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.
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.
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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.”
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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.
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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.
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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)
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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.
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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.
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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.
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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.
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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.”
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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.
No mention of the Rift valley Kenyan Africans consistently winning most marathons.