Our study proposes to examine how stress and emotion recognition interact with a history of maltreatment to influence sensitive parenting behaviors. A sample of 58 mothers and their children aged between 2 and 5 years old were recruited. Parents’ history of maltreatment was measured using the Child Trauma Questionnaire. An emotion recognition task was performed. Mothers identified the dominant emotion in morphed facial emotion expressions in children. Mothers and children interacted for 15 minutes. Salivary cortisol levels of mothers were collected before and after the interaction. Maternal sensitive behaviors were coded during the interaction using the Coding Interactive Behavior scheme. Results indicate that the severity of childhood maltreatment is related to less sensitive behaviors for mothers with average to good abilities in emotion recognition and lower to average increases in cortisol levels following an interaction with their children. For mothers with higher cortisol levels, there is no association between a history of maltreatment and sensitive behaviors, indicating that higher stress reactivity could act as a protective factor. Our study highlights the complex interaction between individual characteristics and environmental factors when it comes to parenting. These results argue for targeted interventions that address personal trauma.

This multi-method longitudinal study evaluated how changes in maternal sensitive parenting may operate as an indirect factor linking family instability and the development of child externalizing problems over time. This study also investigated how mothers’ stress reactivity within the sympathetic nervous system (SNS) may moderate the association between family instability and the development of maternal sensitivity. Participants were 235 families with a young child (Mage = 2.97 years at the first measurement occasion) and these families were followed for two annual measurement occasions. Maternal sensitivity was observed during two discipline tasks (i.e., forbidden toy, discipline discussion tasks), and maternal SNS stress reactivity was indicated by their salivary alpha-amylase (sAA) reactivity to an interpersonal stressor. Findings revealed significant direct effects of family instability and family instability-x-sAA reactivity interaction in association with the change in maternal sensitivity over time. For both tasks, mothers with greater sAA reactivity exhibited stronger associations between family instability and the growth of their sensitivity. Tests of indirect effects indicated that change in maternal sensitivity operated as an indirect factor between family instability-x-sAA reactivity interaction and the change in child externalizing problems. The present findings have important implications for understanding parental and child sequelae associated with unstable family contexts.

Cross-species evidence suggests that the ability to exert control over a stressor is a key dimension of stress exposure that may sensitize frontostriatal-amygdala circuitry to promote more adaptive responses to subsequent stressors. The present study examined neural correlates of stressor controllability in young adults. Participants (N = 56; M age = 23.74, range = 18–30 years) completed either the controllable or uncontrollable stress condition of the first of two novel stressor controllability tasks during functional magnetic resonance imaging (fMRI) acquisition. Participants in the uncontrollable stress condition were yoked to age- and sex-matched participants in the controllable stress condition. All participants were subsequently exposed to uncontrollable stress in the second task, which is the focus of fMRI analyses reported here. A whole-brain searchlight classification analysis revealed that patterns of activity in the right dorsal anterior insula (dAI) during subsequent exposure to uncontrollable stress could be used to classify participants' initial exposure to either controllable or uncontrollable stress with a peak of 73% accuracy. Previous experience of exerting control over a stressor may change the computations performed within the right dAI during subsequent stress exposure, shedding further light on the neural underpinnings of stressor controllability.

Narcissism is a Janusian personality construct, associated with both grandiose self-assuredness and dominance, as well as vulnerable insecurity and reactivity. Central questions of intra- and interpersonal functioning in narcissism are still a matter of debate. Neuroscience could help to understand the paradoxical patterns of experience and behavior beyond the limitations of self-reports. We provide a systematic review of 34 neuroscience studies on grandiose, vulnerable, pathological narcissism, and Narcissistic Personality Disorder (NPD), spanning experimental investigations of intra- and interpersonal mechanisms, research on neurophysiological and neuroendocrine aspects of baseline function, and brain structural correlates. While neuroscience has scarcely directly studied vulnerable narcissism, grandiose narcissism is associated with heightened vigilance to ego threat and stress responses following ego threat, as well as heightened stress indicators in baseline measures. Such responses are not commonly observed in self-reports, highlighting the potential of neuroscience to augment our understanding of self-regulatory dynamics in narcissism. Interpersonal functioning is characterized by deficits in social–affective processes. Both involve altered activity within the salience network, pointing to a double dissociation regarding the expression of narcissism and self/other oriented situational focus. Findings are summarized in an integrative model providing testable hypotheses for future research along with methodological recommendations.

Neuroticism is associated with increased stress reactivity. In autism spectrum disorders (ASD), emotional stress reactivity is increased and there is some evidence for an increased negative affect (NA) when with less familiar people. The aim of this study was to compare adults with ASD and controls on levels of neuroticism and on interactions between neuroticism and appraised stress or social context in models of NA. This is a cross-sectional observational study comprising a group of 50 adults with ASD and 51 controls. Experience sampling method (ESM) reports were collected for 10 days to measure daily life stress, mood, and social context. Multilevel regression analyses revealed significantly higher neuroticism levels in ASD than in controls. Adults with ASD who scored high on neuroticism showed a significantly stronger association between activity/social stress and NA (i.e., higher stress reactivity) than those with low scores. Furthermore, the association between neuroticism and NA was stronger when adults with ASD were with less familiar people compared with being alone or with familiar people. No consistent corresponding significant interactions were found in the control group. In conclusion, in ASD, neuroticism moderates the association between appraised stress and NA as well as the association between social context and NA.

Children who spend their early lives in institutions experience profound psychosocial deprivation that is associated with altered stress response system development. Here, we used data from a longitudinal randomized controlled trial of foster care for institutionally reared children to examine whether caregiving quality and stressful life events (SLEs) in early adolescence (age 12) influence patterns of hypothalamic–pituitary–adrenal (HPA) axis and sympathetic nervous system (SNS) reactivity. Controlling for the effect of institutional care, higher caregiving quality at age 12 was associated with heightened cortisol and SNS reactivity. However, moderation analysis revealed that the latter effect was only observed among never-institutionalized children, whereas ever-institutionalized children demonstrated a persistently blunted SNS response regardless of recent caregiving quality. Among institutionally reared children, SLEs interacted with prior random assignment to foster care, such that those placed in foster care early in development had a SNS response that approximated never-institutionalized children when SLEs at age 12 were low. In contrast, SNS reactivity was persistently blunted among those with prolonged deprivation, regardless of recent SLEs. Early-life deprivation is associated with persistent blunting of stress response systems, but normalization may be achievable if SLEs are limited following placement into enriched family-based care.

We conducted signal detection analyses to test for curvilinear, U-shaped relations between early experiences of adversity and heightened physiological responses to challenge, as proposed by biological sensitivity to context theory. Based on analysis of an ethnically diverse sample of 338 kindergarten children (4–6 years old) and their families, we identified levels and types of adversity that, singly and interactively, predicted high (top 25%) and low (bottom 25%) rates of stress reactivity. The results offered support for the hypothesized U-shaped curve and conceptually replicated and extended the work of Ellis, Essex, and Boyce (2005). Across both sympathetic and adrenocortical systems, a disproportionate number of children growing up under conditions characterized by either low or high adversity (as indexed by restrictive parenting, family stress, and family economic condition) displayed heightened stress reactivity, compared with peers growing up under conditions of moderate adversity. Finally, as hypothesized by the adaptive calibration model, a disproportionate number of children who experienced exceptionally stressful family conditions displayed blunted cortisol reactivity to stress.

The interaction of physical and mental vulnerability and environmental constraints is thought to foster the development of psychiatric disorders such as major depressive disorder (MDD). A central factor in the development of psychopathology is mental stress. Despite some evidence for parasympathetic withdrawal and sympathetic overactivity in MDD, the psychophysiological response to stress in depression is not clear-cut. Given the growing interest in heart rate and heart rate variability as indicators for remote monitoring of patients, it is important to understand how patients with MDD react to stress in a laboratory-controlled environment. We conducted a systematic review of studies using electrocardiography to derive heart rate and heart rate variability during stress in patients with clinical depression. We focused on well-validated stress tasks- the mental arithmetic stress task, the Trier social stress task and public speaking task- to minimize confounding effects due to the nature of the stressor. The majority of studies found hypo-reactivity during stress as a hallmark of depression as evidenced by lower fluctuation in heart rate and heart rate variability in the high-frequency band. We address the potential underlying biological mechanisms, the influence of covariates on these measures and briefly discuss the specificity and potential for remote monitoring by using these variables.

We report on life course stress determinants of overweight in children, using data from the longitudinal follow-up of the nested case–control arm of the SAGE (study of asthma genes and the environment) birth cohort in Manitoba, Canada. Waist and hip measurements were obtained during a clinic visit at age 9–11 years. Multiple linear regression was conducted to determine the relationship between the waist-to-hip ratio and maternal smoking during pregnancy, postpartum maternal distress and stress reactivity in children (cortisol, cortisol-DHEA [dihydroepiandrostrenone] ratio quartiles) following a clinic stressor at age 8–10 years. We found waist-to-hip risk at age 9–11 years to be elevated among boys and girls whose mothers had experienced distress in the postnatal period. This association varied by gender and asthma status. In healthy girls, postpartum distress increased waist-to-hip ratio by a factor of 0.034 (P < 0.01), independent of the child's stage of puberty and adrenarche, cortisol-DHEA ratio and duration of exclusive breastfeeding. Among girls with asthma, maternal smoking during pregnancy was associated with an increased waist-to-hip ratio, if the mother also experienced distress in the postpartum period (0.072, P = 0.038). Among asthmatic boys, an association between maternal distress and waist-to-hip ratio was evident at the highest cortisol-DHEA ratios. Stress-induced changes to leptin and infant over-eating pathways were proposed to explain the postnatal maternal distress effects. Drawing on the theories of evolutionary biology, our findings underscore the significance of postnatal stress in disrupting hypothalamic–pituitary–adrenal axis function in infants and increasing risk for child overweight.

Acute stress elevates blood lipids, with the largest increases among men and postmenopausal women. The mechanisms for the effect are unknown, but may be due to altered lipid metabolism. This study investigated if acute stress induces transient reductions in triglyceride clearance in middle-aged men and women, and determined if gender and menopause affect triglyceride metabolism. Of the 35 women, half were premenopausal, and half were naturally postmenopausal; men (n = 35) were age matched. Clearance of an intravenously administered fat emulsion was assessed twice: once during a nonstress session, and again during a stress-testing session. During the stress session, a battery of behavioral stressors (serial subtraction, speech, mirror tracing, and Stroop) were performed for 40 min. The clearance rate of exogenous fat was significantly diminished during the stress, relative to the nonstress session. Women had more efficient clearance, relative to men, but there were no effects of menopausal status. The diminished ability to clear an intravenous fat emulsion during stress suggests one mechanism for stress-induced elevations in lipids.

Arterialized and venous blood was compared to determine if the arterialization procedure enhances the detection of stress-related changes in catecholamines. Lipid and hematologic measures were also compared for possible distortion by arterialization. Fifteen men completed two stressors. Indwelling venous catheters were placed retrograde in each hand, and the right hand was warmed to a constant temperature. Blood samples were taken simultaneously from both hands, and plasma catecholamines were determined. Arterialization increased baseline epinephrine; there were no effects of arterialization on catecholamines during stress, nor in lipid or hematologic measures during baseline or stress. Thus, arterialization of blood results in small increases in resting epinephrine levels, but does not obscure lipid measures. More importantly, arterialization of venous blood does not enhance the detection of stress-related changes in catecholamines.