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Commentary: The Slavery Hypothesis of Hypertension Among African-Americans

Blackburn, Henry

EPIDEMIOLOGY AND SOCIETY: A Forum on Epidemiology and Global Health

From the School of Public Health, University of Minnesota, Minneapolis, MN.

Address correspondence to: Henry Blackburn, School of Public Health, University of Minnesota, WBOB 300, Minneapolis, MN, 55454;

Editors’ note: Other invited commentaries on the topic appear on pages 120, 122 and 124.

Kaufman and Hall 1 bring to bear a considerable literature and argument critical of the Slavery Hypothesis of Hypertension (that theory purports a short-term selective pressure resulting in susceptibility to hypertension among African-American survivors of the slave trade). 2 They also paint an acerbic picture of bias in the ready acceptance and ongoing dissemination of a thesis they say lacks a strong base either in evolutionary theory or in empiric evidence for its essential parts.

In a 1983 review of hypertension, Prineas and I 3 mentioned the slavery theory without attribution, labeled it “broadly speculative,” and indeed never returned to it. Grim and colleagues, 4 in a wide-ranging, scholarly review of hypertension traced the origins of the theory back to the speculations of pioneer researchers on salt, renin levels and hypertension.

Perhaps the idea of a selective effect of slavery was not much more speculative than a larger subject of our review: that mass phenomena of risk today represent maladaptations to rapid changes in the composition of diet, in the abundance of calories, and in the physical inactivity of industrial societies. These are posited to relate, in turn, to a genetic legacy of adaptations that are fine tuned to hunter-gatherer lifestyles during the major phases of human evolution. That theory, equally difficult of testing or refutation, almost teleologic in its reasoning, has nevertheless informed an entire new field, Evolutionary Medicine, which provides a fresh view of many common afflictions of modern society. With such a fundament, phenotypes among affluent cultures also may be labeled “abnormal” or “maladapted” because of heterogeneous but species-wide susceptibility to current epidemics (for example, hypertension, obesity, diabetes mellitus, atherosclerosis or hormonally related cancers). Geoffrey Rose called this simply, “Sick Populations.”5

I am unable to contribute usefully to a discussion of ethnic or color differences in the alleles so far related to hypertension. Many studies indicate, however, a species—not racial or ethnic—susceptibility to hypertension in migrant cohorts or in populations from rural or island cultures living in urban or Western environs, according to their degree of acculturation. 5–7 It is difficult to ascribe such large group differences to the subtle effects of any genes involved, along with new exposures to demonstrated environmental influences of diet, salting, obesity and social dissonance. Apparently an ethnic paradigm has not been helpful so far in explaining such differences, while the social epidemiology of hypertension, too, remains confounded. It also would be unsuccessful on the face of it to adduce genetic mechanisms as primary in the rapid changes in frequency of disease or the proportion of susceptible phenotypes in the population.

May I suggest a different aspect of this issue and its current polemic, one that might be useful to lower the temperature and temper the language of the ongoing debate on “race” and hypertension? The conflict here, it seems to me, is a classic one between the two major views of science and medicine: one, a view of the uniqueness of the individual (or the “race”?) vs another that sees vast commonalities across the species homo sapiens. On the one hand is the view of those who pursue genetic determinism, whereas on the other is the view of humanity as one species, swept by recurrent tsunamis of social change and cultural pressure. These immense waves determine primarily the average population values of human characteristics, the frequency, and the changes in frequency of hypertensive or other common phenotypes among populations. Genes, on the other hand, influence importantly the individual's rank in the population distribution.

I suggest that these often polar views and the scientists who serve the separate masters of genetic and social determinism reflect a different Weltanschauung and choice of research strategies, maybe even of politics. This observation, if at all legitimate, calls for tolerance of differences in worldview and in strategic approaches to the determinants of common diseases. Of course, it also should encourage sound peer review and discussion on the findings and conclusions from the different approaches, particularly when both are inadequate to explain the population differences.

All this is neither here nor there in respect to the underlying validity of any part or all of the “Slavery Hypothesis,” questioned here so thoroughly and sharply by Kaufman and Hall, 1 nor is it in any obvious way relevant to establishing as fact their inference of bias in the reception and propagation of the theory. The authors leave us contemplative, nevertheless, about the ready acceptance and persistent dissemination of a still largely speculative idea. That, I am sure, is their main intent.

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About the Author

HENRY BLACKBURN is former Mayo Professor and head of the Division of Epidemiology and the Laboratory of Physiological Hygiene at the University of Minnesota School of Public Health. His interests include research on cardiovascular disease epidemiology and prevention, as well as evolutionary medicine.

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1. Kaufman JS, Hall SA. The slavery hypertension hypothesis: dissemination and appeal of a modern race theory. Epidemiology 2003; 14: 111–118.
2. Grim CE, Henry JP, Myers H. High blood pressure in blacks: salt, slavery, survival, stress, and racism. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis, and Management. 2nd ed. New York: Raven Press, 1995; 171–207.
3. Blackburn H, Prineas R. Diet and hypertension: anthropology, epidemiology, and public health implications. Prog Biochem Pharmcol 1983; 19: 31–79.
4. Rose G. Sick individuals and sick populations. Int J Epidemiol 1985; 14: 32–38.
5. Cooper R, Rotini C. Hypertension in blacks. Am J Hypertens 1997; 7: 804–812.
6. Salmond CE, Prior IA, Wessen AF. Blood pressure patterns and migration: a 14-year cohort study of adult Tokelauans. Am J Epidemiol 1989; 130: 37–52.
7. Ward R. Familial aggregation and genetic epidemiology of blood pressure. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis, and Management. 2nd ed. New York: Raven Press, 1995; 67–88.
© 2003 Lippincott Williams & Wilkins, Inc.