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PubMed1992

Verbalized anger and accusatory "you" messages as cues for anger and antagonism among adolescents.

This study investigated the impact of communications of negative feelings between adolescents in close relationships. High school boys and girls were asked to imagine discussing a relationship problem with a personally close partner and to rate likely reactions to four kinds of statements: assertively expressed distress, assertively expressed anger, aggressively expressed distress, and aggressively expressed anger. Accusatory "you" statements were rated as more aversive and evoked stronger antagonistic response inclinations than assertive "I" statements. Statements depicting anger were rated as more aversive and evoked stronger antagonistic response inclinations than statements depicting distress. Results were similar for boys and girls. Implications of the findings and directions for further research are discussed.

Adolescent↗
PubMed2004

On the selective relation of frontal cortical asymmetry and anger-out versus anger-control.

The model of anterior asymmetry and emotion proposes an asymmetric representation of approach and withdrawal systems in the left and right anterior brain regions. Within this framework, 3 different concepts have been related to anterior asymmetry: affective valence, motivational direction, and behavioral activation. The aim of the present study was an empirical investigation into the relation between anterior cortical activity and questionnaire measures related to the 3 dimensions positive versus negative affect, approach versus withdrawal motivation, and behavioral activation versus inhibition. Subjects with relative greater left than right frontal cortical activity showed higher anger-out scores and lower anger-control scores. These results support the hypothesis that motivational direction is related to frontal asymmetry (approach-left and withdrawal-right). Furthermore, subjects with greater bilateral (left and right) frontal cortical activity showed higher behavioral activation scores. This finding might suggest that behavioral activation is related to approach and withdrawal motivation.

Adult↗
PubMed2001

State anger and prefrontal brain activity: evidence that insult-related relative left-prefrontal activation is associated with experienced anger and aggression.

Research has demonstrated that left-prefrontal cortical activity is associated with positive affect, or approach motivation, and that right-prefrontal cortical activity is associated with negative affect, or withdrawal motivation. In past research, emotional valence (positive-negative) has been confounded with motivational direction (approach-withdrawal), such that, for instance, the only emotions examined were both positive and approach related. Recent research has demonstrated that trait anger, a negative but approach-related emotion, is associated with increased left-prefrontal and decreased right-prefrontal activity, suggesting that prefrontal asymmetrical activity is associated with motivational direction and not emotional valence. The present experiment tested whether state-induced anger is associated with relative left-prefrontal activity and whether this prefrontal activity is also associated with aggression. Results supported these hypotheses.

Aggression↗
PubMedDate not supplied

Physician anger, Part 2. More on the dance of anger.

This article is a follow-up to an interview with Charles Dwyer, PhD, which appeared in the 1999 March/April issue of The Physician Executive. He described how physician executives can change the perceptions of today's beleaguered physicians and help them cope with change. We then asked him for some hands-on strategies to deal with physician anger, fear, and resentment. After much contemplation on providing a list of "fixes" that will restore each of us to a state of greater satisfaction, Dr. Dwyer concludes that there are no generalizable solutions because there are too many variables that come into play in each organization, individual, or group. Attending to the self can provide both individual rescue from these turbulent times and the best hope for changes in the system from which patients and health care providers can benefit. If physicians are to regain their power and maintain, or even improve, their quality of life, clearly changes are called for. And these are changes that require persistent effort and uncomfortable adjustments.

Adaptation, Psychological↗
PubMed2003

Differences in anger expression between individuals with and without headache after controlling for depression and anxiety.

OBJECTIVE: To evaluate whether anger and anger expression are different between persons with and without headache after controlling for depression and anxiety. BACKGROUND: Persons with headache may experience more problems with anger and its expression when compared with persons without headache. It is important to establish whether differences exist for persons with and without headache on trait anger and anger expression independent of depression and anxiety. To date, however, this issue has received little attention in the empirical literature. The current study measured trait anger, anger-in, hostility, anxiety, and depression among persons with and without headache, and evaluated whether trait anger and anger-in differentiated groups independent of depression and anxiety. METHODS: Participants were 422 adults recruited from a larger study within a university setting. Of those, 171 suffered from headache (mean age, 21 years; 81% were female; 69% were white; mean years with pain, 7.53). Another 251 sex-matched individuals (mean age, 21 years; 81% female; 62% white) met criteria for the headache-free group. Participants provided information regarding their headache characteristics and were administered affective trait measures (Trait version of the State-Trait Anxiety Inventory, Brief Symptom Inventory-Depression), trait anger measures (Trait Anger Scale, Cook-Medley Hostility Scale), and a measure of the extent to which individuals hold their anger in. RESULTS: Multivariate analysis of variance revealed significant differences between the 2 groups (Wilks lambda =.86, P <.001, eta2 =.14). Step-down analysis revealed that even after controlling for all other variables, those in the headache group had higher levels of anger-in (P <.001, eta2 =.08; mean, 18.98 versus 15.68). Trait anger and hostility did not differ between groups after controlling for depression and anxiety. Logistic regression revealed that anger-in contributed most to predicting headache status (P <.001; partial r =.23). CONCLUSIONS: The current findings indicate that persons with headache hold their anger in more than those without headache even after controlling for levels of trait anger, depression, and anxiety. However, after controlling for depression and anxiety, individuals no longer differed on trait anger. Also, anger-in was the strongest predictor of headache. The current findings suggest that holding anger in is more common among headache sufferers. Given recent findings regarding the negative effect of holding anger in among persons with pain conditions, this may be an important factor to evaluate when considering psychological/emotional factors affecting headache.

Adult↗
PubMed2003

Anger, aggression, risky behavior, and crash-related outcomes in three groups of drivers.

High anger drivers who acknowledged problems with driving anger and were interested in treatment were compared to high and low anger drivers who did not acknowledge problems with driving anger or want treatment. Although high anger drivers who acknowledged problems reported greater anger on two measures than high anger drivers who did not acknowledge problems, both high anger groups tended not to differ from one another and were more frequently and intensely angered when driving, reported more aggressive and less adaptive/constructive forms of expressing anger while driving, engaged in more aggressive and risky behavior on the road, and experienced more of some accident-related outcomes than low anger drivers. High anger groups did not differ from each other, but reported more trait anxiety and anger and more outward negative and less controlled general anger expression than the low anger group. The two groups of high anger drivers, however, require different types of interventions given their state of readiness for driving anger reduction. Results were also interpreted as supportive of the state-trait model of anger and construct validity of the Driving Anger Scale.

Accidents, Traffic↗
PubMed2000

Anger attacks in depressed Turkish outpatients.

Anger attacks have been described as sudden spells of anger accompanied by symptoms of autonomic activation and have been experienced by patients as uncharacteristic of them and inappropriate to the situations in which they had occurred. The aim of this study was to assess the prevalence of anger attacks in a non-Western depressed population. We also wanted to see whether depression in patients with anger attacks was qualitatively different from depression without anger attacks. The Anger Attacks Questionnaire, designed by Fava et al. to assess these attacks, was administered to 88 medication-free consecutive outpatients diagnosed as major depression according to DSM-IV criteria by two psychiatrists. The patients also were assessed by the Beck Depression Inventory, the Beck Anxiety Inventory, the Beck Hopelessness Scale, and the Spielberger's State-Trait Anger Expression Inventory. Forty-three (49%) of these patients had reported having anger attacks. The patients with anger attacks were significantly more depressed and anxious than patients without anger attacks. Anger-out and trait anger measures were significantly higher in depressed patients with anger attacks than patients without anger attacks. Patients with anger attacks also scored higher in hopelessness measure and there was a trend toward statistical significance. Our results are in line with previous literature which show, that anger attacks are prevalent in depressed patients. We also conclude that patients with anger attacks constitute a more depressed population than those without anger attacks. Severity of depression emerges as the strongest predictor of the presence of anger attacks in our study.

Adult↗
PubMed2005

The relation between anger expression, depression, and somatic symptoms in depressive disorders and somatoform disorders.

BACKGROUND: In previous studies, the relationship between either anger suppression and depression or anger suppression and somatic symptoms was examined. However, the relationship between anger expression, depression, and somatic symptoms was not examined in depressive disorders and somatoform disorders. METHOD: The DSM-IV-diagnosed subjects included 73 patients with depressive disorders and 47 patients with somatoform disorders. The Anger Expression Scale was used to assess the level of anger expression or suppression. The severity of depression was assessed using the Symptom Checklist-90-Revised (SCL-90-R). The Somatization Rating Scale and the SCL-90-R somatization subscale were used to assess the severity of somatic symptoms. Data were collected from March 2000 to March 2001. RESULTS: The results of the path analyses showed that in depressive disorder patients, anger expression had a stronger effect on somatic symptoms through depression than did anger suppression, although both anger expression and anger suppression had a significant indirect effect on somatic symptoms. The depressive disorder group also showed a significant but negative direct effect of anger suppression on anger expression in the path from anger suppression to anger expression to depression to somatic symptoms. However, only anger suppression had an indirect effect on somatic symptoms through depression in somatoform disorder patients. CONCLUSIONS: The results suggest that anger expression might play a more predominant role in depression and somatic symptoms of depressive disorder patients than anger suppression, but only anger suppression might be associated with depression and somatic symptoms of somatoform disorder patients. In addition, incomplete anger suppression followed by anger expression is likely to be associated with depression and somatic symptoms in depressive disorders.

Adult↗
PubMed2004

Anger attacks in bipolar depression: predictors and response to citalopram added to mood stabilizers.

BACKGROUND: Of the 2 reports in the literature on anger attacks in bipolar depression, one found them to be uncommon (12%) compared with the rate in bipolar mixed states and unipolar depression (40%-60%), whereas the other found them to be common (62%). We examined anger attacks among participants in an 8-week trial of open-label citalopram added to mood stabilizer for the treatment of bipolar depression. We also examined trait anger, hypomanic symptoms, and depressive symptoms as predictors of anger attacks. We hypothesized that if anger attacks were related to hypomanic symptoms they would respond unfavorably to citalopram, whereas if they were related to trait anger or depressive symptoms they would respond favorably. METHOD: In 45 participants with a DSM-IV diagnosis of bipolar I or II depression, anger attacks, hypomanic symptoms, and depressive symptoms were assessed using a modified Anger Attacks Questionnaire, Young Mania Rating Scale, and Hamilton Rating Scale for Depression, respectively. Trait anger was measured using the State-Trait Anger Inventory. Posttreatment data were collected at the end of 8 weeks of treatment with citalopram or at dropout from the trial. The first participant study visit was in November 1998, and the final participant study visit was in December 2000. RESULTS: Before treatment with citalopram, 17 (38.6%) of 44 participants reported anger attacks (data on anger attacks were missing for 1 participant before treatment and 4 after treatment). Significantly fewer participants reported anger attacks after treatment (6 of 41, 14.6%; McNemar test, p <.05, 2-tailed). At pretreatment and post-treatment, trait anger was the only significant predictor of anger attacks (p <.05). CONCLUSIONS: These findings suggest that in bipolar depression anger attacks are common, may respond favorably to acute treatment with citalopram added to mood stabilizer, and are better predicted by trait anger than hypomanic or depressive symptoms. Further studies are needed to clarify the diagnostic and treatment implications of anger attacks in bipolar depression.

Adult↗
PubMed2006

Suppressed anger is associated with increased carotid arterial stiffness in older adults.

BACKGROUND: Anger and hostility have been implicated in the pathogenesis of heart disease, but the extent to which the large conduit arteries play an intermediate role in this relationship remains to be clarified. The present study investigated associations of anger frequency and expression style with carotid artery intima-media thickness (IMT) and stiffness in healthy adults older than 50 years. METHODS: Two hundred participants (95 men) in the Baltimore Longitudinal Study of Aging completed the Spielberger Anger Expression Inventory, which assesses anger frequency (trait anger), anger expression (anger-out), and anger suppression (anger-in). The carotid artery IMT was assessed by ultrasonography. Carotid stiffness was determined from the log of systolic over diastolic blood pressure (BP) as a function of carotid distensibility. RESULTS: In univariate correlational analysis, a significant positive association of anger-in with stiffness was observed (P < .01), together with a less significant association of anger-in with carotid artery IMT (P < .05). Neither anger-out nor trait anger was significantly associated with carotid artery IMT or stiffness. Moreover, none of the anger measures was significantly associated with resting BP in this normotensive sample. As expected, carotid artery IMT, stiffness, and systolic BP were all positively associated. In multivariate analysis, anger-in remained a determinant of stiffness independent of BP, and a marginally significant determinant of carotid artery IMT. CONCLUSIONS: This is the first known finding that high anger-in is a significant independent determinant of carotid artery stiffness. These results suggest that high anger-in can potentiate the effects of age on stiffening of the central arteries.

Aged↗
PubMed2002

Anger and pain sensitivity in chronic low back pain patients and pain-free controls: the role of endogenous opioids.

The experience of anger (i.e. trait anger) and anger management style (i.e. anger-in, anger-out) are related to sensitivity to acute and chronic pain stimuli, although underlying mechanisms are unknown. This study tested whether anger variables are associated with impaired endogenous opioid antinociceptive activity, and whether these relationships differed between chronic pain patients and healthy normals. Forty-three chronic low back pain (LBP) sufferers and 45 pain-free normals received opioid blockade (8 mg naloxone i.v.) or placebo blockade (saline) in randomized, counterbalanced order in separate sessions. During each session, subjects participated in a 1-min finger pressure pain task followed by an ischemic forearm pain task (maximum duration 5 min), providing pain intensity ratings during and immediately following each task. As a measure of opioid antinociceptive function, drug effects were derived by subtracting placebo from blockade condition pain ratings. Multivariate general linear model analyses indicated that anger-out, but not anger-in, had significant main effects on both finger pressure drug effects (P < 0.05) and ischemic task drug effects (P < 0.05). As hypothesized, high anger-out scores were associated with an absence of opioid analgesia during the acute pain tasks; low anger-out scores were associated with effective opioid analgesia. A similar non-significant trend was noted for trait anger on finger pressure drug effects (P < 0.06). Anger-out x LBP/normal interactions were non-significant, suggesting that links between anger-out and drug effects were similar for patients and normals. Controlling for depression did not eliminate the significant relationship between anger-out and drug effects. Findings suggest that anger-in and anger-out affect pain sensitivity through different mechanisms: only the effects of anger-out may be mediated by endogenous opioid dysfunction.

Acute Disease↗
PubMed1986

The Multidimensional Anger Inventory.

Previous research suggests that anger has important social and health consequences, particularly cardiovascular health. The pathogenic aspects of anger have not been identified, however, in part because of a reliance on unidimensional measures of anger. The present article describes psychometric data for an inventory that is sensitive to the multidimensional nature of the anger construct. It was hypothesized that the newly developed Multidimensional Anger Inventory (MAI) would include scales reflective of the following dimensions of anger: frequency, duration, magnitude, mode of expression, hostile outlook, and range of anger-eliciting situations. The mode of expression dimension was expected to contain separate anger-in, anger-out, guilt, brood, and anger-discuss measures. The inventory was administered to two populations: male and female college students and male factory workers. Factor analyses of the MAI within the two samples showed that the frequency, duration, and magnitude dimensions clustered together to form an anger-arousal factor that accounted for 64% and 71% of the variance in the two samples, respectively. The range of anger-eliciting situations and hostile outlook emerged as separate dimensions, as hypothesized. Mode of anger expression was best described by two dimensions labeled anger-in and anger-out. Psychometric analyses of the scale showed that it possessed adequate test-retest reliability (r = 0.75) and high internal consistency (alpha = .84 and .89 for the two samples). The validity of the scale was supported by the expected pattern of relations with other inventories designed to assess anger or hostility. Comparisons of MAI scores between (college versus factory) and within (male versus female) populations were made.

Adult↗
PubMed2003

Effects of alcohol, personality, and provocation on the expression of anger in men: a facial coding analysis.

BACKGROUND: Research has demonstrated that alcohol-related aggression is modulated by anger-based personality traits. However, it is unclear how anger, as a concomitant of aggression, is affected by an interaction among these variables. The present study evaluated the effects of alcohol, anger-based traits, and physical provocation on anger. METHODS: Participants were 136 male social drinkers who completed measures designed to assess trait anger and anger expression styles and were assigned to an alcohol or no-alcohol control beverage group. Participants engaged in a competitive reaction time task in which electric shocks were received from a fictitious opponent. Participants' experience of anger was assessed unobtrusively via the Facial Action Coding System. RESULTS: Intoxicated participants displayed more facial expressions of anger than sober participants. Interactive effects between anger expression styles and beverage group also were detected in that, among intoxicated participants, a positive relationship between facial expressions of anger and the tendency to express anger outwardly was found after high, but not low, provocation. This relationship was not observed at either provocation level in the no-alcohol control group. Similarly, whereas participants' tendency to control anger resulted in fewer facial expressions of anger by intoxicated participants, no such relationship was found among sober participants. CONCLUSIONS: Findings suggest that alcohol intoxication facilitates the experience of anger after provocation and enhances the relationship between state anger and behavioral tendencies to control anger expression.

Adolescent↗
PubMedDate not supplied

Anger-related personality traits and carotid artery atherosclerosis in untreated hypertensive men.

OBJECTIVE: To determine whether anger-related personality traits are associated with carotid artery atherosclerosis in untreated hypertensive patients. METHODS: Study participants were 237 men with elevated blood pressure (systolic 140-180 mm Hg and/or diastolic 90-110 mm Hg) but untreated for hypertension. Average age was 56 years; 80% of subjects were white. Eighty-six percent had no history of antihypertensive treatment, and the remainder reported median lifetime treatment exposure of 4 months. Subjects were administered the Spielberger State-Trait Anger Expression Inventory, which measures tendencies to experience anger (Trait Anger) and modes of anger expression (Anger-In, Anger-Out, Anger-Control). Mean and maximum intima-medial thickness (IMT) and plaque occurrence in the extracranial carotid arteries were measured by B-mode ultrasonography. RESULTS: Trait Anger was marginally (p =.065) related to mean and significantly (p <.05) related to maximum IMT, independent of standard risk factors (age, race, body mass index, education, smoking, fasting glucose, total:high-density lipoprotein cholesterol ratio). A component of Trait Anger, Angry Temperament, similarly predicted mean (p =.062) and maximum IMT (p <.05) and plaque occurrence (p <.05). Anger-Out predicted both mean and maximum IMT (p values <.01). CONCLUSIONS: An antagonistic disposition (Trait Anger), particularly a tendency to experience anger on minimal provocation (Angry Temperament) and a propensity to express anger outwardly (Anger-Out), are associated with heightened carotid atherosclerosis. These findings suggest that recently reported prospective associations between these anger dimensions and incident cerebrovascular disease may be mediated, in part, by increased atherosclerotic disease.

Age Factors↗
PubMed1997

Factor structure of the State-Trait Anger Expression Inventory.

The assessment of anger has received increased attention because of growing evidence that anger and hostility are related to heart disease. Research on anger assessment has also been stimulated by the development of psychometric measures for evaluating different facets of anger, such as the State-Trait Anger Expression Inventory (STAXI). In this study, factor analyses of the responses of a large sample of university students to the 44 STAXI items identified 7 factors. Of these, the first 6 factors closely corresponded with the 6 STAXI scales and subscales: State Anger (S-Anger); Trait Anger Temperament and Reaction; and Anger-In, Anger-Out, and Anger-Control. All 10 STAXI S-Anger items had salient loadings on the 1st factor for both sexes; the 7th factor also consisted primarily of S-Anger items. Factor analyses of responses to the 10 S-Anger items clearly confirmed two S-Anger factors for both sexes: Feeling Angry (e.g., "I am furious") and Feel Like Expressing Anger (e.g., "I feel like hitting someone").

Adult↗
PubMed2007

Trait anger expressiveness and pain-induced beta-endorphin release: support for the opioid dysfunction hypothesis.

The anger management styles of anger-in (inhibition) and anger-out (direct expression) are positively associated with pain responsiveness. Opioid blockade studies suggest that hyperalgesic effects of trait anger-out, but not those of trait anger-in, are mediated in part by opioid analgesic system dysfunction. The current study tested the opioid dysfunction hypothesis of anger-out using an alternative index of opioid function: pain-induced changes in plasma endogenous opioids. Plasma beta-endorphin (BE) was assessed at rest and again following exposure to three laboratory acute pain tasks (finger pressure, ischemic, and thermal) in 14 healthy controls and 13 chronic low back pain (LBP) subjects. As expected, acute pain ratings correlated positively with measures of anger-in (both groups) and anger-out (LBP group; p's<.05). Greater pain-induced increases in BE were associated with significantly lower pain ratings in both groups (p's<.05). Hierarchical multiple regression indicated that greater anger-out significantly predicted smaller pain-induced BE increases (p<.05). Subject type did not moderate this association (p>.10). Anger-in did not display significant main or interaction effects on pain-induced BE changes (p's>.10). The significant association between anger-out and BE release partially mediated the hyperalgesic effects of anger-out on pain unpleasantness, and was not attenuated by statistical control of general negative affect. This suggests unique associations with expressive anger regulation. Elevated trait anger-out therefore appears to be associated with opioid analgesic system dysfunction, whether it is indexed by responses to opioid blockade or by examining circulating endogenous opioid levels. Possible "statextrait" interactions on these anger-related opioid system differences are discussed.

Acute Disease↗