Anger and fear response to stress have different biological profiles.

ArticleinBrain Behavior and Immunity 24(2):215-9 · October 2009with18 Reads
DOI: 10.1016/j.bbi.2009.08.009 · Source: PubMed
Abstract
In contrast to a general model of stress, a functional model suggests that emotions may regulate stress responses in specific adaptive ways. The current study examined whether anger and fear during a challenging stress task (Trier Social Stress Task) were differentially associated with cortisol and proinflammatory cytokine responses to an acute stressor. Baseline anger and fear were related to greater cortisol and proinflammatory cytokines. However, anger reactions to the stressor were associated with greater stress-related increases in cortisol over time but not proinflammatory cytokines. In contrast, fear reactions to the stressor were associated with increases in stress-related proinflammatory cytokines over time and a decrease in cortisol. Results are consistent with the functional perspective that distinct emotional experiences appear to trigger temporally-patterned adaptive biological processes to mobilize energy in response to anger and to promote withdrawal in response to fear. Discussion focuses on the role of the HPA axis to increase available metabolic fuel and proinflammatory cytokines to prompt behavioral withdrawal.
    • It leads to avoidance behavior and risk aversion (Tiedens & Linton, 2001; Chorpita & Barlow, 1998). Both anger and fear are found to be evoked by stressful experiences, with anger mobilizing energy for confrontation and fear mobilizing energy for retreat (Moons, Eisenberger & Taylor, 2010). Lastly, sadness is related to blaming the situation (Tiedens & Linton, 2001) and to withdrawal behavior (Lazarus, 1991).
    [Show abstract] [Hide abstract] ABSTRACT: Free paper download: http://www.sciencedirect.com/science/article/pii/S0747563216308846 The introduction of new technologies created avenues for new forms of bullying. Despite an impressive body of research on cyberbullying amongst youngsters, studies in the work context have largely neglected its electronic counterpart. In this study, we define workplace cyberbullying and propose an Emotion Reaction Model of its occurrence. Our model aligns with the main proposition of the Affective Events Theory (Weiss & Cropanzano, 1996), that emotions evoked by certain work events may fuel emotion driven behaviors. However, in our model these relationships are further specified combining different literature traditions. Making inferences from the workplace bullying literature, we suggest work stressors to be the work events leading to cyberbullying. Furthermore, building on the literature on cyberbullying amongst youngsters, computer-mediated communication and emotions, we propose discrete emotions of anger, sadness and fear to play a significant role in explaining this stressor-cyberbullying relation. In addition, different moderators (i.e., control appraisal and emotion regulation) of this relationship are suggested and implications of the model are discussed.
    Full-text · Article · Apr 2017
    • Therefore, we conducted a further analysis to control for the presence and degree of depression, the significant differences of cytokine levels between groups remained, which indicates that the inflammatory phenotype in GAD is independent of depression. This finding supports anxiety-specific effects on inflammatory responses and is consistent with the integrated specificity model (Moons et al., 2010) and evidence of anxietyspecific inflammatory response pathway (O'Donovan et al., 2010). Tryptophan metabolism can alter immune activation by modulating Th1/Th2 balance (Steiner et al., 2012;Müller and Schwarz, 2010).
    [Show abstract] [Hide abstract] ABSTRACT: Introduction: Previous investigations have demonstrated that major depression is associated with particular patterns of cytokine signalling. The primary aim of this study was to examine peripheral pro-inflammatory and anti-inflammatory cytokines and immune balance in generalised anxiety disorder (GAD). Methods: A case-controlled cross-sectional study design was employed: 54 patients with GAD and 64 healthy controls were recruited. Participants completed self-report measures of anxiety and depression. Two pro-inflammatory and two anti-inflammatory cytokines were measured using multiplex technology. Results: Case-control logistic regression analyses revealed significant differences in serum levels of IL-10, TNF-α, and IFN-γ between GAD and control groups after adjusting for age, gender, body mass index, smoking and alcohol consumption: these group differences were independent of the presence or degree of depression. Comparison of pro-inflammatory to anti-inflammatory cytokine ratios indicated that there were significantly higher ratios of TNF-α /IL10, TNF-α /IL4, IFN-γ /IL10, and IFN-γ /IL4 in the GAD group compared to the control group. Conclusions: This study is the first to investigate both pro- and anti-inflammatory cytokines and their balance in patients with GAD in comparison to healthy controls. The findings indicate a relatively increased pro-inflammatory response and decreased anti-inflammatory response and provide the first demonstration of an altered cytokine balance in GAD. Serum cytokine levels in GAD were independent of the presence of depression.
    Article · Feb 2017
    • The emotion of fear is induced when one is facing uncertain and existential threat, in which the threat is unpredictable and uncontrollable (Lazarus, 1991; Tiedens and Linton, 2001). In response to a fear-inducing crisis, consumers may benefit from an increase in proinflammatory cytokines that are related with submissive withdrawal (Moons et al., 2010). Additionally, feelings of fear or worried are always associated with uncertain appraisals, which in turn lead people to make pessimistic judgment and precautionary plans (Lerner and Keltner, 2001; Lerner et al., 2003; Skitka et al., 2006).
    [Show abstract] [Hide abstract] ABSTRACT: Three studies examine an emotion fit effect in the crisis communication, namely, the interaction between emotional frames of guilt and shame and consumer emotions of anger and fear on consumer forgiveness. Guilt-framing communication results in higher forgiveness than shame-framing for angry consumers, whereas shame-framing communication results in higher forgiveness than guilt-framing for fearful consumers. These effects are driven by consumers’ accessible regulatory foci associated with anger/fear and guilt/shame. Specifically, feelings of anger activate a promotion focus that is represented by guilt frames, while feelings of fear activate a prevention focus that is enacted by shame frames. Compared with emotion non-fit (i.e., anger to shame and fear to guilt), emotion fit (i.e., anger to guilt and fear to shame) facilitates greater feeling-right and consumer forgiveness. The findings offer novel insights for extant literature on emotion, crisis communication, and regulatory focus theory, as well as practical suggestions regarding the emotional frames.
    Full-text · Article · Nov 2016
    • Therefore, we conducted a further analysis to control for the presence and degree of depression, the significant differences of cytokine levels between groups remained, which indicates that the inflammatory phenotype in GAD is independent of depression. This finding supports anxiety-specific effects on inflammatory responses and is consistent with the integrated specificity model (Moons et al., 2010 ) and evidence of anxietyspecific inflammatory response pathway (O'Donovan et al., 2010). Tryptophan metabolism can alter immune activation by modulating Th1/Th2 balance (Steiner et al., 2012; Müller and Schwarz, 2010 ).
    Article · Oct 2016 · Neuropsychopharmacology
    • Of particular relevance to the present research, several studies show that the extent to which ethnic minority individuals perceive racial stigmatization and discrimination predicts their circulating levels of inflammatory cytokines (Brody et al., 2015;Doyle & Molix, 2014;Lewis et al., 2010;Ratner et al., 2013). Consistent with previous research (e.g.,Moons, Eisenberger, & Taylor, 2010;Ratner et al., 2013), the current research assessed the circulating levels of inflammatory cytokines in oral mucosal transudate (OMT). Both situational and prolonged social stress predict higher levels of inflammatory cytokines in OMT (e.g.,Chiang, Eisenberger, Seeman, & Taylor, 2012;Slavich, Way, Eisenberger, & Taylor, 2010).
    [Show abstract] [Hide abstract] ABSTRACT: We examined participation in an ethnically based residential program or “theme house” during the first year of college as a predictor of downstream immune system inflammation among undergraduates. Using a 4-year prospective design, we compared markers of inflammation among Latino/Latina students in a residential theme program with a matched sample of nonresidents. Students provided oral mucosal transudate samples for the assessment of circulating Interleukin 6 (IL-6), an inflammatory cytokine linked to health vulnerabilities. Findings suggest a protective benefit of theme house residency especially among students with anxious expectations of discrimination. Such expectations predicted higher levels of IL-6 after the first year of college among nonresidents only. In years 2–3, following exit from the theme house, the relationship between expected discrimination and IL-6 levels remained positive among nonresidents and was attenuated among residents, controlling for past IL-6 levels. Culturally based spaces may therefore offset the physiological burden of expected discrimination among undergraduates.
    Article · Aug 2016
    • Indeed, several other studies have shown that the TSST can increase proinflammatory responses from pre-to post-stress (Moons et al., 2010; Slavich et al., 2010: Yamakwa et al., 2009) and that greater experiences of social stress are associated with greater increases in inflammatory responding. For instance, those who reported higher levels of fear or anxiety in response to the TSST also showed greater increases in inflammatory responses to the TSST (IL-6 and sTNFα-RII: Moons et al., 2010; IL-6: Carroll et al., 2011). Similarly, those who reported a greater perceived intensity of stress also showed larger increases in inflammatory activity to the TSST (IL-1β; Yamakawa et al., 2009).
    [Show abstract] [Hide abstract] ABSTRACT: Although it has commonly been assumed that the immune system and the processes that govern social behavior are separate, non-communicating entities, research over the past several decades suggests otherwise. Thus, considerable evidence now shows that inflammatory processes and social behavior are actually powerful regulators of one another. This review first summarizes evidence that inflammatory processes regulate social behavior, leading to characteristic changes that may help an individual navigate the social environment during times of sickness. Specifically, this review shows that inflammation: 1) increases threat-related neural sensitivity to negative social experiences (eg, rejection, negative social feedback), presumably to enhance sensitivity to threats to well-being or safety in order to avoid them and 2) enhances reward-related neural sensitivity to positive social experiences (eg, viewing close others, receiving positive social feedback), presumably to increase approach-related motivation towards others who might provide support and care during sickness. Next, this review summarizes evidence showing that social behavior also regulates aspects of inflammatory activity, preparing the body for situations in which wounding and infection may be more likely (social isolation). Here, we review research showing: 1) that exposure to social stressors increases proinflammatory activity, 2) that individuals who are more socially isolated (ie, lonely) show increased proinflammatory activity, and 3) that individuals who are more socially isolated show increased proinflammatory activity in response to an inflammatory challenge or social stressor. The implications of the co-regulation of inflammation and social behavior are discussed.Neuropsychopharmacology accepted article preview online, 02 August 2016. doi:10.1038/npp.2016.141.
    Full-text · Article · Aug 2016
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