Aberrant positive affect dynamics in individuals with subthreshold depression: Evidence from laboratory and real-world assessments / Dinámica aberrante del afecto positivo en individuos con depresión subumbral: evidencia de evaluaciones de laboratorio y del mundo real

Background/Objective: Reduced positive affect (PA) is a core feature of major depressive disorder (MDD). However, the precursor of MDD, subthreshold depression (StD), has received less attention in this regard. Therefore, we examined PA dynamics in StD, integrating laboratory-based and ecological momentary assessment (EMA) approaches. Method: Participants were college students recruited from Chinese universities (31 with StD, and 39 healthy controls (HC)). Positive mood was induced in the laboratory by an eight-minute comedy clip used to assess PA reactivity and maintenance. To extend findings to the real world and explore mechanisms of PA maintenance, 53 participants with StD and 64 HC reported their emotional states 14 times daily for one week via EMA. Multilevel models were used to test for predictors of PA inertia. Results: In the laboratory, participants with StD achieved the same PA reactivity as HC when facing positive stimuli, yet the curve-fitting revealed difficulties for the StD group in maintaining PA over time. Such reduced capacity was further observed in real-world settings, manifesting in significantly greater PA inertia. Conclusions: High PA inertia in daily life may reflect resistance to mood change in StD, explaining anhedonia and difficulties with emotional maintenance, and highlighting the need for early identification.(AU)

Cortisol interdependence during psychotherapy in major depressive disorder.

The current study explored cortisol interdependence between patients and therapists during psychotherapy, the possible moderating effect of patient alliance ratings on this interdependence, and the associations between cortisol interdependence and treatment outcome. While cortisol interdependence was explored in other interpersonal contexts, its presence in psychotherapy has remained unexplored. We hypothesized that (a) patients' and therapists' cortisol levels at pre-session will predict their own and their partner's subsequent cortisol levels at post-session, (b) patient ratings of their relationship with their therapists will moderate these partner effects, and (c) cortisol interdependence will be associated with better treatment outcome. Fifty dyads undergoing 16 weeks of psychodynamic treatment for major depressive disorder participated in this study. Patient-therapist salivary cortisol samples were collected at eight time points, alongside a post-session patient-rated alliance questionnaire and a symptom severity interview. For analyses we employed the actor-partner interdependence model. Results revealed that (a) patients' and therapists' cortisol levels before sessions predicted their own post-session cortisol changes. However, significant cortisol interdependence was observed in patients' pre-session cortisol levels predicting therapists' post-session cortisol levels. Furthermore, (b) poorer alliance ratings associated with more pronounced cortisol interdependence, and (c) in dyads where patient pre-session cortisol predicted therapist's post-session cortisol, a better treatment outcome was found. This study found novel evidence of cortisol interdependence in psychotherapy and is partially in line with other studies inspecting cortisol interdependence in adjacent research fields. These findings emphasize the intricate psychophysiological interactions within therapeutic relationships and their associations with treatment outcome.

Aberrant positive affect dynamics in individuals with subthreshold depression: Evidence from laboratory and real-world assessments.

Background/Objective: Reduced positive affect (PA) is a core feature of major depressive disorder (MDD). However, the precursor of MDD, subthreshold depression (StD), has received less attention in this regard. Therefore, we examined PA dynamics in StD, integrating laboratory-based and ecological momentary assessment (EMA) approaches. Method: Participants were college students recruited from Chinese universities (31 with StD, and 39 healthy controls (HC)). Positive mood was induced in the laboratory by an eight-minute comedy clip used to assess PA reactivity and maintenance. To extend findings to the real world and explore mechanisms of PA maintenance, 53 participants with StD and 64 HC reported their emotional states 14 times daily for one week via EMA. Multilevel models were used to test for predictors of PA inertia. Results: In the laboratory, participants with StD achieved the same PA reactivity as HC when facing positive stimuli, yet the curve-fitting revealed difficulties for the StD group in maintaining PA over time. Such reduced capacity was further observed in real-world settings, manifesting in significantly greater PA inertia. Conclusions: High PA inertia in daily life may reflect resistance to mood change in StD, explaining anhedonia and difficulties with emotional maintenance, and highlighting the need for early identification.

How do people use reappraisal? An investigation of selection frequency and affective outcomes of reappraisal tactics.

Although the effects of different emotion regulation strategies are well-documented, most studies to date have focused on the selection and implementation of broad strategies, while overlooking the selection and implementation of specific tactics to enact those strategies. The present research investigated the strategy of cognitive reappraisal and the differences in selection frequency and affective outcomes that are associated with the implementation of different reappraisal tactics to enact that strategy. Participants completed a laboratory task in which they were instructed to reappraise or not to reappraise negative images and reported on their use of specific reappraisal tactics for every trial. Using established reappraisal tactic coding, we assessed how people selected from among common tactics for each image (Study 1) and all tactics (Study 2) and implemented those tactics to reappraise negative images. We compared reappraisal tactic selection and implementation when used during instructed reappraisal versus during spontaneous reappraisal, in the nonreappraise condition. Results of both studies indicate that tactics were used more often when instructed to reappraise versus when spontaneously reappraising. Participants used some tactics (e.g., reality challenge) more frequently compared to the rest of the tactics in both conditions. Negative affect was lower following instructed versus spontaneous reappraisal. Some tactics (e.g., change current circumstances) were more effective at decreasing negative affect in both conditions. Knowing which reappraisal tactics are most frequently selected, and their affective outcomes when used when prompted or spontaneously, may help us better understand how to improve people's ability to use reappraisal to achieve their emotional goals. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

The Effect of Dehydroepiandrosterone Administration during Rehabilitation on White Matter Integrity Among Individuals With Polysubstance Use Disorder.

OBJECTIVES: Individuals with polysubstance use disorder (pSUD) exhibit vulnerability to relapse even after prolonged abstinence, with rehabilitation efforts achieving limited success. Previous studies highlighted dehydroepiandrosterone (DHEA) as a putative therapeutic agent that may aid rehabilitation, potentially by impacting white matter (WM) properties. The current study tested, for the first time, the effect of DHEA administration during rehabilitation on WM integrity among pSUD individuals, while assessing its putative association with long-term relapse rates. METHODS: Immediately after admission to rehabilitation, 30 pSUD individuals were assigned to receive either placebo or DHEA (100 mg) daily for 3 months, via a randomized double-blind counterbalanced design. Participants also provided blood samples to assess circulating DHEA levels at treatment initiation and completed a diffusion tensor imaging (DTI) scan approximately 1 month after treatment initiation. Clinical status was evaluated 16 months after treatment initiation. Thirty matched healthy controls also underwent a DTI scan without any intervention. RESULTS: DHEA administration was not associated with reduced relapse rates compared with placebo. Nevertheless, exploratory analysis revealed that DHEA was associated with successful rehabilitation among pSUD individuals with low circulating DHEA levels at treatment initiation. White matter integrity in the splenium corpus callosum (CC) was reduced in pSUD individuals compared with healthy controls, yet pSUD individuals receiving DHEA exhibited recovery of splenium CC WM integrity. CONCLUSIONS: DHEA administration during rehabilitation may restore WM integrity in the CC among pSUD individuals. Although DHEA was not associated with reduced relapse rates in here, its therapeutic efficacy may depend on circulating DHEA levels at treatment initiation.

From childhood adversity to latent stress vulnerability in adulthood: the mediating roles of sleep disturbances and HPA axis dysfunction.

Childhood adversity is a prominent predisposing risk factor for latent stress vulnerability, expressed as an elevated likelihood of developing stress-related psychopathology upon subsequent exposure to trauma in adulthood. Sleep disturbances have emerged as one of the most pronounced maladaptive behavioral outcomes of childhood adversity and are also a highly prevalent core feature of stress-related psychopathology, including post-traumatic stress disorder (PTSD). After reviewing the extensive literature supporting these claims, the current review addresses the notion that childhood adversity-induced sleep disturbances may play a causal role in elevating individuals' stress vulnerability in adulthood. Corroborating this, sleep disturbances that predate adult trauma exposure have been associated with an increased likelihood of developing stress-related psychopathology post-exposure. Furthermore, novel empirical evidence suggests that sleep disturbances, including irregularity of the sleep-wake cycle, mediate the link between childhood adversity and stress vulnerability in adulthood. We also discuss cognitive and behavioral mechanisms through which such a cascade may evolve, highlighting the putative role of impaired memory consolidation and fear extinction. Next, we present evidence to support the contribution of the hypothalamic-pituitary-adrenal (HPA) axis to these associations, stemming from its critical role in stress and sleep regulatory pathways. Childhood adversity may yield bi-directional effects within the HPA stress and sleep axes in which sleep disturbances and HPA axis dysfunction reinforce each other, leading to elevated stress vulnerability. To conclude, we postulate a conceptual path model from childhood adversity to latent stress vulnerability in adulthood and discuss the potential clinical implications of these notions, while highlighting directions for future research.

A mesocorticolimbic signature of pleasure in the human brain.

Pleasure is a fundamental driver of human behaviour, yet its neural basis remains largely unknown. Rodent studies highlight opioidergic neural circuits connecting the nucleus accumbens, ventral pallidum, insula and orbitofrontal cortex as critical for the initiation and regulation of pleasure, and human neuroimaging studies exhibit some translational parity. However, whether activation in these regions conveys a generalizable representation of pleasure regulated by opioidergic mechanisms remains unclear. Here we use pattern recognition techniques to develop a human functional magnetic resonance imaging signature of mesocorticolimbic activity unique to states of pleasure. In independent validation tests, this signature is sensitive to pleasant tastes and affect evoked by humour. The signature is spatially co-extensive with mu-opioid receptor gene expression, and its response is attenuated by the opioid antagonist naloxone. These findings provide evidence for a basis of pleasure in humans that is distributed across brain systems.

Evaluating the Evidence for Brain-Based Biotypes of Psychiatric Vulnerability in the Acute Aftermath of Trauma.

OBJECTIVE: The weak link between subjective symptom-based diagnostic methods for posttraumatic psychopathology and objectively measured neurobiological indices forms a barrier to the development of effective personalized treatments. To overcome this problem, recent studies have aimed to stratify psychiatric disorders by identifying consistent subgroups based on objective neural markers. Along these lines, a promising 2021 study by Stevens et al. identified distinct brain-based biotypes associated with different longitudinal patterns of posttraumatic symptoms. Here, the authors conducted a conceptual nonexact replication of that study using a comparable data set from a multimodal longitudinal study of recent trauma survivors. METHODS: A total of 130 participants (mean age, 33.61 years, SD=11.21; 48% women) admitted to a general hospital emergency department following trauma exposure underwent demographic, clinical, and neuroimaging assessments 1, 6, and 14 months after trauma. All analyses followed the pipeline outlined in the original study and were conducted in collaboration with its authors. RESULTS: Task-based functional MRI conducted 1 month posttrauma was used to identify four clusters of individuals based on profiles of neural activity reflecting threat and reward reactivity. These clusters were not identical to the previously identified brain-based biotypes and were not associated with prospective symptoms of posttraumatic psychopathology. CONCLUSIONS: Overall, these findings suggest that the original brain-based biotypes of trauma resilience and psychopathology may not generalize to other populations. Thus, caution is warranted when attempting to define subtypes of psychiatric vulnerability using neural indices before treatment implications can be fully realized. Additional replication studies are needed to identify more stable and generalizable neuroimaging-based biotypes of posttraumatic psychopathology.

Longitudinal volumetric evaluation of hippocampus and amygdala subregions in recent trauma survivors.

The hippocampus and the amygdala play a central role in post-traumatic stress disorder (PTSD) pathogenesis. While alternations in volumes of both regions have been consistently observed in individuals with PTSD, it remains unknown whether these reflect pre-trauma vulnerability traits or acquired post-trauma consequences of the disorder. Here, we conducted a longitudinal panel study of adult civilian trauma survivors admitted to a general hospital emergency department (ED). One hundred eligible participants (mean age = 32.97 ± 10.97, n = 56 females) completed both clinical interviews and structural MRI scans at 1-, 6-, and 14-months after ED admission (alias T1, T2, and T3). While all participants met PTSD diagnosis at T1, only n = 29 still met PTSD diagnosis at T3 (a "non-Remission" Group), while n = 71 did not (a "Remission" Group). Bayesian multilevel modeling analysis showed robust evidence for smaller right hippocampus volume (P+ of ~0.014) and moderate evidence for larger left amygdala volume (P+ of ~0.870) at T1 in the "non-Remission" group, compared to the "Remission" group. Subregion analysis further demonstrated robust evidence for smaller volume in the subiculum and right CA1 hippocampal subregions (P+ of ~0.021-0.046) in the "non-Remission" group. No time-dependent volumetric changes (T1 to T2 to T3) were observed across all participants or between groups. Results support the "vulnerability trait" hypothesis, suggesting that lower initial volumes of specific hippocampus subregions are associated with non-remitting PTSD. The stable volume of all hippocampal and amygdala subregions does not support the idea of consequential, progressive, stress-related atrophy during the first critical year following trauma exposure.

Reduced anhedonia following internet-based cognitive-behavioral therapy for depression is mediated by enhanced reward circuit activation.

BACKGROUND: Major depressive disorder (MDD) is a highly prevalent psychiatric condition, yet many patients do not receive adequate treatment. Novel and highly scalable interventions such as internet-based cognitive-behavioral-therapy (iCBT) may help to address this treatment gap. Anhedonia, a hallmark symptom of MDD that refers to diminished interest and ability to experience pleasure, has been associated with reduced reactivity in a neural reward circuit that includes medial prefrontal and striatal brain regions. Whether iCBT can reduce anhedonia severity in MDD patients, and whether these therapeutic effects are accompanied by enhanced reward circuit reactivity has yet to be examined. METHODS: Fifty-two MDD patients were randomly assigned to either 10-week iCBT (n = 26) or monitored attention control (MAC, n = 26) programs. All patients completed pre- and post-treatment assessments of anhedonia (Snaith-Hamilton Pleasure Scale; SHAPS) and reward circuit reactivity [monetary incentive delay (MID) task during functional magnetic resonance imaging (fMRI)]. Healthy control participants (n = 42) also underwent two fMRI scans while completing the MID task 10 weeks apart. RESULTS: Both iCBT and MAC groups exhibited a reduction in anhedonia severity post-treatment. Nevertheless, only the iCBT group exhibited enhanced nucleus accumbens (Nacc) and subgenual anterior cingulate cortex (sgACC) activation and functional connectivity from pre- to post-treatment in response to reward feedback. Enhanced Nacc and sgACC activations were associated with reduced anhedonia severity following iCBT treatment, with enhanced Nacc activation also mediating the reduction in anhedonia severity post-treatment. CONCLUSIONS: These findings suggest that increased reward circuit reactivity may contribute to a reduction in anhedonia severity following iCBT treatment for depression.

Resting-state heart rate variability (HRV) mediates the association between perceived chronic stress and ambiguity avoidance.

Chronic stress is associated with profound behavioral and physiological alterations, including intolerance to uncertainty and reduced resting-state heart-rate-variability (HRV). Critically, uncertainty may arise in situations with known probabilities (risk) or unknown probabilities (ambiguity). Whether associations between chronic stress and decision-making under uncertainty are dependent on the specific type of uncertain decisions, and whether physiological alterations play a role in these putative associations is not yet clear. Here, ninety-two healthy adults that exhibit various levels of perceived chronic stress underwent resting-state HRV recording before completing a behavioral task that involves decision-making under either risk or ambiguity. Computational modelling quantified participants' behavioral attitudes of approach and avoidance separately for risk and ambiguity. Results indicate, as expected, that perceived chronic stress is positively associated with intolerance to uncertainty and negatively associated with resting-state HRV. Contrary to expectations, behavioral attitudes towards risk and ambiguity were not directly associated with perceived chronic stress, yet HRV fully mediated the association between chronic stress and ambiguity avoidance. Taken together and given the direction of the associations, elevated HRV despite chronic stress may foster adaptive behavior in the form of avoiding ambiguous situations, and hence contribute to reduced exposure to uncertainty and to lower levels of allostatic load.

Multi-trajectory analysis uncovers latent associations between psychological and physiological acute stress response patterns.

Encounter with an acute stressor elicits multiple physiological and psychological response trajectories that spread at different times-scales and directions. Associating a single physiological response trajectory with a specific psychological response has remained a challenge, due to putative interactions between the different stress response pathways. Hence, multidimensional analysis of stress response trajectories may be better suited to account for response variability. To test this, 96 healthy female participants underwent a robust acute laboratory stress induction procedure while their psychological [positive and negative affect (PANAS)] and physiological [heart rate (HR), heart rate variability (HRV), saliva cortisol (CORT)] responses were recorded before, during and after stress. Combining these data using unsupervised group-based multi-trajectory modelling uncovered three latent classes that best accounted for variability across psychological and physiological stress response trajectories. These classes were labelled based on their psychological response patterns as: A prototypical response group that depict a moderate increase in negative and decrease in positive affect during stress, with both patterns recovering after stress offset (n = 55); A heightened response group that depict excessive affective responses during stress that recover after stress offset (n = 24); and a lack of recovery group that depict a moderate increase in negative and decrease in positive affect during stress, with both patterns not recovering after stress offset (n = 17). With respect to physiological acute stress trajectories, all three groups exhibited comparable increases in HR and CORT during stress that recovered after stress offset, yet only the prototypical group expressed the expected stress-induced reduction in HRV, while the other two groups exhibited blunted HRV response. Critically, focusing on a single physiological stress response trajectory, including HRV, did not account for psychological response variability and vice versa. Taken together, a multi-trajectory approach may better account for the multidimensionality of acute stress response and uncover latent associations between psychological and physiological response patterns. Compared to the other two groups, the prototypical group also exhibited significantly lower overall stress scores based on the DASS-21 scale. This, alongside the uncovered response patterns, suggest that latent psycho-physiological associations may shed light on stress response adaptivity or lack thereof.

Predicting Chronic Stress among Healthy Females Using Daily-Life Physiological and Lifestyle Features from Wearable Sensors.

Background: Chronic stress is a highly prevalent condition that may stem from different sources and can substantially impact physiology and behavior, potentially leading to impaired mental and physical health. Multiple physiological and behavioral lifestyle features can now be recorded unobtrusively in daily-life using wearable sensors. The aim of the current study was to identify a distinct set of physiological and behavioral lifestyle features that are associated with elevated levels of chronic stress across different stress sources. Methods: For that, 140 healthy female participants completed the Trier inventory for chronic stress (TICS) before wearing the Fitbit Charge3 sensor for seven consecutive days while maintaining their daily routine. Physiological and lifestyle features that were extracted from sensor data, alongside demographic features, were used to predict high versus low chronic stress with support vector machine classifiers, applying out-of-sample model testing. Results: The model achieved 79% classification accuracy for chronic stress from a social tension source. A mixture of physiological (resting heart-rate, heart-rate circadian characteristics), lifestyle (steps count, sleep onset and sleep regularity) and non-sensor demographic features (smoking status) contributed to this classification. Conclusion: As wearable technologies continue to rapidly evolve, integration of daily-life indicators could improve our understanding of chronic stress and its impact of physiology and behavior.

Fronto-striatal connectivity patterns account for the impact of methylphenidate on choice impulsivity among healthy adults.

Choice impulsivity depicts a preference towards smaller-sooner rewards over larger-delayed rewards, and is often assessed using a delay discounting (DD) task. Previous research uncovered the prominent role of dopaminergic signaling within fronto-striatal circuits in mediating choice impulsivity. Administration of methylphenidate (MPH), an indirect dopaminergic agonist, was shown to reduce choice impulsivity in animals and pathological populations, although significant inter-individual variability in these effects was reported. Whether MPH impacts choice impulsivity among healthy individuals, and whether variability in the impact of MPH is related to fronto-striatal activation and connectivity patterns, has yet to be assessed. Here, fifty-seven healthy young adults completed the DD task twice during fMRI scans, after acute administration of either MPH (20 mg) or placebo, in a randomized double-blind placebo-controlled design. Acute MPH administration was found to reduce choice impulsivity at the group level, yet substantial variability in this behavioral response was observed. MPH was also found to increase activation in the bilateral putamen and the right caudate, and to enhance functional connectivity between the left putamen and medial prefrontal cortex (mPFC), particularly during non-impulsive choices. Notably, the more putamen-mPFC functional connectivity increased during non-impulsive choices following MPH administration, the less an individual was likely to make impulsive choices. These findings reveal, for the first time in healthy adults, that acute MPH administration is associated with reduced choice impulsivity and increased striatal activation and fronto-striatal connectivity; and furthermore, that the magnitude of MPH-induced change in fronto-striatal connectivity may account for individual differences in the impact of MPH on impulsive behavior.

Assessment of early neurocognitive functioning increases the accuracy of predicting chronic PTSD risk.

Post-traumatic stress disorder (PTSD) is a protracted and debilitating consequence of traumatic events. Identifying early predictors of PTSD can inform the disorder's risk stratification and prevention. We used advanced computational models to evaluate the contribution of early neurocognitive performance measures to the accuracy of predicting chronic PTSD from demographics and early clinical features. We consecutively enrolled adult trauma survivors seen in a general hospital emergency department (ED) to a 14-month long prospective panel study. Extreme Gradient Boosting algorithm evaluated the incremental contribution to 14 months PTSD risk of demographic variables, 1-month clinical variables, and concurrent neurocognitive performance. The main outcome variable was PTSD diagnosis, 14 months after ED admission, obtained by trained clinicians using the Clinician-Administered PTSD Scale (CAPS). N = 138 trauma survivors (mean age = 34.25 ± 11.73, range = 18-64; n = 73 [53%] women) were evaluated 1 month after ED admission and followed for 14 months, at which time n = 33 (24%) met PTSD diagnosis. Demographics and clinical variables yielded a discriminatory accuracy of AUC = 0.68 in classifying PTSD diagnostic status. Adding neurocognitive functioning improved the discriminatory accuracy (AUC = 0.88); the largest contribution emanating from poorer cognitive flexibility, processing speed, motor coordination, controlled and sustained attention, emotional bias, and higher response inhibition, and recall memory. Impaired cognitive functioning 1-month after trauma exposure is a significant and independent risk factor for PTSD. Evaluating cognitive performance could improve early screening and prevention.

Neural Responsivity to Reward Versus Punishment Shortly After Trauma Predicts Long-Term Development of Posttraumatic Stress Symptoms.

BACKGROUND: Processing negatively and positively valenced stimuli involves multiple brain regions including the amygdala and ventral striatum (VS). Posttraumatic stress disorder (PTSD) is often associated with hyperresponsivity to negatively valenced stimuli, yet recent evidence also points to deficient positive valence functioning. It is yet unclear what the relative contribution is of such opposing valence processing shortly after trauma to the development of chronic PTSD. METHODS: Neurobehavioral indicators of motivational positive versus negative valence sensitivities were longitudinally assessed in 171 adults (87 females, age = 34.19 ± 11.47 years) at 1, 6, and 14 months following trauma exposure (time point 1 [TP1], TP2, and TP3, respectively). Using a gambling functional magnetic resonance imaging paradigm, amygdala and VS functionality (activity and functional connectivity with the prefrontal cortex) in response to rewards versus punishments were assessed with relation to PTSD severity at different time points. The effect of valence processing was depicted behaviorally by the amount of risk taken to maximize reward. RESULTS: PTSD severity at TP1 was associated with greater neural functionality in the amygdala (but not in the VS) toward punishments versus rewards, and with fewer risky choices. PTSD severity at TP3 was associated with decreased neural functionality in both the VS and the amygdala toward rewards versus punishments at TP1 (but not with risky behavior). Explainable machine learning revealed the primacy of VS-biased processing, over the amygdala, in predicting PTSD severity at TP3. CONCLUSIONS: These results highlight the importance of biased neural responsivity to positive relative to negative motivational outcomes in PTSD development. Novel therapeutic strategies early after trauma may thus target both valence fronts.

Cognitive and Behavioral Patterns across Psychiatric Conditions.

Psychiatric conditions represent a highly heterogeneous group of disorders associated with chronic distress and a sharp decline in quality of life [...].

Patient and Therapist In-Session Cortisol as Predictor of Post-Session Patient Reported Affect.

The importance of the role of affect in psychotherapy for major depressive disorder (MDD) is well established, but the common use of self-reported measures may limit our understanding of its underlying mechanisms. A promising predictor of patient affect is the stress hormone cortisol. To date, no studies have studied in-session changes in cortisol in psychotherapy for MDD. We investigated whether an increase in patient cortisol over the course of a session correlated with higher negative and lower positive affect. Given previous findings on healthy individuals on the contagious nature of stress, an additional aim was to examine whether these relationships are moderated by therapist cortisol. To this end, 40 dyads (including 6 therapists) provided saliva samples before and after four pre-specified sessions (616 samples). After each session, the patients provided retrospective reports of in-session affect. We found no association between patient cortisol and affect. However, increases in patient cortisol predicted negative affect when the therapists exhibited decreases in cortisol, and increases in patient cortisol predicted positive affect when the therapists showed increases. Our study provides initial evidence for the importance of the social context in the cortisol-affect relationship in MDD.

Now or Later? Stress-Induced Increase and Decrease in Choice Impulsivity Are Both Associated with Elevated Affective and Endocrine Responses.

Exposure to acute stress elicit physiological and psychological responses that can impact decision-making, often expressed as an increased tendency to act in an impulsive manner following stress. Delay discounting (DD) task has emerged as a reliable measure of impulsive behavior in the form of choice impulsivity (CI). Interestingly, studies that examined the effect of acute stress on DD performance reported mixed results. To address this, we conducted a within-subject examination of the impact of acute stress on CI, focusing on individual differences in response patterns. One hundred and fifty healthy female participants completed the DD task twice, before and after undergoing an acute laboratory stress induction procedure. Saliva samples and self-report mood and affect measures were collected at four time points throughout the session. Fifty-nine matched healthy control participants completed only the DD task twice, with no stress in between. Results indicate that the acute stress procedure elicited the expected effects of increased cortisol release and increased negative mood and affect, at the group level. With respect to DD, stress indeed increased CI at the group level, yet participants differed in the magnitude and direction of this effect. Interestingly, regression analysis revealed quadratic relations between stress-induced changes in CI and cortisol release. Indeed, dividing the sample into three sub-groups based on the impact of stress on CI revealed that, compared to participants that exhibited no substantial change in their CI following stress, participants that exhibited either stress-induced increase or decrease in their CI also exhibited more stress-induced cortisol release, as well as more negative affect. Taken together, these findings suggest that elevated physiological and psychological responses to stress are associated with either increased or decreased choice impulsivity, thus depicting quadratic relations between stress and impulsivity.