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Sickle Cell Regents Lesson adapted from Cristina's materials

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Sickle Cell Regents Lesson adapted from Cristina's materials

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https://docs.google.com/document/d/1bhlQ7MJ1V4wi5Gfqwu1vFE-rpl5mwnq7WPVgFoh1AMQ/edit?usp=sharing

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Fall 21 Session 2 Using Biology Class to Promote Racial Justice PLT

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Humane Genetics Summer Institute (BSCS) Reading List

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Humane Genetics Summer Institute (BSCS) Reading List

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data info

Significant Maritime and Industrial Areas

Half-mile buffer to SMIAs

Click the map to explore a neighborhood, or search with the bar below. Click on the map icon on the right to toggle displayed data.

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data info Significant Maritime and Industrial Areas Half-mile buffer to SMIAs Click the map to explore a neighborhood, or search with the bar below. Click on the map icon on the right to toggle displayed data.

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Fight Toxins in Schools
Unfortunately, many children face their highest risks of environmental poisoning in what should be the safest of all venues: at school. A 2001 study by the Center for Health, Environment and Justice entitled "Kids at Risk-Toxic Schools: Creating Safe Learning Zones" revealed that more than 600,000 mostly poor and minority-group students in Massachusetts, New York, New Jersey, Michigan, and California were attending nearly twelve hundred public schools located within half a mile of a federal Superfund- or state-identified contaminated site (2). Contact the EPA if you are concerned that your child's school may be one of them.

In large cities like New York and small communities like Anniston, schools as well as homes have been found to have harbored noxious, brain-damaging chemicals and heavy metals like lead. Because children spend so much time in schools, such environments require attention and immediate detoxification.

Unfortunately, you cannot always rely upon the school administrators to assume leadership. In New York City, school administrations hid their schools' lead contamination by deliberately misleading investigators and workers who were sent to test school lead levels (3). If you ask for information about contamination issues in your child's school and do not receive answers, be prepared to persist and to go higher. The EPA offers information about attaining a lead-free school here.

There is power in numbers, so try to recruit other parents in your search for answers and solutions. Start at the EPA. Its guide to training testing and its "Guide for Community Partners," a blueprint for organizing, can be downloaded here.
Poison-Proof Your Home
You cannot eliminate all sources of toxic exposure, but there are steps you can take to reduce and minimize exposures to environmental poisons within your home.

Air quality. If you live in an area plagued by heavy industrial emissions, the air quality in your home is not completely under your control, but you can improve it. If you can afford to, keep your doors and windows closed and use your air conditioner to minimize emissions, at least during high-traffic hours. Some energy companies and cities have home-energy rebate programs to assist with bills.

Vermin control. Cockroaches and dust mites worsen asthma; rodents carry pathogens that may encourage hypertension, which is linked to lowered cognition. To remove them, hire a professional exterminator and follow his advice to keep these unhealthy visitors at bay. If you rent, check your municipal codes or with the local housing authority or Legal Aid to determine your rights as a renter. Usually it is the landlord's responsibility to ensure vermin-free housing, so she must pay for extermination.

Vacuuming. Use a HEPA vacuum often to minimize your family's exposure to tracked-in toxic substances, dust mites, cockroach parts, and other vermin.

Cleaning supplies. Many cleaners contain volatile toxic chemicals such as halogenated hydrocarbons that harm the lungs and present neurotoxic threats that harm the brain. Others, such as bleach and ammonia, or bleach and various acids, become poisonous when mixed together. Read labels, and whenever possible, choose cleaners that do not contain a long list of chemicals - many are hydrocarbons or poisons that are readily absorbed through the skin.

Diluted bleach (which should always be handled with care), simple detergents, and ammonia can be used, separately, for many household cleaning jobs and are far more economical than complex specialized cleaners. But always use gloves and handle bleach carefully, because it can cause a lot of damage if it's splashed on the body or if it gets in the mouth or eyes.

All cleaning products should be stored in locked, child-safe cabinets: a bad taste will not deter toddlers from sampling these poisons.

Many people use essential oils in cleaning, but these are sometimes toxic as well. Some should not be used by pregnant women, and they can be expensive. For a useful description of low-toxicity cleaning options, see Less Toxic Living: How to Reduce Your Everyday Exposure to Toxic Chemicals-An Introduction for Families, by Kirsten McCulloch (4).

Paper masks. Use paper masks during periods of highest exposure to poor air quality. This might include outdoor activities near toxics-spewing factories, riding the subway in an area of substandard air quality, or outdoor tasks that may heighten your exposure to polluted soil, air, or other pollution "hot spots." Recall the story from Chapter 3 of Shirley Baker, who donned a paper mask to mow her toxics-soaked lawn. City dwellers should emulate commuters in heavily polluted Asian cities who are frequently seen wearing masks on public transportation. Studies show they indeed offer some protection against not only pollutants but also some communicable diseases like the flu and colds.

Shoes. Lead, industrial chemicals, animal dander, pesticides, chemical dust, pathogens, and a wide assortment of uninvited visitors can hitch a ride into your home on the soles of your shoes. Consider leaving your shoes at the door and going shoe-less inside or trading your shoes for flip-flops when you enter. And ask your guests to do the same. But avoid walking barefoot outside, where you can absorb pollutants through your skin and pick up parasites, including hookworms, which have been demonstrated to sap intelligence and are making a resurgence in parts of the United States.

________

(4) Kirsten McCulloch, Less Toxic Living: How to Reduce Your Everyday Exposure to Toxic Chemicals - An Introduction for Families(Canberra, Australia: Green Gables Press, 2013)

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Fight Toxins in Schools Unfortunately, many children face their highest risks of environmental poisoning in what should be the safest of all venues: at school.

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Google Form Lesson: Race and Skin Color 

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Google Form Lesson: Race and Skin Color 

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This goes with the HHMI Biology of Skin Color Video. Click to make a copy of the form: https://docs.google.com/forms/d/10zRuLg-SLlfGWguQtp5Ak8p4czyXPcxOlcrQ4MutgM8/copy

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Google Form Lesson: Single Gene Traits and Race

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Google Form Lesson: Single Gene Traits and Race

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Click to make a copy for yourself: https://docs.google.com/forms/d/1dIZGR9-bC0lFPSKU1yC9684HFX9ppmGA8nf26ttA8PU/copy

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https://www.spps.org/cms/lib/MN01910242/Centricity/Domain/125/racialautobiographyprompts.pdf

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AMNH Genetics Lab Grade 9-12 (45-60 min)

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AMNH Genetics Lab Grade 9-12 (45-60 min)

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Teacher Guide

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AMNH Teacher guide Genetics and Human Variation Student Activity Worksheet

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AMNH Human Evolution Lab Grades 6-8 (30-45 min)

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AMNH Human Evolution Lab Grades 6-8 (30-45 min)

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Teacher Guide

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AMNH Human Evolution Lab 6-8 Teachers Guide

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AMNH Virtual Field Trip around Human Evolution

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AMNH Virtual Field Trip around Human Evolution

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Virtual field trip for Hall of Human Origins--teacher's guide, tour link, and student worksheet.

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Fall 21 Using Biology Class to Promote Racial Justice  - Session 1

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The Most Searched: A Celebration of Black History Makers

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The science of skin color - Angela Koine Flynn

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This three-part documentary by California Newsreel is important for understanding the history of racialization in America and how racial categories came about that we often innacurately equate with biology. InterVarsity has purchased the rights to stream this documentary online for three years.

Race: The Power of an Illusion

( From California Newsreel)

"The division of the world's peoples into distinct groups - 'red,' 'black,' 'white' or 'yellow' peoples - has became so deeply imbedded in our psyches, so widely accepted, many would promptly dismiss as crazy any suggestion of its falsity. Yet, that's exactly what this provocative, new three-hour series by California Newsreel claims. Race - The Power of an Illusion questions the very idea of race as innate biology, suggesting that a belief in inborn racial difference is no more sound than believing that the sun revolves around the earth.

Yet race still matters. Just because race doesn't exist in biology doesn't mean it isn't very real, helping shape life chances and opportunities."
These clips contain some graphic images and sensitive content. Visit the documentary website for more resources.

Episode 1- The Difference Between Us

This episode examines the contemporary science - including genetics - that challenges our common sense assumptions that human beings can be bundled into three or four fundamentally different groups according to their physical traits.

Episode 2- The Story We Tell

Lean about the roots of the race concept in North America, the 19th century science that legitimated it, and how it came to be held so fiercely in the western imagination. The episode is an eye-opening tale of how race served to rationalize, even justify, American social inequalities as "natural."

Episode 3- The House We Live In

If race is not biology, what is it? This episode uncovers how race resides not in nature but in politics, economics and culture. It reveals how our social institutions "make" race by disproportionately channeling resources, power, status and wealth to white people.

By asking, What is this thing called 'race'?, a question so basic it is rarely asked, Race - The Power of an Illusion helps set the terms that any further discussion of race must first take into account. Ideal for human biology, anthropology, sociology, American history, American studies, and cultural studies.

Additional Resources from California Newsreel

Film Discussion Guide Race Literacy Quiz

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Race: The Power of an Illusion Documentary

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This three-part documentary by California Newsreel is important for understanding the history of racialization in America and how racial categories came about that we often innacurately equate with biology. InterVarsity has purchased the rights to stream this documentary online for three years.

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https://www.amazon.com/Darwins-Sacred-Cause-Slavery-Origins/dp/0226144518/ref=sr_1_1?dchild=1&keywords=darwin%27s+sacred+cause&qid=1622067973&sr=8-1

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NY Times article on Darwin's Sacred Cause

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NY Times article on Darwin's Sacred Cause

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Introduction
Unshackling Creation

Global brands don't come much bigger than Charles Darwin. He is the grizzled grandfather peering from book jackets and billboards, from textbooks and TV - the sage on greeting cards, postage stamps and commemorative coins. Darwin's head on British £10 notes radiates imperturbability, mocking those who would doubt his science. Hallow him or hoot at him, Darwin cannot be ignored. Atheists trumpet his 'atheism', liberals his 'liberalism', scientists his Darwinism, and fundamentalists expend great energy denouncing the lot. All agree, however, that for better or worse Darwin's epoch-making book On the Origin of Species transformed the way we see ourselves on the planet.

How did a modest member of Victorian England's minor gentry become a twenty-first-century icon? Celebrities today are famous for being famous, but Darwin's defenders have a different explanation.

To them Darwin changed the world because he was a tough-minded scientist doing good empirical science. As a young man, he exploited a great research opportunity aboard HMS Beagle. He was shrewd beyond his years, driven by a love of truth. Sailing around the world, he collected exotic facts and specimens - most notably on the Galapagos islands - and followed the evidence to its conclusion, to evolution. With infinite patience, through grave illness heroically borne, he came up with 'the single best idea anyone has ever had' and published it in 1859 in the Origin of Species. This was a 'dangerous idea' - evolution by 'natural selection' - an idea fatal to God and creationism equally, even if Darwin had candy-coated this evolutionary pill with creation-talk to make it more palatable. Evolution annihilated Adam; it put apes in our family tree, as Darwin explained in 1871 when he at last applied evolution to humans in The Descent of Man. Secluded on his country estate, publishing book after ground-breaking book, Darwin cut the figure of a detached, objective researcher, the model of the successful scientist. And so he won his crown.

The most that can be said for this caricature is the number of people who credit it. Not only evolutionists and secularists, but many creationists and fundamentalists see Darwin's claim to fame - or infamy - in his single-minded pursuit of science. Doggedly, some say obstinately, he devoted his life to evolution. A zeal for scientific knowledge consumed him, keeping him on target to overthrow God and bestialize humanity. Brilliantly, or wickedly, Darwin globalized himself. By following science and renouncing religion, he launched the modern secular world.

This isn't just simplistic; most of it is plain wrong. Human evolution wasn't his last piece in the evolution jigsaw; it was the first. From the very outset Darwin concerned himself with the unity of humankind. This notion of 'brotherhood' grounded his evolutionary enterprise. It was there in his first musings on evolution in 1837.

Today we are beset by polemics of every stripe, comic attempts to pummel Darwin into this shape or that, to convict or acquit Darwin of beliefs - atrocities even - associated with his name. (A recent title about German history says it all: From Darwin to Hitler.)

To reverse Marx's dictum for a moment: the point is not to change Darwin, the point is to understand him. Darwin was neither saint nor satan. Looked at in his own day, he was complex, sometimes even contradictory, never quite as one imagined, but vastly more interesting and informative. And the real story behind his journey to evolution - human evolution - is much richer than anyone realizes. It is a story we have been piecing together for years, trying to grasp what could have made this gentle naturalist such an anomaly in his age, and so determined in the face of overwhelming odds.

Darwin was the most gentlemanly gentleman anyone had ever met. He was diffident, afraid to ruffle feathers, at home with the conservative Anglican dons, wanting only his own quiet vicarage lifestyle, away from urban tumult and religious harangues. The dons he emulated detested a bestial human evolution - so hysterically that the Cambridge cleric who taught him geology talked of stamping with 'an iron heel upon the head of the filthy abortion' to 'put an end to its crawlings'. Yet even as Darwin listened to his mentors after the Beagle voyage, he was privately musing on a missing 'monkey-man', our ancestor. How could this be? What drove him to deny the cherished tenets of his privileged Christian society? Surely it had to be some overwhelming impulse that outweighed all others, pitching Darwin into words and deeds that frightened even him.

People have been looking in the wrong place for the answer. With the opening up of Darwin's treasure trove of unpublished papers over the past generation, the clues began to appear - some were even there in his most famously little-read book The Descent of Man, and Selection in Relation to Sex (to give its full and telling title). But this was the end point of Darwin's journey, and its contents have so confused readers that they even now call it 'two books' on different subjects, sex and ancestry, and so miss the point entirely. Darwin's human project remains obscure. But it is foundational, and without understanding it, we cannot understand why Darwin came to evolution at all.

'Roots' is where we begin, Roots as in Alex Haley's stirring historical novel - the enslavement of black Africans that so outraged Darwin's generation. It was Darwin's starting point too, his abhorrence of racial servitude and brutality, his hatred of the slavers' desire, as he jotted, to 'make the black man [an]other kind', sub-human, a beast to be chained. Roots were what Darwin's human project was all about. And to understand why he started thinking about the roots - the origin - of black and white races, we have to appreciate his moral anchorage in the noontide of the British anti-slavery movement. It is the key to explain why such a gentleman of wealth and standing should risk all to develop his bestial 'monkey-man' image of our ancestry in the first place.

Always retiring, often unwell, Darwin never threw himself into abolitionist rallies and petitions (as his relatives did). While activists proclaimed a 'crusade' (his word) against slavery, he subverted it with his science. Where slave-masters bestialized blacks, Darwin's starting point was the abolitionist belief in blood kinship, a 'common descent'. Adamic unity and the brotherhood of man were axiomatic in the anti-slavery tracts that he and his family devoured and distributed. It implied a single origin for black and white, a shared ancestry. And this was the unique feature of Darwin's peculiar brand of evolution. Life itself was made up of countless trillions of sibling 'common descents', not only black and white, but among all races, all species, through all time, all joined up in bloodlines back to a common ancestor.

It was in Darwin's most generous, relativistic phase, at the height of Britain's radical political period in the late 1830s, when the slaves in the colonies were finally freed, that he extended the kinship to all groaning, degraded, disparaged races of animals. He saw them sharing our own deep ancestry; 'we may all be netted together', we may all feel a common pain, he jotted in a notebook. He had saved the blacks, stopped the slaves being seen as some 'other kind'. But by embracing the whole of creation - breaking life's shackles and allowing it too to evolve, as black and white men had done from a joint ancestor - he ironically opened himself to vilification by the Christian world whose belief in racial brotherhood he shared. A major criticism of the Origin of Species (particularly during the American Civil War) was that Darwin had now bestialized the white man, by contaminating his ancestral blood. Darwin had upturned the racist logic, only to 'brutalize' his own Anglo-Saxon kind (as it was said), uniting them, not only with black people, but with black apes.

Here was Darwin at his most paradoxical. And in this impasse lies the moral of our story, literally. Rather than seeing 'the facts' force evolution on Darwin (other circumnavigating naturalists had seen similar phenomena all over the globe), we find a moral passion firing his evolutionary work. He was quite unlike the modern 'disinterested' scientist who is supposed (supposed, mark you) to derive theories from 'the facts' and only then allow the moral consequences to be drawn. Equally, he was the reverse of the fundamentalists' parody, which makes his enterprise anti-God, inhuman and immoral. We show the humanitarian roots that nourished Darwin's most controversial and contested work on human ancestry. The ensuing picture is, as a result, dramatically different from previous ones, revealing a man more sympathetic than creationists find acceptable, more morally committed than scientists would allow.

Our reconstruction of Darwin's trajectory - lighting the path he trod after returning with the Beagle, through his private notes and drafts to the Origin itself - finally explains some of his otherwise anomalous statements. Reading the greatest one-origin-for-all-the-races work, by an anti-slavery advocate (James Cowles Prichard's Researches into the Physical History of Mankind), Darwin scribbled, 'How like my Book all this will be.' 'My Book' was of course what became the Origin of Species. And, as this suggests, it too was meant to discuss mankind. The irony is that the Origin ultimately said next to nothing about human origins. Explanations of the human races and of an ape ancestry were dropped at the last moment.

Why, in the book that critics knew was really about mankind, had Darwin decided to say next to nothing on the subject? And why was he forced to come clean twelve years later and write the Descent of Man, and then incongruously fill the book with butterflies and pigeons and 'sexual selection'? Sexual selection is critical to our reading of Darwin's morally-fired 'human brotherhood' approach; it was central and critical, too, in Darwin's answer to the American South's (and London's) proslavery pundits who proclaimed the black and white races as separate species. Understand Darwin's strategy, and the oddities of his books and their anomalous timing make sense.

Today Darwin is the 'scientist' to reckon with. His theories about people and society are debated more widely than ever. The media buzzes with stories about evolutionary psychology, sociobiology and eugenics, about gender, race and sex differences and the possibility of improving human nature.

Some choose to emphasize the darker side to Darwin's evolution, notoriously hinted at in the Origin's subtitle: The Preservation of Favoured Races in the Struggle for Life. From Albania to Alabama, from Russia to Rwanda, Darwin's theories have been used to justify racial conflict and ethnic cleansing. Perpetrators of the worst atrocities have seen themselves as 'favoured races' surviving Darwin's bloody 'struggle'. And so an ocean of ink has been spilt to prove that none of this was in Darwin's works, nor was it a logical consequence. Darwin's was a pure, untainted science.

We aren't out to prove the uncorrupted purity of Darwin's corpus, or indeed deify his corpse. Nor do we celebrate any unsavoury consequences of his work, or coerce him into siding with religious groups or atheists. We undercut all of these contrasting attempts to hijack Darwin for today's ends. The real problem is that no one understands Darwin's core project, the nucleus of his most inflammatory research. No one has appreciated the source of that moral fire that fuelled his strange, out-of-character obsession with human origins. Understand that and Darwin can be radically reassessed.

In sounding the depths of Darwin's anti-slavery we have exploited a wealth of unpublished family letters and a massive amount of manuscript material. We use Darwin's notes, cryptic marginalia (where key clues lie) and even ships' logs and lists of books read by Darwin. His published notebooks and correspondence (some 15,000 letters are now known) are an invaluable source: sixteen of the projected thirty-two volumes of The Correspondence of Charles Darwin have already been published by an international team whose deciphering and transcribing can only be called heroic. Add to this the extraordinary growth of historical studies on transatlantic race, racism and slavery, and we are equipped to connect Darwin for the first time with the most forceful moral movement of his age.

The discovery and recovery of Darwin's letters is still something of a rolling revolution. Even as we write new ones are turning up - not least, from the son of the most famous 'immediatist' abolitionist in the world, the American William Lloyd Garrison. It confirms what we had come to suspect, that Darwin was an admirer of the most uncompromising, non-violent Christian leader in the anti-slavery movement. Garrison was, in Darwin's words, 'a man to be for ever revered'. Darwin was overjoyed on hearing that the blistering anti-slavery passage in his Beagle journal had been read to the elderly Garrison, whose son reported to Darwin how it shed 'a new and welcome light on your character as a philanthropist'. To think, Darwin replied, that a man 'whom I honor from the bottom of my soul, should have heard and approved of the few words which I wrote many years ago on Slavery'. This correspondence shows how much is still to be learned about Darwin.

Not only is the evolutionary upshot of his hatred of slavery unknown, Darwin's humanitarian imperative itself has never been brought adequately to the fore. We try to show how it locks him into the context of nineteenth-century abolitionism, and how it speaks directly to our post-colonial age, with its hatred of ethnic cleansing and apartheid. Ours is a book about a caring, compassionate man who was affected for life by the scream of a tortured slave.

Finally, a word about terminology. Although 'scientific racism' is said to start about 1860 - taking over from an earlier xenophobia - we believe that such a hard-and-fast line is problematic. If 'racism' is taken to mean categorizing difference in order to denigrate, control or even enslave, then its scientific components and rationale can be traced much earlier. It is generally unknown that American slavery-justifying race-agitators were actually booming their hatreds as early as 1841 at the British Association for the Advancement of Science. Even before that they were linking subjugation to the anatomical 'inferiority' of blacks. These ideologies and slaving justifications bathed the cultural debates embroiling Darwin throughout the 1840s and 1850s, and we think that 'racism' is an acceptable historical term in Darwin's context.

We must add to this an apology for our ethnological faux pas. All the actors in our story - Darwin included - held derogatory views of other peoples to some extent, and used terms to match. While we try at times to mention the modern self-appellations of peoples, it would be confusing to mix Darwin's and modern ones, and so we have stuck to contemporary usages in most places. That goes for inclusive language also. We use a mix of contemporary and modern terms for Homo sapiens: 'man', 'mankind', 'humankind', 'humanity' and 'human beings'. Of course we regard such terms, along with 'savages', 'Kaffirs', 'Bantu', 'Hottentot' and so on, together with 'race' and ethnic labels generally, as historically constructed, but it would be tedious to place them in inverted commas every time; so also 'Negro', a respectful period-term for black people, and 'mulatto', a negative term.

This, then, is the untold story of how Darwin's abhorrence of slavery led to our modern understanding of evolution.

(Continues...)
Excerpted from Darwin's Sacred Cause by Adrian Desmond James Moore Copyright © 2009 by Adrian Desmond and James Moore. Excerpted by permission. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher. Excerpts are provided by Dial-A-Book Inc. solely for the personal use of visitors to this web site.

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'Darwin's Sacred Cause' (Published 2009)

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Introduction Unshackling Creation Global brands don't come much bigger than Charles Darwin. He is the grizzled grandfather peering from book jackets and billboards, from textbooks and TV - the sage on greeting cards, postage stamps and commemorative coins. Darwin's head on British £10 notes radiates imperturbability, mocking those who would doubt his science.

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Lactose intolerance is "an impaired ability to digest lactose, a sugar found in milk and other dairy products," according to the National Institutes of Health (NIH).

Lactose intolerance in infants is caused by a mutation in the LCT gene, which results in a life-long intolerance. This condition is inherited, rare, and most common in Finland.

In adults, lactose intolerance is caused by normally decreasing activity of the LCT gene, which means adults may experience increasing inability to digest lactose as they age. About 65% of the adult human population has this sort of lactose intolerance, which results in abdominal pain and other gastrointestinal consequences after eating dairy products.

According to the NIH, in adults lactose intolerance shows up most often in people of East Asian heritage, affecting 70 to 100% of the population. Encyclopaedia Britannica adds that the condition affects about 75 to 90% of Native Americans, Black people, Asians, Mediterraneans, and Jewish people. Only about 5% of Northern and Central Europeans have lactose intolerance.

Sources:

Kelli Glaser, "Lactose Intolerance: Pathology," britannica.com (accessed Mar. 25, 2020)

National Institutes of Health US National Library of Medicine, "Lactose Intolerance" ghr.nlm.nih.gov, Mar. 17, 2020
Global Prevalence of Lactose Intolerance by Country
(percent of country's population with lactose intolerance)

Source: Christian Løvold Storhaug, Svein Kjetil Fosse, and Lars T Fadnes, "Country, Regional, and Global Estimates for Lactose Malabsorption in Adults: A Systematic Review and Meta-Analysis," thelancet.com, Oct. 1, 2017

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Lactose Intolerance by Country - Milk - ProCon.org

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Lactose intolerance is "an impaired ability to digest lactose, a sugar found in milk and other dairy products," according to the National Institutes of Health (NIH). Lactose intolerance in infants is caused by a mutation in the LCT gene, which results in a life-long intolerance. This condition is inherited, rare, and most common in Finland.

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This book has a great article called "Why does the sun make our skin darker, but our hair lighter" which I use to engage students and introduce melanin

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How Science and Genetics are Reshaping the Race Debate of the 21st Century

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How Science and Genetics are Reshaping the Race Debate of the 21st Century

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https://sitn.hms.harvard.edu/flash/2017/science-genetics-reshaping-race-debate-21st-century/

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There is little difference in reluctance to take the coronavirus vaccine among Black and white people in the U.S., according to the latest NPR/PBS NewsHour/Marist survey.

Among those who responded to the survey, 73% of Black people and 70% of White people said that they either planned to get a coronavirus vaccine or had done so already; 25% of Black respondents and 28% of white respondents said they did not plan to get a shot. Latino respondents were slightly more likely to say they would not get vaccinated at 37%, compared with 63% who either had or intended to get a vaccine.

The findings come amid concerns in some states over who is getting vaccinated and who is not, with data in some states suggesting stark racial disparities. The pandemic has had an outsized impact on people of color, especially Black Americans.

The survey of 1,227 adults was conducted March 3 to 8. Respondents were contacted on mobile and landline phones by callers who conducted interviews live in English and Spanish. The poll has a margin of error of 3.4 percentage points, with greater statistical variation possible among subgroups.

Horace Hill, a 61 year old Black man from Tulsa, Okla., said he had an appointment to get his first dose of the coronavirus vaccine on Friday.

He said his health is a high priority for him, and hasn't had issues with the traditional flu vaccine, and so he decided to take the shot when it became available to him.

His parents, who are in their eighties, received their vaccines about two weeks ago.

"I asked them specifically, 'Have you guys had any problems?' " Hill said. "My father was like, 'No, your mother and I, we feel good!' "

Overall, 67% of people said they had either planned to get a coronavirus vaccine, or had done so already. Thirty percent said they did not plan to get a shot.

While there was little racial difference in who wants the vaccine, there were sharp partisan differences, according to the poll.

Among Republican men, 49% said they did not plan to get the shot, compared with just 6% of Democratic men who said the same. Among those who said they supported President Trump in the 2020 election, 47% said they did not plan to get a coronavirus vaccine compared with just 10% of Biden supporters.

Similarly, compared with "big city" respondents, rural residents were more likely to say that they did not plan to take a coronavirus vaccine.

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Little Difference In Vaccine Hesitancy Among White And Black Americans, Poll Finds

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There is little difference in reluctance to take the coronavirus vaccine among Black and white people in the U.S., according to the latest NPR/PBS NewsHour/Marist survey.

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For months, journalists, politicians and health officials - from New York Gov. Andrew Cuomo to Dr. Anthony Fauci - have invoked the infamous Tuskegee syphilis study to explain why Black Americans are more hesitant than white Americans to get the coronavirus vaccine.

"It's 'Oh, Tuskegee, Tuskegee, Tuskegee,' and it's mentioned every single time," says Karen Lincoln, a professor of social work at USC and founder of Advocates for African American Elders. "We make these assumptions that it's Tuskegee. We don't ask people."

When she asks Black seniors in Los Angeles about the vaccine, Tuskegee rarely comes up. People in the community talk about contemporary racism and barriers to health care, she says, while it seems to be mainly academics and officials who are preoccupied with the history of Tuskegee.

" It's a scapegoat," Lincoln says. "It's an excuse. If you continue to use it as a way of explaining why many African Americans are hesitant, it almost absolves you of having to learn more, do more, involve other people - admit that racism is actually a thing today."

It's the health inequities of today that Maxine Toler, 72, hears about when she asks her friends and neighbors in LA what they think about the vaccine. Toler is president of her city's senior advocacy council and her neighborhood block club. She says she and most of the other Black seniors she talks with want the vaccine, but are having trouble getting it. And that alone is sowing mistrust, she says.

Toler says the Black people she knows who don't want the vaccine have very modern reasons for not wanting it. They talk about religious beliefs, safety concerns or distrust for former U.S. president Donald Trump and his contentious relationship to science. Only a handful mention Tuskegee, she says, and when they do, they're fuzzy on the details of what happened during the 40-year study.

"If you ask them what was it about, and why do you feel like it would impact your receiving the vaccine, they can't even tell you," she says.

Toler knows all the details, but she says that history is a distraction from today's effort to get people vaccinated against the coronavirus.

"It's almost the opposite of Tuskegee," she says. "Because they were being denied treatment. And this is like, we're pushing people forward: Go and get this vaccine. We want everybody to be protected from COVID."
Questioning the Modern Uses of The Tuskegee Legacy
The "Tuskegee Study of Untreated Syphilis in the Negro Male" was a government sponsored, taxpayer-funded study that began in 1932. Some people believe that researchers injected the men with syphilis, but that's not true. Rather, they recruited 399 Black men from Alabama who already had the disease.

Researchers told the men they had come to Tuskegee to cure "bad blood," but never told them they had syphilis, and the government doctors never intended to cure the men. Even when an effective treatment for syphilis - penicillin - became widely available in the 1940s, the researchers withheld it from the infected men and continued the study for decades, determined to track the disease to its end point: autopsy.

By the time the study was exposed and shut down in 1972, 128 of the men involved had died from syphilis or related complications, and 40 of their wives and 19 children had become infected.

With a horrific history like this, many scientists assumed that Black people would want nothing to do with the medical establishment again, particularly clinical research. Over the next three decades, various books, articles, and films repeated this assumption until it became gospel.

"That was a false assumption," says Dr. Rueben Warren, director of the National Center for Bioethics in Research and Health Care at Tuskegee University in Alabama, and former associate director of Minority Health at the Centers for Disease Control and Prevention from 1988 to 1997.

A few researchers began to question this assumption at a 1994 bioethics conference, where almost all the speakers seemed to accept it as a given. The doubters asked, what kind of scientific evidence is there to support the notion that Black people would refuse to participate in research because of Tuskegee?

When those researchers did a comprehensive search of the existing literature, they found nothing.

"It was apparently a 'fact' known more in the gut than in the head," wrote lead doubter Ralph Katz, an epidemiologist at the NYU College of Dentistry.

So Katz formed a research team to look for this evidence. They completed a series of studies over the next 14 years, focused mainly on surveying thousands of people across seven cities, from Baltimore to San Antonio to Tuskegee.

The conclusions were definitive: While Black people were twice as "wary" of participating in research, as compared to White people, they were equally willing to actually participate when asked. And, there was no association between knowledge of Tuskegee and willingness to participate.

"The hesitancy is there, but the refusal is not. And that's an important difference," says Warren, who later joined Katz in editing a book about the research. "Hesitant, Yes. But not refusal."

Tuskegee was not the deal breaker everyone thought it was.

These results did not go over well within academic and government research circles, Warren says, as they "indicted and contradicted" the common belief that low minority enrollment in research was the result of Tuskegee.

"That was the excuse that they used," Warren says. " If I don't want to go to the extra energy, resources to include the population, I can simply say they were not interested. They refused."

Now researchers had to confront the shortcomings of their own recruitment methods. Many of them never invited Black people to participate in their studies in the first place. When they did, they often did not try very hard. For example, two studies of cardiovascular disease offered enrollment to more than 2,000 white people, compared to no more than 30 people from minority groups.

"We have a tendency to use Tuskegee as a scapegoat, for us, as researchers, not doing what we need to do to ensure that people are well educated about the benefits of participating in a clinical trial," says B. Lee Green, vice president of diversity at Moffitt Cancer Center in Florida, who worked on the early research debunking the assumptions about Tuskegee's legacy.

"There may be individuals in the community who absolutely remember Tuskegee, and we should not discount that," he adds. But hesitancy "is more related to individuals' lived experiences, what people live each and every day."
'It's What Happened to Me Yesterday'
Some of the same presumptions that were made about clinical research are resurfacing today around the coronavirus vaccine. A lot of hesitancy is being confused for refusal, Warren says. And so many of the entrenched structural barriers that are limiting access to the vaccine in Black communities are not being sufficiently addressed.

Tuskegee is once again being used as a scapegoat, says USC sociologist Karen Lincoln.

"If you say Tuskegee, then you don't have to acknowledge things like pharmacy deserts, things like poverty and unemployment," she says. "You can just say, 'That happened then...and there's nothing we can do about it.' "

She says the contemporary failures of the health care system are more pressing and causing more distrust than the events of the past.

"It's what happened to me yesterday," she says. "Not what happened in the 50s or 60s, when Tuskegee was actually active."

The seniors she works with complain to her all the time about doctors dismissing their concerns, talking down to them, or nurses answering the hospital call buttons for their white roommates more often than for them.

As a prime example of the unequal treatment Black people receive, they point to the recent Facebook Live video of Dr. Susan Moore. When Moore, a geriatrician and family medicine physician from Indiana, got COVID-19, she filmed herself from her hospital bed, an oxygen tube in her nose. She told the camera that she had to beg her physician to continue her course of Remdesivir, the drug that speeds up recovery from the disease.

"He said, 'Ah, you don't need it. You're not even short of breath.' I said 'Yes, I am,'" Moore said into the camera. "I put forward and I maintain, if I was white, I wouldn't have to go through that."

Moore died two weeks later.

"She knew what kind of treatment she should be getting and she wasn't getting it," said Maxine Toler, the 72-year-old from LA, contrasting Moore's treatment with the care Donald Trump received.

"We saw it up close and personal with the president, that he got the best of everything. They cured him in a couple of days, and our people are dying like flies."

Toler and her neighbors say that the same inequity is playing out with the vaccine. Three months into the vaccine roll out, Black people make up just 2.9% of Californians who have received the vaccination, even though they account for 6.2% of the state's COVID-19 deaths.

The first mass vaccination sites set up in the Los Angeles area - at Dodgers Stadium and at Disneyland - are difficult to get to from Black neighborhoods without a car. And you practically needed a computer science degree to get an early dose, as snagging an online appointment required navigating the confusing interface or constantly refreshing the portal.

White, affluent people are snatching up appointments, even at clinics intended for hard-hit Black and Latino communities, while people of color can't get through.

It's stories like these, of unequal treatment and barriers to care, that stoke mistrust, Lincoln says. "And the word travels fast when people have negative experiences. They share it."

To address this mistrust will require a paradigm shift, says Warren of Tuskegee University. If you want Black people to trust doctors and trust the vaccine, don't blame them for distrusting it, he says. The obligation is on health institutions to first show they are trustworthy: to listen, take responsibility, show accountability, and stop making excuses. That, he adds, means providing information about the vaccine without being paternalistic and making the vaccine easy to access in Black communities.

"Prove yourself trustworthy and trust will follow," he says

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Stop Blaming Tuskegee, Critics Say. It's Not An 'Excuse' For Current Medical Racism

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For months, journalists, politicians and health officials - from New York Gov. Andrew Cuomo to Dr. Anthony Fauci - have invoked the infamous Tuskegee syphilis study to explain why Black Americans are more hesitant than white Americans to get the coronavirus vaccine.

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What is race? What is ethnicity? Is there a difference?

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In 1987, 10-year-old Segun Fatumo was on the streets of Lagos, Nigeria, hawking palm oil, yams, and pepper each day after school to help put food on the table. In the evenings, he and his family crowded into a two-room dwelling without running water or electricity. He knew nothing of the plan being hatched by U.S. and U.K. geneticists to sequence the human genome.

Thirteen years later, when researchers completed the draft sequence of the human genome, Fatumo-then an undergraduate studying computer science-heard all about it. "I knew the project would change our world," he recalls. What he didn't realize at the time was how it would change his life.

Fast forward more than 2 decades. Fatumo is now a computational geneticist in Entebbe, Uganda, with the Medical Research Council/Uganda Virus Research Institute and the London School of Hygiene & Tropical Medicine. Genome data by the terabytes flow through his seven-person lab, which is working to pinpoint genes involved in heart, kidney, and other diseases. All members of his team are African, the data come from African donors, and the ultimate goal is to improve the health of the people of Africa.

Until recently, genetic research in Africa was scanty, and most was done by researchers swooping in from afar to gather samples, then leaving to do analyses in well-equipped labs in the United States or Europe. "African genomic study was characterized by ethical dumping, helicopter science, and exploitation," Fatumo says. Researchers gathered samples with little regard for informed consent and without giving back to the communities they studied, he says.

Today, Fatumo and scores of other young Africans are doing a substantial and growing share of this research. "African genomics is a story that's going to be told more and more by Africans," says Charles Rotimi, a genetic epidemiologist at the U.S. National Human Genome Research Institute (NHGRI).

Bolstered by the internationally funded Human Heredity & Health in Africa (H3Africa) Initiative, which sponsored Fatumo as a postdoc, these researchers hope to one day use their data to bring genetically tailored medicine to people who in some places still struggle to get electricity and basic health care. The work is beginning to close a wide gap in who benefits from the human genome revolution. "There's this genomics expansion across the world," says Neil Hanchard, molecular geneticist at Baylor College of Medicine. "Why should Africa be left behind?"

Including African populations is also paving the way for a better understanding of the links between disease and genes in everyone, everywhere, because Africa holds more genomic diversity than any other continent. "The African genome should be used as the reference genome for the entire world," says Tesfaye Mersha, a geneticist at the University of Cincinnati and Cincinnati Children's Hospital Medical Center.

But genomic research in Africa has a long way to go. Researchers have only studied between 5000 and 10,000 whole genomes from Africans, compared with as many as 1 million worldwide. Africa has received less than 1% of the global investment in genomics research and clinical studies, Mersha says.

What's more, funding for all current projects in H3Africa, a $176 million program supported by the U.S. National Institutes of Health (NIH) and the Wellcome Trust that has jump-started African genomics, is set to end in 2022. Fatumo has corralled another prestigious fellowship, but researchers across the continent are scrambling to make sure the nascent genomics community can survive-and grow.

Fatumo decided he wanted to study genetics as a youngster, after a doctor explained sickle cell disease to him. His brother suffered weeklong bouts of pain from the condition. Fatumo learned that his brother had two copies of the responsible gene-and that he himself would be spared because he had just one copy. "The role genes play in disease got me thinking," he recalls.

Sickle cell, which is now being treated through gene therapy, is a classic example of how genetic knowledge can inform medical practice. And it primarily affects people of African descent. Yet most sickle cell studies and medical advances have happened in rich countries. Fatumo wants more Africans doing such research in the future.

One of six children, whose father worked as an unskilled tailor and later as a subsistence farmer and bush hunter, Fatumo moved with his family to the outskirts of Lagos when he was 9 years old. He hiked 2 kilometers early every morning to retrieve water from a river, wielded hoe and cutlass to tend crops, trekked to Lagos for school, then topped off the day hawking.

He and his parents managed to pay the 105 Nigerian naira (about $1) per year for school, thanks, in part, to Fatumo's hawking profits. Fatumo says poverty fueled in him a fierce determination to do better. "The story of my upbringing is the one that propels anger for success."

Later, he earned a B.S. in computer science at the University of Science and Technology in Port-Harcourt, Nigeria. Because little genetics was being done at African universities, he pursued graduate degrees in computer science at Covenant University in Ota, Nigeria. "I was lucky to study at Covenant where they had some key resources and constant electricity," he recalls. Even so, his bioinformatics analyses kept crashing the school's computer system. He spent 1 year studying in Heidelberg, Germany, where "the same analysis was completed in less than 30 minutes" with high-performance computers.

But he was working his way through school at the right time, in the right place. In 2009, the founders of the 6-year-old African Society of Human Genetics met in Cameroon to discuss their vision for an African genome project. "It was a dream we had, but ... we didn't know where the funding would come from," Rotimi says. Francis Collins, who had coordinated the Human Genome Project but was then between jobs, was invited to give the opening talk.

He and other participants knew how much genomics studies in Africa could contribute to research worldwide. Trace any human's family tree back far enough and the roots wind up in Africa, where our species was born some 300,000 years ago. When some groups left the continent over the past 80,000 years or so and spread across the globe, they carried only a subset of human genomic diversity. As a result, the people of Africa today carry more genetic diversity than those of any other continent. "There are parts of our genome that we cannot study any place beside Africa," says Rotimi, who directs NHGRI's Center for Research on Genomics and Global Health.

Those at the 2009 meeting also recognized that Africans needed to lead the way. "The idea that people outside of Africa are going to be able to decide the priorities ... just doesn't work," Collins says. Local investigators are more likely to understand the culture and constraints and to be trusted by the community, Mersha adds.

Some researchers were skeptical about funding African-based research. "People said the money would just disappear," Collins recalls. But "I was pretty convinced we could step away from the colonial perspective where developed nations make the decisions." Collins became NIH director in 2009 and helped launch H3Africa in 2011. NIH has committed $150 million to the initiative through 2022, and Wellcome, a U.K. biomedical philanthropy giant, has kicked in another $26 million.

The initiative aimed to set up a network of laboratories across the continent to explore the relative roles of environment and genes in diseases that plague Africans, such as HIV/AIDS, trypanosome infections, stroke, diabetes, and heart disease. It also established biorepository and bioinformatics networks. To ensure a lasting legacy, it supports training as well as research.

In 2013, with H3Africa funding, Fatumo traveled to the Wellcome Sanger Institute in Hinxton, U.K., and the University of Cambridge as a postdoc in genetic epidemiology. At Sanger, he took part in the largest African genomics project to date, a multimillion-dollar effort to analyze genomic data from 14,126 people from five African countries, including newly collected whole genomes from nearly 2000 Ugandans. The international team of researchers found 9.5 million gene variants not previously spotted, underscoring the diversity of African populations and laying the groundwork for future genomic studies.

The results, published in Cell in 2019, also included specific variants related to cardiovascular diseases in Africans, such as one previously linked to an inherited blood disorder called alpha thalassemia. That single variant could also shape the diagnosis of a third condition: It alters how sugars bind to red blood cells and so affects the results of the blood glucose test often used to track diabetes.

One year later, H3Africa's milestone genome paper came out in Nature. Human geneticist Zané Lombard and bioinformaticist Ananyo Choudhury from the University of the Witwatersrand, along with other African and international colleagues, analyzed 426 genomes, many newly sampled, from 50 populations in 13 countries. They described more than 3 million new human DNA variants, most from previously unsampled populations. The analysis also confirmed the continent's complex migration patterns, tracing the path of Bantu-speaking people as they expanded southward and eastward more than 3000 years ago. That was just one of nearly 300 papers published so far by H3Africa teams, describing results as well as providing curated data sets of African genomes.

Tallying African genomes

Researchers have only just begun to sample the genomes of Africa's 2000 ethnic groups and populations. A handful of whole-genome sequences in 2010 have grown to thousands from multiple projects, many of which are captured on the map below. Their distribution reveals huge gaps in genomic sampling across the continent.

Scroll over points on the map and legend items for more details

H3 Africa: Choudhury et al., Nature ¹, 2020 AGVP²: Gurdasani et al., Nature, 2014 MalariaGEN³: Nature Communications, 2019 SGDP⁴: Fan et al., Genome Biology ⁵, 2019 1000 Genomes⁶: Nature, 2015 UGR⁷: Gurdasani et al., Cell, 2012

Number of

genomes

sequenced

< 10

10-500

> 500

Those databases will illuminate studies of human variation worldwide, in part because the great genomic diversity in Africans can uncover spurious links to medical conditions, explains Concepcion Nierras, an NIH Common Fund geneticist. For example, in Europeans a rare variant of a gene for a low-density lipoprotein that contributes to high cholesterol seemed to raise the risk of heart disease. But Fatumo and his colleagues found that among Africans, the variant was common even in those who did not have heart disease, suggesting it may not have clinical relevance. The Nature paper uncovered 54 such variants that now need re-evaluation.

Scientists say H3Africa has been thoughtful about ethics, vital in a continent with a long history of colonial exploitation and where such concerns remain a flashpoint. For example, until 2019 Sanger was working to develop a DNA chip for scanning African genomes quickly. But whistleblowers said study participants hadn't granted the institute permission to use their DNA in this way. That chip is now not used, although one developed by H3Africa has become a mainstay.

To guard against exploitation, the project brought on bioethicists to discuss the research with local communities and figure out equitable partnerships, addressing concerns from populations worried about misuse of their data. They are also working to establish standards for effective, ethical informed consent. At Makerere University, orthopedic surgeon and bioethicist Erisa Mwaka Sabakaki and colleagues have reviewed hundreds of informed consent and other documents. Projects sometimes came up with unexpected solutions: For a study involving HIV-infected children, comic books proved a great way to communicate to both adults and children.

"There are ongoing and important questions about informed consent, how best to engage communities, benefit sharing, stigma, and many other issues," says Jantina De Vries, a bioethicist at the University of Cape Town who helped set up H3Africa's policies. "But we've started on a really good trajectory."

H3Africa's biggest achievement may be growing a generation of African genomicists, says Harvard University global public health expert Barry Bloom. The project has trained 137 Ph.D.s and 49 postdocs including Fatumo, as well as hundreds of master's students and undergraduates, and gives an incentive for scientists trained abroad to return to Africa. "If not for H3Africa, maybe I wouldn't be a group leader and principal investigator today," Fatumo says.

These efforts have had spillover effects beyond human genetics. For example, the project helped train Christian Happi, a molecular biologist at Redeemer's University in Ede, Nigeria, who runs the African Center of Excellence for Genomics of Infectious Diseases. His team quickly sequenced Nigeria's first Ebola case, identified Lassa fever strains in a 2018 outbreak and-in just 3 days in March 2020-sequenced the first coronavirus genome from an African, showing SARS-CoV-2 had arrived from Europe.

"The program's resources have enabled many African countries to respond to other health challenges," says Clement Adebamowo, a surgical oncologist at the University of Maryland School of Medicine who has been active in African genetics.

But H3Africa's successes highlight how much more work is needed. Most of the project's genomes are from people of Southern, Central, and West African ancestry (see map, above), and many populations haven't been sampled at all, including those in North Africa. "Our studies combined are just the tip of the iceberg," says Sarah Tishkoff, a human geneticist at the University of Pennsylvania who has led the way in sampling remote populations.

Individual studies highlight how much more researchers need to know to understand the intersection of genes and disease. For example, an H3Africa project called the Collaborative African Genomics Network (CAfGEN) aims to come up with a blood test for HIV-positive newborns to show how quickly their infection could progress to AIDS. Researchers scrutinized the genomes of infected children, hoping to find genetic variants associated with slow HIV progression. Children with such variants could postpone treatment and reduce and delay long-term side effects.

But so far, the team has found just one piece of DNA, involved in the immune system, that varies significantly among the children. And candidate variants that popped up in a study of Botswanan children failed to appear in Ugandan children, underscoring the diversity of African genomes. "The African genome is much more complex than we anticipated," says CAfGEN trainee Lesedi Williams, now a genomicist at the University of Botswana, Gaborone.

"The sad reality is that genomics data from Africa [are] still too few," says geneticist Aimé Lumaka of the University of Liège and the University of Kinshasa. So the medical significance of many variants in people of African descent is unknown.

Tishkoff and others are broadening their samples; this year she hopes to publish on 180 more African genomes, while Choudhury and his H3Africa colleagues are coming up with new places to sample, including Mauritius, Réunion, and other islands.

More mundane challenges also loom. "Our supply chains, financial systems, and infrastructure need strengthening," says Iruka Okeke, who studies pathogen genomes at the University of Ibadan. The continent is short of both sequencing capacity and computers powerful enough to analyze giant data sets. These impediments can lead H3Africa investigators to delay making data publicly available in order to do their own analyses, a practice that can create its own problems, says Steven Salzberg, a computational biologist at Johns Hopkins University. "As long as each group keeps its data private, the next group that wants to study these populations has to start over and sequence a new cohort," he says.

With funding scarce, some H3Africa trainees are leaving human genetics for fields where research is cheaper. One CAfGEN trainee, Gerald Mboowa at Makerere University, has shifted away from human genomes-which cost $1000 per sequence-to those of bacteria, which are a mere $90. He recently received a $100,000 Grand Challenges Africa grant funded by the Bill & Melinda Gates Foundation to track drug-resistant bacteria in hospitals.

Others, noting that direct health benefits from genes are often a long way off, wonder whether H3Africa money would be better spent on more immediate public health needs such as antismoking and healthy eating campaigns. "In 2011 we didn't know" whether H3Africa was the best way to spend international resources in Africa, says Richard Cooper, an emeritus epidemiologist at Loyola University Chicago who helped get the project off the ground. "Unfortunately I [now] think the answer is in the negative," because genomics has yet to lead to many concrete boosts in health.

Fatumo is satisfied that his own work is of immediate benefit. As his organization gathered blood samples in rural Uganda, it discovered and treated diseases participants hadn't been aware of, including hepatitis and hypertension.

But a big challenge looms in 2022, when NIH Common Fund support ends. That loss could "be a major blow to everything that's been built up," says Stefan Jansen, a psychologist at the University of Rwanda involved with an H3Africa project on posttraumatic stress disorder. Some support will come from another NIH program, Harnessing Data Science for Health Discovery and Innovation in Africa (DS-I Africa), which is slated to spend $62 million over the next 6 years. And an African genomics startup called 54Gene has gotten $15 million in international backing for a multimillion-dollar facility in Nigeria. But most H3Africa-supported researchers have had little luck finding funding within Africa. It's "really, really challenging getting African funding from private companies or African governments," Rotimi says.

Some of Africa's genomics researchers will manage to win new support from abroad, as Mboowa has done. Fatumo was recently awarded a highly competitive Wellcome International Intermediate Fellowship and now has $1.2 million over the next 5 years plus other support to explore genomic variants linked to chronic kidney disease; he hopes to develop risk scores based on patients' genetic makeup.

He has also teamed up with a South African colleague and applied to become a DS-I Africa research hub. If successful, they will get $1.3 million per year for 5 years to use existing African genetic data to find and validate new drug targets.

Fatumo and others hope their generation's accomplishments will lay the foundation for an even stronger research network. "It is a great time for all of us doing genomics in Africa," Okeke says. "The discovery potential is very high, and the impact that our work could have on health could be huge."
*Correction, 16 February, 3 p.m.: This story has been updated to accurately reflect Segun Fatumo's undergraduate institution.

doi:10.1126/science.abg8903

Liz is a senior correspondent covering many aspects of biology for Science.

More from News

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Africans begin to take the reins of research into their own genomes

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In 1987, 10-year-old Segun Fatumo was on the streets of Lagos, Nigeria, hawking palm oil, yams, and pepper each day after school to help put food on the table. In the evenings, he and his family crowded into a two-room dwelling without running water or electricity.

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https://www.sciencemag.org/news/2021/02/africans-begin-take-reins-research-their-own-genomes

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The Biology of Skin Color — HHMI BioInteractive Video

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Introduction

The genomic research landscape has transformed dramatically since the completion of the human genome project in 2003, but focus in the field has been constrained, in terms of worldwide populations included in this research. Representation in genomics studies has been dominated by populations descending from Europe. The concentration of research and resources within one ancestral group has the potential to further perpetuate and even exacerbate known disparities that negatively affect populations with ancestry that is underrepresented in research (see Box 1: "What do we mean by ancestry?"). There has been increasing recognition of the scientific and equity imperatives to increase the representation of diverse populations in genomic research,1,2,3,4,5,6,7,8,9 and initiatives are underway to address past shortcomings. As these initiatives are beginning to yield results and more findings from studies including diverse populations are accumulating, it is worthwhile to revisit the promises of this inclusion to evaluate whether the anticipated advances are, indeed, emerging. With a focus on the African continent, consistent with the authors' expertise, we evaluate the evidence to support the expected progress from including diverse individuals in genomic research relative to: novel insights into human biology, improvements in clinical care, and enhanced understanding of health disparities (Table 1). The call for increased diversity in genomic research has been accompanied by the need for overcoming related technological challenges and for greater diversity among those conducting research. We also comment on the progress and achievements on these issues.

Table 1 Progress and challenges for achieving scientific promise of diversity and inclusion in genomics.

For clarity, and to be consistent with recently published guidelines for characterizing ancestry in genomic research,10 we here use "individuals of African ancestry" to describe sub-Saharan Africans and those who identify as African American or Afro-Caribbean. Similarly, we use "European ancestry individuals" to describe those who identify as "white" from Europe or America. However, the concepts presented may extend directly to all individuals with any degree of a particular ancestry, as ancestry at a genomic locus of interest may have important health effects, regardless of self-identification.

Box 1 What do we mean by ancestry?

In the context of this paper, ancestry is defined using genetic variants based on the distribution of those variants in worldwide populations. An individual's genome is a mosaic of segments from different ancestral populations. By comparing segments of DNA with the distribution of genetic variants in worldwide populations, it is possible to determine the likely "parental" or source population for each segment of DNA, indicating a component of the individual's overall ancestry. Using this process to interrogate an individual's entire genome, the proportion of an individual's genomic inheritance from specific ancestral populations can be estimated. Importantly, someone's genetic ancestry may have little to do with their identity in terms of race or culture. An individual with a relatively small proportion of African ancestry may not self-identify as "Black" or "African American", yet they may have African ancestry at a specific region of the genome where that ancestry may confer risk, for instance, by carrying a pharmacogenomic risk allele that is more prevalent among those with African ancestry. Based on our most recent analysis of 282 global samples, there are at least 21 ancestries.139 Notably, mixed ancestry is the norm across samples and continents, and the vast majority of individuals (an estimated 97.3%) show ancestral heterogeneity.139 Finally, individuals' ancestry estimates may change over time as our reference datasets become more diverse.

Insights into human biology

A substantial proportion of human genomic variation was left behind during the out-of-Africa migration.11 Therefore, insights into the implications of this variation can only come from research conducted in those of African ancestry. This reservoir of relatively untested African sequence variation has fostered high hopes regarding the potential for novel findings when better representation in genomic research was achieved.6 Notably, expected advances based on findings in those of African ancestry are not limited to those of that ancestry, as can be seen with the discovery of variants in PCSK9 that dramatically reduced low-density lipoprotein cholesterol concentrations. Although these variants were discovered in samples from African Americans, the benefit of drugs targeting PCKS9 extends beyond ancestry-defined subgroups.12,13 In general, common complex diseases require the aggregation of large datasets to yield results. Achieving the needed datasets of participants with African ancestry has been a challenge due to the relatively limited numbers and sample sizes of cohorts from diverse populations. Now that studies of African ancestry individuals are increasing in sample size, are we seeing the expected novel results? A recent evaluation of data included in the NHGRI-EBI GWAS Catalog, which is the most complete record of published genome-wide association studies, found that only 2.4% of the individuals included in the catalog were of African ancestry.10 Even at such a relatively small proportion, the promise of new findings with greater inclusion is clear: they contributed a larger than expected proportion of associations in the catalog (7%).10

New initiatives and large consortia with a focus on increasing the representation of diverse populations in research, such as TopMED and PAGE II, are beginning to bear fruit (Fig. 1; Table 2). In addition to these large-scale efforts, the inclusion of individuals with African ancestry in other studies has led to the identification of novel loci in recent studies of obesity,14 type 2 diabetes,15,16 metabolic syndrome,17 skin pigmentation,18 suicide,19 multiple sclerosis,20 cleft palate,21 and Epstein-Barr virus immune response.22 The National Institutes of Health's recently launched All of Us Precision Medicine Initiative aims to recruit 1 million Americans, with a particular focus on representing the nation's diversity ( http://allofus.nih.gov).23 With estimates of early recruitment showing up to 75% from groups who are underrepresented in health research, this effort promises to yield a considerable number of participants of diverse ancestries.24 Although the development of large, multi-ethnic resources is a clear advance, diligence on the part of researchers, funders, and reviewers is required to ensure that these resources are used to their fullest extent. It is common to exclude non-European ancestry samples from analyses, despite the presence of a sufficient sample size for stratified analysis (such as in UK Biobank),25 or to limit analyses in these samples to replication or confirmation of findings from the analysis of European ancestry samples.

Data for figures taken from the following sources: TOPMed,106 PAGE II,107 Million Veteran Program (MVP),108 CHARGE Gene-Lifestyle Interactions (GLI),109 Cardiovascular H3Africa Innovation Resource (CHAIR),35 CAAPA,110 NeuroGAP-Psychosis,36 All of Us,23 and the GWAS Catalog10.

Table 2 Some insights into human biology from initiatives prioritizing inclusion of participants of African ancestry.

The above projects largely reflect inclusion of African Americans in genomic research, but representation on the African continent, the birthplace of humanity and home to the greatest genomic diversity on the planet, has been more limited. In response to this need, the Wellcome Trust and the National Institutes of Health have supported African-led genomic research through the Human Heredity and Health in Africa (H3Africa) initiative.26,27 Now in its 6th year, H3Africa has received over 170 million USD and sponsored nearly 50 research projects.28 At the time of the writing of this manuscript, H3Africa had reached 54,000 research participants, and convened meetings and workshops with over 2000 attendees.28 This initiative has produced 382 trainees and 219 publications.28 While primary results from the H3Africa projects for the study of complex disease traits have not yet been published, they are poised to make substantial contributions to increasing diversity in genomic research given the following enrollment numbers: a study of over 10,000 individuals for cardiometabolic disease risk (AWI-GEN),29,30 a study of 6000 T2D cases and 6000 controls (H3Africa T2D Study),31 a study of kidney disease ( n = 4000 cases and 4000 controls) (H3Africa Kidney Disease Research Network),32 a study of 3000 stroke cases and 3000 controls (SIREN),33 a study of over 11,000 women on Human Papilloma Virus and cervical cancer risk (African Collaborative Center for Microbiome and Genomics Research),34 and a combined resource for cardiovascular studies with over 30,000 participants (CHAIR).35 Another noteworthy initiative is the Neuropsychiatric Genetics of African Populations-Psychosis (NeuroGAP-Psychosis) project, a study of the genetics of schizophrenia and bipolar disorder recruiting 34,000 participants from Ethiopia, Kenya, South Africa, and Uganda.36 These genomic studies and associated consortia will undoubtedly greatly enhance the detection of novel loci for complex disease risk.

Improvements in clinical care

A key motivation for conducting genomic research is to facilitate improvements in clinical care. A promising outcome of the success of genome-wide association studies (GWAS) of common diseases is the development of polygenic risk scores (PRS): scores that can be calculated for an individual based on the presence or absence of risk variants identified in large GWAS studies. The promise of these scores for clinical use is gaining increased attention.37,38 For instance, risk scores developed using known risk variants have been able to identify the 8.0% of the population with more than a three-fold increased risk of coronary artery disease.39 However, PRS depend on underlying genomic research, which has predominantly been conducted in European ancestry individuals. European ancestry individuals are overrepresented in PRS research at 460% of what it would be if representation matched the proportion of the worldwide population. In contrast, African ancestry individuals are underrepresented (only 17% of expected proportion based on worldwide population).40 As a result, these PRS represent only a subset of the global human population and have limited portability across ancestries.1,41 Some of this lack of portability reflects differences in characteristics of the genome that have accumulated as a result of migration patterns. For instance, as a result of genetic drift and selection pressures, the presence and frequency of alleles vary across ancestry groups.11 PRS can only capture the genetic associations observed in the population in which the underlying GWAS is conducted. An effect of variants that are not sufficiently frequent (or present) in that analysis may influence trait outcomes in a population of a different ancestry, yet the ancestry-unmatched PRS will not reflect those effects and the PRS will give less accurate results. Additionally, population history has led to a generally reduced linkage disequilibrium structure across the genome among those of African ancestry. Although an untested causal variant may be the same across populations, the variant which tags that effect may differ across ancestry groups. In this case, the risk associated with a particular variant may be misattributed and also lead to ancestry-unmatched PRS inaccuracies. The underperformance of the PRS when discovery and target populations are mismatched in ancestry has been demonstrated when PRS constructed based on GWAS findings in European ancestry individuals were tested in those of African ancestry. In UK Biobank data, prediction accuracy was 4.5-fold lower in African ancestry samples compared to European ancestry samples42 (Fig. 2). Similarly, the median effect size for PRS for a variety of traits in African ancestry samples was only 42% of that in matched European ancestry samples in an analysis of published PRS studies.40 In contrast, risk scores based on data derived in African Americans have been demonstrated to perform significantly better in African Americans than risk scores based on studies predominantly including those of European ancestry.43 The PRS could be considered as a new disease biomarker to be evaluated alongside more traditional measures of risk. It is common that the distribution of disease biomarkers varies across ancestries, often leading to adjustments in biomarker calculations (for instance, predicted values for spirometry or estimated glomerular filtration rate). However, PRS uniformly performs more poorly in individuals with African ancestry (and in all understudied populations), and minor ancestry-specific adjustments, such as have been used with other biomarkers, will not be able to make up for this underperformance.42 The complexities of PRS in the context of ancestry and the potential to exacerbate health disparities has been addressed in-depth in recent articles.40,42 Importantly, in addition to limitations in transferability conferred by ancestry-related genomic differences, there can be substantial variation in the performance of PRS for complex genetic traits based on methodological decisions40 and on environmental context.44 If PRS do become useful clinically, the limitations of applying data from a subset of the global population to all global populations are clear. Disparities in clinical care will persist for those with non-European ancestry: medical technology will be less capable of identifying risks, targets, and potential interventions for the majority of patients globally that represent greater genomic heterogeneity. While advances in understanding and adjusting for biases when PRS are applied across ancestries is useful, real progress in PRS for those of African ancestry is tied to increasing the number of large GWAS of African ancestry individuals on which to base these PRS.

Prediction target individuals do not overlap with the discovery cohort and are unrelated. Violin plots show distributions of relative prediction accuracies, points show mean values, and error bars show s.e.m. values. [Reprinted by permission from Springer Nature Customer Service Centre GmbH: Springer Nature, Nature Genetics, "Clinical use of current polygenic risk scores may exacerbate health disparities", Alicia R. Martin et al.42].

Another important area of genomic research in which increased diversity is vital for equitable clinical care is pharmacogenomics: identifying genetic variants that may influence an individual's response to drugs. Depending on the pharmacogenomic variant carried by an individual, treatment outcomes could range from a lack of effect to potentially life-threatening adverse effects. Using genomic data to protect patients from harm or improve their treatment is a key motivation for precision medicine. As the genetic variants present in individuals may vary by their ancestry, limited pharmacogenomic research in diverse populations puts individuals with ancestry from an underrepresented group at more risk of an unanticipated drug response than those in better-studied populations. The African American Cardiovascular Pharmacogenetic Consortium (ACCOuNT) has been established to address this gap and aims to discover novel pharmacogenetic variants in African Americans and to incorporate these variants into clinical recommendations.45 Recent efforts focusing on those of African ancestry have identified novel loci that may help to explain the diminished response to inhaled corticosteroids in African Americans with asthma,46,47,48 though the low number of available studies with individuals of African ancestry to confirm findings was acknowledged as a continuing limitation.47 The first GWAS of neutrophil counts during clozapine treatment (for schizophrenia) conducted in individuals of African ancestry identified a key role for the well-known African ancestry-specific Duffy allele in risk of neutropenia upon treatment, thereby improving our understanding of the differential rates of discontinuation of clozapine by ethnicity.49 Major warfarin-associated bleeding occurs more commonly among those with African ancestry, though genetic risk factors associated with this serious outcome had not been well-studied in these individuals. A recent case-control study among individuals of African ancestry50 was able to identify a locus that associated with more than eight times greater risk of major warfarin-associated bleeding. Risk variants at this locus are relatively common among individuals with African ancestry (minor allele frequency = 0.05) but absent in populations without any African ancestry. Also, potentially relevant warfarin dosing haplotypes, common in Africans but rare in other ancestry populations, have not been systematically evaluated.51,52 Although pharmaceutical drugs can be prohibitively expensive in many African countries, the potential for pharmacogenomic discoveries to increase safety and effectiveness should not be overlooked. Some countries, for instance, consider research findings related to pharmacogenomic alleles that have ramifications for their countries prior to selecting available medicines for use locally. As the prevalence of a CYP2D6 duplication that causes serious adverse outcomes with codeine use is 30% among Ethiopians, and broad genotyping is not feasible, the use of codeine has been banned in Ethiopia.53 It is important to note, however, that because of the great genetic diversity within African ancestry individuals, care must be taken not to group those of African ancestry into broad categories with the expectation of genetic similarity. For instance, HLA-B*5701 is associated with increased incidence of abacavir hypersensitivity, a life-threatening condition among HIV patients being treated with this drug. The frequency of this variant ranges from virtually absent among the Yoruba in Nigeria to 13.6% among the Masai in Kenya. Among the Luhya, also in Kenya, the variant is only present in 3.3% of individuals. In this case, neither "African" nor "Kenyan" are sufficiently precise to describe risk at this pharmacogenomic locus.54 While there are examples of recent progress, continued pharmacogenomics research is needed to form a clearer picture of the distribution of pharmacogenomics variants across diverse African populations.3,54

Inclusion and diversity are also of critical importance for the use of genomic information in clinical diagnosis. Translation of genomics to clinical practice depends upon what genomic studies have been conducted. Analyses of important databases for reporting genomic results illustrate the continuing underrepresentation of populations with significant ancestry outside of Europe: individuals of European ancestry constitute 55.8% of the observations in the Genome Aggregation Database (gnomAD);2 and the Genome-wide Association Study Catalog and the database of Genotypes and Phenotypes both have significantly fewer studies of African, Latin American, and Asian ancestral populations compared to European ancestry populations.2,3,4 This current reality highlights the comparatively reduced ability for clinicians to assess clinically significant variants in individuals with diverse ancestry, particularly when those variants are not shared across populations. Illustratively, genetic testing for cardiomyopathy in European ancestry individuals is more likely to positively identify pathogenic variants than testing conducted in underrepresented minorities in the US, while genetic testing in underrepresented minorities is more likely to be inconclusive.5 African ancestry individuals were also more likely to have variants that were misclassified as pathogenic for hypertrophic cardiomyopathy because of a lack of ancestry-matched controls for comparison.55

Improved understanding of health disparities

Although the social and economic factors are the most significant contributors to health disparities, genomic research has the potential to help unravel disparities in health outcomes that are inappropriately attributed to race. The discovery of kidney disease risk variants in the APOL1 gene that are found predominantly in individuals with African ancestry demonstrated this potential. These variants are thought to have risen in frequency among some African populations through selection pressure due to protection from Human African Trypanomiasis, yet these variants are associated with a marked increase in the risk of kidney diseases of varying etiologies.56 Well-known differences in kidney transplant outcomes that had been attributed to race were found to be better described by APOL1 genotypes. For instance, kidney transplant survival is poorer when the donor is African American compared to European American, but after accounting for those African American donors with the high-risk genotype, African ancestry is no longer associated with such outcomes.57,58,59 While stories like that of APOL1 and kidney disease are likely uncommon, other health disparities are being investigated for genomic contributions, fueled by the increasing availability of genomic data for diverse populations. A G6PD variant that is common among those with African ancestry (but not those without African ancestry) leads to decreased HbA1C levels, irrespective of blood glucose, which may lead to an estimated 2% of African Americans with T2D to remain unidentified by HbA1c screening.60 A separate study reported a role of genetic factors in the difference in distribution of HbA1c by ancestry, also highlighting an association between the variant for hemoglobin S ("sickle cell") in this trait.61 Additional discoveries have been made for the genetic factors underlying differences in the frequency of certain cancers by ancestry. For instance, in a pan-cancer analysis,62 higher degrees of chromosomal instability were observed among African American (vs. European American) patients with breast, head and neck, and endometrial cancers, while less chromosomal instability was observed in African American patients with kidney cancers.62 A study of triple-negative breast cancer identified different mutation profiles in the tumors of African American vs. European American patients, informing the higher prevalence of this subtype of breast cancer observed among African Americans.63 A recent study of prostate cancer disparities identified a protective allele that rose to high frequency in Europe due to linkage with a locus for skin pigmentation under selection pressure.64 The distribution of D-dimer, a cardiovascular disease risk biomarker, is higher among African Americans than among individuals with only European ancestry, and some genetic factors have been identified that contribute to that difference.65 Outcomes with treatment for chronic infection with hepatitis C virus vary, with African Americans having lower rates of treatment response compared to other ethnic groups. The C allele of rs12979860, a variant near IL28B, was found to be associated with improved treatment response among African Americans, European Americans, and Hispanics, and the inter-ancestry differences in frequency of this allele appear to explain approximately half of the disparities in treatment response rate.66 This variant was also associated with spontaneous clearance of the hepatitis C virus, and worldwide allele frequencies suggest that it may have been under selection in human history.67 Fortunately, newer treatment options have increased response to ~90% of patients, regardless of ancestral background.68 With continuing work on understanding how genetic factors contribute to health disparities, inadequate characterizations based on race can be replaced by screening for relevant markers, with improved targeting and the potential for novel biological insights.

Overcoming technological challenges

To efficiently capture the wide range of genomic diversity among African participants, genotyping tools must be optimized for interrogating African genomes. GWAS arrays developed using genetic information derived largely from populations of European ancestry are inefficient when used within the context of research involving non-European populations, particularly the diverse groups that comprise Africa. There have been several notable efforts to improve the genomic diversity represented in commercially available genotyping arrays, including the Multi-Ethnic Genotyping Array (MEGA) produced by Illumina in partnership with the PAGE and CAAPA Consortia69 and the Affymetrix Axiom PanAFR Array, with a focus on coverage of 1000 Genomes AFR populations.70 More recently, the H3Africa Consortium and Illumina have developed a GWAS array with 2.5 million markers based on whole genome-sequencing data from thousands of samples originating from African research participants.3 This genotyping array better represents and reflects the range of common variants in populations across the continent, facilitating the interrogation of variants that had not been previously evaluated as they were not captured by previous tools.

After collection of genome-wide genotype data, it is common practice to impute additional genotypes prior to analysis. Accurate outcomes for imputation are dependent on the selection of the appropriate reference panel, as imputation algorithms incorporate linkage disequilibrium patterns, which vary across ancestries. Due to the generally reduced linkage disequilibrium and greater genetic diversity among African ancestry individuals, imputation accuracy using a comparably sized reference panel is reduced for those of African vs. other ancestries.71 Additionally, the reference panels publicly available for imputing African ancestry samples have been limited, predominated by the 1000 Genomes Project data. The situation has improved, however, with additional reference panels that include African ancestry individuals. High performance and accuracy for imputation with African Americans was observed for reference panels from 1000 Genomes,11 the Haplotype Reference Consortium (HRC, which includes 1000 Genomes data and a large number of predominantly European ancestry samples72), and the Consortium on Asthma among African-Ancestry Populations in the Americas (CAAPA73).74 These reference panels are available at both of the commonly used publicly available imputation servers: the Sanger Imputation Service (1000 Genomes and HRC: https://www.sanger.ac.uk/science/tools/sanger-imputation-service) and the Michigan Imputation Server (1000 Genomes, HRC, and CAAPA: https://imputationserver.sph.umich.edu/index.html#!). Additionally, the Michigan Imputation Server is preparing to offer a reference panel using TOPMed data. The African Genome Resource (AGR), available through the Sanger Imputation Service, is currently the largest publicly available reference panel of African ancestry individuals, including all 1000 Genomes individuals and an additional ~2000 samples from Uganda and ~100 samples each from 5 populations in Ethiopia, Egypt, Namibia, and South Africa. Notably, imputation using the AGR and the 1000 Genomes reference panel was shown to achieve high quality and accuracy even in the presence of five-way admixture in a South African population.75 Additionally, it is anticipated that data from H3Africa will be made available as an imputation resource.76

As the price of sequencing technologies continue to decrease77 and bioinformatic advances reduce the time and expertise burdens associated with processing these data, it is possible that sequencing may become more common. Importantly, the ancestry biases present in GWAS arrays and imputation are not a concern when using sequencing technology.

Infrastructure to include diverse voices

The predominance of European ancestry individuals is observed in those represented in genomic research as well as in the identities of those conducting research.7,78,79,80 In the US, for example, the proportion of those in the academic doctoral workforce (for science, engineering, and health) who are African American has only increased from 5.8% in 1997 to 8.9% in 2017,78 although African Americans represent 13.4% of the population.81 Unfortunately, this lack of diversity among genomic researchers leads to the loss of perspectives that are important in developing hypotheses as well as directing research among diverse individuals, and disparity in terms of research leadership and output among African scientists remains.82 Sustained genomic research capacity in any setting relies on engaged investigators and frameworks that can support the development of datasets relevant to the local population, infrastructure for computation and analysis, and expertise for the translation and implementation of genomics and bioinformatics information into clinical practice. African countries have historically been challenged by poor research infrastructure and limited training and professional opportunities.27 In appreciation of this obstacle faced by African researchers, and with an eye toward the elevation of researchers along with the increased inclusion of African samples, sustained capacity-building is a keystone of the H3Africa Initiative.83 NeuroGAP has also established the Global Initiative for Neuropsychiatric Genetics Education in Research (GINGER), which will support the training of early-career investigators from the countries in which research is being conducted (Ethiopia, Kenya, South Africa, and Uganda).84 The topics for training are determined through the participation of the fellows and their African mentors, so that their needs shape their experiences.84

H3Africa supports the development of large collaborations across multiple centers, leverages synergies between studies, and provides critical training to African researchers. The pan-African bioinformatics network, H3ABioNet, was designed to serve the consortium and assists with data quality control and analysis.85 In addition, it has advanced infrastructure and professional skill development through workshops and meetings and accredited enrichment programs to advance skills related to the conduct of genome-wide association studies and the analysis of next generation sequencing data. Investigators have learned how to conduct GWAS and analyze genome-sequencing data. H3ABioNet has also established infrastructure for computing at different institutions across the continent. Through its monitoring and training efforts, the network has provided bioinformaticians, researchers, medical professionals, systems administrators, and software developers with the tools to utilize and maintain the computing infrastructure.86

One of the ways that the emergence of the voices of African researchers may be observed is in the focus on diseases and traits of significance to Africa among new Africa-led work. For instance, H3Africa-funded projects have supported work on Human African Trypanomiasis87,88,89,90,91,92 and sickle cell disorders.93,94,95 H3Africa provides a model that could be useful to include diversity in leadership in other parts of the world, including in America.

Development of ethical guidelines

As the African genomic research environment expands to examine genetic, environmental, and other contributions to health and diseases, new and familiar ethical questions and concerns will arise that warrant attention to African perspectives. Investigations that employ emerging research tools (e.g., mobile health applications, sensors, wearable devices), for instance, must consider concerns related to genomic research that incorporates behavioral and physiological data.96 For instance, an individual's ability to consent may be complicated in some African cultures by expectations of involvement of family and community in decision-making,97 as has been observed in indigenous people of the Americas.98 Ethical guidelines for these types of scenarios may need to be reevaluated as genomic research capacity grows within African contexts and produces researchers, institutions, and findings that are more accessible locally. Importantly, African countries must have the opportunity to influence the policies for the design and dissemination of genomic research for collaboration to be sustainable. Concerns over parachute or safari research remain where African researchers are left out of the full research process, invited to collaborate only as is useful for sample collection, but without any benefit of the research returning to support African researchers or infrastructure. Community engagement is recognized as a critical strategy for addressing such challenges, understanding research priorities, respecting cultural concerns, and countering concerns of exploitation.99 Others have highlighted the importance of tailoring community engagement strategies to low resource settings, including members of disadvantaged groups in the engagement process, and structuring deliberations in ways that minimize power differentials in community settings.100 Currently there are collaborations between African and non-African researchers "rooted" with a firm foundation within Africa that emphasize capacity building and shared scientific contribution, such as the Viral Hemorrhagic Fever Consortium ( www.vhfc.org) and the African Center of Excellence for Genomics of Infections Disease (acegid.org).101 H3Africa has the formation of equitable collaborations, African researcher-led science, capacity building, and infrastructure development among its central tenets.76,83 Capacity building on the continent addresses concerns related to exploitation and parachute research through concomitant ethics and governance mechanisms, such as those created by H3Africa. Additional questions related to benefit sharing, privacy, confidentiality, and group harm should also be examined with emphasis on concerns specific to African populations.102,103 To address these concerns, H3Africa has provided an excellent foundation by developing guidelines and ethics training modules for ethics committees on the continent that will assess ethical concerns.104

Given the importance of data sharing to genomic research, genotype and phenotype data from the H3Africa research studies are stored in the European Genome Phenome Archive (EGA) but access to data and biological samples is determined by an independent H3Africa Data and Biospecimen Access Committee (DBAC) comprised of mostly African members who consider the informed consent process and stipulations provided by the original ethics committees who approved the studies. Through collective action, members of H3Africa have developed ethical guidelines related to data sharing and processing, consent for the sharing and uses of African samples and data, and issues related to study coordination and the shipping of samples externally.86 Example guidelines include rules and embargos that are sensitive to local infrastructural challenges, thus according to African investigators relatively sufficient time to publish the findings of their primary research questions first.26,105 The training modules and guidelines provide a framework and foundation for existing and future ethics committee members. Strategies to ensure that ethics committee members remain engaged, well-informed, and committed to the committee will be critical to ongoing developments related to ethical guidance.

Conclusion

The need for inclusion of individuals of diverse ancestral backgrounds and identities in genomic research has long been understood, both from the perspective of scientific necessity and equity. Recent initiatives have embraced this call for diversity, including H3Africa, TopMed, CAAPA, PAGE II, and the Million Veteran Program, with more projects, such as large-scale H3Africa projects and the All of Us study seeking to represent US diversity, underway. As results from these and other efforts are reaching the literature, it is warranted to evaluate whether the anticipated benefits of the inclusion of diverse populations in genomics are being realized. Indeed, the increased number of participants with African ancestry is facilitating the discovery of novel genomic loci and establishing new variation of interest within known genomic loci. Importantly, the focus on increasing the number of African ancestry individuals in research is occurring alongside efforts to increase capacity and supporting infrastructure for diverse researchers, and to do so equitably. Clinical and pharmacogenomic studies are improving the data available to accompany integrated social and environmental research on the underlying causes of health disparities. Despite these advances, attaining meaningful representation of diverse populations across the breadth of genomic research that is adequately powered to inform health disparities research will require sustained and continuing efforts.

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Acknowledgements

The contents of this article are solely the responsibility of the authors and do not necessarily represent the official view of the National Institutes of Health. This research was supported in part by the Intramural Research Program of the National Human Genome Research Institute in the Center for Research in Genomics and Global Health (CRGGH-Z01HG200362). CRGGH is also supported by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), the Center for Information Technology, and the Office of the Director at the National Institutes of Health.

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Affiliations

1. Center for Research on Genomics and Global Health, National Human Genome Research Institute, National Institutes of Health, Bethesda, MD, USA

Amy R. Bentley, Shawneequa L. Callier & Charles N. Rotimi

2. Department of Clinical Research and Leadership, The George Washington University School of Medicine and Health Sciences, Washington, DC, USA

Shawneequa L. Callier

Contributions

A.R.B. and S.L.C. wrote the initial draft. C.N.R. provided critical edits and additions. All authors revised and approved the submitted manuscript.

Corresponding author

Correspondence to Charles N. Rotimi.

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Bentley, A.R., Callier, S.L. & Rotimi, C.N. Evaluating the promise of inclusion of African ancestry populations in genomics. npj Genom. Med. 5, 5 (2020). https://doi.org/10.1038/s41525-019-0111-x
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# data[].attributes.attachment_link.title
Evaluating the promise of inclusion of African ancestry populations in genomics

# data[].attributes.attachment_link.description
The lack of representation of diverse ancestral backgrounds in genomic research is well-known, and the resultant scientific and ethical limitations are becoming increasingly appreciated. The paucity of data on individuals with African ancestry is especially noteworthy as Africa is the birthplace of modern humans and harbors the greatest genetic diversity.

# data[].attributes.attachment_link.readable_text
This article is targeted to faculty teaching race and ethnicity, racism, diversity, and multicultural courses. Many students equate race with skin color. The premise of this article is that to teach students about the social construction of race, teachers must first know enough science to teach students that race is not biological. This article examines the biology of race by showing how advances in DNA sequencing led to genetics research that supports arguments that race is not biological. DNA comparisons show that all human populations living today are one species that came from Africa. The article explains the migration of humans out of Africa about 60,000 years ago and how they populated Australia, then Asia, Europe, and the Americas. The article shows how recent research maps the timing of the migration and admixture of specific population groups into Europe and India. The article shows how a mutation in one nucleotide can result in a trait like blue eyes, or Hemoglobin S (which confers resistance to malaria), which can be subject to evolution through natural selection. DNA comparisons show how natural selection shaped the genetics of human skin color to adapt to less UV light in the northern latitudes of Europe and Asia. The article shows that there is no relation between skin color or other "racial" characteristics and complex traits like intelligence. The science in this article will help teachers explain that as race is not biological, race is socially constructed and culturally enacted.

When I began teaching race and ethnicity, I discovered that many of my students believed that race was not an idea, but a fact. Some did not accept the idea that race was socially constructed even by the end of the semester. As I tried to answer their questions, I found that I did not know enough contemporary science to be able to explain why the idea of race was not biological. Consequently, I decided to delve into the scientific literature for answers. When I used the results of my research to teach my students, I was able to reach more of them.

This article argues that to teach students how race is socially constructed, faculty must have mastered enough science to show skeptical students that the idea of race is not biological. Most educators who teach in the areas of anti-racism, cultural competence, diversity, or race and ethnicity are social scientists. Few have backgrounds in biological anthropology, population genetics, or molecular biology. Yet, knowledge that relates to race as biology has exploded with contemporary progress in molecular biology and genomics. The purpose of this article is to present faculty with accurate scientific information on the biology of race to share with their students. This will help students understand that race as biology is not scientifically based. Therefore, the ideas about race that are held as folk concepts in U.S. culture must be socially constructed.

The concept that race does not have a biological basis, but instead is socially constructed, has been accepted among social scientists for three generations (cf. Montagu, 1942). Yet, many U.S. students enter anti-racism, cultural competence, diversity, or race and ethnicity classes in disciplines ranging from business to nursing to sociology, with the underlying assumption that race is biological ( Coleman, 2011). As Goodman, Moses, and Jones (2012) explained, "race seems obviously real to anyone immersed in North America's dominant culture" (p. 2).

We live in a society saturated with race. Racial thinking has infiltrated and now influences in some way or another everyone's experiences of health, education, romance, friendship, work, religion, politics-virtually every arena and aspect of our lives. ( Goodman et al., 2012, p. 9)

Students absorb normative beliefs that "race" is real as part of their culture ( Smedley & Smedley, 2005).

In terms of background assumptions, this article examines the idea of race from the viewpoint of social scientific realism. Social scientific realism asserts that the social world comprises "not only human beings, but also the social relations and structures that are the products of human social interaction" ( Carter, 2000, p. 1). This is to be contrasted with poststructuralist or postmodernist theories of the social world. The implications of social scientific realism include the following: (a) There is a social reality that is "relatively independent of individual social actors" and (b) social structures can "constrain and influence subsequent social actors" ( Carter, 2000, p. 5). As Smedley and Smedley (2005) suggest, while race as biology is fiction, racism as a social problem is real. In the United States, "there are profound and stubbornly persistent . . . differences in socioeconomic status, educational and occupational status, wealth, [and] political power" based on ascribed race ( Smedley & Smedley, 2005, p. 16).

From Traits to Genes to Genomes

Since the end of World War II, biological science has exploded. In 1953, Watson and Crick published the structure of the DNA molecule-the famous double helix. Since then, whole new fields, including molecular genetics, population genetics, epigenetics, and genomics, have developed. Advances in sequencing the human genome can serve as an example of how quickly scientific technology has been developing. The classical Sanger chain-termination DNA sequencing method was introduced in 1977 ( Sanger, Nicklen, & Coulson, 1977). Sanger won a Nobel Prize for it in 1980. Sanger sequencing required a lot of space, and labs could typically run only about 100 reactions at a time. However, it was the most widely used sequencing method for about 25 years. By 1981, Sanger sequencing had been used to fully sequence human mtDNA, which has only 16,569 base pairs organized in a ring, making it easier to sequence. In 1990, the international project to map the human genome was begun. By 1996, the yeast genome was sequenced, followed by the c. elegans roundworm genome in 1998. The first draft of the human genome was announced in 2001. Finally, the first fully sequenced genome of a single person was published in 2003. It took more than 10 years, US$3 billion, and a massive international effort to accomplish the Human Genome Project using Sanger sequencing ( Hayden, 2014b). By 2000, second generation high-throughput sequencing using technologies such as reversible terminator sequencing became commercially available. Technologies have advanced so quickly that, by 2014, a single machine could automatically sequence five full human genomes a day for close to US$1,000 each ( Hayden, 2014a). Exciting new methods are being developed, including a nanopore technology, which uses an enzyme to feed an intact single-stranded length of DNA through a protein nanopore and reads the bases in order in one continuous read. The intact DNA can be hundreds of kilobytes long. All of these new technologies can be brought to bear on the issue of whether race is biological.

There are six accepted scientific arguments as to why race is a biological myth ( Mukhopadhyay, Henze, & Moses, 2014). When students assume that race is a real biological entity, faculty can use these scientific arguments to help students begin to question their assumptions. I typically present the science during the second or third week of the semester.

1. People cannot be reliably divided into racial groups.

2. There are no relationships between traits that are used to categorize people into races (like skin color) and associated stereotypes.

3. Over time, geography and environment influence the genetic structures of human populations through natural selection.

4. There is more diversity within racial groups than between racial groups.

5. All people living today are descended from populations that originated in Africa.

6. All people living today are one biological species.

Considerable scientific evidence that supports these arguments has been published since 2000. The new science will help faculty address student misconceptions that race is biological.

People Cannot Be Reliably Divided Into Racial Groups

Many students enter class assuming that because they can "see" race, it is biological. They assume that by using visible human biological variation like skin color, hair texture, and facial characteristics, they can reliably divide people into racial categories. But McCarthy (2009) emphasizes that "racing" people is not just a visual but also a conceptual process. He states that "real or ascribed somatic markers are taken as signs of deeper differences . . . stereotypical representations combining phenotypic features with cultural and behavioral traits" ( McCarthy, 2009, p. 10). To help students see that they are "racing" people in their minds, I present three ideas.

First, in the United States, the racial categories we use are essentially the same categories used by the Swedish botanist, Linnaeus, 250 years ago. Linnaeus (1758), using his new taxonomic system for categorizing plants and animals, classified people as belonging to the Class- Mammalia, Order- Primates, Genus- Homo, and Species- sapiens. Linnaeus further subdivided Homo sapiens into four types, on the basis of geography and skin color: Europaeus (white skins), Asiaticus (yellow skins), Americanus (red skins), and Afer (black skins; Tattersall & DeSalle, 2011). Linnaeus further suggested that each group had a characteristic temperament due to an excess of one of Galen's four humors: blood, phlegm, yellow bile, and black bile ( Brace, 2005). For example, Linnaeus characterized Europeans as having an excess of phlegm and being "sanguine," "confident, muscular, and inventive." He described American Indians as having an excess of blood and therefore being "choleric," "energetic, upright, and combative." He said that Asiatics had an excess of yellow bile, which caused them to be "melancholic" and "gloomy, thoughtful, inflexible, and avaricious," while Africans were said to have an excess of black bile, which caused them to be "bilious" and as a result, "self-contented, lazy, slow, and relaxed" ( Tattersall & DeSalle, 2011, p. 12). Some of these stereotypes are still in use today.

Second, in class, we talk about how racial categories differ from culture to culture. For example, Barack Obama, the son of an African father from Kenya with dark skin, and a European American mother from Kansas with light skin, would typically be raced as "White" in Brazil but as "Black" in the United States, while he would have been raced as "colored" had he lived under South African apartheid. The idea that in Brazil, people with any European ancestry are raced as White, while in the United States, people who have any African ancestry are raced as Black, often drives discussion toward the "one drop rule" in the United States, and how by 1920, the same person might be raced differently depending on the state. This helps students to challenge their own culturally received notions of the fixedness of racial categories.

Third, we do a class activity to show that many human biological traits are continuous variables, rather than discrete categories. This can be done with a number of easily visible traits, such as height or curliness of hair (have students line themselves up from most straight to most curly), but I always conclude with skin color. Have students line themselves up from most pale to most dark skin (using the inner side of the upper arm works well). Then, let them try to decide where to divide themselves into specific categories. Ask, "How many categories should there be?" and "Why do there need to be categories?"

This exercise lets students see that skin color is an example of a biological cline-the gradual change of a trait across the geographical range of a species. Kittles and Weiss (2003) explain, that "if one examines only the geographic extremes, differences appear large" (p. 38). For example, if you juxtapose people from the Congo in West Africa, and people from Norway, you might conclude that the two peoples looked so different that they were of different "races." However, if you walked all the way from the Congo through Egypt and the Middle East to Norway, you would find that skin color varies very gradually-almost imperceptibly-as you travel. There is no place where one color of skin gives way abruptly to another-no place where you can draw a line and say that people on one side of the line have a different color of skin than people on the other side of the line. Famously, Livingstone (1962), a population biologist, concluded, "there are no races, there are only clines" (p. 279). Scientists have been unable to find a way to objectively and reliably divide people into the same set of racial groupings ( Mukhopadhyay et al., 2014).

"Racial" Traits Do Not Correlate With Other Types of Biological Diversity

A second argument against race as biology is that the visible traits that people use to identify "race," like skin color, hair texture, or facial characteristics, do not correlate with other types of human biological diversity. Students in diversity classes sometimes assume that there is a gene for intelligence, or a gene for athletic ability, or a gene for heart disease. But that is not the case. Even a trait that seems relatively straightforward, like height (which has only one value for each person at a time) is highly complex genetically. For example, in a study of 183,727 adults, Allen et al. (2010) found that "hundreds of genetic variants, in at least 180 loci, influence adult height" (p. 832). However, the genetic variants they identified accounted for only 10.5% of the variation in height in their sample, suggesting that there are many more genes that affect height that have not yet been identified. Height is a classic polygenic trait, meaning that it is controlled by multiple genes, each of which has a very small effect ( Allen et al., 2010).

If hundreds of genes control height, consider how much more complex a trait like "intelligence" is. Psychologists have spent 150 years trying to define and measure intelligence, and they still disagree ( Nisbett et al., 2012). Some scientists believed that because intelligence, as measured by analytic IQ, is 40% to 80% heritable, genes affecting it would be easy to find, once the human genome had been mapped. However, "whereas 282 individual genes responsible for specific forms of mental retardation have been identified, very little progress has been made in finding the genes that contribute to normal variation" in intelligence (p. 135). In fact, Butcher, Davis, Craig, and Plomin (2008) reported that only one gene has been consistently replicated as influencing cognitive ability, and it explains less than 1% of the variance in general cognitive ability.

Cooper (2005) says that all too frequently, "during the last hundred years, the debate over the meaning of race has retained a highly consistent core . . . [built] around the same belief in Black inferiority" (p. 71). Every now and then, he says, someone uses "the latest jargon and half-truths from the margins of science" to reassert that people with the ascribed status of "Blacks" in the United States are inferior ( Cooper, 2005, p. 71; see, for example, Chase, 1977; Hearnshaw, 1981; Hernstein & Murray, 1994; Rowe, 2005). However, Cooper concludes that

despite substantial effort, no genetic polymorphism has yet been found that accounts for any significant proportion of the "racial differences" in the rates of common diseases, IQ, or any other similar trait-nor is there any reason . . . to expect that to be the case. Contrariwise, there is massive and highly consistent evidence of social influences. (p. 74)

In their review of the literature, Nisbett et al. (2012) agree. They conclude that "the direct evidence indicates that the difference between the races is entirely due to environmental factors" (p. 146).

Environment Influences the Genetic Structures of Human Groups via Natural Selection

A fundamental theory of biology is that over time, geography and environment influence the genetic structures of human populations through natural selection. People differ in any number of observable traits, such as height, shape of head, length of arms and legs, stockiness, and facial characteristics, just as they vary in other traits like ABO blood groups and Rh factors. Why is it that traits vary across populations?

Darwin (1876/1902) hypothesized that a single species, spread out over different environmental niches and isolated over time, would adapt to better fit new environments through natural selection. He observed that traits (such as beak shape and size in finches, or skin color or dentition in people) were heritable. However, he had no knowledge of the mechanism of heredity. (Although the work of Mendel outlining the basic mechanics of heredity had been published in an obscure journal in 1866, it was not "rediscovered" until 1900; Darwin died in 1882. So, although Mendel lived at the same time as Darwin, Darwin did not know of his work.)

Today, we know that human DNA consists of some 3.2 billion base pairs (G-C or A-T) arranged in the famous double helix model. During the process of meiosis, when human eggs or sperm cells are created, random copying errors can occur. Most are corrected, but occasionally some errors, or mutations, slip by. Mutations can occur in a single base pair, or through duplication or inversion of a gene (which can have thousands of base pairs), or they can occur through unequal crossing over or duplication of chromosomes (as in Trisomy 21, which causes Down syndrome). A mutation can be neutral, harmful, lethal, or (rarely) beneficial to the individual in whom it occurs. If the individual with the mutation successfully reproduces, the mutation may be passed on to the next generation. Mutations are important for evolution through natural selection because they introduce variety into DNA ( Gould, 1980).

Mutations can be functional or nonfunctional. On one hand, mutations that are located in nonfunctional areas of the genome do not affect genes or parts of the DNA that turn nearby genes on and off. Therefore, as mutations in nonfunctional locations in the genome do not differentially affect successful reproduction, they are not subject to natural selection. However, nonfunctional mutations can be very useful as genetic markers to trace human history. These genetic markers can be used to show ancient human migration patterns; they can also be used to show how closely two population groups are related. For example, genetic markers have been used to determine how closely the Hadza (northern Tanzania), the Sandawe (central Tanzania), and the San (South Africa) peoples, all of whom speak rare click languages, are related ( Tishkoff et al., 2007). Long (2003) concluded that "population history and relationships are read best from DNA sequences without function" (p. 17).

On the other hand, as functional mutations affect genes, or parts of the DNA that turn nearby genes on and off, they are subject to natural selection. Long (2003) concluded that, in contrast to mutations in nonfunctional areas, "DNA sequences that encode expressed genes will show patterns of variation that are more directly related to natural selection and human adaptation" (p. 17).

Scientists are now able to demonstrate how a mutation in a single base pair (one of 3.2 billion) has resulted in a change in a known trait, such as blue eyes. A mutation in a single base pair is called a single nucleotide polymorphism (SNP). In 2008, Eiberg et al. were able to show how the mutation of a single base pair (from A to G) within the HERC2 regulatory gene inhibits the activity of the nearby OCA2 gene. Essentially, the mutation turns off the biosynthesis of melanin (the brown pigment that results in brown eyes) in the iris. People who have two copies of the mutation (the rs12913832*G allele) have blue eyes with no brown pigmentation. People who have two copies of the ancestral allele (the rs12913832*A allele) have brown eyes. The team's research suggests that this is a "founder mutation," meaning that everyone who has the *G allele at this position on chromosome 15q can trace their ancestry back to a single person in whom the mutation first occurred, who most likely lived in the northwest part of the Black Sea region 6,000 to 10,000 years ago ( Eiberg et al., 2008). This type of work is pioneering, because it follows a specific single-point mutation (A to G), through its mechanisms of action, to show how it produces a known human trait. This is an example of the type of random mutation that has recently introduced genetic diversity into a population. However, scientists believe that the rapid increase in blue eyes in Europeans was due to sexual selection, rather than natural selection. They suggest that blue eyes may have been seen as novel, and therefore desirable, in mate selection ( Eiberg et al., 2008). In contrast, let us look at how mutations affect traits that appear to have been beneficial to successful reproduction, and therefore were subject to natural selection.

Hemoglobin S

Hemoglobin S is an abnormal red blood cell which causes sickle-cell anemia. Sickle-cell anemia, a serious, often fatal disease, is also caused by a single-point mutation, from an A to a T. To get sickle-cell anemia, a person must inherit two copies of the mutation (one from each parent). The mutation alters one of the amino acids in the hemoglobin protein which results in abnormal red blood cells, that, under certain conditions, change to a long, sickled shape which causes anemia, pain, and tissue damage (see DNA Learning Center, Cold Spring Harbor Laboratory, n.d.). Prior to modern medicine, sickle-cell anemia was invariably fatal. This should have resulted in people with sickle-cell anemia dying before they could reproduce, thus selecting against the mutation over the generations.

However, instead of being selected against, the sickle-cell mutation is very common in areas with malaria, such as India, the Mediterranean, and sub-Saharan Africa, where 10% to 40% of the population carries it. The reason is that for people who have only one copy of the sickle-cell mutation, the mutation confers tolerance to malaria-people still get malaria, but they do not die from it ( Ferreira et al., 2011). Studies of the distribution of Hemoglobin S and the distribution of malaria show that the higher the prevalence of malaria, the higher the percentage of people with hemoglobin S. Where there is no malaria, 0% of the population has Hemoglobin S. Brace (1996) concluded that the frequency of the sickle-cell mutation in populations "is controlled by the intensity of infestation with falciparum malaria"-the parasite that causes malaria (p. 113). This is a classic example of natural selection. Over time, geography and the environment (areas conducive to malaria) interacted with a random mutation (Hemoglobin S) that conferred a reproductive advantage in people who carried one copy of the gene.

Researchers believe that the Hemoglobin S mutation occurred independently three times in Africa and once in either the Arabian Peninsula or central India between 70,000 and 150,000 years ago ( Desai & Dhanani, 2004). While such mutations are rare, it is likely that over the last 100,000 years or so, this mutation also occurred a few times in areas of the world where there was no malaria. However, as the sickle-cell mutation conferred no advantage in the interaction between people and their (nonmalarial) environment, it died out.

Lactase persistence

All human infants are able to digest lactose, the primary carbohydrate in milk, because their intestines secrete lactase. In most human populations, the ability to secrete this enzyme goes away after weaning. This is the ancestral condition for humans (and all mammals; Itan, Powell, Beaumont, Burger, & Thomas, 2009). Accordingly, in East Asian and Southeast Asian populations, indigenous North and South American populations, and in large parts of Africa, 0% of the adult population has the lactase persistence trait. This makes sense, because, as long as human cultures were based on hunting and gathering, lactase persistence was unnecessary. However, as animals began to be domesticated, nonhuman milk (goat, cow, horse, camel, reindeer) became readily available as a source of food to pastoralists following their herds. Consequently, there was strong natural selection for lactase persistence in herding societies, and so dairying and lactase persistence co-evolved.

In Europeans, lactase persistence is due to a single C to T mutation at −13910*T, upstream from the lactase gene ( Itan et al., 2009). The 13910*T allele accounts for virtually all the variance in lactase persistence frequency in Europe. It ranges in frequency from 73% to 95% in the British Isles and Scandinavia, 56% to 67% in Central and Western Europe, and 6% to 36% in Eastern and Southern Europe. Itan et al. (2009) date the origin of dairying and the co-evolving −13910*T lactase persistence mutation to about 7,500 years ago. Moreover, they conclude that this is a "recent mutation event" ( Ingram, Mulcare, Itan, Thomas, & Swallow, 2009, p. 586); Bersaglieri et al. (2004) concluded that the signals of recent selection for the −13910*T lactase persistence mutation they observed were among the "strongest yet seen for any gene in the genome" (p. 1111).

However, genotype frequency comparisons have shown that the European mutation is not found in African and Middle Eastern dairying populations. Instead, different lactase persistence-associated mutations occurring in the same region of the genome have been identified. For example, Bedouins in Jordan and Saudi Arabia have the −13915*G mutation, while pastoralists in Kenya and Tanzania carry the −13907*G variant and the −14010*C variant ( Ingram et al., 2009; Tishkoff et al., 2008). This is an example of convergent evolution. It is likely that over the last 10,000 years, mutations in the control area upstream of the Lactase (LCT) gene also occurred a few times in areas of the world where there was no dairying. However, as those mutations conferred no advantage to nondairying populations, they died out.

Geography and environment also influenced the genetic structures that resulted in varied skin colors among different human populations. Unlike blue eyes or Hemoglobin S, skin color is a polygenic trait-one whose phenotype is influenced by multiple genes, each one having a relatively small effect ( Sturm, 2009). Observable skin color is determined by the amount and distribution of two types of melanin pigment granules within skin cells-a red-yellow form known as pheomelanin and a black-brown form known as eumelanin ( Barsh, 2003; McEvoy, Beleza, & Shriver, 2006). For example, Beaumont et al. (2007) showed that in Europeans, red hair and fair skin with freckles are associated with loss-of-function alleles of the Melanocortin Receptor (MC1R) gene. These alleles have been shown to decrease the ability of the skin to produce eumelanin (the black-brown melanin) in in vitro functional studies ( Beaumont et al., 2007). Skin color is measured with a hand-held instrument using skin reflectance spectroscopy ( Shriver & Parra, 2000).

Anthropologists assume that the "earliest members of the hominid lineage probably had a mostly unpigmented or lightly pigmented integument [skin] covered with dark black hair, similar to that of the modern chimpanzee" ( Jablonski & Chaplin, 2000, p. 57). They also assume that after our lineage diverged from the lineage of modern chimpanzees, "coincident with the loss of fur . . . there was strong selection for skin darkening" to protect the skin from the ultraviolet rays of the sun ( McEvoy et al., 2006, p. R176). Both of these changes occurred roughly 2 to 5 million years ago ( Fuentes, 2012). Therefore, anthropologists assume that the process of differentiation of skin color started from a population of Homo sapiens with dark skin.

On a global level, skin color in indigenous populations in the Old World tends to be darkest in the tropics. The farther north or south of the tropics, the lighter skin color becomes. The reason appears to be related to the amount of sun light, which is much greater at the equator than at the poles. Melanin absorbs and scatters light ( Jablonski & Chaplin, 2000). Jablonski and Chaplin (2013) found that "86% ( r = 0.927) of the variation in human skin reflectance" can be accounted for by autumn levels of ultraviolet radiation (p. 672). The reason is that humans need enough ultraviolet light to make Vitamin D, but too much ultraviolet light results in sunburn and the destruction of folate, which is necessary for healthy reproduction. The amount of pigment in human skin enables populations to balance these two needs. Therefore, on one hand, in the high latitudes like Sweden or Siberia, there was "positive directional selection" for less melanin in the skin so that people in the high latitudes could make more Vitamin D ( Jablonski & Chaplin, 2000, p. 673). On the other hand, near the equator, in places like Papua New Guinea, Southern India, or the Congo, there was positive selection for more melanin in the skin, so that people could be protected from too much sun and the destruction of folate ( Jablonski & Chaplin, 2000).

Selective sweeps

With regard to how much effect natural selection has had on Homo sapiens in the last 50,000 years or so, at the turn of the 21st century, there were still two camps. Those in the first camp argued that cultural evolution, such as adapting to extreme cold by learning to make thick clothes out of fur skins, had lessened the effects of natural selection. Those in the second camp argued that Homo sapiens continued to benefit from positive natural selection during the last 50,000 years ( Hawks, Wang, Cochran, Harpending, & Moyzis, 2007). Rogers (2011) states that "as recently as the year 2000, it was possible for Stephen Jay Gould to argue that 'natural selection has almost become irrelevant in human evolution. There's been no biological change in humans in 40,000 or 50,000 years'" (p. 93). Gould (1980) had previously argued that "cultural evolution is our primary innovation. It works by the transmission of skills, knowledge and behavior through learning-a cultural inheritance of acquired characters" (p. 137). Rogers states that in 2000, when Gould gave this interview, there was no way to tell which position was correct. However, had Gould lived 10 years longer, advances in genetics would have made Gould's position "untenable," and Rogers believes Gould would have changed his mind. Today, just 15 years later, there is plenty of evidence that natural selection is still affecting humans. Indeed, Hawks et al. (2007) argue that the rapidly expanding world population since the domestication of plants and animals (resulting in shifts from hunter-gatherer cultures to pastoralism and agriculture, about 10,000 years ago) has resulted in a 100-fold increase in mutations, thus increasing the amount of positive natural selection that is occurring.

The way scientists evaluate genomes for evidence of positive natural selection is to look for selective sweeps. Long (2003) states that

a favorable allele may occasionally rise rapidly and sweep through the population replacing all other alleles at that locus. This mode of selection is often referred to as positive selection. One consequence of a selective sweep is that the level of background genetic variation in the vicinity of the favored allele is reduced. (p. 7)

Another way to explain this is that DNA tends to be inherited in chunks or blocks of base pairs grouped around a functional SNP on a chromosome. Functional mutations (SNPs) that occurred earlier in human history tend to have shorter blocks or chunks of unchanged DNA surrounding them, because they had many more generations for recombination to shorten the length of the unchanged stretches of DNA attached to them. However, functional mutations (SNPs) that have occurred relatively recently in human history have much longer chunks of unchanged DNA surrounding them. Several new statistical tests have been developed to evaluate the presence of selective sweeps and their population frequency ( Huff, Harpending, & Rogers, 2010; Pickrell et al., 2009; Sabeti et al., 2002; Voight, Kudaravalli, Wen, & Pritchard, 2006). These tests are particularly effective at identifying selective sweeps at moderate frequency (~50%-80%), and at high frequency (>80% to fixation) within a population ( Pickrell et al., 2009). For example, McEvoy et al. (2006) identified "a 150 kb region surrounding the SLC24A5 gene" that "shows a large drop in heterozygosity in Europeans." This means that the 150 kb region around the gene is unchanged and thus shows evidence of recent selection (p. R177).

McEvoy et al. (2006) were looking for genes within regional populations that affected skin pigmentation. The team studied DNA from three geographically distinct populations from West Africa, East Asia, and Northern Europe. Based on differences among these three groups, they developed a four-step evolutionary model for skin pigmentation. First, they found evidence of mutations in two genes (MITF and EDN3) that occurred in the ancestral human population, prior to any splits between the groups. Second, they found evidence of a split between the African group and the ancestors of Asians and Europeans, who carried the ASIP and BNC2 genes. Third, they identified five genes that showed positive selection only in the East Asian population. Fourth, they identified five different genes that showed positive selection only in the Northern European population. All the genes identified were involved in the pathway for the biosynthesis of melanin. Both Northern Europe and East Asia are at much higher latitudes than Africa, so pale skin with less melanin benefitted humans in both environments. But since mutations are random, nature could only positively select the mutations related to the biosynthesis of melanin that actually occurred in the Northern European and East Asian populations. Thus, the genetic mechanisms that resulted in the pale skin color of East Asians and Europeans are different; this is an example of convergent evolution ( McEvoy et al., 2006). The McEvoy et al. (2006) study shows clear evidence for the operation of natural selection with regard to skin color. As a result of studies like this one, molecular biologists have concluded that "skin colour as a selectable trait has likely occurred multiple times at diverse geographical sites around the globe" ( Sturm, 2009, p. 13).

There Is More Diversity Within Than Between Racial Groups

The fourth argument against race as biology is that there is more diversity among people within groups than between groups. That means that there is more diversity among people within a single population, for example, among Samoans, than there is between regions (or "races") like Europe and sub-Saharan Africa. Lewontin (1972) was the first to demonstrate this. In a landmark article, he examined the frequency of alleles of 17 genes over 101 different populations. First, he established that there were differences in frequencies between populations for each of the 17 genes. For example, he found that the Duffy antigen Fy a occurs in 66% of Europeans and 99% of East Asians but in only 10% of sub-Saharan Africans ( Lewontin, 1972). Then, Lewontin divided the 101 populations into seven "races": Caucasian, African, Mongoloid, South Asian Aborigines, Amerinds, Oceanians, and Australian aborigines. For example, in his Amerind race, he included 21 North, Central, and South American populations; in his Oceanian race, he included 15 populations ranging from the Hawaiians to the Maori.

Lewontin (1972) stated that the statistical question he asked was "How much of human diversity between populations is accounted for by more or less conventional racial classification?" (p. 386). He noted that dividing world populations into seven races (instead of four, for example, as Linnaeus did) and weighting them equally maximizes "both the total human diversity and the proportion of it that is calculated between populations" ( Lewontin, 1972, p. 385). In other words, his assumptions bias the statistics toward showing more diversity between regions or "races." Using the frequencies of different alleles, he calculated diversity within each population (e.g., Basques, or Koreans, or Navaho). Then, he calculated diversity between populations within a region, for example, between all 15 of the Oceanian populations. Then, he calculated the diversity between the seven regions or "races."

Lewontin (1972) concluded that "the results are quite remarkable" (p. 396). Of the total genetic diversity (100%), he found that the average within-population diversity (e.g., within Danes, or within Navaho) was 85.4%. The difference between populations within a region (e.g., between the 15 Oceanian populations) accounted for 8.3% of the total diversity. He found that only 6.3% of the total diversity was accounted for by regional or "racial classification" ( Lewontin, 1972, p. 396). What this means is that most biological variability exists between you and your neighbors in the same population. Lewontin stated that "based on randomly chosen genetic differences, human races and populations are remarkably similar to each other, with the largest part by far of human variation being accounted for by the differences between individuals" (p. 397).

Lewontin's (1972) pioneering findings continue to be borne out by more recent studies. Relethford (2002) summarized six studies looking at within-group variation versus between-group variation. He reviewed studies assessing differences in blood polymorphisms, microsatellite DNA, RFLPs, Alu insertions, mtDNA, Y-chromosome DNA, and craniometrics. He concluded that they all showed the same pattern. Variation within local populations (e.g., Tongans) accounts for 68.9% to 85.4% of total differences found. Variation between populations within a region (e.g., populations of Europe, like the Danes and the Spanish) accounts for 1.3% to 8.4% of the total variation ( Relethford, 2002). Finally, variation between regions or "races" (e.g., Europe vs. sub-Saharan Africa) accounts for 6.3% to 24.9% of total differences found ( Relethford, 2002, p. 396).

Findings also suggest that the more genetic diversity there is within a single population, the older the population is. There is a correlation between frequency of variation, age, and geographic distribution ( Kittles & Weiss, 2003). The greater the variation within a geographic distribution, the greater the age of that population. Using several measures of genetic variation, researchers have determined that sub-Saharan Africans have "almost twice the diversity of non-African populations" ( Kittles & Weiss, 2003, p. 44). In fact, all the genetic diversity of populations from all over the world can be found within sub-Saharan Africa ( Wells, 2003). The San (Bushmen) have the most within-population diversity of any group on the planet and, thus, are considered to be the oldest of all the populations living today ( Li et al., 2008; Tishkoff et al., 2009; Wells, 2003).

The exception to this pattern is skin color. Relethford (2002) found that 88% of the total variation in worldwide skin color is found between regions or "races" (e.g., Europe vs. sub-Saharan Africa), while only 9% of the total variation is within group (e.g., among Tongans, or among San, or among Danes; p. 396). As stated earlier, the observable trait of skin color is not correlated with other traits. What this means is that while there is a relationship between continental ancestry and skin color, the classifications we call "race" are meaningless when it comes to genes and DNA for human traits other than skin color. "Race" is truly only skin deep.

All Humans Living Today Are Descended From Africa

The fifth argument against race as biology is that all humans living today are descended from a small group of ancestors who lived in Africa. This is the "out of Africa" or "recent African origin" model ( Veeramah & Hammer, 2014). In the past, some anthropologists had "argued for the origin of human races through a process of separate speciation events from ape-like ancestors in many parts of the world. This hypothesis became known as multi-regionalism" ( Wells, 2003, p. 33). The multiregionalism hypothesis has not been supported. Evidence from genetics supports the idea that we are all one people, whose ancestors lived in Africa.

The more recently two species have branched from a common ancestor, the more similar their DNA sequences will be. When random mutations occur in nonfunctional areas of DNA, and are passed down to offspring, they stay in the DNA. Thus, they can serve as markers for our ancestry. Wells (2003) explains that

our DNA carries, hidden in its string of four simple letters, a historical document stretching back to the origin of life . . . the differences we see when we compare DNA from two or more individuals . . . are the historical language of the genes. (p. iii)

Molecular biologists compare DNA to find differences, called genetic markers, which they can then use to calculate the genetic distance between two populations ( Cavalli-Sforza, 2000). In some cases, they can use the genetic markers to estimate how long it has been since the populations split into two groups.

For an example of how comparison of DNA can be used, take the Neanderthals. The fossil record shows that they lived in Europe and Asia from about 400,000 years ago to 30,000 years ago, and overlapped with modern humans from about 45,000 to 30,000 years ago ( Green et al., 2010). There have been many questions about how Neanderthals and Homo sapiens were related ( Cavalli-Sforza, 2000; Sykes, 2001). The team that analyzed the first Neanderthal genomes found that humans and Neanderthals share about 99.7% of their DNA, and that humans and Neanderthals shared common ancestors about 500,000 years ago ( Green et al., 2010). The results showed clearly that the Neanderthals were not our direct ancestors ( Cavalli-Sforza, 2000). Instead, the Neanderthals were classified as our "sister" species ( Homo sapiens neandertales, whereas we are Homo sapiens). However, the team found that 1% to 4% of DNA is shared between Neanderthals and Eurasian (but not African) Homo sapiens ( Green et al., 2010). This suggests that there was some interbreeding ( Green et al., 2010; Stewart & Stringer, 2012).

By comparison, the first study to sequence and compare the genome of a chimpanzee with a human genome determined that we share 96% of our DNA with chimpanzees, who are our closest living relatives ( Cheng et al., 2005; Lovgren, 2005). The findings of this team suggested that the ancestors of Homo sapiens (including Neanderthals) and chimpanzees diverged about 6.5 million years ago ( Lovgren, 2005).

The same methods of comparing DNA can be used to tell how closely related two human populations are ( Fairbanks, 2012; Jorde et al., 2000). A decade ago, three teams, led by Cavalli-Sforza, by Sykes and by Wells, reported on years of work looking at relationships among human populations. In 2000, Cavalli-Sforza summarized research conducted over 40 years. His team analyzed gene frequencies on 110 blood system groups and proteins from samples of members of about 2,000 aboriginal populations throughout the world. He concluded that all modern humans are members of one species which originated in Africa. He calculated that some modern humans left Africa between 80,000 and 50,000 years ago and reached Australia by 50,000 years ago. His model of human migration from Africa suggests that after Australia, humans settled Asia, then Europe, and finally, via East Asia, the Americas ( Cavalli-Sforza, 2000).

In 2001, Sykes summarized 25 years of work on mitochondrial DNA (mtDNA), which has the advantage of being passed intact, directly from mother to child. As mtDNA is found within the mitochondria, small "energy factories" within cells, it is not involved in sexual reproduction. When a mutation, such as a change from a G to an A, occurs in the DNA of a mitochrondrion in a woman's germ cell, if that germ cell is passed on to a daughter, the mutation will continue in the daughter's DNA. In other words, your mtDNA is an exact copy of your mother's mtDNA, which is an exact copy of her mother's DNA, which is an exact copy of her mother's DNA, and so on. A mutation occurs in mtDNA about once every 10,000 years, which enables scientists to estimate how long ago two lines shared a common maternal ancestor ( Sykes, 2001).

After analyzing thousands of samples from all over Europe, Sykes (2001) found that nearly all native Europeans could trace their maternal ancestry to one of just seven different women, who lived between 45,000 and 10,000 years ago. Remarkably, 47% of Europeans have mtDNA that traces back to one woman, who lived about 20,000 years ago, most likely in the area of the Rhone River in France. Sykes explained that each of these women was certainly not the only woman living in her hunting and gathering band at the time. But if a woman has no children or only boys, her mtDNA line dies out.

Using mtDNA sequences from all over the world, Sykes (2001) identified 33 women who are the mothers of all people living today, and 13 of them originated in Africa. His findings suggest that a small group from one of the African mtDNA clans left Africa to populate the rest of the world. The 20 women whose mtDNA clans are found in the rest of the world are all descendants of that single woman whose descendants left Africa. Sykes writes,

Incredibly, even though the African clans are easily the most ancient in the world, we are still able to reconstruct the genetic relationships among them . . . the ancestors of the ancestors . . . One by one the clans converge until there is only one ancestor, the mother of all of Africa and of the rest of the world . . . "Mitochondrial Eve." ( Sykes, 2001, p. 276)

Sykes (2001) concluded that "we are all direct maternal descendants" of Mitochondrial Eve, who lived about 150,000 years ago in Africa (pp. 276-277).

Y-chromosome DNA

In 2003, Wells released a book on his research team's findings using DNA from the Y-chromosome. The Y-chromosome is passed down from fathers to sons just as mtDNA is passed down from mothers to daughters. As with maternal lineages, if a man has no children or no sons, his Y-chromosome lineage is lost. The Wells (2003) team studied a "worldwide sample of men, from dozens of populations on every continent" (p. 53).

Wells (2003) concluded that all modern humans originated in Africa. He also concluded that all men alive today can trace their paternal lineage back to one man-"Y-chromosome Adam"-who lived in Africa about 60,000 years ago. While there were other men alive then, their lineages have died out. He noted that the difference between the estimated age of "Mitochondrial Eve" and "Y-chromosome Adam" (who were real people) means that more female lineages survived, unbroken, into the present day. As a result, scientists could trace the maternal line much further back into prehistory (150,000 years) than they could trace the paternal line of all people living today. Wells explained that the greater the diversity, as shown by the accumulation of additional genetic markers, the older the lineage. As a result, he said that "you are more likely to sample extremely divergent genetic lineages within a single African village than you are in the whole of the rest of the world" ( Wells, 2003, p. 39). He emphasized that the real surprise is that as all modern humans lived in Africa until at least 60,000 years ago, our species has only had 60,000 years to populate the globe ( Wells, 2003).

Wells (2003) divided the descendants of men who left Africa into a genealogical tree with 11 lineages. Each genetic marker represents a single-point mutation (SNP) at a specific place in the genome. First, genetic evidence suggests that a small band with the marker M168 migrated out of Africa along the coasts of the Arabian Peninsula and India, through Indonesia, and reached Australia very early, between 60,000 and 50,000 years ago. This very early migration into Australia is also supported by Rasmussen et al. (2011). Second, a group bearing the marker M89 moved out of northeastern Africa into the Middle East 45,000 years ago. From there, the M89 group split into two groups. One group that developed the marker M9 went into Asia about 40,000 years ago. The Asian (M9) group split three ways: into Central Asia (M45), 35,000 years ago; into India (M20), 30,000 years ago; and into China (M122), 10,000 years ago. The Central Asian (M45) group split into two groups: toward Europe (M173), 30,000 years ago and toward Siberia (M242), 20,000 years ago. Finally, the Siberian group (M242) went on to populate North and South America (M3), about 10,000 years ago.

Whole genomes

While the earlier studies compared frequencies of gene alleles for blood proteins, or genetic markers in parts of the mtDNA or the Y-chromosome, second generation sequencing now enables teams to compare whole genomes. For example, Li et al. (2008) analyzed 650,000 base pairs that had been previously identified as having mutations (SNPs), in the genomes of 1,064 individuals from 51 populations. The genomes of members of 51 populations were compared with each other and with chimpanzees. (The chimpanzee genomes were assumed to represent "ancestral allele frequencies"-the frequencies of alleles before humans and chimpanzees began to diverge from a common ancestor.) Li et al. constructed a phylogenetic tree diagram showing the relationships among the populations. The least different from the ancestral allele frequencies were the San (Bushmen) and other sub-Saharan African populations, followed by North African populations, European, Middle Eastern, Central Asian, East Asian, Amerindian, and Oceanian populations. (Australian aboriginal populations were not studied.) They concluded that their findings were consistent with a "serial founder effect, a scenario in which population expansion involves successive migration of a small fraction of individuals out of the previous location, starting from a single origin in sub-Saharan Africa" ( Li et al., 2008, p. 1103). Their study fully supports the recent African origin model.

Second-generation population history studies

Recent work with second generation sequencing and new statistical modeling methods adds much finer detail on migration and admixture of populations. For example, in Europe, Stewart and Stringer (2012) show a cyclical pattern of interglacial expansion of Homo sapiens out of Africa and retreat back to Africa or warmer refuges during ice ages. They showed that populations of Homo sapiens moved out of Africa during warm interglacial periods, then retreated from Europe and Asia into southern areas like Spain, Italy, the Balkans, and the Caspian Sea during the last ice age (about 27,000-11,700 years ago), and then expanded again to repopulate Europe after the climate warmed. Behar et al. (2006) supported these findings by showing that the Basques are a remnant of the Paleolithic hunter-gatherer population that retreated into the area around the Bay of Biscayne during the last ice age. The hunter gatherers then expanded to resettle Central and Western Europe after the end of the last ice age. Using genome-wide data from 94 ancient Europeans who lived 8,000 to 3,000 years ago, Haak et al. (2015) modeled the genetic admixture among the indigenous hunter gatherers, Neolithic farmers expanding into Europe from Anatolia (starting about 8,000 years ago), and the Yamnaya or kurgan culture-a pastoralist culture from the steppes north of the Black and Caspian Seas. The Yamnaya culture had horses, wheeled vehicles, and carried the gene for lactase persistence. Haak et al.'s study showed a massive migration of the Yamnaya people into central Europe about 4,500 years ago, one that could have spread an early form of the Indo-European language, which is the basis of most of today's European languages.

Much of northern India also speaks Indo-European languages. In the first major work on population history in India, Reich, Thangaraj, Patterson, Price, and Singh (2009) used second generation sequencing technology and statistical modeling to compare the genomes of 25 diverse groups from India to the genomes of people from Western Asia, Europe, and the Andaman Islands (who are thought to be closest to the ancestral populations of southern India). They found that the "Ancestral North Indians" (ANI) form a clade with Europeans (meaning that they are closely related), but are genetically distinct from the "Ancestral South Indians" (ASI), who form a clade with the Andaman Islanders ( Reich et al., 2009). Using admixture modeling, they found that different Indian groups inherited different proportions of ancestry from the ANI who are related to western Eurasians, and the ASI, who are related to the Andaman Islanders (p. 491). This parallels the language data-Northern Indian groups speak Indo-European languages, while Southern Indian groups speak Dravidian languages. However, Reich's team called for further investigation to date the beginning of the admixture of Northern Indian and Southern Indian populations.

Thus, the work of teams examining blood group allele frequencies, mtDNA, Y-chromosome DNA, and whole genomes, all shows the same pattern. By comparing the DNA of people from around the world, scientists can determine where their ancestors came from and approximately when migrations took place. And in doing so, they have found that the ancestors of all humans living today came from Africa ( Veeramah & Hammer, 2014). We are all Africans, no matter the color of our skin.

All Humans Living Today Are One Biological Species

The sixth argument against race as biology is that all humans living today are one biological species. The most common definition of a biological species is "a group of interbreeding natural populations that are reproductively isolated from other such groups" ( Fuentes, 2012, p. 108). In other words, one criterion that defines populations as part of the same species is that they can mate and reproduce successfully. By that criterion, it is clear that all humans today are part of the same species. Different species, for example, fox and gray squirrels east of the Mississippi River in the U.S., do not recognize each other as potential mates. All humans, from any population group, can and do mate and reproduce successfully (unlike, for example, horses and donkeys, which can mate, but produce mules, which are infertile). Mukhopadhyay et al. (2014) state that "Contemporary humans are, and always have been, one species, with roots in Africa. There are no subspecies of humans" (p. xvi).

Conclusion

On its face, race seems to be "a concept that is intuitively biologically based" ( Kittles & Weiss, 2003, p. 34). Yet, during the 18th century, the idea that humans could be divided into different biological races that were correlated with different traits and characteristics, such as "intelligent and hard-working" versus "unintelligent and indolent," seems to have appeared about the same time that chattel slavery was rapidly expanding as a money-making opportunity for Europeans ( Smedley & Smedley, 2005). This suggests that the idea of race had a social genesis tied to the justification of slavery. However, even during the time of Linnaeus, there were some authors, e.g., Blumenbach, who recognized that "no absolutely sharp distinction could be expected between different peoples and [that] . . . the varieties of mankind . . . seemed to have been arbitrarily chosen as to both number and definition" ( Boyd, 1950, as cited by Kittles & Weiss, 2003, p. 35). Since then, despite the fact that humans may look very different from each other on the surface, scientists have found that under the skin, we are all alike.

In summary, there are a number of evidence-based reasons why race is not biological. First, there are no objective, identifiable traits by which people can be reliably divided into racial groups. Second, skin color, which is the primary basis of folk conceptions of race in the United States, has been shown to be the result of natural selection; it is a result of the interaction between geographical environment and random mutations in genes that affect the biosynthesis of melanin in the skin. Third, visible traits like skin color do not correlate with traits like blood groups, much less with complex traits like intelligence, athletic ability, or musical ability. Fourth, another way to show that skin color does not correlate with other human traits is to statistically compare within-population variation versus between-region variation. Researchers find that there is much more variation within a single population, like the Yoruba, than there is between geographical regions or "races" (e.g., between Europeans and sub-Saharan Africans).

Fifth, by comparing the genetic markers (mutations or SNPs) of people in populations all over the world, scientists can determine population expansion patterns of the past. Using "molecular clocks," they can also roughly estimate how many thousands of years ago an out-migration or admixture occurred. By comparing genetic markers in mtDNA, Y-chromosome DNA, autosomal DNA or whole genomes, researchers concluded that all humans living today are descended from Africa. Furthermore, all human populations outside of Africa are descended from one hunting and gathering band that migrated from Eastern Africa, probably about 60,000 years ago. Within Africa, the ancestry of sub-Saharan African populations can be traced back to the San, who appear to have the most similarities to the ancestors of all people living today ( Li et al., 2008; Tishkoff et al., 2009). There is no research that supports the theory of polygenesis or multiregionalism, which posited that different "races" arose independently in different geographic regions.

Finally, because members of all human populations living today can successfully interbreed, by definition, humans constitute one species. Although some populations lived long enough in certain geographic environments for natural selection to alter characteristics like skin color, these populations were not isolated long enough to become new species. There is a great deal of both prehistoric and historic evidence for extensive global trading routes, which led to people from different groups meeting and mating over thousands of years of human history ( Fuentes, 2012).

Many students in the United States equate race with skin color. The idea that race is not skin color, or a set of discrete biological types, but instead is socially constructed, is one of the most important ideas of our time. Omi and Winant (2015) conclude as follows:

Race is not something rooted in nature, something that reflects clear and discrete variations in human identity. But race is also not an illusion. While it may not be "real" in a biological sense, race is indeed real as a social category with definite social consequences. (p. 110)

For many students, moving from race-as-biology to race-as-socially-constructed is as profound as learning that the earth is round, when they always knew it was flat ( Goodman et al., 2012). It requires a paradigm shift. While this paradigm shift will not be sufficient to eliminate racism in our time, it is surely a necessary step in the right direction.

When I used these six scientific arguments as to why race is not biological to teach my students, I found that more of them accepted the idea that race is socially constructed. I suspect that I am not the only social scientist teaching diversity classes whose teaching may benefit from increased biological science literacy. Understanding how 21st century science supports arguments against race-as-biology will help educators assist students to make the necessary paradigm shift.

Acknowledgements

Thanks to David Stoesz and Jim Bonacum who thoughtfully reviewed the manuscript prior to submission.

Declaration of Conflicting Interests
The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding
The author(s) received no financial support for the research and/or authorship of this article.

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Author Biography

# data[].attributes.attachment_link.title
Teaching Diversity: The Science You Need to Know to Explain Why Race Is Not Biological - Kay Young McChesney, 2015

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This article is targeted to faculty teaching race and ethnicity, racism, diversity, and multicultural courses. Many students equate race with skin color. The premise of this article is that to teach students about the social construction of race, teachers must first know enough science to teach students that race is not biological.

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Teaching Race (Bioculturally) Matters: A Visual Approach for College Biology Courses

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Race and racism are considered standard subject matter in introductory college courses in the social sciences, but remain relatively absent in biological science courses (Donovan, 2015; Morning, 2011). Given a resurgence of biologically deterministic racial science (e.g., Risch et al., 2002; Shiao et al., 2012) and ongoing racial tensions in the United States, it is imperative that biology professors actively engage students in introductory and upper-level courses.

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Donald Trump's election as the 45th President of the United States has been marked by the brewing storms of racial conflicts. A rise in racial incidents ensued in the immediate aftermath of Trump's victory in November 2016. Since the beginning of 2017, over 100 bomb threats have been made against Jewish community centers and schools. Trump's travel ban, signed in late January 2017, initially affected about 90,000 people from seven Middle Eastern countries; 87,000 of those banned were Muslims. Minorities such as American Muslims and black Americans have expressed fears over racial relations under Trump. Undeniably, the topic of race-and racism-has gripped America and the world throughout.

Over the last decade, there have been hopes that the US has become a post-racial society, free of racial prejudice and discrimination. However, the most recent months indicate the contrary: race remains an incendiary issue. Race and racism are not new issues, but in today's 21 st century Trump-era, discussions about race are distinct from those of the past in that they possess an entirely new dimension: that of genetics and DNA.

Race in the new era of human genetics research

In 2003, scientists completed the Human Genome Project, making it finally possible to examine human ancestry with genetics. Scientists have since tackled topics such as human migrations out of Africa and around the world. And it's not just scientists who are excited about human genetics: widely affordable at-home ancestry test kits are now readily available from companies like 23andMe, Family Tree DNA, and Ancestry. For $99-around the price of a romantic dinner or a pair of Nikes-a customer can receive an analysis from 23andMe indicating that they are, for instance, 18.0% Native American, 65.1% European and 6.2% African.

The soaring popularity of ancestry testing bespeaks a widespread perception that we can use these tests to dissect, delineate, and define our ancestral composition. Indeed, social media is teeming with blog posts, and even livestream videos, from excited customers bursting to broadcast their test results and their reactions. Ancestry test kits are the new "it" item-and with their success is the tacit admission of our belief that our DNA can sort us into categories like the " five races:" African, European, Asian, Oceania, and Native American (Figure 1A).

New findings in genetics tear down old ideas about race

Estimating our ancestral composition down to 0.1% seem to suggest that there are exact, categorical divisions between human populations. But reality is far less simple. Compared to the general public's enthusiasm for ancestry testing, the reaction from scientists has been considerably more lukewarm. Research indicates that the concept of "five races" does, to an extent, describe the way human populations are distributed among the continents-but the lines between races are much more blurred than ancestry testing companies would have us believe (Figure 1B).

A landmark 2002 study by Stanford scientists examined the question of human diversity by looking at the distribution across seven major geographical regions of 4,000 alleles. Alleles are the different "flavors" of a gene. For instance, all humans have the same genes that code for hair: the different alleles are why hair comes in all types of colors and textures.

In the Stanford study, over 92% of alleles were found in two or more regions, and almost half of the alleles studied were present in all seven major geographical regions. The observation that the vast majority of the alleles were shared over multiple regions, or even throughout the entire world, points to the fundamental similarity of all people around the world-an idea that has been supported by many other studies (Figure 1B).

If separate racial or ethnic groups actually existed, we would expect to find "trademark" alleles and other genetic features that are characteristic of a single group but not present in any others. However, the 2002 Stanford study found that only 7.4% of over 4000 alleles were specific to one geographical region. Furthermore, even when region-specific alleles did appear, they only occurred in about 1% of the people from that region-hardly enough to be any kind of trademark. Thus, there is no evidence that the groups we commonly call "races" have distinct, unifying genetic identities. In fact, there is ample variation within races (Figure 1B).

Ultimately, there is so much ambiguity between the races, and so much variation within them, that two people of European descent may be more genetically similar to an Asian person than they are to each other (Figure 2).

Does "race" still mean something?

The divisions between races are doubtlessly blurred, but does this necessarily mean that race is a myth -a mere social construct and biologically meaningless? As with other race-related questions, the answer is multi-dimensional and may well depend on whom you ask.

In the biological and social sciences, the consensus is clear: race is a social construct, not a biological attribute. Today, scientists prefer to use the term " ancestry" to describe human diversity (Figure 3). "Ancestry" reflects the fact that human variations do have a connection to the geographical origins of our ancestors-with enough information about a person's DNA, scientists can make a reasonable guess about their ancestry. However, unlike the term "race," it focuses on understanding how a person's history unfolded, not how they fit into one category and not another. In a clinical setting, for instance, scientists would say that diseases such as sickle-cell anemia and cystic fibrosis are common in those of "sub-Saharan African" or "Northern European" descent, respectively, rather than in those who are "black" or "white".

However, even if scientists agree that race is, at most, a social construct, any cursory search of the internet reveals that the broader public is not convinced of this. After all, if an Asian person looks so different from a European, how could they not be from distinct groups? Even if most scientists reject the concept of "race" as a biological concept, race exists, undeniably, as a social and political concept.

The popular classifications of race are based chiefly on skin color, with other relevant features including height, eyes, and hair. Though these physical differences may appear, on a superficial level, to be very dramatic, they are determined by only a minute portion of the genome: we as a species have been estimated to share 99.9% of our DNA with each other. The few differences that do exist reflect differences in environments and external factors, not core biology.

Importantly, the evolution of skin color occurred independently, and did not influence other traits such as mental abilities and behavior. In fact, science has yet to find evidence that there are genetic differences in intelligence between populations. Ultimately, while there certainly are some biological differences between different populations, these differences are few and superficial. The traits that we do share are far more profound

Science and genetics: Instruments of modern racism

Despite the scientific consensus that humanity is more alike than unlike, the long history of racism is a somber reminder that throughout human history, a mere 0.1% of variation has been sufficient justification for committing all manner of discriminations and atrocities. The advances in human genetics and the evidence of negligible differences between races might be expected to halt racist arguments. But, in fact, genetics has been used to further racist and ethnocentric arguments-as in the case of the alt-right, which promotes far-right ideologies, including white nationalism and anti-Semitism.

Considered a fringe movement for years, the alt-right gained considerable attention and relevance during Trump's presidential campaign. Indeed, Steve Bannon, the current senior counselor and chief strategist to President Trump and the former chief executive officer of Trump's campaign, has notable ties to the alt-right. Once relegated to obscure internet forums, the alt-right's newest pulpit is the White House.

Members of the alt-right are enthusiastic proponents of ancestry testing as a way to prove their "pure" white heritage (with Scandinavian and Germanic ancestry being among the most desirable) and to rule out undesired descent from any other groups (including, unsurprisingly, Africans and the Ashkenazi Jews, but even certain European groups, such as Italians and Armenians). The belief in white superiority, and the need to preserve it, drives the alt-right movement-and genetics is both the weapon and battle standard of this new, supposedly "scientific" racism.

Those who disagree with alt-right ideologies may assume that the alt-right is merely spewing ignorant nonsense. This is certainly true for some of the alt-right. What is perhaps a more difficult truth is that many of the alt-right do, in fact, understand biology and genetics to an impressive extent, even if this understanding is flawed.

For instance, alt-right proponents have stated, correctly, that many people with European and Asian descent have inherited 1-4% of their DNA from Neanderthals ancestors, and those of African descent do not have Neanderthal heritage. They are similarly correct that Neanderthals had larger skulls than humans. Based on these facts, some within the alt-right have claimed that Europeans and Asians have superior intelligence because they have inherited larger brains from their Neanderthal ancestors.

However, this claim ignores that while there is evidence for the effect of Neanderthal DNA on certain traits, there has been no evidence for its effect on intelligence. Furthermore, scientific research indicates that the Neanderthals were not necessarily more intelligent simply because they had larger skulls. Unsurprisingly, the alt-right tends cherry-pick the ideas that align with their preconceived notions of racial hierarchies, ignoring the broader context of the field of human genetics.

Fighting racism with understanding

Just as the alt-right is no longer an easily dismissed fringe group, their arguments have some factual basis, and cannot be swept aside as the babbling of the scientific illiterate. The alt-right is not clumsy in their use of science and genetics in their battle for their "ideals." Those who oppose the alt-right, and other racist entities, must arm themselves with the same weapons: education, namely scientific and genetic literacy.

Mounting scientific evidence has shown that humans are fundamentally more similar than different from each other. Nonetheless, racism has persisted. Scientific findings are often ignored, or otherwise actively misinterpreted and misused to further racist agendas of extreme political groups. Opponents of these forces must, through their own education and awareness, combat these misleading interpretations and representations of scientific findings.

Today, the question of "race" is no longer merely a political and social issue: as science has rapidly advanced, it has become irrevocably intertwined. The genome contains powerful insights about our biology that could unite us as a species, but which could also be dangerous and divisive if used without understanding. As we look forward to 2017 and onwards, it becomes ever more important to understand what our DNA says about what it means to be human.
Vivian Chou is a Ph.D. candidate in the Biological and Biomedical Sciences program at Harvard Medical School.
For more information:

The Atlantic "Will the alt-right promote a new kind of racist genetics?" (December 2016)

Harvard Magazine "Race in a genetic world" (2008)

Livescience "Genetic ancestry tests mostly hype, scientists say" (2007)

Science "The science and business of genetic ancestry testing" (2007; original paper cited in the Livescience article above)

Nature Genetics "Implications of biogeography of human populations for 'race' and medicine" (November 2004)

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How Science and Genetics are Reshaping the Race Debate of the 21st Century - Science in the News

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by Vivian Chou figures by Daniel Utter Donald Trump's election as the 45th President of the United States has been marked by the brewing storms of racial conflicts. A rise in racial incidents ensued in the immediate aftermath of Trump's victory in November 2016.

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In Latin America, Native Americans, Africans, and Europeans have intermixed for centuries. So, a few years back, researchers sought to learn more about the ancestry of more than 7,300 people from Brazil, Chile, Colombia, Mexico and Peru. The volunteers provided DNA samples. And they also answered the question: what do you think your background is?

Turns out that what they thought-that is, their predicted ancestry-told a different story than their genes did-with skin color a key factor.

"Their predicted ancestry is actually very well correlated with their skin color, but poorly with their actual genetic ancestry. So that showed us people are actually trying to predict their whole ancestry by just looking at their skin color, which is a pretty crude thing to do, but that's how the attitude is in Latin America." Kaustubh Adhikari, who studies human genetics at University College London.

In particular, lighter-skinned volunteers tended to overestimate their European ancestry whereas darker-skinned subjects overestimated their Native American or African backgrounds.

Now a new study by Adhikari and his colleagues offers a reason for the mismatch. The skin color data and the DNA sequences led the researchers to identify a genetic variant for lighter skin that arose in Asia 20- to 30-thousand years ago. That event appears to be independent of the evolution of lighter skin in Europe.

What's it all mean? Well, light skin color in Latin Americans could still reflect European ancestry. But it could also indicate Native American ancestry-by way of the original Asian immigrants carrying the trait who crossed the temporary Beringia land bridge into what's now Alaska and became the first Americans.

The researchers were also able to show that this gene variant for lighter skin pigmentation is more prevalent in parts of Asia that do not get much sunlight-indicating a possible way this genetic variant could have been selected for. The new study is in the journal Nature Communications. [Kaustubh Adhikari et al., A GWAS in Latin Americans highlights the convergent evolution of lighter skin pigmentation in Eurasia]

Adhikari says the findings could help modify Latin Americans' social views. "We know for example there's a big socioeconomic stratification in Latin America, and that correlates, because of the history of colonization, to people's European ancestry. And a proxy of European ancestry is often taken to be light skin color. So what we are trying to show is that such a blind attitude to social aspects is also wrong genetically, that there's also big variation of skin color from the native side that such kinds of simplistic attitudes would be ignoring."

A reminder that ancestry, like so much else, is more than skin deep.

-Christopher Intagliata

[ The above text is a transcript of this podcast.]

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Light-Skin Variant Arose in Asia Independent of Europe

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In Latin America, Native Americans, Africans, and Europeans have intermixed for centuries. So, a few years back, researchers sought to learn more about the ancestry of more than 7,300 people from Brazil, Chile, Colombia, Mexico and Peru. The volunteers provided DNA samples. And they also answered the question: what do you think your background is?

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Angélica Dass’s photography challenges how we think about skin color and ethnic identity. In this personal talk, hear about the inspiration behind her portrait project, Humanæ, and her pursuit to document humanity’s true colors rather than the untrue white, red, black and yellow associated with race.

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Used in conjunction with HHMI lactase persistence case study.

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A young man with neo-Nazi tattoos spits milk toward the video camera. Another man, holding a jug of milk, says, "You might not like it, but this is the face of white nationalism."

The group of men were gathered to protest an anti-Trump video installation, " He Will Not Divide Us," in Queens, New York, in February 2017.

Following the protest in New York, depictions of milk alongside white nationalism went viral. Figures affiliated with the alt-right, including Richard Spencer and Tim "Baked Alaska" Gionet, added milk emojis to their Twitter display names and the hashtag "#MilkTwitter" was used as a dumping ground for racist trolls. Later in 2017, Lucian Wintrich, a former correspondent for the right-wing news blog Gateway Pundit who has appeared on a white nationalist podcast, drank from a glass of milk as protesters heckled him during a speech.

These and other incidents have been described as evidence that some white supremacists are co-opting cow's milk as a symbol of their belief that white people are wholesome and pure.

Right-wing news sites like Breitbart have mocked that suggestion. Those who noted milk's popularity with white supremacists have been taunted as fools who fell for what was just a prank that was not meant to be taken seriously.

But whether or not the alt-right was indulging in a trolling exercise, some academics say these events are part of a murky history involving cow's milk.

Iselin Gambert, an associate professor of legal research and writing at George Washington University in Washington, is co-authoring a forthcoming paper that argues milk has long been used as a symbol for and tool of white supremacy. (A draft version can be read online.)

Animal milk products, Gambert told HuffPost, have become ubiquitous around the globe, including in regions with little or no history of a dairy industry. She noted the dairy industry has long marketed milk as universally healthy, even though roughly 65 percent of the world's population has a reduced ability after infancy to digest lactose found in unprocessed milk.

Lactose intolerance is complex and very difficult to measure, but several studies, including a 2010 report produced for the U.S. Department of Health and Human Services, have found that people of color are more likely to report symptoms of lactose intolerance.

Yet milk and milk products have formed the backbone of some food initiatives in the United States. The U.S. Department of Agriculture's National School Lunch Program, School Breakfast Program and Special Milk Program all provide milk to children in public and nonprofit private schools. It's a policy that has been criticized by law professor Andrea Freeman for pushing harmful amounts of saturated fats into the diets of children and disproportionately affecting communities of color.

A USDA spokesperson said the Special Milk Program allows substitutions to be made for children who cannot consume milk if a parent or guardian submits a request in writing. And the National Dairy Council (NDC), a lobbying group for the dairy industry, echoed that, saying that under the federal programs, schools will provide non-dairy milk substitutes to children who report trouble digesting milk.

However, the NDC spokesperson also suggested that more people can drink milk than some critics argue. "In American culture today, limited lactose digestion is common but variable among people of African-American, Hispanic, Asian and Native American descent, but not always a reason to avoid dairy foods," the spokesperson told HuffPost.

The dairy industry has been pushing the idea of milk as an integral part of a healthy diet for a long time. In her book Nature's Perfect Food: How Milk Became America's Drink, sociologist Melanie Dupuis cites an NDC publication distributed in the 1920s that quotes a nutritionist saying, "People who have an appreciation for art, literature and music, who are progressive in science and every activity of human intellect are the people who have used liberal amounts of milk and its products."

Dupuis' book describes how the white beverage was symbolically linked in the early 20th century to white-skinned people, who were better able to digest it due to a genetic mutation known as lactase persistence. "By declaring milk perfect," she wrote, "white northern Europeans announced their own perfection."

The NDC declined to comment on industry marketing materials cited in the various studies. "Milk drinking is not just a practice of Western culture," the spokesperson told HuffPost, "but a shared part of human existence around the world."

Gambert stressed that her research should not be construed to insinuate that people who drink dairy milk are in any way racist or that milk itself is inherently bigoted. But the issues in milk's history, she said, make its co-option as a symbol of white nationalism, whether ironic or not, all the more significant.

"Milk is different than other things, which may be more randomly chosen. There is the reality that milk has historical ties to being used in racist practices," she said.

"There are those who find it funny to use milk as a symbol of white nationalism and tweet offensive content under the hashtag #milktwitter to provoke people," said Gambert. "But saying it's all a prank doesn't mean that milk isn't being used to support racist beliefs."
For more content and to be part of the "This New World" community, follow our Facebook page. HuffPost's "This New World" series is funded by Partners for a New Economy and the Kendeda Fund. All content is editorially independent, with no influence or input from the foundations. If you have an idea or tip for the editorial series, send an email to thisnewworld@huffpost.com.

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The Troubling Link Between Milk And Racism

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A young man with neo-Nazi tattoos spits milk toward the video camera. Another man, holding a jug of milk, says, "You might not like it, but this is the face of white nationalism." The group of men were gathered to protest an anti-Trump video installation, " He Will Not Divide Us," in Queens, New York, in February 2017.

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Used in conjunction with HHMI lactase persistence case study.

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Nowhere on the agenda of the annual meeting of the American Society of Human Genetics, being held in San Diego this week, is a topic plaguing many of its members: the recurring appropriation of the field's research in the name of white supremacy.

"Sticking your neck out on political issues is difficult," said Jennifer Wagner, a bioethicist and president of the group's social issues committee, who had sought to convene a panel on the racist misuse of genetics and found little traction.

But the specter of the field's ignominious past, which includes support for the American eugenics movement, looms large for many geneticists in light of today's white identity politics. They also worry about how new tools that are allowing them to home in on the genetic basis of hot-button traits like intelligence will be misconstrued to fit racist ideologies.

In recent months, some scientists have spotted distortions of their own academic papers in far-right internet forums. Others have fielded confused queries about claims of white superiority wrapped in the jargon of human genetics. Misconceptions about how genes factor into America's stark racial disparities have surfaced in the nation's increasingly heated arguments over school achievement gaps, immigration and policing.

['Could someone please debunk this?' Read about how our reporter grappled with writing about genetics and white supremacists.]
Instead of long-discounted proxies like skull circumference and family pedigrees, according to experts who track the far-right, today's proponents of racial hierarchy are making their case by misinterpreting research on the human genome itself. And in debates that have largely been limited to ivory-tower forums, the scientists whose job is to mine humanity's genetic variations for the collective good are grappling with how to respond.

"Studying human genetic diversity is easier in a society where diversity is clearly valued and celebrated - right now, that is very much on my mind," said John Novembre, a University of Chicago evolutionary biologist who has taken to concluding his visiting seminars by illustrating how one of the field's textbook examples of natural selection has been adopted for illiberal ends.

One slide Dr. Novembre has folded into his recent talks depicts a group of white nationalists chugging milk at a 2017 gathering to draw attention to a genetic trait known to be more common in white people than others - the ability to digest lactose as adults. It also shows a social media post from an account called "Enter The Milk Zone" with a map lifted from a scientific journal article on the trait's evolutionary history.

In most of the world, the article explains, the gene that allows for the digestion of lactose switches off after childhood. But with the arrival of the first cattle herders in Europe some 5,000 years ago, a chance mutation that left it turned on provided enough of a nutritional leg up that nearly all of those who survived eventually carried it. In the post, the link is accompanied by a snippet of hate speech urging individuals of African ancestry to leave America. "If you can't drink milk," it says in part, "you have to go back."

In an inconvenient truth for white supremacists, a similar bit of evolution turns out to have occurred among cattle breeders in East Africa. Scientists need to be more aware of the racial lens through which some of their basic findings are being filtered, Dr. Novembre says, and do a better job at pointing out how they can be twisted.

But the white nationalist infatuation with dairy also heightened Dr. Novembre's concerns about how to handle new evolutionary studies that deal with behavioral traits, such as how long people stay in school.

Anticipating misinterpretations of a recent study on how genes associated with high education attainment, identified in Europeans, varied in different populations around the world, the lead author, Fernando Racimo, created his own "frequently asked questions" document for nonscientists, which he posted on Twitter.

And in a commentary that accompanied the paper in the journal Genetics, Dr. Novembre warned that such research is "wrapped in numerous caveats" that are likely to get lost in translation.

"Great care," his commentary concludes, "should be taken in communicating results of these studies to general audiences."

Already, some of those audiences are flaunting DNA ancestry test results indicating exclusively European heritage as though they were racial ID cards. They are celebrating traces of Neanderthal DNA not found in people with only African ancestry. And they are trading messages with the coded term "race realism," which takes oxygen from the claim that the liberal scientific establishment has obscured the truth about biological racial differences.

Some scientists suggest that engaging with racists would simply lend credibility to obviously specious claims. Many say that they do not study race, in any case: The racial categories used by the United States census correlate only imperfectly with the geographic ancestry groupings of interest to evolutionary geneticists. "Black," for instance, is a socially defined term that includes many Americans who have a majority of European ancestry.

[For more coverage of race, sign up here to have our Race/Related newsletter delivered weekly to your inbox.]
But as the pace of human population genetics research has accelerated, it has yielded results that, to many nonscientists, appear to challenge the idea of race as a wholly social construction.

Genetic ancestry tests advertise "ethnicity estimates" (Senator Elizabeth Warren appealed to the perceived authority of DNA this week to demonstrate her Native American heritage, in response to mocking by President Trump), and some disease-risk genes have turned out to be more common among certain genetic ancestry groups. Doctors use patients' self-identified race as a proxy for geographic ancestry, because individual readouts of DNA are costly, and though the correlation is imperfect, it exists.

As DNA databases tied to medical records and personal questionnaires have reached a critical mass for individuals of European descent, moreover, so-called polygenic scores that synthesize the hundreds or thousands of genes that contribute to many human traits into a single number are being developed to predict health risks, and in some cases, behavior.

Last summer, researchers developed a score that can roughly predict the level of formal education completed by white Americans by looking at their DNA. And while those scores cannot yet be compared among racial or population groups, the new techniques have prompted some scientists to feel it is the field's responsibility to head off predictable misrepresentations.

"You have to make a judgment when you have powerful information that can be misused," said David Reich, a Harvard geneticist who has publicly called on colleagues in a recent book and in a New York Times Op-Ed to more directly address the prospect of identifying genetic differences between populations in socially sensitive traits.

There is no evidence, scientists stress, that environmental and cultural differences will not turn out to be the primary driver of behavioral differences between population groups.

At the same time, the advances in genetic technology have put white supremacists into a kind of anticipatory lather.

"Science is on our side," crowed Jared Taylor, the founder of the white nationalist group American Renaissance, in a recent video that cites Dr. Reich's book.

Dr. Reich was among those to decline an invitation to lead a discussion on the topic at the San Diego meeting. "I really wanted to return to research," he said.

The widespread uncertainty among Americans over what scientists know about genetic differences between racial groups, experts say, has left many flummoxed in the face of white supremacist claims that invoke genetics.

"I was surfing my favorite dumb picture site and I came across a post trying to prove racism with science," a community college student in Florida wrote to Jun Z. Li, a University of Michigan geneticist whose work has been invoked to buttress racist claims of white intellectual superiority. "I read through the paper myself but I do not have the education or experience to understand and make sure I have a coherent counter argument."

For white Americans half-inclined to blame nonwhite immigrants or African-Americans for perceived social problems, the veneer of a scientific rationale for white superiority, researchers say, can tip them toward racial resentment. It can be more effective than base appeals to tribalism, especially for the educated demographic the far-right has been targeting.

And while much of current white nationalist rhetoric is framed in terms of preserving a white cultural identity, experts say it relies on a familiar narrative of immutable biological differences. On a YouTube talk show earlier this year, for instance, Gavin McInnes, founder of the Proud Boys, whose appearance set off a brawl outside a Republican club in Manhattan last week, echoed the pet white supremacist theory that the environmental challenges of cold winters explain the supposed higher intelligence of northern Europeans.

Some geneticists have penned blog posts explaining why new genetic tools will not support white nationalist claims that average behavioral differences between groups are immutable. Others - including Dr. Li - have replied directly to individual queries.

And when a blogger at the far-right Unz Review noted that the DNA variations associated with high IQ in a 2017 study of Europeans were at the lowest frequency among Africans, the study's lead author, Danielle Posthuma, wrote in a published reply that such cross-population comparisons were spurious.

"This," she wrote, "is a very deep-rooted misunderstanding."

Many geneticists at the top of their field say they do not have the ability to communicate to a general audience on such a complicated and fraught topic. Some suggest journalists might take up the task. Several declined to speak on the record for this article.

And with much still unknown, some scientists worry that rebutting basic misconceptions without being able to provide definitive answers could do more harm than good.

"There are often many layers of uncertainties in our findings," said Anna Di Rienzo, a human genetics professor at the University of Chicago. "Being able to communicate that level of uncertainty to a public that often just sees things in black and white is very, very difficult."

As a step toward changing that, Dr. Di Rienzo has helped organize a meeting of social scientists, geneticists and journalists at Harvard next week to discuss the social implications of the field's newest tools.

Participants have been promised that the meeting will be restricted to some three-dozen invitees and that any remarks made there will be confidential.

And David L. Nelson, a Baylor College of Medicine geneticist who is president of the human genetics society, says it will not stay completely quiet on the issue, promising a statement later this week.

"There is no genetic evidence to support any racist ideology," he said.

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Why White Supremacists Are Chugging Milk (and Why Geneticists Are Alarmed) (Published 2018)

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Nowhere on the agenda of the annual meeting of the American Society of Human Genetics, being held in San Diego this week, is a topic plaguing many of its members: the recurring appropriation of the field's research in the name of white supremacy.

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Wendy Roth has been arguing for years that the U.S. Census Bureau should ask about race in a different way. The race box that people check for themselves on the census doesn't always match the box someone else might have checked for them. And that, Roth says, is a problem.

Roth, a sociologist at the University of Pennsylvania, began researching that mismatch in racial identification in the early 2000s. She recruited 60 New Yorkers who had been born in Puerto Rico or the Dominican Republic, showed them the census race question and asked them how they would answer. The responses surprised her.

Consider the case of Salvador, a kitchen worker in the Bronx. " Many Americans observing him would consider him to be black," Roth wrote in December 2010 in Social Science Quarterly. But Salvador told Roth that he checks "white."

While attitudes in the mainland United States have been shaped by the long legacy of the "one-drop rule," in which a single drop of "black blood" conferred "blackness," Puerto Ricans believe the opposite - that even dark-skinned people can't be black if they have "white blood." Puerto Ricans use terms like mulatto or trigueño to describe those falling somewhere between white and black. But when presented with race checkboxes that offer no intermediate options, Salvador simply goes by what he knows.

People from the Dominican Republic, who have long viewed themselves as "whiter" than their Haitian neighbors, likewise avoided checking "black." Roth found that Dominicans selected "white" or "some other race" and then wrote in descriptors, such as Latino or Hispanic.

"There are a lot of other people who don't understand how to complete the U.S. census ... because it doesn't match their way of understanding race," Roth says. "Sometimes they will identify in ways that are the complete opposite of what the U.S. census is trying to capture."

The census race question is trying to capture the changing demographic composition of the country from the federal and state levels down to neighborhood blocks. The stated aim - at least for the last half century - is to help policy makers and demographers assess whether members of different racial groups have equal access to housing, education, employment and other services, as mandated by law.

Population counts from the census, which has run every 10 years since 1790, are used to determine a state's electoral vote count and how many seats a state receives in the House of Representatives. Those data also serve as the denominator for different demographics by age, sex and race. Data gathered by other government agencies provide the numerator, such as the number of children by race in schools or the racial makeup of the prison population, says Katherine Wallman, former chief statistician of the Office of Management and Budget. The OMB makes sure every federal government agency uses the same racial and ethnic categories in data collection.

Imagine, for instance, that the National Center for Education Statistics identifies a high school as having a student body that is 90 percent black and 10 percent white. But the census data show that the school serves a region that is 50 percent black and 50 percent white. That suggests the school is more racially segregated than the surrounding region. Accurately capturing that sort of discrimination in schools requires reliable race data, both for the numerator and the denominator.

The census, though, operates under the premise that people will identify themselves in the same way as those in their society see them. For instance, a person like Salvador will check "black." When a person's view of their own race aligns with that of the broader society, the race data can point to areas of inequality and potential discrimination.

But people who don't identify with the census race boxes may check a box that doesn't reflect how society sees them. Or they may skip the question or fail to return the form, resulting in undercounts, and the race data stop working as intended.

"Discrimination is more about how you're seen by others than how you see yourself," Roth says.

Missing groups

That capture problem is expected to crop up again with the 2020 census. For the race question, a representative from every household, answering online for the first time, will see options within five racial categories: White; Black or African-American; American Indian or Alaska Native; Asian; and Native Hawaiian or other Pacific Islander. The OMB established those categories in 1997. Federal agencies are allowed to ask for more detail within those categories. That's why Asians answering the census can select from Chinese, Filipino, Asian Indian, Vietnamese, Korean, Japanese and other Asian. Native Hawaiians and other Pacific Islanders can choose Native Hawaiian, Samoan, Chamorro or other Pacific Islander. Respondents can also check "some other race" or multiple race boxes.

Missing from that list are two groups that had hoped to find their own race checkbox in the 2020 census: Hispanics and people from the Middle East and North Africa. As in past censuses, members of both groups will mostly select "white" or "some other race," which can make it harder to locate where there may be a need for local bilingual services in schools or during elections, for example.

Plus, there's a new wrinkle brought on by the growing popularity of genetic ancestry tests: Roth's recent work shows that white people have been checking nonwhite boxes on the census as an expression of their newfound genetic history. "They are searching for an identity that is more specific, more interesting than being just white," Roth says.

That murkiness in the race data has prompted Roth and other sociologists to call for more nuanced race questions. There are ways, the researchers say, to get at both how respondents view themselves - which can help build a group's social and political power - and how they are viewed by society, a clearer metric for measuring discrimination against people like Salvador.

"I would love it if [the Census Bureau] actually measured the thing that they were trying to measure," Roth says.

Equity meets frugality

Up until relatively recently, the race question's raison d'être was not to undo racial segregation but to justify practices that separated racial groups, such as the South's Jim Crow laws. But starting about 50 years ago, following the civil rights movement, the purpose of the race question was flipped on its head.

The civil rights movement led to the gradual dismantling of laws and practices that blocked minorities from certain schools, jobs or neighborhoods and led to the passage of new laws, such as the Civil Rights Act of 1964, the Voting Rights Act of 1965 and the Fair Housing Act of 1968, in an attempt to provide equal opportunity for all.

Meanwhile, up through the 1950 census, specially trained enumerators who visited people's homes filled out the form for each family, including the section on race. Asking directly about race was considered rude, says sociologist Carolyn Liebler of the University of Minnesota in Minneapolis. So enumerators eyeballed the person at the door and made a decision.

Library of Congress

Assuming that most people they came across were black or white, enumerators seldom reported American Indian as a race, and they often didn't consider that other family members may be of a different race. In the 1950 census, for instance, enumerators were instructed to "assume that the race of related persons living in the household is the same as the race of your respondent, unless you learn otherwise."

Starting in 1960, though, officials made a money-saving decision with far-reaching consequences: They started cutting back on enumerators. By the 1980 census, almost all households received the census in the mail, and enumerators visited only those households that failed to respond to the questionnaire in a timely manner. Crucially, for the last half century, the vast majority of respondents have been identifying their own race.

So just as the Census Bureau started relying on the race question to quantify discrimination, the agency switched away from using nonfamily members to check the race box. Those seemingly unrelated changes converged to obscure the new-and-improved purpose of the race question.

Most people answering the census don't see the race question as a way for federal agencies to track discrimination, they assume the question is asking them to express their racial identity, says sociologist Ann Morning of New York University who served from 2013 to 2019 on the National Advisory Committee on Racial, Ethnic and Other Populations, a group appointed by the director of the Census Bureau.

Where's my box?

The enumerators who checked boxes for other people had little reason to take offense at the available race categories. But when respondents started filling out the census themselves, the absence of an appropriate checkbox felt like an affront. Consider individuals from Middle Eastern or North African, called MENA, countries, such as Algeria, Egypt, Iran and Lebanon. The OMB defines such individuals as white. But since the 1980s, people who trace their roots to those countries have been calling for a separate MENA checkbox.

"We believe the MENA classification should be its own separate classification divorced from the white classification," says Khaled Beydoun, a law professor and author at the University of Arkansas in Fayetteville.

With the government doling out more than $880 billion in 2016 alone toward census-guided federal programs, a separate designation would enable policy makers to funnel some of that money to MENA communities seeking the American dream. While such dollars are rarely allocated solely on race, except in the case of American Indians, many federal granting agencies will put applications aimed at minority and underserved racial and ethnic populations at the top of the pile, says Andrew Reamer, an economic and statistical policy expert at George Washington University in Washington, D.C. When groups like MENA are folded into the white category, their applications stay buried.

While some worry that checking "MENA" instead of "white" could lead to increased government surveillance of MENA communities, Beydoun and others say the opposite. A separate MENA checkbox would signify that the United States acknowledges such groups outside the lens of counterterrorism and surveillance, Beydoun says. "For the community, it would be symbolic."

Hispanic case study

Hispanics also don't have a race checkbox, but the Census Bureau has been counting that population since 1980. That's when every household in the United States began answering an ethnicity question alongside the race question: It asks if the person is of Hispanic, Latino or Spanish origin.

That data revealed that 14.6 million Hispanics were living in this country in 1980 - accounting for 6.4 percent of the U.S. population. By the last census in 2010, that number had risen to 50.5 million, or 16 percent of the population. As Hispanics' numbers and visibility increased - in large part thanks to their census designation - bilingual Spanish-English schools became more popular, television programs aimed at Spanish-speaking audiences emerged and politicians realized that winning elections often required support from Hispanic voters.

Hispanic people feel "other"

A growing percentage of people with a Hispanic/Latino ethnic identity choose "other" (blue) as their racial identity because they do not see themselves in the available race categories. As a result, "other" has become the third largest racial category in United States census data. Dates in parentheses show the year an option was added.

For Hispanic/Latino populations, the options available for choosing their ethnic identity have expanded. Dates in parentheses show the year an option was added.

Source: U.S. Census

With their new social and political clout, two-thirds of Hispanic adults have come to view their Hispanic origin as part of their race, according to a 2014 survey by the D.C.-based Pew Research Center. Hispanics "don't see themselves as white, black or any of the other races that have boxes on the census race question," Roth says.

In both the 2000 and 2010 censuses, over a third of those who selected a Hispanic ethnicity put themselves in the "some other race" category, making that ambiguous group the nation's third largest for both decades. Absent changes to how the race and ethnicity questions are asked, growth in the country's Hispanic population means "some other race" may become the nation's second largest racial group in 2020, the Census Bureau noted in a 2017 report.

For Hispanic people, at least, the ethnicity data can still reveal where such individuals might be experiencing discrimination - though confusion over the two questions could discourage people from completing the form, further increasing Hispanic undercounts, says sociologist Julie Dowling of the University of Illinois at Urbana-Champaign and chair of the Census Bureau's National Advisory Committee on Racial, Ethnic and Other Populations.

Projections by the Urban Institute, a D.C.-based think tank, made while the current administration was considering adding a citizenship question to the census, showed that the 2020 count could miss 3.6 percent of Hispanics, or over 2.2 million people. Lingering fears over that question could still depress Hispanic participation, says the institute vice president, Rob Santos.

Undercounts translate to lost dollars. For instance, Child Trends, a nonprofit research organization, estimates that 37 states will lose out on funding from five federal child and family programs if there is an undercount of Hispanics on the 2020 census. Texas alone stands to lose $339 million to $1.4 billion annually.

Nonetheless, money still flows into Hispanic communities thanks to the ethnicity question. But for MENA communities - estimated at 3.7 million people according to the Arab American Institute - there is no equivalent channel. In recognition of those difficulties, the Census Bureau recommended adding race checkboxes for both Hispanic and MENA groups to the 2020 census. But the OMB, which must approve such changes, did not do so. (The OMB did not reply to a request for an interview and the Census Bureau did not make anyone available for an interview in the three months it took to report this story.)

One tweak made to the 2020 census could provide some information on MENA and other minority populations hidden within the broader categories, Dowling says. For the first time, those checking "black" or "white" can opt to write in their nationality of origin. But without a checkbox, the information will be in a less accessible form. "Somebody has to comb through that data," Dowling says.

A slippery sense of self

As minority groups fight for greater visibility, and the race question gets wound up in ideas about self-affirmation and group empowerment, the census data have been getting more difficult to decipher since the 1960 shift to self-identification.

With the power to check their own race box, many people previously identified as white have embraced a nonwhite or mixed-race identity. That's evident in the American Indian numbers. From 1890 to 1960, the American Indian population grew from 248,000 to 524,000, with an average annual growth rate of just 1.1 percent. But over the next several decades, and coinciding with the shift to self-identification, that population grew to almost 2 million by 1990 - with an average annual growth rate of 4.3 percent. That meteoric growth extends well beyond what is possible through births alone, Liebler says.

Working with collaborators at the Census Bureau, Liebler looked at changes to the American Indian category between the 2000 and 2010 censuses. Reporting in the April 2016 Demography, the team identified three "types" of American Indians - fewer than one-third reported American Indian on both censuses. The rest either alternated between single-race and mixed-race American Indian or added or dropped American Indian altogether from one census to another. That last category of people was less likely to report tribal affiliation or live in an American Indian area than those in the other two groups.

People with no connection to tribal groups who decide to check "American Indian" can have real-life implications. For instance, American Indians suffer the lowest high school graduation rates of any group in the country, while the education profile of those "new" American Indians resembles that of whites. When education statistics coupled with census race data make it appear as if American Indians in many regions have become more educated, it implies that American Indians no longer require as much government support for education, Liebler says.

Genetic ancestry tests may be contributing to white people adopting American Indian and other minority identities, Roth's recent research suggests. From 2009 to 2010, Roth interviewed 100 individuals who purchased genetic tests and then re-interviewed 89 of those respondents after the 2010 census.

Reporting in the July 2018 American Journal of Sociology, Roth showed that 14 percent of participants changed their race in 2010 from that used in 2000 based on the test results. Though the study is small, the exploding popularity of such tests over the last decade ( SN: 6/23/18, p. 14) means such tests could dramatically alter how people respond to the census race question.

Simple switch

After taking a genetic ancestry test, white respondents were most likely to change how they perceived their own race or ethnicity.

Source: W.D. Roth and B. Ivemark/ Am. J. Sociol. 2018

But extensive interviews with the participants revealed striking group differences. While just 25 percent of black respondents chose a new racial or ethnic identity, about 40 percent of white respondents did so. What's more, white people often chose what new racial information to accept and what to discard. The ability to cherry-pick race is a uniquely white privilege, Roth says. Whites "can claim to be Native American ... or whatever they didn't know about before, and they can go to festivals and they can eat the food, but it's costless. It doesn't bring with it the same kind of discrimination that identity brings for somebody who is seen [by others] as a member of that group."

A more nuanced approach

What Roth is getting at is the idea that discrimination is more about how a person is seen by others than how they see themselves. A white-presenting individual who receives a genetic ancestry test result that reveals American Indian ancestral ties could check "white" and "American Indian" on the 2020 census, but that decision says nothing about the level of discrimination that person has experienced, Liebler says. And that decision makes it harder for policy makers to identify communities in need.

What's more, research over the last few decades has made clear that even for individuals within the same race, light-skinned individuals fare better in American society, receiving more lenient prison sentences and better job opportunities, than their dark-skinned counterparts. So even if "Hispanic," "MENA" or other race checkboxes were added, identifying that sort of discrimination within a group will remain impossible with the current race question.

"We need more than one measure of race," says sociologist Nancy López of the University of New Mexico in Albuquerque. One question should ask respondents to identify their own race so policy makers can continue to identify the country's changing social and political blocs. And another question should ask respondents to gauge how they appear to an outsider, such as an enumerator standing on their doorstep, census form in hand.

But don't expect to see changes to the race question anytime soon, Liebler says. "The push is entirely within the academic world. We've got no traction at all within the Census [Bureau]." Perhaps the place to tack on multiple race questions is on smaller federal surveys, such as those administered by health, education and housing agencies, Liebler says. "That seems plausible."

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Questions or comments on this article? E-mail us at feedback@sciencenews.org

A version of this article appears in the March 14, 2020 issue of Science News.

Citations

D. Murphey et al. Undercounting Hispanics in the 2020 census will result in a loss in federal funding to many states for child and family assistance programs. Child Trends, August 14, 2019.

W.D. Roth and B. Ivemark. Genetic options: The impact of genetic ancestry testing on consumers' racial and ethnic identities. American Journal of Sociology, July 2018, Vol. 124, p. 150, doi: 10.1086/697487.

K. Mathews et al. 2015 National Content Test: Race and ethnicity analysis report. United States Census Bureau, February 28, 2017.

K. Parker et al. Multiracial in America: Proud, diverse and growing in numbers. Pew Research Center, June 11, 2015.

W.D. Roth. Racial mismatch: The divergence between form and function in data for monitoring racial discrimination of Hispanics. Social Science Quarterly, December 2010, Vol. 91, p. 1288, doi: 10.1111/j.1540-6237.2010.00732.x

Margo J. Anderson. The American census: A social history: Second edition, Yale University Press, 2015.

J.S. Passel. The growing American Indian population, 1960-1990: Beyond demography. Population Research and Policy Review, April 1997, Vol. 16, p. 11, doi: 10.1023/A:1005724610787

Sujata Gupta is the social sciences writer and is based in Burlington, Vt.

# data[].attributes.attachment_link.title
To fight discrimination, the U.S. census needs a different race question

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Wendy Roth has been arguing for years that the U.S. Census Bureau should ask about race in a different way. The race box that people check for themselves on the census doesn't always match the box someone else might have checked for them. And that, Roth says, is a problem.

# data[].attributes.attachment_link.readable_text
t seems we can't move for comments about race dominating our media landscape, be it about an actor formerly known as a princess, or by an actor previously unknown to anyone outside of his famous acting dynasty. These are fractious times, and such debates appear to be increasing in frequency. But there are some fights for which you can arm yourself in advance - and when the argument is about race, the weapon of choice is science.

Racism is a prejudice that has a longstanding relationship with science. The invention of race occurred in the age of empires and plunder, when men of the emerging discipline of science classified the people of the world, mostly from their armchairs. Carl Linnaeus is the father of biological taxonomy, having invented the system that we use today: genus and species - Homo sapiens. He was also a central figure in the emergence of scientific racism too, alongside Kant, Voltaire and a host of other European men.

Classifications were based primarily on skin colour, some on a handful of skull measurements, and they also came with some shoddy value judgments: Linnaeus had the people of Africa as lazy and "governed by caprice"; Native Americans were "zealous and stubborn"; East Asians were haughty, greedy, and "ruled by opinions". Voltaire believed that black people were a different species. All of these taxonomies were inherently hierarchical, with white Europeans always on top.

In the 19th century, Darwin's half-cousin Francis Galton and others tightened their scientific arguments for race though, as Darwin noted, no one could agree on how many races there actually were, the range being between one and 63. Galton was an amazing scientist, and a stunning racist. The most delicious irony about him is that the field he effectively established - human genetics - is the branch of science that has demonstrated unequivocally that race is not biologically meaningful. Modern genetics clearly shows that the way we colloquially define race does not align with the biology that underpins human variation. Instead, race is a cultural taxonomy - a social construct. This doesn't mean it is invalid or unimportant, nor does it mean that race does not exist. Humans are social animals, and the way we perceive each other is of paramount importance. Race exists because we perceive it.

No country, people, political power or border is permanent. The only true indigenous Brits were not even our own species

Racism seems to be making a comeback in public life: the prime minister has a well-stocked back catalogue of racist remarks, most notably describing Congolese people as "piccanninies" with "watermelon smiles". Antisemitism is a defining issue for the 21st-century Labour party. Sport has always suffered from racist fans, and in 2018, bananas were thrown on to pitches at black footballers such as Arsenal's Pierre-Emerick Aubameyang, as they were routinely 30 years ago. The England cricketer Jofra Archer was subjected to racist abuse in a Test match in New Zealand in November.

We all know someone who has casually racist opinions: the misattribution of elite athletic success to ancestry rather than training, that east Asian students are naturally better at maths; or that Jews are innately good with money. Racism may be back, so get tooled up, because science is no ally to racists. Here are some standard canards of prejudice, and why science says something different.

What we see with our eyes is the merest fraction of a person. But humans are a highly visual species, and skin colour is the primary factor in allocating race. This idea is modern though, only becoming the primary classifier during the so-called Age of Enlightenment. Modern genetics reveals a much more complicated - and fascinating - picture.

Lighter skin is, at least partially, an adaptation to less sunny skies, as a means of protecting us from folate deficiency. Homo sapiens originated as an African species, but that doesn't necessarily mean that we were ancestrally dark-skinned, nor that everyone was the same colour. Some of the differences we can see and measure between populations are local adaptations to evolutionary pressures such as food availability and disease. Similarly, genes for lighter pigmentation have been selected by an evolution away from the equator. But the palette of skin colour within the African continent is far greater than anywhere else, meaning that a simplistic model of selection based on exposure to the sun only explains a fraction of that diversity. There are 1.3 billion Africans, 42 million African Americans. Not only are these huge numbers, but the people in question are more diverse genetically than anyone else on Earth. And yet westerners refer to all of them as "black". This is a scientifically meaningless classification, and one that is baked into western culture from five centuries of scientific racism. Stereotyping based on pigmentation is foolish, because racial differences are skin deep.

"England for the English" warbled Morrissey in his song The National Front Disco. Now that Mozza has given apparent support to For Britain, a political party even Nigel Farage thinks is full of "Nazis and racists", it's no longer clear the lyrics were ironic. Although Morrissey denies he is a racist, the sentiment is an old racist refrain. In July last year, President Trump suggested that if four elected US congresswomen didn't like it in the US, they should go back to where they came from. Three of them were born in the United States and one is a Somali-born American citizen. Meanwhile, Trump's paternal grandparents were German immigrants, his mother Scottish-born, his first wife Moravian, his third, Slovenian. It is never clear where the benchmark for indigeneity lies.

Indigeneity is a tricky concept. The British Isles have been invaded throughout their history: 1066 was the most recent hostile conquest, but before that, we were occupied by Vikings, who followed Angles, Saxons, Alans, and dozens of other tribes. The Romans ruled for a while, with conscripts not from Rome but from all over their empire, including Gaul, the Mediterranean and sub-Saharan Africa.

About 4,500 years ago, Britain was populated primarily with farmers who had European ancestors. DNA taken from the bones of the long dead suggests they were probably olive-skinned, with dark hair and brown eyes.

Family trees are matted webs, and all the lines of our ancestry get tangled after a few generations

The Beaker folk arrived in Britain about 4,400 years ago, and again according to ancient DNA, within a few centuries had replaced almost the entire population. We don't know how or why, whether it was violence, disease, or something else.

Before them there were darker-skinned hunter-gatherers, who had been there a few thousand years. Then it all gets a bit foggy. The earliest evidence of British humans is in the crumbling coastline of Happisburgh in Norfolk, where size nine footprints of an unknown species of human were set in soft stone 900,000 years ago.

No country, people, political power or border is permanent. The only true indigenous Brits were not even our own species. So, when racists say "England for the English", or when they talk about indigenous people, I do not know who they mean, or more specifically, when they mean. They probably don't either.

White supremacists are obsessed with DNA. I spend time lurking in some of the nastiest corners of the internet, partially so that you don't have to, but also to track their conversations about ancestry. Racist online cesspits such as Stormfront and 4Chan and 8Kun are flooded with thousands of posts about racial purity and ancestry-testing products. Occasionally, these commercial kits reveal previously unknown ancestry from people that white supremacists loathe. White purity is the key idea within white supremacy, and reactions are often conspiracy-fuelled ("the companies are owned by Jews"), or just absurd: "When you look in the mirror, do you see a jew [sic]? If not, you're good," which somewhat undermines the point of the tests.

There are no purebred humans. Our family trees are matted webs, and all lines of our ancestry get tangled after a few generations. All Nazis have Jewish forebears, all racists have African ancestors. Non-racists often think that their ancestry is somehow pure too, and this can be bolstered by misinterpreting commercial genetic ancestry kits. But no matter how isolated or wholesome you think your family tree is, it is a node on a tangled bank, linked directly to everyone else on your continent after only a few centuries, and everyone in the world after a couple of millennia.

Genealogy and genetic genealogy are not perfectly aligned, and due to the way DNA is shuffled during the production of sperm and egg, much is cumulatively lost over the generations. What this means is that you carry DNA from only half of your ancestors 11 generations back. You are genetically unrelated to people from whom you are actually descended as recently as the middle of the 18th century. You are descended from multitudes, most of whom you know nothing about, and many of whom you have no meaningful genetic relationship with.

The last white man to win the 100m final at the Olympics was Allan Wells in 1980, a year when the US boycotted the event. This was also the last time white men competed in the final, five in total. For many, this forms the basis of a long-standing assumption that black people - and more specifically African Americans, Jamaicans or Canadians - have a biological advantage for explosive energy sports.

Unfortunately, elite sportspeople are an abysmal sample on which to make generalisations about populations - they are already wonderfully freakish outliers. The sample size is hopeless, too: the total number of athletes that have competed in the 100m Olympic final since Wells took the gold is 58. Five of them were African, and not from the west African countries from where the enslaved were taken. By this metric, Africans are exactly as successful as white people in the 100m since 1980.

The argument that informs this misguided idea is that centuries of slavery have resulted in selection for explosive energy genes (about which we know very little). This is also a total nonstarter, for many reasons. Most significantly, we can look for the signals of evolutionary selection in African Americans since the beginning of transatlantic slavery, that is, genes that have proliferated in that population. A 2014 study of the DNA of 29,141 African Americans showed no signs of selection across the whole genome for any trait in the time since their ancestors were taken from their African homelands.

But for the sake of argument, let's pretend that genes were selected that related to power and strength. Why then do eastern Europeans dominate weightlifting, yet are absent from sprinting? Why do African Americans dominate in boxing, but not wrestling? Where are all the black sprint cyclists? Why is it that in the 50m freestyle in swimming in the whole history of the Olympics, the number of African American finalists is... one? None of these facts align with the slavery explanation for African American dominance in the 100m.

The transatlantic slave trade also imported millions of West African people to South America. The number of South Americans of any ancestry to have competed in the 100m finals? Zero.

The point is this: sprinters in the Olympics, or indeed any elite sportspeople, are not a dataset on which a statistician could draw any satisfactory conclusion. Yet it is precisely the data on which extremely popular racial stereotypes are based. Elite athletes deserve better praise than the belief that they have auspicious ancestry.

How to Argue With a Racist by Adam Rutherford is published by Orion (£12.99). To order a copy go to guardianbookshop.com. Free UK p&p on all orders over £15

# data[].attributes.attachment_link.description
t seems we can't move for comments about race dominating our media landscape, be it about an actor formerly known as a princess, or by an actor previously unknown to anyone outside of his famous acting dynasty. These are fractious times, and such debates appear to be increasing in frequency.