Delayed effects of psychosocial stress on risk taking.

Several studies found that acute stress leads to increased risk taking in humans. However, this effect appears to be time-dependent because the few studies that examined delayed (>40 min after stress onset) stress effects show in fact a decrease in risk taking. In 32 young healthy women, we intra-individually examined whether psychosocial stress decreases risk taking 80 min after stress induction. All participants performed the Balloon Analog Risk Task (BART) twice: once after exposure to the Trier social stress test (TSST) and once after a control condition Placebo-TSST (P-TSST). The experimental order was randomized across participants. The psychophysiological stress response increased after the TSST compared to the P-TSST, indicated by elevated cortisol concentrations, elevated alpha-amylase activity, and elevated blood pressure. We found a significant interaction of stress condition and experimental order. Compared to the control condition psychosocial stress decreased risk taking in novel decision situations but not when participants were already familiar with the BART from the prior condition. Delayed effects of psychosocial stress lead to a decrease in risk taking in unfamiliar but not familiar conditions 80 min after stress exposure. Lay summary It has been suggested that stress exerts delayed effects on risk taking propensity. We found that individuals who are exposed to psychosocial stress take less risk when confronted with novel decisions even 80 min after the stressor compared to individuals who are not stressed.

C-reactive protein, pre- and postdexamethasone cortisol levels in post-traumatic stress disorder.

BACKGROUND: Dysregulations of the hypothalamic-pituitary-adrenal axis may impact inflammatory processes in post-traumatic stress disorder (PTSD), possibly resulting in a low-grade inflammation as reflected by elevated levels of C-reactive protein (CRP). METHODS: Serum CRP levels and salivary cortisol before and after the dexamethasone suppression test (DST) were assessed in 50 inpatients with main diagnoses PTSD, major depressive disorder or borderline personality disorder. RESULTS: A strong trend for lower CRP levels was found in PTSD positive individuals compared with patients without PTSD. CONCLUSIONS: Our study does not support the hypothesis of elevated serum CRP levels in PTSD compared with other psychiatric patients. However, a dysbalanced immune system with suppressed CRP might contribute to the elevated somatic comorbidity in PTSD.

Non-instrumental information seeking is resistant to acute stress.

Previous research has shown that people intrinsically value non-instrumental information, which cannot be used to change the outcome of events, but only provides an early resolution of uncertainty. This is true even for information about rather inconsequential events, such as the outcomes of small lotteries. Here we investigated whether participants' willingness to pay for non-instrumental information about the outcome of simple coin-flip lotteries with guaranteed winnings was modulated by acute stress. Stress was induced using the Socially Evaluated Cold Pressor Test (SECPT), and information-seeking choices were compared to a warm water control group. Our results neither support the hypothesis that stress decreases information-seeking by directing cognitive resources away from the relevance of the lotteries, nor the opposite hypothesis that stress increases information-seeking by driving anxiety levels up. Instead, we found that despite successful stress induction, as evidenced by increased saliva cortisol levels in the SECPT group, information valuation was remarkably stable. This finding is in line with recent findings that experimentally increased state anxiety did not modulate non-instrumental information seeking. Together, these results suggest that the aversiveness of "not knowing" is a stable cognitive state and not easily modulated by situational context, such as acute stress.

Patients' Perspectives on Artificial Intelligence in Dentistry: A Controlled Study.

Background: As artificial intelligence (AI) becomes increasingly important in modern dentistry, we aimed to assess patients' perspectives on AI in dentistry specifically for radiographic caries detection and the impact of AI-based diagnosis on patients' trust. Methods: Validated questionnaires with Likert-scale batteries (1: "strongly disagree" to 5: "strongly agree") were used to query participants' experiences with dental radiographs and their knowledge/attitudes towards AI as well as to assess how AI-based communication of a diagnosis impacted their trust, belief, and understanding. Analyses of variance and ordinal logistic regression (OLR) were used (p < 0.05). Results: Patients were convinced that "AI is useful" (mean Likert ± standard deviation 4.2 ± 0.8) and did not fear AI in general (2.2 ± 1.0) nor in dentistry (1.6 ± 0.8). Age, education, and employment status were significantly associated with patients' attitudes towards AI for dental diagnostics. When shown a radiograph with a caries lesion highlighted by an arrow, patients recognized the lesion significantly less often than when using AI-generated coloured overlays highlighting the lesion (p < 0.0005). AI-based communication did not significantly affect patients' trust in dentists' diagnosis (p = 0.44; OLR). Conclusions: Patients showed a positive attitude towards AI in dentistry. AI-supported diagnostics may assist communicating radiographic findings by increasing patients' ability to recognize caries lesions on dental radiographs.

Blunted salivary cortisol response to psychosocial stress in women with posttraumatic stress disorder.

Posttraumatic stress disorder (PTSD) is characterized by alterations in the hypothalamic-pituitary-adrenal (HPA) axis and sympathetic nervous system (SNS). There is evidence for a blunted HPA axis reactivity to psychosocial stress. Less is known about how the SNS reacts to psychosocial stress. Here, we compared the HPA axis and SNS responses to psychosocial stress and a non-stressful condition in patients with PTSD and in healthy individuals. Twenty-one women with PTSD and 32 healthy women participated in the Trier social stress test (TSST) and placebo TSST (P-TSST). We measured salivary cortisol, alpha amylase activity and blood pressure before and after the tests. Subjective perceived stress response was also assessed. We found a blunted cortisol response to the TSST in patients with PTSD compared with healthy participants 10 min (t (51) = -2.58, p = .01) and 25 min (t (51) = -2.16, p = .04) after TSST. We found no evidence for an increased SNS reactivity after psychosocial stress in patients with PTSD (all p > .05). Patients with PTSD, but not healthy participants, reported more dissociative symptoms (t (20) = -2.31, p = .03) and being more tired (t (20) = 2.90, p = .01) directly after TSST compared with the placebo condition. Our results suggest a blunted HPA stress reactivity and an increased subjective perceived stress response in female patients with PTSD. Longitudinal studies could test if these altered stress responses constitute a predisposition to or a cause of PTSD. Future studies should investigate whether these results are transferable to men.

Heightened biological stress response during exposure to a trauma film predicts an increase in intrusive memories.

Some people develop symptoms of posttraumatic stress disorder (PTSD) after having experienced a traumatic event, whereas others do not. Intrusive memories are a cardinal symptom of PTSD and a better understanding of encoding and consolidation of intrusive memory may yield important insights on differences in the response to trauma. The primary aim of this study is to investigate whether psychosocial stress induction (Trier Social Stress Test) versus active control (placebo version) leading to respective biological stress responses during the encoding and consolidation of a film-elicited analogue trauma influences the development of intrusive memories over the course of 7 consecutive days. We hypothesized that the activation of the biological stress system increases the number of intrusive memories over the course of 7 days. This single-blind randomized placebo-controlled study examined 122 young healthy women. Biological stress response was measured by salivary cortisol, salivary α-amylase activity, and heart rate variability. Generalized linear mixed models were used to analyze longitudinal effects of activation of biological stress response on self-reported number of intrusive memories. Cross-validated regularized regression (least absolute shrinkage and selection operator) was applied for data-driven feature selection including known biological and psychological predictors. Corroborating our hypothesis, biological stress-responders to the Trier Social Stress Test reported significantly more intrusive memories after trauma film. A priori designed post hoc tests point at significantly more intrusions on Day 1 and 2 in biological stress responders. Least absolute shrinkage and selection operator regression revealed salivary cortisol, salivary α-amylase activity, heart rate variability, subjectively rated distress, fear, and (on trend level) dissociation during the trauma film as relevant predictors of intrusive memories. A heightened biological stress response in young women is associated with more intrusive memories the first days after experiencing a trauma analogue. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Altered cellular immune reactivity in traumatized women with and without major depressive disorder.

Alterations of the hypothalamic-pituitary-adrenal (HPA) axis such as altered glucocorticoid receptor sensitivity and increased immune reactivity might contribute to the pathogenesis of major depressive disorder (MDD). Exposure to adverse childhood experiences (ACE) precipitates vulnerability to MDD and might be associated with endocrine and immune alterations in the disorder. In order to disentangle the effects of ACE and MDD, we recruited 87 women: n = 23 with MDD and ACE as determined by clinical interview and questionnaires (Structured Clinical Interview for DSM-IV, Early Trauma Inventory, Childhood Trauma Questionnaire), n = 24 with MDD without ACE, n = 21 with ACE but no current or lifetime MDD, and n = 26 healthy women without either MDD or ACE. Glucocorticoid signaling and mitogen-stimulated proliferation were analyzed ex vivo in peripheral blood-derived mononuclear cells. Additionally, mRNA expression of the glucocorticoid and the mineralocorticoid receptor (GR / MR) was assessed. Peripheral GR sensitivity as well as GR and MR expression levels were not significantly different between groups. Women with ACE showed an increased immune response after mitogen stimulation independent of the presence of MDD. Our results provide evidence for a functionally altered ex-vivo immune response in cell cultures from women with a history of ACE. Thus, ACE might contribute to the pathogenesis of MDD through inflammatory pathways.

Effects of glucocorticoid and noradrenergic activity on spatial learning and spatial memory in healthy young adults.

BACKGROUND: Acute stress leads to a rapid release of noradrenaline and glucocorticoids, which in turn influence cognitive functions such as spatial learning and memory. However, few studies have investigated noradrenergic and glucocorticoid effects on spatial learning and memory in humans. Therefore, we examined the separate and combined effects of noradrenergic and glucocorticoid stimulation on spatial learning and memory. METHODS: One hundred and four healthy men (mean age = 24.1 years ±SD 3.5) underwent the virtual Morris Water Maze (vMWM) task to test spatial learning and spatial memory retrieval after receiving either 10 mg hydrocortisone or 10 mg yohimbine (an alpha 2-adrenergic receptor antagonist that increases noradrenergic activity), 10 mg hydrocortisone and 10 mg yohimbine combined, or placebo. The vMWM task took place 90 min after yohimbine was administered and 75 min after hydrocortisone was administered. Placebo was given at the same times. Salivary cortisol and alpha amylase levels were measured to check pharmacological stimulation. RESULTS: Hydrocortisone and yohimbine increased salivary cortisol and alpha amylase levels. Participants' task performance improved over time, suggesting successful spatial learning. However, separate and combined noradrenergic and glucocorticoid stimulation had no effect on spatial learning and spatial memory retrieval compared with placebo. CONCLUSIONS: In healthy young men, hydrocortisone and/or yohimbine did not alter spatial learning or spatial memory retrieval. Importantly, pharmacological stimulation took place prior to learning. Further studies should examine the effects of glucocorticoid and noradrenergic stimulation during encoding, consolidation, and retrieval.

Resting-state functional connectivity after hydrocortisone administration in patients with post-traumatic stress disorder and borderline personality disorder.

In a previous study, we found that - in contrast to healthy individuals - patients with borderline personality disorder (BPD) and post-traumatic stress disorder (PTSD) showed better memory retrieval performance after hydrocortisone administration compared to placebo. As these results suggest an altered function of corticosteroid receptors in the brain in PTSD and BPD, we examined the effect of hydrocortisone on brain activation in both disorders. We recruited 40 female healthy controls, 20 female unmedicated patients with PTSD and 18 female unmedicated patients with BPD. We conducted a placebo-controlled cross-over study, in which all participants underwent two resting state MRI measurements after they received either a placebo or 10 mg hydrocortisone orally and in randomized order. There was a time interval of one week between the measurements. We analysed resting state functional connectivity (RSFC) with the hippocampus and the amygdala as seed regions. Compared to healthy controls, both patient groups showed reduced hippocampus RSFC to dorsomedial prefrontal cortex (dmPFC). Positive hippocampus dmPFC RSFC correlated negatively with childhood trauma (r = -0.47) and with severity of clinical symptoms, measured with the Borderline Symptom List (r = -0.44) and the Posttraumatic Stress Diagnostic Scale (r = -0.45). We found neither differences in amygdala RSFC nor an effect of hydrocortisone administration. Childhood trauma might lead to decreased positive hippocampus dmPFC RSFC. This might explain symptoms of PTSD and BPD that are characterized by dysfunctional fear regulation.

Neural correlates of glucocorticoids effects on autobiographical memory retrieval in healthy women.

It is well known that elevated cortisol after stress or after exogenous administration impairs episodic memory retrieval including autobiographical memory (AM) retrieval. This impairment might be mediated by deactivation of a neural network associated with memory retrieval including the prefrontal cortex (PFC) and limbic structures. However, the neural underpinnings of these cortisol effects on AM retrieval have not been investigated yet. In this study, thirty-three healthy women received either placebo or 10 mg hydrocortisone in a double blind cross-over design before completing an AM test during fMRI. In this test, participants are asked to recall specific events from their own past in response to a cue word. In a first step, we analyzed the neural underpinnings of AM retrieval in the placebo condition. We found an activation pattern consistent with core regions involved in autobiographical memory recall, including the ventromedial PFC, anterior medial (am)PFC, inferior frontal gyrus, the posterior cingulate cortex, the tempoparietal junction, the middle temporal gyrus and the hippocampus. Further, we analyzed brain activation during AM retrieval after hydrocortisone compared to placebo. Region of interest (ROI) analyses revealed a hydrocortisone-induced deactivation during AM retrieval in the right amPFC. Results of the ROI analyses were non-significant in the left and right hippocampus, the left and right vmPFC and the left amPFC In sum, during AM retrieval hydrocortisone had the most pronounced effects on the amPFC. This might be explained by the strong involvement of this brain region in self-referential behavior, which is essential for recalling autobiographic information.

HPA axis reactivity and lymphocyte glucocorticoid sensitivity in fibromyalgia syndrome and chronic pelvic pain.

OBJECTIVE: Chronic pelvic pain (CPP) and fibromyalgia syndrome (FMS) have been associated with hypothalamic-pituitary-adrenal (HPA) axis alterations, i.e., mild hypocortisolism and enhanced feedback sensitivity. We tested the hypothesis of reduced cortisol release in response to a psychosocial stressor and pharmacological stimulation. Furthermore, glucocorticoid (GC) sensitivity was evaluated. METHODS: Plasma total and salivary-free cortisol concentrations were measured in response to a standardized social laboratory stressor, the Trier Social Stress Test, and to adrenocorticotropin (ACTH)(1-24) stimulation. In the Trier Social Stress Test, we additionally measured ACTH. GC sensitivity was measured by dexamethasone inhibition of lipopolysaccharide-induced interleukin-6 and tumor necrosis factor-alpha production in whole blood. RESULTS: There were no HPA axis alterations in women with CPP (N = 18) in these tests. Patients with FMS (N = 17) showed lower total cortisol release in response to the social stressor and exogenous ACTH, but normal free cortisol and ACTH levels compared with controls (N = 24). GC sensitivity was similar in all groups. CONCLUSIONS: Our results suggest normal HPA responses to stress and ACTH stimulation in patients with CPP but reduced adrenal reactivity in patients with FMS, namely in total cortisol release. Free cortisol on the other hand was unaltered, possibly reflecting an adaptation to reduced circulating total cortisol.

The dexamethasone corticotropin releasing hormone test in healthy and depressed women with and without childhood adversity.

BACKGROUND: Alterations of the hypothalamic-pituitary-adrenal (HPA) axis are a prominent finding in patients with major depressive disorder (MDD). Inconsistencies regarding a hyper- or hypoactive HPA axis may be explained by the moderating effect of childhood adverse experiences (ACE) which are associated with both HPA axis dysfunction and MDD in adulthood. We aimed to systematically disentangle the effects of ACE and MDD on HPA axis by comparing healthy women with and without childhood adversity and women with MDD with and without ACE. METHODS: The dexamethasone/corticotropin-releasing hormone (DEX/CRH) test was administered in 35 women with MDD and ACE as determined by a clinical interview (SCID, Early Trauma Inventory), 51 women with MDD without ACE, 21 women with ACE but no current or lifetime MDD and 37 healthy women without either MDD or ACE. RESULTS: There were no group differences in age, smoking, body mass index, and intake of oral contraceptives. Free salivary cortisol responses were not significantly different between the four groups. CONCLUSIONS: This study shows no evidence for a dysregulation of the HPA axis as measured by the DEX/CRH test in depressed women with and without childhood adversity as compared to mentally healthy women with or without early life stress. Our results do not support the assumption of distinct neuroendocrine endophenotypes in MDD with regard to ACE.

Stress reactivity and its effects on subsequent food intake in depressed and healthy women with and without adverse childhood experiences.

BACKGROUND: Adverse childhood experiences (ACE) increase the risk to develop major depressive disorder (MDD) and obesity or metabolic syndrome in adulthood. In addition, ACE may be associated with an exaggerated endocrine response to stress, which, in turn, may lead to enhanced food intake resulting in obesity and metabolic problems. METHODS: We systematically examined the stress response and consecutive food intake in 32 women with MDD and ACE as determined by a clinical interview (Early Trauma Inventory), 52 women with MDD without ACE, 22 women with ACE but no current or lifetime MDD and 37 healthy women without either MDD or ACE. All participants underwent a psychosocial stress test (Trier Social Stress Test, TSST) and a control condition (Placebo-TSST) before they were offered a buffet of snacks. Participants were not aware that the primary outcome variable was the amount of consumed kilocalories (kcal). RESULTS: The four groups did not differ in demographic variables. Stress resulted in higher cortisol release and higher blood pressure compared to the control condition. Patients with MDD without ACE had a significantly lower cortisol response to stress compared to controls. Across groups, we found higher kcal intake after stress compared to the control condition. Comparing high and low cortisol responders to stress, higher kcal intake after stress was only seen in those with low cortisol release. CONCLUSIONS: This study provides evidence that blunted rather than enhanced cortisol release to stress might lead to increased food intake, independent from MDD and ACE.

Increased hair testosterone but unaltered hair cortisol in female patients with borderline personality disorder.

A number of studies have reported on dysfunctions in steroid secretion, including altered cortisol and testosterone levels in borderline personality disorder (BDP) patients compared to healthy controls. The present study extends findings from blood and saliva studies to the cumulative measure of hair steroids. We investigated women with BPD (n=18) and age- and education-matched healthy women (n=17). We did not find differences between BPD patients and healthy women (p=0.40) concerning hair cortisol levels but increased hair testosterone levels among BPD patients compared to controls (p=0.03). These results remained when restricting the analyses to unmedicated patients. Our data indicate altered long-term testosterone but not cortisol levels in females with BPD. Future studies should address the possible impact of altered testosterone on medical illness processes including metabolic syndrome in this population.

Impact of exogenous cortisol on the formation of intrusive memories in healthy women.

INTRODUCTION: Stress hormones such as cortisol are involved in modulating emotional memory. However, little is known about the influence of cortisol on the formation of intrusive memories after a traumatic event. The aim of this study was to examine whether cortisol levels during encoding and consolidation of an intrusion-inducing trauma film paradigm would influence subsequent intrusion formation. MATERIAL AND METHODS: In an experimental, double-blind, placebo-controlled study a trauma film paradigm was used to induce intrusions in 60 healthy women. Participants received a single dose of either 20 mg hydrocortisone or placebo before watching a trauma film. Salivary cortisol and alpha-amylase as well as blood pressure were measured during the experiment. The consecutive number of intrusions, the vividness of intrusions, and the degree of distress evoked by the intrusions resulting from the trauma film were assessed throughout the following seven days. RESULTS: Hydrocortisone administration before the trauma film resulted in increased salivary cortisol levels but did not affect the consecutive number of intrusions, the vividness of intrusions, and the degree of distress evoked by the intrusions throughout the following week. CONCLUSIONS: These results indicate that pharmacologically increased cortisol levels during an experimental trauma film paradigm do not influence consecutive intrusive memories. Current data do not support a prominent role of exogenous cortisol on intrusive memories, at least in healthy young women after a relatively mild trauma equivalent.

Mineralocorticoid receptor function in depressed patients and healthy individuals.

BACKGROUND: Many studies have shown disturbed glucocorticoid receptor (GR) in depressed patients. In contrast, only few studies targeted mineralocorticoid receptor (MR) function with inconclusive results. We examined the effects of the MR antagonist spironolactone on cortisol secretion in depressed patients and healthy individuals. METHODS: Forty-eight unmedicated depressed patients (mean age 41.6years) and 45 age- and sex-matched healthy participants (40.7years) received the MR antagonist spironolactone (300mg) or placebo with three days apart in a randomized, double-blind, within-subject cross-over design. We measured salivary cortisol before ingestion of study medication (baseline) as well as +60min, +90min, +120min, +150min and 180min after baseline. RESULTS: Repeated-measures ANOVA for area under the curve (AUCg) cortisol revealed a treatment effect with higher cortisol after spironolactone and a treatment by group interaction. Post-hoc analyses revealed higher cortisol in depressed patients compared to healthy participants in the placebo condition. In the spironolactone condition, the cortisol levels were not significantly different. CONCLUSIONS: Potentially, impaired MR or GR signaling could be responsible for higher cortisol levels in depressed patients in the placebo condition. However, after MR blockade that increased cortisol secretion across groups leading to higher GR occupation, we found no differences between depressed patients and healthy controls. Thus, our results argue for depression-associated alterations in MR signaling rather than disturbed GR-mediated feedback inhibition.

Hair cortisol and cortisol awakening response are associated with criteria of the metabolic syndrome in opposite directions.

Findings on the association between hypothalamic-pituitary-adrenal (HPA) axis activity and metabolic risk are equivocal. Different methods of measuring HPA activity might indicate adverse vs. beneficial effects of HPA activity on metabolic risk thus contributing to heterogenous findings. In this study, we aimed to determine whether (1) the salivary cortisol awakening response (CAR) as a marker of awakening-induced activation of the HPA axis and (2) hair cortisol as a marker of long-term cortisol secretion are associated with criteria of the metabolic syndrome. Therefore, we recruited 41 healthy individuals (26 women, mean age: 41.2 years) and 44 patients with major depression (28 women, 41.4 years) and assessed CAR and hair cortisol values as well as all criteria of the metabolic syndrome (abdominal obesity, blood pressure, plasma glucose, triglycerides and high-density cholesterol levels) according to the International Diabetes Federation. CAR and hair cortisol values were divided into tertiles. Across groups, participants with hair cortisol or hair cortisone in the highest tertile showed significantly more criteria of the metabolic syndrome compared to participants in the medium or low tertile (F2,64=3.37, p=.04). These results were corroborated by significant positive correlations between mean hair cortisol values with waist circumference (r=.29, p=.03), triglycerides (r=.34, p=.01) and systolic blood pressure (r=.29, p=.04) and between mean hair cortisone and triglycerides (r=.46, p<.01). In contrast, mean CAR values correlated negatively with diastolic (r=-.29, p=.03) and systolic blood pressure (r=-.32, p=.02). Our results indicate that higher hair cortisol and hair cortisone levels but lower CAR values are associated with an unfavorable metabolic and cardiovascular risk profile.

Mineralocorticoid receptor stimulation improves cognitive function and decreases cortisol secretion in depressed patients and healthy individuals.

Memory and executive function are often impaired in patients with major depression, while cortisol secretion is increased. Mineralocorticoid receptors (MR) are abundantly expressed in the hippocampus and in the prefrontal cortex, brain areas critical for memory, executive function, and cortisol inhibition. Here, we investigated whether MR stimulation with fludrocortisone (1) improves memory and executive function and (2) decreases cortisol secretion in depressed patients and healthy individuals. Twenty-four depressed patients without medication and 24 age-, sex-, and education-matched healthy participants received fludrocortisone (0.4 mg) or placebo in a randomized, double-blind, within-subject cross-over design. We measured verbal memory, visuospatial memory, executive function, psychomotor speed, and salivary cortisol secretion during cognitive testing between 1400 and 1700 hours. For verbal memory and executive function, we found better performance after fludrocortisone compared with placebo across groups. No treatment effect on other cognitive domains emerged. Depressed patients performed worse than healthy individuals in psychomotor speed and executive function. No group effect or group × treatment interaction emerged on other cognitive domains. Fludrocortisone decreased cortisol secretion across groups and there was a significant correlation between cortisol inhibition and verbal memory performance. Our data suggest a crucial role of MR in verbal memory and executive function and demonstrate the possibility to improve cognition in depressed patients and healthy individuals through MR stimulation.

Early life stress modulates oxytocin effects on limbic system during acute psychosocial stress.

Early life stress (ELS) is associated with altered stress responsivity, structural and functional brain changes and an increased risk for the development of psychopathological conditions in later life. Due to its behavioral and physiological effects, the neuropeptide oxytocin (OXT) is a useful tool to investigate stress responsivity, even though the neurobiological underpinnings of its effects are still unknown. Here we investigate the effects of OXT on cortisol stress response and neural activity during psychosocial stress. Using functional magnetic resonance imaging in healthy subjects with and without a history of ELS, we found attenuated hormonal reactivity and significantly reduced limbic deactivation after OXT administration in subjects without a history of ELS. Subjects who experienced ELS showed both blunted stress reactivity and limbic deactivation during stress. Furthermore, in these subjects OXT had opposite effects with increased hormonal reactivity and increased limbic deactivation. Our results might implicate that reduced limbic deactivation and hypothalamic-pituitary-adrenal axis responsivity during psychosocial stress are markers for biological resilience after ELS. Effects of OXT in subjects with a history of maltreatment could therefore be considered detrimental and suggest careful consideration of OXT administration in such individuals.

Acute glucocorticoid effects on response inhibition in borderline personality disorder.

INTRODUCTION: Growing evidence suggests inhibition dysfunctions in borderline personality disorder (BPD). Moreover, abnormalities in hypothalamic-pituitary-adrenal (HPA) axis functioning have also been found in BPD patients. In healthy individuals, response inhibition has been sensitive to acute stress, and previous research indicates that effects mediated by the HPA axis become particularly apparent when emotional stimuli are processed. This study aimed to explore the influence of acute hydrocortisone administration on response inhibition of emotional stimuli in BPD patients compared to healthy control participants. METHODS: After a single administration of 10mg hydrocortisone or placebo, 32 female BPD patients and 32 healthy female participants performed an adapted emotional go/no-go paradigm to assess response inhibition for emotional face stimuli in a cross-over study. RESULTS: Acute cortisol elevations decreased the reaction times to target stimuli in both BPD patients and healthy controls. Patients and controls did not differ in task performance; however, BPD patients with comorbid posttraumatic stress disorder (PTSD) displayed longer reaction times than patients without PTSD. In contrast, the occurrence of comorbid eating disorder had no significant impact on go/no-go performance. No significant interaction effect between the treatment condition and the emotional valence of the face stimuli was found. CONCLUSIONS: Acute hydrocortisone administration enhances response inhibition of face stimuli in BPD patients and healthy controls, regardless of their emotional valence. Our results agree with the suggestion that moderate cortisol enhancement increases the inhibition of task-irrelevant distracters.