Acute Psychosocial Stress Research Articles

Psychosocial stress affects the change of mental distress under dermatological treatment-A prospective cohort study in patients with psoriasis.

Psoriasis is a chronic-inflammatory, immune-mediated disease leading to a state of increased systemic inflammation. Mental comorbidities often occur in the patients and may additionally affect the therapy outcome. Currently, it is unknown whether the disease severity, psychosocial stress or health-related quality of life determines the manifestation of anxiety/depression, or vice versa, in psoriasis. The interplay between these variables during the dermatological treatment of psoriasis remains to be elucidated in order to initiate appropriate psychological interventions and to identify patients at risk for comorbid anxiety/depression. In a prospective cohort study, the impact of disease severity, health-related quality of life and psychosocial stress on anxiety/depression were examined during the dermatological treatment in patients with moderate to severe psoriasis (patients with psoriasis=PSO). Patients were examined before (T1) and about 3months after (T2) the beginning of a new treatment episode, in most cases by means of systemic therapy. Data were analysed, exploratory, using Bivariate Latent Change Score Models and mediator analyses. Assessments included patient-reported outcomes (Hospital Anxiety and Depression Scale/HADS, Perceived Stress Scale/PSS, Childhood Trauma Questionnaire/CTQ, Dermatology Life Quality Index-DLQI, Body Surface Area-BSA), at both T1 and T2. 83 PSO patients (37.3% women, median age 53.7, IQR 37.8-62.5, median BSA 18.0, IQR 9.0-40.0) with complete data of HADS and DLQI were included. In the total group, a higher anxiety/depression at T1 was associated with a lower improvement in psoriasis severity in the course of the dermatological treatment (γBSA =0.50, p<0.001). In subgroups of PSO with low/high CTQ scores, anxiety/depression at T1 had no impact on the change in psoriasis severity. Only by tendency, in CTQ subgroups, a higher psoriasis severity at T1 was linked with a higher improvement in anxiety/depression at T2 (low/high CTQ, γHADS =-0.16/-0.15, p=0.08). An improvement in the health-related quality of life was positively associated with an improvement in anxiety/depression (Pearson's r=0.49, p=0.02). Here, the reduction of acute psychosocial stress seems to be a decisive factor, mediating this association (β=0.20, t [2,60]=1.87; p=0.07, 95% CI -0.01, 0.41). The results allude, that the initial severity of anxiety/depression may presumably have an impact on the treatment outcome in the total group. In contrast, analysing subgroups of patients with high/low childhood trauma, the impact of the initial disease severity on the course of anxiety/depression after a switch to a new dermatological treatment could not be conclusively ruled out. The latter results from the latent change score modelling should be treated cautiously because of the small sample size. A common aetiopathological mechanism for psoriasis and anxiety/depression might be assumed with impact of dermatological treatment on both. The change in perceived stress seems to play an important role in the manifestation of anxiety/depression, substantiating the need for adequate stress management in patients with increased psychosocial stress during their dermatological treatment.

Developmental Dyslexia and the Stress of Reading: A Social Stress Study of Neuroendocrine Response in Children

AbstractDyslexia is a neurodevelopmental disorder characterized by persistently slow and effortful reading. It is associated with core cognitive deficits in decoding words, but it also presents significant challenges associated with, for example, anxiety and stress related to academic performance. We asked, thus, whether, reading out loud would be associated with elevated stress for readers with dyslexia, relative to good readers, and we investigated stress‐related hormone response in these two groups. We carried out an acute psychosocial stress test (Trier Social Stress Test‐Children adapted for children, TSST‐C), which included a reading out loud task. We carried out a quasi‐experimental study with an experimental group of participants with Developmental Dyslexia (n = 17), and a control group, with good readers (n = 18). During the stress test, we collected six saliva samples for evaluation of two stress‐related hormones, cortisol, and adrenocorticotropic hormone (ACTH) levels. We found a main effect for group for ACTH and for cortisol levels. We also found significantly higher levels of ACTH in the dyslexic group at the end of the task, and during the post‐task recovery period. Results are discussed in the light of the less‐understood emotional impact of dyslexia, and of a recently proposed role for stress as a trigger for increased risk of development of dyslexia. Lastly, we underscore the contribution for the evidence of the emotional impact of learning disorders, especially, as is the case, from a population generally underrepresented in cognitive neuroscience research (i.e., Latin‐American children).

Blunted neurobiological reactivity and attentional bias to threat underlie stress-related disorders in women survivors of intimate partner violence.

Intimate partner violence (IPV) alters women's neurobiological stress response systems. We propose that individual differences early in the attentional processing of threats are associated with these neurobiological mechanisms and contribute to mental illness in this population. We assessed attentional bias in relation to threat (AB) in women survivors of IPV (n = 69) and controls (n = 36), and examined overall cortisol secretion using hair cortisol (HC), and stress responsiveness measuring salivary cortisol and α-amylase (sAA) before (T0), and after (T1, T2) an acute psychosocial stress task (Trier Social Stress Test). We used repeated-measures ANCOVAs to explore the associations between Group (IPV, control) and AB with acute stress response, and regression models to examine the associations with mental health symptoms. There were no between-group differences in HC levels. An interaction between Group and AB was found regarding cortisol reactivity (p < 0.05). IPV women with threat avoidance AB showed a blunted cortisol response compared to controls and to IPV participants with threat vigilance AB. The association between sAA reactivity and the interaction between Group, AB, and time approached significance (p = 0.07), with a trend to lower sAA levels particularly in IPV women with threat avoidance AB. Group and cortisol reactivity were associated with symptoms of depression, generalized anxiety, and post-traumatic stress disorder (8-20% explained variance). Threat avoidance AB is associated with blunted acute cortisol response among women exposed to chronic stress (IPV). Experiencing IPV and acute cortisol response appear to be clearly implicated in long-term mental health problems.

Neuroendocrine response to a psychosocial stress test is not related to schizotypy but cortisol elevation predicts inflexibility of semantic memory retrieval

An altered stress response can contribute to the transition from preclinical psychotic symptoms to the clinical manifestation of schizophrenia and other psychotic disorders. The present study was aimed at testing the hypotheses that (i) the autonomic and neuroendocrine responses under psychosocial stress are dysregulated in individuals with high psychosis proneness (schizotypy); (ii) the magnitude of post-stress autonomic activation and cortisol release predicts alterations in semantic memory retrieval. The study was performed in 73 healthy individuals of both sexes with either high or low schizotypal traits preselected out of 609 individuals using the Schizotypal Personality Questionnaire. A psychosocial stress procedure based on public speech was used as a stress model. We found that individuals with high schizotypy engaged in less adaptive emotional stress-coping strategies than low schizotypy individuals. Yet, the neuroendocrine, immune, and sympathetic activation in response to the stress test was not different between the groups. Irrespective of the exposure to the stressor, individuals with high schizotypy were less fluent when retrieving associations from semantic memory. In addition, we demonstrated that acute psychosocial stress reduced the flexibility of semantic memory retrieval. The post-stress mental inflexibility was reliably predicted by the concomitant elevation of cortisol concentrations in saliva. The present study thus brings novel evidence indicating that the acute psychosocial challenge impairs retrieval flexibility in the semantic domain, which may be due to neuroendocrine activation.

445. Effects of Childhood Adversity on the Relationship Among Resting State Network Dynamics, Cortisol and Subjective Status After an Acute Psychosocial Stressor

445. Effects of Childhood Adversity on the Relationship Among Resting State Network Dynamics, Cortisol and Subjective Status After an Acute Psychosocial Stressor

A Narrative Review on Mental Stress and Cardiovascular Disease: Evidence, Mechanisms, and Potential Interventions

Cardiovascular disease (CVD) is the leading cause of death in the United States and worldwide. Psychosocial stress is an important risk factor implicated in a higher incidence of CVD. There are two prevalent categories of stress – acute psychosocial stress (APS) and chronic psychosocial stress (CPS). APS is typically caused by acute dramatic events such as natural disasters, sexual abuse, terroristic attacks, and sudden death of a loved one, while CPS is usually related to environmental, relationship, and work stressors. Both categories of psychosocial stress are associated with substantial CVD morbidity and mortality that carries a magnitude of risk equal to that of conventional CVD risk factors. As a result, more research is needed to understand the detrimental impacts of psychosocial stress on cardiovascular health and related mechanistic underpinnings that, in turn, would further facilitate the development of novel therapeutic targets. This review aims to elucidate the potential pathophysiological mechanisms by which psychosocial stress can influence CVD. In addition, we aim to discuss the current targeted therapeutic interventions (pharmacological and nonpharmacological) and possible future research directions.

Effects of stress beliefs on the emotional and biological response to acute psychosocial stress in healthy men

BackgroundNegative beliefs about stress (e.g., “stress is bad”) constitute an independent risk factor for increased morbidity and mortality. One potential underlying mechanism are altered responses to acute psychosocial stress. The aim of this study was to investigate whether beliefs about stress are associated with physiological and endocrine stress response patterns. MethodsA total of N = 77 healthy adults were randomised to an experimental and a placebo control group and were subsequently exposed to the Trier Social Stress Test (TSST). Stress beliefs were measured before and after a psychological manipulation aiming at fostering more balanced stress beliefs or a placebo manipulation. Self-reported stress was measured four times before/after the TSST, heart rate was assessed continuously, and cortisol was assessed eight times before/after the TSST. ResultsThere was a significant decrease in negative stress beliefs (p < .001) and increase in positive stress beliefs (p < .001) in participants in the experimental condition, which was absent in participants in the placebo condition. The participants in the experimental group had more pronounced self-reported stress reactions (p = .028) while at the same time also showing more pronounced stress recoveries (p = .036). The findings regarding cortisol were mixed. ConclusionsMore balanced stress beliefs appeared to be associated with more efficient subjective responses to acute psychosocial stress. These findings attest to a potential mechanism translating negative stress beliefs into ill health while at the same time outlining targets for psychological interventions.

P-129 Childhood adversity interacts with the relationship among brain network dynamics, cortisol and subjective status after an acute psychosocial stressor

P-129 Childhood adversity interacts with the relationship among brain network dynamics, cortisol and subjective status after an acute psychosocial stressor

Investigating the effects of maltreatment and acute stress on the concordance of blood and DNA methylation methods of estimating immune cell proportions

BackgroundImmune cell proportions can be used to detect pathophysiological states and are also critical covariates in genomic analyses. The complete blood count (CBC) is the most common method of immune cell proportion estimation, but immune cell proportions can also be estimated using whole-genome DNA methylation (DNAm). Although the concordance of CBC and DNAm estimations has been validated in various adult and clinical populations, less is known about the concordance of existing estimators among stress-exposed individuals. As early life adversity and acute psychosocial stress have both been associated with unique DNAm alterations, the concordance of CBC and DNAm immune cell proportion needs to be validated in various states of stress.ResultsWe report the correlation and concordance between CBC and DNAm estimates of immune cell proportions using the Illumina EPIC DNAm array within two unique studies: Study 1, a high-risk pediatric cohort of children oversampled for exposure to maltreatment (N = 365, age 8 to 14 years), and Study 2, a sample of young adults who have participated in an acute laboratory stressor with four pre- and post-stress measurements (N = 28, number of observations = 100). Comparing CBC and DNAm proportions across both studies, estimates of neutrophils (r = 0.948, p < 0.001), lymphocytes (r = 0.916, p < 0.001), and eosinophils (r = 0.933, p < 0.001) were highly correlated, while monocyte estimates were moderately correlated (r = 0.766, p < 0.001) and basophil estimates were weakly correlated (r = 0.189, p < 0.001). In Study 1, we observed significant deviations in raw values between the two approaches for some immune cell subtypes; however, the observed differences were not significantly predicted by exposure to child maltreatment. In Study 2, while significant changes in immune cell proportions were observed in response to acute psychosocial stress for both CBC and DNAm estimates, the observed changes were similar for both approaches.ConclusionsAlthough significant differences in immune cell proportion estimates between CBC and DNAm exist, as well as stress-induced changes in immune cell proportions, neither child maltreatment nor acute psychosocial stress alters the concordance of CBC and DNAm estimation methods. These results suggest that the agreement between CBC and DNAm estimators of immune cell proportions is robust to exposure to child maltreatment and acute psychosocial stress.

Acute stress alters probabilistic reversal learning in healthy male adults.

Behavioural adaptation is a fundamental cognitive ability, ensuring survival by allowing for flexible adjustment to changing environments. In laboratory settings, behavioural adaptation can be measured with reversal learning paradigms requiring agents to adjust reward learning to stimulus-action-outcome contingency changes. Stress is found to alter flexibility of reward learning, but effect directionality is mixed across studies. Here, we used model-based functional MRI (fMRI) in a within-subjects design to investigate the effect of acute psychosocial stress on flexible behavioural adaptation. Healthy male volunteers (n= 28) did a reversal learning task during fMRI in two sessions, once after the Trier Social Stress Test (TSST), a validated psychosocial stress induction method, and once after a control condition. Stress effects on choice behaviour were investigated using multilevel generalized linear models and computational models describing different learning processes that potentially generated the data. Computational models were fitted using a hierarchical Bayesian approach, and model-derived reward prediction errors (RPE) were used as fMRI regressors. We found that acute psychosocial stress slightly increased correct response rates. Model comparison revealed that double-update learning with altered choice temperature under stress best explained the observed behaviour. In the brain, model-derived RPEs were correlated with BOLD signals in striatum and ventromedial prefrontal cortex (vmPFC). Striatal RPE signals for win trials were stronger during stress compared with the control condition. Our study suggests that acute psychosocial stress could enhance reversal learning and RPE brain responses in healthy male participants and provides a starting point to explore these effects further in a more diverse population.

Revisiting the stress recovery hypothesis: Differential associations of cortisol stress reactivity and recovery after acute psychosocial stress with markers of long-term stress and health

Exposure to excessive and long-term stress may result in dysregulation of the stress system, including the acute stress response. In particular, failure to downregulate stress-related reactivity may lead to prolonged stress responses and the accumulation of allostatic load. However, the contribution of altered acute cortisol recovery to chronic stress and associated health impairments has often been neglected. Addressing this lack of research, we explored whether recovery from – more so than reactivity to – acute stress captures the basal stress load of an individual. Using Piecewise Growth Curve Models with Landmark Registration, we analyzed cortisol reactivity and recovery slopes of 130 healthy participants exposed to a standardized psychosocial laboratory stressor. Reactivity and recovery were predicted by measures indicative of long-term stress and its downstream effects, including self-report questionnaires, diurnal cortisol indices [cortisol awakening response (CAR); diurnal cortisol slope], markers of pro-inflammatory activity (interleukin-6; high-sensitive C-reactive protein), and hippocampal volume (HCV). Among these measures, only an increased CAR was specifically and consistently associated with relatively impaired recovery. Since the CAR represents the physiological enhancement needed to meet the anticipated demands of the forthcoming day, this finding may highlight the contribution of cognitive processes in determining both CAR and acute stress recovery. Furthermore, greater cortisol reactivity covaried with smaller HCV, showing that increased acute reactivity translates to health-relevant downstream effects. The lack of further associations between long-term and acute stress measures may arise from biases in self-reported chronic stress and the rigorously health-screened study sample. Overall, our findings suggest that while cortisol stress recovery might not supersede reactivity as an indicator of the long-term stress load or associated health effects, recovery and reactivity have differential utility in describing individuals’ allostatic states.

The effects of left dorsolateral prefrontal transcranial direct current stimulation on episodic future thinking following acute psychosocial stress

ABSTRACT Introduction Research on stress-related disorders and brain imaging suggests that (acute) stress might impact the capacity to mentally simulate specific episodic future events (EFT) through the effects of cortisol on brain regions supporting this cognitive function, such as the prefrontal cortices. This study aims to examine the mechanisms underlying this link, using transcranial Direct Current Stimulation (tDCS) over the left dorsolateral prefrontal cortex. Methods 60 healthy participants were subjected to the Montreal Imaging Stress Task (MIST), followed by either active or sham tDCS. After stimulation, the EFT task was administered. Salivary cortisol was measured throughout the protocol. Results Higher cortisol AUCi values were linked to less specific episodic future thoughts. Moreover, active tDCS enhanced EFT specificity irrespective of cortisol, especially in high trait ruminators. We did not observe an effect from active tDCS on cortisol AUCi, and equally there was no interaction effect between cortisol AUCi and stimulation condition predictive for EFT specificity. Conclusion Although we did not find evidence for the effects of tDCS on the HPA-system, our data reveal a crucial link between two critical predictors of mental health for the first time, and provide a solution to help rehabilitate EFT deficits. Trial registration: Netherlands National Trial Register identifier: ntr004..

The role of inflammation in acute psychosocial stress-induced modulation of reward processing in healthy female adults

BackgroundAnhedonia, or loss of interest and pleasure, is a pernicious symptom of depression that involves deficits in reward processing. Stress-induced inflammation is a plausible biopsychosocial mechanism of reward deficits, but little is known whether stress-induced inflammation alters reward behavior. The present study (a secondary analysis of a completed randomized controlled trial) tested whether acute stress activated a key pro-inflammatory transcription control pathway, NF-κB, and whether this activation was associated with acute stress-induced modulation of reward processing. MethodsHealthy female adults (age 18–25) were randomized to undergo an acute psychosocial stressor (Trier Social Stress Test; n = 36) or a no-stress active control (n = 16). The Probabilistic Reward Task (PRT) (n = 30 stress; n = 12 control) was administered at baseline and at 90 min post-stress, coinciding with the peak of the stress-induced inflammatory response. Genome-wide expression profiling and bioinformatics analyses of NF-kB transcription factor activity were used to assess pro-inflammatory gene regulation. ResultsRelative to the control condition, stress increased bioinformatic measures of NF-κB transcription factor activity (p = .01) and increased reward response bias scores on the PRT (p = .03). Within the stress condition, greater NF-κB activity was associated with greater increases in PRT scores (p = .01), whereas in the control condition greater NF-κB activity was associated with decreases in PRT scores (p = .002). ConclusionsAcute stress increases inflammatory signaling, and this effect is associated with increased reward processing. This demonstrates the reward system to be highly sensitive to inflammatory signaling, including the relatively mild alterations that occur following a single episode of acute psychosocial stress.

The role of early life adversity and inflammation in stress-induced change in reward and risk processes among adolescents

BackgroundEarly life adversity (ELA) has long been associated with increased risk for stress-related psychopathology, particularly depression. The neuroimmune network hypothesis posits that ELA increases sensitivity to psychosocial stress, moderating the association between increases in peripheral markers of inflammation and decreases in reward outcomes linked to anhedonia and risk-taking behaviors. The present study examined this hypothesis in a sample of adolescents by using acute psychosocial stress to probe the role of inflammatory signaling in behavioral measures of reward and risk processing. Method80 adolescents [13.86 years (SD = 1.54); 45 % female], oversampled for ELA, underwent the Trier Social Stress Test for Children while providing blood samples immediately before and 60-minutes after stress onset. Blood samples were assayed for plasma IL-6. One hour before stress onset, and then 60 min after, participants completed computer-administered behavioral tasks measuring reward (Pirate Task) and risk (Balloon Analog Risk Task). ResultsELA moderated the association between increases in IL-6 and decreases in risk tolerance in pursuit of rewards (p = 0.003) and reward response bias (p = 0.04). Stress-induced increases in IL-6 were associated with decreases in pumps for rewards among adolescents exposed to high, relative to little or no, ELA. Further, greater IL-6 increases were associated with increases in bias toward high relative to low value rewards among adolescents with low adversity exposure but not among those exposed to higher adversity. ConclusionsThe present study provides the first evidence in a pediatric sample that ELA may alter the role of stress-induced inflammation in reward and risk processing, and may extend our understanding of why stress leads to depression in this high-risk population.

Acute psychosocial stress weakens the sense of agency in healthy adults

The sense of agency (SoA) refers to the feeling of being in control of one’s actions and the subsequent consequence of these actions. Emotional context seems to alter the strength of sense of agency. The present study explored the influence of acute psychosocial stress on the SoA by means of the Trier Social Stress Test (TSST). Self-assessment manikin (SAM) and objective physiological indicators (e.g. heart rate, electrodermal activity, and salivary cortisol levels) were utilized to evaluate the effect of the TSST. We also employed the temporal binding effect as an implicit assessment of the participant’s SoA. The results indicated that the stress level of the experimental group after TSST was significantly higher than the control group, whilst the temporal binding scores of the experimental group decreased after TSST manipulation. In short, acute psychosocial stress with intense emotional arousal weakened the sense of agency.

The Forward Testing Effect Is Resistant to Acute Psychosocial Retrieval Stress.

The forward testing effect refers to the finding that testing of previously studied information improves memory for subsequently studied newer information. Recent research showed that the effect is immune to acute psychosocial encoding/retrieval stress, i.e., stress that is induced before initial encoding. The present study investigated whether the forward testing effect is also robust to acute psychosocial retrieval stress, i.e., stress that is induced after encoding but before retrieval of the critical item list. Participants (N = 128) studied three lists of words in anticipation of a final cumulative recall test. Participants were tested immediately on Lists 1 and 2 (testing condition) or restudied the two lists after initial study (restudy condition). After study of the critical List 3, psychosocial stress was induced in half of the participants (stress group), whereas no stress was induced in the other half (control group). The Trier Social Stress Test for Groups (TSST-G) was used for stress induction. Salivary cortisol, alpha amylase, and subjective stress were repeatedly measured. The results of the criterion test showed a generally detrimental effect of psychosocial retrieval stress on List 3 recall. Importantly, the forward testing effect was unaffected by retrieval stress. The findings are discussed with respect to current theories of the forward testing effect.

Cardiovascular stress reactivity, habituation, and adiposity.

The relationship between adiposity and cardiovascular disease morbidity and mortality is complex. One pathway through which adiposity may influence future health outcomes is by altering how biological systems respond to stress. The current study aimed to examine the association between two metrics of adiposity (body mass index and waist-hip ratio) and two indices of cardiovascular stress responses (reactivity and habituation). A sample of 455 participants (Mean age=19.47, SD=1.25 years; BMI=24.32, SD=5.04 kg/m2 ; 62% female; 17.9% Hispanic/Latino; 65.2% White, 18.7% Asian, 7.9% Black, 0.2% American Indian/Alaska Native, and 7% other) completed two acute psychosocial stress tasks. Heart rate (HR), systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded throughout each stressor. In unadjusted and adjusted models, there were no statistically significant associations between adiposity and HR, SBP, or DBP stress reactivity or habituation. The current data do not support the hypothesis that adiposity influences health by altering cardiovascular responses to acute psychological stress. Results are at odds with prior population-level studies and the single prior study examining adiposity and habituation. At the same time, results are in line with mounting evidence that adiposity itself does not drive poor cardiovascular outcomes seen in people classified as overweight or obese.

Blunted cortisol and normal sympathetic nervous system responses to an acute psychosocial stressor in internet addiction

Studies have demonstrated that addiction leads to blunted responses of cortisol and sympathetic nervous system (SNS) to acute stressors; however, limited studies have examined the neuroendocrine and SNS stress responses in Internet addiction (IA). To examine acute stress responses in IA, the current study recruited a total of 76 Japanese university students and staff members (51 females and 25 males, mean age = 22.4 years, SD = 4.7), and measured the salivary cortisol, salivary alpha-amylase (sAA), and blood pressure (BP) responses to an acute stressor under stress or a nonstress placebo conditions in IA and non-IA groups. The results revealed that patients with IA showed a blunted cortisol response to a stressor. In contrast, no differences were found in the sAA and BP responses between the IA and non-IA groups. These results suggest that IA may be characterized by blunted cortisol responses in acute stress settings.

Rapid volumetric brain changes after acute psychosocial stress

Stress is an important trigger for brain plasticity: Acute stress can rapidly affect brain activity and functional connectivity, and chronic or pathological stress has been associated with structural brain changes. Measures of structural magnetic resonance imaging (MRI) can be modified by short-term motor learning or visual stimulation, suggesting that they also capture rapid brain changes. Here, we investigated volumetric brain changes (together with changes in T1 relaxation rate and cerebral blood flow) after acute stress in humans as well as their relation to psychophysiological stress measures.Sixty-seven healthy men (25.8±2.7 years) completed a standardized psychosocial laboratory stressor (Trier Social Stress Test) or a control version while blood, saliva, heart rate, and psychometrics were sampled. Structural MRI (T1 mapping / MP2RAGE sequence) at 3T was acquired 45 min before and 90 min after intervention onset. Grey matter volume (GMV) changes were analysed using voxel-based morphometry. Associations with endocrine, autonomic, and subjective stress measures were tested with linear models.We found significant group-by-time interactions in several brain clusters including anterior/mid-cingulate cortices and bilateral insula: GMV was increased in the stress group relative to the control group, in which several clusters showed a GMV decrease. We found a significant group-by-time interaction for cerebral blood flow, and a main effect of time for T1 values (longitudinal relaxation time). In addition, GMV changes were significantly associated with state anxiety and heart rate variability changes.Such rapid GMV changes assessed with VBM may be induced by local tissue adaptations to changes in energy demand following neural activity. Our findings suggest that endogenous brain changes are counteracted by acute psychosocial stress, which emphasizes the importance of considering homeodynamic processes and generally highlights the influence of stress on the brain.

Vagus activation by Cold Face Test reduces acute psychosocial stress responses

Chronic stress is linked to dysregulations of the two major stress pathways—the sympathetic nervous system and the hypothalamic-pituitary-adrenal (HPA) axis, which could for example result from maladaptive responses to repeated acute stress. Improving recovery from acute stress could therefore help to prevent this dysregulation. One possibility of physiologically interfering with an acute stress reaction might be provided by applying a cold stimulus to the face (Cold Face Test, CFT) which activates the parasympathetic nervous system (PNS), leading to immediate heart rate decreases. Therefore, we investigated the use of the CFT protocol as an intervention to reduce acute stress responses. Twenty-eight healthy participants were exposed to acute psychosocial stress via the Montreal Imaging Stress Task (MIST) in a randomized between-subjects design while heart rate (HR), heart rate variability (HRV), and salivary cortisol were assessed. While both groups were equally stressed during the procedure, participants with CFT intervention showed better recovery, indicated by significant (p<0.05) differences in HR(V). We additionally found a significantly (p<0.05) lower cortisol response to the MIST and less overall cortisol secretion in the CFT condition. Both findings indicate that the CFT can successfully stimulate the PNS and inhibit the HPA axis. To the best of our knowledge, our experiment is the first to successfully use the CFT as a simple and easy-to-apply method to modify biological responses to acute stress.