“I think I shall avoid the whole subject as so surrounded with prejudices”
Letter from Charles Darwin to Alfred Russel Wallace, December 22, 1887
I was Leroy and my sister was Coco when I first encountered racism. We were at the Co-op supermarket in the tiny village of Capel St. Mary in Suffolk, where we lived, when some boys on their bikes shouted out those names to my eight-year-old sister and me, seventeen months younger. Fame was the big hit on television at the time, and Coco and Leroy were the lead characters. I remember two things about what happened next. First, we thought this was excellent, as they were amazing dancers, both African Americans, both supremely attractive: Leroy surly and charismatic with cornrow hair, and Coco tough and beautiful.
The second thing I recall was that my father was livid, splenetic with rage. Maybe his reaction was piqued by the recent murder of his best friend, Blair Peach, by a policeman at an Anti-Nazi League rally in London a year or so earlier. At the time we were utterly baffled by Dad’s reaction, especially as Coco and Leroy were so effortlessly cool. I guess being slightly dark-skinned in rural Suffolk in the 1980s simply made us stand out. My memory is that my sister and I did bad splits all the way home.
Not long after, in the first term at a new school, a fellow seven-year-old called me a “Paki.” By this stage I knew that this was intended as an insult, and I punched him, I think in the stomach.* Like most bullies do when confronted, he went crying off to teacher and I was summoned to the headmaster’s office. With an understandable zero tolerance policy on violence, Mr. Yelland was spittle furious and I was terrified. I told him what happened, he bellowed for me to leave, which I did, still petrified. It seems he had a less-than-zero tolerance level for racism. The other boy got a week of detention.
These two trivial examples of fairly low-level racism are pretty insignificant, and I can’t pretend that I have endured much racial prejudice in my life. My mother is Indian, but I am not very dark, and I sometimes am assumed to be Italian. I have a robustly British name, and the type of accent that gets you a job as a presenter on BBC Radio 4. I have visited India several times, but only as a tourist or for work. I did find my roots of sorts on one trip, but it was of limited scientific interest, revealing that my maternal DNA was likely to have arisen somewhere in the region of Mumbai, probably some 20,000 years ago. There was certainly no spiritual epiphany—I am as Indian as cricket. My mother has never set foot on the subcontinent, nor had her parents. Before they were born, her grandparents immigrated to Guyana in South America, where my mother spent the first twenty years of her life before moving to England, as so many Guyanese women did, when Britain looked to the embers of the colonies to recruit nurses for the neonatal National Health Service. She now lives in Canada.
My father was born in Scarborough, in Yorkshire, and his family tree is rooted in the northeast of England, and north of the border as far back as we can trace, to the seventeenth century. The name Rutherford strongly associates with those areas, and it has its own tartan and motto: nec sorte, nec fato—neither by chance, nor fate—which I suppose is agreeably relevant to evolution and genetics.
His family emigrated to New Zealand when he was five, where there have been plenty of other Rutherford settlers, not least the great physicist Ernest,* but he was drawn back home at twenty. His sister, my aunt, still lives on the other side of Earth and, with an Austrian Jew, had a son, my cousin, who is a full Kiwi, as are his two daughters, my first cousins once removed. My parents divorced when I was about eight, and we soon moved in with my father and his new partner, now wife, who raised us as her own. She is East Anglian, and we can see her maternal family tombstones in a single Essex churchyard all the way back to the seventeenth century. Her father and aunt were orphans raised by Sisters of Mercy in Liverpool, though when we investigated their family tree it looks like their father, her grandfather, was a Russian Jew named Josef Abrahams, but he took (or was given) the naturalized name Joseph Adams—so unceremoniously is heritage abandoned.† She already had two sons, and fused our lineages when together she and my father had another, my youngest brother, sixteen years my junior.
We’re all adults now. My sister married an English South African with Dutch and German/Jewish ancestry, and they have two daughters. My middle brother married a Swede and lives in the birthplace of biological taxonomy, Uppsala,* where they have two dual-nationality bilingual kids. My youngest brother lives with an Iranian woman whose family is in exile. My stepmum’s sister married a man who was adopted by an English family after being found as a baby abandoned in Greece. They have three boys; the eldest married an English woman with a half-German half-Maltese mother. I married an English girl, with Irish and Welsh ancestry on either side of her parents. Our three kids were all delivered by me in London.†
So it goes. In one generation, a Russian Jewish family becomes British Gentile, my cousin is born a New Zealander, and my niece and nephew Swedish. Sometimes, when asked by people or on pull-down menus on official forms, I describe myself as mixed-race Indian British, but is it true? I’m from Ipswich, though now, as I enter my fifth decade, I’ve spent more time in London. I think of my pedigree as mutt—less a tree than an amusing tangled thicket.
Are we unusual? Though through history people have typically married close to home, the progress toward out-breeding has been mostly relentless. At least, this is true in un-royal families. And we’ve seen (in Chapter 4) how inbreeding worked out for the Hapsburgs—that is, not well. It’s no great revelation to point out that racial abuse is idiotic, but being called a “Paki” doesn’t make a great deal of sense given my background. It’s even more absurd to compare my sister and me to African Americans, no matter how awesomely cool Coco and Leroy were, or we might’ve hoped to be.‡ Without knowing the ancestry of the actors, Irene Cara and Gene Anthony Ray, it’s quite possible, extremely probable in fact, that I am more closely related genetically to the racist boys in Suffolk, than those two black kids from Fame are to each other. This applies to both my paternal, that is British, genes, and my Indian maternal ancestry.
In essence, this is because of the small size of the populations that slowly ambled out of Africa some 100,000 years ago, growing and migrating to populate the rest of the world, as discussed in Chapter 1. Only a relative few formed the genetic pool from which we were drawn, far smaller than the people who remained in the nursery of humankind. In statistics this is called a sampling error. By drawing just a small taster from a big population, you select a sample that is not representative of the original group. That small misrepresentative sample was the group of people from whom all DNA would be drawn, apart from those in Africa. This means that in fact, I would be genetically more similar to those Suffolk kids if I were Russian, Swedish, or Maori than many people of largely African descent are to each other.
I guess they didn’t have a working knowledge of human genetic variation and migration, and I feel compelled to conclude that they weren’t intending to make a comment on the evolutionary ascent of man. Racism is hateful bullying, and a means of reinforcing self-identity at the expense of others: Whatever you are, you’re not one of us. If there is one thing that my own tortuous family tree demonstrates it is that families make a mockery of racial epithets, and racial definitions as used in common parlance are deeply problematic. Modern genetics has shown just that, too, and I’ll be navigating through some of the data on that in the next few pages. But here is the idea I will be interrogating: There are no essential genetic elements for any particular group of people who might be identified as a “race.” As far as genetics is concerned, race does not exist.
I am unaware of any group of people on Earth that can be defined by their DNA in a scientifically satisfactory way. There are plenty of genetic differences and physical differences that emerge from those genes between people and peoples, but none that align with the way we talk about “race.” The question of what race means from a scientific point of view is complex, controversial, and still a source of great ire and debate. It is frequently stated that, for the average geneticist, race simply does not exist. This chapter will explore how true that is, not for political reasons, though it is virtually impossible not to feel a sense of right or wrong or injustice or moral indignation when we talk about race. Science’s primary role is to subtract those human characteristics from objective reality, and cast a picture of how things are, rather than how we see them.
The great irony is this: The science of genetics was founded specifically on the study of racial inequality, by a racist. The history of my field is inextricably intertwined with ideas that we now find toxic: racism, empire, prejudice, and eugenics. Like all true stories and histories, like all real family trees, what follows also weaves a meandering path. All geneticists, all statisticians,* and in fact all scientists owe this Victorian racist a profound intellectual debt, for he was a genius on whose foundations much of the modern world rests. His name was Francis Galton, and as all the great stories in biology do, it begins with Charles Darwin.
Darwin had published On the Origin of Species* in November 1859, to immediate blockbuster success. The first edition sold well immediately (though it is unknown whether it sold out, as Darwin wrote in his diaries, and is often repeated), and Darwin amended his work and a second edition of 3,000 copies followed in January 1860. He wasn’t a terribly well man, possibly having picked up a disease (still precisely undiagnosed today) on his travels on HMS Beagle, where he saw evidence of evolution and of the grinding movements of land on the planet, and began to think about the spread of life on Earth, and the similarities and differences between the peoples of the continents. Though voluminous in his correspondence, Darwin didn’t venture out in public often. But his defenders, notably Thomas Huxley and Joseph Hooker, were vociferous in their support for his central idea of evolution by natural selection, descent with modification. By the 1850s, Darwin was already well known from his global travels, but on publication of the Origin, he became a star. The word genius gets bandied around rather casually these days, but Darwin was one unequivocally by any definition—in my view, the greatest of all scientists, across all disciplines. No one singly has done more to reposition life and us in the universe. He described why life on Earth is the way it is, and placed humans very clearly in relation to other animals. Furthermore, though normally I find ranking crude and idolatry disappointing, I’m more than happy to single him out at the very top of the intellectual pile because he was so humble, and credited every Tom, Dick, and Harriet who had the slightest influence on his scheme.
Francis Galton was a genius too, but also a difficult man, and a man more difficult to scrutinize. He was Darwin’s half cousin, and profoundly influenced by the runaway success of Darwin’s work and ideas. Half cousin means that they shared a grandfather, Erasmus Darwin, who married twice. Erasmus was a great thinker and scientist too, and alongside Samuel Galton a founder member of the magnificent Lunar Society, a Birmingham-based intellectual salon of industrialists, such as Josiah Wedgwood and James Watt, and scientists, who would meet by moonlight (to aid potentially drink-wobbly walks home late into the night), and scheme up ideas that would come to stoke the white heat of Victorian ingenuity.
Both branches of Erasmus Darwin’s family were established, wealthy, and successful. The Darwins were scientists and physicians, and the Galtons were Quakers and gunsmiths, which might seem an unlikely combination given that religion’s commitment to nonviolence. Francis was born to Samuel Galton and Frances Darwin in 1822, in a house near Birmingham that was previously occupied by another scientific goliath, the philosopher, theologian, and chemist Joseph Priestley.
Galton had always hero-worshipped his cousin, and was greatly impressed with Darwin’s magnum opus in 1859. It would have a profound impact on his work. Galton wrote warmly within three weeks of publication to offer characteristically Victorian praise:
Pray let me add a word of congratulation on the completion of your wonderful volume, to those which I am sure you will have received from every side. I have laid it down in the full enjoyment of a feeling that one rarely experiences after boyish days, of having been initiated into an entirely new province of knowledge, which, nevertheless, connects itself with other things in a thousand ways. I hear you are engaged on a second edition.
There is a trivial error in page 68, about rhinoceroses . . .
Aside from his rhino blunder, Darwin’s first chapter speaks of breeding in pigeons and plants, and all manner of beasts of the field and fowl of the air. He was demonstrating the mutability of creatures, that they were not fixed in time, but their bodies and behavior could be bent to man’s will through selective breeding. This formed the groundwork from which he would go on to describe the natural process of selection.
After reading his cousin’s masterwork, Galton began pondering whether humankind could be improved by selective breeding. Darwin was a focused scientist compared to Galton, though that title did not exist until 1834. The somewhat arbitrary subject areas of science that we cling to in school today were not so rigid back then, and most dabbled in multiple fields. Darwin was preoccupied with other living things as well as his pigeons, particularly worms, carnivorous plants, and barnacles,* though he was also driven by geology, which was critical to the development of his evolutionary thinking. Galton, by comparison, was more a polymath, and made not insignificant contributions to a whole range of fields. His myriad gifts to the world included the first newspaper weather map,† the scientific basis of fingerprint analysis for forensics, a dizzying number of statistical techniques, many the underpinnings of all statistics used today, foundational work on the psychology of synesthesia, a vented hat to help cool the head while thinking hard,* and much else over his long and distinguished career. He also gave us the word eugenics, more of which later, and the phrase nature versus nurture, which has plagued geneticists ever since, as this whole book I hope makes amply clear. He devised a new way to cut cakes, which was published in Nature, the journal from which both the structure of DNA and the first human genome would break out of the lab and enter the public consciousness.†
My own story, academically speaking, is somewhat enmeshed with Galton’s, not in a particularly special way, merely as it is for many whose intellectual genealogy is rooted at University College London. Like both Darwin and Galton (though this is surely where the comparison ends), I went up to university to study medicine. But I wasn’t that interested in being a doctor, and spent a lot of time gadding around trying to find something else that would gun my engines. Darwin was similarly distracted from his medical studies in Edinburgh by taxidermy and was rather taken by his tutor John Edmonstone, who was a freed black slave; this relationship was part of Darwin’s development as an abolitionist.‡ Instead of lectures, I went to the movies a lot. Galton did a couple of years of medical training in Birmingham and London, but went on to pursue mathematics, and the world of numbers would be the prime determinant of his intellectual legacy.
Over his long and varied career, one thing was consistent among Galton’s traits: He coveted data. He measured. It was in the statistics that he developed, and in his unquenchable thirst for measuring human characteristics, that he tried to formalize and lock down human differences. In Chapter 4 and elsewhere in this book, we explored the new business of genetic ancestry, where for around £100 and a froth of spit in a test tube, one of many companies will draw a sketch of your DNA. The results are, to my mind, of inconsequential interest to an individual, but in collecting these samples the companies behind them, notably 23andMe, are amassing colossal datasets of human genomes in numbers that far outstrip ones available to academic scientific research.
Galton had done it all before. He recognized the power of large collections of measurements—we call it “big data” nowadays—and cannily also recognized our own fascination with ourselves, and willingness to reach into our purses to satisfy those egos.
The huge spectacle of the International Health Exhibition in 1884, at the site now occupied by the Science Museum in South Kensington, featured a replica of an insanitary street, many of the new-fangled drainage systems designed to improve public health, and electrically illuminated fountains. Four million people came to see the new science on show.
Galton was there too. He set up an Anthropomorphic Laboratory, where customers would pay 3 pennies (almost a dollar in today’s money) to enter, and anonymously fill out a card (with carbon copy for Galton to keep the record) with personal details. “The object of the laboratory,” he wrote in Journal of the Anthropological Institute after the expo had ended, “was to show the public the simplicity of the instruments by which the chief physical characteristics of man may be measured and recorded.”
Galton’s biometric equipment.
Figure 1 shows a sickle-shaped layout for testing acuity of vision, first with one eye and then the other. The pages are from the Shilling Diamond edition of the Prayer Book (though he points out that familiar texts are “objectionable” to the test, and—ever the mathematician—“a page of logarithms would be better”). Figure 2 depicts the “color sense” test, in which the participant is asked to identify shades of green wool in the five lengthways cartridges.
They would file through, and be measured and tested for all manner of things. Some metrics were straightforward—height, hair color, arm span, and weight. Others were complex—keenness of sight, punch strength, color perception, and ability to hear high-pitch noises, tested via whistles made by Messrs. Tisley and Co., Brompton Road, and Mr. Hawkesley of Oxford Street. “Hardly any trouble occurred with the visitors.” Galton noted, “though on some few occasions rough persons entered the laboratory who were apparently not altogether sober.”
What a clever scheme. Today, people part with their cash to get some information about their DNA, just as they did for Galton at the Anthropomorphic Laboratory. Our love of navel-gazing means that we not only volunteer to give up our biometrics, but we actually pay for the privilege. Altogether, 9,337 gave up their thruppence to be measured by Galton, who was amassing data on people, hoarding the similarities and differences between people in all of these characteristics.
Mark Twain wrote in 1869 that “travel is fatal to prejudice, bigotry, and narrow-mindedness.” Galton had explored extensively in the 1840s, as privileged young men often did in the nineteenth century, to Turkey and through the Middle East and Egypt. He went further, into what is now Namibia, on a two-year trip with the Royal Geographical Society, and published bestsellers describing his journeys into the heart of darkness. But Galton didn’t adhere to Twain’s maxim. He maintained and grew a deep-rooted sense of hierarchies of the peoples of the world, and formalized it later in his life under a number of auspices. A few years later, in 1873, he submitted a diatribe in the Times about how Africa should be best served if colonized by the Chinese as the characteristics of the “negro race” were not sufficient to foment development in their nations without help from the British. Recognizing that some “negroes” had accumulated wealth and demonstrated decent intellectual chops in a manner that, he asserts, is common among “Anglo Saxons,”
average negroes possess too little intellect, self-reliance, and self-control to make it possible for them to sustain the burden of any respectable form of civilization without a large measure of external guidance and support.
Therefore, he suggests that as colonies of China, Africa would flourish, for
The Chinaman is a being of another kind, who is endowed with a remarkable aptitude for a high material civilization. He is seen to the least advantage in his own country, where a temporary dark age still prevails, which has not sapped the genius of the race.
(though not before pointing out the bountiful negative characteristics of “the Chinaman,” which include deceit, unoriginality, and timidity. “The Arab,” for comparison, he concludes, “is little more than an eater up of other men’s produce; he is a destroyer rather than a creator, and he is unprolific”).
Though wince-inducing now, these sorts of views were not necessarily normal and not necessarily uncontroversial then, and we shouldn’t assume that these were universal British Victorian values. Racism predated Empire, and these were the end times for slavery, which had peaked before Victorian times, even though the British Empire was still robust and proud. William Wilberforce had driven the Abolition of the Slave Trade Act through Parliament in 1807, which largely banned slavery, though only in 1833 was this extended throughout the whole Empire with the Slavery Abolition Act.
The Darwin-Galton-Wedgwood family tree is an impressive canopy. Upward from Charles is Josiah Wedgwood, founder of the pottery dynasty, and Erasmus Darwin. Alongside Charles was Galton, and the descent of Darwin features brilliant scientists, writers, actors and, with marriage into the Keynes family in the 1880s, economists. Galton was aware of his pedigree, and was moved to examine human excellence in families after the publication of On the Origin of Species. Darwin had boiled the bones of fancy pigeons, each displaying absurd and absurdly different plumes or gullets or feet, and in doing so had showed that they were the same species, and that these traits had been bred into the birds by pigeon fanciers for competition over thousands of years. It was crucial for the theory because it showed that species were malleable, not cast immutably in stone never to change. Galton wasn’t thinking about feathers, but of ability and of genius—not least that which was clearly in abundance in his own clan.
Ten years after his cousin changed the world, Galton published Hereditary Genius, in which he carved out the idea that men of eminence—and it was predominantly men—ran in families:
The general plan of my argument is to show that high reputation is a pretty accurate test of high ability; next to discuss the relationships of a large body of fairly eminent men—namely, the Judges of England from 1660 to 1868, the Statesmen of the time of George III, and the Premiers during the last 100 years—and to obtain from these a general survey of the laws of heredity in respect to genius. Then I shall examine, in order, the kindred of the most illustrious Commanders, men of Literature and of Science, Poets, Painters, and Musicians, of whom history speaks. I shall also discuss the kindred of a certain selection of Divines and of modern Scholars.
The measure of reputation is not part of the metrics that includes yards and feet, or volts and amps. So the starting point is questionable. To his credit as a good scientist he did recognize limitations in his methodology, and turned to twins as a means to study the relationship between biology and environment, nature and nurture. Darwin read Hereditary Genius, or more precisely, his wife Emma read it aloud to him, and ever polite, sent effusive letters offering praise on his clarity.
Galton suggests that the betterment of society could be drawn from understanding the role of inheritance of abilities as described in analysis of great men from history, and that the weak could be stored celibate in monasteries or nunneries. In 1883, he invented the word eugenics. It was from these works and from his experiences on his travels that Galton used to formulate ideas about why some people were better than others, why some were successful and others not, ideas articulated so clearly in that letter to the Times. By the last decade of the nineteenth century, politicians and thinkers were expressing concern that the British “stock” were not fit enough to fight in the Boer Wars, which had been raging in Africa since the 1880s. They turned to Galton.
His influence continued for decades. Winston Churchill attended a Galton lecture in 1912, and a few years later raised the topic of British stock in Parliament. Both he and Theodore Roosevelt desired the neutering of the “feeble-minded,” as was the parlance in Edwardian days for all manner of psychological, cognitive, and mental health conditions. Roosevelt, not yet president, expressed the view that purifying the American human stock would be “for the benefit of civilization and in the interests of mankind.”
Marie Stopes is known today as a champion of women’s reproductive rights, and her name adorns hundreds of clinics worldwide that provide essential support for women and their choices regarding pregnancy. But she held some horrifying views, arguing forcefully for the compulsory “sterilisation of those unfit for parenthood,” particularly the Irish in London. During the 1930s, she wrote love poetry to a rising European politician in praise of his policies, which included reform of his country’s population structure using eugenics as part of their radical plans. His name was Adolf Hitler.
Support for eugenics spanned the political spectrum. William Beveridge, principal architect of the welfare state, whose ideas would form the foundations of the National Health Service, said:
Those men who through general defects are unable to fill such a whole place in industry are to be recognized as unemployable. They must become the acknowledged dependents of the State . . . but with complete and permanent loss of all citizen rights—including not only the franchise but civil freedom and fatherhood . . .
George Bernard Shaw, also on the political left, said, “The only fundamental and possible socialism is the socialization of the selective breeding of man.”
The British never did adopt a eugenics policy, despite England being the intellectual birthplace of the idea. Before Darwin and Galton, Thomas Malthus had formally fretted about population growth and control, and therein laid the foundations of improving the “stock” of a people. But in the USA, and a few other countries (notably Sweden), the forced, involuntary, and often secret sterilization of undesirables was embraced enthusiastically. From 1907, when Indiana passed the first mandate, until 1963, forced sterilization was legally administered in thirty-one states, with California the most vigorous adopter. The most recent cases of forced sterilization in that famously liberal state occurred in 2010. In the twentieth century, more than 60,000 men and women, though mostly women, were sterilized for a variety of undesirable traits—men frequently to curtail the propagation of criminal behaviors. Native American women were forcibly sterilized in their thousands, and as late as the 1970s, black women with multiple children were being sterilized under the threat of withheld welfare, or in some cases without their knowledge.
These horrors were all to come in the twentieth century, as were the fullest repercussions of population control via murder and sterilization that occurred during the Holocaust. The Nazis slaughtered not just Jews in their millions, but also homosexual men, Roma, Poles, and people with mental illness.
And to little effect from the point of view of eugenic purification. The Nazis murdered or sterilized more than a quarter of a million with schizophrenia in order to purge them from the German people. The incidence of schizophrenia was measurably lower for a few years after the fall of the Third Reich as a result, but by the 1970s it was unexpectedly high. Schizophrenia is a condition that is associated with dozens if not hundreds of genetic variations, and many people have many of them, without suffering any mental health issues. Furthermore, a high proportion of schizophrenics do not have children, and so a eugenic program appears to have had little long-term effect.
That word, eugenics, did not carry the toxic meaning it has today. At the beginning of the twentieth century, Galton’s influence was formalized with the formation of the Eugenics Records Office in 1904, with him in charge. It was part of University College London, the world’s first secular university, the first to admit women, the first to employ a Jewish professor,* and a bastion of progressive thinking free from the shackles of religious doctrine. After his death in 1911, it was renamed the Francis Galton Laboratory for National Eugenics.
By the time I studied there in the 1990s, it had long since dropped that noxious word to become the Galton Laboratory of the Department of Human Genetics & Biometry. For three decades it was housed in a lackluster 1960s building on Stephenson Way, just north of UCL’s main campus, and typical of universities around Britain, linoleum floors, frosted glass, and orange Formica paneling. The majority of my lectures were in the Galton Lecture Theatre, and that’s where I first did my scientific research as an undergraduate. Every day, I mooched past a humble glass display case of some of Galton’s biometric tools (to which I was largely oblivious), including a head measuring crank, a device for measuring nose straightness, and a copy of his female beauty map of Great Britain (the most attractive women according to his criteria were in South Kensington, the least in Aberdeen).*
The genetics department has now moved half a mile south, across the Euston Road to Gower Street, into the Darwin Building marked with a blue plaque; Charles lived there during the intervallum between the Beagle and his long-term residence at Down House, where he carved out his masterpiece. The building that housed the Galton Laboratory is now largely abandoned, apart from a few offices, one of which hosts the Galton Collection,† an assortment of his letters, notes, and scientific equipment.
It is interesting to draw these comparisons between two nineteenth-century great men of science. Darwin gave us the manner by which we evolved. Galton built the foundational tools for the study of inheritance. He introduced studies of identical twins as a means of extracting the biological from environmental, nature and nurture.
The two men are in many ways perfect opposites. Darwin was dogged by humility; Galton was arrogant. Darwin was beset by doubt; Galton was determined to prove his own ideas. Darwin invented evolutionary biology; Galton founded and formalized many aspects of the biological study of humans. They both worked at a time when great leaps were being made in the study of life, which would lead to further unifying theories of biology. The great nineteenth-century Moravian scientist* Gregor Mendel’s work from exactly the same midcentury time, though ignored until the beginning of the twentieth century, described the rules of inheritance—how characteristics pass down the generations from two parents to one child.
In the first few decades of the twentieth century, primarily at UCL, a new breed of biology emerged that combined statistics and Darwin, and formalized the mechanism by which evolution by natural selection occurs. Not long after, DNA was established as the bearer of the genetic material and, in 1953, Crick and Watson revealed that it was constructed like a twisted ladder, the double helix, which not only was built to be copied from generation to generation, but also harbored information, a code that could be replicated every time a cell divides. Many scientists over the 1960s cracked that code, and showed it to be a means of writing and recording the instructions to make proteins, and this gave us an understanding of why diseases occur, and why people look different from each other: A tweak in the genetic code results in a subtly different protein, which may have a visible effect—eye color, skin color, the curl of hair.
In that century of wonderful, world-changing, glorious science, we had biologized difference. In measuring physical characteristics and subsequently analyzing them in large numbers, Galton set the framework for what was to come: biometrics—the measurement of humans. With genetics, we could peel back the skin and reveal the root causes of difference, and place them in time, in geography, in evolution. We armed ourselves with the tools to scrutinize the difference between individuals and groups of individuals with molecular precision. Surface characteristics—the visible phenotype—would be replaced with the data that underwrote those traits, altogether a more fundamental measure of the true differences between people—the genotype. Mutable and impermanent differences such as nationality or religion could be tucked away as crude anachronisms because DNA and genetics would furnish us with definitive answers to the questions of similarity and difference.
Well, it did and it didn’t.
Biology moved from the shape of bones and features—the morphological—to the molecular long before DNA became the star of the show, in fact well before DNA was even suggested as the material that transmits inheritance. Blood groups began to be established into the A, B, O system we still use today during the First World War. In 1919, the Polish scientists Ludwik and Hanka Hirschfeld looked for a pattern of blood group distribution among soldiers from sixteen different populations they examined (mostly by country, but Jews were also included as a group). What was being measured and differentiated there were proteins, a proxy for the DNA that encodes them, expressed as alleles of the same gene, and they found variation in the frequencies of the different blood groups across their samples.* The same system was employed in the 1970s by the geneticist Richard Lewontin who examined blood groups with a far greater degree of precision, enabled by the emerging field of molecular biology. He looked at a hundred alleles across the genes that constitute blood groups—the subtle differences between people in the same gene. In his landmark 1972 paper, Lewontin quantified the precise differences between the molecules of blood type between peoples, and demonstrated that the highest proportion of genetic differences were seen within racial groups, not between them. Eighty-five percent of human variation, according to the genetic differences in blood groups, was seen in the same racial groups. Of the remaining 15 percent, only 8 percent accounted for differences between one racial group and another.
These numbers have been replicated in other studies of other genes since. What this means is that biology fundamentally deceives our eyes. Genetically, two black people are more likely to be more different to each other than a black person and a white person. In other words, while the physical differences are clearly visible between a white and a black person, the total amount of difference is much smaller than between two black people. If everyone on Earth was wiped out except for one of the traditional racial groups, say, eastern Asians, we would still preserve 85 percent of the genetic variation that humankind bears. They might look more homogeneous, but that fact reveals that the underlying code that causes the characteristics that we use to broadly define race has a disproportionately visible effect. These morphological differences are real, we all know that, but they’re not representative of the genome as a whole.
Of course, there are differences: visible, measurable, and cryptic. It would be intellectually dishonest not to acknowledge them. People from eastern Asia have a darker skin tone than Europeans, as well as having thicker, black hair, and the epicanthic fold, which gives them an eye shape unlike others, and is largely absent in the people of the rest of the world.* In genetics we look for the underlying causes for these variations. Some are merely genetic drift—coded DNA that has changed over time and become fixed in a population not because they are useful, but simply because they were present in the individuals from whom the present-day populations are heavily drawn. Other characteristics may well have a selective advantage, but they are notoriously difficult to prove. Pale skin, prompted by just a couple of genes, is almost certainly an adaptation to lower levels of sunlight, and the subsequent reduced ability to generate vitamin D in the relative gloom of Europe (all discussed in Chapter 2), as well as a host of other proposed or theoretical factors, such as higher resistance to frostbite and simple preference in mating. There is natural variation in whom we fancy, and this might not be solely determined by some form of unconscious selection of a trait that will enhance success in one’s life (such as food foraging skills, or the muscles to fight off a sabre-tooth cat). It might well be that you simply have a slight preference for people with a particular trait—ginger hair, for example—and as a result of that the genetics that code for ginger hair will persist.
The media (and to a lesser extent scientists) tirelessly speculate about the evolution of particular traits or behaviors in humans, with neat explanations as to what the advantage they provided was. Many are silly, and ridiculously unscientific—women like pink because as the gatherer half of hunter-gatherer cultures, being able to spot berries would be useful; babies cry at night to prevent their parents from having sex and therefore create competition for them in the form of siblings.* We label these pseudoscientific fantasies adaptationism, or sometimes a form of panglossianism, after Dr. Pangloss from Voltaire’s Candide. An eternal optimist, he suggested there was a reason for everything, and everything had a reason. Hence our noses were shaped as they are to hold glasses in their place, and we had two legs because that perfectly suits the structure of a decent tailored trouser.
The unglamorous truth is that there are but a handful of uniquely human traits that we have clearly demonstrated are adaptations evolved to thrive in specific geographical regions. Skin color is one. The ability to digest milk is another, which fits perfectly with the emergence of dairy farming (again, discussed in Chapter 2).
The best-understood example of regional adaptation concerns the single greatest cause of death in the human story. Genetic mutations emerged in populations in malaria regions that offer some protection against two versions of the disease, caused by the single-celled parasites Plasmodium falciparum and Plasmodium vivax. An alteration in the gene hemoglobin-B causes a structural change to the shape of blood cells, normally a half-sucked lozenge, which becomes rigid and curved like the blade of a sickle. People with one copy of the mutated gene have sickle cell trait: Their blood contains some of the distorted blood cells, but they are largely unaffected. People with two copies have sickle cell anemia, a serious disease that 300,000 children are born with every year, with symptoms including pain, infections, and increased risk of stroke, and death, all because the misshapen blood cells can get lodged in blood vessels and organs. But sickle cell trait offers protection against infection from malaria. And so, when we look at the distribution of the mutated gene, it perfectly matches the range of malaria all over the world. Furthermore, some researchers have suggested a strong association with the presence of the protective gene in populations who have historically farmed yams. To plant yams, farmers clear forests. Cleared forest means more standing water. More standing water means more mosquitoes. More mosquitoes means more malaria—so the idea goes. The emergence of the disease, and as a consequence the resistance gene, may well have been enabled, or at least nurtured, by yam farming. The persistence of sickle cell anemia is the cost of positive selection for resistance against the most destructive disease in our history.
Interestingly, sickle cell is culturally often thought of as a “black disease,” even to the extent that it comes up in the lyrics of hip-hop frequently, sometimes as a diss.* Sickle cell trait and sickle cell disease are not exclusive to black people, not least because the term black is utterly useless as a descriptor of people whose origin is in Africa. We’ve already established that the vast majority of genetic diversity occurs within that continent, as this was the pool from which only a small sample of humans wandered out to populate the rest of the world. While it is true that the densest concentration of the sickle cell gene is in Sub-Saharan Africa, it is prevalent in the people of every other region that is affected seriously by malaria, including the Middle East, the Philippines, South America, and southern Europe, notably Greece. It seems that disease and evolution have little regard for continents or racial epithets. For the most part, it is not known how adaptive the characteristics we see in specific regions are. That doesn’t mean they haven’t been selected.
Earwax is of great interest to people like me. Stick your little finger in your ear and have a good root around. The stuff that sticks to your finger is called cerumen, and it’s a mixture of dead cells, fluff, dust, and other detritus of a life. We like it because it’s one of a very small handful of traits that has a relatively straightforward relationship between the DNA and its outcome—the genotype and the phenotype.
There are basically two types of earwax, sticky and dry. The gene that determines these two states is called ABCC11, which comes in two alleles to give them their more scientific and less revolting descriptor. The gene is 4,576 base pairs long, and at position 538 there is either a G or an A. If you have a G, the code writes the amino acid glycine, and if you have an A you get an arginine. This simple change slightly nudges the protein into a different shape, and the shape switches the nature of the wax. The inheritance of this terribly important phenotype plays out in a human ear in a straightforward Mendelian way. Wet is dominant: two copies of the G version and you have wet earwax; one of each allele and you have wet earwax; two copies of the A version and you have flaky, crumbly dry earwax. This charming business gets much more interesting when we look at how earwax is smeared across the world.
We think mostly not about the phenotype, but the genotype in genetics, and measure the frequencies that the different alleles have in populations. In the case of earwax, the two relate to each other very directly, so, for example, if the dry allele occurred at a rate of 50 percent, in a population of one hundred people, you’d expect to see twenty-five people with dry and seventy-five with wet wax (not 50:50, because those with one wet and one dry gene have wet wax). In Africa, the proportion of dry genes is effectively zero. In South Korea it’s the other way round. Generally, eastern Asians have a far greater frequency of dry than anywhere else on Earth, and broadly the further east you go, the more likely you are to find dry wax ears, if indeed inspecting people’s ears is your business.
Now, why on earth would this be? Drift might be one explanation—that founding populations of the east had more dry genes than the ones that they left behind in the west as they migrated, and that for no particular reason those proportions spread and became fixed. We can look more closely with genetics, and here is how we do it. Genes occupy locations on chromosomes, but geneticists don’t tend to look at whole genes. They look for SNPs, those individual letters within genes that vary between individual people. These aren’t typos, as they don’t cause disease, they’re just variant spellings—skeptic or sceptic, grey or gray. When tracking the evolution of people, you don’t just look for one SNP, you scan the DNA around the bit you’re interested in for others, because DNA is passed from generation to generation in chunks. A gene that is of advantage to the individual may be selected with flanking bits of DNA in tow.
As well as being a playwright and a vocal eugenics advocate, George Bernard Shaw was a linguaphile, and described the USA and the UK as two countries separated by a common language.* Here are five words with two alternate spellings, some different in UK and US English (but the same number of letters): grey, disk, barbeque, theatre, and adviser. Here they are in a nonsensical sentence:
Your grey disc is a theatre barbecue adviser.
Here’s an alternate version, equally valid (and equally nonsensical), but with five legitimate alterations:
Your gray disk is a theater barbeque advisor.
If each of the variants were independent of each other, and you sampled everyone in the world’s spelling, then you’d expect to see every possible combination of those five variants in the sentence, twenty-five in total, at the same frequency. If some of the words in the sentence are linked to another, for example the adjective grey and noun disc, then you might see these two together more often than not. In genetics, this is one of the key ideas, with a typically wretched and obfuscating technical name: linkage disequilibrium. Grey and disc are linked because they associate with each other in location and meaning, an adjective relating to a noun. In DNA the association has no inherent meaning, but the proximity between two SNPs is all important. We look for variations in DNA that associate with each other in clumps. With the easy access of the full human genome these days, we look not for five differences, but tens, hundreds, thousands, hundreds of thousands. Specific SNPs can undergo linkage disequilibrium as a result of selection (that is, both variants are useful), or by what’s called “genetic hitchhiking”—one variant is useful, and others that are sitting nearby get dragged along into future generations. Because grey disc is preferable to my British eyes, theatre is coming along for the ride too. They have been linked and are now not inherited with an equal probability. They are more likely to be inherited together. These statistical blips are what tells us how we have evolved.
Another related effect that can occur is called a “selective sweep.” This is when one particular variant confers an advantage for the organism, and as a result of hitchhiking over many generations, all other variants are removed until all the variants are deselected, and there’s only one version of the full set: Your grey disc is a theatre barbecue adviser—they have all been linked now.
These concepts are key tools in the geneticist’s toolbox. By taking DNA samples from people spread out over the world, we can use the differences we see in linkage disequilibrium and selective sweeping to suggest patterns of human migration. The patterns are subtle, and it requires delicate math to get these ghosts to emerge. They are hidden in living people, so the (perfectly reasonable) assumption is that the geographical spread shows a degree of recent permanence. It’s not unreasonable because for most genetic variations examined so far, we see them change gradually over landmasses, and more abruptly at seaboards. Although modern movement of people is rapidly messing up these genetic shadings, we can still extract country of origin for previous generations.
Back to earwax. A study in 2011 suggested that with these techniques, the earwax gene had undergone a positive selection as it has moved east. That isn’t necessarily to say that it bestows a clear advantage to those who have it—it’s not easy to even speculate in a panglossian way what benefit flaky ears might bestow. It may merely be positive selection as a migrating population spreads into a new area, has more kids, and the new gene frequency is different from the place whence they came. This is an example of riding the wave of migration, what some geneticists call “surfing.” It might be that it has hitchhiked its way into the east along with something unknown but of much greater benefit.
Japanese researchers in 2009 suggested a reason why the global distribution of earwax is spread the way we see. They proposed it is because we smell. Your axilla is the hairy bit where the arm joins the chest, and we spend billions each year masking the smell that this area naturally generates with deodorant. The wet wax type occasionally associates with a disorder called axillary osmidrosis in a way that is much more rare in our flaky-eared cousins. People with this condition believe their armpits stink, and sometimes seek surgery to remove the glands that generate the sweat that is behind the odor. It seems that ABCC11 may have a role in these apocrine glands, though we don’t know what. Could it be that what was actually being selected was smell (or lack thereof), and the dry wax was merely hitching an evolutionary ride? I am possibly committing what I decry above: This is adaptationist speculation. It may be true, but we simply don’t know. So for now, this remains merely an interesting just-so story. It might render the people of South Korea the least smelly on Earth, though this clearly important study has not yet been published.
While we’re in the Far East, there’s another example of so-called racial characteristics, more visible than earwax, but also concerning sweat, which also have become fixed the further east we travel from Greenwich, and that have also surfed their way into being putatively racial. This one is a gene called EDAR. It’s of similar but different use to us here because it doesn’t just do one thing. The gene EDAR sits on the second human chromosome, and encodes a protein called ectodysplasin A receptor, which typically lies on the surface of some cells of the developing embryo. There it plays a role in communicating between two major classes of cells in the growing flesh of a body, the ectoderm and mesoderm. In this interplay, many tissue types are defined, including hair, teeth, nails, and sweat glands. As with so many human genes, we know how it works by analyzing what happens when it’s broken, and in this case, mutant versions of EDAR cause disorders such as hypohidrotic ectodermal dysplasia, where patients have few or no sweat glands, no hair or fingernails, and peculiar teeth.*
Of the normal versions—the alleles—of EDAR we see in humans, one, referred to as 370A, is almost omnipresent in East Asians and Native Americans, and almost absent in Europeans and Africans. This particular allele associates with thicker hair, an increase in the density of sweat glands, and a particular front teeth shape called “shoveling” (it’s not visible from the smile, but the back of the incisors is scalloped away in a particular way). “Associates with” is not the same as saying “causes,” because it is very tricky to show precisely that a genetic mutation encodes a protein that is altered in such a way that it produces these changes during growth in the womb. Nevertheless, experiments in mice indicate that these characteristics are the result of the 370A mutation.
In 2013, a neat international study did a range of things that set the bar for how to quiz the genetics of our evolution. Geneticists from MIT, Harvard, Fudan University in China, and of course, Galton’s own alma mater, UCL, scanned the genomes of 1,064 people from fifty-two populations around the world, and looked for SNPs that flanked the 370A allele. They ended up with a block of DNA consisting of 139,000 bases, with 280 other SNPs of interest. That’s the ease with which we can now dip into the genome. It has tons of genetic data, and crucially of genetic variation, to play around with to question its origins in human history, and what it enables is the ability to calculate when and where 370A originated. Recall that this is not a common allele in Africa and Europe, so was acquired by an entirely random process at some point as people moved east. The computer simulations include a whole swag bag of input variables, including farming practices, migration, the euphemistic gene flow between distinct populations and other factors, and what comes out the other side is a number. Or, rather, because science is ultra-cautious when it comes to statistical analysis, a range of numbers. What emerges is that this mutation occurred in an individual somewhere between 13,000 and 40,000 years ago, but the most likely date is 31,000 years before today, in what is now central China. This predates the migration across the Bering Strait (which was then terra firma) by the people who would populate the Americas north and south.
The second part tested what the mutation actually does, and they used the standard of genetics for several decades, our old friend the mouse. When a gene is faulty in humans, once identified, it gets tested in mice by inducing the same mutation, and seeing if the result is similar or the same. When the gene is rendered functionless, this is called a knockout, because you eliminate the gene you’re interested in. The opposite test is also useful, a knock-in. A version of the mouse’s EDAR gene was knocked-in with the 370A mutation in place, and it had thicker hair, denser sweat glands, and smaller, more branching mammary glands. Rodents’ incisors grow continuously as they gnaw them down on food, wiring, and skirting boards throughout their lives, so the shape of the teeth is not an informative comparison between us and them. But the other phenotypes were remarkably similar to what we see in East Asian humans.
Speculation as to the reasons why this mutation so successfully spread was rife. Sweat gland density may well relate to climate, as these glands form an effective cooling system in hot and humid conditions, especially for long-distance running or walking, and this might’ve been desirable for the culture of hunter-gathering people of this period. Geological records show China was indeed hot and humid at around the time the mutation arose, and may have retained this heat due to monsoons at a time when temperatures were broadly dropping. One way to address this would be to do more digging. Discover bodies from the time and get their DNA out, and dig up more of China to get better historical climate records. In science, there’s always more digging.
Or it could relate to smell, as suggested with the earwax gene. As ever, speculation in the press looked to the most exciting possibility, and some articles suggested that reduced breast size was visible and therefore possibly a driver of sexual selection that helped fix the new mutation into place. This is pretty flaky science. Breast size is not universal in being a determinant of sexual attractiveness, despite what some strands of contemporary western culture insist upon, and neither mammary gland size nor the internal structure of the ducts of lactation are direct correlates of bra size. But why let the facts get in the way of a good story, especially when it’s got a sexy headline.
Whatever the selective advantage was remains unknown. It is unlikely that all characteristics were advantageous at the same time, and of course we have to try hard not to think of this evolution in a clear linear way. It may be surfing, hitchhiking, or sweeping, and the length of time it took to become omnipresent will be thousands of years and thousands of generations of people. Dan Lieberman, a Harvard professor of evolutionary biology who helped conduct the study, told the press at the time that, “These findings point to what mutations, when, where, and how. We still want to know why.”
What it shows more clearly than ever before is that key physical attributes that we identify as being “race-specific” are superficial and recent. Even with the relatively straightforward EDAR gene, we still don’t really understand why it became so prevalent among more than a billion people, and stayed that way. You could breed out the 370A from a family in a few generations simply by a Taiwanese man marrying a European woman, and their children marrying Europeans until the only allele in that family is the original version. It could conceivably be lost in two generations, with both copies eradicated in successive generations. The children in that family would not have thick black hair, and would have acquired sweat glands like Europeans or Africans. What race are they then? Equally, you could reintroduce it in two generations by marrying into a Vietnamese family. Are they back to being East Asian then? The genetics is not definitional and not essential, and refuses to align with the way we talk about race. And this is just one gene. Behavior is breathtakingly complex to scrutinize.
Yet a book published in 2013 by the former science editor of The New York Times, Nicholas Wade, made a number of questionable assertions relating to the genetics of race. A Troublesome Inheritance posed some ideas that race is not only very clearly defined genetically, but that these distinctions in DNA account for not just the physical characteristics of certain populations, but also some of the social and cultural behaviors.
The book frequently misrepresents much of the work that is used to defend his assertion that recent evolution within so-called races explains why certain people appear to be better or worse at certain things. According to Wade, the English display a “willingness to save and delay gratification” and this is absent from certain tribal cultures. Jewish genes are “adapted for success in capitalism.” The Chinese are predisposed to obey authority (how similar this sentiment is to that of Galton expressed in the letter to the Times in the nineteenth century). These statements are unsupportable in any form based on our knowledge of history, genetics, and cognitive ability. They are also clumsy and gross stereotypes and, in my opinion, straightforward racism. But A Troublesome Inheritance received much press coverage because it laid out controversial and provocative ideas, purportedly based on scientific evidence. Deconstructions in the form of demolition of the book have been universal among geneticists. But some of the fallacies and inconsistencies feebly presented as science are useful for understanding why this is such a sticky area to deal with.
There is no doubt that humans have evolved in the very recent past and are still evolving today. The significance of that change in genetic material over decades, centuries, and millennia is the subject of scientific debate. Wade frequently makes assertions about the changes in genes in his races over very recent human evolution that are simply unsupportable and, moreover, he does not try to support them. Let us not forget that evolution simply means change over time, so the question is really not if we are evolving but we are evolving under the duress of natural selection. Are we adapting to local conditions according to our genetic material? And if we are, do these adaptations correspond with the way we commonly describe races?
What do we mean by race anyway? This is not an easy question to answer: Everyone thinks they know what race means, and can tell the difference between peoples with varying degrees of granularity. The epicanthic folds typical of East Asians are variable within East Asia, and with experience you might be able to, on average, correctly identify a South Korean from a Cambodian. But nobody would classify these as different races. They’re both East Asian. Inuits have an epicanthic fold too, but they’re not East Asian, though we know they came from a population in East Asia. Black, as discussed above, is virtually meaningless as a scientific descriptor, and Africa as a racial group is also of very limited use because black people are more likely to be more genetically different from each other than they are from white people. Nevertheless, you might, with experience, be able to distinguish an Ethiopian from a Senegalese. That distinction, the shape of a face, the color of skin, the breadth of a nose, is precisely why “black” or “race” is a term of little value to science. We use black casually to mean “someone with dark skin whose recent origins have been in Africa” (as opposed to “someone with a similar skin tone from India”). There is not much precision in that statement.
Galton was quite comfortable with broad definitions and crude associated assertions: Hindoos, Negroes, the Arab, the Chinaman, and so on. Already we can see how imprecise the language employed here is. China is a country, so in a sense, the easiest to define—people born inside China. Hindu is broadly a religion or culture, though also generally refers to the largest proportion of members of the Indian subcontinent, and doesn’t include the 180 million Muslim Pakistanis, nor Indian Muslims, both of whom are genetically indistinguishable from Hindu Indians. The Arab? For one so formal in measurement and in categorization, Galton shows his racist hand in being so relaxed about these definitions.
Early attempts at human categorization lumped us all into five, and this endured with remarkable stickiness. The eighteenth-century German anthropologist Johann Blumenbach described Caucasian, Mongolian, Ethiopian (broadly meaning sub-Saharan African), Malayan (roughly Southeast Asian and Pacific Islanders), and Native American. A simplified version arrived at the end of nineteenth century—Caucasoid, Negroid, and Mongoloid. The US anthropologist Carleton Coon stuck with five, but slightly different groups in the mid-twentieth century—Caucasoid; Mongoloid (which included everyone indigenous to the Americas as well as East Asia); Australoid (meaning aboriginal Australians); and Negroid was divided into Capoid and Congoid (from the Cape and the Congo, as a means of distinguishing sub-Saharan Africans of the east and south from central and west).
The minimum number of groups humans can be classified into has never remained static. Nicholas Wade himself vacillates between there being three and seven races on Earth today in his book, and equates them very broadly to continental populations—African, eastern Asian, and Caucasians, but might include Indian and Middle Eastern, and others. This is very broadly what many mean when they talk about race, though clearly it has underlying problems. We know that the emergence of the pale skin we associate with Europe, and particularly northern Europe, only emerged in the last few thousand years, just as the genes for processing milk did. We’ve addressed the single gene EDAR, and how it confers that characteristic thick black hair that is typical of eastern Asians. In terms of genetics, we’re looking at a handful of genes among thousands, and minuscule factors of variation across millions in the whole genome. There is no single gene that underpins the concept of race, just like there are so few genes for any one complex human characteristic, and there are just a few that convey the broad physical differences that render populations very visibly different from each other. Even when there are, such as with EDAR, these represent a superficial and tiny fraction of the total amount of genetic difference between people.
The Human Genome Project moved the field on in a seismic shift, as we could scan not one gene or a handful, or one variation in spelling such as those first assessments using blood group proteins. Instead, we can scan for hundreds and thousands, in thousands of people. Noah Rosenberg from Stanford in California led one of the first major studies that did just that in 2002, and used the new power of genomics and mighty computing to scrape not just beneath the surface, but into the depths of our evolution.
His team sampled SNPs from 1,056 people, from 52 geographic regions, and looked at variations at 377 locations spread across the whole 3 billion letters of each of their genomes. This was a huge study at the time, and though 377 dots in an ocean of 3 billion sounds like a drop, that is plenty enough to determine the spread across nations. They fed this data into a computer program called STRUCTURE that sorts for similarities by clusters—plug the numbers in and then ask it to sort them into a number of categories that you decide. They asked it to give out a range of clusters from two to six—that is, divided into two groups of people based on similarities, then three, four, and so on. When they did two, it grouped all people into those from Africa, Europe, and western Asia, and those from eastern Asia, the Americas, and Australia. That makes sense; these geographically are the places that we populated first. When asking the algorithm for three groups, Africa is hived off as a separate group. That also makes sense; the people who went out of Africa were only a small sample of the total available alleles. With five groupings, Australia becomes a separate group, as does eastern Asia. All of a sudden, the genetics appears to confirm the most traditional racial grouping: African, Europeans and the Middle East, East Asians, Australians, and the Americas.
But push it to six and something weird happens. The Kalasha, a northern Pakistani tribe of around 4,000 people, emerge as the next group. They are a strange population, small and isolated in the highest mountains of the Hindu Kush where it’s barren and glacial, and accessible only by mountain passes and rope bridges. They are largely endogamous—marrying within their community—and have their own language and religion, though many are now converting to Islam, as their neighbors across the border in Afghanistan, the Nuristani, did at the end of the nineteenth century.
The Kalasha are indeed an interesting people, and unusual in many ways. But they’re not that unusual, and certainly not nearly unusual enough to warrant placing them in a whole separate racial grouping, as no one possibly would consider doing, not even the most ardent racialist thinker. If you keep increasing the number of clusters, you get more and more groupings of people, geographically and culturally bound. In fact, the harder you look for this fine-scale architecture within the 3 billion letters of genetic code that each of us has, the more gradients emerge at the boundaries. With these cluster analyses, it is true that the most similarities examined are shared within a group, but plenty overlap with other clusters. The graphical representations of these types of data show blending at the edges. The sharpest delineations coincide with water: Europe, sub-Saharan Africa, and East Asia. But with the addition of more groups, with fewer oceanic gulfs, human variation is pretty continuous. The concept of a discrete or pure race vanishes in the haze.
Rosenberg’s study is a great piece of work and posited the right questions to interrogate the underlying genetics of how the people of the world are distributed. By scanning thousands of single positions spread across the whole genome of more than a thousand people, it reinforced—in fact amplified—Lewontin’s earlier results that the biggest genetic differences in people were seen between people of the same so-called race, rather than between the races. But at exactly the same time, it showed that the differences we do see when picking through the genome with a fine-toothed comb are the same as the basic racial structure that had been suggested for decades, in the era before science, during Galton’s time, during the years of crude surface traits, and throughout the twentieth century. This is not looking for the genetic differences that cause the visible differences between people, but simply hunting for any differences that might exist between them, visible on the outside or not.
Look for clusters, and you’ll find clusters. The fine-tuning of where these clusters exist is fascinating and the question becomes “why?” Why do we see these groupings, especially if the rest of the genome, in fact the majority of the genome, does not show such regional variation?
We often rely on language as a metaphor for explaining genetics, and I’m going to attempt to use it here too. Imagine all the books currently in print in the world. To simplify, let us just refer to those written in English, and nonfiction. Publishers and bookshops like to categorize them in order to help promotion, to push sales, and to help the reader get an idea of what it is that they are buying. You’re holding a science book, though it has plenty of history in it, and it’s primarily a biology book. My last book,* which was about the origin of life, was also science with plenty of history, but while it had plenty of biology, it also featured physics, astrophysics, geology, and chemistry, as befits the study of the transition from inanimate chemicals to living systems on the young earth.
In the classics of science writing, Darwin wrote about geology, Carl Sagan was a cosmologist who wrote eloquently on biology and physics in his masterpiece Cosmos, as does the particle physicist Brian Cox in the modern era, and anatomist Alice Roberts frequently writes about archaeology and history. So while we can agree that this minuscule sample comprises nonfiction books in English, further classification is murky. If we then include all genres of nonfiction—from hokum fad diet books to the Highway Code, via car manuals and celebrity biographies—you begin to see the problem. But we’re not meant to judge books by their covers, or titles, but by their words. Would this help the classification system? If we were to go through the text of all these books and look for the word science, it would appear most frequently in books about science, but not exclusively. Science (misused) is also part of the tool-shed of fad diets and flaky spirituality guides. Context is essential.
So we expand the search criteria and use science and biology, which ought to refine the categorization somewhat. But there will be books that contain the word biology but not science. Do we include them in our science and biology grouping? Say we want to find books about biological evolution, so we might include science, biology, and evolution. Alas, Darwin himself does not use this word in the original text of On the Origin of Species, so that’s not going to work. He does talk about barnacles a lot though, and the ship on which he traveled the world, the Beagle. And indeed there are multiple books—for example Mystics Seafarer’s Trail by Lisa Saunders* and Plant and Animal Alphabet Coloring Book (1979)—that speak of the dogs and the shellfish, and not about Darwin, the explorer ship, or evolution. But these are not in the same category.
And so it goes. Booksellers do their best, and broadly we can say that there are science books, but on close scrutiny it’s a fuzzy definition at best. Certainly the books that sit on the shelf in a bookshop alongside this one you are holding are more likely to contain the words science, biology, and evolution and so on, than the ones in the cookbook section, and so could broadly be lumped together into an appropriate category. But some of them are going to be physics books, or math books. And you wouldn’t have to have gone far to the left or right on the shelf to encounter a “science” book crammed with pernicious unscientific flapdoodle. I do not know where the lines are drawn.
We do this all the time with all things. In art, there’s cubism and Dadaism and surrealism and public art and video installations and portraiture and photography. Politically we’re left wing or right wing or conservative or Conservative or liberal or libertarian. Films are westerns or science fiction or horror or rom coms. And woe betide my ex-girlfriend who said she didn’t like black and white films. It’s not that there aren’t measurable, quantifiable differences between all these categories we impose upon things, it’s just that for the most part they fit not into discrete units, but into a continuum. We are naturally plagued by the tyranny of a discontinuous mind, as Richard Dawkins so eloquently said.
The analogy works up to a point. It fails to recognize that certain genetic groupings do roughly correspond to geography. But not exclusively, and not essentially. The analogy does though satisfy the question of how many races there are: It is unanswerable. It is a meaningless question.
Yet it never goes away. The idea that Native Americans were genetically predisposed to alcoholism persists today, as it has done since the early days of the European occupation of the Americas. Thomas Jefferson wrote a letter in 1802 to an Iroquois chief praising the tribe’s decision to adopt abstinence from “spirituous liquors,” and going on to say “as you find that your people cannot refrain from an ill use of them, I greatly applaud your resolution not to use them at all.” Addiction is a staggeringly complex problem to understand as there are so many biological, social, and cultural factors to consider, including poverty, education, family history, and trauma experienced during childhood. And yes, genetics appears to play a role in about half the total risk for being alcohol addicted. But there’s no evidence that Native Americans have any versions of genes that metabolize alcohol any differently from white people in America, nor is there a simple single genetic factor that might render someone an alcoholic. There is plenty of evidence for brutal social and cultural experiences for many Native Americans, and generations of oppression, resulting in underemployment, poverty, and low socioeconomic status, all of which are risk factors for alcoholism. Yet, the notion that the high rates of alcoholism in Native Americans—almost twice as high as in white European immigrant Americans—are somehow genetic remains an oft-repeated idea.
In the 1880s, two doctors independently identified a new horrible disease, both of them finding it in Jewish families. In London, Waren Tay had spotted red dots in the retina of young children from a single Jewish family, and followed the disease progression through gradual nerve deterioration and death. Bernard Sachs also saw similar symptoms in New York, and proposed a name: amaurotic familial idiocy. The disease they were both seeing is now called Tay-Sachs and is well understood as a recessive disease caused by mutations in the HEXA gene. It’s a terrible syndrome in which the brain deteriorates over a short time in very young children, and they die soon. Within a few years of doctors Tay and Sachs characterizing their disease, children with identical symptoms had been described in Gentile families, but already, because Tay-Sachs was a “Jewish disease,” they were adjudged to have something different.
Tay-Sachs is not a Jewish disease. It’s seen at roughly the same frequency in Cajuns in Louisiana, and French Canadians in Quebec. There’s no such thing as a Jewish disease, because Jews are not a genetically distinct group of people. Certainly there will be higher levels of genetic similarity in families and in related groups, and indeed Tay-Sachs did for a long time have a higher frequency in Ashkenazi Jews than in some other groupings of people. But it’s not exclusive to Jews or Ashkenazi Jews or Sephardic Jews or Cajuns or any single identifiable group of people. Yet the myth persists. When talking about race and genetics in public, as I sometimes do, frequently the question will be asked, “What about Jewish diseases, such as Tay-Sachs?”
Here’s an irony: There has been a great deal of research into the genetics of Jewishness, much more than for many social groups. This is probably to do with a high proportion of Jewish geneticists and scientists in general, and the very unusual history of the Jewish people, whose diasporas and persecution have made them an interesting case study in the way genes and culture interact. Because of this interest, the prevalence of Tay-Sachs has been tackled. In Ashkenazi populations, which make up around a third of Jews in total, careful genetic counseling has effectively eradicated Tay-Sachs. I suppose you could call this a form of soft eugenics in its purest nonjudgmental sense. It was called a Jewish disease at first and that stuck, carried along by prejudice and ignorance. Now, because of an understanding of genetics and inheritance, it most certainly is not a Jewish disease at all.
In sport, similar ideas doggedly persist, despite science. There hasn’t been a white man in the Olympic 100 meters final since Allan Wells won in Moscow in 1980. African American athletes have provided thirteen of the top twenty speeds in the 100 meters in history (the other seven were also by black men, Canadian or Jamaican), and they boycotted the games that year, as the Cold War was as chilly as it would get. These types of numbers have fuelled a notion that the prowess and success of black people in sports is a biological, and therefore genetic advantage that they have over white athletes. Recall Jesse Owens standing on the podium of the 1936 Olympics in Nazi Germany having won the 100 meters in 10.3 seconds, and three other gold medals. Later, Dean Cromwell, the assistant coach to Owen’s team, would attribute this beautiful act of sporting defiance to a crude manifestation of biological destiny:
The Negro excels in the events he does because he is closer to the primitive than the white man. It was not long ago that his ability to sprint and jump was a life-and-death matter to him in the jungle.
The power of that victory in front of a racist murderous regime is sadly undermined by the racism that belittles the achievement itself. Attitudes such as these are extremely common within sports and in the public. Matthew Huey and Devon Goss, two sociologists from the University of Connecticut, forensically took apart a century of attitudes to sporting success of black people, and found that a genetic advantage was a persistent theme.* Throughout the twentieth century, theories arose that attempted to explain the apparently disproportionately high presence of successful black sportsmen. The most persistent is the idea that black people have a higher proportion of “fast twitch” muscle fibers, a type of subcellular protein that is involved with explosive movement.
Of course black is virtually meaningless for the purposes of this argument. The genes that confer skin pigmentation are few, but mask a level of deeper genetic variation within Africa than without. That a Namibian and a Nigerian have more similar skin color than either do to a Swede masks the fact that the majority of their genes are more dissimilar to each other than they are to that same Swede. So if the main classifier is skin color, the differences that underlie dark skin are too great to support an argument of generic athletic superiority. We know, for example, that in parts of Africa, notably the highlands of Ethiopia, many long-standing populations have genetic adaptations to living at altitude. In that specific regard, these people are more genetically similar to Tibetans than to any other Africans, all of whom we would collectively typically describe as black. But this characteristic is unusual in sub-Saharan Africans in general. All other things being equal (which of course they never are), my genetic ability to process oxygen via a gene called ACE is no different from most Africans, though not many East Africans. Similarly, a particular version of the gene alpha-actinin-3, which is associated with the fast-twitch muscle fiber, is present in successful black sprinters, but is not exclusive to Africans, or indeed any particular regional or cultural group within Africa. A thorough 2014 review by the Brazilian sports scientist Rodrigo Vancini of the scientific literature on the genetics of African athletes concluded that the studies of the variation in these two genes, the ones most frequently associated with black sporting success, “do not fully explain the success of these athletes. It seems unlikely that Africa is producing unique genotypes that cannot be found in other parts of the world.”
Part of the cultural argument is based around the possibility that slavery bred in these physical capabilities. The idea that underlies this assertion is that strength and physical prowess would be desirable in slaves, who would then be successful workers and thus procreate, and their genes passed on. This is a kind of “common sense” argument. But science is the opposite of common sense. It’s a set of methodological tools that attempt to extract objective reality from how we perceive it. Science sets aside the bias that we lug around, and separates what feels right from what is.
There are several problems with the idea that slavery bred superhumans. The first is that 400 years is not enough time to establish particular alleles with that effect. Ten or twelve generations might provide the time for the spread (or eradication) of an allele of great biological significance. But as with so many human behaviors, we’re not talking about a single gene of great impact. There are dozens of genes that are involved in the biology of sporting prowess, and these are not uniformly distributed across competitors of different sports: Sprinters do not make good long-distance runners. The second problem is that I am unaware of any data that has analyzed positive selection for these alleles in black people with slave ancestry. Without this, assertions of slavery being effectively a program of selective breeding are merely vaguely racist wish-fulfilment, confirmation bias, or yet another form of adaptationism.
Physical characteristics obviously do play essential roles in sporting success. The average height of an NBA basketball player is six feet seven inches, where being tall is obviously quite handy. Conversely, in horse racing, a sport dominated by white people, jockeys are typically small and light, broadly in accordance with Newtonian rules about speed and mass. Height is heavily influenced by genetics, but these numbers are nothing to do with race, as viewed through the lens of skin color or continental origin. The Dutch are the tallest people on average on Earth, and I have little doubt that if there were similar numbers of Dutch people as there are Americans, and basketball was as culturally important and ubiquitous, then they would produce teams as good as the LA Lakers.
Sport is sometimes cited as the great leveler, a forum in which only talent and sheer grit will win the day. The idea that black people are better at sport because of genetics, and possibly because of breeding during the wicked centuries of slavery, is built upon tissue foundations, and its cultural ubiquity yet another example of the chasm between what we think, and what science says is true.
Some look to the migration and history of our species as a means of suggesting and reinforcing a biological basis for the existence of race. There was, for a time, discussion about where modern humans originated. The question was whether we all spurted out of Africa as one species and grew into the current forms of Homo sapiens we see today, or whether earlier Homos had positioned themselves around the world in earlier migrations, and we have evolved into the current forms from those founding parents. This is known as the “multiregional hypothesis,” but it has been almost universally rejected for many years. The bones don’t say that; they show that the physical differences displayed in the living and the long dead are not significant enough to warrant classifying anyone living on Earth as having had a different route to the present. There are no physical or biological barriers to reproduction for anyone fertile on Earth either; an Aboriginal Australian could happily produce fertile children with an Aboriginal South American, or with anyone in Africa, despite the furthest genetic distance between them that we observe.
In the last couple of years, we’ve seen the addition of a nuance to the preeminently dominant Out of Africa hypothesis via the new ancient genetics discussed in Chapter 1. Modern humans clearly successfully interbred with both Neanderthals and Denisovans, and we carry their DNA to this day. These are not the emergence of other species of humans, but the incorporation of other species into our own. Their genetic contribution to us is not insignificant, and in some cases has furnished modern humans with some specific characteristics that otherwise we would not have. But these contributions are not enough, and not specific enough, to successfully feed into an argument that puts the broad colloquial definitions of race as separate evolutions. Mobility of human species and our excellence at sex have placed the common origin of all humans alive at only 3,400 years ago, or thereabouts. This means that the genetic bases of the characteristics that we class as racial are modern.
I believe that we don’t have the language that allows us to align how we talk about race and what genetics and evolution has shown. Genetics has revealed that human variation and its distribution across the planet is more complex and demands more sophisticated squinting than any attempts to align it with crude and ill-defined terms like race, or even black, or white. It is for this reason that I am comfortable stating that from the point of view of a geneticist, race does not exist. It has no useful scientific value.
In science we crave precision, in measurement and in language. The urge to categorize is very human, and much sought after in science. We don’t have a definition of life; we have inadequate definitions of species. Life does its best to undermine our noble attempts to categorize living and the living—this is what makes it exciting. Yes, variation that we see when measured by scrutiny of the genome broadly matches large landmasses, but even with oceans as barriers, these boundaries are not sharp, and still only account for a fraction of the differences between individuals. To establish these differences between people and peoples may yet have some value in terms of understanding diseases whose penetrance is unevenly distributed across all humans, and has focus on particular populations.
But again, this does not align with the popular concept of race. That, of course, does not mean the racism doesn’t exist. It’s a special thing to experience. Unlike millions, my life has not been blighted by persecution drawn from the tiny fraction of DNA that makes a person look different. But it is difficult to comprehend if you haven’t experienced it. It was trivial in my case, but those experiences set a fire that burns and burns. Genetics has shown that the conflict is with people, and not embedded in biology.
Though Darwin did not discuss humans in On the Origin of Species, his second greatest work, The Descent of Man, was devoted to it. He had seen many of the indigenous populations of the world during his travels on the Beagle, and considered their physical traits carefully. He speaks of races and subspecies, using the language of the era, and embracing soft definitions that we no longer can support:
But since he attained to the rank of manhood, he has diverged into distinct races, or as they may be more fitly called sub-species. Some of these, such as the Negro and European, are so distinct that, if specimens had been brought to a naturalist without any further information, they would undoubtedly have been considered by him as good and true species.
Darwin had used that emotive word race in On the Origin of Species to describe the varieties of types of living thing, “including the several races, for instance, of the cabbage.” But central to his big idea was a recognition of the constant flow of creatures through time, and in 1871 in The Descent of Man, with great, possibly typical, prescience, he also acknowledged that those characters of race in manhood were neither permanent, nor quintessential:
It may be doubted whether any character can be named which is distinctive of a race and is constant.
Not for the first time, genetics has confirmed what Darwin suspected. These were suspicions based on observations, with no concept of the mechanisms of inheritance that would follow him, many of which emerged from the work of his half cousin. Ironically, Galton enacted his own minor form of eugenics. He was married to Louisa Butler until the day he died, but they had no children, and his genetic makeup would not be passed on down the ages.
Galton’s racial definitions are no longer defensible, and indeed none of the ways in which we talk about race today stands up to the scrutiny that genetics has enabled. Families are too untidy, human history is too convoluted, people too motile. The deck has been shuffled and reshuffled. Genetics has shown that people are different, and these differences cluster according to geography and culture, but never in a way that aligns with the traditional concepts of human races. Sometimes in this argument people might say “colors are just social constructs, but you can’t deny that they exist.” It is true that what we call “blue” is merely a convention for what we experience when visible light at a wavelength between 450 and 495 nanometers from the electromagnetic spectrum is processed first in our retinae and then brain. However, the electromagnetic spectrum is continuous, and these arbitrary markers are useful descriptions of what we experience. Human variation is continuous wherever we look too, but unlike light, not in a single line. People do lump together when we look at any single characteristic, and sometimes when we look at multiple traits. But we could equally look at other characteristics within the same groups and find different clustering patterns, and these are never fixed in a population, because populations are not fixed. The Jews once had high (but not exclusively high) rates of Tay-Sachs disease. Now they do not. Some Jews have ginger hair and pale skin, just like plenty of Scots. Others do not. The skin tone of the people of the Andaman Islands is very similar to that of the people of central Africa, but they acquired that hue via different historical and biological routes. Some black Africans are evolved to process oxygen at high altitudes, as are some Tibetans, but most are not. “Black” is no more a race than “long-distance runner” is.
We don’t have to like people to accept that they were correct, or wrong, but Galton remains a tricky fish. Much of his science was utterly brilliant. Much of his insight was equally dazzling. Many of his opinions were horrid. It seems much of his motivation for doing science was born of these ugly views. Science is a process that strives to excise our limited view of the universe and our inbuilt prejudices from understanding an objective reality. Things are often not as they appear to us, but we invented and developed the scientific process to correct our subjective failings: Data is king. Francis Galton’s inclination toward being a data junkie led him to instigate a science that he hoped would affirm his prejudices. The beautiful irony is that it did precisely the opposite.