ROBERT GREEN and I stood inches apart. His eyes scanned across my face, from ear to ear, from forehead to chin.
“What I’m doing,” he murmured, “is looking for any facial features that would suggest an underlying genetic illness.” He looked me over as if I were a horse he was thinking about buying. “The shape of your eyes, whether your ears are low set or not,” he said. “The complexity of your ears.”
Getting my genome was turning out to be a lot more complicated than I had expected. I could not simply spit into a tube and mail it off to a company like 23andMe. In 2007, 23andMe began providing reports on DNA directly to consumers. For $999, they would identify the variants at half a million sites in a person’s genome, analyze them for clues to their ancestry, and even supply a report about how the variants influenced risks for disorders ranging from diabetes to Alzheimer’s disease. Their service was a profound leap from conventional genetic tests. They had to be approved by the FDA and ordered by doctors. Now 23andMe was delivering information straight to customers. In 2013, the FDA told 23andMe to stop selling unvalidated tests or face the consequences. In response, the company cut back their reports to ancestry and nothing more.
Other companies, such as Illumina, took notice. To get my genome from them, I would have to get a doctor to order it for me as a medical test. Green, who had originally invited me to get my genome sequenced, also agreed to sign for the test. First, however, he would put me through a thorough, old-fashioned genetic exam—the kind that Lionel Penrose might have given in the 1950s.
“Future clinicians may judge this to be unnecessarily cautious,” Green told me. “But there is no standard for how we do whole genome sequencing. So this is how I’ve decided to do it.”
I had taken the train to Boston and made my way to Brigham and Women’s Hospital for the exam. I first sat down with a genetic counselor named Sheila Sutti, who took out a form entitled “Family History.” She began asking about my relatives. As we spoke, she filled the page with circles and squares, slashing some of them with the diagonal of death. She noted allergies and surgeries. Question marks recorded the many times I shrugged my shoulders in ignorance. Sutti drew a network of symptoms and uncertainty. When I looked at the form, I could not see any signal of heredity.
Green arrived just as Sutti was finishing up. A looming, silent medical student trailed him. Green peered at my face through his narrow frameless glasses. He was taking advantage of the fact that genes play many different roles in our bodies. A hereditary disease that causes hidden damage to the nervous system may also disrupt the development of the face, leaving behind clues that a geneticist can spot with the naked eye. Green then asked me to walk back and forth from wall to wall. He crossed the arms of his white lab coat as he looked down at my feet, sizing up my gait.
Green told me these conventional exams didn’t reveal any signs that required a test for a specific disease. He signed the request for my genome, and Sutti led me to another wing of the hospital, where a phlebotomist slid a needle into my arm. I watched blood glide like scarlet motor oil out of my arm and into three tubes.
The tubes were shipped across the country to San Diego, where Illumina’s technicians cracked open my white blood cells and pulled out my DNA. They blasted the molecules with ultrasound, shattering them into fragments, and then made many copies of each one. Adding chemicals to the fragments, they were able to determine their sequence.
Now they had to assemble these fragments together like the pieces of a jigsaw puzzle. Just as a puzzle solver can use the picture on the box lid as a guide, the Illumina team consulted a reference human genome to figure out where each of my fragments had come from. Some fragments were too enigmatic to locate, but overall, Illumina was able to rebuild over 90 percent of my genome.
From one person to the next, human genomes are mostly identical. But in a genome stretching over three billion base pairs, the tiny fraction of DNA that varies adds up to millions of differences. Most of these variations are harmless. But some can give rise to a disorder such as PKU. Others raise the risk of more common conditions like cancer or depression. Illumina’s clinical geneticists searched my own collection of variants for any especially worrying ones. A few weeks after my visit to Brigham and Women’s, Sutti called me with the results.
“The reason we’re doing this over the phone and not in person is that we didn’t find anything of clinical importance,” she said. “You had a very benign report, Carl.”
Sutti told me that I didn’t have any dominant mutations known to cause diseases with just a single copy. Nor had I inherited two copies of a dangerous recessive mutation. I did find out a few useful things about my health, though. The sequencing revealed variants that could affect the way I respond to certain medicines. If I ever get hepatitis, I know I shouldn’t get treated with a combination of interferon and ribavirin.
And, like all humans, I’m also a carrier. That is, I carry single copies of recessive variants. If my children inherited the same variants from both me and Grace, they might develop genetic diseases. In the early 2000s, when Grace and I became parents, DNA sequencing technology was far too crude for me to get a full catalog of my carrier variants. The best we could hope for was to have our daughters tested for a few diseases, such as PKU.
It turned out I’m a carrier for two genetic disorders I never heard of: one called mannose-binding lectin protein deficiency, the other familial Mediterranean fever. I had to do a little research to understand this particular inheritance. I learned that mannose-binding lectin protein deficiency weakens the immune system, leaving babies to develop disorders such as diarrhea and meningitis. Familial Mediterranean fever, the result of mutations to a gene called MEFV, causes people to suffer from painful bouts of inflammation in their abdomen, lungs, and joints.
I don’t know which of my parents I inherited those mutations from, but I’d bet that I got my faulty MEFV gene from my father. It is most common among people of Armenian, Arab, Turkish, or Jewish descent. It’s far rarer in other ethnic groups, like the Irish—from whom Grace descends. It would be extraordinarily unlikely that she would have a faulty MEFV gene, too. At worst, my daughters are carriers like me.
And that was all. After more than a century of advances in genetics, I got a glimpse at my genome, something that had been impossible until recently, and there wasn’t much for Sutti and me to talk about. A week after our phone call, I took the train to Boston to attend the “Understand Your Genome” meeting. At lunch, an Illumina representative logged me into a secure web page that elegantly displayed my results. I could compare my own genome to the reference genome, displayed as two rows of colored letters. Where my DNA differed, the colors were brightly mismatched. Along with disease-related variants, Illumina revealed a few more associated with physical traits. They meant little to me. “Your odds of developing male pattern baldness are increased if you are Caucasian,” Illumina told me. You could call me Caucasian, but I have a thick thatch of hair. “Your muscle fibers are built for power,” the website lied.
The whole experience was charming but dull. I certainly didn’t want the excitement that comes from discovering you have cherubism. But getting to see my own genome shouldn’t have been boring. I was pretty sure that if I could dig deeper—or, rather, if I could enlist the help of some scientists to dig deeper—I’d be able to learn much more about heredity.
After a few weeks of wrangling and paperwork, I managed to get all the raw data from Illumina. It showed up at my door one January afternoon in a white cardboard box. Inside was a shroud of green bubble wrap, inside of which was a kidney-shaped black pouch, inside of which was a slim brushed-metal hard drive. It contained seventy gigabytes of data—the equivalent of more than four hundred high-definition movies.
To make sense of that data, I took my genome on the road. On one trip, I drove down I-95 to the Yale campus and walked up Science Hill to reach the office of Mark Gerstein. Gerstein’s office was heaped with scientific bric-a-brac: Galileo thermometers, Klein-bottle coffee mugs, blinking lights that feed off the electric current in your skin. Gerstein’s conversation was packed as well, pinging so quickly between genomes and cloud computing and open-access scientific publishing that I sometimes had to look back at my notebook to remember the question I had just asked him.
The idea of telling me about my own genome intrigued Gerstein to no end. Over the course of his career, he has analyzed thousands of genomes—he helped lead a study called the 1000 Genomes Project, for starters—but he’d almost never looked straight in the face of the person from whom one of those genomes came. As I handed him the drive so that he could copy my genome to his computer, he confessed to a vicarious thrill.
“I’d never have the courage to do this—I’m just too timid,” he said, laughing. “I’m a worrier. Every time there would be a new finding, I’d look in my genome to see if I had it.”
While Gerstein and his team got to work, I went to the New York Genome Center, where a group of scientists were building a genealogical database they called DNA.Land. They created a website where anyone could upload their genetic data for scientific research. In exchange, they would analyze people’s DNA and share whatever genealogical clues they could find.
My brother, Ben, had gotten his DNA sequenced by a company called Ancestry.com—not his whole genome, of course, but 682,549 genetic markers. I asked him to upload his file to DNA.Land in order to compare our genes.
Thanks to meiosis, Ben and I are not genetically identical. Our genomes are made up of different selections from our parents’ chromosomes. Yet, despite our differences, we still have many long stretches of identical DNA in common. DNA.Land could confidently recognize 112 identical segments, each one stretching 100 million bases or more. While we are far from clones, there’s no one on Earth who’s more genetically similar to me than my brother.
If I were to compare myself to one of my first cousins, I’d find fewer identical segments. We share a pair of grandparents, but they also inherited some DNA from their two other grandparents. The segments we share are also smaller, because there have been two generations between us and our grandparents for meiosis to chop our inherited chromosomes into more pieces.
DNA.Land found 45 other people among its 46,675 volunteers who had enough stretches of identical DNA to suggest they might be my cousins. It was also possible they were not closely related at all, our identical DNA a persistent legacy of ancestors who lived centuries ago. I looked at the names of these possible kin and recognized none of their names. Ben was inspired to do some digging and discovered that one of them—a possible fourth cousin named Elias Gottesman—had a harrowing story.
As a child, he had been sent to Auschwitz with his family, and there the camp’s doctor, Josef Mengele, did experiments on him and his twin brother, Jeno. Mengele was especially taken with twins because he believed he could discover the genetic roots of diseases by examining them—sometimes even dissecting them alive. By the end of the war, Gottesman lost his entire family and even lost his name. Only decades later, as an old man in Israel, did he begin searching for them again. A genetic match to cousins in the United States revealed his birth name; his cousins even sent him a picture of his lost parents.
The DNA Gottesman and I inherited from an ancestor might mean we were close kin. But I didn’t contact him, or any of the other possible matches that DNA.Land sent me. A genetic connection did not join our lives together. In fact, if I were to compare my genome to those of my fourth cousins, I’d find that I don’t even share any DNA with some of them. That may sound impossible, but only because in modern Western culture we’ve made the mistake of equating DNA with kinship. That’s not actually how heredity works.
The more distantly a cousin is related to you, the more generations back you have to go to find your common ancestors. It also means that over those generations, the DNA from those ancestors got cut into ever smaller pieces and was mixed with the DNA from ancestors you and your cousin do not share. It’s purely a matter of chance which copy of a DNA segment ends up in an egg or a sperm. And so, in time, one ancestor’s genes may disappear altogether. In 2014, Graham Coop, a geneticist at the University of California, Davis, determined that if you brought together 100 pairs of third cousins, one of those pairs would share no identical segments of DNA at all. If you brought together 100 pairs of fourth cousins, 25 would lack this genetic connection.
The same holds true for our ancestors. If I were to compare my genome to those of my grandparents, I’d be able to find large chunks of identical DNA from all four of them, each totaling roughly 25 percent of my genome. In the next generation back, I have eight great-grandparents, contributing more chunks—but smaller ones. With every generation back, my number of ancestors doubles. Roger Goodspeed is among 1,024 ancestors of mine ten generations back. But according to Coop’s estimates, I inherited only 628 chunks of DNA from that entire generation. There’s only so much room in my genome, and so a lot of their DNA did not finish the journey from my tenth-generation ancestry to me. For any particular ancestor from Roger Goodspeed’s generation, there’s a 46 percent chance I didn’t inherit any of their DNA. I grew up imagining Roger Goodspeed as some kind of American Adam to my family, bestowing Goodspeed genes on all his descendants. But it’s pretty much a coin toss whether I have any of his DNA at all. And even if I did, Coop’s calculations show I’d be able to trace only about 0.3 percent of my DNA to him.
As you move further back in genealogical time, an even bigger paradox looms into view. We think of genealogy as a simple forking tree, our two parents the product of four grandparents, who are descended from eight great-grandparents, and so on. But such a tree eventually explodes into impossibility. By the time you get back to the time of, say, Charlemagne, you have to draw over a trillion forks. In other words, your ancestors from that generation alone far outnumber all the humans who ever lived. The only way out of that paradox is to join some of those forks back together. In other words, your ancestors must have all been related to each other, either closely or distantly.
The geometry of this heredity has long fascinated mathematicians, and in 1999 a Yale mathematician named Joseph Chang created the first statistical model of it. He found that it has an astonishing property. If you go back far enough in the history of a human population, you reach a point in time when all the individuals who have any descendants among living people are ancestors of all living people.
To appreciate how weird this is, think again about Charlemagne. We know for a fact that Charlemagne has some living descendants, thanks to the genealogies proudly drawn by the Order of the Crown. But that fact, according to Chang’s model, means that every European alive today is a descendant of Charlemagne. The order is hardly an exclusive club.
When Chang developed his model in 1999, geneticists couldn’t compare it to reality. They didn’t know enough about the human genome to even guess. By 2013, they had gained the technology they needed. Coop and his colleague Peter Ralph, a statistician at the University of Southern California, set out to estimate how living Europeans are related to people who lived on the continent hundreds or thousands of years ago. They looked at a database of genetic variants collected across Europe from 2,257 living people. They were able to match identical stretches of DNA in different people’s genomes, which they inherited from a common ancestor.
Ralph and Coop identified 1.9 million chunks shared by at least two of the 2,257 people. Some of the chunks were long, meaning they came from recent common ancestors. Others were short, coming from deeper in the past. By analyzing the chunks, Coop and Ralph confirmed Chang’s study, but they also enriched it. They found, for example, that people in Turkey and England shared many fairly big chunks of DNA that they must have inherited from a common ancestor who lived less than a thousand years ago. It was statistically impossible for a single ancestor to have provided them all with all those chunks. Instead, living Europeans must have gotten them from many ancestors. In fact, the only way to account for all the shared chunks Coop and Ralph found was with Chang’s model. Everyone alive a thousand years ago who has any descendants today is an ancestor of every living person of European descent.
Even further back in time, Chang and his colleagues have found, the bigger the ancestral circle becomes. Everyone who was alive five thousand years ago who has any living descendants is an ancestor of everyone alive today. The Order of the Crown may be big, but an early pharaoh of Egypt might be able to get a club seven billion strong.
I asked the scientists at the New York Genome Center to look beyond my cousins and use my genome to tell me something about my ancestry. They started with the simplest pieces of DNA to interpret: the mitochondrial DNA I inherited from my mother, and the Y chromosome I inherited from my father. By 2015, geneticists had built massive databases of both types of DNA, with sequences of hundreds of thousands of people. They organized the sequences in much the same way a taxonomist might classify insects, dividing them into classes, dividing those classes into orders, and so on. Large groups of men across the world have certain Y-chromosome mutations in common—known as haplogroups. I belong to haplogroup E, I learned. Its ranks are made up mainly of African men, but they also include some men from Europe and the Near East. Within that haplogroup, I belong to a smaller one known as E1, and within that, E1b—and so on all the way down to the haplogroup E1b1b1c1.
That particular haplogroup includes some Jewish men. While that certainly jibed with my experiences with my father’s side of the family, the snug fit began wiggling loose when I looked into the haplogroup further. Only a few percent of Jewish men carry E1b1b1c1. Many men who are not Jewish carry it as well; it’s found across a range stretching from Portugal to the Horn of Africa to Armenia. When Napoleon died, one of his followers tucked a few hairs from his beard in a reliquary. In 2011, French researchers managed to extract some of his Y chromosome from them. They found that he belonged to the E1b1b1c1 haplogroup, too. The highest percentage of men with E1b1b1c1 yet found don’t live in Israel. They live in the Jordanian city of Amman. The second-highest percentage can be found among the Amhara, an ethnic group that lives in the highlands of Ethiopia.
The high percentage of men in Jordan with E1b1b1c1 suggests that it first emerged somewhere in the Near East, perhaps as long ago as ten thousand years—long before the Jewish people existed. Thousands of years later, Arabs, Jews, and other peoples of the Near East spread into Africa and Europe, spreading the haplogroup with them. On its own, my E1b1b1c1 haplogroup cannot let me trace its path back through that ancestry (although I’m pretty sure Napoleon isn’t my great-great-great-great-grandfather). All I can know is that there was probably an ordinary Near Eastern farmer some ten thousand years ago who acquired a harmless mutation in his Y chromosome that distinguished a new haplogroup, one that he unknowingly passed down to his son. But even among my male ancestors, that farmer holds no special place. He just happened to be the one from whom I inherited my Y chromosome.
On my mother’s side, I discovered that I have a mitochondrial haplotype called H1ag1. It’s found throughout much of western Europe, and has been found there for quite a while. When a genome sequencing center was built in Hinxton, England, the construction workers dug up across a 2,300-year-old skeleton. It turned out to have some bits of DNA in its bones. The Hinxton skeleton carried H1ag1, just like me. As for the original Ms. H1ag1, however, I can’t say that she lived in Hinxton. I can’t even say she lived in England.
People carrying the H1ag1 haplotype can be found today across northern Europe. I know I am their kin along the maternal line, but I can’t know where our common ancestor lived. Scientists have drawn a tree of all of humanity’s known mitochondrial DNA, and on it my H1ag1 branch sprouts next to other branches common in Europe. The European branches split off from branches common in Asia and the New World. The deepest branches on the tree are found in living Africans. By tracing the mutations along all the branches, scientists can estimate the age of the woman who carried the mitochondrial DNA that gave rise to all haplogroups today. That woman lived in Africa about 157,000 years ago.
The first clues that living humans get their mitochondria from a single woman in Africa first emerged in 1987, thanks to research in the lab of Allan Wilson, a geneticist at the University of California at Berkeley. Reporters swiftly nicknamed this unknown woman Mitochondrial Eve. The name stuck like superglue. Newsweek ran a cover story about the research, illustrating their cover with a brown-skinned Adam and Eve.
It would take years for scientists to trace back the Y chromosome of all living men. According to the latest research, he lived in Africa 190,000 years ago, at the dawn of our entire species. Soon enough that man was christened Y-chromosome Adam. He now enjoys a Wikipedia page of his own. It’s easy to imagine Mitochondrial Eve and Y-chromosome Adam as the parents of all humanity, dropped down into a Pleistocene Garden of Eden. The fact that Eve didn’t show up in the garden until thirty thousand years after Adam died is one of those minor scientific details that cannot undermine a seductive metaphor.
It took a couple of weeks for Mark Gerstein to work over my genome. He and his students wanted to analyze the short fragments of DNA with their own software and create their own map. Once they had pinned down the location of the vast majority of Illumina’s fragments, they could then determine which variants I carried. And they could try to figure out what those variants meant to me. When I paid my second visit to Gerstein, I was surprised that he wasn’t leading me back to his office. Instead, he led me to a conference room down the hall.
Eight of Gerstein’s graduate students and postdoctoral researchers were waiting for us, flanking two sides of a long table, all with laptops and wireless keyboards at the ready. They had me sit down at the head of the table so that they could show me slides on a giant monitor on the wall in front of me.
The first slide was labeled “Individual Z Overview.”
It was only then that I realized why so many of the scientists I contacted for my little project were proving to be so strangely helpful. To them, I am Individual Z. It was as if I was a frog that had hopped into an anatomy class with my own dissecting scalpel, asking the students to take a look inside.
For the next two hours, Gerstein’s team picked over my genome, showing me broken genes and duplicated genes and genes with mutations that altered how my proteins worked. But what struck me most of all was what they found when they compared my genome to two other people’s—a pair of anonymous volunteers who agreed years beforehand to have their DNA sequenced and made publicly available. One of them was from Nigeria and the other from China.
Gerstein’s team identified a total of 3,559,137 bases in my genome that were different from the human reference genome. These variants are known as single-nucleotide polymorphisms, or SNPs for short. They include the variants that make me a carrier for things like familial Mediterranean fever, as well as ones that influence traits that have nothing to do with disease, like my skin color, and ones that have no effect on my biology at all.
The Nigerian and the Chinese had a similar number of single-nucleotide polymorphisms. But those variants did not distinguish the three of us in any clear way. Sushant Kumar, a postdoctoral researcher in Gerstein’s lab, made me a Venn diagram to drive the point home. All three of us have 1.4 million single-nucleotide polymorphisms in common. There were another 530,000 that I shared only with the Chinese person but not with the Nigerian. And there were 440,000 single-nucleotide polymorphisms that I shared with the Nigerian alone. All told, 83 percent of my variants were present in at least one of their genomes.
We were three people of African, Asian, and European descent, from three corners of the world. Three races, some might say. And yet we shared far more than what set us apart.
The concept of race is not like the moon or hydrogen. It is not a feature of the natural world beyond our social experience. Up until the Middle Ages, writers never used the word race in the sense that it would later take on—referring to a sharply defined biological group of people whose members were bound together by heredity. Ancient writers certainly recognized differences among peoples from different parts of the world. But they didn’t explain them with taxonomy.
The word race seems to have first taken on a modern complexion during the Habsburg rule of Spain. The country was filled with people of different ancestries—Christian Celts, Romans, Jews, Africans. When the persecution of the Jews began, other Spanish people began to think of themselves as belonging to a particular group—Old Christians. To prove they were Old Christians, noble Spanish families had to demonstrate that they had no Jewish ancestry. In other words, that they didn’t have a single drop of Jewish blood. Noble families struggled to prove their ancestry had been pure since time immemorial.
When Spain established an empire in the New World, it now had another group of people to distinguish itself from. The Spanish conquistadors, the conquered Indians, and the imported African slaves now shared the same countries. The governments came up with a legal hierarchy with the Spanish on top, Africans in the middle, and Indians at the bottom.
But the people of the New World would not respect those boundaries. Through marriage or rape, people from different races had children together. The colonial governments needed to invent new categories, with new names. In Mexico, the viceroy sliced his subjects into fine distinctions:
Spaniard and Indian beget mestizo
Mestizo and Spanish woman beget castizo
Castizo woman and Spaniard beget Spaniard
Spanish woman and Negro beget mulato
Spaniard and mulato woman beget morisco
Morisco woman and Spaniard beget albino
Spaniard and albino woman beget torno atrás
Indian and torno atrás woman beget lobo
Lobo and Indian woman beget zambaigo
Zambaigo and Indian woman beget cambujo
Cambujo and mulato woman beget albarazado
Albarazado and mulato woman beget barcino
Barcino and mulato woman beget coyote
Coyote woman and Indian beget chamiso
Chamiso woman and mestizo beget coyote mestizo
Coyote mestizo and mulato woman beget ahí te estás
To the north, England brought Africans to their own colonies in the 1600s to work their fields. The Africans worked at first alongside European servants, subject to the same laws, but over the course of decades the colonial governments gradually singled out the people from Africa for harsh treatment. By the early 1700s, free Negroes had lost the right to vote or bear arms, while those still enslaved were recognized by the law as slaves for life, and their children inherited their bondage.
Ham’s curse grew wildly popular in the British colonies as a moral justification for these laws. Ministers proclaimed Noah’s divine prophecy in sermons, and pamphlets circulated in the American South explaining how God turned the skin of Ham’s children dark as a sign of their sin. Africans inherited their enslavement as surely as they inherited their color. Over the course of the 1700s, Ham’s curse became downright biological. Slavery’s defenders now began drawing up catalogs of essential differences between the white and Negro races.
“The Blacks born here, to the third and fourth generation, are not at all different in colour from those Negroes who are brought directly from Africa,” a Jamaican plantation owner named Edward Long observed in 1774. Instead of hair, Long claimed, his slaves had “a covering of wool, like the bestial fleece.” When Long turned to the minds of slaves, the differences from Europeans seemed even more profound. “They have no plan or system of morality among them,” Long declared. “They are represented by all authors as the vilest of the human kind.”
By the late 1700s, slaveholders could apply a scientific veneer to these beliefs. Naturalists argued that, just as animal and plant species could be divided into varieties, so, too, could Homo sapiens. Carl Linnaeus defined four races: Americanus (“reddish, choleric . . . paints himself with fine red lines; regulated by customs”), Asiaticus (“sallow, melancholy . . . haughty, avaricious . . . ruled by opinions”), Africanus (“black . . . women without shame . . . indolent . . . governed by caprice”), and Europeaus (“white . . . inventive . . . governed by laws”).
A few decades after Linnaeus, the German anthropologist Johann Friedrich Blumenbach proposed a new system of five races instead of four. His races were Caucasian, Mongolian, Ethiopian, American, and Malay. Blumenbach came up with the label Caucasian after studying a skull in his collection from a woman who lived in the Caucasus Mountains. It was, he later said, the most beautiful skull he ever laid eyes on. She belonged to the same race as people who lived across Europe, Blumenbach believed. He thought the reason that Caucasians had such beautiful skulls was that they were the first people created by God. They retained humanity’s original glory, while other people degenerated, producing the other four races.
Blumenbach’s system became popular over the nineteenth century, but many of the nuances of his ideas were lost along the way. Blumenbach argued that there was no sharp geographical divide between the races, for example, with each race blending insensibly into neighboring ones. Later anthropologists tried instead to pinpoint fixed anatomical differences. Some even went so far as to reject the idea that humans had a single origin. They argued that every human race had been separately created and forever locked into its place in the divine hierarchy. There was never any question as to how that order was stacked. At the top, one 1852 American textbook explained, was “the white race, who is distinguished above them all: the most perfect type of humanity.”
This racial hierarchy had to remain intact and legally clear-cut, no matter how confusing reality was. For all the imaginary walls that were erected between the races, sex forever threatened to bring them down. Early on in the American colonies, black and white indentured servants would sometimes marry and have children. By the end of the seventeenth century, colonial governments had laws in place to stop that practice. The Virginia House of Burgesses labeled the children of black and white parents as an “abominable mixture and spurious issue.” These interracial children were deemed Negroes as well, and thus slaves. The words that described them had legal weight, even if they were scientifically absurd. Colonial governments were pretending that the flow of heredity from white parent to Negro child could be arbitrarily severed.
Despite all the laws, more interracial children were born—not just to Negro slaves but to free Negroes as well. Some stayed in Negro communities, where their own children ended up inheriting more African ancestry. Others wound up with so much European ancestry that they sometimes chose to “pass” as white. Like the Spanish governors before them, southern states developed a vocabulary to bring some order to their human property. But if they looked closely at their words, they grew uncertain. Was African blood so potent, so poisonous, lawmakers wondered, that inheriting even a drop would overwhelm a much greater portion of white blood? In 1848, a judge in South Carolina tried to answer the question and failed. “When the mulatto ceases, and a party bearing some slight taint of the African blood, ranks as white, is a question for the solution of a jury,” he concluded.
Frederick Douglass took pleasure in forcing his fellow Americans to recognize how badly their racial classifications failed to align with reality. “My father was a white man, or nearly white,” he wrote in his autobiography. “It was sometimes whispered that my master was my father.”
Douglass’s mother was a Maryland slave named Harriet Bailey, who worked as a field hand. His biographers consider it likely that her owner, Aaron Anthony, raped her along with a number of his other female slaves, and then used these children of his for slave labor. Although Douglass may have inherited Anthony’s DNA, he did not inherit the legal status that came with it. Instead, Douglass grew up as a slave, driving cows to grazing fields and keeping them out of his father’s garden. Anthony loaned Douglass out at age eight to his son-in-law’s brother in Baltimore. There Douglass did an assortment of jobs until 1838, when he used false papers to slip aboard a northbound train.
Over the next few years, Douglass started a newspaper and began lecturing across the country in favor of abolition. In 1848, when he traveled aboard a steamboat across Lake Erie to a convention in Buffalo, his fellow passengers recognized him and pleaded for him to give an impromptu speech. Douglass stood up and delivered his case against slavery. “During my remarks, I convicted the slaveholder of theft and robbery,” he reported back to his newspaper.
An actual slaveholder, it turned out, was aboard the ship that evening. The man stood up, “with a most contemptuous sneer on his face,” Douglass recalled, declaring, “‘It was not to be supposed that any white man would condescend to discuss this question with a nigger.’”
Douglass decided to reply with “a somewhat facetious account of my genealogy.” He told the slaveholder “that he was much mistaken in supposing me to be a nigger.”
Instead, Douglass declared, “I was but a half negro—that my Dear father was as white as himself, and if he could not condescend to reply to negro blood, to reply to the European blood.”
The slaveholder could not. He stamped away, astonished, Douglass recalled, that “such sentiments and impudence as he had heard from my lips, could be tolerated and applauded by white men in any part of this Union.”
Two decades later, America’s slaves would be emancipated. The former Confederate states kept searching for a way to oppress them, and to do so they needed a reliable way to identify different races. Even a drop of black blood became enough to exclude a person from whiteness. In 1924, the state of Virginia enshrined this practice as law by passing the Racial Integrity Act, which barred interracial marriages. The law defined whites much like the Spanish had three hundred years earlier: white people were those “whose blood is entirely white, having no known, demonstrable or ascertainable admixture of the blood of another race.”
There was just one problem with this “one-drop rule.” The Virginia law defined whiteness as the absence not only of black blood but of Indian blood, too. Ever since the days of John Randolph, many prominent white Virginians had boasted of being direct descendants of Pocahontas. The Racial Integrity Act would have rendered them no longer white. That would simply not do, and so the state legislature tacked on a so-called Pocahontas exception. Even if Virginians were up to one-sixteenth Native American, the revised law held, they would still be considered white. People who were one-sixteenth black, on the other hand, were still black.
It might be comforting to dismiss the Racial Integrity Act as a monstrosity from a vanished racist past. But when the law was passed in 1924, genetics had already been around for almost a quarter of a century. And some of its most prominent figures gave their support to the law. Many eugenicists not only wanted to stop inferior white people from having children; they also wanted to keep the white race genetically pure.
Racism had been a fundamental feature of eugenics ever since Francis Galton coined the word. When Galton studied the heredity of talent, he compared it in different races. Without any reliable way to actually make such a measurement, he simply used his intuitions. Thinking back on his travels through southern Africa, he concluded that he and his fellow white explorers were far more talented than the Africans they encountered. “The mistakes the negroes made in their own matters, were so childish, stupid, and simpleton-like, as frequently to make me ashamed of my own species,” Galton wrote.
Africans inherited that childishness, Galton believed, in the same way that they inherited their curly hair or dark skin. The great talents of northern Europeans were just as hereditary, he believed. When Galton promoted eugenics, he promised that careful breeding would make northern Europeans even more talented, and the benefits would redound to all the inferior races, too. Throughout their global empires, Galton believed, northern Europeans ought to use eugenics to improve those lower races as much as their heredity would allow.
Galton wrote about race with the cool abstraction of an English gentleman who spent most of his time in London clubs and meetings of scientific societies. For some white American scientists, the question of race was far more urgent and intimate. In the Jim Crow years after the Civil War, millions of blacks boarded trains headed out of the South, to cities like New York and Chicago. Those cities were also taking in immigrants from abroad at the same time—no longer just northern Europeans but huge numbers of Italians, Poles, Russians, and Jews, along with Chinese and Latin Americans. Some white scientists responded to this sudden mixture by trying to put old-fashioned racism on a new scientific footing.
A scientist named Harvey Jordan experienced a fairly typical anxiety for his time. Jordan grew up in the late 1800s in rural Pennsylvania, where, he later wrote, he “was impressed with the importance of heredity, while playing about the barns.” Rather than become a farmer, though, Jordan went to college and became an expert on anatomy, studying at Cornell, Columbia, and Princeton. He spent the summer of 1907 in Cold Spring, New York, where he met Charles Davenport. Davenport taught him the new science of genetics, and, from Cold Spring, Jordan headed straight to the University of Virginia to become an anatomy professor and help modernize its medical school. In all that work, heredity was first and foremost on his mind.
Jordan was appalled to discover in Virginia “the distressing racial conditions in our colored population in the South.” But he didn’t see these conditions as being caused by social forces. Instead, biology was to blame. Its solution must therefore be eugenics—a state-run program of control over who got to have children. Jordan thought it would be especially useful to encourage mulattoes to have children with full-blooded blacks, in order to spread white genes among their children. They would act like yeast in bread dough, he thought, “as a leaven in lifting the colored race to a higher level of innate mental and moral capacity.”
Before such a program could be put in place, Jordan believed it would be necessary to uncover the genetic foundation of the races. He would need the guidance of his eugenic gurus to carry out the task. “I have been wondering if I could be of service in this great work,” Jordan wrote to Davenport in 1910, “perhaps in gathering statistics at close range.”
Just as Davenport had assigned Henry Goddard to study the heredity of feeblemindedness, he tutored Jordan on how to investigate the heredity of race. They agreed that Jordan would start by studying the most obvious feature that appeared to set the races apart: skin color.
Jordan found four families of mulattoes. To measure their skin color, he brought with him a colored top. The top, a child’s toy made by the Milton Bradley Company, had become popular among anthropologists as a way to measure skin color. It had wedges of yellow, black, red, and white. If the top was set spinning fast enough, the colors blurred together into a single hue. By adjusting the size of the wedges, the scientists could change the blurred color. Jordan would have his mulatto subjects hold out their arm and spin his top next to it. He would keep adjusting the colors on the top until he reached a matching shade. Then he would write down the size of the different wedges that produced the match.
Jordan sent his color numbers to Davenport, along with pedigrees of his mulatto families. Their data suggested that the color of children was not simply a blend of their parents’ skin. In a single mulatto family, the children might range from light to dark. The way in which they inherited their color, Davenport realized, hinted that the trait followed Mendel’s Law, passed down through the generations by hidden factors.
Davenport wanted to publish the data, but he was worried that the results might not hold up. If it turned out that the children were illegitimate, Jordan’s pedigrees would be rendered useless. When Davenport told Jordan about his concerns, Jordan assured him he had nothing to worry about. “There isn’t the least doubt, I think, about the legitimacy of the children,” Jordan wrote. “One man is a minister, one principal of the colored school, one a thriving merchant and one a barber, and all seem considerably above the grade of morality and intelligence of the ordinary stupid and irresponsible negro.”
Davenport and his wife, Gertrude, combined Jordan’s data with other pedigree studies and published all the results in the American Naturalist. For the most part, they wrote with clinical detachment about skin color. It would be hard to tell whether they were discussing humans or pea plants. “Skin color in negro x white crosses is not a typical ‘blend’ as conceived by those who oppose the modern direction of research in heredity,” they declared.
In their private correspondences, though, Davenport and Jordan were frank about their ambitions for a greater study of racial heredity. Skin color was just the start. Jordan went on to publish a study in which he claimed blacks are more prone to tuberculosis than whites. In 1913, he amassed an entire catalog of “unit characters” inherited by Negroes, including physical strength, capacity for routine, and “melodic endowment.” Intelligence was not on the list, for “the negro cannot undergo mental development beyond a certain definite maximum,” Jordan said.
Davenport shared Jordan’s faith in fundamental differences in the mental capacities of blacks and whites. In 1917, Davenport laid out his views in an essay called “The Effects of Race Intermingling.” Mixed-race children would suffer because the biology of their parents would be mismatched within them. “One often sees in mulattoes an ambition and push combined with intellectual inadequacy which makes the unhappy hybrid dissatisfied with his lot and a nuisance to others,” Davenport wrote.
When Virginia lawmakers began to draft the Racial Integrity Act, Davenport and Jordan pitched in to make it law. Davenport sent advice to the bill’s architects, while Jordan worked through Virginia’s Anglo-Saxon Club—whose name speaks for itself—to lobby for the bill’s passage. The law would stand until 1967, when an interracial couple named Mildred and Richard Loving were convicted of breaking it. The Supreme Court ruled in their favor and struck down the law. By the time the Lovings won their case, many scientists had already decided that race—in the sense of the word as it was used by biologists like Jordan in early twentieth-century America—did not exist.
As Davenport and Jordan were spinning their color tops and drawing their racial pedigrees, other researchers were drawing a different image of humanity. They saw the variations in our species as too complex, and too interwoven with historical events, to reduce to simplistic racial caricatures. Starting in 1897, the sociologist and activist W. E. B. Du Bois led a massive study on the Negro residents of Atlanta. His team measured their weight, height, skull size, infant mortality rates, and a host of other vital signs. Du Bois combined the survey results with a synthesis of worldwide anthropological research in his 1906 book The Health and Physique of the Negro American.
Du Bois did not present the Negro American as a uniform type of human being. Negro Americans were a population, within which individuals varied tremendously in every regard. In turn, the Negro population itself was intimately connected to other human populations. “The human species so shade and mingle with each other,” Du Bois wrote, “that not only indeed is it impossible to draw a color line between black and other races, but in all physical characteristics the Negro race cannot be set off by itself as absolutely different.”
Like anthropologists before him, Du Bois studied the outward features of humans. But in the early 1900s, other scientists began observing our inner variability. The Polish serologist Ludwik Hirszfeld proved that blood types were inherited according to Mendel’s Law. World War I forced him to put that research on hold, and yet it ultimately provided him with an unprecedented chance to see how blood types varied across human populations.
In 1917, Ludwik and his wife, Hanka, traveled to the Macedonian city of Salonica to work as doctors, treating the thousands of Allied soldiers who were finding refuge in the city. Surrounded by a German cordon, Salonica became “the most crowded and cosmopolitan spot in the universe,” one observer later said.
The Hirszfelds saw an opportunity to get a global view of blood types for the first time. Up until then, they had studied the blood types only of Germans, with little idea of how they compared to people from other parts of the world. In Salonica, they were living alongside soldiers from as far away as Senegal, Madagascar, and Russia. The Hirszfelds began asking soldiers and refugees if they’d give some blood. Eventually the couple ended up with samples from 8,400 people, representing sixteen ethnic groups. If the Hirszfelds had tried to gather that much blood in peacetime, their travels might have taken a decade.
The patterns they discovered did not fit any simple division between races. The four known blood types—A, B, AB, and O—turned up in every country they surveyed. The only distinguishing feature was the proportion of types. In England, 43.4 percent had type A, and 7.2 type B. In India, it was type B that was more common, at 41.2 percent; only 19 percent had type A.
The Hirszfelds calculated a “biochemical race-index” for each country, dividing the frequency of Type A by Type B. The index was highest in northwestern Europe and tapered away to the south and east. The Hirszfelds then grouped these “national types” into three regions: the European type, the Intermediate Type, and the Asio-African type. The Hirszfelds were well aware that the types they were constructing would confuse traditionally minded scientists. How, for example, could Asians and Africans be put in one group? “Our biochemical index in no way corresponds to race in the usual sense of the word,” the Hirszfelds warned.
The complexity that W. E. B. Du Bois saw in the Negroes of Atlanta, that the Hirszfelds saw in the blood of warring nations, demanded a richer view of heredity—one in which genetic variations were liberally spread across populations and had freedom to flow from one population to another. But in the early 1900s, short of bringing thousands of people together in a besieged city, it was impossible to map the genetic geography of our species. Instead, some of the most important early lessons about race came from other species, such as a little brown fly that lived on the west side of North America.
The fly, known as Drosophila pseudoobscura, was studied by a Soviet émigré named Theodosius Dobzhansky. Dobzhansky spent his childhood catching butterflies and became a published expert on beetles at age eighteen. His childhood insect hunts gave him a deep appreciation for nature’s rich complexity. Looking at the markings and colors of his specimens, he could see the enormous variation that a single species could contain. He could spot differences from one insect to another, and he could also observe differences between populations. Biologists sometimes called these recognizable populations subspecies. Sometimes they called them races.
As a young scientist, Dobzhansky learned of Thomas Hunt Morgan’s work on flies. It was a revelation for him. Morgan was tying the visible features of insects that Dobzhansky could see—their wings, their halteres, their spots—to the inner workings of their genes. In 1927, Dobzhansky got a fellowship to spend a year with Morgan in New York. The Soviet Union let Dobzhansky go, assuming he would return home when the fellowship ended. But Dobzhansky cherished his escape from Soviet tyranny and embraced the liberal democracy he found in the United States. He would never set foot in the Soviet Union again.
In 1928, Morgan headed west to the California Institute of Technology, and Dobzhansky went with him to the orange-scented hills of Pasadena. Once Dobzhansky had settled into his new Western home, he drew up a plan to study how genetic variations were spread out over the range of a wild species. He knew he couldn’t study Morgan’s favorite, Drosophila melanogaster. It was a garbage-feeding camp follower. Instead, Dobzhansky picked Drosophila pseuodoobscura, a truly wild animal that lived across a range stretching from Guatemala to British Columbia. Dobzhansky bought a Model A Ford and started driving into remote mountain ranges to catch flies from isolated populations. Back in Pasadena, he bred the flies and inspected their chromosomes under a microscope.
Comparing one fly to another, Dobzhansky sometimes spotted a section of a chromosome that was flipped. These so-called inversions acted like a crude genetic marker. Dobzhansky would find many of the same inversions in different parts of North America. Just as with blood types, the inversions marked no sharp geographical divisions between populations of flies. At best, they were more common or less so from place to place.
As Dobzhansky surveyed his flies, his thoughts turned to his fellow humans. The rise of the Nazis in the 1930s disgusted him intensely. He found the way they used a biological definition of race to persecute Jews both vicious and antiscientific. While Dobzhansky dearly loved his adopted country, he also recognized the racism that still infested it, including among many of the older American geneticists he met.
Dobzhansky confronted America’s race obsession for himself on a visit to Cold Spring in 1936. He met Edward East, a geneticist who had declared a few years earlier that the Negro race possessed undesirable traits that justified “not only a line but a wide gulf to be fixed permanently between it and the white race.” On meeting Dobzhansky, East assured him that, as a brilliant scientist, he could not possibly be a genetically inferior Russian. East was confident Dobzhansky must belong to the small population of Nordics who lived in Russia.
Starting in the late 1930s, Dobzhansky began declaring publicly that popular notions of human races and white superiority “had no basis in biology.” In bestselling books, he explained how populations of any animal were a mix of genetic variants. It might be possible to tell one population from another with statistics, but that was a far cry from claiming that all the animals in one population were alike. In fact, the animals with a single population could be tremendously different, genetically speaking. “The idea of a pure race is not even a legitimate abstraction,” Dobzhansky wrote. “It is a subterfuge to cloak one’s ignorance.”
What was true for flies must be true for humans, Dobzhansky asserted. “The laws of heredity are the most universally valid ones among biological regularities yet discovered,” he declared. Dobzhansky granted that humans certainly varied, and that some of that variation was spread out geographically. But if human races were sharply defined, then you’d expect to find sharp boundaries between them. And that was almost never possible. While it might be possible to tell an Australian Aborigine from a Belgian by a trait like skin color, another trait—like the prevalence of type B blood—might unite them.
Dobzhansky didn’t want to do away with the concept of races completely. He wanted people to see them for just how modest and blurry they really were. Dobzhansky defined races as nothing more than “populations which differ in the frequencies of some gene or genes.”
After World War II, a number of other geneticists and anthropologists joined Dobzhansky’s campaign. Their efforts culminated in an official statement from the United Nations condemning scientific racism as baseless. But Dobzhansky’s new allies pushed the attack further than he had. They demanded scientists give up the term race altogether. It was so fraught with dangerous assumptions that it had to be discarded. The anthropologist Ashley Montagu, for example, switched to using the term ethnic groups. But one of Dobzhansky’s strongest challenges came from one of his own protégés.
In 1951 a young New Yorker named Richard Lewontin came to Dobzhansky’s lab at Columbia to study flies. Dobzhansky was the sort of strong-willed professor who steamrolled his graduate students, pushing them to do the experiments he wanted done and to draw the conclusions he had already reached. But Lewontin pushed right back. He was committed to investigating his own scientific questions. What was most important to Lewontin was finding a new way to measure the genetic diversity in Drosophila pseudoobscura, Dobzhansky’s favorite fly.
In his own work, Dobzhansky had only managed to get a crude measure of the fly’s genetic diversity. He inspected the cells of insects for any that had major changes to their chromosomes. Some flies, for example, had long stretches of DNA that were flipped into reverse order. Lewontin, working with John Lee Hubby at the University of Chicago, developed a new way to look for genetic diversity—one that could detect differences that were invisible under Dobzhansky’s microscope.
Lewontin and Hubby would grind up fly larvae and extract proteins from them. They would then put the proteins in a slab of electrified gelatin. The electric field dragged the proteins across the slab, pulling lighter proteins farther than heavier ones. In some cases, the scientists found that all the flies made proteins of the same weight. In other cases, however, some flies had lighter versions and others had heavier ones. And in still other cases, a single fly made both heavy and light versions of a protein.
The different weights of the proteins were the result of variations in the genes that encoded them. Lewontin and Hubby compared the weight of proteins in six populations of Drosophila pseudoobscura from Arizona, California, and Colombia. Looking at eighteen kinds of proteins, they found that 30 percent existed in different forms within a single population. In other words, these populations were far from genetically uniform. Even individual flies were surprisingly rich in variations: on average, 12 percent of the proteins in a single fly existed in two forms.
Lewontin then applied this same approach to humans. In the early 1900s, scientists knew of only a single protein that varied from person to person: the blood-type protein that determines people’s ABO blood type. By the 1960s, however, scientists had found a number of other kinds of proteins on the surface of blood cells. And these proteins also varied from person to person. A protein called Rh, for example, is present on some people’s cells and missing from others’. Doctors have to make sure the Rh factor is the same in a donor and a patient before transfusing blood. Lewontin reviewed studies on these proteins carried out in England. People there had a surprisingly high level of genetic diversity: A third of the proteins varied from person to person.
These results gave Lewontin the confidence to broaden his research and take on the great question of race. He embarked on a new study to see how well racial groups aligned with the actual genetic diversity of humans. If races were indeed biologically significant, Lewontin argued, each race should have a starkly distinctive combination of genetic variants. Most of the genetic diversity should exist between the races rather than between individuals of the same race.
Lewontin gathered measurements of seventeen different proteins in a wide range of human populations, from the Chippewa to the Zulu, from the Dutch to the people of Easter Island. When he sorted people according to their race, he found that the genetic differences between races accounted for only 6.3 percent of the total genetic diversity in humans. The genetic diversity within populations, such as the Zulu or the Dutch, contained a staggering 85.4 percent.
In 1972, Lewontin published these results in a profoundly influential paper entitled “The Apportionment of Human Diversity.” He concluded that racial classifications had become entrenched in Western society thanks to optical illusions. People defined races based on features “to which human perceptions are most finely tuned (nose, lip and eye shapes, skin color, hair form and quantity).” But these features were influenced by only a small number of genes. It was wrong to assume that all the other genes people carried followed the same patterns.
Given his findings—and given all the suffering that had been justified by racial classifications—Lewontin urged that society set them aside. “Human racial classification is of no social value and is positively destructive of social and human relations,” he declared. “Since such racial classification is now seen to be of virtually no genetic or taxonomic significance either, no justification can be offered for its continuance.”
It was a sweeping statement to make based on fairly little data. But in the years since, younger generations of scientists have revisited Lewontin’s question with better tools. Instead of proteins, they’ve examined DNA. They’ve surveyed more people, from more populations. In 2015, for example, three scientists—Keith Hunley and Jeffrey Long of the University of New Mexico and Graciela Cabana of the University of Tennessee—studied DNA from 1,037 people belonging to fifty-two different populations around the world. In each person, they sequenced the same 645 segments of DNA. They looked for the differences in these segments from person to person, calculating their genetic diversity.
Hunley and his colleagues confirmed, like others had before them, that most human genetic diversity can be found within populations rather than between the so-called races. And thanks to the huge scale of their study, they could measure human diversity with far greater precision. The people who live in African populations tend to be more genetically diverse from one another than people who live on other continents, for example. The population with the lowest genetic diversity was a small Amazon tribe called the Suruí. Yet even the Suruí—who number only about 1,120 people—possess about 59 percent of all the genetic diversity in our entire species. If you wiped out everyone on Earth except the Suruí, in other words, nearly two-thirds of humanity’s genetic variation would survive.
“In sum,” Hunley and his colleagues said, “we concur with Lewontin’s conclusion that Western-based racial classifications have no taxonomic significance.”
The Venn diagram that Sushant Kumar made for me—showing me all the SNPs that are sprinkled over me, a Nigerian, and a Chinese person—felt like a personal emblem of how badly the concept of race explains human genetic diversity. I’d call myself white, and yet 83 percent of my 3.5 million single-nucleotide polymorphisms are shared by either an African or an East Asian. We may inherit some of those shared variants from common ancestors who lived hundreds of thousands of years ago. Some variants may have arisen later, thanks to a new mutation. They then spread from population to population as people mixed their genes the way people always do. All three of us—me and my pair of anonymous far-flung cousins—got showered in the same genealogical glitter.
Race may not be a meaningful biological concept, but it does exist: It has a powerful existence as a tradition of putting people in social categories. Those categories, then, had profound influences on people’s lives. Racial categories served as a legal justification to enslave groups of people and declare their children slaves from birth. Race helped turn other people into scapegoats for economic disasters, justifying their slaughter by the millions. Other people were classified into races judged incompetent to make use of their own land, justifying pushing them off it. And racial categories also gave some people the luxury of enjoying those lands and the profits of slave-based economies without having to learn much about their history. Even after racist institutions and laws were abandoned, their effects have endured for generations, extending race’s power.
Because race is a shared experience, it can join people together who aren’t closely related. American blacks gained their collective identity only when they came together as cargo on slave ships bound for the colonies. Slave traders roamed up and down the coasts of Africa to capture people separated by thousands of years of history, in Senegal, Nigeria, Angola, even Madagascar. Richard Simson, a surgeon who traveled to South America in 1689 on an English privateer, observed that throwing strangers together was a crucial step in making slavery a profitable business.
The way “to keep Negros quiet,” Simson wrote, “is to choose them from several parts of the Country, of different Languages, so that they find they cannot act jointly.”
Leaning on the biological concept of race like a crutch has led doctors into some embarrassing blunders in their studies of diseases. “There is no race which is so subject to diabetes as the Jews,” declared W. H. Thomas, a New York doctor, in 1904. As late as the early 1900s, Jews were considered a distinct race, with its own diseases. To guide their immigration policies, the United States Congress compiled a book called Dictionary of Races or Peoples. The book treated the evidence of the Jewish race as plain to see. “The ‘Jewish nose,’ and to a less degree other facial characteristics, are found well-nigh everywhere throughout the race,” the report declared. Such racial classifications led doctors to look for diseases that were characteristic of each race. Jews, doctors came to agree, had diabetes.
The seed of this notion sprouted in 1870, when a doctor in Vienna named Joseph Seegen observed that a quarter of his patients were diabetic. Other physicians later concluded that Jews died from diabetes at a far higher rate than other groups. German doctors started referring to diabetes as the Judenkrankheit: the Jewish disease.
Between 1889 and 1910, New York saw its rate of diabetes triple. To J. G. Wilson, a physician with the US Public Health Service, the cause was clear: the influx of Jewish immigrants. Jews had “some hereditary defect,” Wilson said, that made them vulnerable. William Osler, the most important clinical doctor of the early 1900s, blamed the vulnerability of Jews to diabetes on their “neurotic temperament,” along with “their racial tendency to corpulence.”
And then, in the middle of the twentieth century, the universally recognized fact that diabetes was a disease of the Jewish race simply disappeared. Historians can’t definitively say why. It’s true that a few scientists questioned the statistical evidence behind the Jewish disease. But no one ever published a definitive takedown. Maybe after Nazis peddled myths that Jews were a naturally disease-ridden race, American doctors quietly decided to retire their own misconceptions.
Myths like Jewish diabetes do not detract from the fact that some people who identify themselves with certain labels—black, Hispanic, Irish, Jewish—have relatively high rates of certain diseases. Ashkenazi Jews have a higher rate of Tay-Sachs disease than other groups, for example. African Americans have a higher rate of sickle cell anemia than European Americans. Hispanics are 60 percent more likely to visit the hospital for asthma than non-Hispanic whites. Researchers have also found significant associations between the race of patients and how their bodies respond to drugs. Chinese people tend to be more sensitive to the blood-thinning drug warfarin than whites, indicating they should get a lower dose.
In some cases, these patterns are the result of the genes people inherited from their ancestors. But sometimes they aren’t.
When Richard Cooper went to medical school at the University of Arkansas in the late 1960s, he was stunned at how many of his black patients were suffering from high blood pressure. He would encounter people in their forties and fifties felled by strokes that left them institutionalized. When Cooper did some research on the problem, he learned that American doctors had first noted the high rate of hypertension in American blacks decades earlier. Cardiologists concluded it must be the result of genetic differences between blacks and whites. Paul Dudley White, the preeminent American cardiologist of the early 1900s, called it a “racial predisposition,” speculating that the relatives of American blacks in West Africa must suffer from high blood pressure as well.
Cooper went on to become a cardiologist himself, conducting a series of epidemiological studies on heart disease. In the 1990s, he finally got the opportunity to put the racial predisposition hypothesis to the test. Collaborating with an international network of doctors, Cooper measured the blood pressure of eleven thousand people. Paul Dudley White, it turned out, was wrong.
Farmers in rural Nigeria and Cameroon actually had substantially lower blood pressure than American blacks, Cooper found. In fact, they had lower blood pressure than white Americans, too. Most surprisingly of all, Cooper found that people in Finland, Germany, and Spain had higher blood pressure than American blacks.
Cooper’s findings don’t challenge the fact that genetic variants can increase people’s risk of developing high blood pressure. In fact, Cooper himself has helped run studies that have revealed some variants in African Americans and Nigerians that can raise that risk. But this genetic inheritance does not, on its own, explain the experiences of African and European Americans. To understand their differences, doctors need to examine the experiences of blacks and whites in the United States—the stress of life in high-crime neighborhoods and the difficulty of getting good health care, for example. These are powerful inheritances, too, but they’re not inscribed in DNA. For scientists carrying out the hard work of disentangling these influences, an outmoded biological concept of race offers no help. In the words of the geneticists Noah Rosenberg and Michael Edge, it has become “a sideshow and a distraction.”
To many people, Rosenberg and Edge may sound as if they’re ignoring the evidence staring them in the face. While I may share millions of single-nucleotide polymorphisms with a Nigerian, no one would mistake me for someone whose family goes back centuries in Lagos. I once went to Beijing, and never on my trip did someone walk up to me and ask for directions in Mandarin. It is true that humans have physical differences, and some of those differences are spread geographically across the planet. But clinging to old notions about race won’t help us understand the nature of those differences—both the ones we can see and the ones we can’t.
What matters is ancestry. A small band of hominins in Africa evolved into Homo sapiens around 300,000 years ago, after which they expanded across that continent and then across the world. Those journeys shaped the genomes that people inherited from their ancestors. And today, if we look at our own genomes, we can reconstruct some of that history, even back to ancestors who weren’t exactly human.