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Kurt Kotrschal - One of the best experts on this subject based on the ideXlab platform.

  • Social context modulates digestive efficiency in greylag geese (Anser Anser).
    Scientific Reports, 2018
    Co-Authors: Didone Frigerio, Kurt Kotrschal, Carla Fabro, Verena Puehringer-sturmayr, Lara Iaiza, Josef Hemetsberger, Federico Mason, Chiara Sarnataro, Stefano Filacorda
    Abstract:

    In group-living animals, social context is known to modulate physiology, behaviour and reproductive output as well as foraging and nutritional strategies. Here we investigate the digestive efficiency of 38 individuals belonging to different social categories of a semi-feral and individually marked flock of greylag geese (Anser Anser). During 9 consecutive days in winter 2017, when the ground was fully covered with snow (i.e. no grass or other natural forage available) and the accessible food was standardized, 184 individual droppings were collected and analysed to estimate the apparent digestibility of organic matter (ADOM). Lignin was used as an indigestible internal marker in the food and droppings. The digestive efficiency was higher in pairs with offspring as compared to pairs without offspring or unpaired birds. Furthermore, individuals with high ADOM were more likely to breed successfully in the following season than those with low ADOM. Our findings demonstrate that social status modulates digestive efficiency, probably via a chain of physiological mechanisms including a dampened stress response in individuals enjoying stable social relationships with and social support by their family members (i.e. their own pair-partner and offspring). Our findings underline the importance of the social network in modulating physiology, such as digestive efficiency, and ultimately reproductive success.

  • Heart rate responses to induced challenge situations in greylag geese (Anser Anser).
    Journal of Comparative Psychology, 2011
    Co-Authors: Claudia A. F. Wascher, Isabella B. R. Scheiber, Anna Braun, Kurt Kotrschal
    Abstract:

    Adequate short-term responses to stressors are of great importance for the health and well-being of individuals and factors modulating the physiological stress response (e.g., controllability, suddenness, familiarity) of a stimulus are well described under laboratory conditions. In the present study we aimed at investigating the stress response in greylag geese (Anser Anser) in the field, confronting individuals with naturally occurring stressors. We measured beat-to-beat heart rate (HR) via fully implanted transmitters during three different experimental challenges: (1) catching and holding, (2) confrontation with a model predator, and (3) approach by different humans. We compared this to a control period and HR during agonistic encounters, a naturally occurring stressor. All three experimental situations evoked a HR increase. Highest HR responses were elicited by catching and holding the animals. In the third experiment, HR responses were greatest when the geese were approached by a human stranger (i.e., somebody the geese have never seen before). Hence, geese discriminated between different kinds of stressors and adjusted their physiological response depending on the type of stressor. Our results show that geese were able to discriminate between individual humans. In line with a number of lab studies, we suggest that particularly the controllability of certain situation determines the intensity of the HR response, also in a natural setting in the field.

  • behavioural and physiological correlates of personality in greylag geese Anser Anser
    Journal of Ethology, 2010
    Co-Authors: Simona Kraljfiser, Brigitte M Weis, Kurt Kotrschal
    Abstract:

    Personality means suites of correlated behavioural traits, also referred to as “behavioural syndromes” or “personality dimensions”. Across animal taxa similar combinations of traits seem to prevail, which may have proximate foundation in common neuroendocrine mechanisms. Hitherto, these have been rarely studied in intact social settings. We investigated personalities of greylag goose males from a free-roaming flock that shows complex social relationships. In connection with our longitudinal study on the consistency of behavioural and physiological responses to multiple challenges, we asked whether and how single, personality-related behavioural traits correlate with each other to form personality dimension(s). We tested whether these dimensions were related to physiological characteristics that previously showed limited plasticity (heart rate (HR), baseline and stress-induced excreted immuno-reactive corticosterone (BM), and testosterone metabolites levels) and, furthermore, to age, body measures, and dominance rank. Principal-components analysis based on behavioural variables revealed two factors: 51.1% of variability was explained by “aggressiveness” and a further 19.1% by “sociability”. “Aggressiveness” comprised correlated measures of aggression, subordinance, boldness, vigilance, and proximity to the mate. This “aggressiveness” positively correlated with stress-induced BM levels, the HR increase during aggressive interactions, and with dominance rank, which may suggest proximate and functional contingencies of this personality dimension.

  • Active and passive social support in families of greylag geese (Anser Anser).
    Behaviour, 2005
    Co-Authors: Isabella B. R. Scheiber, Didone Frigerio, Brigitte M Weiß, Kurt Kotrschal
    Abstract:

    In general, support by social allies may reduce stress, increase success in agonistic encounters and ease access to resources. Social support was mainly known from mammals, particularly primates, and has been studied in birds only recently. Basically two types are known: (i) 'active social support', which describes the participation of a social ally in agonistic encounters, and (ii) 'passive social support' in which the mere presence of a social ally reduces behavioural and physiological stress responses. In greylag geese (Anser Anser) offspring stay with their parents for an entire year or even longer and therefore are a candidate avian model to study support by social allies. We investigated the effects of active and passive social support in ten families (ten males, ten females, 33 juveniles) in a free-roaming, semi-tame flock of greylag geese. Focal individuals were observed during three time periods: (i) re-establishment of the flock in the fall, (ii) stable winter flock, and (iii) disintegration of the flock and break-up of family bonds. We recorded all agonistic interactions of the members of one focal family during morning feedings for two consecutive days: a control day, in which food was distributed widely, and a social density stress situation, in which the same amount of food was spread over a much smaller area. In addition, we collected faeces of all individuals within this family for three hours from the beginning of the feeding situation for determining excreted corticosterone immuno-reactive metabolites by enzyme immuno assay. We found that the small families, i.e. pairs with one or two accompanying young, were involved in more agonistic interactions, mainly through the lack of active social support, as compared to large families in the same situation. Members of greylag goose families lost agonistic encounters significantly less often when actively supported. In addition, the excretion of corticosterone metabolites was significantly decreased in large families during a social density stress situation, probably as an effect of passive social support. Via such a socially induced decrease in hormonal stress response during challenging situations, an individual's long term energy management may benefit.

  • hormonal correlates of being an innovative greylag goose Anser Anser
    Animal Behaviour, 2002
    Co-Authors: Karina Pfeffer, Johannes Fritz, Kurt Kotrschal
    Abstract:

    Abstract A number of studies have focused on the spread of foraging innovations within animal populations, but only rarely have individual dispositions of becoming innovative been considered. With two groups of individually marked, hand-reared greylag goslings we investigated hormonal and behavioural correlates related to the individual's ability to perform operant tasks. During individual tests 6 weeks after hatching, goslings were given small food containers covered by lids. In the following winter the sibling groups were tested in a social set-up at a food dispenser, which the geese could activate by pulling a flap. We analysed individual faecal samples collected at 2, 6 and 12 weeks of age, and also after the individual tests, for excreted corticosterone and testosterone metabolites by enzyme immunoassay. During the individual test, 18 of 23 individuals learned to remove the lids. These 18 birds excreted higher faecal corticosterone concentrations than their respective controls 2 weeks after hatching. At the food dispensers, only four males became food producers; all the others scrounged. These four were in the group of 18 that were successful in the individual test and again tended, although not significantly, to have higher faecal corticosterone 2 weeks after hatching than the scroungers. In one of the groups, excreted corticosterone increased and excreted testosterone decreased after the individual test. Goslings successfully removing lids at 6 weeks raised their faecal corticosterone to a significantly greater extent than the unsuccessful individuals. Our results suggest that becoming an innovator may be contingent upon individual coping styles. Copyright 2002 The Association for the Study of Animal Behaviour. Published by Elsevier Science Ltd. All rights reserved .

Rosario Martin - One of the best experts on this subject based on the ideXlab platform.

Carlo Cantoni - One of the best experts on this subject based on the ideXlab platform.

Stephen Bruehl - One of the best experts on this subject based on the ideXlab platform.

  • anger arousal and behavioral anger regulation in everyday life among patients with chronic low back pain relationships to patient pain and function
    Health Psychology, 2015
    Co-Authors: John W Burns, Stephen Bruehl, James Gerhart, Kristina M Peterson, David A Smith, Laura S Porter, Erik Schuster, Ellen Kinner, Asokumar Buvanendran, Anne Marie Fras
    Abstract:

    For people with chronic pain, anger-related factors are significantly associated with pain intensity, mood and physical function such that greater anger is related to poorer adjustment (Janssen, Spinhoven, & Brosschot, 2001; Kerns, Rosenberg, & Jacob, 1994; Nicholson, Gramling, Ong, & Buenevar, 2003; Wade, Price, Hamer, Schwartz & Hart, 1990). Evidence suggests that how anger is regulated – expression, inhibition – may have greater consequences for chronic pain patients’ pain and function than their level of state anger (Bruehl, Chung, & Burns, 2006; Bruehl, Burns, Chung, Ward, & Johnson, 2002; Burns et al., 2008). Anger expression may be related to pain and function along at least two pathways. First, it has been proposed that people who tend to verbally or physically express anger and who exhibit high pain sensitivity may be characterized by deficits in endogenous inhibitory mechanisms (Bruehl et al., 2002). Findings support this model and indicate that chronic pain patients and healthy people alike who are high in trait anger-expressiveness show evidence of deficient endogenous opioid function, thus leaving them with elevated pain sensitivity (Bruehl et al., 2002). Second, a symptom-specific reactivity model (Flor, Turk & Birbaumer, 1985) has been adapted for anger and chronic pain, and holds that anger arousal may lead to increases in muscle tension near the site of injury, and thereby increase pain (Burns, Bruehl, & Quartana, 2006). In the case of chronic low back pain (CLBP) patients, the relevant muscles would be in the low back (e.g., lower paraspinal [LP] muscles). Results support this model, and indicate that anger arousal among CLBP patients produces greater increases in LP muscle tension than sadness (Burns, 2006), and that CLBP patients with elevated trait anger-expressiveness showed greater increases in LP muscle tension during anger arousal than those low in trait anger-expressiveness (Burns et al., 2006). Anger inhibition may be related to pain and function also along at least two pathways. First, a thought suppression model (Wegner, 1994) was adapted for anger inhibition and pain, and holds that inhibiting anger has the ironic consequence of amplifying and maintaining anger which in turn exerts delayed negative effects on responses to later events (Burns, Quartana, & Bruehl, 2008). Thus, inhibiting anger can worsen later pain perception as ironically sustained thoughts of anger contaminate the experience of pain. Results support this model in that chronic pain patients and healthy people who inhibited anger during anger arousal showed greater increases in anger during anger-induction and reported greater anger and pain intensity during subsequent acute pain-induction than those who did not inhibit anger during anger arousal (Burns, 2008; Quartana & Burns 2007). Second, the symptom-specific reactivity model may also apply to anger inhibition. Findings showed that CLBP patients evinced greater increases in LP muscle tension while inhibiting anger during anger arousal than those not inhibiting, and these increases were shown to predict the frequency of observable pain behaviors during subsequent pain induction (Burns, Quartana, Gilliam, Matsuura, Nappi, & Wolfe, 2012). These conceptual models support hypotheses that both anger expression and inhibition can lead to increased pain sensitivity and intensity, and may do so via distinct pathways. Findings from numerous cross-sectional questionnaire and lab-based studies support these contentions (Bruehl et al., 2006; Burns et al., 2008). However, the questionnaire studies based on traits tell us little about the effects of actual anger regulation behaviors on pain and functioning, and although some lab-based studies did manipulate anger arousal, anger regulation behavior and pain in controlled conditions, ecological validity is limited by the artificial nature of the procedures. Thus, we know little about relationships between what people actually do in everyday life to regulate anger and their pain and function. Results of two recent daily diary studies help address this shortcoming. In the first study (van Middendorp, Lumley, Moerbeek, Jacobs, Bijlsma, & Geenen, 2010), results suggested that behavioral anger expression during an anger-provoking event during the day was related to elevated end-of-day pain. They also reported that state anger was related to higher end-of-day pain. This design did not include true lagged analyses, so it is not clear whether anger predicted pain or vice versa. In the second study (Bruehl, Liu, Burns, Chont, & Jamison, 2012), results of lagged analyses suggested that behavioral anger expression during one period was related to elevated pain in the subsequent period, providing the first evidence of a longitudinal effect. Their assessment was limited, however, only to anger expression and patient rated pain intensity, and, moreover, did not include state anger. In the present study, we used electronic diary methods to replicate and extend prior work, and evaluate the degree to which patient feelings of anger and behavioral anger regulation – both expression and inhibition – occurring in the course of daily life was related to both patient pain and function as rated by patients. In addition, these data were collected as part of a larger study that also included spouse ratings of patient pain and function (Burns et al., in press). Specifically, patients with chronic low back pain (CLBP) and their spouses completed electronic diary entries 5 times/day for 14 days using Personal Data Assistants (PDAs). On one level, if anger arousal and/or behavioral anger regulation, as it occurs in everyday life, are related to pain and function, then concurrent analyses would show relationships between increases in state anger, anger expression and/or inhibition and fluctuations in pain and function. Further, if anger arousal and/or behavioral anger regulation actually influence pain and function, then lagged analyses would show that initial increases in state anger, anger expression and/or inhibition predict later fluctuations in pain and function, particularly in the case of anger inhibition given prior evidence of delayed effects on pain (Burns et al. 2008) (i.e., anger → pain). Alternatively, it may be the case, as suggested by results of Feldman, Downey and Schiffer-Neitz (1999), that initial pain intensity could predispose someone to experience later anger and the need to regulate it, and thus initial increases in pain would predict later fluctuations in anger arousal, anger expression and/or inhibition (i.e., pain → anger). On another level, if increases in anger arousal, anger expression and/or inhibition are indeed related to changes in patient pain and function, these increases should be related to demonstrable pain and function changes that can be observed by reporters other than the patient. We hypothesized that patient-reported increases in their anger arousal, behavioral anger expression and/or inhibition would be related to spouse ratings of observable patient behavior. Finally, the need to regulate anger presupposes the presence of anger arousal. If patient behavioral anger regulation per se is a key phenomenon related to current and later pain and function, then anger regulation factors should exert unique effects beyond those attributable to anger arousal alone. To address this issue, we controlled for either concurrent state anger or lagged state anger where relevant. Note that because anger arousal is a core and necessary constituent of the phenomenon “anger regulation,” statistically controlling for state anger represents a conservative and stringent approach.

  • anger regulation style anger arousal and acute pain sensitivity evidence for an endogenous opioid triggering model
    Journal of Behavioral Medicine, 2014
    Co-Authors: John W Burns, Stephen Bruehl, Melissa Chont
    Abstract:

    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 management style moderates effects of emotion suppression during initial stress on pain and cardiovascular responses during subsequent pain induction
    Annals of Behavioral Medicine, 2007
    Co-Authors: John W Burns, Phillip J Quartana, Stephen Bruehl
    Abstract:

    Background: Suppression of emotion, anger in particular, may be linked to heightened pain intensity during a subsequent painful event, but it is not clear whether an individual’s anger management style (trait anger-out or trait anger-in) moderates effects on pain intensity and cardiovascular responses during pain.Purpose: To determine whether (a) trait anger-out and/or trait anger-in moderate effects of Emotion-Induction (anger, anxiety)×Emotion Suppression (nonsuppression, experiential, expressive) manipulations during mental arithmetic on pain intensity and cardiovascular responses during and following a cold pressor pain task, such that “mismatch” relationships emerge (preferred anger management style is discrepant from situation demands), and (b) general emotional expressivity accounts for these effects.Method: Healthy nonpatients (N=187) were assigned to 1 of 6 conditions for a mental arithmetic task. Cells were formed by crossing 2 Emotion-Induction (anxiety, anger)×3 Emotion Suppression (non-suppression, experiential, expressive) conditions. After mental arithmetic, participants underwent a cold pressor followed by recovery. Systolic blood pressure (SBP), diastolic BP (DBP), heart rate (HR), and pain intensity ratings were recorded. Spielberger Anger Expression Inventory tapped anger management style.Results: General Linear Model procedures tested Emotion-Induction×Emotion Suppression×Anger-Out or Anger-In (continuous)×Period (baseline, cold pressor, recovery) effects on pain intensity, SBP, DBP, and HR. A 4-way interaction emerged for pain intensity: Only for those in the anger-induction/experiential suppression condition, anger-out was related significantly to pain recovery. Three-way interactions emerged for SBP and DBP: Only for those in expressive suppression condition, anger-out was related significantly to SBP during and following cold pressor and to DBP following cold pressor. General emotion expressivity did not account for anger-out effects.Conclusions: A mismatch situation may apply for high anger-out people who suppress emotion in a certain circumstance and thus may suffer greater discomfort and physiological responsiveness to subsequent pain than high anger-out people not having to suppress.

  • trait anger expressiveness and pain induced beta endorphin release support for the opioid dysfunction hypothesis
    Pain, 2007
    Co-Authors: Stephen Bruehl, John W Burns, Ok Yung Chung, Laura Diedrich
    Abstract:

    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 .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.

  • anger management style and hostility among patients with chronic pain effects on symptom specific physiological reactivity during anger and sadness recall interviews
    Psychosomatic Medicine, 2006
    Co-Authors: John W Burns, Stephen Bruehl, Phillip J Quartana
    Abstract:

    OBJECTIVES: We examined whether anger-in, anger-out, and hostility predicted symptom-specific muscle tension reactivity during anger induction (but not sadness induction) among patients with chronic low back pain (CLBP). For patients with CLBP, relevant muscles are the lower paraspinals (LPs). Anger-in x hostility and anger-out x hostility interactions were tested to determine whether particularly reactive groups of patients could be identified with a multivariable profile approach. METHODS: Ninety-four patients with CLBP underwent anger recall (ARI) and sadness recall (SRI) interviews, whereas LP and trapezius electromyography and systolic blood pressure, diastolic blood pressure, and heart rate were recorded. They completed anger-in, anger-out, hostility, and trait anger measures. RESULTS: Hierarchical regressions were used to test anger-in x hostility and anger-out x hostility interactions for physiological changes during the ARI and SRI. A significant anger-in x hostility interaction was found for LP change during the ARI (but not SRI) such that high anger-in/high hostility patients evinced the greatest reactivity. Effects for trapezius reactivity were nonsignificant. Significant anger-in x hostility interactions were also found for systolic blood pressure and diastolic blood pressure changes during the ARI such that high anger-in/low hostility patients showed the smallest changes. The anger-out x hostility interaction for diastolic blood pressure change during ARI was also significant such that high anger-out/low hostility patients showed the smallest changes. All effects remained significant with trait anger controlled. CONCLUSIONS: A multivariable profile approach may help identify especially vulnerable patient groups. Patients with CLBP who tend to suppress anger and are cynically hostile may be more likely to experience high levels of muscle tension near the site of pain and injury during anger, but not during sadness, than other groups.

John W Burns - One of the best experts on this subject based on the ideXlab platform.

  • anger arousal and behavioral anger regulation in everyday life among patients with chronic low back pain relationships to patient pain and function
    Health Psychology, 2015
    Co-Authors: John W Burns, Stephen Bruehl, James Gerhart, Kristina M Peterson, David A Smith, Laura S Porter, Erik Schuster, Ellen Kinner, Asokumar Buvanendran, Anne Marie Fras
    Abstract:

    For people with chronic pain, anger-related factors are significantly associated with pain intensity, mood and physical function such that greater anger is related to poorer adjustment (Janssen, Spinhoven, & Brosschot, 2001; Kerns, Rosenberg, & Jacob, 1994; Nicholson, Gramling, Ong, & Buenevar, 2003; Wade, Price, Hamer, Schwartz & Hart, 1990). Evidence suggests that how anger is regulated – expression, inhibition – may have greater consequences for chronic pain patients’ pain and function than their level of state anger (Bruehl, Chung, & Burns, 2006; Bruehl, Burns, Chung, Ward, & Johnson, 2002; Burns et al., 2008). Anger expression may be related to pain and function along at least two pathways. First, it has been proposed that people who tend to verbally or physically express anger and who exhibit high pain sensitivity may be characterized by deficits in endogenous inhibitory mechanisms (Bruehl et al., 2002). Findings support this model and indicate that chronic pain patients and healthy people alike who are high in trait anger-expressiveness show evidence of deficient endogenous opioid function, thus leaving them with elevated pain sensitivity (Bruehl et al., 2002). Second, a symptom-specific reactivity model (Flor, Turk & Birbaumer, 1985) has been adapted for anger and chronic pain, and holds that anger arousal may lead to increases in muscle tension near the site of injury, and thereby increase pain (Burns, Bruehl, & Quartana, 2006). In the case of chronic low back pain (CLBP) patients, the relevant muscles would be in the low back (e.g., lower paraspinal [LP] muscles). Results support this model, and indicate that anger arousal among CLBP patients produces greater increases in LP muscle tension than sadness (Burns, 2006), and that CLBP patients with elevated trait anger-expressiveness showed greater increases in LP muscle tension during anger arousal than those low in trait anger-expressiveness (Burns et al., 2006). Anger inhibition may be related to pain and function also along at least two pathways. First, a thought suppression model (Wegner, 1994) was adapted for anger inhibition and pain, and holds that inhibiting anger has the ironic consequence of amplifying and maintaining anger which in turn exerts delayed negative effects on responses to later events (Burns, Quartana, & Bruehl, 2008). Thus, inhibiting anger can worsen later pain perception as ironically sustained thoughts of anger contaminate the experience of pain. Results support this model in that chronic pain patients and healthy people who inhibited anger during anger arousal showed greater increases in anger during anger-induction and reported greater anger and pain intensity during subsequent acute pain-induction than those who did not inhibit anger during anger arousal (Burns, 2008; Quartana & Burns 2007). Second, the symptom-specific reactivity model may also apply to anger inhibition. Findings showed that CLBP patients evinced greater increases in LP muscle tension while inhibiting anger during anger arousal than those not inhibiting, and these increases were shown to predict the frequency of observable pain behaviors during subsequent pain induction (Burns, Quartana, Gilliam, Matsuura, Nappi, & Wolfe, 2012). These conceptual models support hypotheses that both anger expression and inhibition can lead to increased pain sensitivity and intensity, and may do so via distinct pathways. Findings from numerous cross-sectional questionnaire and lab-based studies support these contentions (Bruehl et al., 2006; Burns et al., 2008). However, the questionnaire studies based on traits tell us little about the effects of actual anger regulation behaviors on pain and functioning, and although some lab-based studies did manipulate anger arousal, anger regulation behavior and pain in controlled conditions, ecological validity is limited by the artificial nature of the procedures. Thus, we know little about relationships between what people actually do in everyday life to regulate anger and their pain and function. Results of two recent daily diary studies help address this shortcoming. In the first study (van Middendorp, Lumley, Moerbeek, Jacobs, Bijlsma, & Geenen, 2010), results suggested that behavioral anger expression during an anger-provoking event during the day was related to elevated end-of-day pain. They also reported that state anger was related to higher end-of-day pain. This design did not include true lagged analyses, so it is not clear whether anger predicted pain or vice versa. In the second study (Bruehl, Liu, Burns, Chont, & Jamison, 2012), results of lagged analyses suggested that behavioral anger expression during one period was related to elevated pain in the subsequent period, providing the first evidence of a longitudinal effect. Their assessment was limited, however, only to anger expression and patient rated pain intensity, and, moreover, did not include state anger. In the present study, we used electronic diary methods to replicate and extend prior work, and evaluate the degree to which patient feelings of anger and behavioral anger regulation – both expression and inhibition – occurring in the course of daily life was related to both patient pain and function as rated by patients. In addition, these data were collected as part of a larger study that also included spouse ratings of patient pain and function (Burns et al., in press). Specifically, patients with chronic low back pain (CLBP) and their spouses completed electronic diary entries 5 times/day for 14 days using Personal Data Assistants (PDAs). On one level, if anger arousal and/or behavioral anger regulation, as it occurs in everyday life, are related to pain and function, then concurrent analyses would show relationships between increases in state anger, anger expression and/or inhibition and fluctuations in pain and function. Further, if anger arousal and/or behavioral anger regulation actually influence pain and function, then lagged analyses would show that initial increases in state anger, anger expression and/or inhibition predict later fluctuations in pain and function, particularly in the case of anger inhibition given prior evidence of delayed effects on pain (Burns et al. 2008) (i.e., anger → pain). Alternatively, it may be the case, as suggested by results of Feldman, Downey and Schiffer-Neitz (1999), that initial pain intensity could predispose someone to experience later anger and the need to regulate it, and thus initial increases in pain would predict later fluctuations in anger arousal, anger expression and/or inhibition (i.e., pain → anger). On another level, if increases in anger arousal, anger expression and/or inhibition are indeed related to changes in patient pain and function, these increases should be related to demonstrable pain and function changes that can be observed by reporters other than the patient. We hypothesized that patient-reported increases in their anger arousal, behavioral anger expression and/or inhibition would be related to spouse ratings of observable patient behavior. Finally, the need to regulate anger presupposes the presence of anger arousal. If patient behavioral anger regulation per se is a key phenomenon related to current and later pain and function, then anger regulation factors should exert unique effects beyond those attributable to anger arousal alone. To address this issue, we controlled for either concurrent state anger or lagged state anger where relevant. Note that because anger arousal is a core and necessary constituent of the phenomenon “anger regulation,” statistically controlling for state anger represents a conservative and stringent approach.

  • anger regulation style anger arousal and acute pain sensitivity evidence for an endogenous opioid triggering model
    Journal of Behavioral Medicine, 2014
    Co-Authors: John W Burns, Stephen Bruehl, Melissa Chont
    Abstract:

    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 management style moderates effects of emotion suppression during initial stress on pain and cardiovascular responses during subsequent pain induction
    Annals of Behavioral Medicine, 2007
    Co-Authors: John W Burns, Phillip J Quartana, Stephen Bruehl
    Abstract:

    Background: Suppression of emotion, anger in particular, may be linked to heightened pain intensity during a subsequent painful event, but it is not clear whether an individual’s anger management style (trait anger-out or trait anger-in) moderates effects on pain intensity and cardiovascular responses during pain.Purpose: To determine whether (a) trait anger-out and/or trait anger-in moderate effects of Emotion-Induction (anger, anxiety)×Emotion Suppression (nonsuppression, experiential, expressive) manipulations during mental arithmetic on pain intensity and cardiovascular responses during and following a cold pressor pain task, such that “mismatch” relationships emerge (preferred anger management style is discrepant from situation demands), and (b) general emotional expressivity accounts for these effects.Method: Healthy nonpatients (N=187) were assigned to 1 of 6 conditions for a mental arithmetic task. Cells were formed by crossing 2 Emotion-Induction (anxiety, anger)×3 Emotion Suppression (non-suppression, experiential, expressive) conditions. After mental arithmetic, participants underwent a cold pressor followed by recovery. Systolic blood pressure (SBP), diastolic BP (DBP), heart rate (HR), and pain intensity ratings were recorded. Spielberger Anger Expression Inventory tapped anger management style.Results: General Linear Model procedures tested Emotion-Induction×Emotion Suppression×Anger-Out or Anger-In (continuous)×Period (baseline, cold pressor, recovery) effects on pain intensity, SBP, DBP, and HR. A 4-way interaction emerged for pain intensity: Only for those in the anger-induction/experiential suppression condition, anger-out was related significantly to pain recovery. Three-way interactions emerged for SBP and DBP: Only for those in expressive suppression condition, anger-out was related significantly to SBP during and following cold pressor and to DBP following cold pressor. General emotion expressivity did not account for anger-out effects.Conclusions: A mismatch situation may apply for high anger-out people who suppress emotion in a certain circumstance and thus may suffer greater discomfort and physiological responsiveness to subsequent pain than high anger-out people not having to suppress.

  • trait anger expressiveness and pain induced beta endorphin release support for the opioid dysfunction hypothesis
    Pain, 2007
    Co-Authors: Stephen Bruehl, John W Burns, Ok Yung Chung, Laura Diedrich
    Abstract:

    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 .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.

  • anger management style and hostility among patients with chronic pain effects on symptom specific physiological reactivity during anger and sadness recall interviews
    Psychosomatic Medicine, 2006
    Co-Authors: John W Burns, Stephen Bruehl, Phillip J Quartana
    Abstract:

    OBJECTIVES: We examined whether anger-in, anger-out, and hostility predicted symptom-specific muscle tension reactivity during anger induction (but not sadness induction) among patients with chronic low back pain (CLBP). For patients with CLBP, relevant muscles are the lower paraspinals (LPs). Anger-in x hostility and anger-out x hostility interactions were tested to determine whether particularly reactive groups of patients could be identified with a multivariable profile approach. METHODS: Ninety-four patients with CLBP underwent anger recall (ARI) and sadness recall (SRI) interviews, whereas LP and trapezius electromyography and systolic blood pressure, diastolic blood pressure, and heart rate were recorded. They completed anger-in, anger-out, hostility, and trait anger measures. RESULTS: Hierarchical regressions were used to test anger-in x hostility and anger-out x hostility interactions for physiological changes during the ARI and SRI. A significant anger-in x hostility interaction was found for LP change during the ARI (but not SRI) such that high anger-in/high hostility patients evinced the greatest reactivity. Effects for trapezius reactivity were nonsignificant. Significant anger-in x hostility interactions were also found for systolic blood pressure and diastolic blood pressure changes during the ARI such that high anger-in/low hostility patients showed the smallest changes. The anger-out x hostility interaction for diastolic blood pressure change during ARI was also significant such that high anger-out/low hostility patients showed the smallest changes. All effects remained significant with trait anger controlled. CONCLUSIONS: A multivariable profile approach may help identify especially vulnerable patient groups. Patients with CLBP who tend to suppress anger and are cynically hostile may be more likely to experience high levels of muscle tension near the site of pain and injury during anger, but not during sadness, than other groups.

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