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Slavery Hypertension Hypothesis

Slavery Hypertension Hypothesis

A POPULAR HYPOTHESIS

THE SLAVERY HYPOTHESIS TODAY

BEYOND THE SLAVERY HYPERTENSION HYPOTHESIS

BIBLIOGRAPHY

Early in the twentieth century, before chronic high blood pressure (hypertension) was even recognized as a serious medical condition, colonial physicians in Africa had already developed an interest in the apparent absence of hypertension among indigenous black populations. Rather than interpreting these observations as some sort of natural advantage possessed by Africans, they attributed the difference to a carefree traditional life, uncomplicated by the stresses of industrialized society. In the United States, on the other hand, evidence emerged by the 1930s that black Americans had a higher prevalence of hypertension than whites, and this observation spawned many theories about anatomic and physiologic differences that might explain the disparity.

Despite extensive research since the mid-twentieth century on social and behavioral factors that contribute to hypertension, there has been a persistent impulse in American biomedicine to view racial groups as representing human subspecies. Explanations for racial health disparities therefore tend to be couched reflexively in terms of hypothesized genetic factors. This tradition of racial essentialism led to a surfeit of ad hoc hypotheses about hypertension, such as relating blood pressure levels directly to skin pigmentation or to excess testosterone levels in black men. Some authors suggested that because blacks originated from hot and humid environments, they possessed innate capacities for sodium retention that proved maladaptive in other settings. Others proposed that salt supplies for the sub-Saharan progenitors of African Americans were historically limited.

A POPULAR HYPOTHESIS

One of the most widely disseminated of these just so stories is the slavery hypertension hypothesis, an evolutionary theory that relates excess hypertension risk in New World blacks to natural selection during the Middle Passage for the trait of retaining sodium. The theory was posited at least as early as 1983, and it was adopted in the late 1980s by the hypertension researcher Clarence Grim, who has championed the idea energetically in the subsequent decades. Grim speculated that sodium loss from sweating, diarrheal stools, and vomit during the transatlantic voyage led to high levels of mortality from dehydration, and therefore to selection pressure against genes coding for greater sodium excretion in the kidneys.

As this hypothesis grew in popularity, 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. For example, Philip Curtin, a historian of the slave trade on whose work Grim had drawn heavily, denied any historical validity to the proposition that Africa had traditionally been salt-scarce. Curtin asserted that his own work had been misquoted on this point. He also disputed the mortality estimates cited by Grim, noting that these figures were not only incorrect or outdated, but that they were referenced so poorly that their original source could not be identified. Curtin argued that Grims proposition that a majority of deaths were due to diarrheal disease was equally baseless, and he concluded that Grims 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 response 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, admonishing them that race and ethnicity are too important to be ignored or politicized (Dimsdale 2001, p. 325).

THE SLAVERY HYPOTHESIS TODAY

The slavery hypertension hypothesis remains widely accepted, as evidenced by the numerous hypertension textbooks that describe the theory in detail, often without mention of any 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. For example, the editor of the American Journal of Cardiology wrote 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 (Roberts 2001, p. 1344).

The theory also reappears periodically in the popular press. In a 2005 feature about the Harvard economist Roland Fryer Jr. for example, the New York Times Magazine depicted the slavery hypothesis as a new and exciting idea from the young academic superstar. Fryers 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 profiles author, Stephen Dubner. He continued, 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 voyageand who then formed the gene pool of modern African-Americansmay have been disproportionately marked by hypertension (Dubner 2005, p. 56).

In this instance, the reasoning happens to be exactly backwards, as the saltier Africans would be exactly the ones who were not retaining sodium. Disregarding this logical error, what is remarkable is the perpetual recurrence of the theory as so new and exciting that no actual data (e.g., a measurement of a genetic marker for sodium metabolism) is required. The single piece of evidence cited in this account is a 1764 antislavery engraving, the interpretation of which as a depiction of tasting for salt is dubious at best.

BEYOND THE SLAVERY HYPERTENSION HYPOTHESIS

In the case of the slavery hypothesis, a vague suggestion has achieved considerable scientific and popular dissemination, despite a dearth of evidence and denunciations by many critics that have generally gone unanswered. Respected researchers cite the theory readily, in many cases even expressing their aesthetic attraction to the idea. This is echoed in the popular press, where writers have further exaggerated the simplistic genetic determinism and essential black abnormality that are implicit in the hypothesis. Racial groups have been portrayed as fundamentally distinct in physiology, conforming to the stark distinctions that are common in the social sphere. Moreover, the casual acceptance of this outright speculation has become an edifice upon which to construct further elaborations, such as race-specific therapies, and the many facets of this mythology have come to reinforce each other and create the impression of evidence, when in fact there is little or no evidence at all.

SEE ALSO Disease; Hypertension; Race; Slavery

BIBLIOGRAPHY

Curtin, P. D. 1992. The Slavery Hypothesis for Hypertension among African Americans: The Historical Evidence. American Journal of Public Health 82 (12): 1681-1686.

Dubner, S. J. 2005. Toward a Unified Theory of Black America. New York Times Sunday Magazine, March 20: 54-59.

Grim, C. E., J. P. Henry, and H. Myers. 1995. High Blood Pressure in Blacks: Salt, Slavery, Survival, Stress, and Racism. In Hypertension: Pathophysiology, Diagnosis, and Management, eds. John H. Laragh and Barry M. Brenner, 2nd ed., 171-207. New York: Raven Press.

Kaufman, J. S., and S. A. Hall. 2003. The Slavery Hypertension Hypothesis: Dissemination and Appeal of a Modern Race Theory. Epidemiology 14 (1): 111-118.

Roberts, W. C. 2001. High Salt Intake, Its Origins, Its Economic Impact, and Its Effect on Blood Pressure. American Journal of Cardiology 88: 1338-1346.

Jay S. Kaufman

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