Public Health Then and Now
The Slavery Hypothesis for Hypertension among African Americans: The Historical Evidence Philip D. Curtin, PhD Scientific research on disease today rarely turns to historical evidence, especially when that evidence concerns events that occurred more than 2 centuries ago. Within the past decade, however, medical researchers concerned with high rates of hypertension among African Americans have begun to look to the African Americans' ancestors for the possible genetic consequences of an African origin, the experience of the slave trade to America, or conditions of life under slavery. Historians can only welcome the effort of others to use historical evidence to solve current problems. Knowledge today has become so specialized, however, that evidence generated by one discipline is easily misunderstood by another. The theory now recognized as "the slavery hypothesis of hypertension" is a striking case in point. Mistakes in the hypothesis, which would have been caught in the normal process of peer review had the reviewers been historians of Africa, were not caught on the first scientific publication. As a result, they were then picked up and repeated uncritically by the popular scientific press, where the hypothesis was presented as plausible-though still without adequate review by appropriate specialists outside of hypertension studies. The slavery hypothesis began with the widely accepted observation that African Americans have, on the whole, a higher incidence of hypertension than European Americans do-a pattern first detected as long ago as the 1930s. It was only natural in a racist society to look for genetic antecedents in Africa, if only because about 80% of the gene pool of the African-American community is derived from Africa (the other 20% being from Europe).1 Even this is beside the point. Social scientists have long recognized that "African American" is a social rather than
a biological category, and Africanists today try to avoid the racial trap by writing about populations with common elements in their gene pool. Africa contains many different populations of this kind. These populations are superficially similar only when seen from a distance. The association between salt and hypertension has long been recognized as a possibility. Early speculations suggested that a damaging loss of salt may have resulted from sweating in the African heat or from the physical ordeal of the ocean voyage imposed by the Atlantic slave trade.2 More recent research suggested that the blood pressure of some African Americans was more sensitive than that of European Americans to increases in dietary
salt and that African Americans retained an intravenous sodium load longer than European Americans did. It was these observations that drew medical researchers to the African past in search of possible clues to a genetic difference. As the slavery hypothesis developed, it actually became three separate hypotheses. The first hypothesis, which concerns the ancestral experience in Africa, emphasizes the possible genetic consequences of a low-salt diet over many centuries. In the second, which concerns genetic changes caused by the trauma of the ocean passage from Africa to America during the slave trade, the case is made that individuals who were losing salt from sweat, diarrhetic stools, and vomit were more likely to survive if they already had an ability to conserve salt. This ability, which had surPhilip D. Curtin is with the Department of History at The Johns Hopkins University in Baltirnore, Md. Requests for reprints should be sent to Philip D. Curtin, PhD, Department of History, The Johns Hopkins University, 3400 N Charles, Baltimore, MD 21218.
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Salt, mana red on the coast of Senegal by e aring seaw r and packed In the tradMonal manner for shipment Photogmph by author.
vival value in the slave trade, would be passed on to their children and would later cause hypertension and death in the African-American community. For the third hypothesis, which concerns the genetic consequences of life under slavery, the argument is less precise, but it holds that bad conditions caused high death rates and hence genetic change among the survivors. As long ago as 1969, Henry and Cassel had used certain African populations as examples of unusually low blood pressure, and, in 1973, Lillian Gleibermann surveyed published blood pressure figures for 27 different populations in various parts of the world, including tropical Africa. She was concemed with the high blood pressures of African-American and some African-Canibbean peoples, but she failed to point out that the two samples from Liberia and Nigeria-regions that 1682 American Journal of Public Health
had supplied slaves to the New Worldboth showed lower systolic and diastolic rates than her published samples for European Americans did.3 Attention to that point might have squelched the slavery hypothesis before it got started. In 1979, however, Clarence E. Grim, one of the principal authors of the slavery hypothesis, did some research on the blood pressure of African Americans, their sensitivity to salt, and their tendency to retain sodium overload.4 No one but Gleibermann had yet looked for evidence directly from Africa, but Africa became a focal point in 1986 with an article by Thomas W. Wilson in Social Science History. Grim then joined Wilson for their key publication in Hypertension in mid-1991. By October 1991, that article had attracted the attention of Science News, the Journal of theAmerican MedicalAssociation, and Natural History. 5
Wilson began by looking for a salt deficiency in West Africa. In an effort to show that West Africa was historically a salt-deficient region, he wrote that "in most of yesterday's West Africa the only locally available 'salt' was produced from vegetable matter,"7 supporting this contention with three citations to data from the savanna belt near the Sahara. But while some parts of West Africa did lack good local sources of salt, they made up for it through an elaborate set of trade networks.6 All tropical regions near the seacoast have a cheap source of salt in seawater. At high tide, that seawater can be guided into any shallow pan or salt pond, where evaporation will do the rest. Where the terrain is not suitable and fuel is cheap, seawater can also be boiled. From the Senegal River to Benguela in southern Angola, salt was manufactured and exported into the interior over regular trade routes. Rivers and lagoons made transportation to the interior cheap, but even without river transport, there could have been no marked deficiency of salt within 100 or 200 miles of the coast. Indeed, any place in West Africa close enough to the coast to be linked to the Atlantic slave trade was close enough to be supplied with sea salt as well. In the 18th century, 80%o to 90% of all slaves shipped to the New World originated within a hundred miles ofthe coast or a navigable waterway.8 Wilson cites my work on the slave trade to support his argument that, "as the slave trade moved inland from the 16th through the 19th century, progressively more slaves could trace their origins to the 'salt-poor' interior ofthat region."9 However, I said nothing about the "salt-poor" interior. The slave trade to North America, which had begun to be significant in the early 18th century, had effectively ended in 1807. By 1991, Wilson and Grim, writing together, no longer made much of the supposed salt deficiency in West Africa, perhaps because they found out it did not exist. But they did continue to write that, "at present there is not enough published information on salt intake to determine if the slave ships operators provided adequate salt supplies to their captives." 10 Of course there is no record. People do not record the obvious. Salt was cheap; slavers were in business to deliver slaves alive to their American customers. With plenty of salt and water available in African ports, we can assume that the slavers' self-interestwas incentive enough to make them carry adequate salt and water-and food as well, though probably not of the best quality. Food and water for the pasDecember 1992, Vol. 82, No. 12
Public Health Then and Now sage to America was normally loaded in Africa, not brought down from Europe. Part of Wilson and Grim's problem was a simple misunderstanding of African conditions, but another part was a misunderstanding of how historical scholarship is carried out. They would not be likely to cite scientific data from a 30-year-old publication as though it were the latest and best available, but they do just that for historical data-apparently assuming that historical knowledge is unchanging. Their discussion of the total number of slaves to cross the Atlantic is a case in point. They say it was "more than twelve million," a figure about 20% higher than the most carefully researched present estimates.-' The number makes no significant difference, but the way they arrived at it shows the difference between scientific and historical method. Historians are supposed to pay critical attention to numbers of this kind, and to cite their authority in a footnote. For historians, the date of publication is important; it helps to evaluate the evidence. In this instance, Wilson and Grim cite "Davidson, B: The African Slave Trade. Boston, Little, Brown & Co, 1980, pp. 95-101." Although it appears to be a 12-year-old authority, a look at the title page shows that it is, in fact, an American reprint of a London publication of 1961. Furthermore, it was about 1969 that historians began to look carefully at quantitative aspects of the slave trade. Since then, revision has been continuous, and Wilson and Grim cite two of the works that form part of that revision, although in another context and without recognizing that the evidence those works contain puts Davidson out of date.12 The scientific style ofcitation also differs from historical practice in important ways. Because historians often cite books, they have to be careful about page numbers. Because scientists often cite short articles, they cite the whole article and ignore the specific pages. Here, Wilson and Grim cite Basil Davidson's pages 95 to 101, but these pages tell nothing at all about the numbers involved in the slave trade. On page 79, however, Davidson writes that "nobody knows or ever will know" the numbers involved in the slave trade "because the necessary records are either lost or were never made." He then goes on to cite estimates he thinks are reasonable for the total numberwho landed in the Americas, taking 15 million as a minimum and 50 million or more as probable. At least Wilson and Grim's 12-million figure is more accurate than that of the author they cite. Once in the scientific literDecember 1992, Vol. 82, No. 12
ature, however, the outmoded data is accepted as though it represents the most recent research, just as Jared Diamond accepted Davidson's 30-year-old estimate when writing about the Wilson and Grim
thesis.'3 In the mid-1980s, the evidence about hypertension began to change in new ways. The tacit assumption before that time was that hypertension was a racial characteristic, that all African-looking people must share the trait. In 1985, however, 0. 0. Akinkugbe surveyed the existing publications on hypertension in several parts of the world, and his findings show once more-as Gleibermann's did-that hypertension and African appearance are independent variables. Although some African-Caribbean people were similar to African Americans as far as hypertension was concerned, mean arterial pressures in Jamaica, St. Kitts, and the Bahamas were lower than those reported in the United States. Moreover, a Jamaican study showed differences between men and women and rural and urban populations, with rural women having the lowest rates. South African studies of Zulus, Indians, and Whites in Durban showed that urban White males had the highest rates whereas urban White females had the lowest. Cape Town studies showed Africans with high urban rates and low rural rates. And in Nigeria, many studies showed that African hypertension rates were about the same as those of White North Americans.'4 With these data, the earlier speculation about millennia of tropical life before the transfer to the Americas should have disappeared. In 1991, indeed, Wilson and Grim shifted away from Wilson's earlier emphasis on African conditions to look for support in the trauma of the slave trade itself and in the conditions of life under slavery in the New World. Once again, they ran into trouble with the interpretation of historical evidence. First of all, they missed the most important distinction in the literature of comparative slavery-the demographic difference between slave populations in the tropical Americas and those of North America. Well into the 19th century, most slave populations in the tropics had more deaths thanbirths each year, yielding rates of net natural decrease as high as 10 to 40 per thousand per annum.15 On the other hand, the slave population ofNorth America began to grow in the 18th century and grew even more rapidly in the 19th. By that time, its growth rate was higher than that of many European populations and
nearly as high as the European-Americans growth rate of the same period. The population growth rates of slaves and nonslaves in the South were pretty much the same as well, and very different from those of the Caribbean. In fact, most historians of the American South now believe that the diet and disease patterns for slaves in the South was pretty much the same as those for the poor Whites. Thus, the mortality experiences of slave populations in North America and the Carbbean-and any genetic consequences attributable to them-were very different. Thus, evidence from Brazil or Barbados is not relevant to the situation in the United States. Yet Wilson and Grim's evidence is almost entirely from the Caribbean; the United States is barely mentioned. This now leaves the claims that the physiological repercussions of capture and the ocean voyage on slave ships produced genetic selection in favor of hypertension among present-day African Americans. To make this case, Wilson and Grim would have to show that a physiologically traumatic experience lasting less than a year could have genetic consequences more than 2 centuries later. These authors point to the persistence of the sickle-cell trait in African Americans, but that trait was able to develop through about 5000 years of exposure to falciparum malaria, and its incidence has declined steadily among African Americans and West Indians. With Wilson and Grim's treatment of the slave trade, we come again to the differences between scientific and historical traditions in the use of evidence. These authors give some very precise numbersan average death rate of 10% for captives from point of capture to delivery on the coast, of 12% for those awaiting shipment by sea, and of 12% to 15% for slaves at sea. For all this, they cite Herbert Klein's Middle Passage'6 but do not give page numbers in a book of 282 pages. Klein's index has many entries for mortality rates at sea and one for mortality rates on arrival in Brazil, but none for mortality rates between capture and shipment. In fact, it would be impossible to know. The African slave traders kept few records that have survived, and the Europeans bought slaves only at coastal shipping points. Mortality rates between capture and shipment must, in any event, have varied enormously from time to time and place to place. Some guesses have appeared, but these have also been subject to telling criticism in the historical literature.'7 American Journal of Public Health 1683
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Grim had 22% of the slaves dead before shipment, Diamond rounded the figure upward to 37%o-25% en route and 12% awaiting shipment. He also added details Wilson and Grim had not mentioned: "First, slaves captured in raids in the interior of West Africa were chained together, loaded with heavy burdens, and marched for one to two months, with little food and water, to the coast."'21 This raises more questions than it answers. Why take 1 to 2 months to march an average of about 100 miles to navigable water? Why would the African slave dealers withhold water when their clear economic interest was to deliver the slaves in good condition for sale on the coast? Diamond may have been correct, on the other hand, when he lowered the Wilson and Grim estimate for deaths in the middle passage
Ekmina Castle on the coast of Ghana, a fort awith the sae trade, was first under Porgse and then under Dutch control. Photogmph by author. Mortality at sea can be and has been studied far more carefully. Klein discussed a number of data samples for different times and routes across the Atlantic. His figures for the English slave trade are the relevant set because English slavers carried most of the slaves sold in NorthAmerica. His samples show a death rate of around 240 per thousand in the 1680s, a little before the slave trade to North America became important; this rate declined to 56 deaths per thousand in the 1790s.18 Given a median date of about 1770 for arrival of slaves in North America, the probable overall death rate for slaves arriving in what is today the United States would be somewhere around 10%o or perhaps a little less. Iike the discrepancies in the total number of slaves carried by the trade, a shift in the death rate from 10%o to 12% is not crucial to the argument, but it throws some doubt on the method
1684 American Journal of Public Health
Wilson and Grim used to arrive at other
findings. Jared Diamond then reviewed the scientific writing published in Hypertension, which is aimed at a professional audience, for the broader audience of NaturalHistory. In doing so, he left out many important (if inconvenient) points. In 1991, he still believed that salt was scarce in West Africa and that hypertension rates of West Africans were like those of African Americans. He claims, indeed, that "the genetic basis for hypertension in U.S. blacks was already widespread in many of their West African ancestors. It required only the ubiquity of saltshakers in twentieth-century America for that genetic basis to express itself in hypertension."'9 Diamond also extended the Wilson and Grim case with new numbers of unknown provenance.20 Where Wilson and
to 10%S. For the Atlantic passage itself, Wilson and Grim bring in more scientificlooking arguments. They claim that death on shipboard was "often due to conditions that ultimately kill by salt and water depletion."22 Of course, there is no evidence that 18th-century West Africans had a special ability to conserve salt or that salt was in short supply, either on shore or on slave ships. Wilson and Grim nevertheless write that "on slave ships, vomiting due to seasickness was common, and the most common causes of death on the middle passage were recorded as diarrheal (the "flux") and febrile diseases, both salt depletors." Yet it is a curious claim that seasickness, which rarely lasts as long as 48 hours, could affect one's descendants more than 200 years later. As for the fevers, they were mainly falciparum malaria. Like victims of any other fever, its victims may suffer a little loss of salt, but they die because the parasite feeds on hemoglobin in the human bloodstream. Some diseases, like cholera and infantile
diarrhea, kill through dehydration23-not salt depletion alone-but few of the passengers on the slave ships were infants, and cholera was completely absent from the Atlantic basin during the period of the slave trade to North America. So while some deaths from dehydration and salt depletion could have occurred, there is no evidence that either was a significant cause of death on the slave
shipsz24
Similar problems with the historical method appear on the American side of the slave trade. Wilson and Grim give quite precise figures, but all but one of their citations have to do with the West Indies. Their sole citation on the health of slaves in the United States is a false lead December 1992, Vol. 82, No. 12
Public Health Then and Now
to pages that say nothing about that subject.25 And again, Diamond goes them one better, raising their estimated maximum death rate within 3 years of arrival from 30% to 40%o and omiting the crucial fact that even this figure is for the West Indies, not North America. Wilson and Grim also claim that "the high mortality under slavery was caused largely by salt and water-depletive diseases."26 Yet the extensive literature on disease among slaves shows no such thing. The planters and the doctors who cared for slaves had a strong impression that the particular susceptibility of slaves was to the diseases of the lungs, particularly pneumonia and tuberculosis, though many died of malaria and gastrointestinal disease as well.27 What little quantitative data we have from the early 19th century bear this out. From 1819 to 1836, the British army recorded the cause of death among African soldiers on both sides of the Atlantic, and the range of disease shows that a good deal more was happening than salt depletion (Tables 1 and 2, Figure 1). The figures are significant because these soldiers were recruited into the British army as slaves purchased in Africa. Some were left to serve in Africa while others were sent to serve in the West Indies. The statistical picture on the African side shows the diseases that were common among young males in Africa at that time and from which young men were likely to die at sea on the way to the Americas. The main causes of death were eruptive fevers (mainly smallpox) (Table 1) and diseases of the lungs (mainly pneumonia and tuberculosis) (Table 2). The Africans, once they arrived in the New World, died at a higher rate than they did in Africa, aswould be expected of those who moved beyond the disease environment of their childhood, the source
of their range of immunities. This evidence for the West Indies is not truly representative of the disease environment in North America, but it confirms the anecdotal evidence of North American doctors that the serious new threat was lung disease. The increase of 10 deaths per thousand overall was clearly caused by an increase in pneumonia and tuberculosis. Gastrointestinal infections caused less than 20% of all deaths among those recently arrived from Africa. In the decades that followed, American-bom soldiers of African descent developed a much stronger immunity to lung diseases, which dropped to fewer than two deaths per thousand after the 1870s. If the African lack of immunity to these diseases could
18
~16 14
Lz
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[ Windward/Leeward
FIGURE 1-Came of dea anong Afla Troops sevhg In fte Brdsh Anny ln the Srra Leone Cmmand and the Windward and Leewrd Comand, 1817 to 1836.
American Joumal of Public Health 1685
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decline so rapidly, some special explanation would be required to show why a predisposition to hypertension, if it ever existed in Africa, could be so long lasting.28 From the historical point view, the slavery hypothesis to explain AfricanAmerican hypertension not only lacks supporting evidence but also runs counter to what evidence we do have. West Africans had plenty of salt through most of their history. They do not have notably high rates of hypertension today. The mortality during the slave trade was not from salt-depleting causes. No evidence has ever been advanced that the African Americans experienced different conditions of diet and disease from those of other poor southerners. No evidence has been advanced that a dietaxy trauma experienced by 80% of one's ancestors over a period of less than 1 year, 220 years ago, could bring about a genetic change lasting to the present. Yet these hypotheses were published in the serious medical press and picked up by the popular medical literature late in 1991 as though they were possibly true. Perhaps we should try harder to close the gap between scientific and historical knowledge. [
References 1. T. E. Reed, "Caucasian Genes in American Negroes," Science 165(1969):767. 2. 0. M. Helmer, "Hormonal and Biochemical Factors Controlling Blood Pressure," in Les concepts de Claude Bemard sur le miieu interieur (Paris, France: Masson et Compagnie, 1967), 115-28; L. Gleibermann, "Blood Pressure and Dietary Salt in Human Populations," Ecology of Food and Nutriton 2(1973):143-56; H. Blackburn and R. Prineas, "Diet and Hypertension: Anthropology, Epidemiology, and Public Health Implications," Plnss in
Biochemical Pharmacology 19(1982):3179; esp 50-51. 3. J. D. Hemy and J. L. Cassel, "Psychological Factors in Essential Hypertension: Recent Epidemiological and Animal Experimental Evidence," American Journal of
1686 American Journal of Public Health
Epidemiology 90(1969): 172. L. Gleibermann, "Blood Pressure and Dietary Salt," 144 (table). 4. F. C. Luft et al, "Cardiovascular and Humoral Responses to Extremes of Sodium Intake in Normal White and Black Men," Circulktion 60(1979):697-706; F. C. Luft et al, "Effects of Volume Expansion and Contraction in Normotensive Whites and Blacks and Subjects of Different Ages," Circulation 59(1979):643-50. 5. T. W. Wilson, "Africa, Afro-Americans, and Hypertensions: An Hypothesis," Social Science History 10(1986):489-500; T. W. Wilson, "Salt Supplies in West Africa and Blood Pressures Today," Lancet 1(1986):784-86; T. W. Wilson and C. E. Grim, "Biohistory of Slavery and Blood Pressure Differences in Blacks Today: A Hypothesis," Hypertension 17(1991):I122-I-128; K. A. Fackelmann, "The Afican Gene? Searching through History for the Roots of Black Hypertension," Science News 140(1991):254-55; M. F. Goldsmith, "African Lineage, Hypertension Linked," Joumal oftheAmerican Medical Association 266(1991):2049; J. Diamond, "The Saltshaker's Curse," Natural History (October 1991):20-26. 6. E. A. McDougall, "Salts of the Western Sahara: Myths, Mysteries, and Historical Significance," IntemationalJoumal ofAfrican Historical Studies 23(1990):231-57; P. E. Lovejoy, Salt of the Desert Sun A History ofSalt Prdction and Trade in the Central Sudan (New York: Cambridge University Press, 1986). See also S. A. M. Adshead, Salt and Civiliation (London: Macmillan, 1992), 15-26, for an assessment of tropical Africa's comparative place in world salt production and consumption. 7. T. W. Wilson, "Africa, Afro-Americans, and Hypertension," 258. 8. P. D. Curtin, The Atlantic Slave Trade: A Censs (Madison: University of Wisconsin Press, 1969), 191-97, 152-58; D. Geggus, "Sex Ratio, Age and Ethnicity in the Atlantic Slave Trade: Data from French Shipping and Plantation Records," Joumal of African History 30(1989):23-44; D. Richardson, "Slave Exports from West and West-Central Africa, 1700-1810: New Estimates ofVolume and Distribution,"Journal ofAfrican History 30(1989):1-22. 9. T. W. Wilson, "Africa, Afro-Americans, and Hypertension," 262. 10. Wilson and Grim, "Biohistoryof Slavery,"
126. 11. P. E. Lovejoy, "The Volume of the Atlantic Slave Trade: A Synthesis," Jounal of African History 23(1982):473-501; Richardson, "Slave Exports." 12. Curtin Atlantic Slave Trade; H. S. Klein, The MiddlePassage: Comparative Sftdies in theAtlantic Slave Trade (Princeton, NJ: Princeton University Press, 1978). 13. Diamond, "Saltshaker's Curse," 26. 14. 0. 0. Aimkugbe, "World Epidemiology of Hypertension in Blacks," in Hypertension in Blacks: Epidemiology, Pathophysiology and Treatment, ed. W. D. Hall, E. Saunders, and N. B. Shuylman (Chicago: Year Book Medical Publishers, 1985), 8, 9, 11-12. 15. Curtin, Atlantic Slave Trade, 28-34, 73. 16. Klein, Middle Passage. 17. See D. Henige, "Measuring the Unmeasurable: The Atlantic Slave Trade, West African Populations and the Pyrrhonian Critic," Journal of African History 27:
18. 19. 20. 21. 22. 23.
24.
25.
26. 27.
(1986):295-313. Klein, Middk Passage 64, 160. Diamond, "Saltshaker's Curse." 25. Ibid., 26. Ibid. Wilson and Grim, "Biohistory of Slavery," 128. S. G. Wright, "Gastrointestinal Diseases," in Hunter's Tropical Medicine, ed. G. T. Strickland, 6th ed. (Philadelphia: WB Saunders Co, 1984), 16-27; D. R. Nalin, "Cholera," in Hunter's TropicalMedicine, 305-313. R. Steckel and A. Jensen, "New Evidence on the Causes of Slave and Crew Mortality in the Atlantic Slave Trade," Journal of Economic History 46(1986):57-77, esp 6162. The citation is to K F. Kiple and V. H. King,AnotherDimension of the Black Diaspora: Diet, Disease, and Racism (New York: Cambridge Univesity Press, 1981), 147-148. Wilson and Grim, "Biohistoryof Slavery," 126. Kiple and King,AnotherDimension, 137146; R. B. Sheridan,DoctorsandSlaves:A Medical and Demographic History of Slavery in the British West Indies, 1680-1834 (New York: Cambridge University Press, 1985), 185-221; P. D. Curtin, "African Health at Home and Abroad," Social Science History 10(1986):369-98, 130-31, 135.
December 1992, Vol. 82, No. 12
The Slavery Hypothesis for Hypertension among African Americans: The Historical Evidence Philip D. Curtin, PhD Scientific research on disease today rarely turns to historical evidence, especially when that evidence concerns events that occurred more than 2 centuries ago. Within the past decade, however, medical researchers concerned with high rates of hypertension among African Americans have begun to look to the African Americans' ancestors for the possible genetic consequences of an African origin, the experience of the slave trade to America, or conditions of life under slavery. Historians can only welcome the effort of others to use historical evidence to solve current problems. Knowledge today has become so specialized, however, that evidence generated by one discipline is easily misunderstood by another. The theory now recognized as "the slavery hypothesis of hypertension" is a striking case in point. Mistakes in the hypothesis, which would have been caught in the normal process of peer review had the reviewers been historians of Africa, were not caught on the first scientific publication. As a result, they were then picked up and repeated uncritically by the popular scientific press, where the hypothesis was presented as plausible-though still without adequate review by appropriate specialists outside of hypertension studies. The slavery hypothesis began with the widely accepted observation that African Americans have, on the whole, a higher incidence of hypertension than European Americans do-a pattern first detected as long ago as the 1930s. It was only natural in a racist society to look for genetic antecedents in Africa, if only because about 80% of the gene pool of the African-American community is derived from Africa (the other 20% being from Europe).1 Even this is beside the point. Social scientists have long recognized that "African American" is a social rather than
a biological category, and Africanists today try to avoid the racial trap by writing about populations with common elements in their gene pool. Africa contains many different populations of this kind. These populations are superficially similar only when seen from a distance. The association between salt and hypertension has long been recognized as a possibility. Early speculations suggested that a damaging loss of salt may have resulted from sweating in the African heat or from the physical ordeal of the ocean voyage imposed by the Atlantic slave trade.2 More recent research suggested that the blood pressure of some African Americans was more sensitive than that of European Americans to increases in dietary
salt and that African Americans retained an intravenous sodium load longer than European Americans did. It was these observations that drew medical researchers to the African past in search of possible clues to a genetic difference. As the slavery hypothesis developed, it actually became three separate hypotheses. The first hypothesis, which concerns the ancestral experience in Africa, emphasizes the possible genetic consequences of a low-salt diet over many centuries. In the second, which concerns genetic changes caused by the trauma of the ocean passage from Africa to America during the slave trade, the case is made that individuals who were losing salt from sweat, diarrhetic stools, and vomit were more likely to survive if they already had an ability to conserve salt. This ability, which had surPhilip D. Curtin is with the Department of History at The Johns Hopkins University in Baltirnore, Md. Requests for reprints should be sent to Philip D. Curtin, PhD, Department of History, The Johns Hopkins University, 3400 N Charles, Baltimore, MD 21218.
American Journal of Public Health
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Salt, mana red on the coast of Senegal by e aring seaw r and packed In the tradMonal manner for shipment Photogmph by author.
vival value in the slave trade, would be passed on to their children and would later cause hypertension and death in the African-American community. For the third hypothesis, which concerns the genetic consequences of life under slavery, the argument is less precise, but it holds that bad conditions caused high death rates and hence genetic change among the survivors. As long ago as 1969, Henry and Cassel had used certain African populations as examples of unusually low blood pressure, and, in 1973, Lillian Gleibermann surveyed published blood pressure figures for 27 different populations in various parts of the world, including tropical Africa. She was concemed with the high blood pressures of African-American and some African-Canibbean peoples, but she failed to point out that the two samples from Liberia and Nigeria-regions that 1682 American Journal of Public Health
had supplied slaves to the New Worldboth showed lower systolic and diastolic rates than her published samples for European Americans did.3 Attention to that point might have squelched the slavery hypothesis before it got started. In 1979, however, Clarence E. Grim, one of the principal authors of the slavery hypothesis, did some research on the blood pressure of African Americans, their sensitivity to salt, and their tendency to retain sodium overload.4 No one but Gleibermann had yet looked for evidence directly from Africa, but Africa became a focal point in 1986 with an article by Thomas W. Wilson in Social Science History. Grim then joined Wilson for their key publication in Hypertension in mid-1991. By October 1991, that article had attracted the attention of Science News, the Journal of theAmerican MedicalAssociation, and Natural History. 5
Wilson began by looking for a salt deficiency in West Africa. In an effort to show that West Africa was historically a salt-deficient region, he wrote that "in most of yesterday's West Africa the only locally available 'salt' was produced from vegetable matter,"7 supporting this contention with three citations to data from the savanna belt near the Sahara. But while some parts of West Africa did lack good local sources of salt, they made up for it through an elaborate set of trade networks.6 All tropical regions near the seacoast have a cheap source of salt in seawater. At high tide, that seawater can be guided into any shallow pan or salt pond, where evaporation will do the rest. Where the terrain is not suitable and fuel is cheap, seawater can also be boiled. From the Senegal River to Benguela in southern Angola, salt was manufactured and exported into the interior over regular trade routes. Rivers and lagoons made transportation to the interior cheap, but even without river transport, there could have been no marked deficiency of salt within 100 or 200 miles of the coast. Indeed, any place in West Africa close enough to the coast to be linked to the Atlantic slave trade was close enough to be supplied with sea salt as well. In the 18th century, 80%o to 90% of all slaves shipped to the New World originated within a hundred miles ofthe coast or a navigable waterway.8 Wilson cites my work on the slave trade to support his argument that, "as the slave trade moved inland from the 16th through the 19th century, progressively more slaves could trace their origins to the 'salt-poor' interior ofthat region."9 However, I said nothing about the "salt-poor" interior. The slave trade to North America, which had begun to be significant in the early 18th century, had effectively ended in 1807. By 1991, Wilson and Grim, writing together, no longer made much of the supposed salt deficiency in West Africa, perhaps because they found out it did not exist. But they did continue to write that, "at present there is not enough published information on salt intake to determine if the slave ships operators provided adequate salt supplies to their captives." 10 Of course there is no record. People do not record the obvious. Salt was cheap; slavers were in business to deliver slaves alive to their American customers. With plenty of salt and water available in African ports, we can assume that the slavers' self-interestwas incentive enough to make them carry adequate salt and water-and food as well, though probably not of the best quality. Food and water for the pasDecember 1992, Vol. 82, No. 12
Public Health Then and Now sage to America was normally loaded in Africa, not brought down from Europe. Part of Wilson and Grim's problem was a simple misunderstanding of African conditions, but another part was a misunderstanding of how historical scholarship is carried out. They would not be likely to cite scientific data from a 30-year-old publication as though it were the latest and best available, but they do just that for historical data-apparently assuming that historical knowledge is unchanging. Their discussion of the total number of slaves to cross the Atlantic is a case in point. They say it was "more than twelve million," a figure about 20% higher than the most carefully researched present estimates.-' The number makes no significant difference, but the way they arrived at it shows the difference between scientific and historical method. Historians are supposed to pay critical attention to numbers of this kind, and to cite their authority in a footnote. For historians, the date of publication is important; it helps to evaluate the evidence. In this instance, Wilson and Grim cite "Davidson, B: The African Slave Trade. Boston, Little, Brown & Co, 1980, pp. 95-101." Although it appears to be a 12-year-old authority, a look at the title page shows that it is, in fact, an American reprint of a London publication of 1961. Furthermore, it was about 1969 that historians began to look carefully at quantitative aspects of the slave trade. Since then, revision has been continuous, and Wilson and Grim cite two of the works that form part of that revision, although in another context and without recognizing that the evidence those works contain puts Davidson out of date.12 The scientific style ofcitation also differs from historical practice in important ways. Because historians often cite books, they have to be careful about page numbers. Because scientists often cite short articles, they cite the whole article and ignore the specific pages. Here, Wilson and Grim cite Basil Davidson's pages 95 to 101, but these pages tell nothing at all about the numbers involved in the slave trade. On page 79, however, Davidson writes that "nobody knows or ever will know" the numbers involved in the slave trade "because the necessary records are either lost or were never made." He then goes on to cite estimates he thinks are reasonable for the total numberwho landed in the Americas, taking 15 million as a minimum and 50 million or more as probable. At least Wilson and Grim's 12-million figure is more accurate than that of the author they cite. Once in the scientific literDecember 1992, Vol. 82, No. 12
ature, however, the outmoded data is accepted as though it represents the most recent research, just as Jared Diamond accepted Davidson's 30-year-old estimate when writing about the Wilson and Grim
thesis.'3 In the mid-1980s, the evidence about hypertension began to change in new ways. The tacit assumption before that time was that hypertension was a racial characteristic, that all African-looking people must share the trait. In 1985, however, 0. 0. Akinkugbe surveyed the existing publications on hypertension in several parts of the world, and his findings show once more-as Gleibermann's did-that hypertension and African appearance are independent variables. Although some African-Caribbean people were similar to African Americans as far as hypertension was concerned, mean arterial pressures in Jamaica, St. Kitts, and the Bahamas were lower than those reported in the United States. Moreover, a Jamaican study showed differences between men and women and rural and urban populations, with rural women having the lowest rates. South African studies of Zulus, Indians, and Whites in Durban showed that urban White males had the highest rates whereas urban White females had the lowest. Cape Town studies showed Africans with high urban rates and low rural rates. And in Nigeria, many studies showed that African hypertension rates were about the same as those of White North Americans.'4 With these data, the earlier speculation about millennia of tropical life before the transfer to the Americas should have disappeared. In 1991, indeed, Wilson and Grim shifted away from Wilson's earlier emphasis on African conditions to look for support in the trauma of the slave trade itself and in the conditions of life under slavery in the New World. Once again, they ran into trouble with the interpretation of historical evidence. First of all, they missed the most important distinction in the literature of comparative slavery-the demographic difference between slave populations in the tropical Americas and those of North America. Well into the 19th century, most slave populations in the tropics had more deaths thanbirths each year, yielding rates of net natural decrease as high as 10 to 40 per thousand per annum.15 On the other hand, the slave population ofNorth America began to grow in the 18th century and grew even more rapidly in the 19th. By that time, its growth rate was higher than that of many European populations and
nearly as high as the European-Americans growth rate of the same period. The population growth rates of slaves and nonslaves in the South were pretty much the same as well, and very different from those of the Caribbean. In fact, most historians of the American South now believe that the diet and disease patterns for slaves in the South was pretty much the same as those for the poor Whites. Thus, the mortality experiences of slave populations in North America and the Carbbean-and any genetic consequences attributable to them-were very different. Thus, evidence from Brazil or Barbados is not relevant to the situation in the United States. Yet Wilson and Grim's evidence is almost entirely from the Caribbean; the United States is barely mentioned. This now leaves the claims that the physiological repercussions of capture and the ocean voyage on slave ships produced genetic selection in favor of hypertension among present-day African Americans. To make this case, Wilson and Grim would have to show that a physiologically traumatic experience lasting less than a year could have genetic consequences more than 2 centuries later. These authors point to the persistence of the sickle-cell trait in African Americans, but that trait was able to develop through about 5000 years of exposure to falciparum malaria, and its incidence has declined steadily among African Americans and West Indians. With Wilson and Grim's treatment of the slave trade, we come again to the differences between scientific and historical traditions in the use of evidence. These authors give some very precise numbersan average death rate of 10% for captives from point of capture to delivery on the coast, of 12% for those awaiting shipment by sea, and of 12% to 15% for slaves at sea. For all this, they cite Herbert Klein's Middle Passage'6 but do not give page numbers in a book of 282 pages. Klein's index has many entries for mortality rates at sea and one for mortality rates on arrival in Brazil, but none for mortality rates between capture and shipment. In fact, it would be impossible to know. The African slave traders kept few records that have survived, and the Europeans bought slaves only at coastal shipping points. Mortality rates between capture and shipment must, in any event, have varied enormously from time to time and place to place. Some guesses have appeared, but these have also been subject to telling criticism in the historical literature.'7 American Journal of Public Health 1683
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Grim had 22% of the slaves dead before shipment, Diamond rounded the figure upward to 37%o-25% en route and 12% awaiting shipment. He also added details Wilson and Grim had not mentioned: "First, slaves captured in raids in the interior of West Africa were chained together, loaded with heavy burdens, and marched for one to two months, with little food and water, to the coast."'21 This raises more questions than it answers. Why take 1 to 2 months to march an average of about 100 miles to navigable water? Why would the African slave dealers withhold water when their clear economic interest was to deliver the slaves in good condition for sale on the coast? Diamond may have been correct, on the other hand, when he lowered the Wilson and Grim estimate for deaths in the middle passage
Ekmina Castle on the coast of Ghana, a fort awith the sae trade, was first under Porgse and then under Dutch control. Photogmph by author. Mortality at sea can be and has been studied far more carefully. Klein discussed a number of data samples for different times and routes across the Atlantic. His figures for the English slave trade are the relevant set because English slavers carried most of the slaves sold in NorthAmerica. His samples show a death rate of around 240 per thousand in the 1680s, a little before the slave trade to North America became important; this rate declined to 56 deaths per thousand in the 1790s.18 Given a median date of about 1770 for arrival of slaves in North America, the probable overall death rate for slaves arriving in what is today the United States would be somewhere around 10%o or perhaps a little less. Iike the discrepancies in the total number of slaves carried by the trade, a shift in the death rate from 10%o to 12% is not crucial to the argument, but it throws some doubt on the method
1684 American Journal of Public Health
Wilson and Grim used to arrive at other
findings. Jared Diamond then reviewed the scientific writing published in Hypertension, which is aimed at a professional audience, for the broader audience of NaturalHistory. In doing so, he left out many important (if inconvenient) points. In 1991, he still believed that salt was scarce in West Africa and that hypertension rates of West Africans were like those of African Americans. He claims, indeed, that "the genetic basis for hypertension in U.S. blacks was already widespread in many of their West African ancestors. It required only the ubiquity of saltshakers in twentieth-century America for that genetic basis to express itself in hypertension."'9 Diamond also extended the Wilson and Grim case with new numbers of unknown provenance.20 Where Wilson and
to 10%S. For the Atlantic passage itself, Wilson and Grim bring in more scientificlooking arguments. They claim that death on shipboard was "often due to conditions that ultimately kill by salt and water depletion."22 Of course, there is no evidence that 18th-century West Africans had a special ability to conserve salt or that salt was in short supply, either on shore or on slave ships. Wilson and Grim nevertheless write that "on slave ships, vomiting due to seasickness was common, and the most common causes of death on the middle passage were recorded as diarrheal (the "flux") and febrile diseases, both salt depletors." Yet it is a curious claim that seasickness, which rarely lasts as long as 48 hours, could affect one's descendants more than 200 years later. As for the fevers, they were mainly falciparum malaria. Like victims of any other fever, its victims may suffer a little loss of salt, but they die because the parasite feeds on hemoglobin in the human bloodstream. Some diseases, like cholera and infantile
diarrhea, kill through dehydration23-not salt depletion alone-but few of the passengers on the slave ships were infants, and cholera was completely absent from the Atlantic basin during the period of the slave trade to North America. So while some deaths from dehydration and salt depletion could have occurred, there is no evidence that either was a significant cause of death on the slave
shipsz24
Similar problems with the historical method appear on the American side of the slave trade. Wilson and Grim give quite precise figures, but all but one of their citations have to do with the West Indies. Their sole citation on the health of slaves in the United States is a false lead December 1992, Vol. 82, No. 12
Public Health Then and Now
to pages that say nothing about that subject.25 And again, Diamond goes them one better, raising their estimated maximum death rate within 3 years of arrival from 30% to 40%o and omiting the crucial fact that even this figure is for the West Indies, not North America. Wilson and Grim also claim that "the high mortality under slavery was caused largely by salt and water-depletive diseases."26 Yet the extensive literature on disease among slaves shows no such thing. The planters and the doctors who cared for slaves had a strong impression that the particular susceptibility of slaves was to the diseases of the lungs, particularly pneumonia and tuberculosis, though many died of malaria and gastrointestinal disease as well.27 What little quantitative data we have from the early 19th century bear this out. From 1819 to 1836, the British army recorded the cause of death among African soldiers on both sides of the Atlantic, and the range of disease shows that a good deal more was happening than salt depletion (Tables 1 and 2, Figure 1). The figures are significant because these soldiers were recruited into the British army as slaves purchased in Africa. Some were left to serve in Africa while others were sent to serve in the West Indies. The statistical picture on the African side shows the diseases that were common among young males in Africa at that time and from which young men were likely to die at sea on the way to the Americas. The main causes of death were eruptive fevers (mainly smallpox) (Table 1) and diseases of the lungs (mainly pneumonia and tuberculosis) (Table 2). The Africans, once they arrived in the New World, died at a higher rate than they did in Africa, aswould be expected of those who moved beyond the disease environment of their childhood, the source
of their range of immunities. This evidence for the West Indies is not truly representative of the disease environment in North America, but it confirms the anecdotal evidence of North American doctors that the serious new threat was lung disease. The increase of 10 deaths per thousand overall was clearly caused by an increase in pneumonia and tuberculosis. Gastrointestinal infections caused less than 20% of all deaths among those recently arrived from Africa. In the decades that followed, American-bom soldiers of African descent developed a much stronger immunity to lung diseases, which dropped to fewer than two deaths per thousand after the 1870s. If the African lack of immunity to these diseases could
18
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FIGURE 1-Came of dea anong Afla Troops sevhg In fte Brdsh Anny ln the Srra Leone Cmmand and the Windward and Leewrd Comand, 1817 to 1836.
American Joumal of Public Health 1685
Public Healh Tben and Now
decline so rapidly, some special explanation would be required to show why a predisposition to hypertension, if it ever existed in Africa, could be so long lasting.28 From the historical point view, the slavery hypothesis to explain AfricanAmerican hypertension not only lacks supporting evidence but also runs counter to what evidence we do have. West Africans had plenty of salt through most of their history. They do not have notably high rates of hypertension today. The mortality during the slave trade was not from salt-depleting causes. No evidence has ever been advanced that the African Americans experienced different conditions of diet and disease from those of other poor southerners. No evidence has been advanced that a dietaxy trauma experienced by 80% of one's ancestors over a period of less than 1 year, 220 years ago, could bring about a genetic change lasting to the present. Yet these hypotheses were published in the serious medical press and picked up by the popular medical literature late in 1991 as though they were possibly true. Perhaps we should try harder to close the gap between scientific and historical knowledge. [
References 1. T. E. Reed, "Caucasian Genes in American Negroes," Science 165(1969):767. 2. 0. M. Helmer, "Hormonal and Biochemical Factors Controlling Blood Pressure," in Les concepts de Claude Bemard sur le miieu interieur (Paris, France: Masson et Compagnie, 1967), 115-28; L. Gleibermann, "Blood Pressure and Dietary Salt in Human Populations," Ecology of Food and Nutriton 2(1973):143-56; H. Blackburn and R. Prineas, "Diet and Hypertension: Anthropology, Epidemiology, and Public Health Implications," Plnss in
Biochemical Pharmacology 19(1982):3179; esp 50-51. 3. J. D. Hemy and J. L. Cassel, "Psychological Factors in Essential Hypertension: Recent Epidemiological and Animal Experimental Evidence," American Journal of
1686 American Journal of Public Health
Epidemiology 90(1969): 172. L. Gleibermann, "Blood Pressure and Dietary Salt," 144 (table). 4. F. C. Luft et al, "Cardiovascular and Humoral Responses to Extremes of Sodium Intake in Normal White and Black Men," Circulktion 60(1979):697-706; F. C. Luft et al, "Effects of Volume Expansion and Contraction in Normotensive Whites and Blacks and Subjects of Different Ages," Circulation 59(1979):643-50. 5. T. W. Wilson, "Africa, Afro-Americans, and Hypertensions: An Hypothesis," Social Science History 10(1986):489-500; T. W. Wilson, "Salt Supplies in West Africa and Blood Pressures Today," Lancet 1(1986):784-86; T. W. Wilson and C. E. Grim, "Biohistory of Slavery and Blood Pressure Differences in Blacks Today: A Hypothesis," Hypertension 17(1991):I122-I-128; K. A. Fackelmann, "The Afican Gene? Searching through History for the Roots of Black Hypertension," Science News 140(1991):254-55; M. F. Goldsmith, "African Lineage, Hypertension Linked," Joumal oftheAmerican Medical Association 266(1991):2049; J. Diamond, "The Saltshaker's Curse," Natural History (October 1991):20-26. 6. E. A. McDougall, "Salts of the Western Sahara: Myths, Mysteries, and Historical Significance," IntemationalJoumal ofAfrican Historical Studies 23(1990):231-57; P. E. Lovejoy, Salt of the Desert Sun A History ofSalt Prdction and Trade in the Central Sudan (New York: Cambridge University Press, 1986). See also S. A. M. Adshead, Salt and Civiliation (London: Macmillan, 1992), 15-26, for an assessment of tropical Africa's comparative place in world salt production and consumption. 7. T. W. Wilson, "Africa, Afro-Americans, and Hypertension," 258. 8. P. D. Curtin, The Atlantic Slave Trade: A Censs (Madison: University of Wisconsin Press, 1969), 191-97, 152-58; D. Geggus, "Sex Ratio, Age and Ethnicity in the Atlantic Slave Trade: Data from French Shipping and Plantation Records," Joumal of African History 30(1989):23-44; D. Richardson, "Slave Exports from West and West-Central Africa, 1700-1810: New Estimates ofVolume and Distribution,"Journal ofAfrican History 30(1989):1-22. 9. T. W. Wilson, "Africa, Afro-Americans, and Hypertension," 262. 10. Wilson and Grim, "Biohistoryof Slavery,"
126. 11. P. E. Lovejoy, "The Volume of the Atlantic Slave Trade: A Synthesis," Jounal of African History 23(1982):473-501; Richardson, "Slave Exports." 12. Curtin Atlantic Slave Trade; H. S. Klein, The MiddlePassage: Comparative Sftdies in theAtlantic Slave Trade (Princeton, NJ: Princeton University Press, 1978). 13. Diamond, "Saltshaker's Curse," 26. 14. 0. 0. Aimkugbe, "World Epidemiology of Hypertension in Blacks," in Hypertension in Blacks: Epidemiology, Pathophysiology and Treatment, ed. W. D. Hall, E. Saunders, and N. B. Shuylman (Chicago: Year Book Medical Publishers, 1985), 8, 9, 11-12. 15. Curtin, Atlantic Slave Trade, 28-34, 73. 16. Klein, Middle Passage. 17. See D. Henige, "Measuring the Unmeasurable: The Atlantic Slave Trade, West African Populations and the Pyrrhonian Critic," Journal of African History 27:
18. 19. 20. 21. 22. 23.
24.
25.
26. 27.
(1986):295-313. Klein, Middk Passage 64, 160. Diamond, "Saltshaker's Curse." 25. Ibid., 26. Ibid. Wilson and Grim, "Biohistory of Slavery," 128. S. G. Wright, "Gastrointestinal Diseases," in Hunter's Tropical Medicine, ed. G. T. Strickland, 6th ed. (Philadelphia: WB Saunders Co, 1984), 16-27; D. R. Nalin, "Cholera," in Hunter's TropicalMedicine, 305-313. R. Steckel and A. Jensen, "New Evidence on the Causes of Slave and Crew Mortality in the Atlantic Slave Trade," Journal of Economic History 46(1986):57-77, esp 6162. The citation is to K F. Kiple and V. H. King,AnotherDimension of the Black Diaspora: Diet, Disease, and Racism (New York: Cambridge Univesity Press, 1981), 147-148. Wilson and Grim, "Biohistoryof Slavery," 126. Kiple and King,AnotherDimension, 137146; R. B. Sheridan,DoctorsandSlaves:A Medical and Demographic History of Slavery in the British West Indies, 1680-1834 (New York: Cambridge University Press, 1985), 185-221; P. D. Curtin, "African Health at Home and Abroad," Social Science History 10(1986):369-98, 130-31, 135.
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