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Hostility and caffeine: cardiovascular effects during stress and recovery
Personality and Individual Differences 30 (2001) 1125±1137
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Hostility and caeine: cardiovascular eects during stress and recovery Barry D. Smith *, David Cranford, Lee Green Department of Psychology, University of Maryland, College Park, MD 20742, USA Received 10 November 1999; received in revised form 23 March 2000
Abstract Both hostility and caeine are frequently cited as potential factors in coronary heart disease (CHD). The present study examined the independent and interactive eects of these important variables on cardiovascular functioning. The Cook±Medley Scale was used to select 24 high and 24 low hostile subjects, who received caeine (400 mg) or a placebo (lactose) in a double-blind design. All completed mental arithmetic (MA) and anagram stress tasks during which they experienced periods of verbal harassment and non-harassment. Blood pressure and heart rate were recorded. The combination of high hostility and harassment increased diastolic blood pressure (DBP) and maintained elevated levels of mean arterial pressure (MAP) during task periods, while reducing DBP recovery during rest periods. Caeine increased systolic blood pressure (SBP) and interacted with harassment to create an inverted-U eect, reducing blood pressure. Finally, hostility and caeine interacted to maintain elevated levels of DBP during recovery periods. These results support the dual-interactional theory of personality and behavior, which suggests an interaction of genetic and environmental factors and of dispositional and situational factors. # 2001 Elsevier Science Ltd. All rights reserved. Keywords: Hostility; Caeine; Cardiovascular; Heart rate; Blood pressure; Arousal; Stress; Harassment
1. Introduction Three factors frequently cited in the development of coronary heart disease (CHD) are hostility (Smith, Tola & Mann, 2000; Kop, 1997), gender (Smith, Cranford & Mann, 2000) and caeine use (Smith & Tola, 1998). In a recent study in which heart rate and blood pressure were monitored while subjects were exposed to physical, emotional, and cognitive stressors, we found evidence
* Corresponding author. Tel.: +1-301-776-3983; fax: +1-301-314-9566. E-mail address: [email protected] (B.D. Smith). 0191-8869/01/$ - see front matter # 2001 Elsevier Science Ltd. All rights reserved. PII: S0191-8869(00)00097-0
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supporting the hostility and gender hypotheses (Smith, Cranford, et al., 2000). Men had consistently higher blood pressures than women, and high and low hostile subjects diered in heart rate and blood pressure. The purpose of the present study was to examine the independent and interactive eects of hostility with the third factor, caeine, on cardiovascular functioning. The hostility hypothesis has recently been con®rmed by a number of studies and meta-analyses (Everson et al., 1997; Lahad, Heckbert, Koepsell, Psaty & Patrick, 1997; Miller, Smith, Turner, Guijarro & Hallet, 1996), including our work (Smith, Cranford, et al., 2000). Hostility appears to be associated with increased cardiovascular and neuroendocrine responses to stress and possibly also with reduced parasympathetic antagonism of sympathetically mediated arousal (Smith, Cranford, et al., 2000; Smith, Tola, et al., 2000; Williams, 1987). Based on the senior author's theoretical arousal model (Smith, 1983, 1994; Smith & Tola, 1998), the authors therefore hypothesized that excessive arousal may have a dierentially greater adverse cardiovascular impact on those who are high in trait hostility. Supportive studies have shown that the hostility eect may include both the dierential reactivity of the cardiovascular system to stress and dierences in resting cardiovascular values (Benotsch, Christensen & McKelvey, 1997; Bongard, al'Absi & Lovallo, 1998; Carels, Sherwood & Blumenthal, 1998; Shapiro, Jamner & Goldstein, 1997; Voegele, 1998). The present study employed a drug Ð caeine Ð and two experimental stress tasks Ð mental arithmetic and anagrams Ð to increase arousal in participants high and low in hostility under verbal harassment and non-harassment conditions. The authors hypothesized that caeine, hostility, and their interaction aect cardiovascular functioning, with the combination of high hostility and caeine producing the greatest blood pressure elevations. Although the relevant literature is somewhat mixed, it was expected that caeine would have greater in¯uence on systolic and hostility on diastolic pressure (Bongard et al., 1998; Green & Suls, 1996). 2. Method 2.1. Subjects Twenty-four high hostile (11 male and 13 female) and 24 low hostile (10 male and 14 female) participants, ranging in age from 18 to 25, were selected from a screening group of 218 students in lower-level psychology courses, who completed the Cook±Medley Hostility Scale. The high-hostility (HH) group had scores of 27 or higher X 30:79; while the low-hostility (LH) group had scores of 19 or lower X 13:75: These means are consistent with those found in similar studies (Hardy & Smith, 1988; Smith, Cranford, et al., 2000). 2.2. Apparatus Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and heart rate (HR) were measured, using a Dinamap Vital Signs monitor (Critikon Model 8100). All visual stimuli appeared on a high resolution color monitor, and auditory stimuli were computer-generated, recorded tones. They were delivered through a speaker in an Audio Suttle, Model AS-109 (Type 40 C) sound booth.
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2.3. Questionnaire The Cook±Medley Hostility Scale was employed to assess what is probably best described as cynical hostility (Smith & Frohm, 1985). Participants with high scores tend to be higher in neuroticism (Costa, Zonderman, McCrae & Williams, 1986), which is also correlated with ischaemic heart disease (Marusic, Gudjonsson, Eysenck & Starc, 1999). 2.4. Experimental tasks and harassment intervention Two cognitive stress tasks were used in the experiment. The ®rst was a mental arithmetic (MA) task, in which subjects serially subtracted 7 from a number on the computer screen. Subjects heard a tone every 2 sec and attempted to make verbal subtractions within that time interval. There were two verbal harassment (at 2 and 3 min) and two non-harassment (at 1 and 4 min) trials. This pattern of trials allowed us to obtain control (non-harassment) readings before and after the two harassment trials. The second task involved 30 ®ve-letter anagrams, each displayed on the screen for 15 sec. There were three harassment (minutes 1, 5, and 7) and three non-harassment (minutes 2, 3, and 6) trials. 2.5. Procedure A double-blind procedure was employed for both hostility group and drug condition. Equal numbers of HH and LH subjects were randomly assigned to the caeine and placebo conditions. Following informed consent, subjects completed screening questionnaires assessing health factors, caeine sensitivity, and recent drug usage (Smith, Davidson & Green, 1993). Two subjects were dropped, one due to reported lack of sleep, the other due to reported caeine sensitivity, and randomly replaced. The subject was next given either caeine (400 mg) or an equal amount of placebo (lactose) mixed in fruit juice. The experiment proper began 45 min after caeine ingestion (Davidson & Smith, 1989). A blood pressure cu was secured to the non-dominant arm and initial instructions given. Counterbalancing the order of presentation of the two tasks, the experiment that followed consisted of ®ve phases: A 10-min baseline, ®rst task (MA or anagrams), ®rst 5-min recovery period, second task, second 5-min recovery period. Blood pressure and heart rate were taken at 60-sec. intervals throughout all ®ve phases. Following the experiment, a questionnaire assessed emotions experienced during the study. 3. Results The four cardiovascular measurements (DBP, SBP, MAP, and HR) were determined separately for each participant on each trial (two trials of each type of Intervention for MA and three of each for anagrams). All scores were range-corrected (Lykken, 1972), then subjected to analyses of variance and covariance. The principal between-subject factors were Hostility Group (high vs low) and Drug Condition (caeine vs placebo). The principal within-subject factors were Intervention (harassment vs non-harassment) and Repetitions of harassment or non-harassment.
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Baseline scores were covaried. In analyses of non-task intervals, a Periods factor, with three levels (Baseline, Recovery 1, and Recovery 2) replaced the Repetitions and Intervention factors. Univariate ANOVA and ANCOVA results are reported only when the appropriate omnibus F in the relevant MANOVA or MANCOVA was signi®cant. 3.1. Diastolic blood pressure Analysis of MA data yielded a signi®cant Drug ConditionInterventionRepetition interaction [F(1, 44)=4.59, p<0.05]. Harassment had no overall eect on DBP under placebo and produced a decrease across trials under caeine (Fig. 1). With no harassment, there was a decrease under
Fig. 1. Dierential change in DBP as an interactive function of Drug Condition and Harassment Intervention.
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placebo and a substantial increase under caeine conditions. For the anagram task, there was a signi®cant Hostility GroupInterventionRepetition interaction [F(2, 88)=3.87, p<0.025]. The LH subjects showed a gradual decrease in DBP under non-harassment conditions and a slight increase on the third trial under harassment conditions (Fig. 2). By comparison, HH subjects
Fig. 2. Interactive eects of Hostility Group and Harassment Intervention on the change in DBP over trials.
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showed a crossover eect, in which there was a decrease in DBP under non-harassment and an increase under harassment conditions. The ®nal analysis examined DBP during non-stimulation periods, including the pre-task Baseline, Recovery 1 and Recovery 2. The analysis yielded signi®cant eects of Hostility Group [F(1, 44)=4.32, p<0.05] and the Hostility GroupConditionPeriod Interaction [F(2, 88)=3.18, p<0.05]. The Group eect was due to higher DBP in the HH group X 66:86 than in the LH group (60.61). The interaction showed that caeine maintained higher blood pressures in both groups, but with highest pressures occurring when hostility and caeine were combined (Fig. 3).
Fig. 3. Change in DBP across baseline and recovery periods as an interactive function of Hostility Group and Drug Condition.
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3.2. Systolic blood pressure Data for the MA task yielded a signi®cant main eect of Drug Condition [F(1, 44)=6.97, p<0.025] due to higher mean SBP under caeine X 135:9 than placebo (125.36) conditions. A
Fig. 4. Dierential change in MAP as an interactive function of Hostility Group and Harassment Intervention.
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signi®cant ConditionInterventionRepetition crossover interaction, F(1, 44)=4.96, p<0.05 was the same as that for DBP: caeine caused a clear increase in SBP across trials when no harassment occurred and a clear decrease when harassment did occur (cf Fig. 1). Anagram task data yielded a signi®cant main eect of Drug Condition [F(1, 44)=4.51, p<0.05], with SBP again higher under caeine X 127:8 than under placebo (119.72). An analysis of the baseline and recovery periods yielded a signi®cant main eect of Drug Condition, F(1, 44)=4.14, p<0.05. Mean SBP was higher under caeine X 119:85 than under placebo (113.56) conditions. 3.3. Mean arterial pressure For the MA task, there was a signi®cant main eect of Drug Condition [F(1, 44)=7.15, p<0.025] due to higher MAP under caeine X 102:01 than placebo (95.30). A Drug ConditionInterventionRepetition Interaction [F(1, 44)=9.80, p<0.005] re¯ected the same pattern of increase in MAP in the placebo group but decrease in the caeine group under harassment as was seen for DBP and SBP (cf Fig. 1). Anagram task data yielded signi®cant eects of Drug Condition [F(1, 44)=6.42, p<0.025] and the GroupInterventionRepetition Interaction [F(2, 88)=6.84, p<0.005]. Mean MAP was higher under caeine X 95:05 than placebo (88.80) conditions. Fig. 4 shows that with no harassment, both groups demonstrated a decrement in MAP over trials. With harassment, low hostiles still decreased, but high hostiles increased substantially on the third trial. Baseline and recovery period data showed a signi®cant eect of Drug Condition [F(1, 44)=4.60, p<0.05]. Means were 87.80 and 83.41 for caeine and placebo, respectively, demonstrating the arousal eect of caeine. 3.4. Heart rate There were no signi®cant Hostility Group or Drug Condition eects for either the MA or the anagram task. Baseline and recovery period data, however, yielded three signi®cant interactions. The Drug Condition by Period eect [F(2, 88)=3.87, p<0.025] re¯ected the steady increase in heart rate from baseline through and including Recovery 2 for the placebo group and an increase followed by a decrease in the caeine group. The interaction of Hostility Group with Period [F(2, 88)=3.18, p<0.05] showed a steady increase in HR from Baseline through Recovery 2 for the low hostiles and a slight decrease to a stable and lower baseline in high hostiles. Finally, the signi®cant Drug ConditionGroupRepetition Interaction [F(2, 88)=4.07, p<0.025] shows an interesting reversal of the two hostility groups under placebo and caeine conditions (Fig. 5). With caeine, high hostiles started at a much lower heart rate and increased slightly to a rate that was still considerably lower than that of the placebo group. The latter showed a decremental trend. 3.5. Questionnaire data The post-experimental questionnaire assessed subjective aect before and during the experiment for each of ®ve emotions: happiness, anger, depression, anxiety, and frustration (Table 1).
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Fig. 5. Change in HR across trials under the interactive in¯uence of Drug Condition and Hostility Group.
The experimental manipulation produced signi®cant perceived increases in intensity for the negative emotions and a decrease in happiness. In addition, caeine caused higher overall levels of anxiety [F(1,44)=10.91, p<0.005]. There were no Hostility Group dierences. 4. Discussion Present results con®rmed our hypothesis that both hostility and caeine impact cardiovascular functioning. Moreover, independent eects of the two variables were observed during stressful task performance, and interactive eects were seen during recovery. Finally, questionnaire data supported the eectiveness of the experimental stress manipulations in that negative emotion
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Table 1 Perceived emotional intensity Emotion
Before experiment
During experiment
F
p
Happiness Anger Anxiety Depression Frustration
2.81 1.19 2.00 1.65 1.21
2.31 1.96 3.23 2.40 3.25
11.47 22.58 45.97 23.60 99.66
<0.005 <0.0001 <0.0001 <0.0001 <0.0001
increased and positive emotion decreased. Interestingly, however, anger increased no more than other negative emotions, and the signi®cant group dierences in blood pressure were not accompanied by group dierences in perceived emotional intensity. 4.1. Hostility eects Blood pressure data in the present study validated the earlier ®nding that high hostility, when combined with interpersonal stress, increases cardiovascular arousal (Miller et al., 1996) and extended that ®nding to demonstrate recovery eects that included interactions with caeine. The anagram stress task produced BP habituation overall, but high-hostile participants faced with harassment experienced increases in DBP and were unable to sustain decreases in MAP. This ®nding is consistent with other work showing selective increases in the blood pressures of high hostile subjects during a stressful task, particularly one involving interpersonal con¯ict (Hardy & Smith, 1988; Smith & Allred, 1989; Suarez & Williams, 1989). For high hostile subjects in the present study, interpersonal stress also aected the recovery of diastolic pressure. There was less DBP reduction during recovery in high hostiles than in their low hostile counterparts. Both this ®nding and the observed BP elevations in high hostiles during task periods suggest that hostility increases arousal and inhibits recovery under conditions of stress. This conclusion is supported by data from earlier studies (Hardy & Smith, 1988; Smith & Allred, 1989) and may suggest that hostility should be included among such other arousal-related personality dimensions as sensation-seeking (Smith, Davidson, Perlstein & Gonzalez, 1990) and extraversion (Smith, Concannon, Rockwell, Bozman & Kline, 1990). It was not, of course, hostility alone, but rather the interaction of hostility with the situational stress factor that produced the group dierences. This observation supports the theories of Williams (1987), Siegman (1988), and the present senior author (Smith, Cranford, et al., 2000; Smith, Tola, et al., 2000). Moreover, it is consistent with other work showing that high hostility is associated with increases in blood pressure under stress (Pettit, Marchand & Graham, 1999), particularly when the stressor involves an interpersonal element (Morris-Prather et al., 1996). These eects can be interpreted within the context of a dual-interactional theory of personality and behavior (Smith, 1994). This theory basically suggests that genetic and environmental factors interact to produce stable dispositions, such as the hostility trait. These dispositions then interact with speci®cally relevant current situational factors to produce behavior. We would accordingly hypothesize that hostility has a genetic predisposition (Carmelli, Rosenman & Swan, 1988; Matthews, Manuck & Saab, 1986), probably expressed in part in terms of arousal or arousability (Smith &
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Tola, 1998). This predisposition combines with experience to produce an individual who is suspicious, cynical, and resentful. Such characteristics lead to increased vigilance, which is associated with elevated arousal (Cantero, Atienza, Salas & Gomez, 1999) and, correspondingly, with increases in vasoconstriction, norepinephrine, and testosterone (Williams et al., 1982). Thus primed by genetics, experience, and physiology, high hostile subjects react more strongly to situational stressors with at least increases in diastolic pressure and the derivative mean arterial pressure. The reason for the selective increase in DBP is not entirely clear. However, there is some evidence that the vigilance hypothetically characteristic of high hostiles causes muscular vasoconstriction without associated changes in cardiac output (Harms et al., 1998), leading to increases in DBP alone. The previously observed association of DBP with anger arousal (Kop, 1997) and with hostility (Smith, Cranford, et al., 2000) further supports this interpretation. 4.2. Caeine eects The eects of caeine in the present study were largely independent of those of hostility. There were consistent caeine-induced increases in systolic pressure and in mean arterial pressure across both task and recovery periods, with no accompanying increase in heart rate. Other work has also shown selective increases in systolic pressure (Myers, Shapiro, McClure & Daims, 1989), consistent with the well-documented arousal eects of caeine (Myers & Reeves, 1993; Smith & Tola, 1998). A more interesting ®nding was the interaction of caeine with harassment on all three blood pressure measures. In all cases, caeine increased blood pressure under non-harassment conditions but decreased it under harassment. While this result may at ®rst appear counter-intuitive, it is consistent with a theoretical inverted-U-shaped arousal function. Basically, increasing arousal causes an increment in physiological activation up to a point. A further increase in arousal intensity then produces transmarginal inhibition (Nebylitsyn, 1972; Watters, Martin & Schreter, 1997), causing arousal indicators to asymptote or even decrease. In the present study, the combined eect of two arousal agents, caeine and harassment, pushed arousal past the peak of the inverted-U-shaped function, causing a decrease in arousal output. This ®nding is consistent with the recent theory that caeine acts to enhance a variety of other sources of arousal (Smith, 1994). If the arousal increment produced by caeine is relatively small, the overall arousal output should be high. However, if caeine and stress increase arousal further, arousal output may decrease as transmarginal inhibition develops. 4.3. Hostility and caeine Hostility and caeine interacted to aect physiology only during recovery periods. Heart rate under caeine increased across baseline and recovery periods in high hostile participants and decreased from a higher starting point in lows. For blood pressure, it was the combination of caeine and high hostility that maintained the highest levels of diastolic pressure during recovery. In addition, both placebo and low hostility conditions were associated with decreases in DBP across recovery periods. Only the combination of caeine and high hostility maintained elevated pressure across periods. Applied to actual situations, these data would suggest that the blood pressure of high hostile subjects taking caeine is not dierentially aected while performing
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tasks. However, task-induced elevations in this group will not recover as quickly when there is caeine in the system or perhaps when other arousal sources are present. Further research is clearly needed to better understand the interactive eects of caeine and hostility during periods of task performance. It was frankly surprising to ®nd no such interactive eects in the present study. It may, of course, be that the two variables act entirely independently during tasks. However, it is also possible that interactions will be found during less stressful tasks or in the absence of an interpersonal stress manipulation. 5. Conclusions Present results showed that, as hypothesized, hostility aects primarily diastolic blood pressure, while caeine aects principally systolic pressure, at least under the experimental conditions represented here. This may suggest that DBP under stress is aected by more chronic conditions, such as those represented by a personality trait variable, while systolic pressure is more responsive to such acute conditions as caeine-induced arousal. More data will be needed, however, before any ®rm conclusions can be drawn. References Benotsch, E. G., Christensen, A. J., & McKelvey, L. (1997). Hostility, social support, and ambulatory cardiovascular activity. Journal of Behavioral Medicine, 20, 163±176. Bongard, S., al'Absi, M., & Lovallo, W. R. (1998). Interactive eects of trait hostility and anger expression on cardiovascular reactivity in young men. International Journal of Psychophysiology, 28(2), 181±191. Cantero, J. L., Atienza, M., Salas, R. M., & Gomez, C. M. (1999). Alpha EEG coherence in dierent brain states: An electrophysiological index of the arousal level in human subjects. Neuroscience Letter, 271(3), 167±170. Carels, R. A., Sherwood, A., & Blumenthal, J. A. (1998). Psychosocial in¯uences on blood pressure during daily life. International Journal of Psychophysiology, 28, 117±129. Carmelli, D., Rosenman, R. H., & Swan, G. E. (1988). The Cook and Medley HO Scale: A heritability analysis in adult male twins. Psychosomatic Medicine, 50, 165±170. Costa, P. T., Zonderman, A. B., McCrae, R. R., & Williams, R. B. (1986). Cynicism and paranoid alienation in the Cook and Medley Ho scale. Psychosomatic Medicine, 48, 283±285. Davidson, R. A., & Smith, B. D. (1989). Arousal and habituation: Dierential eects of caeine sensation seeking and task diculty. Personality and Individual Dierences, 10, 111±119. Everson, S. A., Kauhanen, J., Kaplan, G. A., Goldberg, D. E., Julkunen, J., Tuomilehto, J., & Salonen, J. T. (1997). Hostility and increased risk of mortality and acute myocardial infarction: The mediating role of behavioral risk factors. American Journal of Epidemiology, 146, 142±152. Green, J. J., & Suls, J. (1996). The eects of caeine on ambulatory blood pressure, heart rate, and mood in coee drinkers. Journal of Behavioral Medicine, 19, 111±128. Hardy, J. D., & Smith, T. W. (1988). Cynical hostility and vulnerability to disease: Social support, life stress, and physiological response to con¯ict. Health Psychology, 7, 447±459. Harms, C. A., Wetter, T. J., McClaran, S. R., Pegelow, D. F., Nickele, G. A., Nelson, W. B., Hanson, P., & Dempsey, J. A. (1998). Eects of respiratory muscle work on cardiac output and its distribution during maximal exercise. Journal of Applied Physiology, 85, 609±618. Kop, W. J. (1997). Acute and chronic psychological risk factors for coronary syndromes: Moderating eects of coronary artery disease severity. Journal of Psychosomatic Research, 43, 167±181. Lahad, A., Heckbert, S. R., Koepsell, T. D., Psaty, B. M., & Patrick, D. L. (1997). Hostility, aggression and the risk of nonfatal myocardial infarction in postmenopausal women. Journal of Psychosomatic Research, 43, 183±195.
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Lykken, D. A. (1972). Range correction applied to heart rate and GSR data. Psychophysiology, 9, 151±159. Marusic, A., Gudjonsson, G. H., Eysenck, H. J., & Starc, R. (1999). Biological and psychosocial risk factors in ischaemic heart disease: Empirical ®ndings and a biopsychosocial model. Personality and Individual Dierences, 26, 285±304. Matthews, K. A., Manuck, S. B., & Saab, P. G. (1986). Cardiovascular responses of adolescents during a naturally occurring stressor and their behavioral and psychophysiological predictors. Psychophysiology, 23, 198±209. Miller, T. Q., Smith, T. W., Turner, C. W., Guijarro, M. L., & Hallet, A. J. (1996). A meta-analytic review of research on hostility and physical health. Psychological Bulletin, 119, 322±348. Morris-Prather, C. E., Harrell, J. P., Collins, R., Leonard, K. L., Boss, M., & Lee, J. W. (1996). Gender dierences in mood and cardiovascular responses to socially stressful stimuli. Ethnicity Discourse, 6(12), 123±131. Myers, M. G., & Reeves, R. A. (1993). The eect of caeine on daytime ambulatory blood pressure. American Journal of Hypertension, 4, 427±431. Myers, H. F., Shapiro, D., McClure, F., & Daims, R. (1989). Impact of caeine and psychological stress on blood pressure in black and white men. Health Psychology, 8, 597±612. Nebylitsyn, V. D. (1972). Fundamental properties of the human nervous system. Oxford: Pergamon Press. Pettit, S. E., Marchand, I., & Graham, T. (1999). Gender dierences in cardiovascular and catecholamine responses to cold-air exposure at rest. Canadian Journal of Applied Physiology, 24, 131±147. Shapiro, D., Jamner, L. D., & Goldstein, I. B. (1997). Daily mood states and ambulatory blood pressure. Psychophysiology, 34, 399±405. Siegman, A. W. (1988). Typ A und danach: Die Bedeutung von Feindseligkeit Neurotizismus und Sprechstil fur koronareHerzerkrankungen. Z Klin Psychol Psychopathol Psychother, 36, 3±24. Smith, B. D. (1983). Extraversion and electrodermal activity: Arousabilty and the inverted-U. Personality and Individual Dierences, 4, 411±419. Smith, B. D. (1994). Eects of acute and habitual caeine ingestion on physiology and behavior: Tests of a biobehavioral arousal theory. Pharmacopsychoecologia, 7, 75±84 Invited article. Smith, T. W., & Allred, K. D. (1989). Blood pressure reactivity during social interaction in high and low cynical hostile men. Journal of Behavioral Medicine, 11, 135±143. Smith, B. D., Concannon, M., Rockwell, S., Bozman, A., & Kline, R. (1990). Regression and criterion measures of habituation: A comparative analysis in extraverts and introverts. Journal of Research on Personality, 24, 123±132. Smith, B. D., Cranford, D., & Mann, M. (2000). Gender, cynical hostility, and cardiovascular functioning: Implications for dierential cardiovascular disease risk. Personality and Individual Dierences. Smith, B. D., Davidson, R. A., & Green, R. L. (1993). Eects of caeine and gender on physiology and performance: Further tests of a biobehavioral model. Physiology and Behavior, 54, 415±422. Smith, B. D., Davidson, R. A., Perlstein, W., & Gonzalez, F. (1990). Sensation-seeking: Electrodermal and behavioral eects of stimulus content and intensity. International Journal of Psychophysiology, 9, 179±188. Smith, T. W., & Frohm, K. D. (1985). What's so unhealthy about hostility? Construct validity and psychosocial correlates of the Cook and Medley Ho Scale. Health Psychology, 4, 503±520. Smith, B. D., & Tola, K. (1998). Caeine: Eects on psychological functioning and performance. In G. Spiller, Caeine (pp. 251±299). New York: CRC Press. Smith, B. D., Tola, K., & Mann, M. (2000). Caeine and arousal: A biobehavioral theory of physiological, behavioral, and emotional eects. In B. S. Gupta, Caeine and behavior: Current views and research trends. CRC Press. Suarez, E. C., & Williams, R. B. (1989). Situational determinants of cardiovascular and emotional reactivity in high and low hostile men. Psychosomatic Medicine, 51, 404±418. Voegele, C. (1998). Serum lipid concentrations, hostility and cardiovascular reactions to mental stress. International Journal of Psychophysiology, 28(2), 167±179. Watters, P. A., Martin, F., & Schreter, Z. (1997). Caeine and cognitive performance: The nonlinear Yerkes±Dodson Law. Human Psychopharmacology, 12, 249±257. Williams, R. B. (1987). Re®ning the type A hypothesis: Emergence of the hostility complex. American Journal of Cardiology, 60, 27J±32J. Williams, R. B., Lane, J. D., Kuhn, C. M., Melosh, W., White, A. D., & Schanberg, S. M. (1982). Type A behavior and elevated physiological and neuroendocrine responses to cognitive tasks. Science, 218, 483±485.
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Hostility and caeine: cardiovascular eects during stress and recovery Barry D. Smith *, David Cranford, Lee Green Department of Psychology, University of Maryland, College Park, MD 20742, USA Received 10 November 1999; received in revised form 23 March 2000
Abstract Both hostility and caeine are frequently cited as potential factors in coronary heart disease (CHD). The present study examined the independent and interactive eects of these important variables on cardiovascular functioning. The Cook±Medley Scale was used to select 24 high and 24 low hostile subjects, who received caeine (400 mg) or a placebo (lactose) in a double-blind design. All completed mental arithmetic (MA) and anagram stress tasks during which they experienced periods of verbal harassment and non-harassment. Blood pressure and heart rate were recorded. The combination of high hostility and harassment increased diastolic blood pressure (DBP) and maintained elevated levels of mean arterial pressure (MAP) during task periods, while reducing DBP recovery during rest periods. Caeine increased systolic blood pressure (SBP) and interacted with harassment to create an inverted-U eect, reducing blood pressure. Finally, hostility and caeine interacted to maintain elevated levels of DBP during recovery periods. These results support the dual-interactional theory of personality and behavior, which suggests an interaction of genetic and environmental factors and of dispositional and situational factors. # 2001 Elsevier Science Ltd. All rights reserved. Keywords: Hostility; Caeine; Cardiovascular; Heart rate; Blood pressure; Arousal; Stress; Harassment
1. Introduction Three factors frequently cited in the development of coronary heart disease (CHD) are hostility (Smith, Tola & Mann, 2000; Kop, 1997), gender (Smith, Cranford & Mann, 2000) and caeine use (Smith & Tola, 1998). In a recent study in which heart rate and blood pressure were monitored while subjects were exposed to physical, emotional, and cognitive stressors, we found evidence
* Corresponding author. Tel.: +1-301-776-3983; fax: +1-301-314-9566. E-mail address: [email protected] (B.D. Smith). 0191-8869/01/$ - see front matter # 2001 Elsevier Science Ltd. All rights reserved. PII: S0191-8869(00)00097-0
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supporting the hostility and gender hypotheses (Smith, Cranford, et al., 2000). Men had consistently higher blood pressures than women, and high and low hostile subjects diered in heart rate and blood pressure. The purpose of the present study was to examine the independent and interactive eects of hostility with the third factor, caeine, on cardiovascular functioning. The hostility hypothesis has recently been con®rmed by a number of studies and meta-analyses (Everson et al., 1997; Lahad, Heckbert, Koepsell, Psaty & Patrick, 1997; Miller, Smith, Turner, Guijarro & Hallet, 1996), including our work (Smith, Cranford, et al., 2000). Hostility appears to be associated with increased cardiovascular and neuroendocrine responses to stress and possibly also with reduced parasympathetic antagonism of sympathetically mediated arousal (Smith, Cranford, et al., 2000; Smith, Tola, et al., 2000; Williams, 1987). Based on the senior author's theoretical arousal model (Smith, 1983, 1994; Smith & Tola, 1998), the authors therefore hypothesized that excessive arousal may have a dierentially greater adverse cardiovascular impact on those who are high in trait hostility. Supportive studies have shown that the hostility eect may include both the dierential reactivity of the cardiovascular system to stress and dierences in resting cardiovascular values (Benotsch, Christensen & McKelvey, 1997; Bongard, al'Absi & Lovallo, 1998; Carels, Sherwood & Blumenthal, 1998; Shapiro, Jamner & Goldstein, 1997; Voegele, 1998). The present study employed a drug Ð caeine Ð and two experimental stress tasks Ð mental arithmetic and anagrams Ð to increase arousal in participants high and low in hostility under verbal harassment and non-harassment conditions. The authors hypothesized that caeine, hostility, and their interaction aect cardiovascular functioning, with the combination of high hostility and caeine producing the greatest blood pressure elevations. Although the relevant literature is somewhat mixed, it was expected that caeine would have greater in¯uence on systolic and hostility on diastolic pressure (Bongard et al., 1998; Green & Suls, 1996). 2. Method 2.1. Subjects Twenty-four high hostile (11 male and 13 female) and 24 low hostile (10 male and 14 female) participants, ranging in age from 18 to 25, were selected from a screening group of 218 students in lower-level psychology courses, who completed the Cook±Medley Hostility Scale. The high-hostility (HH) group had scores of 27 or higher X 30:79; while the low-hostility (LH) group had scores of 19 or lower X 13:75: These means are consistent with those found in similar studies (Hardy & Smith, 1988; Smith, Cranford, et al., 2000). 2.2. Apparatus Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP), and heart rate (HR) were measured, using a Dinamap Vital Signs monitor (Critikon Model 8100). All visual stimuli appeared on a high resolution color monitor, and auditory stimuli were computer-generated, recorded tones. They were delivered through a speaker in an Audio Suttle, Model AS-109 (Type 40 C) sound booth.
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2.3. Questionnaire The Cook±Medley Hostility Scale was employed to assess what is probably best described as cynical hostility (Smith & Frohm, 1985). Participants with high scores tend to be higher in neuroticism (Costa, Zonderman, McCrae & Williams, 1986), which is also correlated with ischaemic heart disease (Marusic, Gudjonsson, Eysenck & Starc, 1999). 2.4. Experimental tasks and harassment intervention Two cognitive stress tasks were used in the experiment. The ®rst was a mental arithmetic (MA) task, in which subjects serially subtracted 7 from a number on the computer screen. Subjects heard a tone every 2 sec and attempted to make verbal subtractions within that time interval. There were two verbal harassment (at 2 and 3 min) and two non-harassment (at 1 and 4 min) trials. This pattern of trials allowed us to obtain control (non-harassment) readings before and after the two harassment trials. The second task involved 30 ®ve-letter anagrams, each displayed on the screen for 15 sec. There were three harassment (minutes 1, 5, and 7) and three non-harassment (minutes 2, 3, and 6) trials. 2.5. Procedure A double-blind procedure was employed for both hostility group and drug condition. Equal numbers of HH and LH subjects were randomly assigned to the caeine and placebo conditions. Following informed consent, subjects completed screening questionnaires assessing health factors, caeine sensitivity, and recent drug usage (Smith, Davidson & Green, 1993). Two subjects were dropped, one due to reported lack of sleep, the other due to reported caeine sensitivity, and randomly replaced. The subject was next given either caeine (400 mg) or an equal amount of placebo (lactose) mixed in fruit juice. The experiment proper began 45 min after caeine ingestion (Davidson & Smith, 1989). A blood pressure cu was secured to the non-dominant arm and initial instructions given. Counterbalancing the order of presentation of the two tasks, the experiment that followed consisted of ®ve phases: A 10-min baseline, ®rst task (MA or anagrams), ®rst 5-min recovery period, second task, second 5-min recovery period. Blood pressure and heart rate were taken at 60-sec. intervals throughout all ®ve phases. Following the experiment, a questionnaire assessed emotions experienced during the study. 3. Results The four cardiovascular measurements (DBP, SBP, MAP, and HR) were determined separately for each participant on each trial (two trials of each type of Intervention for MA and three of each for anagrams). All scores were range-corrected (Lykken, 1972), then subjected to analyses of variance and covariance. The principal between-subject factors were Hostility Group (high vs low) and Drug Condition (caeine vs placebo). The principal within-subject factors were Intervention (harassment vs non-harassment) and Repetitions of harassment or non-harassment.
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Baseline scores were covaried. In analyses of non-task intervals, a Periods factor, with three levels (Baseline, Recovery 1, and Recovery 2) replaced the Repetitions and Intervention factors. Univariate ANOVA and ANCOVA results are reported only when the appropriate omnibus F in the relevant MANOVA or MANCOVA was signi®cant. 3.1. Diastolic blood pressure Analysis of MA data yielded a signi®cant Drug ConditionInterventionRepetition interaction [F(1, 44)=4.59, p<0.05]. Harassment had no overall eect on DBP under placebo and produced a decrease across trials under caeine (Fig. 1). With no harassment, there was a decrease under
Fig. 1. Dierential change in DBP as an interactive function of Drug Condition and Harassment Intervention.
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placebo and a substantial increase under caeine conditions. For the anagram task, there was a signi®cant Hostility GroupInterventionRepetition interaction [F(2, 88)=3.87, p<0.025]. The LH subjects showed a gradual decrease in DBP under non-harassment conditions and a slight increase on the third trial under harassment conditions (Fig. 2). By comparison, HH subjects
Fig. 2. Interactive eects of Hostility Group and Harassment Intervention on the change in DBP over trials.
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showed a crossover eect, in which there was a decrease in DBP under non-harassment and an increase under harassment conditions. The ®nal analysis examined DBP during non-stimulation periods, including the pre-task Baseline, Recovery 1 and Recovery 2. The analysis yielded signi®cant eects of Hostility Group [F(1, 44)=4.32, p<0.05] and the Hostility GroupConditionPeriod Interaction [F(2, 88)=3.18, p<0.05]. The Group eect was due to higher DBP in the HH group X 66:86 than in the LH group (60.61). The interaction showed that caeine maintained higher blood pressures in both groups, but with highest pressures occurring when hostility and caeine were combined (Fig. 3).
Fig. 3. Change in DBP across baseline and recovery periods as an interactive function of Hostility Group and Drug Condition.
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3.2. Systolic blood pressure Data for the MA task yielded a signi®cant main eect of Drug Condition [F(1, 44)=6.97, p<0.025] due to higher mean SBP under caeine X 135:9 than placebo (125.36) conditions. A
Fig. 4. Dierential change in MAP as an interactive function of Hostility Group and Harassment Intervention.
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signi®cant ConditionInterventionRepetition crossover interaction, F(1, 44)=4.96, p<0.05 was the same as that for DBP: caeine caused a clear increase in SBP across trials when no harassment occurred and a clear decrease when harassment did occur (cf Fig. 1). Anagram task data yielded a signi®cant main eect of Drug Condition [F(1, 44)=4.51, p<0.05], with SBP again higher under caeine X 127:8 than under placebo (119.72). An analysis of the baseline and recovery periods yielded a signi®cant main eect of Drug Condition, F(1, 44)=4.14, p<0.05. Mean SBP was higher under caeine X 119:85 than under placebo (113.56) conditions. 3.3. Mean arterial pressure For the MA task, there was a signi®cant main eect of Drug Condition [F(1, 44)=7.15, p<0.025] due to higher MAP under caeine X 102:01 than placebo (95.30). A Drug ConditionInterventionRepetition Interaction [F(1, 44)=9.80, p<0.005] re¯ected the same pattern of increase in MAP in the placebo group but decrease in the caeine group under harassment as was seen for DBP and SBP (cf Fig. 1). Anagram task data yielded signi®cant eects of Drug Condition [F(1, 44)=6.42, p<0.025] and the GroupInterventionRepetition Interaction [F(2, 88)=6.84, p<0.005]. Mean MAP was higher under caeine X 95:05 than placebo (88.80) conditions. Fig. 4 shows that with no harassment, both groups demonstrated a decrement in MAP over trials. With harassment, low hostiles still decreased, but high hostiles increased substantially on the third trial. Baseline and recovery period data showed a signi®cant eect of Drug Condition [F(1, 44)=4.60, p<0.05]. Means were 87.80 and 83.41 for caeine and placebo, respectively, demonstrating the arousal eect of caeine. 3.4. Heart rate There were no signi®cant Hostility Group or Drug Condition eects for either the MA or the anagram task. Baseline and recovery period data, however, yielded three signi®cant interactions. The Drug Condition by Period eect [F(2, 88)=3.87, p<0.025] re¯ected the steady increase in heart rate from baseline through and including Recovery 2 for the placebo group and an increase followed by a decrease in the caeine group. The interaction of Hostility Group with Period [F(2, 88)=3.18, p<0.05] showed a steady increase in HR from Baseline through Recovery 2 for the low hostiles and a slight decrease to a stable and lower baseline in high hostiles. Finally, the signi®cant Drug ConditionGroupRepetition Interaction [F(2, 88)=4.07, p<0.025] shows an interesting reversal of the two hostility groups under placebo and caeine conditions (Fig. 5). With caeine, high hostiles started at a much lower heart rate and increased slightly to a rate that was still considerably lower than that of the placebo group. The latter showed a decremental trend. 3.5. Questionnaire data The post-experimental questionnaire assessed subjective aect before and during the experiment for each of ®ve emotions: happiness, anger, depression, anxiety, and frustration (Table 1).
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Fig. 5. Change in HR across trials under the interactive in¯uence of Drug Condition and Hostility Group.
The experimental manipulation produced signi®cant perceived increases in intensity for the negative emotions and a decrease in happiness. In addition, caeine caused higher overall levels of anxiety [F(1,44)=10.91, p<0.005]. There were no Hostility Group dierences. 4. Discussion Present results con®rmed our hypothesis that both hostility and caeine impact cardiovascular functioning. Moreover, independent eects of the two variables were observed during stressful task performance, and interactive eects were seen during recovery. Finally, questionnaire data supported the eectiveness of the experimental stress manipulations in that negative emotion
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Table 1 Perceived emotional intensity Emotion
Before experiment
During experiment
F
p
Happiness Anger Anxiety Depression Frustration
2.81 1.19 2.00 1.65 1.21
2.31 1.96 3.23 2.40 3.25
11.47 22.58 45.97 23.60 99.66
<0.005 <0.0001 <0.0001 <0.0001 <0.0001
increased and positive emotion decreased. Interestingly, however, anger increased no more than other negative emotions, and the signi®cant group dierences in blood pressure were not accompanied by group dierences in perceived emotional intensity. 4.1. Hostility eects Blood pressure data in the present study validated the earlier ®nding that high hostility, when combined with interpersonal stress, increases cardiovascular arousal (Miller et al., 1996) and extended that ®nding to demonstrate recovery eects that included interactions with caeine. The anagram stress task produced BP habituation overall, but high-hostile participants faced with harassment experienced increases in DBP and were unable to sustain decreases in MAP. This ®nding is consistent with other work showing selective increases in the blood pressures of high hostile subjects during a stressful task, particularly one involving interpersonal con¯ict (Hardy & Smith, 1988; Smith & Allred, 1989; Suarez & Williams, 1989). For high hostile subjects in the present study, interpersonal stress also aected the recovery of diastolic pressure. There was less DBP reduction during recovery in high hostiles than in their low hostile counterparts. Both this ®nding and the observed BP elevations in high hostiles during task periods suggest that hostility increases arousal and inhibits recovery under conditions of stress. This conclusion is supported by data from earlier studies (Hardy & Smith, 1988; Smith & Allred, 1989) and may suggest that hostility should be included among such other arousal-related personality dimensions as sensation-seeking (Smith, Davidson, Perlstein & Gonzalez, 1990) and extraversion (Smith, Concannon, Rockwell, Bozman & Kline, 1990). It was not, of course, hostility alone, but rather the interaction of hostility with the situational stress factor that produced the group dierences. This observation supports the theories of Williams (1987), Siegman (1988), and the present senior author (Smith, Cranford, et al., 2000; Smith, Tola, et al., 2000). Moreover, it is consistent with other work showing that high hostility is associated with increases in blood pressure under stress (Pettit, Marchand & Graham, 1999), particularly when the stressor involves an interpersonal element (Morris-Prather et al., 1996). These eects can be interpreted within the context of a dual-interactional theory of personality and behavior (Smith, 1994). This theory basically suggests that genetic and environmental factors interact to produce stable dispositions, such as the hostility trait. These dispositions then interact with speci®cally relevant current situational factors to produce behavior. We would accordingly hypothesize that hostility has a genetic predisposition (Carmelli, Rosenman & Swan, 1988; Matthews, Manuck & Saab, 1986), probably expressed in part in terms of arousal or arousability (Smith &
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Tola, 1998). This predisposition combines with experience to produce an individual who is suspicious, cynical, and resentful. Such characteristics lead to increased vigilance, which is associated with elevated arousal (Cantero, Atienza, Salas & Gomez, 1999) and, correspondingly, with increases in vasoconstriction, norepinephrine, and testosterone (Williams et al., 1982). Thus primed by genetics, experience, and physiology, high hostile subjects react more strongly to situational stressors with at least increases in diastolic pressure and the derivative mean arterial pressure. The reason for the selective increase in DBP is not entirely clear. However, there is some evidence that the vigilance hypothetically characteristic of high hostiles causes muscular vasoconstriction without associated changes in cardiac output (Harms et al., 1998), leading to increases in DBP alone. The previously observed association of DBP with anger arousal (Kop, 1997) and with hostility (Smith, Cranford, et al., 2000) further supports this interpretation. 4.2. Caeine eects The eects of caeine in the present study were largely independent of those of hostility. There were consistent caeine-induced increases in systolic pressure and in mean arterial pressure across both task and recovery periods, with no accompanying increase in heart rate. Other work has also shown selective increases in systolic pressure (Myers, Shapiro, McClure & Daims, 1989), consistent with the well-documented arousal eects of caeine (Myers & Reeves, 1993; Smith & Tola, 1998). A more interesting ®nding was the interaction of caeine with harassment on all three blood pressure measures. In all cases, caeine increased blood pressure under non-harassment conditions but decreased it under harassment. While this result may at ®rst appear counter-intuitive, it is consistent with a theoretical inverted-U-shaped arousal function. Basically, increasing arousal causes an increment in physiological activation up to a point. A further increase in arousal intensity then produces transmarginal inhibition (Nebylitsyn, 1972; Watters, Martin & Schreter, 1997), causing arousal indicators to asymptote or even decrease. In the present study, the combined eect of two arousal agents, caeine and harassment, pushed arousal past the peak of the inverted-U-shaped function, causing a decrease in arousal output. This ®nding is consistent with the recent theory that caeine acts to enhance a variety of other sources of arousal (Smith, 1994). If the arousal increment produced by caeine is relatively small, the overall arousal output should be high. However, if caeine and stress increase arousal further, arousal output may decrease as transmarginal inhibition develops. 4.3. Hostility and caeine Hostility and caeine interacted to aect physiology only during recovery periods. Heart rate under caeine increased across baseline and recovery periods in high hostile participants and decreased from a higher starting point in lows. For blood pressure, it was the combination of caeine and high hostility that maintained the highest levels of diastolic pressure during recovery. In addition, both placebo and low hostility conditions were associated with decreases in DBP across recovery periods. Only the combination of caeine and high hostility maintained elevated pressure across periods. Applied to actual situations, these data would suggest that the blood pressure of high hostile subjects taking caeine is not dierentially aected while performing
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tasks. However, task-induced elevations in this group will not recover as quickly when there is caeine in the system or perhaps when other arousal sources are present. Further research is clearly needed to better understand the interactive eects of caeine and hostility during periods of task performance. It was frankly surprising to ®nd no such interactive eects in the present study. It may, of course, be that the two variables act entirely independently during tasks. However, it is also possible that interactions will be found during less stressful tasks or in the absence of an interpersonal stress manipulation. 5. Conclusions Present results showed that, as hypothesized, hostility aects primarily diastolic blood pressure, while caeine aects principally systolic pressure, at least under the experimental conditions represented here. This may suggest that DBP under stress is aected by more chronic conditions, such as those represented by a personality trait variable, while systolic pressure is more responsive to such acute conditions as caeine-induced arousal. More data will be needed, however, before any ®rm conclusions can be drawn. References Benotsch, E. G., Christensen, A. J., & McKelvey, L. (1997). Hostility, social support, and ambulatory cardiovascular activity. Journal of Behavioral Medicine, 20, 163±176. Bongard, S., al'Absi, M., & Lovallo, W. R. (1998). Interactive eects of trait hostility and anger expression on cardiovascular reactivity in young men. International Journal of Psychophysiology, 28(2), 181±191. Cantero, J. L., Atienza, M., Salas, R. M., & Gomez, C. M. (1999). Alpha EEG coherence in dierent brain states: An electrophysiological index of the arousal level in human subjects. Neuroscience Letter, 271(3), 167±170. Carels, R. A., Sherwood, A., & Blumenthal, J. A. (1998). Psychosocial in¯uences on blood pressure during daily life. International Journal of Psychophysiology, 28, 117±129. Carmelli, D., Rosenman, R. H., & Swan, G. E. (1988). The Cook and Medley HO Scale: A heritability analysis in adult male twins. Psychosomatic Medicine, 50, 165±170. Costa, P. T., Zonderman, A. B., McCrae, R. R., & Williams, R. B. (1986). Cynicism and paranoid alienation in the Cook and Medley Ho scale. Psychosomatic Medicine, 48, 283±285. Davidson, R. A., & Smith, B. D. (1989). Arousal and habituation: Dierential eects of caeine sensation seeking and task diculty. Personality and Individual Dierences, 10, 111±119. Everson, S. A., Kauhanen, J., Kaplan, G. A., Goldberg, D. E., Julkunen, J., Tuomilehto, J., & Salonen, J. T. (1997). Hostility and increased risk of mortality and acute myocardial infarction: The mediating role of behavioral risk factors. American Journal of Epidemiology, 146, 142±152. Green, J. J., & Suls, J. (1996). The eects of caeine on ambulatory blood pressure, heart rate, and mood in coee drinkers. Journal of Behavioral Medicine, 19, 111±128. Hardy, J. D., & Smith, T. W. (1988). Cynical hostility and vulnerability to disease: Social support, life stress, and physiological response to con¯ict. Health Psychology, 7, 447±459. Harms, C. A., Wetter, T. J., McClaran, S. R., Pegelow, D. F., Nickele, G. A., Nelson, W. B., Hanson, P., & Dempsey, J. A. (1998). Eects of respiratory muscle work on cardiac output and its distribution during maximal exercise. Journal of Applied Physiology, 85, 609±618. Kop, W. J. (1997). Acute and chronic psychological risk factors for coronary syndromes: Moderating eects of coronary artery disease severity. Journal of Psychosomatic Research, 43, 167±181. Lahad, A., Heckbert, S. R., Koepsell, T. D., Psaty, B. M., & Patrick, D. L. (1997). Hostility, aggression and the risk of nonfatal myocardial infarction in postmenopausal women. Journal of Psychosomatic Research, 43, 183±195.
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Lykken, D. A. (1972). Range correction applied to heart rate and GSR data. Psychophysiology, 9, 151±159. Marusic, A., Gudjonsson, G. H., Eysenck, H. J., & Starc, R. (1999). Biological and psychosocial risk factors in ischaemic heart disease: Empirical ®ndings and a biopsychosocial model. Personality and Individual Dierences, 26, 285±304. Matthews, K. A., Manuck, S. B., & Saab, P. G. (1986). Cardiovascular responses of adolescents during a naturally occurring stressor and their behavioral and psychophysiological predictors. Psychophysiology, 23, 198±209. Miller, T. Q., Smith, T. W., Turner, C. W., Guijarro, M. L., & Hallet, A. J. (1996). A meta-analytic review of research on hostility and physical health. Psychological Bulletin, 119, 322±348. Morris-Prather, C. E., Harrell, J. P., Collins, R., Leonard, K. L., Boss, M., & Lee, J. W. (1996). Gender dierences in mood and cardiovascular responses to socially stressful stimuli. Ethnicity Discourse, 6(12), 123±131. Myers, M. G., & Reeves, R. A. (1993). The eect of caeine on daytime ambulatory blood pressure. American Journal of Hypertension, 4, 427±431. Myers, H. F., Shapiro, D., McClure, F., & Daims, R. (1989). Impact of caeine and psychological stress on blood pressure in black and white men. Health Psychology, 8, 597±612. Nebylitsyn, V. D. (1972). Fundamental properties of the human nervous system. Oxford: Pergamon Press. Pettit, S. E., Marchand, I., & Graham, T. (1999). Gender dierences in cardiovascular and catecholamine responses to cold-air exposure at rest. Canadian Journal of Applied Physiology, 24, 131±147. Shapiro, D., Jamner, L. D., & Goldstein, I. B. (1997). Daily mood states and ambulatory blood pressure. Psychophysiology, 34, 399±405. Siegman, A. W. (1988). Typ A und danach: Die Bedeutung von Feindseligkeit Neurotizismus und Sprechstil fur koronareHerzerkrankungen. Z Klin Psychol Psychopathol Psychother, 36, 3±24. Smith, B. D. (1983). Extraversion and electrodermal activity: Arousabilty and the inverted-U. Personality and Individual Dierences, 4, 411±419. Smith, B. D. (1994). Eects of acute and habitual caeine ingestion on physiology and behavior: Tests of a biobehavioral arousal theory. Pharmacopsychoecologia, 7, 75±84 Invited article. Smith, T. W., & Allred, K. D. (1989). Blood pressure reactivity during social interaction in high and low cynical hostile men. Journal of Behavioral Medicine, 11, 135±143. Smith, B. D., Concannon, M., Rockwell, S., Bozman, A., & Kline, R. (1990). Regression and criterion measures of habituation: A comparative analysis in extraverts and introverts. Journal of Research on Personality, 24, 123±132. Smith, B. D., Cranford, D., & Mann, M. (2000). Gender, cynical hostility, and cardiovascular functioning: Implications for dierential cardiovascular disease risk. Personality and Individual Dierences. Smith, B. D., Davidson, R. A., & Green, R. L. (1993). Eects of caeine and gender on physiology and performance: Further tests of a biobehavioral model. Physiology and Behavior, 54, 415±422. Smith, B. D., Davidson, R. A., Perlstein, W., & Gonzalez, F. (1990). Sensation-seeking: Electrodermal and behavioral eects of stimulus content and intensity. International Journal of Psychophysiology, 9, 179±188. Smith, T. W., & Frohm, K. D. (1985). What's so unhealthy about hostility? Construct validity and psychosocial correlates of the Cook and Medley Ho Scale. Health Psychology, 4, 503±520. Smith, B. D., & Tola, K. (1998). Caeine: Eects on psychological functioning and performance. In G. Spiller, Caeine (pp. 251±299). New York: CRC Press. Smith, B. D., Tola, K., & Mann, M. (2000). Caeine and arousal: A biobehavioral theory of physiological, behavioral, and emotional eects. In B. S. Gupta, Caeine and behavior: Current views and research trends. CRC Press. Suarez, E. C., & Williams, R. B. (1989). Situational determinants of cardiovascular and emotional reactivity in high and low hostile men. Psychosomatic Medicine, 51, 404±418. Voegele, C. (1998). Serum lipid concentrations, hostility and cardiovascular reactions to mental stress. International Journal of Psychophysiology, 28(2), 167±179. Watters, P. A., Martin, F., & Schreter, Z. (1997). Caeine and cognitive performance: The nonlinear Yerkes±Dodson Law. Human Psychopharmacology, 12, 249±257. Williams, R. B. (1987). Re®ning the type A hypothesis: Emergence of the hostility complex. American Journal of Cardiology, 60, 27J±32J. Williams, R. B., Lane, J. D., Kuhn, C. M., Melosh, W., White, A. D., & Schanberg, S. M. (1982). Type A behavior and elevated physiological and neuroendocrine responses to cognitive tasks. Science, 218, 483±485.