Commentary: Salt, Slavery and Survival— Hypertension in the African Diaspora

Kaufman and Hall 1 raise important issues about scientific and media racism in their discussion of research reports—especially reports on populations of sub-Saharan descent. We completely agree that the words “defect” or “abnormality” should never be used in describing variations in population phenotypes or genotypes. Even the terms “African gene” or “African genome” come with racist baggage. Although some of our earlier publications have used these terms, in recent years we have made a concerted effort to avoid them and we urge others to do the same. Even so, we believe that history can help to refute or support modern physiologic hypotheses, as long as sensitivities to past racially inspired abuses are taken into account. In Kaufman and Hall's critique, 1 we and others who have discussed the “Slavery Hypothesis” are taken to task for the media's interpretation of our reports on variation in blood pressure control systems and the genetic influences on these systems in populations around the world. We suggest this is out of our control. When we speak with the media we always reinforce that we are not talking about genetic defects, but about genetic variations in the human population. What is in our control is the review and synthesis of information on population variations in blood pressure. We hypothesize that these variations are attributable to variation in the genes that dictate the physiology of the tightly integrated control systems for blood pressure and blood volume. We suggest that this genetic variation has evolved to protect humans against fatal sodium depletion from low sodium intake or high sodium losses attributable to sweating, diarrhea and vomiting, especially when combined with conditions of high environmental temperature and high physical work demands. This is a complex interdisciplinary area, and we recommend several key references. The first is Denton's Hunger for Salt, 2 an elegant synthesis of the role of sodium in physiology and evolution. Next is Cavalli-Sforza's The History and Geography of Human Genes, 3 which includes maps of many types of genetic variation around the world. Miller's Way of Death4 describes in great detail the most brutal Brazilian trade from Angola. Finally, for a view of the American slave experience before the 19th century, we recommend Berlin's Many Thousands Gone5 and an on-line issue of The William and Mary Quarterly devoted to new evidence on mortality in the slave trade. 6 We do not feel that accusations of racism belong in a scientific discussion of populations that differ in physiology or gene frequency, in particular a discussion of what is perhaps the most important health problem in the African Diaspora—hypertension. We agree with Risch et al., who argue that categorization of humans by ethnicity is a useful tool to learn about health and disease differences among humans. 7 The power of studying African populations lies in the fact that Africa contains the most genetically and ethnically diverse populations in the world. This diversity has been shaped by ancient and recent evolutionary forces. Investigations of African populations are likely to make substantial contributions to our understanding of the genetic and environmental causes of complex diseases such as hypertension and diabetes. 8 Sometimes a new hypothesis will lead to a dead end. Other times new hypotheses point the way to the “truth.” For almost all of medical science, the “truth” is still down the road, awaiting new hypotheses to guide the way. We believe that the “selective survival during slavery” hypothesis is such a hypothesis. Only by disproving hypotheses can science advance. Kaufman and Hall 1 would have us stop all genetic research (hypothesis testing) for fear that we may discover information that “marks a group as permanently distinct from other groups, thus cementing an uncomfortable fragile group identity into an immutable categorization that can perpetuate indefinitely.” Would they have us stop research into the genetic and environmental causes of Tay-Sach's disease, cystic fibrosis, diabetes, sickle-cell disease, prostate cancer or asthma because they affect different populations? We doubt it. We believe the use of history to help refute or support modern physiologic hypotheses is a valid exercise, as long as sensitivities to past racially inspired abuses are taken into account. Do African populations metabolize sodium differently than Europeans or African-Americans? We do not know. What we do know more about are African-Americans. When given an intravenous or oral sodium load, African-Americans retain the sodium load longer and their blood pressure goes up sooner and higher. Wedler et al. 9 reported no differences between blacks and whites when going from a high- to a low-sodium diet. However, when going from low- to a high-sodium intake, African-Americans retained more sodium than whites (909 vs 385 mm). Thus, African-Americans appear to store more sodium when presented with an increasing sodium intake. This would have survival advantages, as the stored sodium (a sodium “hump,” if you will) provides a buffer for the next challenge of sodium depletion (caused by sweating, diarrhea, vomiting or inadequate sodium intake) to meet physiologic demands. It is likely that this “hump” resides in the stores of sodium. Similar studies on populations of various areas of African will be of interest. It is clear that mortality among slaves differed markedly by region of origin from Africa, and those with the lowest salt intake or stores would be more likely to die—especially during the Middle Passage. The issues of mortality are key to the hypothesis. Curtin elegantly outlines the basis of this whole issue in his landmark book The Atlantic Slave Trade: A Census. 10 “The cost of the slave trade in human life was many times the number of slaves landed in the Americas. For every slave that landed alive, other people died in warfare, along the bush paths leading to the coast, awaiting shipment, or in the crowed and unsanitary conditions of the middle passage. Once in the New World, still others died on entering a new disease environment.” We have used Miller's detailed estimates of mortality of the Angolan-Brazil trade to estimate that perhaps only 28% of captives survived the first 4 years. 5 Kaufman and Hall, 1 as well as Curtin, 10 have objected to these data as not representative of the United States. Let us look at the most recent analysis of the historical evidence on mortality at each stage, as gleaned from The William and Mary Quarterly review: March to the coast: assume 10% mortality. Baracoons waiting for sale: assume 10% mortality. Coasting period (sailing up and down the coast of Africa to get a full load): Miller (and the present authors) did not include this as a mortality point. Assume 12%11 mortality. Middle Passage (to the Chesapeake area of the United States) 11: About 75% came from the Bight of Biafra or Angola, which had the highest mortalities. (Senegambia = 12%, Bight of Biafra = 18%). Assume 15% mortality into the southern United States. Before Sale in the West 11: 6% mortality. “Seasoning”: year 1: 5% mortality. “Seasoning”: year 2: 5% mortality. Cumulative survival = 0.9 × 0.9 × 88 × 0.85 × 0.94 × 0.95 × 0.95 = 51%; thus, 49% died in the first 3 years. If death was not random, then those who died were different from those who lived. Only those who lived transmitted their genes to America. Mortality of the slaves continued after the seasoning period (the initial years of adjustment in America). While working in the sugar plantations in the southern United States, 12 “sooner or later excessive labor was bound to take its toll.” In the heat of mid-summer, slaves who could not bear hard driving without sufficient rest at noon simply collapsed in the fields. In Mississippi, a planter reported “numerous cases” of sunstroke in his neighborhood during a spell of extreme heat. His slaves “gave out.” On a southern plantation, a number of hands “fainted in the field” one hot August day. Even in Virginia, hot weather and heavy labor caused “the death of many Negroes in the harvest field.” If death were related to sodium depletion, as we assume, then those who were the best at storing sodium would be at an advantage. Thus it seems reasonable that the genotype for surviving sodium depletion would continue to be selected until the end of slavery. Kiple, a major contributor to information about the health of slaves, has suggested that simple dehydration caused many deaths. 13 Yet Curtin states, “So while some deaths from dehydration and salt depletion could have occurred, there is no evidence that either was a significant cause of death.”14 Clearly Curtin does not understand the pathophysiology of sodium depletion from sweating, diarrhea, vomiting and heat stroke. Support of the role of heat in many deaths is given in a report by Hales 15 on the beneficial effects of placing human-powered ventilators on slave ships resulting in marked reductions in mortality. Kaufman and Hall 1 (and others) contend the hypothesis cannot be proven. We disagree. We predict that new genetic techniques and salt sensitivity testing will find as follows: 1) the genotypes for salt sensitivity differ between ethnic/language groups in Africa; 2) these genetic variations will be predictive of salt sensitivity in African-Americans; and 3) the genes for salt sensitivity will be more common in Western hemisphere descendants of the Diaspora. We await such new information. If it disproves the hypothesis, then we will move on. About the Author CLARENCE GRIM is Professor of Medicine and Epidemiology at the Medical College of Wisconsin. He has published over 220 papers and conducted research on salt sensitivity, especially in African-Americans. Current NIH funding includes studies among African-Americans on the genetics of hypertension and heart disease, as well as intervention trials of the effects of classic transcendental meditation on heart disease and preventing high blood pressure.