Published on: Jun 07, 2006
Jay Kaufman is an associate professor of epidemiology at the University of North Carolina School of Public Health and a fellow of the Carolina Population Center. He has written a number of articles on the ways in which health status varies by race, class and other socioeconomic quantities, and has co-written an important essay for the New England Journal of Medicine called "Race and Genomics."
There are countless instances in the history of science when widespread and uncritical embrace of a myth or fallacy has retarded progress, sometimes for centuries. For example, following Newton’s work in the early 18th century it could have been deduced that the universe must be expanding or contracting, yet the notion of a static universe remained dominant. Even into the early 20th century this was so entrenched that Albert Einstein fudged his General Theory of Relativity in 1917, including a "cosmological constant" that would make gravity repulsive at large distances. When Edwin Hubble demonstrated in the 1920's that the universe was indeed expanding, Einstein declared that this fudge was his "biggest blunder."
In biomedicine we may eventually recognize our biggest blunder to be the stubborn idea that socially recognized racial groupings, such as "White," "Black" and "Asian," have some clinical or epidemiologic utility. The belief that continental races are genetically distinct in ways that are relevant to medicine remains prevalent in clinical research, training and practice. Psychiatrist Sally Satel declared in The New York Times Magazine in 2001, for example, that she is a "racially profiling doctor," arguing that basing diagnosis and treatment on racial classification is supported by contemporary biomedical research. More recently, evolutionary biologist Armand Marie Leroi wrote in The New York Times that “…the recognition of race may improve medical care. Different races are prone to different diseases…[G]eneticists have started searching for racial differences in the frequencies of genetic variants that cause diseases. They seem to be finding them.”
Closer inspection of the putative evidence supporting such assertions reveals a more ambiguous picture, however, and illustrates how the normative process of scientific research may permit myths to endure. Just as Einstein fudged his work to make it consistent with a mistaken assumption, modern researchers err by privileging the premise of essential differences between continental populations in disease etiology. In this essay I recount one illustrative example in which a contemporary theory of genetic predisposition became a dominant paradigm for understanding racial variation in disease.
Racial Differences in Hypertension
By the 1960s there was extensive survey evidence indicating that black Americans experienced nearly twice the level of clinically defined hypertension as white Americans. Because sodium metabolism plays a key role in blood pressure regulation, many researchers sought explanations for excess African-American hypertension in factors related to renal handling of sodium, presumably under genetic control. Several authors in the 1960s and 1970s posited that blacks were more likely to suffer from a genetic mutation affecting sodium excretion. Some suggested that since blacks originated from hot and humid environments, they may possess innate capacities for sodium retention that would prove maladaptive in other settings. Others proposed that salt supplies for the sub-Saharan progenitors of African-Americans were historically limited.
Epidemiologic surveillance in West Africa soon demonstrated that most of these populations had comparatively low average blood pressures. It was reasoned that African-Americans bore a strong genetic similarity to modern West Africans, given the recent era of forced migration, and yet New World blacks evidenced more prevalent hypertension even in comparably tropical climates. Researchers struggled to accommodate the apparently conflicting pieces of information, and under the sway of a paradigm that favored genetic explanations for the black-white disparity, several authors began to formulate a hypothesis that would provide a genetic explanation for the black-black disparity. Something had to be different about New World blacks, and speculation soon focused on selection processes in the slave trade and the trans-Atlantic voyage.
The Slavery Hypertension Hypothesis
In 1983 it was hypothesized that an exaggerated hypertensive response to salt in black Americans might be traced to selective mortality during the period of Atlantic slavery. If mortality from salt and water deprivation, accompanied by excessive electrolyte loss from sweating, diarrhea and vomit during the brutal voyage across the sea, was reduced in those with the genetic good fortune to retain sodium, it was reasoned, might not descendents of these survivors fare worse in a high sodium environment in which this trait would become disadvantageous? This explanation soon became known as the "Slavery Hypothesis," and became intimately linked to its primary proponent, Clarence Grim.
Grim's 1988 conference presentation of this hypothesis attracted considerable media attention, with headlines such as "Black Slave Heritage Linked to Hypertension," and "High Blood Pressure, Most Deadly Among Blacks, Is Inherited." In 1990 a detailed account of the hypothesis made its first appearance in a clinical textbook, and a year later appeared for the first (and last) time as the subject of a peer-reviewed scientific paper. Media response remained energetic. In a medical news column, JAMA reported on the hypothesis declaring "African Lineage, Hypertension Linked." Another headline declared "Gene Linked to Hypertension," even though no genetic variants were identified or measured. Moreover, the unspecified "gene" was portrayed as a foreign villain: "Researchers…have found a genetic link that may explain why blacks in the Western Hemisphere suffer abnormally from high blood pressure. A 'salt retention' gene or genes of African origin may be the culprit," explained one article. This nonsensical description of the putative variant was echoed by an article in Science News: "The African Gene? Searching Through History for the Roots of Black Hypertension." Popular science writer Jared Diamond published an adulatory treatment in a 1991 issue of Natural History, including what appeared to be compelling historical data on African salt-scarcity and high slave-trade mortality.
As the Slavery Hypothesis grew in popularity in professional and popular circles, some researchers began to voice skepticism, arguing against the theory on the basis of population genetics, details of the physiology of hypertension, and basic evolutionary biology. The most scathing rebuttal, however, came from Philip Curtin, an historian of the slave trade on whose work Grim had drawn heavily. Curtin denied any historical validity to the proposition that Africa had traditionally been salt-scarce, and asserted that his own work had been misunderstood or misquoted on this point. He also disputed the mortality estimates cited by Grim, noting that these figures were not only incorrect or outdated, but cited so poorly that their original source could not be identified. Indeed, he disparaged Diamond’s impressive statistics as "numbers of unknown provenance." Further, Curtin argued that Grim's proposition that a majority of deaths were due to diarrheal disease was equally baseless. He concluded that the Slavery Hypothesis not only lacked supporting evidence, but that what little evidence did exist directly contradicted the theory.
Grim has largely avoided responding to specific criticisms, and in reply to these arguments he countered vaguely that Curtin had "failed to grasp several key physiological and epidemiological principles underlying the hypothesis." Other defenders of the hypothesis have been similarly oblique in print. The editor of the journal Psychosomatic Medicine, for example, dismissed critics of the Slavery Hypothesis as "left-thinking" people, and followed with the admonition that race and ethnicity are "too important to be ignored or politicized."
The Slavery Hypothesis Today
Despite these refutations, the Slavery Hypothesis remains widely accepted, as evidenced by the numerous hypertension textbooks that describe the theory in detail, often without mention of criticism. The hypothesis is frequently invoked in the medical literature to justify the more general proposition of innate biologic difference in cardiovascular disease risk and treatment efficacy. The editor of the American Journal of Cardiology declared in 2001 that "[i]t is this selective survival among the descendants of surviving slaves of genes responsible for an increased ability to hold on to salt that is now responsible for the exceptionally high prevalence of hypertension in African-Americans." The reflexiveness with which researchers invoke the hypothesis to justify notions of racial essentialism was exemplified in a radio interview at the 1999 Society for Human Genetics Meeting. Responding to a reporter’s question about hypertension in African-Americans, a genetic epidemiologist answered, “There must be something that sets them apart, and I come from the assumption that what sets them apart is their genes." The reporter then clarified that there was a "logical basis for pursuing this line of research," and returned to the epidemiologist who explained: "There is a theory that African-Americans who survived the slave trading trips over on the ships actually made it over if they were able to conserve salt."
Similarly, in a feature about Harvard economist Roland Fryer, Jr. published in March 2005, The New York Times Magazine depicted the Slavery Hypothesis as a new and exciting idea from the young academic superstar. “Fryer's notion that there might be a genetic predisposition at work was heightened when he came across a period illustration that seemed to show a slave trader in Africa licking the face of a prospective slave…,” wrote the profile’s author, Stephen Dubner. “A person with a higher capacity for salt retention might also retain more water and thus increase his chance of surviving. So it may have been that a slave trader would try to select, with a lick to the cheek, the ''saltier'' Africans. Whether selected by the slavers or by nature, the Africans who did manage to survive the voyage—and who then formed the gene pool of modern African-Americans—may have been disproportionately marked by hypertension.” In this instance, the reasoning happens to be exactly backwards, as the ''saltier'' Africans would be exactly the ones who were not retaining sodium, and therefore, based on the theory, the least able to endure the voyage. Regardless, what is remarkable is the perpetual recurrence of the theory as so new and exciting that no actual data (for example, measurement of a genetic marker for sodium metabolism) is required. The single piece of “evidence” cited in this account is a 1764 anti-slavery engraving, the interpretation of which as a depiction of tasting for salt is dubious at best.
Our Biggest Blunder?
The Slavery Hypothesis is a single example, but an illuminating one. A vague suggestion has achieved remarkable scientific and popular dissemination, enjoying the credibility accorded biomedical research, despite a dearth of evidence and denunciations from a range of critics that have generally gone unanswered. Respected researchers cite it readily, in many cases even expressing their aesthetic attraction to the theory. This is echoed in the popular press, where writers further exaggerate the simplistic genetic determinism and essential black abnormality that are implicit in the hypothesis. Racial groups are portrayed as fundamentally distinct in physiology, conforming to the stark distinctions with which we have become comfortable in the social sphere. Just as Einstein didn’t question the static nature of the universe because this appeared to be a matter on which there was consensus among knowledgeable people, so too does the utter normalcy of racial essentialism in biomedical science act to reinforce its legitimacy.
How often contemporary scientists may actually fudge their results to conform to a racial paradigm is impossible to know. We certainly have many historical examples of both conscious fraud and unconscious distortion in the scientific study of racial differences. Our most important blunders may less commonly take the form of overt fudging, however, and more often consist simply of extending credibility too quickly. Casual acceptance of an outright speculation such as the Slavery Hypothesis can become an edifice upon which we construct further elaborations (such as race-specific therapies), until the many facets of this process come to reinforce each other and create the impression of evidence when in fact there is little or none.