Anger regulation style,anger arousal and acute pain sensitivity: evidence for an endogenous opioid “triggering” model

Findings suggest that greater tendency to express anger is associated with greater sensitivity to acute pain via endogenous opioid system dysfunction, but past studies have not addressed the role of anger arousal. We used a 2 × 2 factorial design with Drug Condition (placebo or opioid blockade with naltrexone) crossed with Task Order (anger-induction/pain-induction or pain-induction/anger-induction), and with continuous Anger-out Subscale scores. Drug × Task Order × Anger-out Subscale interactions were tested for pain intensity during a 4-min ischemic pain task performed by 146 healthy people. A significant Drug × Task Order × Anger-out Subscale interaction was dissected to reveal different patterns of pain intensity changes during the pain task for high anger-out participants who underwent pain-induction prior to anger-induction compared to those high in anger-out in the opposite order. Namely, when angered prior to pain, high anger-out participants appeared to exhibit low pain intensity under placebo that was not shown by high anger-out participants who received naltrexone. Results hint that people with a pronounced tendency to express anger may suffer from inadequate opioid function under simple pain-induction, but may experience analgesic benefit to some extent from the opioid triggering properties of strong anger arousal.     

Anger Regulation Style, Postoperative Pain, and Relationship to the A118G Mu Opioid Receptor Gene Polymorphism: A Preliminary Study

Greater trait anger-out is associated with elevated pain responsiveness. Previous work suggests this effect may be mediated by deficient endogenous opioid analgesia, possibly reflecting diminished opioid receptor sensitivity. The A118G single nucleotide polymorphism (SNP) of the mu opioid receptor gene influences both opioid receptor sensitivity and clinical responsiveness to opioid analgesics. Therefore, this study tested whether this SNP either mediated or moderated the effects of anger-out on postsurgical pain outcomes. Forty-eight patients undergoing coronary artery bypass graft surgery provided genetic samples, and completed measures of anger-out and postsurgical pain. Postsurgical opioid analgesic use was also recorded. Anger-out was positively associated with postsurgical pain ratings (p < 0.05). Anger-out was not associated with A118G SNP status (p > 0.10), suggesting the latter is unlikely to mediate anger-out's pain-related effects. A significant anger-out × A118G interaction was observed on analgesic use (p < 0.05), due to a much stronger positive relationship between anger-out and analgesic demands in patient with the A118G SNP (b = 0.53) than those with the wild-type receptor (b = 0.07). These results suggest that the A118G SNP may moderate but not mediate the effects of anger-out on postoperative pain responses.     

Anger Expression and Pain: An Overview of Findings and Possible Mechanisms

A tendency to manage anger via direct expression (anger-out) is increasingly recognized as influencing responses to pain. Elevated trait anger-out is associated with increased responsiveness to acute experimental and clinical pain stimuli, and is generally related to elevated chronic pain intensity in individuals with diverse pain conditions. Possible mechanisms for these links are explored, including negative affect, psychodynamics, central adipose tissue, symptom specific muscle reactivity, endogenous opioid dysfunction, and genetics. The opioid dysfunction hypothesis has some experimental support, and simultaneously can account for anger-out’s effects on both acute and chronic pain. Factors which may moderate the anger-out/pain link are described, including narcotic use, gender, and genetic polymorphisms. Pain exacerbating effects of trait anger-out are contrasted with the apparent pain inhibitory effects of behavioral anger expression exhibited in anger-provoking contexts. Conceptual issues related to the state versus trait effects of expressive anger regulation are discussed.     

Anger Management Style and Hostility: Predicting Symptom-Specific Physiological Reactivity Among Chronic Low Back Pain Patients

It was hypothesized that anger management style (anger-in or anger-out) and hostility affect the aggravation of chronic low back pain (CLBP) through symptom-specific (i.e., lower paraspinal muscle) reactivity during stress. Subjects were 102 CLBP patients who performed mental arithmetic and an Anger Recall Interview (ARI) while trapezius and lower paraspinal EMG, SBP, DBP, and HR were recorded. Results showed anger-in × hostility and anger-out × gender interactions for lower paraspinal but not trapezius reactivity, and only during the ARI. Further analyses revealed that (1) hostility was related positively to lower paraspinal reactivity among high anger suppressors, (2) hostility was related negatively to lower paraspinal reactivity among low anger suppressors, and (3) anger expression was related positively to lower paraspinal reactivity only among men. Anger management style and hostility may contribute to the exacerbation of CLBP by influencing stress reactivity only in muscles near the site of pain or injury.     

Anger Management Style and Endogenous Opioid Function: Is Gender a Moderator?

This study explored possible gender moderation of previously reported associations between elevated trait anger-out and reduced endogenous opioid analgesia. One hundred forty-five healthy participants underwent acute electrocutaneous pain stimulation after placebo and oral opioid blockade in separate sessions. Blockade effects were derived reflecting changes in pain responses induced by opioid blockade. Hierarchical regressions revealed that elevated anger-out was associated with smaller pain threshold blockade effects (less opioid analgesia) in females, with opposite findings in males (interaction p < .001). Similar marginally significant interactions were noted for blockade effects derived for nociceptive flexion reflex threshold, pain tolerance, and pain ratings (p < .10). Anger-in was also associated negatively with pain threshold blockade effects in females but not males (interaction p < .05). Across genders, elevated anger-in was related to smaller pain tolerance blockade effects (p < .01). Overlap with negative affect did not account for these opioid effects. The anger-in/opioid association was partially due to overlap with anger-out, but the converse was not true. These findings provide additional evidence of an association between trait anger-out and endogenous opioid analgesia, but further suggest that gender may moderate these effects. In contrast to past work, anger-in was related to reduced opioid analgesia, although overlap with anger-out may contribute to this finding.     

Anger-coping styles and blood pressure in black and white males: Buffalo, New York

Data from a random survey of household residents in the urban area of Buffalo, stratified by race and education, showed relations between anger-coping styles and age-weight adjusted blood pressure (BP) among males (N = 720). Findings show that older black males with a high reflective mode of anger (constrain anger and try to solve the problem) had significantly lower blood pressure than those with low scores on this mode. In contrast, older black males with a high Anger-out mode (impulsive anger strongly expressed) had significantly higher blood pressure than those low on this mode. This Anger-out pattern was also found for older white men; but for younger whites, only higher alcohol and lower education were significantly related to higher BP levels. An Anger-in mode (impulsive anger not expressed) was not significantly related to blood pressure. The limitations of the Anger-in measures are examined. and a concept of a resentful anger style is discussed and presented for further research.     

Is postoperative pain a self-fulfilling prophecy? Expectancy effects on postoperative pain and patient-controlled analgesia use among adolescent surgical patients

OBJECTIVE: To explore relationships among anxiety, anticipated pain, coping styles, postoperative pain, and patient-controlled analgesia (PCA) use among adolescent surgical patients and their parents. METHODS: Sixty-five 12- to 18-year-old surgical patients undergoing surgery with postoperative PCA pain management were included. Before surgery, adolescents and parents reported anxiety and expected levels of postoperative pain. Pain catastrophizing and coping style were assessed within 48 hr after surgery, with pain scores and PCA use recorded through the end of the second postoperative day. RESULTS: Adolescents' preoperative psychological characteristics (anxiety and anticipated pain) predicted postoperative pain scores, number of PCA injections and demands, and the PCA injections:demands ratio, with reports of anticipated pain associating most closely with these postoperative pain outcomes. Parental anxiety and anticipated pain did not predict teens' postoperative pain. Coping style did not moderate the relationship between anticipated pain and pain outcomes. CONCLUSIONS: Findings are interpreted as suggesting a self-fulfilling prophecy in adolescents' postoperative pain experience wherein teens who expect to have high levels of postoperative pain ultimately report more pain and use more opioid PCA medication than those who report lower levels of pain.     

Is anger management style associated with descending modulation of spinal nociception?

Anger management styles (i.e., anger‐in and anger‐out) characterize a person's typical response to anger. Anger‐in, the suppression of anger, and anger‐out, the outward expression of anger, have been associated with increased acute and chronic pain. Previous research suggests that anger‐in is related to pain because of its shared variance with negative affect; anger‐out is believed to be related to pain because of a disruption of endogenous opioid systems. It is currently unknown whether anger management styles promote pain by facilitating central sensitization or spinal nociception. This study assessed the relationship between anger management styles and markers of central sensitization (i.e., temporal summation of pain [TS ‐pain] and nociception flexion reflex [TS ‐NFR ]), spinal nociception (nociception flexion reflex [NFR ] threshold), and measures of pain experience. One hundred nine healthy pain‐free individuals completed the study. A bootstrapped mediation analysis was conducted to test whether negative affect mediated relationships with anger‐in. Results suggested that anger‐in and anger‐out were associated with lower NFR thresholds (facilitated spinal nociception), but no other outcome. Negative affect did not mediate either of these relationships. These results suggest that anger management styles may amplify spinal nociceptive processes in healthy humans without altering central sensitization.     

Pain catastrophizing,physiological indexes,and chronic pain severity: tests of mediation and moderation models

Catastrophizing about pain is related to elevated pain severity and poor adjustment among chronic pain patients, but few physiological mechanisms by which pain catastrophizing maintains and exacerbates pain have been explored. We hypothesized that resting levels of lower paraspinal muscle tension and/or lower paraspinal and cardiovascular reactivity to emotional arousal may: (a) mediate links between pain catastrophizing and chronic pain intensity; (b) moderate these links such that only patients described by certain combinations of pain catastrophizing and physiological indexes would report pronounced chronic pain. Chronic low back pain patients (N = 97) participated in anger recall and sadness recall interviews while lower paraspinal and trapezius EMG and systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) were recorded. Mediation models were not supported. However, pain catastrophizing significantly interacted with resting lower paraspinal muscle tension to predict pain severity such that high catastrophizers with high resting lower paraspinal tension reported the greatest pain. Pain catastrophizing also interacted with SBP, DBP and HR reactivity to affect pain such that high catastrophizers who showed low cardiovascular reactivity to the interviews reported the greatest pain. Results support a multi-variable profile approach to identifying pain catastrophizers at greatest risk for pain severity by virtue of resting muscle tension and cardiovascular stress function.     

Interactive effects of traits,states, and gender on cardiovascular reactivity during different situations

Interactive effects of anger and anxiety traits, negative affect state, different situations, and gender on cardiovascular reactivity (CVR) to stress were examined. Subjects (91 men, 92 women) performed a reaction time task under either a Social Evaluation, a Harassment, or a Control condition; SBP, DBP, and HR were recorded continuously. Hierarchical multiple regressions revealed intricate interactions. The interaction of anger expression style and anger experience was significant only among men, such that anger suppressors with high trait anger showed the largest CVR of any group during Harassment; anger expressors exhibited generally high CVR across conditions. However, anger expression style and state negative affect interacted to affect CVR in both men and women. Finally, the fear of negative evaluation predicted elevated DBP responses only among men in the Social Evaluation condition. Results imply that the extent to which traits of anger and anxiety contribute to coronary risk may depend on interactions with other traits, gender, and the environment.     

Anger inhibition and pain: conceptualizations, evidence and new directions

Anger and how anger is regulated appear to affect acute and chronic pain intensity. The inhibition of anger (anger-in), in particular, has received much attention, and it is widely believed that suppressing or inhibiting the verbal or physical expression of anger is related to increased pain severity. We examine theoretical accounts for expecting that anger inhibition should affect pain, and review evidence for this claim. We suggest that the evidence for a link between trait anger-in (the self-reported tendency to inhibit anger expression when angry) and acute and chronic pain severity is quite limited owing to a number of factors including a inadequate definition of trait anger-in embodied in the popular anger-in subscale of Spielberger's Anger Expression Inventory, and a strong overlap between trait anger-in scores and measures of general negative affect (NA). We argue that in order to determine whether something unique to the process of anger inhibition exerts direct effects on subsequent pain intensity, new conceptualizations and approaches are needed that go beyond self-report assessments of trait anger-in. We present one model of anger inhibition and pain that adopts elements of Wegner's ironic process theory of thought suppression. Findings from this emerging research paradigm indicate that state anger suppression (suppression manipulated in the laboratory) may indeed affect sensitivity to subsequent painful stimuli, and we outline potentially productive avenues of future inquiry that build on this model. We conclude that although studies employing correlational designs and self-reports of trait anger-in have not upheld the claim that anger inhibition affects pain severity, evidence from studies using new models suggests that actually inhibiting anger expression during a provocative event may increase perceived pain at a later time.     

Gender, anger expression style, and opportunity for anger release determine cardiovascular reaction to and recovery from anger provocation.

This study represents an extension of Hokanson's research, which showed that for men anger release after provocation tends to accelerate cardiovascular recovery. The objective of this study was to investigate how gender and habitual style for anger-in or anger-out behavior modulate the effect of anger provocation and release. Male and female subjects (N = 105) were classified as anger-in/anger-out only when a double criterion (i.e., self-report and peer evaluation) was satisfied. Following a state anger rating at pre-test, subjects were harassed during the performance of a 12-minute math task. After task completion, subjects were randomly assigned to one of two 10-minute recovery protocols a) having an opportunity to release negative affect, and b) not not having such an opportunity. All groups (including the anger-ins) that had an opportunity to express negative affect did in fact express similar levels of anger. Men reacted more strongly to the math task performed under anger provocation on all cardiovascular indices. Anger expression style as a trait-type disposition was important for the recovery process in women whereas the situational manipulation (i.e., the opportunity to release anger) had specific effects on the recovery process of men. Opportunity to release anger facilitated heart rate recovery (and to a lesser degree diastolic pressure recovery) in men but not in women. Women with anger-in tendencies on the other hand displayed better systolic pressure recovery than female anger-outs whereas no such effects were observed in men.     

Trait anger and blood pressure recovery following acute pain: evidence for opioid-mediated effects

Previous work has suggested that positive associations between trait anger (TRANG) and pain sensitivity are due to dysfunctional endogenous opioid analgesic systems. In this study, we examined whether TRANG is associated with impaired opioid modulation of blood pressure (BP) recovery. A total of 46 pain-free normotensive controls and 69 normotensive chronic low back pain (LBP) sufferers received opioid blockade (8mg naloxone IV) or placebo in randomized, counterbalanced order in separate sessions. During each, participants underwent a 1-min finger pressure pain task followed by an ischemic forearm pain task. Opioid blockade impaired post-pain BP recovery in controls but not LBP participants (ps < .001). In controls, low TRANG was associated with blockade-induced recovery impairments, with no blockade effect in high TRANG participants. In LBP participants, blockade did not alter recovery regardless of TRANG (interaction ps < .05). Results support dysfunctional opioid modulation of BP recovery in healthy high TRANG controls and further suggest chronic pain-related impairments in opioid-mediated cardiovascular recovery.     

Lymphocyte Proliferation Is Associated with Gender, Caregiving, and Psychosocial Variables in Older Adults

We examined lymphocyte responses to mitogens [phytohemagglutinin (PHA), concanavalin A, pokeweed] in spouse caregivers of persons with Alzheimer's disease (n = 82; mean age = 69.4) and noncaregiver spouses (n = 83) group matched on age and gender. Data were collected at study entry (T1) and 15–18 months later (T2). In men (n = 52), a depressed mood factor was negatively related to all mitogen responses at T1 and PHA at T2. Loneliness was the most important variable in the depressed mood factor. No relationships occurred in women (n = 113). At T2 an anger expression factor (anger-out – anger-control) was negatively related to all mitogen responses in caregivers. Anger-out was the most important variable for anger expression. Depressed mood at T1 predicted residualized changes in PHA at T2 in men. In conclusion, men with higher depressed mood and caregivers with higher anger expression may be at risk for lower proliferation responses.     

Opioid peptides in peripheral pain control

Opioids have a long history of therapeutic use as a remedy for various pain states ranging from mild acute nociceptive pain to unbearable chronic advanced or end-stage disease pain. Analgesia produced by classical opioids is mediated extensively by binding to opioid receptors located in the brain or the spinal cord. Nevertheless, opioid receptors are also expressed outside the CNS in the periphery and may become valuable assets in eliciting analgesia devoid of shortcomings typical for the activation of their central counterparts. The discovery of endogenous opioid peptides that participate in the formation, transmission, modulation and perception of pain signals offers numerous opportunities for the development of new analgesics. Novel peptidic opioid receptor analogs, which show limited access through the blood brain barrier may support pain therapy requiring prolonged use of opioid drugs.     

The Outward Expression of Anger, the Inward Experience of Anger and CVR: The Role of Vocal Expression

Two hypotheses were tested: (1) that only the outward expression of anger, not its mere experience, is associated with heightened cardiovascular reactivity; and (2) that the discussion of anger-arousing experiences in a mood incongruent speech style (soft and slow) attenuates the subjective experience of anger and its cardiovascular correlates. Each of 24 subjects participated in three experimental conditions: (1) Anger-out, in which previously experienced anger-arousing events were described loudly and quickly; (2) Anger-in, in which anger-arousing events were relived inwardly, in subject's imagination; and (3) mood-incongruent speech, in which anger-arousing events were described softly and slowly. Only the Anger-out condition was associated with high cardiovascular reactivity levels. The Anger-in and the mood-incongruent conditions were associated with near-zero and very low reactivity levels, respectively. Subjective anger ratings were highest in the Anger-out condition, moderate in the Anger-in condition, and lowest (not angry) in the mood-incongruent condition. All differences were significant. These findings suggest that the full-blown expression of anger, in all of its paraverbal intensity, is pathogenic and that the mere inner experience of anger is not.     

Experiences of patients requiring strong opioid drugs for chronic non-cancer pain: a patient-initiated study

BACKGROUND: Chronic non-cancer pain is an increasing problem in health care. This study was initiated by a patient wanting to discover more about the experiences of other patients requiring strong opioid analgesia for such pain. AIM: To determine the attitudes and experiences of patients receiving long-term strong opioid medication for chronic non-cancer pain in primary care. Design of study: Qualitative study using interpretative phenomenological analysis. SETTING: A semi-rural general practice in southwest England. METHOD: The study data came from a focus group and 10 individual patient interviews. A patient researcher was involved in the design, conduct, and analysis of the project. RESULTS: The impact of pain affected participants in every aspect of their daily lives. Attitudes to strong opioid medication were both positive and negative. Concerns about starting medication usually centred on fears of addiction, being seen as an addict, or that the patients may have a more serious condition than they had previously thought. However, these fears were tempered by an appreciation of the benefits that strong opioids brought in terms of pain relief and consequent gains in a nearer-to-normal existence. The data did not produce any evidence of addictive behaviour or of tolerance despite these initial fears. Patients adopted a trade-off approach, balancing pain relief with medication side effects, accepting more pain for a reduction in sedation and nausea. All patients described coping strategies they developed themselves and learned from outside influences, such as pain clinic courses and support from the GP. There was realism that total pain relief was not possible, but that a balance could be struck. CONCLUSION: Chronic non-cancer pain is associated with high levels of distress and psychosocial impairment. Patients in this study appreciated the benefits of strong opioid medication, having come to terms with fears of addiction and learned coping strategies. These findings should encourage GPs to consider strong opioid medication for patients with severe chronic pain in line with published evidence-based guidelines.     

Anger expression, hostility, anxiety, and patterns of cardiac reactivity to stress.

The majority of studies investigating the relationships between psychological characteristics and cardiovascular reactivity to stress use a research strategy in which discrete traits are evaluated in isolation. The present study examined the effects of additive and/or interactive relationships among traits on cardiac reactivity to a mental arithmetic task. In addition, impedance cardiographic techniques were employed to examine potential relationships between such psychological traits and a specific measure--pre-ejection period (PEP)--of sympathic influence on the heart. Forty-nine undergraduate men performed a mental arithmetic task while continuous measures of PEP and interbeat interval (IBI) were collected. The subjects then completed questionnaires measuring anger expression, hostility, and trait anxiety. Analyses of variance (ANOVAs) showed a significant main effect for anger-out on PEP change from baseline, but not for IBI. Results also showed that anger-in interacted with anger-out and hostility to affect both PEP and IBI changes significantly. Other results indicated that subjects in the high anger-in/low anger-out and high anger-in/low hostility groups did not show significant PEP change, although they nevertheless showed significant IBI change. These results highlight the importance of the consideration of interactions among traits in predicting cardiac reactivity and of the importance of measuring specific indexes of sympathetic arousal.