Abstract

The excess of hypertension among blacks has been recognized since early in this century and explains a substantial portion of the black health disadvantage. In a cohort study begun in the 1970s, hypertension accounted for 20% of all-cause mortality among blacks, compared to 10% among whites. National data on trends in hypertension (140/90 mm Hg or treatment) prevalence from 1960 to 1990 suggest a decline from 44% to 32%, although differences in survey technique likely account for this pattern. During this period the prevalence ratio of black:white remained constant at 1.5, suggesting that secular trends in causal factors, if any, effected both groups equally. Recent data demonstrate a gradient in risk across the African diaspora, with standardized prevalences of 14% in West Africa and 26% in the Caribbean, compared to 33% in the US. This pattern parallels the gradient in known risk factors, with obesity alone accounting for a third of the excess in the US compared to Africa.

Why the black excess of hypertension in the US? Despite widespread speculation, unique characteristics of hypertension among blacks have yet to be established. Consistent evidence demonstrates a similar impact of the known risk factors in all population groups. Epidemiologic evidence likewise suggests that a similar risk of complications exists with blood pressure elevation among blacks and whites, level for level. Although the genetic epidemiology of hypertension is still in its infancy, no clear cross-population differences are yet apparent. Pathophysiologic traits that are known to be part of the causal etiologic pathway have not been shown to vary across groups. Unique features of this condition among blacks are likely to be restricted to the different mixes and intensities of risk factors. In the absence of evidence to support the hypothesis, it is perhaps surprising that credence continues to be given to the notion of black exceptionalism. Am J Hypertens 1997;10:804–812 © 1997 American Journal of Hypertension, Ltd.

The underlying processes that define the pathophysiology of hypertension have proved exceedingly difficult to identify, and this challenge is equally daunting for the physiologist and the epidemiologist. Although a series of sociodemographic risk factors have been identified, overall they account for little more than 25% to 30% of the interindividual variation in blood pressure.1,2 At the same time, despite detailed knowledge of blood pressure control mechanisms, it has not been possible to specify the central physiologic alterations that lead to hypertension. In contrast, variation in hypertension risk among population groups has been detected in a wide range of studies, and the excess risk experienced by black Americans is among the most fundamental observations on the distribution of blood pressure in human populations.3–10

Despite the consistency of the epidemiologic findings on racial and ethnic variation in hypertension, relatively little is known with certainty about the causes of the black predicament. In this setting the “ethnic paradigm” has been applied, in an often uncritical manner, to suggest the inference that any group differences in blood pressure control systems are causally linked to the differential in hypertension risk.5 It is surprising, however, that the explanation of the black excess is so consistently divorced from the problem of our ignorance of the etiology of hypertension in general. In the absence of knowledge of epidemiologic exposures that account for a large proportion of risk within populations, or a coherent description of the pathophysiologic process, it will remain impossible to explain differences between populations.

Despite this obvious limitation in the evidence, the cause of excess hypertension in blacks has been the subject of many speculative interpretations.11,12 While not intended to be exhaustive, this review is undertaken to suggest the perimeters of empirical knowledge on the causes of hypertension in blacks. We are particularly concerned about the use of explanations that rely on the notion of “intrinsic inferiority” among persons of African origin. Given the crucial role of the epidemiologic findings, and the emerging importance of molecular genetics, we will focus primarily on those two topics.

Prevalence

The descriptive epidemiology of hypertension remains a slow-moving scientific field. Two essential areas of inquiry are addressed: documentation of prevalence and identification of risk factors. The remarkable set of national probability surveys carried out by the National Center for Health Statistics has provided a comprehensive description of the prevalence of hypertension in the major racial/ethnic groups in the US.6–10 Hypertension, defined by the cutpoint of 140/90 mm Hg or treatment, is 50% more common among blacks than whites or Hispanics, whereas it is twice as common using the definition of 160/90 mm Hg or treatment.6–10,13 Despite the comprehensiveness of these surveys, their major strength lies in the ability to provide comparative estimates of hypertension prevalence by age, gender, and race/ethnicity at a given point in time. As can be seen in Fig. 1, prevalence has varied markedly over the course of the four relevant national surveys. These trends are even apparent among the youngest age group, and most likely represent varying methods of measuring blood pressure. Nonetheless, the black:white ratio has been essentially unchanged,10 suggesting that either the force of the disease has remained constant for both groups, under the assumption that all of the trends are driven by methodology, or the secular patterns in risk have effected both groups equally.

Trends in hypertension prevalence, blacks and whites, 1960 to 1991. Hypertension = 140/90 mm Hg + treatment. Adapted from Burt et al.10

In the current era of effective treatment, the disease burden should be measured in the prevalence of individuals with uncontrolled hypertension. Depending on which direction one approaches this problem from, we have achieved a great deal or face an enormous unmet challenge.9,10,14 Instead of the “rule of halves,” surveys from the 1990s suggest that we have moved closer to the “rule of two thirds” (Table 1). Among blacks over the age of 18, 23% of the population currently has uncontrolled hypertension, whereas for whites the corresponding figure is 18%.9,14 This burden falls disproportionately on men (Table 2), and increases to 45% among persons 50 to 69 years of age. At the same time, remarkable progress has been made in pharmacological control. Because the target blood pressure was reduced from 160/95 to 140/90 mm Hg in the 1970s, for trend analysis only the earlier standard is appropriate. With this cutpoint, a slightly different picture emerges in terms of black:white comparisons than was apparent in the data summarized in Table 1. Although control rates had previously been higher among blacks, they have decreased in recent surveys, relative to whites (Fig. 2). 10

Percentage of hypertensives who were treated and controlled, blacks and whites, US, 1960 to 1991, ages 18 to 74. Hypertension = 106/95 mm Hg. Adapted from Burt et al.10

Table 1

Hypertension Treatment and Control in the 1990s (Percent)

 NHANES III* (1988–91)  
 Blacks Whites Maywood, IL (1991–93) 
Aware 74 70 81 
Treatment of those aware 57 54 66 
Control of those treated 25 24 36 
Control on pharmacologic treatment 44 45 55 
 NHANES III* (1988–91)  
 Blacks Whites Maywood, IL (1991–93) 
Aware 74 70 81 
Treatment of those aware 57 54 66 
Control of those treated 25 24 36 
Control on pharmacologic treatment 44 45 55 
*

From Burt et al.10

From Freeman et al.14

Table 2

Percentage of U.S. Population with Uncontrolled Hypertension, NHANES III

 Blacks Whites 
SBP Level (mm Hg) Men Women Men Women 
140–159 18 13 16 11 
160–179 
≥180 
Total 25 21 21 15 
Both sexes 23 18 
 Blacks Whites 
SBP Level (mm Hg) Men Women Men Women 
140–159 18 13 16 11 
160–179 
≥180 
Total 25 21 21 15 
Both sexes 23 18 

From Burt et al.10

Estimates of hypertension risk among blacks in the US have been framed almost exclusively in terms of a comparison to whites.3,6–9 Even setting aside the obvious heterogeneity within each of these groups, epidemiology does not have sufficient descriptive power to characterize aggregate risk of environmental exposures for hypertension at the population level, and black:white comparisons are subject to substantial residual confounding. The persistence of an “unexplained” residuum in turn has prompted many investigators to propose intrinsic, ie, genetic, differences.3,11,12 Given that the basis for this hypothesis lies in the differentials in prevalence, it is important to recognize the extent to which observations in the US are culture-specific. Recent data provide standardized comparisons among several of the populations that comprise the African diaspora.15 A consistent gradient can be described, with the prevalence rising from 10% to 15% in Africa, to 20% to 25% in the Caribbean, to 33% in the US.15 Rural Africa thus remains one of the social environments that is kindest to the human cardiovascular system; across the age span mean pressures rise very little, although a minority of individuals will develop hypertension. The known sociodemographic factors, particularly obesity, provide a clear explanation for this transition in risk (Fig. 3). 2,15,16 While these data shed no light on the intrinsic susceptibility to hypertension among persons of African origin relative to other groups, they do demonstrate the paramount role of socially mediated exposures.

Prevalence of hypertension by mean body mass index among populations of West African origin. The ICSHIB study.

Blacks and Hispanics share minority status in the US, and similar social and economic disadvantage based on measures of income and education. Comprehensive national data on Hispanics have become available in recent years and it comes as something of a surprise that the prevalence of hypertension is similar to whites, and therefore lower than blacks (Table 3). 9 Does this disparity support the notion that blacks are uniquely susceptible to hypertension? The comparisons among the three major demographic groups that are now possible for a number of major health conditions highlight our lack of understanding of the determinants of risk in US subpopulations (Table 4). Obesity is equally common in blacks and most Hispanic groups.17,18 Non–insulin-dependent diabetes mellitus, which shares many of the risk factors of hypertension, occurs at a similar frequency in blacks and Hispanics, twice that of whites.18 At the same time, Hispanics have rates of infant mortality comparable to whites, therefore half that of blacks18; Hispanics also experience lower mortality from most cancers and life expectancy is high.18,19 These data suggest that the causal factors underlying population-group differentials in common diseases are very heterogeneous, and offer no simple explanations at either the genetic or environmental level. Likewise, despite the similarities in crude proxies of social status, like income and education, the black and Hispanic populations have obvious historical and cultural differences. Detailed comparisons of hypertension risk factors between blacks and Hispanics have not been carried out, so we have no direct evidence that can be used to resolve the apparent prevalence paradox, although the psychosocial dimension stands out as the obvious candidate.

Table 4

Risk Factors for Hypertension, NHEFS: Ten-Year Incidence of Hypertension (Percent)

 Men Women 
 Black White Black White 
Education     
 <12 years 41 24 42 30 
 >12 years 29 16 20 14 
 Ratio of black:white 1.4 1.5 2.1 2.1 
Overweight     
 Overweight 51 27 46 33 
 Normal weight 29 18 30 17 
 Ratio of black:white 1.8 1.5 1.5 1.9 
 Men Women 
 Black White Black White 
Education     
 <12 years 41 24 42 30 
 >12 years 29 16 20 14 
 Ratio of black:white 1.4 1.5 2.1 2.1 
Overweight     
 Overweight 51 27 46 33 
 Normal weight 29 18 30 17 
 Ratio of black:white 1.8 1.5 1.5 1.9 

From Ford et al.26

Table 3

Prevalence of Hypertension in US Hispanics (Percent)

 Mexican Americans Puerto Ricans Cubans 
Men 29 30 31 
Women 25 27 19 
 Mexican Americans Puerto Ricans Cubans 
Men 29 30 31 
Women 25 27 19 

Age-adjusted, persons 35 to 64 years old.

Adapted from reference 13.

The impact of elevated blood pressure among blacks compared to whites has also been a vexed topic. Numerous investigators have stated that hypertension is “more severe” among blacks.3,20,21 This conclusion derives from what should be a straightforward comparison of the relative risk of complications in blacks and whites. In fact, these comparisons have generally not been adjusted for severity, duration, or comorbidity. In the first National Health and Nutrition Examination Survey (NHANES-I), for example, mean systolic blood pressure for black male hypertensives was 157 mm Hg, whereas it was 151 mm Hg among white males, and this residual confounding can account for all of the differential mortality risk.22 The extent to which adequate control for differences in risk can be achieved by these methods remains an open question, however. Additional reports that have focused on specific outcomes, like renal disease, have not been able to control carefully for these inherent differences.23 Given the potential impact of other coexisting conditions, like diabetes mellitus, that are more likely to be present among blacks, an accurate assessment of the independent contribution of hypertension becomes difficult, particularly in the face of interactions.22 A recent biracial cohort study based on a sample of patients from Veteran's Affairs hospitals, which did attempt to control for severity, degree of drug control, and age of onset, demonstrated no residual black excess in risk of all-cause mortality.23 Despite the theoretical interest of this question, in the current era of widespread treatment, the “natural history” aspect of hypertension is probably moot anyway.

Are the risk factors for hypertension the same for blacks and whites? Representative national data suggest that overweight and education have a similar impact (Table 5). 26 The contentious areas, of course, are electrolyte intake and psychosocial factors. In a recent metaanalysis on the impact of sodium, for example, it was asserted that “blood pressures seem to be higher in black populations at any level of sodium intake,” a difference that was thought to be “genetically determined.”27 Again, despite its widespread currency, rigorous tests of differential responsiveness of black Americans to changes in sodium and potassium intake are not available. A summary of the experience with a salt loading protocol suggested no differences among normotensive blacks and whites, and a slight excess of “salt sensitivity” among hypertensive blacks compared to hypertensive whites.28 On the other hand, data have been presented that suggest that blacks may have greater reductions in blood pressure with potassium supplementation.29 Multivariate assessment of the risk associated with these exposures is complex, however, because the outcome of all of these interventions are likely to be conditioned by other factors. It is well recognized, for example, that age and baseline blood pressure strongly influence the responsiveness to changes in both sodium and potassium intake.30,31 It seems entirely possible that if blacks are on average more exposed to the factors that cause hypertension, they would experience greater changes in blood pressure with a given single intervention; this differential outcome need not imply any greater intrinsic responsiveness.

Table 5

Rates of Common Health Conditions in Blacks, Whites, and Hispanics

 Rate Ratio* 
Health Condition Blacks Whites Hispanics 
Prevalence    
 Hypertension 1.5 1.0 1.0 
 Obesity 1.2 1.0 1.3 
 NIDDM 2.0 1.0 2.0 
Mortality    
 Coronary heart disease 1.1 1.0 1.0 
 Stroke 2.0 1.0 0.9 
 Breast cancer 1.2 1.0 0.8 
 Lung cancer 1.4 1.0 0.5 
 Prostate cancer 2.1 1.0 0.8 
 Infant mortality 2.0 1.0 1.0 
 Rate Ratio* 
Health Condition Blacks Whites Hispanics 
Prevalence    
 Hypertension 1.5 1.0 1.0 
 Obesity 1.2 1.0 1.3 
 NIDDM 2.0 1.0 2.0 
Mortality    
 Coronary heart disease 1.1 1.0 1.0 
 Stroke 2.0 1.0 0.9 
 Breast cancer 1.2 1.0 0.8 
 Lung cancer 1.4 1.0 0.5 
 Prostate cancer 2.1 1.0 0.8 
 Infant mortality 2.0 1.0 1.0 

NIDDM, non–insulin-dependent diabetes mellitus.

Data from the US Public Health Service.17,18

*

All conditions compared to whites.

Despite the enormous effort devoted to physiologic studies of hypertension, there have been very few attempts to apply sophisticated laboratory assays in the setting of population surveys. Even fewer such attempts have been made among blacks. As a result, most studies involve convenience samples and case-control studies of hypertension clinic patients. This work has created a large body of contradictory data. The approach, in fact, is well characterized by Kuhn's definition of a scientific discipline that has not yet reached maturity and is “engaged in more or less random fact gathering.”32 In the area of ion transport, for example, it is usually asserted that the sodium-lithium countertransport has no relationship to blood pressure in blacks; however, the available data do not support this conclusion.33 At the same time, another metabolic marker of hypertension risk—intracellular calcium—is found be to higher in blacks than whites by some groups,34 but not by others.35 A particularly widespread belief in the field holds that insulin is not related to blood pressure in blacks.36 The data that support this contention, however, were generated from a very unusual convenience sample, and have not been confirmed in a community sample.37 Even the well accepted differences in renin among blacks and whites have not been demonstrated in representative samples, and may well not exist among normotensives.38,39 Again, it appears that below the level of prevalence relatively few well substantiated differences, which both relate to blood pressure and vary consistently across groups, can be identified.

An even greater challenge faces the attempt to account for psychosocial factors.40 Although the limitations of the measurement tools dominate efforts to account for the impact of the social environment as transmitted through emotional experience, a number of basic observations suggest that psychogenic arousal can influence vascular tone.40,41 Among black populations, data now exist that psychosocial factors influence hypertension risk in Africa, the Caribbean, and the US.41–44 On the other hand, the search for psychosocial determinants of the black:white differential in the US has been notably unsuccessful. While social class measures themselves can explain a portion of the differential risk,45 that does not help estimate the “race difference.” This result follows from the very construction of the question—if racial prejudice is the exposure, then whites are totally unexposed and there is no means of estimating the effect across groups, any more than one could estimate the impact of pregnancy on male:female differences. Although one might be able to demonstrate a gradient of risk associated with the intensity of racial discrimination among blacks, the contribution of this risk to group differences will remain unknown. On close examination, therefore, the attempt to “explain” black: white differences founders on this unavoidable epidemiologic contradiction: you cannot estimate the contribution of the variable used to create strata.

The important contribution of hypertension to mortality risk among blacks has been widely recognized. The data on this question is not particularly robust, however. An essential requirement for the study of this question is longitudinal follow-up data on a representative cohort. To our knowledge, only two such cohorts exist—the Evans County Study and the NHANES National Epidemiologic Follow-up Study (NHEFS).26,27,46 Enrolled in the 1960s, the participants in the Evans County study were sharecroppers from the rural South, and although the findings have been useful, they are not informative about contemporary populations.46 The NHEFS sample was nationally representative; however, only 737 black men and 1,243 black women were enrolled.22,27 The longitudinal component of NHANES II is now complete, although, there were only 447 black men and 547 black women in that study.47 The paucity of available longitudinal data on population samples makes it almost impossible to test hypotheses related to specific risk factors, although ongoing studies should ameliorate that situation to some degree.

Based on patient series and vital statistics data, however, a firm basis exists for the conclusion that the sequelae of hypertension are more common among blacks, and that they make a crucial contribution to the black health disadvantage. All-cause mortality rates among blacks are twice those of whites, and rates among black men are four times higher than among white women.17,18 During the 1980s mortality increased for black men and life expectancy fell,48,49 primarily as a result of rising mortality in large urban areas.49 Cardiovascular diseases are coded as the single most important cause of death for blacks and the decline has been less steep for blacks than for whites.50 Death rates for coronary heart disease—the most important fatal outcome related to hypertension—are now substantially higher.48,50 In black communities like Harlem, where life expectancy is less than Bangladesh, cardiovascular disease is still the largest contributor to mortality.51 Although coronary disease and stroke are the most frequent rubrics coded on death certificates,49 left ventricular hypertrophy—resulting from uncontrolled hypertension—plays a very substantial role in the causal sequence, even while not appearing in the public health data. In a hospital series from Chicago, left ventricular hypertrophy accounted for 40% of the population-attributable risk for mortality.52 Renal failure continues to increase as a cause of morbidity, although diabetes mellitus—in combination with hypertension—probably accounts for this upward trend in recent years.53 It is obvious, therefore, that the urgency to control hypertension in the black community, by preventing its occurrence and treating it when it develops, remains as important as ever.

Genetics

Before the current era of research in molecular genetics, indirect measures of heritability and group differences were the only analytic tools available. Based on family studies, it is generally estimated that 30% of the interindividual variance in blood pressure in Westernized societies can be attributed to inherited factors.54,55 These estimates are, of course, conditioned on the precision with which environmental factors are measured, and are likely to vary widely from one social environment to another. Unfortunately, as implied above, given the strength of this evidence on heritable determinants for individuals, many investigators have also asserted that the excess risk among blacks that remains unexplained after adjusting for measured environmental factors is likely to be genetic.12,27 These assertions are entirely unwarranted. The degree of individual heritability has no necessary relationship to effects at the population level.56 The classic example offered by population biologists relates to height. While a highly heritable trait, at approximately 90%, mean attained height for populations is primarily a result of nutrition and other social factors.57

Molecular genetics has now made it possible to move from the level of speculation and inference about the genetic underpinnings of hypertension to direct measurement. Despite the initial surge of enthusiasm, it is now clear that the genetic determinants of hypertension are exceedingly complex, and may lie beyond the resolving power of current techniques. The current data available from black populations is fragmentary and contradictory. Following the report by Jeunemaitre et al,58 several groups have investigated the angiotensinogen locus.59–62 The M235T mutation is common among blacks, but not associated with hypertension risk.59 Recent evidence from our group suggests that the mutation at amino acid postion 174 may weakly influence circulating angiotensinogen and blood pressure among Jamaicans.61 Although Caulfield et al have reported positive findings in a Caribbean population,62 we were unable to demonstrate association at the angiotensinogen locus in a combined sample of Nigerians, Jamaicans, and US blacks (unpublished observations). Other investigators have noted associations at both the atrial natriuretic peptide and α2-adrenergic receptor loci in blacks, although the numbers of patients involved has been small.63,64 As noted, much has been made of the potential selective pressure for sodium retention occurring during the European slave trade as a cause for black hypertension.12 Molecular data should provide a test of this hypothesis. Based on markers currently available, the frequency of the alleles of the renin-angiotensin system are similar in West Africa, the Caribbean, and the US,61 arguing against selective pressure on this physiologic system. It should be noted that, while invoking unmeasured genetic effects, the “slavery hypothesis” represents another version of the theory of “intrinsic inferiority” as an explanation of phenotypic traits among persons of African origin. As we have argued, it is precisely this premise that has led to great confusion in the study of population differentials, whether it be for intelligence quotient (IQ), low birthweight, or hypertension.65,66

A crucial limitation in the study of human hypertension is the unavailability of large epidemiologic family data sets. In addition, the high level of treatment in the US reduces the precision with which the phenotype can be characterized. These disadvantages are overcome in Africa, where families are large, participation rates are high, and treatment is less common. An ongoing family study in Nigeria recently demonstrated very high estimates of familial aggregation of blood pressure (Table 6). While the impact of shared environment cannot be separated from shared genes, these data do suggest that the determinants of blood pressure at the individual level can be characterized with greater precision in African families. This epidemiologic setting could thus provide an unusually effective field setting in which to search for genes related to hypertension among blacks.

Table 6

Estimates of Familial Aggregation of Blood Pressure Among Nigerian Families

 Systolic BP Diastolic BP 
Father:mother 0.20 [0] 
Father:son 0.35 0.17 
Mother:son [0.35] 0.36 
Father:daughter ” 0.32 
Mother:daughter ” 0.30 
Son:daughter ” 0.52 
Son:son ” 0.60 
Daughter:daughter ” 0.10 
t2 66% 68% 
 Systolic BP Diastolic BP 
Father:mother 0.20 [0] 
Father:son 0.35 0.17 
Mother:son [0.35] 0.36 
Father:daughter ” 0.32 
Mother:daughter ” 0.30 
Son:daughter ” 0.52 
Son:son ” 0.60 
Daughter:daughter ” 0.10 
t2 66% 68% 

Represents the parsimonious model from univariate path analysis; correlations below “mother:daughter” are not different from the common estimate.

t2 = general heritability.

Conclusions

Few important new insights have been forthcoming on the differential risk of hypertension experienced by black Americans in recent years. We have argued that much of the speculative superstructure that has been erected on the descriptive observations suffers from flawed logic, and cannot sustain careful scrutiny. While perhaps not at an impasse, the study of this condition with classic epidemiologic techniques is currently making very limited progress. International studies among populations of the African diaspora have provided new insights into the range of prevalence rates experienced by blacks, highlighting the role of variation in the exposure to socially mediated risk factors.

In the absence of important breakthroughs in epidemiologic methods, studies that elucidate the physiologic mechanisms of hypertension may provide the best clues to the etiology. At present, most bets are on molecular biology to provide access to this new knowledge. The European fascination with race has intruded into the study of many biological questions, often obscuring the more pressing and testable questions. A similar context exists for hypertension. Given the enormous challenges facing genetic research in complex diseases, and the degree of interindividual heterogeneity that can be anticipated, intergroup heterogeneity may be exceedingly difficult to define. A focus on what causes hypertension in blacks, rather than the distraction of why blacks have more hypertension than whites, is likely to be a more productive strategy.

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Author notes

*
This work was supported by grants from the National Institutes of Health (HL 45508 and HL 47910).
Presented in part at the Eleventh Annual Meeting of the American Society of Hypertension, New York, May 1996.