Malaria and Muscle Fibers
Compared with Europeans, Jamaicans have longer legs relative to body height, and more narrow hips. This, Morrison says, is inarguable.
That Jamaicans would have a more linear build than Europeans is no surprise, nor is it specific to Jamaicans. As Allen’s rule of body proportions dictates, men and women with recent ancestry from low latitudes and warm climates generally have proportionally long limbs. Another ecogeographic principle, known as Bergmann’s rule—named for nineteenth-century biologist Carl Bergmann—indicates that humans with recent low latitude ancestry will also tend to be more narrow, with slimmer pelvic bones. Both long legs and narrow hips are advantageous for running and jumping. All other factors being equal, maximum running speed scales with the square root of leg length. But the theory of western African sprint dominance that Morrison coauthored is a thesis entirely apart from these anatomical concerns.
In 2006, Morrison, with Patrick Cooper, proposed in the West Indian Medical Journal that rampant malaria along the west coast of Africa, from where slaves were taken, led to specific genetic and metabolic alterations beneficial for sprint and power sports. The hypothesis: that malaria in western Africa forced the proliferation of genes that protect against it, and that those genes, which reduce an individual’s ability to make energy aerobically, led to a shift to more fast-twitch muscle fibers, which are less dependent upon oxygen for energy production. Morrison helped with the biology details, but the fundamental idea originally came from Cooper, a writer and childhood friend of Morrison’s.
Cooper was a polymath who had professional success in jobs ranging from music recording to writing speeches for Norman Manley, an architect of Jamaica’s independence, and then for his son, Prime Minister Michael Manley. Early in his career, Cooper had been a reporter for The Gleaner, Jamaica’s largest newspaper. Working at The Gleaner’s sports desk, he first surmised that white athletes had historically dominated sprint and power sports only by systematically excluding or dodging black athletes, like boxing champion Jack Johnson. In later writing, Cooper meticulously documented the fact that athletes with western African heritage become highly overrepresented in sprint and power sports almost immediately once they are allowed a fraction of their white counterparts’ access to sports. Cooper highlighted trends that continue today: At every Olympics after the U.S. boycott of 1980, every single finalist in the men’s Olympic 100-meters, despite homelands that span from Canada to the Netherlands, Portugal, and Nigeria, has his recent ancestry in sub-Saharan West Africa. (The same has been true for women at the last two Olympics, and all but one female winner since the U.S.-boycotted 1980 Games has been of recent western African descent.) And there has not been a white NFL player at cornerback, football’s speediest position, in more than a decade.*
As a speechwriter during Michael Manley’s combative 1976 reelection campaign, Cooper and his family were under constant threat. Cooper stopped sitting with his back to windows, and when his wife, Juin, was held up at gunpoint, he moved the family away from Jamaica, for good. Living in Houston in the late 1980s, Cooper haunted the library, stalking historical and biological explanations for the dominance of black athletes in sprint sports. Cooper read voraciously from scientific publications in biology, medicine, anthropology, and history in a manner that few ever did prior to the advent of electronic databases that sift scholarly journals with a keystroke.
Cooper found the famous body types study of 1968 Olympians, and he latched on to a curious side note recorded by the scientists. The researchers had been surprised to find that “a sizeable number of Negroid Olympic athletes manifested the sickle-cell trait.” That is, some black Olympians had, in one of two copies of the gene that codes for hemoglobin—the oxygen-carrying molecule in red blood cells—a mutation that causes round red blood cells to curl up in a sickle shape in the absence of oxygen, potentially impairing blood flow through the body during vigorous exercise. The gene variant that causes sickle-cell trait is found most often in people with recent sub-Saharan ancestry in west or central Africa, and scientists had previously believed that the high altitude of the 1968 Mexico City Olympics would prevent athletes with sickle-cell trait from performing well. “Sickle-cell was supposed to be a deterrent,” Morrison says. But it made no difference at the Olympics in events of short duration, like sprints and jumps.
In the decades since, epidemiological studies have found that athletes with sickle-cell trait (they have one copy of the mutant gene and are known as “sickle-cell carriers”) are indeed underrepresented in athletic endeavors that require aerobic endurance. In competitive running, sickle-cell carriers all but disappear in events longer than 800 meters. They are genetically disadvantaged for long-distance sports. In a small number of sickle-cell carriers, blood flow is inhibited to such a degree as to become deadly if they work out too hard for too long. Since 2000, the sudden deaths of nine college football players—all of them black and in Division I—during training have been tied to sickle-cell trait, and the NCAA now requires screening for the gene variant that causes it. (According to a panel at the 2012 Big East Conference Sports Medicine Society, white college athletes, on the advice of a team doctor, will often sign a waiver to forgo the testing, given the unlikelihood that they carry the sickle-cell gene variant.)
In 1975, the year after the Mexico City Olympics data was published, another study appeared that Cooper would dissect two decades later, this one showing naturally low hemoglobin levels in African Americans. The work was published in the Journal of the National Medical Association, run by the Maryland-based National Medical Association, which promotes the interests of physicians and patients of recent African descent. Using data from nearly 30,000 people in ten different states, with ages ranging from the first year to the ninth decade, it reported that African Americans have lower hemoglobin levels at every stage of life than white Americans, even when socioeconomic status and diet are matched. (Errol Morrison’s wife, Fay Whitbourne, formerly head of Jamaica’s National Public Health Laboratory Services, says that hemoglobin levels among Jamaicans are in line with those of African Americans.) Numerous studies, as well as population data from the U.S. National Center for Health Statistics, have replicated this result in the years since, including in athletes. In a colossal 2010 study of 715,000 blood donors across America, researchers wrote that African Americans exhibit a “lower genetic set point for hemoglobin,” regardless of environmental factors like nutrition.* Like sickle-cell trait, genetically low hemoglobin—all else being equal—is a genetic disadvantage for endurance sports. Runners of recent western African descent are very much underrepresented at high levels of distance running. (The Jamaican record in the 10K would not even have qualified for the 2012 Olympics)
The authors of the Journal of the National Medical Association paper wrote that lower hemoglobin levels raise the possibility that African Americans employ more of some alternate energy pathway to compensate for a relative lack of oxygen-carrying hemoglobin. Two years later, in the same journal, another group of scientists insisted: “some compensatory mechanism must exist to counteract this relative deficiency in hemoglobin, since a significant difference has even been demonstrated in healthy athletes.” Cooper set out to find that compensatory mechanism.
His tireless perusal of medical journals took on greater urgency in 1996, when he was diagnosed with terminal prostate cancer. Cooper and Juin moved to New York City in 2000 so that Cooper could spend every day at the New York Public Library. “My office,” he called it. Weekend trips to Baltimore to visit his daughter doubled as visits to the University of Maryland library.
And then Cooper found just the potential “compensatory mechanism” he was looking for, in a 1986 study from Laval University in Quebec published in the Journal of Applied Physiology and coauthored by Claude Bouchard, who would go on to become the most influential figure in the field of exercise genetics, and the leader of the HERITAGE Family Study that documented aerobic trainability differences among families. Bouchard and colleagues took muscle samples from the thighs of two dozen sedentary Laval students, primarily from countries in western Africa, as well as from two dozen sedentary white students, who were identical to the African students in age, height, and weight. The researchers reported that a higher proportion of muscle in the African students was composed of fast-twitch muscle fibers, and a lower proportion was slow-twitch muscle fibers compared with the white students. The African students also had significantly higher activity in the metabolic pathways that rely less on oxygen to create energy and that are engaged during an all-out sprint. The scientists concluded that, relative to the white students, the students from western Africa “are, in terms of skeletal muscle characteristics, well endowed for sport events of short duration.”
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 throws.”
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.
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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.