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 elevated hypertension prevalence are not described as suffering “abnormally.” Another 1991 article in The Washington Post, also focusing on the twin study, quoted Charles Curry of Howard University describing the Slavery Hypothesis as “a beautiful idea,” although he went on, “but the problem is…you can't prove it.”43,p.Z7
After initial press reports on Grim's articles and conference presentations in 1991 came more elaborate treatments in magazines and periodicals, including publications directed to African-American audiences. 44 Popular science writer and UCLA physiologist Jared Diamond published an adulatory treatment of the hypothesis in a 1991 issue of Natural History, 45,p.20 posing the question “What is it about American blacks that makes them disproportionately likely to develop hypertension and then to die of its consequences?” His subsequent description of Grim's theory involved compelling use of historical data on African salt scarcity and high slave-trade mortality (∼70%), estimates that a historian would later disparage as “numbers of unknown provenance.”46,p.1684
Critics of the Slavery Hypothesis
The 1991 paper by Wilson and Grim 36 in a supplement of the American Heart Association journal Hypertension was the first full-length paper in a scientific journal to focus on the Slavery Hypothesis. It was also the last time that these authors would publish a peer-reviewed article on this specific topic. Wilson appears to have largely abandoned his theory of historical salt scarcity in Africa by the mid-1990s, and Grim continued advocating for his theory of selection for salt conservation largely through media interviews, lectures, conference presentations and book chapters. Although various expressions of caution and skepticism regarding the hypothesis were voiced in the late 1980s, the first published criticism appeared alongside Wilson and Grim's 1991 Hypertension article. Fatimah L.C. Jackson, a biological anthropologist, questioned the theory on the basis of population genetics, especially with respect to the notion that a genetic “bottleneck” (ie, a vast restriction in variability) imposed at one point in history would persist over subsequent generations characterized by novel environmental stresses and substantial admixture. 47 Indeed, she suggested, the imposition of such intense environmental stress from so many infectious causes of death may well have acted to increase diversity.
The most scathing rebuttal, however, came from an historian of the slave trade, Philip Curtin, on whose work Wilson and Grim had drawn heavily. 46 Curtin denied any historical validity to the hypothesis that Africa had traditionally been salt scarce, and asserted that his own work had been misunderstood or misquoted on this point. Indeed, after this stinging critique, Wilson and Grim apparently avoided this formerly key element of their hypothesis, although other authors have laid claim to the salt scarcity notion as their own. 48,49 Curtin also disputed the mortality figures cited by Wilson and Grim, asserting that these figures were not only incorrect or outdated, but also often cited in such a way that their original source could not be clearly identified. Further, he contended that the Wilson and Grim proposition that a majority of deaths were attributable to diarrheal disease was equally baseless. Curtin concluded that the Slavery Hypothesis not only lacked supporting evidence, but that what little evidence did exist directly contradicted the theory.
Although Curtin's critique focused on historical evidence, other critical perspectives on the Slavery Hypothesis emerged over the next 5 years from the hypertension research community. Questioning the notion with respect to physiology and pathology of the disease, Weder and Schork 50 invoked numerous objections, noting that it would be naive to assume that sodium retention and excretion are both controlled by the same unitary genetic mechanism. Furthermore, they questioned the evolutionary biology of the theory, dismissing the possibility of so rapid an evolution for such a complex trait. Likewise, James and Baker 51 judged the Slavery Hypothesis to be improbable, arguing that the theory is premised on an ill-considered analogy with malaria and sickle-cell trait. The adaptive mechanism in the case of endemic malaria is not a modification of the symptoms of disease, but rather a modification of the susceptibility to infection by the plasmodium that attacks red blood cells. Were there high mortality pressures from infectious disease in the slave trade, they reasoned, individuals would likewise be selected for resistance to infection rather than for moderation of symptoms.
Cooper and Rotimi expressed similar objections, 12 noting in addition that for the several hypertension candidate genes that have now been identified, African-Americans do not show the restricted allele frequencies relative to Africans that would be predicted by the Slavery Hypothesis. 52 Indeed, it appears to be whites who show evidence of a genetic “bottleneck,” having experienced severe restriction of genetic variability when a relatively small number of individuals (perhaps on the order of a few thousand) founded the modern European population some 30 to 50 thousand years ago, 53 whereas no such restricted variability has been described for the modern African-American population. Further elaborations on these critiques are provided by Cooper et al. 54 and Cooper and Zhu. 55
Persistence of the Slavery Hypothesis
Grim's published defense of the hypothesis has been limited to a brief response to Curtin in a 1995 textbook chapter 56 and a general defense of genetic explanations for the excess prevalence of hypertension among blacks. 57 In the 1995 book chapter, 56,p.178 Grim provided a detailed accounting of the Slavery Hypothesis, although he attributed the hypothesis of salt scarcity in Africa only to Wilson and others, and identified his own unique contribution as having realized the importance of rapid selection during slavery as a crucial element. With respect to critics, he cited only Curtin by name, averring that he and others “failed to grasp several key physiological and epidemiological principles underlying the hypothesis.”56,p.179 In the paragraphs that followed, however, there were no specific rebuttals concerning these principles. Rather, Grim reviewed the dangers of sodium depletion, clarified that the Slavery Hypothesis referred not only to deaths during the Middle Passage but rather to the entire period from captivity through “seasoning,” and finally questioned Curtin's assertion that poor whites in the American South would have shared comparable conditions of heavy agricultural labor, poor diet and sodium depletion: “[Curtin] suggests that individual freedom and an intact family milieu are not important to health!”56,p.180 In his review coauthored with Robinson, Grim made no specific defenses of the Slavery Hypothesis beyond simply reiterating the basic details of the theory and extolling those researchers who “champion a genetic cause of the black-white difference in hypertension incidence.”57,p.84
Although the Slavery Hypothesis remains widely cited, few authors have actively defended the theory in print. In 2000, Dimsdale 58 published a review essay in which he restated the hypothesis, asserted that Middle Passage mortality averaged 30% (ie, twice the mortality proportion cited by Grim) and, while admitting that the theory remained highly speculative, concluded that “The data….are suggestive of a genetic legacy from the Middle Passage, a historical legacy accounting for increased salt retention and thereby increased salt sensitivity in blacks.”58,p.166 Kaufman 59 disputed this evidence and cited several of the published criticisms, as well as a criticism of the 30%-mortality figure. Regarding the level of mortality experienced during the transatlantic journey, Dimsdale countered that “…the exact mortality rates on the Middle Passage are uncertain to everyone,” thus effectively denying that extant historical evidence on the mortality experience of African slaves might be used either in support or in criticism of the Slavery Hypothesis. Dimsdale concluded with an enigmatic reference to critics of the Slavery Hypothesis as “left-thinking” people, followed by the admonition that race and ethnicity are “too important to be ignored or politicized.”60,p.325
The Slavery Hypothesis Today
Despite these criticisms, the Slavery Hypothesis remains widely accepted in the hypertension community as an active, serious and plausible scientific and historical proposition. Evidence of this acceptance can be found in the various hypertension textbooks that contain detailed accountings of the theory. The Fray and Douglas 61 text, for example, devotes 25 pages to a detailed argument by Grim, with no mention of criticism. The theory is also cited in a chapter by Blaustein and Grim 62,p.98 in Saunders’Cardiovascular Diseases in Blacks, again with no mention of criticism. The Textbook of Hypertension by Swale 63,pp.813–814 likewise provides a long quote from the 1991 Wilson and Grim paper stating the Slavery Hypothesis, with no mention of criticism.
A comparison of two editions of Normal Kaplan's Clinical Hypertension provides an illuminating historical perspective. In the fourth edition (published in 1986, before Grim's theory had been articulated), Kaplan wrote that (emphasis added) “[A] very attractive case can be constructed, all based upon a genetic defect in sodium excretion that is more prevalent among blacks. Perhaps blacks, who originally lived in hot, arid climates wherein sodium conservation was important for survival, have evolved the physiologic machinery which protects them in their original habitat but makes it difficult for them to handle the excessive sodium they ingest when they migrate.”64,pp.114–115 By the sixth edition in 1994, a section on the Slavery Hypothesis had been inserted, although the larger portion of the text was still devoted to the acclimation of blacks to “a hot environment” with “little access to salt.” Kaplan concluded: “As attractive as the Slavery Hypothesis seems to be, it has been vigorously denied in all of its major parts by a Johns Hopkins historian.”65,pp.128–129
More recent sources continue to cite the Slavery Hypothesis, often uncritically. The book Salt, Diet and Health by MacGregor and de Warndener, 66,p.122 for example, devotes several pages to the Slavery Hypothesis and describes slaves as having originated in “very low-salt areas of West Africa.” They repeat the same distorted historical data contained in previous treatments, such as a march of a distance of “100 to 200 miles to the coast,” and the same untenable mortality figures cited by Diamond 45 but never attributed to a specific source. Indeed, despite their utter denunciation by an eminent historian, 46 these slave-trade statistics have achieved a virtual immortality in the hypertension literature. For example, citing MacGregor and de Warndener, 66 a 2001 editorial in the American Journal of Cardiology repeats the litany of historical inaccuracies in its entirety, concluding, “It 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.”67,p.1344 A chapter by Wilson and Grim 68,p.851 on sodium in the 2000 edition of The Cambridge World History of Food was somewhat more cautious, describing the Slavery Hypothesis as “controversial,” and referencing Curtin's critique 46 without further comment.
Popular media attention to the Slavery Hypothesis has also continued, although sometimes accompanied by discussion of criticisms as well. Under the subheading “Genetic Links Hinted,” one 1993 newspaper article covered the theory but gave prominent attention to critic John Flack, 69 who opined “That's a nice historical story based on not a lot of science.” A 1997 article, on the other hand, gave a somewhat more essentialist spin with the title “Dealt a Bad Hand, Black Males Can Beat the Odds.”70 Another 1997 article 71 discussed the theory under the subheading “A Legacy of Slavery,” citing Grim and Wilson as well as criticism by anthropologist William Dressler. Also in 1997, Diamond's Natural History article 45 was the subject of a syndicated radio essay entitled “Black Salt” in which author and narrator John Lienhard 72 described the selection for sodium retention during the Middle Passage as “…a death sentence now that we load our diets with salt and sugar.”
In the peer-reviewed medical literature, the Slavery Hypothesis continues to be cited frequently as a paradigm for justifying the proposition of innate biological difference in cardiovascular disease risk and treatment efficacy. For example, Brownley and colleagues 73,p.611 refer to the hypothesis as an explanation for why diuretic therapy is preferred for black patients. Similar arguments based on various elements of the hypothesis have similarly been invoked to justify variation in recommended therapy by race of patient. 74,75 Lackland et al. 76,p.62 cite the work of Wilson and Grim to support the suggestion that there may have been “transmission of genetic susceptibility for stroke among blacks originally immigrating from West Africa.” Shields and Mann 77 posit selection for smaller salivary glands among African slaves as a mechanism that would have provided the necessary protection against fluid and electrolyte losses during the Atlantic transit. Finally, widespread awareness among hypertension researchers of the Slavery Hypothesis provides a constant rationale for focusing on genetic determinants of the racial/ethnic variation in disease. This phenomenon was exemplified in a recent radio interview conducted at the 1999 Society for Human Genetics Meeting. The reporter interviewed a prominent genetic epidemiologist as she stood by her poster: “There must be something that sets them apart,” explained the epidemiologist, when asked about excess prevalence of hypertension among African-Americans, 78 “and I come from the assumption that what sets them apart is their genes.” The reporter then explained that there was a “logical basis for pursuing this line of research,” and returned to the epidemiologist for clarification: “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,” she explained. The radio report then continued with a critique of this idea from Stanford geneticist David Cox. Nonetheless, the epidemiologist's explanation bespeaks an enduring faith in the Slavery Hypothesis by many prominent scientists.
What Does the Slavery Hypothesis Tell Us About the Racialized Epistemology of Science?
The Slavery Hypothesis is an unusual theory by any reckoning. It has achieved remarkable dissemination, and yet only a single peer-reviewed scientific article has ever focused on the details of the theory. 36 The bulk of the written work on this topic by Wilson and Grim is confined to conference abstracts and book chapters, which are not generally peer reviewed, and which themselves tend to rely on references to other non–peer reviewed material. In the Fray and Douglas 61 textbook, for example, the Wilson and Grim chapter contains 10 citations authored by Wilson, four of which are abstracts that apparently never proceeded to journal publication, and three of which are books or book chapters. Furthermore, despite a barrage of criticism from a number of disciplines that have generally gone without response, the theory remains viable, and respected researchers cite it without apparent hesitation. It has been incorporated as a standard feature of many hypertension textbooks, often with minimal reference to published criticisms. In many cases, authors go out of their way to express their admiration of the theory and their aesthetic attraction to the paradigm. This is echoed in the popular press, where writers provide further exaggeration to the notions of genetic determinism and essential black abnormality that are implicit in the Slavery Hypothesis.
Clearly, the theory is one that can neither be readily refuted nor confirmed, which perhaps helps to account for its enduring attraction. Some authors have remarked on this with subtle ambiguity about whether the impossibility of resolution might not, in fact, constitute one of its most endearing features (“[A] beautiful idea…but the problem is…you can't prove it”). 43 Wilson and Grim 36,p.I-125 cite Grollman 18 as lamenting that the precursor theory would be “impossible to verify,” but they continue: “We disagree with Grollman; our knowledge of the extensive material available of the biohistory of blacks makes it possible to test the hypothesis against the historical record.” Thus, they identified historical material as the primary evidentiary basis for their argument, materials that historian Philip Curtin would subsequently assert were wholly misunderstood or misused. 46 This stands in contrast to Dimsdale, who asserted that historical arguments could not be used to argue against the Slavery Hypothesis because “…the exact mortality rates on the Middle Passage are uncertain to everyone.”60,p.325 What constitutes “evidence” is therefore very much a key question in this discussion, as are the uses and abuses of such evidence. Grim, for example, apparently relied heavily on historian Joseph Miller's estimates for mortality in the trade of slaves from Angola to Brazil, 79,pp.437–442 estimates that have then been bandied about as if they apply to all places for all time, especially by popular writers such as Diamond. 45,72
The intellectual resilience of the Slavery Hypothesis may be attributable to several of its ideologic components. As reflected in several press accounts, perhaps the most influential of these in the modern era is the beguiling allure of a simplistic genetic determinism. Nelkin and Lindee have suggested that what makes these popular notions so enticing is that “…genetic explanations…exonerate the individual, removing moral responsibility by providing a biological ‘excuse.’ Genes are the agents of destiny: We are the victims of a molecule, captives of our heredity.”80,p.129 The notion of being circumscribed by one's ancestral past may be particularly salient for a group whose historical connection to African origin and the epoch of Atlantic slavery are central components of ethnic affiliation. As in the case of sickle-cell anemia, the presence of a biological trait that is understood to derive directly from Africa or from the initial passage from Africa may therefore become an authenticating characteristic. 81,p.139 The myth of genetic determinism cuts both ways, however, for although it absolves the individual from responsibility, it also absolves the society at large. “Deterministic biological explanations (‘it's in my genes’)—much like theological explanations (‘the devil made me do it’)—locate problems (and, therefore, solutions) within individuals.”80,p.130
Finally, the seemingly irresistible siren song of the Slavery Hypothesis may derive in part from its implications for scientific conceptions of race and identity. Once Grim devised the evolutionary hypothesis of rapid genetic selection during the period of slavery, it provided a basis for exceptionalism in the discussion of African-American hypertension, a basis for treating American blacks as a group that had been uniquely and intractably transformed, genetically mutilated. The essential “defect” or “abnormality” in this group therefore achieved not only a rational basis, but became something innately pathologic, thereby reinforcing blacks’ essential physical inferiority in the modern world. Given the common African origins for all of humanity, therefore, the Slavery Hypothesis may serve not merely to provide an explanation for biological distinction between racial/ethnic groups, but to judge that distinction as a deformity rather than a mere divergence. The idea that a whole people could carry through history the permanent scar of a momentous event is one previously advanced by Freud. 82 Grim's theory effectively recapitulates this narrative, replacing the psychoanalytic paradigm of collective guilt as a group psychologic property with the contemporary biomedical paradigm of genetic legacy as a group biological property. In both cases, the achieved difference marks the group as permanently distinct from other groups, thus cementing an uncomfortably fragile group identity into an immutable categorization that can perpetuate indefinitely.
Helpful comments were provided by Tim Carey, Vic Schoenbach, Sherman James, and John Flack. Christiane Voisin provided assistance in acquisition of archival materials.
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