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We conduct a laboratory experiment among male participants to investigate whether rewarding schemes that depend on work performance—in particular, tournament incentives—induce more stress than schemes that are independent of performance—fixed payment scheme. Stress is measured over the entire course of the experiment at both the hormonal and psychological level. Hormonal stress responses are captured by measuring salivary cortisol levels. Psychological stress responses are measured by self-reported feelings of stress and primary appraisals. We find that tournament incentives induce a stress response whereas a fixed payment does not induce stress. This stress response does not differ significantly across situations in which winners and losers of the tournament are publically announced and situations in which this information remains private. Biological and psychological stress measures are positively correlated, i.e. increased levels of cortisol are associated with stronger feelings of stress. Nevertheless, neither perceived psychological stress nor elevated cortisol levels in a previous tournament predict a subsequent choice between tournaments and fixed payment schemes, indicating that stress induced by incentives schemes is not a relevant criterion for sorting decisions in our experiment. Finally, we find that cortisol levels are severely elevated at the beginning of the experiment, suggesting that participants experience stress in anticipation of the experiment per se, potentially due to uncertainties associated with the unknown lab situation. We call this the novelty effect.
Rationality is a fundamental pillar of Economics. It is however unclear if this assumption holds when decisions are made under stress. To answer this question, we design two laboratory experiments where we exogenously induce physiological stress in participants and test the consistency of their choices with economic rationality. In both experiments we induce stress with the Cold Pressor test and measure economic rationality by the consistency of participants’ choices with the Generalized Axiom of Revealed Preference (GARP). In the first experiment, participants delay the decision-making task for 20 min until the cortisol level peaks. We find significant differences in cortisol levels between the stressed group and the placebo group which, however, do not affect the consistency of choices with GARP. In a second experiment, we study the immediate effect of the stressor on rationality. Overall, results from the second experiment confirm that rationality is not impaired by the stressor. If anything, we observe that compared to the placebo group, participants are more consistent with rationality immediately after the stressor. Our findings provide strong empirical support for the robustness of the economic rationality assumption under physiological stress.
Many important decisions are made under stress and they often involve risky alternatives. There has been ample evidence that stress influences decision making, but still very little is known about whether individual attitudes to risk change with exposure to acute stress. To directly evaluate the causal effect of psychosocial stress on risk attitudes, we adopt an experimental approach in which we randomly expose participants to a stressor in the form of a standard laboratory stress-induction procedure: the Trier Social Stress Test for Groups. Risk preferences are elicited using a multiple price list format that has been previously shown to predict risk-oriented behavior out of the laboratory. Using three different measures (salivary cortisol levels, heart rate and multidimensional mood questionnaire scores), we show that stress was successfully induced on the treatment group. Our main result is that for men, the exposure to a stressor (intention-to-treat effect, ITT) and the exogenously induced psychosocial stress (the average treatment effect on the treated, ATT) significantly increase risk aversion when controlling for their personal characteristics. The estimated treatment difference in certainty equivalents is equivalent to 69 % (ITT) and 89 % (ATT) of the gender-difference in the control group. The effect on women goes in the same direction, but is weaker and insignificant.
Individual willingness to enter competitive environments predicts career choices and labor market outcomes. Meanwhile, many people experience competitive contexts as stressful. We use two laboratory experiments to investigate whether factors related to stress can help explain individual differences in tournament entry. Experiment 1 studies whether stress responses (measured as salivary cortisol) to taking part in a mandatory tournament predict individual willingness to participate in a voluntary tournament. We find that competing increases stress levels. This cortisol response does not predict tournament entry for men but is positively and significantly correlated with choosing to enter the tournament for women. In Experiment 2, we exogenously induce physiological stress using the cold-pressor task. We find a positive causal effect of stress on tournament entry for women but no effect for men. Finally, we show that although the effect of stress on tournament entry differs between the genders, stress reactions cannot explain the well-documented gender difference in willingness to compete.
This is the story of how I circuitously journeyed into my life’s work. I began as a music major, then thought I would be a music therapist, then decided on psychology as the major because I was better at it. A graduate school sojourn in Michigan, a fateful conversation with John Hagen, nabbing a summer research position with Eleanor Maccoby and spending the summer trying to scare babies with a cymbal-clapping monkey. Chutzpah! Telling Eleanor I would help with the next phase of their study if she made me a graduate student. From scaring babies to giving them control over a scary toy to realizing I was studying the key factor in stress regulation to cortisol to a seminar offered by Seymour Levine and the discovery of the field of developmental psychoneuroendocrinology. I was in my fourth year of graduate school before I knew where I was going. Take heart students. You will figure it out if you keep asking questions.
This study investigated the psychometric properties of the Highly Sensitive Child-Rating System (HSC-RS), the existence of sensitivity groups, and the characterization of sensitivity at behavioral, genetic, and physiological levels in 541 preschoolers (M(SD)age = 3.56(0.27); 45%male; 87%Caucasian). Temperament, genetic, cortisol, and electroencephalography asymmetry data were collected in subsamples (n = 94-476). Results showed a reliable observational measure of sensitivity. Confirmatory factor and latent class analysis supported a one-factor solution and three sensitivity groups, that are a low (23.3%), medium (54.2%), and a high (22.5%) sensitivity group. Hierarchical regression analyses showed moderate associations between HSC-RS and observed temperament traits (i.e., behavioral level). In addition, a small negative association between HSC-RS and a genome-wide association study polygenic risk score (GWAS PGS) for Attention Deficit Hyperactivity Disorder was found. No relations with candidate genes, other GWAS PGS phenotypes, and physiological measures were found. Implications of our findings and possible explanations for a lack of these associations are discussed.
Using [18F]altanserin, a serotonin 2A receptor (5-HT2AR) antagonist Positron Emission Tomography (PET) tracer, a positive association between cortical 5-HT2AR binding and the inward-directed facets of neuroticism has been demonstrated in healthy individuals. Psilocybin, a 5-HT2AR agonist, shows promise for the treatment of depression, reducing neuroticism and mood symptoms potentially via hypothalamic-pituitary-adrenal (HPA) modulation. 5-HT2AR and neuroticism are both modulated by HPA axis function.
Aims
In this study, we examined whether the association between 5-HT2AR binding and the inward facets of neuroticism can be replicated in an independent healthy cohort using the new 5-HT2AR agonist tracer [11C]Cimbi-36, and if their association is moderated by cortisol awakening response (CAR), an index of HPA axis function. If so, this could advance mechanistic insights into interventions that target the 5-HT2AR and reduce neuroticism.
Method
Eighty healthy volunteers underwent [11C]Cimbi-36 PET scans and completed the NEO personality inventory (NEO-PI-R) for the assessment of neuroticism. Salivary samples were available for determination of CAR in 70 of the participants. Using linear latent variable models, we evaluated the association between 5-HT2AR binding and inward facets of neuroticism, namely depression, anxiety, self-consciousness and vulnerability to stress, and whether CAR moderated this association.
Results
The study confirms the positive association between 5-HT2AR binding and the inward facets of neuroticism (β = 0.01, 95% CI = [0.0005: 0.02], P = 0.04), and this association is independent of CAR (P = 0.33).
Conclusions
The findings prompt consideration of whether novel interventions such as psilocybin that actively targets 5-HT2AR and causes changes in personality could be particularly beneficial if implemented as a targeted approach based on neuroticism profiles.
Despite the added value of multisystem (relative to traditional single-system) approaches for characterizing biological processes linked to risk for psychopathology (e.g., neuroendocrine stress responsivity; Buss et al., 2019; Quas et al., 2014), no study to date has evaluated whether multisystem processes may serve as viable biological targets of intervention. Utilizing a multiple-levels-of-analysis approach (Cicchetti & Dawson, 2002), this person-centered study examined whether stress-adapted patterns of hypothalamus–pituitary–adrenal (HPA) axis and sympathetic-adrenomedullary (SAM) system co-activation were amenable to change following the Building a Strong Identity and Coping Skills intervention (BaSICS; Wadsworth et al., 2022). Preadolescents exposed to concentrated poverty (n = 112, Mage = 11.78 years, 57.1% female, 54% assigned to intervention; 40% Hispanic, 63% Black, 20% White) completed questionnaires and the Trier Social Stress Test at both pre- and posttest. Multitrajectory modeling of cortisol and alpha-amylase levels identified four pretest and posttest HPA-SAM co-activation profiles. At pretest, youth exhibiting Asymmetric Nos. 1 & 2 HPA-SAM co-activation reported greater maladjustment relative to youth with Symmetric Nos. 1 & 2 co-activation. Youth exhibiting Asymmetric No. 1 co-activation at pretest were more likely to exhibit Symmetric No. 1 co-activation following BaSICS relative to control. Findings highlight the potential of BaSICS to restore neuroendocrine stress response function in impoverished youth, pointing to HPA–SAM co-activation as a potential biological target of preventive intervention in this population.
The endorsement of conspiracy theories may be increased by subjectively perceived stress. Yet, it is not known whether this correlation is caused by the effects of the acute stress reaction on the brain or other psychological, social, or methodological factors. The effect of an experimentally induced acute stress reaction on conspiracy thinking was tested on a sample (n = 115) of students of medicine. Although the stress procedure caused a substantial increase in salivary cortisol, there was no significant effect on endorsing conspiracy theories or adopting conspiracy interpretations of novel information. The results confirmed no effect of the acute stress reaction on conspiracy thinking, suggesting it may be absent or weaker than expected. The study demonstrated the viability of psychophysiological experimental design in conspiracy research and may inspire further examination of the physiological mechanisms underlying susceptibility to conspiracy theories.
Terrorism and trauma survivors often experience changes in biomarkers of autonomic, inflammatory and hypothalamic-pituitary-adrenal (HPA) axis assessed at various times. Research suggests interactions of these systems in chronic stress.
Study Objective:
This unprecedented retrospective study explores long-term stress biomarkers in three systems in terrorism survivors.
Methods:
Sixty healthy, direct terrorism survivors were compared to non-exposed community members for cardiovascular reactivity to a trauma script, morning salivary cortisol, interleukin 1-β (IL-1β), and interleukin 2-R (IL-2R). Survivors’ biomarkers were correlated with psychiatric symptoms and diagnoses and reported functioning and well-being seven years after the Oklahoma City (OKC) bombing.
Main outcome measures were the Diagnostic Interview Schedule (DIS) Disaster Supplement for Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) diagnoses, Impact of Events Scale-Revised (IES-R), Beck Depression Inventory-II (BDI-II), Distress and Functioning Scale (DAF), and General Physical Well-Being Scale.
Results:
Survivors had higher inflammatory IL-1β, lower anti-inflammatory IL-2R, lower cortisol, higher resting diastolic blood pressure (BP), and less cardiovascular reactivity to a trauma script than comparisons. Survivors’ mean posttraumatic stress (PTS) symptom levels did not differ from comparisons, but survivors reported worse well-being. None of survivors’ biomarkers correlated with PTS or depressive symptoms or diagnoses or reported functioning.
Conclusions:
Alterations of biological stress measures in cardiovascular, inflammatory, and cortisol systems coexisted as an apparent generalized long-term response to terrorism rather than related to specific gauges of mental health. Potential interactions of biomarkers long after trauma exposure is discussed considering relevant research. Longer-term follow-up could determine whether biomarkers continue to differ or correlate with subjective measures, or if they accompany health problems over time. Given recent international terrorism, understanding long-term sequelae among direct survivors is increasingly relevant.
Depressive disorders in adolescents affect all aspects of life and impose a very large burden of disease. Sleep is frequently affected by depression and is crucial for facing challenges during development. One of the postulated reasons for depression-induced sleep disruption is dysregulation of the physiological stress system.
Aims
To investigate the links of adolescent depressive disorders with subjective sleep quality, objective sleep quality, and the course of cortisol and alpha-amylase after awakening.
Method
We compared subjective sleep quality (via daily questionnaires) and objective sleep quality (via actigraphy measurement) of 35 adolescents with depressive disorders and 29 healthy controls over 7 consecutive days. In addition, saliva samples were collected on 3 days to examine cortisol and alpha-amylase patterns after awakening.
Results
No significant differences in cortisol or alpha-amylase awakening responses were observed between participants with depressive disorders and healthy controls. We found severe reductions in subjective sleep quality in the depression group (Z = −5.19, P < 0.001, d = 1.80) and a prolonged actigraphy-measured sleep onset latency (Z = −2.42, P = 0.015, d = 0.64) compared with controls. Reductions in subjective sleep quality were partially correlated with objective sleep measures (sleep onset latency: r = −0.270, P = 0.004, sleep efficiency: r = 0.215, P = 0.017).
Conclusions
Sleep onset latency seems to aggravate depressive symptoms and to have an important role in perception of sleep quality. Adolescents with depressive disorders should be supported regarding the establishment of good sleep hygiene and avoiding activities that may impede falling asleep.
High-risk pregnancies elevate maternal stress, impacting offspring neurodevelopment and behavior. This study, involving 112 participants, aimed to compare perceived stress, neurodevelopment, and behavior in high-risk and low-risk pregnancies. Two groups, high-risk and low-risk, were assessed during pregnancy for stress using hair cortisol and psychological analysis. At 24 months post-birth, their children’s neurodevelopment and behavior were evaluated. Results revealed higher perceived stress and pregnancy-related concerns in high-risk pregnancies, contrasting with low-risk pregnancies. Offspring from high-risk pregnancies displayed elevated internalizing behavior scores, while low-risk pregnancies showed higher externalizing behavior scores. Additionally, women in low-risk pregnancies exhibited increased cortisol concentrations 24 months post-delivery. These findings underscore the necessity for early stress detection and prevention programs during pregnancy, particularly in high-risk cases, to enhance maternal and infant health.
Dante Cicchetti’s remarkable contributions to the field of developmental psychopathology include the advancement of key principles such as the interplay of typical and atypical development, multifinality and equifinality, the dynamic processes of resilience, and the integration of multiple levels of analysis into developmental theories. In this paper we assert that person-centered data analytic methods are particularly well-suited to advancing these tenets of developmental psychopathology. We illustrate their utility with a brief novel empirical study focused on underlying patterns of childhood neuroendocrine regulation and prospective links with emerging adult functioning. Results indicate that a childhood neuroendocrine profile marked by high diurnal cortisol paired with low diurnal DHEA was uniquely associated with more adaptive functioning in emerging adulthood. We discuss these findings, and person-centered methods more broadly, within the future of developmental psychopathology.
Adrenal insufficiency can be either primary, resulting from destruction of the adrenal gland, or secondary, resulting from a deficiency of ACTH (adrenocorticotropic hormone, corticotropin).
Adrenal crisis is either the acute development of severe adrenal insufficiency or a rapid deterioration from baseline chronic adrenal insufficiency (which is often insidious) brought on by a stressor.
The adrenal gland (made up of cortex and medulla) produces three categories of steroids: glucocorticoids (cortisol), mineralocorticoids (aldosterone) and gonadocorticoids (sex hormones). Aldosterone levels change in response to volume status and sodium intake. Aldosterone maintains sodium and potassium concentration and regulates water balance.
Suicide is a complex public health problem driven by a multitude of biopsychosocial factors and is the result of gene–environment interactions. Psychosocial variables like chronic stress and trauma have biologic ramifications and can contribute to various forms of pathophysiology, dysregulation, and degradation, represented by allostatic load (AL). AL is the wear and tear that stress exerts on the body, and it has been associated with mental health problems and suicide. Fortunately, there are pharmacological and non-pharmacological interventions that may be effective at reducing AL and reversing its effects. Incorporating AL into efforts to promote early risk identification, prevention, and treatment of suicide is an important consideration. Critical next steps are identifying which AL biomarkers are most malleable, which effective treatments reduce AL, and if these reductions of AL are associated with decreased suicide.
Preliminary evidence shows that discordance in stress experience, expression, and physiology (EEP) in adolescents is linked to depression, suicidal ideation (SI), non-suicidal self-injury (NSSI), and brain functioning. This study employs person-centered analysis to probe the relationship between stress responses, psychopathology, and neural patterns in female adolescents who are oversampled for engagement in NSSI.
Methods
Adolescent females (N = 109, ages 12–17) underwent a social stress test from which self-report measures of stress experience, observer ratings of stress expression, and physiological metrics of stress (via salivary cortisol) were obtained. Multi-trajectory modeling was employed to identify concordant and discordant stress EEP groups. Depressive symptoms, SI and attempt, NSSI engagement, frontal and limbic activation to emotional stimuli, and resting state fronto-limbic connectivity were examined in the EEP groups derived from the multi-trajectory models.
Results
Four groups were identified, three of which demonstrated relatively concordant EEP and one which demonstrated discordant EEP (High Experience-High Expression-Low Physiology). Further, replicating past research, the High Experience-High Expression-Low Physiology discordant group exhibited higher depressive symptoms, SI, suicide attempt, and NSSI episodes (only for sensitivity analyses based on past year) relative to other EEP groups. No significant group differences in brain functioning emerged.
Conclusion
Results indicate that within-person, multi-level patterns in stress responding capture risk for dysfunction including depression and self-injurious thoughts and behaviors. Further interrogating of system-level stress functioning may better inform assessment and intervention efforts.
Increasing age and puberty affect the hypothalamic pituitary adrenal (HPA) axis maturation, which is likely associated with an increase in environmental demands (e.g., social) and vulnerability for the onset of psychiatric conditions (e.g., depression). There is limited research as to whether such patterns are consonant in youth with autism spectrum disorder (ASD), a condition marked by social challenges, dysregulation of the HPA axis, and higher rates of depression setting the stage for enhanced vulnerability during this developmental period.
The current study interrogated diurnal cortisol by examining (1) cortisol expression longitudinally over the pubertal transition between autistic and neurotypical youth, (2) the trajectory of diurnal cortisol and the unique contributions of age vs. puberty, and (3) potential sex differences. As hypothesized, results indicate autistic compared to typically developing youth demonstrate a shallower diurnal slope and elevated evening cortisol. These differences were in the context of higher cortisol and flatter rhythms based on age and pubertal development. Also, sex-based differences emerged such that females in both groups had higher cortisol, flatter slopes, and higher evening cortisol than males. The results show that despite the trait-like stability of diurnal cortisol, HPA maturation is impacted by age, puberty, sex, as well as an ASD diagnosis.
A blunted hypothalamic–pituitary–adrenal (HPA) axis response to acute stress is associated with psychiatric symptoms. Although the prefrontal cortex and limbic areas are important regulators of the HPA axis, whether the neural habituation of these regions during stress signals both blunted HPA axis responses and psychiatric symptoms remains unclear. In this study, neural habituation during acute stress and its associations with the stress cortisol response, resilience, and depression were evaluated.
Methods
Seventy-seven participants (17–22 years old, 37 women) were recruited for a ScanSTRESS brain imaging study, and the activation changes between the first and last stress blocks were used as the neural habituation index. Meanwhile, participants' salivary cortisol during test was collected. Individual-level resilience and depression were measured using questionnaires. Correlation and moderation analyses were conducted to investigate the association between neural habituation and endocrine data and mental symptoms. Validated analyses were conducted using a Montreal Image Stress Test dataset in another independent sample (48 participants; 17–22 years old, 24 women).
Results
Neural habituation of the prefrontal cortex and limbic area was negatively correlated with cortisol responses in both datasets. In the ScanSTRESS paradigm, neural habituation was both positively correlated with depression and negatively correlated with resilience. Moreover, resilience moderated the relationship between neural habituation in the ventromedial prefrontal cortex and cortisol response.
Conclusions
This study suggested that neural habituation of the prefrontal cortex and limbic area could reflect motivation dysregulation during repeated failures and negative feedback, which might further lead to maladaptive mental states.
Childhood adversity has been associated with hypothalamic–pituitary–adrenal axis dysregulation, which is associated with mental and physical health consequences. However, associations between childhood adversity and cortisol regulation in the current literature vary in magnitude and direction. This multilevel meta-analysis examines the association between childhood adversity and diurnal cortisol measures, as well as potential moderators of these effects (adversity timing and type, study or sample characteristics). A search was conducted in online databases PsycINFO and PubMed for papers written in English. After screening for exclusion criteria (papers examining animals, pregnant women, people receiving hormonal treatment, people with endocrine disorders, cortisol before age 2 months, or cortisol after an intervention), 303 papers were identified for inclusion. In total, 441 effect sizes were extracted from 156 manuscripts representing 104 studies. A significant overall effect was found between childhood adversity and bedtime cortisol, r = 0.047, 95% CI [0.005, 0.089], t = 2.231, p = 0.028. All other overall and moderation effects were not significant. The lack of overall effects may reflect the importance of the timing and nature of childhood adversity to adversity’s impact on cortisol regulation. Thus, we offer concrete recommendations for testing theoretical models linking early adversity and stress physiology.