We Are All Black (Sort Of)
Race and Genetic Diversity
Race and Genetic Diversity
ou could carry a bag of blood onto an airplane in 1986. So the handoff that would help alter scientists’ understanding of race and human ancestry took place at John F. Kennedy International Airport, in a rugged nook of Queens, New York.
Two colleagues of Yale geneticist Kenneth Kidd were traveling back from Africa with connecting flights at JFK, so he met them to collect the blood samples taken from the Biaka, a people from the Central African Republic, and the Mbuti, a people from the Democratic Republic of the Congo.
Growing up in Taft, California, the son of a gas station manager, Kidd had been fascinated by genetics since he was a twelve-year-old puttering around in the garden, marveling at what happened when he cross-bred different color irises. As an adult, he graduated to studying human DNA. Even before that handoff at JFK, Kidd had an inkling of what he would find.
At a scientific symposium in Italy in 1971 dedicated to the one hundredth anniversary of Darwin’s Descent of Man, Kidd had presented data showing that some African populations have more variations—different possible spellings of the same gene or area of the genome—in their DNA than populations from East Asia or Europe. At the time, many scientists contended that Africans, East Asians, and Europeans had all reached the Homo sapiens stage independently; that Homo erectus—the precursor to modern man—had evolved separately on each continent to become the distinct ethnic variations that we see today.
Over the next two decades, Kidd filled his lab with the DNA of native populations spanning the globe. The Masai of northern Tanzania, the Druze of Israel, the Khanty of Siberia, the Cheyenne Native Americans of Oklahoma, Danes, Finns, Japanese, Koreans—all in translucent plastic containers color-coded by continent. Kidd collected some of the samples himself. Others, like DNA from the Hausa people of Nigeria, came from a Nigerian physician who was trying to figure out why women of certain ethnicities in southwest Nigeria give birth to twins at a higher frequency than women anywhere else on the planet.
Part of Kidd’s goal was to categorize genetic variation around the world by looking at corresponding stretches of DNA in many different populations and examining how they differ. Every time he zoomed in on a portion of the double helix, a particular pattern held: more variation in the populations from Africa. For any piece of text in the DNA recipe book, there were almost always more possible spellings and phrasings in African populations than anywhere else in the world. In many areas of the genome, there was more genetic variation among Africans from a single native population than among people from different continents outside of Africa. On one particular stretch of DNA, Kidd observed more variation in one population of African Pygmies than in the entire rest of the world combined.
With geneticist Sarah Tishkoff, Kidd drew a family tree to represent everyone on earth. While African populations fanned out to form the bulk of the tree, all the European populations were clustered on tiny branches on the fringes. “From that genetic point of view,” Kidd says, “I like to say that all Europeans look alike.” This is because nearly the entirety of human genetic information was contained in Africa not so very long ago.
Kidd’s work, along with that of other geneticists, archaeologists, and paleontologists, supports the “recent African origin” model—that essentially every modern human outside of Africa can trace his or her ancestry to a single population that resided in sub-Saharan East Africa as recently as ninety thousand years ago. According to estimates made from mitochondrial DNA—and the rate at which changes to it occur—the intrepid band of our ancestors who ventured out from Africa en route to populating the rest of the world might have consisted of just a few hundred people.
Humans split from our common ancestor with chimpanzees five or so million years ago. So relative to that time span, people have been outside of Africa for less—much less—than the equivalent of a two-minute drill in a football game. Because that band of our ancestors left not so very long ago in evolutionary terms, and took only a tiny fraction of the population along, they left behind most of humanity’s genetic diversity. For millions of years, DNA changes had accumulated—both randomly and by natural selection—in the genomes of our ancestors inside Africa. But with only ninety thousand years for unique changes to occur outside of Africa, there simply hasn’t been as much action in many stretches of the genome. People outside of Africa are descendants of genetic subsets of a group that was itself just a subset in Africa in the recent past.* Each time modern humans expanded to a new region of the globe, it appears that the pioneering emigrants were small in number and carried just a fraction of the genetic variation of their home en route to founding new populations. Data from around the world shows that the genetic diversity of native populations generally decreases the farther the population is along the human migratory path from East Africa, with populations native to the Americas tending to have the least genetic diversity.
This has momentous implications for classifying people according to their skin color. In some cases, the fact of an individual’s black skin might indicate very little specific knowledge about his genome other than that he has genes that code for the dark skin that protects against equatorial sunlight. One African man’s genome potentially contains more differences from his black African neighbor’s than does Jeremy Lin’s genome from Lionel Messi’s.
There might also be implications for sports. Kidd suggests that for any skill that has a genetic component, theoretically, both the most and least athletically gifted individuals in the world might be African or of recent African descent, like African Americans or Afro-Caribbeans. Both the fastest and slowest person might be African. Both the highest and lowest jumper might be African. In athletic competition, of course, we seek to identify only the fastest runners and highest jumpers. “One can certainly find individual genes where there’s more variation outside of Africa,” Kidd says, “but the general picture is that there’s more variation in Africa. . . . So you would expect out at the extremes there will be a greater proportion of people.”
That said, there are clearly also average differences between populations, which is why Kidd does not recommend scouting for the next Olympic sprinter or NBA All-Star amid the staggering genetic diversity of African Pygmies. “There are certain anatomical features of the Pygmies that would intervene,” Kidd says, referring to their extremely short stature. “But you might find the best basketball players in some of those populations in Africa where height and coordination are on average very high, and where you have a lot of other genetic variation within that group.”
Kidd is suggesting that certain Africans, or people of recent African ancestry, do have a genetic advantage in sports performance at the upper end of athleticism. But because he is not professing an average genetic advantage, Kidd’s supposition is intellectually palatable and has been touted as such both by scientists and in the press.
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In the New Haven, Connecticut, lab that Kidd shares with his wife, Yale geneticist Judith Kidd, are the stainless steel refrigerators and garbage-bin-size liquid nitrogen containers that preserve the world’s DNA, all neatly color-coded. The Yoruba people from Nigeria are there in their translucent yellow plastic box, the Han Chinese in a green box, and, in a purple box, Ashkenazi Jews. If Kidd had my DNA, it would be in the purple box.
In 2010, I had a portion of my genome analyzed by a private company that accurately traced my recent ancestry to eastern Europe and informed me that I carry a mutation on one copy of my HEXA gene. If I procreate with a woman who also carries the same mutation on one of her HEXA genes, each of our children would have a one-in-four chance of receiving two mutant versions of the HEXA gene and having Tay-Sachs disease, a nervous system disorder that results in death by age four. The HEXA mutation is uncommon throughout most of the world, but around one in every thirty Jews with Polish or Russian ancestors (like me) are carriers. The HEXA mutation is one among a batch of DNA signatures that make the people in Kidd’s purple plastic box identifiable by their genes. Every one of the colorful boxes contains the DNA of populations with their own distinct genetic profiles.
“This is a genetic locus [a location on the genome] that affects how well you degrade Tylenol,” Kidd says, through his handlebar mustache, as he clicks on a desktop file to open a study he coauthored. “There are certain mutations on this gene [CYP2E1] that cause acetaminophen poisoning of an individual.” A rainbow-colored diagram appears on Kidd’s monitor.
In this study, as in numerous others he has conducted, Kidd documented how common particular DNA spellings of sections of a gene are in fifty native populations from around the world. As expected, all sixteen of the spelling variations of CYP2E1 that Kidd examined—each represented by a different color—can be found in people in Africa, as can a number of other DNA spelling combinations that are found nowhere else in the world. As the populations get farther from East Africa, through southwest Asia, Europe, northeast Siberia, Pacific Islands, East Asia, and the Americas, more and more of the colors drop out.
“You see, in Africa you have the lavender, the magenta, the yellow, the black, whatever,” Kidd explains. “But when you get to Europe almost everybody is going to have at least one copy of the green one.” Among the Nasioi people, who are confined to the island of Bougainville in the Pacific Ocean near Papua New Guinea, every single member has the “green” DNA sequence in the CYP2E1 gene. “There are also Africans who have two copies of the green, so at that particular location [on the genome], one in a hundred Africans will be more similar to a European than another African,” Kidd says. “But overall they’re going to be very different from a European.” Not only because they have unique spellings in their genetic code, but also because the frequency of gene variations is different in different populations. By looking at just one segment of one single gene, Kidd can start the process of homing in on a person’s geographic and ethnic ancestry.
As ancestral humans spread across the world and became separated by all manner of obstacles—mountains, deserts, oceans, social affiliations, and later national boundaries—populations developed their own DNA signatures. For nearly our entire history, people lived, married, and procreated predominantly where they were born. As pioneers set up civilizations in new locales, gene variants became more or less common in populations both by random chance, or “genetic drift,” as well as by natural selection when a version of a gene helped humans survive or reproduce in a new environment.
The gene variant that allows some adults to digest lactose, the sugar in milk, is one example. The general rule for mammals is that the lactase enzyme is shut down after the weaning period, and milk can no longer be fully digested. That held true for essentially all humans just nine thousand years ago, before the domestication of cattle. Once humans kept dairy cows, though, any adult who could digest lactose was at a reproductive advantage, so gene variants for lactose tolerance spread like brushfire through societies that relied on dairy farming to thrive during winter, like those in northern Europe. Almost all present-day Danes and Swedes can digest lactose, but in populations in East Asia and West Africa, where cattle domestication is more recent or nonexistent, adult lactose intolerance is still the norm. Comedian Chris Rock famously joked that lactose intolerance is a luxury of wealthy societies: “You think anybody in Rwanda’s got a f——g lactose intolerance?!” Rock asked in one of his routines. In fact, most people in Rwanda are lactose intolerant.
In an example particularly relevant to sports, about 10 percent of people with European ancestry have two copies of a gene variant that allows them to dope with impunity. The most common sports urine test that probes for illicit testosterone doping analyzes the ratio of testosterone to another hormone called epitestosterone—the “T/E ratio.” A normal ratio is one-to-one. Injecting synthetic testosterone upsets the ratio by pushing the T higher than the E, and drug testers consider a ratio above four-to-one to signify possible cheating. But carriers of two copies of a particular version of the UGT2B17 gene pass the test no matter what. The gene is involved in testosterone excretion and one version of it causes the T/E ratio to remain normal no matter how much testosterone one injects. So 10 percent of European athletes can cheat and still have no chance of failing the most common drug test. And the get-out-of-drug-testing-free gene is more rule than exception in other parts of the world, like East Asia. Two thirds of Koreans have the genes that confer immunity to T/E ratio testing.
Despite our differences, because all humans have common ancestry that is not so distant in the past, we are exceedingly similar, more similar across the entire genome than chimpanzees are to one another. At the DNA level, of the three billion letters in the recipe book, humans are generally about 99 to 99.5 percent the same. In a sense, you probably knew that intuitively. If you had to build two human beings from scratch, no matter where in the world they were from, most of the instructions would be identical: two eyes, ten fingers and toes, a liver and two kidneys, all the same bones and brain chemicals. For that matter, just about every page would be the same for a human and a chimp, as we are 95 percent similar to chimps at the DNA level. But it is a mistake to take all that to mean that the differences are unimportant.
At least 15 million letters of the DNA code differ on average between individuals, and the actual length of people’s genomic recipe book can differ by millions of letters as well. It is plenty enough difference to cause all the variation we see in the world. In 2007, as genome sequencing became faster and cheaper, Science, one of the two most prestigious scientific journals in the world, named as its breakthrough of the year the revelation of “how truly different we are from one another” at the genetic level. As genome sequencing has become cheaper still, that point has only been amplified. Wherever humans have set up civilizations, they have rapidly differentiated themselves.
Though natives have inhabited Iceland for just a single millennium, the company deCODE Genetics showed that it could identify which of eleven regions of Iceland a resident’s grandparents hailed from using just forty areas along the genome. In 2008, scientists looking at much larger swaths of DNA pinpointed the geographic ancestry of nearly all of a sample of three thousand Europeans to within a few hundred miles. And, to a degree, DNA can identify the construct we call “race” as well.
A 2002 study published by a team of researchers (including Kidd) in Science directed a computer to peruse 377 spots on the genomes of 1,056 people from around the world and then automatically separate the people into groups based on genetic differences. The groups that the computer delineated corresponded with the world’s major geographic regions: Africa, Europe, Asia, Oceania, and the Americas. A subsequent Stanford-led study asked 3,636 Americans to self-identify as either white, African American, East Asian, or Hispanic, and found that the self-identification matched a blind DNA identification in 3,631 cases. “This shows that people’s self-identified race/ethnicity is a nearly perfect indicator of their genetic background,” geneticist Neil Risch said in a press release issued by the Stanford University School of Medicine.*
Skin color, which is primarily determined by latitude, can be an imprecise marker of geographical ancestry, as there are spectrums of skin color on each continent. But geography and ethnic affiliation have most certainly left a trail of genetic crumbs.
In some areas of medicine, like pharmacogenetics—the study of how and why people with different genes respond differently to the same drugs—skin color is already being used as a proxy, albeit often a crude one, for underlying genetic information, and medical researchers now recognize the importance of testing the efficacy of drugs separately on different ethnic groups.
In 2004, Kidd and Tishkoff wrote that the main genetic and geographic clusters of people do “correlate with the common concept of ‘races,’” but added that if every population on earth were included, the genetic differences would look more like a continuous spectrum as opposed to a collection of discrete groups.
In 2009, Tishkoff and an international team published a landmark study that characterized the genetic backgrounds of African Americans. They found that adults who identify as African American are highly genetically diverse on the whole, with ancestry ranging from 1 percent to 99 percent West African. African Americans are particularly diverse in the amount of European ancestry they have in their DNA. But almost all African Americans were found to have African X chromosomes, consistent with the idea that the mothers of African Americans have historically been of very recent African ancestry, while fathers were sometimes African and sometimes European. The African Americans studied were from Baltimore, Chicago, Pittsburgh, and North Carolina, and the African components of their genetic ancestry showed “little genetic differentiation,” according to Tishkoff, and were similar to one another and often to the genetic profiles of West African people like the Igbo and Yoruba of Nigeria; not a surprise, as the Igbo and Yoruba show up frequently in records of the slave trade as Africans who were wrenched from their homes and taken to the Caribbean and the United States.*
One’s ancestry can be traced through one’s genes, but to go further down the path of Kidd’s thought experiment about African athletes, we must know not only that the genotypes of African people are the most diverse, but whether their phenotypes are also the most diverse. A phenotype is the physical manifestation of underlying genes. Geneticists still have scant clue what most of the billions of bases (each “letter” is one base) in our DNA do. Some may do little or nothing at all. Kidd’s suggestion is that because the greatest diversity of genotypes is contained in African populations, the greatest diversity of athletic phenotypes—both the slowest and the fastest runners—might also be there. So far, though, there is no easy, blanket conclusion to Kidd’s thought experiment.
In 2005, the U.S. government’s National Human Genome Research Institute weighed in on the issue of race and genetics and the question of whether most of the physical variation in the world occurs among individual people within ethnic groups, or among entire ethnic populations themselves. The institute directly addressed the question of whether the high degree of genetic diversity in African populations also means that most of the physical diversity in the world is contained in those populations. The answer: it depends on the specific physical trait you’re looking at.
About 90 percent of the variation in the shape of human skulls occurs within every major ethnic group—only 10 percent separates ethnicities—with Africans indeed showing the greatest variation. But the exact opposite is true for skin color: only 10 percent of the variation occurs within ethnic groups, and 90 percent of the difference is between groups. Thus, in order to discuss whether Africans or African Americans have specific genes that are advantageous in certain sports, scientists should first identify specific genes and innate biological traits that are important for sports performance, and then examine whether they occur more frequently in some populations than in others.
They have begun to do just that.
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Kathryn North had the letter to Nature Genetics all ready to go, and her report would be a breakthrough.
A few years earlier, in the summer of 1993, North had left Australia to train as a pediatric neurologist and geneticist at Boston Children’s Hospital, where she worked in a lab that had discovered the genetic mutation that causes Duchenne muscular dystrophy, a devastatingly virulent muscle-wasting disease. When North examined the muscle fibers of muscular dystrophy patients, she saw that they had a normal ration of fast-twitch muscle fibers, but that about one in five patients was missing a particular structural protein called alpha-actinin-3 that should have been in those explosive muscle fibers.
Her letter to Nature Genetics would document the case of two Sri Lankan brothers North examined in her lab in Sydney in 1998 and who had congenital muscular dystrophy. The brothers’ parents, who did not have the disease, were cousins, so the case appeared to be one of recessive genetic inheritance. Neither of the boys had any alpha-actinin-3, so North and colleagues sequenced in each boy the gene that codes for it, the ACTN3 gene. Sure enough, each boy had a “stop codon,” a genetic stop sign, at the same spot on both copies of the ACTN3 gene. The stop sign—just one single letter switch in the DNA—prevented the alpha-actinin-3 protein from being produced in muscles. North and her team, it appeared, had discovered a new gene mutation that caused muscular dystrophy. “I started drafting a letter to Nature Genetics, and I was literally drafting a paper to report a new disease gene,” she says. “But if you’re a good geneticist, you bring in the whole family.”
So North invited the parents and their other two, healthy children and probed their ACTN3 genes too. The version of the gene that the ill brothers had that stopped alpha-actinin-3 production is known as the X variant, and North expected the parents each to have one X variant, which they had passed to their sons, and one R variant, which functioned normally and facilitated production of the protein. To her surprise, both parents and the two healthy siblings also each had two X variants of the ACTN3 gene. Nobody in the family had any alpha-actinin-3 in their muscles whatsoever, yet only the two brothers had muscular dystrophy. North had not found a new muscular dystrophy gene after all. “That was a Friday when we found out,” she says, “and it was really, really depressing.”
That Sunday, she went to a movie and afterward took a walk to ponder the previous week. Never, not in the lab nor in the scientific literature, had she found an example of a healthy person with genes that left them entirely devoid of a structural protein. Structural proteins are critical. They make fingernails, hair, skin, tendons, and muscle. Humans tend to be diseased or to die when the genes that code for them are not functioning. “So I started reading the evolution literature,” North says, “and I thought, well, maybe alpha-actinin-3 is redundant. Maybe we don’t need it and it’s on its way out.”
North cold-called Simon Easteal, an Australian researcher with a specialty in molecular evolution. Together they yanked from storage two hundred samples of muscle with all manner of disease, from muscles that did not contract properly to others that had malfunctioning nerves. Just as she had seen with muscular dystrophy patients in Boston, about one in five of the diseased muscles had two copies of the X version of the ACTN3 gene, and thus no alpha-actinin-3. But about one in five samples of normal, healthy muscle had two X variants as well, so the gene could not be the cause of disease. Perhaps, then, alpha-actinin-3 had some other purpose in muscle. “That’s when we started to pull in different groups of people,” North says. “And that’s when we found this different ethnic distribution of the gene.”
North saw that one quarter of people of East Asian descent had two copies of the X variant of ACTN3 and about 18 percent of white Australians had two X variants. But when she tested Zulu people from South Africa, less than 1 percent had two X variants. Nearly all had at least one copy of the R variant, which codes for alpha-actinin-3 in fast-twitch muscle. And that was true of every African population. With respect to this particular gene variant, Africans or people of recent African ancestry happen to be extraordinarily uniform.
North was convinced that alpha-actinin-3 was not a meaningless protein, even though its absence did not lead to disease. Like the myostatin protein—of Superbaby fame—alpha-actinin-3 was highly conserved in evolutionary terms. It is in the explosive muscle fibers of chickens, mice, fruit flies, and baboons, among other animals, including our closest primate relatives, chimps. The absence of alpha-actinin-3, then, is a very recent and very human trait. North and colleagues estimated that the X variant spread through humans within the last thirty thousand years, and only outside of Africa. The gene, it appears, had been favored by natural selection only in non-African environments for some reason. Fast-twitch fibers must need it for something, North thought.
So she and her colleagues collected DNA from subjects with ample fast-twitch fibers: elite sprinters. They partnered with the Australian Institute of Sport to do ACTN3 testing on international-level athletes. While 18 percent of Australians had two X copies of the gene, almost none of Australia’s competitive sprinters did. Nearly every sprinter produced alpha-actinin-3 in their fast-twitch fibers. “I waited for years to publish that study,” North says. “The result came out the first time we did the analysis, and then we repeated it again and again internally.” And it held. Not only did sprinters in general tend not to have two X copies of ACTN3, but the better they were, the less likely it was they were XX. In one sample, just 5 out of 107 Australian sprinters were XX, and zero of the 32 sprinters who had gone to the Olympics were XX.
After that work was published, sports scientists around the world hustled to test their local sprinters, and the association showed up everywhere. With almost no exceptions, sprinters from Jamaica and Nigeria all had alpha-actinin-3 in their fast-twitch muscles, but so did distance runners from Kenya—no surprise given that nearly all of the control subjects from African populations did as well. Scientists in Finland and Greece took DNA from their Olympic sprinters, and, again, not a single one was XX. In Japan, a few sprinters were XX, but none who had run faster than 10.4 seconds for 100 meters.
ACTN3, North concluded, is a gene for speed. Why that may be so is not exactly clear. Alpha-actinin-3 may have a structural impact on how explosively a muscle fiber can contract, or it may influence the configuration of the muscular system. Mice as well as—in several studies—Japanese and American women who are deficient in alpha-actinin-3 have smaller fast-twitch muscles and less muscle mass over all. When North bred mice to have no alpha-actinin-3, compared with normal mice they had far less active glycogen phosphorylase, the enzyme that mobilizes sugar for explosive actions, like sprinting. The fast-twitch muscle fibers in those mice also took on some of the properties of slow-twitch, endurance fibers.
Given the approximate timing of when the X version of ACTN3 appears to have spread through humans—fifteen to thirty thousand years ago—North has toyed with the idea that the variant may have proliferated during the last ice age. Absence of alpha-actinin-3 may make fast-twitch muscle fibers more metabolically efficient, like their slow-twitch neighbors, a boon, perhaps, in frigid, food-scarce northern latitudes outside of Africa. Two anthropologists have suggested that the X version may have spread when humans outside of Africa transitioned from the hunter-gatherer lifestyle to an agricultural one, where they would have had less need to sprint in war or hunting but more need to be metabolically efficient and to work at a steady rate for long hours.
But North is cautious. Though we share the vast majority of our DNA sequence with mice, genetically manipulated rodents are not ideal models of human genetic variation. “We don’t know the whole story,” North says. “Right now, it looks like ACTN3 is one gene that contributes a little to sprinting, and there may be hundreds, and of course there are other factors like diet, environment, and opportunity.”
Private gene-testing companies have been less circumspect. As soon as the ACTN3-and-Olympians study appeared, companies rushed into the sparsely regulated direct-to-consumer genetic testing market. Genetic Technologies, of Fitzroy, Australia, led the way. For $92.40, the company would tell a customer what versions of the ACTN3 gene they carry. (I have two R copies.) In 2005, the Manly Sea Eagles of Australia’s National Rugby League became the first team to admit publicly that it was testing players for ACTN3 and tailoring training programs accordingly, giving more explosive weight lifting and less cardio to the guys with sprinter variants.
Atlas Sports Genetics, of Boulder, Colorado, has made headlines for selling parents an ACTN3 test for their children. According to Kevin Reilly, president of Atlas, the test is particularly useful for “those younger athletes who don’t have the motor skills yet.” By “younger,” Reilly means that just because baby Kobe doesn’t know how to walk yet, that should not mean his DNA can’t begin charting his athletic career. If Kobe has no R versions of the gene, his parents can start nudging their little bundle of DNA toward endurance sports. The genetic-testing-in-diapers market barely materialized for Atlas, but the company did manage a preteen customer base. Says Reilly, “We have had some impact on athletes in the eight-to-ten age group,” in terms of influencing their sport choices.
Unfortunately for those eight-to-ten-year-olds, though, consumer genetic testing for athleticism is nearly worthless.* Scientists have increasingly realized that the inherited component of complex traits, like athleticism, is most often the result of dozens or even hundreds or thousands of interacting genes, not to mention environmental factors. If you are XX for the ACTN3 gene, “you probably won’t be in the Olympic 100-meters,” North says. But you already knew that, without a genetic test. Though the ACTN3 gene does appear to influence sprinting ability, making a sports decision based on it is like deciding what a puzzle depicts when you’ve only seen one of the pieces. You need that piece to complete the puzzle, but you certainly can’t see a meaningful picture without more pieces.
As Carl Foster, director of the Human Performance Laboratory at the University of Wisconsin–La Crosse and coauthor of several ACTN3 studies, puts it: “If you want to know if your kid is going to be fast, the best genetic test right now is a stopwatch. Take him to the playground and have him race the other kids.” Foster’s point is that, despite the avant-garde allure of genetic testing, gauging speed indirectly is foolish and inaccurate compared with testing it directly—like measuring a man’s height by dropping a ball from a roof and using the time it takes to hit him in the head to determine how tall he is. Why not just use a tape measure?
All that ACTN3 can tell us, it seems, is who will not be competing in the 100-meter final in Rio de Janeiro in 2016. And it is not even doing a very specific job of that, given that it is only ruling out about one billion of the seven billion people on earth.
Still, if only that one gene is taken into account, it is also telling us that there are almost no black people anywhere in the world who are ruled out.
Two colleagues of Yale geneticist Kenneth Kidd were traveling back from Africa with connecting flights at JFK, so he met them to collect the blood samples taken from the Biaka, a people from the Central African Republic, and the Mbuti, a people from the Democratic Republic of the Congo.
Growing up in Taft, California, the son of a gas station manager, Kidd had been fascinated by genetics since he was a twelve-year-old puttering around in the garden, marveling at what happened when he cross-bred different color irises. As an adult, he graduated to studying human DNA. Even before that handoff at JFK, Kidd had an inkling of what he would find.
At a scientific symposium in Italy in 1971 dedicated to the one hundredth anniversary of Darwin’s Descent of Man, Kidd had presented data showing that some African populations have more variations—different possible spellings of the same gene or area of the genome—in their DNA than populations from East Asia or Europe. At the time, many scientists contended that Africans, East Asians, and Europeans had all reached the Homo sapiens stage independently; that Homo erectus—the precursor to modern man—had evolved separately on each continent to become the distinct ethnic variations that we see today.
Over the next two decades, Kidd filled his lab with the DNA of native populations spanning the globe. The Masai of northern Tanzania, the Druze of Israel, the Khanty of Siberia, the Cheyenne Native Americans of Oklahoma, Danes, Finns, Japanese, Koreans—all in translucent plastic containers color-coded by continent. Kidd collected some of the samples himself. Others, like DNA from the Hausa people of Nigeria, came from a Nigerian physician who was trying to figure out why women of certain ethnicities in southwest Nigeria give birth to twins at a higher frequency than women anywhere else on the planet.
Part of Kidd’s goal was to categorize genetic variation around the world by looking at corresponding stretches of DNA in many different populations and examining how they differ. Every time he zoomed in on a portion of the double helix, a particular pattern held: more variation in the populations from Africa. For any piece of text in the DNA recipe book, there were almost always more possible spellings and phrasings in African populations than anywhere else in the world. In many areas of the genome, there was more genetic variation among Africans from a single native population than among people from different continents outside of Africa. On one particular stretch of DNA, Kidd observed more variation in one population of African Pygmies than in the entire rest of the world combined.
With geneticist Sarah Tishkoff, Kidd drew a family tree to represent everyone on earth. While African populations fanned out to form the bulk of the tree, all the European populations were clustered on tiny branches on the fringes. “From that genetic point of view,” Kidd says, “I like to say that all Europeans look alike.” This is because nearly the entirety of human genetic information was contained in Africa not so very long ago.
Kidd’s work, along with that of other geneticists, archaeologists, and paleontologists, supports the “recent African origin” model—that essentially every modern human outside of Africa can trace his or her ancestry to a single population that resided in sub-Saharan East Africa as recently as ninety thousand years ago. According to estimates made from mitochondrial DNA—and the rate at which changes to it occur—the intrepid band of our ancestors who ventured out from Africa en route to populating the rest of the world might have consisted of just a few hundred people.
Humans split from our common ancestor with chimpanzees five or so million years ago. So relative to that time span, people have been outside of Africa for less—much less—than the equivalent of a two-minute drill in a football game. Because that band of our ancestors left not so very long ago in evolutionary terms, and took only a tiny fraction of the population along, they left behind most of humanity’s genetic diversity. For millions of years, DNA changes had accumulated—both randomly and by natural selection—in the genomes of our ancestors inside Africa. But with only ninety thousand years for unique changes to occur outside of Africa, there simply hasn’t been as much action in many stretches of the genome. People outside of Africa are descendants of genetic subsets of a group that was itself just a subset in Africa in the recent past.* Each time modern humans expanded to a new region of the globe, it appears that the pioneering emigrants were small in number and carried just a fraction of the genetic variation of their home en route to founding new populations. Data from around the world shows that the genetic diversity of native populations generally decreases the farther the population is along the human migratory path from East Africa, with populations native to the Americas tending to have the least genetic diversity.
This has momentous implications for classifying people according to their skin color. In some cases, the fact of an individual’s black skin might indicate very little specific knowledge about his genome other than that he has genes that code for the dark skin that protects against equatorial sunlight. One African man’s genome potentially contains more differences from his black African neighbor’s than does Jeremy Lin’s genome from Lionel Messi’s.
There might also be implications for sports. Kidd suggests that for any skill that has a genetic component, theoretically, both the most and least athletically gifted individuals in the world might be African or of recent African descent, like African Americans or Afro-Caribbeans. Both the fastest and slowest person might be African. Both the highest and lowest jumper might be African. In athletic competition, of course, we seek to identify only the fastest runners and highest jumpers. “One can certainly find individual genes where there’s more variation outside of Africa,” Kidd says, “but the general picture is that there’s more variation in Africa. . . . So you would expect out at the extremes there will be a greater proportion of people.”
That said, there are clearly also average differences between populations, which is why Kidd does not recommend scouting for the next Olympic sprinter or NBA All-Star amid the staggering genetic diversity of African Pygmies. “There are certain anatomical features of the Pygmies that would intervene,” Kidd says, referring to their extremely short stature. “But you might find the best basketball players in some of those populations in Africa where height and coordination are on average very high, and where you have a lot of other genetic variation within that group.”
Kidd is suggesting that certain Africans, or people of recent African ancestry, do have a genetic advantage in sports performance at the upper end of athleticism. But because he is not professing an average genetic advantage, Kidd’s supposition is intellectually palatable and has been touted as such both by scientists and in the press.
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In the New Haven, Connecticut, lab that Kidd shares with his wife, Yale geneticist Judith Kidd, are the stainless steel refrigerators and garbage-bin-size liquid nitrogen containers that preserve the world’s DNA, all neatly color-coded. The Yoruba people from Nigeria are there in their translucent yellow plastic box, the Han Chinese in a green box, and, in a purple box, Ashkenazi Jews. If Kidd had my DNA, it would be in the purple box.
In 2010, I had a portion of my genome analyzed by a private company that accurately traced my recent ancestry to eastern Europe and informed me that I carry a mutation on one copy of my HEXA gene. If I procreate with a woman who also carries the same mutation on one of her HEXA genes, each of our children would have a one-in-four chance of receiving two mutant versions of the HEXA gene and having Tay-Sachs disease, a nervous system disorder that results in death by age four. The HEXA mutation is uncommon throughout most of the world, but around one in every thirty Jews with Polish or Russian ancestors (like me) are carriers. The HEXA mutation is one among a batch of DNA signatures that make the people in Kidd’s purple plastic box identifiable by their genes. Every one of the colorful boxes contains the DNA of populations with their own distinct genetic profiles.
“This is a genetic locus [a location on the genome] that affects how well you degrade Tylenol,” Kidd says, through his handlebar mustache, as he clicks on a desktop file to open a study he coauthored. “There are certain mutations on this gene [CYP2E1] that cause acetaminophen poisoning of an individual.” A rainbow-colored diagram appears on Kidd’s monitor.
In this study, as in numerous others he has conducted, Kidd documented how common particular DNA spellings of sections of a gene are in fifty native populations from around the world. As expected, all sixteen of the spelling variations of CYP2E1 that Kidd examined—each represented by a different color—can be found in people in Africa, as can a number of other DNA spelling combinations that are found nowhere else in the world. As the populations get farther from East Africa, through southwest Asia, Europe, northeast Siberia, Pacific Islands, East Asia, and the Americas, more and more of the colors drop out.
“You see, in Africa you have the lavender, the magenta, the yellow, the black, whatever,” Kidd explains. “But when you get to Europe almost everybody is going to have at least one copy of the green one.” Among the Nasioi people, who are confined to the island of Bougainville in the Pacific Ocean near Papua New Guinea, every single member has the “green” DNA sequence in the CYP2E1 gene. “There are also Africans who have two copies of the green, so at that particular location [on the genome], one in a hundred Africans will be more similar to a European than another African,” Kidd says. “But overall they’re going to be very different from a European.” Not only because they have unique spellings in their genetic code, but also because the frequency of gene variations is different in different populations. By looking at just one segment of one single gene, Kidd can start the process of homing in on a person’s geographic and ethnic ancestry.
As ancestral humans spread across the world and became separated by all manner of obstacles—mountains, deserts, oceans, social affiliations, and later national boundaries—populations developed their own DNA signatures. For nearly our entire history, people lived, married, and procreated predominantly where they were born. As pioneers set up civilizations in new locales, gene variants became more or less common in populations both by random chance, or “genetic drift,” as well as by natural selection when a version of a gene helped humans survive or reproduce in a new environment.
The gene variant that allows some adults to digest lactose, the sugar in milk, is one example. The general rule for mammals is that the lactase enzyme is shut down after the weaning period, and milk can no longer be fully digested. That held true for essentially all humans just nine thousand years ago, before the domestication of cattle. Once humans kept dairy cows, though, any adult who could digest lactose was at a reproductive advantage, so gene variants for lactose tolerance spread like brushfire through societies that relied on dairy farming to thrive during winter, like those in northern Europe. Almost all present-day Danes and Swedes can digest lactose, but in populations in East Asia and West Africa, where cattle domestication is more recent or nonexistent, adult lactose intolerance is still the norm. Comedian Chris Rock famously joked that lactose intolerance is a luxury of wealthy societies: “You think anybody in Rwanda’s got a f——g lactose intolerance?!” Rock asked in one of his routines. In fact, most people in Rwanda are lactose intolerant.
In an example particularly relevant to sports, about 10 percent of people with European ancestry have two copies of a gene variant that allows them to dope with impunity. The most common sports urine test that probes for illicit testosterone doping analyzes the ratio of testosterone to another hormone called epitestosterone—the “T/E ratio.” A normal ratio is one-to-one. Injecting synthetic testosterone upsets the ratio by pushing the T higher than the E, and drug testers consider a ratio above four-to-one to signify possible cheating. But carriers of two copies of a particular version of the UGT2B17 gene pass the test no matter what. The gene is involved in testosterone excretion and one version of it causes the T/E ratio to remain normal no matter how much testosterone one injects. So 10 percent of European athletes can cheat and still have no chance of failing the most common drug test. And the get-out-of-drug-testing-free gene is more rule than exception in other parts of the world, like East Asia. Two thirds of Koreans have the genes that confer immunity to T/E ratio testing.
Despite our differences, because all humans have common ancestry that is not so distant in the past, we are exceedingly similar, more similar across the entire genome than chimpanzees are to one another. At the DNA level, of the three billion letters in the recipe book, humans are generally about 99 to 99.5 percent the same. In a sense, you probably knew that intuitively. If you had to build two human beings from scratch, no matter where in the world they were from, most of the instructions would be identical: two eyes, ten fingers and toes, a liver and two kidneys, all the same bones and brain chemicals. For that matter, just about every page would be the same for a human and a chimp, as we are 95 percent similar to chimps at the DNA level. But it is a mistake to take all that to mean that the differences are unimportant.
At least 15 million letters of the DNA code differ on average between individuals, and the actual length of people’s genomic recipe book can differ by millions of letters as well. It is plenty enough difference to cause all the variation we see in the world. In 2007, as genome sequencing became faster and cheaper, Science, one of the two most prestigious scientific journals in the world, named as its breakthrough of the year the revelation of “how truly different we are from one another” at the genetic level. As genome sequencing has become cheaper still, that point has only been amplified. Wherever humans have set up civilizations, they have rapidly differentiated themselves.
Though natives have inhabited Iceland for just a single millennium, the company deCODE Genetics showed that it could identify which of eleven regions of Iceland a resident’s grandparents hailed from using just forty areas along the genome. In 2008, scientists looking at much larger swaths of DNA pinpointed the geographic ancestry of nearly all of a sample of three thousand Europeans to within a few hundred miles. And, to a degree, DNA can identify the construct we call “race” as well.
A 2002 study published by a team of researchers (including Kidd) in Science directed a computer to peruse 377 spots on the genomes of 1,056 people from around the world and then automatically separate the people into groups based on genetic differences. The groups that the computer delineated corresponded with the world’s major geographic regions: Africa, Europe, Asia, Oceania, and the Americas. A subsequent Stanford-led study asked 3,636 Americans to self-identify as either white, African American, East Asian, or Hispanic, and found that the self-identification matched a blind DNA identification in 3,631 cases. “This shows that people’s self-identified race/ethnicity is a nearly perfect indicator of their genetic background,” geneticist Neil Risch said in a press release issued by the Stanford University School of Medicine.*
Skin color, which is primarily determined by latitude, can be an imprecise marker of geographical ancestry, as there are spectrums of skin color on each continent. But geography and ethnic affiliation have most certainly left a trail of genetic crumbs.
In some areas of medicine, like pharmacogenetics—the study of how and why people with different genes respond differently to the same drugs—skin color is already being used as a proxy, albeit often a crude one, for underlying genetic information, and medical researchers now recognize the importance of testing the efficacy of drugs separately on different ethnic groups.
In 2004, Kidd and Tishkoff wrote that the main genetic and geographic clusters of people do “correlate with the common concept of ‘races,’” but added that if every population on earth were included, the genetic differences would look more like a continuous spectrum as opposed to a collection of discrete groups.
In 2009, Tishkoff and an international team published a landmark study that characterized the genetic backgrounds of African Americans. They found that adults who identify as African American are highly genetically diverse on the whole, with ancestry ranging from 1 percent to 99 percent West African. African Americans are particularly diverse in the amount of European ancestry they have in their DNA. But almost all African Americans were found to have African X chromosomes, consistent with the idea that the mothers of African Americans have historically been of very recent African ancestry, while fathers were sometimes African and sometimes European. The African Americans studied were from Baltimore, Chicago, Pittsburgh, and North Carolina, and the African components of their genetic ancestry showed “little genetic differentiation,” according to Tishkoff, and were similar to one another and often to the genetic profiles of West African people like the Igbo and Yoruba of Nigeria; not a surprise, as the Igbo and Yoruba show up frequently in records of the slave trade as Africans who were wrenched from their homes and taken to the Caribbean and the United States.*
One’s ancestry can be traced through one’s genes, but to go further down the path of Kidd’s thought experiment about African athletes, we must know not only that the genotypes of African people are the most diverse, but whether their phenotypes are also the most diverse. A phenotype is the physical manifestation of underlying genes. Geneticists still have scant clue what most of the billions of bases (each “letter” is one base) in our DNA do. Some may do little or nothing at all. Kidd’s suggestion is that because the greatest diversity of genotypes is contained in African populations, the greatest diversity of athletic phenotypes—both the slowest and the fastest runners—might also be there. So far, though, there is no easy, blanket conclusion to Kidd’s thought experiment.
In 2005, the U.S. government’s National Human Genome Research Institute weighed in on the issue of race and genetics and the question of whether most of the physical variation in the world occurs among individual people within ethnic groups, or among entire ethnic populations themselves. The institute directly addressed the question of whether the high degree of genetic diversity in African populations also means that most of the physical diversity in the world is contained in those populations. The answer: it depends on the specific physical trait you’re looking at.
About 90 percent of the variation in the shape of human skulls occurs within every major ethnic group—only 10 percent separates ethnicities—with Africans indeed showing the greatest variation. But the exact opposite is true for skin color: only 10 percent of the variation occurs within ethnic groups, and 90 percent of the difference is between groups. Thus, in order to discuss whether Africans or African Americans have specific genes that are advantageous in certain sports, scientists should first identify specific genes and innate biological traits that are important for sports performance, and then examine whether they occur more frequently in some populations than in others.
They have begun to do just that.
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Kathryn North had the letter to Nature Genetics all ready to go, and her report would be a breakthrough.
A few years earlier, in the summer of 1993, North had left Australia to train as a pediatric neurologist and geneticist at Boston Children’s Hospital, where she worked in a lab that had discovered the genetic mutation that causes Duchenne muscular dystrophy, a devastatingly virulent muscle-wasting disease. When North examined the muscle fibers of muscular dystrophy patients, she saw that they had a normal ration of fast-twitch muscle fibers, but that about one in five patients was missing a particular structural protein called alpha-actinin-3 that should have been in those explosive muscle fibers.
Her letter to Nature Genetics would document the case of two Sri Lankan brothers North examined in her lab in Sydney in 1998 and who had congenital muscular dystrophy. The brothers’ parents, who did not have the disease, were cousins, so the case appeared to be one of recessive genetic inheritance. Neither of the boys had any alpha-actinin-3, so North and colleagues sequenced in each boy the gene that codes for it, the ACTN3 gene. Sure enough, each boy had a “stop codon,” a genetic stop sign, at the same spot on both copies of the ACTN3 gene. The stop sign—just one single letter switch in the DNA—prevented the alpha-actinin-3 protein from being produced in muscles. North and her team, it appeared, had discovered a new gene mutation that caused muscular dystrophy. “I started drafting a letter to Nature Genetics, and I was literally drafting a paper to report a new disease gene,” she says. “But if you’re a good geneticist, you bring in the whole family.”
So North invited the parents and their other two, healthy children and probed their ACTN3 genes too. The version of the gene that the ill brothers had that stopped alpha-actinin-3 production is known as the X variant, and North expected the parents each to have one X variant, which they had passed to their sons, and one R variant, which functioned normally and facilitated production of the protein. To her surprise, both parents and the two healthy siblings also each had two X variants of the ACTN3 gene. Nobody in the family had any alpha-actinin-3 in their muscles whatsoever, yet only the two brothers had muscular dystrophy. North had not found a new muscular dystrophy gene after all. “That was a Friday when we found out,” she says, “and it was really, really depressing.”
That Sunday, she went to a movie and afterward took a walk to ponder the previous week. Never, not in the lab nor in the scientific literature, had she found an example of a healthy person with genes that left them entirely devoid of a structural protein. Structural proteins are critical. They make fingernails, hair, skin, tendons, and muscle. Humans tend to be diseased or to die when the genes that code for them are not functioning. “So I started reading the evolution literature,” North says, “and I thought, well, maybe alpha-actinin-3 is redundant. Maybe we don’t need it and it’s on its way out.”
North cold-called Simon Easteal, an Australian researcher with a specialty in molecular evolution. Together they yanked from storage two hundred samples of muscle with all manner of disease, from muscles that did not contract properly to others that had malfunctioning nerves. Just as she had seen with muscular dystrophy patients in Boston, about one in five of the diseased muscles had two copies of the X version of the ACTN3 gene, and thus no alpha-actinin-3. But about one in five samples of normal, healthy muscle had two X variants as well, so the gene could not be the cause of disease. Perhaps, then, alpha-actinin-3 had some other purpose in muscle. “That’s when we started to pull in different groups of people,” North says. “And that’s when we found this different ethnic distribution of the gene.”
North saw that one quarter of people of East Asian descent had two copies of the X variant of ACTN3 and about 18 percent of white Australians had two X variants. But when she tested Zulu people from South Africa, less than 1 percent had two X variants. Nearly all had at least one copy of the R variant, which codes for alpha-actinin-3 in fast-twitch muscle. And that was true of every African population. With respect to this particular gene variant, Africans or people of recent African ancestry happen to be extraordinarily uniform.
North was convinced that alpha-actinin-3 was not a meaningless protein, even though its absence did not lead to disease. Like the myostatin protein—of Superbaby fame—alpha-actinin-3 was highly conserved in evolutionary terms. It is in the explosive muscle fibers of chickens, mice, fruit flies, and baboons, among other animals, including our closest primate relatives, chimps. The absence of alpha-actinin-3, then, is a very recent and very human trait. North and colleagues estimated that the X variant spread through humans within the last thirty thousand years, and only outside of Africa. The gene, it appears, had been favored by natural selection only in non-African environments for some reason. Fast-twitch fibers must need it for something, North thought.
So she and her colleagues collected DNA from subjects with ample fast-twitch fibers: elite sprinters. They partnered with the Australian Institute of Sport to do ACTN3 testing on international-level athletes. While 18 percent of Australians had two X copies of the gene, almost none of Australia’s competitive sprinters did. Nearly every sprinter produced alpha-actinin-3 in their fast-twitch fibers. “I waited for years to publish that study,” North says. “The result came out the first time we did the analysis, and then we repeated it again and again internally.” And it held. Not only did sprinters in general tend not to have two X copies of ACTN3, but the better they were, the less likely it was they were XX. In one sample, just 5 out of 107 Australian sprinters were XX, and zero of the 32 sprinters who had gone to the Olympics were XX.
After that work was published, sports scientists around the world hustled to test their local sprinters, and the association showed up everywhere. With almost no exceptions, sprinters from Jamaica and Nigeria all had alpha-actinin-3 in their fast-twitch muscles, but so did distance runners from Kenya—no surprise given that nearly all of the control subjects from African populations did as well. Scientists in Finland and Greece took DNA from their Olympic sprinters, and, again, not a single one was XX. In Japan, a few sprinters were XX, but none who had run faster than 10.4 seconds for 100 meters.
ACTN3, North concluded, is a gene for speed. Why that may be so is not exactly clear. Alpha-actinin-3 may have a structural impact on how explosively a muscle fiber can contract, or it may influence the configuration of the muscular system. Mice as well as—in several studies—Japanese and American women who are deficient in alpha-actinin-3 have smaller fast-twitch muscles and less muscle mass over all. When North bred mice to have no alpha-actinin-3, compared with normal mice they had far less active glycogen phosphorylase, the enzyme that mobilizes sugar for explosive actions, like sprinting. The fast-twitch muscle fibers in those mice also took on some of the properties of slow-twitch, endurance fibers.
Given the approximate timing of when the X version of ACTN3 appears to have spread through humans—fifteen to thirty thousand years ago—North has toyed with the idea that the variant may have proliferated during the last ice age. Absence of alpha-actinin-3 may make fast-twitch muscle fibers more metabolically efficient, like their slow-twitch neighbors, a boon, perhaps, in frigid, food-scarce northern latitudes outside of Africa. Two anthropologists have suggested that the X version may have spread when humans outside of Africa transitioned from the hunter-gatherer lifestyle to an agricultural one, where they would have had less need to sprint in war or hunting but more need to be metabolically efficient and to work at a steady rate for long hours.
But North is cautious. Though we share the vast majority of our DNA sequence with mice, genetically manipulated rodents are not ideal models of human genetic variation. “We don’t know the whole story,” North says. “Right now, it looks like ACTN3 is one gene that contributes a little to sprinting, and there may be hundreds, and of course there are other factors like diet, environment, and opportunity.”
Private gene-testing companies have been less circumspect. As soon as the ACTN3-and-Olympians study appeared, companies rushed into the sparsely regulated direct-to-consumer genetic testing market. Genetic Technologies, of Fitzroy, Australia, led the way. For $92.40, the company would tell a customer what versions of the ACTN3 gene they carry. (I have two R copies.) In 2005, the Manly Sea Eagles of Australia’s National Rugby League became the first team to admit publicly that it was testing players for ACTN3 and tailoring training programs accordingly, giving more explosive weight lifting and less cardio to the guys with sprinter variants.
Atlas Sports Genetics, of Boulder, Colorado, has made headlines for selling parents an ACTN3 test for their children. According to Kevin Reilly, president of Atlas, the test is particularly useful for “those younger athletes who don’t have the motor skills yet.” By “younger,” Reilly means that just because baby Kobe doesn’t know how to walk yet, that should not mean his DNA can’t begin charting his athletic career. If Kobe has no R versions of the gene, his parents can start nudging their little bundle of DNA toward endurance sports. The genetic-testing-in-diapers market barely materialized for Atlas, but the company did manage a preteen customer base. Says Reilly, “We have had some impact on athletes in the eight-to-ten age group,” in terms of influencing their sport choices.
Unfortunately for those eight-to-ten-year-olds, though, consumer genetic testing for athleticism is nearly worthless.* Scientists have increasingly realized that the inherited component of complex traits, like athleticism, is most often the result of dozens or even hundreds or thousands of interacting genes, not to mention environmental factors. If you are XX for the ACTN3 gene, “you probably won’t be in the Olympic 100-meters,” North says. But you already knew that, without a genetic test. Though the ACTN3 gene does appear to influence sprinting ability, making a sports decision based on it is like deciding what a puzzle depicts when you’ve only seen one of the pieces. You need that piece to complete the puzzle, but you certainly can’t see a meaningful picture without more pieces.
As Carl Foster, director of the Human Performance Laboratory at the University of Wisconsin–La Crosse and coauthor of several ACTN3 studies, puts it: “If you want to know if your kid is going to be fast, the best genetic test right now is a stopwatch. Take him to the playground and have him race the other kids.” Foster’s point is that, despite the avant-garde allure of genetic testing, gauging speed indirectly is foolish and inaccurate compared with testing it directly—like measuring a man’s height by dropping a ball from a roof and using the time it takes to hit him in the head to determine how tall he is. Why not just use a tape measure?
All that ACTN3 can tell us, it seems, is who will not be competing in the 100-meter final in Rio de Janeiro in 2016. And it is not even doing a very specific job of that, given that it is only ruling out about one billion of the seven billion people on earth.
Still, if only that one gene is taken into account, it is also telling us that there are almost no black people anywhere in the world who are ruled out.
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