1. health and fitness
2. disease

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 rsjorgen@syr.edu.
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-
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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. P. Shapiro and Miller's (1987) belief that efforts to
specify the physiologic and behavioral aspects of EH show
promise of being a vibrant research area. With greater precision
in design, use of longitudinal designs, and measurement of behavioral and physiologic factors, the biopsychosocial synergism
underlying EH may be revealed. Likewise, behavioral assessment and ambulatory BP monitoring in the daily environment
(e.g., Jamner et al., 1991) are likely to provide a clearer picture
of the linkages among personality, stress, coping efforts, and EH
than can be derived from BP and behavioral assessments performed in a laboratory or clinic. Finally, such information can
be used to enhance biobehavioral interventions for EH or its
prevention by tailoring intervention strategies to the person
(Linden & Chambers, 1994).
315
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Received February 21,1995
Revision received January 30, 1996
Accepted January 31,1996 •