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.
"Drawing some early conclusions, our results suggest that anger and anxiety may be characterized as motivational behavior which triggers different endocrine and IL-1b salivary release (Moons et al., 2010). Our data are in accordance with findings that propose a role for C in anxiety responses; they also argue the implication of T, T/C ratio and IL-1b in the expression of anger in a sporting context . "
"This suggests that a tendency to respond to stress in an irritable manner may be associated with a distinct pattern of physiological activation. However, self-reported anger and fear were moderately correlated in the Moons et al. (2010) study, making disentanglement of the two emotions difficult. Studies that induced stress experimentally in children with ASD, using psychosocial stress paradigms such as the Trier Social Stress Test (TSST; Kirschbaum, Pirke, & Hellhammer , 1993), have been inconsistent. "
[Show abstract][Hide abstract] ABSTRACT: Background
Irritability in people with autism spectrum disorders (ASD) is common and impairing, yet its mechanisms remain understudied. We investigated symptom reporting and mechanisms of irritability in ASD, focusing on the relation between irritability and physiological stress responses.Methods
Forty-seven unmedicated boys with high-functioning ASD (hfASD) and 23 typically developing boys aged 10–16 years completed a psychosocial stress test. Changes in cortisol, heart rate and heart rate variability throughout the test were recorded. Self- and parent-reported measures of irritability were obtained. Irritability symptom reporting in the hfASD group was compared to two groups of boys without ASD: highly irritable boys (severe mood dysregulation, SMD; n = 40) and healthy-control boys (HC; n = 30).ResultsBoys with hfASD scored significantly higher on irritability than HC boys, and they reported a pattern of irritability symptoms closely resembling that of boys with SMD. The internal consistency of irritability in hfASD was high by parent- and self-report. Although boys with hfASD showed significant stress-induced changes in cortisol and heart rate, those who rated themselves as highly irritable had lower cortisol levels throughout the test compared to those low on irritability. Participants rated as highly irritable by their parents showed blunted cortisol and heart rate responses to stress. The effects of irritability on heart rate, but not cortisol, were accounted for by trait anxiety.Conclusions
Irritability can be measured reliably in hfASD and is associated with distinct biological responses to stress.
Journal of Child Psychology and Psychiatry 01/2015; DOI:10.1111/jcpp.12382 · 6.46 Impact Factor
"LPS-stimulated TNFα expression was positively correlated with physical aggression, verbal aggression, and hostility. In other studies, LPS-induced increases in TNFα correlated with stress-induced emotion arousal,(Moons et al., 2010; Suarez et al., 2006) and interferon-induced labile anger (Lotrich et al., 2010). "
[Show abstract][Hide abstract] ABSTRACT: The mechanisms underlying aggression in adolescents with bipolar disorder have been poorly understood. The present study has investigated the associations among TNF gene expressions, functional brain activations under the frustrative non-reward task, and aggression in adolescents with bipolar disorder. Baseline gene expressions and aggressive tendencies were measured with the RNA-sequencing and Brief Rating of Aggression by Children and Adolescents (BRACHA), respectively. Our results show that activity levels of left subgenual anterior cingulate gyrus (ACG) right amygdala, left Brodmann area 10 (from the orbitofrontal cortex), and right thalamus were inversely correlated with BRACHA scores and were activated with frustrative non-reward during the affective Posner Task. In addition, eleven TNF related gene expressions were significantly correlated with activation of amygdala or ACG during the affective Posner task. Three TNF gene expressions were inversely correlated with BRACHA score while one TNF gene (TNFAIP3) expression was positively correlated with BRACHA score. Therefore, TNF-related inflammatory cytokine genes may play a role in neural activity associated with frustrative non-reward and aggressive behaviors in pediatric bipolar disorder.
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