The study was small, as usual with biopsy studies that require the surgical removal of a gobbet of muscle tissue. The few similar studies over the years have generally agreed with the Laval findings, but each one has relied on a small number of subjects.*
In his 2003 book, Black Superman: A Cultural and Biological History of the People Who Became the World’s Greatest Athletes, and then in his 2006 paper with Morrison, Cooper first made the argument that West Africans evolved characteristics like a high prevalence of the sickle-cell gene mutation and other gene mutations that cause low hemoglobin for protection from malaria, and that an increase in fast-twitch muscle fibers followed from that, providing more energy production from a pathway that does not rely primarily on oxygen, for people who have reduced capacity to produce energy with oxygen. The former part of Cooper’s hypothesis—that sickle-cell trait and low hemoglobin are evolutionary adaptations to malaria—now seems undeniable.
In 1954, the same year Sir Roger Bannister broke the four-minute mile, British physician and biochemist Anthony C. Allison, who had been raised on a farm in Kenya, showed that sub-Saharan Africans with sickle-cell trait have far fewer malaria parasites in their blood than inhabitants of the same region who do not have sickle-cell trait. Normally, the sickle-cell gene variant seems like a bad thing to carry. If two people who each have one copy have kids together, one in four of their children will have two copies of the gene and therefore sickle-cell disease—also known as sickle-cell anemia—a condition in which sickled blood cells exist even without exercise, and life expectancy is reduced. And yet, this gene mutation has hung around—proliferated, actually—in the malaria danger zones of sub-Saharan Africa.
That is because people who have one copy of the sickle-cell gene variant are generally healthy, but have red blood cells that sickle when infected with the malaria parasite, which in turn protects the host from the parasite’s devastating effects. (Because sickle-cell disease shortens lives, the sickle-cell gene will never spread through an entire population. Among African Americans who have lived in the malaria-free United States for generations, the sickle-cell gene variant is steadily disappearing.) Today, the sickle-cell balance with malaria resistance is one of biology’s textbook examples of an evolutionary tradeoff, propagating an otherwise harmful gene variant because of an associated protection.
Cooper and Morrison’s suggestion that low hemoglobin in African Americans and Afro-Caribbeans is a second adaptation to malaria has been proven true as well, in a deadly manner.
Even as evidence mounted that low hemoglobin levels in Africans native to malarial zones is at least partly genetic, aid workers in Africa looked upon low hemoglobin as a sign purely of a diet with too little iron. In 2001, the United Nations General Assembly charged the world with reducing iron deficiency among children in developing nations. And so, in a well-intended effort to improve nutrition, health-care providers descended on Africa with iron supplements, which raise the hemoglobin levels of those who consume them. (Hemoglobin is an iron-rich protein, so levels fall if insufficient iron is consumed. Often the first thing elite endurance athletes check for if they start performing poorly is a low iron level.)
The problem was that doctors who studied malarial regions saw increased cases of severe malaria wherever iron supplements were dispensed. Since the 1980s, scientists working in Africa and Asia had documented lower rates of malaria death in people with low hemoglobin levels. In 2006, following a large, randomized, placebo-controlled study in Zanzibar that reported a stark increase in malaria illness and death among children given iron supplements, the World Health Organization issued a statement backtracking from the earlier UN position and cautioning health workers about giving iron supplements in areas with high malaria risk. Low hemoglobin, like sickle-cell trait, is apparently protective against malaria. And, in keeping with Cooper and Morrison’s hypothesis, many Africans who were forcibly taken to the Caribbean and North America came from the precise parts of the west coast of sub-Saharan Africa that suffer the highest rates of malaria illness and death in the world, as well as the greatest frequency of the sickle-cell gene.
It is the coda of the Cooper and Morrison hypothesis—that fast-twitch muscle fibers moved in as hemoglobin moved out—that is highly speculative.
To the end of his life, Patrick Cooper remained dedicated to his research and writing. Up until the day in 2009 that cancer finally overwhelmed him, Cooper was dictating to Juin from his bed. I had been hoping to meet Cooper on my trip to Jamaica before I learned that he had passed away and hadn’t been living in Jamaica for years anyway. Instead, I met with Morrison and then presented the paper he and Cooper coauthored to five scientists who were not previously familiar with it, and asked their opinions. One insisted that the theory was too speculative to discuss. The other four said that it was a reasonably constructed hypothesis, but also that it had never been directly tested and was not proven. (In 2011, though, scientists from the University of Copenhagen proposed that a high proportion of fast-twitch muscle fibers could account for several physical traits that have been documented in African Americans and Afro-Caribbeans, including low resting and sleeping metabolism, and less metabolism of fat for energy and more of carbohydrates as compared with Europeans.)
Pitsiladis—the gene hunter who collects DNA from world-class sprinters—argues that such a theory could not hold true because of the tremendously diverse genetic background of African Americans and Jamaicans that shows they aren’t some genetically monolithic block. But they do have the traits in question—significant prevalence of sickle-cell trait and low average hemoglobin—in common, so the issue of general genetic diversity is irrelevant. Africans are, on average, much more genetically diverse than Europeans. But with respect to certain genes, like the ACTN3 sprint gene variant, they can be more homogenous. So genetic diversity in itself does not imply that an ethnic group cannot share a common trait, as many certainly do. As Yale geneticist Kenneth Kidd said of African Pygmy groups: they are among the most genetically diverse people in the world, and yet they share the trait of diminutive stature that will prevent them from dominating the NBA.
Because I could not follow up with Cooper himself, I decided to follow up on his work to see if any evidence had emerged that might affirm or dismantle his theory since it was published. First stop: do athletes with sickle-cell trait perform any differently in explosive sports?
French physiologist Daniel Le Gallais, former medical director of the National Center for Sports Medicine in Abidjan, Ivory Coast, posed that question long before Cooper. About 12 percent of Ivorian citizens are sickle-cell carriers, and in the early 1980s Le Gallais noticed that the top three female Ivorian high jumpers (one of whom won the African championship) became abnormally exhausted during workouts. Le Gallais tested the athletes and found—“surprisingly,” he wrote in an e-mail—“these three athletes were sickle cell trait carriers, despite originating from different ethnic groups in the country.”
Le Gallais later coauthored studies that screened for sickle-cell trait in elite sprinters and jumpers. In 1998, he reported that nearly 30 percent of 122 Ivorian national champions in explosive jumping and throwing events were sickle-cell trait carriers, and that they collectively accounted for thirty-seven national records. The top male and female in the group were both sickle-cell carriers. In a 2005 study of sprinters from the French West Indies who made the French national team, about 19 percent of the athletes tested were sickle-cell carriers, and they accounted for an outsized proportion of titles and records held by the team.
“What is my standpoint currently?” Le Gallais wrote me. “Studies have clearly shown that athletes with [sickle-cell trait] were less numerous than non-SCT athletes in long endurance races. In contrast, athletes with SCT are more numerous in jumps and throws. . . . The oxygen transport system impairment explains the poor performances in long distance races. On the contrary, we don’t know the cause of their advantage in jumps and t
hrows.”
As for whether low hemoglobin in itself might prompt a switch to more fast-twitch fibers, there is evidence that it can in rodents. A UCLA study of mice that were put on iron-deficient diets showed a drop in hemoglobin and displayed a shift of type IIa fast-twitch muscle fibers to type IIb “super fast twitch” muscle fibers in their lower legs. In another study in Spain, rats were made to have low hemoglobin through periodic blood draws, and a shift to a higher proportion of fast-twitch fibers occurred in their lower legs. But no one has conducted such a study in humans, and mice have a greater ability to swap muscle fiber types than humans do. Plus, that is a developmental effect within the lifetime of a mouse, not an evolutionary one caused over generations by changing genes.
And that is all the science there is. A single mouse study and a single rat study demonstrating in rodents that low hemoglobin can induce a switch to more explosive muscle fibers. No scientist has attempted to test Cooper and Morrison’s idea in humans, so there are simply no human studies at all.
•
Several scientists I spoke with about the theory insisted that they would have no interest in investigating it because of the inevitably thorny issue of race involved. One of them told me that he actually has data on ethnic differences with respect to a particular physiological trait, but that he would never publish the data because of the potential controversy. Another told me he would worry about following Cooper and Morrison’s line of inquiry because any suggestion of a physical advantage among a group of people could be equated to a corresponding lack of intellect, as if athleticism and intelligence were on some kind of biological teeter-totter. With that stigma in mind, perhaps the most important writing Cooper did in Black Superman was his methodical evisceration of any supposed inverse link between physical and mental prowess. “The concept that physical superiority could somehow be a symptom of intellectual inferiority only developed when physical superiority became associated with African Americans,” Cooper wrote. “That association did not begin until about 1936.” The idea that athleticism was suddenly inversely proportional to intellect was never a cause of bigotry, but rather a result of it. And Cooper implied that more serious scientific inquiry into difficult issues, not less, is the appropriate path.
Cooper and Morrison’s hypothesis, that reduced oxygen-carrying capacity induced a shift to more explosive muscle properties, was never intended as simply a “black” phenomenon. Even if the hypothesis is correct, there is still tremendous physiological variation within any ethnic group, and Cooper and Morrison were theorizing about a set of black athletes with very specific geographic ancestry.
On the side of Africa opposite the ancestry of sprinters, and by the serendipity of geography, a different faction of the world’s greatest athletes were spared potentially endurance-harming genetic adaptations. They live at altitudes where the mosquitoes are scarce, and so are malaria and the sickle-cell gene.
Those black athletes came to dominate in an entirely different realm.
12
Can Every Kalenjin Run?
Every summer, John Manners returns to Kenya, and every July—after the 1,500-meter time trial—there are tears. Most of them stream down the cheeks of the kids who just ran. But, says Manners, “some of the tears are mine. It’s a pretty emotional business.”
It’s hard to imagine Manners sad. His eyes glitter under a newsboy cap. Together with his pointed white goatee and his buoyant walking stride, the eyes lend a puckish delight to his conversations.
The 1,500-meter race that makes Manners cry is the capstone of a unique college application process for sixty or so impoverished Kenyan kids each year, and Manners and his KenSAP program have to leave all but a dozen of them behind.
Begun in 2004, KenSAP—the Kenya Scholar-Athlete Project—is the brainchild of Manners, a New Jersey–based writer, and Dr. Mike Boit, a bronze medalist for Kenya in the 800-meters at the 1972 Olympics and now a professor of exercise and sports science at Kenyatta University in Nairobi. The idea is to get top Kenyan students from the western Rift Valley Province into premier colleges in the United States.
Each year, Manners peruses the list in the newspaper of the highest scorers on the Kenya Certificate of Secondary Education (KCSE) exam—a high school exit exam that accounts for 100 percent of the college admissions process in Kenya—for names of students with the best marks in the western Rift Valley. He also goes on local Kass FM radio and solicits applications from students who scored an “A plain,” the highest possible mark. Still, recruitment has challenges. “Because the program’s free,” Manners says, “some of the [applicants’] parents assume it’s a scam.”
Manners invites selected students who complete an application to the High Altitude Training Center, in the Rift Valley town of Iten. There they are interviewed, and then made to run a 1,500-meter race at an altitude around 7,500 feet. All of the students have succeeded in high school despite coming from destitute rural families. The majority are boys—the patriarchal nature of Kenyan culture affords girls less opportunity to prepare for the KCSE exam—and some come from tiny subsistence farms and attend school in classrooms with mud or stone floors. All have both the academic skill and the college-essay fodder to knock the argyle socks off East Coast admissions officers. After the interview and 1,500, Manners confers with Boit and a group of American instructors and local Kenyan elders, and within hours reads aloud the names of the kids who are accepted. That’s where the tears come in, from those who missed the cut.
The dozen kids KenSAP accepts undertake two months of intensive SAT prep and college application work. Thus far, the KenSAP plan has worked brilliantly. Between 2004 and 2011, seventy-one of the seventy-five students accepted by KenSAP gained entrance to U.S. colleges. Every Ivy League university has had a KenSAP kid. Harvard leads the league with ten, followed by Yale at seven, and Penn with five. Others have gone to prestigious liberal arts colleges, on the order of Amherst, Wesleyan, and Williams. “I love NESCAC,” says Manners, referring to the New England Small College Athletic Conference. “We’re very strong in NESCAC.”
The 1,500-meter time trial is, obviously, an unprecedented piece of a college application process. Kenyan kids who score an A plain usually come out of government-supported boarding schools, and most have no running experience at all. In a letter sent to KenSAP applicants months before the interviews, Manners explains that there will be a running test, and that they should dress accordingly. And yet, without fail, some boys will show up in long pants, and a few girls in calf-length skirts and pumps.
Manners’s hope with the 1,500 is to find undiscovered athletic prodigies with the running chops that will persuade an American coach to put a word in with the admissions committee. “We’re looking for everything we can to strengthen an application,” Manners says. If a kid with no running background shows promise, Manners will contact college coaches to see if any might be interested.
If forcing the academic all-stars of a geographic sliver of East Africa to run a 1,500-meter time trial on a dirt track at 7,500 feet seems a little strange, well, it is. Imagine a college admissions counselor taking the American kids who scored a perfect 2400 on the SAT and lining them up for a time trial.
But then, this is no random geographic sliver.
•
In 1957, when Manners was twelve, he moved with his father from Newton, Massachusetts, to Africa. Robert Manners, an anthropology professor and founder of the anthropology department at Brandeis University, had intended to study the Chaga people of Tanzania. But another anthropologist beat him to it, so Manners ventured west to the Rift Valley of Kenya to study the Kipsigis, a traditionally pastoral people who are a subgroup of a larger tribe, the Kalenjin. The Kipsigis held fiercely to their traditional culture in the face of British colonization, which lasted until 1963.
Robert Manners found a house in Sotik, in western Kenya, surrounded by tea and cattle farms, and at an altitude of six thous
and feet. There was one mud street, enclosed by verandas over raised sidewalks, like a town from the Old West. In short order, John Manners became like any other Kipsigis child, speaking Swahili and running two to three miles to school with his friends so they could avoid being caned for showing up late. He also attended his first track meet, as a spectator.
As was the case in Jamaica, British colonialism imported the sport of track and field. The Kenya Amateur Athletics Association was founded in 1951, and by the time the Manners family arrived, regional track meets—on dirt or grass tracks—were common. At one of the first meets Manners saw, in seventh grade, he was delighted by the stellar performances of Kipsigis runners—his people.
In the fall of 1958, Manners returned to Massachusetts for eighth grade, but his fascination with track and field, and with Kenya, remained. In the 1964 Olympics, just the third ever in which Kenya competed, a Kipsigis runner named Wilson Kiprugut won bronze in the 800-meters. Four years later, in the altitude of Mexico City, Kenya was the dominant distance running power, winning seven medals in middle- and long-distance events. The very same month of those Olympics, Manners, having just graduated from Harvard, was in upstate New York training for the Peace Corps. “I saw the names of the Kenyan runners who were winning those medals,” Manners says, “and I saw that almost all of them were Kalenjin.”
The Sports Gene: Inside the Science of Extraordinary Athletic Performance Page 20
