Tài liệu tâm lý học sức khỏe: Nhân cách và các yếu tố nguy cơ

9 Personality Traits as Risk Factors forPhysical llness The belief that stable patterns of thought, emotion, and behavior contribute to the development of physical illness has been prese

9 Personality Traits as Risk Factors for

Physical llness

The belief that stable patterns of thought, emotion, and behavior contribute

to the development of physical illness has been present throughout thehistory of medicine (McMahon, 1976) Hippocrates, for example, arguedthat four basic temperaments or personality types reflected excesses ofspecific humors and caused corresponding medical disorders Manycenturies later, Sir William Osler (1892) suggested that coronary heartdisease befell “not the neurotic, delicate person …but the robust, thevigorous in mind and body, the keen and ambitious man, the indicator ofwhose engine is always at full speed ahead” (p 839) The descriptions ofpersonality, disease, and the nature of their relation have varied widely, butthe essence of this psychosomatic hypothesis has remained unchanged

Earlier in this century, the hypothesis was refined by the psychoanalyticschool in psychosomatic medicine (Alexander, 1950; Dunbar, 1943) Thesemodels assigned a pathophysiological role to unconscious personalitydynamics, and suggested a correspondence between specific emotionalconflicts and medical conditions Unlike previous psychoanalyticformulations of hysteria or hypochondriasis (Freud, 1933), these modelsidentified causes for actual disease, rather than unfounded physicalsymptoms For example, an unconscious conflict between aggressiveimpulses and anxiety concerning the consequences of their expression wasdescribed as a cause of essential hypertension Although a weak scientific

foundation limited the impact of this approach on the mainstream of eithermedicine or psychology (Surwit, R B Williams, & Shapiro, 1982), it set thestage for current research on personality and illness

During the same period, developments in the physiology of stress provided

an essential, scientifically credible set of mechanisms connecting personalityand disease (Ax, 1953; Cannon, 1939; Seyle, 1936, 1952; Wolff, 1950) Notsurprisingly, the psychophysiology of stress and emotion remains an integralcomponent of this research area (Contrada, Leventhal, & O'Leary, 1990).The immediate predecessor of the current interest in the issue is undoubtedlythe seminal work of M Friedman and Rosenman (1959) on the Type Acoronary prone behavior pattern Although M Friedman and Rosenmanactively avoided describing their work in the language of personality traits,their work is now recognized as involving personality characteristics (Suls &Rittenhouse, 1987) Friedman and Rosenman's version of the centuries- oldpsychosomatic hypothesis was a major force in the early development of thelarger fields of behavioral medicine and health psychology (G C Stone, F.Cohen, & Adler, 1979; Weiss, Herd, & Fox, 1981)

An often overlooked forerunner to current research on personality traits asrisk factors for illness are early studies that used psychometrically soundmeasures of personality in large, prospective designs (e.g., Ostfeld, Lebovits,Shekelle, & Paul, 1964) Effects of personality variables on subsequentdisease were examined while attempting to control statistically the possibleconfounding medical or demographic variables Studies of this typeprovided important evidence of the merit of the hypothesis and the outlines

of a methodology for constructing a credible epidemiological foundation forthe field

The current state of research on the hypothesis that personality traits caninfluence physical health comprises notable achievements and clearlimitations On the one hand, several literatures have matured to the pointthat the evidence is compelling; specific personality characteristics areindeed associated with increased risk of serious illness and premature death(e.g., T Q Miller, T W Smith, Turner, Guijarro, & Hallet, 1996) Further,plausible mechanisms accounting for this association have been articulatedand evaluated, at least in a preliminary manner (S Cohen & Herbert, 1996;Manuck, 1994) On the other hand, a steady climate of skepticism persists inmuch of the medical community (e.g., Angel, 1985), and the empiricalsupport for the health relevance of some personality traits discussed in thisliterature is quite limited Further, the implications of this work for thetreatment and prevention of illness are largely unknown Fortunately,conceptual, methodological, and analytic tools in personality psychologyand behavioral medicine have evolved to the point where future studies willaddress these limitations in an increasingly compelling manner

This chapter provides an overview and critique of the literature concerningpersonality traits as risk factors for physical disease It begins by addressingsome basic issues regarding the nature of personality, disease, and theirpotential association After reviewing models of this association, it turns totheory and research on the major personality attributes in the field Finally, itconcludes with a critical evaluation of the state of the literature and issues to

be addressed in its future

BASIC ISSUES

What Is Personality?

Allport (1937) succinctly argued that “personality is something andpersonality does something” (p 48, emphasis added) Personality traits arestable patterns of thought, emotion, and behavior that characterize anindividual across time and situations Traits are presumed to be based inpsychological and/or biological structures within the individual, and theyform a dimensional basis for comparing individuals For example, somepeople are generally friendly and warm, whereas others are cold anddisagreeable, presumably because of differences in their biologic and/orpsychologic “make-up.” Thus, from this perspective, personality traits arethings that people “have” (Cantor, 1990)

In Allport's other, more active meaning, personality refers to the processesthrough which an individual's thoughts, emotions, and behavior cohere intomeaningful patterns over time and across situations These processes includethe ways in which individuals select and interpret the contexts and situations

of their lives, the goals they pursue, the strategies and tactics they employ indoing so, and the ways in which they evaluate and react to the outcome ofthese activities These more circumscribed and dynamic psychologicalprocesses are closely associated with the stable patterns of thought, emotion,and behavior that are indicators of traits Yet, this other sense of personality

is obviously much more concerned with how traits operate, rather than theirdescription Thus, the study of personality as “doing” rather than having(Cantor, 1990) focuses on describing both the psychological mechanismsunderpinning more broadly defined, static personality traits and the ways inwhich these “middle units” of personality are dynamically interrelated andexpressed

Current personality psychology reflects both of Allport's meanings, andrecent developments of both types have the potential to make enormouslyvaluable contributions to the study of personality and health (T W Smith &

P G Williams, 1992) In the classic trait perspective, a far-reachingdevelopment is the emergence of the five-factor model of personality as anadequate taxonomy of basic personality characteristics (Digman, 1990; John,1990; McCrae & John, 1992) Although descriptions vary across versions ofthis model, and despite several notable critics (e.g., Block, 1995), there isgeneral consensus regarding the traits listed in Table 9.1- Extraversion,Agreeableness, Conscientiousness, Neuroticism, and Openness toExperience These traits have been recovered in factor analyses of self- andother- ratings, and several reliable and valid measures of these broaddimensions and their subcomponents have been developed (Digman, 1990;John, 1990)

The validity and potential impact of this taxonomy are evident in the factthat these traits are clearly not simple mental abstractions or linguisticconveniences used by raters (e.g., Funder & Colvin, 1991; Moskowitz,1990) Rather, they reflect verifiable, general dimensions of individualfunctioning Further, these broadly defined traits are stable (McCrae &Costa, 1990), show patterns of variability consistent with genetic influences(Bouchard, Lylkken, McGue, Segal, & Tellegen, 1990), and predict behavior

in many circumstances (Kendrick & Funder, 1988)

The elements of this taxonomy can provide a useful guide for organizing thegrowing array of otherwise conceptually isolated traits suggested as riskfactors for physical illness (Costa & McCrae, 1987b; Marshall, Wortman,Vickers, Kusulas, & Hervig, 1994; T W Smith & P G Williams, 1992)

Traits studied as risk factors are often described and studied individually,without attention to their overlap or even redundancy with other traits Oneimportant application of the five-factor taxonomy is the conceptual andempirical description of traits suggested as potential risk factors This use ofthe five-factor taxonomy might reveal similarities and differences amongotherwise isolated traits In addition, the five traits themselves might beviable candidates as risk factors (e.g., Costa, McCrae, & Dembroski, 1989).

In either of these applications of the model, the well-validated assessmentdevices are likely to be useful to health researchers

One important variation on the five-factor model substitutes the dimensions

of Friendliness versus Hostility and Dominance versus Submissiveness forAgreeableness and Extraversion, respectively (Trapnell & Wiggins, 1990).This permits the integration of the five-factor approach with theinterpersonal approach to personality (Carson, 1969; Kiesler, 1983; Leary,1957; Wiggins, 1979) As depicted in Fig 9.1, the dimensions of dominanceand friendliness define a two-dimensional space, or circumplex Thecircumplex model has been used, conceptually and empirically, to describe avariety of personality characteristics, interactional behaviors, and socialstimuli (Kiesler, 1991; Wiggins, 1991; Wiggins & Broughton, 1991) As aresult, it has considerable potential for facilitating the integration ofpersonality and social risk factors for disease (Gallo & Smith, 1998; T W.Smith, Gallo, Goble, Ngu, & Stark, 1998; T W Smith, Limon, Gallo, &Ngu, 1996) That is, personality traits and aspects of the social environmentcan be described and even assessed through a common framework

Although the five-factor model and its variants are potentially invaluable inidentifying and organizing traits in the study of personality and health, they

have less to say about the mechanisms through which traits influencebehavior, emotion, and ultimately health It is here that the second majoremphasis in personality psychology is of use Unfortunately, less agreementexists regarding an adequate taxonomy of the “middle units” of personalityprocesses (Cantor, 1990) However, several overlapping sets have beenarticulated, and clear themes have emerged in the related research Theseapproaches follow from the cognitive social learning tradition in personalitypsychology (Kelly, 1955; Mischel, 1973; Rotter, 1954), and they share manyconceptual similarities to interpersonal approaches in personality andclinical psychology (Kiesler, 1996; Westen, 1991) Examples of theconstructs described in this literature are mental representations (i.e.,schemas) of the self, others, relationships, and social interaction sequences(i.e., scripts); life tasks, motives, and goals; appraisals, values, and beliefs;strategies, tactics, and competencies in goal-directed behavior; and copingstyles and behaviors (Cantor, 1990; McAdams, 1995; Mischel & Shoda,

1995, 1998; Oglevie & Rose, 1995; Westen, 1995)

An underlying premise in this tradition is that characteristics of the personare reciprocally related to the social environment Intentionally or not,people choose to enter some situations and not others, and their actions andovert expressions of emotion elicit responses from their interaction partners

in ways that reflect their personality traits (Asendorpf & Wilpers, 1998).These selected, evoked, and intentionally manipulated features of theindividual's social environment in turn influence the individual (Bandura,1977; Buss, 1987; Ickes, Snyder, & Garcia, 1997) Thus, an individual'sthoughts, emotions, and behavior are seen as highly responsive tocharacteristics of the specific situation, and many situations are modified by

the individual's actions Through these recurring, reciprocal patterns,individuals foster social environments that maintain central features of theirpersonalities over time (Caspi et al., 1989; Kiesler, 1996; Wachtel, 1994;Wagner, Kiesler, & Schmidt, 1995) A further implication of this view isthat personality processes are best understood in the contexts that compriseand surround these reciprocal interactions between people and socialenvironments (Revenson, 1990), such as characteristics of the physicalenvironment, subculture, and socioeconomic factors Personalitydescriptions are likely to be more accurate and informative to the extent thatthey consider individuals, their recurring social circumstances, and thecontext in which they are embedded

Current versions of the cognitive-social approach to personality offer thepotential for a comprehensive description of broad traitlike characteristicsand recurring patterns of situationally specific responding (e.g., Mischel &Shoda, 1995, 1998) That is, the approach has the potential to describe themechanisms through which traits, such as those in the five-factor taxonomy,influence thought, emotion, and behavior in interaction with socialsituations Another important advantage of the cognitive-social perspective

is its overlap with current stress and coping theory, given their mutualemphasis on cognitive appraisal processes, self- regulation of emotionalresponses, and strategies for managing situational threats and demands(Contrada, 1994) The general stress and coping model (e.g., Lazarus &Folkman, 1984; Lazarus, 1991) has become a cornerstone of healthpsychology and behavioral medicine, and it provides an importantconceptual and empirical connection to the psychophysiological responseshypothesized to link personality traits and subsequent disease

Another benefit of the cognitive-social approach is its relevance forinterventions Although the general trait approach is useful in identifying thepersonality characteristics that might be useful foci in interventions intended

to prevent or manage illness, it has less to say about specific targets forchange With its increased attention to specific psychological mechanismsand dynamic patterns, the cognitive-social approach is likely to aid in thearticulation and refinement of intervention techniques For example, whereasthe five-factor taxonomy might identify neuroticism and (low) agreeableness

as useful targets for change, the cognitive-social perspective could suggestspecific patterns of appraisals, beliefs, interaction tactics, and copingbehaviors to be included in such interventions

What Are the Appropriate Indications of Illness?

A revolutionary difference between psychoanalytic writing on hysteria andhypochondriasis as opposed to the later work of Alexander, Dunbar, andtheir colleagues lies in the nature of the health endpoint under consideration-abnormal illness behavior versus actual illness This distinction was clearlydrawn more recently in conceptual discussions of the potential effects ofpersonality on health (e.g., F Cohen, 1979) Outcomes such as symptomreports, utilization of health care resources (e.g., physician visits), takingmedication, or receiving other treatments typically reflect the presence ofillness, but are fallible indicators In evaluating the role of personality inphysical illness, care must be taken to avoid mistaking an associationbetween personality traits and illness behavior for an association with actualillness The former may or may not reflect the latter

Despite the early and clear articulation of this issue, many influentialempirical reports on the association between personality and physical illnessrelied heavily on these less definitive indices (e.g., Haynes, Feinleib, &Kannel, 1980; Kobasa, 1979; Scheier & Carver, 1985) Similarly, severalimportant reviews of this literature (e.g., H S Friedman & Booth- Kewley,1987) have been criticized for the potential misinterpretation of associationsbetween personality traits and illness behaviors-especially somaticcomplaints-as reflecting the effects of personality on actual physical health(e.g., Matthews, 1988; Stone & Costa, 1990; T W Smith & Rhodewalt,1991)

In the most notable example of this issue, several investigators havedemonstrated that neuroticism is consistently related to somatic complaints,even in the absence of actual illness (Costa & McCrae, 1985a, 1987; Watson

& Pennebaker, 1989) If the personality characteristic under consideration isassociated with neuroticism and if the disease endpoint studied wholly oreven partly reflects illness behavior rather than objectively documenteddisease, then this interpretive ambiguity arises; the association observedmight involve personality traits and actual illness, or personality and illnessbehavior Given this concern and its potential negative impact on theidentification of robust causal influences on actual illness, symptom reportsand other illness behaviors are no longer considered an acceptableoperational definition of illness Although illness behaviors are importanttopics for research, cumulative progress in the study of personality traits asrisk factors requires less ambiguous methodologies

A second major development in this literature is the recognition that thepathophysiology of the major diseases studied varies considerably across

their progression For example, the beginning stage of coronary heart disease(CHD) is characterized by microscopic injuries to the endothelial lining ofthe coronary arteries The potential psychophysiological influences on thisprocess might differ from those of the next stage-the slow progressivebuildup of fatty deposits at the injury sites Further, the factors thatprecipitate the emergence of overt symptoms of CHD (i.e., angina,myocardial infarction, sudden cardiac death) may differ still from those thathasten the progression of previously asymptomatic coronary artery disease(CAD; S Cohen, J R Kaplan, & Manuck, 1994; Kamarck & Jennings,1991) The natural histories of many forms of cancer and the course of HIVinfection and AIDS include similar possibilities for heterogeneouspsychophysiological influences over time This poses two challenges forresearchers in the area First, biologically plausible mechanisms linkingpersonality and disease must be articulated, and second, mechanisms must

be tied to identifiable points in the etiology of the illness

How Do We Evaluate the Personality-Disease Hypothesis?

In order to reach valid conclusions about the presence or absence of ahypothesized relation between a personality trait and illness, severalcommon methodological issues must be addressed These can be groupedinto the classic, four categories of validity in research design specified byCook and Campbell (1979)-statistical conclusion validity, internal validity,construct validity, and external validity (or generalizability)

Statistical associations between personality traits and illness are generallysmall, at least by the standards typical in behavioral research (J Cohen,1990) These effects are often at least as large as those involving more

conventional risk factors for disease Given the prevalence and cost of thediseases studied, even small effects can have important public healthimplications However, small effects, multifactorial etiologies, and changinginfluences across the course of disease can make it difficult to detectsignificant covariation between personality characteristics and disease As aresult, large epidemiological studies and quantitative combination ofindependent results (i.e., meta-analysis) are essential in the development andevaluation of this literature The results of individual studies must beconsidered with caution, especially if they employ small, select samples T.

Q Miller and his colleagues (1991) demonstrated that the use of high risksamples and the associated restriction of range in disease prevalence andseverity (i.e., disease-based spectrum bias) can mask the statisticalassociation of personality traits and other risk factors with disease

Given that personality characteristics are rarely manipulated experimentally,the issue of internal validity is central in this literature A common strategy

in early stages of investigation of a risk factor is the concurrent case controldesign, in which individuals with the disease (or more severe disease) arecompared with controls on the trait of interest However, given the manypossible consequences of serious illness, the alternative interpretation thatcognitive, emotional, and behavioral correlates of a disease might reflectconsequences rather than causes of the condition often seems equallyplausible(S Cohen & Rodriguez, 1995) Prospective designs eliminate thisambiguity to a large extent, but because of their cost are oftenunderrepresented in the literature on specific traits Further, the possibility ofunmeasured third variables a& counting for statistical associations betweenpersonality and disease remains as a threat to internal validity even in

prospective designs Biologic, psychologic, and sociodemographic variablescould exert simultaneous effects on personality and health, therebyproducing a noncausal association

As previously noted, many studies have relied on symptom reports ordiagnoses in which somatic complaints are primary criteria (e.g., angina tooperationalize CHD) This poses the threat to construct validity describedearlier; the statistical associations might involve illness behavior rather thanillness itself The field has shown an increasing recognition of this concernover time

However, the construct validity of the personality variables studied aspredictors of illness is still often underemphasized Scales are sometimesspecifically developed to assess an individual trait described in a newlyproposed model of personality and health Sometimes such scales areemployed prior to thorough construct validation As a result, it is oftenuncertain if the statistical associations examined actually involve thepersonality trait(s) under study, as opposed to some other characteristic(s)assessed unintentionally Similarly, the distinct versus overlapping nature ofthe growing array of traits in the field is largely neglected (H S Friedman etal., 1995) Thus, it is often unknown whether or not scales intended to assesssimilar characteristics actually do so (i.e., convergent validity), and whether

or not scales with dissimilar names and conceptual descriptions actuallyassess distinct traits (i.e., discriminant or divergent validity) Carefulattention to the issue, possibly using the five-factor model as an integrativetool and source of validated indicators (Gallo & Smith, 1998; Marshall et al.,1994; T W Smith & P G Williams, 1992), could improve the quality ofthis literature considerably

Finally, as with much medical research, the literature on personality traits asrisk factors can be rightfully criticized as employing samples that aredisproportionately White, middle- class, and male (N B Anderson, 1989; N.

B Anderson & Armstead, 1995; Stanton, 1995) Thus, the generalizability

of effects across sexes, races, and socioeconomic status is often unknown.Once apparently robust relationships are identified, their generalizability tomore diverse groups should be examined Given that many of thesepersonality traits vary systematically as a function of age, race, sex, andsocioeconomic status (e.g., Siegler, 1994), and that these demographiccharacteristics are themselves risk factors, the issue is likely to be important

in the future of the research area

MODELS OF THE ASSOCIATION BETWEEN PERSONALITY AND DISEASE

Even if reliable and valid associations between personality traits andsubsequent illness can be established, the processes or mechanisms thatunderlie these effects have yet to be determined Several models have beenproposed to describe the association of personality characteristics andsubsequent health (F Cohen, 1979; S Cohen & Rodriquez, 1995; Krantz &Glass, 1984; Suls & Sanders, 1989) The interactional and transactionalstress moderation models suggest that physiological reactivity is the criticallink underlying this statistical association Likewise, the constitutionalvulnerability model posits a physiological influence on disease, butidentifies personality as a noncausal correlate or epiphenomenon of thisresponsivity The health behavior model suggests that personality influenceshealth by affecting health practices Finally, the illness behavior modelindicates that personality impacts the subjective experience of illness and the

behavioral responses to perceived symptoms The subsequent sectionelaborates on each of these models It is important to note that they are notnecessarily mutually exclusive, and that for any given personalitycharacteristic, several models may explain health effects in a complementarymanner

Stress Moderation Models

Stress moderation models are based on the premise that stress is afundamental component of the relation between personality and disease(e.g., F Cohen, 1979; S Cohen & Rodriquez, 1995; Contrada, Leventhal, &O'Leary, 1990; Houston, 1989; Suls & Rittenhouse, 1987) To explain thehistorically modest association of stress and illness (Rabkin & Struening,1976), the interactional stress moderation model goes beyond a direct ormain effect model by suggesting that individuals will differ in their degree

of vulnerability to the detrimental effects of stress, as a consequence (in part)

of their personality characteristics Thus, personality traits are seen asmoderators (Baron & Kenney, 1986) of the stress-illness relation, in thatillness is more accurately predicted by the statistical interaction ofenvironmental stress and personality traits Further, the interactive effect ofstress and personality on illness is, in turn, seen as mediated by differentialpsychophysiological responses to stressors as a function of an individual'sstanding on the personality dimension(s)

Given its central role in this model, it is important to describe the currentstatus of the hypothesis that the psychophysiology of stress can influencedisease The prevailing theory suggests that psychological stress elicitsincreases in activity in the sympathetic adrenomedullary and hypothalamic,

pituitary adrenocortical axes Over time, pronounced, repetitive, orprolonged physiological responses are thought to contribute to the etiology

of illness Cardiovascular illnesses (e.g., CHD, hypertension, stroke) arebelieved to be fostered by activation of neuroendocrine (e.g.,catecholamines, cortisol) and cardiovascular (e.g., blood pressure) responses(Barnett, Spence, Manuck, & Jennings, 1997; Kamarck & Jennings, 199 I;Manuck, 1994; Markovitz, Raczynski, Wallace, Chettur, & Chesney, 1998).Infectious illnesses and cancer are presumed to be influenced by the effects

of stress on the immune system (Herbert & S Cohen, 1993; Kiecolt-Glaser

& Glaser, 1995) Although definitive evidence is lacking, these pathways arebiologically plausible and the research to date provides considerable, albeitpreliminary, support for their role in pathophysiology

Personality may serve to attenuate or exacerbate (i.e., moderate) theconnection between stress and pathophysiology at several places in the stressand coping sequence (see Fig 9.2 ) First, the degree to which a given eventwill be experienced as stressful depends on an individual's subjectiveappraisal of harm or loss, as well as the resources believed to be availablefor managing the situation (Lazarus and Folkman, 1984) Certain personalitycharacteristics are thought to influence this subjective appraisal Forexample, Type A individuals frequently appraise situations as involvingmore threat or demand than do Type B persons-a tendency thought to linkTABP to cardiovascular disease (Houston, 1989) In contrast, hardyindividuals are believed to perceive life events to be challenging, rather thanthreatening, which may decrease their vulnerability to disease (e.g., Kobasa,1979) Through these appraisals, personality influences the emotional andmotivational responses to events (Houston, 1992), and emotions and aroused

motives influence psychophysiological response (Wright, 1996) Second,personality may influence the coping mechanisms that the individual applies

in managing the stressor Specific coping mechanisms probably cannot becategorically regarded as adaptive or maladaptive (e.g., Lazarus, 1990).However, personality may influence the likelihood that the individual willemploy strategies that are adaptive in a given circumstance (Bolger &Zuckerman, 1995)

Although the succinctness of the interactional stress moderation approach isappealing, the model is somewhat limited Fundamentally, it is a model ofindividual differences in responses to potentially stressful circumstances.These responses are viewed as the result of the static or statistical interaction

of personality traits and aspects of the situation Several researchers haveadvocated a more process-oriented approach (e.g., Bolger, 1990; Contrada etal., 1990, Houston, 1989; Lazarus, 1990; Revenson, 1990) that emphasizesthe ongoing interplay between personality, coping, and contextual factors.Such models move beyond the static or statistical interactional approach byacknowledging the type of reciprocal transactions between persons and theirenvironments typical of the cognitive-social learning and interpersonalmodels of personality already described Thus, transactional views of thestress moderation process emphasize the ways in which people influence theobjective features of their environments by actively choosing situations andsubsequently responding to them in characteristic ways (Bandura, 1977;Buss, 1987; Cantor, 1990; Mischel, 1973) For example, because of theirantagonistic interactional style, hostile persons are likely to evoke frequentinterpersonal strain Such conflicts probably confirm hostile expectations

and increase the likelihood of future antagonistic behavior (Wagner et al.,1995)

The transactional approach submits that personality influences thestress/illness relation at three points in the stress and coping cycle (see Fig.9.3 ) As in the interactional stress moderation approach, personality isthought to alter the appraisal of events and to influence the choice of copingresponses In addition, personality is thought to affect exposure to stressfulevents, through the individual's selection, evocation, and intentionalprovocation of characteristics of the situations they encounter (Buss, 1987).Personality characteristics that expose the individual to increased stressthrough these processes will also elicit the increased psychophysiologicalreactivity and subsequent potential for disease discussed earlier Thus, fromthis perspective, psychosomatic processes are not simple consequences ofspecific personality characteristics, but reflect a dynamic process emergingfrom the recurring transactions between people and the social contexts theyinhabit (Revenson, 1990; T W Smith, 1995)

Health Behavior Model

The stress moderation and transactional models rest on the assumption thatthe physiological components of stress mediate the association betweenpersonality and disease In contrast, the health behavior model posits that theeffects of personality traits on health are indirect, mediated by theintervening effects of health practices (see Contrada et al., 1990; F Cohen,1979) (See Fig 9.4 ) This model is derived from research suggesting thatcertain behaviors (e.g., smoking, leading a sedentary lifestyle, and practicingpoor nutrition habits) are reliably associated with disease risk (e.g., Blair et

al., 1989; Holroyd & Coyne, 1987; Paffenbarger & Hale, 1975) Further, themodel draws on research suggesting that personality traits, includinghardiness (Wiebe & McCallum, 1986), neuroticism (Costa & McCrae,1987a; McCrae, Costa, & Bosse, 1978), and hostility (Leiker & Hailey,1988; Siegler, 1994) affect the likelihood that one will practice negativehealth habits

Personality might influence the choice of health practices in several ways.First, psychological factors presumed to guide lifestyle choices may becomponents or correlates of personality constructs Examples includevariables such as locus of control, health beliefs and values, and self-efficacy(Bandura, 1989; Lau, 1988; Strickland, 1978) Alternatively, negative healthpractices may reflect ineffectual coping practices That is, personalitycharacteristics, such as hostility, may not only increase the likelihood thatsubjective stress will be experienced, but also that maladaptive behaviors,such as smoking or substance use, will be utilized as emotion-focusedcoping strategies Research suggesting that individuals often adopt morenegative health habits when exposed to stress is consistent with thishypothesis (Horowitz et al., 1979; Langlie, 1977; Shachter, Silverstein,Kozlowski, Herman, & Liebling, 1977)

As noted earlier, the health behavior model does not suggest that a directphysiological pathway connects personality to health However, there may

be physiological correlates of health behaviors that operate through the set ofpsychophysiological responses described in the stress moderation models

As portrayed in the lower panel of Fig 9.4, many health practices producephysiological changes similar to those generated by stress For example,stress-related alterations in nutrition or sleep habits appear to attenuate

immune functioning (Hall et al., 1998; O'Leary, 1990) Furthermore, certainhealth practices, such as smoking, leading a sedentary lifestyle, andconsuming caffeine, appear to intensify laboratory-induced stress responses(e.g., Blumenthal et al., 1990; MacDougall, Musante, Castillo, & Acevedo,1988; M D Davis & Matthews, 1990) Thus, it is possible that the effects ofstress on health behaviors produce pathophysiological responses similar tothose described in the stress moderation models

The health behavior model suggests that the common practice of controllingtraditional risk factors (e.g., smoking, exercise, etc.) in epidemiologicalresearch might lead to an underestimate of the effects of personality onillness, as some of the impact of personality traits on health may occurthrough unhealthy lifestyles Contrada et al (1990) described several othermethodological concerns with evaluations of this model In particular, theyemphasized the problems associated with utilizing self-report indices toassess health practices Methodological artifacts such as social desirabilitymay be particularly problematic in these studies, given the widespreadpublicity about the detrimental effects of health practices like smoking Inaddition, Contrada and colleagues noted that the health behaviors commonlyassessed in this research often exhibit only modest intercorrelations (e.g.,Leventhal, Prochaska, & Hirshman, 1985; Norris, 1997), and that healthbehaviors appear to be inconsistent over time (Mechanic, 1979) Failure torecognize the limitations of most measures of health behavior could lead to

an underestimate of their role as a mediator of the association betweenpersonality traits and subsequent illness

Constitutional PredisposXon Model

Regardless of whether or not the connection is direct, viapsychophysiological responses, or indirect, via intervening effects on healthbehavior, the stress moderation and health behavior models share thecommon assumption that the statistical association between personality andhealth reflects a causal relation Several researchers have suggested that itmay not be causal, but instead may reflect the existence of a third variable(Krantz & Durel, 1983; Suls & Sanders, 1989; R B Williams, 1994) Asdepicted in Fig 9.5, this model proposes that an underlying constitutionalvulnerability causes a predisposition for autonomic lability, whichsubsequently influences both personality processes (e.g., emotionalresponses, etc.) and health problems Thus, this model considers statisticalassociations between personality and subsequent health to be artifactsresulting from the existence of a biologic third variable

Given the growing body of evidence suggesting that certain personality factors and physiological stress responses may be at least partiallydetermined by genetic factors (Bouchard et al., 1990; Smith et al., 1987;Turner & Hewitt, 1992), this model may be p, articularly important Thisapproach has been applied to the relation of Type A behavior and coronaryheart disease (Krantz & Durel, 1983)) and more recently, to the association

-of hostility and disease (R B Williams, 1994) Future research is necessary

to clarify possible genetic influences on other personality-disease relations

Illness Behavior Model

In contrast to the previous models, the illness behavior approach suggeststhat personality does not actually affect illness, but that it influencesbehaviors related to the subjective perception of physical health This model

is derived from evidence indicating that objective health versus illness doesnot fully explain illness behaviors such as health care utilization, symptomreporting, work absenteeism, and self-medication (e.g., G A Kaplan &Camacho, 1983; Kaplan & Kotler, 1985; Maddox & Douglas, 1973) On thecontrary, psychological variables strongly affect the likelihood thatindividuals will attend to physiological sensations and perceive that they areindicative of illness (Cioffi, 1991; F Cohen, 1979; Pennebaker, 1982;Watson & Pennebaker, 1989)

Fig 9.6 depicts the potential effects of psychological variables on variousmanifestations of illness behavior Symptom reports, which are reliably butweakly predictive of objective health outcomes (Idler, Kasl, & Lemke,1990), provide the clearest example of the less than perfect relation betweenillness behaviors and disease Self-reports of physical symptoms areinfluenced by various psychological factors, including health beliefs anddifferences in focus of attention (Pennebaker, 1982) For example,individuals higher in neuroticism are more likely to be concerned withsomatic sensations, and subsequently, to report symptoms (Costa & Mc-Crae, 1985a, 1987; Watson & Pennebaker, 1989) Furthermore, behavioralhealth indices such as health care visits may be influenced by somaticperceptions and other psychological processes This phenomenon may beparticularly relevant to studies comparing samples selected through medicalclinics to control groups solicited from the community These samples may

be biased by psychological characteristics that relate to self-selection intohealth care settings Any observed association between a targetedpersonality trait and illness may be confounded by the relation of the trait tohealth care utilization behaviors

The preceding discussion illustrates the distinction between actual illnessand illness behavior, and suggests the necessity of carefully evaluating themethodology utilized in studying personality and disease As discussedpreviously in the section on validity threats, before the mechanism(s) bywhich personality contributes to disease can be classified, the research mustdemonstrate that illness-and not simply illness behavior-is influenced bypersonality

TRAITS LINKED TO HEALTH

The following sections review literature regarding several specificpersonality traits studied as risk factors The list is not exhaustive; sometraits discussed in this literature are not included The criteria for includingtraits are that research published in refereed outlets shows considerableevidence of a prospective association of the trait with objective indicators ofserious illness, or that despite the lack of such evidence, the trait is widelystudied in the field For each trait, a description of its usual measurement,the findings linking it to illness outcomes, and theory and research regardingthe processes underlying this association are presented

Type A Behatior

As noted earlier, the Type A behavior pattern (TABP) occupies a centralplace not only in the modern literature on personality and health, but also inthe evolution of the larger fields of behavioral medicine and healthpsychology The recent history of research on the topic illustrates most ofthe central conceptual and methodological issues in this area of research

Assessment Following M Friedman and Rosenman's (1959) description of

an inaction-emotion complex” consisting of achievement striving,competitiveness, excessive job involvement, time urgency, and easilyprovoked hostility, two assessment procedures quickly achieved widespreaduse The Structured Interview (SI; Rosenman, 1978) is a semistandardizedinterview intended to elicit a behavioral sample of the behaviors comprisingthe TABP, or their relative absence (i.e., the Type B pattern) With sufficientraining in administration and scoring, reliable ratings can be achieved Avariety of studies indicate that valid ratings can be made with the procedure,with the caveat that the style of administration can affect the quality ofratings (Scherwitz, 1988) The second principal measure is the JenkinsActivity Survey (JAS; Jenkins, Rosenman, & Zyzanski, 1974) This self-report measure primarily assesses achievement striving, competitiveness, jobinvolvement, and hard-driving behavior Unlike the SI, it does notadequately sample individual differences in hostility However, many years

of research with various versions of the JAS have indicated that it is areliable and valid measure of the other aspects of the TABP (Rhodewalt &

T W Smith, 1991)

Because of its availability in a large, prospective study of corontly risk, theFramingham Type A scale (Haynes et al:, 1980) is also recognized as apotentially important measure However, it is poorly correlated with the SIand is more closely associated with both neuroticism and symptom reportingthan either the SI or JAS (T W Smith, O'Keeffe, & Allred, 1989; Suls &Marco, 1990) Thus, some of the association between the FTAS and illnessendpoints involving symptom reports (e.g., angina vs myocardial infarction

or cardiac death) might involve the association between neuroticism andsymptom reports already described

Notably, the convergence among the three principal measures is moremodest than would be expected if they are to be interpreted as reflecting asingle construct Thus, a basic measurement concern-poor convergentvalidity-limits much of the literature on the TABP (Rhodewalt & T W.Smith, 1991)

Assocition With Diseage After nearly 20 years of cross-sectional andprospective research, a panel of experts convened by the American HeartAssociation concluded that the TABP was a robust risk factor for CHD(Cooper, Detre, & Weiss, 1981), with Type As having about a twofoldgreater risk than Type Bs Several notable failures to replicate this relationappeared soon after the expert panel's conclusion These included not onlyseveral prospective, multicenter studies (Shekelle, Gale, & Norusis, 1985;Shekelle, Hulley, et al., 1985), but a long-term follow-up from the originalprospective study of the TABP (Ragland & Brand, 1988)

These and other negative endings (e.g., Barefoot, Peterson, et al., 1989)called into question the status of the TABP as a risk factor, and prompted amore fine-grained analysis of the broadly defined pattern The negativereports also prompted skepticism in both the medical and popular healthliterature However, skepticism about the TABP may have been bothpremature and too general In a carefully rendered quantitative review of thisliterature, T Q Miller and his colleagues (1991) demonstrated that when it

is assessed via the SI as opposed to self-report methods, the TABP is indeed

a reliable risk factor for the subsequent development of CHD, even when the

illness is defined in terms of objectively verified events (i.e., MI and SCD).This conclusion echoed the results of a previous quantitative review byMatthews (1988)

Additional analyses by T Q Miller et al (1991) indicated that the historicaltrend toward more frequent negative findings was probably related to a shiftover time in the types of populations studied Whereas early studies includedlarge proportions of initially healthy, low risk subjects, the later studiesincluded a greater propotion of high risk subjects The resultingoverrepresentation of Type As in the samples and the restriction of range inthe disease endpoint (i.e., disease-based spectrum bias) is likely to havereduced the statistical power for finding the association between the TABPand CHD

The potential clinical importance of the TABP was suggested by the results

of the Recurrent Coronary Prevention Project (RCPP; M Friedmann et al.,1984) In this clinical trial, group therapy not only reduced Type A behavior

in CHD patients, but also successfully reduced the rate of recurrent coronaryevents by nearly 50% (M Friedman et al., 1984) Among patients with amild previous infarction, treatment reduced the occurrence of cardiac death(Powell & Thoresen, 1988) Thus, in one of a very few attempts toexperimentally alter a personality risk factor for serious illness, the resultswere quite encouraging

Models of Association Each model of the mechanisms linking the TABP toCIID has been based on a specific description of the psychologicalunderpinnings of the pattern For example, Glass (1977) suggested that theseovert behaviors reflect a heightened motivation to exert control over

environmental events, a low threshold for perceiving potential threats to thiscontrol, and an aggressive style in reasserting it Powell (1992) elaboratedthis view, arguing that Type As see external events and other people as theprimary cause of their difficulties and distress When combined with theType As' exaggerated belief in their ability to control others and the viewthat exerting control is the only coping strategy available to them, thisexternal attribution leads Type As to engage in vigorous attempts to exertcontrol and manage the events of their lives

Price (1982) argued that a set of core beliefs is the foundation of the overtbehavior pattern For example, Type As are seen as believing thatindividuals must constently prove themselves worthy trough Gontinualachievement, resorces and opportunities for such achievements are limited,and no universal moral principles exist to ensure that people will be fair As

a result, Type As are engaged in an ongoing struggle to bolster theirtentative sense of self-worth through what they perceive as a competitionwith potentially ruthless adversaries

In all three models, appraisals of enviromental threat and engagement ineffortful coping are seen as activating psychophysiological reactivity-thefinal common pathway between the TABP arid CHD In the dozens ofstudies examining differences between Type As and Bs in theircardiovascular and neuroendocrine responses to threat and challenge, themajority have supposed the basic prediction that Type As are more reactive(Harbin, 1989; Houston, 1988) These effects are most reliable when the SI

is used to assess the TABP, and when the situation is at least mildlyprovoking or challenging Thus, the results are generally consistent with theinteractional stress moderation model discussed earlier

A transaction model of the association between the TABP and CHD has alsobeen outlined (T W Smith & N B Anderson, 1986; T W Smith &Rhodewalt, 1986) From this perspective, Type As are seen not only asoverresponding to environmental stressors, but also as creating morefrequent, severe, and enduring stressors Thus, the increasedpsychophysiological responsiveness believed to link the pattern to diseasecomes from two sources: the stressors that most individuals experience, andthe additional stressors Type As create for themselves through their stressengendering behavior Examples of Type A stress engendering behaviorsinclude selection of more demanding tasks, appraisal of tasks as requiring agreater level of achievement, eliciting or provoking competitive anddisagreeable behavior from others, and evaluating their own performancesharshly Such cognitive and overt behaviors would increase the cumulativeamount of exposure to threat and demand, increase psychophysiologicalresponses, and perpetuate the Type A style itself (T W Smith &N B.Anderson, 1986; T W Smith & Rhodewalt, 1986)

Another important view of the association between the TABP and illnesstakes the form of a constitutional predisposition model From thisperspective, overt Type A behaviors are seen as the consequence-rather thancause-of heightened sympathetic nervous system responsivity (Krantz &Durel, 1893) Likewise, this underlying biologic responsivity is thoughteventually to cause disease Thus, the statistical association between theTABP and CHD is a noncausal one, as both are influenced by a thirdvariable Some evidence suggests that there may be genetic influences on theTABP (Matthews, Rosenman, Dembroski, Harris, & MacDougall, 1984), aswell as basic physiologic differences between Type As and Bs (R B

Williams, Suarez, Kuhn, Schanberg, & Zimmermann, 1991) However, even

if an underlying biologic substrate does account for the phenotypicbehavioral differences between As and Bs, these overt behaviors are likely

to remain important in the development of disease For example, asdescribed in the transactional view, biologically vulnerable Type As would

be prone to exposing themselves to additional stressors Such increasedexposure to threats and demands would exert a negative effect on health,especially among individuals who are constitutionally hyperreactive

Hostility as the Toxic Component of Type A

Concern about the inconsistent findings regarding the health effects of theTABP has had one invaluable effect on subsequent work in the field; itprompted the examination of the individual elements or components withinthe pattern Beginning with a seminal paper by Matthews, Glass, Rosenman,and Bortner (1977), efforts to isolate a “toxic” component of the TABPquickly converged on hostility (Dembroski, MacDougall, Costa, & Grandits,1989; Hecker, Chesney, Black, & Frautchi, 1988) This developmentsparked a resurgence of interest in the centuries-old hypothesis that chronicanger and hostility contribute to the development of CHD (Dembroski et al.,1989; Siegman, 1994)

Assessment Although this area of research is usually identified by the label

of hostility, that term is more accurately reserved for one of three closelyrelated constructs (T W Smith, 1994) Anger refers to an unpleasantemotion, varying in intensity from mild irritation to rage It can be construed

as either a transitory state or a more enduring disposition (i.e., trait) Closelyrelated emotions include contempt and resentment In contrast, hostility

refers to a cognitive phenomenon In part, it refers to a negative attitudeabout others, consisting of enmity, denigration, and ill will Cynicism-thebelief that others are motivated by selfish concerns-and mistrust are closelyrelated cognitive processes Aggression refers to verbal behavior andphysical actions that are destructive or hurtful Although these three broadconstructs are clearly related and often co-occur, they are distinct

As with the TABP, two assessment procedures have become central indices

of this trait (Barefoot & Lipkus, 1994; T W Smith, 1992) Several differentbehavioral rating systems have been developed, primarily in the context ofsystems for scoring individual components of the TABP (Dembroski et al.,1989; Hecker et al., 1988) The most thoroughly developed and validated ofthese is the Interpersonal Hostility Assessment Technique (IHAT; Barefoot

& Lipkus, 1994; Haney et al., 1996) This rating system scores four specificaspects or manifestations of hostility in the Structured Interview- directchallenges or confrontations with the interviewer, hostile or uncooperativeevasions of questions, indirect challenges, and expression of irritation Theseratings can be made reliably, and have been found to correlate withangiographically documented coronary artery disease (Barefoot et al., 1994;Haney et al., 1996)

The second widely used measure is the Cook and Medley Hostility (Ho)Scale (W Cook & Medley, 1954) It consists of 50 true-false items, selectedfrom the Minnesota Multiphasic Personality Inventory (MMPI) based ontheir ability to discriminate between teachers with good versus poor rapportwith students (W Cook & Medley, 1954) Subsequent research with thescale has shown that it correlates highly with other self-report measures ofhostility, and correlates significantly, but less closely, with measures of

other negative affects (e.g., Pope, T W Smith, & Rhodewalt, 1990; T W.Smith & Frohm, 1985) The scale has also been found to be reliablyassociated with other affective, cognitive, and behavioral indicators ofhostility (Allred & T W Smith, 1991; Pope et al., 1990; Rosenberg et al.,1998; T W Smith, Sanders, & Alexander, 1990)

One troublesome psychometric characteristic of the scale is its poorlydefined internal structure (Contrada & Jussim, 1992) This has led someinvestigators to explore various approaches to identifying morehomogeneous subsets of items (e.g., Barefoot, Dodge, et al., 1989; Costa,Zonderman, Mc- Crae, & R B Williams, 1986) The scale's poor internalstructure and its correlation with characteristics other than anger andhostility are clear limitations of the scale However, the availability of largeMMPI data sets in which previously established cohorts can be reevaluatedregarding health status has permitted the rapid development of anepidemiological database on the health consequences of hostility, albeit with

a somewhat flawed measure of the construct

As in the case of the TABP, the primary behavioral and self-report measures

of the construct are only modestly intercorrelated (Dembroski, MacDougall,

R B Williams, Haney, & Blumenthal, 1985) Thus, the questionableconvergence of these measures raises a concern about the nature of theconstruct(s) under study There are a variety of other self-report and ratingscale measures of anger, hostility, and aggressive behavior used in thisliterature (for a review, see Barefoot & Lipkus, 1994; T W Smith, 1992),but only a few of these have been used in large, follow-up studies ofobjective health outcomes (e.g., Barefoot et al., 1987)

Association With Disease The initial studies of the prospective associationbetween behavioral ratings of hostility and subsequent CHD all suggestedthat hostility was indeed an important risk factor (Dembroski et al., 1989;Hecker et al., 1988; Matthews et al., 1977) Similarly, several early studiessuggested that self-reported hostility as measured by the Ho scale alsopredicted CHD and premature mortality (e.g., Barefoot, Dahlstrom, & R B.Williams, 1983; Shekelle, Gale, Ostfeld, & Paul, 1983) However, severalfailures to replicate the latter effect soon appeared in the literature (Hearn,Murray, & Leupker, 1989; Leon, Finn, Murray, & Bailey, 1988), againraising concerns about the consistency and importance of the risk associatedwith this trait

A recent meta-analysis of the literature on hostility and health supports thebasic conclusion that this characteristic is associated with increased risk ofserious illness and early death (T Q Miller et al., 1996) For example,behavioral measures of hostility were significantly associated withobjectively defined CHD (i.e., MI, coronary death), as was the Ho scale.Interestingly, the association between the Ho scale and subsequent CHD wassmall, suggesting that negative findings in some studies may be due tolimitations in sample size and the resulting low statistical power The Hoscale and other measures of cognitive aspects of hostility were also reliable-and stronger-predictors of all-cause mortality This suggests that there may

be pathways between hostile attitudes and beliefs and serious illness that areoutside the pathophysiology of CHD

Mechanisms of Association Several models of the association betweenhostility and health have been presented in the literature (T W Smith, 1992,1994) Similar to the process described in the interactional stress moderation

model and in the description of psychophysiological correlates of the TABP,

R B Williams, Barefoot, and Shekelle (1985) suggested that hostile personsare likely to respond to everyday stressors with exaggerated cardiovascularand neuroendocrine responses Further, heightened reactivity could facilitatethe development of CVD Some initial studies of the psychophysiologicalcorrelates of hostility suggested that this trait was not associated with greaterreactivity to standard laboratory stressors, such as mental arithmetic (e.g.,Sallis, Johnson, Trevorrow, Kaplan, & Hovell, 1987; M A Smith &Houston, 1987) However, subsequent studies have indicated thatinterpersonal stressors (e.g., harassment, conflict, self-disclosure) elicitreliably larger psychophysiological responses from hostile than nonhostilepersons (Christensen & T W Smith, 1993; Hardy & T W Smith, 1988; S

B Miller et al., 1998; Powch & Houston, 1996; T W Smith & Gallo, 1999;Suarez & R B Williams, 1989; Suarez, Kuhn, Schanberg, R B Williams,

& Zimmermann, 1998) This literature generally supports the conclusion thathostility is associated with psychophysiological reactivity to interpersonal,but not nonsocial, stressors (Houston, 1994; Suls & Wan, 1993) In aninteresting extension of this pattern, Lepore (1995) found that the provision

of social support attenuated cardiovascular reactivity in nonhostile persons,Hostile subjects did not benefit from the availability of support Thus,hostility may be associated with both heightened reactivity to social stressorsand decreased psychophysiological benefit from social resources

Hostility has also been linked to physiological stress responses in the naturalenvironment For example, Pope and T W Smith (1991) demonstrated thathostility is associated with larger daily excretion of cortisol, and Jamner,Shapiro, Goldstein, and Hug (1991) found that hostility is associated with

larger ambulatory blood pressure responses to interpersonally stressfulsituations Several ambulatory studies have indicated that hostility isassociated with higher levels of blood pressure and/or heart rate during dailyactivities (Benotsch, Christensen, & McRelvey, 1997; Linden, Chambers,Maurice, & Lenz, 1993; Guyll & Contrada, 1998) Recent research has alsoshown that hostility is associated with stress-induced changes in immuneresponses, perhaps suggesting a mechanism through which this trait mightinfluence noncardiovascular illnesses (Christensen, Edwards, Wiebe,Benotsch, & McKelvey, 1996)

Anger and hostility, considered either as individual difference variables or astransient, situationally evoked responses, have also been linked to theprecipitation of myocardial ischemia among patients with significantcoronary artery disease The arousal of anger, irritation and frustration canprecipitate ischemic changes during laboratory tasks (Ironson et al., 1992)and during routine daily activity, as assessed with ambulatory monitoring(Gabbay et al., 1996; Gullette, Blumenthal, & Babyak, 1997) Episodes ofanger have also been found to precipitate acute myocardial infarctions(Mittleman et al., 1995) Further, ischemic changes have been found to bemore pronounced among hostile patients, both in response to laboratorystessors (Burg, Jain, Soufer, Kerns, & Zaret, 1993), and during the course ofdaily activities (Helmers et al., 1993) One study suggested that thecombination of high hostility and defensiveness as measured by theMarlowe-Crown Social Desirability Scale, was associated with greaterischemia among heart patients both in response to laboratory stressors andduring ambulatory monitoring (Helmers et al., 1995) Thus, regardless ofwhether or not hostility can initiate and hasten the development of CAD, it is

likely to contribute to CHD through the precipitation of ischemic events.Behavioral ratings of hostility have also been found to predict more rapidrestenosis following coronary angioplasty (Goodman, Quigley, Moran,Meilman, & Sherman, 1996)

In addition to these direct psychophysiological connections between hostilityand disease, research has addressed behavioral links For example, hostilityhas been found to be consistently associated with increased experience ofstressful life circumstances and decreased levels of social support, a patterndescribed as psychosocial vulnerability (T W Smith & Frohm, 1985; T W.Smith, Pope, Sanders, Allred, & O'Keeffe, 1988) Compared with their moreagreeable counterparts, hostile persons report more major life stressors andminor events (i.e., daily hassles), and fewer and less satisfactory socialsupports (Barefoot et al, 1983; Houston & Kelly, 1989; Scherwitz, Perkins,Chesney, & Hughes, 1991; T W Smith et al., 1988; Suls, Martin, & David,1998) Hostility is also associated with self-reports and behavioral displays

of marital conflict (Houston & Kelly, 1989; T W Smith, Sanders, &Alexander, 1990) This pattern of high conflict and low support also appears

in hostile persons' descriptions of their work environments (T W Smith etal., 1988) and families of origin (Houston & Vavak, 1991; McGonigle, T

W Smith, Benjamin, & Turner, 1993; T W Smith et al., 1988)

Although most of this research on psychosocial vulnerability has relied oncross-sectional or even retrospective methodologies, recent studies foundevidence of a prospective association between hostility and subsequentincreases in marital conflict (T Q Miller, Marksides, Chiriboga, & Ray,1995; Newton & Kiecolt-Glaser, 1995) So, in addition to the heightenedreactivity to interpersonal stressors described in the psychophysiological

reactivity model, the psychosocial vulnerability model suggests that the riskassociated with hostility might also reflect a greater degree of exposure tosuch situations and a concurrent lack of resources or buffers in facing them

The transactional approach has also been applied to hostility (T W Smith,1995; T W Smith &Pope, 1990) From this perspective, the heightenedinterpersonal conflict and reduced support experienced by hostile personsreflects a reciprocal relation between their actions and the responses ofothers Through their expectations of mistreatment and outwardlydisagreeable behavior, hostile persons are likely to create conflict,undermine cooperation and support, and foster opposition from others (T

W Smith, 1995; T W Smith & Pope, 1990) Once created, such anenvironment would likely be interpreted as confirming the accuracy of thehostile person's interpersonal “world view, “ as well as the apparentnecessity of an antagonistic behavioral style in dealing with others Suchdynamic patterns are likely to be seen in momentary interactions lasting afew minutes, in more enduring relations, and in repeating patterns over manyyears (Caspi et al., 1989; Henry, 1996; Kiesler, 1991; Wachtel, 1994)

Another psychological connection between hostility and health is consistentwith the health behavior model Several studies have indicated that hostilepersons engage in unhealthy practices, such as smoking and excessivealcohol use (Siegler, 1994) Epidemiological studies attempting to controlstatistically the possible role of such health practices have suggested that thehealth behavior model does not account for the health consequences of thistrait (T Q Miller et al., 1996) However, as noted earlier, compelling tests

of such mediational models are extremely difficult to conduct (Contrada et

al., 1990), and some studies do support the health behavior model of theeffects of hostility on health (Evenson et al., 1997)

Constitutional models of the health consequences of hostility have also beenpresented For example, R B Williams (1994) argued that low brain levels

of serotonin could underlie the affective and behavioral features of hostility(cf Coccaro, Kavoussi, Cooper, & Hauger, 1997), the autonomic labilityidentified as a psychophysiologic mechanism linking hostility and health,and unhealthy behaviors associated with this trait (e.g., smoking, alcoholconsumption, excessive calorie and fat intake) Thus, a single central deficit-reduced brain levels of a specific neurotransmitter-is seen as responsible forthis cluster of biobehavioral characteristics and the statistical associationbetween hostility and health J R Kaplan, Botchin, and Manuck (1994)similarly suggested that reduced central serotonergic drive might be thebasis of the associations between aggressive behavior and related affect,physiological responsivity, and CHD in animal models

Unlike the early literature on the global TABP, descriptions of thesemechanisms linking hostility and health have not included detaileddiscussion of the psychological underpinnings of hostility Certainly, hostilebehavior can be seen as a strategy for exercising interpersonal control(Averill, 1982) or attempting to secure desired outcomes during competitivestruggles (Bandura, 1973) Further, hostility is associated with endorsement

of the beliefs related to the TABP (P L Watkins, Ward, Southard, & Fisher,1992) Thus, the psychological perspectives on coronary prone behaviorproposed by Glass (1977), Powell (1992), and Price (1982) described earlierare also relevant to hostility However, other perspectives from outsidetraditional health psychology and behavioral medicine are relevant as well