24 Sociocultural Influences on Health Caroline A Macera Centers for Disease Control and Prevention Cheryl A Armstead University of South Carolina Norman B Anderson National Institutes of Health The health experience of Americans has improved enormously over the course of the 20th century Communicable and infectious diseases, the major causes of premature death in the United States prior to 1930, have been replaced by chronic illnesses such as heart disease and cancer Furthermore, age-adjusted mortality from heart disease has decreased from 307.2 per 100, 000 in 1950 to 138.3 per 100, 000 in 1995 Similarly, infant mortality has decreased from 12.6 per 1, 000 live births in 1980 to 7.6 per 1, 000 live births in 1995 These changes mean that a majority of people in this country can expect to live a long and productive life In fact, a child born in 1995 could expect to live 75.8 years compared to 47.3 years for a child born in 1900 (National Center for Health Statistics, 1997) Unfortunately, these astounding improvements in health status have not affected all Americans equally Lagging behind are many of the underserved and minority populations (Kington & Smith, 1997; Liao & Cooper, 1995) The ethnic composition of the U.S population has changed from being primarily White to include a large percentage of African Americans (or Blacks), Hispanics, and Asian and Pacific Islanders This cultural diversity will continue to increase because of high immigration and birth rates among minority populations Each ethnic group views health within its own cultural context, which complicates the decision to seek and continue treatment, and to use preventive measures Additionally, social conditions may put minorities at higher risk for specific health problems The purpose of this chapter is to first present basic demographic and health characteristics of the major ethnic groups in this country, and then to describe a contextual model of hypertension in Blacks as an example of how ethnic disparities in health status may occur and be understood DISTRIBUTION OF ETHNIC MINORITIES Although there is a great deal of diversity within ethnic groups, this chapter uses the five general categories as collected and reported by the National Center for Health Statistics (1997): White, Black, American Indian or Native Alaskan, Asian and Pacific Islander, and Hispanic origin When possible, data is presented by non-Hispanic White and non-Hispanic Black groups Because there is no consistent agreement on terminology, this chapter uses African American and Black interchangeably throughout African Americans, or Blacks, the largest minority group in the United States, number almost 34 million and represent 12.8% of the population (U.S Bureau of the Census, 1995) During 1994, the African American population grew at a faster rate than the White population (1.5% compared to only 0.8%), but not as fast as the Hispanic population (3.5%) Blacks are projected to be the second largest minority group in this country by 2025 ( Fig 24.1 ) -427FIG 24.1 The term Hispanic is used to summarize information about people of all races whose ancestry can be traced to Spain, Mexico, Puerto Rico, Cuba, or to any of the Spanish-speaking Latin American countries The 1990 census enumerated 29.2 million Hispanics classified as Mexican Americans, Puerto Ricans, Cuban Americans, and about 30 additional Hispanic- origin groups aggregated as Other Hispanics (U.S Bureau of the Census, 1995) Hispanics in the United States represent about 10.9% of the population and are the nation's second largest minority group However, because of high immigration and birth rates, Hispanics are expected to replace American Americans as the largest ethnic minority group in the United States by 2025 Asians and Pacific Islanders in the United States number about 10 million (representing 3.7% of the population), and speak more than 30 major languages or dialects (U.S Bureau of the Census, 1995) The major groups in this category include Chinese, Filipinos, Japanese, Koreans, and Native Hawaiians Furthermore, about two thirds of the persons in this population group speak their native language at home, and more than 60% of Southeast Asians (Vietnamese, Cambodian, Hmong, and Laotian) have limited proficiency in English Although a small proportion of the U.S population, this diverse minority group is expected to increase to more than five times its current size and represent 10.3% of the population by 2050 (US Bureau of the Census, 1995) Native Americans in the United States number about 2.3 million, just less than 1% of the population Although this group is expected to grow steadily over the next 50 years, the percent of the population that is American Indian or Alaskan Native would only rise to 1.1% by 2050, remaining the smallest minority group in the United States (U.S Bureau of the Census, 1995) LIFE EXPECTANCY One measure of the health of a population is its life expectancy, a value that heavily weights early morality, but does not incorporate quality of life issues Throughout the 20th century, African Americans experienced substantial improvements in life expectancy, but they still have an estimated life span of to years less than Whites (Table 24.1) For both Whites and Afican Americans, women live longer than men, resulting in a higher proportion of women alive, especially in the older age groups The life expectancy at birth for African American men increased 2.2% (or 1.4 years) from 1980 to 1995 compared to a 38% (or 2.7 years) increase for White men The increase in life expectancy for African American women during this same period was identical to that for White women, 1.9% (about 1.5 years; National Center for Health Statistics, 1997) Although comparable national data are not available for the other ethnic groups, information on residents of Texas suggests that life expantancy at birth for Hispanics is the same as non-Hispanic Whites and higher than non- Hispanic Blacks (Centers for Disease Control and Prevention, 1994; Markides, 1989) Similarly, area-specific studies have found life expectancy for Asian and Pacific Islanders in the United States to be higher than that of Whites However, data on life expectancy for Asians may be particularly subject to -428- misclassification and underestimates of the number of deaths within ethnic groups (Gardner, 1994; Hahn, Truman, & Barker, 1996) Life expectancy for Native Americans is lower than for Whites primarily because of the high death rate for persons under age 45 This higher rate is due to excess mortality from intentional and unintentional injuries rather than from chronic diseases The death rates for Native Americans are based on death certificate identification of the decedent as a member of this minority group Unfortunately, it has been demonstrated that many Native Americans have been classified as White on death certificates (Classification of American Indian race on birth and death certificates, 1993; Frost, Taylor, & Fries, 1992; Hahn et al., 1996; Sugarman $I Lawson, 1993), thereby artificially reducing the death rate for persons in this group MAJOR CAUSES OF DEATH As shown in Table 24.2, the highest death rate in 1995 is found for Black men (1, 016.7 per 100, 000) Although most men and women in all ethnic groups experienced a decline in overall mortality rate from 1985 to 1995, the largest decline was among White men (9.6%) Ethnic differences are apparent for mortality, but also for other health indicators such as preventable hospitalizations (Pappas, Hadden, Kozak, & Fisher, 1997) By examining the top five causes of death (Table 24.3), it is clear that all ethnic groups share some common characteristics in spite of the differences in mortality rates Among the leading causes of death for both men and women in most ethnic groups are diseases of the heart and cerebrovascular disease (stroke) A major chronic condition associated with these conditions is hypertension After heart disease and stroke, the major contributors to the high mortality rate among Black men are HIV infection, violence, and unintentional injuries HEALTH STATUS Unlike identifying the major causes of death, measuring good health is a complicated task Often health status is simply defined as the absence of disease, even though a complex of physical, social, cognitive, and psychological factors are involved in determining overall health This chapter uses high blood pressure, or hypertension, as a marker for health status because of its association with the major causes of death and disability for all ethnic groups Hypertension is usually defined as having a systolic pressure of at least 140 mm Hg or a diastolic pressure of at least 90 mm Hg, or taking antihypertensive medication About half the people who have hypertension are undiagnosed Furthermore, only about one fourth of those who know they have the disease have controlled through lifestyle modification or medication (Havas et al., 1996) Uncontrolled hypertension increases the risk of circulatory diseases (particularly heart disease and stroke), and kidney disease (Burt et al., 1995) Because it is an important marker of health, questions about hypertension are routinely included in national surveys, thus providing comparable estimates of the prevalence of hypertension for White, African American, and Mexican American subgroups As shown in Fig 24.2 and Table 24.4, African Americans have the highest prevalence of hypertension, almost 1.5 times that of Whites, whereas Mexican Americans have an intermediary prevalence (Burt et al., 1995; National Center for Health Statistics, 1997) The percentage of the population with hypertension has decreased between 1976 and 1980 and 1988 and 1994 for Whites and African Americans, but has remained constant for Mexican Americans: The decrease was over 40% among Whites, but less than 30% among Blacks Consequently, Blacks will continue to experience disproportionately higher rates of morbidity and mortality from heart disease, stroke, and renal disease compared to the other ethnic groups -429- FIG 24.2 Percent of population with hypertension among persons from age 20 to 74, in the United States from 1976 to 1980 and 1988 to 1994 (Hypertension is defined as either systolic pressure of at least 140 mm Hg or diastolic pressure of at least 90 mm Hg, or taking antihypertensive medication.) From National Center for Health Statistics (1997) -430- For less than 10% of those with hypertension, there is a definite cause However, for over 90% of people with hypertension, the cause is unknown and it is termed essential hypertension (Frohlich, 1994) Hypertension occurs more frequently among Blacks, older individuals, less educated individuals, those who are obese or have gained weight, those who are physically inactive, and those who use alcohol excessively Additionally, some individuals with augmented sodium metabolism may develop hypertension (Frohlich, 1994) Because none of these risk factors alone explains a majority of the risk for developing hypertension, it is clear that this disease develops from multiple interacting mechanisms rather than from a single source (Calhoun & Oparil, 1995; Flack et al., 1995) Among the contributors to this disorder are genetic, biological, nutritional, behavioral, social, environmental, and psychological factors SOCIAL AND CULTURAL FACTORS RELATED TO HEALTH STATUS Given the changing demographic makeup of the United States, it is necessary to examine subpopulations within the major ethnic groups that may be at high risk for disease The rest of this chapter focuses on the development and description of a model that may explain how social and cultural influences interact to affect health status, using the example of hypertension in Blacks Although this model focuses on Black/White differences in hypertension risk, many elements of the model may be generalizable to other ethnic subpopulations and other health problems Contextual Model of Hypertension in Blacks The contextual model of hypertension in Blacks reflects the contribution of sociology, psychology, and the natural sciences in attempting to systematically understand the key determinants of ethnic differences in the development and maintenance of hypertension The unacceptableness of unidimen sional or strictly genetic accounts of the determinants of hypertension in Blacks is exemplified in the Report of the Secretary's Task Force on Blacks and Minority Health (1986): Black, in the United States is a sociological category Some investigators have confused ethnic identity with genetic constitution, simplistically equating them The heterogeneity of blood pressure levels and hypertension prevalence in Black populations in Africa, the Caribbean, and the Americas casts doubt on the proposition that genetic factors are primarily responsible for the blood pressure excess in U.S Blacks …It becomes clear that any explanation of blood pressure differences between Black populations must take into explicitly account of environmental Within the contextual model, hypertension risk factors interact with ethnicity in the context of the environment and culture Cardiovascular Reactivity In recent years, researchers in health psychology and behavioral medicine have explored the role of cardiovascular reactivity as a potential contributor to the high rates of hypertension Reactivity is defined as the magnitude and pattern of acute changes in cardiovascular activity (reactivity) in response to behavioral, social, and environmental stressors According to Krantz and Manuck (1984), the measurement of reactivity contributes unique information regarding the physiological functioning of the individual beyond that provided by resting or baseline levels alone The reactivity hypothesis rests on the assumption that acute changes in cardiovascular reactivity to laboratory procedures are analogous to cardiovascular challenges encountered in daily life (Anderson, McNeilly, Armstead, Clark, & Pieper, 1993) Reactivity studies also suggest that exaggerated changes in cardiovascular parameters, which occur when individuals are exposed to behavioral, psychological, or physical challenges precede the development of sustained hypertension (Julius & Schork, 197 I) Individuals at risk for hypertension show greater sympathetic nervous system reactivity to stressors In animal as well as human research, groups at risk for hypertension have shown greater stress reactivity than groups with relatively lower risk For example, “hyperreactivity” has been observed in Blacks as compared to Whites, in anxious versus nonanxious persons, in anger suppressors versus anger expressors, and in chronically stressed versus nonstressed individuals Hyperreactivity is thought to be a risk marker for hypertensive risk and may be also directly implicated in the pathogenesis of hypertension There have been a substantial number of studies on Black- White differences in autonomic reactivity (Anderson, McNeilly, & Myers, 1992) These studies have been conducted with both children (Dysart, Treiber, Pflieger, Davis, & Strong, 1994; Murphy, Stoney, Alpert, & Walker, 1995) and adults (Anderson, 1989) and have utilized a wide variety of laboratory -431stressors, experimental designs, physiological measures, and population subgroups Despite the diversity of approaches used, most studies have demonstrated that Blacks show a greater blood pressure reactivity to laboratory stressors as compared to Whites Perhaps more important, is that the mechanisms responsible for producing the stress-induced blood pressure response may be different in Blacks than in Whites Blacks have been found to exhibit greater blood pressure reactivity mediated by peripheral vasoconstriction (characteristic of the vascular pattern of reactivity; Girdler, Hinderliter, & Light, 1993; Terrell & Manuck, 1996), whereas the blood pressure response of Whites has shown a greater cardiac involvement (characteristic of the cardiac pattern of reactivity) These results, particularly the heightened peripheral vasoconstrictive responses in Blacks, have been observed among children, adults, normotensives, and borderline hypertensives It has been most clearly seen in studies using stressors, such as the forehead cold pressor test, that are specifically designed to produce a predominantly vascular pattern of reactivity among Blacks The studies have not consistently found greater reactivity in Black adults with a positive family history (Anderson, Lane, Taguchi, & Williams, 1989; Anderson, Lane, Taguchi, Williams, & Houseworth, 1989) Augmented Reactivity in Blacks Thus far, research using the reactivity paradigm has been largely concerned with describing racial differences in reactivity The next logical step is to identify the variables that are predictive of heightened vascular reactivity among Blacks Anderson et al (1991) noted that physiological and psychophysiological responses obtained in an experimental laboratory are partly a function of the socioecological niche that the individual occupies at that time The principal tenet of the proposed contextual model is that the exaggerated peripheral vascular reactivity observed in many Blacks relative to Whites is a function of a number of biological, psychological, behavioral, environmental, and sociocultural factors The model begins with the premise that in reactivity research, race should be viewed as a proxy for the effects of differential exposure to chronic social and environmental stressors rather than as a proxy for the effects of genetic differences Black Americans, on average, are exposed to a wider array of chronic stressors than their White counterparts These chronic stressors interact with nervous system activity, which in turn leads to the release of neuroendocrine substances, including norepinephrine and adrenocorticotrophin hormone (ACTH), augmented sodium retention, and enhanced vasoconstriction The resulting higher levels of endogenous sodium and ACTH not only increase blood volume but also act to potentiate the vasoconstrictive effects of norepinephrine on the peripheral vasculature Over time, the repeated stressor- induced episodes of vascular reactivity may lead to structural changes in the vascular wall (e.g., increased wall-to-lumen ratio), which further augments reactivity If repeated frequently over a number of years, this process has the potential to lead to the development of sustained hypertension The remainder of this chapter is devoted to describing each component of this model Chronic Stressors and the Social Environment Many writers view race as a sociological designation that indicates exposure to common life experiences According to the model presented here, one distinguishing feature of the life experiences between Black and White Americans is exposure to chronic life stressors As a consequence of historical factors and the continued race consciousness of society, Blacks currently experience a greater array of chronic stressors relative to Whites These chronic socioecological stressors include, among others, higher unemployment, higher poverty rates and lower income levels, lower status occupations and lower social status, residential crowding, and substandard housing (Bullard, 1994; Farley, 1984; Farley & Allen, 1989; Harris, 1982; McLoyd, 1990) Many of these chronic social and environmental stressors have been associated with hypertensive status among Blacks For example, socioeconomic status shows a strong inverse relation with hypertension among Blacks (Adams-Campbell, Brambilla, & Minlay, 1993) Racial Stress Racism represents one of the most pernicious forms of chronic psychosocial stress facing African Americans today A burgeoning body of literature identifies racism as a macrosocial factor contributing to the vast racial disparity of health outcomes found among African Americans and Whites (Jackson et al., 1996; McNeilly et al., 1996) Racial stress has been found to be related to both blood pressure status (Krieger, 1990; Krieger & Sidney, 1996) and cardiovascular reactivity (Armstead, 1991; Armstead, K A Lawler, Gorden, Cross, & Gibbons, 1989; Jones, Harrell, Morris-Prather, Thomas, & Omowale, 1996; McNeilly et al., 1995; Morris-Prather et al., 1996) Historically, African Americans often received severe punitive sanctions for expressing emotions they experienced when exposed to racism Anger suppression may be a historical coping style that presently serves as a moderator of the interaction between racism and blood pressure status and reactivity Gentry, Chesney, Gary, Hall, and Harburg (1982) found that males who are high in interracial hostility and who tend to keep anger suppressed have the highest mean diastolic pressure Krieger (1990) found that Black women who reported usually accepting and keeping quite about racist treatment were 4.4 times more likely to report being hypertensive than were Blacks who talked to others Among Whites, this relation did not hold true In another study, Krieger and Sidney (1996) found that hypertension was significantly higher among working-class Blacks reporting that they typically “accepted” unfair treatment and had not experienced racial discrimination in one of seven situations relative to those reporting that they “challenged” unfair treatment and experienced racial discrimination Among professional Black adults, systolic blood pressure was to 10 mm Hg higher among those reporting a higher frequency of discrimination -432and those reporting that they “accepted” unfair treatment Black-White differences in blood pressure were partially explained by incorporating variables for exposure and coping styles utilized with racial discrimination Armstead (1991) and Armstead et al (1989) found that anger suppression was related to increased diastolic reactivity to racist stimuli and to a speech stressor Vascular activation may be end products of chronic anger suppression as a result of coping with racism Chronic exposure to racial stress may contribute to concomitant changes in the peripheral vasculature in ways similar to other chronic stressors Anger kinetics may play a role in catecholamine release and subsequent hemodynamic changes associated with racial laboratory stressors Lower Socioeconomic Status The health history of African Americans in the United States is filled with accounts of pervasive disease morbidity and mortality associated with social stratification (Anderson & Armstead, 1995) In U.S society, social stratification occurs as a function of ethnicity, gender, or socioeconomic status The term socioeconomic status (SES) is typically used to describe stratified inequality in ranking that exists in society Educational attainment is also one of the strongest predictors of health outcomes in the United States Higher educational attainment does not consistently bring comparable health benefits for minorities (Pappas, Queen, Hadden, & Fisher, 1993) For example, Blacks have significantly lower SES than Whites by every measure What is often not recognized, however, is that at most levels of SES, morbidity and mortality rates are higher for Blacks than for Whites (Lillie-Blanton & Laveist, 1996; Williams, 1996) At present, it is unclear how SES differentially influences hypertension risk behaviors or blood pressure-related knowledge, attitudes, and beliefs of minorities Stratification and discrimination may directly and/or indirectly interact with socioeconomic status to create a highly vulnerable underclass of African American citizens with poorer overall health, poorer health behaviors, increased daily life stress, and lack of access to health care (Williams, 1992) Lower SES Blacks may not only receive more exposure to environmental risk factors, psychosocial risk factors, and deficits in medical care, but also may be more vulnerable to them Dressler (1996) found diastolic blood pressure levels were associated with an interaction between lower socioeconomic status and increased exposure to stressful life events In the case of essential hypertension, a consistently strong gradient for SES exists, especially for African Americans Among both Blacks and Whites, hypertension is higher at the lower end of the SES spectrum, yet the relation clearly reflects an interaction of gender, ethnic, and socioeconomic stratification (Adams-Campbell et al., 1993; Williams, 1992) If SES is linked to hypertension in a causative way, it should be expected that it is also linked to physiological systems relevant to hypertension One possible biological mediator of SES effects on hypertension effect is cardiovascular reactivity Carroll, Davey-Smith, Sheffield, Shipley, and Marmot (1997) examined the relation of SES, hostility, and blood pressure reactions to mental stress in British men They found that systolic pressure reactivity was positively associated with SES Higher SES was associated with greater reactivity Armstead, Anderson, and Lawler (1994) found an interaction between SES and ethnicity for laboratory reactivity to a speech stressor among African American and White women Lower socioeconomic status Black women demonstrated greater reactivity than White women or higher SES Black women This indicates that being Black and poor may physiologically predispose individuals to hyperreactivity, which may be a risk marker for essential hypertension SES is related to several factors known to enhance reactivity, such as emotional suppression (Armstead et al., 1989; Durel et al., 1989; Johnson, 1989), lower levels of social support (Kamarck, Manuck, & Jennings, 1990), and greater exposure to chronic stress (James & Kleinbaum, 1976) The contextual model of hypertension suggests that lower SES may be an index of exposure to these reactivity-enhancing factors, especially among Blacks, and may serve as a predictor of augmented cardiovascular responsivity in this group If SES is related to reactivity, then ethnic group differences in SES might partially account for the mixed reactivity results among African Americans and Whites Calhoun, Mutinga, Wyss, and Oparil (1994) suggest that SES-related stress may cause sympathetic nervous system hyperreactivity by vascular mechanisms Socioecological Stressors Harburg et al (1973) found that Detroit Blacks residing in neighborhoods high in socioecologic stress, characterized by low SES and high social instability (SIS; defined as high crime and divorce rates), exhibited significantly higher blood pressures than Blacks living in low SES but more stable neighborhoods Among Whites, socioecologic stress did not influence blood pressure Similarly, James and Kleinbaum (1976) found that for Black men from age 45 to 54, high stress counties (low SES, high SIS) of North Carolina were associated with significantly higher hypertension- related mortality (e.g., hypertensive heart disease and stroke) than low stress counties As in Harburg's Detroit studies, no stress-mortality relation was found for White men In a study of residential crowding, Fleming, Baum, and Weiss (1987) found that individuals living in densely populated neighborhoods had higher blood pressure and greater heart rate reactivity during a challenging behavioral task than those who lived in less crowded neighborhoods Family environment is a socioecological stressor that has been found to influence hemodynamic reactivity in children prospectively (Wright et al., 1993) For example, parental reports of greater conflict and control were associated with vascular reactivity among 6- to 8-year-old children at a 2year follow-up Thus, not only are Blacks exposed more frequently to chronic stressors, but these socioenvironmental factors may have greater health consequences for Blacks Chronic Stress and Vascular Reactivity: Physiologic Mediators If the differential exposure to chronic stressors is related to acute cardiovascular reactivity as proposed, it should be possible -433to identify specific physiological mechanisms linking these phenomena in Blacks It is proposed that exposure to chronic stressors enhances sympathetic nervous system activity that results in augmented sodium retention and catecholamine release Augmented sodium retention and catecholamine release may, in addition to increasing blood volume, contribute to the greater vascular responses in Blacks Sympathetic Nervous System (SNS) Effects Of critical importance is whether exposure to chronic stress is associated with this hypothesized physiological scenario In support of this, research from animal and human studies has demonstrated that exposure to acute and chronic uncontrollable stress may augment resting SNS tone; enhance sympathetic reactivity to acute, novel stressors; elevate plasma levels of catecholamines, ACTH, and opioid peptides; and augment sodium retention (Baum, Gatchel, & Schaeffer, 1983; Davidson, Fleming, & Baum, 1987; Fleming, Baum, Davidson, Rectanus, & McArdle, 1987; Koepke & DiBona, 1985; Koepke, Light, & Obrist, 1983; J E Lawler, Naylor, & Abel, 1993; Lawler, Zheng, Li, Wang, & Edgemon, 1996; Light, Koepke, Obrist, & Willis, 1983; McCarty, Horwatt, & Konarska, 1988) Studies of reactivity indicate that norepinephrine elicits elevations in blood pressure through vasoconstrictive effects on the peripheral vasculature (Goldstein, 1983) ACTH has been shown to potentiate norepinephrine's vasoconstrictive effects, particularly in humans and animals with reduced renal excretory capacity (Bassett, Strand, & Cairncross, 1978; Strand Jz Smith, 1980; Whitworth, Coghlan, Denton, Hardy, & Scoggins, 1979), and to augment norepinephrine-induced contractions of a striated muscle (Bassett et al., 1978; Strand & Smith, 1980) Importantly, ACTH also induces sodium and water retention (Lohmeier & Caroll, 1985) In a series of studies at the University of North Carolina and the University of Iowa, investigators examined the role of stress and sodium retention in dogs and spontaneously hypertensive rats (Grignolo, Koepke, & Obrist, 1982; Koepke & DiBona, 1985; Koepke et al., 1983; Light, 1987) In these studies, animals who were exposed to chronic stress showed significant reductions in sodium and fluid excretion and an associated rise in blood pressure that was mediated by renal sympathetic nerves In perhaps the first study of stress and sodium retention in humans, Light et al (1983) discovered that a stressful laboratory task (competitive reaction time) led to decreased urinary sodium excretion in men with risk factors for hypertension (positive parental history of hypertension and/or borderline hypertension) but only if these men showed evidence of high SNS activity as indicated by above average heart rate increases It has also been found that low intake of dietary potassium enhances vasopressor responses to cold stress in African Americans, but not in Whites (Sudhir et al., 1997) Ionic mediation of reactivity by sodium, calcium, and potassium interactions is implicated, but remains largely unstudied Sodium Effects sodium as a principal physiological mediator of heightened vascular reactivity in Blacks First, considerable evidence exists that heightened sympathetic activity may induce sodium retention (Weinberger, Luft, & Henry, 1982) Although the dietary sodium intake of Blacks may not be significantly higher than that of Whites (Grim et al., 1980), Blacks excrete less sodium in urine and exhibit greater pressor response to sodium loading (Luft et al., 1979; Luft, Grim, & Weinberger, 1985) Thus, Blacks may be more susceptible to the blood pressure effects of sodium despite a similar dietary intake relative to Whites Research suggests that sodium may augment cardiovascular reactivity in subjects at risk for hypertension (Ambrosioni et al., 1982; Ambrosioni, Costa, Montebugnoli, Borghi, & Magnani, 1981; Falkner, Onesti, & Angelakos, 1981) Finally, studies in both humans and spontaneously hypertensive rats indicate that sodium may exert its influence on blood pressure via heightened vasoconstriction rather than by increasing cardiac output (Nilsson, Ely, Friberg, Kalstrom, & Folkow, 1985) Therefore, given the influence of the SNS on sodium retention, the greater sodium sensitivity among Blacks, and the effects of sodium on both reactivity and vascular resistance, sodium may be the pivotal physiological mechanism responsible for the observed race differences in vascular reactivity How might sodium contribute to increased vascular resistance? Sodium may lead to heightened vascular resistance through its effects on plasma norepinephrine release and action Although in normotensive individuals sodium loading has been shown to decrease plasma and urinary norepinephrine levels, the opposite effect has been observed for saltsensitive and hypertensive individuals In these individuals, sodium loading increases plasma and urinary norepinephrine levels, whereas sodium deprivation has the opposite effect (Koolen & Van Brummelen, 1984; Luft et al., 1979; Takeshita, Imaizumi, Ashihara, & Nakamura, 1982) Furthermore, high sodium intake has been shown to potentiate the effects of norepinephrine on the vasculature (Rankin, Luft, Henry, Gibbs, & Weinberger, 1981), and has also been associated with increased pressor responses to infused norepinephrine in Black hypertensives relative to White hypertensives (Dimsdale, Graham, Ziegler, Zusman, & Berry, 1987) Thus, if Blacks exhibit an exaggerated antinatriuresis, this may lead to an increased release vasoconstrictive action of plasma norepinephrine This chain of events would increase peripheral vascular resistance in Blacks Moreover, chronic stressors that stimulate the release of plasma norepinephrine would interact with higher prevailing sodium levels to further stimulate vascular reactivity (Henry, 1988) Deter et al (1997) found that salt sensitivity was related to increased anger irritation levels and increased reactivity to an information-processing task They suggested that salt sensitivity, psychosocial, and psychophysiological traits, such as reactivity, interact to play a role in the pathogenesis of hypertension It is hypothesized that the heightened vascular reactivity observed in Blacks may ultimately result in structural changes (i.e., hypertrophy) in the peripheral vasculature, which in turn may further augment vascular hyperactivity (Folkow, 1982, 1987) A long-term consequence of this process could be sustained hypertension -434In summary, compelling evidence exists that Blacks in American society are systematically exposed to a wider array of chronic social stressors compared to their White counterparts These stressors involve lower SES, higher rates of poverty, higher unemployment, lower status occupations, exposure to racism, and more crowded and ecologically stressful residential environments Many have been related to elevated blood pressure and increased hypertension prevalence Research with humans and animals suggests that exposure to chronic stress may increase tonic SNS activity, acute autonomic reactivity, and urinary sodium retention Future studies may determine whether the types of stressors that many Blacks are exposed to on a daily basis are related to these potentially pathological sequelae Bheamoral and Psychological Factors It is conceivable that chronic social stressors may increase catecholamine release and sodium retention through specific behavioral or psychological factors Early research demonstrated an association between, anger, Type A behavior, and higher levels of plasma norepinephrine and blood pressure among Whites (Friedman, Byers, Diamant, & Rosenman, 1975) To date, only one study has examined these relations in Blacks (Durel et al., 1989) Although this study yielded nonsignificant relations between norepinephrine and anger for both Blacks and Whites, it did demonstrate positive correlations between anger and cardiovascular reactivity in these individuals Several studies have shown that behavioral and psychological factors are linked to elevated blood pressure and hypertension among Blacks (Anderson, Myers, Pickering, & Jackson, 1989; James, 1985) For example, suppressed anger and hostility have been associated with elevated blood pressure and hypertension in both adolescents and adults (Harburg, Blakelock, & Roeper, 1979; Johnson, Schork, & Spielberger, 1987; Johnson, Spielberger, Worden, & Jacobs, 1987) In general, this literature has indicated that Blacks who frequently suppress their anger when provoked, or who express their anger without reflection, have higher resting blood pressure levels than those who routinely express their anger when provoked or who express it only after some reflection (Gentry et al., 1982) Recently, the experience of frequent anger has been related to higher ambulatory blood pressures among Black women while at work (Durel et al., 1989) At this time, research has not examined whether inhibited anger expression is related to sodium excretion or catecholamine release among Blacks Another behavioral factor associated with high blood pressure among Blacks is the “John Henryism” behavioral pattern of hard work and determination against overwhelming odds James, Hartnett, and Kalsbeek (1983) speculated that Blacks who exhibit this type of determination, but who also have few resources to help them achieve their goals, may be at greatest risk for developing hypertension (James, LaCroix, Kleinbaum, & Strogatz, 1984) Furthermore, it has been found that low SES Blacks who are high in John Henryism have a higher percentage of hypertension than persons who are low in John Henryism or have a high SES (James, Strogatz, Wing, & Ramsey, 1987) Interestingly, no interaction of John Henryism with education or blood pressure has been found for Whites, suggesting, as James and colleagues (1983) noted, that this coping style may be particularly relevant to Black populations The behavior of individuals high in John Henryism may actually increase their exposure to stressful social and environmental circumstances That is, these individuals may continually strive to gain control over their environment in spite of numerous barriers, thereby potentially exposing themselves more frequently to frustrating and stressful situations Whether this exposure to behaviorally mediated chronic stress results in enhanced SNS and altered sodium regulation remains to be empirically determined It has been reported, however, that active behavioral coping with acute laboratory stressors enhances sodium retention (Light et al., 1983) It is this active coping with real-life stressors that is the sine qua non of the John Henryism pattern Several studies support the notion of active coping as a moderating variable in laboratory reactivity and ambulatory monitoring situational effects Saab et al (1997) found that during a speech stressor (active coping), Black men responded with lower blood pressure, cardiac output, and heart rate changes than did White men, White women, or Black women They also reported more inhibitory-passive coping, hostility, pessimism, and less social support than other groups Light et al (1995) found that high effort coping in addition to high job status predicted diastolic blood pressure at work and in the laboratory for both Black and Whites Job strain coupled with lower status is also implicated in reactivity (K A Lawler & Schmied, 1992) Chronic social stressors may also have other psychological and emotional effects that could potentially influence sodium retention and neuroendocrine release For example, low income Blacks have been found to report more psychological distress than low or high income Whites and high income Blacks, perhaps due to the combined burden of poverty and racism (Kessler & Neighbors, 1986) Additionally, the stressful residential environments to which many Blacks are exposed (e.g., crowding and crime) are related to stress symptoms, such as anxiety, depression, somatic complaints, lower levels of perceived control, and enhanced sympathetic nervous system activity (Baum et al., 1983; Davidson et al., 1987; Fleming et al., 1987; Schaeffer & Baum, 1984) It has been suggested that urban Black youths have decreased quality and quantity of social support In fact, African Americans residing in high poverty areas have a higher percentage of people who report being unmarried, having no current partner, and having no best friend compared with those living in nonpoverty areas These findings on the relative lack of potentially supportive social relationships have also been observed in Whites (Belle, 1982) Social support has been found to have both direct and indirect stress buffering effects on resting blood pressure (Strogatz et al., 1997) and on cardiovascular reactivity (Gerin, Milner, Chawla, & Pickering, 1995; Kamarck, Manuck, & Jennings, 1990; McNeilly et al., 1995) -435- Biological and Genetic Factors Although genetic variables have been identified as important in determining sodium excretion in both Blacks and Whites (Luft, Miller, Cohen, Fineberg, & Weinberger, 1988; Grim et al., 1984), epidemiologic evidence suggests that the association of parental history and risk for hypertension may not be as strong among Blacks relative to Whites (R Stamler, J Stamler, Riedlinger, Algera, & Roberts, 1979) In fact, no published studies have reported the expected relation between parental history of hypertension and cardiovascular reactivity among Black adults (Anderson et al., 1986; Anderson, Lane, Taguchi, & Williams, 1989; Anderson, Lane, Taguchi, Williams, & Houseworth, 1989; Rowlands et al., 1982), although this relation has been found fairly consistently among Whites (Fredrikson & Matthews, 1990) A possible explanation for these somewhat puzzling findings may be the substantial influence of psychosocial factors in the development of hypertension among Blacks That is, psychosocial factors, such as chronic stress, may overshadow the influence of parental history such that risk for hypertension and hyperactivity are augmented even in persons with a negative parental history This could result in a diminished ability to detect differences between parental history groups among Blacks Second, although sodium retention has a clear genetic component (Grim et al., 1984), it may also be stimulated by psychosocial stress To the degree that Blacks, particularly low income Blacks, experience more psychological stress than Whites or upper income Blacks (Kessler & Neighbors, 1986), they may consequently be more susceptible to inhibited sodium excretion Finally, the genetic distinction between Black and White Americans is, at best, ambiguous It has been noted that the gene pool of American Blacks is comprised of a heterogeneous mixture of genes from genetically diverse populations in Africa (Hiernaux, 1975; Mourant, 1983) and the U.S Caucasian population (Glass & Li, 1953; Pollitzer, 1958) In fact, Reed (1969) estimated that up to 505 of the genes of Black Americans are derived from Caucasian ancestors, whereas Lewontin and associates (Lewontin, 1973; Lewontin, Rose, & Kamin, 1984) reported that genetic differences between individuals within a race have a substantially greater impact on the total species genetic variation than genetic differences between races Therefore, although genetic factors no doubt play a role in reactivity among Blacks, their influence on between- race differences is likely to be considerably less Coping Resources Thus far, the chapter has been discussing the various physiologic, social, and behavioral factors that may contribute to the augmented sodium retention, greater vascular reactivity, and higher hypertension prevalence among Blacks as compared to Whites It is important to note, however, that there may be factors inherent in the culture and traditions of Black Americans that may counteract the sympathetic and hypertensinogenic effects of chronic stress A number of researchers have advocated the view that minorities share many characteristics (contextual, social, and behavioral) associated with unique intra- and interethnic stress coping mechanisms (Armstead, 1991; Dressler, 1993; Smyth & Yarandi, 1996; Williams, 1996) According to the contextual model, certain cultural traditions such as strong kinship ties, unique forms of emotional expressiveness, social support, and spirituality could decrease the effects of stress and consequently the effects of stress on SNS activity, sodium retention, and blood pressure level It has been found, for instance, that resting blood pressure levels among Whites who attend church regularly are lower than among those with less frequent attendance (Graham et al., 1978) It would be of interest to determine whether Blacks exposed to chronic life stressors (e.g., low income Blacks) but who also have a high cultural “buffer” (e.g., strong religious orientation, social support, or an extended family network) exhibit lower tonic SNS activity, lower sodium retention, and lower cardiovascular reactivity than those individuals less connected with cultural resources Because of the paucity of coping, stress, vulnerability, and resiliency measures, the complexity of behavior in this population is often misrepresented and misunderstood (Stevenson, 1997) It is important that researchers perform ethnographic studies of culture, stress, and coping in minority populations before making generalizations about psychosocial mediators of cardiovascular reactivity Furthermore, studies of behavioral risk factors, adaptive behaviors, and maladaptive behaviors are warranted from a culturally sensitive perspective (Bagley, Angel, Dilworth-Anderson, Liu, & Schinke, 1995; Myers, Kagawa-Singer, Kumanyika, Lex, & Markides, 1995) It is imperative to understand how culture and ethnicity may interact with the laboratory environment, the perceptions of laboratory stressors, and the psychological and physiological coping responses to stressors TESTING THE CONTEXTUAL MODEL Directions for Research The contextual model presented here was designed to provide a stimulus for examining both the basis for racial differences in vascular reactivity as well as for exploring within-race variability in vascular responses among Blacks Toward these ends, the model suggests a number of testable hypotheses and research questions Various components of the model could be tested using either field or laboratory methodologies For example, the model would predict that Blacks who are exposed to higher levels of chronic stress should have higher resting stress hormone levels (e.g., catecholamines, ACTH) and exaggerated responses to novel stimuli, suggesting increased SNS activity compared to Blacks experiencing lower levels of chronic stress Second, chronic stress should also be positively associated with increased sodium retention (i.e., slower sodium excretion rates) and greater vascular reactivity in Blacks Third, the combination of chronic stress exposure and behavioral and psychological factors, such as anger suppression and John Henryism, should be positively associated with both increased SNS activity and greater sodium retention Dietary sodium loading (or saline infusions) should potentiate -436vascular reactivity in Blacks experiencing chronic stress Furthermore, macrosocial phenomenon, such as lower SES, residence in socially unstable communities, and chronic exposure to racial stress should be positively associated with increased SNS activity and greater sodium retention Finally, the contextual model would predict that Blacks with more coping resources (e.g., high social support, strong religious orientation, and racial identity) will show lower SNS activity and decreased sodium retention relative to those with fewer coping resources CONCLUSIONS In summary, according to the proposed model, race is viewed as a sociocultural designation that denotes differential exposure to chronic social stressors It is proposed that Black Americans are exposed to significantly more chronic social stressors than White Americans Many of these chronic social stressors have been associated with hypertension prevalence in epidemiological studies Furthermore, chronic stress has been shown to augment cardiovascular reactivity to acute stress in both animals and humans and to increase sodium retention in SHRs Acute stress has also been demonstrated to increase sodium retention in humans The essential element of this model is that chronic social stressors that are overrepresented within the Black American population due to historical factors are related to an increase in sodium retention and enhanced reactivity This altered sodium metabolism and reactivity may be further augmented by biological, behavioral, and psychological risk factors for hypertension and modulated by stress coping resources It is hoped that this model will serve as a stimulus for further research on the biopsychosocial aspects of autonomic reactivity and hypertension in minorities Disparity in health status will remain a problem in this country until researchers begin to look at ethnic- specific pathways using this type of contextual modeling approach This is a challenge directed at researchers to test the applicability of this model to other minority populations  ... relevant to hypertension One possible biological mediator of SES effects on hypertension effect is cardiovascular reactivity Carroll, Davey-Smith, Sheffield, Shipley, and Marmot (1997) examined... methodologies For example, the model would predict that Blacks who are exposed to higher levels of chronic stress should have higher resting stress hormone levels (e.g., catecholamines, ACTH) and exaggerated... TO HEALTH STATUS Given the changing demographic makeup of the United States, it is necessary to examine subpopulations within the major ethnic groups that may be at high risk for disease The rest