Copyright 1996 by the American Psychological Association, Inc. 0033-2909/96/S3.00 Psychological Bulletin 1996. Vol. 120, No. 2, 293-320 Elevated Blood Pressure and Personality: A Meta-Analytic Review Randall S. Jorgensen, Blair T. Johnson, Monika E. Kolodziej, and George E. Schreer Syracuse University A meta-analysis of 295 relevant effect sizes obtained from 25,469 participants confirmed expectations that elevated blood pressure (BP) and essential hypertension (EH) would be associated with lower affect expression but with more negative affectivity and defensiveness. The strongest associations occurred for defensiveness and measures of anger and affect expression linked to an interpersonal context (s). However, a number of other factors also were found to moderate associations of BP with personality measures, including awareness of BP status, gender, occupation, and diastolic versus systolic BP assessment. Given these moderators, the authors conclude that a traditional view of personality causing EH is untenable and that, not incorporating multifactorial, synergistic approaches is likely to obscure associations of personality-behavior with EH. BP is enhanced by matching "individually-relevant etiological factors with treatment rationales" (p. 41). Our meta-analysis shows promise of contributing to this "individualizing of treatment rationales" by empirically testing the significance of each marker of "individuality" (i.e., markers of personality). However, attempts to link personality factors to the pathophysiology of EH have produced a large body of conflicting findings (Harrell, 1980; Sommers-Flanagan & Greenberg, 1989; Steptoe, 1981;Weiner, 1979; Weiner & Sapira, 1987). Discussions of the psychological correlates of high BP (cf. Anderson, Myers, Pickering, & Jackson, 1989; Diamond, 1982; Harrell, 1980; Myers & McClure, 1993; Sommers-Flanagan & Greenberg, 1989; Steptoe, 1981; Suls et al., 1995; Wiener, 1979) suggest that inconsistent findings relate to sample characteristics (race, gender, age, awareness of diagnostic status, and socioeconomic status [SES]) and methods (type of psychological instrument, adequacy of casual BP readings, and SBP or DBP as the criterion). As detailed below, we undertook analyses of moderator variables in which we had theoretically driven predictions, as well as exploratory analyses of potential moderator variables. We conducted these moderator analyses in an attempt to delineate the sample and methodological characteristics associated with significant links between one or more of the personality domains and high BP. In this article, we first detail three paradigms used to explain linkages of personality with EH and high BP: namely, the psychogenic, somatogenic, and biopsychosocial synergism perspectives. As shown later, these three paradigms converge to predict negative relations among blood pressure, anger expression, and submissiveness. However, psychogenic and somatogenic paradigms differ in the direction of the expected correlation of dispositional negative affect with high BP (positive for the former, negative for the latter). In contrast to the other two paradigms, biopsychosocial synergism emphasizes the study of interactions and bidirectional links (i.e., a factor is affected by the changes it induces in another factor). After we present these paradigms, we discuss our theoretically driven and exploratory sets of moderator analyses. Finally, we use the results of our meta-analysis According to N. M. Kaplan (1989), in general, hypertension presents the largest risk for cardiovascular disease. As blood pressure (BP) increases from normal to severe elevations, the risk for accelerated atherosclerosis, left-ventricular hypertrophy, coronary heart disease, and stroke increases markedly (Castelli, 1984;Frohlichetal., 1992; N.M. Kaplan, 1990; Sambhi, Chobanian, Julius, Noth, Borhani, & Perry, 1988). Arterial hypertension is denned as a chronic elevation of systolic blood pressure (SBP) at or above 140 mm Hg, a chronic elevation of diastolic blood pressure (DBP) at or above 90 mm Hg, or both; an estimated 20% of the American population has arterial hypertension (N. M. Kaplan, 1989; Mohrman & Heller, 1991). However, in 90% of the people with diagnosed arterial hypertension, the cause for their condition is unknown (Guyton, 1981; Mohrman & Heller, 1991). Essential hypertension1 (EH) is the diagnostic label for elevated BP of unknown origins. Because EH is a significant risk factor for morbidity and mortality, the etiology and pathophysiology of EH has been a major focus of biomedical and psychosomatic research for decades (E. H. Johnson, Gentry, & Julius, 1992). In particular, attempts to link personality factors to the pathophysiology of high BP has been a major area of inquiry and dispute (E. H. Johnson et al., 1992; Linden, 1984; SommersFlanagan & Greenberg, 1989; Suls, Wan, & Costa, 1995). Because of EH's possible links to stress reactivity and personality, researchers and clinicians have treated it with psychological interventions, ranging from biofeedback and relaxation techniques to individualized therapy (Linden & Chambers, 1994). Based on their meta-analysis, Linden and Chambers argued that the efficacy of psychological interventions for high Randall S. Jorgensen, Blair T. Johnson, Monika E. Kolodziej, and George E. Schreer, Department of Psychology, Syracuse University. We thank Kate Carey, Larry Jamner, and Steve Maisto for their comments on a draft. Preparation of this article was facilitated by National Institute of Mental Health Grant K21-MHO 1377-01 to Blair T. Johnson. Correspondence concerning this article should be addressed to Randall S. Jorgensen, Department of Psychology, 430 Huntington Hall, Syracuse University, Syracuse, New \brk 13244-2340. Electronic mail may be sent via Internet to [email protected]. 1 Note that some researchers prefer the term primary hypertension over EH (see Folkow, 1982). 293 294 JORGENSEN, JOHNSON, KOLODZIEJ, AND SCHREER as a framework for future research directions. As shown later, a traditional view of personality causing EH is untenable, and, not incorporating a multifactorial, synergistic approach is likely to obscure associations between personality (or even behaviors themselves) and EH. Historical Roots: The Psychogenic Paradigm Psychogenic paradigms posit that disturbances in physical function result from such psychological factors as conflict, frustration, and repression (Shontz, 1975). This paradigm assumes a direct linear relationship between personality and physical disfunction. In the case of EH, a specific set of conflicts and traits maintained across the life span are thought to eventually induce EH (Jern, 1987). As discussed by Jern, this direct linear assumption argues for a main effect of personality, in lieu of examining other factors that may moderate the association of personality with high BP and EH (i.e., the study of interactions). Early psychosomatic views theorize that a neurotic interpersonal style, designed to safeguard against the conflict between dependency needs and hostile impulses, fosters the development of EH (Alexander, 1939; Dunbar, 1943; Saul, 1939). Accordingly, persons prone to EH inhibit hostile and aggressive impulses in an attempt to avoid interpersonal conflict and maintain dependent, interpersonal relationships (Alexander, 1939; Diamond, 1982; E. H. Johnson & Spielberger, 1992). Furthermore, pent-up hostility, repression of threatening hostile impulses, and the anxiety and tension related to potential agonistic and competitive transactions contribute to a tonic level of physiologic activation characteristic of Cannon's (1936) fight-orflight response (Alexander, 1939; Diamond, 1982; E. H. Johnson & Spielberger, 1992). Alexander proposed that chronic activation of the fight-or-fiight response over an extended time period eventually induces the pathological changes associated with sustained elevated BP. Alexander's (1939) theoretical formulations provided a heuristic framework for the three main foci of studies on the personality correlates of EH (Boutelle, Epstein, & Ruddy, 1987; Cochrane, 1973; Jern, 1986, 1987; Sommers-Flanagan & Greenberg, 1989). One line of inquiry pertains to the inhibition of overt behavior and affect expression, with anger expression as a major focus; we labeled such traits anger-affect expression. A second area centers on such markers of negative affectivity as anxiety, covert angry feelings, guilt, dysphoria, and depression; we labeled such traits negative affectivity. In light of Alexander's discussion of a proneness of persons with EH to block from awareness the hostile impulses that may trigger antagonistic behavior, defensiveness and denial emerged as a third area of research; we labeled such traits defensiveness. Anger-Affect Expression In his narrative review, Diamond (1982) presented a lucid integration of theoretical perspectives on the inhibition of agonistic and assertive behavior. Briefly, stern yet loving parents who do not exhibit frequent displays of affection foster conflicts centering on dependency and the attainment of status. Interpersonal frustration of these status and dependency needs elicits strong angry emotions, including rage. Although the angry and hostile impulses are mobilized in preparation for overt aggression, this heightened state of physiologic activation is not discharged through verbal and motor activity because people with EH ostensibly fear retaliation and loss of social approval by those who provoke interpersonal distress. From this perspective, persons with EH have been described as passive, unassertive, submissive, and prone to suppress anger and hostility (Diamond, 1982; Jern, 1986; E. H. Johnson & Spielberger, 1992; Sommers-Flanagan & Greenberg, 1989). A psychogenic perspective predicts inverse associations between high BP and the overt behavior associated with assertion, dominance, angerhostility, and the emotional expression designed to influence the behavior of others (see Jern, 1986). Consistent with theoretical and case study descriptions of persons with high BP, high BP levels have been correlated with low anger expression (Esler et al., 1977; Gentry, Chesney, Gary, Hall, & Harburg, 1982; Sommers-Flanagan & Greenberg, 1989), low levels of dominance (Esler et al., 1977), and unassertive behavior (Morrison, Bellack, & Manuck, 1985; Sommers-Flanagan & Greenberg, 1989). However, in their recent meta-analysis of part of this literature, Suls et al. (1995) concluded that "there is little consistent support for a connection between anger and chronically elevated BP" (p. 454) and that this inconsistency is not attributable to age, race, or gender. However, it is possible that this conclusion of Suls et al. relates, in part, to their focus on trait anger self-report scores derived by averaging across items, varying in their linkage to or specification of an interpersonal context (see Table 1, p. 447); only 5 of the 33 summary scores were calculated with a method closely linked to an interpersonal context (viz., scores derived from the Structured Interview for Type A Behavior Pattern and the angerin-anger-out vignettes developed by Harburg et al., 1973). As discussed later, it is quite possible that methods with stronger interpersonal foci or contexts (e.g., structured interviews or vignettes containing a provocateur) may affect the strength of the association between anger and EH.2 Our moderator analyses were designed to help shed light on factors contributing to the often reported, confusing and contradictory findings reported in the literature on anger and EH. Negative Affectivity A psychogenic perspective predicts positive associations between BP and markers of negative affect.3 As discussed by Byrne 2 Note that our meta-analysis differs from Suls et al.'s (1995) in that we (a) incorporated a larger set of studies; (b) excluded studies that studied only persons with EH or screened out people with elevated causal BP (see p. 445); (c) compared the magnitude of the anger-affect expression effect size with the effect sizes for negative affectivity and defensiveness; (d) examined whether anger-affect expression measures with a greater interpersonal focus, due to the ostensible role of interpersonal stress in the pathophysiology of some forms of EH. would provide a stronger prediction of BP than summary scores not as tightly linked to a more specific interpersonal context(s); and (e) examined whether race (Black vs. White) would moderate the association of anger-affect expression with EH and high BP for measures linked more closely to interpersonal contexts. 3 Although the trait categories of neuroticism (Costa & McCrae, 1985) and negative affectivity (Watson & Clark, 1984) are global categories that include items related to anxiety, depression, hostility, anger, low self-esteem, and guilt, we use negative affectivity in an effort to avoid the connotations of psychopathology. BLOOD PRESSURE AND PERSONALITY (1992) in his narrative review, some empirical research has linked interpersonal sensitivity, anxiety, tension, depression, and guilt proneness to high levels of BP. Others reported high casual BP levels to covary with the covert negative affective states of anger, resentment, irritability, and hostility (Baer, Collins, Bourianoff, & Ketchel, 1979; Durel et al., 1989; E. H. Johnson, Schork, & Spielberger, 1987; E. H. Johnson, Spielberger, Worden, & Jacobs, 1987). Theoretically, the occurrence of these negative affective experiences among persons with EH is triggered by a conflict between unfulfilled competitive and status needs and the dependency on the approval of others (Byrne, 1992; Diamond, 1982; E. H. Johnson & Spielberger, 1992). On the one hand, some significant people in the life of people with EH are viewed as blocking the competitive acquisition of status; this frustration of status needs can then induce covert angry and hostile reactions, as well as depressive affect. On the other hand, fear of retaliation by these significant others (i.e., loss of social approval and favor) for anger expression induces anxiety and worry. Guilt may contribute to the suppression of anger and hostility (Diamond, 1982;Esleretal., 1977). 295 Both the psychogenic and somatogenic perspectives are unidirectional (i.e., recursive). The psychogenic perspective assumes that behavior and personality factors precede and cause the development of disease, and a somatogenic perspective stipulates that alterations in behavior and personality are the result of ongoing pathophysiologic alterations, previous pathophysiologic alterations, or both in physical function. A. P. Shapiro and Miller (1987) discussed two somatogenic perspectives. One focuses on changes in behavior and personality, resulting from the pathophysiologic changes (e.g., cerebral vascular changes as white matter lesions; Elias & Elias, 1993) induced by arterial hypertension. The second relates to the modulation of cardiovascular, behavioral, and affective adjustments to environmental stressors by central (endogenous opioids) and peripheral (baroreceptors) mechanisms involved with the experience of pain. We now discuss each of these perspectives in relation to the covariation of measures of personality and BP. Anger-Affect Expression: Cognitive Deficits Hypothesis EH is associated with subtle neurological impairments as measured by tests of cognitive function (see Elias, Robbins, & Defensiveness Elias, 1991). The association of EH and elevated BP with vitiated cognitive performance is most pronounced for responses Among persons with EH, inhibition of the expression of inrequiring immediate memory and rapid information processtense angry cognitive and emotive reactions might occur as a ing (Blumenthal, Madden, Pierce, Siegel, & Appelbaum, means of avoiding the triggering of interpersonal conflict (Alexander, 1939; Diamond, 1982; Jorgensen, Gelling, & 1993), shifting of response sets (Wilkie, Eisdorfer, & Nowlin, Kliner, 1992; Jorgensen & Houston, 1986; Weiner & Sapira, 1976), serial discrimination under time constraints (Light, 1975; Speith, 1964), and the use of nonverbal visual memory 1987), the loss of social approval following disclosure of psyand attention (Elias, Robbins, Schultz, & Pierce, 1990; Wilkie chological symptoms (Sommers-Flanagan & Greenberg, 1989), or both. This defensive and chronic inhibition of verbal et al., 1976). A. P. Shapiro and Miller (1987) argued that deficits in perception, processing, and recall of information impairs and motoric expression of intense emotions is thought to foster the rapid and efficacious responding to demanding and conflicta chronic activation of the sympathetic nervous system that is laden interpersonal situations. A history of difficulties with the primarily expressed in the cardiovascular system; this chronic state of high physiologic activation is thought to contribute to management of interpersonal stress and conflict is likely to foschanges in the vasculature underlying EH (Alexander, 1939; Diter expectancies of not being efficacious (i.e., low self-efficacy amond, 1982). Consequently, a psychogenic perspective preexpectations) at coping with interpersonal conflict (cf. Bandicts a positive association between defensiveness and high BP. dura, 1977). As discussed by Bandura (1982), perceptions of low personal self-efficacy induce psychological distress and augConsonant with this theoretical perspective, Sommers-Flanagan and Greenberg's narrative review concludes that markers of ment physiological responses during, following, and in anticidenial, the defensive production of socially desirable responses, pation of situations associated with the inefficacious execution of behavior. Low self-efficacy also can induce an active avoidand "alexithymia" (i.e., a proneness of not labeling and reporting emotions) are positively associated with casual BP levels. ance of situations associated with suboptimal performance (Bandura, 1982). Consequently, some people with EH (i.e., those whose hypertension has induced cognitive deficits in the Somatogenic Perspective processing of exteroceptive and interoceptive information) may In contrast to a psychogenic perspective, a somatogenic peravoid and retreat from cognitively and emotionally taxing interspective assumes that associations of physical health with patpersonal situations, in an effort to circumvent the distress of exhibiting a suboptimal execution of adaptive, self-cued behavterns of behavior and personality stem from shared abnormal physiological processes, disease-related morphological (struciors. Such avoidant behavior is likely to be negatively reinforced tural) changes (cf. Jern, 1987; Rau & Brody, 1994; Shontz, by reducing or escaping the aversive psychological and physio197 5), or both. Because the variables of vitiated health and patlogical reactions linked to inefficacious coping. This avoidance terns of personality and behavior are correlated only through of conflict may result in others labeling these people with EH each variable's common association with abnormal physiology, as timid, submissive, and prone to retreat from interpersonal physical structure, or both, any association of disease with beconflict (A. P. Shapiro & Miller, 1987). Conflict avoidance also havior and personality is spurious (i.e., reflects the confound of may extend to an attenuated processing of angry and irritable a third factor correlation). There is no direct causal link bebehavioral cues in others and oneself in an attempt to avert tween signs of disease and patterns of personality and behavior, the intensification of agonistic interpersonal transactions and any obtained association is the result of common, underly(Jorgensen et al., 1992; Sapira, Scheib, Moriarty, & Shapiro, ing physiological factors, morphological factors, or both. 1971; A. P. Shapiro & Miller, 1987). In summary, among peo- 296 JORGENSEN, JOHNSON. KOLODZIEJ, AND SCHREER pie whose hypertension has impaired the cognitive processing and management of interpersonal conflict, low self-efficacy expectations and impaired processing of anger in oneself and others may combine to produce a profile of submissiveness, conflict avoidance, and low levels of anger experience and expression. Like the psychogenic paradigm, this somatogenic paradigm predicts high BP to covary with low levels of anger-affect expression and high levels of submissiveness. However, it is important to note the significant differences in the implications of these paradigms. First, in the case of the somatogenic paradigm, these personality characteristics are seen as the consequence rather than the cause of hypertension and are expected to become more pronounced with the progression of hypertension induced central nervous system (CNS) deficits (A. P. Shapiro & Miller, 1987). Second, whereas a psychogenic paradigm is incompatible with the presence of statistical moderation, the somatogenic perspective is not. That is, although an association between EH and anger-affect expression may be stronger for a particular group of people, this stronger association could still be the result of these two variables sharing an underlying biological third factor or set of factors. Pain Perception, Defensiveness, and Reported Affect Negative affective states and associated behaviors (defensiveaggressive behavior, behavioral freezing, and escape behavior) induced by fear-producing stimuli are intimately connected to central and peripheral neural pathways linked to pain and harm-avoidance (Lang, 1995). Moreover, neurophysiological and neuroanatomical studies have shown close connections between pain and cardiovascular regulatory systems that include the nucleus tractus solitarii and nuclei of the vagus nerve (Maixner, 1991; Sheps et al., 1992; Szilagyi, 1989). Because exogenous opiates (e.g., morphine) are known to reduce both the nociceptive and emotional responses to the stress of pain, the modulation of psychological and physiological stress reactions probably reflects one function of endogenous opioids; that is, opioid mechanisms appear to be involved with the central modulation of the sympathetic and parasympathetic effector pathways that are related to the cardiovascular and affective adjustments necessary for behavioral adaptation to environmental stressors, as well as with peripheral (i.e., baroreceptors) modulation of BP and pain (Maixner, 1991; McCubbin, 1993). Given these linkages among the cardiovascular system, CNS, peripheral nervous system, opioid mechanisms, and affective and behavioral adjustments to stress, it is possible that associations of personality with EH involve these overlapping regulatory systems designed to modify the behavioral, affective, and cardiovascular adjustments to stressors (cf. Maixner, 1991; McCubbin, 1993; A. P. Shapiro & Miller, 1987; Sheps et al., 1992). One discussion of connections of opioid mechanisms with behavioral factors focuses on central mechanisms (Jamner, Schwartz, & Leigh, 1988), whereas another centers on the impact of baroreceptors (mechanoreceptors sensitive to increases in either BP or blood volume) on the instrumental conditioning of high BP (Dworkin et al., 1994; Dworkin, Filewich, Miller, Craigmyle, & Pickering, 1979; Maixner, 1991; Sheps etal., 1992). Opioid antagonists have been shown to increase levels of reported negative affective states as tension, anger, hostility, and anxiety (Jamner et al., 1988; McCubbin, 1993). Persons who minimize or deny the experience of negative affect (i.e., score high on measures of defensiveness or low on measures of anxiety) are reported to show a greater tolerance for painful electrical stimulation (Jamner & Schwartz, 1986; Schalling, 1971) and to show high levels of casual BP (Sommers-Flanagan & Greenberg, 1989) and ambulatory BP in a natural setting (Jamner, Shapiro, Goldstein, & Hug, 1991; Linden, Chambers, Maurice, & Lenz, 1993). The covariation of low levels of reported negative affect and increased pain tolerance with measures of defensiveness has been related to an opioid-peptide theory of defense and self-deception (Jamner & Schwartz, 1986; Jamner et al., 1988; Schwartz, 1990). On the basis of this view, higher levels of endorphins, increased numbers of opiate receptors, or both within the CNS are thought to contribute to the low reports of psychological distress and high pain tolerance among defensive people (Jamner & Schwartz, 1986; Jamner et al., 1988; Schwartz, 1990). Note that, in comparison with people who are normotensive, people with EH show higher pain thresholds to a variety of painful stimuli (Ghione, Rosa, Mezzasalma, & Panattoni, 1988; Rau et al., 1994; Rosa, Vignocchi. Panattoni, Rossi, & Ghione, 1994;Zamir&Shuber, 1980). Furthermore, people who are normotensive and have a parental history of hypertension have shown lower pain sensitivity to a constrictive thigh cuff than persons without this risk for EH (France, Ditto, & Adler, 1991; France & Stewart, 1995). Research also suggests that people at high risk for EH (elevated but nonhypertensive mean arterial BP) are at risk because of an impaired ability of the central opiodergic systems to modulate stressor induced activity of the sympatho-adrenal-medullary and pituitary-adrenal-cortical systems; that is, disordered opioid function may contribute to frequent bouts of neuroendocrine and cardiovascular hyperreactivity that, over the course of life, is conducive to the morphological changes (e.g. vascular hypertrophy) associated with EH (McCubbin, Surwit, & Williams, 1985, 1988; McCubbin, Surwit, Williams, Nemeroff, & McNeilly, 1989). Finally, Jorgensen and Houston (1986), Jorgensen et al. (1992), and D. Shapiro, Goldstein, and Jamner (1995) have shown that high levels of stressor induced cardiovascular reactivity are associated with a combination of a positive parental history of hypertension and high levels of defensiveness. If endogenous CNS opioids underlie the linkages among high BP, defensiveness, low reports of negative affect, increased pain tolerance, and stress induced physiologic hyperreactivity, then BP and EH should correlate positively with defensiveness but negatively with negative affectivity. A proposed peripheral mechanism linking pain, low negative affect, and high BP is based on research showing that stimulation of baroreceptors covaries with increased pain tolerance in rats (Dworkin et al., 1979; Randich & Maixner, 1984) and in humans (Apkarian, Jyvasjarvi, Kniffki, Mengel, & Stiefenhofer, 1989; Droste et al., 1994; Dworkin et al., 1994; Rau et al., 1994). Reflexes triggered by this stimulation also contribute to deceases in sympathetic tone, contribute to increases in parasympathetic tone, and produce such CNS-related changes as electroencephalographic synchronization, sleeplike behavior, and reductions in anxiety (Dworkin et al., 1994; Sheps et al., 1992). The effects of barostimulation on vasodilation, vagally mediated heart rate decreases, and decreases in pain and emotional arousal has been presented as a supplementary negative BLOOD PRESSURE AND PERSONALITY feedback mechanism, designed to reduce stressor induced BP elevations to safer levels (Dworkin et al., 1979, 1994). Dworkin et al. (1979), Maixner (1991), Rau and Brody (1994), and Sheps et al. (1992) proposed that progressive elevations in casual BP are instrumentally reinforced by reductions in the psychological and physical aversive sensations associated with environmental stressors. In other words, relief from stressorevoked aversive sensations may foster conditioning mechanisms that "gradually modify the short-term coping pattern of acute BP reactivity into chronic disease. Such mechanisms may utilize endogenous opioids as part of a reward system" (Sheps et al., 1992, p. 5F). Instead of high negative afTectivity and neuroticism causing high BP—as proposed by a traditional psychogenie paradigm—the baroreceptor-instrumental conditioning perspective suggests that low negative affectivity and BP are associated as a consequence of laws of conditioning (Maixner, 1991). Like the opioid-peptide hypothesis, the instrumental conditioning hypothesis indicates an inverse association of negative affectivity with EH and high BP. Note that mechanisms related to endogenous opioids and baroreceptor stimulation are complicated by a number of biological and methodological factors (McCubbin, 1993; Szilagyi, 1989). For example, baroreceptor stimulation does not induce increased pain tolerance for all types of painful stimuli (Droste et al., 1994; France et al., 1991; Rau et al., 1994), different strains of rat may not show blunted pain perception involving sinoaortic baroreceptors (Maixner, Touw, Brody, Gebhart, & Long, 1982), and the effects of endogenous opioids reflect multiple systems (e.g., the existence of different types of opioid substances and receptors; McCubbin, 1993; Szilagyi, 1989). Furthermore, in the case of persons with normotension at low risk for EH, the negative association of BP with pain perception may reflect nonopioid-peptide mechanisms (McCubbin & Bruehl, 1994). Despite the complexities related to theory and research on stress, endogenous opioids, cardiovascular regulation, behavioral factors, and such diseases as EH, McCubbin (1993) concluded that this area of research shows promise for improvements in the understanding of stress and the development of behavioral and pharmacologic interventions for stressrelated disease. In terms of markers of personality, expectations derived from the opioid-peptide hypothesis and baroreceptorinstrumental conditioning hypothesis are inconsistent with viewing neurosis as playing a causal role in EH; specifically, both perspectives suggest a negative association of negative affectivity with high BP, resulting from the trans-situational attenuation of negative emotional reactions to aversive stimuli. Note that although A. P. Shapiro and Miller (1987) discussed potential somatogenic factors linking EH to personality and behavior, they concluded that "the behavioral aspects of hypertension include both contributions to causation of this multifactorial disease, and functional and organic consequences of this disorder" (p. 256). This dual aspect of behavior and personality is consonant with biopsychosocial synergism. Biopsychosocial Synergism In Folkow's (1982) discussion of historical landmarks related to the investigation of the etiology of arterial hypertension, he stated that "around the 1950's and 1960's it slowly dawned on experienced investigators that virtually any unitary concept of 297 primary hypertension ended in a blind alley" (p. 358). People with hypertension are now viewed as varying in terms of etiology and pathogenesis; that is, hypertension is a heterogeneous condition resulting from a complex interplay of polygenetic vulnerability (e.g., salt sensitivity, overactivity of the sympathetic nervous system, or both) and environmental factors (e.g., salt intake, stress, or both; Folkow, 1982; A. P. Shapiro & Miller, 1987;Weiner, 1979; Weiner & Sapira, 1987). According to this view, the interaction of heredity and environmental conditions induces insidious changes underlying sustained arterial hypertension (Folkow, 1982). Contributors to arterial hypertension are thought to include changes in the (a) cardiovascular system (e.g., high arterial resistance related to vascular hypertrophy), (b) sympathetic nervous system (SNS; e.g., alterations in adrenergic receptors), (c) renal functioning (e.g., increased fluid volume), and (d) the interaction of the CNS with the SNS (Egan, 1987, 1992; Folkow, 1982,1987a, 1987b;Guyton, 1992; S. Julius, Amerena, Smith, & Petrin, 1995; S. Julius & Weder, 1989). It is likely that these neurophysiologic and morphologic changes are not uniform across people and, therefore, reflect different pathophysiologic pathways (Weiner & Sapira, 1987). Given the empirical evidence showing the existence of subtypes of EH, Weiner and Sapira cogently argued for discarding the psychogenic approach, in favor of the study of subtypes of personality and behavioral tendencies. As elucidated by Folkow (1987b) and Weiner and Sapira (1987), psychogenic and somatogenic perspectives, due to their unitary and recursive orientations, cannot explain the myriad of mechanisms, lifestyle factors (e.g., carbohydrate consumption, salt intake, exercise, and alcohol consumption), sociocultural stressors, personality styles, and behavioral tendencies that synergistically influence the pathophysiology and etiology of arterial hypertension. Instead of searching for the existence of main effects, researchers argued that a biopsychosocial synergistic approach's interaction terms are necessary to predict high BP (Myers & McClure, 1993; Weiner & Sapira, 1987). Moreover, a biopsychosocial synergistic perspective encourages the analysis of bidirectional links; for example, stress-induced SNS reactivity may increase salt appetite and intake, which in turn can enhance SNS reactivity (Folkow, 1987a; Henry, 1988). Moderator Analyses As previously noted, we computed moderator analyses to examine a priori expectations related to person and assessment factors and to undertake exploratory analyses as a means of increasing the precision of prediction. We conducted the moderator analyses of person-related variables to examine the adequacy of the psychogenic perspective. Because a psychogenic perspective is an unitary, main effect model, whereas both biopsychosocial synergism and somatogenic perspectives are compatible with interactive models, statistical moderation (i.e., significant interactions involving person variables such as race, age, or—as discussed below—awareness of diagnostic status) would support the latter perspectives in lieu of the former perspective. That is, if personality is the cause of EH, then associations should be equivalent in terms of direction and magnitude across all samples. Because of the evidence showing that EH reflects a variety of biological and psychosocial factors, we expected that the moderator analyses would reveal interactions 298 JORGENSEN, JOHNSON, K.OLODZIEJ, AND SCHREER consistent with biopsychosocial synergism or a somatogenic perspective rather than support the psychogenic paradigm. As a "mediational" model, somatogenic perspectives require (a) identification and assessment of the biological and structural variables accounting for the covariation of a personality factor with BP-EH and (b) the statistical removal of these variables' variance from the correlation of personality variables with EH to assess whether the strength of the correlation substantially drops (see Baron & Kenny, 1986). Regrettably, because there is a paucity of research reporting the relationships among biological variables, morphological variables, personality, and EH, we are unable to address any mediating hypotheses derived from the somatogenic perspectives discussed earlier. Likewise, in terms of a biosynergistic perspective, we are unable to evaluate the notion of bidirectional links due to the paucity of intensive longitudinal studies. Specifically, a biosynergistic examination of bidirectional links requires the repeated assessment of personality, lifestyle, and physiological and morphological variables across the life span (cf, Elias, Elias, & Elias, 1990). Affect Expression and Covert Anger Assessment Procedures Differences in methodology of assessment procedures are thought to contribute to the heterogeneity of published findings on affect expression, anger, and EH (see Diamond, 1982; Ewart, 1991; Harrell, 1980; E. H. Johnson & Spielberger, 1992; and Suls et al., 1995). We therefore developed and coded distinct general categories related to the experience of anger and management of overt behavior. Ewart (1991) pointed out that a major problem with research on the personality correlates of EH relates to an excessive reliance on global-trait, self-report measures that do not capture the behavioral tendencies linked to the suppression of anger within specific social contexts. It is significant that each perspective discussed above (viz., psychogenic, somatogenic, and biopsychosocial synergism) emphasizes the importance of management and expression of strong negative emotions within an interpersonal context. Therefore, one important distinction pertains to the anchoring of responses to a specific context or set of items focusing on interpersonal situations. Examples include the vignettes used by Harburg, Blakelock, and Roeper (1979) to assess anger expression; the Rosenzweig (1978) Picture-Frustration Study, telling stories in response to pictures with interpersonal content (e.g., pictures from the Thematic Apperception Test; McClelland, 1979); and evaluation of assertiveness as assessed from standardized role-play situations (Keane et al., 1982; Morrison et al., 1985). These methods share a common element of people creating a response following consideration of an interpersonal context. We labeled such measures interpersonal analogue assessment. Given that theory specifically links submissive behavior and the suppression of agonistic behavior and strong negative emotions as anger to interpersonal contexts and that greater specificity in the assessment of behavioral tendencies should be more sensitive to associations posited by theory (cf. Ewart, 1991), we predicted that the interpersonal analogue assessment category would show the strongest association and lowest level of heterogeneity of the four categories. A second category is use of self-report measures designed to assess anger management or dominance that do not anchor the items to vignettes, pictures, or role-play contexts of an interpersonal nature. Examples include the Dominance/Submissiveness scale of the 16-PF (Cattell, Eber, & Tatsuoka, 1970), Verbal Hostility scale of the Buss-Durkee Hostility Inventory (BDHI; Buss & Durkee. 1957), the Extrapunitive Hostility scale of the Hostility and Direction of Hostility Questionnaire (HDHQ; Caine, Foulds, & Hope, 1967), and the Anger-Out scale of the Anger Expression Inventory (AX; Spielberger et al., 1985). We labeled such measures "reported overt reactions." We expected a negative association with BP, similar to the interpersonal analogue assessment category. Although such labels as anger-in, suppressed anger, and intropunitive hostility connote an inhibition or suppression of anger, a perusal of item contents and scale descriptions suggests that some scales with these labels primarily assess such covert angry and negative affective reactions as harboring of grudges, irritation, resentment, guilt, and cynicism in lieu of the inhibition of aggressive-angry behavior. Examples include the Anger-In scale of the AX, the Intropunitive Hostility scale of the HDHQ, and the Irritation and Resentment scales of the BDHI. We labeled scales of this type as reported covert anger. Finally, some scales include a combination of ratings of overt angry behavior-anger expression and covert angry reactions; the Suppressed Anger scale used by Cottington, Matthews, Talbott, and Kuller (1986) is an example ("Even after I have expressed my anger, I have trouble forgetting about it"; "When I am angry with someone, I take it out on whoever is around"; and so on). We labeled such measures ambiguous because of the difficulty in specifying whether expression, covert reactions, or both are responsible for obtained associations with BP. We expected a positive association for reported covert anger. Likewise, because high scores from scales classified as ambiguous reflect the covert anger dimension, we thought it likely that this category would also show a positive association with BP. Note that the reported covert anger and ambiguous categories overlap with the negative affectivity category described above. Race In comparison to other groups living in the United States, samples of Black people have consistently shown a disproportionate risk for hypertension and the mortality, morbidity, and sequelae of this disease (Myers & McClure, 1993). Within industrialized nations, Black people are more likely to experience chronic sociocultural stressors (e.g., racism, living in high crime neighborhoods, and lower SES) than White people (Anderson & McNeilly, 1993; Anderson et al., 1989; Dressier, 1993; Myers & McClure, 1993). As discussed by Anderson and McNeilly; Anderson, McNeilly, and Myers (1992); and Anderson et al. (1989), chronic sociocultural stressors are thought to interact with psychological risk factors (e.g., suppressed anger, anxiety, and depression) in the frequent triggering of the physiological stress reactions (e.g., SNS mediated sodium retention and vasoconstriction) thought to contribute to the development of EH (Anderson & McNeilly, 1993; Anderson et al., 1989, 1992; Myers & McClure, 1993). That is, the combination of chronic sociocultural stress and a psychological risk as suppressed anger may induce greater pathophysiologic activity related to EH than either factor alone; this augmentation of a psy- 299 BLOOD PRESSURE AND PERSONALITY chological factor's triggering of pathophysiologic reactions by chronic sociocultural stressors has been termed the stress augmentation hypothesis (Anderson & McNeily, 1993). Because Black people are more likely to experience chronic sociocultural stress and because this stress may augment the association of psychological risk with the actual development of EH, we predict that race (Black vs. White) would moderate the association of BP with anger-affect expression and negativity affectivity. Specifically, we predict that BP would correlate negatively with anger-affect expression and positively with negative affectivity and that because of the augmenting influence of chronic sociocultural stress, these associations would be significantly greater for Black samples than for White samples. Recall that Suls et al. (1995) reported no moderating relations of race on associations of trait anger with BP. However, these researchers used fewer studies to examine race as a moderator and did not use the interpersonal analogue category in their analyses. We therefore also examined if race would interact with the subcategory of interpersonal analogue assessment in the prediction of EH and BP. Awareness of High BP Status The influence of knowledge of EH status on the correlation of high BP with negative affectivity has been termed the labeling effect (Irvine, Garner, Olmsted, & Logan, 1989; MacDonald, Sackett, Haynes, & Taylor, 1984; Sommers-Flanagan & Greenberg, 1989; Suls et al., 1995; Wagner & Strogatz, 1984). For example, Irvine et al. reported that only persons with EH who were aware of their high BP scored significantly higher on measures of neuroticism and negative affectivity than a demographically matched group of persons who are normotensive and a group of persons unaware of their high BP status; persons unaware of their hypertensive status did not differ from a demographically matched group of people who are normotensive on any measures of negative affectivity. Interestingly, among a large community sample of persons who are normotensive, Wagner and Strogatz reported that persons who were either informed by a medical professional that they had high BP or simply believed they had high BP reported more depressive symptoms and poorer health than people who are normotensives who were never labeled, either by themselves or medical personnel, as having high BP. Studies were categorized with respect to study participants being aware or unaware of their BP status. For the associations involving negative affectivity, we predicted that the strongest associations would be obtained for studies of people who are aware of their BP status. In their narrative review, SommersFlanagan and Greenberg (1989) concluded that the labeling effect does not account for associations of BP with anger management and emotional expressive behavior. Likewise, for measures of anger expressiveness, Suls et al. (1995) reported that a selection bias (i.e., persons attending a medical clinic vs. persons selected from a community) did not affect the obtained effect sizes. A number of possible factors might account for why the labeling effect apparently affects more strongly associations involving negative affectivity than those involving anger-affect expression. First, markers of behavioral expression may be less sensitive to sampling biases as measures of neuroticism and negative affectivity. For example, people low in anger expression and assertiveness may be as likely to visit physicians as people high in anger expression and assertiveness. Second, measures of negative affectivity may be more sensitive to drug side effects than measures focusing on anger expression, assertiveness, and dominance. Likewise, measures of negative affectivity may be more reactive to the anxiety and worry associated with knowledge of having a life-threatening disease than measures focusing on the behavioral aspects of anger expression, assertiveness, and emotional expression. It therefore is conceivable that the awareness dimension may serve as a moderator only for the negative affectivity dimension. Exploratory Analyses A number of other person-related factors have been linked to EH. Men are at greater risk for EH than premenopausal women; it has been posited that an apparent attenuation of stressor-induced, physiologic reactivity by female sex hormones may partially account for this gender difference (Saab, 1989). Another factor is the well-documented increase in BP with aging (Mohrman & Heller, 1991). Moreover, the underlying mechanisms contributing to high BP change across the life span (S. Julius, 1992; Mohrman & Heller, 1991). A third factor relates to SES. Specifically, SES has been found to be inversely related to BP levels (Anderson et al., 1989; James, 1987). We thought it likely that sample variations in gender, age, and SES contribute to the heterogeneity of findings reported on the personality correlates of BP. We therefore conducted exploratory analyses to examine whether associations of personality with BP were moderated by these factors that are thought to influence the manifestation of EH. Although the post hoc analyses by Suls et al. (1995) suggest that age and gender do not influence the associations of anger with BP, we thought it likely that our larger database and use of direct tests of interactions would provide more sensitive tests of gender and age. Another possible factor contributing to inconsistent results relates to the adequacy of BP assessment or diagnosis of EH (Sommers-Flanagan & Greenberg, 1989; Suls, etal., 1995). We therefore coded studies regarding the degree of adequacy of BP assessment or diagnosis of hypertensive status. Finally, SBP and DBF may behave differently depending on complex interactions among such factors as environmental stressors (e.g., BP cuff inflation, worry over receiving a diagnosis of EH, or both), arterial hypertrophy, and activity of the autonomic nervous system (cf. Obrist, 1981). Because SBP and DBP readings do not necessarily reflect the same psychophysiologic reaction to BP assessment, we computed effect sizes separately for SBP and DBP when results were presented for both variables. Method Overview We attempted to locate all studies containing trait measures of affect expression, negative affectivity, defensiveness, or a combination of the three. To be included in the meta-analysis, a study had to be a published empirical article written in English and containing sufficient information to allow for estimation of effect sizes (sample sizes, sample descriptions, descriptive statistics, probability values, and inferential statistics). Studies that only contained sampled persons with high BP 300 JORGENSEN, JOHNSON, KOLODZIEJ, AND SCHREER (i.e., associations between BP and personality based on only samples of people with high BP) were excluded from the meta-analysis. Likewise, case studies of individuals with EH were not included in our review (for a review of these studies, see Diamond, 1982). We had to examine resting BP values, diagnostic status (normotension vs. hypertensive status), or both, with reference to at least one of the trait categories. Because our review focused on associations with the diagnosis of EH, casual BP, or both, we did not analyze studies that only presented associations of a trait with stressor-induced pressor reactivity; that is, we excluded cardiovascular reactivity studies if there was insufficient information to determine the association between a marker of personality and a pretask rest period. Our aim was to focus on the theory and research directly relevant to the personality correlates of EH and elevated casual BP. Consequently, Type A behavior was not analyzed because it is viewed as a predictor of coronary heart disease, which is independent of casual BP elevations (Dembroski & Costa, 1987; Rosenman, 1992; Williams & Barefoot, 1988). Furthermore, Type A behavior does not consistently predict coronary heart disease (Dembroski & Costa, 1987; Williams & Barefoot, 1988). As discussed earlier, elevated BP is thought to be associated with the frequent and trans-situational inhibition of emotional expression and covert experience of dysphoric reactions. Consequently, we did not analyze state-related variables (e.g., state anxiety or state hostility responses to psychological stressors) that were designed to assess the affective reactions during the time of assessment. Sample of Studies To obtain a sample of studies, we conducted computer-based information searches using the keywords hypertension, high blood pressure, or elevated blood pressure, combined with personality, psychosocial variable, or any of a number of specific trait terms (e.g., hostility, anger, depression, anxiety, stress, and defensiveness) on the PsycINFO (19671989) and PsycLIT (1990-1995), Medline (1966-1995) databases.4 We also searched through (a) the reference lists of numerous review articles, including Booth-Kewley and Friedman (1987), Diamond (1982), Harrel (1980), and Sommers-Flanagan and Greenberg (1989); (b) the reference lists of all located studies; and (c) Psychological Abstracts (1965-1967), Current List of Medical Literature (1959), and Cumulative Index Medicus (1960-1964; 1965) databases. Only studies that were available by August 1995 were included in the sample. Sample Selection Criteria Criteria for including studies or portions of studies in the sample were that (a) the study was published, (b) participants were human beings, (c) participants' range of BP was not restricted (i.e., the sampling procedures did not exclude people with normotension or with hypertension), and (d) hypertensive-normotensive diagnostic status or casual BP was related to a trait measure. These criteria meant that we excluded studies or portions of studies that (a) used non-trait-like variables (e.g., psychological states such as anxiety); (b) used measures of global Type A as trait predictors (see Overview of the Mela-Analysis above); (c) presented stressor-induced BP reactivity without examining associations of a trait (s) with BPs of a nonstressor, baseline period (e.g., Delehanty, Dimsdale, & Mills, 1991; Lovallo & Pishkin, 1980); and (d) examined only people with hypertension (e.g., Pilowski, Spalding, Shaw, & Korner, 1973; Thailer, Friedman, Harshfield, & Pickering, 1985) or excluded them (e.g., Jorgensen et al., 1992; Wagner & Strogatz, 1984). On the basis of these criteria, 83 studies qualified for the meta-analysis. Variables Coded From Each Study To the extent that each report permitted it, we coded the following theoretical and descriptive information from each study. The theoreti- cal and exploratory dimensions, used for moderator analyses, included (a) type of trait assessed (see below for details), (b) affect expressionanger measurement technique (also described later), (c) race of participant (White, Black, or ambiguous), (d) proportion of men or boys in sample, (e) mean age of sample, ( f ) occupation of participant (student, blue collar, white collar, other-mixed, or unknown), (g) awareness of hypertension, and ( h ) type of BP assessed (SBP, DBF, both, or unclear). For descriptive purposes, we also coded each studie's (a) year of publication, (b) type of population (precollege, college undergraduate, noncollege adult, or other), (c) type of noncollege adult population (inpatient, outpatient, nonpatient, or other), (d) nationality of participant (United States, Canada, Europe, Australia, Asia, or Africa), (e) U.S. region of study (northeast, midwest, southeast, southwest, west, nationwide, or irrelevant), ( f ) presence of potential confounds related to hypertension (age, medication, health-related problems, psychiatric history, or other), (g) type of design (hypertension as a categorical predictor variable, hypertension as a categorical criterion variable, and correlational study in which both predictor and criterion variables are continuous), and (h) degree of study blindness (single-blind experiment, participant not aware of treatment or hypothesis; double-blind experiment, participant and experimenter not aware of treatment or hypothesis; or unknown-ambiguous). The trait measure(s) used in each study were coded as follows: (a) psychometric predictors: anger-affect expression (e.g., anger-in-out, assertiveness, expressed-suppressed anger, social competence, or submissiveness), negative affect (e.g., feelings of anxiety-tension, anger-hostility, depression, or neuroticism), defensiveness (e.g., defensiveness, denial, repressive coping, other, or ambiguous); (b) affect expression-anger measurement technique: interpersonal analogue assessment (including role-playing, projective tests, interviews, etc.); reported overt reactions (including self-report measures of anger, assertion, or dominance); covert anger (including self-ratings of the covert experience of angry affect); and ambiguous (a combination of the reported overt reactions and covert anger reactions dimensions); (c) type of trait measurement (standardized or custom made for study); (d) trait measurement techniques (self-report ratings, interview, projective tests, a combination of two or more, or other); (e) trait measure reliability (coefficient alpha, split-half reliability, interrater reliability, test-retest correlation, or none reported); and ( f ) presence of potential confounds related to trait measures (medication specified, health-related problems, psychiatric history, other, or unknown). We used five dimensions to code adeqacy of BP assessment. The superior dimension corresponds to use of two casual readings or more (following 3 min or more of rest) obtained on at least 2 separate days plus a medical diagnosis (e.g., Steptoe, Melville, & Ross, 1984). Good corresponded to a medical diagnosis of hypertension based on two visits with a physician or more (e.g., Esler et al., 1977) or to two BP determinations or more obtained on 2 days or more (e.g., Drummond, 1982). In the case of studies with only one assessment session, a study was labeled as marginal if two readings of BP or more were obtained following 2 min or more of rest (e.g., Melamed, 1987; Siegel & Leitch, 1981) or during a rest period of 5 min or more (e.g., Waal-Manning, Knight, Spears, & Paulin, 1986). The insufficient information code reflects the ambiguous presentation of assessment methods (e.g., time intervals between BP readings or amount of time before the readings are clearly 4 We used these search terms because they reflect common terms in this literature. To assuage readers who may conclude that we underrepresented the big five personality variables (e.g., McCrae & Costa, 1986) in our sample, we also specifically searched for BP or hypertension studies that included the term big five in their title or abstract. Although the PsycLIT database yielded 130 instances of big five for the period of January 1990-September 1995. none of these studies included bloodpressure or hypertension in their titles or abstracts. BLOOD PRESSURE AND PERSONALITY specified; Insel, Fraser, Phillips, & Williams, 1981). Finally, a study was labeled as inadequate when neither causal BP readings nor medical diagnoses were used to determine the BP status of participants who are normotensives (e.g., van der Ploeg, van Bluuren, & van Brummelen, 1985) or when only the first reading of an unspecified time of sitting was used as the BP measure (Monk, 1980). As detailed below, adequacy ratings were used to categorize effect sizes in terms of high-quality BP assessment (studies judged as good or superior) and lower quality BP assessment (studies judged as marginal, insufficient information, or inadequate). The following characteristics were coded about each study's participant sample: (a) time with hypertension (<5 years, 5-15 years, >15 years, unknown, or irrelevant); (b) family history of hypertension (no, yes, or unknown); (c) participants' awareness of BP levels (aware, unaware, or unknown); (d) severity of hypertension based on World Health Organization (1989) criteria, using DBF ("normal" <90 mm Hg, mild 90-104 mm Hg, moderate 105- 114mm Hg, severe > 115 mm Hg); (e) severity of hypertension based on SBP (normal < 140 mm Hg, mild 140-159 mm Hg, moderate 160-179 mm Hg, severe >180 mm Hg); and ( f ) whether a measure of life event stress was included in the study (occupational stress, neighborhood or environmental stress, or family stress). Two of the authors independently coded these characteristics with a mean agreement of 99.35%; discrepancies were resolved through discussion. Computation and Analysis of Effect Sizes The effect size calculated is g, the difference between the means of the higher and lower BP groups divided by the pooled standard deviation (SD: see Hedges & Olkin, 1985; and B. T. Johnson, 1989). Therefore, effect sizes with positive signs indicate that higher levels of BP were associated with higher amounts of the trait dimension in question. Reports of correlations were transformed into the g value. To reduce computational error, at least two of us calculated these effect sizes separately using a computer program (B. T. Johnson, 1989) and met to resolve discrepancies. Multiple effect sizes from single studies. Nearly every study permitted the computation of more than one comparison of the traits of individuals with higher versus lower BP. Specifically, if the report contained sufficient information, then we calculated effect sizes separately for the (a) three relevant trait dimensions; (b) different groups of participants (e.g., races, men or women, occupations, and awareness of BP), and (c) type of BP assessed (e.g., systolic vs. diastolic). When a study had more than one assessment of the same measurement dimension (e.g., two measures of defensiveness), we calculated effect sizes for each of these measures and combined effect sizes over those measures, using Rosenthai and Rubin's (1986) strategy that adjusts the mean effect size for the correlation of the trait measures. When the correlation was unknown, we estimated it based on the average correlation of trait measures obtained in the sample (r = .35). However, when a study included more than one measure of a trait dimension and one of the measures was atypical of the literature (e.g., Keane et al.'s, 1982, positive assertion measure), we omitted these atypical dimensions. Our strategy of using different trait measures available for individual samples of participants (e.g., both negative affectivity and defensiveness traits may have occurred in a given study) meant that we often calculated more than one effect size for a particular sample of participants, implying that some of our analyses were based on somewhat nonindependent observations. However, the questions we desired to answer necessitated partitioning the data into these ways. On the basis of these rules, 26 studies yielded 1 effect size, 24 studies yielded 2, 6 yielded 3, 14 yielded 4, 1 yielded 5,2 yielded 6, 3 yielded 8, 1 yielded 10,2 yielded 12, 3 yielded 16, and 1 yielded 24; thus, 83 studies yielded 295 effect 301 Analysis of effect sizes. Our analysis of effect sizes implemented the techniques presented by Hedges and Olkin (1985; see B. T. Johnson, 1989). The gs were converted to rfs by correcting them for bias (i.e., g's overestimate of the population effect size, which occurs especially in small samples). To obtain an overall estimate of the extent to which hypertensive and normotensive groups differed on the various trait measures in the available research, we then combined the study outcomes by averaging the d values. To determine whether the ds shared a common effect size (i.e., consistent across the studies), we calculated a homogeneity statistic, Q, which has an approximate x 2 distribution with k - 1 degrees of freedom (rf/), where k is the number of effect sizes. We accounted for variability in heterogeneous effect sizes by relating them to the attributes of the studies. To determine the relation between these study characteristics and the magnitude of the effect sizes, we tested both categorical and continuous models (Hedges & Olkin, 1985). Categorical models, which are analogous to analyses of variance (ANOVAs), may show that heterogeneous effect sizes are homogeneous within the subgroups established by dividing studies into classes based on study characteristics. The techniques for calculating categorical models provide a between-classes effect (analogous to a main effect in an ANOVA) and a test of the homogeneity of the effect sizes within each class. The between-classes effect is estimated by QB, which has an approximate x 2 distribution with p - 1 df, where p is the number of classes. The homogeneity of the effect sizes within each class is estimated by £)w, which has an approximate x 2 distribution with m - 1 df, where m is the number of effect sizes in the class. The continuous models are least-squares, simple linear regressions, calculated with each effect size weighted by the reciprocal of its variance. Each such model yields a test of the significance of a predictor as well as a test of model specification, which evaluates whether significant systematic variation remains unexplained in the regression model (Hedges & Olkin, 1985). As a supplementary analysis, we attained homogeneity by identifying outliers among the effect sizes and sequentially removed those that reduced the homogeneity statistic by the largest amount (cf. Hedges, 1987). Inspection of the percentage of effect sizes removed to attain homogeneity allows one to determine whether the effect sizes are homogeneous, aside from the presence of relatively few aberrant values. Under such circumstances, the mean attained after removal of such outliers may better represent the distribution of effect sizes than the mean based on all of the effect sizes. Results Characteristics of Studies Each study's effect sizes and important coded characteristics appear in Table 1. As is shown by the central tendencies of the variables listed in Table 2, most studies (a) were published about 10 to 12 years ago, (b) tested noncollege, nonpatient adults as participants, (c) who resided in the United States, (d) usually in the northeast or southeast (rather than southwest or west). The participants in these studies tended (e) to be adults somewhat younger than middle age, (f) White, (g) men, (h) and not students or blue- or white-collar workers (instead, studies tended to draw on populations of unknown or mixed occupations). The participants (i) tended to be aware of their BP status (although many studies provided too little information to determine this feature); (j) usually had DBF and SBP of unknown or mixed levels; and (k) when BP levels were known, participants in the hypertensives group tended to fall into the (text continues on page 306) 302 JORGENSEN, JOHNSON, KOLODZIEJ. AND SCHREER Table 1 Study Effect Sizes and Moderator Information Participant characteristics Study Adams etal. (1986) Adams etal. ( 1987) Baer etal. (1979) Bergland etal. (1975) Boutelle etal. (1987) Brunswick & Collette (1977) Buck &Stenn( 1979) Bulpitt etal. (1976) Burakovskaya(1984) Burke etal. (1992) Cochrane(1973) Cottington etal. (1985) d -0.14 -0.20 0.20 -0.14 0.00 0.16 -0.10 0.32a -0.22 -0.20 0.10 -0.26 0.24 -0.22 -0.08 0.04 0.58a 0.16 -0.41" 0.28 0.55a -0.25 0.16 0.29 0.09 0.00 0.20 -0.03 0.46a 0.22a 0.67a 0.05 0.03 0.17 0.08 0.04 0.01 0.10 0.05 0.08 0.03 0.19 0.11 -0.07 -0.08 0.10 0.04 0.02 0.02 0.12 0.04 0.07 -0.00 0.18 0.08 -0.17 0.00 0.12 0.06 0.45a -0.05 0.06 -0.02 Trait category Neg Neg Neg Neg Neg Neg Aff Aff Neg Neg Aff Aff Neg Neg Aff Aff Neg Neg Aff Aff Neg Aff Neg Neg Aff Def Neg Aff Neg Neg Neg Neg Neg Neg Neg Aff Aff Aff Aff Neg Neg Neg Neg Neg Neg Neg Neg Aff Aff Aff Aff Neg Neg Neg Neg Neg Neg Aff Aff Aff Neg Neg Aff Anger measurement technique Cov Cov Cov Cov NA Rep Cov Rep NA Rep Cov Rep NA Rep Cov Rep NA Rep Cov Rep NA Rep Amb NA Rep NA NA Int NA NA NA NA NA NA NA Int Int Int Int Cov Cov Cov Cov NA NA NA NA Int Int Int Int Cov Cov Cov Cov NA Cov Rep Amb Amb NA NA Amb Age (in years) 18.10 17.90 18.10 17.90 18.40 18.40 18.40 18.40 18.40 18.40 18.40 18.40 18.50 18.50 18.50 18.50 18.50 18.50 18.50 18.50 43.85 50.00 50.00 47.25 47.25 47.25 14.34 15.07 43.40 45.21 14.60 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 71.10 52.60 52.60 52.60 44.00 44.00 44.00 44.00 44.00 Race B B B B B B B B B B B B B B B B B B B B W W W W W W B Amb Amb Amb W W W W W W W W W W W W W W W W W W W W W W W W W Amb Amb Amb W W W W W Proportion men or boys 1.00 0.00 1.00 0.00 1.00 1.00 .00 .00 .00 .00 .00 .00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.50 1.00 1.00 0.50 0.50 0.50 0.50 0.59 1.00 0.00 1.00 0.00 1.00 0.00 1.00 0.00 1.00 0.00 1.00 0.00 1.00 0.00 1.00 0.00 1.00 0.00 1.00 0.00 1.00 0.00 1.00 0.00 1.00 0.00 .00 .00 .00 .00 .00 .00 .00 .00 0.00 Occupation s s s s s s s s s s s s s s s s s s s s o u u u u u u s u u s 0 o o o 0 o o o 0 o o o o o o o o o 0 0 o o 0 o u u u o 0 o o o BP awareness U u u u u u u u u u u u u u u u u u u u A A A A A A U A A A A U U A A A A A A U U A A U U A A A A A A U U A A A A A Una Una ' Una Una Una Type ofBP assessed SBP SBP DBF DBF SBP SBP SBP SBP DBP DBP DBP DBP SBP SBP SBP SBP DBP DBP DBP DBP Unc Unc Unc Unc Unc Unc DBP SBP Unc Unc SBP SBP SBP SBP SBP SBP SBP SBP SBP SBP SBP SBP SBP DBP DBP DBP DBP DBP DBP DBP DBP DBP DBP DBP DBP DBP DBP DBP SBP DBP SBP DBP SBP BLOOD PRESSURE AND PERSONALITY 303 Table 1 (continued) Participant characteristics Study Cottingtonetal. (1985) (continued) Cottingtonetal. (1986) Cumes-Rayner & Price (1989) Davies(1970) Dembrowski et al. (1989) Dimsdaleetal.(1986) Drummond(1982) Dureletal.(1989) Esleretal.(1977) Francis etal. (1989) Friedman & Bennett (1977) Diastolic BP > 100 mm Hg Diastolic BP > 90 mm Hg Goldstein etal. (1988) Hafner& Miller (1991) Handkins & Munz (1978) Harburg etal. (1979) Harburg etal. (1964) Haynes etal. (1978) d Trait category Anger measurement technique 0.36" 0.11 0.06 0.07 1.07" -0.75" 0.00 0.07 -0.46 -0.45 -0.17 -0.06 0.21 0.41 0.99a 0.69a 0.42 0.71a 0.60 0.65" -0.52a -0.29 -0.87a -0.53 0.21 0.18 0.34" 0.20 Aff Neg Neg Amb Aff Amb NA 0.07 0.04 -0.85 -0.68 0.43 0.22 0.76a 0.24 0.57a 0.97a -0.66 -0.09 -0.09 -0.18 0.09 0.57 0.80" -0.34a -0.38" 0.07 -0.04 -0.09 -0.21a 0.11 0.13 0.11" -0.06 0.02 0.1 2a -0.08 0.00 0.06 -0.08 Def Neg Def Aff Aff Aff Aff Aff Neg Def Neg Neg Neg Neg Neg Neg Neg Neg Aff Aff NA NA NA NA Int Int Int Int Int NA NA Cov Cov Cov Cov Cov Cov Cov Cov Int Rep Neg Neg Cov Cov Aff Aff Amb Amb Neg Neg NA NA Amb Amb Aff Aff Aff Aff Rep Cov Neg NA Aff Aff Rep Cov Neg NA Aff Aff Aff Aff Aff Aff Neg Aff Aff Aff Aff Aff Aff Aff Aff Int Neg NA Aff Aff Neg Aff Aff Neg Aff Rep Cov Int Int Int Int Rep NA Rep Rep Rep Rep Rep Rep Rep Rep NA Rep Cov NA Rep Age (in years) Race 44.00 44.00 44.00 52.50 29.30 49.80 49.80 46.00 40.00 40.00 40.00 40.00 24.00 24.00 34.50 34.50 34.50 34.50 34.50 34.50 34.50 34.50 26.50 26.50 26.50 26.50 29.65 29.65 W W 46.00 46.00 50.16 50.16 51.35 51.35 51.35 50.60 50.60 50.60 43.00 36.67 36.67 36.67 36.67 21.30 21.30 55.00 55.00 23.50 23.50 55.00 55.00 23.50 23.50 57.50 57.70 57.70 57.70 57.70 57.70 58.18 58.18 W W W Amb Amb Amb Amb W B W B W W B B B B W W W W Amb Amb Amb Amb Amb Amb W Amb Amb Amb Amb Amb Amb Amb Amb W Amb Amb B W W W B B B B W W W W Amb Amb Amb Amb Amb Amb Amb Amb Proportion men or boys Occupation BP awareness 0.00 0.00 .00 1.00 1 .00 .00 .00 .00 1.00 1.00 0.00 0.00 .00 1.00 0.00 0.00 .00 .00 0.00 0.00 .00 .00 .00 .00 1.00 .00 0.49 0.49 O O O BC S BC BC O O O O O U U U U U U U U U U U U U U O O Una Una Una U U U 1.00 .00 0.47 0.47 .00 .00 .00 0.00 0.00 0.00 .00 .00 0.00 0.65 0.58 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 0.00 0.00 U U U U BC BC BC BC BC BC O O O O O S S 0 O O O O O O O O O O O O O O O A A A A A A A U A A A U U A A A A U U U U U U U U U U U U U U U U U U U U U U DBF SBP DBF DBF Unc - U Una Una Una Una A A U U U U U U U U A Type ofBP assessed DBF DBF DBF SBP SBP SBP SBP SBP SBP SBP DBF SBP DBF SBP DBF SBP DBF Unc Unc Unc Unc SBP DBF DBF DBF SBP DBF Unc Unc Unc Unc Unc Unc Unc DBF DBF DBF DBF SBP SBP SBP DBF SBP DBF SBP DBF SBP DBF SBP SBP SBP Unc Unc Unc DBF DBF (table continues) 304 JORGENSEN, JOHNSON, KOLODZIEJ, AND SCHREER Table 1 (continued) Participant characteristics Study Haynesetal. (1978) (continued) Heine & Sainsbury ( 1 970) Inseletal.(1981) Irvine etal. (1989) James etal. (1984) Jern(1982) E H. Johnson, Schork et al. (1987) E H. Johnson, Spielberger et al. (1987) M.Julius etal. (1986) Kalis, etal. (1957) S. M.Kaplan etal. (1961) Keane etal. (1982) d -0.02 0.13" -0.04 0.18" 0.37 -0.13 -0.36 I.64 a 0.93" 0.06 -0.1 7a -0.20a 0.07 0.66a 0.00 0.32a 0.14 0.15 0.00 0.02 -0.03 0.02 -0.49 0.89a 0.87a 0.01 -0.14 -0.49a -0.41s 0.32" -0.04 -0.54a -0.34" 0.32a -0.32" -0.63a -0.24a -0.07 -0.08 -0.22a -0.02 -0.12 0.04 -0.67a -0.10 0.47a 0.30a -0.54a -0.26" 0.30a -0.14 -0.87a -0.28a 0.65a 0.08 -0.493 0.16 0.45a 0.00 0.54 1.03a -1.45a Trait category Anger measurement technique Aff Neg Aff Aff Rep NA Neg Neg Neg NA NA NA NA NA Rep Neg Neg Aff Aff Neg Neg Neg Aff Aff Aff Neg Aff Aff Aff Neg Neg Neg Neg Aff Neg Aff Aff Aff Neg Aff Aff Aff Neg Aff Aff Aff Neg Aff Aff Aff Neg Aff Aff Aff Neg Aff Aff Aff Neg Aff Aff Aff Neg Aff Aff Aff Aff Aff Neg Aff Rep Rep Rep NA NA NA Rep Cov Amb NA Rep Cov Amb NA NA Amb Cov Rep NA Int Rep Cov NA Int Rep Cov NA Int Rep Int NA Int Rep Int NA Int Rep Cov NA Int Rep Cov NA In' Rep Cov NA Int Rep Cov Rep Int NA Int Age (in years) Race Proportion men or boys 58.18 58.18 58.18 58.18 54.09 54.09 54.09 54.09 54.09 13.00 13.00 13.00 13.00 46.20 46.20 46.20 46.20 46.10 46.10 46.10 46.10 38.50 38.50 26.64 26.64 26.64 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 16.00 45.00 25.00 45.30 47.36 Amb Amb Amb Amb W W W W W W W W W Amb Amb Amb Amb Amb Amb Amb Amb B B W W W B B B B B B B B W W W W W W W W B B B B B B B B W W W W W W W W W Amb Amb Amb 0.00 0.00 0.00 0.00 0.38 .00 .00 0.00 0.00 0.47 0.47 0.41 0.41 0.75 0.75 0.75 0.75 0.89 0.89 0.89 0.89 .00 .00 .00 .00 .00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 0.00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 .00 0.46 0.00 0.50 .00 Occupation O O O O U U U U U S S S S O O O O O O O O BC BC O O 0 S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S S O O BC O BP awareness U U U Type ofBP assessed Una DBP DBP DBP DBP DBP SBP DBP SBP DBP DBP SBP SBP DBP DBP DBP DBP DBP DBP DBP DBP DBP SBP DBP Unc Unc Unc SBP SBP Una SBP Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una Una U SBP DBP DBP DBP DBP SBP SBP SBP SBP DBP DBP DBP DBP SBP SBP SBP SBP DBP DBP DBP DBP SBP SBP SBP SBP DBP DBP DBP DBP Both Both Unc Unc U U U U U U U U U U A A A A Una Una Una Una U U U U U Una A A A BLOOD PRESSURE AND PERSONALITY 305 Table 1 (continued) Participant characteristics Study Kidson(1973) King etal. (1990) Kronetal. (1980) Lazaro etal. (1993) Linden & Feuerstein (1983) Unmedicated Medicated Unmedicated participants Medicated participants Lyketsos etal. (1982) Mann (1977) McClelland (1979) Sample 1 Sample 2 Sample 3 Melamed(1987) Meyer etal. (1978) C.L. Miller etal. (1979) Monk (1980) Morrison etal. (1985) Myers & Miles (1981) Netter(1983) Netter & NeuhauserMetternich(1991) Ostfeld & Lebovits ( 1 959) Osti etal. (1980) Pagotto etal. (1992) Perini etal. (1990) Perini etal. (1994) Rabkin etal. (1983) Robbins etal. (1990) Trait category d a Anger measurement technique 0.90 1.34a 0.33 0.82" 0.18 0.93" 0.50 -0.10 0.46 0.51 0.62" Neg Neg Def Def Def Def Def Aff Aff Aff Neg NA NA NA NA NA NA NA -0.95" -0.18 0.95a 0.18 0.67a 1.12" -0.48" -0.23 Neg Neg Def Def Aff Neg Aff Aff NA NA NA NA Amb NA -0.46" Aff -0.14 Aff Aff -0.33 a -0.94 Aff -0.72 Aff Aff -0.83 0.22 Neg 0.08 Neg 0.28 Neg 0.10 Neg -0.26a Neg a 0.55 Aff 0.30 Aff a 0.55 Neg 0.05 Neg -0.1 3a Neg -0.14 Aff a -0.82 Aff 0.46 Neg 0.49 Neg 0.40 Def a -0.5 l Aff -0.32 Aff -0.19 Neg 0.13 Def a 0.87 Neg 0.81a Def 0.60 Neg a -0.71 Aff Aff -0.61" -0.61" • Neg Aff -0.28 -0.16 Neg 0.32 Neg 0.74a Def 0.26 Neg -0.25 Neg -0.09 Neg -0.16 Neg 0.09 Neg -0.19 Neg Int Rep Cov NA Cov Amb Int Int Int Int Int Int NA NA NA NA NA Rep Rep NA NA NA Int Rep NA NA NA Rep Rep NA NA NA NA NA Int Rep NA Cov Cov NA NA NA NA NA NA NA NA Age (in years) Race Proportion men or boys 44.38 44.38 44.38 49.00 49.00 47.00 47.00 12.00 50.64 50.64 50.64 W W W Amb Amb Amb Amb Amb Amb Amb Amb .00 .00 .00 .00 .00 .00 .00 — 0.43 0.43 0.43 0 O O 42.14 45.38 42.14 45.38 36.89 36.89 44.67 44.67 Amb Amb Amb Amb Amb Amb Amb Amb 1.00 1.00 1.00 1.00 0.34 0.34 — — u u u u u u 45.00 19.00 19.00 52.00 52.00 52.00 49.67 30.00 49.67 30.00 39.90 41.28 41.28 41.28 41.28 54.50 33.94 33.94 35.20 36.72 36.72 41.00 41.00 39.00 39.00 44.50 44.50 44.00 21.33 21.33 21.33 46.83 46.83 46.83 46.83 38.88 38.88 53.13 31.06 53.13 31.06 Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb B Amb Amb Amb Amb B B Amb Amb Amb W W W Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb .00 .00 .00 .00 .00 .00 .00 .00 0.00 0.00 0.36 0.00 1.00 0.00 1.00 0.07 1.00 1.00 0.39 — — 1.00 0.00 0.11 0.11 0.55 0.55 0.65 0.63 0.63 0.63 0.85 0.85 0.85 0.85 0.00 1.00 0.52 0.53 0.52 0.53 Occupation BP awareness A Type ofBP assessed we we we we A A U U U U S O O O A A A Both Both Both SBP SBP SBP DBP SBP Both Both Both A A A A A A A A Unc Unc Unc Unc Unc Unc DBP DBP O 0 O S S O O 0 O O O 0 BC O 0 O O u u u BC u u u u BC BC O O U u u u O 0 0 O u u 0 O 0 O U A Unc U SBP U DBP A SBP A DBP A Unc A SBP A SBP A SBP A SBP A Unc A Unc A Unc A Unc A Unc Una Unc A Unc A Unc A Unc A Unc A Unc A Unc A Unc A Unc A Unc A Unc A Unc A Both A Unc A Unc A Unc A Both A Both A Both A Both A Unc A Unc A SBP A SBP A DBP A DBP (table continues) 306 JORGENSEN, JOHNSON. KOLODZIEJ, AND SCHREER Table 1 (continued) Participant characteristics Study Robinson (1962) Roter&Ewart(1992) Safaretal. (1978) Sainsbury(1964) Santonastaso et al. ( 1 984) Schalling & Svensson ( 1 984) Siege! &Leitch( 1981) Sparacino et al. (1982) Steptoeetal. (1984) Sullivan et al. (1981) Theorell et al. (1986) van derPloegetal. (1985) Vlachakis, DeGuia et al. ( 1 974) Vlachakis, Schiari et al. ( 1 974) Waal-Manning et al. ( 1 986) Warrenburg et al. (1989) Wennerholm & Zarle ( 1 976) Wheatley et al. (1975) Wood etal. (1979) YePanin & Sokolov ( 1 980) d 0.79° -0.56a 0.00 0.88a 0.24 -0.45" 0.08 0.22 -0.95" 1.01" -0.07 -0.49" 0.61a 0.49 0.57 0.03 0.12 0.52 -0.36 -0.69 0.99a 0.43a 0.29 0.04 0.06 -0.09 0.35 0.06 -0.37a -0.07 0.04 -0.32a -0.17" 0.10 -0.39a -0.11 0.22a -0.22a 0.07 0.00 0.00 0.86° 0.00 0.37 0.66a 0.15 0.09 1.18" 1.32" Trait category Neg Aff Neg Neg Neg Anger measurement technique Neg Neg NA Int NA NA NA NA NA Aff Aff Amb Rep Neg Def NA NA Aff Int Cov Neg Neg Neg Neg Neg Aff NA NA NA NA Amb Neg Aff Neg Aff NA Int NA Neg Neg Neg Neg NA NA NA NA NA NA Neg Neg Aff Aff Rep Rep Neg Cov NA Aff Aff Rep Cov Neg Aff Aff Neg Aff Aff Neg Neg NA Def Def Neg Def Neg Neg Neg Neg Rep Cov NA Rep Cov NA NA NA NA NA NA NA NA NA NA Age (in years) 45.50 59.39 59.39 36.99 39.50 34.67 40.67 18.00 18.00 18.00 18.00 15.43 15.43 40.47 40.47 40.47 40.47 42.55 42.55 36.43 36.43 28.00 49.90 49.90 43.31 38.43 38.43 40.26 40.26 40.26 40.26 40.26 40.26 40.94 40.94 40.94 40.94 40.94 40.94 57.17 57.17 57.17 57.17 40.49 40.49 55.88 54.07 26.57 44.50 Race Amb Amb Amb Amb Amb Amb Amb W W W W Amb Amb W W W W Amb Amb Amb Amb Amb W W Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Amb Proportion men or boys 0.49 — — 1.00 — 0.59 0.49 1.00 .00 1.00 1.00 — — 1.00 1.00 0.00 0.00 1.00 1.00 0.54 0.54 1.00 1.00 0.00 0.63 1.00 0.00 1.00 1.00 1.00 1.00 1.00 1.00 0.00 0.00 0.00 0.00 0.00 0.00 .00 .00 .00 .00 .00 .00 — 0.58 0.50 1.00 Occupation BC 0 0 u o 0 0 o o o 0 s s s s ' S s BC BC U u u u u u u u u u u u u u u u u u u u u u u u o 0 o 0 0 o BP awareness A A A A A Una A A A A A U U U u u u Una Una A A U A A A A A U U U U U U U U u u u u u u u u A A A A A U Type ofBP assessed DBP Unc Unc DBP Unc Unc Unc Unc Unc Unc Unc Unc Unc DBP SBP DBP SBP Unc Unc Unc Unc SBP Unc Unc Unc Unc Unc SBP SBP SBP DBP DBP DBP SBP SBP SBP DBP DBP DBP SBP DBP SBP DBP Unc Unc Unc Unc Unc Unc Note. Effect sizes are positive when participants with higher blood pressure had more of the trait dimension than did participants with lower blood pressure. A = aware; Aff = affect expression; Amb = ambiguous; B = Black; BC = blue collar; BP = blood pressure; Both = DBP + SBP; Cov = covert anger; DBP = diastolic; Def = defensiveness; Int = interpersonal analogue; Neg = negative affect; O = other; Rep = reported overt; S = student; SBP = systolic, U = unknown; Una = unaware; Unc = unclear; W = white; WC = white collar. a Differs significantly (p < .05 or smaller) from 0.00 (exactly no difference). mild hypertension category.5 (1) There were some, although a minority, of studies in which BP levels were confounded with either the ages of the hypertensive and normotensive categories (i.e., groups differed in mean age) or with the fact that people with hypertension were medicated (i.e., associations of personality markers with BP levels might be due to medication side effects), (m) The BP assessment technique tended to be mar- ginal. ( n ) The studies usually used hypertension or BP as a predictor variable, usually comparing people known to have hypertension with people known to not have hypertension, although many studies treated both BP and traits as continuous mea5 Thus, BP levels suffered from restriction of range in many of the studies in the literature, which served to truncate observed relationships. BLOOD PRESSURE AND PERSONALITY sures. Finally, (o) the studies were usually only single blind. These patterns generally held up within the category of the type of trait assessed, with the following exceptions: (a) Negative affectivity and defensiveness have been less frequently examined in Black samples than in White samples; (b) defensiveness has been examined with regard to white-collar occupations but neither affect expression nor negative affectivity have, and (c) defensiveness has probably never been examined in participants who were unaware of their BP levels (whereas it has been studied for the other two trait types). Across the 295 effect sizes in the sample (with a total of 25,469 independent participants), BP was unrelated to personality (d + = — 0.01), and there was considerable variation around the mean weighted effect size, as shown in the significant homogeneity test, 0(294) = 1,726.38, p < .0001. Thus, as expected, study findings in this literature conflicted greatly. Theoretical Moderators of Trait-Hypertension Relations To test our hypothesis that BP would be positively related to negative affectivity and defensiveness but negatively related to affect expression, we fit a model for type of trait to the effect sizes. This model showed that BP-trait associations did depend on the trait under consideration, QB(2) = 162.22, p< .0001. As Table 3 shows, the prediction was confirmed: Individuals with higher BP tended to have lower affect expression but higher negative affectivity and defensiveness than those with lower BP. The mean effect sizes for these three classes differed significantly from each other (ps < .001, for contrasts). The homogeneity tests within each of these classes were significant, and, consistent with these tests, relatively large numbers of outliers needed to be removed (ranging from 11% to 40%) to achieve homogeneity. Thus, overall, this model is not correctly specified: The mean differences between the classes' means should only be considered as general trends among the studies (as is the case for each of the reported moderator analyses in this article). To test our hypothesis that awareness of hypertensive status also would moderate BP-trait relations, we fit several models using awareness as a moderator. As the first column in Table 4 shows, there was a general trend for BP levels to relate positively to the traits when participants were aware as opposed to unaware of their BP levels, QB(2) = 82.02, p < .0001. When they were aware, participants with higher BP were significantly higher on the traits than those with lower BP, but when they were unaware, this relationship reversed (p < .0001, for contrast). To examine whether these general patterns were also present for each type of personality trait, we used awareness as a moderator within the trait classes and type of trait as a moderator within levels of awareness. These analyses determined that awareness was a significant predictor of study outcomes for both affect expression and negative affectivity but not for the defensiveness category, which contained no studies with participants who were known to be unaware of their BP levels. As Table 4's column for the affect expression studies shows, those with higher BP were lower on affect expression than those with lower BP, whether they were aware or unaware of their BP levels. However, as Table 4's column for the negative affectivity trait studies shows, when participants were aware of their status, those with higher BP exhibited significantly more negative affectivity than 307 did those with lower BP, but when they were unaware of their hypertensive status, they exhibited significantly less negative affectivity than those with lower BP (p < .0001, for contrast). Finally, as the model tests in Table 4 for type of trait show, type of trait remained a significant predictor of the BP-trait association when the studies' participants were aware and when it was unknown whether participants were aware of their BP, but type of trait did not moderate associations when participants were unaware of BP levels. We next examined our hypothesis that the technique of assessing affect expression and trait anger moderates associations of BP with these traits. For the 165 effect sizes for which we could code this moderator (including all affect expression cases and several negative affectivity cases), it proved a strongly significant moderator of effect sizes, £> B (3) = 295.01, p < .0001. As the first column in Table 5 shows, when the studies' researchers assessed affect and anger expression with measures of interpersonal analogue assessment or reported overt reactions, those with higher BP tended to exhibit significantly less anger and affect expression than those with lower BP. In fact, this pattern was significantly stronger on the interpersonal analogue assessment measures than on the reported overt reactions measures (p < .001, for contrast). In comparison, when the studies' researchers assessed anger using self-report measures that best measure the covert experience of angry affect (or ambiguous dimensions of anger), those with higher BP reported significantly more anger than did those with lower BP. The means for each of the four classes differed from each other (contrast ps < .001). Finally, to show that these patterns were not dependent on the quality of BP assessment, we fit models for measurement technique within studies that had what we judged good or superior measures of BP and within studies that had what we judged marginal, insufficient information, or inadequate measures of BP. As the second and third columns of Table 5 show, measurement technique remained a significant predictor of BP-trait associations in both high- and lower quality BP assessment classes. Moreover, each model produced the same pattern, whereby the interpersonal analogue and reported overt techniques produced negative associations and the covert anger and ambiguous techniques produced positive associations. As shown in Table 6, the overall test of race was statistically significant (p < .01) for the combination of negative affectivity and anger-affect expression effect sizes. Although the test for the Black-White comparison is significant for negative affectivity, this result is difficult to interpret. First, the largest positive significant effect size was obtained for the ambiguous category; second, whereas the positive effect size for White samples is significant, the somewhat larger, positive effect size for Black samples is nonsignificant, which is a likely reflection of the larger number of effect sizes associated with the White category. As shown in Table 6, the overall comparison for the three categories is significant for anger-affect expression. Consistent with the augmentation hypothesis, for studies that assessed angeraffect expression using the interpersonal analogue assessment, those testing Black participants produced a stronger and more negative, d+ = -0.51, mean effect than did studies testing White participants, d+ = -0.37), (?„( 1) = 5.94, p < .05. Likewise, for the reported overt anger subcategory, those testing Black participants produced a stronger and more negative, d+ = -0.13, mean effect than did studies testing White participants, 308 JORGENSEN, JOHNSON, KOLODZIEJ, AND SCHREER Table 2 Characteristics of Study Effect Sizes Overall and Divided for Type of Trait Type of trait assessed Characteristic (and class) Overall" Affect expression6 Negative affectc Defensivenessd Publication and sample characteristics M year of publication Education level Precollege College undergraduate Noncollege adult Other Noncollege adult status Inpatient Outpatient Nonpatient Other Nationality United States Canada Europe Australia Asia U.S. region Northeast Midwest Southeast Southwest West Nationwide Not in the United States Mage Race White Black Ambiguous M proportion of men Occupation Student Blue collar White collar Other-mixed Unknown Years with hypertension <5 5 to 15 >15 Unknown or not relevant Family history of hypertension Yes No Unknown Awareness of hypertension Aware Unaware Unknown DBF level Normal Mild Moderate Severe Unknown or mixed SBP level Normal Mild Moderate Severe Unknown or mixed 1984.17 1985.20 1983.34 1983.16 45 29 13 62 30 14 18 76 34 2 2 10 5 1 19 8 28 38 68 33 148 69 10 51 84 150 41 73 177 89 13 50 48 7 77 18 2 161 39.14 103 53 139 70 19 11 3 0 1 2 0 2 5 0 9 7 1 47 36.55 69 41.17 55 25 62 44 27 63 .64 4 36 8 18 3 29 0 6 1 47 5 10 2 5 40 11 21 5 9 78 4 30 25 16 20 2 7 1 4 .63 40 6 42.90 4 1 14 .61 29 11 .89 1 2 5 2 4 117 78 62 50 5 24 47 7 10 4 4 2 1 7 1 3 2 130 0 2 16 2 2 275 0 129 4 82 209 0 40 98 40 2 100 15 123 52 44 36 54 68 16 58 11 0 8 120 35 112 11 8 129 38 78 43 6 130 16 18 1 37 1 2 78 70 7 5 15 28 10 0 81 6 41 17 45 30 6 44 3 0 10 6 5 3 0 5 309 BLOOD PRESSURE AND PERSONALITY Table 2 (continued) Type of trait assessed Affect expression11 Overall2 Characteristic (and class) Negative affect0 Defensivenessd Measurement and study design characteristics Potential confounding of hypertension with e Age Medication Neither BP assessment quality Inadequate Insufficient information Marginal Good Superior Study design Hypertension or BP is predictor variable Hypertension or BP is criterion variable Correlation study in which predictors are continuous Study blindness degree Single Double Unknown-ambiguous 112 53 130 46 17 71 59 30 53 7 6 11 19 8 176 76 16 9 4 86 26 9 9 4 80 44 5 1 0 10 6 2 145 24 125 49 17 67 83 2 57 13 5 1 233 22 39 106 14 13 114 7 21 13 1 5 Note. Except where noted, values represent the number of effect sizes for the given class. BP = blood pressure; DBP = diastolic blood pressure; SBP = systolic blood pressure. DBP level coding: normal = <90 mm Hg, mild = 90-104 mm Hg, moderate = 105-114 mm Hg, severe = > 115 mm Hg; SBP level coding: normal = < 140 mm Hg, mild = 140-159 mm Hg, moderate = 160-179 = mm Hg, severe = >180mmHg. a /t = 295. hk= 134. C A:= 142. d A : = 1 9 . e Effect sizes may be tallied more than once. d+ = -0.03, GB( 1) = 7-38, p < .025. The Black versus White comparison was nonsignificant for the covert anger dimension. Other Models for Effect Sizes Age, gender, occupation, and type of BP assessment also related to the magnitude and direction of effect sizes. Across all 295 effect sizes, the mean age of the sample related positively, 0 = .15, p < .001, to the magnitude and direction of effect sizes. Thus, for older participants, higher BP tended to be associated with high scores on the traits that we examined in this review. Similar models that fit within each of the three trait categories indicated that this positive relationship was positive and significant for anger-affect expression, ft = .12, p < .001, and for negative affectivity trait studies, /3 = .14, p < .001, but not for defensiveness. Thus, as age increased, higher BP tended to be associated with more affect expression and negative affect. Across all effect sizes, gender of sample, represented as the proportion of men in the study sample, was unrelated to the magnitude and direction of effect sizes, /? = .01. Within the trait categories, the proportion of men was also unrelated to the magnitude and direction of effect sizes. Thus, the observed patterns appear to generalize across gender of participant. However, results did depend on the occupation of participants: Blue-collar workers exhibited relatively large (and positive) associations between BP levels and affect expression but not negative affectivity, whereas other known categories of occupations showed negative or nonsignificant associations (see Table 6). However, when participants were college students, those with higher BP levels tended to be less affect expressive than those with lower BP levels. Finally, SBP and DBP also were differentially linked to trait levels. Those with higher SBP or DBP tended to be less affect expressive than those with lower BP. Individuals with higher Table 3 Test of Categorical Model for Type of Trait Assessed 95% CI for di+ Variable and class Type of trait Affect expression Negative affectivity Defensiveness Between-classes effect (CB) k Mean weighted effect size (di+) Lower Upper Within-class homogeneity (2wi)a 134 142 19 -0.07 0.07 0.39 -0.09 0.05 0.27 -0.06 0.09 0.51 915.29*** 615.32*** 33.54* 162.22*** Note. CI = confidence interval. a Significance indicates a rejection of the hypothesis of homogeneity. */><.05. ***p<.001. 310 JORGENSEN, JOHNSON, KOLODZIEJ, AND SCHREER Table 4 Tests of Categorical Models Relating to Awareness of Blood Pressure (BP) Levels Overall Awareness of BP levels Aware U na ware Unknown QB for awareness k 123 52 120 Affect expression k C?wia d+ 0.10" 514.41*** -0.09" 536.55*** -0.01 593.38*** 82.02*** 44 36 54 d+ Negative affectivity a <2wi -0.12" 184.67*** -0.1 l b 488.83*** -0.06b 232.17*** 9.62** ' Significance indicates a rejection of the hypothesis of homogeneity. **/x.01. ***/><.001. b Defensiveness a (2w, k d+ 65 16 58 0.1 8b -0.06b 0.06" 241.86*** 44.53*** 270.51*** 58 .41*** k i/+ C?wia 11 0.35" 13.10 0.45" 19.78* 0.66 8 OB for type of trait 74.78*** 3.19 70.92** Differs significantly (p < .05 or smaller) from 0.00 (exactly no difference). DBF tended to be higher on negative affectivity than those with lower DBF; however this relation did not attain significance with SBP, p < .001, for contrast, (see Table 6). Discussion From the data of 83 studies and 25,469 participants, resulting in 295 effect sizes computed for associations between BP levels and personality variables, we obtained a huge amount of variation of individual study findings. Like the results from a metaanalysis of studies focusing on only anger (Suls et al., 1995), our results empirically substantiate the view that research in the personality correlates of BP is marked by substantial amount of inconsistency and confusion (Harrell, 1980; Sommers-Flanagan & Greenberg, 1989; Steptoe, 1981; Weiner, 1979). Nevertheless, a number of characteristics reported in the literature were found to influence the strength and direction of association. Furthermore, due to our analysis of all three dimensions commonly linked to elevated BP, and our assessment of moderators linked to high BP, our meta-analysis to date is the most comprehensive evaluation of the empirical validity of the psychogenic perspective with regard to hypertension. We next discuss the evident shortcomings of this approach. Personality as the Unitary Cause The traditional psychogenic paradigm assumes that EH results from a neurotic disorder that is characterized by the con- flict between status and dependency needs and the high negative affectivity, defensiveness, submissiveness, and inhibition of anger expression induced by this conflict (Alexander, 1939; Cochrane, 1973; Diamond, 1982; Saul, 1939). To the extent that negative affectivity covaries with a prevalence of neurotic disorders, our meta-analysis is inconsistent with the linkage of EH with neurosis. If a "neurotic" style is the cause of EH, then the association of EH-high BP with variables thought to covary with neurosis should generalize across different kinds of people. However, analyses showed that negative affectivity and angeraffect expression were positively associated with BP for older samples but negatively associated for younger samples. Furthermore, persons unaware of their BP-EH diagnostic status showed a negative association of negative affectivity with BP, whereas persons aware of their BP status showed a positive association. These reversals of signs are inconsistent with a psychogenic assumption of a positive correlation of BP with markers thought to reflect neurotic problems. Accordingly, the moderating influence of such person variables as awareness of hypertension, age, and job status (blue collar vs. college student) empirically supports assertions (Weiner, 1979; Weiner & Sapira, 1987) that the psychogenic perspective of neurotic conflict does not account for the multifactorial nature of EH. We conclude that the occurrence of significant moderators is compatible with somatogenic and biopsychosocial synergistic perspectives in lieu of a psychogenic one. We now turn to a discussion of the moderators and their implications. Table 5 Tests of Categorical Models for Technique of Measuring Trait Anger Overall and Both High and Lower Quality Blood Pressure (BP) Assessment Studies. Overall High quality BP assessment" Measurement technique class and model Interpersonal analogue assessment Reported overt Covert anger Ambiguous QB Lower quality BP assessment11 k 34 64 49 17 -0.36" -0.07d 0.08d 0.1 8d 295.00*** 178.72*** 283.21** 230.60*** 48.89** 12 12 16 7 -0.27" -0.07 0.21" 0.03 39.10*** 68.81*** 43.72*** 46.37*** 19.89** 24 52 33 10 -0.39d -0.07d 0.07d 0.21d 269.26*** 105.45*** 239.48*** 178.83*** 25.49** Note. Only studies that assessed trait anger are included in the models. CI = confidence interval. a Includes studies judged to have "good" or "superior" measures of BP. blncludes studies judged to have "marginal," "inadequate," or "insufficient information" measures of BP. 'Significance indicates a rejection of the hypothesis of homogeneity. d Differs significantly (p < .05) from 0.00 (exactly no difference). **/?<.01. ***p<.001. BLOOD PRESSURE AND PERSONALITY 311 Table 6 Tests of Categorical Models for Race and Occupation, and Type of Blood Pressure (BP) Assessment Overall Variable and class Race White Black Ambiguous Between class Occupation Students Blue collar White collar Other Unknown Between class Type of BP assessment Systolic Diastolic Both Unknown Between class Affect expression Negative affectivity k d+ Ow,' k 646.41*** -0.01 342.63*** -0.06b 0.01 725.88*** Gn(2) = 1 1 .46** 44 27 63 -0.05" -0.1 3b -0.07b 367.85*** 219.28*** 319.27*** 47 25 62 0.03" 256.28*** 0.05 97.56*** 0.10" 250.06*** GB(2) = 11.41** 70 19 11 117 78 -0.07" 638.21*** 82.23*** -0.00 0.03" 35.15*** 0.04" 473.85*** -0.02 436.22*** QB(4) = 60.71*** 40 6 -0.11" 496.55*** 3.54 0.25" 0.49" 0.02 -0.01 226.30*** -0.20" 103.65*** (?B(3) = 85.25*** 29 9 5 50 -0.02 118.18*** 0.02 70.17*** -0.07 9.76 0.12" 186.67*** 0.1 2b 174.97*** £?n(3) = 55.58*** 94 103 13 85 -0.07b 644.29*** 496.84*** 0.01 0.18" 82.73*** b 434.94*** 0.06 <2i>(3) = 67..57*** 45 53 420.12*** -0.1 2b -0.04" 314.37*** 0.01 11.62* -0.10" 140.83*** <2n(3) = 24.22*** 46 45 k 103 53 139 d+ Qwi' Significance indicates a rejection of the hypothesis of homogeneity. kJlg,lll ll^«ll\,V» 1 1HJ1\,C41^O tl 1 VJV.V, 11 \_Jll Ul <2e(2) = 8.90* 2 62 24 5 31 b 47 6 45 d+ Cw,a 0.01 151.00*** 0.08b 144.63*** b 0.72 24.33*** 0.15" 222.02*** Gn<3) = 73.33*** Differs significantly (p < .05 or smaller) from 0.00 (exactly no difference). *p<.05. **/><.01. ***/><.001. Type of Trait As expected, anger-affect expression was inversely related to BP, whereas negative affectivity and defensiveness correlated positively with BP. Similar to Suls et al. (1995), the anger-affect expression and negative affectivity associations are weak. Note that the mean weighted effect sizes differed significantly from each other, with defensiveness showing the largest effect size. Our results suggest that defensiveness is the most robust predictor of high BP; however, the mean weighted effect size for defense is based on fewer effect sizes than the others, and additional studies are needed to examine whether this association persists with a more diverse set of samples, varying in such important dimensions as awareness, age, and race. Nonetheless, the association of defensiveness with high BP is consistent with the involvement of central opioid-peptide mechanisms in the covariation of EH with defensiveness. Because the weak association of BP with negative affectivity changes sign for different categories of people (e.g, awareness of diagnostic status, student vs. blue-collar status, and older vs. younger people), the instrumental conditioning of high BP by reductions in negative affect may relate to only certain groups of people (e.g., younger people). Note that baroreceptor sensitivity decreases with age (Mohrman & Heller, 1991). If baroreceptor sensitivity attenuates stressor-evoked negative affect and if this decrease in perceived aversive affective reactions influences how people construe their disposition to experience negative affectivity, then it is possible that dysregulation of baroreceptors could contribute to the covariation of high BP and high negative affectivity among older people. Interestingly, among young men who are normotensive, Vogele and Steptoe (1992) found that only a combination of high risk for EH (upper quartile of mean arterial pressure) and anxious-emotional inhibition predicted stressor evoked cardiac baroreflex inhibition and SBP and HR reactivity. No differences were obtained for ratings of negative affect following the stressors; however, these nonsignificant differences may reflect not assessing state affect during the tasks, these stressors (mental arithmetic and mirror tracing) did not evoke enough interpersonal discomfort, or both. In summary, the Vogele and Steptoe study is consistent with linkages among baroreceptor sensitivity, BP regulation, and negative affectivity; it is possible that these linkages may become more evident as vascular hypertrophy and decreased vascular compliance associated with aging contribute to a greater dysregulation of BP control by baroreceptors. Awareness ofBP Status Recall that factors related to awareness of BP status may influence the covariation of BP with personality measures. Our overall analyses found a positive correlation between BP and the examined traits when individuals were aware and a negative correlation when they were unaware of their BP levels. Our more specific analyses showed that this overall pattern held especially for the negative affectivity trait category but not for the anger-affect expression trait category. A number of factors could account for the impact of awareness. First, the positive association of negative affectivity with BP among people aware of their BP status may reflect the effects of having a life-threatening disease on measures of anxiety and dysphoria (Irvine et al., 1989; Sommers-Flanagan & Greenberg, 1989; Wagner & Strogatz, 1984). Second, cognitive and somatic side effects of antihypertensive medications can confound correlations between EH status and measures of psychological well-being (Cochrane, 1973; Davies, 1970; Irvine et al., 1989). It also is possible that persons higher in negative affectivity are more likely to routinely visit physicians, with the net result being a greater likelihood of people with high negative affectivity receiving a diagnosis of hypertension than people with low negative 312 JORGENSEN, JOHNSON. KOLODZIEJ. AND SCHREER affectivity (Suls et al., 1995; Wagner & Strogatz, 1984). However, such a selection bias may not hold for people with high versus low anger-affect expression. Along these lines, Suls et al. (1995) concluded that their meta-analysis of anger shows that sampling biases related to medical treatment of EH "cannot account for all of the positive findings in the literature, because some supportive evidence emerges from studies using representative samples" (p. 453). Longitudinal and experimental research is needed to address the hypotheses above. For example, people with normal BP and people without severe EH, who, for a limited time, can be unmedicated without negative health consequences can be randomly assigned to be treated with medication or to a wait-list control; measures of negative affectivity can be assessed before and after treatment to assess the impact of medication on selfreported anxiety and dysphoria. If the threat of having a diagnosis of EH is a factor, then assignment to an intervention demonstrated to reduce threat (in contrast to a wait-list control group) should nullify the association of negative affectivity with BP. A combination of longitudinal and cross-sectional designs is also needed to establish that the covariation of negative affectivity with BP only develops following diagnosis of EH or is an artifact of sampling bias. That is, BP, markers of negative affectivity, medical records (i.e., examination of severity of health problems), and frequency of physician visits need to be tracked in people without hypertension who eventually receive the diagnosis of EH and people who remain normotensive. Regarding the trend of an inverse relationship between BP and negative affectivity among persons unaware of their BP status, it is possible that some of these studies included individuals prone to suppress emotional expression (Davies, 1970) or to not disclose personal information as a means of maintaining social approval (Cumes-Rayner & Price, 1989). The positive relationship of BP with defensiveness is congruent with both the emotional suppression hypothesis and the low self-disclosure hypothesis. Regrettably, there were not enough studies to partition the defensiveness effect sizes into the categories of aware versus unaware to evaluate whether effect sizes for defensiveness were moderated by the labeling effect. Nevertheless, if an accumulation of research eventually shows that (a) BP levels correlate with defensiveness mostly among persons unaware of their BP status, (b) the inverse relationship of BP with emotional expression becomes nonsignificant following diagnosis, and (c) an increase in negative affectivity is obtained following diagnosis, this pattern of findings would suggest that the threat of hypertensive morbidity and mortality contributes to a reduction in defensiveness with a coextensive increase in anxiety and dysphoria. Research is needed to address this important area of inquiry. Anger Subcategories Along the lines of Ewart's (1991) discussion of assessment procedures, measures categorized as interpersonal analogue assessments showed the strongest association with high BP; this negative association was significantly greater than the significant negative association obtained for the more global self-report measures of anger expression (i.e., the reported overt reactions category). Both the covert anger and ambiguous categories showed the expected positive association, with the ambiguous category showing a significantly greater association than the covert anger category. Finally, the pattern of these associations were consistently replicated across the lower and high-quality BP assessment categories. In summary, our analysis of anger assessment subcategories supports Ewart's strategy of maximizing the prediction of EH by using anger-suppression measures that are linked to specific social contexts. Race The moderating role of race (Black vs. White) is most clearly associated with the anger-affect expression subcategories of interpersonal analogue assessment and reported overt reactions. Because of the paucity of reported demographic information, we were unable to partition the studies into high versus low chronic stress environments to test Personality Domain X Race X Stress three-way interactions or additive models of these three factors, which are more direct tests of the stress-augmentation hypothesis. Nevertheless, with the more interpersonally oriented category of assessment (interpersonal analogue assessment) and with measures focusing on expression, low levels of anger-affect expression showed a stronger association with high BP in Black people compared with White people, which is quite remarkable given the complex interrelations among culture, race, biologic-physiologic, and demographic factors. Analyses of the Harburg et al. (1979) vignettes by Gentry, Harburg, and Hauenstein (cited in Gentry et al., 1982) partially illustrate these complex interrelations. These researchers reported that among a sample of Detroit women, low anger expression interacts with race, socioecological stress (e.g., crime and poverty), and type of person delivering an unfair interpersonal attack. For Black women, high DBF was associated with high sociological stress, and low anger expression related to an angry boss or housing discrimination; whereas for White women, high DBP was associated with low socioecological stress and low anger expression toward an angry boss or police officer. When combined with the work of Harburg et al. (1973, 1979) and of Gentry et al. (1982), our analysis of the interpersonal analogue assessment category suggests that a robust test of the stress-augmentation hypothesis requires using assessment procedures grounded in the interpersonal and sociocultural context of people's lives. Given that none of the more global measures of affect experience (viz., self-report measures of negative affectivity and covert anger) interacted with race and that interpersonal analogue assessment procedures are stronger predictors of BP than reported overt reaction measures, we favor the use of interpersonal analogue assessment procedures for testing components of the stress-augmentation hypothesis, consistent with Ewart's ( 1 9 9 1 ) recommendations. In other words, use of instruments that focus on the interpersonal context (e.g., high vs. low crime neighborhoods) associated with the salubrious (e.g., assertiveness) versus pathogenic (e.g., anger inhibition) management of anger should provide a more robust test of linkages of EH with anger management. As indicated by Anderson and McNeilly (1993) and Myers and McClure (1993), examining the role of anger expression in EH among Black people requires a combination of longitudinal and crosssectional designs with repeated measures of life-style factors (e.g., dietary habits), neuroendocrine measures (e.g., plasma renin, cortisol, and catecholamines), hemodynamic activity BLOOD PRESSURE AND PERSONALITY (heart rate, stroke volume, and peripheral resistance), sociocultural stressors (e.g., amount of crime and frequency of being the recipient of bigotry), and anger measures sensitive to the sociocultural context of Black people (e.g., role-playing dealing with an arbitrary confrontation with a police officer or workplace discrimination). Other Moderator Analyses Whereas measures of anger-affect expression showed a negative association for college students, it showed a positive association with BP for blue-collar workers. Because higher BP tended to be associated with more anger-affect expression as age increased and because college students are usually younger than blue-collar samples, it is difficult to assess whether the observed difference in effect sizes relates to developmental-maturational factors, work strain, SES, or some combined effect of these factors. Regrettably, we were unable to adequately examine effect sizes for white-collar workers because so few studies clearly separated out the results along SES dimensions. Anger-affect expression shows a modest inverse association for SBP, and a very weak inverse association for DBF. Whereas DBF shows a weak positive association with negative affectivity, SBP is unrelated to negative affectivity. Without information related to neuroendocrine activity (e.g., catecholamines and assessment of adrenergic receptor activity), hemodynamics (heart rate, stroke volume, and vascular peripheral resistance), and renal activity (e.g., plasma renin and salt sensitivity), it is difficult to interpret why effect sizes varied as a function of SBP versus DBF. Trait associations with BP were not moderated by gender. However, as age increased, higher BP tended to be associated with more affect expression and negative affectivity. Schulz (1985) suggested that the experience of negative affective states, particularly in response to unfamiliar negative life events, could be exacerbated by age-related declines in behavioral (e.g., slower responses to external stressors) and cognitive (e.g., problems with retrieval of new information; Poon, 1985) function. EH may augment these cognitive and behavioral declines associated with aging, which in turn could vitiate coping with novel negative life events (Eisdorfer & Wilkie, 1977). Hence, the stronger associations of the experience and expression of negative affect with BP could reflect, in some cases, increases in the experience of negative affect related to an acceleration of cognitive and behavioral declines by EH. Williams (1994) presented research indicating that low serotonin (a neurotransmitter) levels covary with a "hostility complex," which is characterized by irritability, anger, and aggressive behavior. Interestingly, serotonin levels have been reported to decrease with normal aging (Ferrier & McKeith, 1991). It is conceivable that the stronger association of BP with negative affect and anger-affect expression among older samples could reflect two processes linked together only by age: Namely, EH related to age-induced changes in the vasculature (arteriosclerosis and hypertrophy) and an increased susceptibility to negative affect and agonistic behavior related to ageinduced changes in the CNS (cf. Ferrier & McKeith, 1991; Williams, 1994). Nevertheless, a myriad of additional biologic and methodologic factors can account for associations of age, health, and behavior (see Elias, Elias, et al., 1990). 313 Personality and High BP: A Biopsychosocial Synergistic View As stated earlier, without the ability to isolate and adjust for salient physiological and anatomical variables, it is impossible to draw conclusions regarding the somatogenic versus biopsychosocial synergistic bases of linkages of EH with personality and behavior. As discussed by A. P. Shapiro and Miller (1987), even if EH contributes to changes in behavior and personality, these changes could vitiate coping ability. In turn, this reduced ability to adapt to stressors could increase the frequency and severity of pathogenic physiologic reactivity associated with the severity of EH and its sequelae. With reference to personality, we now turn to a discussion of some possible bidirectional links associated with biopsychosocial synergism. Figure 1 is based on a number of reviews discussing behavioral factors in the pathophysiology of EH (Anderson & McNeilly, 1993; Egan, 1987, 1992; Folkow, 1982, 1987a, 1987b; Henry, 1988; S.Julius, 1988, 1991, 1992; S. Julius etal., 1995; Manuck, Kasprowicz, & Muldoon, 1990; Maixner, 1991; Pickering & Gerin, 1990, 1992; A. P. Shapiro & Miller, 1987; Weiner & Sapira, 1987) and illustrates some of the possible bidirectional links related to personality and EH. Bidirectional arrows illustrate bidirectional links between one or more factors in two separate boxes. Furthermore, a factor within a box may influence or be influenced by one or more other factors within the box. Because the brain is central to personality functioning (Eysenck, 1990) and the regulation of BP (Folkow, 1987b; Henry, 1988; S.Julius, 1988; Weiner & Sapira, 1987), Figure 1 emphasizes the brain's role of integrating information from the internal and external environments to adjust to environmental (e.g., threat of physical harm) and physical (e.g., running) exigencies. Cortical and limbic structures are implicated in the storage and retrieval of patterns of coping, defense, affect management, motives (e.g., need for approval), and expectancies (e.g., self-efficacy); these patterns likely affect the appraisal of harm-loss and threat (see Lazarus, 1991; and N. E. Miller, 1995). Interpersonal exchanges construed as threatening or harmful involve transactions among cortical, limbic (e.g., hypothalamus and amygdala), and brain-stem structures (vasomotor centers in the medulla oblongata) as a means of preparing for the execution of defensive behavioral adaptations (cf. Folkow, 1987b; Lang, 1995; Mohrman & Heller, 1991). To prepare for muscular action, CNS structures trigger an autonomically mediated shift in blood flow from the viscera and skin to large muscles with the aid of such neuroregulators as norepinephrine, a neurotransmitter and hormone; cardiac output and BP increase to perfuse tissues with oxygen, glucose, free fatty acids, and other substances for the execution of adaptive behavior. To facilitate coping reactions, other neuroregulators (central opioids) are thought to ready a stressed person for the possibility of experiencing pain during the stressful encounter (Maixner, 1991). As discussed by Folkow (1987b), this pattern of vigorous psychophysiologic reactivity is appropriate for the "harsh realities of primitive life" (p. 1-11) but is frequently inappropriate for the largely symbolic challenges faced in industrialized countries. Because overt somato-motor reactions designed for attack or retreat are not culturally sanctioned, "social demands often lead to a forced dissociation of normal psycho- 314 JORGENSEN, JOHNSON, KOLODZIEJ, AND SCHREER • Information processing • Expectancies (e.g., sell -efficacy) • Defensiveness and cop ng • Motives • Anger expression • Affect expression PSYCHOSOCIAL STIMULI • Cortex • Limbic system • Vasomotor control sys em - Neuroregulators • Pathological factors (e. >., white matter lesions, arteriosclerosis) BACKGROUND PHYSIOLOGICAL PROCESSES REACTIVITY TO STRESSORS Psychosocial • Cognitive • Affective • Behavior Physiological • Cardiovascular • Neuroendocrine • Sodium retention VASCULAR HYPERTROPHY Sympathetic tone Parasympathetic nervous system Sodium-to-fluid balance Vascular adrenergic tone Baroreflex sensitivity Aging CONTRIBUTING FACTORS Environmental • Chronic stressors • Dietary intake • Low social support Constitutional • Autonomic nervous system dysregulation • Vascular stiffness • Sodium retention • Insulin resistance • Central opiodergic mechanisms Figure 1. A biopsychosocial synergistic model for personality factors, behavior, and high blood pressure. biological response patterns" that are triggered by psychosocial stressors (Folkow, 1987b, p. 1-11); that is, in the absence of physical exertion, BP reactivity is not buffered by exercise induced vasodilation, and neurohormonal substances associated with the stress reaction are not cleared rapidly. It has been suggested that frequent and intense elicitation of this forced dissociation associated with BP reactivity contributes to a thickening of arterial walls (vascular hypertrophy), which in turn augments vasoconstrictive reactivity to any vasoconstrictive stimulus (Folkow, 1987b; Manuck et al., 1990; Obrist, 1981). These chain of events are reflected in the left side of Figure 1. However, this reactivity hypothesis is considered by some researchers to be highly untenable (S. Julius, 1991; Pickering & Gerin, 1990, 1992). When stress reactivity has been correlated with EH or risk for EH, Pickering and Gerin (1990, 1992) indicated that these differences are secondary to such genetically influenced factors as sodium transport, vascular stiffness, and underlying disease processes. The box in the lower middle of Figure 1 reflects this possibility. Others (Egan, 1987, 1992; S. Julius, 1988, 1991) discussed the CNS and sympathetic tone (sympathetic drive times adrenergic receptor sensitivity; Egan, 1987) in relation to the pathophysiology of EH. Briefly, earlier phases of hypertension (where the hypertension is not chronic) are thought to reflect factors related to increased sympathetic tone, coupled with decreased parasympathetic tone; this increased sympathetic tone is likely of central origins and is recognized as a contributor to vascular hypertrophy (Egan, 1987, 1992; S. Julius 1991). As discussed above, the development of vascular hypertrophy makes resistance vessels hyperresponsive to any vasoconstrictive stimulus. S. Julius (1988,1992) theorized that the brain reduces the sympathetic drive because, as a consequence of the vascular hyperreactivity, less sympathetic drive is required to maintain the high BP through high levels of tonic vasoconstriction. Theoretically, this adjustment by the brain accounts for why a high proportion of people with EH are characterized by high total peripheral resistance but normal levels of sympathetic tone. According to S. Julius ( 1 9 9 1 ) , a personality of profile of vigilance, submissiveness, and inhibition of anger expression could contribute to increased sympathetic tone associated with the early stages of EH. Other factors such as insulin resistance, sodium sensitivity, and dietary patterns (carbohydrate and sodium consumption) also are potential contributors to overactivity of the SNS. The perspectives of Egan and of S. Julius are reflected in the right side of Figure 1. We now use Figure 1 to briefly discuss a possible example of a series of interlocking factors related to hypertension and personality. First, inherited (e.g., autonomic nervous dysregulation, impaired sodium transport, and vascular stiffness), family, and environmental influences (e.g., high carbohydrate and sodium diet, poor models for anger management, or living in a dangerous neighborhood) may contribute to tonic elevations of BLOOD PRESSURE AND PERSONALITY sympathetic drive, reduced baroreflex sensitivity, and insulin resistance. Likewise, these factors, in combination with background (viz., tonic) physiological processes, may contribute to frequent and intense bouts of stressor evoked reactivity. If strongly punished by significant others, the behavioral manifestations of the acute physiological reactivity (i.e., overt aggressive behavior) could be suppressed as a means of avoiding further punishment; this sets the stage for the learning of the "forced dissociation" discussed by Folkow (1987b). This sort of punishment also can lead to a learned inhibition of the cue-producing responses (thoughts and images stored in memory) that trigger overt, agonistic behavior; in other words, suppression of covert and overt angry reactions are negatively reinforced by (a) reducing the discomfort of high levels of physiologic and psychologic activation and (b) avoiding the social, physical, or both harm-loss consequences of agonistic behavior (cf. N. E. Miller, 1995; Jorgensen et al., 1992; Sapira et al., 1971). Vigilance for aggression and punishment also may result from these chains of events (Julius, 1991) that, when combined with ineffective coping and low self-efficacy expectations related to resolution of interpersonal conflict, predispose the at-risk person to high levels of sympathetic tone and hyperreactivity to interpersonal stress. As hypertrophy of the cardiovascular system develops and increases, sustained high BP and its sequelae follow. As discussed by Folkow (1987b), the vascular hypertrophy augments cardiovascular reactivity, and this in turn may accelerate further thickening of the arterial wall and contribute to higher levels of hypertension. High levels of chronic hypertension may then cause the brain to adjust tonic autonomic activity (S. Julius, 1988, 1992) as well as induce cognitive deficits. These cognitive deficits could contribute to an additional lowering of selfefficacy expectancies due to the awareness of an impaired ability to rapidly process information during interpersonal conflict. Because low self-efficacy expectations can induce physiologic activation and psychological distress, there could be an augmentation of anger suppression, submissiveness, and avoidance of conflict. Likewise, chronic increases in distress linked to low self-efficacy or cognitive deficits could, in turn, foster tonic elevations in central opioid activity and opioid dysregulation (cf. Jamneretal., 1988; McCubbin, 1993). As enumerated by Weiner and Sapira (1987), a mosaic of factors, interacting and changing synergistically across the life span, is likely to produce a number of different pathophysiologic manifestations of links among behavior, personality, and EH. Instead of "putting to rest" research on the behavioral and personality aspects of EH, we believe our meta-analysis supports A. 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Received February 21,1995 Revision received January 30, 1996 Accepted January 31,1996 •
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