The Slavery Hypertension Hypothesis: Dissemination and Appeal of a Modern Race Theory

In this essay we present a case study of a recent etiologic hypothesis that was advanced in an effort to explain observed racial/ethnic variation in hypertension prevalence. We trace the historical development of this hypothesis, from early statements to current expressions. We examine the debate that has transpired in scientific journals and been disseminated through medical textbooks and the popular press, and the relation of these arguments to putative evidence from population genetics, historical demography and other fields. Despite criticism, this hypothesis has sustained some considerable degree of popular and scientific acceptance. We discuss this phenomenon in relation to broader themes in the epidemiology of racial/ethnic disparities. These include the use and misuse of various types of data, the role of peer review and its potential deficiencies in evaluating extradisciplinary material, and the ways in which popular notions about “race” contribute to epidemiologists’ credulity in the case of a controvertible hypothesis. Hypertension in African-Americans Observations of an African-American excess in mean blood pressure or in clinically diagnosed hypertension arose over a century ago, with primitive survey results dating back to at least as early as 1932. 1 By the 1960s there was extensive evidence from population-based surveys to indicate that black Americans experienced nearly twice the level of clinically defined hypertension observed among white Americans. 2 Although survey results in the 1960s began to suggest that most population groups in Africa had low mean pressures, 3,4 a presumed racial equivalence between Africans and African-Americans led many authors to assert that blood pressures in Africa were similarly elevated. Numerous cardiovascular surveys conducted subsequently in many parts of Africa have confirmed a generally low hypertension prevalence compared with Western populations. 5 Nonetheless, this continued presumption of the racial equivalence of various black populations still allows some current authors to mischaracterize African populations as endemically hypertensive. Halberstein wrote, for example: “The more frequent occurrence of hypertension in black (Afro-Caribbean) subsamples throughout the Caribbean has been traced to ancestral populations in West Africa and is thus at least partially attributable to gene flow from an originally high-prevalence area…”. 6,p.676 Another consequence of the observation of racial/ethnic disparity in hypertension prevalence has been the continued use of language that reveals an unambiguous tendency to view blacks and whites as fundamentally distinct in terms of innate biology or physiology. For example, articles bear titles such as “Is the Pathogenesis of Hypertension Different in Black Patients?”, 7 “Hypertension in Blacks. Is it a Different Disease?”, 8 and “Hypertension in African-Americans: A Paradigm of Metabolic Disarray.”9 Language in the published articles similarly reflects this doctrine of essential difference, and especially of “defects” or “abnormalities” in blacks. For example, “…hypertension in black subjects is linked to abnormalities of control of intracellular sodium,”10,p.291 and “…hypertension in blacks is associated with abnormalities of renal sodium and hydrogen exchange…”. 11,p.455 As Cooper and Rotimi 12 noted, other ethnic groups (such as Finns) with hypertension prevalences comparable with that of African-Americans are not described similarly as harboring a genetic defect or physiologic abnormality. This predominant ideology of essential difference has precipitated numerous unsubstantiated assertions in the peer-reviewed literature. For example, the disease is often described as intrinsically more virulent among blacks: “[B]lacks tend to experience greater cardiovascular and renal damage at any level of [blood] pressure,”13,p.450 a claim with no obvious empiric basis. 14 Likewise, following the long-standing paradigm of viewing racial/ethnic groups as primarily distinguished by genetic factors, the observed disparity in hypertension prevalence is frequently asserted matter-of-factly to be genetic in origin, 15 and a proliferation of bizarre theories has arisen as to the nature of this genetic predisposition, including hypotheses relating blood pressure disregulation directly to skin pigmentation 16 or to excess testosterone levels in black men. 17 The Slavery Hypothesis As it became increasingly clear that sodium metabolism played a key role in blood-volume regulation and barostasis, many researchers sought explanations for excess African-American hypertension prevalence 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 natriuresis. 18 Helmer 19 suggested that because blacks originated from hot and humid environments, they might possess innate capacities for sodium retention that would prove maladaptive in other settings. Gleiberman 20 added to this theory by suggesting that salt supplies for the sub-Saharan progenitors of African-Americans were historically limited, an idea further developed by Wilson. 21,22 With the increasing awareness that hypertension was rare in Africa, researchers struggled to accommodate the apparently conflicting pieces of information. It was reasoned that African-Americans bore a strong genetic similarity to modern Africans, given the relatively recent era of forced migration, and yet New World blacks evidenced more prevalent hypertension even in comparably tropical climates. 23 Locked in 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 the speculation soon focused on selection processes in the slave trade and the transatlantic voyage: “There are also hypothetical effects of genetic selection which could lead to an unusual population susceptibility to salt. Could an exaggerated hypertensive response to salt be related, for example, to selective effects in blacks of slavery? First came the forced recruitment of Africans from central, low salt-use areas; subsequently came a selective wastage from heat stress and salt and water deprivation during the brutal voyage across the sea. Among survivors, likely those most fit to withstand the acute stress, there followed an abrupt exposure to a poor quality diet with heavy salting on which the southeastern American slaves subsisted. Salt-saving renal-adrenal adaptations to a low salt environment, and selection, would be, by this idea, overwhelmed in the new salt-rich environment. Excess pressor responses to sodium might result not only from these sorts of selection processes, but from the stress of social dissonance among the slaves. But all these ideas too are broadly speculative.”24,pp.50–51 This brief comment by Blackburn and Prineas contained the central elements of what was to become the “Slavery Hypothesis.” It appears that neither author ever wrote again on the topic, and the theory has become more closely associated with its primary proponent, Clarence Grim. Grim elaborated on the Blackburn and Prineas hypothesis in a 1988 conference presentation, considering not only sodium loss from sweating but also the more substantial potential loss from diarrheal stools and vomit during the transatlantic voyage. 25 His presentation at the American Heart Association meeting that same year attracted immediate media attention. The United Press International (UPI) newswire story carried the headline “Black Slave Heritage Linked to Hypertension,”26 and the story ran in newspapers under headlines such as “High Blood Pressure, Most Deadly Among Blacks, Is Inherited.”27 The UPI newswire story stated that up to 40 million Africans were captured in the slave trade, and that of these only 11 million survived to be transported to the Western hemisphere, estimates that differ remarkably not only from those reported by most historians and demographers, but also from those in Grim's own published work on the topic. In 1989 and 1990, Grim 28–30 continued to present his theory at various professional and research meetings, and again the story was picked up in the popular press. 31,32 Also in 1990, Laragh and Brenner published the first edition of their hypertension textbook, which contained a chapter coauthored by Grim 33 in which the Slavery Hypothesis was described in detail. The specific idea that selection for a genetic trait had occurred during the capture and transport of individuals to the New World had still not been mentioned in a single peer-reviewed scientific journal article since the “broadly speculative” statement by Blackburn and Prineas 24 in 1983. In a 1990 article on a study of twins in Barbados, Grim and coauthors 34 made a passing reference to this hypothesis, citing conference abstracts, Blackburn and Prineas and a 1986 paper by Thomas Wilson on salt scarcity in Africa. Wilson, who appeared as coauthor with Grim on several articles throughout the late 1980s and early 1990s, had published a doctoral dissertation and two articles in which he linked excess African-American hypertension to salt scarcity in Africa through an adaptive response that he termed a “genetic proclivity” to retain body sodium. 21,p.494;22,35 The notion of a slow evolutionary adaptation to chronic salt scarcity in Africa proffered by Wilson, however, was soon overshadowed by the notion that was favored by Grim of a rapid selection process attributable to high mortality during slave transport and slave labor. Wilson and Grim 36 finally situated the Slavery Hypothesis as the central focus of a peer-reviewed journal article in 1991. Once again, the article attracted attention in both the secondary scientific literature and the popular media. In a 1991 review article, for example, Beevers and Prince cited the theory as “attractive.”37 In a “Medical News and Perspectives” column, The Journal of the American Medical Association reported on the Slavery Hypothesis, along with Grim's American Heart Association meeting presentation that year on the Barbados study of black twins, under the headline “African Lineage, Hypertension Linked.”38 The column included the results of a study by George Bakris “that fits with the Grim hypothesis,” and Bakris’ conclusion: “[S]o maybe what we're looking at in these hormone profiles is a reflection of the fact that, intrinsically, salt may be handled differently by blacks and whites.”38,p.2049 Popular media accounts often linked the Slavery Hypothesis to numerous other theories associated with the general theme of racial predisposition to hypertensive disease. The New York Times, for example, carried a story explaining the Slavery Hypothesis in which they also reported that researcher Roger Allen had “linked a chemical produced by the body during stress with the high prevalence of hypertension in blacks. The chemical, a blood vessel–constricting hormone called norepinephrine, is formed as a byproduct of production of the skin pigmentator melanin, which is much more abundant in blacks than in whites.”39,p.B6 This work by Allen described in The New York Times article appears never to have been published in a scientific journal. In other news articles focusing on Grim's related Barbados twin study, language tended to focus on the putative sodium-retention gene, which, despite being completely hypothetical, precipitated the headline “Gene Linked to Hypertension.”40 Furthermore, this unspecified gene was portrayed not only as a villain, but also as a foreign one. “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 the article (emphasis added). 41,p.B3 That this human gene should be an “African” gene was also echoed in a contemporaneous article in Science News, “The African Gene? Searching Through History for the Roots of Black Hypertension.”42 Furthermore, it bears repeating that other demographic or ethnic groups with hypertension prevalence are not described as Another 1991 article in The also focusing on the twin study, of the Slavery Hypothesis as he the prove on Grim's articles and conference in 1991 came more in and including to African-American Popular and published an of the hypothesis in a 1991 of the is it about American blacks that likely to hypertension and to of its His of Grim's theory use of historical on African salt scarcity and high mortality estimates that a would as of of the Slavery Hypothesis The 1991 paper by Wilson and Grim 36 in a of the American Heart Association journal Hypertension was the first paper in a scientific journal to focus on the Slavery It was also the that these authors would a peer-reviewed article on this specific topic. Wilson appears to have his theory of historical salt scarcity in Africa by the and Grim continued for his theory of selection for salt through media conference and Although various of and the hypothesis were in the late the first published appeared Wilson and Grim's 1991 Hypertension a the theory on the of population genetics, especially with to the notion that a genetic a in at in would over by and substantial the of such stress from many of may have to The most however, came from an of the slave trade, on work Wilson and Grim had any historical to the hypothesis that Africa had been salt and asserted that his own work had been or on this this Wilson and Grim apparently this key of their hypothesis, other authors have claim to the salt scarcity notion as their also the mortality cited by Wilson and that these were not only or but also often cited in such a that their could not be he that the Wilson and Grim that a of were attributable to diarrheal disease was that the Slavery Hypothesis not only but that what evidence directly the Although focused on historical other on the Slavery Hypothesis over the 5 from the hypertension research the notion with to and of the and numerous that it would be to that sodium retention and are both by the same genetic Furthermore, they the evolutionary biology of the the of rapid an for such a Likewise, and the Slavery Hypothesis to be that the theory is on an with and The adaptive in the case of is not a of the of but a of the susceptibility to by the that blood there high mortality pressures from disease in the slave trade, they individuals would be for to than for of Cooper and Rotimi 12 in that for the several hypertension genes that have been African-Americans not the to Africans that would be by the Slavery it appears to be whites who evidence of a genetic experienced of genetic a relatively of individuals on the of a the modern population some to ago, no such has been described for the modern African-American on these are by Cooper and Cooper and of the Slavery Hypothesis Grim's published of the hypothesis has been to a brief response to in a chapter and a general of genetic explanations for the excess prevalence of hypertension among blacks. In the Grim a of the Slavery Hypothesis, he the hypothesis of salt scarcity in Africa only to Wilson and and his own as the of rapid selection during as a With to he cited only by that he and to several key and the In the that however, there were no specific these Grim the of sodium that the Slavery Hypothesis not only to during the but to the from through and finally that poor whites in the American would have comparable of heavy poor diet and sodium that and an are not to In his review coauthored with Grim made no specific of the Slavery Hypothesis the of the theory and those researchers who a genetic of the black-white difference in hypertension Although the Slavery Hypothesis authors have the theory in In published a review essay in which he the hypothesis, asserted that mortality twice the mortality cited by that the theory that “The of a genetic from the a historical for salt retention and salt in this evidence and cited several of the published as as a of the the level of mortality experienced during the transatlantic that mortality on the are to thus that historical evidence on the mortality experience of African slaves might be in or in of the Slavery with an reference to of the Slavery Hypothesis as followed by the that and are to be or The Slavery Hypothesis Despite these the Slavery Hypothesis in the hypertension as an and scientific and historical of this be found in the various hypertension textbooks that of the The and for example, 25 to a by with no of The theory is also cited in a chapter by and Grim in in Blacks, again with no of The of Hypertension by a from the 1991 Wilson and Grim paper the Slavery Hypothesis, with no of A of two of Hypertension an historical In the edition in Grim's theory had been wrote that (emphasis case be all a genetic defect in sodium that is more prevalent among blacks. blacks, who originally in sodium was for have the physiologic which in their but it for to the sodium they they By the edition in a on the Slavery Hypothesis had been the of the was still to the of blacks to hot with to as the Slavery Hypothesis to be, it has been in all of its parts by a recent to the Slavery Hypothesis, often The and by and for example, several to the Slavery Hypothesis and slaves as originated in of West the same historical contained in such as a of a of to to the and the same mortality cited by but never to a specific despite their by an these have a in the hypertension literature. For example, citing and a in the American Journal of the of historical in its is this selective among the of slaves of genes for an to on to salt that is for the high prevalence of hypertension in A chapter by Wilson and Grim on sodium in the edition of The World History of was more the Slavery Hypothesis as and further Popular media attention to the Slavery Hypothesis has also by of as the article the theory but attention to who a historical story on not a of A article, on the other a more with the a Black the Another article the theory under the of citing Grim and Wilson as as by Also in History article was the of a essay “Black in which author and described the selection for sodium retention during the as that we with salt and In the peer-reviewed medical the Slavery Hypothesis to be cited frequently as a paradigm for the of innate difference in cardiovascular disease and For example, and to the hypothesis as an explanation for why is for black arguments on various elements of the hypothesis have similarly been to variation in by of the work of Wilson and Grim to the that there may have been of genetic susceptibility for among blacks originally from West and selection for among African slaves as a that would have the and during the awareness among hypertension researchers of the Slavery Hypothesis a for focusing on genetic of the racial/ethnic variation in disease. 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