
know the exact cause of the changes, in recent years, the Dutch have far
surpassed Americans in their average height, and the children of first-
generation Koreans now have average heights equivalent to those of Amer-
icans, even though the parents of that generation had average height less
than that of Americans.
What about variation in genotypes? First, all human beings are identical
at about 99.9 percent of the DNA nucleotides. There are differences at an
average of only about one of every thousand letters.
Consider these random changes in a passage from Harriet Beecher
Stowe’s Uncle Tom’s Cabin. The first three passages show single-letter changes
(mutations) in different words. The fourth shows a deletion of an entire
word, “old.” Note that the fourth sentence still makes sense despite the loss
of the word; if the word “sobbing” had been lost, the sentence would make
less sense.

Passage 1: “O, now, don’t—don’t, hy boy!” said the old man, almost sob-
bing as he spoke.
Passage 2: “A, now, don’t—don’t, my boy!” said the old man, almost sob-
bing as he spoke.
Passage 3: O, now, don’t—don’t, my boy!” said the old man, almost sob-
bing as he spjke.
Passage 4: O, now, don’t—don’t, my boy!” said the man, almost sobbing as
he spoke.

Now let’s move this analogy from a book to the human genome. As noted
earlier, our genome contains approximately 3.3 billion nucleotides. Of these,
about 10 million differ between any two individuals, thus making each indi-
vidual unique. Below is an example of a random change in a DNA sequence.
The sequences of the three individuals show single changes relative to one
another. Given that each set of three nucleotides (or triplets) codes for amino
acids in the protein resulting from the sequence, we have shown the amino
acids that would result from each sequence.
 11
INTRODUCTION

Individual 1 DNA: ATG GGA TTC AGA GGG CCG TCA TAG
Amino acids: methionine, glycine, phenylalanine, arginine, glycine, pro-
line, serine, stop code.
Individual 2 DNA: ATG GGC TTC AGA GGG CCG TCA TAG
Amino acids: methionine, glycine, phenylalanine, arginine, glycine, pro-
line, serine, stop code.
Individual 3 DNA: ATG GGA TTC AGA GGT CCG TCA TAG
Amino acids: methionine, glycine, phenylalanine, arginine, glycine,
proline, serine, stop code.
Individual 4 DNA: ATG GGA TTC AGA ___ CCG TCA TAG
Amino acids: methionine, glycine, phenylalanine, arginine, proline,
serine, stop code.

The DNA sequence change between individuals 1 and 2 does not change
the amino acid sequence. This is because the triplet code is redundant with
64 possible codes for only 23 naturally occurring amino acids, along with
one start and three stop codes. Notice that the changes between the first
three individuals’ DNA sequences did not change the resulting amino acid
sequence. However, the fourth individual is missing an entire triplet, result-
ing in the loss of the amino acid glycine in the final protein sequence. The
loss or change of an amino acid in a protein often has severe consequences,
as in the case of the mutation that causes sickle cell anemia, where glutamic
acid is replaced by valine.
Recognizing that individuals differ in their DNA also raises the question
of whether those differences are associated with membership in a “race.” In
other words, could the ~3.3 million nucleotide differences be used to neatly
define racial groups within our species? It turns out that the answer is “no.”
A quick way to understand this is to break down the approximately 10 mil-
lion nucleotide differences by geography: worldwide, by continent (Africa,
Americas, Asia, Europe, and Oceania), and by regions within the continents
(see figure 0.1). Genetic variations are most often shared throughout the
world. Others are specific to local environmental conditions. For example,
genes associated with resistance to malaria (e.g., blood group O and glu-
cose six phosphate deficiency) occur in higher frequency in zones where
malaria transmission is still common (the tropics, including sub-Saharan
 12
INTRODUCTION

100

Percentage of total genetic variation 90

80

70

60

50

40

30

20

10

0
From the same Among populations From different
population on the same continents
continent

FIGURE 0.1. Of the roughly ~3.3 million genetic variants, the vast majority are found within the same local
group or population, and a small percentage is found among populations within a continent and among con-
tinents. Moreover, the variation among populations and continents is attributable to geographic distance, not
race. Source: Courtesy of George Armelagos.

Africa, the Middle East, and India). Genes associated with lactose persis-
tence occur at higher frequencies in populations that domesticated cattle
(northern Europeans and East African Masai). There are also genes that help
populations survive at high altitude (such as observed in Ethiopians, Tibet-
ans, and Andeans).
Finally, for an example of pattern of variation among traits within indi-
viduals, let’s consider height, weight, and hair color. Traits having to do with
color tend to be correlated. Similarly, traits having to do with size, such as
height and weight, also tend to correlate. However, size traits are not cor-
related with color traits, and color and size traits are generally not correlated
with any other traits. The pattern of independence is the factual rule, and it
is important. It should cause us to exercise great caution about extrapolating
from a single trait, such as skin color or, really, any single trait.
In summary, variation includes genotypes and phenotypes. Although we
are all unique, and we certainly look unique, genetically, humans are rather
homogeneous. Most of that tiny genetic variation is found within any group.
 13
INTRODUCTION

The largest amount of our genetic variation is cosmopolitan: it has spread

throughout the world.

HOW DOES HUMAN VARIATION COME ABOUT?

Variation is amazing and amazingly important. So, how did we get to the
pattern of variation seen today? The short answer is that variation evolved.
Human variation came about through evolution.
Charles Darwin was the first to clearly demonstrate, in On the Origin of
Species, that evolution by natural selection results from the existence of
variation within species. Some variants lead to greater survival and repro-
ductive success and are therefore selected over other variants. For example,
modern humans originally evolved in the tropics. After losing the protection
of a hairy body that our ancestors surely shared with their primate cousins,
these first humans almost certainly evolved dark skin to better protect them
from damage to folic acid, one of the B vitamins. Folic acid, also known as
folate, is a compound that is essential to the successful completion of preg-
nancy (live birth, reducing birth defects). Exposure to ultraviolet radiation
from sunlight can damage folate, and the melanin in darker skin provides
protection.
Darwin had a rudimentary idea about the origin of variation in living things,
particularly the importance of variation for adaptation. Today, scientists have
a much deeper and broader understanding of how variation comes into exis-
tence and evolves. The variation in all biological traits in any group of organ-
isms (including humans) is determined by the complex interaction of three
major sources: genes, environment, and chance. For purposes of this book,
we’re not interested in all biological variation, such as that associated with sex
or age. Rather, we’re interested in variations among groups and regions that
are often associated with socially defined race. How did humans who lived and
evolved in different locations come to be different from one another?
Because our species began in sub-Saharan Africa, Africans account for
the greatest amount of genetic variation within our species. The rate of muta-
tion in the human genome is constant, so the more time has passed, the
greater the number of mutations and accumulation of new genetic variants.
Conversely, when smaller groups of humans left Africa and traveled around
the world, these founder groups left behind some of the genetic variation
that was in the larger population. As a result, the group that migrated lost
some genetic variants.
 14
INTRODUCTION

Consider a deck of playing cards as a model of the genetic variants in a

large population. If you deal out all the cards, you will find an equal distribu-
tion of spades, clubs, diamonds, and hearts. If you deal only four cards, you
are highly likely to deal something like two hearts, one club, and one spade.
The diamonds have been lost by chance simply because of the small number
of cards dealt. If you try this a second time, you might deal two diamonds,
one heart, and one club; this time, the spades have been lost. And so on.
This evolutionary process is called genetic drift and refers to a random
change in allele frequencies due to small population size. An allele is an
alternative form of a gene, such as in the case of brown, blue, and green eye
color. A consequence of genetic drift is that the farther people migrated from
Africa, the more genetic variation (alleles) they lost. But despite the loss of
some genetic variants, and the introduction of new variants through muta-
tion during the movement of people to different parts of the globe, at the end
of the day, genetically, we all remain Africans.
It is also important to understand that our geographical entities are human
creations as well. Australia, as a separate land mass, is somewhat zoologically
distinct, whereas Asia and Europe are connected and not so distinct from
each other. For example, the best way to understand the distribution of the
hemoglobin S (HbS) genetic variant is not by which continents it is found
on but by its association with ecological conditions such as stagnant water,
which provided a breeding ground for the mosquito that carries the malaria
parasite. Individuals who are heterozygous or carriers (one copy of the HbS
and one copy of the HbA allele) are resistant to malaria and do not display
sickle cell anemia. Individuals without a HbS allele have elevated death rates
due to malaria. Individuals with two HbS alleles have elevated death rates
due to sickle cell anemia. Thus, in malaria zones, it is best to be a carrier.
Early agriculturalists came in contact with and actually expanded the
breeding grounds of malaria on several continents and regions, including
west central Africa, the Middle East, the Mediterranean, and the Indian
subcontinent. As a result, the frequency of the HbS allele in Nigeria (west-
ern Africa) is 0.14, in Saudi Arabia (Arabian Peninsula) it is 0.12, and in
Greece (Mediterranean) it is 0.12. Conversely, the frequency of this allele
in South Africa (southern Africa) is only 0.02. The difference between the
former and latter countries is that the former all have high levels of malaria
transmission, whereas there is virtually none in South Africa. The bottom
line: continent or race does not explain sickle cell trait, but evolution does
beautifully.
 15
INTRODUCTION

Finally, human variation in physical appearance and other phenotypes is

also due to how genetics is expressed under different conditions. The envi-
ronment in which an organism lives always influences the expression of its
genes. Picture a tree that lives on a windy slope. The tree grows in a tangled
and twisted form because of the constant pressure of the wind. If one takes
the seeds of such trees and plants them in a calm environment, the trees will
grow to have a more typical, straight trunk.
Throughout human history, people have lived in unique, varied, and often
unequal environments. Even in modern times, the probability that a person
will die (at any age) in the United States is strongly stratified by socioeco-
nomic environment. A person who lives in a household that brings in less
than $15,000 a year is over three times more likely to die than a person who
lives in a family whose income is greater than $70,000 annually.
In the United States, socioeconomic status is strongly stratified by socially
defined race, so that compared with people of European descent, racial
minorities experience more environmental insults, such as heavy-metal pol-
lution and pesticide exposure, during their life spans. The take-home point
is that we cannot assume that differences in health or other physical traits
(the phenotype) are due to differences in genes and genomes (the geno-
type). This confusion is one of the most nefarious parts of race science—the
assumption that the differences we see in wealth, health, and other measures
are attributed to genetic differences when, in fact, they are due to environ-
mental differences.
In summary, genetic variation arises from mutations. Some of these are
beneficial, such as in the example of the sickle cell trait in the presence of
endemic malaria. Other mutations (or variants) are neutral and simply car-
ried as part of the genome without functional consequences. These variants
can change in frequency through time, distance, and random events. Finally,
much of what we see, such as differences in life spans, are nongenetic varia-
tions that are due to environmental conditions.

IF RACE ISN’T BIOLOGICAL, HOW DO YOU

EXPLAIN THE DIFFERENCES WE SEE?

Examples such as the sickle cell allele and skin color (see chapter 3) demon-
strate that geographically based genetic variation exists within the human
species. However, the existence of these variations should not be confused
with socially defined races. Complex forces—ancestry, natural and sexual
 16
INTRODUCTION

selection, genetic drift, and environmental effects—alter the physical appear-

ance and other attributes of various populations of human beings. However,
it’s worth repeating that none of these differences, alone or combined, scien-
tifically justifies the partitioning of people into racial groups. Nor does the
underlying genetic variation encoding the physical differences we observe
in people justify the clustering of humans into biological races. Both pheno-
typic and genetic variation is found within and among human groups—but
that variation is not racial. It is geographic and is explained by evolution
and history. Variation exists. It is wonderful and ripe for exploration. But it
is not race.

WHAT IS A SOCIAL CONSTRUCTION?

You might have heard people say that race is “just” a social construct and
therefore is not “real.” But equating a social construction with not being real
is a mistake. A social construction becomes real in that it has real effects.
Our world is socially constructed. How we see our world, our reality, is
the result of how our society trains us to see that world. For example, we are a
very visual species and see skin color as telling a good deal about an individ-
ual. That’s not because skin color is inherently more important. It is because
skin color is readily seen and has become imbued with cultural meaning.
Anthropologists often study how cultures and subcultures view the world
in different ways. A ready example includes attitudes toward race. Within
the broad culture of the United States, white people are more likely to see
race as biologically based but believe that great progress has been made in
reducing racism. In contrast, African Americans and other racial and ethnic
minorities are less likely to see race as biologically based, and they are far
more pessimistic about progress in race relations.
In Brazil, it is said that money “whitens.” Race and class are more tightly
wound in the Brazilian compared with the American consciousness. In
Europe, anti-Semitism is more closely equated with racism. In medieval
Europe, Jews were treated as a separate race of humans. They were thought
to have tails, and males were thought to menstruate. Pogroms (organized
massacres) against Jews occurred consistently throughout European history.
In the Jewish quarter of Paris, the Marais, one frequently encounters plaques
dedicated to places where Jewish families once lived who were sent to con-
centration camps and their deaths. The legacy of European anti-Semitism
lives in these places. The difference in how anti-Semitism is understood in
 17
INTRODUCTION

America and Europe results from the fact that people see the world differ-
ently based on personal experiences. Our social brains train our eyes to see
significance.
Social constructions make our reality. Race might not be based on biol-
ogy, but, paradoxically, dividing individuals into races has biological effects.
Individuals whom our society classifies as Black or brown are treated dif-
ferently. They have different barriers to achieving a quality education, being
hired in meaningful employment, and living in a safe environment. There-
fore, as a result, they are exposed to more stress and greater health problems
than people who are classified as white. In the United States, the chance that
a baby will die before its first birthday is over two times greater if its mother
is classified as Black versus white. And the average life expectancy of whites
in 2016 approached seventy-nine years, which gives them an extra four years
of life compared with Native Americans and Blacks. Social constructions
have real consequences for our bodies and our lives.
Another way of understanding social construction is to begin by recog-
nizing that all knowledge is socially constructed. Science operates from the
proposition that objective reality exists, and scientists attempt to understand
that reality through the use of scientific methods. The scientific method is the
most reliable intellectual program to understand how nature works. Among
its successes are outlining the rules of motion (by Newton and Einstein),
the understanding of the conservation of matter (Lavoisier), cell theory
(Schwann), the significance of the cell surface (Just), the origin of species by
the means of natural selection (Darwin), and the nature of genetic material
itself (Watson, Crick, and Franklin).
The degree to which the people who live in modern industrialized societ-
ies enjoy relative ease and comfort is partly the result of the fact that science
works. Today, fewer people die of the fatal synergy of malnutrition and infec-
tion compared with just decades ago. The worldwide rate of infant mortal-
ity has dropped from about one hundred fifty per thousand in the 1950s to
under thirty today. At the same time, average worldwide life expectancy has
increased from under fifty to over seventy years.
The greatest strength of science is that it requires skeptical analysis and
the testing of hypotheses, and therefore it must be self-correcting. However,
science is conducted by human beings, and humans always exist in societ-
ies. Therefore, as all human beings operate using various levels of flawed
thinking, societal biases often enter into the enterprise of science. What’s
wrong with socially defined race schemes is that they were produced without
 18
INTRODUCTION

proper adherence to the scientific method. This deviation from the scientific
method was a human flaw, driven by the realization that the idea of race
provided justification for the existing sociopolitical hierarchy.
We are left to practice science as best we can, and that includes trying to
be clear about our biases. That isn’t easy. Scientists are not generally trained
to recognize their own biases, which are like the air we breathe.
In hindsight, we can recognize the biases of American and European sci-
entists who tried to justify slavery by making racial hierarchies. And even
though seeing one’s own biases is difficult, we, too, have our biases. Martin
Wobst, one of Alan’s graduate school professors, was fond of saying that see-
ing one’s own bias is like jumping over one’s shadow. Culture makes and
shapes reality.

WHAT IS RACISM?

Racism is systematic discrimination by a powerful individual or institu-

tion against individuals based on their perceived membership in a socially
defined racial group. Only governments, corporations, social groups, and
individuals who have collective political and social power can implement
racism. Institutional racism, a predominant form of racism, is alive and
well in American society and can be observed in a variety of aspects of our
lives, such as discrimination in housing, employment, and income; expo-
sure to toxic wastes; likelihood of incarceration; and death by police inter-
vention. Furthermore, globalization has allowed American-style racism to
spread and combine with indigenous racisms to degrade the lives of even
more people.
It’s important to distinguish bigotry from racism. Anyone can be a bigot—
that is, anyone can have an irrational hatred for individuals who belong to a
different socially defined racial group. Racism, on the other hand, requires
having, and using, social power.
Racism as a worldwide phenomenon dates to the period of the European
voyages of colonization. There is no evidence that racism (or the concept of
race) existed in the ancient world (~1200 BCE–400 CE). Societies displayed
various sorts of ethnocentrism; for example, the Greeks considered all non-
Greeks as barbarians. Generally, all cultures thought that their people were
somehow better than others with whom they came into contact. Slavery
in the ancient world was not racial; rather, it was associated with conquest
 19
INTRODUCTION

during war and with poverty. For example, in the Roman Empire, poor peo-
ple often left at the city dump babies that they couldn’t afford to take care
of. Slave traders were aware of this practice and congregated at the dump to
collect these unfortunate infants.
During the Crusades, the slave trade was balanced between Islamic peo-
ple entering the Christian trade and Christians entering the Islamic trade.
The transatlantic slave trade was unique in the history of humanity in that
it targets a specific group based on its geographic location and reliance on
social definitions of race. Africans of widely different ethnicities, language
groups, and cultures began to be lumped together as a race. European phi-
losophers, such as Giordano Bruno (1548–1600), thought that this group of
people had been created separately from Adam and Eve. Others, such as
Comte de Buffon (1707–1788), felt that all humans were created from Adam
and Eve. Buffon believed that the environment created the different aspects
of human physiology, such as skin color and stature. He thought that a sav-
age tribe captured and brought to Europe, fed on European food, would
gradually become civilized and their skin would whiten.
The ideology of race always supports those in power. So, it is not surpris-
ing that variants of this ideology spread and now it is not solely the prov-
ince of individuals of European descent. The Japanese imperial class saw
the Japanese as the “master race” of Asia and used this ideology to justify
its conquest and genocide against other East Asians during the Asia-Pacific
War (1933–45). Another horrific example of this thinking was the Rwandan
genocide of the 1990s.
Unfortunately, there are several examples in modern history of what hap-
pens when racist ideology becomes the policy of the state. When the sub-
ject is broached with Americans, most think of Nazi Germany. However,
the United States was founded on white supremacy and racial ideology. It
maintained de jure (by law) white supremacy until the Civil Rights Act of
1964; in fact, we argue, in contradiction to remarks by Tucker Carlson on
his FOX News show that white supremacy is a hoax, that this ideology still
plays a major role in American social life and foreign policy.
In summary, hating another group is one thing. That’s ethnocentrism.
Feeling that your hate is justified because people are biologically inferior
(and science proves it) is quite another. That’s racism. The idea of race
is essential for racism. And the idea of race is based on deeply flawed
science.
 20
INTRODUCTION

CONCLUSIONS

Race is an idea that people made real by constant use. It was a useful idea to
those in power to promote slavery and colonization and, in current times,
to maintain a racial status quo of differences in opportunity. Historically,
scientists thought of race as equivalent to the biological subspecies concept.
Today, many people still think that races are biologically different and have
different attributes. However, that view of race is scientifically incorrect.
Human biological variation is real, complex, and wondrous. But race nei-
ther describes nor explains human variation. Race is a social idea, not a
biological one.
Our country was built on the hard work and brilliance of many. And it
was also built on the myth of race that enslaved and colonized many more. In
his poem “Let America Be America,” Langston Hughes writes of the United
States that it is “the land that never has been yet.” We have never come to
face the myths of race and the history of racism. We hope this chapter and
chapters to follow help to bring us closer to what this land could be.
 Chapter One

HOW DID RACE BECOME BIOLOGICAL?

The old, mythical idea of race as consisting of distinct biological groups of

humans, what we here call biological race or biologized race, slowly took hold
in Europe, then the Americas, and finally other parts of the globe. It became
reified, especially by those with power and authority, eventually including
scientists. Today, it seems that this dominant worldview of race as somehow
rooted in biological and genetic differences is so accepted that it must be
scientifically true. It seems so obvious. We can see difference. But what seems
obvious can deceive.
Here, we focus on how and why this false idea of biological races devel-
oped through historical places and periods. This chapter is a short, capsu-
lized history of the big lie: how the mythic idea that races are biological came
about and became dominant. In the next chapter, we explain the science of
why this idea of biologized race is incorrect and harmful.
We begin with a brief overview. It is probably true that for the vast major-
ity of human history, each group of people thought of others as somehow
different from themselves. From the first humans some 300,000 years ago
to the thirteenth century, individuals rarely traveled more than forty miles
from their place of birth. That’s still true for many today. Individuals would
rarely encounter anyone whose physical appearance was noticeably differ-
ent from their own group. People in the out-group might speak a different
language or dialect, have slightly different customs and ways of doing things,
and rarely might even have looked a bit different. But those in the out-group
 22
H OW D I D R AC E B E CO M E B I O LO G I C A L?

were not racially different; that is, the differences were not thought to be
innate, based on biology, and not necessarily hierarchical.
Members of early agricultural groups and ancient civilizations might have
considered others outside of their group as less than those in their group.
Throughout history, “the other” was often mythologized as uncivilized, sav-
age, or even cannibalistic. However, physical or phenotypic differences were
of little importance. The concept of races as biologically distinct groups had
not yet found a foothold.
The idea of race started around five hundred years ago, and the fully
formed idea of biologized races is only about two or three hundred years
old. In the next section, we outline three key steps related to the idea of
biologized race: folk, legal, and scientific.
First, race developed as a folk idea to characterize different groups as
fundamentally different types. These were general ideas used to explain
similarities and differences. How these notions started is difficult to trace.
They likely started with explorer tales and reports. Fantastic tales were com-
mon of wild men and bloodthirsty cannibals. The explanations these tales
provided for these peoples were that they were entirely different creations
(pre-Adamites) or that they were remnant, devolved humans from after the
Flood. In either case, the differences were fundamental and innate. That
view of difference took hold in the Christian world and became common
and a dominant worldview.
This folk idea of race slowly emerged over centuries and millennia. By
1492, it had become clear that a shift was in process, from seeing out-groups
not as just culturally different but as something more inherent and biologi-
cally different. In that year, Jews were expelled from the Iberian Peninsula
because they were not merely religiously but fundamentally different. And,
of course, we all know that Columbus sailed from Spain and landed on the
island of San Salvador in the Bahamas. There, and in his further explora-
tions, Columbus and those who sailed with him encountered peoples who
were remarkably different in customs, dress, language, and looks from any
they had known. They must be a fundamentally different type.
Second, race became a legal entity. Fast-forward two hundred years after
Columbus’s voyages, and economies throughout the Americas became
increasingly dependent on slavery and indentured servitude for labor. To
stabilize these systems of oppression, race became legal. Laws in Virginia
and the other colonies in the 1600s were used to legally separate Indians
from enslaved Africans and enslaved Africans from indentured Europeans.
 23
H OW D I D R AC E B E CO M E B I O LO G I C A L?

It became legal for one individual, a European, to own another, an African,

based on their race alone.
Third, race became scientific. Guided by Christian special creationism, in
the mid-1700s, naturalists made a variety of attempts to name and describe
racial types. Soon after, natural scientists and early anthropologists tried to
justify slavery and colonization by proving that races were fundamentally dif-
ferent and, by extension, that some races were meant by God to rule others.
Racist science and theology made the case that races could be classified in
a repeatable way and that those innate racial differences were based on bio-
logical differences in skin and hair and thought to extend to the inner body
and brain. Races became inherent, universal, biological, and hierarchical.
In the nineteenth century, a handful questioned the reality and hierarchi-
cal view of race. Frederick Douglass wrote that the conditions of slavery
made the slave, and Charles Darwin overcame his own Eurocentric ten-
dencies and came to the revolutionary understanding of natural selection
as a process that countered idealism and the inevitability of humans’ place
in nature. However, it would take another century before the data would
be available—and understood—to fully and scientifically dismantle racial
thinking in biology and anthropology.
Today, we have made progress in changing the legal status of race. Laws
in the United States have eliminated racial slavery, followed by the elimina-
tion of “separate but equal” laws and the passing of voting rights legislation.
Scientists have shown that biological races do not exist within our species.
Yet, the folk ideology of biologized race remains. It might change from time
to time and place to place. It is a chameleon of a concept. However, most
fundamentally, the worldview of biologized race remains. And that is funda-
mentally why racism remains.

DID THE ANCIENT EGYPTIANS, GREEKS, AND

ROMANS HAVE A CONCEPT OF RACE?

No.
The idea of biological races formed after these periods and places. In fact,
no civilization or group from any part of the world had a concept of race at
least until the late Middle Ages, from the Crusades, which began in 1095,
through 1492.
The Indian caste system is older than race, and although it, too, is based
on family inheritance, it is not biological in the way that race becomes
 24
H OW D I D R AC E B E CO M E B I O LO G I C A L?

biological. There simply is no record that groups were thought of as dis-

tinct because of their innate biological differences. Audrey Smedley writes,
“Expansion, conquest, exploitation and enslavement have characterized
much of human history of the past 5000 years or so, but none of these events
before the modern era resulted in the development of ideologies or social
systems based on race.”
“Race” or an equivalent term does not exist in the Hebrew Bible or Chris-
tian New Testament. The world of the people who wrote these texts makes
it clear that they had not encountered the full scope of human biological
diversity. The Levantine people, who produced the Hebrew Bible (1200–722
bce), described persons of African descent. The prophets Nahum and Amos
described Ethiopia, which meant the region south of the Blue Nile. Their
description of the people of that area in Nahum 3:9 or Amos 9:7 lacked any
negative aspect.
The world of the New Testament was considerably larger, which expanded
in the first century with the growth of the Roman Empire. The farthest
northern region in their world was Scythia (modern-day Russia), and they
knew of northern Africa and Lusitania (in modern Spain) to the west. There
is some evidence that Rome traded with China via the Silk Road, and some
archaeological remains show that persons of Chinese descent might have
inhabited the Roman Empire.
Greek philosophers thought that within people could be found various
ratios of humors and essences. Based on their essences, individuals were
suited for specific positions in society. According to this idealist worldview,
individuals and groups were essentially their specific melding of humors.
That essentialist thinking provides some of the background for typological
thinking. One could say this was proto-racial thinking, but it wasn’t yet racial
thinking, because the essences were not specific to individuals of different
family groups and cultures.
The Greek Herodotus (called the “father of history,” 484–425 bce) consid-
ered non-Greeks as barbarians, but one could change their status by adopting
Greek cultural norms. The ancient Arabs were aware of ethnic differences
but did not describe them in “racial” terms. Finally, neither Marco Polo of
Venice, who traveled from Europe through Central Asia to China and back
by Southeast Asia and India, or the Moroccan Ibn Battuta, who traveled
through the Balkans, Black Sea, southern Russia, India, China, the Middle
East, Egypt, and North Africa, described peoples they encountered in racial
terms. Thus, the ancients did not view others as bioracially different.
 25
H OW D I D R AC E B E CO M E B I O LO G I C A L?

Throughout history and across the globe, it appears to have been common
to use derogatory terms to name other groups and to think of one’s own
group as superior. This is ethnocentrism. Although ethnocentrism is hurt-
ful and potentially harmful, especially as it carries over into an increasingly
interconnected world, it is not racism simply because it is not based on the
idea of biological races.
There is abundant evidence for this sort of thinking through the Mid-
dle Ages and the Renaissance (1300–1600). Outside groups were frequently
described as barbarians and worse. In this period, European Jews were
treated in ways that resemble modern racism. Yet, although there was fear
and loathing of those outside one’s own group, or xenophobia, it is also
clear that humans merged and mingled through time and also evidence of
acceptance, admiration, desire, love, and reproduction. Wherever humans
roamed, be it in search of new lands or foods or for conquest and subjuga-
tion, humans ended up mingling and mating.
What we know of Egyptians’ art and writing makes it clear that they were
aware that people from different lands looked different. Egyptian hiero-
glyphics portray humans with a wide range of features that look like those
of individuals from areas including southern Russia to the equator. They
saw differences, but no concept or word equivalent to “race” existed in their
language. They enslaved individuals, usually the captives from wars. But
there is no evidence that they thought of these differences as racial; that is,
distinct biological differences. Like Moses in the Bible, one could become an
Egyptian simply by living as an Egyptian.
The same is true for the ancient Greeks and Romans. Their empires
expanded as they conquered foreign lands, spreading at times to the British
Isles and Northern Europe and into the Middle East and North Africa. Like the
Egyptians, they saw the peoples of captured lands as different in their ways of
life and language but not racially different. Others might be heathens or could
be enslaved, but being a heathen or slave was not based on biology or race.

WHAT CHANGED IN SPAIN IN 1492?

First, the Jews and Moors were expelled. Second, Columbus left Spain and
encountered the Taino of San Salvador. Indeed, the expulsion of the Jews and
Moors provided some of the funds for Columbus’s voyage.
The Alhambra Decree, or the Edict of Expulsion, was the punctuation
mark ending Jewish life in Spain, the result of over a century of religious
 26
H OW D I D R AC E B E CO M E B I O LO G I C A L?

persecution and pogroms. Issued in March 1492 by Catholic monarchs Isa-

bella I of Castile and Ferdinand II of Aragon, the same monarchs who sent
Columbus to find the Far East, the edict required all practicing Jews to leave
Spain within four months. Prior to 1492, Jews had been allowed to convert
to Catholicism, and an estimated half of all Spanish and Portuguese Jews,
called conversos, did so. But the Catholic monarchs worried that conversos
would continue to secretly practice Judaism. These Jews were called Mar-
ranos (swine).
These actions against Spanish Jews, as horrific as they are, were based on
religious rather than racial intolerance. The expulsion might be considered
to be based on proto-racial beliefs, in that a Jew will remain a Jew even if a
converso. Jews could change their religion but not their essentialness as dif-
ferent. The expulsion was not based on thinking that the Jews were a race but
is a sort of preview of the connection between race and racist acts.
Similarly, Columbus’s contact with Taino Indians of San Salvador in 1492
is a single act. What is significant for the history of race has to do with long-
distance travel, especially by boat, and exemplified by Columbus’s journey.
Prior to the age of European exploration, which began in the early fifteenth
century, travel was typically slow and covered shorter distances by land.
Travelers such as Marco Polo (1254–1324) and Ibn Battuta (1304–68/69)
encountered people who were not perceivably different from people living
in the lands from which they came. The differences were not profound or
noteworthy. Dialects, dress, and diets changed, but they did so in ways that
were subtle, continuous, and undramatic.
Marco Polo famously traveled along the Silk Road into China, discover-
ing peoples who were different in looks, language, and customs. The same
is especially true for early seafaring explorers such as Columbus and Vasco
da Gama during the so-called Age of Exploration, which spanned the 1400s
to the 1600s.
The effect of the sudden change from light-skinned and -eyed Europe-
ans to brown-eyed and -skinned Native Americans almost certainly gave the
impression that variation was discontinuous and that the latter had to be a
distinct type.
Columbus kept a journal that included his thoughts on those he encoun-
tered in October 1492 in San Salvador. He describes the Taino by their physi-
cal features (well-made and handsome bodies), hair (like a horse’s tail), and
color. He described them later as simple and opined that they easily would be
made Christians. He did not recognize that they had their own religion. To
 27
H OW D I D R AC E B E CO M E B I O LO G I C A L?

Columbus, the Taino and other Native Americans were less than Europeans,
to the extent that they could be enslaved. Indeed, he kidnapped and enslaved
several of them to present as spoils to Queen Isabella to justify his voyage
and tempted her with the lure of additional wealth that could be plundered
from the new lands. Although he did not yet have law and science on his
side, he had an ideology that could bend to political power and that allowed
him and those like him to designate Indios, Native Americans, as a different
kind of non-Christian people, either separately created or devolved.

WHAT LED TO THE IDEA OF BIOLOGICAL RACE?

Race is not the type of invention that is marked by a patent, stamped as

officially invented by a person at a specific moment in history. Ideas and
concepts are not invented by one person in one place and time. Rather, ideas
emerge slowly and are slow to be adopted and solidified. That’s almost cer-
tainly how the idea came about that different human groups are delimited
by differences in biology and that those differences might also be ranked in
worth. Also, the sciences of biology and anthropology did not develop all
at once. As discussed by Terence Keel in his book Divine Variations, these
emerging disciplines were intimately linked with and driven by religious
beliefs. It is important to recognize that prior to the nineteenth century,
people simply did not have the scientific knowledge and understanding of
evolutionary processes to correctly understand human biological variation.
Table 1.1 provides a timeline of important scientific discoveries and con-
troversies that had to be resolved before the modern views of biological vari-
ation and its significance could be developed. Most important in this regard
(in bold font) were the 1859 publication of Charles Darwin’s On the Origin
of Species and Gregor Mendel’s discovery of particulate genetic inheritance
in 1868.
Two main conceptual roots of racial thought began to come together
around 1492. The first is an idealist worldview. Idealism was the dominant
worldview up to the nineteenth century. As exemplified by Plato (427–337
bce), idealism is a view of the material world as secondary to or derived
from a more fundamental world of ideal things. Plato called these ideals
forms, or eidos. In the history of philosophical ideas, this worldview is most
often referred to as Plato’s theory of forms or doctrine of ideas. In biology, it
became known as essentialism and gave rise to the essentialist species con-
cept (table 1.1).
TABLE 1.1ġ
Biological Conceptions of Race Timeline

Year Event

428–348 bce Plato, Greek philosopher, eidos—diversity of living things is the reflection of a limited number
of unchanging universals.
384–322 bce Aristotle, Greek philosopher, scale of nature, De Partibus animalium.
1520 ce Paracelsus, Swiss physician, pre-Adamite races.
1583 Andrea Cesalpino, Italian, de Plantis, downward classification of organisms by logical division.
1591 Giordanno Bruno, Italian priest, philosopher, pre-Adamite races.
1619 Lucilio Vanini, Italian, Africans descended from apes and had once walked on all fours.
1696 John Ray, essentialist (Plato) species concept.
1735 Carolus Linnaeus, Systema Naturae, essentialist species and varieties.
1700–1800 Naturalists disagree about African inferiority, unclear on the heritability of racial traits, effect
of the environment, primarily monogenists.
1749 Georges Louis LeClerc, Compte de Buffon, Histoire Naturelle, forerunner of modern biological
species concept, infertility criterion.
1760–1830 Lamarkian evolution, races as distinct lineages at different levels of perfection.
1800–1860 Naturalists agree on African inferiority, heritability of racial traits, polygenists.
1812 Georges Cuvier, correlation of animal parts.
1830 Paris Academy debate, Cuvier vs. Etienne Geoffroy Saint-Hilaire.1
1850–60 Four horsemen of craniometry: Louis Agassiz, Samuel Morton, Josiah Nott, and George R.
Gliddon.
1854 Frederick Douglass, The Claims of the Negro Ethnologically Considered.
1859 Charles Darwin, On the Origin of Species, or, the Preservation of Favored Races in the
Struggle for Life.
1868 Gregor Mendel, principles of particulate inheritance.
1870–73 Mitosis, meiosis, German cytogeneticists.
1871 Darwin, The Descent of Man and Selection in Relation to Sex, chapter 7, the races of man.
1918–51 Neo-Darwinian synthesis (unification of natural selection with Mendel’s genetics); population
genetics; J. B. S. Haldane, Julian Huxley’s clines, Sewell Wright’s F-statistics.
1930 Chromosomal theory of inheritance, Thomas Hunt Morgan and others.
1942 Ashley Montagu, Man’s Most Dangerous Myth: The Fallacy of Race.
1944 DNA as material of heredity; Avery, MacLeod, McCarthy experiment.
1950–51 UNESCO race statements.
1962 Frank Livingstone, nonexistence of human races, Current Anthropology.
1972 First protein electrophoretic studies of human genetic variation.2
2002 Publication of human genome by Sanger sequencing technology, announced by project leaders
J. Craig Ventor and Francis Collins.
2006–14 Illumina sequencing technology reduces time and cost of human genome sequencing,
announces $1,000 human genome.

Note: Entries in bold represent the most significant events.

1The Paris Academy debate of 1830 concerned whether animals could be thought to have a unified body plan; such a plan was
an idea associated with evolution and common descent. Saint-Hilaire argued for a unified body plan, opposing Cuvier, who
was thought to be the most brilliant man of that age. Cuvier used the example of the human races as evidence for the separate
creation of species.
2R. C. Lewontin, “The Apportionment of Human Diversity,” in Evolutionary Biology, ed. T. Dobzhansky, M. K. Hecht, and W. C.
Steere, 381–98 (New York: Springer, 1972).
 29
H OW D I D R AC E B E CO M E B I O LO G I C A L?

Plato wrote that the things that were all around him, such as a chair
and a tree, were not the true essences of “chair-ness” or “tree-ness.” Rather,
the true chair is an ideal chair, and a real tree is an ideal tree. Ideal types
are an abstraction that humans must imagine, as their essences come from
the gods.
There is an undeniable appeal to ideal thinking. Our brains seem to be
drawn to categorizing things into their types or slots. It is not a far reach
from ideal types to naming practices; for example, naming diseases provides
a sense that we know or at least can recognize them. The same goes for nam-
ing types of peoples.
The first problem with idealism is that it is entirely subjective. For exam-
ple, is the piece of furniture in Alan’s living room a large six-legged chair, a
small couch, or a loveseat? There is no objective way to decide. How many
separate ideal things are there, and how does one account for intermediates?
And who is to say what the ideal is? What is the ideal tree?
The second problem is that idealism does not involve a process. There is
no mechanism for change: essences are static, fixed and eternal. Idealism is
unscientific because the nature of things is beyond human comprehension.
Finally, idealism was a barrier to the discovery of a theory of change (or
evolution) simply because few natural historians were concerning them-
selves with the question of change in the observable material world. Ideal-
ism was a barrier that Charles Darwin and Alfred Wallace had to overcome
to work out the origin of species.
That said, the idea of biological races is aided by all of those problems:
idealism, subjectivity, and changelessness. It’s a small step from Platonic
idealism to ideal types of humans, each with a unique set of properties.
The Greeks came close to thinking that there are ideal types of men and
women and ideal rulers and peasants; Aristotle’s concept of the “natural
slave” comes to mind. Ideal types set a part of the intellectual stage for bio-
racial types.
The other main root of racial thinking was later set by the “Great Chain
of Being,” a related view of the natural world whereby all God’s creatures
were seen as occupying a rung on a ladder of creation. The higher on the lad-
der, the closer to God. This great chain was built off Greek notions of ideals
and added a god into the equation, placing animals and human groups as
distinct in proximity to the deity. Some depictions of the great chain place
women below men, and others clearly draw in different types of people, with
Europeans occupying the higher rungs on the “Great Chain of Being.” The
 30
H OW D I D R AC E B E CO M E B I O LO G I C A L?

importance of the “Great Chain of Being” is that it clearly added the dimen-
sion of hierarchy to proto-racial, idealist thinking.

DID SLAVERY MAKE RACE NECESSARY,

OR DID RACE MAKE SLAVERY ACCEPTABLE?

Both!
The connection between race and slavery is central to understanding both
the idea of biological races and the acceptance of chattel slavery, the type of
slavery in which enslaved individuals are possessions of the owner. The story
of the codevelopment of slavery and racial ideology is well documented in
Virginia.
In August 1619, an English ship, the White Lion, arrived near Hampton,
Virginia, and twenty or so enslaved Africans eventually found their way
to Jamestown. So, slavery in the English colonies began at least four hun-
dred years ago. In reality, racial slavery is older; countless other slave ships,
mainly Portuguese, had already brought enslaved people to the Caribbean,
Florida (then under Spanish rule), Brazil, and other locations in Central
and South America. You can learn a great deal about the voyages that
carried enslaved people to the Western Hemisphere at the Slave Voyages
website.
There is an important historical debate about whether these first Africans
who toiled at Jamestown, as well as other early North American colonies,
could be properly thought of as chattel slaves or simply indentured servants.
Many Africans of this period were granted freedom after a period of servi-
tude. The important point is that in the early days of Jamestown, it wasn’t
clear that there needed to be a legal difference between enslaved Africans and
indentured Irish and other indentured Europeans.
Starting in 1661, Virginia began to pass laws that legally separated Afri-
cans from indentured Europeans and made slavery a permanent state for
enslaved Africans. This was done to reduce the organizing power of both
groups. Although indentured Europeans did not have political power, at
least they eventually could become free. This was the first time European
or Christian was established as an identity and in opposition to the label of
Native American or enslaved African.
Is race the parent of racism, or is racism, in the form of slavery and colo-
nization, the parent of race? Both. The idea of race was made out of political
necessity to justify continued enslavement and colonization.
 31
H OW D I D R AC E B E CO M E B I O LO G I C A L?

HOW COULD EUROPEAN COLONISTS JUSTIFY ENSLAVEMENT

AND THE DECIMATION OF NATIVE PEOPLES?

Race.
The concept of race justified the inhumane treatment of people of differ-
ent races. At the time Columbus arrived in the Caribbean, European society
was emerging from feudalism. In this social system, the members of the rul-
ing class had relatively absolute power over peasants and artisans. Europeans
felt that they had the right to conquer non-Christians, and with the voyages
of discovery, more and more non-Christians who were not white were being
discovered. Originally, the debate was whether these new people had souls
and could be converted to the Christian faith. The question of the status of
non-Christians has its roots in debates from the Middle Ages and the pos-
sibility of redemption for Jews and Muslims in Spain. The forced conversion
view had its roots with Aristotle and his idea of the natural slave and St.
Augustine’s intolerance of other religions.
The opposition to forced conversion and conquest of the American Indi-
ans came mainly from the Dominican order of the Catholic Church. Domin-
icans opposed such conversion on the basis of both natural and divine law.
The opposition included Francisco de Vitoria, considered the father of inter-
national law; Bartolomé de las Casas, bishop of Chiapas and apostle of the
Indians; Domingo de Soto, a theologian at Salamanca University; Bartolomé
Carranza, bishop of Toledo; and Antonio de Montesinos, a friar on the Island
of Hispaniola whose preaching led to the conversion of de Las Casas. The
Dominican appeals to the Catholic kings led to the Laws of Burgos of 1512.
That law proposed that:

(a) the American Indians were free,

(b) they were to be instructed in the Christian faith, and
(c) the Spanish monarch could utilize them to work, but the work must be of a nature
that would not be detrimental to their physical or spiritual well-being.

However, secular interests overpowered the spiritual intentions of the

church, and the laws were never implemented. Thus, the debate during the
seventeenth into the nineteenth century was not about whether the Indi-
ans had souls, but how to best justify their being decimated and enslaved.
This discussion was closely related to biblical questions on the origin of
human races.
 32
H OW D I D R AC E B E CO M E B I O LO G I C A L?

Essentially, there were two answers to the question of how the races came
to be: monogenism and polygenism. Monogenists believed that all humans
were created by God at the same time. They followed the Genesis story in the
Bible: we are all descendants of Adam and Eve. However, the races separated
after the sons of Noah dispersed after the great Flood. The different races
were descended from different sons; Africans were descended from Ham’s
son Canaan, who was cursed by Noah.
It is interesting in this context to understand that Genesis does not mention
which sons gave rise to which races. This is easy to understand because, as we
discussed earlier, the ancients had no concept of race. The tribes mentioned
in Genesis all inhabited the Levantine world, and the descendants of each son
overlapped in their residence within the Mediterranean basin, Middle East, and
Arabian Peninsula. This explains why medieval scholars consistently disagreed
about which people were descended from which son. The idea that the curse
of Ham was visited solely onto the “darker races” took hold after the age of
discovery and was used as an argument to justify the enslavement of Africans.
In polygenism, the different human races were created separately (the
pre-Adamite races; see table 1.1). The Bible is not necessarily incorrect, it just
isn’t about those other creations.
In monogenism, the races are closer to different varieties of humans, and
in polygenism, they are closer to the modern notion of different species. In
some sense, polygenism offered the strongest ideological cover for subjuga-
tion, because it suggests that the different races are outside of the Bible and
more like different species. In this scheme, killing an individual of a different
race would not be murder but equivalent to killing a hog or dog.
In summary, both monogenists and polygenists owned slaves and colo-
nized lands. Monogenists might have made more of an effort to rehabilitate
individuals of different races and turn them into Christians. But everyone
bought into the justification for inhumanity. In both monogenism and poly-
genism, races were considered separate and unequal. The difference was in
degree: greater in polygenism. For everyone, the idea of races as separate and
unequal had high stakes. It still does.

HOW DID EIGHTEENTH- AND NINETEENTH-CENTURY

SCIENTISTS TURN A FOLK IDEA OF RACE INTO A SCIENTIFIC
CONCEPT? WHY DID THESE SCIENTISTS DO THAT?

Scientists didn’t invent the idea of biological races among humans. But
they certainly did a lot to solidify the reification of race, to make race seem
 33
H OW D I D R AC E B E CO M E B I O LO G I C A L?

unquestionably real. Before scientists got involved, race was a folk idea, and
then it became a legal entity. A folk idea is one that is common but does
not necessarily come from any one place; it is just widely shared, common
wisdom. That was likely part of what made race seem real. It was simply that
different peoples are essentially different.
Then race became a legal entity. It became legal to separate race in the
colonies. Being white eventually gave poor whites legal rights and social
status—to vote, own land, own other people, and a lot more—that were
legally denied to individuals of other races.
And then scientists got into it! Scientists were instrumental in moving
race from a folk idea and legal entity to an unquestioned real thing. How-
ever, it must be remembered that biology and other sciences in this period
were practiced by individuals who believed in the literalness of the Bible and
were members of the Christian church. The schism between Christian and
biological views of human origins and diversity did not begin until well after
the publication of On the Origin of Species in 1859.
Before science got into the race business, races were already seen and
accepted as discrete and unchanging types with separate places on the Great
Chain of Being. That view had been made real by constant use. The power
of rulers and the clergy, state and church, made it true. Virginia laws then
codified it and made it legally true.
But some still wondered if it was natural fact that races would be for-
ever separate and unequal. At the end of his Voyage of the Beagle (1839), a
young Charles Darwin asked, “If the misery of the poor be caused, not by
the laws of nature, but by our institutions, [then] great is our sin.” Science
was employed by those in power who asserted that it was indeed nature that
made, and would continue to make, misery.
It is important for the reader to understand that what we think of as sci-
ence, and specifically biological science, in the eighteenth century is vastly
different from modern science. In the Western world, biological and anthro-
pological science at that period was not independent from theology. Thus,
the origin of human beings was thought to be the result of a divine act of
special creation, and explanations for the different biological characteris-
tics of human beings had to relate to the book of Genesis. As noted above,
those naturalists who felt that humans of all types shared common descent
were called monogenists. Thus, in this worldview, the differences observed
in human beings had to do with degeneration resulting from either the mark
of Cain (Gen. 4:15) or the curse of Ham (Gen. 9:25–27). Samuel Stanhope
Smith, a Presbyterian minister and professor of moral philosophy at the
 34
H OW D I D R AC E B E CO M E B I O LO G I C A L?

College of New Jersey, wrote in 1788 that all humans were descended from
Adam and Eve and that differences in human complexion and form were the
result of climate, geography, and custom.
Mary Wollstonecraft, best known for A Vindication of the Rights of Woman,
was also a monogenist. Most of the prominent naturalists of the eighteenth
century were monogenists, including Carolus Linnaeus (1707–78); Georges
Louis LeClerc, Compte de Buffon (1707–88); and Johann Friedrich Blumen-
bach (1752–1840).
Polygenist (or the pre-Adamite race concept) ideas began to surface in the
sixteenth century. Isaac La Peyrère wrote Pre-Adamite (Men before Adam) in
1655. By the nineteenth century, the tenor of naturalist thought had shifted
to favor this worldview. As this view was considered in opposition to the
Christian scriptures, it caused considerable controversy. However, promi-
nent men of science such as Louis Agassiz and the Episcopalian Samuel
George Morton (1799–1851) backed it. This is one of the reasons that Dar-
win did not discuss human beings in On the Origin of Species. Not until 1871,
when he had achieved the position as one of the most prominent scientists,
did he dismantle the pseudoscience of polygenism in The Descent of Man.
The science of taxonomy (classification of living things) goes at least as
far back as the ancient Greeks. The main principle used in this science by
the sixteenth century was the idea of logical division. This simply means
that if two organisms share a common characteristic, they are included in
the same group. This, of course, requires the scientist to decide which traits
are important to classification. Note that classifying organisms together does
not require that one think the organisms share a common descent. The early
taxonomists thought that the groups were fixed, eternal, and unchanging
and based on the Great Chain of Being. For example, when Italian anatomist
Andrea Cesalpino started classifying plants (see table 1.1), he did so within
a creationist framework. Similarly, European naturalists such as John Ray
thought they were cataloging God’s creation. Linnaeus began his work in
the 1730s, and his purpose was to develop a system to classify all organisms
(not just humans). Similarly, leading French naturalists such as Comte de
Buffon, Georges Cuvier, and Jean-Baptiste Lamarck were not simply inter-
ested in the classification of humans; rather, they were attempting to develop
a comprehensive system of all living things within the framework of natural
theology.
Thus, when taxonomy was applied to humans, it also was driven by ideas
that had been developed and applied to all of the natural world. Of course,
 35
H OW D I D R AC E B E CO M E B I O LO G I C A L?

European naturalists also brought into the process biases that had been
developed due to manifestly unequal social conditions. So, when the science
of taxonomy was applied to humans, it had two main goals. The first goal
was to figure out the names, numbers, and essential characteristics of human
varieties (or races). Once those were classified, some eighteenth-century sci-
entists had a second goal, which was to prove by the rather newly adopted
methods of science—measuring and comparing things—that the races were
unequal and had always been so.
It is important to note that not all eighteenth-century European natural-
ists felt that human races were ranked hierarchically, François Bernier of
France (1625–88); Gottfried Wilhelm von Leibnitz of Germany, co-inventor
of calculus; and Blumenbach of Germany considered the father of anthro-
pology, did not think that human races should be ranked hierarchically.
Leibnitz’s personal experience convinced him that Africans were not inferior
to Europeans. One of his most gifted students was Wilhelm Anton Amo.
Amo was born in Ghana and raised as a house boy (read as “pet”) of a Ger-
man noble. He went on to study mathematics at university. Amo’s career
never developed, as there was no place in eighteenth-century European soci-
ety for an African mathematician. He eventually died penniless on the west
coast of Africa.
Many scientists named, numbered, and described the races. This was a
cottage industry in the seventeenth to the nineteenth century. These early
scientists were known as naturalists for their study of the natural world,
including the natural varieties of humans. The aforementioned Bernier, a
physician and amateur naturalist, might well have been the first to develop
a clear and comprehensive classification of human races. His races are more
akin to species: Europeans, Far Easterners, Negroes, and Lapps. Yes, Lapps.
Bernier obviously was not very familiar with much of the world.
Until the 1800s, it was clear to the Christian world that God must have
created some number of different human types/species (polygenism) or that
some human types degraded after the Flood (monogenism). Remember, this
is a world in which everything seemed to be fixed and more or less as God
created. Thus, no one gave much consideration to the problem of intermedi-
ates. For example, the idea at that time of gradual variation that we know so
well today made less conceptual sense than seeing the world as consisting of
distinct types. The goal was not to understand the process by which things
came about; that was a given: God created the world. The classifiers’ goal was
to understand which things were created.
 36
H OW D I D R AC E B E CO M E B I O LO G I C A L?

One of those who wondered about intermediate forms was German sci-
entist Blumenbach the “great-grandfather” of anthropology. Blumenbach
organized humans into five races: Caucasian, Mongolian, Malayan, Ethio-
pian, and American. He is credited with naming the white or European race
“Caucasian” after a beautiful skull from the Caucasus mountains. Although
Blumenbach’s concern for intermediates was shoved aside, his classification
of five races was influential, and the name Caucasian stuck.
Linnaeus was a Swedish naturalist who is credited with the notion that
races are separate subspecies. Linnaeus traveled in his early life and later
relied on reports from explorers and conquerors. He is the father of modern
taxonomy and envisioned himself as having categorized what God created.
God created, and Linnaeus classified.
Linnaeus’s race categories included Americanus, Africanus, and even
Monstrosus (for wild and feral individuals and those with birth defects). To
Linnaeus, their essential defining traits included a biocultural mélange of
color, personality, and modes of governance. Linnaeus described Europeaus
as white, sanguine, and governed by law and Asiaticus as yellow, melancholic,
and ruled by opinion. These descriptions highlight just how much ideas of
race are formulated by social ideas of the time. The goal was to describe and
classify. Many did.
Around 1800, the center of race science shifted from Europe to the Amer-
icas and from classification and naming the different racial types to describ-
ing the essential, everlasting hierarchical differences. The shift happened for
a simple reason: the need to justify slavery and colonization and, after slavery
ended, institutional and structural inequalities.
In the United States, the contradiction of the country’s freedom from Eng-
land and its enslavement of Africans was all too apparent. The Abolitionist
movement gained steam at about the same time as the war for independence
from England. Abolitionism was a movement of importance, with ethics on
its side. How could one man ethically enslave another? Perhaps they could
do so if the other was meant by God to be controlled.
Here, the work of Samuel George Morton is illustrative and central. It also
demonstrates the growing ideological power of science to make something
real. Morton, a Philadelphia physician and self-styled natural scientist, was
famous for collecting skulls from around the world. He was not seen as a
thorough racist scientist. Rather, working in Philadelphia, he was considered
to be neutral, objective, and data driven regarding questions about race and
intelligence.
 37
H OW D I D R AC E B E CO M E B I O LO G I C A L?

Thinking that intelligence is the most important human capacity and that
it could be measured by the size of the brain, Morton set about measuring
the brain sizes—or, more precisely, the cranial capacities—of skulls that he
had collected of different races, including ancient and contemporary Egyp-
tians and Native Americans. He wanted to show that (a) the races could be
separated and ranked on cranial capacity (= intelligence) and (b) those rank-
ings were permanent through time.
Morton tabulated the cranial capacities of different “races,” both in the
present or near term as well as in the past, by measuring ancient Egyptians
and Native Americans. Showing also that ancient skulls had cranial capaci-
ties comparable to their contemporaries made it clear to Morton that his
results supported polygenism. Morton’s work, emerging just before the Civil
War, was influential. One of the only individuals who stepped up to chal-
lenge Morton was Frederick Douglass. Douglass, born a slave, taught him-
self to read and had very little formal education. Yet, he brilliantly saw that
one’s conditions in life helped to create the person one became. Environ-
ments worked to shape man.
Douglass’s writings point clearly to the importance of environment in
shaping organisms and in this sense is early evolutionary thinking. More-
over, he was also aware of the biases in writing: “Scientific writers, not less
than others, write to please, as well as to instruct,” “and even unconsciously
to themselves (sometimes) sacrifice what is true to what is popular.” Finally,
although we focus on Morton, it is important to know he was not alone.
Other individuals were to echo his results and, more so, his sentiments.
Picking up on Douglass’s insights into bias and before we move on, you
might be aware that Morton’s results were re-examined by Steven Jay Gould
(1941–2002). Gould claimed that Morton finagled his results to fit his pre-
conceived notions. Others think that Gould might have also finagled his
restudy of Morton. What’s important is not Morton’s objectivity. After all,
his equating of cranial capacity with intelligence is incorrect. Rather, what is
important is that science was used to prove what the culture of those scien-
tists supported: slavery and polygenism.

DID THE END OF SLAVERY CHANGE IDEAS ABOUT RACE?

No.
In fact, what changed was that the end of legal slavery increased the fervor
of those in power to prove the races are separate and unequal and thereby
 38
H OW D I D R AC E B E CO M E B I O LO G I C A L?

to justify other forms of racism. Races became more equal under the law,
but those laws were often averted. Races remained unequal in power and all
aspects of life. With less legal support for slavery, scientists worked harder to
prove that races were inherently unequal. Indeed, Agassiz, one of the most
virulent racists in the history of American science, was hired to work with
the Freedman’s Bureau after the Civil War had concluded.
The ideology of race certainly did not end when slavery was declared
to be illegal with the passage of the Thirteenth Amendment of 1865. More-
over, no longer protected by the legal sanctioning of slavery, many scientists
continued to study racial differences with preconceived notions of racial
hierarchies.
There are many examples of the continuation of racist science. Efforts
were made to find the root of racial differences in all sorts of glandular sub-
stances and parts of the body. Researchers continued to focus on efforts to
prove differences in intellectual abilities both by examining brains and test-
ing cognitive abilities.
The research of Robert Bennett Bean (1974–44) provides a clear example
of the shift from skulls to brains and the continued drumbeat of racist sci-
ence. Bean, a professor of anatomy at the University of Virginia, wrote exten-
sively on subjects such as the biological uniqueness of the Philippines, the
Jewish nose, and black brains. In 1906, Bean published an eighty-page article
titled “Some Racial Peculiarities of the Negro Brain” in the American Journal
of Anatomy. This is a piece of science that has all the trappings of objective
science: there are lots of numbers, and its conclusions are clear and precise.
Bean makes four concluding points:

1. The brain of the American Negro is smaller than that of the American Caucasian,
the difference being primarily in the frontal lobe, and it follows that the anterior
association center is relatively and absolutely smaller.
2. The Negro brain can be distinguished from the Caucasian with a varying degree
of accuracy according to the amount of admixture of white blood.
3. The area of the cross section of the corpus callosum varies with the brain weight.
However, in the Negro its anterior half is relatively smaller than in the Caucasian,
to correspond with the smaller anterior association center; the genu is relatively
larger and the splenium relatively smaller.
4. From the deduced difference between the functions of the anterior and posterior
association centers and from the known characteristics of the two races the con-
clusion is that the Negro is more objective and the Caucasian more subjective.
 39
H OW D I D R AC E B E CO M E B I O LO G I C A L?

The Negro has the lower mental faculties (smell, sight, handcraftsmanship, body-
sense, melody) well developed, the Caucasian the higher (self-control, will power,
ethical and Esthetic senses and reason).

Bean’s career, including his service as chair of the Department of Anatomy,

is honored by the Robert Bennett Bean Award of the University of Virginia
School of Medicine. The award has been given annually since 1968 to a mem-
ber of the faculty for excellence in teaching the basic medical sciences. Bean
is buried in the university cemetery.
Work such as Bean’s in the tradition of anatomy and physical anthropol-
ogy was soon to be joined by work in the growing field of psychology and
mental testing by paper-and-pencil intelligence tests, and ultimately by the
growing field of hereditarian studies and eugenics.

IN THE TWENTIETH CENTURY, WERE JEWS, ITALIANS, AND

IRISH THOUGHT TO BE SEPARATE RACES?

Yes, but not in any consistent way.

Efforts were made to characterize different groups of Europeans as differ-
ent races. For example, William Z. Ripley characterized some dozen races
of Europeans in his “The Races of Europe” (1899), and Carleton Coon did
the same forty years later in his 1939 book of the same title. In between
these books were efforts to restrict immigration from Southern and Eastern
Europe and elevate the Nordic and Aryan racial type, and the genocide of
Gypsies and Jews as degenerate races.
Grasping at straws, practitioners of racist science tried to restrict the
composition of the club of whiteness and guard the borders between
white and nonwhite. The rise of eugenics in the 1910s and 1920s led to
efforts to protect the purity of the white race, white being so-called Native
Born whites. This purity was to be maintained by restricting immigration
from Eastern and Southern Europe and passing laws to prohibit marriage
between individuals of different races. Scientists such as Bean were explicit
and unequivocal in their desire to prove the superiority of the white race.
But who is white? And is there also a ranking and separation of European
racial types?
The greatest efforts were made to prove the separateness of Jews. Bean
pitched in and wrote on the unique features of the Jewish nose: “The nose of
the Jew is large. . . . That it is a Jewish feature cannot be doubted.”
 40
H OW D I D R AC E B E CO M E B I O LO G I C A L?

In 1927, E. O. Manoiloff of Leningrad published “Discernment of Human

Races by Blood: Particularly of Russians from Jews” in the American Journal
of Physical Anthropology. Manoiloff claimed that Jews and Russian blood
can be identified by adding reagents and watching their color change. He
proposed this method because it was difficult to make this discernment
based on physical features. Although Manoiloff wrote that he was success-
ful, his methods were entirely nonsensical and easily disproven. The paper
is a fraud and should have been so recognized by the journal editors. This is
the type of science that led Hitler to believe that the Jews were a separate race
that needed to be expunged from the Aryan population.
After the 1960s, eugenics began to fade, and race once again solidified
along the lines of protecting whites. Although prejudice still exists against
“Whites of a Different Color” in the United States, the category of white-
ness expanded to include the Irish, Polish, Jews, and others from Southern
and Eastern Europe.

ALTHOUGH CULTURAL IDEAS ABOUT THE NUMBER AND

TYPES OF RACES CHANGE, WHY DOES THE FUNDAMENTAL
CONCEPT—THAT HUMANS ARE DIVISIBLE BY DISCRETE
BIOLOGICAL GROUPS—PERSIST?

Scientists were never able to establish a replicable classification of races

because human variation is simply not racial. In the absence of an objec-
tive method, cultures are free to make up racial classifications to fit their
needs.
What needs to be understood is racial classifications as a cultural category
are subjective and will change over time and place as the dynamics of racial
interactions and racism change. These changes are seen in different classifi-
cations of race in different countries and even in the change in official clas-
sifications over time in the United States.
Yet, most Americans think that racial classifications are based in biology.
Biological race persists because it is a powerful ideology for maintaining the
status quo. If, for example, one can explain racial differences in infant mor-
tality as due to genes and inherent differences, rather than lived experiences
and racism, then one need not address this inequality. It is natural. A lot is
at stake in the belief in inherent biological differences, and that is why it is
so intractable.
 41
H OW D I D R AC E B E CO M E B I O LO G I C A L?

CONCLUSIONS

The existence of biological races in our species came to be the dominant

worldview. This worldview started to gain traction around 1492 and did so
in three phases: folk ideology, backed by the idea of types and a racial hier-
archy; legal separation of races; and scientific reification. Fully formulated
biological races (subspecies) did not come about until the 1800s and was
most virulently promulgated by pro-slavery scientists and those in support
of racist Jim Crow and anti-immigration laws. Today, the idea of biological
races has been disproved by science. Yet, the worldview that race is based on
biological differences persists and continues to hold back social justice and
science.
 Chapter Two

EVERYTHING YOU WANTED TO KNOW ABOUT

GENETICS AND RACE

This chapter focuses on the science of human genetic variation and why
humans are not divided into biological races. The big truth is that race
neither explains nor describes human genetic variation. Race-as-biology
is a myth and should never be used as a substitute for human genetic
variation.
To understand why humans do not have biological races, we clarify the
evolutionary forces that create and maintain genetic diversity (mutation,
natural selection, and genetic drift). In case you’re concerned about getting
bogged down in a lot of scientific lingo, we will attempt to explain these con-
cepts using clear, accessible language. We also encourage you to look up any
terms you don’t understand in one of the online glossaries that we referenced
in the preface.
We then point out why common notions of race are completely at odds
with the modern scientific understanding of human variation. Along the
way, you’ll be introduced to important concepts such as continuous variation
and discordant variation. We explain the importance of understanding the
structure of human variation and how it is measured. Finally, we state the
reasons that the existence of regional biological variation within our species
is not equivalent to the existence of biological races within our species. First,
let’s start with some basic genetics!
 43
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

WHAT IS THE HUMAN GENOME, AND HOW DID

WE COME TO READ IT?

To understand differences among individuals and groups, let’s make clear

what is being measured: differences in human genomes. A genome is an
organism’s complete set of DNA. The complete human genome contains
about 3.3 billion base pairs of DNA strung together on twenty-three pairs of
chromosomes of different sizes. One set of chromosomes is inherited from
the biological mother and the other from the biological father, totaling 46
chromosomes. The bases are paired sugars that make up the structure of
DNA. The four base pairs that you might be familiar with are adenine (A),
cytosine (C), guanine (G), and thymine (T).
Everyone except identical twins varies genetically. Recent advances in
human genetics have shown us just how similar all humans are genetically.
On average, about 999 of the 1,000 letters in base pairs of the genome are
the same among individuals. Alan and Joe, or Alan and you, or Joe and you,
whoever you might be, are about 99.9 percent similar genetically. This means
that each person differs from any other in about 3.3 million base pairs. So,
two questions arise. First, are two individuals who are purported to be in the
same race significantly more alike than two individuals in different races?
Second, what is significant?
Knowing that letters are different is akin to having a list of individuals who
attended a party. Useful information that might be, but if you want to solve a
murder that occurred at the party, it is important to know what every indi-
vidual was doing at the time the murder was committed. Gene expression is
like knowing what every individual was doing at any given time at the party.
In organisms like us, our DNA molecules are associated with a group of pro-
teins called histones. Histones play an important role in how these genes are
expressed in various tissues throughout the body. Of the 3.3 billion base pairs
in your DNA, only about 1.5 percent of them are directly involved in coding for
a protein. Another 7 to 8 percent regulates the expression of the protein-coding
DNA; in other words, about 90 percent of your DNA is not related to encoding
your proteins. Going back to our murder analogy, the 90 percent that are non-
coding could not have been involved in the crime. However, this noncoding
DNA plays an important role in how genetic ancestry, the genetic connections
that have developed through history, is determined by genetic tests.
 44
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

The second question is a tricky one, in part because “significant” has multi-
ple meanings, such as in statistics and significance with regard to a process or
context. For example, is being 99.92 percent genetically similar significantly
different from being 99.88 percent similar? The short answer is, it depends.
So, consider this a tease, and let’s save any more of this discussion for later.
It is amazing that we can answer the first question about how similar each
of us is genetically, thanks to a lot of hard work, technical breakthroughs,
and creativity. It is answerable because we have now read the full genomes of
tens of thousands of individuals from around the globe.
Here’s some backstory to how we got here. Do you remember The Human
Genome Project (HGP), which started in 1990 and ended in 2003? As a
reminder, it was the largest collaborative biological project in history, with a
final tally of $3 billion. The first draft of the human genome was announced
as complete on June 26, 2000, making local and national news. It was on the
front page, above the fold, of the New York Times. The accomplishment was
vaunted as unraveling the long book of life. That was hyperbole; it really isn’t
the book of life, but it was important. To our surprise, Craig Venter, president
of Celera Genomics and one of the captains of the HGP ship, announced on
that day that the new genomic information showed that race was a myth.
Actually, we knew already that race was a myth based on prior studies of
blood groups and the like, which we discuss later in this chapter. And his
finding, based on three individuals, added little to the scientific proof that
humans do not have biological races. But it was a headline that we agreed
with, and it did usher in many subsequent studies that examined the DNA
of many more individuals from different groups of peoples. These studies
put an exclamation point on the short declarative statement that “race is a
(biological) myth.”
After 2003, the National Institutes of Health’s National Human Genome
Research Institute (NHGRI) initiated a program to bring down the cost of
whole genome sequencing to $1,000 in ten years. This accelerated the devel-
opment of new sequencing technologies (called next generation sequencing, or
NGS), resulting in unimaginably fast genome sequencing speeds. By 2014, the
$1,000 genome had been achieved. Since the dramatic reduction of sequenc-
ing costs, hundreds of studies of human genetic variation have been con-
ducted. These studies compared the nucleotide sequences of specific genes, as
well as entire genomes, including comparisons of the genomes of populations
from all over the globe. The results further validated Venter’s original claim
that the notion of biological races within our species is a myth.
 45
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

HOW MUCH DO HUMANS VARY GENETICALLY FROM ONE

ANOTHER AND BY POPULATION?

The ultimate sources of all genetic variation are mutations. Mutation refers to
random changes in the genetic code due to an error in DNA replication. The
enzymes responsible for replicating DNA are like any other machine: they
usually replicate DNA with great fidelity, but every now and then, mistakes
happen. The mutation rate for organisms most like ourselves (mammals) is
incredibly low, about 1 mutation per one hundred million (108) base pairs.
From that point, the fate of mutations varies. The vast majority of muta-
tions within coding regions of genes are harmful and are therefore removed
or kept at low frequencies by natural selection. Next in frequency are neu-
tral mutations; many of these are found in the noncoding portions of the
genome. This is where most genetic variation will be observed in any species.
This variation is largely neutral, but it is useful for determining ancestry (see
chapter 9). Finally, a small proportion of mutations are beneficial, and these
are increased in frequency by natural selection. Their frequency will differ
by geographical region as well as other aspects of environments (such as diet
or the presence of parasites).
As a result of the NGS revolution, we know that on average about 99.9
percent of the genomes of all living humans are the same. There may be a
higher amount of difference between individuals due to copy number vari-
ants (CNV), making humans 99.4 similar in these variants. Copy num-
ber variants result from the genetic processes of duplication, deletions,
insertions, and inversions. The global differentiation of SNPs and CNVs
are pretty much the same, meaning that there is more variation within
populations than there is between populations for these types of genetic
variants. Of those differences, the majority are shared in all populations
across the globe, smaller amounts are unique to continental origin, such
as Africa, Asia, or Europe; and even less are unique to a region within a
continent, such as East or West Africa. The distribution of these differ by
population.

HOW DO SCIENTISTS EVALUATE GENETIC DIFFERENCES

AMONG GROUPS OF INDIVIDUALS?

There are a number of ways to think about, and tools to measure, the genetic
similarity (or difference) among groups (or populations). One of the most
 46
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

tried and best known is the population subdivision statistic (FST), which was
invented by the American population geneticist Sewall Wright (1889–1988).
This statistic quantifies the difference in the frequencies of alleles in a popu-
lation compared with the allele frequency of the entire species. Remember
that at the level of the DNA, an allele is an alternative spelling of a gene. For
example, sickle cell allele is an alternative spelling of the gene that codes for
the beta chain of the hemoglobin molecule.
FST is mathematically simple. FST is the variation within a population over
the total variation. Results can range from 0 (no population subdivision) to
1.00 (complete population subdivision). The higher the FST, the more differ-
ences among populations. For a number of theoretical reasons, Wright felt
that an FST value exceeding 0.25 would indicate the presence of something
akin to subspecies or biological races within a species.
Whole genome studies of humans show that our population subdivision
between major continental groups is much less than 0.25. Exactly how much
lower varies by study and what is being studied. For example, it is about
0.110 for protein-coding genes. These values are much smaller than those
observed in other large-bodied mammals.
However, it would be a mistake to think that the FST values for all human
genes are low. Humans display geographically based genetic variation, such
that some genes are strongly differentiated between population groups. For
example, for one single nucleotide polymorphism (SNP) associated with
a greater risk of Crohn’s disease (rs10761659), the global FST is 0.351, with
the frequency of this risk allele worldwide at 0.542. In Africa it is 0.015; the
Middle East, 0.427; Europe, 0.507; and East Asia, 0.759. For another SNP
associated with Crohn’s (rs100777885), the FST is 0.062, with the frequency
of the risk allele worldwide at 0.820; in Africa, 0.975; the Middle East, 0.809;
Europe, 0.812; and East Asia, 0.898. In the former case, the frequency in
Africa is different from the rest of the world, whereas in the latter case, the
frequencies are similar in these different regions of the world.

HOW DOES THE TOTAL AND APPORTIONED HUMAN

VARIATION COMPARE WITH THE VARIATION AMONG
GORILLAS AND OTHER MAMMALS?

We humans are a young species. One clear result is that we have very little
genetic variation compared with that of other species. What’s most interest-
ing about humans is that despite their global range, they exhibit less variation
 47
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

1.00
0.90
0.80
0.70
Average FST

0.60
0.50
0.40
0.30
0.20
0.10
0.00
ril ral e

ia
Bo ort st A a

es out , Ke l
No st A a

ya

S pe

nt ra

r, E ia
ica
ca

an ca
ca

st ica
ild h A ica

n, por ee, a
rn ise rica
a

nd ny
i

ic
p

as
al lo, E mib

pa ob

ge as
ha at
fri

C Gira en
, W fri

fri
o

an uro

d, Gaz Afr
r

or an Afr
fr

a a Ke
eb me

Af

ur
Ti Eur
r

ep um
A
Hu st A

Or Zeb Im , gl
, C Eu

K
a Na

eo , E

,
an arb imp fe,
,

ric e,
la
bo rn
a

rn ea
e

Af ell
f
Go nt

ee
Bu ah,

d
z
no he

t
h

Bo po
e

r
t

la
ee

El
f
Ch

, w a, s
,N

H h
te
r
se

ar
op
or

ta
ca
rb

Le
gu
Ha

Or

FIGURE 2.1. Average FST values for humans and other large mammal populations. Source: Courtesy of Alan
Templeton.

among regions and continents than most other mammals. For example, the
human FST of about 0.15 is considerably less than in geographically limited
species such as orangutans and gazelles (fig. 2.1).
The chimpanzees of tropical Africa also contain within-species varia-
tion. These animals are considered to have subspecies or geographical races.
The FST value between Western and Nigerian-Cameroonian chimpanzees is
0.270, greatly exceeding Wright’s 0.250 threshold.
The amount of genetic variation within any species is determined by the
mutation rate, the amount of time the species has existed, and demographic
events such as a population bottleneck that occurred during the time that
it existed. There is some evidence that mammalian mutation rates differ by
climate, such that mammals that evolved in the tropics have slightly higher
rates than those that evolved in the temperate and Arctic zones. Thus, we
would expect humans (who evolved in the tropics) to have slightly higher
rates than polar bears (which evolved in the Arctic).
Modern humans have been on this planet for about 300,000 years. This
duration is typical of animal species. About 90 percent of all existing species
formed in the last 100,000–200,000 years. This is consistent with what we
know about the fossil record of complex organisms on Earth. It shows that
 48
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

most complex species—especially hominids—had relatively short durations

in the history of life. Examples include Homo ergaster (1.8–1.5 Mya, dura-
tion 300,000 years), Homo erectus (1.2–0.4 Mya, duration 800,000 years),
Homo heidelbergensis (0.6–0.2 Mya, duration 400,000 years), and Homo
neanderthalensis (0.3–0.03 Mya, duration 270,000 years). Thus, the small
(0.1 percent) difference between any two humans who currently reside on
this planet is similar to what we observe in most other animal species. By
comparison, if genetic diversity is simply a function of species duration, we
would expect that H. erectus was probably the most diverse and H. neander-
thalensis the least diverse of all human species.
Thus, considering that 200,000 of our 300,000-year existence was spent
in Africa, it makes sense that sub-Saharan Africans contain more genetic
diversity than all other human groups. In addition, non-African humans left
Africa in the late Pleistocene and lost genetic variation due to the founder
effect (genetic drift).
Comparing the sister species of chimpanzees (Pan troglodytes) and bono-
bos (Pan paniscus) helps to understand how the demographic history of a
species affects its genetic variability. These species share a recent common
ancestor with humans, between five and thirteen million years ago. The two
chimp species are thought to have diverged approximately one to two mil-
lion years ago and have experienced different demographic histories since
their divergence. The history of bonobos is marked by population bottle-
necks (sharp reduction in numbers) in the past and a smaller long-term
effective population size. They were also geographically isolated in central
Africa for a long time. Bottlenecks, isolation, and small population size all
serve to decrease genetic diversity.
On the other hand, chimpanzees inhabited a much wider region across
Africa (from Tanzania to Guinea, at the east and west edges of Africa). Most
chimpanzee subspecies, except the western population, had larger population
sizes, and not surprisingly, they maintained a greater level of genetic diversity
compared with bonobos. The western chimpanzees are thought to have spread
from a very small ancestral population, whereas central chimpanzees con-
tinuously inhabited central Africa. Thus, these demographic events mean that
chimpanzees are more genetically diverse than their sister species, bonobos.

WHAT EXPLAINS HUMAN GENETIC DIFFERENCES?

As we discussed previously, genetic differences in our and all other species

start with mutations. A combination of selective and random events then
 49
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

determines the frequency of the mutations in any given population. Our

species originated in sub-Saharan Africa and stayed there for 200,000 of
its 300,000-year existence. Due to climate changes in the late Pleistocene,
humans were able to migrate out of Africa. Migration also occurred within
Africa. It is the second-largest continent and spans the greatest amount of
latitude compared with all other land masses (37° N to 35° S). Today, there are
at least seven vegetation zones: tropical forest, wooded savannah, subtropi-
cal moist lands, subtropical dry lands, thorn brush vegetation, low altitude
desert, and highlands.
At the end of the Pleistocene, the Sahara occupied considerably less area
than its current confines. This means that human populations that migrated
within Africa faced new environmental conditions. This in part explains why
sub-Saharan Africans display greater genetic diversity than all other world
populations. More time equates to more opportunity to build up variation.
The migration out of Africa was also bidirectional. Studies of ancient DNA
indicate that back-and-forth migration occurred between regions within
sub-Saharan Africa, between sub-Saharan Africa and the Middle East, and
between the Caucasus/Southern European regions and sub-Saharan Africa
during the first great migration of modern humans. The migrating popu-
lations were smaller than their originating populations. Thus, by statistical
necessity, these migrants contained less genetic variation (founder effect/
genetic drift) than the populations from which they originated.
Migration between populations is an additional factor that works against
strong genetic differentiation. Thus, gene flow among human population
centers is one of the reasons that humans never formed geographically based
biological races (or subspecies). Unlike other species that separate geograph-
ically and, once separated, remain so, humans have a history of back-and-
forth migration and continual interchange across geographic areas.
As human populations established themselves in new regions, they also
began to accumulate new mutations. Some of these mutations were benefi-
cial and increased until fixation in these populations. Fixation means that all
individuals within the population would have the same allele at the locus in
question. As all new mutations are rare, the rate at which they achieve fixa-
tion is dependent on their evolutionary fitness or differential survivorship
and reproduction (see fig. 2.2). Generally, in nature, the force of selection on
complex traits is very weak. Thus, changes in traits like behavior take a very
long time. Genomic studies over the last decade have allowed us to gain a
better understanding of how much and where adaptation occurred in our
species over the last 200,000 years. A list of these traits appears in table 2.1.
 50
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

1.0

0.8
Frequency

0.6

0.4

0.2

0.0

0 10 20 30 40 50 60
Generations
Frequency of wild type gene
Frequency of beneficial mutation

FIGURE 2.2. A selective sweep of a rare beneficial mutation with a strong fitness effect. As the beneficial
mutation increases in frequency, the “wild type” gene must decrease as the frequency of p + q = 1, where p is
the frequency of the wild type and q is the frequency of the beneficial mutation. The algebra governing this
relationship shows that even a weakly beneficial mutation will eventually replace the wild type. The number
of generations required for this to happen is a function of the selective pressure.

Most of them are not surprising. Humans adapted to altitude, new climates,
diets, pathogens, solar intensity, and toxins. What might be surprising to
some is that these adaptations generally have a relatively simple genetic basis.
For example, a single mutation, a substitution of A to T at the sixth position
on the beta chain of the hemoglobin molecule, causes an amino acid change
from glutamic acid to valine. That change leads to a different folding of the
molecule that confers resistance to malaria. These types of mutations are rare
but do occasionally occur!
Skin color variation is greatest among Africans, considering that Africa
passes through the largest latitude. One variant associated with fair skin,
SNP rs1426654 (G to A), is found in modest frequency in East Africa (0.571
in Somalis), but it went through strong selection in fair-skinned populations
such as Europeans, Central Asians, and North Indians (frequency of A =
1.00). Thus, modern human genetic diversity is explained by natural selec-
tion for variants, allowing adaptation to various features of the environment
in different portions of the globe, combined with aspects of population his-
tory, as further explained in the next question.
What explains variation? In the end, it is the processes of adaptation to
local conditions, gene flow, and genetic drift, all of which are dependent on
 51
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

TABLE 2.1
Adaptation in Modern Humans

Trait Genes Locus Locations

Lactose tolerance MCM6 2q21.3 E. Africa, ME, N. Europe

Arctic environment CPT1A, LRP5, 11q13.3, 11q13.2, 2p21, Siberia
THADA, PRKG1 10q11.23-10q21.1
High-fat diet FADS1, FADS2, FADS3 11q12–11q13.1 Greenland
Thick hair EDAR1 2q13 E. Asia
Starchy food AMY1 1p21.1 E. Asia
Skin pigmentation SLC24A5, SLC45A2, 15q21.1, 5p13.2, 11q14.3, Europe
TYR, MC1R 16q24.3
High altitude VAV3, ARNT2, THRB, 1p13.3, 15q25.1, 3p24.2, E. Africa, Himalayan Mts,
EGLN1, EPAS1 1q42.2, 2p21 Andes Plateau
Trypanosome resistance APOL1 22q12.3 W. Africa
Malaria resistance G6PD, HBB, GYPA, Xq28, 11p15.4, 4q31.21, Tropical Africa,
GYPB, GYPC 2q14.3 Mediterranean, ME
Toxic arsenic AS3MT 10q24.32 Argentina
Increased BMI CREBRF 5q35.1 Melanesia
Height (shorter) CISH, DOCK3, STAT5, 3p21.2, 3p21.2, 17q21.2, W. and C. Africa
HESX1, POU1F1 3p14.3, 3p11.2
Height (taller) Polygenic 294,831 SNPs across N. Europe
multiple chromosomes
accounted for 45 percent
of variance in height.
Note: Adaptation in modern humans is supported by strong genomic and evolutionary evidence. The table shows the type of
adaptation and specific genes (where possible) that are associated with it. The chromosomal locations of the genes involved
in the specific adaptation are also provided. Note that relatively simple genetic mechanisms are associated with the examples
is this table.
Data are modified from S. Fan, M. E. Hansen, Y. Lo, and S. A. Tishkoff, “Going Global by Adapting Local: A Review of
Recent Human Adaptation,” Science 354, no. 6308 (2016): 54–59. SNPs for variation in height are discussed in J. Yang, B.
Benyamin, B. P. McEvoy, et al., “Common SNPs Explain a Large Proportion of the Heritability for Human Height,” Nature
Genetics 42, no. 7 (2010): 565–69.

variables such as time and population size. And none of these processes has
made for deep separations and variations among people on different conti-
nents. This is why we do not consider variation within our species to have
created human races.

ARE HUMAN GENETIC DIFFERENCES CLUSTERED INTO

GEOGRAPHIC AREAS, OR DO WE CONTINUOUSLY VARY, LIKE
A WEATHER REPORT OF TEMPERATURES?

Short answer: humans vary continuously. This is because of a process called

isolation by distance. The rule of human evolution is continuous variation
 52
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

across geographic areas. Geographic closeness is very highly correlated with

genetic similarities.
The first thing to know is the history of human occupation of the globe.
We are an amazing species in our ability to occupy virtually all land masses.
Modern humans, those individuals who led to us, arose in and left sub-
Saharan Africa sometime between 50,000 and 100,000 years ago. They might
have traveled by foot in multiple waves, and some might have left Africa by
different routes.
These modern humans encountered other species of humans, such as Nean-
derthals in southern Europe. Although the groups might have competed and
made war, the genetic evidence makes it clear that they also reproduced with
each other, and most people of Eurasian descent have a small (1–3) percent of
Neanderthal gene sequences (see chapter 9 for more details). The first modern
humans arrived in Europe around 43,000 years ago. These people did not con-
tribute much genetic information to modern Europeans. The ancestors of those
who currently live in Europe arrived around 7,000–10,000 years ago. Those
first modern humans who arrived in Europe were primarily hunter-gatherers.
Later, humans who had developed farming replaced the hunter-gatherers. A
third wave of migration into Europe occurred about 4,500 years ago (during
the early Bronze Age). These migrants were descendants of hunter-gatherers
who originated in what today is modern Russia and the Caucasus Mountains.
In addition to being populated by part of the wave of peoples coming
through the Middle East, Asia was home to at least two early waves of migra-
tion: first by the ancestors of Australians and the Papuans, followed by other
ancestors of East Asians.
The archaeological evidence suggests that modern humans were present in
Oceania 47,500–55,000 years ago. The extensive genomic study of Papuan and
aboriginal Australians suggests that genetic divergence between these groups
might have been driven by climate changes and that the aboriginal Austra-
lians were living in a relatively high level of isolation until modern times.
The earliest arrival of modern humans in the Americas is accepted to be
about 14,000–15,000 years ago. The widespread occupation of the Americas
is associated with the Clovis culture (~12,600–13,000 years ago). It is likely
that the genomic divergence of Siberians and the American Indian popula-
tions began around 23,000 years ago. This suggests that American Indians
moved into the Western Hemisphere earlier than indicated by the dating of
archaeological remains; however, by what means and routes this occurred is
still uncertain and has generated a considerable degree of disagreement.
 53
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

The migratory paths of humans around the world led to divergences in

their gene frequencies, driven primarily by their population history (par-
ticularly genetic drift). The answer to the foregoing question focused on the
role of natural selection in producing adaptation to new environmental chal-
lenges that were faced by our migrating ancestors, but this amounts to the
smaller part of the differences in the gene frequencies we observe in modern
humans. Also, as people migrated around the globe, the distance between
populations reduced the amount of gene flow between them, allowing natu-
ral selection to increase the frequency of local adaptations and for genetic
drift to differentiate populations from one another by random chance.
The best way to explain the distribution of human gene frequencies is the
isolation-by-distance model. This means that the genetic similarity of popula-
tions is directly a function of how geographically close they are (fig. 2.3). This
figure shows that the value of the FST statistic between any two populations
of humans increases linearly with the distance between them. Thus, sub-
Saharan Africans and Europeans are more similar to each other than either
is to Amerindians. The distance from Lagos, Nigeria, to Berlin, Germany, is
4,555 km. The distance from Lagos to the eastern portion of North America
is more than 18,000 kilometers (via the early human migration route). East-
ern Europeans and western Asians would be more similar to each other than
either is to sub-Saharan Africans, and so on. This change is also continuous,
displaying no gaps or clusters in populations. It is also worth noting that the
FST values in figure 2.3 never exceed Wright’s critical value for the existence
of biological races (0.25). The maximum value of the regression line is ~0.15.
The figure also shows that the genetic diversity of humans declines with
distance from Africa. This results from the founder effect (genetic drift) phe-
nomenon. Each newly founded population contains a subset of the genes
of the parental population. As this process continued in a series of found-
ing events, each population continued to lose alleles, becoming less diverse.
For example, for the human histocompatibility A locus (HLA), there are
31, 23, 20, 21, and 9 alleles for Africa, Europe, East Asia, South Asia, and
the Kolla people of northwest Bolivia, respectively. Researchers believe that
the extreme lack of HLA diversity in the Kolla resulted from the original
population bottleneck that resulted from the migration of humans to the
Americas, not some recent event associated with the colonization of Bolivia
by Europeans.
There is some debate concerning the processes that explain the isola-
tion-by-distance pattern we see in humans. In the 1990s, the predominant
 54
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

0.25
Genetic distance (FST)

0.20
0.15
0.10
0.05
R2 = 0.7679
0
0 5000 10,000 15,000 20,000 25,000 30,000
(a) Pair-wise distance between populations (km)
Gene diversity (Hs)

0.9
0.8
0.7
0.6
0.5
0.4 R2 = 0.8493
0.3
0 5000 10,000 15,000 20,000 25,000 30,000
(b) Distance from East Africa (km)

FIGURE 2.3. The genetic distances (FST) between populations is a linear function of the geographic distance
separating the pairs (a). The genetic diversity found within a population declines with distance from East
Africa (b). Source: L. J. Lawson Handley, A. Manica, J. Goudet, and F. Balloux, “Going the Distance: Human
Population Genetics in a Clinal World,” Trends in Genetics 23, no. 9 (2007): 432–39.

explanation for isolation by distance was the serial founder event model
described earlier. However, new data resulting from technology that allows
for the study of ancient DNA has called into question a simple serial founder
events explanation (more details are provided in chapter 9). David Reich and
his coworkers suggest that this model will need to be modified to account
for remixing of “significantly” diverged populations, or some combination
of both models. In either case, a few barriers to migration, such as oceans,
mountain ranges, and deserts, modify genetic continuity. But the overriding
fact is that human genetic variation is continuous.

WHY DO SOME GENETIC TRAITS CORRELATE WITH EACH

OTHER, WHEREAS MOST TRAITS ARE INDEPENDENT (NOT
CORRELATED) WITH OTHER TRAITS?

Genetic correlation can result from two processes: linkage or pleiotropy. Of

these, the first term is easiest to understand. Linkage refers to the fact that
genes are found in the same region of a chromosome. For this reason, during
 55
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

crossing over in meiosis (the process that produces egg and sperm cells from
the ovaries and testes, respectively), the genes are inherited as a block. If
selection favors one gene in a given region, then the nearby genes will also
increase in frequency along with the gene under selection. In table 2.1, the
genes for adaptation to an Arctic environment (CPT1A, LRP5) are found at
11q13.3 and 11q13.2, respectively. Furthermore, the genes associated with tol-
erance to a high-fat diet (FADS1, FADS2, I) are found nearby at 11q12–11q13.1.
Finally, a gene associated with lighter skin pigmentation (which could in
turn be associated with better vitamin D synthesis in lower solar intensity)
is found at 11q14.3.
It turns out that populations such as the Inuit have high frequencies of the
alleles associated with survival and reproduction in the Arctic at all of these
loci. This could have resulted from selection that favored any one of them
and carrying along all the others. The Inuit managed to live in the Arctic, eat
high-fat diets, and evolve lighter skin. The HBB gene that confers resistance
to malaria is found at 11p15.4. This locus is on the other end of chromosome
11 and is therefore not linked to Arctic tolerance genes. Thus, selection for
Arctic tolerance had no impact on malaria resistance.
In pleiotropy, one gene is involved in producing multiple traits. For exam-
ple, having the capacity to tolerate a high-fat diet allows the body to generate
greater fat stores, which in turn might produce a greater capacity to retain
heat, also allowing for better survivability at Arctic temperatures. This is an
example of positive pleiotropy.
On the other hand, negative (or antagonistic) pleiotropy occurs when a
gene influences traits in opposite directions. There is abundant evidence
from the literature on experimental evolution that antagonistic pleiotropy
played a major role in influencing the survival and reproduction of model
organisms (nematodes, fruit flies, yeast). It is likely that antagonistic plei-
otropy plays an important role in driving the evolution of genes that cause
cancer at a later age (because they are beneficial at earlier ages). It is possible
that the increase in frequency of the mutations that causes cystic fibrosis
in northern Europeans resulted from antagonistic pleiotropy (beneficial in
increasing reproduction and lowering infection, but detrimental in causing
cystic fibrosis).
But most of the traits that we see in humans are not at all consistently
correlated with one another. This is called discordance. Traits that are found
on different chromosomes (or arms of chromosomes) will be inherited inde-
pendently (such as the TYR 11q14.3 and HBB 11p15.4 genes). If these genes
 56
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

influence different traits, there is no reason that they would be genetically

correlated. In addition, the various aspects of environment faced by human
beings are not always correlated. For example, latitude (solar intensity) and
altitude are not correlated. The altitudes of Ethiopia and Tibet are around
4,550 and 5,000 meters (9.14° N and 31.86° N), respectively. Both Ethiopians
and Tibetans have high-altitude adaptations but differ in skin color as well
as biometric proportions of their skeletons. Thus, Ethiopians are a domi-
nant force in world long-distance running due to their combination of high-
altitude adaptation, biometrics, and culture. But no such dominance is
observed in Tibetans, because although they have high-altitude adaptation,
their biometrics and culture were not conducive to success at long-distance
running. However, if you were attempting to climb Everest, you would be
better off with a Tibetan Sherpa helping to carry your gear than an Ethiopian.
There is an important implication of discordance; namely, that one can-
not extrapolate from one trait to almost any other trait. For example, we
might be able to extrapolate from skin color to hair and eye color because of
pleiotropy, but we cannot extrapolate almost anything else from skin color.

IS THERE ONE HUMAN SPECIES? CAN WE DEFINE SUBUNITS

WITHIN OUR SPECIES? IF SO, WHAT DO WE CALL THEM?

At present, there is only one human species on Earth. You have already
learned that this was not always so. Around 300,000 years ago, our species
shared the planet with at least six other archaic human species (H. erectus,
H. floresiensis, H. antecessor, H. heidelbergenesis, H. neanderthalensis, and
H. naledi). It is unclear whether the Denisovan humans should be considered
a subspecies or a species in their own right. The evidence suggests that our
species became hybridized through reproduction with the archaic humans
H. naledi (in sub-Saharan Africa), H. neanderthalensis (in Eurasia), and the
Denisovans (in East Asia, Melanesia, and Australia). In modern humans,
about 1.0 to 2.0 percent of genes originated in these other species.
How one decides to classify human subgroups within anatomically mod-
ern humans is not as objective as we might prefer. Modern genomics has
allowed the sequencing of thousands of genomes from around the world.
The sequence data allow for the application of computational methods to
sort individuals into groups. In one popular program called STRUCTURE,
one can sort them into any number of groups. But because variation is con-
tinuous, some individuals will seem to be made up of more than one group.
 57
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

However, it is clear that whatever the methods used, no group within

our species can be considered a biological race. Interestingly, when genomic
methods are used to divide humans into nineteen ancestry groups, it turns
out that most, twelve of the nineteen, are sub-Saharan Africans. Why?
Because of the greater variation within Africa.

WHY IS IT THAT YOU CAN ALMOST ALWAYS TELL A NIGERIAN

FROM A NORWEGIAN, YET A NIGERIAN AND A NORWEGIAN
DO NOT GENETICALLY DIFFER THAT MUCH?

Nigerians and Norwegians differ in the frequencies of several physical traits.

The most apparent of these are skin and eye color. Yet the genetic foundation
of these traits is very simple. There are only five or six major genes associated
with skin color and one or two associated with eye color. As there are around
23,000 protein-coding genes in the human genome, only 0.03 percent of the
genome accounts for these apparent physical differences.
Also, the differences in allele frequencies along the geographic distance
from Nigeria to Norway are continuous. If you were to walk from Lagos to
Oslo, you would have a very hard time figuring out where dark skin begins
to shade into lighter skin tones. Rather than an abrupt change in skin color
or any physical feature, what you’d find is continuous change in the physical
appearance of the people you meet.
Yes, if you had a room full of Nigerians and Norwegians you could proba-
bly sort them out. But that has nothing to do with “race.” Your success in sort-
ing is based simply on the fact that Norwegians and Nigerians live far away
from each other and have evolved obvious differences in skin and eye color.

DO OUR SOCIAL CATEGORIES OF RACE MAP ONTO

“BIOLOGICAL UNITS”? THAT IS, HOW CLOSE ARE OUR SOCIAL
DEFINITIONS AND IDEAS ABOUT RACE TO SOME SORT OF
BIOLOGICAL GROUP?

For all the reasons that have been discussed in this chapter, the social defini-
tions of race utterly fail to describe the underlying biological variation found
in human beings. In addition, social definitions of race are historically and
culturally contingent. The meaning of Black differs in various societies. In
the United Kingdom, Black includes Pakistanis and East Indians. In Bra-
zil, it includes many persons of African descent, who would be classified as
 58
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

something else in the United States. In the United States, Black includes any-
one with detectable African descent. In the Caribbean, white includes any-
one with any European descent, including people who would be classified as
Black in the United States. Social races change over time and place. That is
fine and appropriate. But science requires stable classifications in order to be
replicable. These categories are clearly not biologically justified.

CONCLUSIONS

Human genetic and phenotypic variations are real and measurable. Humans
are unusual in that one species has colonized the globe. Yet, humans in dif-
ferent regions have not formed discrete subspecies or biological races. That
is a measurable reality. The reasons we have not formed biological races
include that we are a young species with little time to develop differences,
especially outside sub-Saharan Africa, and the continuous exchange of genes
and contact of humans across wide geographic areas.
Human variation is not explained by race. Rather, variation is explained
by evolution. Evolution acts locally, not on social races or continents. Race
also does not describe human variation. Variation is nonracial. It is almost
always continuous, without clear breaks, and it is nonconcordant. Finally,
variation within a continent, social race, or local group is much greater than
variation among them.
The bottom line is that human biological race is wrong and continued
use of the concept in scientific and public discourse is ultimately harmful.
 Chapter Three

EVERYTHING YOU WANTED TO KNOW

ABOUT RACISM

Is that racist? Am I a racist? What, if anything, is reverse racism?

“Racism” and “racist” are common terms. Not too long ago, racism was
unapologetically embraced by the nation’s leaders and most of its popula-
tion. We remember watching Alabama Governor George Wallace on TV as
he proclaimed in his inauguration speech on January 14, 1963, to a cheering
crowd, “Segregation now, segregation forever.” Now, almost no one wants to
be called or considered a racist. Donald Trump, despite his public actions,
declares himself “the least racist person.” Ignoring or being oblivious to rac-
ism is obviously damaging. It is also problematic to be paralyzed by the epi-
thet of being called a racist. By neither ignoring nor cowering from the label
of racist, we move toward antiracism. And in focusing endlessly on racism
as personal, these discussions move us away from some hard work and the
focus on racism as a historical and present-day system.
In chapter 1, we outlined the history of the cocreation of race and racism.
The preposterous idea of biological races was needed to justify what phi-
losopher Charles Mills calls the “racial contract” and what Isabel Wilkerson
refers to as a U.S. caste system. Racism results from the operation of a caste
system or levels of closeness to God, the old Great Chain of Being. In this
chapter, we move to the present and provide you with basic definitions that
help to differentiate among some crucially important but commonly con-
fused terms. We break down the difference between prejudice and racism
 60
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

as well as forms of racism, such as racist actions and thoughts, individual

and institutional racism, and how they all connect into a system. We provide
clear and concrete examples to help you recognize when ideas and behaviors
are racist and when they are not, as well as how individual racist thoughts
and behaviors relate to systemic and structural levels of racism.
To be sure, racism is in the ideological air we breathe. We end with a dis-
cussion of white supremacy and data showing the persistence of racism and
racial inequalities. It is time for all of us to look in the mirror, take on racism,
and move together toward antiracism.

WHAT ARE THE DIFFERENCES AMONG THE TERMS “BIGOTRY,”

“BIAS,” “PREJUDICE,” “XENOPHOBIA,” “ETHNOCENTRISM,” AND
“RACISM”? HOW ARE THEY DEFINED AND CONNECTED?

These terms are interrelated and have overlapping meanings. Bigotry refers
to intolerance of any belief or opinion that differs from one’s own. For exam-
ple, one can be a religious bigot. One can be aware of one’s own bigotry,
or it can be unconscious. Prejudice, related to bigotry, refers to an opinion
against a group that is typically based on preconceived notions rather than
actual experience or reason. It is a preconceived notion that can result from
the elementary, logical fallacies of composition and division. The fallacy of
composition results when one takes the characteristics of an individual and
then infers that all members of a group have that characteristic. The fallacy of
division takes a statistical characteristic of a group and infers that all mem-
bers of the group have that characteristic.
Bias is similar to prejudice and bigotry but slightly more inclusive: it refers
to beliefs and actions for or against any object, thing, person, or group com-
pared with another based on preconceived notions. One can also be biased
toward an explanation or mode of thinking, and reckoning with such biases
is also of great importance. We all have biases and preconceived notions
that act as shortcuts. That is, because our biases result from the fact that our
brains were produced by natural selection (descent with modification), and
many of them are predictable. That is why when we think we’ve seen some-
thing before, our tendency is to take a shortcut to explanation. Guarding
against bias is important in science as well as in daily life. One might have a
bias toward simple and genetic explanations for racial inequalities in health.
These are very common in our culture. Most people prefer simple, genetic
explanations for biology and behavior.
 61
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

Finally, biases might be conscious and explicit. We are aware of our biases.
Alan’s favorite basketball player is Jaylen Brown of the Boston Celtics. Joe’s
favorite is LeBron James. Both Alan and Joe love spaghetti and meatballs,
one of their favorite suppers as children. But more often, bias is unconscious
and implicit. We are not even aware that our brains are pushing us in certain
directions because of lessons we learn without thinking of them throughout
our lives. When a job applicant is selected over other applicants because he
or she has a white-sounding name, that is an implicit bias. The recruiter
probably has no idea that he or she is making an unconscious decision based
on associations with a name. A great deal of our ideological and personal
racism is unconscious or implicit.
Xenophobia is a fear or hatred of others. It appears to be common that
some individuals approach those in other groups with some degree of cau-
tion. We are, after all, less familiar with the customs and behavior of people
in other groups. The Athenians were definitely cultural xenophobes, calling
other groups uncivilized or savages, which are xenophobic epithets. Some
evolutionary theorists and anthropologists consider fear of strangers (xeno-
phobia) as a sort of hard-wired behavior used for protection of the cultural
group. There is evidence for this view, as xenophobia exists in all anthropoid
apes (humans, chimpanzees, gorillas, and orangutans) and therefore might
have originated in their common ancestor. But make no mistake: even if
xenophobia might have some support based on evolution, it is not inevitable,
and it certainly is not an explanation for racism. If anything, xenophobia
has been used as an excuse for institutional racism. Finally, there is just as
much evidence from evolution for the desire of others and the evolutionary
importance of exogamy, mating outside one’s group.
Xenophobia also lapses into ethnocentrism, a preference for one’s own
culture and the evaluation of other cultures according to preconceptions
derived from one’s own. However, humans also seem to have an attraction
to others. The other is often seen as exotic and attractive. Although there
might be some evolved and genetic basis for xenophobia and ethnocentrism,
the specifics are highly cultural. For example, Donald Trump’s stated prefer-
ence for immigrants from Norway or Eastern Europe rather than the Middle
East or Mexico is his personal, learned expression of his ethnocentrism and
xenophobia.
These ideologies and behaviors intersect with one another, as they all
have to do with negative preconceptions and behaviors toward individuals
in other groups, whether different genders, social classes, castes, ethnicities,
 62
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

citizens of other states or countries, or race. These negative perceptions are

often unconscious.

Defining Racism

As we discussed in chapter 1, the most common and simple definition of

racism is prejudice plus power. This definition highlights that racism is a
form of prejudice against people of another socially defined race. However,
to be racist requires a power differential or an ability to move the wheels of
institutions that have power over individual lives. By this definition, within
the contemporary U.S. power structure, a Black or brown person can hold
prejudices against a white person, but they have no or limited power to act
on their prejudice and to be racist against a white person. By this definition,
reverse racism is not a thing (see the later discussion). The cultural legacy of
the United States is responsible for the moronic concept of reverse racism.
For most of our history, it was normal for whites to unashamedly enact racist
policies and laws against Blacks, browns, and reds.
We like the short definition of racism (prejudice plus power) but want
to go further and make sure it is clear how racism is linked to the belief in
biological races. The “rocket fuel” of racism is the belief that biological races
are different, innate, and hierarchically arranged by God and/or evolution.
Ibram X. Kendi says that if you believe in biological race, you are a racist.
We would say you are an ideological racist or racialist. However, there is a
strong correlation between racialism and racism. The belief in innate biolog-
ical differences can then justify racial differences in wealth and health as just
part of those innate differences rather than being attributable to structural
and institutional forms of racism. The belief in biological race can become
an excuse for racism.
To clarify, there are two intersecting forms of racism. One is more per-
sonal and ideological and includes the varied and everyday notions of racial
difference and hierarchy. It is what individuals think, consciously or sub-
consciously, which form patterns of thought and actions that are inherited
through history and culture. Kendi says that this is a simple descriptor of
“racist.” Most people harbor racist ideas. In the words of Beverly Tatum, we
all breathe the ideological smog of racism. However, a primary purpose of
this book is to maintain that it is possible to cure oneself of racist ideology. It
does take work, however, as so much in our society continues to reify racial
thinking and to reward racist behavior.
 63
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

Personal or individual racism is important because without it, the second

and most important form of racism—institutional and structural racism—
would lose ideological support. In her bestselling book White Fragility, Robin
DiAngelo makes the important point that racism is not about individuals, it
is not an action, and it does not require intent. Rather, racism is systemic
and institutional. We agree that the racism that affects human lives is sys-
temic and institutionalized. And we think DiAngelo would agree with our
addition that individual-level racism—especially the worldview of innate,
unchanging, and hierarchically arranged biological races—however implicit
and buried it might be, is the ideological fuel for institutional racism. That
kind of racism in employment, for example, rests on the many managers
who, time after time, reject applicants based on Black-sounding names. You
might not think you see color, but we all do. Racism is like oxygen in the air
we breathe. You might not see it, but science can measure it.

ARE THERE DIFFERENT FORMS OF RACISM?

Yes, racism takes a variety of forms with different central elements. One
typology developed by sociologists identifies four prominent, intersect-
ing types: biological racism, symbolic racism, ethnocentrism, and aversive
(color-blind) racism. In addition, as noted earlier, racism can be individual-
ized (interpersonal and internalized) and institutional. Racism can also vary
in being entirely intentional to entirely unintentional. All of these types of
racism intersect and can support one another, so they are all part of a system.
They all contribute to suffering and limit human and societal potential.
Biological racism rests on the premise that races exist in the human spe-
cies and that these races differ in their innate (genetic) capacities. It purports
that the social status of these groups results not from discrimination but
from their innate capacities. Among these innate capacities are traits such
as intelligence, morality, and longevity. Thus, biological racism posited that
certain races are more likely to produce criminals than others, providing
a handy justification for the preponderance of African American convict
laborers in the 1930s and the mass incarceration of African Americans to the
present day. In the late nineteenth century, this ideology also predicted that
“Negroes” would go extinct due to their lack of “persistence.” Frederick Hoff-
man predicted, in Race Traits and Tendencies of the American Negro, that
the Negro would become extinct because he was unable to adapt to the rig-
ors of northern cities and American civilization. We believe that biological
 64
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

racism is the foundational racism, because all the other forms of racism rely
on the notion the underlying biological differences exist between racialized
groups of human beings.
Symbolic racism is a form of prejudice held by individuals of European
descent against those of African descent. Other American ethnic groups also
adhere to this belief system, being prejudiced against any group that is dif-
ferent from their own. Symbolic racism is usually described as a coherent
system that can be expressed in several beliefs: that individuals of African
descent no longer face serious prejudice or discrimination, that their fail-
ure to progress results from their unwillingness to work hard enough, that
they make excessive demands, and that they have received more help from
the government than they deserve. Symbolic racism feeds into biological
racism.
Ethnocentrism is the tendency to evaluate other ethnic groups by the
standards of behavior and qualities displayed in one’s own ethnic group.
Judging standards of beauty by physical traits inherent to one’s own eth-
nic group (hair type and skin color, for instance) is one example. Judging
another group’s patterns of expression as vulgar, based on how one’s own
group expresses itself, is another. Ethnocentrism in and of itself is not a form
of racism, because it does not always involve a power dynamic. However,
ethnocentrism is aligned with symbolic racism, and with the added element
of power and belief that differences are innate, it leads to racism.
Cultural racism is the belief that different races have different cultures
that lead to particular outcomes, such as better education, more wealth, and
a better society. It is an effort to separate from biologizing differences. There
are three fundamental problems with the notion of cultural racism. First, it is
a sort of oxymoron. As we discuss, a fundamental aspect of race and racism
is biologization. Linnaeus was culturally racist, in that he confused cultural
and biological traits in his racial classifications, thinking they were all essen-
tial to racial types. But today, few have this problem. Second, just as there is
no essential whiteness, there is no essential white culture. Cultures, by their
very definition, are constantly mixing and changing. Finally, cultures do not
form in vacuums. For example, one cannot know or evaluate a health behav-
ior, diet, exercise, and the like without thinking about housing and access to
healthy foods. Those things are cultural but also consequences of regional,
national, and global flows of people, ideas, and things.
Color-blind or aversive racism is an ideology that allows those of the domi-
nant socially defined race (those of European descent) to claim that racism
 65
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

is no longer the central factor determining the life chances of people of non-
European descent (particularly dark-skinned individuals of African descent).
This position argues that instead of the ongoing institutional and individual
racism of American society, nonracial factors such as market dynamics,
naturally occurring phenomena, and the cultural attitudes of racial/ethnic
minorities themselves are the main causal factors of their social subordina-
tion. Indeed, recent studies have shown that although there is near universal
endorsement of racial equality as a core value, aversive racism persists.
People practicing aversive racist behavior would never describe them-
selves as racists, but this form of subtle, indirect racism operates across a
wide variety of settings, such as in employment, legal decisions, group prob-
lem-solving, and everyday helping decisions. An example of an everyday
helping decision is whether or not a white person stops to hold a door open
for a person who is not white, or which persons someone decides to help,
such as when white rather than nonwhite homeless people are given more
donations of money or food.
Our culture tends to focus on individual racism, that is, the racism that
individuals undertake as actions, behaviors, and underlying racist thoughts
and ideas that determine their behavior. Recent studies have found that all
humans harbor unconscious stereotypes or implicit biases. When most of us
think about racism, we think about individual racism. And, yes, individual
racism is important.
The main importance of individual racism is not just in how it impacts
one’s thoughts and actions but in how it ramps up into institutional racism.
When individual ideas become socially agreed “fact,” powerful institutions
can act to discriminate. Take redlining as an example. It became a wide-
spread practice in the United States to deny loans and housing to families of
color, and this practice of redlining led to different capacities for accumulat-
ing wealth. Specifically, redlining influenced who was able to receive loans to
buy a home. Considering that homeownership has been seen as one of the
avenues by which wealth is generated and transmitted to the next generation,
redlining explains, more than any other recent racist practice, the difference
in wealth between whites and Blacks in the United States.
In 2014, the median household income for whites was $71,300, compared
with $43,000 for Blacks. The difference is almost the same when we control
for education. For college-educated whites, median income was $106,600
compared with $82,300 for college-educated Blacks. However, worse than
just the household income difference is the disparity in overall wealth, which
 66
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

includes all assets a family owns, including stocks, bonds, and properties
minus outstanding loans and other debts. The median wealth in 2016 was
$13,204 for Blacks and $149,703 for whites—a ratio of 1 to 11.5—and has not
changed since 1968.
Finally, it is easy to recognize the violent racism of slave owners and Nazis.
If they were the only racists, racism would be a problem that we could more
easily isolate. Unfortunately, the ideology of race as biological and hierarchi-
cal has permeated society for so long that we hardly notice how pervasive
it is. As we’ve said, it is reified. The doctor who refused to diagnose sclero-
derma and the physician who failed to give orders for a bone density test
(see the introduction) are not overt racists. Rather, they are following their
medical training, which is racialized in ways that disempower individuals
and communities of color.
Consider the idea of mean and kind racists. Mean racists are those who
recognize their hate and intentionally do harm. Kind racists include pretty
much everyone else, who might see racism as an evil yet fail to fully rec-
ognize the humanity of individuals of different races. Kind racists support
mean racists, and both contribute to systemic racism.

WHEN DID RACISM BEGIN?

Racism and race began together. As race evolved from a folk belief to a legal
entity to a set of pseudoscientific facts, both institutional and ideological
racism became more established. Racism requires race, and biological race
provides intellectual cover for racism.
Given that formulation, racism cannot have existed before race. The treat-
ment of Jews throughout medieval Europe and their expulsion from Spain
in 1492 are acts that presage racism. These acts were ethnocentric, intoler-
ant, and bigoted. The belief that a Jew will always be a Jew, that Jews can-
not change their essential Jewishness, and that Jews differed physically from
Christians is close to believing Jews are a distinct race. But these actions
certainly are not full-blown racism as at this time Jews were not fully con-
sidered to be a race.
The enslavement of Africans and the start of the triangle trade was an
indication of the beginning of full-blown racism. Enslaved Africans were
thought to be subhuman and of an entirely different type of human. They
were commodities that could be enslaved, traded, owned, and put to death.
Slavery is an economic system that is supported by the ideology that the
 67
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

enslaved individual will always be of less value than the slave owner. The
enslaved person was either degraded (monogenism; e.g., the mark of Cain or
curse of Ham) or created separately (polygenism; e.g., pre-Adamite races).
Chattel slavery is often pointed to as the essential form of institutional
racism. We have no argument with that. However, in the seventeenth and
eighteenth centuries, ideological racism had not completely developed. Race
was not fully reified. Theologians, scientists, and politicians struggled to jus-
tify their belief that Native Americans and Africans were less than Europe-
ans. One sees evidence of this ideological struggle in the words of Darwin,
Jefferson, and many other influencers of their time.
Jefferson, in Notes on the State of Virginia, pondered the ethics of slav-
ery. He found himself in the contradictory position of writing in support
of liberty yet owning slaves, not to mention his sexual relationship with Sally
Hemings. As we noted in chapter 1, in The Voyage of the Beagle, Darwin
made a number of comments on the gap between the English gentlemen
and native South Americans, but he also said, “If the misery of the poor be
caused, not by the laws of nature, but by our institutions, [then] great is our
sin.” Jefferson held to the idea of the inferiority of Africans but was more
sympathetic to the notion of Amerindian equality with Europeans. On
the other hand, the young Darwin was raised in an abolitionist family. His
grandfather, Josiah Wedgewood, designed the British Anti-Slavery Society
medal. Darwin, unlike Jefferson, later in his career would contribute major
scholarship that helped to debunk the polygenist views of this period con-
cerning the existence of separately created species and an innate hierarchy
among human types.
Perhaps it is surprising that we observe that racist ideology—the ideol-
ogy of different races hierarchically arranged—might be as great now as at
any time in history. That is because the idea of race is at full strength today.
Since at least the time of Jefferson, a counter ideology of egalitarianism and
democracy has tried to chip away at the ideology of racism. Racial equality
is in the Constitution. A plethora of laws prohibit discrimination by race.
Scientists have even proven that our species does not have biological races.
Evolution is the main scientific discipline that demonstrates that biological
races do not exist within in our species. Yet, in the United States, the major-
ity of Americans either do not accept that evolution is true or simply do not
understand it.
A significant sector of American society draws its belief concerning
human biological variation from religious teachings, particularly special
 68
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

creationism. The racial attitudes of religious denominations in the United

States vary considerably, with some of the most racist beliefs and behav-
iors exhibited by evangelical Christians. For example, in 2020, Quan
McLauren, the diversity and retention director at Liberty University,
resigned, citing university president Jerry Falwell Jr.’s racist and oppres-
sive leadership.
Throughout our careers, we have been fighting an uphill battle against
racism. That is because the ideology of race and racism has history and
power on its side. In table 3.1 we visualize the history of racism in America
as occurring during a single day. Laws that attempted to chip away at the
lived experience of racism didn’t start appearing until late in the after-
noon. The most significant of these laws did not appear until after 8:00 p.m.
Eroding biological racism is difficult, because when scientists present
their findings concerning biological variation, most individuals think they
see race when what they actually see is skin color variation. Race is rei-
fied, and institutionalized white supremacy rewards racist behavior. This
is exactly the ideological fuel needed to keep America’s racial hierarchy
in place.

TABLE 3.1
African American Social Experience Presented as a Single Day

Event Year Clock Time

First Africans in Jamestown, VA 1619 12:00 a.m.

Virginia laws differentiating Africans from other servants by race 1682 4:47 a.m.
Fugitive Slave Act 1850 1:50 p.m.
13th Amendment ends slavery 1865 2:43 p.m.
Plessy v. Ferguson—separate but equal 1896 3:33 p.m.
Red Summer—race riots massacre of African Americans, Tulsa massacre 1919 5:57 p.m.
Black vs white incarceration ratio is 4:1 1950 7:49 p.m.
Emmett Till lynched 1955 8:07 p.m.
Mass incarceration ratio reaches 5:1 1960 8:25 p.m.
Civil Rights Act 1964 8:29 p.m.
Voting Rights Act 1965 8:42 p.m.
Mass incarceration ratio reaches 6:1 1970 9:01 p.m.
Joe Graves earns PhD in evolutionary biology 1988 10:03 p.m.
Mass incarceration ratio reaches 7:1 1989 10:04 p.m.
Killing of George Floyd, Breonna Taylor, Ahmaud Aubrey 2020 11:59 p.m.
 69
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

WHAT ARE EXPLICIT AND IMPLICIT BIASES?

Quotes such as “I’m not racist,” “I treat everyone the same,” and “I don’t see
color” are commonplace. Making fun of these color-blind notions, late night
comedian Steven Colbert said, “I don’t see race. People tell me I’m white, and
I believe them.”
Explicit biases refer to the attitudes and beliefs that people have about a
person or group on a conscious level. Much of the time, these biases and
their expression arise as the direct result of a perceived threat. For example,
a white woman might say that she wants a white female teenager to babysit
her child because she feels more comfortable with a white girl than a Black
boy. But more often, these biases are unconscious. She might not consciously
realize why she picked the white girl, or that she crossed the street to avoid
coming close to a Black male.
As a graduate student in 1981, Joe had a door slammed in his face as
he attempted to enter the University of Michigan’s Museum of Zoology.
The woman who slammed the door assumed that as a Black male, he had
no legitimate reason to be in the building on the weekend. When he pro-
duced his key and entered the building, she continued to interrogate him
about his purpose for being there. She assumed that there were no Black
graduate students in evolutionary biology. He explained to her as gently
as he could that he was going back to his laboratory to take care of his
animals.
Implicit biases are unconscious attitudes, beliefs, and stereotypes that
affect our understanding, actions, and decisions. We all have unconscious
biases. They help us to make decisions. From birth, our brains collect infor-
mation. We come to have expectations about what is safe to eat, what is a
soothing sound, and what a friendly face looks like. We also tend to classify
individuals. We grow up to associate lots of behaviors and characteristics
with females and males. And we apparently do the same based on skin color
and race.
Project Implicit, the developer of tests of implicit bias, starts with the
example of someone who smokes a pack of cigarettes a day. One could hide
this information because of embarrassment. That is an explicit bias; it is a
purposeful deceit. On the other hand, one might not be aware of the amount
that one smokes and thus might underestimate it. That is implicit bias.
Studies of implicit racial biases have recently mushroomed, uncovering
the breadth and depth of such bias and how it influences decision-making
 70
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

and actions in education, health care, employment, and law enforcement.

Implicit racial bias, we now objectively know, is everywhere.
One early example of implicit bias concerned physician recommendations
to patients who reported heart problems. The researchers recruited white
and Black cardiologists at a medical conference and had them observe four
actors who were trained to act like patients: a Black female and male and a
white female and male. The researchers asked the cardiologists to recom-
mend tests and treatments. The authors found that both Black and white car-
diologists treated the Black patients less aggressively than the white patients.
After being asked about their different diagnoses and treatment suggestions,
the physicians discovered that they were unaware that they had made them.
Similarly, a 2016 study examined interactions between Black patients and
white oncologists who had been administered a test for their levels of implicit
bias. The authors found that oncologists who rated higher in implicit racial
bias had shorter interactions with their patients, and their patients rated the
interactions as “less patient-centered and supportive” than doctors with less
implicit bias. The study also found links between a physician’s bias level and
their patients’ confidence in the physician’s recommended treatments, as well
as more perceived difficulty in completing them. These and other examples
of implicit bias might contribute to decreased effectiveness of health care of
Black patients and the huge racial inequalities in disease and death rates.
One of the most powerful examples of the harm caused by implicit bias
comes from its role in determining death sentences. Previous research on
homicide sentencing had shown that when the offender was Black and the
victim was white, the offender was more likely to receive the death penalty.
Stanford professor Jennifer Eberhardt and her team examined more than six
hundred death penalty cases from Philadelphia, Pennsylvania, from 1979 to
1999. They found within this dataset that the more the offender displayed
stereotypically “Black” physical features, the more likely they were to receive
the death penalty.
Consider the difference between David Duke, the former grand wizard
of the Ku Klux Klan, and Donald Trump. Duke is an explicit racist. He
does not hide his hopes for unequal and as separate as possible. Every-
one knows where he stands. He is an explicit white nationalist and white
supremacist. Conversely, Trump claims to be “the least racist person.” Let’s
assume that he believes that to be true. If so, then his racism is implicit. His
words and actions, including his association with and failure to speak out
against white supremacists like Duke, his enacting of the Muslim ban, and
 71
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

his support for building a border wall, make clear that he implicitly fears
Black and brown people.
To summarize, biases, whether explicit or implicit, are important because
biases or preconceived notions directly influence actions. These biases have
been shown to influence who gets hired for a job. The résumés of individu-
als with traditional Black names are rejected more often than those with tra-
ditionally white-sounding names. These biases constrict opportunities from
the cradle to the grave. They contribute to institutionalized racism because
these biases are deeply cultural and get stuck in the minds of those with the
greatest political power.

AM I A RACIST IF I . . . ?

Questions that start with “Am I racist if ” are, in truth, a little off. As we’ve
said, racism is not so much about individuals as it is about a system. Racism
is not so much about thoughts and personal behaviors as it is about histories
and institutions. That said, the question “Am I a racist?” is a common one
and important to answer. If you are reading this book, we assume you do not
want to be a racist.
Nobody is purely a racist or an antiracist. We all, one hopes, are striving
to be more antiracist. But sometimes we have racist thoughts and, worse, act
in ways that perpetuate racism. Our parents probably repeated racial ste-
reotypes, which got stuck in our brains. We live in racial smog. And our
thoughts and actions are connected to systemic, institutional racism. As a
house is built on brick and beam, so a system of institutional racism is built
on racist idea and racist action.
Yes, we all harbor some racist thoughts. Some might be explicit, and most
are probably implicit. We live in a society and time that make it impossible to
not be infected by racist memes and not breathe the air of racial differences,
codes, and racism. All of us—but perhaps especially folks with so-called
white skin privilege, like Alan—need to be aware of them, to be sensitized to
them, and then to call them out. Do not be afraid to address them.
Actions that typically come from unconscious thoughts can do harm.
Denying a job interview because of a Black-sounding name might be an
unconscious thought that leads to an action. It is not yelling and threatening
to call the cops on a Black bird-watcher, and it is not a policeman with a knee
on the neck of a Black man. Those actions are different. Actions arising from
unconscious thoughts probably will not make the evening news. However,
 72
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

such everyday racism as denying a job is one of the myriad hidden bricks of
systemic racism.
If you do something that, in retrospect, is racist, we recommend that you
consider the difference between an act of racism and being a racist. A single
act does not make you a racist. As Ibram Kendi says, we all do racist stuff.
For our culture, that is a norm. The point is to be more aware and, we hope,
move from more to less.
Now, why is this all a little off? If you’ve been reading other sections, you
might know what we are about to say. Pause. It is because being racist is not
about a specific action. Rather, it is about a system and operating within a
system that perpetuates racial inequality.

IS THERE SUCH A THING AS KIND RACISM?

The distinction that historian Donal Muir makes between kind and mean
racism is close to the distinction between conscious (explicit) and uncon-
scious (implicit) racism. Muir argues that few individuals are intentionally
racist. The policies of the KKK are mean, explicitly racist. Nazi laws and
genocide were explicitly racist. Jim Crow laws were explicitly racist. The
banning of Colin Kaepernick from the NFL was most likely explicitly racist
because it was planned—perhaps not formally but nonetheless planned—as
a punishment for his activism.
But as Muir argues, most racism is not mean. Perhaps it is not exactly kind
either, but that is his term. This racism is often paternalistic. It is thought to
be helpful, or at least not harmful. For example, dividing research subjects
into races might be seen as kind because it provides separate results by race.
If the researcher is focused on genetic differences, it is also racist in think-
ing that races might respond differently to a drug or treatment. It would not
be racist to recognize that socially defined races experience different social,
cultural, and physical environments and therefore might respond differently
to a drug or treatment. In the former case, the researcher is assuming a bio-
logical, innate, and immutable difference between these groups. In the latter
case, the researcher is concerned with how institutional racism harms racial-
ized individuals.
Kind racism is also, well, sort of kind. It is the complement of “oh, Blacks
have such great rhythm” or “the Asians are so hard working” or “those Jews
are great with money.” Kind racisms leave the door open for mean racism.
 73
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

IS USING THE “N WORD” RACIST? IS IT RACIST IF I AM WHITE?

IS IT RACIST IF I AM BLACK?

Yes, the N word is racist if you are not Black. No, the N word is not rac-
ist if you are Black. However, the continued use of this word by African
Americans has links to deep self-hatred that was internalized through years
of racial subordination in America.
The N word is a virulent epithet. It harks back to the time of slavery and
the Jim Crow era. It harks back to the Negroid race and racial rankings. It
is pure hierarchy. It has hurtful overtones. It is not unlike epithets for other
minorities and ethnic groups. We need not repeat them here. The N word is
at the far end of a continuum of hurtful epithets. Let it die.
If you are Black, uttering the N word might not be polite. It might still
shock, and it might still hurt. But it is also a way to defang the short word
by embracing it and making it one’s own. Fair enough. It is for Blacks only.
But Joe would say that Black people will never be truly liberated until they
forever erase this word from their vocabulary.

IS ANTI-SEMITISM A FORM OF RACISM?

Yes, and it is a unique form of racism. Anti-Semitism is its own unique form
of intolerance and hate and, at the same time, a form of racism.
First, a bit on the illuminating history of the term anti-Semitism. From
the German Antisemitismus, the word was coined in 1879 by William Marr, a
German political agitator, to replace Judenhass (literally “Jew hatred”). The
linguistic move was to hide hatred of Jews behind the façade of science. With
anti-Semitism, Jews became a Semitic people, or the Semitic people, a race
or subrace, and hatred of Jews could then be fit into a scientific hierarchy,
Nordics and Aryans at the top and Semitic peoples near the bottom. Anti-
Semitism was rationalized.
Some have debated whether anti-Semitism remains the appropriate term
for hatred of Jews. Its advantage, racializing Jew hatred, is also its disadvan-
tage. It continues to highlight the old trope that a Jew is always a Jew. In the
following, we use “anti-Semitism” or “Jew hatred” when one or the other
seems most appropriate.
Why, then, is Jew hatred different from racism? The answer is that Jew
hatred does not fit the classic definition of racism: prejudice plus power.
 74
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

Jews experience lots of anti-Jewish prejudices and hate. Jews have been
victims of hate longer than any other group. But unlike other oppressed
groups, Jews are seen as both less than (dirty, disgusting, infectious) and as
a powerful cabal.
A common trope of Jew hatred is that they are inordinately powerful,
somehow in control of the media, banks, and other industries. This lie of
Jewish power dates from the Protocols of the Elders of Zion, a fabrication
produced in Russia before the revolution, widely circulated by Henry Ford
in the 1920s, and still frequently reproduced. This myth of Jewish power is
articulated on the political left, such as in the Sociology of Freedom, the 2020
book by Abdullah Öcalan, the imprisoned leader of the Kurdistan Workers’
Party. Öcalan writes, without citations, about an eternal and essential Jew
with a powerful ideology. Given Öcalan’s stature on the left, his words gained
credibility. A widely circulated lie takes on a life, it continues to act. And this
leftist anti-Semitism feeds the right and rightists’ chant that the (powerful)
“Jews will not replace us” (with Black and brown people).
However, Jews are neither powerful, as they have been thought to be in
imaginary works, nor do they have an ideology. Jews differ from place to
place and time to time. Under Christianity, Jews gravitated toward jobs and
positions that were open to them. But there is no Jewish cabal. Believing in
such is Jew hatred and lacking in facts. Jews are thought to be both commu-
nists and, at the same time, virulent capitalists, and hated for both. Jews are
what whites imagine them to be.
Here are some facts about Jews. The number of Jews alive today is less
than fifteen million. (It was more than sixteen million before the Holocaust.)
More than half a million Jews reside in just two countries: the United States
and Israel. Jews make up about 1.8 percent of the U.S. population. That’s
because Jews escaped from Jew hatred in Europe and the Middle East to
Israel and United States. That’s hardly the stuff of worldwide control.
Judaism is a religion practiced by people of varied genetic ancestries. That’s
confusing to many who blanketly call Jews white or think that all Jews have
white skin privilege. Many Jews do indeed pass as white and have white skin
privilege. These Jews, including Alan, are eastern European or Ashkenazi.
Development of the Jewish diaspora led other groups to join, including Sep-
hardic Jews of Iberia, northern Africa, and locals throughout Asia, the Medi-
terranean, and Africa. The stereotypical Jew is Ashkenazi. After World War II,
they became categorized as white, perhaps honorary whites or whites of a
different shade, as Jacobson aptly describes—but, most important, white.
 75
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

And although not all Jews are middle or upper class, many are. They have
some economic power. The result is that on measures of impact of racism,
such as education and economic status, Jews in the United States and most
European countries seem to be doing okay. Once they could not gain accep-
tance into certain country clubs, live in certain locations, be admitted to
certain hotels, or go to certain schools (like Harvard), but now they can,
explicitly if not always implicitly.
Why, then, is the answer to the question, “Is anti-Semitism racism?” a
yes? As has been clear since the Middle Ages, Jews have been persecuted.
Throughout history, they have been victims of religious persecution, from
their expulsion from Spain, to pogroms throughout Eastern Europe, Hitler’s
Holocaust, and the rise of anti-Semitic tweets, desecrations, and murders
in the United States. These add up to ethnic and racial discrimination and
more.
The “more” is captured in stereotypes. The Jew is often seen as a racial
type, as having inherent qualities that are biological. In Spain, a Jew would
always be a Jew. In Nazi Germany, Jewish blood needed to be avoided at all
cost and Aryan blood needed to be protected. Science got involved to study
the Jewish type. Efforts were made to recognize Jews and to explain how they
became the way they were. And these efforts supported their eradication. As
they often do to support racist institutions, science and law worked together.
In a research report published in the American Journal of Physical Anthro-
pology in 1929, Manoiloff, a Russian scientist, wrote that he could discern
Jewish from Russian blood. He declared that Jewish blood was paler than
Russian blood, which also contained more adrenaline. Manoiloff added
reagent to the blood of known Jews and Russians and was able to deduce
that they changed color so he could with almost perfect accuracy detect Jew-
ish from Russian blood. Of course, this is the quintessential unrepeatable
experiment. We do not know what reagent he used, and the results are pre-
posterous. But, as Hitler was soon to seize power, it would be important to
discern who is a Jew, and the thought is that it was in the blood.
Anti-Semitic science flourished on both sides of the Atlantic. At the Uni-
versity of Virginia Medical School, Robert Bennett Bean, head of the Depart-
ment of Anatomy, joined a chain of scientists who were fascinated by Jewish
noses. His 1913 paper in the Anatomical Record, a well-respected publication,
is devoted to the study of the unique characteristics of the Jewish nose, com-
plete with an analysis of the surrounding muscles and a theory about which
factors accounted for how the Jewish nose form evolved.
 76
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

Given how much anti-Jewish racism exists today, we recommend letting

the term “anti-Semitism” die and instead use either “Jew hate” or “anti-Jew-
ish racism.” Because that’s what it is.

IS ISLAMOPHOBIA RACISM?

Similar to the answer regarding Jew hate, Islamophobia—fear or dislike of and

prejudice against individuals who identify as followers of Islam, or Muslims—
is and is not a form of racism. Islamophobia has not yet taken on the same
degree of racist tinge as anti-Semitism. Fear of such individuals focuses more
on Islam as a culture, religion, and political power than as a racial essence.
However, Islamophobia is a form of virulent ethnocentrism that could be con-
sidered a form of cultural racism, that being a Muslim is culturally essential.
In 2019, the Institute for Social Policy and Understanding reported that
Islamophobia in the United States had increased from the previous year. The
increase differed by socially defined race, ethnicity, and religion. Jewish and
Hispanic Americans had the most favorable views of Muslims, whereas white
evangelicals had the least favorable view (44 percent favorable versus 20 percent
unfavorable). On the other hand, Jews had greater than five times more favorable
than unfavorable views (53 versus 13 percent), Hispanics had about five times
more favorable than unfavorable (51 versus 10 percent), and African Americans
seven times more favorable than unfavorable views (35 versus 5 percent).
At the level of politics, our fear is that the attempt of former President
Trump to guard the borders and try to ban travel for individuals from so-
called Muslim countries feeds into existing misrepresentations and fears of
Muslims. It seems to us that Islamophobia at the political level generalizes
from cultural and political intolerance to stereotypes about more than one
billion followers of Islam. That is certainly prejudice, and with differential in
power, it is also a form of racism.

PEOPLE KEEP TALKING ABOUT “REVERSE DISCRIMINATION,”

BUT WHAT IS IT?

Nothing.
This one is easy. Reverse racism, or reverse discrimination, is not a thing.
It is a myth. The idea of reverse racism refers to the assumed overreach
of affirmative action programs that are aimed at equalizing past injustices
against minorities of color. But that is not true.
 77
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

Now for some history. The idea of affirmative action effectively began in
1961, when President John F. Kennedy issued an executive order creating
the Committee on Equal Employment Opportunity. This very limited order
called only for all hiring programs supported with federal funds to ensure
that they are free of racial bias. A year after the passing of the Civil Rights
Act of 1964, President Lyndon Johnson framed affirmative action this way in
his 1965 Howard University commencement address:

You do not wipe away the scars of centuries by saying: “now, you are free to go
where you want, do as you desire, and choose the leaders you please.” You do
not take a man who for years has been hobbled by chains, liberate him, bring
him to the starting line of a race, saying, “you are free to compete with all the
others,” and still justly believe you have been completely fair. . . . This is the
next and more profound stage of the battle for civil rights. We seek not just
freedom but opportunity—not just legal equity but human ability—not just
equality as a right and a theory, but equality as a fact and as a result.

From the 1960s to today, the idea of affirmative action has been hard to
enforce, widely debated, and widely misunderstood. The most important
legal case to challenge affirmative action is known as Regents of the Uni-
versity of California v. Bakke. In this 1978 case, Allan Bakke claimed that he
was denied admission to medical school because of his race. He is white and
challenged that positions in the entering class of Davis Medical School had
been set aside for disadvantaged minorities, thus disadvantaging him.
But Bakke had the advantages of his white skin privilege. This did not go
away. All that was being tried was to make the advantage a bit less.
What Johnson was aiming for over a half century ago was not equal-
ity, that everyone is given an equal chance but starts from widely different
places. Rather, he was trying to take small steps toward equity, that everyone
has an equal chance of admission to school and a job and an equal ability to
own a home and build equity in it.

CAN ANYONE BE A RACIST? CAN A PERSON WITH LITTLE

ACCESS TO POWER BE RACIST?

No. Like the answer to the reverse racism question, this one is easy. Again,
we are helped by the useful definition of racism as prejudice plus power.
By definition, those without power cannot be racist. They can—and are
 78
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

often—prejudiced. We all hold some prejudices. Prejudices are cognitive

shortcuts. Without power, you can think like a racist, you can be a cognitive
racist, but you cannot set in motion the levers of institutional racism. Your
racism does not act on the world.
The most important thing to take away is that racism is not about indi-
vidual skin colors but about all of our silent collusions and complicities in
institutions that change lives.

IS WHITE SUPREMACY ON THE RISE, AND IF SO, WHAT’S

GOING ON?

First, let’s look at the question, “Is white supremacy on the rise?” Our answer
unfortunately seems to be yes: white supremacy is on the rise. It is doubt-
lessly increasingly visible, and more and more individuals are joining white
supremacist groups. The harder question is, “What’s going on?” There are a
number of theories and ideas about why white supremacy is on the rise and
what is in the heads of people who think white supremacist thoughts and act
in supremacist ways.
The U.S. State Department has tracked the rise in hate crimes. The
Anti-Defamation League tracks anti-Semitic incidents and found that they
reached an all-time high in 2019, the last year for which the organization
has data. Similar increases have been seen in hate crimes against Black and
brown people. The most egregious of these were the 2020 killings of Ahmaud
Arbery, Breonna Taylor, and George Floyd. Many of those who stormed
the Capitol building on January 6, 2021, held white supremacist beliefs and
belonged to white supremacist militias.
Our sense is that whites—especially working-class whites—feel increas-
ingly threatened by Black and brown people. They feel that they have less
control over their lives. As we write, COVID-19 is still rampant in the United
States (and elsewhere in the world). There are huge political divides in Amer-
ica. We live in uncertain and stressful times. It is easier to blame the loss of
control on scapegoats, so Black and brown people are portrayed as taking
jobs from whites and somehow robbing others of the American dream. This
situation has unsettling parallels with how anti-Semitism was used as a cata-
lyst to fuel the growth of the Nazi movement in Germany. On August 11–12,
2017, there were more white supremacists marching in Charlottesville, Vir-
ginia, than there were fascists marching with Hitler in the Munich Beer Hall
Putsch of November 1923. We believe that in the current situation, we must
 79
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

pay careful attention to the growth of white supremacy and the hate that it
generates or we risk being caught off guard, as were Germans in 1933. We
also warn that the lack of a strenuous response to the storming of the Capitol
has actually emboldened the white supremacist movement.

WHAT IS WHITE FRAGILITY?

White fragility is a framework popularized and used by Robin DiAngelo

to describe a common pattern of behavior and feeling expressed by whites
when engaging with race and racism. DiAngelo writes that white people
are protected from dealing with race and racism. They are insulated by their
majority status and the sense that white is not a race, the result of growing
up with the expectation that race is not their problem and thus lowers their
ability to endure racial discussions and deal with racial situations. As a result,
they are frail.
White fragility is a condition in which any degree of racial stress becomes
overwhelming and intolerable and thereby triggers a defensive posture.
Instead of dealing with hard discussions about the racial world order, whites
often say “I am not racist” or “That’s not me” and change the subject.
DiAngelo believes that white fragility is a major impediment to becoming
antiracist.

WHAT ARE THE DIFFERENCES AND SIMILARITIES BETWEEN

RACE AND CASTE?

Most scholars view a racial contract and castes as different and parallel forms
of social and politically sanctioned hierarchies. A few scholars and writers,
most notably Isabel Wilkerson and Michelle Alexander, argue that the West-
ern racial hierarchy is a form of caste.
One’s caste in India is determined by birth and is permanent. Intermar-
riage among castes is discouraged, if not prohibited. This has resulted in
genetic divergence to occur between the castes to the extent that they can be
identified through genetic markers. Caste is like class but far more immuta-
ble. In India, Dalits are the lowest caste, previously known as “untouchables.”
In the United States, race is associated with class hierarchy and is cer-
tainly caste-like. This is an old observation. Both Swedish sociologist Gunnar
Myrdal and British anthropologist Ashley Montagu made this observation
in the 1940s. Caste is like race, in that it is assigned at birth based on the
 80
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

caste into which one is born. It is like a class system, in that social immobil-
ity leads to a trap that makes it hard to escape one’s class and caste. Liberal
thinkers might say that class mobility is possible, whereas caste mobility,
moving out of one’s caste, is not possible. However, the data on low class
mobility in America refutes the notion that these are so different. Sociolo-
gists have long recognized that capitalist economies operate with dual labor
markets. In America, racially subordinated groups have been differentially
relegated to the secondary market, which is characterized by menial and
irregular labor. To make the situation even worse, in the later portion of
the twentieth century, the irregular labor market grew, as well as the percent-
age of people who are structurally unemployed. This means that upward
social mobility for most racially subordinated persons in America is gradu-
ally ceasing to exist.
Wilkerson recently wrote that race in America is much like the caste sys-
tem of India. One is born into one’s race, and the expectations and limits of
race are the same as in a caste. She formulates that race is a visible manifes-
tation of an underlying system and that caste and inequality make up the
invisible structure. Race is the skin, and caste is the bones.

WHAT IS INSTITUTIONAL RACISM? HOW DO WE KNOW THAT

IT STILL EXISTS?

Institutional racism refers to the work of institutions such as education,

health care, and law enforcement to treat individuals differently based on
race. The differential access and engagement with institutions is a major way
that racism becomes real. Institutional racism highlights the ways that insti-
tutions, rather than individuals, drive racial inequalities. Some prefer terms
such as “structural racism” or “systemic racism” to highlight how racism is
part of the structure of society and a system that promotes inequality.
Some forms of institutional racism are explicit. For example, mortgage
companies were clear about their practices of giving home mortgages to
white families in certain areas while denying them to families of color with
the same credentials and means. This practice, as noted earlier, was referred
to as redlining.
Often, institutional racism is a silent code—whereby individuals and
groups are treated differently. Predominantly Black schools lack the resources
of predominantly white schools. In chapter 4, we discuss how toxic waste
dumps are often located closer to predominantly Black and brown than
 81
E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

white areas. Policing is less effective in communities of color than in white

communities. No one in America has ever viewed a video on television of a
white person being choked to death by Black officers (the opposite of what
happened to Eric Garner), or heard a report of Black officers breaking into
the apartment of a white nurse and shooting her dead (as opposed to what
happened to Breonna Taylor), or watching a white citizen having his neck
crushed by a Black officer (such as the opposite of what happened to George
Floyd). And on and on.
The proof of the existence of institutional racism is in the facts of differen-
tial treatment in almost all aspects of life. Black life expectancy, for example,
is less than white life expectancy (see chapter 5). And this is not just a matter
of having less money or lower socioeconomic class, although money and
class are important. The data show that Blacks live shorter lives than whites
at all educational levels. This is proof of systemic racism. One sign of the
elimination of systemic racism is equality of life expectancy. The gap has
closed slightly, and we look forward to it closing more and to all of us living
our potential for as full a life as possible.
 Chapter Four

WHY DO RACES DIFFER IN

DISEASE INCIDENCE?

In early March 2020, before the COVID-19 pandemic grabbed our attention,
Joe was interviewed on Roland Martin’s show, Unfiltered. He stated that as
soon as sufficient data became available on COVID-19 infection and death
rates, it would show large disparities by socially defined race and ethnicity.
We didn’t need a crystal ball to foresee this, because racial inequalities have
always existed for virtually every disease in our society. Moreover, during
crises and hardships, poor and nonwhite communities are invariably hit the
hardest.
Joe, of course, was right. The COVID-19 data were soon to show that 24
percent of those who died were African Americans, whereas African Ameri-
cans made up 13 percent of the U.S. population. On July 5, 2020, the New
York Times reported that the virus positivity rates for African Americans
and Latinos were 2.7 and 3.2 times greater than that for European Ameri-
cans, respectively. The rate of vaccination of African Americans and Latinos
has fallen behind that of European Americans. In North Carolina, African
Americans are 22 percent of the total population and 26 percent of the health
care workforce but had received only 11 percent of vaccinations by January
30, 2021. More recently, the CDC reports that, nationally, Blacks and Latinos
still trail other ethnic groups in the rate of vaccination.
As some of you might know, racial disparities in sickness and death have
been a consistent feature of American society. You might have heard a variety
of explanations for this, including the notion that if races differ genetically,
 83
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

it is only logical that they should differ in rates of sickness and death. This
is a core premise of so-called racial medicine. We place this idea under a
microscope in this chapter and focus on the life-and-death consequences of
living in a racialized society. We unpack the relationship between genetic
variation and disease predisposition and demonstrate that any associations
between genes and disease have nothing to do with race. On the contrary,
the history and current reality of life in a racially stratified and racist society
make people sick and shorten their lives.
In the United States, we routinely collect health data by race. Time after
time, these data show glaring racial inequalities in disease and death. But the
inequalities are not due to biological race; rather, they are due to the experi-
ence of living in a society that treats individuals differently based on their
socially defined race. Racism has always been and is still a public health crisis.

MY DOCTOR’S OFFICE INTAKE FORM ASKS FOR MY AGE, SEX,

AND RACE. WHY DOES IT ASK FOR MY RACE?

Socially defined races differ in their patterns of disease prevalence and rates
of death. Thus, from the standpoint of current medical practice, it is rea-
sonable for a physician to ask about a patient’s socially defined race. The
problem, of course, is that a patient’s socially defined race is a poor proxy
for understanding their predisposition for disease. Worse, there is still much
confusion between social and biological conceptions of race in the medical
community.
In May 2002, Sally Satel wrote a provocative article in the New York Times
magazine titled “I Am a Racially Profiling Doctor.” With that title, she was
proudly playing off the notion of racial profiling that is a routine part of
law enforcement. Satel made the point that it is appropriate and efficient to
racially profile in health care because different races get different diseases
and react differently to drugs and treatments. Unfortunately, Satel chalks up
these differences to genetic factors, though often these differences do not
hold up on closer inspection, and they differ over time and place.
For example, one of the oldest myths is that Blacks have thicker skin and
are less sensitive to pain, leading to their being undertreated for pain. In this
example, we see two mistakes: one about genetics and the other about the
conjunction of race and genetics. First, there is a racial biological assump-
tion that skin thickness and lower pain perception is due to genetics. Pain
perception could be due to all sorts of factors and might have very little to
 84
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

do with skin thickness, and skin thickness might have very little to do with
genetics. Second, even if genetics is somehow important in determining skin
thickness and pain perception, we are aware of no data showing that these
unknown genetic factors vary by frequency in different races. It is, in short,
one racial assumption built on another and another.
A recent study conducted at the University of Virginia (UVA) Medical
School found that false beliefs about racial differences in medically relevant
traits persisted in first- to third-year medical students and residents (table 4.1).
For example, a third or more of first-year students thought that Blacks aged
more slowly, their blood coagulated faster, and they had thicker skin and
stronger immune systems than whites. Some of these misconceptions, such
as the rate of aging and thicker skin, persist among the medical school’s resi-
dents. These results are far from trivial. This is a premier medical school, so
it is highly likely that the prevalence of these misconceptions is as great or
greater among nurses and other health professionals and in less prestigious
medical programs. Let’s cease to make these conceptual errors.
The good news is that there has been movement toward reforming medi-
cal curricula to incorporate more nuanced understandings of human genetic
variation and how such variation does not map onto socially defined race.
We have authored several articles on this topic. Many of our colleagues who
understand the problems of racialized medicine work in medical schools,
and others are giving talks at these schools. Alan has lectured at many medi-
cal schools and consulted with the University of Illinois Medical School. Joe
has been active in the International Society for Evolution, Medicine, and
Public Health (ISEMPH). ISEMPH is a consortium of scientists and physi-
cians dedicated to reforming medical instruction and practice so that it bet-
ter incorporates evolutionary and anthropological perspectives, which are

TABLE 4.1
Some False Racial Beliefs Among Recent UVA Medical Students (percentages)

False Belief 1st Year 2nd Year 3rd Year Residents

Blacks age more slowly than whites. 33.3 38.9 20.3 50.0
Black nerve endings are less sensitive than white. 12.7 19.4 0.0 14.3
Black blood coagulates more quickly than white. 46.0 23.6 5.1 14.3
Black skin is thicker than white. 63.5 58.3 37.3 100.0
Blacks have stronger immune system than whites. 33.3 20.8 5.1 14.3
Note: In general, medical students’ false beliefs decline with years of training. The residents’ pattern of false belief is
not directly related to that for medical students, as many of these individuals were trained at other medical schools.
 85
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

crucial in improving patient outcomes. These efforts are relatively new, and
much work is still needed, but we are optimistic that instead of promoting
racial biological thought, medical schools could become sites in support of
antiracism.

WHEN DOCTORS, EPIDEMIOLOGISTS, AND OTHER

MEDICAL SCIENTISTS SAY THAT RACE IS A RISK FACTOR,
WHAT DO THEY MEAN?

A risk factor for disease simply means that having a condition or any “fac-
tor,” such as being male, having a specific gene, living in a certain zip code,
or having a bald spot, is statistically associated with an increased probability
(or risk) of a disease. There is, or should be, no assumption of causality.
However, with any risk factor, there is an association that might be worth
exploring. Why do males have shorter life expectancies? The reasons—the
processes and mechanisms—could be many.
For well over twenty years, we have contributed to a growing professional
literature on the confusion in medical practice and biomedical research on
the meaning of race as a risk factor. Just as not asking why baldness is associ-
ated with disease, not digging further to ask why race is a risk factor is not
good science. It is giving up too soon. Why? Because not asking often leads
to the assumption that the risk is due to genetics. And it certainly fails to take
the next step to explore the reasons that race is a risk factor, those processes
and mechanisms.
Socially defined race includes an individual’s ancestry, position in society,
and cultural practices. Thus, the raced and racialized experiences that people
experience in our society result from these practices and much more. Due to
the fact that socially defined races experience different social and environ-
mental conditions, it is understandable that races might vary in disease rates
and therefore that race would be a statistically valid risk factor in a variety
of diseases, such as infectious (smallpox, tuberculosis, yellow fever, H1N1
influenza, HIV, COVID-19) or complex diseases such as cancer, diabetes,
heart disease, and stroke.
Figures 4.1a and 4.1b show the ratio or relative risk of mortality (death)
by age for Blacks compared with whites in 2015 for infectious diseases
(influenza and septicemia) and complex, chronic diseases (heart disease
and cancer). Septicemia is blood poisoning resulting from systematic bac-
terial infection. These graphs show that people who are socially defined as
 2.5
Heart disease
Cancer
2.0 Identity line
Mortality ratio

1.5

1.0

20 30 40 50 60 70 80 90
Age

FIGURE 4.1A. The ratio of Black/white mortality by age in the United States in 2015 for heart disease and
cancer, which are ranked as the number 1 and 2 sources of mortality in the United States. These diseases
become the most significant contributors to mortality at later ages (so the youngest ages are not shown on
this graph). From age twenty-two on, Blacks die from heart disease at a ratio of 2.3 - 1.1 times that of whites
and from cancer at a ratio of 1.4 - 1.0 times that of whites. These ratios were more disproportionate in the
twentieth century. See J. L. Graves, “Looking at the World through ‘Race’ Colored Glasses: The Influence of
Ascertainment Bias on Biomedical Research and Practice,” in Mapping “Race”: A Critical Reader on Health Dis-
parities Research, ed. Laura Gomez and Nancy Lopez (New Brunswick, NJ: Rutgers University Press, 2013).
Source: Adapted and updated from Centers for Disease Control and Prevention, National Center for Health
Statistics, National Vital Statistics System, “Leading Causes of Death 2015,” https://www.cdc.gov/nchs/data
/nvsr/nvsr66/nvsr66_05.pdf.

2.5
Influenza
Septicemia
2.0 Identity line
Mortality ratio

1.5

1.0

20 30 40 50 60 70 80 90
Age

FIGURE 4.1B. The ratio of Black/white mortality by age in the United States in 2015 for influenza and
septicemia, which rank in the top fifteen causes of death in the United States. They become the most sig-
nificant contributors to mortality at later ages (so the youngest ages are not shown on this graph). From age
twenty-two on, Blacks die from influenza at a ratio of 2.3:1.0 times that of whites, and from septicemia at
a ratio of 2.17:1.46 times that of whites. These ratios were more disproportionate in the twentieth century.
See J. L. Graves, “Looking at the World through ‘Race’ Colored Glasses: The Influence of Ascertainment Bias
on Biomedical Research and Practice,” in Mapping “Race”: A Critical Reader on Health Disparities Research, ed.
Laura Gomez and Nancy Lopez (New Brunswick, NJ: Rutgers University Press, 2013). Source: Centers for Dis-
ease Control and Prevention, National Center for Health Statistics, National Vital Statistics System, “Leading
Causes of Death 2015,” https://www.cdc.gov/nchs/nvss/index.htm.
 87
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

Black in the United States display higher rates of death from these diseases
across age. These ratios are also true for other leading causes of death, such
as cerebrovascular disease, diabetes, chronic lower respiratory disease, HIV/
AIDS, and, now, COVID-19. Thus, for virtually every kind of disease in the
United States, socially defined race is and always has been a risk factor for
developing and dying from that disease. It was this knowledge that led to
Joe’s prediction that COVID-19 data would also show significant disparity
by socially defined race.
Yes, race is a risk factor. Almost every disease we are aware of varies by
race. But that is just the first question. The more important questions to ask
have to do with how consistent those results are and why disease and death
rates vary by race.

ARE THERE RACE-SPECIFIC DISEASES?

No.
However, as we noted earlier, the prevalence of diseases and mortality rates
differs in various socially defined racial groups. For example, infectious disease
was a major source of death for Amerindian nations after the colonization of
the Americas by Europeans. Smallpox first appeared in the Amerindian popu-
lations of Santo Domingo in 1518. It is likely that the English brought smallpox
to the northeast by the early seventeenth century. As Snow and Lanphear note,
John Josselyn wrote that by the 1630s, the Sagamore nation was reduced from
30,000 to about 300 by smallpox. The high susceptibility of Amerindians to
smallpox resulted from the fact that the virus was new to their populations,
their means of subsistence had been disrupted because of colonialism, and the
lower human leucocyte antigen (HLA) diversity of Amerindians compared
with Africans, Europeans, and East Asians. The HLA system is encoded by
the histocompatibility gene complex (MHC) and is responsible for the regu-
lation of the immune response in all mammals. The lower HLA diversity of
Amerindians resulted from the serial founder effects that established them in
the Western Hemisphere and lowered their genetic diversity compared with
the Eurasian populations from which they descended.
African Americans also suffered higher death rates compared with Euro-
pean Americans in the smallpox epidemic of 1862–65. W. E. B. DuBois’s
sociological study, The Philadelphia Negro, published in 1899, also traced the
disparate rates of tuberculosis to the poor social conditions experienced by
African Americans in that city.
 88
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

Similarly, the disproportionate incidence of COVID-19 in African Ameri-

cans and Latinos results from differential exposure to the virus, not increased
genetic susceptibilities. The 2019 coronavirus is new to humans, most likely
having originated in bats. Bioinformatic analysis of HLA loci that might
confer resistance to or greater severity of COVID-19 found some HLA vari-
ants that were extremely rare and not differentiated by population. Finally,
in summer 2020, genome-wide association studies (GWAS) of Italian and
Spanish patients identified variants that led to more severe cases. Later
that summer, it was determined that a segment of chromosome 3 associated
with greater severity of COVID-19 most likely originated in Neanderthals
(who once interbred with modern humans in Eurasia, not Africa). Afri-
can Americans can display these segments as well but at lower frequency,
because the variants result from their European ancestry (derived from the
rape of African women during slavery).
The prevalence of diseases with relatively simple genetic foundations such
as sickle cell anemia, Tay-Sachs, and cystic fibrosis differs by population (but
not race). For example, populations that live in high malaria transmission
zones have elevated frequencies of the sickle cell (HbS) allele. Individuals
who are heterozygous for this trait (HbA/HbS)—that is, have one copy of
the sickle cell allele—display resistance to malaria; homozygous individuals
without a copy of the sickle cell allele (HbA/HbA) display elevated death
rates due to malaria; and individuals that are homozygous (HbS/HbS) with
two copies of the sickle cell allele are at greater risk of death.
Sickle cell allele rates vary by region and population. Kenyans living
at high altitude have very low frequencies of HbS, whereas low-altitude
Kenyans have elevated frequencies of this allele. Greeks and Saudi Arabians
have higher frequencies of HbS than native South Africans, as the former
climates supported malaria transmission and the cape of southern Africa
did not. The frequency of the HbS allele in African Americans in the United
States is about 5 percent. This is lower than the frequency of the mutation
(12–14 percent) in western and central African populations from which
African Americans are descended, as malaria transmission in the United
States dropped steadily over the nineteenth and twentieth centuries. Without
malaria transmission, the HbS allele conferred no advantage and was there-
fore reduced in frequency by natural selection.
Earlier, we noted that the prevalence and mortality rates for complex dis-
eases (e.g., heart and cancer) differ by socially defined race in the United
States. A strong indication that these differences are not driven by genes is
 89
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

the fact that the rates of complex disease differ within groups of the same or
similar ancestry by country of origin. Indeed, the rates of heart and other
complex diseases in western Africa are considerably lower than those expe-
rienced by persons of African descent in the United States.
However, within a single generation, West African immigrants take on
the disease pattern observed among African Americans. Prior to 1960, vir-
tually no persons of African descent immigrated to the United States. This
changed when biased immigration quotas were struck down by the Hart-
Celler Immigration Act of 1965. Today, individuals of African descent are
one of the largest groups entering the country. A series of studies have shown
that although persons of African descent not born in the United States ini-
tially have a health advantage compared with African Americans, after liv-
ing in the United States, these groups begin to take on the health profile of
African Americans. These studies also showed that the health decline was
greatest for immigrants from nations in which Europeans were the majority,
suggesting that it resulted from their previous experience with racism. Spe-
cifically, it is thought that these individuals experienced early-life adversity
due to institutional racism in their countries of origin, making them even
more vulnerable to the racialized health conditions in the United States. The
role of early-life adversity is well established in accounting for disease in
later life.

DOES BLOOD DIFFER BY RACE? CAN I DONATE TO OR RECEIVE

A BLOOD TRANSFUSION OR AN ORGAN FROM A PERSON OF
ANOTHER RACE?

Former Hawaiian Senator Daniel Inouye was critically wounded in World

War II. He was a member of the 100th Infantry, 442nd Regimental combat
team. They were an all-Japanese-American unit, called the “Nisei soldiers,”
and many were recruited from internment camps. He received a life-sav-
ing blood transfusion from the Negro blood supply. At this time, the U.S.
Army continued to mistakenly segregate blood supplies of whites and Blacks
despite full awareness that anyone could receive blood from anyone else if
their blood group genotype/phenotype matched, and that blood groups had
nothing to do with race.
The ability of an individual to receive a blood transfusion (red blood cells)
depends on variation at two major loci: blood group (A, B, O) and Rh factor
(+ or −). Furthermore, variation at the Kell, Kidd, MNS, Duffy, and HLA
 90
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

(major histocompatibility) loci can influence blood group compatibility.

Also, the capacity to successfully receive blood platelets depends on varia-
tion in the human platelet antigen system (HPA).
Human populations differ in their allele frequencies in all these systems.
However, blood transfusion compatibility depends on the genotypes of the
individuals at the key loci, not their socially defined race. Individual-level
variation determines compatibility.
Given that genes are inherited in families, the best choice for a blood or
tissue donor will always be a close relative. For example, if a man has chil-
dren with two different women (one socially defined as white and the other
as Black), it is more likely that the siblings will be good blood donor matches
than unrelated individuals in either socially defined race.
The major human blood groups (A, B, O) were discovered by Karl Land-
steiner in 1900. These groups are characterized by antigens (molecules such
as proteins or sugars that elicit an immune response). The A and B antigens
are sugars, and O is the absence of either the A or B antigen. The frequency
of the ABO alleles differs in human populations. For example, recent surveys
have found that the frequencies of blood type O are 70.9, 65.6, and 34.0 per-
cent in African Americans, European Americans, and Chinese (in China),
respectively. Furthermore, blood group compatibility requires the matching
of at least both ABO genotype and Rh genotype. Determining the frequency
of the two locus blood group phenotypes requires multiplying the frequen-
cies of the individual loci (by the rules of independent assortment). The
frequency of the Rh+ allele in these populations is 97 to 99 percent, 83 to
85 percent, and 93 to 99 percent, respectively. Thus, the frequency of the
ORh+ phenotype in these groups would be 68.7–70.1, 54.0–55.7, and 31.6–
33.7 percent, respectively. It follows that if ABO and Rh phenotype are the
primary factors determining blood transfusion compatibility, a person of
East Asian descent, such as Senator Inouye, with the ORh+ phenotype,
would have a greater probability of getting the right blood transfusion from
someone of African American descent in the United States than someone of
East Asian descent.
For patients who receive multiple transfusions, genetic variation at the
secondary (and tertiary) blood compatibility loci become important. These
are the Kell, Kidd, MNS, Duffy, HPA, and HLA gene systems. As with the
major blood compatibility loci, the frequencies of the gene encoding the
antigens produced by these systems differ by population. For example,
the Kell system has two major codominant alleles: K and k. Codominance
 91
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

means that both the K and k proteins (antigens) are made in persons with
the Kk genotype. An antigen is any molecule (protein or carbohydrate) that
elicits an immune response. The K antigen occurs at the lowest frequency in
African Americans (0.02), is slightly higher in European Americans, and is
highest in some Middle Eastern Arab populations (0.250). The K antigen, Rh
phenotype frequencies are KRh−/kRh+ 0.91, 0.98; KRh+/KrRh− 0.0002, not
detected; and KRh+/KRh+ 0.088, 0.02 in European Americans and African
Americans, respectively.
The take-home message here is that blood transfusion is determined not
by socially defined race but by an individual’s genotype at the primary com-
patibility loci A, B, O and Rh, as well as the secondary and tertiary loci.
Individuals who carry the more common alleles at these genetic systems will
find it easier to find a suitable blood donor. Individuals with rare alleles will
find it more difficult to find a suitable donor. In all cases, close relatives will
be the most likely suitable blood donors.
The ability to receive tissue donations is similar to blood donation. In this
case, the major compatibility loci are the human leucocyte antigens (HLA)
system. The HLA antigens are proteins found on the surface of virtually
every cell in animals. The purpose of these proteins is to allow the recogni-
tion of foreign proteins and sugars from organisms (such as viruses, bacteria,
and other parasites).
In humans, there are three major HLA loci (HLA-A, HLA-B, and HLA-C),
and five class 2 loci (HLA-DPA1, HLA-DQA1, HLA-DQB1, HLA-DRA, and
HLA-DRB1), along with some minor loci. At the HLA-A locus, 68 com-
mon alleles account for about 4,340 antigens, HLA-B, 125 common alleles
account for 5,212 antigens; and HLA-C, 44 common alleles for 3,930 anti-
gens. These staggering numbers explain how our HLA system protects
us from pathogens but also why tissue donation is so difficult. The Be the
Match Foundation requires that at least 6 of 8 HLA markers match to facili-
tate a successful bone marrow donation. In some cases, more matches are
required.
Just as in blood donation, tissue donation works best with a close relative
(brother, sister, first cousins), who share more genes with an individual by
descent and thus have a greater likelihood of sharing HLA genotypes. HLA
allele frequency varies by population, and sub-Saharan Africans have the
greatest diversity of HLA alleles. African Americans are less likely to find
a suitable donor match for tissue transplantation due to the fact that low
numbers of this group have registered for tissue donation and because of
 92
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

their greater HLA diversity. In some cases, individuals have received tissue
donations across socially defined race.
A study published in 2004 found that the number of cadaveric renal trans-
plants performed between 1996 and 2001, white-white, white-Black, Black-
white, and Black-Black transplants accounted for 66, 23, 5, and 6 percent,
respectively. This meant that Black patients received 17 percent more renal
transplants across socially defined race than from within socially defined race.
With regard to the tissue match genetics, this makes sense, as Europeans have
lower genetic diversity at HLA-A loci compared with Africans and because
African Americans have on average 16 percent European genetic ancestry.
In conclusion, the idea that blood varies by race is a myth that we can put
to rest. Race is not in the blood.

ARE CERTAIN MEDICINES MORE EFFECTIVE DEPENDING ON

YOUR RACE? SHOULD A PILL BE COLOR-BLIND?

Yes, a pill should be color-blind. The efficiency and rate of metabolism of

medicines might vary by genes, but that has nothing to do with social race.
The genes that are involved in an individual’s drug metabolism are
ancient. Many of them are conserved across vertebrate animals. Their pri-
mary purpose was to detoxify compounds associated with plant and fun-
gal foods. However, ancestral mammals never encountered these natural
sources of toxins at the concentration that we see in modern drugs. Thus,
our body’s lack of capacity to react to modern high-purity and -potency
drugs is an example of an evolutionary mismatch. Evolutionary mismatches
in humans often result from the fact that our technology and cultures have
evolved at a much faster rate than our genomes. This is why in virtually
every ad you watch on television for a medication, the small print and low-
volume narration for its potential side effects might last the entire length of
the commercial.
Genes associated with drug metabolism could vary in frequency by popu-
lation and therefore can be a factor in how socially defined races respond to
specific drugs. For example, in 2014, the attorney general for Hawaii, David
Louie, filed a lawsuit against Bristol-Myers Squibb and Sanofi-Aventis, the
manufacturers and distributors of the drug Plavix (brand name for clopido-
grel). In the suit, Louie alleged that the manufacturers engaged in unfair
and deceptive marketing of the blood-thinning drug. Plavix is designed to
prevent strokes and heart attacks. The suit claimed that the manufacturers
 93
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

did not disclose information related to how certain genetic traits alter the
effectiveness of the drug and potentially lead to complications such as gas-
trointestinal bleeding. Studies of the drug found that 38–79 percent of Pacific
Islanders and 40–50 percent of East Asians might respond poorly to Plavix.
The inability to successfully metabolize clopidogrel is associated with
variation in the cytochrome P450 (CYP) enzymes. These enzymes are part
of the cellular respiration chain. The CYP2C19*2 allele produces a defective
protein, resulting in poor metabolism. The allele occurs in high frequency in
East Asians, South Indians, and Pacific Islanders but at very low frequency in
Africans and Europeans. Genetic variation at the CYP2D6 locus is particu-
larly important because it enables a variety of drugs to be metabolized. There
is also considerable genetic variation at this locus.
To demonstrate that variation at this locus is not “racial” in the context of
social definitions, the frequency of allele *1 is 83 percent in African Ameri-
cans (of western and central African and European descent) but 27.8 percent
in Tanzanians (East Africans) and 85.6 percent in Zimbabweans (south-
east Africans). It is 27 percent in East Asians, 43 percent in Han Chinese,
43 percent in Japanese, and 0.49 in Koreans. Thus, this allele occurs both
more and less frequently in Africans than Asians, depending on the African
population.
Understanding how human genetic variation impacts drug metabolism
reveals how ridiculous the notion of a “race-specific” medicine actually is.
The drug BiDil was designed to be more effective than traditional medi-
cines for congestive heart failure. BiDil is a combination pill that included
an antioxidant and nitric oxide inhibitor. It was originally designed as a bet-
ter therapeutic for anyone with heart disease. However, it became racial-
ized when it was shown that although the drug didn’t significantly improve
heart disease outcomes for the overall population tested, it did so for the
African American subsample in the study. The drug was then tested in the
African American Heart Failure Trial (A-HeFT). As a result of the strong
performance in that study, the manufacturer, NitroMed, sought and received
permission from the FDA to market BiDil as the first “race-specific” drug.
This right was granted despite the fact that BiDil was never extensively tested
with other racial or ethnic groups. BiDil failed to capture a significant por-
tion of the market for a number of reasons, including the fact that it was a
self-limited market, its cost was high ($1,200–$2,800 per year), generics were
available that could do the same job, and, finally, African American patients
for the most part did not desire a “race-tailored” drug.
 94
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

The lesson of BiDil has changed the conversation in medicine from race
as a proxy for biological, environmental, and social variation to the notion
of personalized medicine. This sea change resulted in part from recognition
that the key variables determining how a drug will metabolize in a specific
patient are related to the individual’s genome and their own environmental
history and current situation. The advent of cheap whole-genome-sequenc-
ing technology is ushering in the day when this sequencing will be routinely
offered to patients with sufficient financial resources, allowing for therapies
tailored to a patient’s specific genome and environmental exposures.

IN THE UNITED STATES, RACES DIFFER IN THE RATES

OF THE MOST COMPLEX DISEASES, SUCH AS DIABETES,
HIGH BLOOD PRESSURE, CONGESTIVE HEART FAILURE, AND
CANCER. WHAT EXPLAINS THESE DIFFERENCES IF THE GENETIC
DIFFERENCES ARE SO MINIMAL?

The short answer is that disease rates vary by race because growing up Black
or brown takes a toll on the body. Both racism and being racialized cause
health inequalities.
Now let’s step back. An individual’s disease risk is influenced by three
sources:

1. genes,
2. the environment, and
3. chance.

The racial health disparity observed in modern societies is primarily driven

by the first two causes, but not in ways that most people appreciate. The
disparities we see in complex disease rates in the United States cannot be
explained by allele frequency differences between socially defined racial
groups. If we were to posit a simple genetic explanation of disease differen-
tial by socially defined race, we would expect persons of primarily European
ancestry to bear a higher disease burden than those of African ancestry. This
is because genome-wide studies show that Europeans actually carry a greater
load of deleterious mutations than Africans.
This is illustrated by examining risk alleles for hypertension and their fre-
quency in African Americans and European Americans. Joe examined thirty-
three such loci associated with hypertension in a prior paper and found that
 95
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

African Americans actually had higher frequencies of the protective alleles

at many loci. Other studies have shown that when African Americans had
higher frequencies of the risk allele, this was only true for persons of African
descent in the United States. Persons of African descent with the risk allele
living in western Africa showed no such elevation of risk. Therefore, it is
not genetic predisposition that accounts for African American health dispar-
ity; rather, it is American institutional racism that produces a toxic environ-
mental effect on otherwise healthy genomes.
The reason that allele frequency differences do not readily tell us much
about complex disease causality and risk is because of the complicated
genomic foundations of these diseases. The more complicated the genomic
foundation, the harder it is to compare populations, particularly those that
significantly differ in linkage disequilibrium (LD) levels. Linkage disequilib-
rium is the nonrandom association between two alleles in a population due
to the linkage of their loci along a segment of the chromosome. LD breaks
down with time due to crossing-over events in meiosis (gamete formation).
This means that older populations (sub-Saharan Africans) have smaller
linkage blocks compared with newer populations such as Eurasians, Pacific
Islanders, and Amerindians.
It’s important to note that for this reason, a genetic variant that might be
associated with a disease in one group might have no relationship at all with
that disease in another group. For example, SNP rs9264942, which is associ-
ated with control of HIV, is located in the HLB-C gene in Europeans, but it
has no effect on this trait in Africans. Although SNP rs2523608 is associated
with the same trait in Africans, it is located in HLB-B.
In addition, the polygenic character of disease predisposition means that
these traits are strongly influenced by environment. Thus, in any genome-
wide association study, before genetic causality can be assigned to any
variant, it is crucial that the environment experienced by the organisms in
question be equalized. This is always true in Joe’s experimental work on life
span and physiological performance in the fruit fly (Drosophila melanogaster)
and bacterium Escherichia coli.
These complexities and gene–environment interactions are prime reasons
to take all claims of genetic causation of disease differential among any human
populations—particularly socially defined races in the United States—with a
heavy dose of skepticism. Racially subordinated populations (such as Amer-
indians, Latinx, and African Americans) have never lived in environments
that are equivalent to the socially dominant European population.
 96
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

Table 3.1 presented the African American social experience as a single

day. As emotionally traumatizing as these events were, we also know that
they have had powerful effects on the health of persons who experienced
them. A review of health literature between 2003 and 2013 showed that per-
ceived racism impacted the health of African American women. This study
found consistent evidence for the relationship between perceived racism and
adverse birth outcomes (discussed later), illness incidence, and cancer and
tumor risk. Inconsistent results were found for heart disease, and none of
the studies could validate a relationship between high blood pressure and
perceived discrimination. These relationships are not unique to persons
of African descent. It has also been documented for aboriginal Australians,
who, though they share a dark skin phenotype with sub-Saharan Africans,
are actually among the populations furthest in genetic distance from African
Americans. Racial discrimination is a form of social subordination, and
social subordination has been shown to effect health status in a variety of
animals (mammals and birds).
Today, the mechanisms by which traumatic events affect physical and
mental health are also better understood. One way that traumatic events
(including racism) make their way “under the skin” is via epigenetic changes
to the genome. Epigenesis refers to non-nucleotide-based changes to the
DNA molecule. This includes DNA methylation, short interfering RNAs
(siRNA), micro RNAs (miRNA), and histone modification. DNA methyla-
tion refers to the addition of methyl (-CH3) groups to DNA chain in places
where a cytosine (C) is connected to a guanine (G) nucleotide. These modi-
fications occur over an individual’s life span. Epigenetic changes impact how
genes are expressed and are known to play a substantial role in a variety
of complex diseases such as heart, cerebrovascular, peripheral artery, liver,
and inflammatory bowel disease, as well as cancer and a variety of mental
illnesses.
Researchers examined more than two hundred fifty African American
women and found a highly significant association between perceived racial
discrimination and DNA methylation levels. In that study, the increased
DNA methylation was associated with elevated levels of schizophrenia, bipo-
lar disorder, and asthma. There is evidence that epigenetic modifications
play a major role in a variety of diseases that display racial disparities, includ-
ing the big killers of heart disease and cancer.
Finally, in chapter 1, we discussed how the environment had powerful
effects on any organism’s physical traits. The social subordination of racial
 97
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

minorities has had significantly impacted the physical and biotic environ-
ments in which they have lived over the course of U.S. history. And in turn,
these physical and biotic environments have profound influences on the pat-
terns of disease and mortality experienced by these minorities.
A glaring historical example of the importance of ecological conditions is
the dispossession of the Five Civilized Tribes (Cherokee, Chickasaw, Choc-
taw, Creek, and Seminole), who once occupied much of the modern states
of the Carolinas, Georgia, Kentucky, Tennessee, and Virginia during Andrew
Jackson’s administration. The Indian Removal Act of 1830 was premised on
Jackson’s deep racial mistrust of American Indians. This removal occurred
despite the fact that these tribes had agreed to change their way of life (many
adopting Christianity) to adhere to the cultural norms of white Americans.
The removal began with armed men seizing horses, cattle, and houses and
ejecting their occupants, assaulting any who dared to resist. Along the “trail
of tears,” the tribes suffered from poor weather, inadequate food, disease,
depression (due to the loss of loved ones and homes), and mistreatment by
soldiers. The estimates of death from this forced removal of the Cherokees,
Choctaw, Creeks, and Seminoles was 4,000–5,000 (25 percent), 6,000 (15
percent), 500 (50 percent), and 500 (50 percent), respectively.
This kind of environmental violence still occurs in the United States,
though perhaps not so blatantly. This is illustrated by the pattern of exposure
to the toxic wastes generated by our society. In 2007, it was estimated that
more than 9,222,000 people lived in neighborhoods within three kilome-
ters of our nation’s documented 413 commercial hazardous waste facilities.
More than 5.1 million nonwhites—including 2.5 million Hispanics or Lati-
nos, 1.8 million African Americans, 616,000 Asians/Pacific Islanders, and
62,000 American Indians—live in neighborhoods with one or more com-
mercial hazardous waste facilities.
Host neighborhoods of commercial hazardous waste facilities are 56 per-
cent nonwhite, whereas nonhost areas are only 30 percent nonwhite. The
percentages of African Americans, Hispanics/Latinos, and Asians/Pacific
Islanders in host neighborhoods are 1.7, 2.3, and 1.8 times greater (20 percent
vs. 12 percent, 27 percent vs. 12 percent, and 6.7 percent vs. 3.6 percent),
respectively, than their representation in the U.S. population.
Poverty rates in the host neighborhoods are 1.5 times greater than nonhost
areas (18 percent vs. 12 percent). More than 600,000 students in Massachu-
setts, New York, New Jersey, Michigan, and California attend nearly 1,200
public schools whose enrollment is largely made up of African American
 98
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

and other ethnic minority children, and these schools are located within a
half mile of federal Superfund or state-identified contaminated sites.
More than 68 percent of African Americans live within thirty miles of a
coal-fired power plant—the distance within which the maximum effects of
the smokestack plume are expected to occur—compared with 56 percent of
European Americans. Exposure to toxic materials such as heavy metals and
pesticides has well-known impacts on complex diseases. It is possible to look
up the exposure of various communities at the EPA’s Toxic Release Inventory
website. One study found that in Southern California, census tracts with
more than 15 percent Latino residences were exposed to 84.3 percent more
toxic waste than those with less Latino residence. Similarly, census tracts
with greater than 15 percent Asian residences were exposed to 33.7 percent
more toxic waste. Finally, census tracts with more than 15 percent recipients
with a bachelor’s degree had 88.8 percent less exposure than those with less
than a bachelor’s degree.
In conclusion, the answer to why health disparities for complex disease
persist for racially subordinated communities in America can be found in
the toxic social and physical environments that these communities have
been forced to endure.

WHY ARE RESULTS FROM A BONE DENSITY TEST

RACE-SPECIFIC?

It has long been thought that there are biologically based racial differences
in bone density. Examples of this thinking go back to at least the 1800s. And
it continues today. One day, the father of one of Alan’s students, a practicing
dentist, came to visit his osteology lab. The dentist saw a mandible (lower
jawbone) and politely asked if he could pick it up. He then declared with
confidence that the jaw, being robust and dense, must be from an African
American male. It wasn’t. But the myth of greater bone density of all African-
derived individuals persists.
Possibly the most frequently cited study on race and bone density was
published in a series of articles by biological anthropologist Mildred Trot-
ter in the late 1950s and early 1960s. Trotter and colleagues measured the
bone densities of the long bones from cadavers that are still in the collections
of the Cleveland Museum of Natural History. Information on age, sex, and
race is available for the cadavers, as far as this demographic information
could be ascertained. Most of the individuals were unclaimed bodies from
 99
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

the Cleveland morgue from the late 1800s and early 1900s. These individuals
mainly seem to have lived around Cleveland in the mid- to late 1800s.
Trotter produced a number of graphs for different bones showing their
densities on one axis and age on the other, with demarcations of individu-
als by sex (male or female) and race (white or Black). Her total sample was
eighty individuals, with twenty in each of the four race/sex groups.
Her main conclusions were that (a) peak bone mass was greater in males
than females and in Blacks than whites and (b) the rates of bone loss with
age were rather comparable by race. Trotter’s graphs contain regression lines
for each race/sex group illustrating that bone density decreases in parallel
fashion, at much the same rate, for each group.
What subsequent scientists seem to have taken from her study is the first
part, that peak average densities vary by race and sex, and not the second
part, that the rates of bone loss are similar for all groups.
Because Alan has a condition that effects his bone turnover, about a
decade ago, one of his doctors thought he should have his bone density
tested. Alan traveled down Route 91 from western Massachusetts to Yale-
New Haven Medical Center. There, the receptionist handed him a question-
naire to fill out with lots of the usual questions: name, address, sex, and age.
He answered a bunch of additional questions about risk factors for low bone
density, such as smoking, alcohol consumption, activity level, and diet. The
form also asked him for his race.
He knew why they asked about his race. Simply, it is because race is con-
sidered a risk factor for osteoporosis or low bone density. But is it? What did
this physician mean by “race”?
Alan has returned for a bone density test every summer. Each time, he
fills out the questionnaire, and each time he asks the technician why they
want to know his race. Answers range from a shrug of the shoulder to an
explanation that it is needed so that the data can be interpreted, to an expla-
nation that bone density varies by race. When he asks a follow-up question
about why race is needed or why bone density varies by race, he sometimes
gets an explanation that points to genetic differences. At this point, the tech-
nician usually gives him the same pamphlet on osteoporosis and risk factors
that he always receives. Race is listed as a risk factor along with sex, age,
genetics, and lifestyle. Is race different from genetics? Is it different from
lifestyle?
So, what is under the hood of the machine that measures bone density?
Bone densitometry, also called dual-energy x-ray absorptiometry (DEXA or
 100
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

DXA), uses a very small dose of ionizing radiation to produce pictures, sort
of like x-rays, typically focused on key bone density sites (spine and hips) to
estimate bone density. One beam of x-rays is mainly absorbed by soft tissue
and the other by bone, so from these, bone mineral density can be quanti-
fied. The technique is widely used throughout the world. It is simple, quick,
and noninvasive.
So, why race? It has long been known that men have denser bones at a
given age than women. Women are at increased risk of osteoporosis and
bone fractures due to low density. The same is true of age: we lose bone with
age. And the same is generally thought to be true of race.
Alan gets his results. They include a graph with a dot that shows his bone
density. On one axis, from the bottom of the page to the top, is bone mineral
density from low to high; on the other axis, across the bottom, is age from 20
to 85. Three color zones run across the graph: green starts at the higher bone
densities red at the lowest bone densities, and yellow in the middle. He finds
a dot of his density, the point that crosses his age and bone density, right at
the border of the green and yellow zones.
Now, the results are not purely about bone density; rather, they are
“adjusted” based on comparing his results with those of other individuals of
his age, sex, and race. It makes sense to compare him with others like him:
apples to apples. It would not make sense to compare a twenty-year-old with
an eighty-year-old or a male with a female.
But race? The calculation is based on an algorithm called FRAX. FRAX is
widely available, and one can put one’s own results into FRAX or even make
up results and enter them into FRAX. Alan did both. It turns out that if he
had said he was African American, his risk of osteoporosis would be seen as
much greater, because the comparative database for Blacks has higher bone
densities.
The use of race here as a risk factor is illustrative of a common set of mis-
takes, actually two leaps of faith: that racial differences in osteoporosis risk
are genetic and that genetic differences break along racial lines.
Certainly, there are some genetic factors that could lead to greater or lesser
peak bone mass and the rate of bone loss from that mass. But, of course,
there are a host of other factors, like the ones Joe was asked about, including
exercise and diet, that can affect a person’s bone health.
In the end, what does race mean? Is it standing in for genetics? If so, we
know that this is a deep problem. If genetics is the issue, why not ask instead
about family history or collect some actual genetic information?
 101
WHY DO RACES DIFFER IN DISEASE INCIDENCE?

Let’s also be clear that FRAX and osteoporosis is not the only example of
how race gets baked into the science. Race is a demographic factor that is all
too frequently used to “adjust” for risk. Lundy Braun of Brown University
has written about how the spirometer has separate adjustment points for
race. Also, the interpretation of iron deficiency takes race into account,
with the highly likely result of undercounting African American iron defi-
ciency. Finally, it has recently come to light that the diagnosis of a con-
cussion is based on separate standards for African Americans than white
football players. Race is in the algorithms. It is baked into biomedicine.
In conclusion, we think we know why you are being asked your race,
and that is because race is assumed to be a biologically stable risk factor for
osteoporosis. But we see no reason that this should be the case despite how
it is embedded in FRAX. So, the answer is bad medicine.
We hate to call out an entire industry and profession for making the con-
ceptual error in thinking that race is a useful genetic construct. So, here’s
a simple challenge: prove to us that asking one’s race helps to understand,
diagnose, or treat bone loss. In particular, show us that this is the case after
you have corrected for easily obtainable (and repeatable) information such
as diet, exercise, and known genetic risk factors.
 Chapter Five

LIFE HISTORY, AGING, AND MORTALITY

Death and taxes. Both are guaranteed to happen. The former is guaranteed
for everyone and all living things. It is the last of what biologists refer to
as “life history events.” The other important events include birth, matura-
tion, menarche and menopause (the beginning and end of the ability to give
birth), and aging (or senescence). In this chapter, we focus on myths about
life history differences among races.
Evolutionary fitness is defined as “differential reproductive success.” For
organisms like ourselves, this involves how long we live and how much we
reproduce. We calculate evolutionary fitness as the product of the probability
of survival at a given age (lx) times the average reproduction of individuals at
that age (mx). For example, if 100,000 babies are born in a given year, some
fraction of them will not survive the first year. Similarly, of those who survive
to age one, some fraction will not survive to their second birthday. We can
continue following that group until every one of them has died (for humans,
usually about one hundred years; see fig. 5.1).
Similarly, the average reproduction of the cohort is calculated by the num-
ber of live births to the females in that group each year. For humans, repro-
duction generally doesn’t begin until females are around age thirteen, but this
continues, with peak reproduction occurring in the twenties and declining
until no reproduction occurs sometime in the fifties. Life histories are impor-
tant because variation in the timing of life events might greatly shift fitness.
 103
L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

FIGURE 5.1. The age-specific probability of survival for Americans is plotted. The probability of survival
drops steadily until all individuals of the original birth cohort (100,000 individuals) have died. Data from
National Center for Vital Statistics, 2008.

Traits associated with life history include age of reproductive maturity,

age-specific reproduction, survival rate, aging, and number and size of off-
spring at birth. The study of life histories in a variety of organisms (animals,
plants, fungi) demonstrates that many life history traits are in opposition
to one other, an adaptive trade-off. For example, life span and reproduc-
tive effort generally trade off against each other. In other words, traits and
environmental conditions that tend to increase average reproduction gener-
ally decrease health and life span. We now know that these trade-offs play
a crucial role in the health profiles of organisms. Thus, at different points
throughout a person’s life, increased investment in reproductive function by
either physiology or behavior affects the risk of many diseases and therefore
life span.
Genetic factors contribute to interindividual and interpopulation vari-
ation in reproductive traits; however, the dominant source of variability
is how the environment influences physical traits (phenotypic plasticity)
during development and adult life. In our species, reproductive traits in
both sexes evolved sensitivity to ecological conditions. This is reflected in
contemporary associations of hormone concentrations with geographical
setting, nutritional status, and physical activity level. Also, lifetime expo-
sure to increased concentrations of sex hormones is associated with the
risk of some cancers. As well, faster sexual maturation and higher number
 104
L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

of births per age interval (parity) increases one’s risk of diabetes and car-
diovascular disease.
To illustrate this compromise, one recent study examined progesterone
(one of the reproductive hormones) levels in reproductively healthy females
from different populations (Democratic Republic of the Congo, Bolivia,
Nepal, Poland, and the United States). Women in the Congo are gener-
ally Africans; in Bolivia, Amerindian/European; in Nepal, Eurasian; and in
Poland, European. The race/ethnic identity of women from the United States
was not identified. This study showed that women from the Congo, Bolivia,
Nepal, and Poland had statistically significantly lower levels of progesterone
(200–250 picomoles/liter compared with 350 picomoles/liter) than Ameri-
can women. The authors suggest that this is due to the higher physical work-
load and lower energy balance of the non-American women. Thus, although
genetic variation exists between these different groups of women, it was not
a primary factor in determining their progesterone levels. In turn, the life
history trade-off theory would predict that all other factors being equal, the
non-American women would display lower average reproduction and longer
average life span compared with American women. However, we know that
in the countries represented in this study, all other factors are not equal.

WHY DO BLACKS SEEM TO AGE SLOWER

THAN WHITES? (AND IS THAT TRUE?)

No. It is not true that Blacks age slower than whites. Indeed, the evidence we
reviewed concerning sickness and death rates of African Americans in the
previous chapter speaks volumes against this mistaken idea. In 1999, the life
expectancy for whites was ~77 years compared to only 72 years for blacks.
From 1999 to 2013, the life expectancy increased for both groups but the gap
still remained. Thus, the data clearly show that longevity for Blacks has his-
torically been lower than for whites in the United States.
This myth of slower aging of African Americans most likely tracks to the
popular expression, “Black don’t crack,” which is associated with African
American skin. It is true that darker skin sustains less ultraviolet damage
than lighter skin. This means that as darker-complexed individuals age, they
show less wrinkling in their skin, giving the appearance of younger age. This,
of course, will be true of all dark-complexed individuals whose ancestry can
be traced to any of the populations of tropical equatorial regions (Africa,
Middle East, India).
 105
L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

Life expectancy from birth

84
Life expectancy Hispanic
81 White
Black
78

75

72

2005 2010 2015 2020

Year

FIGURE 5.2. Life expectancy at birth from 2006 to 2020. The life expectancy for all socially defined racial
groups increased and then declined in that period. Hispanics had the highest life expectancy, followed by
white, with Blacks displaying the lowest. The drop for all groups in 2020 was due to COVID 2019. Blacks
showed the steepest decline due to the virus.

However, to truly understand that this idea is false requires a better under-
standing of what aging actually is. Surprisingly, most people (including med-
ical doctors and biomedical scientists) do not fully understand aging. The
evolutionary theory of aging has been validated in a large number of experi-
ments in model organisms such as bacteria, round worms, and fruit flies.
The first misconception that people often make is to associate aging with
chronological time. If this assumption held, we would have a really difficult
time explaining the life span of organisms with cellular structures similar to
our own whose maximum life spans vary over orders of magnitude (May
flies, one day; mice, three years; humans and lake sturgeon, 100-plus years;
redwoods, more than 300 years; fungal fairy rings, 3,000 or more years; pop-
lar clones, more than 10,000 years). In humans and organisms like us, it is
better to think of our life spans as punctuated by stages: development, ado-
lescence, adulthood, senescence (aging), and late life. Senescence does not
begin until our net future expected reproduction has dropped to zero. At
that point, the power of natural selection to correct the expression of genetic
systems that might reduce our evolutionary fitness (the product of our age-
specific survival and reproduction) consistently declines. This results in an
increasing dysregulation of our molecular, cellular, and physiological func-
tion, eventually ending in death.
The inability of natural selection to address such late-life genetical disas-
ters allowed our genome to accumulate alleles that contribute to aging
 106
L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

via two mechanisms, mutation accumulation and antagonistic pleiotropy.

Alleles governed by mutation accumulation have no effect during develop-
ment, adolescence, and adulthood but negative effects during aging. Those
that are governed by antagonistic pleiotropy are beneficial during the first
three stages of life but detrimental during senescence (see table 5.1). Genes
governed by antagonistic pleiotropy would be found in all world populations
(although different variants and frequencies); those determined by muta-
tion accumulation might be specific to certain populations. These genes
would contribute to a variety of pathologies that begin to accelerate at later
ages, including those impacting the leading sources of mortality in Western
nations, such as cancer and heart disease.
However, aging is a complex phenomenon, with contributions from vir-
tually every gene in the human genome, and therefore is strongly influenced
by environmental factors. The best studies of the genetic contributions to
life span find a maximum contribution of about 30 percent from genes and
70 percent from environment. In this chapter, we have already discussed the
differential environments experienced by persons due to socially defined race.
In this regard, studies of mortality rates with age have shown consistently that
African Americans die sooner than European Americans and Asian Ameri-
cans. Insight into this pattern has been provided by new genomic methods
that have been developed to measure biological (as opposed to chronologi-
cal) age. Recent studies have found that DNA methylation can be used as a

TABLE 5.1
Population Genetic Mechanisms That Account for Aging

Mechanism Early life Late life Examples

Mutation/selection − NA Genes, such as progeria, do not contribute

balance to aging; individuals rarely live to reproduce;
frequency will vary in populations by mutation
rate.
Mutation accumulation 0 − Alzheimer’s disease, Huntington’s chorea; have
no negative effects on early life; frequency in
populations will be determined by genetic drift.
Antagonistic pleiotropy + − Cancer genes play a beneficial role in
development and maintenance of tissues. All
populations will have these genes, although the
variants might be different in specific groups.
Note: Mutation/selection balance is not an aging mechanism and doesn’t really affect average life span (these alleles
will be rare). Mutation accumulation effects will vary by population and could contribute to variation in rates of
aging. Antagonistic pleiotropy governs genes that had beneficial effects early in life. These genes would be present
in all humans (and in many related species) as well.
 107
L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

proxy for biological aging. We know that DNA methylation can result from
differential stress and exposure to toxic environments.
One recent study found that in genes associated with age-specific cellular
pathways, African Americans showed 4,930 methylation sites compared with
only 469 in European Americans. The authors calculated that the increase
in biological aging was gender-specific, with an increase of biological age of
2.04 years in a sample of middle-aged African American compared with age
matched European American men. Results from these kinds of studies tell us
that the “Black does not crack” metaphor is just skin deep. Data on age-spe-
cific sickness and death in the United States explains that although Joe’s skin
might look good for someone his age, he is far more likely to die sooner than
Alan or any other white male with a comparable occupation and social status.
Another general measure of aging (or weathering) is telomere length.
Telomeres are the ends of chromosomes and are made up of repeated nucle-
otide sequences that act to protect chromosomes from deterioration or from
fusion with other chromosomes. Telomeres shorten with age, but their rate
of shortening varies and is accelerated by psychological stress. Shortened
telomeres are associated with cellular health and aging. A recent commu-
nity that engaged in a collaborative study in Tallahassee, Florida, found that
self-reported unfair treatment attributed to race (or racial discrimination) is
associated with shorter telomere lengths.
The take-home message is that institutional racism still kills racially sub-
ordinated groups faster than those of the socially dominant populations.
Racism, not biological race, increases aging.

WHY ARE THERE MORE BLACK THAN WHITE BABIES

WITH LOW BIRTH WEIGHT?

Infant birth weights and infant mortality tell another vital story about how
racism, not biological race, persists.
First, we present some facts and definitions. The average birth weight in
the United States is around 7.5 pounds (3,400 grams). Birth weights are a
function of the rate of growth and amount of time in utero (the longer or
closer to full term, the higher the weight). Early birth is defined as prematu-
rity, and being born small for the length of pregnancy is called intrauterine
growth retardation.
The average birth weight of a Black baby in the United States in 2016–18
was about a pound (454 grams) less than that of a white baby. And the rate
 108
L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

of low-birth-weight babies born to Black women (less than 2,500 grams) is

nearly twice that of babies born to white women. These inequalities have
persisted pretty much unchanged since the United States began to systemati-
cally collect birth weight and infant mortality data.
Infant birth weights are of great importance because they are the clearest
risk factor for infant mortality (death before the first birthday) and future
developmental problems. Today, Black babies die at a rate over two times
that of white babies.
Study after study has shown that in the United States, the birth weights
of infants of Black women are lower than those of infants of white women.
The extent to which the lower birth weights gap is due to life circumstances
or genetic factors is unclear. However, given the consistency of the difference
over time, regions of the country, and social strata and economic classes—
combined with a bias toward genetic explanations— physicians and biomed-
ical researchers have all too often favored a racial-genetic explanation.
In one study, the birth weight records of more than 90,000 infants from
1980 to 1995 from Illinois were used to test the importance of lived experi-
ence versus race. Most of the infants were born to white (n = 44,046) and
Black (n = 43,222) mothers who were themselves born in the United States.
As in prior studies, the investigators found a clear difference in birth weights,
such that babies born to the white women had an average weight of 7.58
pounds compared with 6.80 pounds for babies of Black women.
Notice this study specified the mothers’ place of birth. That is because
the authors wanted to test whether growing up in the United States, a rac-
ist country, with stresses from racism, might be a cause of the lower birth
weights. Thus, the authors of this study, neonatologists Richard David and
James Collins, added to their study the birth weight records of 3,135 infants
of African-born Black women who had given birth in Chicago but spent at
least part of their lives in Africa.
Because of the history of white men having babies with Black slaves, Afri-
can Americans are genetically part white (we discuss this in more detail in
chapter 9), whereas this is not the case with African women. Therefore, if
racial genetics is the predominant explanation for the birth weight differ-
ence, one would expect that the babies of “purer” African women, those
born in Africa and with less European admixture, would have the lowest
birth weights.
However, the study found that the babies of Black women who were born
in Africa had an average birth weight of 7.33 pounds, or just a quarter pound
 109
L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

less than the babies born to white women. The close tracking of the dis-
tributions of babies born to white women and those of Black women who
grew up in Africa is strikingly clear, as is the lag in birth weights of babies
born to Black women who were born in the United States (figure 5.3). David
and Collins conclude, “The birth-weight patterns of infants of African-born
black women and U.S.-born white women are more closely related to one
another than to the birth weights of infants of U.S.-born black women.”
Moreover, the results strongly—and dramatically—smash a genetic hypoth-
esis and support a hypothesis that growing up under conditions of racism
takes a lifelong toll.
What, then, explains these differences? The results we suggest strongly
point to a lifelong consequences of living in a racist society. This has been
called “weathering” by Geronimus. Others have called this the develop-
mental origins of health and disease (DoHaD). These hypotheses are simi-
lar in that they consider how early life stresses can have lasting effects on
life events, aging, and adult disease. These impacts have been shown in
other mammals and birds, not just humans. Thus, we now know that the

25
African-born Blacks
U.S.-born Blacks
U.S.-born whites
20
Percentage of births

15

10

0
0 500 1000 1500 2000 2500 3000 3500 4000 4500 5000 5500
Birth weight (g)

FIGURE 5.3. The distribution of birth weights for babies born to African-born Black women is very similar
to that of babies born to U.S.-born whites. The birth weight distribution for both groups is higher than that
of babies born to U.S.-born Black women. These results strongly suggest that African ancestry is not the pri-
mary factor contributing to the birth weight differential of U.S.-born Blacks and whites. Source: Richard David
and James Collins, “Differing Birthweight Among Infants of U.S. Born Blacks, African-Born Blacks, and U.S.
Born Whites,” New England Journal of Medicine 337, no. 17 (1997): 1209–14
 110
L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

weathering of moms (and the epigenetic mechanisms of institutional rac-

ism) affects their babies’ development in utero and forever.

DOES LIFE EXPECTANCY VARY BY RACE?

Yes. And this is one of the main areas in which we see the effects of persistent
racism.
First, the overall average life expectancy from birth in the United States is
shockingly low compared with other countries. In 2015, the life expectancy
was 78.8 years. That was actually a slight decline from the prior year and a
long-term trend of increasing life expectancy. Researchers point to problems
like death from opioid addiction. The United States currently ranks around
forty-sixth in the world for life expectancy, almost six years below Japan and
about four to five years below most countries in the European Union. It is
almost four years below Canada as well as Cuba, Costa Rica, and Chile. Yet,
we spend almost twice as much as any country on health care.
In addition to the overall poor record in health, there is a huge dispar-
ity in life expectancy by race and socioeconomic status. African American
life expectancy has typically been about 5 to 10 percent shorter than that of
whites. Recent data suggest some closing of the gap—to about four years—
but much of that is due to increased deaths from addiction among whites.
However, the differential death toll on Blacks due to COVID-19 might fur-
ther widened the gap beyond four years (figure 5.1). These are real minutes,
hours, days, months, and years of real lives lost.
Figure 5.4 shows the impact of race, gender, and educational attainment
on life expectancy in the United States. First, note that Hispanic females and
males have relatively high life expectancies. This is an example of what has
been called the “Hispanic paradox.” Hispanics generally have better health
than one might expect given their position in U.S. society. They might be
protected from more virulent forms of stress. And their being recent immi-
grants might insulate them from the weathering effects of U.S. racism.
Education is a huge predictor of life expectancy. For all groups, increasing
education from less than a high school degree to a college degree increases
life expectancy by around a decade. Stay in school!
Finally, Blacks have lower life expectancies than whites and Hispanics
at all levels of education. For example, Black males without a high school
degree have life expectancies in the mid-sixties. Even with a college degree,
 111
L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

90 Hispanic females
Life expectancy at birth (years)

White females
Hispanic males
White males
80 Black females
Black males

70

60
< 12 12 13–15 16 or more
Years of education

FIGURE 5.4. Life expectancy by race and years of education. Life expectancy increases with years of educa-
tion for all groups, but the gap between that for whites and Blacks remains. Hispanic males and females show
greater life expectancy than either whites or Blacks. Source: S. J. Olshansky, T. Antonucci, L. Berkman, R. H.
Binstock, A. Boersch-Supan, J. T. Cacioppo, and J. Rowe, “Differences in Life Expectancy Due to Race and Edu-
cational Differences Are Widening, and Many May Not Catch Up,” Health Affairs, 31, no. 8 (2012): 1803–13.

their life expectancy is less than the average white life expectancy and below
that of a Hispanic male without a high school degree.
Yes, life expectancy varies by race. This is one of the most important indi-
cators of racial inequality.

IF RACES ARE NOT BIOLOGICAL, WHY ARE THERE SUCH

PERSISTENT DIFFERENCES IN HEALTH AMONG RACES?

The simple answer to this question is that the social and physical aspects
of the environment that contribute to health disparities have not changed
enough to eliminate the disparities. This reality has been brought into
sharper focus by the COVID-19 pandemic. As this virus was new to
our species, no population had genetically based resistance to it, in the
way that endemic diseases such as malaria (sporozoan parasite), yellow
fever (flavivirus), or sleeping sickness (trypanosomiasis) do. The rates
of infection and death from COVID-19 that we are now experiencing
are explained by differential exposure and lack of adequate health care.
Indeed, the rates we see in Latinx populations is also associated with a
fear among undocumented people to seek medical treatment because they
might be deported.
 112
L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

Thus, the differential patterns of sickness and death that we see in the
United States is one of the most powerful signs of institutional racism. The
killings of George Floyd, Breonna Taylor, and Ahmaud Aubrey are just the
tip of the iceberg of this murderous system. These stark ongoing disparities
are a call for all people of goodwill to take immediate action.

CONCLUSIONS

Humans have a specific life history marked by a long period of early develop-
ment and slow maturation. However, there is no evidence that this pattern
varies by continent. Rather, there is strong evidence that life histories vary
depending on the stresses of different environments. Adaptations to early
stresses can have impacts on later events such as birth weight and telomere
length. These results show that racism, once it gets into the body, can have
long-lasting effects.
 Chapter Six

ATHLETICS, BODIES, AND ABILITIES

How do we think about the connection between athletic ability and intel-
ligence? Are they connected in any way? Do individuals who are smart tend
to be more athletic and physically able, or is the reverse more likely? And
what about races? Are some races more athletic than others? Are members
of some races more intelligent?
Up to the 1930s, the general idea was that there was a connection between
athletic ability and intelligence. Whites from elite schools such as Harvard,
Yale, and Princeton were viewed as smart and intelligent as well as handsome
and athletic. They played football and other sports. The Kennedy clan, Bos-
ton Brahmins and mainly Harvard educated, were often photographed and
filmed playing football and sailing. President John Kennedy was handsome,
trim, and smart.
After the Age of Discovery, individuals of European decent thought that
they were more intelligent than those of African and Asian descent. That’s
perhaps the oldest and most central myth of race. And until the 1930s, they
also thought that they were the most athletic, strongest, and most virile of the
races. Whites dominated the Olympics and professional sports. Of course,
few non-European countries fielded a full-fledged and well-trained Olym-
pics team, but that did not seem to impact the view of European athletic
superiority. And in the United States, all of the professional sports leagues
barred nonwhites. It is easy to dominate when you have no competition.
 114
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

There were always counter facts to European athletic superiority. Heavy-

weight boxer Jack Johnson (1878–1946) was a champion and without doubt
the best boxer in the age of Black terror (the Jim Crow era). Satchel Paige
(1906–82) started playing baseball in the Negro Leagues in the 1920s and
might well have been the best pitcher of all time.
The myth of European athletic superiority took a tumble in the 1930s. In
1936, African American Jesse Owens won four gold medals at the Berlin Olym-
pics, to the dismay of Adolf Hitler. Two years later, African American heavy-
weight boxer Joe Lewis knocked out Max Schmeling, the German champion,
to recapture the world heavyweight boxing crown. Boxing required feats of
speed, strength, and cunning; thus it was no longer possible to hide the fact
that non-Europeans might be the athletic equals of Europeans.
Instead of an acknowledgment that excellent athletic performance might
be found in individuals of all socially defined races, another myth emerged:
that there is an inverse relationship between athletic and intellectual ability.
And it was racialized. Whites are smart and Black and brown folks are ath-
letic. Here, we unpack this myth.

DO RACES DIFFER IN THEIR ATHLETIC ABILITY?

No. Individuals certainly do vary in athletic abilities. There also are data
suggesting that genetic variation among groups might play a role in group
differences in specific athletic feats. But that variation is not racial variation.
In prior chapters, we established that human beings cannot be classified
into biological races. So, we could stop right here. The question of different
abilities of any sort by biological race makes no sense, because biological
races make no sense. They do not exist.
But clearly, many individuals today wonder about the dominance of
African Americans in sports such as basketball and whether that could be
explained by genetic differences among groups of people. A common ques-
tion we hear in private conversations is some version of “If race is not genet-
ics, then why are there so many excellent Black athletes?” So, let’s explore
these ideas head on!
First, to answer the question about the reality and likely roots of any pur-
ported racial differences in athletic ability, we have to be clear about what
is meant by “athletic ability” and how it is measured. A general definition is
“the strength, co-ordination, speed of reflexes and other qualities and skills
which are required for a person to excel in a sport.” By that definition, many
 115
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

sports require much the same things: coordination the same muscle groups,
as well as stamina, to be successful. However, we quickly see how the defini-
tion gets racially subverted.
The 2008 Summer Olympics in Beijing saw stellar performances by Usain
Bolt (Jamaica, primarily of African descent) and Michael Phelps (United
States, European descent), but only Bolt’s athletic accomplishment was racial-
ized. Phelps’s success was discussed in the context of the sacrifices made by
his single mother and the outstanding coaching he received throughout his
career. His success was due to circumstances and perseverance. Bolt’s suc-
cess, on the other hand, was discussed in the context of genomic variants
associated with superior Jamaican sprinting ability.
What is clear is that athletic performance, just like aging or intelligence,
however defined, is a complex physical and mental trait involving a set of
interacting genes of interacting genes, environment, culture, and opportu-
nities. For example, a 2006 study of the genetics of athletic performance
found 165 autosomal, 5 X-linked, and 17 mitochondrial loci that had some
relationship to performance. A year later, the same research group found 214
autosomal, 7 X-linked, and 18 mitochondrial loci that related to athletic per-
formance. These genetic markers were found by comparing elite athletes and
nonathletes using candidate gene methods, a standard method at that time.
After reviewing these studies, in 2013, Joe found that there was no basis for
differentiating socially defined racial groups according to genes associated
with athletic performance. Several more recent studies have failed to find
any racial component to the genomic foundation of athletic performance.
For example, a review of the literature from 1997 to 2014 found 120 genetic
markers (77 endurance, 43 power/strength) associated with elite athlete sta-
tus. A genome-wide association study (GWAS) found 6 markers associated
with athleticism in a sample of African-American, Jamaican, Japanese, and
Russian elite athletes. The fact that these markers were found in persons of
widely divergent descent also shows that there is no racial basis for athletic
performance.
Furthermore, these genetic variants are pretty evenly distributed across
continents. For example, the FST value for one variant, the nuclear factor
1 transcription factor SNP, rs1572312, is only 0.065. (Remember that an FST
below 0.25 suggests that there is little variation among groups.) Indeed, for
the seventy-six populations in the ALFRED (allele frequency) database, the
frequencies of the allele are virtually the same in all populations. Also, the FST
value for the SNP associated with muscle power (rs1815739) in the ACTN3
 116
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

(alpha-actinin 3) gene that is expressed in type II muscle fibers is 0.139. The

range of this SNP in Africa is 1.00–0.65; in Europe, 0.760–0.500; and in East
Asia, 0.650–0.500. This means that in virtually every country measured, at
least half the population carries the SNP for increased muscle power.
Thus, the science of human genetic variation does not support the idea
that any large (continental) human groups are necessarily more athletic
overall than others. Elite athletes’ ability is the complex result of genomic
variants, gene expression (including epigenetic effects), and metabolic effi-
ciency, as well as access to training facilities and coaching.
Biomechanical differences also influence the capacity of specific popu-
lations to produce world-class athletes. For example, although ancestry
associated with high-altitude adaptation is a definite advantage for endur-
ance events, due to the need to maximize oxygen metabolism, excellence in
long-distance running is more likely to some groups such as Ethiopians as
opposed to others, such as Himalayans or Andeans. This is because other
biometric attributes, such as body mass and proportion, favor Ethiopians.
Culture also plays a significant role in which sports athletes from different
societies engage in. The success of Ethiopians and Kenyans in long-distance
running is directly related to the lack of transportation available in the com-
munities that have spawned the recent wave of world-class runners from
those nations.
Similarly, the success of male and female Jamaican sprinters can be
directly related to the cultural influences that funnel athletes into this sport.
Of the men who have completed the 100-meter dash in under 9.8 seconds,
six are from Jamaica and three are African Americans. There are 41 million
African Americans and only 2.8 million Jamaicans. For example, since 1910,
Jamaica’s premier athletic event has been the boy’s high school track and field
championship. Success breeds success.
Another example of how opportunity and culture influence sport is the
way in which basketball transitioned from a sport dominated by various
European ethnic groups to an inner-city game dominated by African Ameri-
cans. In the early part of the twentieth century, basketball was dominated by
Jewish, Irish, and Italian teams before it became “integrated.”
Now, the complexion of basketball is changing again, rising in popular-
ity in Eastern Europe and throughout the world. As a result, some of the
brightest stars of today’s NBA, such as Luka Dončić from Slovenia and Rudy
Gobert from France, come from Europe. During the 2019–20 NBA season,
108 foreign-born players were on NBA rosters. Europeans now outnumber
 117
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

European-Americans in the NBA. Is that because Europeans are more natu-

ral basketball players? This is highly unlikely. Rather, we believe that most
European-Americans have shifted away from basketball while Europeans are
embracing the sport.

ARE FINNS THE WORLD’S BEST ATHLETES?

Finns? If you were envisioning sprints, I bet you thought we were going
to say Jamaicans, or if you are a fan of marathons, you might be inclined
to answer “Ethiopians.” Or Americans if you are into total Olympic medal
counts. Finns? Let’s get to it!
How do we evaluate extraordinary athletic ability? We could examine
direct test strength, speed, and jumping ability, but those data are not avail-
able for random samples. Another way to think about athletic ability is via
Olympic medal counts—flaws, biases (which we will discuss), and all.
The highest Finland has ever ranked in the medal count in the Winter
Olympics is second, in 1924. Since 1992, the medal count for Finland has
placed its athletes between eighth and twenty-fourth. The pattern for the
Summer Olympics is similar. In 1924, when Finns ranked second in total
medal count, the Finnish team was led by Paavo Nurmi, one of the greatest
distance runners of all time. Nurmi won gold in the 1,500- and 5,000-meter,
individual cross-country, 3,000-meter team, and men’s cross-country team
races. If we asked you whether Finns were the world’s best athletes in 1928,
what do you suppose your answer might be?
Since 1992, the Finnish medal totals have been between twenty-ninth and
seventy-eighth highest. In the Winter Olympics, the Finns’ best sport has
been cross-country skiing, which makes sense given this country’s climate,
with 80 medals earned. In the Summer Olympics, the best performance has
been in track and field, with a total of 114 medals. Only 16 nations partici-
pated in the 1924 Winter Olympics compared with 92 in 2018. The 2016 Sum-
mer Olympics had 205 nations competing.
Based on everything we know about athletic performance as a complex
trait, we would never expect a country with a population as small as Fin-
land’s to produce the world’s best athletes. The population in 1924 was only
3,272,000, and in 2020 it was 5,553,000. Finland was settled by founder pop-
ulations from northern Europe, so it has less genetic diversity than the rest of
Europe. For example, its frequency of the genetic diseases common to north-
ern Europeans is considerably lower. For example, the frequency of cystic
 118
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

fibrosis in Finland is a tenth that of its neighbors. It is possible that some

adaptation unique to Finland occurred, but that is highly unlikely. And, too,
countries are not populations.
Athletic ability as a quantitative trait is distributed in a normal (bell
curve) shape. Using the tools of classic genetics, we can calculate the number
of physical classes of quantitative traits. Applying the formula for physical
classes (2N + 1) using the 239 loci that have been associated with athletic
ability results in 479 categories of athletic ability. This means that 239 classes
fall above the central point (mean, median, and mode constitute a normal
distribution) and 239 below. Elite athletes would be individuals who fall into
the highest physical classes. The size of a population and its genetic diversity
might be factors in producing people who fall into the extreme high ends of
the athletic distribution, again, where we would expect to find people who
are elite athletes.
The NCAA listed about 35,000 female and male basketball players. If we
assumed there were fifty sports in the United States, all with 35,000 athletes
(a generous assumption), and calculated them as a fraction of the age classes
of where we observe major sports activity (18–44), less than 1.4 percent of
Americans would be considered elite athletes.
One way of determining the performance of a nation’s elite athletes is the
number of medals earned in the Olympics. In 2007, Joe ran a statistical anal-
ysis of total Olympic medal count and showed that a nation’s population size
and gross domestic product were highly significant variables in determin-
ing how many medals its athletes earned. Nations such as the United States,
China, France, Germany, Japan, Russia, and the United Kingdom dominate
the Olympics because of their combination of large population size and
economic power. Additionally, because of their size and waves of immigra-
tion from other countries, these nations might have higher genetic diversity
than smaller countries. Finally, there is considerable variation between the
national medal counts in the summer versus the winter games. Tropical/
desert nations rarely, if ever, win medals in the Winter Olympics. That is a
clear bias!
On the other hand, if one viewed Finland’s Olympic medal count against
its population size, then Finnish athletes do extremely well. The ratio of total
winter medals per million individuals for Finland is 85.5 compared with only
8.5 for the United States! Similarly, the summer medal count per million
individuals for Jamaica is 26.8 and 16.3 for Kenya compared with only 7.6
for the United States. So, by these metrics, maybe the Finns, Jamaicans, and
 119
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

Kenyans are among the greatest athletes in the world? Assuming that they
might be, race clearly explains nothing.
Are Finns the world’s best athletes? In 1924, one might have concluded
that the answer was yes. But then the Olympics changed, and the answer to
the question, as silly as it is, changed to no. What changed? The genetics of
Finns did not change. What changed was culture and the political economy
of Olympic sports.

DO AFRICANS RUN FASTER AND JUMP HIGHER THAN

EUROPEANS AND ASIANS?

No. Although this trope is common and seems true to many, there simply
is no data to support its veracity. Variation exists, but that variation is not
racial. Here is why.
When people ask this question, they usually think about sprint events
such as the 100-meter races that are run on land by elite athletes. However,
we would not be pondering this question if we were thinking about sprint
events in water (tables 6.1a and 6.1b), even though the necessary muscles are
much the same.
World records in land sprint events are dominated by individuals whose
ancestry is primarily from western and central African descent. Note that we
said ancestry, not race. Ancestry is more specific. African Americans, most
of whom do indeed have western and central African ancestry, also have

TABLE 6.1Aġ
Male (M) and Female (W) World Record Holders: Land Sprint Events (< 400 Meters)

Event Time Name Country Ancestry

100 m (M) 9.58 Usain Bolt Jamaica African/European

100 m (W) 10.49 Florence G. Joyner USA African/European
200 m (M) 19.19 Usain Bolt Jamaica African/European
200 m (W) 21.34 Florence G. Joyner USA African/European
400 m (M) 43.03 Wayde Van Niekerk RSA European
400 m (W) 47.60 Marita Koch GDR European
110 m hurdles (M) 12.80 Aries Merritt USA African/European
100 m hurdles (W) 12.20 Kendra Harrison USA African/European
400 m hurdles (M) 46.78 Kevin Young USA African/European
400 m hurdles (W) 52.16 Dalilah Muhammad USA African/European
 120
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

TABLE 6.1B
Male (M) and Female (W) World Record Holders: Water Sprint Events (< 200 Meters)

Event* Time Name Country Ancestry

50 m FS (M) 20.91 César Cielo Brazil European

50 m FS (W) 23.67 Sarah Sjöström Sweden European
100 m FS (M) 46.91 César Cielo Brazil European
100 m FS (W) 51.71 Sarah Sjöström Sweden European
50 m BFly (M) 22.27 Andriy Govorov Ukraine European
50 m BFly (W) 24.43 Sarah Sjöström Sweden European
100 m BFly (M) 49.50 Caeleb Dressel USA European
100 m BFly (W) 55.48 Sarah Sjöström Sweden European
50 m BS (M) 24.00 Kliment Kolesnikov Russia European
50 m BS (W) 26.98 Liu Xiang China Han Chinese
100 m BS (M) 51.85 Ryan Murphy USA European
100 m BS (W) 57.57 Regan Smith USA European
50 m BrS (M) 25.95 Adam Peaty UK European
50 m BrS (W) 29.40 Lilly King USA European
100 m BrS (M) 56.88 Adam Peaty UK European
100 m BrS (W) 1:04.13 Lilly King USA European
*BFly = butterfly, BrS = breaststroke, BS = backstroke, FS = freestyle.

on average 16 percent of genes resulting from their European descendants.

Jamaicans have slightly less European ancestry, about 12.4 percent, but still
a good amount.
Conversely, world records in swimming sprint events are dominated
by persons of European descent. It is important to understand that the
biomechanics of sprinting on land and in the water are not very differ-
ent. Performance is strongly correlated with muscle strength in both land
and water sprinting events. Swimmers tend to be stronger in the arms and
shoulders than runners but equivalent in leg strength. This makes sense,
as it is much harder to propel oneself through water than through air. Thus,
if we were to make a claim about which continental group is fastest, these
data would support the contention that Europeans are faster than Africans.
It takes more athletic strength to be an elite swimmer than a runner, and
the world record-holding persons of African descent also have consider-
able European ancestry. Of course, this is a biased test, because it looks
 121
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

only at an infinitesimally small number, the top fraction of the total popu-
lation, and does not say anything about the average or variation around
the average.
One can also ask why are there so few elite U.S. African American swim-
mers. The answer is simple: racism and classism. The history of slavery and
racial segregation in the United States has made it difficult for African Amer-
icans to gain access to pools, and safe places to swim as well as lessons and
coaches. This pattern remains. In 2014, USA Swimming reported that only
5.3, 2.9, and 1.0 percent of its membership was Asian, Hispanic, and Afri-
can American, respectively. This lack of participation of racial minorities in
competitive swimming also has a bearing on the rate of accidental death by
drowning in the United States.
Because swimming is an important skill to prevent drowning, Joe and
his wife made sure that their children took lessons. Soon after, their eldest
son’s smooth stroke was noticed by his coach, previously with the Cana-
dian Olympic Swim program, and at that time of the Sun West Swim Club
in Glendale, Arizona. Eventually, both of Joe’s children became competitive
swimmers. Joe’s older son excelled at middle distances of 200 to 400 meters,
particularly medley events. Joe’s younger son was a sprinter, excelling at free-
style and the butterfly. Joe’s dream of watching the U.S. flag go up with his
sons on the medal platform at the 2020 Summer Olympics faded when his
older son chose to pursue mathematics and his younger son switched to
concert piano.
African American swimmers, including Cullen Jones, Lia Neal, Simone
Manuel, and Reece Whitley, are beginning to make their mark in com-
petitive swimming. Jones was the first African American to win a gold
medal, in the 4 × 100-meter relay with Michael Phelps, Jason Lezak, and
Garrett Weber-Gale at the 2008 Summer Games in Beijing. He took the
silver medal in the 50-meter freestyle at the London games in 2012. Simone
Manuel tied for the gold medal in the 100-meter freestyle with Penny Olek-
siak (Canada) at the 2016 Summer Olympics, also earning a silver medal in
the 4 × 100-meter freestyle relay (with Abbey Weitzeil, Dana Vollmer, and
Katie Ledecky). At the 2017 World Championships, Manuel anchored the
4 × 100-meter relay (with Kathleen Baker, Kelsi Worrell Dahlia, and Lilly
King), setting a new world record at 3:51.55. She also anchored the mixed
4 × 100-meter freestyle (with Caeleb Dressel, Zach Apple, and Mallory
Comerford), with a world record of 3:19:97 in 2019. The Australians and
Americans were dead even when Manuel entered the pool. She totaled
 122
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

seven medals in that meet (two individual gold, two team gold, and three
individual silver).
Finally, it should be noted that the specific sports at the Olympics and
World Championships have been dominated by only a few countries in given
periods, and these have changed over time. For example, swimming has been
dominated by the United States and Australia for the last fifty years, but
Japan and China are beginning to make inroads. China has earned forty-
three Olympic swimming event medals since 1984. Since the 1990s, China
has also begun to be a force in diving.
Similarly, female gymnastics was once dominated by teams from East-
ern Europe and China, but this trend has been overturned by the United
States, with African American gymnasts like Gabby Douglas and Simone
Biles making major contributions. In addition, U.S. men once topped inter-
national basketball competitions, but now teams from western and eastern
Europe are legitimate competitors, as noted by the number of stars from
those areas who have signed NBA contracts.
A final nail in the coffin of “racial” claims of athletic dominance is the per-
formance of various populations by gender. For example, U.S. men’s soccer
(football) has been disappointing, whereas the American women’s team has
dominated world competition for the last two decades. (The socially defined
race compositions of these teams is similar.) Similarly, U.S. women’s vol-
leyball has maintained consistently higher rankings over the last fifty years
compared with men’s volleyball.
Popular mythology tells us that “white men can’t jump.” This is sup-
ported primarily by observations of NBA and NCAA basketball (but not of
volleyball). Persons of European descent are rarely seen in the slam dunk
competitions. Performances in this event by former NBA players Domi-
nique Wilkins, Spud Webb, Michael Jordan, and Larry Nance (all of pri-
marily African descent) are legendary. However, we cannot conclude from
this anecdotal evidence that persons of European and East Asian descent are
genetically less capable of jumping than those whose ancestry is primarily
African. (Remember that all the individuals listed earlier also have European
ancestry.)
Table 6.2 lists the male and female world record holders in the three track
and field jumping events: high jump, long jump, and triple jump. Perfor-
mances are dominated by persons of European and not African descent.
Once again, we cannot conclude that superior jumping ability is found only
in persons of African descent.
 123
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

TABLE 6.2
Male (M) and Female (W) World Record Holders in Jumping Events

Event Distance (m) Name Country Ancestry

High jump (M) 2.45 Javier Sotomayor Cuba African/European

High jump (W) 2.09 Stefka Kostadinova Bulgaria European
Long jump (M) 8.95 Mike Powell USA African/European
Long jump (W) 7.52 Galina Christyakova USSR European
Triple jump (M) 18.29 Jonathan Edwards UK European
Triple jump (W) 15.50 Inessa Kravets UKR European

WHY ARE THERE SO MANY AFRICAN AMERICAN BASKETBALL

PLAYERS AND LATIN AMERICAN BASEBALL PLAYERS?

Basketball was invented by Canadian-born James Naismith in 1891. Due to

the racially segregated character of American society, almost all of the early
basketball clubs were organized around ethnic groups. This included teams
such as the Smart Set (African Americans from New York City), the Buf-
falo Germans (German Americans, Buffalo, NY), the Original Celtics (Irish
Americans from the Hell’s Kitchen area of New York City), and the South
Philadelphia Hebrew Association (Jewish Americans from Philadelphia). In
the 1930s, there was also a highly successful barnstorming team composed
of Chinese Americans.
Powerful evidence against the genetic racial theory of basketball includes
the fact that as the social and cultural conditions of American society
changed, so did the ethnic composition of top basketball players. Basketball
took root in the inner cities of America and in the farm fields of the Midwest
during the 1950s. Unlike tennis, golf, and swimming, basketball required lit-
tle specialized equipment and space. In the 1980s, the sport began to spread
from the Midwest to inner cities around the world. As an international nutri-
tion postdoctoral student, Alan was surprised to find basketball courts in the
remote village of the Solis Valley, Mexico.
Further evidence against the genetic racial theory of basketball is that the
biomechanics required to become a great basketball player are very simi-
lar to those required to be a great volleyball player. Support for this claim
comes from the fact that these athletes routinely sustain similar types of
injuries resulting from movement during these sports. Joe grew up playing
 124
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

basketball in the tough working-class, racially segregated urban/suburban

environments of north central New Jersey. He played in community center
club leagues and faced many athletes who went on to NCAA Division 1 and
professional basketball careers.
During his years as a graduate student and assistant professor, Joe con-
tinued to play in pick-up games against Division 1 and professional bas-
ketball players, including NBA players B. J. Armstrong (Chicago Bulls),
Scott Brooks (Minnesota Timberwolves and current Washington Wiz-
ards coach), and Richard Jefferson (New Jersey Nets). His team even won
some games.
However, in college, he did not play basketball but learned to play vol-
leyball, first as an undergraduate at Oberlin College and then as a graduate
student at the University of Michigan in the Midwest Intercollegiate Volley-
ball Association (MIVA). At that time, the vast majority of MIVA teams were
clubs and therefore did not play on the same schedule as the school’s varsity
male sports. So, Joe got to play against Division I schools (including Miami
University of Ohio, the University of Toledo, Michigan State, Purdue, North-
western, and Notre Dame) and nationally ranked teams such as Ohio State
and Penn State. The point of this personal note is that Joe has direct experi-
ence to claim that basketball and volleyball skills are virtually identical and
that the latter were harder to acquire than the former. Yet, if one looks at the
demographics of these sports, men’s basketball is disproportionately African
American, and men’s volleyball is disproportionately European American.
On the other hand, it is telling that women’s basketball and volleyball are
more equally balanced by race and ethnicity. Finally, at the international
level, volleyball dominance shows no association with socially defined race.
Again, this demonstrates that performance in elite sports cannot simply be
reduced to the athletes’ racial origin.

Baseball

Joe’s autobiography could well be called “The Thick Gray Line.” That line
refers to the gray bricks that made up part of the rear wall of McKinley
Elementary school in Westfield, New Jersey. Almost every day of the sum-
mer, the kids of its ethnically mixed student body—Irish American, Italian
American, and African American—played slow-pitch baseball with a tennis
ball on the field behind the school. A fly ball that landed over the thick gray
line was a home run.
 125
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

The fifth and sixth graders hit home runs on that field at about the same
frequency of major leaguers in professional baseball, and yes, they kept stats!
However, even in slow-pitch, as a third-grader, Joe struggled to get on base.
The pitchers threw great stuff, particularly curves and sinkers that would
cause Joe to regularly ground or fly out.
Joe and friends also played fast-pitch stickball on the other side of the
school. They played with sponge balls, baseballs shaped with seams, and
regular baseball bats. This was not stickball in the classic sense of using a
broomstick. They played with teams of three kids per side: a pitcher and
two fielders. You could strike out, ground out, or fly out. A strike zone was
marked on the wall in chalk. Hits were calculated by distance (singles, dou-
bles, triples, and homers). Joe struggled in this game as well, but his younger
brother, Warren, was outstanding. He went on to play varsity baseball at
Westfield High School and then switched to its tennis team.
Many American kids of Joe’s generation could describe a similar expe-
rience. Baseball has been called the “American game.” It had been played
since at least 1857. The National League (originally known as the National
League of Professional Baseball Clubs) was founded in 1876. The American
League was founded in 1901. Baseball spread to the Caribbean during the
Spanish-American War in 1898. World War II spread baseball to Japan and
the Pacific.
American baseball was never officially racially segregated. However, in
1887, one minor baseball league voted against offering contracts to Negro
players, sending an important signal that Negroes were not welcome in
major league baseball. Latinos (here defined as persons from North or Cen-
tral America, the Spanish-speaking Caribbean, or Mexican Americans with
a shared cultural heritage of colonization by Spain and use of the Span-
ish language) also began to appear in baseball in the 1880s. These athletes
walked a precarious line of being acceptable to “whites” while participating
in the Negro leagues.
Baseball’s official color line fell in 1947, when Jackie Robinson signed with
the Brooklyn Dodgers. The Boston Red Sox considered signing Robinson,
but Jackie had a disastrous tryout with that team due to its racial attitudes.
Indeed, one prominent Boston sportswriter suggested that the real “curse” of
the Red Sox was not from trading Babe Ruth to the Yankees but the inability
of the franchise to deal with its own and the broader city’s racism.
By 1968, major league baseball was composed of 15 percent African Ameri-
cans and 7 percent Afro-Latinos. Like many major league sports, it suffered
 126
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

from “stacking,” the assignment of players to fielding positions by socially

defined race. African Americans outperformed European Americans by objec-
tive statistics by position, but they were overrepresented as outfielders and at
first base and underrepresented as pitcher and catcher. The latter positions,
like the quarterback in football, are thought to need greater cognitive capacity.
The percentage of African Americans in the major leagues declined
steadily from this period. In 2018, only 8.2 percent of major league rosters
were made up of African Americans. Conversely, the percentage of Latinos
has grown steadily. By 2018, 28.2 percent of major league players were Latino,
and these players are overrepresented at second base and as shortstops. Yet,
they are also less likely to be drafted than European Americans.
Once again, we are left with the question of whether representation in
baseball or the stacking of positions results from genetically determined
differences in socially defined races. We have established why this is highly
unlikely. The genetic composition of people who are described as “Latino”
is another example of strong evidence against this claim. Due to the history
of colonialism and slavery in Latin America, the genetic ancestry of indi-
viduals varies considerably and included Amerindian, African, and Euro-
pean elements. For example, Colombians have on average 64, 29, and 7
percent European, Amerindian, and African ancestry, respectively. Puerto
Ricans have 72, 16, and 12 percent European, Amerindian, and African
ancestry, respectively. Cubans range from being virtually all European with
some Amerindian ancestry to virtually all African with some Amerindian
ancestry. Baseball players from all of the places and ancestry combina-
tions have excelled at the sport. Once again, this exposes a supposed racial
theory of baseball performance as patently ridiculous. The arenas of base-
ball and basketball show the social influence on sports participation and
excellence.

ARE EUROPEANS STRONGER THAN AFRICANS AND ASIANS?

As with previous questions, people who ask are usually thinking about the
performance of elite athletes in sports associated with strength, such as
offensive linemen in American football or wrestling and weightlifting com-
petitors. If we examine the Olympic world records in weightlifting, a strik-
ing pattern emerges for male and female athletes. Records are kept for three
categories: snatch, clean and jerk, and total weight. Persons of East Asian
 127
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

TABLE 6.3ġ
Male (M) and Female (W) World Record Holders for Weightlifting (Total Weight) in 2019

Name Ratio* Country Ancestry

Li Fabin (M) 5.21 China East Asian
Shi Zhiyong (M) 4.97 China East Asian
Lü Xiaojun (M) 4.67 China East Asian
Jiang Huihua (W) 4.33 China East Asian
Kuo Hsing-Chun (W) 4.17 Chinese Taipei East Asian
Liao Qiuyun (W) 4.13 China East Asian
NoteĻġAll females listed with a world record were from China or North Korea. For males, notable performance by
persons not from China or North Korea were Lasha Talkhadze, Georgia (4.40 ratio, Eurasian), and Sohrab Moradi
(1.80 ratio, Eurasian).
*Represents the ratio of the weight category to the athlete’s body weight.
SourceĻġWikipedia, “List of World Records in Weightlifting,” accessed April 29, 2021, https://en.wikipedia.org/wiki
/List_of_world_records_in_Olympic_weightlifting.

descent—specifically from China and North Korea—dominate this sport,

along with a few Middle Easterners, North Africans, and Europeans. When
we calculate the strength of individuals by the relationship of the total weight
category to their body weight, we find that persons of Chinese descent win
hands down (see table 6.3). There are no sub-Saharan Africans holding any
of the world records. So, to answer this question, East Asians’ elite perfor-
mance in strength fares better than Europeans’, with no evidence of world-
record-level achievements by sub-Saharan Africans (or any other tropically
derived population) in these events.
But, once again, we cannot ascribe the differences in performance in
weightlifting to biological race. Not all East Asian nations claim records in
weightlifting: there are no record holders from Vietnam, Laos, or Cambodia.
The biomechanical requirements for elite-level weightlifting are associated
with a shorter limb-to-height ratio. This provides a mechanical advantage to
lifting heavy loads. Thus, populations that evolved in climates that produced
body proportions with shorter limb-to-height ratios would have an advan-
tage in this sport. We know that human (and other large-bodied mammal)
body proportions were influenced by adaptation to climate. Bergmann’s rule
states that for homeotherms (mammals, birds), body mass is inversely related
to ambient temperature (as temperature goes down, body mass goes up).
 128
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

In addition, Allen’s rule states that species or populations that have adapted
to warmer climates tend to have longer body extremities (feet and arms)
compared with those who adapted to colder climates. Thus, the combi-
nation of these rules strongly suggests that individuals with ancestry from
warmer, tropical climates will not have body proportions that are conducive
to elite weightlifting.
This is similar to what we learned about the advantage of persons
adapted to high altitudes for excelling in sports that require endurance.
Thus, the absence of athletes from populations of tropical ancestry from
the highest levels of weightlifting competition is unsurprising. It should
also be noted that other temperate-zone populations that are closely
related to Chinese and North Koreans, such as Japanese and South Kore-
ans, did not produce any world record holders in Olympic weightlifting
either. This again indicates that there is a social and cultural aspect to
achievement in this sport.
It is well established that physical strength is a heritable trait. One recent
study attempted to use GWAS to identify genetic variants associated with
the greater strength of elite Russian weightlifters. The researchers found
three SNPs that were statistically significant: rs120554409, G allele near the
MLN gene that encodes promotilin, associated with contraction of smooth
muscle; rs4626333, G allele near the ZNF608 gene, which encodes a zinc fin-
ger transcription factor protein; and rs2273555, A allele in the GBF1 gene,
which encodes the Golgi-specific brefeldin A-resistance guanine nucleotide
exchange factor 1 protein. They found in a follow-up study of sub-elite Polish
weightlifters that GG homozygotes at rs4626333 SNP showed better compe-
tition results and greater cross-sectional type II muscle fiber area than the
other genotypes. The FST values for these SNPs worldwide are 0.103, 0.198,
and 0.116, respectively, meaning that if variation alone in these genes were
responsible for elite strength performance, then virtually every population
would have lots of people who are capable of performing at elite levels of
strength athleticism.
In summary, elite-level performance in strength-related athleticism is
related to body proportions and muscle mass composition. Temperate-zone
populations are more likely to have the combination of body mass and limb
proportions for elite performance compared with those from tropical zones.
The outcome of world competition in strength-related events is also influ-
enced by social and cultural factors. Climate and culture are important. Race
is not.
 129
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

ARE ASIANS MORE FLEXIBLE THAN AFRICANS AND

EUROPEANS?

This is a particularly hard question to answer, because there doesn’t seem to

be a generally accepted definition in the sport or medical literature for the
physical trait known as flexibility. There seems to be some agreement that
genetic variants might have something to do with the mechanical properties
of musculoskeletal soft tissue that are associated with the range of motion
of particular joints. Alan’s wife and daughter are hypermobile because of a
genetic condition called Ehlers Danlos syndrome, which affects collagen. But
that is a rare condition. The question of the greater flexibility of East Asians is
often associated with claims of their superiority in sports such as gymnastics
and diving, which require high degrees of contortion.
Once again, if we turn to the records of elite performance in the sports of
gymnastics and diving, we find no data to support the conclusion of greater
East Asian flexibility, as least as related to performance in gymnastics. Tables
6.4a and 6.4b present data for total medals in Olympic individual all-around
competition. There’s no evidence of dominance by East Asians in gymnas-
tics. Indeed, Europeans of both sexes dominate these events. Japan’s suc-
cess in male gymnastics (thirteen medals) is countered by the failure of its
women (no medals) and China’s performance (only three bronze medals).
The recent emergence of African American women Gabby Douglas, the 2012
Olympic all-around gold medalist, and Simone Biles, the 2016 gold medalist
in vault, floor, and all-around as two of the finest female athletes in the his-
tory of this sport severely erodes this stereotype.

TABLE 6.4Aġ
Total 2019 Olympic Medals for Women in the Gymnastics Individual All-Around Event

Country Medals Ancestry

USSR/Russia 20 European
Romania 8 European
Czechoslovakia 2 European
Germany 2 European
Hungary 2 European
USA 8 European (6), African American (2)
China 3 East Asian
Note: It is notable that the three medals won by China were all bronzeį
 130
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

TABLE 6.4B
Total 2019 Olympic Medals for Men in the Gymnastics Individual All-Around Event

Country Medals Ancestry

USSR/Russia 19 European
Japan 13 East Asian
France 6 European
Switzerland 6 European
Italy 5 European
Germany 4 European
Finland 3 European
USA 2 European
Note: A number of countries earned only one medal, including China, South Korea, Hungary, Yugoslavia, and
Austria.

Diving

The data for Olympic medals in diving (10-meter platform, synchronized

10-meter platform, 3-meter springboard, and synchronized 3-meter spring-
board) mirror those found for gymnastics (tables 6.5a and 6.5b). Europeans
have long dominated the sport in total medal counts. Chinese divers have
recently started to earn medals, particularly in synchronized diving, but other
East Asian nations—notably Japan and South Korea—have not done well.
In summary, all that we know about the continuous nature of human
genetic variation and how it affects physical traits does not support the idea
that there are genetically racial differences in flexibility. East Asians show
no dominance in gymnastics. In addition, both diving and gymnastics are
associated with specific cultural and social norms throughout the world.

TABLE 6.5A
Total Medals for Women in 2019 Olympic Diving Events (Top Five)

Country Medals Ancestry

ŖŔł ĵĵ ņŶųŰűŦŢů
ńũŪůŢ ĴĶ ņŢŴŵġłŴŪŢů
œŶŴŴŪŢİŖŔŔœ IJĶ ņŶųŰűŦŢů
ňŦųŮŢůź IJĶ ņŶųŰűŦŢů
ŔŸŦťŦů ġġĹ ņŶųŰűŦŢů
Note: Notable countries not making the top five were Canada (7), Australia (6), Malaysia (2), and Mexico (3).
 131
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

TABLE 6.5B
Total Medals for Men in 2019 Olympic Diving Events (Top Five)

Country Medals Ancestry

USA 73 European
China 34 East Asian
Russia/USSR 17 European
Germany 17 European
Mexico 11 European, Amerindian, African
Note: Notable countries not making the top five were Italy (9), Sweden (6), and Australia (5).

In the United States, African Americans have been excluded from both
sports until recently. The emergence of a new generation of African Ameri-
cans in gymnastics (but not yet in diving) at the elite level is evidence against
racial theories.

DO AFRICANS HAVE THICKER BONES, EXTRA MUSCLES,

OR EXTRA TENDONS?

No.
All human populations are anatomically the same with regard to the
number of muscles and tendons. Bone density varies by population but not
socially defined race. It is a complex trait, influenced by genetics, epigenetics,
endocrine function, and environmental factors (especially nutrition and
disease). A variety of hormones positively influence bone density including
insulin, growth hormone, insulin-like growth factor I, estrogen, testosterone,
vitamin D3, and calcitonin. Parathyroid hormone, cortisol, and thyroid hor-
mones will negatively impact bone growth.
Much of what we know about variation in bone density has been driven
by studies of bone-associated diseases, such as osteoporosis or risk of frac-
ture injuries. These studies were organized within the socially defined race
paradigm that is still utilized in medicine. For example, a 1995 study of bone
mineral density (BMD) in Black and white men took measurements in the
lumbar spine, femoral neck, and radial shaft. The study, which used only 34
Black and 160 white men, controlled for education level, smoking, exercise,
and fractures. The researchers found no significant Black/white differences
in mean weight, height, or body mass index (BMI). They also found that
 132
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

the Black men had higher BMDs than the white men at every site: 5 percent
greater for the radius, 10 percent greater for the lumbar spine, and 20 per-
cent greater for the femoral neck. The study concluded that Black men had
higher BMD than white men and that this was not due to greater body size.
The investigators also concluded that the lower hip fracture risk reported
for Black than for white men was not due to a difference in hip axis length;
rather, it was the result of greater BMD in the former group.
Studies such as this contributed to the false belief that Blacks have always
had greater bone density than whites. A more recent study demonstrated
that this was incorrect. The motivation for the study was the fact that ref-
erence populations from the United States are often used around the world
for representative measures of BMD by sex, age, and race. Mukwasi and col-
leagues examined BMD in adult Black Zimbabwean women and compared
it with that of Black and white U.S. women. They examined 289 participants
age 20–69 years, controlling for BMI. In the 20–59-year age range, compared
with U.S. white women, mean BMD for Black Zimbabwean women was 4.5
to 7.4 percent lower for the lumbar spine but 2.0 to 4.8 percent higher for
the total hip and 0.2 to 10.2 percent higher for the femur neck. The authors
also compared the Zimbabwean with U.S. Black women of ages 20–59 and
found that the mean BMD for the former was 9.1 to 11.5 percent lower for the
lumbar spine and 1.4 to 8.1 percent lower for the total hip. Black Zimbabwean
women also had lower mean weight and BMI compared with U.S. women.
Thus, from these results we learn that there is no simple way to generalize or
predict the bone density of human populations.
In addition, given the complexity of the determinants of bone density,
the genomic foundation of this trait has been shown to be just as complex.
Recent GWAS identified more than one hundred genetic loci associated with
bone density. In addition, given that bone density is profoundly influenced
by the conditions under which an individual develops, epigenetic influences
have been demonstrated. Thus, given the enormity of genetic variation on
the continent of Africa, along with the tremendous variation in environmen-
tal circumstances that influence bone development, there is no simple way to
claim or predict a specific bone density for any African population.

CONCLUSIONS

Since the 1940s, people have seemed to adhere to the stereotype of the “dumb
jock.” Athletic ability and intelligence seem to be polar opposites among
 133
AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

individuals. We didn’t fit that stereotype. Alan was a halfback, and Joe was
a wide receiver in junior high school. Alan’s high school team was unde-
feated and co-state champions. In college, Joe went on to excel in a variety
of sports: basketball, rugby, softball, and volleyball. He was also his college’s
chess champion and still is a highly rated United States Chess Federation
player. Alan was a member of his college’s intramural football team, which
won three consecutive championships. Having never played lacrosse until
college, he made the varsity lacrosse team (ranked eleventh in the nation).
Alan is five foot five and was likely the shortest and lightest-weight person
on all of these teams.
As harmful as the stereotype of the dumb jock is, it is made worse when
racialized.
 Chapter Seven

INTELLIGENCE, BRAINS, AND BEHAVIORS

In this chapter, we dive into what is possibly the most destructive myth of
race: that there are innate differences in intelligence among racialized groups.
This is often considered the flip-side of believing that races differ in ath-
letic ability. We examine what is meant by intelligence, how it is measured,
and what we actually know about the genomics of intelligence and cogni-
tive abilities. We also address related questions about behaviors and traits
including personality, mental health, violence, and criminality. The bottom
line is this: there is absolutely no evidence that differences in any of these
traits or behaviors have to do with genetic differences among social races.
Any thoughts that there are racial differences in intelligence due to genetics
are hurtful and false.

WHAT IS INTELLIGENCE?

Not surprisingly, there is no general agreement on how to define the complex

trait that we often reduce to one word: intelligence. Is intelligence a thing
that you have or don’t have, or have in varying degrees? Or are there multiple
types of intelligence that might or might not be related to each other?
Three definitions of and frameworks for thinking about intelligence are
commonly used. The first is Cattell-Horn-Carrol (CHC) theory. This holds
that there are three strata of intelligence, which are hierarchically linked:
narrow abilities (I), broad abilities (II), and general ability (III). Stratum III
 135
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

is referred to as general intelligence or g. The second stratum, fluid ability,

allows one to cope with novelty and to think rapidly and flexibly. Finally,
crystallized or narrow ability refers to the general store of knowledge.
The second commonly used concept is multiple intelligence theory. This
holds that intelligence resides in eight or so different components, includ-
ing linguistic, mathematical, spatial, musical, bodily/kinesthetic, naturalist,
interpersonal, and intrapersonal.
The third commonly used definition is triarchic theory, which holds that
intelligence consists of three components: creative, analytical, and practical.
There are variations on all of these themes. The key point is that even
though we often think of intelligence as a single attribute, everyone knows
someone who is gifted at some tasks (say, being good at directions, memoriz-
ing lines, or hitting a golf ball) and at the same time very bad at others. All
themes highlight various forms of intelligence.

DO RACES DIFFER IN THEIR COGNITIVE ABILITIES AND

INTELLIGENCE?

As stated in our responses to previous questions in this book, humans do

not have biological races, and therefore there can be no genetically based
racial differences in intelligence. However, some have reframed the question,
avoiding the racial claim and changing the focus to genetically defined popu-
lations. Again, we answer “no” to that reformulation. Intelligence, however
defined and measured, is the wondrous result of a complex mix of multiple
genes, chance events during development, and environments.
Most claims of racial differences in intelligence refer to the CHC defini-
tion; specifically, generalized intelligence or g. Intelligence testing has a long
history in the United States, beginning with conversion of the intelligence
quotient (IQ) score into a tool for eugenics. In 1917, Henry Goddard pub-
lished a paper titled “Mental Tests and the Immigrant.” He administered IQ
tests to steerage passengers at Ellis Island and determined that those enter-
ing could be classified as “normal,” “borderline,” “feeble-minded,” “moron,”
or “imbecile.” He found that these categories differed by nationality, with
just 10, 0, 7, and 0 percent of Jews, Hungarians, Italians, and Russians clas-
sified as “normal,” respectively. Conversely, over 83, 80, 79, and 87 percent
of immigrants from those countries were thought to fall into the categories
of “feeble-minded” or worse. Seven years later, eugenicist Lothrop Stod-
dard reported to the U.S. Congress that more than 46 percent of American
 136
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

Negroes from the North and 75 percent of those from the South displayed
inferior intelligence.
Discussion of the intellectual inferiority of European immigrants shifted
through the early portion of the twentieth century, particularly as these
groups became “white.” However, the IQ test scores for African Americans
improved more slowly. As early as 1932, IQ testing had shown a fifteen-
point (about 1 standard deviation) difference between whites and Blacks in
the United States. In the 1990s, Richard Herrnstein and Charles R. Mur-
ray argued in The Bell Curve (1994) that this IQ test gap had been stable
throughout the twentieth century, also observing that East Asians scored
about three points higher on average than Europeans and that Latinos fell
between Europeans and Africans. Throughout this narrative of IQ test dif-
ference was a constant claim that the IQ test score was a singular, unbiased
measure of intelligence (g) and that the racial IQ test gaps were driven pri-
marily by genetic differences influencing cognitive performance. However,
the history of IQ testing is far from unbiased, and we have already discussed
the numerous fallacies of believing that there are genetically based racial
groups in our species (chapter 3).

IS THERE A GENETIC BASIS FOR INTELLIGENCE?

Yes, but. . . . it is wrong to say that intelligence is caused by genes. How

genetics is supposedly causally linked to degrees and types of intelligence is
complex and varies for each person. And, of course, this has nothing to do
with socially defined race.
Intelligence, however defined or measured, is related to brain function. Spe-
cifically, it is related to the function of the prefrontal cortex, neocortex, and
superior parietal, temporal, and occipital cortexes. In addition, the subcortical
regions of the brain, such as the striatum, and the integration of the parietal
and frontal lobes are especially important. The complexity of gene involve-
ment is indicated by the fact that more than 82 percent of the estimated total of
23,000 human genes are expressed in the brain, nearly double the 46 percent of
genes that are expressed in other tissue types. However, even this is an under-
estimate of genetic contributions to cognitive function, as a wide variety of
physiological systems outside of the brain also contribute to what we call intel-
ligence. In addition to genetic influence on cognitive function, a large number
of environmental factors influence brain function, such as nutritional state,
exposure to neurotoxins such as lead, and infectious disease.
 137
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

The heritability of intelligence has been consistently shown to be between

0.50 and 0.80; in other words, greater than 50 percent of intelligence is gen-
erally attributable to heredity. Estimates of heritability also differ for com-
ponents: verbal aptitude (0.70) seems to be higher than spelling (0.50) and
mathematical aptitude (0.30).
However, these heritability estimates should be taken with a large lump
of salt. Heritability, or h2, is typically measured in humans by comparing
similarities between monozygotic and dizygotic twins. As noted earlier,
monozygotic twins share all genomes, whereas dizygotic twins share half of
their genomes. Studies of twins tend to overestimate the genetic contribu-
tion attributable to the unintended correlation of twin environments. First,
identical twins share the same physical attributes, so any aspects of the envi-
ronment associated with how one is treated due to physical appearance are
shared. Also, of specific importance for identical twins socially defined as
white in America, there are rigorous requirements concerning the attributes
of potential adoptive parents. Thus, such twins tend to be adopted into fami-
lies with shared socioeconomic characteristics. So, we can say with confi-
dence that there definitely is a genetic component to cognitive performance,
but cognitive performance as a complex trait is also strongly influenced by
environmental conditions. Finally, it is really important to understand that
stating that intelligence is heritable is not the same as saying that the genetic
basis of the trait must differ among socially defined races, as many people
who should know better do, including Murray.
At present, GWAS of intelligence (measured by various IQ tests) predicts
only 1–4 percent of the variation in the trait. Such genome-wide association
studies also have failed to discover many genomic variants that are consis-
tently associated with the trait even within populations of the same ancestry.
For example, a study examining 549,692 SNPs from 3,511 unrelated adults
in the Lothian Birth Cohorts (1921, 1936), Aberdeen Birth Cohort (1936),
and the Manchester and Newcastle Longitudinal Studies of Cognitive Aging
Cohorts showed that none of the individual SNPs they discovered showed
a replicable genome-wide association. One gene with a suggestive associa-
tion with fluid intelligence was statistically significant in a binding protein
(FNBP1L). However, this result was not replicated in the Norwegian Cogni-
tive Neurogenetics sample.
A 2015 GWAS examined exonic (genes that are expressed) variation
associated with extremely high intelligence (HiIQ). HiIQ individuals were
selected from the Duke University Talent Identification Program (TIP). This
 138
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

study used the top 1 percent of this group who had very high IQ scores. A
control group was generated from the Minnesota Twin Family Study: 3,253
individuals identified as white with IQ scores distributed between 70 and
150. This resulted in just a single nonsynonymous SNP in the PLXNB2 locus,
whose gene product has been associated with neuronal migration, explain-
ing only 0.16 percent of the variance in IQ between the controls and the
high-IQ group.
Attempts to improve the power of GWAS to discover genomic variants
associated with cognitive function have utilized proxies for the intelligence
(g), such as educational attainment, or highest-level math course taken. There
are obvious problems with these traits as proxies for cognitive function, as
they clearly are influenced by differing opportunities and circumstances.
However, even if we accept these limits, these new indicators perform only
slightly better than IQ tests. For example, a study of a European population
demonstrated that 74 genetic markers (SNPs) contributed to individual dif-
ferences in educational attainment and explained about 20 percent of the
variance in education levels. However, even with a 20 percent genetic con-
tribution to educational attainment, if the effects are additive (and equal), we
would expect that each SNP contributed only 0.27 percent to the variance
in the trait.
In another large GWAS of Icelandic people, it was shown that 35 of 120
significant SNPs had a strong association with age of first child for women.
The SNP rs192818565 had the highest association with lower educational
attainment but was highly associated in women with having more children
and having them at an earlier age. This suggests that what is at play here is
not intelligence; rather, it is that female educational attainment is often nega-
tively associated with having more children.
One of the largest studies to date showed that 1,271 SNPs accounted for 11
percent of the variance in educational attainment (EA) in a sample of 1.1 mil-
lion individuals of European descent. These results suggest that the roughly
1,200 SNPs explain as much variation in EA as family socioeconomic status
(SES). They showed that 225 SNPs were significantly associated with cogni-
tive test performance, 618 with self-reported math ability, and 365 with hard-
est math class taken. Again, if we accept these results as true, they really say
only that genes and environmental factors are equally important in deter-
mining someone’s educational attainment. This is not a shocking conclusion.
Finally, one of the few genome-wide association studies that examined
a cognitive trait in populations of different ancestry examined cognitive
 139
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

flexibility in a sample of more than 3,000 African Americans and 2,500

European Americans. The variants found to be associated with this trait
in African Americans were not significant in European Americans (and no
significant SNPs were found for this group.) Nongenetic factors in this study
were actually more significant than the SNPs. Older age and recent tobacco
use were shown to make performance worse (for both groups); and years
of education made performance better for both groups. Frankly, given the
small size of the cohorts examined, it is amazing that this study found any
significant genetic variants. Of course, the results were not replicated in these
socially defined groups or in any other population. Therefore, after this long
trip through many studies, we cannot make much of the results. Effects of
single genes are small and typically fail to repeat across studies. Given what
we know about genes and brains, that’s actually not surprising.
Taken as a whole, these GWAS results on cognitive function support that
idea that although genes are associated with individual IQ, the relation is
extremely complex. Furthermore, the relationship between intelligence and
genetics is likely to vary by population (due to different patterns of linkage
disequilibrium). And even though there is a real but variable genetic contri-
bution, the environmental contribution is just as real and equally, if not far
more, important. Finally, whatever we now know about the intelligence and
genetics is independent of and unrelated to social race. More on this in the
next question.

DO GENES ASSOCIATED WITH INTELLIGENCE

DIFFER AMONG RACES?

No.
A mainstay of psychometrics is the assertion that intelligence differs
among biological races. Past reasoning was that because human groups dif-
fered in some physical traits, or at least were thought to differ, they must
also differ in their intellectual capacity. When it became clear that the physi-
cal traits used to ascribe difference (such as skull angle and volume) did not
differ in a way consistent with notions of racial classification, new tools to
measure intelligence were invented. However, once studies of genetic mark-
ers in humans demonstrated the fallacy of grouping human beings into bio-
logical races, many psychometricians continued to ignore the genetic data,
suggesting genetic differences accounting for intelligence among Blacks,
whites, and Asians.
 140
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

Recently, Harvard geneticist David Reich alluded to the possibility that

genetic variants exist that are differentiated by population and that might
account for differences in intelligence. In making this claim, he directly dis-
missed Joe’s analysis suggesting that the measured IQ differences in human
populations cannot result from genetic differences among them. His dis-
missal was rooted in the idea that natural selection can act on complex traits
(such as intelligence).
On this point we agree. Yes, natural selection can act effectively on com-
plex traits; indeed, Joe spent his early career demonstrating it with regard to
life history traits in fruit flies. What we question is whether this ever hap-
pened in the human species for the quantitative trait we call intelligence.
There are two ways that natural selection could have accounted for altering
the genomic foundation of cognitive performance in humans: there could
have been direct selection for improved performance, or improvement could
have resulted from selection on some other trait (correlated selection).
It is generally agreed that the greater intelligence of humans compared
with other animals is the key adaptation of our species. Our evolution-
ary lineage was characterized by increased brain size and complexity. Our
skulls changed in ways that decreased the size of the face, specifically bones
and muscles that allow for powerful chewing, and allowed more space for
larger brains. Furthermore, it is argued that the primary driving force of
all primate intelligence (including our own) is social interactivity. Thus,
most of the evolution of our intelligence capacity occurred long before any-
one left Africa. This raises the question about whether direct selection for
greater intelligence occurred after some humans left Africa, particularly for
life in Eurasia.
Two theories have been used to claim greater natural selection for intel-
ligence in Eurasia: the so-called winter hypothesis and r versus K selection.
According to the winter selection hypothesis, which dates to the turn of the
twentieth century, the unique problems of winter (such as shelter, food stor-
age, and lack of food) required greater cognitive sophistication to solve than
life in the “easygoing” tropics, resulting in natural selection for greater cogni-
tive capacity in Eurasians. The problem with this theory is that sub-Saharan
Africans did not stay put in one place while Eurasians roamed the world
solving new problems. Africa has eight climatic zones (equatorial, humid
tropical, tropical, Sahelian, desert, and Mediterranean). The distribution of
these zones differed in the Pleistocene period, but migration and survival in
any of the zones required solving new problems as well.
 141
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

The r/K selection theory, a variant of the winter selection hypothesis,

was championed by Canadian psychologist J. Phillipe Rushton (1943–2012).
It posited that humans could be arrayed along a spectrum of reproductive
investment, which in turn was in opposition to somatic investment. Africans
were r-selected (high reproduction, low investment in brain mass, lower
altruism, lower social organization), and Eurasians were K-selected (lower
reproduction, higher investment in brain mass, higher altruism, higher
social organization). Rushton utilized this model to explain why Blacks were
not found in high-IQ professions as well as various social pathologies that
he claimed existed in Black societies worldwide. The problem with Rushton’s
theory was that he applied it backwards. The theory actually predicted that
species in the temperate zones should be r-selected and those in the trop-
ics should be K-selected. Moreover, it is a misapplication of an ecological
idea applied across species to variation within a species. Finally, that eco-
logical idea has been challenged, because it does not work in a wide array
of situations.
Therefore, no one has presented a credible model for why some people
should have evolved greater cognitive performance than others. Without a
direct theory of selection, one is left to explain that evolution of greater intel-
ligence in Eurasians resulted from an accident of evolutionary history. This
approach does not work either. Methods have been developed to assess the
signature of natural selection on complex traits. Classic quantitative genet-
ics tells us that selective sweeps reduce the heterozygosity of nearby neutral
polymorphisms and provides a strong genetic signature of selection. How-
ever, in organisms like us, there is increasing evidence that “soft” selective
sweeps, particularly adaptation resulting from changes in allele frequen-
cies of existing genetic variation, could be the major mechanism of adap-
tive events. It is particularly hard to detect these signals in humans due to
incomplete knowledge of our genetic architecture and weak selection signals
of individual loci.
To overcome these difficulties, investigators in one study utilized a combi-
nation of FST and branch analysis on thirty-eight complex traits to determine
if there was evidence of directional selection in humans. Branch analysis
refers to examination of the lengths and patterns of branches in phyloge-
netic trees of the genes that are undergoing positive natural selection among
the populations being studied. The traits fell into six categories: quantitative
physical traits, quantitative physiological traits, inflammatory or autoim-
mune disorders, mental disorders, cancers, and miscellaneous traits related
 142
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

to menstruation. This study concluded that (a) natural selection on standing

variants associated with complex traits is common in humans; (b) signatures
of selection for any particular trait that is enriched in different human lin-
eages indicating recent adaptation are most likely associated with temporary
and geographically specific environmental challenges (e.g., malaria adapta-
tion); and (c) there is a strong correlation between the strength of selection
and how much the trait has changed (such as height and some physiologi-
cal traits). The study also found that for traits without correlation between
the estimated strength of selection and how much the trait changed (thirty-
four of the thirty-eight traits they studied), selection on the trait was acting
through selection on a correlated trait.
The second and third conclusions have particular relevance in consider-
ing whether consistent directional selection for any complex trait is possible.
These data indicated that the genetic response to natural selection (change
in allele frequencies) could be highly driven by chance, meaning that we
should not expect any consistent or predictable changes for allele frequen-
cies over the course of human evolution. This is also due to the fact that the
evolutionary forces impacting any specific trait are heterogeneous (multiple
mechanisms operating at the same time). These conclusions are entirely con-
sistent with our assertion that it is highly unlikely that directional selection
for greater or lesser intelligence, no matter how defined, drove observed dif-
ferences in this trait among supposed human races.
Therefore, if no genes have been identified to date that differentiate human
populations (or socially defined races) for cognitive function, why are there
observed differences in IQ? The answer to this question is the same as the one
we provided for health disparity. Cognitive performance is a complex trait
with a strong environmental component. The environments of America’s
socially defined races have never been equalized. This has particular signifi-
cance (as we have explained in a number of scholarly works) for estimating
the genetic effects on any complex trait. Any estimate of a genetic effect
on a physical trait will be incorrect if the groups being compared are not
reared in the same environment. This is an elementary principle of quantita-
tive genetics, one that psychometricians have never bothered to heed when
making claims about the genetic basis of intelligence differentials in socially
defined races.
In summary, the persistent belief that there are racial differences in intel-
ligence are based on a series of fallacies and unsupported assumptions,
including these:
 143
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

(a) races are genetically real,

(b) IQ (g) measures intelligence (assuming that we truly understand the meaning of
this term), and
(c) IQ (g) differences among socially defined races are measured in an unbiased and
consistent way.

All of these assumptions are highly problematic and unsupported. Instead,

it is clear that cognitive ability, like most traits that result from contribu-
tions from genes, environments, and chance, varies among the individual
members in any group. However, intelligence is a requirement of all cultures.
Cultures are all complex, and success within them often requires the effective
use of one’s intellectual ability.

DOES MUSICAL ABILITY DIFFER BY RACE?

Musical ability is considered one of the components in the multiple theory of

intelligence. Similar to other complex traits, musical ability is hard to define.
However, some biologic traits are associated with musical ability that display
genomic variation within our species. What we know so far coincides with
other complex traits: variation within populations exists, but we have no
evidence that there is significant variation for these traits among populations
or socially defined races.
Evidence for genetic contributions to musical ability can be found in
unusual conditions, such as tone-deafness, the inability to detect notes that
are out of key; and the opposite condition, absolute pitch (AP), the ability to
identify and reproduce a musical note without reference to an external stan-
dard. Both conditions are rare in human populations (tone-deafness occurs
in about 3 percent), and their genomic foundation is therefore very differ-
ent from the normal range of musically related traits in humans. Here we
note that genes might be the foremost reason for variation in great ability or
inability (the extreme ends of the spectrum) but not necessarily the small
variation observed in almost everyone else.
Evidence for the genetic foundation of tone-deafness comes from the fact
that it is clustered in families. A candidate gene analysis examining Europe-
ans and East Asians found that it was associated in the former with varia-
tion at chromosome position 8q24. Studies of families in Finland using tools
such as the Karma music test, Seashore pitch test, and the Seashore rhythm
subtest found heritability performance on these tests at 0.42, 0.51, and 0.21,
 144
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

respectively. Other studies in this population found genetic associations for

musical abilities with chromosome positions and specific genes. Another
study of musical ability in Finnish musicians found evidence of positive
selection in another set of genes. Yet a further study of the ability to dis-
criminate pitch, duration, and sound patterns in seventy-six Finnish fami-
lies found significant genetic associations at position 3q21.3 (SNP rs9854612),
which is upstream of the GATA2 (GATA binding protein 2) gene. This gene is
involved in regulating the development of cochlear hair cells and the interior
colliculus. The strongest genetic association was for sound patterns at posi-
tion 4p14 (rs13146789, rs13109270) within the protocadherin (PCDH7) gene,
which also regulates cochlear and amygdaloid complexes.
The combination of the heritability of performance on these musical tests
and evidence that so many of the candidate genes are associated with cog-
nitive processes suggests that for these families, there is an actual genetic
component to the variation in their musical abilities. However, it is criti-
cally important to understand that these estimates come from a set of fami-
lies in Finland, a country whose genetic composition is strongly influenced
by genetic drift (see chapter 6). Therefore, there is absolutely no reason to
believe that these genetic associations would replicate across other Europe-
ans, let alone the rest of the world.
For example, the frequency for the SNP rs13146789 associated with the
PCDH7 gene varies between 0.473 in Siberians and 0.213 in Koreans, and
rs13109270 varies from 0.475 in northern Swedes to 0.228 in Koreans in
dbSNP. These values indicate that there should be adequate variation in all
of these groups to allow for people with the musically associated phenotypes
that might result from these variants. In summary, although genetic varia-
tion associated with musical ability has been discovered through modern
genomic techniques, there is no reason to believe that there are significant
differences in the genomic foundation of this trait among populations or
socially defined races.

DO RACES DIFFER IN PERSONALITY?

Now do you think that’s the wrong question to be asking?

We don’t want to sound like a broken record, but personality is extremely
difficult to define and therefore extremely difficult to measure. Definitions
of personality commonly highlight variations in enduring patterns and
thoughts, feelings, and behaviors that tend to allow an individual to respond
 145
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

in individually specific ways to specific circumstances. An individual’s per-

sonality is associated with their cognitive processes, just as intelligence is
a complex phenotype influenced by genetic, epigenetic, and environmen-
tal factors. In the case of personality, it is also important to focus on the
components of environment, such as its physical and social/cultural aspects.
Much of the biomedical literature focuses on aspects of personality that are
associated with mental illness, whereas the literature in industrial psychol-
ogy tends to focus on personality with regard to its application to improving
institutional effectiveness. In either case, stereotypical views of personality
associated with socially defined race are disastrous.
The five-factor personality model is widely used in both biomedical
and industrial psychology. This model includes scales associated with neu-
roticism or emotional stability, extroversion, openness to new experience,
agreeableness, and conscientiousness. The scales also have subdimensions.
Subdimensions of neuroticism/emotional stability include self-esteem, low
anxiety, and even temperedness; extroversion includes dominance and
sociability; openness, agreeableness, and conscientiousness subdimensions
are achievement, dependability, degree of caution, and desire for order.
Table 7.1 summarizes data from a meta-analysis of the five-factor person-
ality scale conducted with a large sample of individuals (> 300,000) from five
socially defined races in America. On positive personality metrics, whites
and East Asians tended to score highest, and Blacks and American Indi-
ans tended to score lowest. Despite the large sample, there are serious issues
with the design of this study. Specifically, the data used in this study were
distributed among individuals from the general population (50 percent),
business occupations (31 percent) and students in colleges (19 percent).
In addition, the distribution of individuals in these categories by socially
defined race is unequal. The data also indicate that there is a great deal of
representation by individuals from each of the socially defined races in each
score category in each component of the five-factor system. For example,
for the dependability trait, there is virtually no difference among socially
defined races. However, for traits having to do with need and desire, East
Asians scored much higher than whites, who scored the same as Hispanics
and Blacks.
An aspect of personality that has important implications for how socially
defined race is lived in societies is social dominance orientation (SDO).
SDO is related to the order and dominance subscales of the five-factor per-
sonality scale, but it is designed to evaluate an individual’s comfort with
 146
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

TABLE 7.1
Five-Factor Personality Scale Ratings for Americans by Socially Defined Race

Factor W-B W-As W-H W-AI Order

Emotional stability −0.90 −0.12 0.03 −0.21 H > W >A > AI > B
Global measures −0.12 −0.16 −0.04 ND W>H>B>A
Self-esteem 0.17 0.30 0.25 ND A>H>B>W
Low anxiety −0.23 0.27 0.25 ND A>H>W>B
Even tempered 0.06 −0.38 0.09 ND H>B>W>A
Extroversion −0.16 −0.14 −0.02 −0.21 W > H > A > B > AI
Global measures −0.21 −0.07 0.12 ND H>A>W>B
Dominance −0.03 −0.19 −0.04 ND W>B>H>A
Sociability −0.39 −0.09 −0.16 ND W>A>H>B
Openness −0.10 0.11 −0.02 ND A>W>H>B
Agreeableness −0.03 0.63 −0.05 −0.28 A > W > B > H > AI
Conscientiousness −0.07 0.11 0.08 ND A>H>W>B
Global measures 0.17 0.04 0.20 ND H>B>A>W
Achievement −0.03 0.14 0.10 ND A>H>W>B
Dependability −0.05 −0.01 0.00 ND W=H>A>B
Caution 0.16 ND ND 0.25 AI > B > W
Order 0.01 0.50 0.00 ND A>B>H=W
NoteĻġ The values listed are proportions of the standard deviation in the distribution of the response. All groups
are compared with whites, allowing the ranking of nonwhite groups relative to one another. Whites, East Asians,
Hispanics, American Indians, and Blacks rank first or second at eight, nine, ten, one, and five times, respectively.
Whites, East Asians, Hispanics, American Indians, and Blacks rank fourth or fifth at four, three, two, three, and
nine times, respectively. For American Indians, low ranking on these personality variables occur in three of the four
studies in they were included.
AI = American Indian, A = East Asian, B = Black, H = Hispanic, ND = no data, W = whiteį
Source: H. J. Foldes, E. E. Dueher, and D. S. Ones, “Group Differences in Personality: Meta-Analyses Comparing
Five US Racial Groups,”ġPersonnel Psychologyġ61 (2008): 579–616, https://onlinelibrary.wiley.com/doi/abs/10.1111/
j.1744-6570.2008.00123.x.

social dominance. SDO survey instruments contain items questioning an

individual’s attitudes about gender and sexism, ethnic and racial prejudice,
nationalism, cultural elitism, political and social conservatism, distribution
of resources, meritocracy, military policy, punitive policies, social welfare,
civil rights, and environmental policies. SDO has been validated across cul-
tures and tends to show consistent results, with men displaying greater SDO
than women and members of dominant racial and ethnic groups showing
higher SDOs than subordinated populations.
 147
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

For example, in Taiwan, SDO was significantly correlated with an indi-

vidual’s sexism, traditional attribution for poverty, attribution of economic
inequality, support for the existing political system, support for the mili-
tary and police, support for hegemonic nations, and opposition to college
students. In Canada, SDO had significant correlations with sexism, ethnic
prejudice, opposition to gay rights, environmental protection, punishment
for police brutality, more equalitarian distribution of resources, support for
capital punishment and more defense spending.
In summary, we once again conclude that personality is a complex trait
whose components are far from agreed on. Studies of personality routinely
show differences and similarities in these metrics among socially defined
races. Certainly, the overlap between the distribution of these metrics dem-
onstrates that one cannot use socially defined race as an accurate predictor
of the personality traits of any individual.

DO GENES ASSOCIATED WITH PERSONALITY DIFFER

AMONG RACES?

Not surprisingly, as with intelligence, personality as measured by a variety

of means has been shown to be heritable. The range for h2 reported in
the recent literature varies from 0.17 to 0.65. The higher estimates tend to
come from more biomedically related mental illness metrics. However,
similar to the case with intelligence, the existence of genetic variation that
influences various aspects of personality does not mean that a genetic
basis for the distribution of such aspects exists among socially defined
races. So far, genome-wide association studies that have attempted to find
a genomic foundation for various components of the five-factor scale
have been limited in scope and found few positive associations (table 7.2).
Table 7.2 shows that eleven SNPs were identified as statistically signifi-
cantly associated with five-factor traits from ten studies of Europeans and
East Asians.
Even these minimal results need to be taken with yet another large grain
of salt. One major difficulty that is immediately apparent with these data
is that the social/cultural environments of these groups (as well as physi-
cal environments) are not equalized. Thus, even if we were to believe these
results, we have no way of really determining the robustness of their effects
across environments and cultures. Thus, similar to the GWAS results for
intelligence, we know there is a genomic contribution to the personalities of
 148
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

TABLE 7.2
GWAS Meta-Analysis Results for Five-Factor Scale Ratings for Various Populations

Trait SNP Gene Population Size Replicated?

Agreeable None Sardinians 3,572 ŏŰ
Agreeable rs9650241, rs2701448, Chromosome 8 Europeans 4,595 ŏŰ
kgp6080068
Agreeable None East Asians 3,898 ŏŰ
Agreeable rs8015351 RPS29 Koreans 4,919 ŏŰ
Conscientious None Sardinians 3,572 ŏŰ
Conscientious rs2576037 Europeans 17,375 ŏŰ
Conscientious rs912765, NS. LMO4 Koreans 4,919 ŏŰ
Extroversion None Sardinians 3,572 ŏŰ
Extroversion rs57590327, rs2164273, GBE1ĭġMTMR9ĭġ Europeans 122,886 ŏŰ
rs6481128, rs1426371 PCDH15ĭġWSCD2
Extroversion rs12537271, NS PTPN12 Koreans 4,919 ŏŰ
Excitement seeking rs7600563 CTNNA2 Europeans 7,860 ŏŰ
Openness None Sardinians 3,572 ŏŰ
Openness rs1477268, rs20332794 RASA1 Europeans 17,375 ŏŰ
Openness rs16321695 IMPAD1 Koreans 4,919 ŏŰ
NoteĻġThe limitations of the studies include the fact that only Europeans and East Asians were sampled (and certainly not all
groups within these regions of the world) and that the studies were not replicated.
NS = not statistically significant.
The data are summarized from B. H. Kim, H. N. Kim, S. J. Roh, et al., “GWA Meta-Analysis of Personality in Korean Cohorts,”ġ
Journal of Human Geneticsġ60, no. 8 (2015): 455–60, https://www.nature.com/articles/jhg201552.

individuals but no reason to suppose that the genomic foundation of person-

ality differs among populations or socially defined races.

DO GENES ASSOCIATED WITH MENTAL ILLNESS DIFFER

AMONG RACES?

At the risk of sounding like a skipping record, we again start with this dis-
claimer: the definition of mental illness influences both the capacity to iden-
tify its prevalence within human populations and also to identify any genes
associated with variation in this trait. The modern conception of mental
illnesses identifies these as otherwise normal behaviors that, under certain
circumstances, become pathological.
 149
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

A more fruitful way of understanding mental health is to envision it as

brain health. The paradigm of brain health makes it easier to understand
what makes us vulnerable to mental illness. Just as the other organs of our
body are vulnerable, so is the brain. Evolutionary biology has demonstrated
that the six factors that make us vulnerable to illness include evolution-
ary mismatch, infection (viruses/bacteria), evolutionary constraints (limi-
tations in the power of natural selection), trade-offs (all parts of the body
have their advantages and disadvantages), reproduction (all of our body sys-
tems evolved to promote differential reproductive success), and defensive
responses (pain and anxiety can be useful responses to threats). The conse-
quence of the combination of these factors is that by the turn of the twenty-
first century, one in five Americans (children and adults) had a diagnosable
mental disease as defined by the Diagnostic and Statistical Manual of Mental
Disorders (DSM-IV-TR) or International Classification of Disease (IDC-10)
tools. The major classes of mental illness are mood and anxiety disor-
ders (major depressive disorder, or MDD, bipolar disorder, panic disorder,
obsessive compulsive disorder); psychotic disorders (schizophrenia); eating
disorders (anorexia nervosa); and childhood disorders (attention deficit/
hyperactivity disorder, or ADHD).
Given what we already know about the social determinants of health and
health disparity in the United States (see chapter 5), no one should be sur-
prised that this disparity also exists with regard to mental disease. However,
the direction in which the disparity exists is surprising. For example, despite
the fact that African Americans suffer from more psychological distress, they
show lower levels of diagnosed MDD. This conclusion was drawn from
comparing measures of psychological distress and MDD in studies spanning
1970–2008, with well over 500,000 subjects. Additional evidence for this
paradox is that suicide rates (which are associated with MDD) have always
been higher for European Americans.
The rates of post-traumatic stress disorder (PTSD) show no clear pat-
terns of differentiation by socially defined race. PTSD is twice as com-
mon in women as it is in men. The environmental risk factors associated
with this condition are childhood mistreatment, sexual assault (SA), and
intimate partner violence (IPV). The prevalence of PTSD among women
who have experienced IPV is six times that of women in the general
population. Some studies have found a lower prevalence of PTSD among
African Africans and Hispanics compared with European Americans, but
 150
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

those studies were not disaggregated by sex. Others have found the oppo-
site pattern.
National survey data suggest that Africans and Hispanics are more likely
than European Americans to be exposed to PTSD risk factors. African Amer-
ican women are more likely to be exposed to IPV, but Hispanic women had
a lower rate of assaultive violence than European American women. Other
studies have found that European American women were at a greater risk of
IPV than African American women. Data from a 2006 study examining
the risk of PTSD and MDD in a sample of women included in the National
Epidemiological Survey on Alcohol and Related Conditions showed that the
risk of a lifetime history of PTSD was 12.79 percent for all women in the
sample and 12.68, 13.89, and 12.29 percent for European American, African
American, and Hispanic women, respectively. There was no statistically sig-
nificant difference between the groups. However, for MDD, the lifetime risk
was 27.66 percent for all women, and 29.08, 21.78, 24.90 percent for European
American, African American, and Hispanic women, respectively. These dif-
ferences were highly significant. The results are consistent with studies that
have routinely found that European Americans are more likely to develop
MDD compared with African Americans and Hispanics.
Schizophrenia is a severe and disabling brain disorder characterized by a
combination of delusions (erroneous beliefs), hallucinations in every sense
(e.g., sight, hearing), disorganized speech, grossly disorganized behavior, nega-
tive symptoms (such as flat affect), and, in some cases, catatonic motor behav-
iors (although the latter might result from the side effects of the drugs used to
control the condition). This disease severely impairs social and occupational
functioning. Schizophrenia affects one in one hundred Americans, although
there is evidence that the rate is higher in African Americans. This higher
prevalence is partly influenced by bias among psychiatrists, who are three
times more likely to diagnose an African American with schizophrenia com-
pared with a European American patient with the same set of symptoms.
The heritability of schizophrenia is estimated at around 0.80; however,
inflammation levels, date of birth, place of birth, seasonal effects, infectious
disease (Toxoplasma gondii and herpes viruses: cytomegalovirus, Varicella-
zoster, and herpes simplex type 1), complications during pregnancy (this
actually might be a genetic effect), complications during delivery, substance
abuse, and stress contribute to the roughly 0.20 environmental effect. The
infectious disease association is also consistent with the inflammation mech-
anism that influences schizophrenia risk.
 151
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

Over the last decade, important developments in discovery of the evolu-

tionary origins of schizophrenia have been made. Specifically, we now see
schizophrenia and autism as different ends of a spectrum of mental activ-
ity. On the psychotic side of the spectrum, the brain produces auditory
hallucinations, megalomania, paranoia, delusion, major depression-elation,
thought disorder, and mania. On the autism side, the brain produces no or
reduced speech, reduced sense of self, lack of mentalistic skill, basic emo-
tions, mechanical logic, and lack of or little goal pursuit.
These disease conditions have their origin in genomic imprinting that
results from the fitness conflict between males and females in sexual spe-
cies. The mechanism of genomic imprinting is epigenetic. DNA methylation
can silence or activate genes. Male and female parents imprint genes dif-
ferently in their offspring to improve their fitness. Male imprinting favors
slower growth and larger size at birth, whereas female imprinting upregu-
lates growth genes favoring faster growth and smaller size at birth. This con-
flict leads to a stable equilibrium in which growth rates and sizes evolve that
balance the needs of both sexes. However, mutations can occur that disrupt
the equilibrium, and this disruption causes mental disease when the genes
involved are expressed in brain tissue.
There is strong theoretical and experimental evidence for this perspec-
tive, including genomic experiments with mice and data from human birth
cohorts. For example, it has been shown that many of the same genes are
associated with autism and schizophrenia; but, more important, a deletion
in the gene in question is associated with schizophrenia, and a duplication in
the gene in question is associated with autism. Furthermore, the patterns of
DNA methylation in genes associated with these conditions differ between
persons who have and those who lack them.
Given that the fitness conflicts between males and females and the mecha-
nism of genomic imprinting predates the evolution of our species, it is highly
unlikely that specific populations—let alone socially defined races—dramat-
ically differ in the prevalence of autism/schizophrenia spectrum disorder or
the genomic variants associated with those conditions. For example, a 2019
study found a common genetic architecture for schizophrenia in Europe-
ans and East Asians. Another study found shared genomic foundations for
schizophrenia in Europeans and sub-Saharan Africans.
In summary, envisioning mental illness in the framework of brain health
helps us to better understand it as a complex physical trait, similar to intel-
ligence and personality. Furthermore, given the complexity of the human
 152
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

brain, the fact that one in five Americans currently suffers from a diagnos-
able mental disease in one sense should not be shocking. However, there
might be some evidence that evolutionary mismatch is contributing to rising
rates of mental illness worldwide. If that is the case, it calls into question
ways in which our modern environments differ from those of our ancestors
in ways that cause us to be sick. In this vein, it is interesting to note that
social injustice has been associated with increased risk of disease (including
depression) in a cohort of German workers who were examined between
2005 and 2013. Those who perceived income injustice showed an elevated
risk of diabetes, stroke, cardiopathy, asthma, hypertension, and depression.
To make the point clear, social injustice makes people sick.
Here, we have not attempted to summarize all the literature on the preva-
lence of the various mental illnesses observed in the human species. These
conditions vary in their heritability, with schizophrenia on the high end
(~0.80) and mood and anxiety disorders ranging from 0.20 to 0.60. As with
other complex brain-associated traits, the genomic foundations of these dis-
orders are shared across the human species, with populations differing in
the frequency of risk-associated variants. Thus, as with other health-related
traits, levels of mental health differ in socially defined races, and this varia-
tion is not driven by genomic differences. However, the different physical
and social environments that socially defined racial groups experience prob-
ably play a major role in determining the patterns and prevalence of mental
illnesses observed within them, as in the cases of MDD and PTSD.

DO RACES DIFFER IN CRIMINAL BEHAVIOR AND VIOLENCE?

Another enduring myth of race is that criminality and violent behavior run
along a skin color gradient from light to dark. The false belief that violence
and criminality differ by race is part of the discourse that dark-skinned indi-
viduals are more physical and unable to control their physical selves, tend-
ing toward aggressive behavior. This aggression could be sexual and also
result in homicides and other forms of physical harm. The fear of the sexual
aggression of Black men was clearly in the mind of D. W. Griffith when he
directed the infamous rape scene in Birth of a Nation, his 1915 blockbuster
that was shown at the White House. This trope of Black criminality was also
a component of J. P. Rushton’s life-history theory of racial difference. Based
on the shoddiest of data, Rushton asserted that Blacks are innately more
prone to criminal behavior than whites and East Asians.
 153
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

In an earlier time, this myth of criminality was routinely used to segre-

gate Europeans of a “color” other than white, including the Irish, Italians,
and Jews. Jews were less physical but more cunning in their criminal behav-
ior. The Irish and Jews, and especially the Italians, became criminal mob-
sters. During an 1881–82 lecture tour of the United States, Oxford University
professor Edward Freeman proposed a simple remedy for what he saw as
the social assault against the Teutonic races: “that every Irishman should
kill a Negro and be hanged for it.” The belief in a higher tendency toward
criminal behavior was often supported by junk racist and eugenic science. It
was central to efforts to limit immigration by less desirable Europeans, and
although the science has been discredited, the ideology remains.
Today, the greatest myths of criminality are used against brown and Black
peoples. There are two separate questions we want to answer: (1) is criminal-
ity greater in African Americans and Latinos, and (2) if so, why? A belief in
the inherent nature of criminality and race would lead to yes answers for the
first question. We find that the prevalence of acts defined as criminal might
be greater in these groups, but the reasons have nothing to do with biology
and a lot to do with racism.
Similar to our discussion of intelligence and personality, we must begin
with a definition of crime. Legal definitions describe crime as behavior by an
act or omission, as defined by statute or common law, deserving of punish-
ment. Sociology takes a broader view, describing crime as deviant behavior
that violates prevailing norms concerning how an individual ought to behave.
In both cases, we have the problem that depending on the law or social norm
in question, an individual acting morally can be considered a criminal. For
example, Lutheran theologian Dietrich Bonhoeffer (1906–45) was hanged
for his opposition to Nazism, Rosa Parks (1913–2005) was arrested for defy-
ing the city of Montgomery’s segregation ordinances, and Nelson Mandela
(1918–2003) was imprisoned for most of his adult life for opposition to apart-
heid in South Africa.
On the other hand, clearly immoral acts such as financial crimes are often
applauded by society even though they violate the law. Business Insider listed
the ten biggest financial white-collar crimes from 2000 to 2009. Each of
the individuals listed was a man of European descent, including people like
Kenneth Lay, who, with the accounting firm Arthur Anderson, mispresented
Enron, losing shareholders $1 billion. Lay was never convicted of a crime.
Others, such as New York City money manager Bernie Madoff, ran a classic
Ponzi scheme for over two decades, defrauding investors of an estimated
 154
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

$65 billion. He was convicted and sentenced to 150 years in prison. How-
ever, whenever racial theories of crime are discussed, they usually focus on
violent crime, such as rape, homicide, and serious assault. For example, a
review of the 2020 tables of contents in the academic journal Criminal Jus-
tice and Behavior did not reveal a single article associated with white-collar
crime.
What causes one to be a violent criminal? This question is also conflated
with the issue of what counts as criminal behavior and what is more properly
understood as mental illness. For example, are antisocial behavior, conduct
disorder, callous unemotional affect, and antisocial personality disorders
predictors of crime? Or are these best understood as mental disorders that
might or might not be associated with an individual who commits a violent
crime? As with intelligence, there have always been competing hypotheses,
with nature on one side and nurture on the other. Are criminals born that
way, or are they made so by their life experiences? Those supporting the
idea of an inborn tendency to criminality have pointed—often with flawed
data—to how crime runs in families. They have used skull shapes (phrenol-
ogy), hormone levels (Rushton’s theory, mentioned earlier), and, recently,
genes to detect criminals.
Our broken-record analogy shows that genome-wide association stud-
ies of traits possibly linked to criminal behavior do not show any evidence
of genomic differentiation between socially defined racial groups. A 2019
review of genes associated with aggressive behavior (antisocial behavior,
conduct disorder, callous unemotional affect, and antisocial personality dis-
orders) examined about 59,000 individuals (mostly of European descent,
with some African Americans) across six studies published between 2011
and 2017 and found only five statistically significant SNPs for the four traits
under study. Those data do not make for a very strong genomic foundation
for a criminal behavior argument.
In 1992, with crime increasing in many urban areas in the United States,
the National Institutes of Mental Health (NIMH) began its Violence Initia-
tive to study the biology of crime and violence. Black and brown inner-city
youth were compared to animals roaming the urban jungle. It was in this
ideological climate that the case of the so-called Central Park Five emerged.
In this horrific injustice, five Black and brown teenagers were accused of the
rape of a white Central Park jogger and convicted by coerced confessions
and the slimmest of evidence.
 155
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

TABLE 7.3ġ
Probability of Homicide by Race of Victim and Race of Offender

White Black Other Unknown offender

White 0.81 0.09 0.02 0.02

Black 0.08 0.89 0.01 0.03
Other 0.25 0.18 0.55 0.02
Unknown victim 0.42 0.22 0.06 0.30
NoteĻġThe boldface numbers show the homicide probability within socially defined group. Thus, a white American
is nine times more likely to be killed by a white than a Black American, whereas a Black American is ten times more
likely to be killed by a Black than a white American.
The data are modified from U.S. Department of Justice, Federal Bureau of Investigation, Criminal Justice Informa-
tion Services Division, “2018 Crime in the United States,” table 6: Expanded Homicide Data, https://ucr.fbi.gov
/crime-in-the-u.s/2018/crime-in-the-u.s.-2018/tables/expanded-homicide-data-table-6.xls.

Although the panic over the alleged criminality of Black and brown men
is almost entirely about fear of whites being the victims, such occurrences
are actually rather rare. What is unfortunately more frequent is that victims
of Black and brown crime are most often also Black and brown. For example,
homicide in America occurs mainly within socially defined racial catego-
ries (table 7.3). In 2018, 3,315 whites and 2,925 Blacks were murdered in the
United States. However, whites make up 61 percent in the U.S. population,
whereas Blacks account for 13.4 percent. So, to generate equivalent numbers,
you would have to divide the white number by 4.55, resulting in about 728
whites murdered for equivalent population sizes. Even more telling is what’s
revealed when examining deaths due to homicide by race (fig. 7.1). Blacks
show the highest mortality rate by homicide across age. For all other groups,
there is no detectable homicide from ages one to nineteen. Indeed, the rank
of these groups for homicide mortality tracks with their median net wealth
per family.
The question is, why? If one does not study in detail the causes of vio-
lent crime, one could be left with the impression that the racial variation is
innate. It isn’t.
Two studies by epidemiologist Brandon Centerwall show how important
it is to try to control for environment when comparing racial differences in
violent crime. Centerwall, working at the Centers for Disease Control in
the 1990s, came across federal data on rates of domestic homicide in differ-
ent cities. A domestic homicide is the murder of one individual by another
 156
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

60
Age vs. Black
Age vs. white
50 Age vs. As/PI
Age vs. Hispanic
Age vs. Amlnd
40
Mortality rate

30

20

10

0 10 20 30 40 50
Age

FIGURE 7.1. The homicide rate per 100,000 individuals by socially defined race in 2017. These figures
include both sexes. The greatest gap is observed at ages 15–19, when the rate for Blacks is 35.5 and for
whites is 2.4, with all other groups at about 0.0. At later ages, American Indians come closest to the rate
for Blacks at 23.4 from ages 25–34. Source: Melonie Heron, “Deaths: Leading Causes for 2017,” National
Vital Statistics Reports 68, no. 6 (June 24, 2017): 1–77, https://www.cdc.gov/nchs/data/nvsr/nvsr68/nvsr68
_06-508.pdf.

living in the same domestic unit (typically the same apartment). Centerwall
first studied intraracial domestic homicides in Atlanta, Georgia, and New
Orleans, Louisiana, for a number of years from the late 1970 to the mid-1980s.
Centerwall found that for both cities, the risk of intraracial domestic
homicide was almost six times greater in the Black than white communi-
ties. Others are aware of these data and have left open the interpretation
as to why homicide rates vary so much. This study went further; Center-
wall developed a simple measure to control for crowding by stratification of
the socioeconomic status of different census tracts. He found that nearly all
white residents of these cities lived in areas with low crowding (and higher
SES), whereas Blacks often lived in areas with much greater crowding, and
the rate of Black domestic homicide increased dramatically with crowding.
Furthermore, if one controls for crowding, comparing the rate of Black ver-
sus white domestic homicide in census tracts with equal crowding, the rate
of homicide is almost equal. Centerwall concluded that domestic homicide
 157
I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

has nothing to do with race but a whole lot to do with crowded conditions,
which are themselves attributable to racism and class.
The myth of criminality is powerful in how it has burdened Black and
brown families. Police are not helpful or friendly; they are more likely to
harass, arrest, and even kill. Police encounters lead to incarceration, and incar-
ceration leads to further struggles for families of the incarcerated individual
to maintain anything close to a healthy lifestyle. This is systemic racism.

CONCLUSIONS

Individuals vary in complex traits such as musical ability, personality, and

intelligence. The cause of these traits is equally complex. Modern genomics
has demonstrated that although genes play a role, individual variants are
likely to make a very small contribution to complex traits. Rather, genes
work together with chance and environmental conditions. After all, these
complex traits, including brain diseases and violent criminality, are the result
of a cascade of events that might stretch back generations and continue to
trigger specific violent events.
There are some measured differences in these complex traits across popu-
lations and socially defined races. Where we have failed intellectually is in
gravitating too quickly to the simplified assumption that these differences
are due to more consequential biogenetic differences. This assumption is
unfounded. Indeed, much simpler environmental factors, such as poverty,
have been demonstrated as explaining most of the variation in violent crime
rates. Indeed, the UN Global Study of Homicide shows a clear inverse rela-
tionship between a country’s gross domestic product (GDP) and its homi-
cide rate. To underscore the complexity of the association between homicide
rate and social, cultural, and environmental factors, some of the countries
with the highest GDPs (Germany, Switzerland, Japan, Hong Kong) have the
highest proportions of female homicide victims. Simplistic genetic theories
of violent crime are scientifically untenable and have done tremendous harm
in supporting the status quo and worldwide racial hierarchies.
 Chapter Eight

DRIVING WHILE BLACK AND OTHER

DEADLY REALITIES OF INSTITUTIONAL AND
SYSTEMIC RACISM

The existence of racism is not up for debate. An overwhelming abundance of

facts demonstrate the reality of structural racism in America. Unfortunately,
we have not reached racial equality. We are not postracial. The truth is in the
facts of racial inequalities.
This chapter is about racial inequality in life circumstances and
opportunity—today. These inequalities have histories and origins in the
past. They have a legacy. They are part of the long and continuing history of
institutionalized and systematized unequal treatment by race. Here, at the
onset, we remind you that racism isn’t about individuals, or thoughts, or spe-
cific acts, or even intention. Rather, racism is about systematic maltreatment
by groups with access to power over groups without equal access to power.
Thoughts and ideas, no matter to what degree they are explicit and implicit,
are important because they solidify into ideologies and worldviews that jus-
tify institutions and systems. And the consequences of racism result from
institutions and systems of racial oppression. This means that addressing
one’s own racial misconceptions is an important start but very far from the
end of eliminating racial injustice. We also need to go beyond the individual
awakening, because ending racial injustice requires systemic and concerted
political and social action.
The consequences of systemic racism are found pretty much everywhere
one looks. One finds, without much digging, that racial inequalities are at
every step of medical care and health outcomes (see chapter 5), from general
 159
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

causes including unhealthy diets and air, pollutants, dangerous streets, and
lifelong psychological stresses, to lack of health insurance and lower-quality
and less aggressive medical care. Racial inequalities are also found in edu-
cation, beginning with less access to quality childcare and early-childhood
enrichment programs, impoverished schools from pre-kindergarten to col-
lege, and systemic lower expectations and ability to stay in school. Inequalities
are part of the housing and neighborhoods of racially subordinated commu-
nities. These environments include heavy metals in soils and chipping paints
in buildings, unsafe streets, and houses without proper heating, cooling, and
ventilation, all of which are among the various aspects of environmental rac-
ism. Racism puts up obstacles to secure, prestigious, and well-paid jobs. Biases
become institutional racism when an employment selection process results in
choosing applicants and advancing workers whose résumés look white, whose
names sound white, and who fit most seamlessly into the white club.
All of these biases and actions contribute to a silent system that leads to
inequalities in family wealth. Poor education, health, and environments lead
to lower-paying jobs. And the trend extends from the past, as less inherited
wealth and building of wealth through homeownership and other long-term
investments perpetuates intergenerational cycles of family poverty. The
cycle continues, with lower wealth leading to poor education, poor diets,
exposure to toxic environments, and poor health.
Inequality of opportunity by race is central to our history. It is intergen-
erational. It is a cultural inheritance. It is part of the social contract of the
United States. Just as in genetics, DNA is not destiny; racial inequalities and
racism in societies are not forever, and acting to eliminate them is under
our control. In fact, part of what excites us is that social ideas can change.
We are a flexible species with brains that adapt. We can and must change.
Racial inequality is ours to overcome. The future of our species is at stake.
To understand why overcoming racism is so imperative, let’s take a look at
the depth and breadth of racial inequalities and racism.
In prior chapters, we have defined and discussed racism and its various
forms. We have explored in depth how racism, rather than biological race,
impacts health and longevity (chapter 5). In this chapter, we examine some
of the other consequences of the lived experiences of racially subordinated
people in a society with endemic racism. We bring to the forefront some
of the many everyday experiences of racism in society. Our focus is on five
interrelated arenas where racism lives today: the criminal justice system,
education, employment, environments, and wealth accumulation.
 160
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

DRIVING WHILE BLACK, OR WHY DO AFRICAN AMERICAN

MEN GET PULLED OVER BY THE POLICE MORE OFTEN
THAN OTHERS?

On July 6, 2016, Philando Castile, a thirty-two-year-old Black man, was driv-

ing in a suburb of Saint Paul, Minnesota, when he was pulled over at 9:00 p.m.
by police officer Jeronimo Yanez and his partner. Castile was driving with his
partner, Diamond Reynold, and her four-year-old daughter. Once stopped,
Castile, with his seat belt on, is heard on a video telling the officers that he
had a firearm that he was licensed to carry. The video shows Yanez becoming
agitated, screaming “Don’t pull it out!” Both Castile and Reynold try to assure
Yanez that Castile is not pulling out his gun. But the agitated officer shot Cas-
tile at close range seven times, hitting him five times and piercing his heart.
Castile died at 9:37 p.m. This was Castile’s forty-sixth traffic stop.
Driving while Black (DWB) sounds kind of cool and flip. It is a word play
on driving while intoxicated (DWI). And it is also equally serious. Driv-
ing while Black refers to a part of the system of differential treatment that
Black- and brown-skinned individuals, especially Black men, receive from
law enforcement. Statistics repeatedly show that Black men are more often
stopped and searched by police officers than other men. A study conducted
about a decade ago in St. Louis, Missouri, showed that searches were more
likely in stops of Black drivers than of white drivers, especially those con-
ducted by white officers; the study controlled for other characteristics of the
officer, driver, and reason for the stop. In predominantly Black communities,
however, stops of white drivers by white officers were more likely to result
in a search. The reason for this was that officers have assumed that a likely
reason for white drivers to be in Black communities was to purchase drugs.
A recent study of more than 20 million traffic stops in North Carolina
across multiple decades showed a pattern of more aggressive targeting of
racially subordinated youth, despite the fact that the stops were not justi-
fied by differential crime rates among those youths compared with whites.
Finally, to demonstrate that this problem does not reside only in the former
Confederate states, the stop-and-frisk policy of New York City police was
also shown to be racially biased (controlling for social areas, neighborhoods,
and precincts).
Scholars and activists have pointed out that over-policing of racially
subordinated people is rarely comprehended by middle-class whites. This
 161
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

might have contributed to the grief and anger many white Americans expe-
rienced when they saw the full video of George Floyd’s murder on televi-
sion news and social media feeds. Routinely being pulled over while DWB
is part of systematic unequal treatment in the criminal justice system. Black
and brown communities are differentially targeted, accused, arrested, found
guilty, and incarcerated. Black and brown people receive unequal treatment
at every stage in the criminal justice system.
Why? Driving while Black is justified as part of racial profiling, the use
of perceived race as grounds for suspecting someone of having committed
an offense. However, the problem is that racial profiling is based on a false
supposition that Black and brown people are more likely to be breaking the
law. For example, the war on drugs, the increased criminalization of not just
selling but being caught in possession of small quantities of marijuana and
other illegal drugs, targets Black and brown communities.
In Suspect Citizens, Frank Baumgartner and co-authors document race
inequalities in traffic stops. Hispanic drivers are pulled over about as often
as white drivers, but once pulled over and perhaps identified as Hispanic,
they are more likely to be searched. Even though whites drive more often on
average than Blacks, the authors found that Blacks are nearly twice as fre-
quently pulled over as whites. It doesn’t stop there. Blacks, once pulled over,
are twice as likely to be subject to search. So, overall, the chance of a Black
driver being searched is about four times that of a white driver.
Many might think that this sort of profiling is justified. It is common, but
it is not effective. After these traffic stops, police are less likely to find guns,
drugs, or illegal substances in the cars driven by African Americans or His-
panics. The contraband hit rates are 36, 33, and 22 percent for whites, Blacks,
and Hispanics, respectively. In fact, if anything, the cause-and-effect relation-
ship is reversed. Racial profiling of Black and brown men and women leads
to further arrests, convictions, and jailings, as individuals without white skin
privileges go through a system of inequalities. The real reason for the driving
while Black phenomenon is racism.
Sandra Bland, a twenty-eight-year-old Black woman with a new job, died
in her jail cell of an apparent suicide. Three days earlier, July 10, 2015, Bland
was stopped for changing lanes by a Texas State Trooper. She said she had
changed lanes to let the trooper’s car pass. After an exchange with the officer,
Bland was handcuffed and jailed. Records indicate that this was Bland’s tenth
routine traffic stop. Bland, we guess, was done with DWB.
 162
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

WHY IS THERE A RACIAL DIFFERENCE IN

INCARCERATION RATES?

On the warm spring night of April 19, 1989, Trisha Meili was out for a jog in
Central Park when she was assaulted and raped. Meili was found early the
next morning, so badly injured that she remained in a coma for twelve days.
Initially, her identity was hidden from the public. Meili came forward years
later to reveal her identity.
This rape took place at a time of heightened fear of Black and brown
youth, who were accused of “wilding,” a term for running wild in the streets.
Some, like Donald Trump, imagined these youth, the Central Park Five and
other young boys, as no more than a pack of hunting animals out to destroy
property and needlessly harm people. And these packs of youth were said to
be Black and brown. Trump publicly railed against the Central Park Five.
He paid $85,000 to run ads in New York’s four premier daily newspapers
calling for the reintroduction of the death penalty. He said, “I want to hate
[them]. They should be forced to suffer. . . . I am looking to punish them.”
All this was said even before a trial date had been set.
Worse, of course, is that these underage men never committed this crime.
Feeling pressure to solve the so-called Central Park Jogger case, the police
arrested ten suspects. Ultimately, five Black and brown youth, ages fourteen
to sixteen, were illegally interrogated and eventually tried, found guilty, and
sentenced to five to ten years for the four boys under age fifteen and five to
fifteen years for Korey Wise, then sixteen years old. Wise was classified as an
adult due to the violent nature of the crime, one we later learned he never
committed. He served thirteen years. All the boys had been framed by the
New York Police Department, sentenced, and jailed before eventually being
cleared of the crime after the true rapist, a convicted murderer and serial
rapist, came forward in 2001 and confessed in 2002. His DNA matched
DNA found in semen on Meili. He said he had committed the crime alone.
Other evidence corroborated his confession.
The case of the Central Park Five shows the logical conclusion of the trope
of Black and brown men as bestial rapists and criminals. In the 1990s, the
National Institutes of Mental Health (NIMH) focused on aggressive, violent
criminal behavior as arising from abnormally high hormones and genetic fac-
tors. In 1992, NIMH was beginning to formalize a “violence initiative,” except
that Frederic Goodwin, a psychiatrist and head of the Alcohol, Drug Abuse
and Mental Health Administration, made very clear what such an initiative
 163
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

was about. At a NIMH advisory committee meeting, Goodwin discussed

the parallels, as he saw them, between violent behavior by young male rhe-
sus monkeys and young men. He suggested that this parallel might provide
insight into the increasing level of violence in inner cities. Goodwin noted
that this rise in violence might be the result of a loss of civilizing social fac-
tors that typically keep human and monkey aggression in check: “That is the
natural way of it for males, to knock each other off . . . maybe it isn’t just care-
less use of the word when people call certain areas of certain cities jungles.”
Of course, this sort of reasoning betrays the most simple-minded under-
standing of violence as part of primate behavior. Social behavior drove the
evolution of intelligence in primates. Violence, or its threat, similarly plays a
role in all primate behavior and is one of many tactics that can be deployed
in the pursuit of social goals. Given that all primates, including humans, are
social strategists, they evaluate the costs and benefits of any tactic for obtain-
ing a desired social outcome. Thus, episodes of violence do not result from
an individual’s “losing control” or from the “beast within” overwhelming
the fragile control of civilization. Rather, it is a tactic that individuals rarely
choose to deploy because of the very high costs and lower efficiency of other
tactics to achieve social goals. This further suggests that in situations of
uneven social power, the costs of violent acts might be nil.
This argument would explain the large number of lynchings conducted
against Blacks during the era of Jim Crow laws, or the recent wave of shoot-
ings of Blacks by white police officers. Alternatively, innocent black and
brown men have been jailed or executed by the state for alleged rapes of
white women throughout American history. Conversely, a white man has
never received the sentence of execution for the rape of black woman in all
of America’s history.
Racial differences in incarceration follow from racial disparities in all
stages in law enforcement and criminal justice, from differences in traffic
stops to searches, arrests, convictions, and sentencing. Racial profiling hap-
pens on highways and at traffic lights and also in homes, parks, and neigh-
borhoods. Incarceration rate differences are the end result of the system of
unequal treatment. But the harm continues for the incarcerated individual
and their families, especially their children.
The United States has the largest prison population in the world and also
the higher per-capita incarceration rate. In 2016, 2.2 million individuals
were in U.S. jails and prisons. As Michelle Alexander aptly puts it, imprison-
ment is the new Jim Crow. It was not always this way. In 1970, only about
 164
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

800 7

Prision admission rate per 100,000 700 6

600
5

Black/white ratio
500
4
400
3
300
2
200
100 1

0 0
1920 1930 1940 1950 1960 1970 1980 1990 2000

White rate Black rate Ratio

FIGURE 8.1. The rise in rates of prison admission in white and Black populations and the rise in the Black/
white ratio. In the 1930s, prison admissions were relatively low, and Black admissions were three times the
white admissions rate. By 2000, the Black admissions rate had skyrocketed, especially after 1980, and is now
over six times the rate of white admissions. Source: Makheru Bradley, “America’s Jails Are the Foundation of
the Prison Industrial Complex,” July 9, 2015, Makheru Speaks (blog), http://makheruspeaks.blogspot
.com/2015/07/americas-jails-arethe-foundation-of.html.

400,000 individuals were incarcerated. As shown in figure 8.1, rates began

to increase in 1971 with Nixon’s war on drugs. Then it skyrocketed further
in 1984 with the Sentencing Reform Act. From 1970 to 2016, the number of
individuals in prisons and jails grew more than fivefold.
In 1970, the U.S. prison population was not particularly high compared
with other countries, especially other Western countries. Now it is. No other
country on the planet has a higher rate or number of incarcerated indi-
viduals. The rates of incarceration in Cuba, Brazil, and Russia are among
the highest but only about half to three quarters of the U.S. rate. Prisons in
Europe have about a fifth to less than a tenth the number of inmates com-
pared with the United States.
Why are American incarceration rates so high? The traditional answer is
that incarceration is an appropriate punishment for a crime. Slogans such as
“let’s get tough on crime” are common, uttered by politicians such as Trump
and many of his predecessors, and not just Republicans. Getting tough is
thought to take criminals off the streets and protects other citizens.
In 1988, Michael Dukakis lost his bid for the presidency to George H. W.
Bush largely because of ads suggesting that he was soft on crime. Dukakis
was pilloried by a series of ads revolving around a violent crime committed
 165
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

by Willie Horton, a Black inmate on furlough. The Massachusetts Correc-

tional Reform Act (MCRA) of 1972 (which passed due to the leadership of
the Republican governor) allowed an inmate who had served more than ten
years for first-degree murder to have eighteen to forty-eight hours of unsu-
pervised furlough. During one of his furloughs, Horton broke into the home
of Cliff and Angela Barnes, terrorizing and robbing the couple and raping
Angela. The ad featuring Horton held Dukakis responsible for allowing this
crime to happen because he supported the MCRA.
Many viewed this ad as having played a crucial role in Bush’s landslide
victory. Although we cannot be certain how much this ad or the public per-
ception of Dukakis’s views on crime changed the outcome of that election,
clearly, it sounded a warning to American politicians. Now Republicans and
Democrats are sure to be seen as tough on crime. William Clinton, the next
Democratic president, as well as Hilary Clinton, his wife and future Dem-
ocratic presidential candidate, established their stances as being tough on
crime. Hilary Clinton played on fears by referring to “super predators.” Seen
as being soft on crime is a sure way to kill a politician’s career.
The hope is that incarceration leads to rehabilitation. Unfortunately, that
is well known to be a myth. Imprisonment more often leads to a life of
crime. It is hard—a small miracle—to escape the cycle because imprison-
ment leads to impoverishment and a severe restriction of opportunities for
a decent, law-abiding life.
Incarceration is big business. There is money to be made in the privati-
zation of prisons. For example, in 2011, corruption at a private prison in
Arizona led to a prisoner escape and the murder of a family in Oklahoma.
However, because the private prison system is profitable, events such as that
did not slow its rise. But there are also economic costs to federal, state, and
local governments to incarcerate prisoners. In 2015, the average cost was
about $33,000 per year, all paid for by taxes and individual citizens sending
financial support to their incarcerated family members. Whether prisons are
privately or publicly funded, ultimately, we taxpayers pay for incarceration.
That is part of the problem of incarceration. Less well understood are the
costs of conviction and imprisonment borne by both those who are sent to
prison and their families. Once a person has a criminal record, it is harder to
get a decent job. That much should be obvious. However, what isn’t obvious
is that socially defined race is a determinant of how much a prison sentence
impacts one’s employability. One study found that white males with a prison
record were more likely to receive a callback for an employment opportunity
 166
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

than Black males without a prison record. This study utilized equivalent
résumés, so the Black and white individuals could not be differentiated by
any features other than their socially defined race.
Once one enters prison, it is much harder to support a family and provide
for dependents. Thus, it also should not be surprising how much the children
of incarcerated parents suffer from poorer education and health. About ten
million children in the United States have a parent who has been incarcer-
ated. The chance of having an incarcerated parent is twice as high for His-
panic children and six times higher for Black children. This institutional
violence is largely hidden from us.
And who goes to prison? Poor people, whites, and especially Black and
brown people. Data for 1978–2014 from the Sentencing Project show that the
rate of incarceration is over five times greater for Blacks versus whites. As
shown in figure 8.2, Hispanics and especially Blacks are disproportionately
imprisoned. Of the total male prison population in 2018, 33 percent were
Black, 30 percent were white, and 23 percent were Hispanic.
Bryan Stevenson and Michelle Alexander write that imprisonment today
is nothing more than the continuation of Jim Crow and slavery. More Black
men are in prison now than were slaves in the 1850s! Of course, this is partly
due to the growth of the U.S. population, but that fact is still alarming. Today,
an astonishing one in three Black men will spend some time behind bars.
Such a rate of incarceration is facilitated by an increasing militarization of
the police and the differential patrolling of this force in Black and brown

White 64%

Black 33%
White 30%
Hispanic 23%
Hispanic 16%
Black 12%

Share of U.S. Share of U.S.

adult population prison population

FIGURE 8.2. Share of the U.S. adult population versus share of the U.S. prison population by race and His-
panic origin. Source: U.S. Bureau of the Census, Bureau of Justice Statistics.
 167
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

communities. It is a way to exert control. It is not about safety. It is not

about rehabilitation. It is about control. It is about racism.
When criminal (in)justice ends in prisons and jails, the consequences
continue in the lives of the former inmates, their families, and their com-
munities. That is why the criminal justice system is the clearest example of
institutional racism. But, as we shall soon discuss, it is not the only system.

WHY IS THERE A RACIAL DIFFERENCE IN EDUCATIONAL

ATTAINMENT?

First, there is a huge difference in level of education by race. Here, we are

talking not about quality of education but simply about final grade com-
pleted by age 25. As shown in figure 8.3 from from the National Center for
Education Statistics, between 2010 and 2016, 8 percent of whites do not have
a high school degree and 35 percent have a college degree. By comparison,

100
15 18 15
21
31 35 34
80 6 9
8
8 54
18
8 26
9 25 10
Percentage

60 25
21
21 28
7 25
40
12 33
31 35
27
20 27 15 22
33
15 13 13 17
13 8 9
0
Total White Black Hispanic Asian Pacific American Two or
Islander Indian/ more races
Alaska native
Race/ethnicity

Bachelor’s or higher degree Associate’s degree Some college, no degree

High school only Less than high school completion

FIGURE 8.3. Education by race/ethnicity. Overall (left column), 40 percent of those over age twenty-five
in the United States have no college experience, and 60 percent have some experience. Whites and Asians
are most likely to have high school experience (65 and 72 percent, respectively), whereas Blacks, Hispanics,
Pacific Islanders, and American Indians/Alaska Natives are more likely to have just a high school degree or
less education. Source: National Center for Education Statistics, https://nces.ed.gov/programs/raceindicators
/indicator_RFA.asp.
 168
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

nearly twice as many Blacks and American Indians and four times as many
Hispanics do not have a high school degree. Blacks are 50 percent more likely
to not have a college degree, and brown and American Indians are twice as
likely to not have a college degree.
The racial difference in education is due to a complex set of causes, all part
of the web of racism and socioeconomic inequalities. Clearly, educational
attainment is related to socioeconomic class. But it is also related to culture,
politics, and racism. Let’s break it down.

Education and Social Class

Public school systems are largely funded by local taxes, mainly from real
estate taxes, which are related to home value. Wealthier communities with
more expensive houses pay higher taxes, which they are able to afford (in part
because their houses increase in value, thus building wealth), and with these
extra funds they are able to spend more for better schools, more teachers,
and more educational resources. They can afford special education teach-
ers, teachers with advanced degrees and enthusiasm for their subjects and
students, and teachers with resources including books, computers, musical
instruments, and science labs. Their students have more opportunities to be
engaged with educational subjects in ways that are exciting, often individual-
ized, and hands-on.
On the other hand, students from poor communities go to underfunded
schools. We have already established that the poverty rate of Black, brown,
and American Indian families is much greater than that of white families.
The schools in these communities are under-resourced and under-stimu-
lated. School and learning are to be avoided rather than enjoyed. Schools are
not stimulating. Today, increasingly, as wealth varies, students with means
can afford better schools, whereas poorer families are left with less. Students
from wealthier families can attend special charter and private schools. If
higher education ever was an institution that allowed for social mobility, it
no longer does so.
Public schools in poorer communities typically have fewer resources.
This might be particularly true for schools on American Indian reservations.
Because white families are less likely to live in such places, poor white chil-
dren are less likely to attend these schools.
Alan’s daughter Ruby was fortunate to go to elementary school in Leverett,
a small rural community that is part of the Amherst, Massachusetts, school
 169
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

system. Amherst is a liberal town with many families associated with the Uni-
versity of Massachusetts (UMass), by far the largest employer. Leverett Elemen-
tary School was built for more than one hundred fifty students but currently
has only about one hundred, almost entirely white students. Opportunities
are abundant for learning and getting individualized attention. Similarly, Joe’s
children (Joey and Xavier) attended elementary school in an upscale neigh-
borhood in Glendale, Arizona. Most of the students’ parents held professional
jobs. An outstanding feature of the school was the fact that several college-
educated moms were available to provide in-classroom support to teachers.
Ruby was having trouble hearing and retaining instructions. One of her
teachers had an idea. Perhaps her issue was with central auditory process-
ing. The school district made plans for Ruby to be tested at a UMass labora-
tory. And, yes, that was the problem. Next, they had her work with a speech
pathologist and purchased an expensive computer program. Ruby’s auditory
processing improved dramatically. She was lucky. But her luck is also part of
an unequal system.
In addition, the double whammy of being poor and nonwhite results in
teachers’ having low expectations. One of the biggest myths of race (see chap-
ter 7) is that there is a racial (and class) difference in intelligence. Joe began
school in 1960 in an integrated school district in Westfield, New Jersey. At
that time, students were tracked into slow, intermediate, and advanced learn-
ing classes. Joe began kindergarten in a slow class (all the Black kids in the
school were assigned to this class). As a young child who was not challenged
by his work, he soon was identified as a discipline problem. The school orga-
nized a parent-teacher conference and recommended to his mother that Joe
be placed in a remedial class. “Remedial,” at the time, was a code word for
mental retardation or learning disability. Joe’s mother, who had been raised
in the Jim Crow South, would not allow it. Three years later, a student teacher
found Joe in the library reading The Crusades by Harold Lamb. Lamb’s
book was used in college-level history courses. The rest of the teachers had
assumed that Joe was pretending to read such books due to his inability to
read. However, this student teacher was bold enough to sit down next to him
and ask him about what he was reading. Joe then proceeded to explain the
main points of the book, his favorite events, and historical characters. The
next day, Joe was reassigned to the advanced classes, the only Black kid to be
so placed. The rest is history. Unfortunately, we have no idea how many other
Joes were never discovered. That is a loss for our society and an especially
painful loss for the undiscovered Joes.
 170
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

The Pseudoscience of Low Expectations

In 1967, Arthur Jensen began a long, widely read, and attention-grabbing

article in the Harvard Educational Review with this sentence: “Compensatory
education has been tried and it apparently has failed.” What Jensen meant
by compensatory education were efforts such as the Head Start program,
intended to provide resources for children of poorer families and communi-
ties. He cites Head Start’s own statistics showing that an initial gain in IQ
test scores of five to ten points in children from these programs tended to
diminish over time.
Was that a failure? We think not. First, a gain in five to ten IQ points for
just a little enrichment is astonishing. The failing is in considering that a little
educational enrichment for a short time could overcome a life of unequal
treatment—in home environments, diets, medical care, and educational
resources, among other areas.
Joe has personal experience of this. In the mid-1990s, he helped to direct
a National Science Foundation–funded project, the Phoenix Urban Systemic
Initiative. Its goal was to provide greater opportunities for racially subordi-
nated urban youth to enter the science career trajectory. In one of the poor-
est neighborhoods of the city, an elementary school with primarily Mexican
American enrollment was performing as well as or better than the other
schools in the district. Many of the children were from families headed by
a single mother. The secret to their success was that the school was located
in the shadow of Sky Harbor Airport and was receiving funding from taxes
paid by the airport. As a result, this school was abundantly provisioned with
teachers, supplies, and other resources. However, after these children left that
elementary school, they were funneled into middle and high schools without
that sort of support. Without great surprise, their test scores began to fall,
such that their scores were equivalent to those observed for other poor Mexi-
can Americans in the Phoenix School District.
Despite the glaring examples of “savage inequalities” in school funding,
it is convenient to blame unequal education and educational attainment on
genes and racial differences. Jensen’s article echoed prior pronouncements
going back to Samuel Morton’s study of cranial capacities and going forward to
Richard Herrnstein and Charles Murray’s The Bell Curve in 1994 and Nicholas
Wade’s ideas that societal successes are based on genes and race.
No, gaps in educational achievement have simple, systemic explana-
tions. Wealth is a determinant of educational achievement, and educational
 171
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

achievement leads to wealth. Low expectations, a part of systemic racism,

lead to low educational achievement. They are parts of a system that rein-
forces and reproduces itself throughout history.
As we were writing this chapter, then-President Trump was telling all who
would listen that the coronavirus will just go away soon. Just like that. Just
as we know that was a lie, it is misleading and incorrect to think that educa-
tional gaps by race and class are due to genes. We discussed the poor science
behind genetic and racial claims of intelligence and educational attainment
in chapter 7. In the case of both the COVID-19 pandemic and inequalities
in education, action to address them is sidelined. But the truth is that edu-
cational inequalities are fed by inequities in environments and expectations
that feed employment and income inequities, and all of these systems of
inequalities work together.

DOES PERCEIVED RACE AFFECT EMPLOYMENT OPPORTUNITIES?

Yes. There are two parts to consider, the immediate and the systemic. The
immediate is evidence that individuals with Black-sounding names are far
less likely to have their résumés taken seriously. This impact has been docu-
mented over and over again. For example, Bertrand and Mullainthan sent out
fictitious résumés in response to help wanted ads in Boston and Chicago.
They randomly gave the résumés, which were otherwise identical, African
American or white-sounding names: Lakisha and Jamal versus Emily and
Greg. White names received 60 percent more callbacks for interviews. The
gap is unaffected by occupation, employer size, and industry. It is universal.
Although it is studied a bit less often, the same is true of Latinx- and
Asian-sounding names. Common practice today, especially in the Asian
community, is to “whiten” résumés by adding white-sounding hobbies and
making subtle changes in names, for example, from Lee to Luke.
The longer-term, systemic aspect relates to the “old boys clubs” of cor-
porations. Class and gender can intersect with race. As a long-time fac-
ulty member, Alan can attest to the number of times an applicant has been
deemed comfortable and thought to “fit in” better. Joe lost a lot of faculty
appointment opportunities early in his career because he had the reputation
of being “too Black.” The applicants who make predominantly white faculty
members comfortable tend to be from the upper class, have come from elite
schools, and, most notably, are white. This injustice persists for science fac-
ulty, as discussed by Joe and Erich Jarvis.
 172
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

A good part of the reason that African Americans and Latinx are over-
represented in some types of employment is that they are steered away from
stable, well-paying, and high-status jobs. For decades, it was difficult for non-
whites to get a job in a union or a solid blue-collar job as a policeperson or
firefighter. Federal laws opened up these jobs, slowly. However, over the lat-
ter part of the twentieth century, the American labor force began to polarize,
with high-skilled occupations that require many years of education at one
end and low-skilled, precarious employment at the other. Due to inequities
in educational opportunity, Black and brown people have been differentially
regulated into the precarious workforce. This is also an example of a color-
blind racial inequity. On the surface, it appears as if this pattern results from
blind forces of the market, but in reality, it has been created by the structural
racism of the American educational system.

WHAT IS ENVIRONMENTAL RACISM?

Environmental racism refers to the differential exposure to pollution and

unsafe environments by race. Poor communities and communities of color
are most likely to be near polluted areas and exposed to chemicals, such
as lead, that might stunt development and cause health problems such as
asthma.
Like a lot of undergraduates, Joseph Jones was not sure what he wanted
to study at Howard University. The son of a minister with lots of enthusiasm
for ideas, Joseph had a whole host of intellectual interests. He loved history,
especially African American history, and philosophy, sociology, and the sci-
ences. He thrived at Howard, taking courses in a variety of departments but
without a singular direction. Then, one day, he took Introduction to Physical
Anthropology with Professor Michael Blakey. Blakey is a leading African
American anthropologist and perhaps the best-known African American
anthropologist working on race and slavery. Jones was invited to see if he
might like to work in Blakey’s lab, named after famous African American
scientist W. Montagu Cobb, looking at the bones of enslaved Africans from
lower Manhattan. Jones was hooked on the scientific study of bones to tell
something about the hidden history of enslaved Africans.
Years later, as a graduate student, Jones worked with Alan at the University
of Massachusetts. His main goal for his dissertation was to try to figure out
who was born into slavery in New York and the American colonies and who
might have grown up in Africa, became enslaved, made the middle passage,
and came to New York as an adolescent or adult. His novel method to answer
 173
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

this question was to assess the unique chemistry of growth rings in teeth that
calcified in early life. Different landscapes lead to different chemical signa-
tures in these tooth rings. For example, West Africa has a ratio of strontium
isotopes different from those of the eastern shores of North America.
Jones was able to find these signals and separate who had been born
enslaved from those who became enslaved after their birth in Africa. He
also found that the lead levels in the teeth of those born in Africa were low,
not at all surprising for individuals from the eighteenth century. And then
came the surprise: the lead levels of those born in the Americas were high,
even in their first years of life. It was often off the charts.
Now, three hundred years later, lead pollution is still getting into poor
bodies, and those poor bodies are often from poor communities of color.
Lead has long been known to be a neurotoxin. In any amount, it affects
neurological development. There is no safe amount. And the more lead, the
worse and more irreversible the effects. Despite early suspicions about the
toxicity of lead, from the 1920s to 1973, it was added to gasoline in the United
States (to prevent engine knocking) and to paints that went on houses, win-
dows, and almost everywhere else. Lead was not phased out of gasoline until
1986. In many of the houses painted with lead, coats of lead paint are still
chipping and peeling. Lead is now in soils. Lead also remains in water pipes,
such as in Flint, Michigan, and it continues to be found in the bones of preg-
nant women and released into their fetuses.
A recent study compared blood lead levels of young Black, white, and
Hispanic children based on a national sample from 1988–91, 1991–94, 1999–
2002, and 2010. In 1988–91, around 18 percent of Black, 7 percent of brown,
and 6 percent of white children ages one to five years were shown to have at
least 10 μg/dL (micrograms per deciliter) of lead in their blood, a criminally
toxic level. Black children were three times more likely to have high blood
lead levels than white children.
The overall levels have dropped from the time of that study, but in 2010,
young Black children were still 2.8 times as likely as non-Black children to
have elevated blood lead levels, after adjusting for other risk factors. The
source of the lead exposure could not be ascertained. However, it is likely to
not be a single source, possibly from the bones of mothers, soil, paint in old
buildings that have not had lead paint removed, and pipes such as in Flint
and other cities with unattended infrastructures. Lead pollution is silent, yet
it is a potent example of environmental racism.
There are a number of aspects and forms of environmental racism. In gen-
eral, poor communities of color are more crowded. Apartments and other
 174
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

types of housing might have less ventilation. Communities also might be

food “deserts,” places where it is difficult to find high-quality foods. These
places also might be where it is easier to buy liquor than a fresh apple. It is
easier to get a cheap taco, soft drink, or burger than a peach or tomato.
Poor communities are also safety deserts. Residents lack places to hang
out. These communities might even lack shade trees, which are taken for
granted in white communities. The trees provide protection from the sun
and cooling.
As industrialization has increased, factories have released pollutants into
the air, water, and soil. These factories are most often located near poor com-
munities. Environmental racism is racism because it is the result of a differ-
ence in power. Wealthy and white communities have the political power to
resist factories. They have a tax base of sufficient size that they do not need
industrialization.

IS THERE A RACIAL DIMENSION TO CLIMATE CHANGE?

Yes. A crisis, whatever it might be, is almost certainly going to be amplified in

poor and nonwhite communities. And climate change is bringing on crises.
Liberal whites and many others often think that ecology and the exis-
tential threat of climate crisis are not as important to Black and brown as
to white communities. The environmental movement, until very recently,
is led largely by liberal whites. And, indeed, poorer communities face other
threats that compete with threats to ecological conditions and global warm-
ing. However, poorer communities are also the most vulnerable to and will
be most impacted by climate change.
One need only to look back to Hurricane Katrina in August 2005. We
will not get deeply into how much Katrina was aggravated by global warm-
ing. The degree that one attributes anthropogenic climate change with caus-
ing the greater frequency and intensity of severe weather is inconsequential,
even though, at the time of this writing, two hurricane-force storms— Laura,
at category 4, and Marco—were bearing down on the Gulf Coast. We are
concerned here with the response and human costs of Hurricane Katrina to
the residents of New Orleans.
Katrina’s storm surge caused as many as fifty-three flood protection struc-
tures in and around New Orleans to fail. The result was that 80 percent of
the city was under water. The total damage was estimated at $125 billion. The
human toll in suffering and loss of life is harder to pin down.
 175
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

Quite simply, most New Orleans residents in wealthier, predominantly

white communities were able to safely escape and ultimately return quickly
to their pre-Katrina lives. On the other hand, residents of nearly the entire
lower Ninth Ward were stranded, many lost their homes, and many lost
loved ones. The problem is both where individuals live—the conditions
under which they live—and how federal and state agencies respond.
On the other end of the scale are wealthy (predominantly white) individ-
uals who choose to live in dangerous environments, such as the coastal scrub
of California. These locations have beautiful views of the Pacific Ocean. How-
ever, during the Santa Ana winds or lightning storms in the summer, these
ecosystems are susceptible to fires. At the time of this writing, wildfires have
burned 1.25 million acres in California. Few people recognize these natural
disasters as yet another example of white and class privilege. The decision to
expand housing into these dangerous ecosystems is driven not by any dire
need for new housing but, rather, the power of real estate developers and the
market for luxury homes. With the expansion of populations in this fragile
ecosystem, water resources are strained, leading to the increase in burnable
plant material. This continues to occur despite the well-established scientific
knowledge concerning the historic combustion of these ecosystems. The
cost of fighting these fires is not shouldered by the wealthy alone but also by
the tax dollars of the poor, who do not benefit in any way from the luxury
homes of the rich.
The disparity between the politically powerless victims of Katrina and the
politically powerful victims of California coastal wildfires is not unusual.
Globally, the most dangerous environments are usually occupied by the
poor. For example, in countries where poverty is associated with socially
defined race or caste, you find disproportionate numbers of these individu-
als living in low-lying communities that are most vulnerable to hurricanes,
rising tides, and infectious disease. Alternatively, wealth allows people the
opportunity to choose to live in beautiful but often dangerous ecosystems.
The capacity to do so is often subsidized at public expense, thus doubly vic-
timizing poor people.

WHY IS THERE A RACIAL DIFFERENCE IN FAMILY WEALTH?

Here’s the short answer: history. A history of racism and unequal treatment
now has consequences for the accumulated wealth of families of different
social races.
 176
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

The gap in wealth between white families and Black, brown, and Ameri-
can Indian families is huge and hugely significant. The example of how the
Five “Civilized Tribes” (chapter 5) were dispossessed of their farms and live-
stock and forced to take a hazardous journey into inhospitable lands west of
the Mississippi River demonstrates how wealth is influenced by a history of
subordination. Contrary to most people’s understanding, the federal govern-
ment has done far more to help white people gain wealth than it ever has for
nonwhites.
Wealth is the total amount of monetary assets one owns minus all that one
owes, or debt. Alan and Joe differ in social race but share class backgrounds.
Their current wealth includes the value of their homes (minus what they
owe in mortgages) and all of their other assets, such as retirement accounts
minus any other debts like car loans, credit card debt, and student loans.
Both of us are one generation out of the working class. This means that we
had debt (college loans) to cover. Alan paid his off when he became a full
professor. Joe has still not finished paying his loans. They cannot pass on an
inheritance in the same way that a person who is descended from the middle
class (professionals, doctors, lawyers) or upper class (business owners) can
pass on to their children.
By comparison, income or annual income is the amount of money one
gets in salaries, wages, investments, and the like. Income obviously can make
wealth, especially if one has income above what is needed to live, which
can be invested. As well, individuals in the top income brackets often earn
income not just from their jobs (employment income) but also from the
return on their investments. Money makes money.
Wealth is more important than income, because it is wealth that one can
use to invest in the future. Or wealth can be passed on, inherited.
Wealth is sort of like mortality, the end result of a process that likely
involves one or more diseases. Wealth is where we see the most glaring racial
disparities.
As we write, the average wealth of a Black or brown family is decreas-
ing. In 2016, white families had median wealth (that is, half had greater and
half had less) of $171,000, whereas Hispanic families had median wealth of
$20,700 and Black families had median wealth of $17,600, or about a dime
for every white dollar.
White families are more likely to own their homes, to have accumu-
lated wealth in homeownership through appreciation, and to own busi-
nesses, stocks, and retirement accounts. The wealth disparity has huge
 177
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

implications for how race is lived in America. It determines access to edu-

cation, comfortable and safe housing, and health care. This in turn deter-
mines how long a person will live. Indeed, the disparities we are currently
observing from COVID-19 infection and mortality are strongly correlated
with wealth.

CONCLUSIONS

There are only two ways to explain all of these racial differences in health,
incarceration, educational achievement, employment, and wealth. One can
explain that they are all due to genetic differences, or one can explain that
they are due to systemic inequalities. Throughout this book, we have shown
that the first explanation—genetic differences—lacks any support. None. Zip.
So, the only explanation is that the differences are due to systemic inequali-
ties. We hope that is sobering, clarifying, and ultimately liberating.
The truth is plain. We once had a written racial contract that has led to
differential access to resources by race for 400 years. African Americans who
came to the United States as enslaved persons starting in 1619 have had it
the worst. They were enslaved for almost two hundred fifty years and since
then have been subject to racist ideologies and systems, such as incarcera-
tion and voter suppression, that have kept them relegated to the lowest caste.
(Remember the calendar in chapter 5.) Those facts are clear in all the socio-
logical statistics that have been gathered by the nation’s finest scholars with
appointments at our finest universities.
American Indians were decimated by contact and colonization. They are
still recovering from the loss of lands and self-governance. Although the
people of these nations often are admired in white imaginations, they none-
theless continue to suffer, often far from the eyes and experiences of the
white majority.
Latinx groups have come to the United States at different times and from
different areas. But remember that for most Mexican Americans, the bor-
der crossed them, not the other way around. The war with Mexico was a
blatant act of manifest destiny fueled by southern slaveholders who wanted
to expand territory for their peculiar institution. Some Latinx have become
“honorary” whites, particularly those light-skinned individuals who immi-
grated from countries whose political systems our government disfavors. But
most suffer as brown people in brown communities, sometimes as much as
African Americans.
 178
D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

Asians also have come to America at different times and from different
areas. South Asians with darker complexions (e.g., from India) face racism
that is similar to that of African Americans. East Asians began arriving
in the United States in the nineteenth century (before many white Ameri-
cans). All faced racist immigration policies and the violation of their rights
to become citizens under laws favoring whites. Yet, they have been possibly
the most successful in keeping out of the direct line of racist fire. They have
achieved a decent level of education. But they are far from free of racism.
Witness the way that Trump insisted on calling COVID-19 the “Chinese flu.”
What is important to come away with is that racism is a system that inter-
sects different institutions. The exact way the intersection takes place differs
by time, place, and racial group. But it is always a system that perpetuates
racial inequalities.
 Chapter Nine

DNA AND ANCESTRY TESTING

Advances in genomic science have allowed us to conduct a finer examina-

tion of the human genome and its variations. We have already established
that geographically based genetic variation exists within the human species.
We have also shown why this variation is nonracial. Most variation occurs
within continents and smaller regions and populations rather than among
continents or social races. However, signatures of one’s geographical ances-
try have been found within our genomes. This might seem like a paradox,
but it is not. Ancestry is real. Biological races are not.
In this chapter, we explore why genetic ancestry and biological race
are not the same thing. We also examine the methods and claims of DNA
ancestry-testing companies. We conclude by putting into perspective the
results of ancient DNA research that shows how much humans mixed and
mated in the past. These results further clarify why there are not—and never
have been—biological races within anatomically modern humans.

WHAT IS ANCESTRY?

Ancestry refers to an individual’s history that connects them to past indi-

viduals, families, traditions, and places. Ancestry is a concept that is used
in popular discourse and by many cultures and religions to trace individual
and family connections. Many of us build family trees and now take DNA
 180
DNA AND ANCESTRY TESTING

“ancestry” tests to help us figure out one type of ancestry that can be traced
through genomes. We humans have a yearning to make these connections.
We find it useful to think about three types of ancestry: cultural, geo-
graphic, and genetic. Cultural ancestry refers to the linguistic, social, cultural,
and religious traditions that one follows and is connected to. These might
include dialects, ways of preparing food, residential patterns, and beliefs that
both connect us to the past and changes with the times. Culture does not sit
still. Cultures and components of cultures can fade, merge, and grow. Cul-
tures evolve and change.
Geographic ancestry refers to where one’s ancestors came from. This might
be known through family histories, as well as through written records such
as shipping information and archaeological evidence such as artifact sim-
ilarities. Recent advances in paleo-geochemistry have made it possible to
trace ancient migrations and the movements of individuals and groups by
matching the chemistry of early-forming bones and teeth to water and soil.
For example, in a study of enslaved individuals from the New York African
Burial Ground, Alan and his colleagues were able to determine which indi-
viduals were born and spent their infancies in the Americas and those who
were born in Africa and the Caribbean.
What these studies cannot tell is where one’s ancestors grew up. This
information can come from family histories and sometimes written sources.
Alan’s grandparents came to the United States sometime in the early 1900s
from somewhere in Russia or Poland, escaping pogroms and anti-Semitism.
His family history pretty much stops with his parents. That’s probably not
unusual. Geographic ancestry is complicated, because we humans tend to
move around and often do not think to pass the information down the
generations.
We most often think of the third type, genetic ancestry. Genetic ancestry is
written in DNA and passed through both maternal and paternal lines. Getting
information about one’s genetic ancestry, currently referred to as finding one’s
ancestry or roots, has become extremely popular with the advent of inexpen-
sive sequencing technologies. For example, African Americans can now get
information about the group in Africa from which they might have come.
Finally, it is important, when thinking about these types of ancestries, to
recognize that they might or might not be related. Geographic, cultural, and
genetic ancestries are often confused with one another. In the earlier exam-
ple, individuals born in what today is Ghana and enslaved as adolescents
in the eighteenth century spent their adult lives as slaves in America. Their
 181
DNA AND ANCESTRY TESTING

geographic and cultural ancestries shifted, but their genetic ancestries did
not. Similarly, individuals fleeing poverty in Ireland or China in the nine-
teenth century came to Boston or San Francisco, and their genetic ances-
tries tie them to their natal homes. Their bones and teeth also have telltale
signs of their natal homes, but their culture slowly shifted to Irish American
and Chinese American. A child adopted from Korea by European American
parents grows up in their parent’s Euro-American culture, but that child is
genetically and geographically connected to East Asians.

IF RACE ISN’T GENETIC, HOW COME MY DNA TEST RESULTS

ARE TELLING ME MY ANCESTRY?

As of February 11, 2019, more than twenty-six million people had taken a
direct-to-consumer (DTC) genetic ancestry test. As we write, at least thirty-
eight companies offer such tests. Many of these companies employ the con-
cept of continental ancestry in reporting ancestry results to their customers.
This concept assumes the existence of a small number (typically four or five)
of ancient parental populations that gave rise to our current populations. It
is frequently equated with race in the biological sense. On the other hand,
biogeographic ancestry is the association of a person’s origin with the geo-
graphic location(s) of presumed ancestors. This is inferred by comparing the
relative similarities of an individual’s genetic markers with those found in
contemporary populations.
To understand how one can make this inference, it is important to under-
stand the nature of the genetic markers being used. We have already pointed
out that only about 1.5 percent of the human genome is composed of protein-
coding sequences. It has been estimated that the total amount of human
DNA that is exposed to natural selection is less than 10 percent. This means
that variation in the remaining DNA is effectively neutral. Thus, that portion
of DNA can accumulate mutations, and the specific mutations will be associ-
ated with the population in which they first appeared. Of the polymorphic
genetic variation within humans, 85–95 percent is found in all world popula-
tions. That leaves variation that is associated with continental origin at about
10 percent on the high end and 5 percent on the low end. This means that the
variation within subregions of continents is less than 5 percent.
Polymorphism refers to those portions of the genome that can have alter-
native alleles without causing a major loss in evolutionary fitness. Most loci
within our genomes (~67 percent) are monomorphic. This means that a SNP
 182
DNA AND ANCESTRY TESTING

in this position would likely result in death or sterility. Given that the human
genome contains about 3.3 billion nucleotides, and that all humans share
99.9 percent of their DNA, the 0.1 percent that is differentiated provides at
most 4-5 million genetic markers that could be differentiated by continent
and region.
However, for a marker to be useful, its frequency must be strongly differ-
entiated between regions in question, so the amount used by specific DTC
DNA companies is less than this amount. For example, the 2015 Bryc et al.
study, which examined continental ancestry in Americans, used around
2,020,000 SNPs. The same panel of genetic markers was used in the Miche-
letti et al. 2020 study examining the distribution of genetic ancestry in per-
sons of African descent now living in the Western Hemisphere.

HOW IS ANCESTRY DETERMINED BY DNA? ARE GENETIC

ANCESTRY AND RACE THE SAME THING?

Ancestry typically represents a generational narrative about one’s relatives

through their maternal, paternal, or both lines of descent. Sexual organisms
such as ourselves display biparental inheritance. Our offspring are composed
of diploid (2N) genomes whereby one copy (1N) of the genetic code origi-
nates from each parent. This means that in each generation, an individual
has two ancestors. Going backwards through generations, this amounts to
a maximum of 2N ancestors, where N is the number of generations in the
past (two parents, four grandparents, eight great-grandparents, and so on).
Therefore, about half of your genome came from each parent, a quarter from
each grandparent, and one eighth from each great-grandparent. The logic
of this process means that all modern humans are related going back to the
first humans who lived in sub-Saharan Africa 200,000 to 300,000 years ago.
Because our species began as hunter/gatherers, population growth was
very low until the advent of agriculture and the Industrial Revolution. Esti-
mates of world population in 1500 range from 425 to 540 million. Consider
this in comparison with our current population level, which exceeds 7.8 bil-
lion people! Approximately ten human generations have passed since the
year 1700. This means that you have had about 210 = 1,024 ancestors, assum-
ing no inbreeding in your lineage. However, because everyone’s genealogy
contains marriages between cousins, your actual number of ancestors is con-
siderably less than that.
 183
DNA AND ANCESTRY TESTING

Mitochondrial DNA (mtDNA) is a genetic marker that children inherit

from their mother. The Y chromosome SNP haplotypes are passed from
father to son. These tracing methods allow direct comparison of the lineages
of sampled and referenced individuals. For mtDNA, the genetic markers
are from the D-loop region of the molecule. This method has been used in
forensics (more on this later in the chapter).
For example, mtDNA was used to identify the son of deposed French
monarchs Marie Antoinette and Louis XVI. The boy supposedly died in
prison at age ten. In 1845, he was given a royal burial, but some suspected
that an imposter was buried instead. His desiccated heart was preserved by
the royal family. In 2001, researchers utilized heart and hair follicle tissue
from the bodies of Marie Antionette, two of her sisters, and the still living
queen of Romania (a descendant of Marie Antionette) to determine that the
body was really that of her son.
Another historical debate was resolved using Y chromosome sequences.
This was the long-standing claim concerning whether President Thomas Jef-
ferson fathered the children of Sally Hemings, one of his slaves. Annette
Gordan Reed recounted this saga in 1998. A genomic study showed that
Jefferson’s Y chromosome matched Sally’s last son, Eston Hemings, but did
not match the Y sequence of Thomas Woodson, Sally’s first son. This result
is interesting in that Sally became pregnant with Thomas while she was Jef-
ferson’s servant in France. Given that France had outlawed slavery, Sally was
a free woman in that country and could not be compelled to return to slavery
in Virginia. Gordan Reed recounts that to get Sally to return to America,
Jefferson agreed to free all of her children. This indicates that Jefferson must
have thought that he was the father of this child.
The DNA results show only that someone carrying a “Jefferson” Y chro-
mosome fathered Sally Hemings’s last son, but it could have been another
male in the Jefferson family. This case also underscores the difference
between socially defined race and genetic ancestry. Hemings was a half-sister
of Thomas Jefferson’s first wife. She was fathered by Jefferson’s father-in-law
and born to one of the enslaved women on his plantation. This woman also
had at least half European ancestry, so Sally had three quarters European
and one quarter African ancestry; yet by Virginia law she was still a slave. All
of her children were fathered by men of European descent and thus would
have been seven-eighths European and one-eighth African. Her daughter,
Harriet, was also most likely fathered by Thomas Jefferson.
 184
DNA AND ANCESTRY TESTING

Harriet was eventually allowed to leave Monticello in 1822 at age twenty-

one and moved to Philadelphia. She married a man of European descent.
Harriet must have passed as white, as no one knew her mother was enslaved
on the Jefferson plantation. Her children were therefore fifteen-sixteenths
European and one-sixteenth African. If anyone had known of the ancestry of
Harriet and her children, their legal racial status would have differed by their
state of residence. Some states would have declared them white, but in Loui-
siana (with its one thirty-second rule), they would have been declared Black.
Finally, is modern genomic technology, which enables us to learn about
an individual’s ancestry, just another way of classifying humans into biologi-
cal races? How can a DNA ancestry company say what percentage of your
DNA is from each continent? Isn’t that race? No, it is not. That is geographic
variation divided into continents. It is not biological race.
The method used by DNA ancestry companies takes advantage of the
distribution of genetic variations within and between groups and continents,
as well as whether human groups can be considered unique lineages (due to
lack of gene flow). The ability to look at millions of SNPs has not changed
our conclusions that humans do not divide into biological races. If anything,
whole-genome studies confirm that modern humans do not contain biological
races. For example, sequencing studies have shown that the Khoisan hunter-
gatherers are different from sub-Saharan Africans to a greater extent than
the latter group is from Europeans and East Africans, and the Maasai people
are more similar to Europeans than they are to the Khoisan. Within Africa,
the Sandawe are closer to Europeans than they are to the Hadza. This shows
that genomic data disagree with older physical race classification schemes,
as several groups with African physical features (Khoisan, Sandawe, Hadza,
and East Africans in general) do not group together by ancestry.

ARE SOME ANCESTRY-TESTING SERVICES BETTER THAN

OTHERS?

This is hard to answer, because the genetic markers and algorithms used by
these companies are proprietary. This means that not all of the DNA pan-
els that these companies use to infer ancestry are open to scientific peer
review. Therefore, we can only describe attributes of testing methods that
would make them better estimates of “real” ancestry and in which popula-
tions ancestry testing should work best. Clearly, the more genetic markers
used, the more repeatable the estimates of ancestry will be. (For example,
 185
DNA AND ANCESTRY TESTING

in the studies cited earlier, 23andMe used more than two million markers.)
The markers should also be well dispersed across the twenty-three pairs of
human chromosomes. In this way, the SNPs mark more segments of each
chromosome that are inherited together.
Also, it is important to know something about the populations being
tested and their demographic history. In theory, the methods should work
best for populations that have been relatively stable in size (no recent major
reductions) and that have experienced little migration/emigration recently
(which would introduce new markers or reduce the frequency of older
markers). Unfortunately, human groups tend to change in size and to move
and mix. So, the assumption of stability on which ancestry testing is based
are shaky in some groups.
With these caveats in mind, certain socially defined groups are more
likely to get more accurate DNA ancestry test results than others. Individu-
als whose ancestry is from large European groups (such as English, French,
German, and Italian) and East Asian (Han Chinese, Japanese) that have seen
little population reduction or gene flow should get results that are more
accurate than persons with substantial western African ancestry. (The reason
is that west African societies were disrupted by wars, and large numbers of
individuals were removed by the transatlantic slave trade.)
This effect would differ by the specific western and central African group in
question. During the transatlantic slave trade, growth in the total population
of this region stagnated. In other words, the birth rate equaled the death
rate, for an intrinsic rate of increase (symbolized as r) that would have been
zero or negative. However, the births and deaths in this region were not
equally distributed, so some groups might have seen serious reduction of
their numbers, with the resulting allele frequencies determined by genetic
drift (random chance). Indeed, this is highly likely to have been true for
the Amerindian populations of North America and the Caribbean (whose
populations were drastically reduced by colonialism, war, and epidemics; see
chapter 5). Ironically, African Americans or American Indians taking DNA
ancestry tests are likely to get a more accurate assessment of their European
ancestry that their western or central African or Amerindian ancestry.
Data on the within-company reliability of DNA ancestry testing indicate
that applying the same set of genetic markers to an individual almost always
produces similar results. That is because the same algorithm is used on the
same data. A recent study examined the reliability of DNA-testing results
of identical twins who were tested by the same company. Identical twins
 186
DNA AND ANCESTRY TESTING

have identical genomes (although they might differ by small amounts due to
somatic mutations accrued over their lifetime). The study examined results
from 23andMe, Ancestry, and MyHeritage and showed that within-company
tests had from 94.2 to 99.2 percent agreement between the identical twins.
However, when the twins were tested by different companies, the agree-
ment among the estimates resulting from the different companies fell to only
52.7–84.1 percent. This decline in replicability is due to the use of differ-
ent data sets and algorithms. In addition, the three companies characterize
ethnicity differently. For example, to describe ancestry from the British Isles:
Ancestry used Ireland/Scotland and England/Wales as categories; MyHer-
itage used Irish, Scottish, Welsh, and English; and 23andMe used British and
Irish. For West African ancestry, Ancestry had no panel, MyHeritage used
Nigerian, and 23andMe used Nigerian, Coastal West African, Senegambian,
and Guinean categories. In the latter case, the 23andMe categories are clearly
more accurate than those of MyHeritage and Ancestry for western African
ancestry.
Finally, a counterintuitive result of genetic ancestry testing is how it has
undermined claims of racial identity by individuals whose racial identity was
central to their worldview. Very early in the history of these DTC companies,
Afrocentric individuals received results showing that their DNA indicated
substantial European ancestry. We know that the flow of genetic information
between Africans and Europeans in the Western Hemisphere was mainly
unidirectional due to laws that defined racial status. One study found that the
European genetic contributions were highest in African Americans for the
Y chromosome (28.46 percent), followed by the autosomes (19.99 percent),
then the X chromosome (12.11 percent) and mtDNA (8.51 percent). This
means that European males were far more likely to impregnate women of
African descent (such as in the story of Thomas Jefferson and Sally Hemings)
than vice versa. A 2015 23andMe study of socially defined European Ameri-
cans found only 0.19 percent genome-wide recent African ancestry.
The ubiquitous TV ads for genetic ancestry testing all sell these tests as
somehow revealing some true (genetic) self. One of the most historically
inaccurate TV ads was run by Ancestry.com in early 2019. The spot revolves
around a fictionalized man of European descent imploring a woman of
African descent to escape with him from slavery. The reason he wants the
woman to go with him is because she is carrying his child. Although it is
entirely possible that some men of European descent had consensual love
affairs with women of African descent during the time of chattel slavery,
 187
DNA AND ANCESTRY TESTING

historical records clearly demonstrate that the vast majority of these preg-
nancies resulted from the rape of enslaved women. After a massive public
uproar, the advertisement was removed on April 15, 2019.
The fact that some persons of African descent managed to pass as white
played out in the story of Davis Knight, the grandson of Newton Knight.
Newton, played by Matthew McConaughey, was the main character in the
2016 film, Free State of Jones. Mississippi charged Davis with miscegenation
due to his alleged one-eighth African ancestry when he married a white
woman, Junie Lee Spradley, in 1946. Newton’s second wife was reputed to be
a Negro, and the state claimed that Davis was descended from this woman
(Rachel Knight), not Newton’s first wife. Davis challenged both the state mis-
cegenation law and his racial status. He and his wife eventually left the state
after Mississippi dropped the charges against him in return for his agreement
to stop challenging the miscegenation law.
Probably the most ironic case of DTC testing resulted when the DTC
ancestry results of Craig Cobb, a white supremacist, were revealed on televi-
sion. They showed that he had 14 percent African ancestry, an amount con-
sistent with having one great-grandparent with 100 percent African ancestry.
Of course, Cobb denied the validity of the results and eventually recast them
in an attempt to rescue his white identity.

HOW IS ANCIENT DNA (DNA OBTAINED FROM

ARCHAEOLOGICAL AND FOSSIL MATERIALS) CHANGING OUR
UNDERSTANDING OF HUMAN EVOLUTION?

Recent developments in technology are now allowing scientists to extract

and analyze DNA, including ancient DNA (aDNA), from humans and for-
merly living organisms. The genetic material has now been extracted from
relatively recently deceased individuals, such as historical figures, as well as
from fossils that are tens of thousands of years old. Once an organism dies,
its DNA begins to break down. For this reason, the fossilization conditions
that allow adequate amounts of genetic material to be preserved are rare.
In addition, there is frequent contamination of the sample with DNA that
originated from outside the sample. A bone lying in the soil accumulates
DNA from various microbes as well as from any individuals who might have
handled the fossil in the recovery process.
However, in the last decade, researchers have substantially improved
both experimental and computational methods that correct for the effect
 188
DNA AND ANCESTRY TESTING

of contamination on these ancient samples. The process includes extracting

the sample’s DNA under strict clean-room conditions, using UV radiation
to degrade microbial DNA, bleaching all surfaces where the extraction takes
place, and using filtered air systems. In addition, computational methods are
used that allow researchers to identify the degradation associated with the
ends of ancient DNA that is not found in modern DNA.
Over the last few decades, researchers have recognized that we cannot
understand past human migration by studying only the genomes of the
people who are alive today. People move! The ancient DNA revolution has
recently allowed geneticists and anthropologists to test models of ancient
human migration in ways not possible a few decades ago. The new data show
that human migration in the ancient world was complex, just as it is in the
modern world. Some researchers suggest that modern human populations
are the result of the admixture (interbreeding) of highly differentiated exist-
ing populations. They further claim that these population admixture events
occurred repeatedly in the evolutionary history of our species.
This view of ancient human migration is more complex than the serial
founder effect model. In the latter model, small populations leave large
populations to found new populations, which are dispersed from the ances-
tral population (see fig. 9.1). When modern humans began to migrate from
Africa, our species’ population size was estimated to be between fifty and
one hundred thousand individuals. This migration was possible because
of changing weather patterns near the end of the Pleistocene era. Glacial ice
sheets began to recede, allowing subgroups of modern humans to exit Africa.
For example, one can imagine the populating of the Australian continent as
beginning in East Africa around 50,000–60,000 years ago and progressing
through the founding of subsequent populations in the Arabian peninsula,
Indian subcontinent, Indochina, the islands of New Guinea, and, finally, to
the Australian mainland. In the original model of human expansion, hybrid-
ization with other human species was not thought to play a major role.
On the other hand, in the more complex admixture model of the popu-
lating of the Australian continent by modern humans, hybridization with
other human species plays a prominent role. Ancient DNA reveals that the
individuals who founded the ancient Australian populations had genomic
elements from anatomically modern humans: Neanderthals, Siberian Den-
isovans, and a group dubbed Australo-Denisovans. These were Denisovan
humans who lived southeast of Huxley’s line, a demarcation between animals
undergoing adaptation in mainland Asia and those undergoing adaptation
 189
DNA AND ANCESTRY TESTING

A1, A2, A3, A4, A5, A1, A7,

A6, A7, A8 A8, A4

Second founder population loses

A2, A3, and A6 by chance alone. A1,
A1, A2,
A4
A3,
Original large population contains A4, A6, Third founder population loses
8 alleles at a given locus. A7, A8 A7 and A8 by chance alone.

First founder population loses

A5 allele by chance alone.

A4

Final population lost A1 through founder event,

grows to large size but only contains the A4 allele.

FIGURE 9.1. Potential population genetic effects of the serial founder effect. The initial large population
contains eight alleles. Alleles are lost as each smaller population migrates to new territory, ending with only
one allele (A4) remaining at the end of the migratory journey. As a result, the genetic diversity of each serial
founded population declines with distance from the original large population. (The founder population would
have thirty-six possible genotypes, whereas the final population would have only one genotype, A4A4.)

in the transitional ecological zones from Asia to Australia. These different

hominid species were separated by hundreds of thousands of years of evo-
lution, a much greater time span than the separation between San hunter-
gatherers and the rest of modern humans (about 70,000 years).
Thus, during the migration of our species around the world about 100,000
years ago, different groups encountered and mated with other groups, archaic
human species, as they traveled. The decrease in the percentage of archaic
DNA that originated from these species in modern humans results from the
fact that these other species went extinct. Therefore, mating with them ceased.
By genetic recombination, each generation would have the amount of archaic
DNA reduced by 50 percent. Thus, in the genome of modern East Asians,
Denisovan DNA is about 0.2 percent and in South Asians, 0.3–0.6 percent.
Some of the genes that were acquired by hybridization with other spe-
cies were beneficial. There is evidence that in Tibetans, the genomic vari-
ant associated with high-altitude adaptation is more closely aligned with
ancient Denisovan DNA than it is with the modern human sequence of that
 190
DNA AND ANCESTRY TESTING

gene. Movement of genes between species resulting from hybridization is

well known. Generally, in the case of “true” species, hybrid individuals have
lower evolutionary fitness compared with their parental species. An extreme
case of this is the mule, the offspring of a horse and a donkey. Most mules
are sterile.
However, in many closely related species, the hybrids are only slightly
less viable than the parental species, as in the case of the fruit fly species
Drosophila melanogaster and Drosophila simulans. If a D. melanogaster/simu-
lans hybrid mates with either a D. melanogaster or a D. simulans individual,
genes that originated from one of the species can move into the other. If the
new gene is beneficial compared with the ancestral one, natural selection
will increase its frequency within the species that acquired the new gene.
An example of this has been shown recently with killifish. Adaptive toxicant
resistance rapidly evolved in Gulf killifish (Fundulus grandis) that live in pol-
luted habitats. There is a clear relationship between the amount of resistance
in the fish populations and the pollution level they experience. Two loci with
the strongest signatures of recent selection encode genes that provide resis-
tance to the specific toxin the fish experience, and the resistant alleles moved
between the species recently (eighteen to thirty-four generations ago) from
the Atlantic killifish (F. heteroclitus).
Adaptive introgression would account for the high frequencies of genes
that originated from Denisovans or Neanderthals in some modern human
populations. Of course, it must also be understood that parallel or conver-
gent evolution could have easily produced the high-altitude genetic adapta-
tion displayed in Tibetans. In that case, it is likely that the Tibetan variant
originated in Denisovans.
This was not true of the Andean and Ethiopian high-altitude variants
of this gene, which originated in modern humans. Indeed, to give you a
sense of the power of convergent evolution, the cold temperature adapta-
tions observed in ancient Neanderthals are also found in mastodons!
Mastodons are extinct members of the same order as modern elephants
(Proboscidea). Both species originated in tropical conditions, and some of
their subpopulations migrated to colder climates. As the temperature regula-
tion mechanisms of mammals are deeply conserved, both Neanderthals and
mastodons would have begun their adaptation to colder climates utilizing
similar genetic mechanisms.
By the beginning of the twentieth century, naturalists had come to under-
stand that all species were composed of populations (groups of organisms
 191
DNA AND ANCESTRY TESTING

inhabiting specific space and time) that exhibited a continuity of interbreed-

ing across their range. Modern humans are somewhat unique among land
mammals, in that our range extends over most of the planet. The only place
that does not feature indigenous human beings is Antarctica.
There is general agreement that our species originated in sub-Saharan
Africa. Therefore, what is at issue now is our exact understanding of how
modern humans expanded across the planet. The current consensus is that
modern humans (Homo sapiens sapiens) originated in eastern, central, or
southern Africa around 300,000 years ago. The first fossil evidence of mod-
ern humans found outside Africa dates from 100,000 years ago in the Mid-
dle East and 80,000 years ago in southern China. There are several ideas
about how and when modern humans left sub-Saharan Africa, with esti-
mates ranging from 50,000 to 100,000 years ago. Some debate about whether
there were multiple waves of migration, as well as by which route the migra-
tion occurred (northern or southern). It is also clear that during these
migrations, modern humans hybridized with various species of archaic
humans in Africa, Europe, and Asia.
Modern humans arrived in Europe around 43,000 years ago, but most
likely these first Europeans did not contribute much to the people who cur-
rently live in Europe, whose ancestors arrived around 7,000–10,000 years
ago. The first Europeans were primarily hunter-gatherers, and these pop-
ulations were replaced by humans who had developed farming. A third
wave of migration into Europe occurred about 4,500 years ago (Early Bronze
Age). These migrants were descendants of hunter-gatherers who originated
in what today is modern Russia and the Caucasus mountains.
Asia was populated by at least two early waves of migration: first by ances-
tors of Australians and the Papuans, followed by other ancestors of East
Asians with modern populations resulting from admixture between all the
individuals and groups that were parts of these two waves of migration.
However, many details about migration into Asia are yet to be resolved. These
details may emerge with further studies of aDNA. At present, the archaeo-
logical data place modern humans in Oceania 47,500–55,000 years ago. The
extensive genomic study of Papuan and aboriginal Australians suggests that
genetic divergence between these groups might have been driven by climate
changes and that the aboriginal Australians were living in a relatively high
level of isolation until modern times.
Finally, the earliest arrival of modern humans in the Western Hemisphere
is accepted to be about 14,000–15,000 years ago. The widespread occupation
 192
DNA AND ANCESTRY TESTING

of that region is associated with the Clovis culture (12,600–13,000 years ago).
It is likely that the genomic divergence of Siberians and the Amerindian
populations began around 23,000 years ago. This suggests that Amerindi-
ans moved into the Western Hemisphere earlier than the dating of archaeo-
logical remains indicates; however, by what means and route this occurred is
still the source of considerable controversy. The earliest archaeological sites
could be buried under ice or in the Pacific Ocean (because the ancient shore-
line has changed) or simply not found and accepted by the archaeological
community.
The migratory paths of humans around the world led to divergences in
their gene frequencies, primarily driven by genetic drift. In addition to
drift, great distances between populations reduced the amount of gene flow.
Also, as humans migrated away from sub-Saharan Africa, new environmen-
tal conditions, including extreme cold, altered exposure to sunlight intensity,
and new pathogens were experienced. This also occurred as humans moved
around sub-Saharan Africa.
As noted in chapter 2, Africa is the second-largest continent, covering
more latitude than all other landmasses (about 37o N to 35o S) with highly
diverse vegetation zones. However, at the end of the Pleistocene, the Sahara
was reduced in size. As we previously noted, human populations that
migrated within Africa faced new environmental conditions and habitat
diversity, and this partly explains why sub-Saharan Africans display greater
genetic diversity than all other populations. Also, throughout human migra-
tion, cultural evolution introduced new methods of hunting, along with plant
and animal domestication, creating changes in diet. That process leads to
the genetic structure within the human species that we see today. However,
modern human populations are not just the result of ancient migrations.
Events such as the expansions by the Bantu and Mongol Empires and the
transatlantic slave trade have altered populations in the last thousand years
or so. These events altered the genetic structure within our species, as they
increased the gene flow between populations located in different regions of
the world.
In summary, ancient DNA has provided us with a new perspective on
how human populations expanded and merged around the world. On the
global scale, the best way to understand human genetic variation is to recog-
nize that it was driven by genetic drift resulting from serial founder events.
Interspersed with genetic drift was adaptation to new local conditions.
Because ancient migration was not unidirectional, gene flow among human
 193
DNA AND ANCESTRY TESTING

populations maintained genetic uniformity, such that our species never

formed biological races. Finally, the coming of technological and cultural
innovations in the modern age accelerated gene flow among global regions,
further reducing the possibility that biological races would ever form in
modern humans.

HOW CAN MORPHOLOGY AND DNA BE USED IN FORENSICS?

One of the main goals of forensic science is to identify individuals who are
either victims of crime or perpetrators. Typical FBI forms for filing victim
reports include questions about estimated age, sex, height, and “race” of the
perpetrator. In cases in which only bones and teeth are present, a foren-
sic anthropologist is typically called in to make all of these determinations.
Standard methods are available to estimate height (based on long-bone
lengths), sex (based on features such as the size and shape of the pelvis), and
age (determined from multiple signs of aging in teeth and bones). But what
about race?
Forensic anthropologists have made a number of suggestions that race
can be determined from skeletal remains. These include the size and shape
of the cranium, harking back to old studies of cranial shape and intelligence.
What we call racial anthropology is an anthropology that maintains the
fiction of biological races and is obsessed with determining differences
among biological races. Many forensic anthropologists are still heavily into
racial anthropology. They might argue that this is because forms from the
FBI ask them to fill in a victim’s race. The problem is, of course, that race is
a biological fiction. And it is reinforced by the fact that as much as forensic
anthropologists attempt to reliably determine race from bones and teeth,
they continue to fail to do so.
A good example of this failure revolves around the use of discriminant
functions of skull shape as a way to distinguish sex and race. The gold stan-
dard method was developed by Giles and Elliot and published in 1962.
These two, then anthropology graduate students at Harvard, determined that
a set of measurements could distinguish males from females. Then another
set of measurements could distinguish among three races: Black, white, and
American Indian. They were able to do so with almost 90 percent accurate
“racial classification” in their original study. So far so good.
The problem comes in efforts to apply their method to different locations
and samples. Alan studied this problem and located four restudies. He found
 194
DNA AND ANCESTRY TESTING

that on average, the American Indians were correctly classified in the four
restudies about one third of the time and misclassified as white or Black the
remaining two thirds of the time. Given that random classification would
return about the same results, the method is no better than chance when it
comes to determining “race.” It’s not even good enough for government work.
Why were retest results so bad? These data point to a couple of problems
of racial anthropology. First, these are efforts to biologize a social category of
race. They assume that there is a good fit between the two, but there is not.
Second, the studies assume that race is universal and the same in all times and
places. But that’s not true. Indeed, a Black or white person in St. Louis and
Cleveland in the twentieth century is different socially and genetically from
a Black and white individual elsewhere at other times. Color lines change.
More recently, DNA evidence has begun to supplant phenotypes such as
skull shape in efforts to determine the identities of victims of crime and
especially the perpetrators. Previously, efforts were made to study any sort of
information that might have been left behind by a possible perpetrator; for
example, footprints or fingerprints. DNA has been shown to be more precise
in making these determinations. For example, if a 100 base pair segment of
noncoding DNA is used, the possible number of sequences is 4100, or about
1.6 × 1060 possibilities! This is greater than the number of stars in the known
universe. To identify some of the victims of the World Trade Center bomb-
ing, Myriad Genetics utilized thirteen short tandem repeat (STR) loci. Short
tandem repeats are segments of DNA (2–7) base pairs long. The chance
that any two individuals share the same thirteen STR genotypes is 1 in 250
trillion (2.5 × 1014). This means that no two people on Earth (other than
identical twins) can share the same set of thirteen STR markers.
Now, with millions of individuals in DNA databases, we have approached
a time when DNA left at a crime scene, perhaps from a single hair, can be
sequenced and matched. The matching need not be to the individual; it
could even be to a potential cousin or more distant relative. This is precisely
how the Golden State Killer was identified. Conversely, the lack of a match
between the DNA of someone previously incarcerated with the genetic evi-
dence found at the crime scene is leading to overturning previous convic-
tions, most often of Black men.
However, there is a dark side to DNA databases. Specifically, many states
retain DNA profiles of people who were accused of a crime but never con-
victed. In the United States, you are presumed innocent until proven guilty.
Unfortunately, disproportionate numbers of racially subordinated people
 195
DNA AND ANCESTRY TESTING

(African Americans, Latinos) are arrested. As a result, the genetic informa-

tion of these innocent individuals and, by extension, their families remains
in DNA databases.
In 2008, the European Court of Human Rights ruled that the indefinite
retention of the DNA of convicted and innocent persons was disproportion-
ate. However, to get around this ruling, in 2012, England and Wales passed
the Protection of Freedom Act, which allows the indefinite retention of the
DNA of convicted persons and the temporal retention of DNA of first-time
convicted minors and innocent individuals in the country’s database.
Recent events in China are even more disturbing. There the government
is collecting DNA from men and boys across the country to build a data-
base targeting ethnic minorities and other groups. This database will allow
the tracking of individuals (and their families) from any of their biological
material. This is being accomplished with the help of American biotechnol-
ogy company ThermoFisher. What should be clear is that this recent use of
DNA in forensics has little to do with race. However, DNA databases are cur-
rently being deployed in racist ways. Their use is consistent with the existing
patterns of social dominance in various nations, resulting in intensifying the
disparity in social justice in these societies.

CONCLUSIONS

In this chapter, we have tried to answer questions about what ancestry is and
have presented three types: cultural, geographic, and genetic. Just as social
race does not always map onto biological ideas about human variation, so,
too, cultural, geographic, and genetic ancestries do not always map onto one
another.
Recreational genomics, and specifically genetic ancestry testing, is now
a large and expanding industry. We explained how genetic ancestry might
be determined and especially why being able to do so has nothing to do
with biological race. Rather, these tests take advantage of the fact that there
is geographic and population-level variation in genomes. The key problem
is that the ancestry companies often give a false sense of precision, and the
results are interpreted in racial terms. This shouldn’t be a surprise, given that
biological race remains such a dominant worldview. That’s why it is impor-
tant to be clear that ancestry and biological race are very different constructs.
Studies of past individuals, directly through bones and teeth and their
archeological remains and now through their ancient DNA (aDNA), provide
 196
DNA AND ANCESTRY TESTING

a clearer view of human history. Perhaps the biggest lesson we are learning is
that humans always moved and merged. Thus, what might be called English
at one time might look very different physically from English today or at any
other time. Moreover, there is no reason to continue to think that social defi-
nitions of race neatly map onto the mythic idea of biological races. Finally,
as W. E. B. DuBois said well over a century ago, the problem of the twentieth
century is the problem of the color line. Indeed, the color line is still shifting
and continues to be a problem well into the twenty-first century.
 Chapter Ten

RACE NAMES AND “RACE MIXING”

Some years ago, psychologist Jefferson Fish brought his daughter and her
Brazilian boyfriend to his class at St. John’s University in New York. Profes-
sor Fish had often accompanied his wife, anthropologist Dolores Newton,
to Brazil, where she did her fieldwork. Fish noticed that his wife, an African
American, seemed to become white when she got off the plane and entered
Brazilian society. In his cross-cultural psychology class, Fish, the son of
Eastern European Jewish immigrants, asked his daughter and her Brazilian
friend point blank if they were Black. His daughter said without hesitation
that she was Black. Her Brazilian friend, who is considerably darker-skinned
than her, said no. How can that be so?
This chapter examines how we have talked—and how we should be
talking—about socially defined race, ancestry, and identity. We discuss the
use of race as a census question in the United States, other forms of racial
classifications, ideas about “racial” purity and whiteness, and confusing
racial categories. We examine how and why the U.S. government collects
data (head counts) by race and ethnicity and the differences and similari-
ties between official data and everyday, street-level classifications. We discuss
changes in racial classifications over time and variation by countries, as in
the comparison between the United States and Brazil.
In race classifications, we find both an old, color-coded system that har-
kens back to Linnaeus and the early classifiers and, at the same time, one
that changes over time and in different locations. Who is classified as white
 198
RACE NAMES AND “RACE MIXING”

changes, over time in Europe and the United States, and over space, as when
Professor Newton boards a plane from New York to São Paulo. The color
lines shift, but they are still there and remain heavily guarded. Race is both
stable and a chameleon that conveniently changes to fit the local political and
social power structure.

WHY DOES THE UNITED STATES COLLECT

CENSUS DATA BY RACE?

First, we collect data on the social race of those living in the United States
because in 1787, Congress mandated that we do so. But that, of course, is just
the first, superficial pass at an answer. Why we continue to abide by the law
has changed through time. In 1790, the year of the first census, we counted the
number of free white men over sixteen years of age in order to establish taxes
and representation in the new states. In addition to counting the white men,
it was thought, why not count slaves and women? We did that. Infamously,
in one of the oddest of compromises in U.S. history, enslaved Africans were
counted as three-fifths of a person. That compromise gave the slaveholding
states greater representation in Congress than would have been allowed by
their white male population alone. As such, this was one of the original hypoc-
risies of American social life. The war for independence had been fought based
on taxation without representation. Yet, enslaved Africans were counted to
bolster the representation of their owners, not for the slaves’ benefit.
Now, more than two hundred thirty years later, we continue to count all
citizens by race, not only in the decennial census but for most federal pro-
grams including housing, employment, health and health care, and education.
We do so in order, at least in theory, to provide equal representation and track
inequalities by race as well as ethnicity. Oddly, in federal data, Latinx individ-
uals are considered to be an ethnicity. For example, collecting health data by
race allows us to track inequalities in infant mortality and life expectancy as
well as educational attainment and to track labor practices and housing loans.
There is a potential contradiction at the heart of collecting data by race:
we thereby affirm that race must be a useful and real category. And socially
defined race is real. However, many continue to think that biological races
are real. However, as we have shown in prior chapters, humans do not have
biological races, but race is real because people have made it real. Moreover,
the consequence of being asked one’s race suggests that race categories are
fixed and stable when, in fact, they are anything but.
 199
RACE NAMES AND “RACE MIXING”

The official census categories show just how unstable race categories are.
In 1790, the categories were Indian, slave, and white. In 1810, the category
of free colored persons was added. Later, categories such as mulatto (half
Black and half white, 1850), quadroon (one-quarter Black and three-quarters
white), and octoroon (one-eighth black and seven-eighths white) were added
in 1890. Asians—specifically Chinese—were added in 1870 and Japanese in
1890. Mexican, even though many had been living in the United States since
1848, was added in 1930 and removed in 1940.
In 1970, a question about Hispanic ethnicity was added. Note the term
“ethnicity.” As a group of individuals who generally result from the intermix-
ing of individuals from the Iberian Peninsula, indigenous Americans, and
enslaved Africans, it must have seemed wrong to call Hispanics a race. If so,
what race are they? The two largest groups of Hispanics in the United States
are Mexican Americans (who are more American Indian than European,
with little African descent) and Puerto Ricans (who have less American
Indian, about the same European, but more African descent than Mexican
Americans). The percentage of these three ancestry groups in Caribbean
Hispanics can differ widely.
Of course, by that reasoning, it is just as wrong to call Blacks or African
Americans a race, as this group also has African (about 83 percent), European
(16 percent), and indigenous American ancestry (1 percent; see chapter 9).
It seems the primary reason for identifying “Hispanic” as an ethnicity is
that many of these individuals come from cultures in which Spanish was
the primary language. So, the U.S. census now includes the option to select
Hispanic ethnicity and a race of one’s choosing.
Slowly, the race categories expanded further (fig. 10.1) and now include
multiracial options. Sometimes names change to keep up with changes in
common usage. However, it is clear that the census categories have always
been driven by the political needs of the government. They have nothing
to do with the biological ancestry of the people being classified. They are
also not backed by science and anthropology. In fact, in the Office of Man-
agement and Budget Directive 15, the section in which the categories are
laid out and defined specifically states that they are “neither scientific nor
anthropological”!
Finally, the United States is among a minority of countries that are
obsessed with recordkeeping by race. For example, in the United Kingdom,
data on class and occupation are much more available. One can better track
health changes there by class rather than race, for instance; the opposite is
 200
RACE NAMES AND “RACE MIXING”

Census year

1790

1800

1810

1820

1830

1840

1850

1860

1870

1880
1890

1900

1910

1920

1930

1940

1950

1960

1970

1980

1990

2000
2010
Indian
Slave
White
Free colored
person
Black
Mulatto
Chinese
Japanese
Octoroon
Quadroon
Other
Mexican
Negro
American Indian
Race categories

Filipino
Hawaiian
Korean
Aleut
Asian Indian
Eskimo
Guamanian
Hispanic*
Samoan
Vietnamese
Other Asian or
Pacific Islander
African American
Alaska native
Chamorro
Latino*
Other Asian
Other Pacific
islander

FIGURE 10.1. Official U.S. census categories by decade. Source: A. H. Goodman, Y. Moses, and J. Jones,
Race: Are We So Different?, 2nd ed. (New York: Wiley, 2019).

true in America. This makes sense given the enduring dynamics of class dis-
crimination in the UK and racial discrimination in the United States. How-
ever, it obscures the lived significance of social class in America and the lived
significance of racism in the UK.
Still, although imperfect, the collecting of data by socially defined race is
very important because it is the only way we can track racial inequalities and,
we hope, progress toward equality.

ARE RACIAL CLASSIFICATIONS THE SAME

IN DIFFERENT COUNTRIES?

Yes and no.

We first say yes because the classification of three to five main races that
has come down from natural scientists such as Linnaeus and Blumenbach
 201
RACE NAMES AND “RACE MIXING”

still dominates. These racial classifications or names sometimes correspond

to continents, but not always. Some variation, sometimes small and some-
times a bit more significant, are found in almost every place we are aware of.
For example, race classifications in European countries are rather simi-
lar. Racial distinctions are almost always made between European, African,
and Asian derived populations. In 2019, Joe gave a lecture in Poland and
was informed that the public education system there still taught the three-
race classification scheme as if it were state-of-the-art science. Sometimes
Native Americans are lumped in with Asians, sometimes they are ignored,
and sometimes they are added as a separate race. Native Americans are a
separate race in the United States because their histories are very different
from those of other Asians. Sometimes Native Australians, Pacific Islanders,
and Middle Easterners are added as separate races.
Racial classifications tend to differ more outside the West, where there
are different histories of colonization and slavery. Race might even be less
important. For example, in India, a country that did not experience the
importation of Africans or other non-Indians as laborers, the caste system
functions a bit like a mix of race and class. Not unlike race, one’s caste is
inherited and passed down through generations. Castes are also like classes,
in that they are tied to occupations.
However, Western ideologies have spread throughout the world, and part
of that ideology is the myth that biological races are real. Thus, we still almost
always see the big three races—European, African, and Asian—referred to in
almost every corner of the globe. Classifications also take on a more local
flavor based on the dynamics of different locations. For example, throughout
Central and South America, physical signs that we hold to be signifiers of race,
such as hair form and skin color, merge with signifiers of social class, such as
education and economic status. Socioeconomic class tends to correlate with
skin color (and admixture). Lighter-skinned individuals, the descendants of
conquering Europeans, tend to be more educated and wealthier. This is also
why Dolores Newton, the African American anthropologist mentioned ear-
lier, becomes whiter when she travels to Brazil. This dynamic is largely true
in Puerto Rico, where any European ancestry turns you white, and in Brazil,
where there are several categories of race that would be classified as Black in
the United States. In addition, the amount of “Indian-ness” is more impor-
tant in countries such as Mexico, Guatemala, Bolivia, and Peru, all of which
have deep histories of admixture.
So, our racial classifications are similar throughout the world because
of the dominance of Western racial classifications. And they also vary over
 202
RACE NAMES AND “RACE MIXING”

time and place as chameleon-like adaptations to the needs of local power

structures.

WHAT IS THE “ONE-DROP RULE”?

The one-drop rule is an informal classification traditionally followed in the

United States whereby having a single drop of “Negro” blood makes one a
Negro. It is an extreme version of hypodescent, a practice in many cultures by
which children of mixed race are classified as members of the less dominant
race. The one-drop rule is a guide to social classification. It is explainable if
you believe that African ancestry is a pollutant. Interestingly, Negro blood is
the most potent type and able to pollute a white body, whereas this is not as
true for the blood of other races.
The one-drop rule is anachronistic. There is no such thing as Negro blood
or blood of any so-called race. However, this as well as other rules of hypo-
descent have had great historical importance and continue to be observed in
informal yet powerful ways.
The percentage of inheritance (or blood) from a Negro was often used to
determine the legality of marriage across races. Protecting the color line or,
more accurately, the white race, was paramount. Thus, at different times, it
became important to be clear about the percentage of Negro blood in each
person and to guard against a Black with only a drop of Negro blood passing
as white (see chapter 9). A drop of Negro blood was defined differently by
state. In Louisiana, it was one thirty-second, or just one great-great-grand-
parent. Other states allowed it to be one-quarter (one grandparent) or one-
sixteenth blood (a great-grandparent). The consequence of different legal
thresholds for classification as white or nonwhite meant that a person could
change their race simply by moving from one state to another. Note that we
use the term “blood,” not “genes” or “genetics.” That is because at this time—
the early 1800s through into the twentieth century—the nature of genetic
inheritance had not been fully developed. Eugenicists became obsessed with
protecting and maintaining the purity of the white race.
Many individuals have traced the origins of the Nuremberg Laws of 1933
and 1935, which classified individuals as Aryan or Jewish, to the U.S. one-
drop rule. In Germany, individuals with partial Jewish heritage, generally
one or two grandparents, were called Mischlinge (or mixed). One required
a certificate of German ancestry to join the Nazi Party. Interestingly, Nazi
Germany’s Nuremberg Laws allowed for some flexibility in determining
 203
RACE NAMES AND “RACE MIXING”

Jewish blood or parentage. Having one or even two Jewish grandparents did
not automatically classify one as a Jew; thus, one could say that Jewish blood
was less powerful than Negro blood.
The effectiveness of hypodescent statutes and cultural practices is illus-
trated by the fact that socially defined whites in the United States have on
average just 0.19 percent recent African and 0.18 percent American Indian
ancestry. Of course, the opposite was far from true; due to rape and sexual
coercion during chattel slavery, African Americans have on average 16 to 24
percent European ancestry (see chapter 9).
Today, the U.S. state and federal governments have overturned all legal
references to the one-drop rule. All of the thirty-three states that had out-
lawed marriages across races, so-called miscegenation laws, overturned these
laws mostly between the end of World War II and 1967, when the Supreme
Court ruled them illegal.
Although the U.S. census and other legal documents no longer classify
individuals by their percentage Negro blood, the one-drop rule had many
lasting effects. Some individuals with parents from different ancestry groups
can now call themselves multiracial. There is now a multiracial category on
the census, and it is expanding. However, the ancestral origins of these mul-
tiracial individuals are still influenced by America’s racial hierarchy. Individ-
uals with a European American father and East Asian mother are far more
common than those with a European American father and African Ameri-
can mother (despite Hollywood’s and Madison Avenue’s best intentions). But
when push comes to gentle shove, most individuals with an African Ameri-
can parent or grandparent identify themselves, and are indexed by others, as
Black. This is true of Barak Obama (whose father was Kenyan, not African
American) and Kamala Harris (whose father is from Jamaica and mother is
from India). Harris, affirming her Black identity, went to Howard University,
a prestigious historically Black college.

WHAT DO I CALL PERSONS WITH AFRICAN,

LATIN AMERICAN, AND ASIAN ANCESTRY?

We have repeatedly pointed out that humans don’t have biological races.
Thus, what we “call” people results from cultural, historical, and social forces.
These forces are constantly moving, so group names within societies change.
For example, Joe is “colored” on his 1955 birth certificate. This was the term
in use across the country for children of African descent in the mid-1950s.
 204
RACE NAMES AND “RACE MIXING”

As a child, he identified as “colored” until 1968, when James Brown released

Say It Loud: I’m Black and I’m Proud. Listening to Brown was an awakening
for Joe, a moment when he and many of his peers began to identify with the
Black Power Movement.
Like many, later in his, life Joe shifted his identity to “Afro-American.” This
was spurred by his recognition of the significance of his African heritage.
Today, Joe calls himself an “African American,” again recognizing his Afri-
can cultural and genetic roots and the significance of his family’s American
experience in forming his identity. The American experience also includes
his European genetic ancestry through known ancestors; he estimates that
he has about 18.75 percent European ancestry (see chapter 9).
We have previously discussed the confusing inadequacy of the term
“Hispanic.” Those who fall into that census category come from all over the
Southwestern United States, Caribbean, and Central and South America. A
historical fact that gives perspective to this discussion is that most people
in this category have significant amounts of Amerindian ancestry. Addi-
tionally, Spain was the first European power with colonies in the Western
Hemisphere. Spaniards began their exploration of North America as early
as 1513 with Ponce de Léon; Francisco Vázquez de Coronado explored the
Southwest in 1541; and Pedro Menéndez de Avilés founded St. Augustine,
Florida, in 1565.
By comparison, Jamestown, Virginia, the first permanent English settle-
ment, was not founded until 1607. Furthermore, Mexico had established
cities in the Southwest that were occupied by the beginning of the eighteenth
century. Mexico outlawed chattel slavery in 1829. Mexico was conquered
by the United States in the Mexican-American War of 1846–48, after which
slaveholders in the United States moved into these teritories in order to
expand slavery into the Southwest.
Many Americans seem to forget that the residents of the island of Puerto
Rico are U.S. citizens (Immigration and Nationality Act of 1952, § 302, 8
U.S.C. § 1402). Similar to the Mexican southwest, Puerto Rico became part
of the United States through an act of war against Spain; the 1898 Treaty of
Paris ceded Guam, the Philippines, and Puerto Rico to America. Parallel-
ing the struggle for African American liberation, anticolonial and antiracist
struggle among those in the census category of “Hispanic” has altered the
way they think about themselves and therefore what they wish to be called.
Our general rule for addressing individuals in the Hispanic category
is to ask them how they wish to be addressed. Some Mexican Americans
 205
RACE NAMES AND “RACE MIXING”

prefer the term “Chicano,” others prefer the generic terms “Latino, Latina,
or Latinx.” Still others wish to be referred to by their country of origin, such
as Dominican or Cuban. The process of asking someone how they wish to
ethnically and culturally self-identify demonstrates that you have an interest
in their story. You might find out a great deal by simply asking this question.
Finally, the term “Asian” is possibly even more inadequate than “His-
panic” to describe persons with ancestry in this census group. The continent
of Asia spans 17.21 million square miles, and depending on one’s perspec-
tive, it includes the geographical regions including the Middle East, Eurasia,
India, East Asia, and some islands of the Indian and Pacific Ocean. As we
write, the population of Asia is around 4.5 billion people or about 60 percent
of the world population. Thus, the label of “Asian” encompasses a huge vari-
ety of groups without specificity.
The 2020 U.S. census form lists the following options: “Chinese, Fili-
pino, Asian Indian, Vietnamese, Korean, Japanese, Other Asian—Print,
for example, Pakistani, Cambodian, Hmong, etc.” According to the U.S.
Bureau of the Census, persons identifying as Asian numbered about 21 mil-
lion (about 7 percent of the population). Although Chinese and Japanese
immigrants began to arrive in significant numbers in the nineteenth century,
most Asian Americans entered the country after 1965. The largest groups are
Chinese, Filipino, Indian, Vietnamese, Korean, and Japanese Americans (in
that order). Our general rule applies here as well: the best practice is to ask
individuals who fall within this category how they wish to be addressed. For
example, Joe’s wife simply refers to herself as “Korean.”
In conclusion, the old race classifications are generally inadequate for cap-
turing the lived experiences of individuals or how they self-identify. Clas-
sifications require more specificity and can change over time and by place.
Finally, as a general rule, if you are unsure of how someone wishes to be
identified, it is okay to ask.

WHAT WILL SOCIETY CALL MY CHILDREN?

American society remains mired in institutional racism. Underlying societal

racism is the dominance of biological essentialist ideas held by the majority of
Americans. A core notion of biological essentialism is the belief in the reality
of biological races and the notion of racial purity. Even DNA ancestry test-
ing, with results showing that almost everyone is mixed, fails to improve the
general level of genetic essentialism among Americans. A recent study of U.S.
 206
RACE NAMES AND “RACE MIXING”

whites showed that for people with high levels of understanding of genet-
ics, direct-to-consumer (DTC) ancestry testing did not reduce their level of
genetic essentialism. Conversely, for people with low levels of prior genetic
knowledge, such testing actually increased their level of genetic essentialism.
Surprisingly, despite the centrality of race in American social life, the
twentieth century saw the loss of legislation that defined races. Louisiana
was the last state with a statute that defined “Black.” That law played a major
role in the case of Susie Guillory Phipps, who, in 1983, sued to have her
racial status changed to white and to overturn the one thirty-second African
descent rule.
Throughout our history, the courts have used various racial notions to
decide cases in which racial identity was a central factor. These include what
we can call (a) status race, whereby the central premise is of Black inferiority
and allows private individuals to discriminate on the basis of this belief; (b)
formal race, holding that race is different based on appearance; (c) histori-
cal race, whereby race depends on an individual’s or group’s historical rela-
tionship to oppression and unequal power in society; and (d) cultural race,
prioritizing a group’s culture, community, and consciousness. The lack of
consistency allowed courts and judges to make rules that fit their biases and
need to retain power and protect the white race.
It is probably even more shocking that cases can still be decided on the
“status race” criterion. For example, in 1992, a white woman was awarded full
worker’s compensation disability for her phobia of Black men. She claimed
to suffer from post-traumatic stress disorder because she had been mugged
by a person she believed was Black. Of course, one can only wonder why
her PTSD was not just about men, as crimes by men against women are more
common than those by Blacks against whites.
Title VII of the Civil Rights Act of 1964 directs the federal government to
collect data on race and ethnicity. The current categories, their definitions,
and the means of collecting these data are determined by the Bureau of the
Census and the Office of Management and Budget (Directive 15). The OMB
categories are as follows:

• “White: A person having origins in any of the original peoples of Europe, the
Middle East, or North Africa.
• American Indian or Alaska Native: A person having origins in any of the origi-
nal peoples of North and South America (including Central America) and who
maintains tribal affiliation or community attachment.
 207
RACE NAMES AND “RACE MIXING”

• Black or African American: A person having origins in any of the Black racial
groups of Africa.
• Asian: A person having origins in any of the original peoples of the Far East,
Southeast Asia, or the Indian subcontinent including, for example, Cambodia,
China, India, Japan, Korea, Malaysia, Pakistan, the Philippine Islands, Thailand,
and Vietnam.
• Native Hawaiian or Pacific Islander: A person having origins in any of the original
peoples of Hawaii, Guam, Samoa, or other Pacific Islands.”

State agencies often have to decipher the self-reports that they receive for
federal reporting requirements. For example, in 2004, the North Carolina
Department of Public Health collected data on self-reported race at birth.
From 118,000 live births, the mothers (or their representatives) reported 600
versions of racial categories for their children. As the federal government does
not use 600 categories, the state workers collapsed these reports into the ten
standard categories. This was not accomplished in an unbiased manner. Two-
thirds of the Hispanic mothers reported the race of their baby as “other.” As
a result, the workers reassigned these children to the white racial category.
Robert Hahn studied linked birth and death certificates. He found that
over 40 percent of infants who died in the first year and were listed as Native
American on their birth certificates had their race changed to white on their
death certificates. He attributes this to the fact that although the mother was
present at birth, the coroners might have filled out the death certificate with-
out knowing the ethnicity of the mother or father. What especially worries
us about this example is that it directly implies a serious undercounting of
Native American infant mortality.
With the decline of laws forbidding interracial marriage, there has been
an increase in the number of marriages between people of different socially
defined racial groups. This increase is nowhere near as large as one might
expect from the recent glut of television commercials featuring such couples
and their children. A recent study of 543 advertisements found that the
percentage of these couples in ads was much greater than the percentage
of such marriages in U.S. society. In addition, nonwhite male/white female
couples were underrepresented. No commercial with this dyad was found on
the Disney Channel.
In 2013, about 3.1 percent of Americans claimed “interracial” ances-
try. Within this group, the most common dyads were Black/white (> 2.4
million), followed by Asian/white (> 1.8 million), and Native American/
 208
RACE NAMES AND “RACE MIXING”

white (> 1.7 million). However, among these individuals, 61 percent did
not identify as “multiracial.” In response to the question about how they
identified themselves, most responded that they identified with the “race”
that they most physically resemble. This is easy to explain, as the racial
essentialism in which these individuals are immersed tend to generate
that result.
Alan is friends with a couple, a white woman and a Black man. They refer
to their daughter as Black (she has dark skin) and their son as Caucasian (he
has much lighter skin). Joe has seen this in his own sons. One does not iden-
tify at all as African American. His appearance is closer to that of his mother,
but he also does not identify as Korean. The other son identifies as African
American (his skin is darker and his hair is curlier than his brother’s). He
feels the racism directed at his Blackness more acutely than his brother does.
These responses differ by the dyad of the parents, as East Asians have social
and cultural experiences different from those of African Americans. One
study found that Asian Americans are actually more likely to classify mul-
tiracial (white/Asian) individuals as an out-group and not Asian. This, of
course, would lead such individuals to have a greater tendency to identify as
white, but that is counterbalanced by the lack of acceptance by whites of any
multiracial individuals as white.
So, the answer to the question about what people will call the children
is unfortunately driven by our society’s rampant genetic essentialism. The
majority of Americans still accept the idea that races have a biological essence
(and purity). There are no laws that classify individuals by race at either the
state or federal level. Race identity is self-reported. Multiracial individuals
respond to the genetic essentialism of our society in a variety of ways, which
might change over their lifetimes. Some will cling to one ancestry and not
the other (often associated with their own appearance). Some will honor
both ancestries equally. Joe’s experience suggests that the latter course is the
more psychologically healthy choice.

WILL MY CHILDREN BE HEALTHY AND GOOD-LOOKING

IF I REPRODUCE WITH SOMEONE OUTSIDE MY RACE?

Sorry, but we cannot answer that question. What we can say definitively is
that your children’s health will not be negatively impacted by the socially
defined race of your partner. However, even this statement must be taken
with a grain of salt, as we have established that a person’s socially defined
 209
RACE NAMES AND “RACE MIXING”

race might place them in an environment that is not conducive to good

health. We explained the impact of the environment on health in chapters 3,
5, and 7. There is no evidence that reproduction with any human from any
part of the globe is harmful. Indeed, the general expectation is that repro-
duction with someone whose ancestry is different from your own should
minimize the number of deleterious (bad) genes that are homozygous. In
virtually every organism ever studied, an increase in heterozygosity leads to
an improvement of the health of the offspring.
Through all the centuries of efforts to document that there might be some
biological reason that two individuals of different races should not repro-
duce, none has ever been found. It is flat-out myth, flat-out wrong to think
there is anything biologically problematic. Of course, there is the potential
for discrimination and feeling socially ostracized by different communities.
This can certainly influence your own and your child’s mental health, but it
does not have to.
In the nineteenth century, some scientists tried to invent biological
reasons for why individuals of different races should not reproduce. They
even came up with a popular term for it: miscegenation, a term used for the
interbreeding of two individuals from different races, which they treated as
separate species. The “fertility of the hybrids” was an argument that Charles
Darwin used to debunk the idea that human races actually represented
separate species. He relied on data that he received from South Carolina
slaveholder John Bachman. Bachman’s plantation records showed no loss
of viability in the children of enslaved African women and white males. We
need look no further than Thomas Jefferson, Sally Hemings, and her family
to see that reproduction between individuals of different genetic ancestries
does not cause biological harm.
Even though polygenism was disproven, the idea that cross-race children
would be unhealthy only gained speed. The end of chattel slavery drove this
idea. During slavery, the impregnation of Black women by white men was
frowned on, but no law prevented it. However, once slavery ended, South-
ern states rapidly enacted miscegenation statutes, primarily to prevent Black
men from impregnating white women. The census categories took care to
document the portion of blood by race, mainly to identify those who would
be denied their rights under separate and unequal Jim Crow laws. How-
ever, it was also thought that Blacks were a reservoir of disease that could be
passed into the white community by sexual relations, including the genetic
disease sickle cell anemia and the infectious disease syphilis.
 210
RACE NAMES AND “RACE MIXING”

In the first half of the twentieth century, scientists rolled up their sleeves
to study miscegenation. For example, Charles Davenport, then head of the
Cold Spring Harbor lab, studied race crossing and concluded that the result
of the race cross was always worse than the parent races. He initially studied
immigrant communities in New York (1917) and then headed to Jamaica.
He considered race crosses to be disharmonious. Davenport was influen-
tial and not alone: he had the weight of the Eugenics Record Office at Cold
Spring Harbor behind him.
And this fake science led to laws. In fact, as noted earlier, thirty-three
states passed anti-miscegenation laws. An anti-miscegenation amendment
to the U.S. Constitution was proposed at various times but never passed into
law. The last of these state laws was overthrown by the Supreme Court in
1967 in the case of Loving v. Virginia.
The United States was not the only country to legislate against sexual
unions between individuals of different races. South Africa did so with
national laws in 1949 and 1950. The first eugenics act of the Nazi government
was to sterilize the progeny of African soldiers who fathered children with
German women after WWI. In 1935, they banned sexual relations between
Jews and Germans.

WHY DO SOME PEOPLE SAY THAT INTERRACIAL

CHILDREN ARE BETTER LOOKING?

Don’t be confused: there has never been a time in America when people
weren’t having interracial sex and bearing children. However, because of
miscegenation laws, it was rare for these couples to marry. Now it is more
common. One can legitimately ask whether this trend will have any impact
on the future of the race. As we have become increasingly more cosmopoli-
tan, the number of so-called interracial marriages has increased. As noted
earlier, President Barack Obama is the result of an interracial marriage. His
mother, Ann Dunham (1942–95), who went on to become an anthropolo-
gist, was from Wichita, Kansas. His father, Barack Obama, Sr. (1936–82), was
from Kenya. His parents met in 1960 while students in a Russian language
class at University of Hawaii, Manoa.
The same story, though different, is true for Vice President Kamala Devi
Harris. Her mother, Shyamala Gopalan (1938–2009), was a biologist from
India. Her father, Donald Harris (1938–), is an economist and emeritus pro-
fessor at Stanford University. He was an immigrant from Jamaica of African
 211
RACE NAMES AND “RACE MIXING”

descent. They met at a protest in San Francisco. How crazy are these stories?
These days, not very crazy. The rest is history.
These are two public examples of the products of interracial marriage who
are now in their fifties. Evidence suggests that what was somewhat unusual
in the 1960s has become more common in the 2010s and 2020s. Indeed,
when communities and individuals come together, desire happens. However,
no one should jump the gun on this trend yet, because it accounts for only
about 3 percent of marriages. And, as discussed earlier, who marries whom
in interracial marriage dyads is strongly influenced by ongoing patterns of
racial inequality.

WHAT DOES “CAUCASIAN” MEAN?

Alan was at home listening to a National Public Radio show during which
individuals were being interviewed about their attitudes toward the Black
Lives Matter movement. One person identified as Caucasian and another did
not but said her husband was Caucasian. Alan’s friends often use the term
“Caucasian.” What do they mean by that?
Doctors and forensic anthropologists use Caucasian. It shows up on police
forms and medical intake records. In our research on multiple myeloma, we
found that various websites list race as a risk factor. Some specify that being
a member of the Black race is such a factor. Blacks have twice the prevalence
of multiple myeloma as Caucasians. Caucasians? Who are they?
To the ancient Greeks, “Ethiopian” meant all Africans. However, modern-
day Ethiopians are genetically closer to Europeans than to many western
African populations. Today, in studies of multiple myeloma, they might
be labeled as individuals of African ancestry. Asian was once just Chinese.
Negroid (and Negro) and Mongoloid have gone largely out of favor in public
discourse, but these nineteenth-century anthropological categories can still
be found as search terms in library systems. “Caucasian,” by contrast, is still
in popular use. Is it not weird how white folks don’t even know how to name
their own group?
As we noted in earlier chapters, the term “Caucasian” originated in the
eighteenth century. German anatomist Johann Blumenbach declared that
a skull in his possession from the Caucasus Mountains, an area between
the Caspian and Black Seas, was close to the most beautiful that could be
found. To Blumenbach, the human skull was created in God’s image. Thus,
he determined that the particular skull was of the type for individuals like
 212
RACE NAMES AND “RACE MIXING”

him and in his race. By “type” we mean that it would stand for what God
created. All other skulls could then be considered to have changed somehow
from the original type. We have previously talked about how eighteenth-
and nineteenth-century naturalists generally thought that such change was a
degeneration from the ideal type. Blumenbach called the people of this type
Caucasians, after the location of the skull. In addition, individuals of other
races would need other types, but those could be graded on the degree to
which they varied from the skull from the Caucasus, with the further down
they were on the typological ladder of life, the greater the variation. It is
notable that Georges Cuvier was the only named person in the central plate
of Nott and Gliddon’s 1857 work, Indigenous Races of the Earth.
What constitutes who is Caucasian, or white, has never been determined
scientifically. It is the wrong question, because there is nothing there. However,
it has been hotly debated for centuries, because the stakes have always been
high. Typically, Caucasian included only Europeans, then scientists and others
debated the extent of the Caucasian classification. Did it include Middle East-
erners? A medical anthropologist colleague of Alan’s from Egypt was shocked
to find out that when she came to the United States, she became a Caucasian.
Northern Indians were thought by physical anthropologists and linguists
to be Caucasians. But that was not so for those who policed the color line.
This was well illustrated by the Supreme Court case United States v. Bha-
gat Singh Thind. In 1923, Thind, an Indian Sikh, sued the United States for
citizenship, citing his identity as a “free white person.” His evidence for this
claim was that anthropological science held that Europeans and Indians
shared common descent from Proto-Indo-Europeans. Chief Justice George
Sutherland summarized the position of the majority. They held, in effect,
that the science of Thind’s ancestry did not matter, because he did not meet
the common white man’s definition of Caucasian.
The Thind case exemplifies the sort of contradiction that stands in the
middle of the classification. Blumenbach and later scientists knew that
peoples residing in Europe, which had arbitrary boundaries, moved around
and intermixed with individuals from Asia and the Middle East. Remember
Homer’s Iliad? Troy was located in modern Turkey. So, would these indi-
viduals who mixed with Europeans be Caucasians as well? Ancient DNA
(chapter 10) also demonstrates that the modern inhabitants of Europe are
descended from farmers who originated in the Middle East.
Blumenbach’s fivefold classification of races, which included Caucasian
along with Ethiopian, Mongoloid, Malayan, and Native American, had great
 213
RACE NAMES AND “RACE MIXING”

influence. Many of the descriptions changed. Ethiopian became African and

Mongoloid became Asian. But the mythical Caucasian is still kicking around.
One of the great myths associated with the term was the idea that all humans
are descended from Caucasians. James Cowles Prichard (1786–1848), a pio-
neer of the typological race concept, believed, as almost everyone did during
his time, that humans must have originated in Europe. This commonly
agreed-upon notion played a major role in the rejection of Raymond Dart’s
discovery in 1924 of Australopithecus africanus (a close human relative)
in Taung, in the northwest province of South Africa. However, as more
and more of the oldest fossils of human relatives and anatomically modern
humans were discovered in Africa, European and American anthropologists
finally had to give up on the myth of Caucasian origins.
It is time to put the term Caucasian to rest. It was never defined, its roots
are pure typology, and it invokes a fake science suggesting that the category
has some scientific validity. “European” or “European American” is a useful
political and social category. One can self-identify as German American or
German, Polish American, or Polish, and so on. It is your choice. However,
Caucasian serves no purpose but to reify biological race as a typological con-
cept and to obfuscate. Let’s make a promise to one another to never again
use the term.

ARE “JEWS” A RACE? WHAT ABOUT PEOPLE OF

ITALIAN AND IRISH DESCENT?

No. Jews are not a race. Italians and the Irish are not a race. These groups are
not races in either the biological or the cultural sense. Italian and Irish are
ethnicities in the U.S. context of ethnicities, the lumping together of immi-
grants from existing countries. Jews are a religious group that also incorpo-
rates a couple of ethnicities based on their diasporic locales.
Jews—or, better, Ashkenazi Jews—are a subset of Jews who migrated from
Palestine and the Middle East and lived for centuries mostly in isolated vil-
lages in central and eastern Europe. Sephardic Jews also left the Middle East
and lived in North Africa and the Iberian Peninsula. Most left or converted
to Christianity after their expulsion from the peninsula in 1492. A third and
smaller branch, the Mizrahi, remained in the Middle East. The diaspora
also spun off some smaller and even more isolated branches in modern-
day India, Yemen, Ethiopia, and even China. All of these diasporic branches
maintained some version of Judaism but came to speak different languages
 214
RACE NAMES AND “RACE MIXING”

and develop unique customs. They can be considered ethnic groups, in that
they share lots of customs and beliefs. The same goes for Irish Catholics and
Irish Protestants; they are ethnic groups. Italians are an ethnic group that
might be broken down into smaller groups, such as Sicilians and northern
Italians.
This view of various Europeans as being ethnic groups is relatively new.
Before World War II, it was common to think of all of these groups as races
or racial types. Unfortunately, some of this thinking is still promoted in the
popular media and among individuals who have not had the opportunity to
consider why these groups are not races.
In his influential book, The Races of Europe (1899), William Z. Ripley clas-
sified Jews, Italians, and the Irish as members of races. The same occurred
in 1939 when Harvard physical anthropologist Carleton Coon counted these
individuals among his various racial types of Europe. Coon was a walking
contradiction in trying to have it both ways: In addition to listing some
dozen races of Europe, he kept to the five main quasi-continental races,
including the racist notion, outlandish even at the time, that the five races
stepped over the threshold to become Homo sapiens at different times. Of
course, by Coon’s theory, Caucasians became human first, with Africans in
last place. Following the tradition of Nott, Gliddon, and Ripley, in his books,
Coon included lots of side and front view mug shots of individuals to display
the different racial types.
Despite the fact that Adolph Hitler knew that race science was bogus, he
and Nazi Party officials weaponized race science to support their program of
blaming Germany’s problems on the Jewish racial element, with the ultimate
goal of seizing power in Germany. Jews and Gypsies were studied to deter-
mine the faults of these aliens (compared with the mythical Aryans racial
types). In a parallel with the ongoing science of Black and brown bodies,
Nazi scientists examined bodies and minds of Jews and Gypsies, working
hard to pinpoint what was wrong with the Jews and to eradicate the Jewish
problem. Jewish blood was a pollutant.
But all of that work is fake science. It is based on ideology and belief. It
is wrong in its facts and especially the assumption that Jews, Italians, Irish,
and other groups are anything close to closed-breeding populations. Yes,
there are some small differences in allele frequencies among these groups
(see chapter 2). Yes, some Jews are prone to certain simple Mendelian dis-
eases, such as Tay-Sachs and Gaucher disease. However, through genetic
counseling, American Jews have reduced their frequency of Tay-Sachs, to
 215
RACE NAMES AND “RACE MIXING”

the extent that it now matches other populations of European descent. But
the propensity to these diseases constitute small genetic differences in the
greater scheme. We have explained in chapters 5 and 9 how human popula-
tions (ethnic groups) carry small genetic differences that have little impact
on complex traits. So, once again, as Ashley Montagu told the world in 1942,
the Jews and European ethnic groups are not races. Some genetic differ-
ence? Yes. Race? Absolutely not.

AM I WHITE?

Maybe. The answer depends not just on where you are from and your skin
color but also on where you live and especially when you live. The color line
between white and various forms of nonwhite has changed over time and
from place to place.
First, white is one of those color terms that is used informally to lump
together individuals of European ancestry. Of course, nobody is really white,
and in fact, some Europeans are closer to beige or light brown. White seems
to have become the chosen descriptor of Europeans, as it provided the maxi-
mum contrast to Black. The gulf between races might not have seemed so
insurmountable if the labels had been beige and brown.
“White,” rather than strictly being European, has in some quarters
replaced “Caucasian” as a term that has implications for being somewhat
genetic and not merely geographic. It is a more social and less anachronistic
term than Caucasian for a hard-to-define group of people. Thus, one could
be a European—say, an ethnic Pole or an Irish Catholic—in the early twenti-
eth century, but one’s whiteness was still questioned. Finally, white has stood
for some sort of trans-European white culture. In this regard, white as a
designation is fascinating. As most sociologists will tell you, it is really hard
to pin down what white culture is, yet it is often fetishized and seen as in
need of defending. Sociologists have also begun to examine whiteness as an
object of study. This, we feel, is an interesting variation on the study of race
and racism, as white is often also unmarked and taken for granted. White
individuals often feel that they have no race and, even more often, that they
are not constrained or described by their race.
After the horrors of the Holocaust, the distinction among European
types began to fade. The United States was to be a melting pot where indi-
viduals from different countries and with different religions could go to
school and work together, and even love one another. The result was that
 216
RACE NAMES AND “RACE MIXING”

many European groups became honorary whites, and the category of white
expanded beyond Nordic, Anglo-Saxon, and Aryan. However, at the same
time, the sharpness of the color line between whites and others became even
more significant.

WHAT IS WHITE SUPREMACY?

White supremacy is the belief that white people are superior to those of
other races. It claims that because of their intellectual and cultural superior-
ity, whites should be at the top of the social, political, and cultural ladders.
White supremacy is the most pernicious myth of the Western world. Behind
it is the myth that races are natural and real and that they are ranked hierar-
chically. Thus, white supremacy is just a new version of eighteenth-century
racist thought. It is our time’s big lie.
It is hard to quantify how much suffering has been and continues to be
caused by adherence to white supremacy. Here, we are not just referring to
the more egregious acts, such as the attempted takeover of the U.S. Capital
on June 6, 2021, which have resulted from this false belief. The victims of
a false ideology are not just persons of color, the intended victims; white
supremacy hurts poor and middle-class whites. And frankly, by maintaining
a hierarchy supported by a myth rather than merit, it hurts everyone.
White supremacy sits at the core of racism because it reifies that there is
such a thing as a white race. Furthermore, it harks back to basic typological
thinking in arranging races on a ladder of inferior to superior, with whites at
the top as a result of evolution or God’s will. We are firm in our conviction
that white supremacy is one of the major factors impairing white American
Christians from actually following the core tenets of their belief system to
“love God and love your neighbor as yourself.”
It is also hard to quantify the extent of white supremacist thinking. Only
those individuals on the tip of the white supremacist iceberg openly identify
as such. However, studies suggest that this is a significant issue in Amer-
ica. Data suggest that virtually every white person who voted for Donald
Trump in the 2016 and 2020 elections was, in part, unconsciously moti-
vated by white supremacist thinking. Trump received more than 62 million
votes in 2016 and over 74 million votes in 2020, the majority of which were
cast by whites. This was indicated by exit polls as well as graphic represen-
tations of the percentage of voters by county across the nation. Analy-
sis of why individuals voted for Trump in 2016 at first focused on issues
 217
RACE NAMES AND “RACE MIXING”

associated with the economy; however, a more detailed study showed that
a significant number of Trump voters were primarily motivated by their
racial attitudes and support for blocking the immigration of individuals
from the Middle East and Central and South America. One of the clear-
est political links to white supremacy is the belief that America should be
a white, Christian country.
Further evidence of the resurgence of white supremacy in America is pro-
vided by the analysis of individual and group racial attitudes that are more
freely expressed on the internet. In addition, the last decade has witnessed
ongoing and intensifying racist incidents on college campuses throughout
the country. In November 2019, all fraternity activities at Syracuse University
were suspended after video captured fraternity members calling an African
American female student by a racial slur. Finally, there is growing evidence
that white supremacy has made a resurgence in the military and that little
to nothing is being done by commanders to stop it. These examples make
clear that white supremacy is more than those committed to white racial
hegemony. It is also widespread among those who wish to turn a blind eye
to it. And as long as the big lie of white supremacy continues to be oxygen-
ated, we are pessimistic about the future of racial equality and democracy in
America.
It is common to think that certain people, such as members of the KKK,
are white supremacists. Maybe some older Southerners also harbor white
supremacist thoughts. But most whites do not. Then came the riots in Char-
lottesville in 2017 and the attempted overturn of the 2020 presidential elec-
tion results and storming of Congress January 6. And the world was exposed
to a vast underground of a well-organized white supremacist movement that
now also plants its propaganda online.
But those events are just the tip of the iceberg. White supremacy is the air
we breathe in the United States. White supremacy is the dominant form of
racial thought. It is everywhere. White supremacy is the underlying ideology
of racism. We need to understand and face the size and shape of the iceberg
of white supremacy.

WHAT IS WHITE NATIONALISM?

White nationalism is a political stance based on white supremacy and

strives for either separation of the races or complete control of the govern-
ment by whites. Despite the cameo appearances of African Americans and
 218
RACE NAMES AND “RACE MIXING”

Latinx individuals at the 2020 Republican National Convention, the GOP

became the party of white people in the 1960s. Richard Nixon conquered
the White House using the same strategy that Donald Trump is attempting
to resuscitate for the 2024 election, by playing on white suburban fear of
urban racial unrest.
“People are terrified . . . sooner or later the white community is going to
retaliate and all the patient work will be undone. And the majority of law-
abiding Negroes are going to take the heat.” Nixon became the spokesper-
son for the so-called silent majority, those who wanted a return to normalcy
and law and order. However, Nixon was flanked on the right by an even
more violent racist, third-party candidate George Wallace, the former anti-
integration governor of Alabama.
Prior to Nixon’s move to win over Southern whites, that group mostly
aligned with the Democratic Party, “Dixiecrats.” For example, Franklin Del-
ano Roosevelt struggled to get his New Deal legislation passed with South-
ern Democrats. They forced him to limit the labor classifications to which
the New Deal would apply, specifically removing those categories that were
most crucial for keeping African Americans economically subservient and
disenfranchised in the South. With Nixon, the positions of the two parties
changed over the twentieth century; the Democrats now command more
support from nonwhites than do Republicans.
The Southern Poverty Law Center monitors white nationalist groups, or
hate groups. They write that white nationalists’ core belief is that countries
should be organized around individuals identifying as white and that there
should be a turn away from multiculturalism. Thus, one objective of the
movement is to return to a country that is more completely dominated by
whites. Some advocate the removal of nonwhites from America or the cre-
ation of white homelands. Of course, the example of Nazi Germany informs
us that it is one short step from these objectives to genocide. Nazi ideol-
ogy tried to eliminate all non-Aryans from Germany. It played on the myth
of purity to justify its eugenic sterilization and eventually extermination of
non-Aryans.
Short of purging nonwhites, the objective of white nationalism is to
restrain the numbers and political power of non-whites. Thus, it is closely
aligned with immigration restrictions to maintain a white majority. It also
employs a host of other methods to restrict the rights of nonwhites, includ-
ing purging voter rolls, gerrymandering, and vigilantism. Racial gerryman-
dering has the effect of diluting the vote of racial minorities. As a result of
 219
RACE NAMES AND “RACE MIXING”

this practice, the Republican Party now holds some sixteen additional seats
in the House of Representatives.
Racial vigilantism has taken a dangerous turn over the last few years. In
its most benign form, it consists of white people calling the police to report
Black and brown people who are engaged in everyday activities, such as lay-
ing their head down in the common room of their college dorm or bird-
watching. On the opposite side of privilege, pro-gun whites feel as if it is
their obligation to display their AR-15s while shopping at Walmart. In the
summer of 2020, a pro-Trump vigilante shot and killed two and severely
wounded a third individual in Kenosha, Wisconsin. This occurred follow-
ing a call for white militants to come to Kenosha to “protect businesses”
in danger from anti-police brutality protestors. The protests erupted after
an unarmed black man, Jacob Blake, was shot in the back seven times by a
police officer. Later that week, a caravan of some six hundred armed pro-
Trump demonstrators descended on Portland, Oregon. Their charge was to
demonstrate support for the president’s “get tough” policy on demonstrators.
The demonstrations in Portland were an ongoing response to the murder of
George Floyd, reignited by the shooting of Blake. This precipitated an armed
clash between the pro-Trump forces and the protesters, leaving one person
dead. The dead man, Aaron J. Danielson, belonged to the right-wing group
Patriot Prayer. Trump praised the militias for their actions in Portland and
defended Kyle Rittenhouse, the young man who allegedly shot and killed
demonstrators in Kenosha.

CONCLUSIONS

Naming races carries a lot of weight. Who gets to be counted in the U.S.
census and federal programs such as fair housing and employment have con-
sequences for whether and how inequality is tracked. The process of nam-
ing is the first step to making something real, to reification. Where society
goes from there is up to the individuals in that society. Our past practices
are cause for pessimism. Science, as we have seen so often, got involved to
try and prove that racial crosses were biologically harmful. These fake stud-
ies helped to justify anti-miscegenation laws. In Nazi Germany and South
Africa, naming races was the first step to banning interracial sexual relations,
and the same was true in the majority of U.S. states.
In the United States today, communities are largely separated by race. Thus,
marriages across color lines are still relatively rare, but they are increasing.
 220
RACE NAMES AND “RACE MIXING”

And slowly the stigma and stress of being interracial is decreasing. On the
other hand, more concerning is the resurgence of white supremacy and
white nationalism which threaten to destabilize our democracy. In a worst-
case scenario, the United States could return to a de jure white supremacist
nation. History is rife with lessons about people who thought the worst-case
scenario could never happen to them. We wrote this book because we felt
that it was crucial for us to prevent a repetition of these tragedies. What hap-
pens from here is up to all of us.
 Chapter Eleven

A WORLD WITHOUT RACISM?

In much of the Democratic Party, it’s now fashionable to say that America is racist.
That is a lie. America is not a racist country.
—NIKKI HALEY, FORMER UN AMBASSADOR, 2020.

What the people want is simple. They want an America as good as its promise.
—BARBARA C. JORDAN, U.S. CONGRESSWOMAN, 1977

Nikki Haley was born Nimrata Nikki Randhawa, the daughter of Sikh par-
ents who immigrated to the United States from Punjabi, India. Like many
women, she changed her last name upon marriage. Later in her speech, she
described how her parents, and she herself, experienced discrimination as
Indian Americans. That seems like an example of systemic racism to us.
Democratic vice presidential candidate Kamala Harris’s mother was also an
Indian American. Aside from their mothers and that they both went into
politics, their similarities seem to end there. Harris’s mother married a man
from Jamaica of African descent. Her parents met at a civil rights rally in
Oakland. She strongly identifies with her African heritage, and attended
Howard, a historically Black university. Harris, as evidenced by her speaking
and writing, is well aware of her personal experiences of racism as well as
institutional racism in the United States. She is now the first Afro-Indian and
female vice president of the United States.
Whether institutional racism still exists and is a major problem is not
something that is decided by anecdotal experiences of famous people.
Recently, Mark Robinson, the African American lieutenant governor of
North Carolina, assailed the new inclusive K–12 social studies curriculum as
“political in nature” and that it unfairly portrayed America as systematically
racist. Robinson is known for his support of various conspiracy theories as
well as his Islamophobic and homophobic views.
 222
A WORLD WITHOUT RACISM?

Throughout this book, we have documented the existence of institutional

and systemic racism in the United States. It is a topic that appears in virtu-
ally every sociology textbook used at the university level. A Google Scholar
search on the phrase “institutional racism United States” turns up more than
fifty pages of journal articles and books on the topic. Denying the existence
of institutional racism in the United States is like denying the existence of
gravity or claiming that the Earth is flat. QAnon conspiracy theorists and
others who believe that Trump won the 2020 presidential election freely
ignore facts and science.
We did not write this book for Nikki Haley, Donald Trump, Mark Robin-
son, or Stephen Hsu (Asian supremacist, eugenicist, and former vice presi-
dent of research at Michigan State University). We know that no evidence
of any kind exists that can change the views of people who are deeply com-
mitted to the notion that America is the land of the “free.” In this respect,
these individuals resemble special creationists and flat-Earthers. They might
well be science deniers and believe what they hear on Alex Jones’s InfoWars.
Some research suggests that persons displaying extreme racist tendencies
have a mental disease.
However, as we have shown, the vast majority of Americans who harbor
racial supremacist views are not crazy. Rather, they have absorbed a cultural
lie about biological racial differences in athleticism, personality, and intel-
lect. They have bought into the mantra that the position that individuals and
groups occupy in society are the result of those people’s attributes, rising and
falling as if in a color-blind meritocracy, rather than facing up to systems
that bias opportunity on the basis of socially defined race.
It is precisely this mantra that needs to be unpacked and relegated to the
scrap heap of human history. Socially defined race was invented to support
social dominance. It has never served any other purpose. The proof of that
claim is found in American history. We began writing this chapter a week
after thousands of people gathered at the Lincoln Memorial for the Com-
mitment March of 2020. Despite the fact that the nation was still in the
midst of the COVID-19 pandemic, people gathered to address the issue of
ongoing police brutality aimed at African Americans. Most of the individu-
als observed at this gathering were wearing masks, although social distanc-
ing was compromised at the large gathering. At that moment, Jacob Blake,
paralyzed from the waist down after a Kenosha, Wisconsin, police officer
shot him seven times in the back, was shackled to his hospital bed despite
not having been charged with a crime.
 223
A WORLD WITHOUT RACISM?

The following day, then President Trump appeared at a campaign event in

New Hampshire. Most of the gathered supporters were not wearing masks
and booed when a public address announcement reminded them that wear-
ing a mask was required by Trump’s own Coronavirus Task Force and New
Hampshire law. None of the unmasked individuals were arrested or shot
by police.
An even worse manifestation of Trumpism materialized on January 6,
2021. A mob of thousands, brought to Washington, D.C. by the former presi-
dent’s ongoing denial of the legitimacy of the election of Joe Biden as the
new president of the United States, stormed the Capitol building. They had
been prompted by Trump’s speech that day. During the insurrection, five
people died. We might never know the true death toll that resulted from
the insurrection, because most of the people in the mob were not wearing
masks. Their actions demonstrated that they intended to capture members
of Congress and Vice President Mike Pence. We can only guess that if they
had captured any of the officials they were looking for, mock trials and public
executions would have followed.
These events are powerful evidence that systemic racism and white
supremacy continue to be significant problems in America. How do we
move forward? Nothing can be achieved without a vision. In this final chap-
ter, we present our vision.

HOW DOES ONE BECOME ANTIRACIST?

We hope that this book has outlined steps toward developing antiracist
thinking. This starts by recognizing that one simply needs to apply standard
methods of critical thinking to the issue of race and racism. When Joe was
dean of general education at North Carolina A&T University, he insisted on
implementing a course in critical thinking for every entering student. Alan
teaches at Hampshire College and was its dean of natural science and of
faculty. Hampshire College focuses on teaching critical thinking and engage-
ment. Critical thinking—being able to gather information and evaluate facts
and ideas—should be a standard part of all high school and university cur-
ricula. Many programs rely on adding critical thinking competencies as
learning objectives across disciplinary coursework. However, we suggest that
requiring at least one course in which the focus is on critical thinking (free
of specific disciplinary content) is a better way to improve students’ skills. A
number of excellent texts can be used at the university level for this purpose.
 224
A WORLD WITHOUT RACISM?

Antiracism is also a moral decision. It starts with a fundamental question

regarding whether you believe that we should have a nation that provides
everyone with equal opportunity for life, liberty, and the pursuit of happi-
ness. A country is judged by how it treats its poorest and most disadvan-
taged. This moral sentiment is in our Constitution. We have unfortunately
fallen short and seem to be backsliding. It is more common to ignore the
poor and foment racism.
Antiracism requires that we all stand together against ongoing racialist
and racist practices. America is in the midst of a racial crisis. The police and
vigilante killings of Breonna Taylor, George Floyd, and Ahmaud Arbery, as
well as the excessive force shooting of Jacob Blake have led to thousands of
demonstrations across the country and internationally. Three of these events
were caught on video, but they represent only the tip of the iceberg of racial
violence in America. They are the canaries in the coal mine of an ongoing
and systematized violence that includes mass incarceration, health disparity,
hunger, and hopelessness.
With racism and white supremacy operating in so many aspects of Ameri-
can society, one does not have to march in protest demonstrations to make
a difference. Indeed, it can be debated that beyond bringing attention to sys-
temic racial violence, protest marches have little impact on making lasting
societal change. As well, not everyone has the ability to march and protest.
On the other hand, before, during, and after such protests, the most impactful
antiracist activities must take place in the communities where we live, work,
worship, and play. We discuss what such activity might look like in this chapter.

ISN’T FOCUSING ON RACE MAKING IT EVEN MORE REAL?

We don’t believe that we can make race any more real than it is. We could
say we wish race was less real, but just wishing it will not make it happen.
The simple and more important point is to be clear about what race is and
what it is not.
We have shown how socially defined race operates to diminish the life
chances of people in virtually every aspect of our society. Social race is real.
Racism is real. What an antiracist perspective requires is accurately under-
standing exactly how racism and white supremacy operate in specific con-
texts and developing programs of action to redress these injustices.
This is a project that we dare not fail. The United States—and, seemingly,
most of the world—is rapidly polarizing around racial justice issues, and
 225
A WORLD WITHOUT RACISM?

this polarization has put democracy at risk. A 2020 survey found that ethnic
antagonism strongly erodes Republicans’ commitment to democracy. In the
survey, 1,151 Republicans and Independents were asked whether they agreed
or disagreed with the statement, “The traditional American way of life is
disappearing so fast that we may have to use force to save it.” The response
showed that 50.7 percent strongly agreed or agreed with that statement. An
additional 27.7 percent were unsure about whether force would be required.
Another closely related statement was, “A time will come when patri-
otic Americans will have to take the law into their own hands.” Responses
showed that 41.3 percent strongly agreed or agreed, and 26.3 percent were
unsure. Recently, we have seen examples of right-wing racially inspired
vigilante action, as in the case of Kyle Rittenhouse, who killed two protesters
and wounded another in Kenosha, Wisconsin (discussed in chapter 10), and
of the January 6 mob attacking the Capitol while prominently displaying
white supremacist symbols. In this regard, the comment from Tony Caniglia
in response to Black Lives Matter protests against his father’s restaurant in
Omaha, Nebraska, was sobering: “Get rid of the rubber bullets and it’s time
to go lethal. . . . I promise you that when the first body hits the ground, reality
will set in for 95 percent of the rioters and you can use the other 5 percent
as target practice.” Talking about race does not make it more real, but accu-
rately and effectively talking about race could make it far less dangerous. We
can’t stop talking about social race until it is insignificant.

WHEN WILL WE KNOW WE HAVE REACHED RACIAL EQUALITY?

HOW DO WE GET TO RACIAL EQUALITY?
WHAT IS POSTRACIAL?

Answering the “when” question is easier than answering the “how” question.
One way we can determine that we have achieved racial equality would be
if all the various measures of social achievement—such as the number of
billionaires, CEOs of major corporations, those in management positions,
university presidents, doctors, lawyers, computer scientists, Senators, and
Congresspeople—were represented at the same level in each socially defined
race in the general population. Doing so would be good for everyone, because
we would draw on the talents of more individuals, and decisions would be
made by a more representative and diverse set of these talented folks.
Similarly, we would expect equality in measures of social dysfunction, such
as incarceration rates, police killings of unarmed persons, unemployment,
 226
A WORLD WITHOUT RACISM?

exposure to toxic pollutants, domestic violence cases, disability days, and

shortened lives. Achieving this equality does not mean increasing any of
these measures for whites. Indeed, we would very much like to see a decrease
for every group. For example, the white incarceration rate is much too high,
and the same is true for white infant mortality and chronic diseases. The
wealth and resources of this nation allow us all to have safer, longer, and
more productive lives. Racism holds us all back.
We would argue that only the most hardened white supremacists would
be against our metric of what racial equality should look like. With this in
mind, the real challenge is determining exactly how we can move from our
current racially stratified society toward racial justice. Some might think it is
counterintuitive that the mistaken idea that we have already achieved a post-
racial color-blind society is one of the major impediments to progress. In the
opening chapter, we discussed color-blindness, the idea that society should
treat everyone the same way. We described how this idea relies on the claim
that instead of the ongoing institutional and individual racism that exists
in American society, nonracial factors such as market dynamics, naturally
occurring phenomena, and the cultural attitudes of minorities themselves
are the main causal factors of their social subordination.
One way to gain a sense of the popularity of such ideas is to examine data
associated with race relations. For example, figure 11.1 shows the percentage
of people who are very satisfied, satisfied, dissatisfied, and very dissatisfied
with the position of Blacks and other racial minorities in America between
the years 2000–20. The wording of the question is such that it is hard to know
what someone might have been thinking when they answered it. One way
of thinking might have been motivated by the Obama presidency during the
years 2008–16. Yet, during those same years, the killing of unarmed Blacks by
police was unabated, mass incarceration continued, and the median wealth
of a Black family was only one-tenth that of whites. Thus, the percentage of
those who answered “very satisfied” or “satisfied” in this poll (always between
53–45 percent, summed together in fig. 11.1) is disconcerting.
One of the most illuminating studies of current views in the United States
concerning race relations addressed the primary reasons that white voters
chose Donald Trump over Hillary Clinton in the 2016 presidential election.
Since the 1960s, Republicans have generally fared slightly better than Demo-
crats with college-educated whites. The 2016 exit polls showed that Trump
had an edge of 4 percentage points in this group over Clinton. However, the
gap between the candidates for non-college-educated whites was 40 percent!
 227
A WORLD WITHOUT RACISM?

60

55

50
Percentage

45

40

35

30
1998 2001 2004 2007 2010 2013 2016 2019
Year

Year vs. satisfied

Year vs. dissatisfied

FIGURE 11.1. Responses to the Gallup poll question, “Next, we’d like to know how you feel about the state of
the nation in each of the following areas. For each one, please say whether you are—very satisfied, somewhat
satisfied, somewhat dissatisfied or very dissatisfied. If you don’t have enough information about a particular
subject to rate it, just say so. How about—the position of blacks and other racial minorities in the nation?”
Source: Gallup, “In Depth: Topics A–Z, Race Relations,” accessed May 4, 2021, https://news.gallup.com/poll
/1687/race-relations.aspx.

These sorts of results make it clear that whether or not America moves in
the direction of antiracism is a political issue. Throughout this work, we have
demonstrated that biological racism is false. If it is, then white supremacists
in America have nothing on which to base their claims. Even if biological
races existed within our species, and if some races were smarter than oth-
ers, there still would be no moral justification for denying all human beings
equal treatment under the law. The unanswered question is, how do we move
toward a society in which equal treatment under the law is possible?
We argue that answering this question requires dismantling institutions
within our society that buttress racial injustice. Many of you who are reading
this book might take exception when we begin to outline specific examples
of institutions and practices that must be eliminated or significantly altered
if we are to ever become a just society. Some of these recommendations exist
 228
A WORLD WITHOUT RACISM?

within the political parties (mainly among Democrats, as the Republicans

have so thoroughly hitched their elephant to pull the war chariot of white
supremacy). Several go well beyond what most of the Democratic Party
would support. Some will begin to make a difference immediately, and oth-
ers will take longer to have an impact. None of these recommendations is
ideal, but achieving them will challenge the way that most people think a
society should operate. Indeed, much of what we suggest will have intersec-
tional impacts, impacts on multiple oppressions, such as class, gender, sexual
orientation, and racial oppression. In the following sections, we list some
actions that we believe will move us in the direction of a less racist and even
antiracist society. These recommendations are not all-encompassing or the
only ones that we or you could make. Indeed, we encourage you to envision
other changes that could help move us toward a more antiracist society.

Voting and Elections

Antiracism starts with fair and equal representation. To that end, we propose
the following:

1. All gerrymandering should be immediately struck down. If this simple and obvi-
ous action were to be taken, state and federal legislatures would begin to more
accurately reflect the racial composition of their constituents.
2. Voter registration should be automatic on every citizen’s eighteenth birthday.
3. Everyone should have their voting rights immediately restored on completion of
any time served for a crime.
4. All voter suppression tactics (requiring identification, police patrols of voting
precincts) should be immediately struck down.
5. Everyone should be able to vote without hardship. Election days should be
national holidays. Early voting and absentee voting should be expanded. The
number of polling places in low-income neighborhoods should be increased.
6. The Electoral College should be eliminated. It overcounts the votes of states with
primarily rural and white majority populations and undercounts those that are
more urban with more diverse (Black, brown, yellow) populations. Election of
the president should be determined by popular vote. If the Electoral College is
retained, “winner takes all” should be eliminated, with electoral votes appor-
tioned based on the percentage of votes each candidate received in each state.
7. Strict limits should be placed on campaign spending. At present, money, more than
programs, determines the outcome of elections. Private donations to campaigns
 229
A WORLD WITHOUT RACISM?

should be eliminated. A fund for local, state, and federal elections should be
established, with equal apportionment of funds for all qualified candidates.
8. All campaign ads on television and the internet must be rigorously fact-checked
by independent entities before airing. Ads that do not pass fact-checking cannot
be aired.

Justice and Policing

The criminal justice system has caused unconscionable harm to poor and
especially Black and brown individuals and families. It must be reformed.
Specifically, the mission of policing must change from a militarized and
often hostile presence in racial minority communities to one that serves
and protects all citizens equally. Instead of breaking up peaceful protests
or strikes, we propose that the mission of law enforcement be focused—
as it always should have been—on protecting all people and all communities
from violent crime.

1. Police forces must be diversified to reflect the demography of the communities in

which they are assigned to work.
2. Ongoing diversity and equity training must be required within all ranks of the
police. It is very important to understand psychological problems and to deal
properly with them, and police need more mental health training and more assis-
tance from professionals who are devoted to mental health interventions.
3. Bail reform must be implemented now. The bail system as currently constructed
forces hundreds of thousands of poor, predominantly racial minority individuals
to sit in jail before they have been convicted of a crime. This has resulted in the
creation of a predatory bail bond system that is based on economic means and
not on fairness.
4. The death penalty must be eliminated in all states. Racial minorities are differen-
tially impacted by death penalty sentencing. Brian Stevenson and his group have
shown that one in nine persons executed was innocent of the crime for which
they were sentenced to death. Jennifer Eberhardt and her group have shown that
African Americans are more likely to receive the death penalty due to ongoing
racist stereotypes concerning their supposed subhuman character.
5. Drugs must be decriminalized and/or legalized. There is no evidence that any
socially defined race sells or uses drugs at a substantially different rate. Data
from 2015 suggest that about 18 percent of adult whites versus 16 percent of adult
 230
A WORLD WITHOUT RACISM?

Blacks use drugs. About 2 percent of both groups sell drugs, but Blacks are 6.5
times more likely to be incarcerated at the state level for drug-related offenses.
Colorado legalized marijuana in 2012, and by 2020, eleven states had done so.
Marijuana is still fully illegal in just eight states. The remaining states have either
decriminalized or allowed marijuana use for medical reasons with a prescrip-
tion. On February 1, 2021, Oregon became the first state to decriminalize small
amounts of “hard” drugs. Fully legalizing drugs nationwide would allow taxes
to be generated from their sale and distribution. This money can used for fund-
ing prevention and addiction treatment programs. Most important, this is money
that will not be flowing into organized crime, also reducing the violence associ-
ated with the drug trade.

Employment Opportunities: A Massive Job Creation Program

One clear way of improving race relations in this country is to prevent or

reduce competition for economic resources. The Reverend Martin Luther
King Jr., in his speech in Montgomery, Alabama, pointed out (based on
the work of C. Vann Woodward) that segregation gave white supervisors
of plantations and factories a backup labor force of poor Blacks. These
Black workers could be used to prevent the formation of labor unions or
to break up strikes by white workers. This resulted in keeping the wages
of Southern whites “almost unbearably low.” This has been a consistent
theme in the development of capitalism. In the Northern cities, industrialists
could always threaten white union workers with employing racial minority
strikebreakers.
Competition for jobs has accelerated neo-liberalism. This phase of capi-
talism has been driven by both the export of labor to foreign countries and
the growth of new technology allowing the unparalleled automation of labor.
This means that jobs in the manufacturing sector of industrialized nations
has been steadily declining. The moniker “rust belt” now describes the cities
that were centers of American manufacturing in the mid-twentieth century.
The loss of high-paying labor jobs in the American economy is intensifying
racial divisions.
Automation via new computer technology has been likened to the steam
engine, electricity, and the internal combustion engine. Jobs have disap-
peared that will never come back in our present economic system. For
example, automation has been introduced in American industry to compete
with the cost and productivity of labor in underdeveloped nations, such as
 231
A WORLD WITHOUT RACISM?

Mexico. In 1997, the total manufacturing output per dollar of labor cost for
Mexico was 2.7 and only 1.3 for the United States. Via automation, in 2013,
that value was 2.9 for Mexico and 2.5 for the United States. So, what hap-
pened to displaced American labor? Much of this has moved into the pre-
carious workforce.
Between 1980 and 2004, more than 30 million Americans lost their jobs.
Many of these individuals transitioned to long-time unemployed, temporary,
and now “gig” economic sectors. People who are employed by companies
are protected by minimum wage laws, cannot be dismissed unfairly, can
unionize, and receive Social Security and pension benefits. The gig economy
does not offer any of that. Even academia has entered the gig world as a result
of the unparalleled growth in “adjunct” instructors.
We believe that a false scarcity of jobs severely inhibits real progress
toward antiracism in the United States and globally. We are in agreement
with the speech by then nominee and now President Joe Biden at the 2020
Democratic National Convention: a commitment must be made to provide
meaningful employment for all.
Additionally, insecurity would decrease and development would improve
if we could include free early child care and expand Head Start centers,
increase the number of public schoolteachers (and their wages), repair
infrastructure (such as roads, bridges, and water pipes), and create farms
that utilize human labor close to or within inner cities. Indeed, making
these changes might have an additional benefit of slowing the production
of potentially pandemic-causing viruses. Finally, we support the plan for a
“Green New Deal,” which promises to create exciting jobs that help to stop
global warming and protect our environment. And we need to build a public
health system that provides jobs where they are needed and also maximize
health, not profits.
Our society needs to envision a new sort of innovation and entrepreneur-
ship. Work need not be full-time. Indeed, most estimates are that efficiencies
should lead to the need for less work. But work should be meaningful and
well compensated. Instead of driving productivity through decreasing the
workforce, innovation should be used to invent new ways of bringing people
back into meaningful jobs. The economic advantages of putting people back
to work are obvious: more people employed increases the demand for goods
and services, which in turn stimulates economic growth. The antiracism
benefits are also obvious: reducing economic competition in turn reduces
the conflict among socially defined groups.
 232
A WORLD WITHOUT RACISM?

Education

We wrote this book in hopes of providing an accessible means for individ-

uals to educate themselves and their communities about race and racism.
Surveys show that there is still considerable confusion about the meaning
of “race” and its influence on society. And indeed, these misunderstandings
convinced us of the need for this book. We further propose the following
steps to improve education around human variation, race, and racism:

1. K–12 science standards that are associated with human biological variation
should be adopted nationwide. Specifically, the standards should address the fail-
ure of the biological race concept to describe biological variation within our spe-
cies. Alan and colleagues Joseph Jones and Maddie Marquez initiated “rethinking
race” as a teacher-training program. However, they could not secure funding to
continue it. A pilot program headed by Brian Donovan has demonstrated both
why this work is so important and how it can be effectively done.
2. K–12 social science and history standards nationwide that accurately address race
and racism should be adopted. We must face our history. Specifics include the
role of chattel slavery in the formation of the United States, the political fight
over slavery as the primary cause for the Civil War, and fuller coverage of recon-
struction, the terror of Jim Crow laws, and more recent fights for voting rights
and protections. In addition, we advocate for inclusion in K–12 curricula of the
racism faced by diverse groups, as illustrated by the Mexican-American War,
the wars against American Indian nations, exploitation of Chinese laborers in
the building of the Transcontinental Railroad, Japanese internment during World
War II, and restrictions on immigration based on faulty racism and eugenics laws
of some “European races,” such as Jews, Irish, and Poles. Finally, K–12 education
should address the expansion of whiteness, further illustrating the role of racism
in American history.
3. School funding by real estate values within the district must be eliminated. All
public school districts should receive equitable funding. As well, public funding
to support charter schools must be eliminated. Charter schools have played a
major role in reinstituting school segregation, particularly in the former Confed-
erate states.
4. A kind of “Marshall Plan” for America’s public schools is needed. This should
include rebuilding and modernizing infrastructure, raising the wages of teachers
to competitive levels (particularly in science, technology, engineering, and medi-
cine); expanding the number of teacher aides in the classroom (as part of the jobs
 233
A WORLD WITHOUT RACISM?

initiatives); expanding the number of counselors and social workers associated

with schools; and restoring programs in athletics, arts, and music. This plan will
make possible the formation of a labor force for meaningful skilled jobs.
5. Institute truth and reconciliation projects similar to those in many countries,
including Germany and South Africa. Susan Neiman’s Learning from the Ger-
mans beautifully illustrates how a nation can face up to its past. These proj-
ects should not be seen as scary or anxiety-producing but as opportunities for
communities to know and confront their past and move together into a more
just future. The pushback by Trump about teaching the history of slavery—
specifically the New York Times “1619 Project”—shows just how much we need to
address, not avoid, our shared history.

Health Care

Access to quality health care ought to be a fundamental human right. This

country spends 18–20 percent of its gross domestic product on health care,
yet the system is geared to making money rather than eliminating disease
and suffering. Moreover, the cost of health care plans is a major contributor
to racial health disparity. In addition, in the age of pandemics, the lack of
access to health care for the poor threatens everyone, as untreated individu-
als will act as a reservoir for infectious disease. We propose the following:

1. Adopt a plan of universal health care coverage. The Medicare for All program of
Senator Bernie Sanders is a template for the creation of a truly universal health
care insurance system by which all Americans will have access to quality and
affordable health care.
2. Expand the training and licensing of physicians and physician assistants. There is
considerable debate about whether the United States is experiencing a physician
shortage. This, of course, is under the current health care model (in which many
people do not have access to needed health care, and this shortage differentially
impacts racial minorities). It is clear that the number of physicians from racially
subordinated groups is inadequate to meet their need. The expanded health
care system we envision would require greater numbers of primary care physi-
cians and nurse practitioners. More health care facilities would need to be built
in primarily minority and rural communities.
3. Per our discussion in chapter 4, physician training and ongoing professional
development programs need curricula that correctly address human biologi-
cal variation and the causes of disease. Specifically, there must be a focus on
 234
A WORLD WITHOUT RACISM?

dismantling racial determinist misconceptions concerning disease prevalence

and, in its place, an understanding of how racism is a public health problem.

Faith Communities

It is our fervent hope that this book will have some traction within faith
communities. The three largest religions in the United States (Christianity,
Judaism, and Islam) have tenets that are consistent with antiracism. How-
ever, in practice, all have fallen short with regard to their beliefs.
To be clear that what follows is not an attack on Christianity, Joe is a
confirmed Episcopalian. He has served on the Racial Justice and Reconcili-
ation Commission of the Episcopal Diocese of North Carolina (RJCR), as
well as the Racial Justice Ministry of his own church. That said, white Chris-
tians (Evangelicals, Mainline Protestants, and Catholics) have failed the
most to face the toxicity of white supremacy in America. Speaking to this
claim, Robert Jones commented, “White Christian churches have not just
been complacent; they have not only been complicit; rather, as the dominant
cultural power in America; they have been responsible for constructing and
sustaining a project to protect white supremacy and resist black equality.
This project has framed the entire American story.”
There is much work to be done in faith communities. Much of this work
centers around developing a productive dialog between science and religion.
This is not as difficult as it sounds, and tools are available to help facilitate
it. Joe serves as the science adviser for both the Chicago and New Bruns-
wick Theological Seminaries (as part of the American Association for the
Advancement of Science’s Dialogue on Science, Ethics, and Religion). He has
discussed science and antiracism before church audiences and for BioLogos.
Following are some things you can do:

1. Start or join an antiracist group in your faith community. There are a number of
useful tools. For Christians, Joe recommends Joseph Barndt’s Becoming the Anti-
Racist Church. Although the book is written for Christians, many of its lessons
would translate across any faith tradition, or all organizations, for that matter.
2. Engage in real efforts to learn about other faith traditions besides your own. Many
faiths are primarily associated with different human populations, such as Islam
with Middle Easterners, Europeans, Africans, and East Asians; or Daoism and
Buddhism with East Asians. Yet, all traditions include diverse individuals. Learn
about the lives of others and their faiths.
 235
A WORLD WITHOUT RACISM?

INTERSECTIONALITY: HOW DOES ANTIRACISM FIT WITH THE

FIGHT AGAINST OTHER FORMS OF OPPRESSION AND SOCIAL
INJUSTICE?

We see the fight against racism as hand in hand with the fight against all
forms of injustice. The term intersectionality is used by scholars to describe
the interactions among various forms of social dominance (e.g., classism,
racism, sexism, anti-gay bigotry). Women consistently earn less than men,
and pay rate also differs by socially defined race. In 2013, female median
annual incomes were $46,000 for Asian/Pacific Islanders, $40,000 for whites,
$38,000 for people of two or more races, $31,000 for American Indians, and
$28,000 for Hispanics.
Homicide rates against transgender individuals also differ by socially
defined race. We do not think that we can (or should) make progress against
all of these forms of oppression in isolation from one another. For example,
one of the drawbacks of the original woman’s movement in the United States
was its racism. Rampant sexism was one of the most glaring drawbacks of the
Civil Rights movement. Finally, we think that it will be difficult or impossible
to make lasting change in any form of oppression within the context of capi-
talism. As discussed earlier, the dynamics of this economic system operate to
exacerbate the intersectional antagonisms that exist within our society. Nei-
ther do we think that socialism is a guaranteed solution to these social antag-
onisms. Countries that have made real progress with regard to democratic
socialism, such as Norway, have neither large, ethnically diverse populations
nor a history of racial slavery. The simple fact is that there is no road map that
we can turn to for how to build a more just society. We know the things that
we need to dismantle (e.g., classism, racism, sexism, anti-gay bigotry).
Finally, we end with this warning. If democracy should fall in America,
there will be no one to rescue us. In World War II America, we had the “arse-
nal of democracy” to provide both materials and people to bring down the
fascist and racist Axis forces in Europe and Asia. Joe’s dad landed on Utah
Beach during the Normandy invasion of 1944. His maternal uncles fought
in the Pacific against the empire of Japan. Alan’s father was wounded in the
war and awarded the Purple Heart. Today, no other nation has the economic
means or interest to rescue America from a fascist dictatorship. We are all
we have, and therefore the battle against racism is one that we dare not lose.
How we do (or do not) engage in this struggle will determine the future of
our species and our precious planet.
 CONCLUSIONS

Our primary message is that in our species, biological races are a myth. This
idea is not supported by modern science. It fails to describe, explain, or tell
us how to properly utilize human variation in biomedical research. Yet, race
is a social and historical means of classifying and dividing individuals and
has many consequences. The belief in biological races has a synergetic rela-
tionship to racism. It has provided, and still provides, ideological coverage
for racism. Dismantling the myth of race as a biological idea is a first step
toward antiracism.
We have tried to clarify what race is and isn’t and the connections among
race, racism, and human genetic variation. We have endeavored to do so by
answering questions that our students, friends, family, and colleagues have
asked us, and we have tried to answer them in a straightforward way without
skimping on the underlying facts and details. In the following, we present
our major takeaways. In this age of elevator pitches and Twitter, we start with
some short take-home messages or sound-bites and conclude with some elab-
orations on the fundamental concepts of race, racism, and human variation.

TEN FACTS

1. Human biological variation is real. It is patterned, important, and a thing of

beauty to be celebrated.
2. Race neither describes nor explains human biological variation.
 238
CONCLUSIONS

3. Humans do not have biological races.

4. Human biological races are a relatively recent idea that was reified—made real
legally and scientifically—to justify racism.
5. Racial classifications developed historically as a politically important means to
categorize and divide individuals.
6. Many individuals still believe in the myth of race as being “obviously” biological,
in the blood and genes. Race is a powerful illusion. That myth provides ideologi-
cal justification for systemic racial inequalities.
7. Racism is an ideology that is built on a myth and widely shared, with institutional
and structural manifestations.
8. The proof of the impact of racism is found in the data on inequalities in almost
all aspects of life, including education, employment, health, and wealth.
9. Race will become less salient when racial ideology is overcome and races reach
equality in measures of life such as health and wealth.
10. We cannot have a civil and just society without racial equality. Racial equality will
be good for everyone.

HUMAN BIOLOGICAL VARIATION

By this we refer to the pattern of phenotypic and genetic differences and

similarities among individuals and groups. Some authors, such as Nicholas
Wade, imagine that showing that humans do not have biological races is the
same as saying that individual and group genetic variation does not exist or
that this variation is always insignificant. Nothing could be further from our
position and the facts.
Wade says that the critique of race comes mostly from politically moti-
vated social scientists. He fails to realize that biological anthropologists and
evolutionary biologists such as Ashley Montagu, Richard Lewontin, Alan,
and Joe have led the critique of biological races. Let’s be clear: human varia-
tion exists. But race does not describe or explain human variation.
It is true that our overall genetic variation is less than we might have
expected. Any individual—of the same or different social race—is sur-
prisingly similar to any other individual on a genetic level. This is mainly
because we are a relatively young species and one that has experienced few
geographic blocks to the flow of people and their genes.
We are a species with a worldwide distribution. And there is evidence that
individuals who occupy different parts of the world differ from one another.
These local variations leave some genetic signatures of ancestry, not race.
 239
CONCLUSIONS

But these differences are small, found primarily in noncoding genes, and are
well explained by geographical distance and specific ancestries. Ancestry is
not the same as race.
Biological anthropologists and human population geneticists study the
evolutionary forces and mechanisms that produce variations and the vari-
ous consequences of that variation. As for how variation comes about, most
is selectively neutral; thus, groups randomly differ in allele frequencies via
genetic drift. The genetic distance between groups is understood by the
amount of gene flow between them (isolation by distance). As we showed in
chapter 1, the genetic difference between any two groups is highly correlated
with the geographic distance between them.
Some variations are adaptive and appear to be the result of natural selec-
tion related to environments in different parts of the world. Skin color and
sickle cell anemia are two well-studied examples that we previously reviewed.
Skin color varies by amount of solar radiation and appears to be a com-
promise between folate destruction due to too much radiation (most likely
to occur in less pigmented skin) and low vitamin D3 (a more likely result
for darker skin). Sickle cell trait is a balanced polymorphism. Having one
copy of the sickle cell allele is a winning compromise, providing resistance
to malaria but not the debilitating consequences of sickle cell disease. It is a
genetic compromise.
Other disease risk genes differ in frequency among groups (not races!).
However, what is most astonishing is the relatively high amount of variation
among individuals within any given group. Because there is so much varia-
tion between two individuals in a so-called race, the concept of race ceases to
be meaningful. By all objective measures, such as Wright’s population subdi-
vision statistic (FST), humans fail the test of “race-ness.”
Finally, individuals vary in simple Mendelian genetic traits such as sickle
cell, as well as complex traits such as height, weight, and disease predisposi-
tion (determined by many genes). Even the simple traits can be affected by
life courses and developmental conditions. The complex traits are just that—
complex unfolding of the interactions of multiple genes and environmental
conditions over time.
In summary, human biological variation is complex, patterned, impor-
tant, and incredibly interesting. We are excited to be contributing to the rev-
olution in understanding genomes and genomic differences. Our concern,
first, is that we not over-react to genetic information. Indeed, as we explore
genomes, what is becoming clearer is just how complex and interactive genes
 240
CONCLUSIONS

are. And second, we want to make clear (if anything is clear) that human
variation is nonracial. Viva la difference.

HUMAN BIOLOGICAL VARIATION ≠ RACE

If you’ve learned one thing from this book, we hope it is this: although
human biological and genetic variation is real, humans simply do not divide
into races.
The structure of human genetic variation—how it is patterned on a
worldwide level—is profoundly nonracial. If humans had races, we would
expect clear variations among purported races. But no matter how races are
described and delineated, we do not find clear demarcations.

• Human variation is typically continuous from one individual to the next and
from one group to the next. For example, skin color around the globe varies
slowly from one shade to slightly lighter or darker shades. Allele frequencies also
vary slowly from one group to the neighboring groups. Race implies clear breaks
or discontinuities, but that is not the truth of human global variation.
• We tend to think of race as identified by phenotypes—outward signs of
differences—such as skin color. Biological race implies that skin color is simply
the outward manifestation of deeper and more complex traits and abilities. But
the truth is that skin color fails to predict almost anything else save the color of
one’s eyes and hair. This is because traits are largely inherited independently.
• Finally, we now know just how much genetic variation there is among continents,
among groups within a continent, and among individuals within any given group.
Almost fifty years ago, Richard Lewontin found that only about 6 percent of varia-
tion was apportioned to variation among continents and most of the remaining
variation was within any local group. Variation among continents and anything
we might think of as biological races, Lewontin concluded, are biologically rather
meaningless. His results have been corroborated over and over in the last fifty years.
• Variation among groups is mainly a result of geographic distance.
• The average genetic difference between any two individuals has almost nothing to
do with race. In fact, two individuals from Africa are on average more different
genetically from each other than one of them is from a European or Asian.

RACISM

A main aim of this book is to combat racism as both ideology and insti-
tutional practices. Some have argued that racism is a thing of the past and
 241
CONCLUSIONS

that we are postracial. Others have suggested that racism is a natural part of
evolution. Yet others think racism is just a part of the “natural” competition
among groups. Some have even argued in the courts and centers of public
discourse that favoring individuals of color now overshadows racism against
individuals of color. All of these suggestions and ideas are totally unsup-
ported by the facts of inequalities by race in health, wealth, and virtually all
important aspects of life.
Ibram X. Kendi makes the important point that racial inequalities in, say,
incarceration rates and educational achievements can be explained in only
two ways: by genetic differences among races or by unequal historical and
continuing social conditions of life. As a naturalist aboard HMS Beagle, a
young Charles Darwin came to the same conclusion almost two hundred
years ago. He wrote, “If the misery of the poor be caused not by the laws of
nature, but by our institutions, great is our sin.” Indeed, great are our sins.
We have answered questions about why genetic differences among races
fail to explain a wide range of inequalities and explain that it is a myth to
think that there are genetically based racial differences in attributes such as
intelligence, athletic performance, and more. Having shown that genes do
not explain racial differences frees us to examine how institutions and sys-
tems continue to promote inequalities.
And there are many inequalities. In the United States, there are tremen-
dous differences in wealth and health by class, education, and race. We have
tried to show how the race differences in criminal justice and incarceration
affect lives and families. Race differences in education, employment, and liv-
able environments perpetuates a permanent caste-like system of inequality.
Americans think there is a race difference in wealth but seriously underes-
timate the size of the gap. There is not a wealth gap; rather, there is wealth
hoarding. Everyone suffers without movements toward more economic
equality by class and race. Wealthy families become literally fenced and
walled off. They live in fear and the nagging reality that their wealth is not
sustainable. And, of course, the greater consequence of wealth inequalities
is borne by poor families and Black and brown families. Poverty takes away
security, leading to stress, and presents a wide range of hindrances to devel-
opment. Wealth is inherited.
Life expectancy differences between white and Black individuals, now an
average of about four years, decreased in the early years of the twenty-first
century. That is a great sign, but the difference, on top of class-based inequal-
ity, represents an unconscionable loss of opportunity and life. A 2012 paper
showed a sixteen-year gap in life expectancy if one combines education and
 242
CONCLUSIONS

race. And, sadly, now we must add that the racial gap in life expectancy is
growing again as a consequence of the grossly unequal impact of COVID-19.
A recent estimate is that the reduction in life expectancy at birth in 2020
for whites will be .68 years and 2.10 and 3.05 years for Blacks and Latinos,
respectively. Those lost years are of someone’s child, spouse, and parent. The
loss of opportunity is a drag on society, a drag that everyone pays for.

BEYOND RACIAL THINKING AND RACISM

Racism has its origins in the worldview that races are biologically real and
differ in abilities. That view of humankind provided false justifications for
enslavement and colonization. It still functions in providing cover for police
violence and countless everyday acts that promote the status quo. The most
important step to combat racism, therefore, is to expose racial ideology to
the light of facts and science.
There are many challenges facing Americans and our globe. We are still in
the midst of the COVID-19 pandemic. Climate disruptions are becoming all
too evident. A pandemic and climate change are incredibly important global
threats. We submit that there is a reason that the United States has failed to
come together to fight these threats: racism. Until we change our mindsets
to see one another as equals, we are doomed. We will not be able to address
existential threats until we address the roots of racism.
Antiracism starts with understanding what race is and isn’t.
Antiracism is not just an ethical and scientifically correct position; it is
necessary to our survival.
 NOTES

PREFACE
1. A. Hassan, “Hate-Crimes Violence Hits 16-Year High, FBI Reports,” New York Times,
November 12, 2019, https://www.nytimes.com/2019/11/12/us/hate-crimes-fbi-report
.html.
2. “Antisemitic Incidents Hit All-Time High in 2019,” Anti-Defamation League, May 12,
2020, https://www.adl.org/news/press-releases/antisemitic-incidents-hit-all-time-high
-in-2019.
3. B. Tatum, “Why Are All The Black Kids Sitting Together in the Cafeteria?”: A Psycholo-
gist Explains the Development of Racial Identity (New York: Basic Books, 1997).

INTRODUCTION
1. Scleroderma Foundation, accessed April 6, 2021, https://www.scleroderma.org/site
/DocServer/About_Scleroderma.pdf?docID=660 and Sclero.org, https://sclero.org
/scleroderma/causes/genetics/geography.html.
2. “Osteoporosis: Are You at Risk?” WebMD, November 20, 2020, https://www.webmd
.com/osteoporosis/guide/osteoporosis-risk-factors.
3. K. Gewertz, “Taxonomist Carl Linnaeus on Show at HMNH,” Harvard Gazette, Novem-
ber 1, 2007, https://news.harvard.edu/gazette/story/2007/11/taxonomist-carl-linnaeus
-on-show-at-hmnh-2/.
4. C. Linnaeus, Systema Naturae, 10th ed., 1758.
5. S. Outram, J. L. Graves, J. Powell, et al., “Genes, Race, and Causation: US Public
Perspectives About Racial Difference, Race and Social Problems,” Race and Social
Problems 10 (2018): 79–90, https://doi.org/10.1007/s12552-018-9223-7. This study also
showed that whites were more likely to believe that race was more biological than
social and Blacks were less likely to believe that race was more biological than merely
a social classification.
 244
INTRODUCTION

6. M. F. Jacobson, Whiteness of a Different Color (Cambridge, MA: Harvard University

Press, 1989).
7. We go more deeply into this subject in chapter 3.
8. M. F. Fraga, E. Ballestar, M. F. Paz, et al., “Epigenetic Differences Arise During the
Lifetime of Monozygotic Twins,” Proceedings of the National Academy of Sciences
of the United States of America 102, no. 30 (2005): 10604–9, https://doi.org/10.1073
/pnas.0500398102.
9. K. J. Wu, “Twins with Covid Help Scientists Untangle the Disease’s Genetic Roots,”
New York Times, January 18, 2021, https://www.nytimes.com/2021/01/18/health/covid
-twins-genetics.html.
10. C. Darwin, On the Origin of Species, or the Preservation of Favored Races in the Struggle
for Life (London: John Murray, 1859).
11. N. Jablonski and G. Chapin, “The Evolution of Human Skin Coloration,” Journal of
Human Evolution 39 (2000): 57–106.
12. R. Nielsen, J. M. Akey, M. Jakobsson, J. K. Pritchard, S. Tishkoff, and E. Willerslev,
“Tracing the Peopling of the World Through Genomics,” Nature 541, no. 7637 (2007):
302–10, https://doi.org/10.1038/nature21347.
13. P. M. McDonough, G. J. Duncan, D. Williams, and J. House, “Income Dynamics and
Adult Mortality in the United States, 1972–1989,” American Journal of Public Health 87
(1997): 1476–83.
14. Numerous scholarly studies have demonstrated differential exposure of ethnic minor-
ities to toxic environmental conditions. These studies are reviewed in J. L. Graves,
“Looking at the World Through ‘Race’-Colored Glasses: The Influence of Ascertain-
ment Bias on Biomedical Research and Practice,” in Mapping “Race”: A Critical Reader
on Health Disparities Research, ed. L. E. Gómez and N. López (New Brunswick, NJ:
Rutgers University Press, 2003).
15. “On Views of Race and Inequality, Blacks and Whites Are Worlds Apart,” Pew
Research Center, Social and Demographic Trends, June 27, 2016, https://www
.pewsocialtrends.org/2016/06/27/on-views-of-race-and-inequality-blacks-and-whites
-are-worlds-apart/.
16. Centers for Disease Control and Prevention, National Center for Health Statistics,
“Data Table for Figure 1. Life Expectancy at Birth, by Sex, Race, and Hispanic Origin:
United States, 2006–2016,” in Health, United States, 2017, https://www.cdc.gov/nchs
/data/hus/2017/fig01.pdf.
17. This is well explained in J. L. Graves, The Emperor’s New Clothes: Biological Theories of
Race at the Millennium (New Brunswick, NJ: Rutgers University Press, 2005).
18. This perspective is explored in E. Bonilla-Silva, “Rethinking Racism: Toward a Struc-
tural Interpretation,” American Sociological Review 62, no. 3 (1997): 465–80.
19. J. A. Glancy, Slavery in Early Christianity (Minneapolis: Fortress, 2006).
20. J. L. Graves, “Genocide (Japanese Occupation),” in Encyclopedia of Race and Racism,
2nd ed., ed P. L. Mason (Farmington Hills, MI: Gale-Cengage Learning, 2013).
21. The genocide in Rwanda was a complex and strange application of racialist/racist ide-
ology. For a thorough discussion, see H. H. Hintjens, “Explaining the Genocide in
Rwanda,” Journal of Modern African Studies 37, no. 2 (1991): 241–86.
22. See E. Rueb and D. Taylor, “Tucker Carlson of Fox Falsely Calls White Supremacy a
‘Hoax,’ ” New York Times, August 8, 2019, https://www.nytimes.com/2019/08/08/business
/media/tucker-carlson-white-supremacy.html.
 245
1 . H OW D I D R AC E B E CO M E B I O LO G I C A L?

1. HOW DID RACE BECOME BIOLOGICAL?

1. See the discussion in J. L. Graves, The Emperor’s New Clothes: Biological Theories
of Race at the Millennium (New Brunswick, NJ: Rutgers University Press, 2005),
15–20.
2. J. E. H. Smith, “The Pre-Adamite Controversy and the Problem of Racial Difference
in Seventeenth-Century Natural Philosophy,” in Controversies Within the Scientific
Revolution, ed. E. Dascal and N. D. Boantza (Amsterdam: John Benjamins Publish-
ing, 2011).
3. F. Douglass, Claims of the Negro Ethnologically Considered (Rochester, NY: Lee, Mann
& Co., 1854).
4. Graves, The Emperor’s New Clothes, chap. 4, “Darwinism Revolutionizes Anthropol-
ogy,” 55–73.
5. A. Smedley, Race in North America: Origin and Evolution of a Worldview (Boulder,
CO: Westview, 1993).
6. R. McLaughlin, The Roman Empire and the Silk Routes: The Ancient World Economy
and the Empires of Parthia, Central Asia, and Han China (Barnsley, UK: Pen & Sword
History, 2016); and R. C. Redfern, D. R. Gröcke, et al., “Going South of the River:
A Multidisciplinary Analysis of Ancestry, Mobility and Diet in a Population from
Roman Southwark, London,” Journal of Archaeological Science 74 (2016): 11–22, http://
dx.doi.org/10.1016/j.jas.2016.07.016.
7. Graves, The Emperor’s New Clothes, 17–20.
8. C. L. Brace, “Race” Is a Four-Letter Word: The Genesis of the Concept (New York:
Oxford University Press, 2005), 19–20.
9. Brace, “Race” Is a Four-Letter Word.
10. I. Hannaford, Race, The History of an Idea in the West (Washington, DC: Woodrow
Wilson Center Press, 1996).
11. J. Reston, Dogs of God: Columbus, the Inquisition, and the Defeat of the Moors (New
York: Anchor, 2006).
12. H. Zinn, A People’s History of the United States (New York: Harper Perennial Modern
Classics, 2015). See the chapter titled “Columbus and the Indians.”
13. J. Tisby, “What Columbus Really Thought About Native Americans,” The Witness,
October 8, 2018, https://thewitnessbcc.com/columbus-and-his-fellow-europeans
-imported-their-ideas-of-racial-superiority-into-relationships-with-native-americans/.
14. T. Keel, Divine Variations: How Christian Thought Became Racial Science (Palo Alto,
CA: Stanford University Press, 2019).
15. L. Eiseley, Darwin’s Century: Evolution and the Men Who Discovered It (New York:
Anchor Doubleday, 1958).
16. A. O. Lovejoy, The Great Chain of Being: A Study of the History of an Idea (Cambridge,
MA: Harvard University Press, 1936).
17. D. B. Domingues da Silva and N. Radburn, eds., Slave Voyages, 2008–Present, https://
www.slavevoyages.org/.
18. W. M. Wiecek, “The Origins of the Law of Slavery in British North America,” Cardozo
Law Review 17 (1995): 1711.
19. I. F. Gomez, “International Law, Ethno-Cultural Diversity and Indigenous People’s
Rights,” in Ethno-Cultural Diversity and Human Rights: Challenges and Critiques, ed.
G. Pentassuslia (Leiden: Brill Nijhoff, 2018).
 246
1 . H OW D I D R AC E B E CO M E B I O LO G I C A L?

20. D. M. Goldenberg, The Curse of Ham: Race and Slavery in Early Judaism, Christianity,
and Islam (Princeton, NJ: Princeton University Press, 2003).
21. C. Darwin, Voyage of the Beagle (London: Henry Colburn, 1839).
22. E. Mayr, The Growth of Biological Thought: Diversity, Evolution, and Inheritance (Cam-
bridge, MA: Belknap Press of Harvard University Press, 1982).
23. S. S. Smith, “An Essay on the Causes of the Variety of Complexion and Figure in the
Human Species” (Philadelphia: Printed and sold by Robert Aitken, at Pope’s Head,
Market Street, MDCCLXXXVII [1787]), http://resource.nlm.nih.gov/2572030R.
24. S. Juengel, “Countenancing History: Mary Wollstonecraft, Samuel Stanhope Smith, and
Enlightenment Racial Science,” ELH 68, no. 4 (2001): 897–927, http://www.jstor.com
/stable/30031999.
25. Graves, The Emperor’s New Clothes, 39, table 3.1.
26. Graves, The Emperor’s New Clothes, 44, table 3.2.
27. I. Duncan, Pre-Adamite Man; Or, the Story of Our Old Planet and Its Inhabitants, Told
by Scripture and Science (Edinburgh: W. P. Kennedy, 1860).
28. C. Irmscher, Louis Agassiz: Creator of American Science (Boston: Houghton Mifflin
Harcourt, 2013); see the chapter entitled “A Pint of Ink.”
29. A. Desmond and J. Moore, Darwin: The Life of a Tormented Evolutionist (New York:
Time Warner, 1991). See also the discussion of Darwin’s concern about retaliation
from Irmscher, Louis Agassiz, 442–43.
30. A. Desmond and J. Moore, Darwin’s Sacred Cause: How a Hatred of Slavery Shaped
Darwin’s Views on Human Evolution (Boston: Houghton Mifflin Harcourt, 2009).
31. Mayr, The Growth of Biological Thought, 254–63.
32. Graves, The Emperor’s New Clothes, 44, table 3.1.
33. W. Abraham, “The Life and Times of Anton Wilhelm Amo,” Transactions of the His-
torical Society of Ghana 7 (1964): 60–81, http://www.jstor.com/stable/41405765; and B.
Brentjes, “Anton Wilhelm Amo, First African Philosopher in European Universities,”
Current Anthropology 16, no. (1975): 443, https://doi.org/10.1086/201577.
34. J. F. Blumenbach, “De Generis Humani Varietate Native Liber” [On the Natural Variet-
ies of Mankind], 1775. In The Anthropological Treatises of Johann Friedrich Blumenbach
and the Inaugural Dissertation of John Hunter, ed. and trans. T. Bendyshe (Lon-
don: Longman, Green, Longman, Robers, & Green, 1865), 65–144, http://dx.doi.org
/10.5962/bhl.title.50868.
35. Douglass, Claims of the Negro, Ethnologically Considered.
36. S. Morton, Crania Americana, or, A Comparative View of the Skulls of Various Aboriginal
Nations of North and South America (Philadelphia: J. Dobson, 1839), https://collections
.nlm.nih.gov/catalog/nlm:nlmuid-60411930R-bk.
37. S. J. Gould, The Mismeasurement of Man (New York: Norton, 1980).
38. Irmscher, Louis Agassiz, see the chapter titled “A Pint of Ink.”
39. R. Bean, “Some Racial Peculiarities of the Negro Brain,” American Journal of Anatomy
5 (1906): 353–431.
40. Joe summarized the history of racial science in his book The Emperor’s New Clothes.
41. W. Z. Ripley, The Races of Europe: A Sociological Study (New York: D. Appleton, 1899).
42. C. S. Coon, The Races of Europe (New York: Macmillan, 1939).
43. R. Bean, “The Nose of the Jew and the Qudratus Mabii Spererioris Muscle,” Anatomi-
cal Record 7 (1913): 47–49.
44. E. O. Manoiloff, “Discernment of Human Races by Blood: Particularly of Russians
from Jews,” American Journal of Physical Anthropology 10 (1927): 11–21.
 247
2 . E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

45. M. F. Jacobson, Whiteness of a Different Color: European Immigrants and the Alchemy
of Race (Cambridge, MA: Harvard University Press, 1998).

2. EVERYTHING YOU WANTED TO KNOW ABOUT

GENETICS AND RACE
1. But even identical twins can vary epigenetically, non-nucleotide changes in DNA, that
affect whether DNA is “read” and might eventually code for a protein.
2. Identical twins have identical genomes because the chromosomes they inherited are
identical. Identical twins are formed when, after fertilization of an egg by a sperm
cell and at the two-cell stage of development, the embryo splits. Each cell now begins
development as a separate organism, but both contain an identical set of chromo-
somes. However, everyone else varies genetically.
3. Ancestry is different from race and should not be confused with the concept of race.
We all have ancestries; that is, we come from different places and have parents, grand-
parents, and ancestors further in our past. Those genetic connections can be traced.
This is further discussed in chapter 9.
4. We are also genetically 99 percent the same as chimpanzees, our nearest living nonhu-
man relatives.
5. R. Redon, S. Ishikawa, K. R. Fitch, L. Feuk, G. H. Perry, T. D. Andrews, H. Fiegler, et
al, “Global Variation in Copy Number in the Human Genome,” Nature 444, no. 7118
(November 23, 2006): 444–54, https://doi.org/10.1038/nature05329.
6. The 1000 Genomes Project Consortium, A. Auton et al., “A Global Reference for
Human Genetic Variation,” Nature 526, no. 7571 (October 1, 2015): 68–74, https://doi
.org/10.1038/nature15393.
7. S. Wright, Evolution and Genetics of Populations: A Treatise in Four Volumes. 4: Variabil-
ity Within and Among Natural Populations (Chicago: University of Chicago Press, 1978).
8. This is not an exact science, because populations can be arbitrarily decided on. For
example, one could calculate subdivision for a range of ethnic populations within a
region of a continent (English, French, Basques), or across regions within a continent
(Han Chinese, Japanese, or Mongolians), or among continents (Africa, Asia, Austra-
lia, Europe, etc.). Still, FST does tell us something!
9. S. Garte, “Human Population Genetic Diversity as a Function of SNP Type from Hap-
Map Data,” American Journal of Human Biology 22, no. 3 (2010): 297–300, https://doi
.org/10.1002/ajhb.23324.
10. S. Myles, D. Davison, J. Barrett, M. Stoneking, and N. Timpson, “Worldwide Popu-
lation Differentiation at Disease-associated SNPs,” BMC Medical Genomics 1, no 22.
(2008), https://doi.org/10.1186/1755-8794-1-22.
11. A. R. Templeton, “Genetics and Recent Human Evolution,” Evolution 61, no. 7 (2007):
1507–19, https://doi.org/10.1111/j.1558-5646.2007.00164.x. However, it is important to
avoid making the common error that small amounts of genetic variation within a
species necessarily means that the species could not have formed biological races.
Unfortunately, this misconception is seen in many popular treatments of biologi-
cal race. An example is in the description on the race and racial identity section of
the National Museum of African American History and Culture’s website, “Talking
About Race,” https://nmaahc.si.edu/learn/talking-about-race/topics/race-and-racial
-identity; accessed April 20, 2021.
 248
2 . E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T G E N E T I C S A N D R A C E

12. A. Fischer, K. Prüfer, J. M. Good, et al., “Bonobos Fall Within the Genomic Variation
of Chimpanzees,” PLoS One 6, no. 6 (June 29, 2011): e21605, https://doi.org/10.1371
/journal.pone.0021605.
13. S. Theodoridis, D. A. Fordham, S. C. Brown, et al., “Evolutionary History and Past
Climate Change Shape the Distribution of Genetic Diversity in Terrestrial Mammals,”
Nature Communications 11, no. 2557 (2020), https://doi.org/10.1038/s41467-020-16449-5.
14. D. Thaler, “Why Should Mitochondria Define Species?,” Human Evolution 33, nos. 1–2
(2018): 1–30, doi:10.14673/HE2018121037.
15. J. Herron and S. Freeman, Evolutionary Analysis, 5th ed. (New York: Pearson, 2013).
16. P. Gagneux, M. K. Gonder, T. L. Goldberg, and P. A. Morin, “Gene Flow in Wild Chim-
panzee Populations: What Genetic Data Tell Us About Chimpanzee Movement Over
Space and Time,” Philosophical Transactions of the Royal Society of London, Series B,
Biological Sciences 356, no. 1410 (2001): 889–97, https://doi.org/10.1098/rstb.2001.0865.
17. R. Kuper and S. Kropelin, “Climate-Controlled Holocene Occupation in the Sahara:
Motor of Africa’s Evolution,” Science 313, no. 5788 (2006): 803–807.
18. R. Nielsen, J. M. Akey, M. Jakobsson, et al., “Tracing the Peopling of the World
Through Genomics,” Nature 541, no. 7637 (2017): 302–10, https://www.nature.com
/articles/nature21347.
19. Indeed, human activity in reducing the size of other large-bodied mammal popula-
tions, their geographical ranges, and their ability to migrate between their locations
played a major role in these species’ forming biological races.
20. S. Fan, M. E. Hansen, Y. Lo, and S. A. Tishkoff, “Going Global by Adapting Local: A
Review of Recent Human Adaptation,” Science 354, no. 6308 (2016): 54–59, https://doi
.org/10.1126/science.aaf5098.
21. N. G. Crawford, D. E. Kelly, M. E. B. Hansen, et al., “Loci Associated with Skin Pig-
mentation Identified in African Populations,” Science 358, no. 6365 (2017): eaan8433,
https://doi.org/10.1126/science.aan8433. Corrections published December 15, 2017, and
January 17, 2020.
22. L. J. Handley, A. Manica, J. Goudet, and F. Balloux, “Going the Distance: Human
Population Genetics in a Clinal World,” Trends in Genetics 23, no. 9 (2007): 432–39,
https://doi.org/10.1016/j.tig.2007.07.002.
23. L. Quintana-Murci, O. Semino, H. J. Bandelt, et al., “Genetic Evidence of an Early Exit
of Homo sapiens sapiens from Africa Through Eastern Africa,” Nature Genetics 23, no.
4 (1999):437–41.
24. This is what is known as a Neanderthal admixture.
25. T. Günther and M. Jakobsson, “Genes Mirror Migrations and Cultures in Prehistoric
Europe: Population Genomic Perspective,” Current Opinions in Genetics & Develop-
ment 41 (2016): 115–23, https://doi.org/10.1016/j.gde.2016.09.004.
26. M. Rasmussen, X. Guo, Y. Wang, et al., “An Aboriginal Australian Genome Reveals
Separate Human Dispersals Into Asia,” Science 334, no. 6052 (2011): 94–98, https://doi
.org/10.1126/science.1211177.
27. A. S. Malaspinas, M. C. Westaway, C. Muller, et al., “A Genomic History of Aboriginal
Australia,” Nature 538, no. 7624 (2016): 207–14, https://doi.org/10.1038/nature18299.
28. M. Raghavan, M. Steinrücken, K. Harris, et al., “Genomic Evidence for the Pleistocene
and Recent Population History of Native Americans,” Science 349, no. 6250 (2015):
aab3884, https://doi.org/10.1126/science.aab3884.
29. A. M. Little, I. Scott, S. Pesoa, et al., “HLA Class I Diversity in Kolla Amerindians,” Human
Immunology 62, no. 2 (2001): 170–79, https://doi.org/10.1016/S0198-8859(00)00248-2.
 249
3 . E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

30. D. Reich, Who We Are and How We Got Here (New York: Pantheon, 2018).
31. S. G. Byars and K. Voskarides, “Antagonistic Pleiotropy in Human Disease,” Journal of
Molecular Evolution 88, no. 1 (2020): 12–25, https://doi.org/10.1007/s00239-019-09923-2.
32. M. F. Hammer, A. E. Woerner, F. L. Mendez, et al., “Genetic Evidence for Archaic
Admixture in Africa,” Proceedings of the National Academy of Sciences 108, no. 37
(2011): 15123–28, https://www.pnas.org/content/early/2011/08/29/1109300108.
33. J. K. Pritchard, M. Stephens, and P. Donnelly, “Inference of Population Structure Using Mul-
tilocus Genotype Data,” Genetics 155: 945–59, https://www.genetics.org/content/155/2/945.
34. S. Tishkoff, F. A. Reed, F. R. Friedlaender, et al., “The Genetic Structure and His-
tory of Africans and African Americans,” Science 324: 1035–44, https://doi.org/10.1126
/science.1172257.
35. Recent research supports this claim. See T. Günther, C. Valdiosera, H. Malmström, et
al., “Ancient Genomes Link Early Farmers from Atapuerca in Spain to Modern-Day
Basques,” Proceedings of the National Academy of Sciences112, no. 38 (2015): 11917–22,
https://doi.org/10.1073/pnas.1509851112; E. R. Jones, G. Gonzalez-Fortes, S. Connell, et
al., “Upper Palaeolithic Genomes Reveal Deep Roots of Modern Eurasians,” Nature
Communications 6: 8912, https://doi.org/10.1038/ncomms9912; J. Paganini, L. Abi-
Rached, P. Gouret, et al., “HLAIb Worldwide Genetic Diversity: New HLA-H Alleles
and Haplotype Structure Description,” Molecular Immunology 112 (2019): 40–50,
https://doi.org/10.1016/j.molimm.2019.04.017; F. A. Reed and S. A. Tishkoff, “African
Human Diversity, Origins and Migrations,” Current Opinions in Genetics & Develop-
ment 16, no. 6 (2006): 597–605, https://doi.org/10.1016/j.gde.2006.10.008; A. K. Roy-
choudhury and M. Nei, Human Polymorphic Genes: World Distribution (New York:
Oxford University Press); O. Thalmann, D. Wegmann, M. Spitzner, et al., “Historical
Sampling Reveals Dramatic Demographic Changes in Western Gorilla Populations,”
BMC Evolutionary Biology 11 (2011): 85, https://doi.org/10.1186/1471-2148-11-85; and J.
Yang, B. Benyamin, B. P. McEvoy, et al., “Common SNPs Explain a Large Propor-
tion of the Heritability for Human Height,” Nature Genetics 42, no. 7 (2010): 565–69,
https://www.nature.com/articles/ng.608.

3. EVERYTHING YOU WANTED TO KNOW ABOUT RACISM

1. (1963) G. Wallace, “Segregation Now, Segregation Forever,” BlackPast, January 22,
2013, https://www.blackpast.org/african-american-history/speeches-african-american
-history/1963-george-wallace-segregation-now-segregation-forever/.
2. C. Mills, The Racial Contract (Ithaca, NY: Cornell University Press, 1997).
3. I. Wilkerson, Caste: The Origins of Our Discontents (New York: Random House, 2020).
4. B. N. Moore and R. Parker, Critical Thinking, 9th ed. (Boston: McGraw-Hill, 2009).
5. G. Marcus, Kluge: The Haphazard Construction of the Human Mind (Boston: Hough-
ton Mifflin, 2008).
6. W. D. Roth, Ş. Yaylacı, K. Jaffe, and L. Richardson, “Do Genetic Ancestry Tests Increase
Racial Essentialism? Findings from a Randomized Controlled Trial,” PLoS One 15, no.
1 (January 29, 2020): e0227399, https://doi.org/10.1371/journal.pone.0227399.
7. See, for example, I. W. Maina, T. D. Belton, S. Ginzberg, A. Singh, and T. J. Johnson,
“A Decade of Studying Implicit Racial/Ethnic Bias in Healthcare Providers Using the
Implicit Association Test,” Social Science & Medicine 199 (2018): 219–29, https://doi
.org/10.1016/j.socscimed.2017.05.009.
 250
3 . E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

8. H. D. Fishbein and N. Dess, “An Evolutionary Perspective on Intercultural Conflict:

Basic Mechanisms and Implications for Immigration Policy, in Evolutionary Psychol-
ogy and Violence: A Primer for Public Policymakers and Public Policy Advocates, ed. R.
W. Bloom and N. Dess (Westport, CT: Praeger, 2003).
9. I. X. Kendi, How To Be an Antiracist (New York: One World, 2019).
10. B. Tatum, Can We Talk About Race?: And Other Conversations in an Era of School
Resegregation (New York: Beacon, 2008).
11. R. DiAngelo, White Fragility: Why It’s So Hard for White People to Talk About Racism
(Boston: Beacon, 2020).
12. F. Hoffman, Race Traits and Tendencies of the American Negro (New York: Macmillan,
1896).
13. D. O. Sears, “Symbolic Racism,” in Eliminating Racism: Profiles in Controversy. Per-
spectives in Social Psychology: A Series of Texts and Monographs, ed. P. A. Katz and D.
A. Taylor (Boston: Springer, 1988).
14. H. Long and A. Van Dam, “The Black-White Economic Divide Is as Wide as It Was
in 1968,” Washington Post, June 4, 2020, https://www.washingtonpost.com/business
/2020/06/04/economic-divide-black-households/.
15. D. Muir, “Race: The Mythic Root of Racism,” Sociological Inquiry 63 (1993): 339–50.
16. K. W. Deutsch, “Anti-Semitic Ideas in the Middle Ages: International Civilizations in
Expansion and Conflict,” Journal of the History of Ideas 6, no. 2 (1945): 239–51.
17. D. Goldenberg, The Curse of Ham: Race, Slavery, in Early Judaism, Christianity and
Islam (Princeton, NJ: University of Princeton Press, 2003).
18. J. L. Graves, The Emperor’s New Clothes: Biological Theories of Race at the Millennium
(New Brunswick NJ: Rutgers University Press, 2005), 39–44.
19. T. Jefferson, Notes on the State of Virginia (Oxford: University of Oxford Text Archive,
1787).
20. C. Darwin, The Voyage of the Beagle (New York: Penguin, 1989). First published in 1839.
21. Jefferson’s racism is well discussed in Graves, The Emperor’s New Clothes, 42–43.
22. A. Desmond and J. Moore, Darwin’s Sacred Cause: How a Hatred of Slavery Shaped
Darwin’s Views on Human Evolution (Boston: Houghton Mifflin, 2009).
23. C. Darwin, The Descent of Man and Selection in Relation to Sex (Princeton, NJ: Princ-
eton University Press, 1981), first published in 1871.
24. R. Moore, “The Dark Side of Creationism,” American Biology Teacher 66, no. 2 (2004):
85–87.
25. D. R. Sharpe, “Evangelicals, Racism, and the Limits of Social Science Research,” Chris-
tian Scholars Review 33, no. 2 (2004): 237–51.
26. K. Mangan, “A Diversity Director Quit Liberty University. Then He Started ‘LUnder-
ground Railroad’ for Employees,” Chronicle of Higher Education, June 9, 2020, https://
www.chronicle.com/article/a-diversity-director-quit-liberty-university-then-he
-started-lunderground-railroad-for-employees.
27. Project Implicit, Harvard University, accessed April 22, 2021, https://implicit.harvard
.edu/implicit/.
28. K. A. Schulman, J. A. Berlin, W. Harless, et al., “The Effect of Race and Sex on Physi-
cians’ Recommendations for Cardiac Catheterization,” New England Journal of Medi-
cine 340, no. 8 (1999): 618–26; slight correction noted in 340, no. 14 (April 8, 1999): 1130.
29. L. A. Penner, J. F. Dovidio, R. Gonzalez, et al., “The Effects of Oncologist Implicit
Racial Bias in Racially Discordant Oncology Interactions,” Journal of Clinical Oncology
34, no. 24 (2016): 2874–80, https://ascopubs.org/doi/abs/10.1200/JCO.2015.66.3658.
 251
3 . E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

30. J. L. Eberhardt, P. G. Davies, V. J. Purdie-Vaughns, and S. L. Johnson, “Looking Death-

worthy: Perceived Stereotypicality of Black Defendants Predicts Capital-Sentencing
Outcomes,” Psychological Science 17, no. 5 (May 2006): 383–86, https://doi.org/10.1111
/j.1467-9280.2006.01716.x.
31. Donald Trump’s relationship with white nationalist Stephen Bannon is described in
J. Green, Devil’s Bargain: Steve Bannon, Donald Trump, and the Nationalist Uprising
(New York: Penguin, 2017).
32. For an excellent example of how implicit bias operates in hiring see: D. Pager, Marked:
Race, Crime, and Finding Work in an Era of Mass Incarceration (Chicago: University of
Chicago Press, 2007).
33. Kendi, How To Be an Antiracist.
34. Muir, “Race: The Mythic Root of Racism.”
35. R. Kennedy, Nigger: The Strange History of a Troublesome Word (New York: Vintage,
2003).
36. M. Zimmerman, Wilhelm Marr: The Patriarch of Anti-Semitism (New York: Oxford
University Press, 1986).
37. The Protocols of the Elders of Zion is believed to have been published first in Russia
in 1903 and translated into English in 1919. It was instrumental in Nazi anti-Semitic
restrictions and eventually the Holocaust.
38. A. Ocalan, The Sociology of Freedom: Manifesto of the Democratic Civilization (Chi-
cago: PM Press, 2020).
39. M. F. Jacobson, Whiteness of a Different Color: European Immigrants and the Alchemy
of Race (Cambridge, MA: Harvard, 1998).
40. E. O. Manoiloff, “Discernment of Human Races by Blood: Particularly of Russians
from Jews,” American Journal of Physical Anthropology 10 (1927): 11–21.
41. R. Bean, “The Nose of the Jew and the Quadratus Labii Superioris Muscle,” Anatomi-
cal Record 7 (1913): 47–49.
42. D. Mogahed and A. Mahmood, American Muslim Poll: Key Findings 2019, Insti-
tute for Social Policy and Understanding, April 29, 2019, https://www.ispu.org
/american-muslim-poll-2019-key-findings/.
43. DiAngelo, White Fragility.
44. W. S. Watkins, R. Thara, B. J. Mowry, et al., “Genetic Variation in South Indian Castes:
Evidence from Y-Chromosome, Mitochondrial, and Autosomal Polymorphisms,”
BMC Genetics 9 (2008): 86, https://doi.org/10.1186/1471-2156-9-86.
45. G. Myrdal, An American Dilemma: The Negro Problem and Modern Democracy (New
York: Harper, 1944); M. F. Ashley Montagu, Man’s Most Dangerous Myth: The Fallacy
of Race (New York: Columbia University Press, 1942), xi.
46. E. Bonacich, “Advanced Capitalism and Black/White Race Relations in the United
States: A Split Labor Market Interpretation,” American Sociological Review 41 (1976):
34–51.
47. W. P. O’Hare and B. Curry-White, “Is There a Rural Underclass?,” Population Today 20
(1992): 6–8.
48. H. Queneau and A. Senc, “On the Structure of US Unemployment Disaggregated by
Race, Ethnicity, and Gender,” Economics Letters 117 (2012): 91–95.
49. B. Hardy and T. Logan, “Race and the Lack of Intergenerational Economic Mobility in
the United States,” Washington Center for Equitable Growth, February 18, 2020, https://
equitablegrowth.org/race-and-the-lack-of-intergenerational-economic-mobility
-in-the-united-states/.
 252
3 . E V E RY T H I N G YO U WA N T E D TO K N O W A B O U T R A C I S M

50. This is an ongoing discussion in America. See K. Meatto, “Still Separate, Still
Unequal: Teaching About School Segregation and Educational Inequality,” New York
Times, May 2, 2019, https://www.nytimes.com/2019/05/02/learning/lesson-plans/stil
l-separate-still-unequal-teaching-about-school-segregation-and-educational
-inequality.html.

4. WHY DO RACES DIFFER IN DISEASE INCIDENCE?

1. J. Graves, interview by Roland Martin, Unfiltered, March 2020, https://youtu.be
/rtRI5hLJ7hc.
2. J. Abbasi, “Taking a Closer Look at COVID-19, Health Inequities, and Racism,” JAMA
324, no. 5 (2020): 427–29, https://doi.org/10.1001/jama.2020.11672.
3. R. A. Oppel Jr., R. Gebeloff, K. K. Rebecca Lai, W. Wright, and M. Smith, “The Fullest
Look Yet at the Racial Inequality of the Corona Virus,” New York Times, July 5, 2020,
https://www.nytimes.com/interactive/2020/07/05/us/coronavirus-latinos-african
-americans-cdc-data.html.
4. C. K. Johnson, A. Kastanis, and K. Stafford, “AP Analysis: Racial Disparities Seen
in US Vaccination Drive,” Associated Press, January 30, 2021, https://apnews.com
/article/race-and-ethnicity-health-coronavirus-pandemic-hispanics-d0746b028cf562
31dbcdeda0fba24314.
5. CDC Data Tracker, https://covid.cdc.gov/covid-data-tracker/#vaccination-demographics
-trends, accessed May 25, 2021.
6. J. L. Graves and M. R. Rose, “Against Racial Medicine,” in “Race and Contemporary
Medicine: Biological Facts and Fictions,” ed. S. Gilman, special issue, Patterns of Preju-
dice 40, nos. 4–5 (2006): 481–93.
7. S. Satel, “I Am a Racially Profiling Doctor,” New York Times, May 2, 2002, https://www
.nytimes.com/2002/05/05/magazine/i-am-a-racially-profiling-doctor.html.
8. K. M. Hoffman, S. Trawalter, J. R. Axt, and M. N. Oliver, “Racial Bias in Pain Assess-
ment and Treatment Recommendations, and False Beliefs About Biological Differ-
ences Between Blacks and Whites, Proceedings of the National Academy of Sciences 113,
no. 16 2016): 4296–301, https://doi.org/10.1073/pnas.1516047113.
9. Hoffman et al., “Racial Bias in Pain Assessment and Treatment Recommendations.”
10. For example, see A. H. Goodman, “Why Genes Don’t Count (for Racial Differences
in Health),” American Journal of Public Health 90, no. 11 (2000): 1699–702, https://doi
.org/10.2105/AJPH.90.11.1699.
11. J. L. Graves Jr., C. Reiber, A. Thanukos, M. Hurtado, and T. Wolpaw, “Evolution-
ary Science as a Method to Facilitate Higher Level Thinking and Reasoning in
Medical Training,” Evolution, Medicine, & Public Health 2016, no. 1 (January 2016):
358–68, https://doi.org/10.1093/emph/eow029. This article resulted from a think-
tank discussion about medical education that included prominent scientists and
physicians.
12. D. R. Snow and K. M. Lanphear, “European Contact and Indian Depopulation in the
Northeast: The Timing of the First Epidemics,” Ethnohistory 35, no. 1 (1988)): 15–33.
13. J. Downs, Sick from Freedom: African American Illness and Suffering During the Civil
War and Reconstruction (New York: Oxford University Press, 2012).
14. W. E. B. DuBois, The Philadelphia Negro: A Social Study, with an introduction by Eli-
jah Anderson (Philadelphia: University of Pennsylvania Press, 1899).
 253
4. WHY DO RACES DIFFER IN DISEASE INCIDENCE?

15. A. Nguyen, J. K. David, S. K. Maden, et al., “Human Leukocyte Antigen Susceptibil-

ity Map for SARS-CoV-2,” Journal of Virology 94, no. 13: e00510-20, https://doi.org
/10.1128/JVI.00510-20.
16. D. Ellinghaus, F. Degenhardt, L. Bujanda, et al., “Genomewide Association Study
of Severe Covid-19 with Respiratory Failure,” New England Journal of Medicine 383
(2020): 1522–34, https://doi.org/10.1056/NEJMoa2020283.
17. H. Zeberg and S. Pääbo, “The Major Genetic Risk Factor for Severe COVID-19 Is
Inherited from Neandertals,” Nature 587 (2020): 610–12, https://www.nature.com
/articles/s41586-020-2818-3.
18. J. G. Read, M. O. Emerson, and A. Tarlov, “Implications of Black Immigrant Health
for U.S. Racial Disparities in Health,” Journal of Immigrant Health 7, no. 3 (2005):
205–12, https://doi.org/10.1007/s10903-005-3677-6; T. G. Hamilton and R. A. Hum-
mer, “Immigration and the Health of U.S. Black Adults: Does Country of Origin Mat-
ter?” Social Science & Medicine 73, no. 10 (2011): 1551–60, https://doi.org/10.1016/j.
socscimed.2011.07.026; and M. J. Brown, S. A. Cohen, and B. Mezuk, “Duration of U.S.
Residence and Suicidality Among Racial/Ethnic Minority Immigrants,” Social Psy-
chiatry and Psychiatric Epidemiology 50, no. 2 (2015): 257–67, https://doi.org/10.1007
/s00127-014-0947-4.
19. R. Nusslock and G. E. Miller, “Early-Life Adversity and Physical and Emotional Health
Across the Lifespan: A Neuroimmune Network Hypothesis,” Biological Psychiatry 80,
no. 1 (2016): 23–32, https://doi.org/10.1016/j.biopsych.2015.05.017.
20. L. Dean, Blood Groups and Red Cell Antigens (Bethesda, MD: National Center for
Biotechnology Information, 2005), https://www.ncbi.nlm.nih.gov/books/NBK2270/.
21. Be the Match, “HLA Basics,” https://bethematch.org/transplant-basics/matching-patients
-with-donors/how-donors-and-patients-are-matched/hla-basics/.
22. A. R. Sehgal, “The Net Transfer of Transplant Organs Across Race, Sex, Age, and
Income,” American Journal of Medicine 117, no. 9 (2004): 670–75, https://doi.org
/10.1016/j.amjmed.2004.05.025.
23. J. Blakely, “Hawaii Attorney General Sues Maker of the Drug Plavix Alleging Unfair and
Deceptive Marketing,” Pacific Business News, March 19, 2014, https://www.bizjournals
.com/pacific/news/2014/03/19/hawaii-attorney-general-files-lawsuit-against.html.
24. The most common alleles are *1, *2, *9, *10, and *17. See table 2.6 in S. Stearns and R.
Medzhitov, Evolutionary Medicine (Sunderland, MA: Sinauer, 2016), 45.
25. J. Kahn, “Race-ing Patents/Patenting Race: An Emerging Political Geography of Intel-
lectual Property in Biotechnology,” Iowa Law Review 92 (2007): 355–415.
26. K. E. Lohmueller, A. R. Indap, S. Schmidt, et al., “Proportionally More Deleterious
Genetic Variation in European than in African Populations,” Nature 451, no. 7181
(2008): 994–97, https://doi.org/10.1038/nature06611.
27. J. L. Graves, The Race Myth: Why We Pretend Race Exists in America (New York: Dut-
ton, 2005).
28. R. Cooper and D. Rotimi, “Hypertension in Blacks,” American Journal of Hypertension
10, no. (7,pt. 1 (1997)): 804–12, https://doi.org/10.1016/S0895-7061(97)00211-2.
29. See table 2.5 in Stearns and Medzhitov, Evolutionary Medicine, 40–41.
30. J. L. Graves, K. L. Hertweck, M. A. Phillips, M. V. Han, L. G. Cabral, T. T. Barber, L.
F. Greer, M. F. Burke, L. D. Mueller, and M. R. Rose, “Genomics of Parallel Experi-
mental Evolution in Drosophila,” Molecular Biology and Evolution 34, no. 4 (2017):
831–42, https://doi.org/10.1093/molbev/msw282; and J. L. Graves, A. J. Ewunkem, M.
D. Thomas, J. Han, K. L. Rhinehardt, S. Boyd, R. Edmondson, L. Jeffers-Francis, and S.
 254
4. WHY DO RACES DIFFER IN DISEASE INCIDENCE?

H. Harrison, “Experimental Evolution of Metal Resistance in Bacteria,” in Evolution in

Action: Past, Present, and Future, ed. Banzhaf et al., 91–106 (Cham, Switzerland: Springer,
2020).
31. J. L. Graves, “Why the Nonexistence of Biological Races Does Not Mean the Nonex-
istence of Racism,” American Behavioral Scientist 56, no. 5 (2015): 1474–95, https://doi
.org/10.1177/0002764215588810.
32. L. L. Black, R. Johnson, and L. VanHoose, “The Relationship Between Perceived Rac-
ism/Discrimination and Health Among Black American Women: A Review of the
Literature from 2003 to 2013,” Journal of Racial and Ethnic Health Disparities 2, no. 1
(2015): 11–20, https://doi.org/10.1007/s40615-014-0043-1.
33. A. Markwick, Z. Ansari, D. Clinch, and J. McNeil, “Perceived Racism May Partially
Explain the Gap in Health Between Aboriginal and Non-Aboriginal Victorians: A
Cross-Sectional Population Based Study,” SSM—Population Health 7 (April 19, 2018):
100310, https://doi.org/10.1016/j.ssmph.2018.10.010.
34. N. Snyder-Mackler, J. R. Burger, L. Gaydosh, et al., “Social Determinants of Health
and Survival in Humans and Other Animals,” Science 368, no. 6493 (2020): eaax9553,
https://doi.org/10.1126/science.aax9553.
35. J. L. Graves, “Great Is Their Sin: Biological Determinism in the Age of Genomics,”
Annals of the American Academy of Political and Social Science 661, no. 1 (2015): 24–50,
https://doi.org/10.1177/0002716215586558.
36. V. Barcelona de Mendoza, Y. Huang, C. A. Crusto, et al., “Perceived Racial Dis-
crimination and DNA Methylation Among African American Women in the Inter-
GEN Study,” Biological Research for Nursing 20, no. 2 (2018)): 145–52, https://doi.org
/10.1177/1099800417748759.
37. S. Oyama and S. F. Terry, “Epigenetics and Racial Health Inequities,” Genetic Testing and
Molecular Biomarkers 20, no. 9 (2016): 483–84, https://doi.org/10.1089/gtmb.2016.29021.sjt.
38. R. Thornton, “Cherokee Population Losses During the Trail of Tears: A New Perspec-
tive and a New Estimate,” Ethnohistory 31, no. 4 (Autumn 1984): 289–300.
39. R. D. Bullard, P. Moha, R. Saha, and B. Wright, Toxic Wastes and Race at Twenty 1987–
2007: A Report Prepared for the United Church of Christ Justice and Witness Ministries
(Cleveland, OH: United Church of Christ, 2007), https://www.nrdc.org/sites/default
/files/toxic-wastes-and-race-at-twenty-1987-2007.pdf.
40. Bullard et al., Toxic Wastes and Race at Twenty.
41. Toxic Release Inventory, U.S. Environmental Protection Agency, https://www.epa.gov
/toxics-release-inventory-tri-program.
42. J. R. Hipp and C. M. Lakon, “Social Disparities in Health: Disproportionate Toxicity
Proximity in Minority Communities Over a Decade,” Health & Place 16, no. 4 (2010):
674–83, https://doi.org/10.1016/j.healthplace.2010.02.005.
43. M. Trotter, G. E. Broman, and R. R. Peterson, “Densities of Bones of White and Negro
Skeletons,” Journal of Bone and Joint Surgery 42, no. 1 (1960): 50–58.
44. For example, WebMd lists ethnicity as a risk factor for osteoporosis: “Research shows
that Caucasian and Asian women are more likely to develop osteoporosis than women
of other ethnic backgrounds. Hip fractures are also twice as likely to happen in Cau-
casian women as in African-American women”; “Osteoporosis: Are You at Risk?,”
https://www.webmd.com/osteoporosis/guide/osteoporosis-risk-factors. In its entry
on risk of osteoporosis, the Mayo Clinic states, “You’re at greatest risk of osteoporo-
sis if you’re white or of Asian descent”; “Osteoporosis,” https://www.mayoclinic.org
/diseases-conditions/osteoporosis/symptoms-causes/syc-20351968.
 255
5 . L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

45. In Savage Africa, a book published in 1864 in London, W. Winwood Reade, who listed
himself as a Fellow of the Geographical and Anthropological Societies of London,
wrote, “The skull is extremely thick. If a negro wishes to break a stick, he does not
break it across his knee as we do, but across his head. The power of the skull in resist-
ing blows is something marvelous.” That same year, Dr. Carl Vogt, professor of natural
history at the University of Vienna, wrote that “he [the Negro], like a ram, uses his
hard skull in a fight.” A year earlier, in the 1863 edition of Introduction to Anthropology,
Dr. Theodor Waitz wrote, “The skeleton of the Negro is heavier, the bones thicker.”
Further, he said, “This is especially the case with regard to the skull, which is hard and
unusually thick, so that in fighting, Negroes, men and women, butt each other like
rams without exhibiting much sensibility.”
46. L. Braun, Breathing Race into the Machine: The Surprising Career of the Spriometer
from Plantation to Genetics (Minneapolis: University of Minnesota Press, 2014).
47. R. T. Jackson et al., “Comparison of Hemoglobin Values in Black and White Male U.S.
Military Personnel,” Journal of Nutrition 113 (1983): 165–71.
48. K. Belson, “Black Former N.F.L. Players Say Racial Bias Skews Concussion Payouts,” New
York Times, August 25, 2020, https://www.nytimes.com/2020/08/25/sports/football
/nfl-concussion-racial-bias.html.
49. For more support of these claims, see A. M. Amin, L. Sheau Chin, D. A. Mohamed
Noor, et al., “The Effect of CYP2C19 Genetic Polymorphism and Non-Genetic Factors
on Clopidogrel Platelets Inhibition in East Asian Coronary Artery Disease Patients,”
Thrombosis Research 158 (2017): 22–24, https://doi.org/10.1016/j.thromres.2017.07.032;
G. Hempel, ed., Handbook of Analytical Separations, vol. 7: Methods of Therapeu-
tic Drug Monitoring Including Pharmacogenetics (Amsterdam: Elsevier Science,
2020), 321–53; J. Kahn, “Race, Pharmacogenomics, and Marketing: Putting BiDil
in Context,” American Journal of Bioethics 6, no. 5 (2006): W1–W5, https://doi
.org/10.1080/15265160600755789; C. Roselli, M. D. Chaffin, L. C. Weng, et al., “Multi-
Ethnic Genome-Wide Association Study for Atrial Fibrillation,” Nature Genetics 50,
no. 9 (2018): 1225–33, https://doi.org/10.1038/s41588-018-0133-9; B. Séguin, B. Hardy,
P. A. Singer, and A. S. Daar, “BiDil: Recontextualizing the Race Debate,” Pharma-
cogenomics Journal 8, no. 3 (2008): 169–73, https://doi.org/10.1038/sj.tpj.6500489;
D. R. Snow and K. M. Lanphear, “European Contact and Indian Depopulation in
the Northeast”; D. Zou and K. L. Goh, “East Asian Perspective on the Interaction
Between Proton Pump Inhibitors and Clopidogrel,” Journal of Gastroenterology and
Hepatology 32, no. 6 (2017): 1152–59, https://doi.org/10.1111/jgh.13712; and Z. Shao,
L. G. Kyriakopoulou, and S. Ito, “Chapter 14—Pharmacogenomics,” in Handbook
of Analytical Separations, vol. 7: Methods of Therapeutic Drug Monitoring Including
Pharmacogenetics, ed. G. Hempel (Amsterdam: Elsevier, 2020), https://doi.org/10.1016
/B978-0-444-64066-6.00014-9.

5. LIFE HISTORY, AGING, AND MORTALITY

1. S. Stearns and R. Medzhitov, Evolutionary Medicine (Sunderland, MA: Sinauer, 2016),
57–64.
2. G. Jasienska, R. G. Bribiescas, A. S. Furberg, S. Helle, and A. Núñez-de la Mora,
“Human Reproduction and Health: An Evolutionary Perspective,” Lancet 390, no.
10093 (2017): 510–20, https://doi.org/10.1016/S0140-6736(17)30573-1.
 256
5 . L I F E H I S T O R Y, A G I N G , A N D M O R T A L I T Y

3. Joe is one of the scientists who helped to establish the scientifically correct modern
evolutionary theory of aging. See M. R. Rose, T. Flatt, J. L. Graves, et al., “What is
Aging? (opinion),” Frontiers in Genetics (July 20, 2012), https://doi.org/10.3389/fgene
.2012.00134.
4. M. R. Rose, Evolutionary Biology of Aging (New York: Oxford University Press, 1991);
J. L. Graves, “General Theories of Aging: Unification and Synthesis,” in Principles of
Neural Aging, ed. S. F. Dani, A. Hori, and G. F. Walter (London: Elsevier, 1997); and M.
R. Rose, M. Matos, and H. B. Passananti, Methuselah Flies: Case History of the Evolu-
tion of Aging (New York: World Scientific, 2004).
5. C. J. Murray, S. C. Kulkarni, C. Michaud, et al., “Eight Americas: Investigating Mortal-
ity Disparities Across Races, Counties, and Race-Counties in the United States,” PLoS
Medicine (September 12, 2006): 3:e260, https://doi.org/10.1371/journal.pmed.0030260.
6. S. M. Tajuddin, D. G. Hernandez, B. H. Chen, et al., “Novel Age-Associated DNA
Methylation Changes and Epigenetic Age Acceleration in Middle-Aged African
Americans and Whites,” Clinical Epigenetics 11, no. 1 (2019): 119, https://doi.org/10.1186
/s13148-019-0722-1.
7. P. H. Rej, HEAT Steering Committee, C. C. Gravlee, and C. J. Mulligan, “Shortened
Telomere Length Is Associated with Unfair Treatment Attributed to Race in African
Americans Living in Tallahassee, Florida,” American Journal of Human Biology 32, no.
3 (2020): e23375, https://doi.org/10.1002/ajhb.23375.
8. R. Coutinho, R. J. David, and J. W. Collins Jr., “Relation of Parental Birth Weights to
Infant Birth Weight Among African Americans and Whites in Illinois: A Transgen-
erational Study,” American Journal of Epidemiology 146, no. 10 (1997): 804–9, https://
doi.org/10.1093/oxfordjournals.aje.a009197.
9. R. David and J. Collins, “Differing Birthweight Among Infants of U.S. Born Blacks,
African-Born Blacks, and U.S. Born Whites,” New England Journal of Medicine 337,
no. 17 (1997): 1209–14. Also see P. D. Gluckman, M. A. Hanson, C. Cooper, and K. L.
Thornburg, “Effect of in Utero and Early-Life Conditions on Adult Health and Dis-
ease, New England Journal of Medicine 359, no. 1 (2008): 61–73, https://doi.org/10.1056
/NEJMra0708473.
10. A. T. Geronimus, “The Weathering Hypothesis and the Health of African American
Women and Infants: Evidence and Speculation,” Ethnicity & Disease 2, no. 3 (1992):
207–21: A. T. Geronimus, “Deep Integration: Letting the Epigenome Out of the Bottle
Without Losing Sight of the Structural Origins of Population Health,” American Journal
of Public Health 103, suppl. 1(2013): S56–S63, https://doi.org/10.2105/AJPH.2013.301380.
11. DOHaD was initially known as the “Barker hypothesis” after David Barker. See S. W.
Limesand, K. L. Thornburg, and J. E. Harding, “30th Anniversary for the Develop-
mental Origins of Endocrinology,” Journal of Endocrinology 242, no. 1 (2019): E1–4.
12. Centers for Disease Control and Prevention, National Center for Health Statistics,
“Life Expectancy Increases in 2018 as Overdose Deaths Decline Along with Several
Leading Causes of Death” (press release), January 30, 2020, https://www.cdc.gov/nchs
/pressroom/nchs_press_releases/2020/202001_Mortality.htm.

6. ATHLETICS, BODIES, AND ABILITIES

1. Olympic Diary, “Jamaicans Built to Beat the Rest,” Herald.ie, August 19, 2008, https://
www.herald.ie/sport/other-sports/jamaicans-built-to-beat-the-rest-27882487.html.
 257
6 . AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

2. T. Rankinen, M. S. Bray, J. M. Hagberg, et al., “The Human Gene Map for Perfor-
mance and Health-Related Fitness Phenotypes: The 2005 Update,” Medicine & Sci-
ence in Sports & Exercise 38, no. 11 (2006): 1863–88, https://doi.org/10.1249/01.mss
.0000233789.01164.4f; and M. S. Bray, J. M. Hagberg, L. Pérusse, et al., “The Human
Gene Map for Performance and Health-Related Fitness Phenotypes: The 2006–2007
Update,” Medicine & Science in Sports Exercise 41, no.1 (2009): 35–73, https://doi
.org/10.1249/MSS.0b013e3181844179.
3. J. L. Graves, “Theories of Athletic Performance (General),” in Encyclopedia of Race and
Racism, 2nd ed., ed. P. L. Mason (Detroit: Macmillan Reference, 2013).
4. The markers were CREM, cAMP responsive element modulator, rs1531550 A; DMD,
encodes the gene dystrophin found in muscle tissue, rs939787 T; GALNT13, encodes
polypeptide N-acetylgalactosaminyltransferase 13 protein, rs10196189 G; NFIA-AS1,
encodes the nuclear factor 1 transcription factor, rs1572312 C; RBFOX1, RNA binding
protein, rs7191721 G; TSHR, receptor for thyroid-stimulating hormone, rs7144481 C; I.
I. Ahmetov and O. N. Fedotovskaya, “Chapter Six: Current Progress in Sports Genom-
ics,” in Advances in Clinical Chemistry 70, ed. G. S. Makowski (San Diego: Academic,
2015), 247–314, https://doi.org/10.1016/bs.acc.2015.03.003.
5. The data identified that the polymorphism rs55743914 located in the PTPRK gene
(which encodes the receptor-type tyrosine protein phosphatase kappa) was the most
significant. Seven of the discovered SNPs were also associated with sprint test perfor-
mance in 126 Polish women, and four were associated with power athlete status in 399
elite Russian athletes. Six SNPs were associated with muscle fiber type in 96 Russian
subjects. They also examined genotype distributions and possible associations for six-
teen SNPs previously linked with sprint performance. Four of the SNPs (AGT rs699,
HSD17B14 rs7247312, IGF2 rs680, and IL6 rs1800795) were associated with sprint
test performance. In addition, the G alleles of two SNPs in ADRB2 (rs1042713 and
rs1042714) were significantly overrepresented in these players compared with British
and European controls; see C. Pickering, B. Suraci, E. A. Semenova, et al., “A Genome-
Wide Association Study of Sprint Performance in Elite Youth Football Players,” Journal
of Strength and Conditioning Research 33, no. 9 (2019): 2344–51, https://doi.org/10.1519
/JSC.0000000000003259. Another piece of evidence for the lack of genomic racial
differentiation in alleles associated with athletic ability is a GWAS study that found
no difference between elite endurance athletes and nonathletes for alleles supposedly
related to athletic performance. This study examined 1,520 elite athletes and 2,760
controls from Ethiopia, Kenya, Spain, Poland, Russia, Japan, and Australia. By modern
GWAS protocols, this study was underpowered for finding significant genetic differ-
ences, because of the small number of people classified as elite athletes. The power
to uncover significant differences in the frequency of genetic markers in GWAS is
directly influenced by the number of people studied. By modern standards, studies
that examine on the order of a million (cases and controls) would be considered very
strong, and those examining less than 10,000 (cases and controls) would be consid-
ered weak. Alternatively, a GWAS to identify SNPs associated with speed or power in
European youth football (soccer) players found twelve SNPs.
6. M. S. Sarzynski, S. Ghosh, and C. Bouchard, “Genomic and Transcriptomic Predictors
of Response Levels to Endurance Exercise Training,” Journal of Physiology 595, no. 9
(2017): 2931–39, https://doi.org/10.1113/JP272559.
7. J. Bale and J. Sung, Kenyan Running: Movement, Culture, Geography, and Global
Change (London: Frank Cass, 1996).
 258
6 . AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

8. R. Irving and P. Bourne, “The Ecological Model of Sprinting Determinants of Jamai-

can Athletes,” Austin Emergency Medicine 2, no.1 (2016): 1009, https://austinpublishing
group.com/emergency-medicine/fulltext/aem-v2-id1009.php.
9. All medal counts were gathered from the Wikipedia “All-time Olympic Games medal
table,” accessed April 29, 2021, https://en.wikipedia.org/wiki/All-time_Olympic_Games
_medal_table.
10. H. Kääriäinen, J. Muilu, M. Perola, and K. Kristiansson, “Genetics in an Isolated Popu-
lation Like Finland: A Different Basis for Genomic Medicine?,” Journal of Community
Genetics 84, no. 4 (2017): 319–26, https://doi.org/10.1007/s12687-017-0318-4.
11. K. Bryc, E. Y. Durand, J. M. Macpherson, D. Reich, and J. L. Mountain, “The Genetic
Ancestry of African Americans, Latinos, and European Americans Across the United
States,” American Journal of Human Genetics 96, no. 1 (2015): 37–53, https://doi.org
/10.1016/j.ajhg.2014.11.010.
12. J. Benn-Torres, C. Bonilla, C. M. Robbins, et al., “Admixture and Population Stratifi-
cation in African Caribbean Populations,” Annals of Human Genetics 72, pt. 1 (2008):
90–98, https://doi.org/10.1111/j.1469-1809.2007.00398.x.
13. J. A. Hawley, M. M. Williams, M. M. Vickovic, and P. J. Handcock, “Muscle Power
Predicts Freestyle Swimming Performance,” British Journal of Sports Medicine 26,
no. 3 (1992): 151–55, http://dx.doi.org/10.1136/bjsm.26.3.151; H. C. Emslander, M.
Sinaki, J. M. Muhs, et al., “Bone Mass and Muscle Strength in Female College Ath-
letes (Runners and Swimmers),” Mayo Clinic Proceedings 73, no. 12 (1998): 1151–60,
https://doi.org/10.4065/73.12.1151; and R. Van Schuylenbergh, B. V. Eynde, and P.
Hespel, “Prediction of Sprint Triathlon Performance from Laboratory Tests,” Euro-
pean Journal of Applied Physiology 91, no. 1 (2004): 94–99, https://doi.org/10.1007
/s00421-003-0911-6.
14. M. Lloyd, “Exploring the Racial Disparities in Competitive Swimming,” Swimming
World, February 3, 2016, https://www.swimmingworldmagazine.com/news/exploring-
the-racial-disparities-in-competitive-swimming/; S. L. Myers Jr., A. M. Cuesta, and Y.
Lai, “Competitive Swimming and Racial Disparities in Drowning,” Review of Black
Political Economy 44, no. 1–2 (2017): 77–97, https://doi.org/10.1007/s12114-017-9248-y.
15. NBC Sports, “US Sets World Record in 4 x 100 Freestyle Relay” (video), July 27, 2019,
https://www.youtube.com/watch?v=D7L9T6LuQrA.
16. Joe’s history of basketball can be found in J. L. Graves, “Sports (Basketball)” in Encyclo-
pedia of Race and Racism, 2nd ed., ed. P. L. Mason (Detroit: Macmillan Reference, 2013).
17. K. Sinsurin, R. Vachalathiti, W. Jalayondeja, and W. Limroongreungrat, “Altered Peak
Knee Valgus During Jump-Landing Among Various Directions in Basketball and Vol-
leyball Athletes,” Asian Journal of Sports Medicine 4, no. 3 (2013): 195–200, https://doi
.org/10.5812/asjsm.34258.
18. H. Bryant, Shut Out: A Story of Race and Baseball in Boston (New York: Routledge,
2013); and R. K. Barney and D. E. Barney, “ ‘Get Those Niggers off the Field!’: Racial
Integration and the Real Curse in the History of the Boston Red Sox,” NINE: A
Journal of Baseball History and Culture 16, no. 1 (2007): 1–9, https://doi.org/10.1353
/nin.2007.0030.
19. G. L. González, “The Stacking of Latinos in Major League Baseball: Does It Matter
If a Player Is Drafted?,” Journal of Hispanic Higher Education 1, no. 4 (2002): 320–28,
https://doi.org/10.1177/153819202236976.
20. E. T. Norris, L. Wang, A. B. Conley, et al., “Genetic Ancestry, Admixture and Health
Determinants in Latin America,” BMC Genomics 19, suppl. 8 (2018): 861, https://doi
.org/10.1186/s12864-018-5195-7.
 259
6 . AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

21. C. Fortes-Lima, J. Bybjerg-Grauholm, L. C. Marin-Padrón, et al., “Exploring Cuba’s

Population Structure and Demographic History Using Genome-Wide Data,” Scientific
Reports 8, no. 1 (2018): 11422, https://doi.org/10.1038/s41598-018-29851-3.
22. Wikipedia, “List of World Records in Weightlifting,” accessed April 29, 2021, https://
en.wikipedia.org/wiki/List_of_world_records_in_Olympic_weightlifting.
23. A. Storey and H. K. Smith, “Unique Aspects of Competitive Weightlifting: Perfor-
mance, Training and Physiology,” Sports Medicine 42, no. 9 (2012): 769–90, https://doi
.org/10.1007/BF03262294.
24. W. R. Leonard and P. T. Katzmarzyk, “Body Size and Shape: Climatic and Nutritional
Influences on Human Body Morphology,” in Human Evolutionary Biology, ed. M. P.
Muehlenbein (Cambridge: Cambridge University Press, 2010).
25. In a recent analysis of literature estimating the heritability of various types of strength
(isometric grip, isometric strength, isotonic strength, isokinetic strength, jump-
ing ability, and other measures of power), the heritability (or h2) for these kinds of
strength was determined to be 0.56, 0.49, 0.49, 0.49, 0.55, and 0.51 respectively. All of
these estimates of h2 included their 95 percent confidence intervals. Heritability can
vary from 0 to 1.00 and is a measure of how much of a physical trait is determined by
genes. This trait is determined by studies of monozygotic twins (those who share all
of their genetic information) versus dizygotic twins (who share half of their genetic
information), as well as parent–offspring comparisons. The populations examined in
this study were primarily European (with some Japanese studies). The h2 results for
these strength traits mean that an individuals’ strength is determined as much by their
genetic inheritance as the environment in which they live. We also know that due to
the relationship between genetic and environmental determinants of physical traits,
changing either of these components will result in different estimates of heritabil-
ity. So, the take-home message is that we cannot easily generalize the results of this
study to the rest of the world’s populations. See H. Zempo, E. Miyamoto-Mikami,
N. Kikuchi, et al., “Heritability Estimates of Muscle Strength-Related Phenotypes: A
Systematic Review and Meta-Analysis,” Scandinavian Journal of Medicine and Science
in Sports 17, no. 12 (2017): 1537–46, https://doi.org/10.1111/sms.12804.
26. E. E. Grishina, P. Zmijewski, E. A. Semenova, et al., “Three DNA Polymorphisms
Previously Identified as Markers for Handgrip Strength Are Associated with Strength
in Weightlifters and Muscle Fiber Hypertrophy,” J Strength Cond Res. 33, no. 10 (2019):
2602–7, https://doi.org/10.1519/JSC.0000000000003304.
27. M. Collins, K. O’Connell, and M. Posthumus, “Genetics of Musculoskeletal Exercise-
Related Phenotypes,” in Genetics and Sports, Medicine and Sports Science 61, 2nd ed.,
ed. M. Posthumus and M. Collins (Basel: Karger, 2016); also see M. J. Alter, Science of
Flexibility, 3rd ed. (Champaign, IL: Human Kinetics, 2004).
28. D. A. Nelson, G. Jacobsen, D. A. Barondess, and A. M. Parfitt, “Ethnic Differences
in Regional Bone Density, Hip Axis Length, and Lifestyle Variables Among Healthy
Black and White Men,” Journal of Bone and Mineral Research 10, no. 5 (1995): 782–87,
https://doi.org/10.1002/jbmr.5650100515.
29. C. Mukwasi, L. Stranix Chibanda, J. Banhwa, and J. A. Shepherd, “US White and Black
Women Do Not Represent the Bone Mineral Density of Sub-Saharan Black Women,”
Journal of Clinical Densitometry 18, no. 4 (2015): 525–32, https://www.sciencedirect
.com/science/article/abs/pii/S1094695015001213?via3Dihub.
30. N. Lovšin, J. Zupan, and J. Marc, “Genetic Effects on Bone Health,” Current Opinion in
Clinical Nutrition and Metabolic Care 21, no. 4 (2018): 233–39, https://doi.org/10.1097
/MCO.0000000000000482.
 260
6 . AT H L E T I C S , B O D I E S , A N D A B I L I T I E S

31. L. Michou, “Epigenetics of Bone Diseases,” Joint Bone Spine 85, no. 6 (2018): 701–7,
https://doi.org/10.1016/j.jbspin.2017.12.003.
32. Supporting references for the chapter include T. Rankinen, N. Fuku, B. Wolfarth, et
al., “No Evidence of a Common DNA Variant Profile Specific to World Class Endur-
ance Athletes,” PLoS One 11, no. 1 (January 29, 2016): e0147330, https://doi.org/10.1371
/journal.pone.0147330; and A. Vander, J. Sherman, and D. Luciano, Human Physiol-
ogy: The Mechanisms of Body Function, 8th ed. (Boston: McGraw Hill, 2001).

7. INTELLIGENCE, BRAINS, AND BEHAVIORS

1. R. Sternberg, “Intelligence: State of the Art,” Dialogues Clinical Neuroscience 14, no. 1
(2012): 19–27.
2. H. H. Goddard, “Mental Tests and the Immigrant,” Journal of Delinquency 5, no. 2
(1917).
3. See Lothrop Stoddard report: “Europe as an Emigrant Exporting Continent and the
United States as an Emigrant Receiving Nation,” Hearings, Committee on Immigra-
tion and Naturalization, March 8, 1924.
4. A. J. Onwuegbuzie and C. E. Daley, “Racial Difference in IQ Revisited: A Synthesis of
Nearly a Century of Research,” Journal Black Psychology 27, no. 2 (2001): 209–20.
5. R. Herrnstein and C. R. Murray, The Bell Curve: Intelligence and Class Structure in
American Life (New York: Free Press, 1994).
6. M. Hout, “Test Scores, Education, and Poverty,” in Race and Intelligence: Separating
Science from Myth, ed. J. Fish (Mahwah, NJ: Lawrence Erlbaum, 2002).
7. See table 7.2 in R. Lewis, Human Genetics: Concepts and Applications, 5th ed. (Boston:
McGraw-Hill, 2003).
8. C. Murray, Human Diversity: The Biology of Gender, Race, and Class (New York:
Twelve, 2020).
9. R. Plomin and S. von Stumm, “The New Genetics of Intelligence,” Nature Reviews
Genetics 19, no. 3 (2018): 148–59, https://doi.org/10.1038/nrg.2017.104.
10. G. Davies, A. Tenesa, A. Payton, et al., “Genome-Wide Association Studies Establish
That Human Intelligence Is Highly Heritable and Polygenic,” Molecular Psychiatry 16,
no. 10 (2011): 996–1005, https://doi.org/10.1038/mp.2011.85.
11. S. L. Spain, I. Pedroso, N. Kadeva, et al., “A Genome-Wide Analysis of Putative Func-
tional and Exonic Variation Associated with Extremely High Intelligence,” Molecular
Psychiatry 21, no. 8 (2016): 1145–51, https://doi.org/10.1038/mp.2015.108.
12. A. Okbay, J. P. Beauchamp, M. A. Fontana, et al., “Genome-Wide Association Study
Identifies 74 Loci Associated with Educational Attainment,” Nature 553, no. 7694
(2016): 539–42, https://doi.org/10.1038/nature17671; and A. Kong, M. L. Frigge, G.
Thorleifsson, et al., “Selection Against Variants in the Genome Associated with Edu-
cational Attainment,” Proceedings of the National Academy of Sciences 114, no. 5 (2017):
E727-32, https://doi.org/10.1073/pnas.1612113114.
13. J. J. Lee, R. Wedow, A. Oakbay, et al., “Gene Discovery and Polygenic Prediction from
a Genome-Wide Association Study of Educational Attainment in 1.1 Million Individu-
als,” Nature Genetics 50, no. 8 (2018): 1112–21, https://doi.org/10.1038/s41588-018-0147-3.
14. H. Zhang, H. Zhou, T. Lencz, et al., “Genome-Wide Association Study of Cognitive
Flexibility Assessed by the Wisconsin Card Sorting Test,” American Journal of Medi-
cal Genetics, Part B: Neuropsychiatriatic Genetics 117, no. 5 (2018): 511–19, https://doi
 261
7. I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

.org/10.1002/ajmg.b.32642. This study found two significant SNPs associated with

cognitive flexibility in African Americans (rs7165213 and rs35633795). The SNPs were
located downstream of a noncoding gene, LOC101927286.
15. D. Reich, Who We Are and How We Got Here: Ancient DNA and the New Science of the
Human Past (New York: Doubleday, 2018), 255:
The indefensibility of the orthodoxy is obvious at almost every turn. In 2016,
I attended a lecture on race and genetics by the biologist Joseph L. Graves Jr.
at the Peabody Museum of Archaeology and Ethnography at Harvard. At one
point, Graves compared the approximately five mutations known to have large
effects on skin pigmentation and that are obviously different in frequency
across populations to the more than ten thousand genes known to be active in
human brains. He argued that in contrast to pigmentation genes, the patterns at
genes active in the brain would surely average out over so many locations, with
some mutations nudging cognitive and behavioral traits in one direction and
some pushing in the other direction. But that argument doesn’t work.
16. J. J. McKee, F. E. Poirer, and S. McGraw, Understanding Human Eolution, 5th ed.
(Upper Saddle River, NJ: Prentice/Pearson, 2005).
17. R. Boyd and J. B. Silk, How Humans Evolved, 3rd ed. (New York: Norton, 2003).
18. J. L. Graves, “What a Tangled Web He Weaves: Race, Reproductive Strategies, and
Rushton’s Life History Theory,” Anthropological Theory 2, no. 2 (2002): 131–54; and J.
L. Graves, “In Defense of the ‘Orthodoxy’: Who We Really Are and Why Some Folks
Have a Problem With It,” in Critical Race Theory in the Academy, ed. V. L. Farmer and
E. S. W. Farmer (Charlotte, NC: Information Age, 2020).
19. G. Zhang, L. J. Muglia, R. Chakraborty, J. M. Akey, and S. M. Williams, “Signatures of
Natural Selection on Genetic Variants Affecting Complex Human Traits,” Applied &
Translational Genomics 2 (2013): 78–94.
20. P. C. Sabeti, S. F. Schaffner, B. Fry, et al., “Positive Natural Selection in the Human
Lineage,” Science 312, no. 5780 (2006): 1614–20.
21. See J. L. Graves Jr., K. L. Hertweck, M. A. Phillips, et al., “Genomics of Parallel Experi-
mental Evolution in Drosophila,” Molecular Biology and Evolution 34, no. 4 (2017):
831–42, https://academic.oup.com/mbe/article/34/4/831/2897202; J. K. Pritchard, J.
K. Pickrell, and G. Coop, “The Genetics of Human Adaptation: Hard Sweeps, Soft
Sweeps, and Polygenic Adaptation,” Current Biology 20, no. 4 (2010): R208—15, https://
doi.org/10.1016/j.cub.2009.11.055; and Zhang et al., “Signatures of Natural Selection on
Genetic Variants.”
22. Zhang et al., “Signatures of Natural Selection on Genetic Variants.”
23. This is well summarized in J. L. Graves, The Emperor’s New Clothes: Biological Theories
of Race at the Millennium (New Brunswick, NJ: Rutgers University Press, 2005); and J.
L. Graves, The Race Myth: Why We Pretend Race Exists in America (New York: Dutton,
2005).
24. The basic principles of equalizing environment for the estimation of genetic con-
tributions to complex traits is explained in the classic work, by D. S. Falconer and
T. MacKay, Introduction to Quantitative Genetics, 4th ed. (Essex, UK: Longman,
1996).
25. The genes associated with these traits are AVPR1 (receptor for arginine vasopres-
sin), SLC6A4 (membrane protein that transports the neurotransmitter serotonin),
COMT (encodes catechol-O-methyltransferase), DRD2 (encodes the D2 subtype of
 262
7. I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

the dopamine receptor), and TPH1 (encodes the protein that is involved in step 1 of the
sub-pathway that synthesizes serotonin from the amino acid L-tryptophan); see B. Gin-
gras, H. Honing, I. Peretz, L. J. Trainor, and S. E. Fisher, “Defining the Biological Bases
of Individual Differences in Musicality,” Philosophical Transactions of the Royal Soci-
ety B Biological Sciences 370, no. 1664 (2015): 20140092, https://royalsocietypublishing
.org/doi/10.1098/rstb.2014.009.
26. The chromosome positions were 4p14-13, 4p12-q12, 4q22, 8q13-21, 18q12-21, 16q21-22,
and 22q11. Specific genes were GPR98 (encodes a G protein coupled superfamily),
USH2A (encodes usherin, a protein that is an important component of basement
membranes that support cells and separate tissues; both genes are involved in audi-
tory reception), GRIN2B (encodes the protein Glu2B, which works in nerve cells,
IL1A (interleukin 1 alpha releases by macrophages and stimulates production of cells
from the thymus gland), IL1B (a potent inflammatory cytokine), and RAPGEF5 (gua-
nine nucleotide exchange factor for cognition, memory). See X. Liu, C. Kanduri, J.
Oikkonen, et al., “Detecting Signatures of Positive Selection Associated with Musi-
cal Aptitude in the Human Genome,” Scientific Reports 6 (2016): 21198, https://www
.nature.com/articles/srep21198.
27. J. Oikkonen, Y. Huang, P. Onkamo, et al., “A Genome-Wide Linkage and Associa-
tion Study of Musical Aptitude Identifies Loci Containing Genes Related to Inner Ear
Development and Neurocognitive Functions,” Molecular Psychiatry 20, no. 2 (2015):
275–82, https://www.nature.com/articles/mp20148.
28. Oikkonen et al., “A Genome-Wide Linkage and Association Study of Musical Aptitude.”
29. Available through the National Center Biological Information (NCBI), https://www
.ncbi.nlm.nih.gov/snp/?cmd=search.
30. S. Sanchez-Roige, J. C. Gray, J. MacKillop, C. H. Chen, and A. A. Palmer, “The Genet-
ics of Human Personality,” Genes, Brain and Behavior 17, no. 3 (2018): e12439, https://
onlinelibrary.wiley.com/doi/full/10.1111/gbb.12439; and H. J. Foldes, E. E. Dueher, and
D. S. Ones, “Group Differences in Personality: Meta-Analyses Comparing Five US
Racial Groups,” Personnel Psychology 61 (2008): 579–616, https://onlinelibrary.wiley
.com/doi/abs/10.1111/j.1744-6570.2008.00123.x.
31. Foldes et al., “Group Differences in Personality.”
32. J. Sidanius and F. Pratto, Social Dominance: An Intergroup Theory of Social Heirarchy
and Oppression (Cambridge, UK: Cambridge University Press, 1999).
33. F. Pratto, J. L. Liu, S. Levin, et al., “Social Dominance Orientation and the Legitima-
tization of Inequality Across Cultures,” Journal of Cross-Cultural Psychology 31, no. 3
(2000): 369–409, https://journals.sagepub.com/doi/abs/10.1177/0022022100031003005.
34. B. H. Kim, H. N. Kim, S. J. Roh, et al., “GWA Meta-Analysis of Personality in Korean
Cohorts,” Journal of Human Genetics 60, no. 8 (2015): 455–60, https://www.nature.com
/articles/jhg201552.
35. D. G. Amen, The End of Mental Illness: How Neuroscience Is Transforming Psychiatry
and Helping to Prevent or Reverse Mood and Anxiety Disorders, ADHD, Addictions,
PTSD, Psychosis, Personality Disorders, and More (Carol Stream, IL: Tyndale Momen-
tum, 2020).
36. R. Nesse, Good Reasons for Bad Feelings (New York: Dutton, 2019).
37. T. A. LaVeist, Minority Populations and Health: An Introduction to Health Disparities
in the United States (San Francisco: Jossey-Bass, 2005).
38. S. J. Bartels and P. DiMilia, “Why Serious Mental Illness Should Be Designated
a Health Disparity and the Paradox of Ethnicity,” Lancet Psychiatry 4, no. 5 (2017):
 263
7. I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

351–52, https://www.thelancet.com/journals/lanpsy/article/PIIS2215-0366(17)30111-6
/fulltext.
39. D. M. Barnes and L. M. Bates, “Do Racial Patterns in Psychological Distress Shed
Light on the Black-White Depression Paradox? A Systematic Review,” Social Psychia-
try and Psychiatric Epidemiology 52, no. 8 (2017): 913–28, https://link.springer.com
/article/10.1007/s00127-017-1394-9.
40. Barnes and Bates, “Do Racial Patterns in Psychological Distress Shed Light on the
Black-White Depression Paradox?”
41. S. Lipsky, M. A. Kernic, Q. Qiu, and D. S. Hasin, “Traumatic Events Associated with
Posttraumatic Stress Disorder: The Role of Race/Ethnicity and Depression,” Violence
Against Women 22, no. 9 (2016): 1055–74, https://journals.sagepub.com/doi/10.1177
/1077801215617553.
42. Lipsky et al., “Traumatic Events Associated with Posttraumatic Stress Disorder.”
43. M. Bresnahan, M. D. Begg, A. Brown, et al., “Race and Risk of Schizophrenia in a US
Birth Cohort: Another Example of Health Disparity?,” International Journal of Epide-
miology 36, no. 4 (2007): 751–58, https://academic.oup.com/ije/article/36/4/751/665657.
44. K. Plowden, “Schizophrenia Spectrum Disorder Disparity Among African-Americans,”
Journal of the National Black Nurses Association 5*30, no. 1 (2019): 14–20.
45. E. F. Torrey and R. H. Yolken, “Schizophrenia and Infections: The Eyes Have It,”
Schizophrenia Bulletin 43, no. 2 (2017): 247–52, https://doi.org/10.1093/schbul/sbw113;
and J. Janoutová, P. Janácková, O. Serý, et al., “Epidemiology and Risk Factors of
Schizophrenia,” Neuroendocrinology Letters 37, no.1 (2016): 1–8.
46. B. Crespi, P. Stead, and M. Elliot, “Evolution in Health and Medicine Sackler Col-
loquium: Comparative Genomics of Autism and Schizophrenia,” Proceedings of the
National Academy of Science 107, suppl. 1 (2010): 1736–41, https://www.pnas.org/content
/early/2010/01/14/0906080106.
47. S. G. Byars, S. C. Stearns, and J. J. Boomsma, “Opposite Risk Patterns for Autism and
Schizophrenia Are Associated with Normal Variation in Birth Size: Phenotypic Sup-
port for Hypothesized Diametric Gene-Dosage Effects,” Proceedings of the Royal Soci-
ety B: Biological Sciences 281, no. 1794 (2014): 20140604, https://royalsocietypublishing
.org/doi/10.1098/rspb.2014.0604.
48. L. K. Pries, S. Gülöksüz, and G. Kenis, “DNA Methylation in Schizophrenia,” in Del-
gado-Morales R. (eds) Neuroepigenomics in Aging and Disease, Advances in Experi-
mental Medicine and Biology 978, ed. R. Delgado-Morales (Cham, Switzerland:
Springer), https://doi.org/10.1007/978-3-319-53889-1_12.
49. M. W. Tremblay and Y. H. Jiang, “DNA Methylation and Susceptibility to Autism
Spectrum Disorder,” Annual Review of Medicine 70 (2019): 151–66, https://www.annual
reviews.org/doi/10.1146/annurev-med-120417-091431.
50. M. Lam, C.-Y. Chen, Z. Li, et al., “Comparative Genetic Architectures of Schizophre-
nia in East Asian and European Populations,” Nature Genetics 51, no. 12 (2019): 1670–
78, https://www.nature.com/articles/s41588-019-0512-x.
51. T. R. de Candia, S. H. Lee, J. Yang, et al., “Additive Genetic Variation in Schizophrenia
Risk Is Shared by Populations of African and European Descent,” American Journal
of Human Genetics 93, no. 3 (2013): 463–70, https://www.sciencedirect.com/science
/article/pii/S000292971300325X.
52. B. H. Hidaka, “Depression as a Disease of Modernity: Explanations for Increas-
ing Prevalence,” Journal of Affective Disorders 140, no. 3 (2012): 205–14, https://doi
.org/10.1016/j.jad.2011.12.036.
 264
7. I N T E L L I G E N C E , B R A I N S , A N D B E H AV I O R S

53. C. Boscher, L. Arnold, A. Lange, and B. Szagun, “Die Last der Ungerechtigkeit. Eine
Längsschnittanalyse auf Basis des SOEPs zum Einfluss subjektiv wahrgenommener
Einkommensgerechtigkeit auf das Risiko einer stressassoziierten Erkrankung [The
load of injustice: A longitudinal analysis of the impact of subjectively perceived
income injustice on the risk of stress-associated diseases based on the German
Socio-Economic Panel Study],” Gesundheitswesen 80, S 02 (2018): S71-S79, http://
doi:10.1055/s-0043-107876.
54. J. P. Rushton, Race, Evolution, and Behavior: A Life History Perspective (New Bruns-
wick, NJ: Transaction, 1994).
55. A. Chase, The Legacy of Malthus: The Social Costs of the New Scientific Racism (Cham-
pagne-Urbana, IL: University of Illinois Press, 1980).
56. L. Delevingne, “The Decade’s 10 Biggest Financial Crimes,” Business Insider, December 21,
2009, https://www.businessinsider.com/the-decades-10-biggest-financial-crimes-2009
-12#7-scott-rothstein-4.
57. The home page for Criminal Justice and Behavior is found at https://journals.sagepub
.com/home/cjb.
58. A. M. Gard, H. L. Dotterer, and L. W. Hyde, “Genetic Influences on Antisocial Behavior:
Recent Advances and Future Directions,” Current Opinion in Psychology 27 (2019): 46–55,
https://www.sciencedirect.com/science/article/pii/S2352250X18300952?via3Dihub.
Two of the SNPs (rs16891867, rs1861046) are on chromosome 4 (and seem to be linked),
as they show the same frequencies in each population listed in the Single Nucleotide
Polymorphism Database (dbSNP). The frequency of the risk SNPs are 0.357 in Sibe-
rians, 0.200 in Koreans, and 0.042 in northern Swedes. The SNP on chromosome 13
(rs11838918) has an FST of 0.014, and the risk allele has a frequency ranging from 0.000
to 0.130 in Africa and essentially the same frequency (around 0.030) in the rest of
the world. The most strongly differentiated SNP, rs7950811, is on chromosome 11 and
has an FST of 0.135, with a range of 0.294–0.07 in Africa, 0.125–0.00 in Europe, and
0.130–0.00 in East Asia.
59. S. L. Davies, “The Reality of False Confessions—Lessons of the Central Park Jogger
Case,” New York University Review of Law and Social Change 2 (2006): 209–54.
60. Tax Policy Center, Urban Institute and Brookings Institution, Fiscal Facts, “Median
Value of Family Net Worth by Race or Ethnicity, 2016,” March 11, 2019, https://www
.taxpolicycenter.org/fiscal-fact/median-value-wealth-race-ff03112019.
61. B. S. Centerwall, “Race, Socioeconomic Status, and Domestic Homicide,” Journal of
the American Medical Association 273, no. 22 (1995): 1755–58.
62. B. Dong, P. H. Egger, and Y. Guo, “Is Poverty the Mother of Crime? Evidence from
Homicide Rates in China,” PLoS One 15, no. 5 (2020): e0233034, https://journals.plos
.org/plosone/article?id=10.1371/journal.pone.0233034.
63. United Nations Office on Drugs and Crime, “Global Study on Homicide, 2019 Edition,”
https://www.unodc.org/unodc/en/data-and-analysis/global-study-on-homicide.html.

8. DRIVING WHILE BLACK AND OTHER DEADLY REALITIES OF

INSTITUTIONAL AND SYSTEMIC RACISM
1. United Church of Christ, “Toxic Wastes and Race at Twenty,” accessed May 2, 2021,
https://www.ucc.org/environmental-ministries_toxic-waste-20. This is also well
explained in the documentary film Unnatural Causes: Is Inequality Making Us Sick?,
 265
8 . D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

California Newsreel, accessed May 2, 2021, http://newsreel.org/video/UNNATURAL

-CAUSES.
2. R. L. Wagmiller and R. M. Adelman, “Childhood and Intergenerational Poverty:
The Long-Term Consequences of Growing Up Poor,” Columbia Academic Commons
(November 2009), https://doi.org/10.7916/D8MP5C0Z.
3. Joe discussed the role of systemic racism in the United States as a factor fuel-
ing the COVID-19 pandemic in J. L. Graves, “Their Money, Our Lives,” Science for
the People, August 23, 2020, https://magazine.scienceforthepeople.org/web-extras
/covid-19-coronanvirus-wealth-race-public-health/.
4. There is an overabundance of evidence to support this fact. See A. Gelman, J. Fagan,
and A. Kiss, “An Analysis of the New York City Police Department’s ‘Stop-and-Frisk’
Policy in the Context of Claims of Racial Bias,” Journal of the American Statistical
Association 102, no. 479 (2007): 813–23, https://doi.org/10.1198/016214506000001040;
J. Rojek, R. Rosenfeld, and S. Decker, “Profiling Race: The Racial Stratification of
Searchers in Police Traffic Stops,” Criminology 50, no. 4 (2012): 993–1023, https://doi
.org/10.1111/j.1745-9125.2012.00285.x; F. R. Baumgartner, D. A. Epp, and K. Shoub, Sus-
pect Citizens: What 20 Million Traffic Stops Tell Us About Policing and Race (Cam-
bridge: Cambridge University Press, 2018).
5. Gelman et al., “An Analysis of the New York City Police Department’s ‘Stop-and-Frisk’
Policy”; Rojek et al., “Profiling Race”; and Baumgartner et al., Suspect Citizens.
6. A classic study of this problem is J. G. Miller, Search and Destroy: African American Males
in the Criminal Justice System (Cambridge: Cambridge University Press, 1996). This work
is more than twenty years old but accurately describes much of what is still going on today.
7. Miller, Search and Destroy.
8. F. R. Baumgartner, D. A. Epp, and K. Shoub, Suspect Citizens: What 20 Million Traffic
Stops Tell Us About Policing and Race (Cambridge: Cambridge University Press, 2018).
9. N. J. Duru, “The Central Park Five, the Scottsboro Boys, and the Myth of the Bestial
Black Man,” Cardozo Law Review 25 (2004): 1315, available at SSRN: https://papers
.ssrn.com/sol3/papers.cfm?abstract_id=814072.
10. S. L. Davies, “The Reality of False Confessions—Lessons of the Central Park Jogger
Case,” N.Y.U. Review of Law and Social Change 30, no. 2 (2005–2006): 209.
11. R. Stone, “HHS ‘Violence Initiative’ Caught in a Crossfire,” Science 258, no. 5080
(1992): 212–13, https://doi.org/10.1126/science.1411519.
12. B. Rensberger, “Science and Sensitivity,” Washington Post, March 1, 1992, https://www
.washingtonpost.com/archive/opinions/1992/03/01/science-and-sensitivity/285e7541
-3b66-48c4-9cc9-55fb37d013f9/.
13. J. Silverberg and J. P. Gray, “Violence and Peacefulness as Behavioral Potentialities of
Primates” in Aggression and Peacefulness in Humans and Other Primates, ed. J. Silver-
berg and J. P. Gray (Oxford: Oxford University Press, 1992).
14. P. Dray, At the Hands of Persons Unknown: The Lynching of Black America (New York:
Random House, 2002).
15. At the time of this writing, another unarmed black man, Jacob Blake, was shot in the
back seven times in front of his children in Kenosha, Wisconsin; B. Booker, “Man
Shot by Kenosha, Wis., Police Paralyzed from the Waist Down, Lawyer Says,” https://
www.npr.org/sections/live-updates-protests-for-racial-justice/2020/08/25/905786759
/another-night-of-clashes-and-unrest-in-kenosha-wis-following-jacob-blake-shootin.
16. D. M. Summerville, Rape and Race in the Nineteenth-Century South (Chapel
Hill: University of North Carolina Press, 2004); and M. Marable, How Capitalism
 266
8 . D R I V I N G W H I L E B L A C K A N D O T H E R D E A D LY R E A L I T I E S

Underdeveloped Black America: Problems in Race, Political Economy, and Society (Chi-
cago: Haymarket, 2015).
17. P. Wagner and W. Sawyer, “States of Incarceration: The Global Context 2018,” Prison
Policy Initiative, June 2018, https://www.prisonpolicy.org/global/2018.html.
18. T. Mendelberg, “Executing Hortons: Racial Crime in the 1988 Presidential Campaign,”
Public Opinion Quarterly 61, no. 1 (1997): 134–57, https://doi.org/10.1086/297790.
19. J. Esherick, Prison Rehabilitation: Success Stories and Failures (Broomall, PA: Mason
Crest, 2015).
20. M. Brickner and S. Diaz, “Prisons for Profit: Incarceration for Sale,” 38 Human Rights
Magazine 13 (July 1, 2011).
21. D. Pager, Marked: Race, Crime, and Finding Work in the Era of Mass Incarceration
(Chicago: University of Chicago Press, 2007).
22. J. Tucker, “Captive Lives,” San Francisco Chronicle, September 16, 2016, https://projects
.sfchronicle.com/2016/captive-lives/.
23. A. Nellis, “The Color of Justice: Racial and Ethnic Disparity in State Prisons,” The Sen-
tencing Project, June 14, 2016, https://www.sentencingproject.org/publications/color
-of-justice-racial-and-ethnic-disparity-in-state-prisons/.
24. M. Alexander, The New Jim Crow: Mass Incarceration in the Age of Colorblindness
(New York: New Press, 2010); B. Stevenson, Just Mercy: A Story of Justice and Redemp-
tion (New York: One World, 2014).
25. R. Balko, Rise of the Warrior Cop: The Militarization of America’s Police Forces (New
York: Public Affairs, 2013).
26. National Center for Education Statistics, Status and Trends in the Education of Racial
and Ethnic Groups, “Indicator 27: Educational Attainment,” updated February 2019,
https://nces.ed.gov/programs/raceindicators/indicator_RFA.asp.
27. H. Lamb, The Crusades (New York: Bantam, 1967, originally published in 1931).
28. A. Jensen, “How Much Can We Boost IQ and Scholastic Achievement?,” Harvard Edu-
cational Review 39, no. 1 (1969): 1–123.
29. J. Kozol, Savage Inequalities: Children in America’s Schools (New York: Broadway
Books, 2012).
30. S. Morton, Crania Americana; or, a Comparative View of Skulls of Various Aboriginal
Nations of North and South America; to which Is Prefixed an Essay on the Varieties of the
Human Species (Philadelphia: J. Dobson, 1839); and R. Herrnstein and C. R. Murray, The
Bell Curve: Intelligence and Class Structure in American Life (New York: Free Press, 1994).
31. M. Bertrand and S. Mullainthan, “Are Emily and Greg More Employable Than Laki-
sha and Jamal? A Field Experiment on Labor Market Discrimination,” American Eco-
nomic Review 94, no. 4 (2004): 991–1013.
32. J. L. Graves and E. Jarvis, “An Open Letter: Scientists and Racial Justice,” Scientist,
June 19, 2020, https://www.the-scientist.com/news-opinion/an-open-letter-scientists
-and-racial-justice-67648.
33. H. Queneau and A. Sen, “On the Structure of US Unemployment Disaggregated by
Race, Ethnicity, and Gender,” Economics Letters 117, no. 1 (October 1, 2012): 91–95,
https://doi.org/10.1016/j.econlet.2012.04.065.
34. Centers for Disease Control and Prevention, “Morbidity and Mortality Weekly
Reports,” 54, no. 20 (May 27, 2005): 513–516.
35. United Church of Christ, “Toxic Wastes and Race at Twenty.”
36. B. Chappell and S. Nuyen, “2 Hurricanes Could Form in the Gulf of Mexico Next Week—
An Apparent First,” NPR, https://www.npr.org/2020/08/21/904674353/2-hurricanes
-could-be-in-gulf-coast-early-next-week-weather-service-says.
 267
9. DNA AND ANCESTRY TESTING

37. ESRI, “Aftermath of Katrina: A Time of Environmental Racism,” accessed May 2, 2021,
https://www.arcgis.com/apps/Cascade/index.html?appid=2106693b39454f0eb0abc5c2
ddf9ce40.
38. J. Hanna and S. Chan, “California Wildfires Have Burned 1.25 Million Acres, But Fire-
fighters Say the Weather Is Now Helping,” CNN, August 25, 2020, https://www.cnn
.com/2020/08/25/us/california-fires-tuesday/index.html.
39. J. E. Keely, H. Safford, C. J. Fotheringham, J. Franklin, and M. Moritz, “The 2007
Southern California Wildfires: Lessons in Complexity,” Journal of Forestry 107, no. 6
(2009): 287–96, https://doi.org/10.1093/jof/107.6.287.
40. J. L. Graves, The Race Myth: Why We Pretend Race Exists in America (New York: Dut-
ton, 2004), 194–203.
41. K. McIntosh, E. Moss, K. Moss, R. Nunn, J. Shambaugh, “Up Front: Examining the
Black-White Wealth Gap,” Brookings, February 27, 2020, https://memphis.uli.org/wp
-content/uploads/sites/49/2020/07/Examining-the-Black-white-wealth-gap.pdf.
42. N. T. Sharma, Hip Hop Desis: South Asians, Blackness, and a Global Race Consciousness
(Durham, NC: Duke University Press, 2010).
43. L. Salyer, Laws as Harsh as Tigers: Chinese Immigrants and the Shaping of Modern
Immigration Law (Chapel Hill: University of North Carolina Press, 1995).

9. DNA AND ANCESTRY TESTING

1. A. Regalado, “More Than 26 Million People Have Taken an At-Home Ancestry
Test,” MIT Technology Review, February 11, 2019, https://www.technologyreview
.com/2019/02/11/103446/more-than-26-million-people-have-taken-an-at-home
-ancestry-test/.
2. C. M. Rands, S. Meader, C. P. Ponting, and G. Lunter, “8.2 Percent of the Human
Genome is Constrained: Variation in Rates of Turnover Across Functional Element
Classes in the Human Lineage,” PLoS Genetics 10, no. 7 (2014): e1004525, https://doi
.org/10.1371/journal.pgen.1004525.
3. G. Barbujani and C. Colonna, “Human Genome Diversity: Frequently Asked
Questions,” Trends in Genetics 26, no. 7 (2010): 285–95, https://doi.org/10.1016/j.tig
.2010.04.002.
4. K. Bryc, E. Y. Durand, J. M. Macpherson, D. Reich, and J. L. Mountain, “The Genetic
Ancestry of African Americans, Latinos, and European Americans Across the United
States,” American Journal of Human Genetics 96, no. 1 (2015): 37–53, https://doi
.org/10.1016/j.ajhg.2014.11.010; and S. J. Micheletti, K. Bryc, S. G. Ancona Esselmann,
et al., “Genetic Consequences of the Transatlantic Slave Trade in the Americas,” Amer-
ican Journal of Human Genetics 107, no. 2 (2020): 265–77, https://doi.org/10.1016/j
.ajhg.2020.06.012. The first study utilized the V1, V2 variants of the Illumina Human-
Hap 550 + Bead Chip, which included 25,000 custom SNPs chosen by 23andMe, total-
ing 560,000 SNPs. The researchers also used the V3 platform Illumina OmniExpress
+ Bead Chip + custom content, which included 950,000 SNPs; and the V4 platform,
which had an additional custom 510,000 SNPs.
5. You can watch world population grow in real time at the Current World Population
Clock, https://www.worldometers.info/world-population/.
6. E. Jehaes, H. Pfeiffer, K. Toprak, et al., “Mitochondrial DNA Analysis of the Putative
Heart of Louis XVII, Son of Louis XVI and Marie-Antoinette,” European Journal of
Human Genetics 9, no. 3 (2001): 185–90, https://doi.org/10.1038/sj.ejhg.5200602.
 268
9. DNA AND ANCESTRY TESTING

7. A. Gordon Reed, Thomas Jefferson and Sally Hemings: An American Controversy

(Charlottesville: University Press of Virginia, 1998).
8. E. A. Foster, M. A. Jobling, P. G. Taylor, et al., “Jefferson Fathered Slave’s Last Child,”
Nature 396, no. 6706 (1998): 27–28, https://doi.org/10.1038/23835.
9. S. A. Tishkoff, F. A. Reed, F. R. Friedlaender, et al., “The Genetic Structure and History
of Africans and African Americans,” Science 324, no. 5930 (2009): 1035–44, https://doi
.org/10.1126/science.1172257.
10. B. M. Henn, C. R. Gignoux, M. Jobin, et al., “Hunter-Gatherer Genomic Diver-
sity Suggests a Southern African Origin for Modern Humans,” Proceedings of the
National Academy of Sciences 108, no. 13 (2011): 5154–62, https://doi.org/10.1073
/pnas.1017511108.
11. P. Manning, “Slavery and the Slave Trade in West Africa: 1450–1930,” in The History of
African Development. An Online Textbook for a New Generation of African Students and
Teachers, ed. E. Frankema, E. Hillbom, U. Kufakurinani, and F. Meier zu Selhausen,
African Economic History Network, accessed May 4, 2021, https://www.aehnetwork
.org/textbook/; also see P. Lovejoy, “The Impact of the Atlantic Slave Trade on Africa:
A Review of the Literature,” Journal of African History 30, no. 3 (1989): 365–94, https://
doi.org/10.1017/S0021853700024439.
12. A. M. Huml, C. Sullivan, M. Figueroa, K. Scott, and A. R. Sehgal, “Consistency of Direct-
to-Consumer Genetic Testing Results Among Identical Twins,” American Journal of
Medicine 133, no. 1 (2020): 143–46.e2, https://doi.org/10.1016/j.amjmed.2019.04.052.
13. J. M. Lind, H. B. Hutcheson-Dilks, S. M. Williams, et al., “Elevated Male European
and Female African Contributions to the Genomes of African American Individu-
als,” Human Genetics 120, no. 5 (2007): 713–22, https://doi.org/https://doi.org/10.1007
/s00439-006-0261-7.
14. Micheletti et al., “Genetic Consequences of the Transatlantic Slave Trade in the
Americas.”
15. L. M. Holson, “Ancestry.com Apologizes for Ad Showing Slavery-Era Interracial
Couple,” New York Times, April 19, 2019, https://www.nytimes.com/2019/04/19/us
/ancestry-dna-slavery-commercial.html.
16. The story of Patsy is well recounted in Solomon Northup’s Twelve Years a Slave (New
York: Graymalkin Media, 2014), originally published in 1853. This character was also
brought to the screen in the 2013 film Twelve Years a Slave with Kenyan-born actress
Lupita Nyong’o in the role of Patsy. (By the way, Kenyans were never sold in the trans-
atlantic slave trade.)
17. V. E. Bynum, “ ‘White Negroes’ in Segregated Mississippi: Miscegenation, Racial
Identity, and the Law,” Journal of Southern History 64, no. 2 (1998): 247–76, https://
doi.org/10.2307/2587946; also see R. Grant, “The True Story of ‘Free State of Jones,’ ”
Smithsonian (March 2016), https://www.smithsonianmag.com/history/true-story-free
-state-jones-180958111/.
18. A. Panofsky and J. Donovan, “Genetic Ancestry Testing Among White Nationalists:
From Identity Repair to Citizen Science,” Social Studies of Science 49, no. 5 (2019):
653–81, https://doi.org/10.1177/0306312719861434.
19. M. Slatkin and F. Racimo, “Ancient DNA and Human History,” Proceedings of the
National Academy of Sciences 113, no. 23 (2016): 6380–87, https://doi.org/10.1073/pnas
.1524306113.
20. L. Cavalli-Sfroza, P. Menozzi, and A. Piazza, The History and Geography of Human
Genes (Princeton, NJ: Princeton University Press, 1994).
 269
9. DNA AND ANCESTRY TESTING

21. D. Reich, Who We Are and How We Got Here: Ancient DNA and the New Science of the
Human Past (New York: Pantheon, 2018).
22. Reich, Who We Are and How We Got Here.
23. S. Sankararaman, S. Mallick, N. Patterson, and D. Reich, “The Combined Landscape
of Denisovan and Neanderthal Ancestry in Present-Day Humans,” Current Biology 26,
no. 9 (2016): 1241–47, https://doi.org/10.1016/j.cub.2016.03.037.
24. E. Huerta-Sánchez, X. Jin, Asan, et al., “Altitude Adaptation in Tibetans Caused by
Introgression of Denisovan-Like DNA,” Nature 512, no. 7513 (2014): 194–97, https://doi
.org/10.1038/nature13408.
25. Huerta-Sánchez et al., “Altitude Adaptation in Tibetans.”
26. E. M. Oziolor, N. M. Reid, S. Yair, et al., “Adaptive Introgression Enables Evolutionary
Rescue from Extreme Environmental Pollution,” Science 364, no. 6439 (2019): 455–57,
https://doi.org/10.1126/science.aav4155.
27. B. Kislev, “Neanderthal and Woolly Mammoth Molecular Resemblance: Genetic Simi-
larities May Underlie Cold Adaptation Suite,” Human Biology 90, no. 2 (2019): 115–28,
https://doi.org/10.13110/humanbiology.90.2.03.
28. J. K. Pickrell and D. Reich, “Toward a New History and Geography of Human Genes
Informed by Human DNA,” Trends in Genetics 30, no. 9 (2014): 377–89, https://doi
.org/10.1016/j.tig.2014.07.007.
29. R. Nielsen, J. M. Akey, M. Jakobsson, et al., “Tracing the Peopling of the World
Through Genomics,” Nature 541, no. 7637 (2017): 302–10, https://doi.org/10.1038
/nature21347.
30. M. F. Hammer, A. E. Woerner, F. L. Mendez, J. C. Watkins, and J. D. Wall, “Genetic
Evidence for Archaic Admixture in Africa,” Proceedings of the National Academy of
Sciences 108, no. 37 (2011): 15123–128, https://doi.org/10.1073/pnas.1109300108.
31. T. Günther and M. Jakobsson, “Genes Mirror Migrations and Cultures in Prehistoric
Europe—A Population Genomic Perspective,” Current Opinion in Genetics & Develop-
ment 41 (2016): 115–23, https://doi.org/10.1016/j.gde.2016.09.004.
32. T. Günther, C. Valdiosera, H. Malmström, et al., “Ancient Genomes Link Early Farmers
from Atapuerca in Spain to Modern-Day Basques,” Proceedings of the National Acad-
emy of Sciences 112, no. 38 (2015): 11917–922, https://doi.org/10.1073/pnas.1509851112.
33. E. R. Jones, G. Gonzalez-Fortes, S. Connell, et al., “Upper Palaeolithic Genomes Reveal
Deep Roots of Modern Eurasians,” Nature Communications 6 (2015): 8912, https://doi
.org/10.1038/ncomms9912.
34. M. Rasmussen, X. Guo, Y. Wang , et al., “An Aboriginal Australian Genome Reveals
Separate Human Dispersals Into Asia,” Science 334, no. 6052 (2011): 94–98, https://doi
.org/10.1126/science.1211177.
35. A. S. Malaspinas, M. C. Westaway, C. Muller, et al., “A Genomic History of Aboriginal
Australia,” Nature 538, no. 7624 (2016): 207–14, https://doi.org/10.1038/nature18299.
36. M. Raghavan, M. Steinrücken, K. Harris, et al., “Genomic Evidence for the Pleistocene
and Recent Population History of Native Americans,” Science 349, no. 6250 (2015):
aab3884, https://doi.org/10.1126/science.aab3884.
37. K. L. Hunley and G. S. Cabana, “Beyond Serial Founder Effects: The Impact of Admix-
ture and Localized Gene Flow on Patterns of Regional Genetic Diversity,” Human
Biology 88, no. 3 (2016): 219–31, https://doi.org/10.13110/humanbiology.88.3.0219.
38. R. Kuper and S. Kropelin, “Climate-Controlled Holocene Occupation in the Sahara:
Motor of Africa’s Evolution,” Science 313, no. 5788 (2006): 803–7, https://doi.org/10.1126
/science.1130989.
 270
9. DNA AND ANCESTRY TESTING

39. S. Fan, M. E. Hansen, Y. Lo, and S. A. Tishkoff, “Going Global by Adapting Local: A
Review of Recent Human Adaptation,” Science 354, no. 6308 (2016): 54–59, https://doi
.org/10.1126/science.aaf5098.
40. D. Smay and G. Armelagos, “Galileo Wept: A Critical Assessment of the Use of Race
in Forensic Anthropology,” Transforming Anthropology 9, no. 2 (2000): 19–29, https://
doi.org/10.1525/tran.2000.9.2.19.
41. E. Giles and O. Elliot, “Race Identification from Cranial Measurements,” Journal of
Forensic Sciences 7, no. 2 (1962): 147–57.
42. A. H. Goodman, “Bred in the Bone?,” The Sciences 37 (1997): 20–25, https://doi
.org/10.1002/j.2326-1951.1997.tb03296.x.
43. R. Lewis, Human Genetics: Concepts and Applications, 5th ed. (Boston: McGraw-Hill,
2003).
44. C. Phillips, “The Golden State Killer Investigation and the Nascent Field of Foren-
sic Genealogy,” Forensic Science International: Genetics 36 (2018): 186–88, https://doi
.org/10.1016/j.fsigen.2018.07.010.
45. B. Scheck, “The Innocence Project at Twenty: An Interview with Barry Scheck. Inter-
view by Jane Gitschier,” PLoS Genetics 9, no. 8 (2013): e1003692, https://doi.org/10.1371
/journal.pgen.1003692.
46. P. A. Chow-White and T. Duster, “Do Health and Forensic DNA Databases Increase
Racial Disparities?,” PLoS Medicine 8, no. 10 (2011): e1001100, https://doi.org/10.1371
/journal.pmed.1001100.
47. A. O. Amankwaa and C. McCartney, “The UK National DNA Database: Implementa-
tion of the Protection of Freedoms Act 2012,” Forensic Science International 284 (2018):
117–28, https://doi.org/10.1016/j.forsciint.2017.12.041.
48. S.-L. Wee, “China Is Collecting DNA from Tens of Millions of Men and Boys, Using
U.S. Gear,” New York Times, June 17, 2020, https://www.nytimes.com/2020/06/17/world
/asia/China-DNA-surveillance.html.

10. RACE NAMES AND “RACE MIXING”

1. J. M. Fish, “Mixed Blood: An Analytical Look at Methods of Classifying Race,” Psychol-
ogy Today, November 1, 1995, https://www.psychologytoday.com/us/articles/199511
/mixed-blood.
2. D. I. Ketzer and D. Arel, “Censuses, Identity Formation, and the Struggle for Politi-
cal Power,” in Census and Identity: The Politics of Race, Ethnicity, and Language in
National Census, ed. D. I. Ketzer and D. Arel (New York: Cambridge University Press,
2002).
3. See Office of Management and Budget Directive 15, https://wonder.cdc.gov/WONDER
/help/populations/bridged-race/directive15.html.
4. S. Arasaratnam, “Weavers, Merchants and Company: The Handloom Industry in
Southeastern India 1750–1790,” Indian Economic and Social History Review 12, no. 3
(1980): 257–81.
5. F. V. Harrison, “Unraveling Race for the Twenty-First Century,” in Exotic No More:
Anthropology for the Contemporary World, 2nd ed., ed. J. MacClancy (Chicago: Uni-
versity of Chicago Press, 2019).
6. C. C. Gravlee and W. W. Dressler, “Emic Ethnic Classification in Southeastern Puerto
Rico: Cultural Consensus and Semantic Structure,” Social Forces 83 (2005): 949–70;
 271
10. RACE NAMES AND “RACE MIXING”

R. L. Reichmann, Race in Contemporary Brazil: From Indifference to Inequality (State

College, PA: Pennsylvania State University Press, 2010).
7. L. Wright Jr., “Who’s Black, Who’s White, and Who Cares: Reconceptualizing the
United States’s Definition of Race and Racial Classifications,” Vanderbilt Law Review
48, no. 2 (1995): 513.
8. T. Pegelow, “Determining ‘People of German Blood’, ‘Jews’ and ‘Mischlinge’: The Reich Kin-
ship Office and the Competing Discourses and Powers of Nazism, 1941–1943,” Contempo-
rary European History 15, no. 1 (2006): 43–65, https://doi.org/10.1017/S0960777306003092.
9. K. Bryc, E. Y. Durand, J. M. Macpherson, D. Reich, and J. L. Mountain, “The Genetic
Ancestry of African Americans, Latinos, and European Americans Across the United
States,” American Journal of Human Genetics 96, no. 1 (2015): 37–53, https://doi.org
/10.1016/j.ajhg.2014.11.010.
10. J. Brown (with P. Ellis), Say It Loud—I’m Black and I’m Proud, https://en.wikipedia
.org/wiki/Say_It_Loud_E28093_I27m_Black_and_I27m_Proud.
11. Bryc et al., “The Genetic Ancestry of African Americans, Latinos, and European
Americans.”
12. L. R. Arana, “The Exploration of Florida and Sources on the Founding of St. Augus-
tine,” Florida Historical Quarterly 44, no. 1/2 (1965): 1–16; R. J. Weber, Myth and History
of the Hispanic Southwest (Albuquerque: University of New Mexico Press, 1988); and
J. L. Allen, “From Cabot to Cartier: The Early Exploration of Eastern North America,
1497–1543,” Annals of the Association of American Geographers 82, no. 3 (1992): 500–21,
https://doi.org/10.1111/j.1467-8306.1992.tb01972.x.
13. J. W. Davidson, B. DeLay, C. L. Heyman, M. H. Lytle, and M. B. Stoff, Nation of
Nations: A Narrative History of the American Republic (Boston: McGraw-Hill Higher
Education, 2008).
14. S. Kelley, “ ‘Mexico in His Head’: Slavery and the Texas-Mexico Border, 1810–1860,”
Journal of Social History 37, no. 3 (2004): 709–23, https://doi.org/10.1353/jsh.2004.0010;
and J. D. P. Fuller, “The Slavery Question and the Movement to Acquire Mexico, 1846–
1848,” Mississippi Valley Historical Review 21, no. 1 (1934): 31–48.
15. E. Guzman, “Igartua de la Rosa v. United States: The Right of the United States Citizens
of Puerto Rico to Vote for the President and the Need to Re-Evaluate America’s Ter-
ritorial Policy,” Journal of Constitutional Law 14, no. 1 (2001), https://scholarship.law.
upenn.edu/jcl/vol4/iss1/3.
16. P. Cabán, Constructing a Colonial People: Puerto Rico and the United States: 1898–
1932,(New York: Routledge, 1999).
17. “Census Bureau Releases Updates on Race Categories for 2020 Census,” https://
2020census.gov/en/about-questions/2020-census-questions-race.html.
18. These race categories are found at U.S. Bureau of the Census, https://2020census.gov
/en/about-questions/2020-census-questions-race.html.
19. W. D. Roth, Ş. Yaylacı, K. Jaffe, and L. Richardson, “Do Genetic Ancestry Tests Increase
Racial Essentialism? Findings from a Randomized Controlled Trial,” PLoS ONE 15, no.
1 (2020): e0227399, https://doi.org/10.1371/journal.pone.0227399.
20. M. Omi and H. Winant, “Racial Formations,” in Race, Class, and Gender in the United
States, ed. P. S. Rothenberg (New York: Worth, 2007).
21. S. Hoffman, “Is There a Place for Race as a Legal Concept,” Faculty Publications 227
(2004), https://scholarlycommons.law.case.edu/faculty_publications/227.
22. W. Booth, “Phobia About Blacks Brings Worker’s Compensation Award,” Washington
Post, August 13, 1992, https://www.washingtonpost.com/archive/politics/1992/08/13
 272
10. RACE NAMES AND “RACE MIXING”

/phobia-about-blacks-brings-workers-compensation-award/5bff7057-22c3-4b45
-ad32-0f58d0fd9b1f/.
23. P. Buescher, Z. Gizlice, and K. Jones-Vessey, “Self-Reported Versus Published Data on
Racial Classification in North Carolina Birth Records,” SCHS Studies no. 139—Racial
Classification (February 2004), https://schs.dph.ncdhhs.gov/schs/pdf/schs139.pdf.
24. R. A. Hahn, “Why Race Is Differentially Classified on U.S. Birth and Infant Death Cer-
tificates: An Examination of Two Hypotheses,” Epidemiology 10, no. 2 (1999): 108–11.
25. E. Hackenmueller, “The (Mis)Representation of Interracial Couples in Television
Advertisements” (master’s thesis, University of Alabama, Department of Advertising
and Public Relations, 2020), http://ir.ua.edu/handle/123456789/6982.
26. K. Parker, J. M. Horowitz, R. Morin, and M. H. Lopez, “Multiracial in America: Proud,
Diverse, and Growing in Numbers,” Pew Research Center, June 11, 2015, https://www
.pewsocialtrends.org/2015/06/11/multiracial-in-america/.
27. J. M. Chen, N. S. Kteily, and A. K. Ho, “Whose Side Are You On? Asian Ameri-
can Distrust of Asian-White Biracials Predicts More Exclusion from the Ingroup,”
Personality and Social Psychology Bulletin 45, no. 6 (2019): 827–41, https://doi.org
/10.1177/0146167218798032.
28. S. Outram, J. L. Graves, J. Powell, et al., “Genes, Race, and Causation: US Public Perspec-
tives About Racial Difference,” Race Soc. Probl. (2018), https://doi.org/10.1007/s12552
-018-9223-7.
29. A discussion of hybrid vigor or heterosis can be found in any standard genetics text;
e.g., see D. S. Falconer and T. Mackay, Introduction to Quantitative Genetics, 4th ed.
(Essex, UK: Addison Wesley Longman, 1996), 258.
30. C. Darwin, The Descent of Man and Selection in Relation to Sex (Princeton, NJ: Princ-
eton University Press, 1981), first published in 1871. His discussion of the fertility of the
hybrids is on 221–23.
31. K. Wailoo, Sickle Cell Disease: Dying in the City of the Blues (Chapel Hill: University of
North Carolina Press, 2001); and J. H. Jones, Bad Blood: The Tuskegee Syphilis Experi-
ment, new and exp. ed. (New York: Free Press, 1993).
32. C. B. Davenport and M. Steggerda, Race Crossing in Jamaica (Washington, DC: Carn-
egie Institution of Washington, 1929).
33. See discussion of Charles Davenport and the Eugenics Record Office in J. L. Graves,
The Emperor’s New Clothes: Biological Theories of Race at the Millennium (New Bruns-
wick, NJ: Rutgers University Press, 2005), 115–25.
34. A discussion of how this sterilization was conducted can be found in S. F. Weiss, “The
Race Hygiene Movement in Germany 1904–1945,” in The Wellborn Science: Eugenics
in Germany, France, Brazil, and Russia, ed. M. Adams (New York: Oxford University
Press, 1990).
35. WedMd, “Multiple Myeloma: Causes and Risk Factors,” https://www.webmd.com
/cancer/multiple-myeloma/are-you-at-risk-for-multiple-myeloma.
36. S. A. Tishkoff, F. A. Reed, F. R. Friedlaender, et al., “The Genetic Structure and History
of Africans and African Americans,” Science 324, no. 5930 (2009): 1035–44, https://doi
.org/10.1126/science.1172257.
37. J. Nott and G. R. Gliddon, Indigenous Races of the Earth or New Chapters of Ethnologi-
cal Inquiry (Philadelphia: Lippincott and Grambo, 1857).
38. J. Snow, “The Civilization of White Men: The Race of the Hindu in United States v.
Bhagat Singh Thind,” in Race, Nation, and Religion in the Americas, ed. H. Goldschmidt
and E. McAllister (New York: Oxford University Press, 2004).
 273
10. RACE NAMES AND “RACE MIXING”

39. J. C. Prichard, Researches Into the Physical History of Mankind, vol. III. Researches Into
the Origin of the European Nations (London: Sherwood, Gilbert, and Piper, 1841).
40. R. Dart, “Australopithecus africanus: The Man-Ape of South Africa,” Nature 115, no.
2884 (1925).
41. J. K. McKee, F. E. Poirier, and W. S. McGraw, Understanding Human Evolution, 5th ed.
(New York: Routledge, 2004).
42. C. Coon, The Origin of Races (New York: Knopf, 1962).
43. A. Montagu, Mankind’s Most Dangerous Myth: The Fallacy of Race, 6th ed. (Palo Alto,
CA: Alta Mira, 1997). He quotes an interview by Herman Rauschning with Adolph
Hitler; see H. Rauschning, The Voice of Destruction (New York: Putnam, 1940).
44. M. Kaback, J. Lim-Steele, D. Dabholkar, et al., “Tay-Sachs Disease—Carrier Screening,
Prenatal Diagnosis, and the Molecular Era. An International Perspective, 1970 to 1993.
The International TSD Data Collection Network,” Journal of the American Medical
Association 270, no. 19 (1990): 2307–15.
45. Montagu, Mankind’s Most Dangerous Myth.
46. P. Kolchin, “Whiteness Studies: The New History of Race in America,” Journal of
American History 89, no. 1 (2002): 154–73, https://doi.org/10.2307/2700788.
47. See the classic historical work on this phenomenon, D. R. Roediger, Working Toward
Whiteness: How America’s Immigrants Became White; The Strange Journey from Ellis
Island to the Suburbs (New York, Basic Books, 2005).
48. Joe is not alone in thinking this way; see J. Barndt, Becoming an Anti-Racist Church:
Journeying Towards Wholeness (Minneapolis: Fortress, 2011).
49. P. Bump, “Presenting the Least Misleading Map of the 2016 Election,” Washington
Post, July 30, 2018, https://www.washingtonpost.com/news/politics/wp/2018/07/30
/presenting-the-least-misleading-map-of-the-2016-election/.
50. T. T. Reny, L. Collingwood, and A. A. Valenzuela, “Vote Switching in the 2016 Elec-
tion: How Racial and Immigration Attitudes, Not Economics, Explain Shifts in White
Voting,” Public Opinion Quarterly 83, no. 1 (2019): 91–113, https://doi.org/10.1093/poq
/nfz011.
51. J. Daniels, Cyber Racism: White Supremacy Online and the New Attack on Civil Rights
(Lanham, MD: Rowman & Littlefield, 2009).
52. “Fraternity Activities Suspended at Syracuse University Following Latest Racist Inci-
dent, Investigation Into Graffiti Ongoing,” DiversityInc, November 18, 2019, https://www
.diversityinc.com/syracuse-university-racist-graffiti/?utm_source=hs_email&utm
_medium=email&utm_content=79571173&_hsenc=p2ANqE280A6.
53. R. Ralston, M. Motta, and J. Spindel, “When OK Is Not OK: Public Concern About
White Nationalism in the U.S. Military,” Armed Forces & Society (April 2020): 1–12,
https://doi.org/10.1177/0095327X20918394.
54. Daniels, Cyber Racism.
55. J. D. Mayer, Running on Race: Racial Politics in the Presidential Campaigns, 1960–2000
(New York: Random House, 2002). The Nixon quote is on 69.
56. P. Sullivan, Days of Hope: Race and Democracy in the New Deal Era (Chapel Hill: Uni-
versity of North Carolina Press, 1996).
57. Southern Poverty Law Center, “White Nationalist,” https://www.splcenter.org/fighting
-hate/extremist-files/ideology/white-nationalist.
58. E. Levenson, “The Realities of Being a Black Bird Watcher,” CNN, May 27, 2020,
https://www.cnn.com/2020/05/27/us/birdwatching-black-christian-cooper/index
.html.
 274
10. RACE NAMES AND “RACE MIXING”

59. T. McCoy, “In Jim Cooley’s Open-Carry America, Even a Trip to Walmart Can
Require an AR-15,” Washington Post, September 17, 2016, https://www.washingtonpost
.com/national/guns-and-sodas/2016/09/17/805e0db4-79e9-11e6-bd86-b7bbd53d2b5d
_story.html.
60. M. Macaya, M. Wagner, and M. Hayes, “The Latest on Kenosha Police Shooting of
Jacob Blake,” CNN, August 31, 2020, https://www.cnn.com/us/live-news/jacob-blake
-kenosha-police-shooting-08-31-2020/index.html.
61. M. Holcombe, S. Nottingham, and E. Levenson, “Man Killed in Portland Shooting
Identified by Police as Aaron J. Danielson,” CNN, August 31, 2020, https://www.cnn
.com/2020/08/31/us/governor-brown-portland-plan-curb-protests/index.html.
62. A. Wise, “Trump Defends Kenosha Shooting Suspect,” NPR, August 31, 2020, https://
www.npr.org/sections/live-updates-protests-for-racial-justice/2020/08/31/908137377
/trump-defends-kenosha-shooting-suspect.

11. A WORLD WITHOUT RACISM?

1. G. Childress, “State Board of Education OKs New Social Study Standards; Lt. Gov-
ernor Calls It ‘Irresponsible,’ ” NC Policy Watch, February 5, 2021, http://pulse
.ncpolicywatch.org/2021/02/05/state-board-of-education-oks-new-social-study
-standards-lt-governor-calls-it-irresponsible/#sthash.jKcKVCHx.dpbs.
2. W. Guzman, “Michigan State Vice President of Research Stephen Hsu Resigns,” State News,
June 19, 2020, https://statenews.com/article/2020/06/michigan-state-vp-of-research
-stephen-hsu-resigns.
3. A. F. Poiussaint, “Is Extreme Racism a Mental Disorder?,” Western Journal of Medicine
176, no. 4 (2002).
4. S. Barnes, Washington Staff, and Associated Press, “Commitment March on Wash-
ington: Crowds at National Mall Call for Justice,” NBC, August 28, 2020, https://www
.nbcwashington.com/news/commitment-march-on-washington-2020-thousands-to
-converge-on-national-mall/2403921/.
5. “Trump Holds NH Rally After Accepting Republican Presidential Nomination,” NBC,
August 28, 2020, https://www.nbcboston.com/news/politics/decision-2020/trump-to
-hold-rally-in-nh-friday/2185378/.
6. As of January 8, 2021.
7. One of our favorites is T. Schick Jr., and L. Vaughan, How to Think About Weird Things:
Critical Thinking for a New Age, 5th ed. (Boston: McGraw-Hill, 2008).
8. L. M. Bartels, “Ethnic Antagonism Erodes Republicans’ Commitment to Democracy,”
Proceedings of the National Academy of Sciences 117, no. 37 (2020): 22752–759, https://
doi.org/10.1073/pnas.2007747117.
9. D. Searcey, “The Battle Over Biscuits and Gravy at the 11-Worth Cafe,” New York Times,
September 5, 2020, https://www.nytimes.com/2020/09/05/us/politics/omaha-cafe
-confederate-protests.html?searchResultPosition=1.
10. B. F. Schaffner, M. Macwilliams, and T. Nteta, “Understanding White Polarization in
the 2016 Vote for President: The Sobering Role of Racism and Sexism,” Political Science
Quarterly 133, no. 1 (2018): 9–34, https://doi.org/10.1002/polq.12737.
11. S. Coll, “The Case for Dumping the Electoral College,” New Yorker, September 13, 2020,
https://www.newyorker.com/magazine/2020/09/21/the-case-for-dumping-the-electoral
-college.
 275
11. A WORLD WITHOUT RACISM?

12. Joe once participated in such training for the Portland Oregon police force (com-
manders and sergeants).
13. See the American Civil Liberties Union (ACLU) bail reform site, https://www.aclu
.org/issues/smart-justice/bail-reform.
14. B. Stevenson, Just Mercy: A Story of Justice and Redemption (New York: Random
House, 2014).
15. J. L. Eberhardt, P. G. Davies, V. J. Purdie-Vaughns, and S. L. Johnson, “Looking Death-
worthy: Perceived Stereotypicality of Black Defendants Predicts Capital-Sentencing
Outcomes,” Cornell Law Faculty Publications 41 (2006), https://scholarship.law.cornell
.edu/lsrp_papers/41.
16. Hamilton Project, “Rate of Drug Use and Sales, by Race; Rates of Drug Related Criminal
Justice Measures, by Race,” October 26, 2016, https://www.hamiltonproject.org/charts
/rates_of_drug_use_and_sales_by_race_rates_of_drug_related_criminal_justice.
17. J. Hudak, “Colorado’s Rollout of Legal Marijuana Is Succeeding: A Report on the State’s
Implementation of Legalization,” Case Western Reserve Law Review 65, no. 3 (2015): 649.
18. A. Selsky, “Oregon 1st State to Decriminalize Possession of Hard Drugs,” Associated Press,
February 1, 2021, https://www.usnews.com/news/politics/articles/2021-02-01/oregon-1st
-state-to-decriminalize-possession-of-hard-drugs.
19. M. L. King Jr., “Our God Is Marching On” (speech), American Public Media, March 25,
1965, http://americanradioworks.publicradio.org/features/prestapes/mlk_speech.html.
20. W. C. Whatley, “African-American Strikebreaking from the Civil War to the New
Deal,” Social Science History 17, no. 4 (1993): 525–58.
21. C. J. Walley, “Trump’s Election and the ‘White Working Class’: What We Missed,”
American Ethnologist 44, no. 2 (2017): 231–36, https://doi.org/10.1111/amet.12473.
22. K. Harris, A. Kimson, and A. Schwedel, “Labor 2030: The Collision of Demograph-
ics, Automation and Inequality,” Bain & Company, February 7, 2018, http://www.bain
.com/publications/articles/labor-2030-the-collision-of-demographics-automation
-and-inequality.aspx.
23. A. L. Kalleberg, “Precarious Work, Insecure Workers: Employment Relations in Tran-
sition,” American Sociological Review 74 (2009): 1–22.
24. J. Prassl, Humans as a Service: The Promise and Peril of Work in the Gig Economy (New
York: Oxford University Press, 2018).
25. E. P. Bettinger and B. T. Long, “Does Cheaper Mean Better? The Impact of Using
Adjunct Instructors on Student Learning Outcomes,” Review of Economics and Statis-
tics 92, no. 3 (2010): 598–613.
26. R. Wallace, Dead Epidemiologists: On the Origins of COVID-19 (New York: Monthly
Review Press, 2021).
27. B. Donovan, “Reclaiming Race as a Topic of the U.S. Biology Textbook Curriculum,”
Science Education 99, no. 6 (2015): 1092–117.
28. R. Bifulco and H. F. Ladd, “School Choice, Racial Segregation, and Test-Score Gaps:
Evidence from North Carolina’s Charter School Program,” Journal of Policy Analysis
and Management 26, no. 1 (2006): 31–56.
29. S. Neiman, Learning from the Germans (New York: Farrar, Straus and Giroux, 2019).
30. P. Hayner, Unspeakable Truths: Transitional Justice and the Challenge of Truth Com-
missions (New York: Routledge, 2011).
31. See news coverage, including J. Zelizer, “Why President Trump Is Targeting the 1619 Proj-
ect,” CNN, September 25, 2020, https://www.cnn.com/2020/09/21/opinions/patriotic
-education-1776-commission-zelizer/index.html.
 276
11. A WORLD WITHOUT RACISM?

32. B. Smedley, A. Y. Stith, and A. R. Nelson, eds., Unequal Treatment: Confronting Racial
and Ethnic Disparities in Health Care (Washington, DC: National Academies Press,
2004); and P. R. Rose, Health Equity, Diversity, and Inclusion: Context, Controversies,
and Solutions (Burlington, MA: Jones & Bartlett Learning, 2021).
33. See J. Fodeman and P. Factor, “Solutions to the Primary Care Physician Short-
age,” American Journal of Medicine 128, no. 8 (2015): 800–801, doi:10.1016/j.
amjmed.2015.02.023; R. B. Cooper, “What Does It Mean to Have a Physician Short-
age?,” Journal of the American Academy of Physician Assistants 28, no.3 (2015): 17–18,
https://doi.org/10.1097/01.JAA.0000460925.13380.92; and A. Grover, J. M. Orlowski,
and C. E. Erikson, “The Nation’s Physician Workforce and Future Challenges,” Ameri-
can Journal of the Medical Sciences 352, no. 1 (2016): 11–19, https://doi.org/10.1016/j
.amjms.2015.10.009.
34. G. Sánchez, T. Nevarez, W. Schink, and D. E. Hayes-Bautista, “Latino Physicians in
the United States, 1980–2010: A Thirty-Year Overview from the Censuses,” Academic
Medicine 90, no. 7 (2015): 906–12, https://doi.org/10.1097/ACM.0000000000000619;
L. M. Hamel, R. Chapman, M. Malloy, et al., “Critical Shortage of African Ameri-
can Medical Oncologists in the United States,” Journal of Clinical Oncology 33, no. 32
(2015): 3697–700, https://ascopubs.org/doi/abs/10.1200/JCO.2014.59.2493.
35. See, for example, J. L. Graves, “Biological V. Social Definitions of Race: Implications
for Modern Biomedical Research,” Review of Black Political Economy 37, no. 1 (2009):
43–60, https://doi.org/10.1007/s12114-009-9053-3; and J. L. Graves, C. Reiber, M.
Hurtado, A. Thanukos, and T. Wolpaw, “Evolutionary Science as a Method to Facili-
tate Higher Level Thinking and Reasoning in Medical Training,” Evolution, Medicine,
& Public Health no. 1 (January 2016): 358–68, https://doi.org/10.1093/emph/eow029.
36. R. Jones, White Too Long: The Legacy of White Supremacy in American Christianity
(New York: Simon & Schuster, 2020).
37. See, for example, E. H. Ecklund, Why Science and Faith Need Each Other: Eight Shared
Values That Move Us Beyond Fear (Grand Rapids, MO: Brazos, 2020).
38. See “Our Mission,” BioLogos, accessed May 4, 2021, https://biologos.org/about-us#our
-mission; also see Joe’s discussion, “The Genetics of Race (Part 1),” https://biologos
.org/podcast-episodes/joseph-graves-the-genetics-of-race-part-1, and “The Genetics
of Race (Part 2),” https://biologos.org/podcast-episodes/joseph-graves-the-genetics-of
-race-part-2.
39. J. Barndt, Becoming the Anti-Racist Church: Journeying Toward Wholeness (Minneapo-
lis: Fortress, 2011).
40. P. H. Collins and S. Bilge, Intersectionality, 2nd ed. (Cambridge, UK: Polity Press,
2020).
41. Status of Women in the States, https://statusofwomendata.org/explore-the-data
/employment-and-earnings/employment-and-earnings/#eefigure2.3.
42. A. Dinno, “Homicide Rates of Transgender Individuals in the United States: 2010–
2014,” American Journal of Public Health 107, no. 9 (2017): 1441–47, https://doi.org
/10.2105/AJPH.2017.303878.

CONCLUSIONS
1. N. Wade, A Troublesome Inheritance: Genes, Race, and Human History (New York:
Penguin, 2014).
 277
CONCLUSIONS

2. C. Darwin, Narrative of the Surveying Voyages of the Adventure and Beagle, vol. III
(London: Henry Colburn, 1839).
3. S. J. Olshansky, T. Antonucci, L. Berkman, R. H. Binstock, A. Boersch-Supan, J. T.
Cacioppo, . . . and J. Rowe. “Differences in Life Expectancy due to Race and Educa-
tional Differences Are Widening, and Many May Not Catch Up,” Health Affairs 31, no.
8 (2012): 1803–13.
4. T. Andrasfay and N. Goldman, “Reductions in 2020 US Life Expectancy Due to
COVID-19 and the Disproportionate Impact on the Black and Latino Populations,”
Proceedings of the National Academy of Sciences 118, no. 5 (2021): e2014746118, https://
doi.org/10.1073/pnas.2014746118.
 INDEX

Aberdeen Birth Cohort, 137 mechanisms accounting for, 106;

abolitionism, 36 telomeres, 107
absolute pitch (AP), 143 agreeableness, five-factor personality
adaptive introgression, 190 model, 145–46
adenine (A), 43 Alaska natives: education of,
admixture, 7, 188 167
Africa, 15; climatic zones of, 140; human Alexander, Michelle, 79, 163, 166
origins in, 191; human species in, 13 ALFRED (allele frequency), 115
African American Heart Failure Trial Alhambra Decree, 25–26
(A-HeFT), 93 alleles, 15
African Americans, 123–26; criminality, “Am I racist if,” 71–72
152–57; disease rate variation in, American Indians, 97, 145, 177, 185, 194;
94–98; false racial beliefs about, education of, 167; homicide rate,
84; identifying individuals, 203–5; 156; intersectionality, 235; justifying
methylation sites, 107; mortality by enslaving, 31–32
age for disease, 85–86; origins of American Journal of Physical
racism, 66–67; PTSD among, Anthropology, 75
149–50; schizophrenia in, 150–52; amino acids, 10
social experiences, 68; thick skin Amo, Wilhelm Anton, 35
myth, 83–84; wealth disparity and, Anatomical Record (Bean), 75
65–66. See also Blacks ancestry, 186; ancient DNA, 187–93;
Age of Discovery, 113 defining, 179–81; determining,
Age of Exploration, 26 182–84; DNA testing of, 181–82;
aging: associating chronological time forensics, 193–96; “racial
with, 105–6; population genetic classification,” 193
 280
INDEX

ancient DNA (aDNA), 187–93 Battuta, Ibn, 26

animals, FST values of, 47 Baumgartner, Frank, 161
antagonistic pleiotropy, 106 Bean, Robert Bennett, 38–39, 75
anthropology, 36 Bell Curve, The (Herrnstein/Murray),
antigens, 90–91 136
antiracism, 221–22; defining racial Bernier, François, 35
equality, 225–34; intersectionality, bias, defining, 60–61
235; requirements for, 223–24; Biden, Joe, 223, 231
talking about race, 224–25 BiDil, 93–94
anti-Semitism, 73–76 bigotry, defining, 60; distinguishing
Antoinette, Marie, 183 racism from, 18–20
Arbery, Ahmaud, 78, 224 Biles, Simone, 122, 129
Arctic environment, genes representing, biological race, 3, 21: conception
55 of, 27–30; consistent race
Aristotle, 29 characterization, 39–40; end
Armstrong, B. J., 124 of slavery, 37–39; in ancient
Ashkenazi (stereotype), 74–75 civilizations, 23–25; justifying
Asians: education of, 167; flexibility, enslavement, 31–32; overview of,
129–31; identifying individuals, 21–22; persistence of, 40–41; and
203–5; sprinting, 119–23; strength, slavery, 30; solidifying scientific
126–28 concepts, 32–37; Spain (1492),
Asia-Pacific War, 19 25–27; timeline of development
Athenians, 61 of, 28
athletic ability, defining, 114–15, 118 biological racism, 63; eroding, 68
athletics: baseball, 123–26; basketball, biological units, mapping, 57–58
123–26; biomechanical differences, biologized race, 21
116; bone density, 131–33; culture, BioLogos, 234
116; diving, 130–31; Finns as world’s birth certificates, 207–8
best athletes, 117–19; flexibility, Birth of a Nation (film), 152
129–31; “racial” dominance claims, birth weight: distribution of, 109;
122; sprinting variation, 119–23; lowness of, 107–10
strength, 126–28; studying genetics Black Lives Matter, 225
of, 115; variation among races, 114–17; Blacks: alleged criminality, 155; birth
“white men can’t jump,” 122 weight, 107–10; education of, 167;
Atlantic killifish (F. heteroclitus), 190 family wealth, 175–77; flexibility,
Australo-Denisovans, 188–89 129–31; life expectancy from birth of,
Australopithecus africanus, discovering, 103, 105; life expectancy of, 110–11;
213 looking Black, 1; negroid race, 2; and
automation, 230–31 one-drop rule, 202–3; percentage of
Avilés, Pedro Menéndez de, 204 inheritance, 202; prison; admission
rates among, 164; probability of
Bakke, Allan, 77 homicide, 155; slow aging, 104–7;
Barnes, Angela, 165 and strength, 126–28; U.S. adult
baseball, 123–26 population, 166
basketball, 123–26; transitions in, 116–17 Blake, Jacob, 224
 281
INDEX

Blakey, Michael, 172 Central Park Five, 154

Bland, Sandra, 161 Central Park Jogger, 162
blood groups, 89–90 Cesalpino, Andrea, 34
blood, transfusion of, 89–92 Charlottesville, Virginia, march in, 78
Blumenbach, Johann Friedrich, 34, chattel slavery, 30, 67
211–13 Chicano, term, 205
body mass index (BMI), 131–32 children: physical appearance of, 210–11;
Bolt, Usain, 115 racial identity of, 205–8; securing
bone mineral density (BMD), 131–32 health of, 208–10
bones, density of, 131–33; tests, 98–101 chimpanzees, genetic variation of, 48
Bonhoeffer, Dietrich, 153 Civil Rights Act (1964), 5, 206
Boston Brahmins, 113 climate change, racial dimension to,
Boston Red Sox, “curse” of, 125 174–75
branch analysis, 141–42 Clinton, Hillary, 165
brancos, 7 Clinton, William, 165
Braun, Lundy, 101 Clovis culture, 52, 192
Brazil, categories recognized in, 6–7; Cobb, Craig, 187
incarceration rate in, 164; money Cobb, W. Montagu, 172
in, 15 Collins, James, 108–9
Bristol-Myers Squibb, 92 color-blind (aversive) racism, 64–65
British Anti-Slavery Society, 67 Columbus, Christopher, 25–27 , 31
Bronze Age, 52 conscientiousness, five-factor
Brooklyn Dodgers, 125 personality model, 145–46
Brooks, Scott, 124 conversos, 26
Brown, Jalen, 61 Coon, Carleton, 7, 39, 214
Brown, James, 204 copy number variants (CNV), 45
Bruno, Giordano, 19 Coronado, Francisco Vázquez de, 204
Buffalo Germans, 123 COVID-19, 83–88, 171, 222
Buffon, Comte de, 19, 34 crime, defining, 153–54
Bush, George H. W., 164 Criminal Justice and Behavior, 154
criminality, races differing in, 152–57
Cain, 33 Crohn’s disease, 46
cancer, mortality by age for, 85–86 Crusades, The (Lamb), 169
Caniglia, Tony, 225 Cuba, incarceration rate in, 164
Carlson, Tucker, 19 cultural ancestry, 180
Carranza, Bartolome, 31 cultural racism, 64
Casas, Bartolome de las, 31 Cuvier, Georges, 34, 212
caste system, Indian, 23–24 cytochrome P450 (CYP) enzymes, 93
castes, comparing race with, 79–80 cytosine (C), 43
Castile, Philando, 160
Cattell-Horn-Carrol (CHC) theory, Danielson, Aaron J., 219
134–35 Dart, Raymond, 213
Caucasian, defining, 211–13 Darwin, Charles, 13, 23, 27
Celera Genomics, 44 Davenport, Charles, 210
Centerwall, Brandon, 155–57 David, Richard, 108–9
 282
INDEX

Davis Medical School, 77 “dumb jock,” stereotype, 132–33

death certificates, 207–8 Dunham, Ann, 210
death rates, 15
death sentence, biases concerning, 70 education, 167; low expectations,
deoxyribonucleic acid (DNA), 43: 170–71; social class, 168–69
ancestry and, 181–93; forensics, educational attainment (EA), 138
193–95; human genome, 43–44; Egyptians, concept of race by, 23–25
methylation, 96, 107, 151; random Ehlers Danlos syndrome, 129
change in, 10–12 eidos, 27
developmental origins of health and Elliot, O., 193
disease (DoHaD), 109–10 emotional stability, five-factor
Diagnostic and Statistical Manual of personality model, 145–46
Mental Disorders (DSM-IV-TR), employment, systemic racism in,
149 171–72
DiAngelo, Robin, 63, 79 environmental racism, 172–74
direct-to-consumer (DTC): ancestry epigenetics, 8
testing, 206; genetic ancestry test, equality: defining, 225–27; education,
181 232–33; employment opportunities,
“Discernment of Human Races by 230–31; faith communities, 234;
Blood Particularly of Russians and health care, 233–34; justice/policing,
Jews” (Manoiloff) 229–30; voting/elections, 228–29
discordance, 55 Escherichia coli, 95
disease indifference, 82–83; blood essentialism, 27
transfusion, 89–92; bone density Ethiopians: high-altitude adaptation of,
tests, 98–101; disease rate variation, 56; term, 211
94–98; intake forms, 83–85; pills, ethnocentrism, 25; defining, 64
92–94; race as risk factor, 85–87; European Americans: PTSD among,
race-specific disease, 87–89; 149–50
“race-specific” medicine, 92–94 European Court of Human Rights, 195
Divine Variations (Keel), 27 Europeans: “color,” 153; sprinting,
diving, flexibility in, 130–31 119–23; and strength, 126–28
Dixiecrats, 218 evolutionary fitness, 102
Dončić, Luka, 116 explicit biases, 69–71
Douglas, Gabby, 121, 129 extroversion, five-factor personality
Douglass, Frederick, 23, 37 model, 145–46
driving while Black (DWB), 160–61
driving while intoxicated (DWI), 160 family wealth, racial differences in,
drug metabolism, drugs associated 175–77
with, 92–93 Ferdinand II, 26
dual-energy x-ray absorptiometry “fertility of the hybrids,” 209
(DEXA), 99–100 Finland, athletics in, 117–19
DuBois, W. E. B., 87 Five Civilized Tribes, 97
Duffy, 89–90 five-factor personality model,
Dukakis, Michael, 164–65 145–48
Duke, David, 70 fixation, 49–50
 283
INDEX

Flood (monogenism), 35 school system, 168–69; studying

Floyd, George, 78, 161, 219, 224 sports, 123–26
FNBP1L (binding protein), 137 Goodwin, Frederic, 162–63
folate, 13 Gopalan, Shyamala, 210
food “desert,” 174 Gould, Steven Jay, 37
forensics, 193–96 Graves, Joseph L., Jr.: analyzing total
FRAX, 100 Olympic medal count, 118; and
Free State of Jones, movie, 187 biases, 69; disease rate variation,
Freedman’s Bureau, 38 94–98; family wealth, 175–77;
fruit fly (Drosophila melanogaster), 95; human genome, 43; identifying,
hybrids of, 190 203–5; low expectations, 170;
public school system, 168–69;
GATA2 (GATA binding protein 2), studying athletic performance
144 genetics, 115; studying sports,
genetic ancestry, 43, 180 123–26
genetic drift, 15 Great Chain of Being, 4, 29–30, 59
genetic traits, correlation of, 54–56 Greeks, concept of race by, 23–25
genetics: defining human genome, Green New Deal, 231
43–44; defining subunits, 56–57; Griffith, D. W., 152
evaluating differences, 45–46; guanine (G), 43
explaining human genetic Gulf killifish (Fundulus grandis), 190
differences, 48–51; geography Gypsies, 39, 214
clustering, 51–54; mapping
biological units, 57–58; modern Hahn, Robert, 207
adaptations, 51; mutations, 45; other hair color, pattern of variation, 12
mammals, 46–48; physical trait Haley, Nikki, 221
frequencies, 57; trait correlation, Ham, 33
54–56 Harris, Donald, 210–11
genome-wide association study Harris, Kamala, 203, 210, 221
(GWAS), 88, 115, 132, 137–39 Hart-Celler Immigration Act (1965),
genotype, phenotype versus, 9–10 89
geographic ancestry, 180 Harvard Educational Review, 170
geography, genetic differences and, heart disease, mortality by age for,
51–54 85–86
Geronimus, A.,109 heart problems, biases concerning,
gerrymandering, 218–19 70
“gig” economic sectors, 231 height: pattern of variation, 12;
Giles, E., 193 phenotypic variation, 9–10
Gliddon, G. R., 212, 214 Hemings, Eston, 183
Goddard, Henry, 135 Hemings, Sally, 67, 183
Goodman, Alan H.: anti-Semitism, heritability, 137; of intelligence, 137; of
74–75; becoming antiracist, 223–24; musical ability, 143–44; of racial
bone density tests, 98–101; family traits, 28; of schizophrenia, 150–52
wealth, 175–77; human genome, Herodotus, 24
43; interracial ancestry, 208; public Herrnstein, Richard, 136, 170
 284
INDEX

high-fat diet, genes representing Hurricane Katrina, 174–75

tolerance of, 55 hypodescent, 202–3
HiIQ (extremely high intelligence),
137 “I Am a Racially Profiling Doctor,”
Hispanics: addressing individuals, 83
204–5; census question, 199; Ibn Battuta, 24
education of, 167; inadequate term, idealist worldview, 27, 29
204; in federal data, 198; Hispanic Immigration and Nationality Act,
paradox, 110; life expectancy from 204
birth of, 103; life expectancy of, implicit biases, 69–71
110–11; PTSD among, 149–50; U.S. incarceration, business of, 165–66
adult population, 166. See also Latin incarceration, racial differences in,
Americans 162–67
histocompatibility A locus (HLA), Indian Removal Act, 97
53 Indian-ness, 201
histocompatibility gene complex Indios. See Native Americans
(MHC), 87 individuals, identifying, 203–5
histones, 43 Industrial Revolution, 182
Hitler, Adolf, 114, 214 influenza, mortality by age for, 85–86
HLA, 89–90 InfoWars, 222
HLB-C gene, 96 Inouye, Daniel, 89
Hoffman, Frederick, 63 institutional racism, 80–81, 222
homicide, probability of, 155–57 intelligence quotient (IQ), 135
Homo erectus, 48 intelligence: cognitive ability
Homo ergaster, 48 differences, 135–36; criminal
Homo heidelbergensis, 48 behavior, 152–57; defining, 134–35;
Homo neanderthalensis, 48 genetic basis for, 136–39; mental
Homo sapiens, 4 illness genes, 148–52; musical ability,
Horton, Willie, 165 143–44; personality genes, 147–48;
Hsu, Stephen, 222 personality, 144–47; racial difference
Hughes, Langston, 20 with, 139–43
Human Genome Project (HGP), 44 International Classification of Disease
human genome: defining, 43–44; letters (IDC-10), 149
in, 9; reading, 44 International Society for Evolution,
human leucocyte antigen (HLA), 87 Medicine, and Public Health
human platelet antigen system (HPA), (ISEMPH), 84
90 intersectionality, 235
human variation: facts, 237–42; origins intimate partner violence (IPV),
of, 13–15; in physical appearance, 15; 149
structure of, 7–13 intrauterine growth retardation,
humans: defining subunits, 56–57; FST 107
value, 47; early migration, 190–91; Inuit, 55
explaining genetic differences, 48–51; Isabella, I., 26
migratory patterns of, 53; modern Islamophobia, 76
adaptations in, 51 isolation-by-distance, model, 51–54
 285
INDEX

Jacobson, Frye, 74–75 lead, presence of, 173

Jacobson, Matthew Frye LeClerc, Georges Louis, 34
James, LeBron, 61 Leibnitz, Gottfried Wilhelm von, 35
Jamestown, Africans in, 30 Léon, Ponce de, 204
Jarvis, Erich, 171 Levantine people, 24
Jefferson, Richard, 124 Lewis, Joe, 114
Jefferson, Thomas, 67, 183 Lezak, Jason, 121
Jensen, Arthur, 170 life history, 102–4; birth weight, 107–10;
Jews: anti-Semitism, 73–76; health differences, 111–12; life
characterizing separateness of, expectancy, 110–11; reproductive
39–40; expulsion of, 25; identifying traits, 103; slow aging, 104–7; traits
as race, 213–15; origins of racism, associated with, 103
66 linkage, 54
Jim Crow, 41, 72 – 73, 114, 163, 166, 169, linkage disequilibrium (LD), 95
209, 232 Linnaeus, Carl, 3–4, 34, 197
Johnson, Jack, 114 Longitudinal Studies of Cognitive
Johnson, Lyndon, 77 Aging Cohorts, 137
Jones, Cullen, 121 Lothian Birth Cohorts, 137
Jordan, Michael, 122 Louis XVI, 183
Loving v. Virginia, 210
Kaepernick, Colin, 72 low expectations, pseudoscience of,
Karma music test, 143–44 170–71
Keel, Terence, 27
Kell, 89–90 Madoff, Bernie, 153–54
Kendi, Ibram X., 62, 72 Mandela, Nelson, 153
Kennedy clan, 113 Manoiloff, E. O., 40, 75
Kennedy, John F., 77 Manuel, Simone, 121
Kidd, K., 89–90 Marr, William, 73
kind racists, 66 Martin, Roland, 82
King, Martin Luther, Jr., 230 Massachusetts Correctional Reform Act
Knight, Davis, 187 (MCRA), 165
knowledge, social construction of, 17–18 mastodons, adaptations of, 190
Ku Klux Klan, 70 Match Foundation, 91
McConaughey, Matthew, 187
Lamarck, Jean-Baptiste, 34 mean racists, 66
Lamb, Harold, 169 Mediterranean, 14, 32, 51, 140
land sprint events, world record holders Meili, Trisha, 162
in, 119 Mendel, Gregor, 27
Landsteiner, Karl, 90 mental illness, genes associated with,
Lapps, 35 148–52
Latin Americans, 123–26; criminality, “Mental Tests and the Immigrant,” 135
152–57; genetic classification of, methylation, 151
125–26; identifying individuals, 203–5 micro RNAs (miRNA), 96
Laws of Burgos, 31 Middle East, 12, 14, 24–25, 32, 46, 49,
Lay, Kenneth, 153 104, 191, 205–6, 212–13
 286
INDEX

Midwest Intercollegiate Volleyball New York Times, 44, 82–83, 233

Association (MIVA), 124 Newton, Dolores, 197, 201
migration, 49 next generation sequencing (NGS),
Mills, Charles, 59 44–45
Minnesota Twin Family Study, 138 Nigerians, genetic differences of, 57
miscegenation, 209 NitroMed, 93
mitochondrial DNA (mtDNA), 183, 186 Nixon, Richard, 218
MLN gene, 128 North Carolina Department of Public
MNS, 89–90 Health, 207
monogenism, 32 Norwegians, genetic differences of,
Montagu, Ashley, 79, 215 57
Montesinos, Antonio de, 31 Notes on the State of Virginia, 67
Moors, expulsion of, 25 Nott, J., 212, 214
Morton, Samuel George, 34, 36, 170 Nuremberg Laws, 202–3
Muir, Donal, 72 Nurmi, Paavo, 117
mulatto, 6
multiple intelligence theory, 135 Obama, Barack, 203, 210
Murray, Charles R., 136, 170 Obama, Barack, Sr., 210
music, ability in, 143–44 Öcalan, Abdullah, 74
mutations, 13–15; accumulation, 106; Office of Management and Budget
genetic variation, 45, 48–50 (OMB), categories defined by, 206–7
MyHeritage, 186 Oleksiak, Penny, 121
Myrdal, Gunnar, 79 On the Origin of Species (Darwin), 13,
27, 33
N word, 73 one-drop rule, 202–3
Naismith, James, 123 openness, five-factor personality model,
Nance, Larry, 122 145–46
National Center of Education Statistics, Origin of Races, The (Coon), 7
167 Original Celtics, 123
National Epidemiological Survey on Owens, Jesse, 114
Alcohol and Related Conditions, 150
National Institutes of Health’s National Pacific Islanders, education of, 167
Human Genome Research Institute pardos, 7
(NHGRI), 44 Parks, Rosa, 153
National Institutes of Mental Health Pence, Mike, 223
(NIMH), 154; violence initiative, 162 personality: genes associated with,
Native Americans, 37; justifying 147–48; racial differences in, 144–47
enslavement of, 31–32 Peyrère, Isaac La, 34
natural slave, 29 Phelps, Michael, 115, 121
naturalists, 35 phenotype, genotype versus, 9–10
Nazi Germany, 19; joining, 202 Philadelphia Negro, The, 87
NCAA, listings in, 118 philosophers, views of, 24
Neal, Lia, 121 Phipps, Susie Guillory, 206
Neanderthals, 188 Phoenix Urban Systemic Initiative, 170
negative pleiotropy, 55 pills, color of, 92–94
 287
INDEX

Plato, 27, 29 characterizing, 39–40; defining, 3;

pleiotropy, 55 disease indifference, 82–101; facts,
Pleistocene, 49, 188 237–42; genetic variation, 7–13;
pogroms, 15 genetics, 42–58; health differences,
Polo, Marco, 26 111–12; in Hebrew Bible, 24; human
polygenism, 32 variation origins, 13–15; idea of,
polymorphism, 181–82 67; intelligence, 134–57; justifying
poplar clones, 105 enslavement, 31–32; life expectancy
population subdivision statistic, 45 variation, 110–11; Linnaeus varieties
post-traumatic stress disorder (PTSD), of, 4; number of, 6–7; as parent of
149–50 racism, 30; as risk factor, 85–87;
poverty rates, 97–98 “race-specific” medicine, 92–94;
Pre-Adamite (Men before Adam), 34 as social construction, 15–18;
prejudice, defining, 60 turning into scientific concept,
prematurity, 107 32–37; as worldview/social
pretos, 7 classification, 3–6
Prichard, James Cowles, 213 Races of Europe, The (Ripley), 39, 214
progesterone, studying presence of, racial classifications, 200–202
104 racial contract, 59
Project Implicit, 69 Racial Justice and Reconciliation
protocadherin (PCDH7) gene, 144 Commission of the Episcopal
Protocols of the Elders of Zion, 74 Diocese of North Carolina (RJRC),
public school system, 168–69 234
racial medicine, 83
r- versus K-selection, 140 racism: “Am I racist if,” 71–72; anti-
race naming/mixing: addressing Semitism, 73–76; biases, 69–71;
children, 205–8; counting citizens by caste comparison, 79–80; defining,
race, 198–200; defining “Caucasian,” 18–19, 62–63; different forms of,
211–13; identifying individuals, 63–66; facts, 237–42; imagining life
203–5; identifying whiteness, without, 221–35; institutional racism,
215–16; interracial marriages, 210–11; 80–81; interrelated terms related
interracial physique, 210–11; Jews to, 60–63; Islamophobia, 76; kind
as race, 213–15; one-drop rule, racism, 72; lack of power, 77–78; N
202–3; racial classifications, 200–202; word, 73; origins of, 66–68; parent
securing children’s health, 208–10; of race, 30; recognizing presence
white nationalism, 217–20; white of, 71–72; reverse discrimination,
supremacy, 216–17 76–77; systemic racism, 158–78;
Race Traits and Tendencies of the white fragility, 79; white supremacy,
American Negro (Hoffman), 63 78–79
race: athletics, 113–33; becoming recreational genomics, 195
scientific, 23; biological view of, redlining, 80
21–41; castes, 79–80; categories of, Reed, Annette Gordan, 183
36; census data collection, 198–200; Regents of the University of California v.
colonization, 4–5; connection Bakke, 77
with slavery, 30; consistency of rehabilitation, myth of, 165
 288
INDEX

Reich, David, 54, 140 social dominance orientation (SDO),

remedial, term, 169 145–47
résumés, “whitening,” 171 social race, 3, 6–7, 92, 139, 224
reverse discrimination, 76–77 socially defined race, risk factors of,
Reynold, Diamond, 160 85–87
Ripley, William Z., 39, 214 socioeconomic status (SES), 138
risk factors, 85–87 Sociology of Freedom (Öcalan), 74
Rittenhouse, Kyle, 219, 225 “Some Racial Peculiarities of the Negro
Robinson, Mark, 221 Brain” (Bean), 38–39
Romans, concept of race by, 23–25 Soto, Domingo de, 31
Roosevelt, Franklin Delano, 218 South Africa, 15
Rushton, J. Phillipe, 141, 152 South Philadelphia Hebrew Association,
Russia, incarceration rate in, 164 123
Ruth, Babe, 125 Southern Poverty Law Center, 218
Spain (1492), 25–27
Sanofi-Aventis, 92 Spanish-American War, 125
Satel, Sally, 83 Spradley, Junie Lee, 187
Saudi Arabia, 15 sprinters, studying, 116
Say It Loud: I’m Black and I’m Proud sprinting, variation in, 119–23
(James Brown), 204 “stacking,” 126
schizophrenia, heritability of, 150–52 “status race” criterion, 206
Schmeling, Max, 114 Stevenson, Bryan, 166
scleroderma, 1–22 Stoddard, Lothrop, 135–36
Scythia, 24 Stowe, Harriet Beecher, 10
Seashore pitch test/rhythm subtest, Stratum III, 134–35
143–44 STRUCTURE (program), 56
selection balance, aging, 106 subunits, locating, 56–57
senescence, 102 Superfund, 98
Sentencing Project, data from, 166 Suspect Citizen, 161
Sentencing Reform Act, 164 Sutherland, George, 212
septicemia, mortality by age for, swimming, 120–21
85–86 symbolic racism, 64
serial founder effect, 189 Systema Naturae (Systems of Nature), 4
sexual assault (SA), 149 systemic racism, 158–59; climate
short interfering RNAs (siRNA), 96 change, 174–75; driving
short tandem repeat (STR) loci, 194 while Black (DWB), 160–61;
Siberian Denisovans, 188 education, 167–71; employment,
sickle cell anemia, alleles rates for, 88 171–72; environmental racism,
single nucleotide polymorphisms 172–74; family wealth, 175–75;
(SNPs), 45–46 incarceration, 162–67
slavery: justifying, 31–32; end of, 37–39
smallpox, 87 Taino, physical features of, 26–27
Smedley, Audrey, 24 Talent Identification Program (TIP),
Smith, Samuel Stanhope, 33 137
social construction, 15–18 Tatum, Beverly, 62
 289
INDEX

taxonomy, origins of, 34–35 University of Virginia (UVA), 84–85

Taylor, Breonna, 78, 224 untouchables, 79
Tay-Sachs disease, 214–15
telomeres, 107 variation, explaining, 50–51
terms, interrelation of, 60–63 Venter, Craig, 44
Teutonic races vigilantism, racial, 219
ThermoFisher, 195 Vindication of the Rights of Women,
thymine (T), 43 A, 34
Tibetans, high-altitude adaptation of, volleyball, 123–24
56, 189–90 Voyage of the Beagle, 33
tissue, donation of, 91–92
traffic stops, frequency of, 160 Wade, Nicholas, 170
triarchic theory, 135 Wallace, Alfred, 29
triplets, 9 Wallace, George, 59, 218
Trotter, Mildred, 98–99 water sprint events, world record
“true” species, 190 holders in, 120
Trump, Donald, 70, 162, 171, 178, weathering, 109
222–23; white supremacy and, 216–17 Webb, Spud, 122
TV ads, genetic ancestry testing in, Wedgewood, Josiah, 67
186 weight, pattern of variation, 12
23andMe, 185–86 weightlifting, world record holders for,
127
U.S. Census: categories enumerated in, Western Hemisphere, 52
6; official categories, 199, 205 White Fragility (DiAngelo), 63
Uncle Tom’s Cabin (Stowe), human “Whites of a Different Color,” 40
genome and, 10 whites: alleged criminality of,
United States v. Bhagat Singh Thind, 212 155; birth weight, 107–10; and
United States: addressing children, DWB 160–61; education of, 167;
205–8; adult population, 166; birth European athletic superiority,
weight studies in, 108; census 113–14; family wealth, 175–77;
categories (by decade), 200; “honorary” whites, 177; identifying,
Committee on Equal Employment 215–16; life expectancy from
Opportunity, 77; disease rates in, birth of, 103, 105; life expectancy
94–98; environmental violence of, 110–11; mortality by age for
in, 97; Hurricane Katrina, 174–75; diseases, 85–86; prison admission
interracial ancestry, 207–8; lead rates among, 164; probability of
pollution in, 173; New York African homicide, 155; slow aging, 104–7;
Burial Ground, 180; North Carolina U.S. adult population, 166; white
vaccinations, 82; prison population, fragility, 79; white nationalism,
163–64; recordkeeping by race, 217–20; white supremacy, 19,
198–200; religious teachings 78–79, 216–17
in, 67–68; “separate but equal,” Whitley, Reece, 121
23; socioeconomic status in, 15; “wild type” gene, 50
Virginia laws, 30; wealth disparity wilding, 162
in, 65–66; white supremacy in, 19 Wilkerson, Isabel, 59, 79–80
 290
INDEX

Wilkins, Domonique, 122 Wright, Sewall, 46

winter hypothesis, 140
Winter Olympics, 117 xenophobia, defining, 25, 61
Wise, Korey, 162
Wollstonecraft, Mary, 34 Yanez, Jeronimo, 160
work, reimagining, 231
World War II, 203 ZNF608 gene, 128