Racial Differences in Life Expectancy: The Impact of Salt, Slavery, and Selection *

Transcription

1 Racial Differences in Life Expectancy: The Impact of Salt, Slavery, and Selection * David M. Cutler, Roland G. Fryer, Jr., and Edward L. Glaeser Harvard University and NBER March 1, 2005 Abstract The life expectancy of blacks is 6 years less than that of whites. Over half of this disparity is accounted for by differences in mortality rates attributable to cardiovascular related diseases. We estimate that racial differences in salt sensitivity can account for 78 percent of the difference in mortality due to cardiovascular-linked diseases between blacks and whites, and 45 percent of the difference in overall life expectancy. Evidence suggests that the underlying racial differences in sensitivity to salt are partially due to the transatlantic slave trade and living conditions thereafter. * Authors names are in alphabetical order, all contributed equally to this project. We are grateful to Elizabeth Avery, Lisa Boulanger, Glenn Chertow, Angus Deaton, Stephen Dubner, Arnold Epstein, Claudia Goldin, Theodore Joyce, Srikanth Kadiyala, Lawrence Katz, Sarah Levin, Steven Levitt, Glenn Loury, Adrianna Lleras-Muney, Amy Finkelstein, Sendhil Mullainathan, Jesse Shapiro, Jonathan Skinner, Andrei Shliefer, David Williams, and Heidi Williams for helpful comments and suggestions. Patricia Foo, Alex Kaufman, Lia Larson, Roland Pongou, Laura Rees, and Lisa Vura-Weis provided truly exceptional research assistance. Correspondence can be directed to any of the authors at Department of Economics, Harvard University, 1875 Cambridge Street, Cambridge MA

2 I. Introduction At birth, blacks can expect to live 72 years, six years fewer than whites. This differential is similar in magnitude to the growth of life expectancy in the past 30 years among whites or the difference in life expectancy between individuals with less than 12 years of schooling and individuals with 16 or more years of schooling (1). Life expectancy of blacks in the US is comparable to life expectancy in Lebanon, Sri Lanka, or Thailand (2). A wide variety of possible explanations for racial differences in life expectancy have been put forth including differences in socioeconomic status (3,4), stress and overt or perceived racial discrimination (5,6), and physician discrimination and access to health care (7,8). To date, these explanations have met only mixed support, and consensus reports in the field conclude that further work is needed (9). Age-adjusted mortality for blacks is 1,083.3 per 100,000 compared to for whites, implying a 31 percent higher age-adjusted mortality rate for blacks relative to whites (10). Figure 1 shows the sources of this difference. Over 40 percent of the mortality difference is accounted for by cardiovascular disease. Diabetes and kidney disease are another 17 percent combined, making the total for cardiovascular-related death well over 50 percent. Cancer, especially prostate cancer, is another 19 percent, and external causes and HIV are the bulk of the remainder. Researchers have speculated for some time about a genetic basis for health differences between ethnic groups (11-13). We posit that genetic differences in sensitivity to salt, due perhaps to the transatlantic slave trade, is a major piece of the puzzle of low black life expectancy. While there is a sizeable literature on racial 1

3 differences in salt sensitivity and the effects of salt sensitivity on health outcomes, the two strands of this argument have yet to be put together and evaluated rigorously. We undertake an empirical evaluation of the salt sensitivity theory and present evidence on its origins. II. Salt Sensitivity and Health Salt is essential for human life. The balance between salt intake and excretion is crucial in the control of extracellular fluids. Salt aids in the contraction of muscle tissue and serves as a vital ingredient of blood plasma and digestive secretions. People without sufficient salt intake can have difficulty maintaining hydration, suffer from muscle cramps, or have chronic fatigue. Modern populations typically consume too much, rather than too little salt. In many people, the kidneys regulate high salt intake, disposing of the salt with no increase in arterial blood pressure (14). In populations that consume the most sodium (the inhabitants of the northern Japanese islands, for example, whose sodium intake averages 435 meq/day), over 60% of the population remains normotensive (15). In other individuals, however, this regulation does not fully occur. The extent to which blood pressure rises with salt intake is termed salt sensitivity. The typical experiment to measure salt sensitivity involves two phases (16,17): (1) a lowsalt diet (15 mmol of sodium per 140 lbs of body weight) and (2) salt loading (250 mmol of sodium per 140 lbs of body weight). Depending on the study, these stages take as little as hours or as long as 3 weeks. A person is typically defined as salt 2

4 sensitive if they experience a salt-induced increase of mean arterial blood pressure of greater than or equal to 3mm Hg (or 5 mm Hg in some studies). Salt sensitivity is a leading cause of hypertension. Weinberger et. al estimate that roughly 60 percent of hypertensives are salt sensitive, and that blacks are particularly likely to have low-renin hypertension (17). Hypertension itself is a risk factor for left ventricular hypertrophy, kidney damage, and cerebrovascular disease (14,18). Salt sensitivity also has other deleterious effects on health, beyond the impact on hypertension. The precise mechanism behind salt sensitivity is not completely known, but may involve suppressed plasma renin activity, increased activity of the sodium-hydrogen exchanger mediating sodium reabsorption in the proximal tubule, or other genetic polymorphism defects still under investigation (19). Studies by Rapp et. al. have established that salt sensitivity is associated with alterations in the renin genotype, which is associated with low levels of renin and salt sensitivity (20). III. The Impact of Salt Sensitivity on Racial Differences in Life Expectancy It is well known that salt sensitivity increases with age and is more marked in African-Americans, obese individuals, and patients with renal insufficiency (14). The link between salt sensitivity and race is the issue we address. To calculate the impact of differential salt sensitivity on overall racial differences in mortality, we use two sources of data: salt sensitivity differences between blacks and whites (17,21), and the impact of salt sensitivity on mortality (22). 3

5 Table 1 estimates the impact of salt sensitivity on racial differences in life expectancy. The first column reports the prevalence of hypertension among blacks and whites between the ages of 20 and 74; 39 percent of blacks are hypertensive compared to 30 percent of whites. Using these estimates and data from 2 clinical studies (17,21), we estimate that 50 percent of blacks between the ages 18 and 65 are salt sensitive, compared to 31 percent of whites. Similar observations of a greater frequency of salt sensitivity among blacks have been reported in other studies (16,17). In a long term follow-up of 430 normotensive and 278 hypertensive subjects in whom assessment of salt sensitivity had been previously performed, Weinberger et al. estimate that individuals who were initially diagnosed with salt sensitivity were 73 percent more likely to die over the follow-up period (p-value =.042), even controlling for their initial blood pressure (22). Combining racial differences in sensitivity to salt with estimates of the effect of this sensitivity on health, implies a 14 percent higher mortality rate due to differential salt retention. Relative to the 31 percent overall mortality difference between blacks and whites, our results show that salt sensitivity can account for 45 percent of the overall racial mortality gap. Put another way, this is 78 percent of the mortality difference attributable to cardiovascular related diseases, although the impacts of salt sensitivity might extend beyond these causes of death. We have demonstrated that racial differences in sensitivity to salt are stark, and these differences explain a large share of differential mortality rates between blacks and whites. We now discuss the origins of these underlying differences in salt sensitivity. 4

6 IV. Salt, Slavery, and Selection A key factor that might explain differential salt sensitivity among American blacks and whites is the legacy of the slave trade, and in particular the arduous journey from Africa to the Americas (23). The middle passage, as it is called, was particularly dangerous for African slaves. About 13 million Africans left for the Americas from Africa during the slave trade, with nearly 15 percent dying during the passage (24). Further estimates suggest that between 50 and 70 percent of slaves obtained in Africa died less than 4 years after their capture (25,26). Dehydration was a fundamental cause. As T. Buxton writes nobody suffered more intensely from thirst than the poor little slaves, who were crying for water. Exhausted by their sufferings and their lamentations, these unhappy creatures fell to the ground, and seemed to have no power to rise (27). Perspiration is once source of dehydration. Between May and November, when most of the slaves were likely to be shipped (avoiding hurricane season), the temperature in coastal Nigeria was over 80 degrees, with humidity of about 77 percent (28). Slaves were generally kept below deck (29,30), where one slave trader estimated the temperature was between 120 and 130 degrees (31). After the slaving vessel was clear of the African coast, the custom was to bring slaves on deck to let them cool off, but slaves were required to sleep below deck. In addition to perspiration, vomiting from seasickness and various gastrointestinal diseases and fever -- diseases which spread in part through the close quarters in which slaves were kept -- affected many slaves. Amoebic dysentery was commonplace, and gastrointestinal disease and fever were the two leading causes of death during the slave voyage (32). 5

7 In a setting of profuse water loss, the ability to retain salt and hence water substantially increased the chances of survival. Contemporary accounts indicate that at least some slave traders were aware of this, and selected slaves on the basis of the salt on their skin. Figure 2 captures a slave trader licking a slave s face to assess his fitness for the voyage across the Atlantic. Most of the selection on the basis of salt sensitivity was likely unintentional, however. Salt depleting environments and diseases were ubiquitous throughout the slave trade, favoring individuals able to retain salt (33). Blacks selected for salt sensitivity are likely to pass the trait along to their children. Given an interracial birth rate of less than 2 percent a figure that was even lower throughout the 20 th century genetic differences across races will tend to persist (34). Further, salt sensitivity is highly heritable. Svetkey et al. enrolled 20 families comprised of 30 parent-offspring pairs and 115 adult sibling pairs to estimate the heritability of salt sensitivity among blacks (35). Their estimates of heritability ranged from.26 to.84, depending on how the data were weighted (36). The plausibility of swift evolution of salt sensitivity is supported by observations in Dahl and Shackow (37), who demonstrated that artificial selection of rats could, in three generations, produce one strain with extreme salt sensitivity and another with extreme salt resistance. Dahl et. al discovered that the population of Sprague-Dawley rats had considerable variation in the prevalence of salt sensitive blood pressure. To test the importance of genetics, Dahl and colleagues examined the effect of selective breeding on salt sensitivity. They began by establishing baseline salt sensitivity among the rats. Matings were then assigned between a pair with the lowest blood pressure response to salt loading and another pair with the greatest increase. The first generation of the 6

8 selective pairs demonstrated discernible differences in the prevalence of salt sensitivity. This process was repeated for two additional generations, at which time there was no overlap between the two strains. Renin levels in the salt sensitive rats were significantly lower and they exhibited higher mortality due to hypertension. All of this is suggestive that salt sensitivity could be a major factor in the differential health of blacks relative to whites today. In addition to this circumstantial evidence, three types of direct evidence support this theory. Blacks from the slave trade are more salt sensitive than whites and than blacks in Africa. Most American blacks are descendants of the slave trade, rather than recent immigrants. Thus, the 19 percentage point greater prevalence of salt sensitivity among blacks today is largely indicative of slave trade survivors. Such high levels of salt sensitivity do not seem to be characteristic of blacks in Africa, though different methodologies and definitions of salt sensitivity make direct comparison difficult (38-39). For example, in a study of 48-hour urinary electrolyte excretion, Barlow et. al. show that there is no difference in urinary sodium emission between black and white South African men. Further, Wilson et. al. (40) demonstrate the rarity of hypertension in adult black men in a rural village in Eastern Nigeria who consume as much salt as US blacks, providing evidence that salt sensitivity may be very low in West Africa. This suggests that salt sensitivity is not intrinsically different across races, but rather that the selection of blacks who survived the passage to the Americas is particularly salt sensitive. 7

9 Blacks from the slave trade have higher blood pressure than whites and than blacks in Africa. Hypertension is the leading endpoint for salt sensitivity. It is thus a natural way to gauge the importance of salt sensitivity. Clinical data on hypertension among American blacks and whites, taken by physical examination, are available in the NHANES. We use data from the third national survey, which includes adults aged 25 and over in the years (n=5,486 blacks and 8,483 whites). We compare the US population to two others: blacks in the Caribbean (Jamaica, St. Lucia, Barbados) and West Africa (rural and urban Nigeria and Cameroon), using data from the International Collaborative Study of Hypertension in Blacks (ICSHIB) (41). As a robustness check, we also include data on US blacks living in Metropolitan Chicago, also surveyed in ICSHIB. Caribbean blacks largely arrived through the slave trade, but live in very different circumstances today, without many of the social inequalities experienced in US society (42). West African blacks are not descendants of slaves and were not subject to the conditions of the slave trade. We have 3,159 blacks in the Caribbean, 5,337 blacks in West Africa, and 1,518 blacks in Chicago. The sample in each survey is the population aged 25 and older. To make the data comparable, we weight the US data from the NHANES to the age and sex distribution of the other countries. Figure 3 presents hypertension rates in these populations. Consistent with the salt sensitivity theory, US and Caribbean blacks, both of whose ancestors likely arrived during the slave trade, have higher rates of hypertension than do whites in the US and blacks in Africa. The NHANES data show that 38 percent of US blacks are hypertensive, compared to 23 percent of US whites (p-value<.001). The prevalence of hypertension in 8

10 the Caribbean is 26 percent (43). Hypertension rates in Africa are the lowest, at only 16 percent. Blacks in metropolitan Chicago have hypertension rates of 33 percent, 3 percent below the average for US blacks as a whole. Hypertension is caused by factors in addition to salt sensitivity, most importantly weight and salt intake. Using NHANES data on self-reported salt intake in the previous 24 hours and clinically measured BMI, we can evaluate how important these factors are for differential rates of salt sensitivity among blacks and whites. Blacks consume 85/mg more salt per day than whites. Compared to the unadjusted differential in hypertension rates of 15 percentage points, the differential when controlling for salt intake and a quadratic in BMI is still 13 percentage points (p-value<.001). Further adjustments for differences in age, gender, region of the country, education, and income hardly affect the difference at all. Even with all of these adjustments, hypertension rates are 11 percentage points higher among blacks than among whites (p-value <.001). African Immigrants Have Better Health than Blacks Descended from the Slave Trade. A final test is to compare health among American blacks descended from the slave trade versus blacks who are themselves immigrants, and thus came long after the slave trade had ended (44). The NHANES data, along with most health data sets, do not indicate immigrant status. The only data set that allows us to compare health outcomes for a representative sample of African-Americans versus black immigrants is the National Longitudinal Mortality Study (NLMS), a national population sample drawn from the Current Population Surveys (CPS) of March 1979, April 1980, August 1980, December 1980, and March 1981, and linked to the National Death Index through Because 9

11 the CPS surveys are large, our sample size is 637,162. In all cases, logit estimation of cause-specific mortality is performed and odds ratios are reported. Table 2 shows the difference in all-cause mortality, and mortality from cardiovascular, diabetes, stroke, kidney disease, and all other causes among domestic born blacks, foreign born blacks, foreign born whites, and domestic born whites. In addition to the racial identification and place of birth variables, each of our regressions control for extensive background factors such as age, education, income, and urbanicity (the coefficients on race and place of birth are not sensitive to whether these variables are included or how they are specified). Foreign-born blacks have lower mortality rates than whites, while domestic blacks have significantly higher mortality. This is true for both deaths from any cause, and for mortality from cardiovascular disease, stroke, diabetes, and kidney disease. For the foreign born black population, overall mortality is roughly 50 percent below mortality for whites (p-value <.001). Blacks born in the United States have a 15 percent higher mortality than whites (p-value <.001), yielding a difference of 65 percent between domestic and foreign born blacks (p-value <.001). Foreign born whites have a 23 percent lower mortality than native whites (p-value <.001). Importantly for the salt-selection theory, domestic-born blacks are more likely to die of cardiovascular disease (5 percent), stroke (32 percent), diabetes (49 percent), and kidney disease (113 percent) all of which are influenced by sensitivity to salt. Foreign born blacks exhibit the opposite patterns. On all other causes of death, domestic born blacks have a slightly higher mortality rate relative to foreign born blacks (45). 10

12 One again worries about the impact of any omitted socioeconomic and environmental factors on mortality. To examine this possibility, we look at data from the United Kingdom. The UK has a significant population of blacks from the Caribbean, largely descendents of the slave trade, and another large population of blacks who immigrated from Africa. Most importantly, the social environment for blacks in the UK is very different from that in the US. The Health Survey of England contains data on measured blood pressure (n=18,412) and on a physician s overall assessment of the person s health (n=33,900) for a random sample of the British population. We focus on adults aged Table 3 reports racial differences in these measures of health, controlling for a variety of socioeconomic factors including age, income, education, and occupation (though our conclusions are the same if these factors are omitted). Caribbean blacks have substantially higher rates of hypertension and poor health than do whites or African blacks. For example, hypertension rates among Caribbean blacks are 29 percent higher than rates among whites (p-value =.003). In contrast, the hypertension rates of African blacks are statistically indistinguishable from whites (p-value =.300). On the measure of general health, the patterns are the same. V. Implications for Health Policy and Future Research These results have several implications. First, they suggest that physicians should be particularly attuned to salt sensitivity, especially among blacks. Salt sensitivity cannot be measured with a simple blood test the way that cholesterol or PSA levels can. Still, salt sensitivity testing is not so onerous that it is inconceivable for physicians to 11

13 substantially increase its use. A related implication is the need for dietary changes, especially in the black community. For people who are salt sensitive half the black community and one-third of the white community -- salt intake should be cut to recommended levels or perhaps lower. For the typical person, this is a percent reduction in daily salt intake (46). Finally, to the extent that genetics or environment influence salt sensitivity, it is important to understand which genes or environmental factors are related to salt sensitivity and how such forces might be regulated. Modern genetic techniques could potentially yield an answer to this, if applied to the problem. All of these steps offer significant promise for reducing racial differences in mortality. 12

14 Figure 1: Sources of Mortality Differences Between Blacks and Whites, 2002 External 4% Other 11% HIV 8% Cardiovascular 41% Cancers 19% Diabetes 10% Kidney 7% Notes: Age-adjusted death rates for U.S. Population. Sample used for computing death rates are postcensal estimates based on the 2000 Census. 12

15 Figure 2: Slave Trader licking a slave s face to assess his fitness for the voyage across the Atlantic. Source: Chambon, Le Commerce de l'amerique par Marseille (Avignon, 1764). 13

16 Figure 3: Hypertension Rates Among Blacks and Whites US Whites US Blacks Caribbean Africa Metropolitan Chicago Note: Data for US Whites and Blacks is drawn from a sample of US Population, years old. Data for the Caribbean, Africa, Metropolitan Chicago are drawn from the International Collaborative Study of Hypertension in Blacks. The sample consists of adults over the age of 20. Hypertension is defined as having either systolic blood pressure greater than 140, diastolic blood pressure greater than 90, or taking anti-hypertensive medication. Age and Gender distributions between the two datasets have been equalized. 14

17 Table 1: The Effect of Salt Sensitivity on Racial Differences in Mortality Mortality Salt Sensitivity Implied Mortality Difference Race Total Cardiovascular Percent Hypertensive Percent Salt Sensitive Black % 50% 14% White Ratio: Black / White Note: Mortality rates are age adjusted and are expressed per 100,000 people. 15

18 Table 2: Mortality Among Domestic and Foreign Born Blacks, NLMS Race and Ethnicity All Causes Cardiovascular Diabetes Stroke Kidney Other Domestic Born Blacks 1.156** ** 1.318** 2.138** 1.147** (.027) (.035) (.179) (.092) (.321) (.041) Foreign Born Blacks.555**.620* ** (.085) (.138) (.821) (.255) (1.980) (.133) Foreign Born Whites.773**.868** ** (.019) (.028) (.142) (.067) (.174) (.032) Observations (Pseudo) R Squared Notes: Robust standard errors in parentheses. * implies significance at 5%; ** significant at 1%. Coefficients are odds ratios from logistic regressions. All Regressions control for demographic and socioeconomic factors, including age, urbanicity, income, and education. We include dummies for all missing values. 16

19 Table 3: The Relationship Between Ancestry and Health in England, HSE Race and Ethnicity Blood Pressure "Bad Health" Caribbean Blacks 1.292** 1.579** (.110) (.096) African Blacks (.284) (.154) Female.618**.943* (.022) (.025) Observations R Squared Notes: Robust standard errors in parentheses. * implies significance at 5%; ** significant at 1%. Coefficients are odds ratios from logistic regressions. All Regressions control for demographic and socioeconomic factors, including age, income, education, and occupation. Coefficients on Caribbean and African Blacks are relative to Whites. We include dummies for all missing values. 17

20 References 1. Elo, I. and S. Preston. Educational differences in mortality, Social Science and Medicine, 42 (1) 47-57, Based on Data from the World Bank: ( 3. Nettleton, S. and R. Burrows Mortgage Debt, Insecure Home Ownership and Health: an Exploratory Analysis, Sociology of Health and Illness, 20, 5, , Williams, D. Racial/ethnic variations in women s health: The social embededness of health. American Journal of Public Health, 92(4), , Broman, C. The Health Consequences of Racial Discrimination: A Study of African Americans. Ethnicity and Disease, 6 (Winter/Spring), , Ellison, C. J. Boardman, D. Williams, and J. Jackson. Religious Involvement, Stress, and Mental Health: Findings from the 1995 Detroit Area Study, Social Forces, 80 (1) , Balsa A and McGuire T. Statistical Discrimination in Health Care. Journal of Health Economics, 20: , Bird. S. and L. Bogart. Perceived Race-Based and Socioeconomic Status(SES)- Based Discrimination in Interactions with Health Care Providers, Ethnicity and Disease, 11 (Autumn) , Kington, R. and H. Nickens. Racial and Ethnic Differences in Health: Recent Trends, Current Patterns, Future Directions in America Becoming: Racial Trends and Their Consequences, Vol. II, S. Smelser, W. Wilsion, and F. Mitchel Eds, National Vital Statistics Reports, Vol. 53, No. 5, October 12, Brandon, D., K. Whitfield, J. Sollers, S. Wiggins, S. West, G. Vogler, G. McClearn and J. Thayer. Genetic and Environmental Influences on Blood Pressure and Pulse Pressure among Adult African Americans. Ethnicity and Disease 13(2) , Jacobson, K and D. Rowe Genetic and Shared Environmental Influences on Adolescent BMI: Interactions with Race and Sex. Behavioral Genetics, 28 (4) , 1998, 13. Nazaroo, J. Genetic, cultural, or socio-economic vulnerability? Explaining ethnic inequalities in health, in The Sociology of Health Inequalities, M. Bartley, D. Blane, and G. Smith eds. Oxford, UK: Blackwell Publishers, Braunwald, et. al. Harrisons Principles of Internal Medicine, 15 th edition. NY: McGraw Hill. 15. Sasali, N. The Relationship of Salt Intake to Hypertension in the Japanese. Geriatrics, (19) , Sullivan, J. Salt Sensitivity: Definition, Conception, Methodology, and Long Term Issues. Hypertension, 17 (1) I-61 I68, Weinberger, M. Salt Sensitivity of Blood Pressure in Humans. Hypertension, ,

21 18. MacGregor, G. and H. Wardener. Salt, Diet, and Health. Cambridge, UK: Cambridge University Press 19. Wu, X. et. al. An association Study of Angiotensinogen Polymorphisms with Serum Level and Hypertension in an African-American Population. Journal of Hypertension, 21: , Rapp, P. S. Wang, and W. Dene. A Genetic Polymorphism in the renin gene of the Dahl Rats Co-segregates with Blood Pressure. Science 243: , Morris, R., A. Sebastian, A. Forman, A. Tanaka, and O. Schmidlin. Normotensive Salt sensitivity: Effects of Race and Dietary Potassium. Hypertension, 18-23, Weinberger, M. N. Fineberg, S. Fineberg, M. Weinberger. Salt Sensitivity, Pulse Pressure, and Death in Normal and Hypertensive Humans. Hypertension, 37 (part 2) , This theory has been discussed in the physiology literature for some time, but not evaluated rigorously. See Grim, C. and T. Wilson. Salt, Slavery, and Survival: Physiological Principles Underlying the Evolutionary Hypothesis of Salt Sensitive Hypertension in Western Hemisphere Blacks, in Fray JCS, Douglas JG, eds. Pathophysiology of Hypertension in Blacks. New York, NY: Oxford University Press; 1993: Klein, H. The Atlantic Slave Trade. Cambridge, UK: Cambridge University Press, Wilson, T. and C. Grim. The Bio-history of Slavery and Blood Pressure Differences in Blacks Today: A Hypothesis. Hypertension 17 (Suppl I): I-122-I- 128, Miller, C. Way of Death: Merchant Capitalism and the Angolan Slave Trade, Madison: University of Wisconsin Press, Buxton, T. The African Slave Trade and its Remedy. London: John Murray, Wilmott, C., J. Mather, and C. Rowe. Average Monthly Temperature and Precipitation Data for the World, vol 1, Eastern Hemisphere. Elmer, NJ: C.W. Thornwaite Assoc. 29. Falconridge, A. Account of the Slave Trade on the Coast of Africa. London: J.Phillips., Donnan, E. Ed. Documents Illustrative of the Slave Trade to America. Four Volumes, New York: Octagon Books, Kiple, K. and B. Higgins. Mortality Caused By Dehydration During the Middle Passage. Social Science History, 13 (4) , Gastrointestinal diseases are major outlets of water and electrolytes, and fevers often accompany extreme dehydration. For evidence on causes of death during the middle passage, see Steckel, R. and R. Jensen. New Evidence on the Causes of Slave and Crew Mortality in the Atlantic Slave Trade. The Journal of Economic History, 46 (1) 57-77, It is likely that salt selection continued to occur on the plantation, as excessive salt loss was customary. Perspiration from labor in the fields siphoned salt, though the major cause of death continued to be dysentery. Cholera, another major outlet of electrolytes and waters, attacked the Americas and Caribbean killing thousands of Blacks. 18

22 34. Calculations done using the 2000 Census, which allowed individuals to indicate whether they were mixed race. Unfortunately, we do not have estimates of the magnitude of interracial mixing in the 17 th through 19 th centuries. 35. Svetkey, L., S. McKeown, and A. Wilson. Heritability of Salt Sensitivity in Black Americans. Hypertension, , Heritability of hypertension among all racial groups is approximately Dahl, K., and E. Shackow. Effects of Chronic Salt Ingestion: Experimental Hypertension in the Rat. Canadian Medical Association Journal. 90: , Barlow, R, M. Connel, and F. Milne. A Study of 48-Hour Faecal and Urinary Electrolyte Excretion in Normotensive Black and White South African Males. Journal of Hypertension, , Fumo, M., S. Teeger., R. Lang., J. Bednarz, P. Sareli, and M. Murphy. Diurnal Blood Pressure Variation and Cardiac Mass in American Blacks and Whites and South African Blacks. American Journal of Hypertension, , Wilson, T., et. al. Blood Pressure Does Not Increase with Age in a High Sodium Intake, Rural Population in Imo State, Nigeria. (abstract). Circulation 82:III-21, Cooper, R. et. al. The Prevalence of Hypertension in Seven Populations of West African Origin. American Journal of Public Health, 87 (2) , Loury, G. T. Modood, and S. Teles. Ethnicity, Social Mobility and Public Policy Cambridge, UK: Cambridge University Press (in press) 43. There are several reasons that the prevalence of hypertension of Caribbean blacks is less than US blacks, including differences in diet, body mass, and the degree of interracial mixing. 44. Black immigrants from Africa and the Caribbean comprise 89.9% of all foreign born blacks residing in the US (calculations based on the 2000 Census). 45. This could be due to the fact that immigrants who return to their home country during the follow-up period will not be linked to the death index. Thus, the foreign deaths may be under-reported. 46. Panel on Dietary Reference Intakes for Electrolytes and Water. Dietary Reference Intakes for Water, Potassium, Sodium, Chloride, and Sulfate. Washington, DC: National Academies Press,