Journal: Stress (Amsterdam, Netherlands)
Experiences during early life are suggested to affect the physiological systems underlying stress responses, including the hypothalamic-pituitary-adrenal axis (HPA axis). While stressful early experiences have been associated with dysregulated HPA-axis functioning, positive early experiences, i.e. high maternal caregiving quality, contribute to more optimal HPA-axis functioning. Influences of other early caregiving factors, however, are less well documented. The goal of this study was to examine whether breastfeeding and co-sleeping during the first 6 months of life were associated with infant cortisol regulation, i.e. cortisol reactivity and recovery, to a stressor at 12 months of age. Participants were 193 infants and their mothers. Information on breastfeeding and co-sleeping was collected using weekly and daily sleep diaries, respectively, for the first 6 months of life. Co-sleeping was defined as sleeping in the parents' bed or sleeping in the parents' room. At 12 months of age, infants were subjected to a psychological stressor [Strange Situation Procedure (SSP); Ainsworth et al. 1978]. Salivary cortisol was measured prestressor and at 25, 40, and 60 min poststressor to measure reactivity and recovery. Regression analyses showed that after controlling for maternal sensitivity, infant attachment status, feeding, and sleeping arrangements at 12 months of age and other confounders, more weeks of co-sleeping predicted lower infant cortisol reactivity to the SSP. Also, more weeks of breastfeeding predicted quicker cortisol recovery. These results indicate that an early history of co-sleeping and breastfeeding contributes positively to cortisol regulation in 12-month-olds.
Abstract Acute psychological stress has primarily been investigated regarding its effects on conventional lymphocytes such as natural killer (NK) cells and CD4(+) and CD8(+) T cells. However, it might be important, to focus on more “specialized” lymphocyte subsets, playing a role, for instance, in allergic conditions and autoimmunity, to identify links between stress, the immune system, and somatic diseases. Using flow cytometry we determined frequencies of circulating T helper (Th)1- (CD226(+)) and Th2-type (CRTH2(+)) T cells, γδ T cells, conventional CD56(+) natural killer T (NKT) cells, and invariant NKT cells (iNKT) in healthy young males (N=31; median age 26 years) undergoing a laboratory computer-based stressor lasting 12 minutes. We found that acute psychological stress induced a prolonged increase in CD4(+) and CD8(+) T cells expressing a Th2 phenotype. We also detected an acute increase in CD4- and CD8-double negative γδ T cells. Finally, we found that the well-known increase in NK cells under stressful conditions was paralleled by a significant increase in numbers of conventional CD56(+) NKT cells. In contrast, numbers of iNKT was not altered by stress. This study adds further evidence to a psychoneuroimmunological model proposing that under stressful conditions certain lymphocyte subsets, including iNKT and less mature T cells, are retained in lymphoid tissues while antigen-experienced effector-type T cells with a Th2 phenotype, γδ T cells, and conventional CD56(+) NKT cells are mobilized into the peripheral blood. We suggest that in case of frequent stress exposure this might result in the promotion of, for example, allergic conditions.
Given the well-documented deleterious health effects, poor sleep has become a serious public health concern and increasing efforts are directed toward understanding underlying pathways. One potential mechanism may be stress and its biological correlates; however, studies investigating the effects of poor sleep on a body’s capacity to deal with challenges are lacking. The current study thus aimed at testing the effects of sleep quality and quantity on cortisol responses to acute psychosocial stress. A total of 73 college-aged adults (44 females) were investigated. Self-reported sleep behavior was assessed via the Pittsburgh Sleep Quality Index and salivary cortisol responses to the Trier Social Stress Test were measured. In terms of sleep quality, we found a significant three-way interaction, such that relative to bad sleep quality, men who reported fairly good or very good sleep quality showed blunted or exaggerated cortisol responses, respectively, while women’s stress responses were less dependent on their self-reported sleep quality. Contrarily, average sleep duration did not appear to impact cortisol stress responses. Lastly, participants who reported daytime dysfunctions (i.e. having trouble staying awake or keeping up enthusiasm) also showed a trend to blunted cortisol stress responses compared to participants who did not experience these types of daytime dysfunctions. Overall, the current study suggests gender-specific stress reactivity dysfunctions as one mechanism linking poor sleep with detrimental physical health outcomes. Furthermore, the observed differential sleep effects may indicate that while the body may be unable to maintain normal hypothalamic-pituitary-adrenal functioning in an acute psychosocial stress situation after falling prey to low sleep quality, it may retain capacities to deal with challenges during extended times of sleep deprivation.
Abstract Hormesis is the process by which small stresses build resilience to large stresses. We pre-exposed rats to various parameters of mild-to-moderate stress prior to traumatic stress in the present experiments to assess the potential benefits of hormetic training on resilience to traumatic, uncontrollable stress. Rats underwent varying stress pre-training parameters prior to exposure to uncontrollable traumatic stress in the learned helplessness procedure. The ability to prevent the exaggerated fear responding and escape deficits that normally follow experience with traumatic stress were used as a measure of the benefits of hormetic training. Four experiments examined the effects of number of training sessions, stressor severity, and pattern of rest between pre-training stress sessions. Repeated exposure to mild restraint stress or moderate shock stress eliminated both the enhanced fear conditioning and shuttle-escape deficits that result from exposure to traumatic, inescapable shock. The pattern of rest did not contribute to resilience when the pre-exposure stressor was mild, but was vital when the pre-exposure stressor was moderate, with an alternation of stress and rest being the most effective procedure. The data also suggests that the level of resilience may increase with the number of pre-exposure sessions.
For centuries philosophical and clinical studies have emphasized a fundamental dichotomy between emotion and cognition, as, for instance, between behavioral/emotional memory and explicit/representative memory. However, the last few decades cognitive neuroscience have highlighted data indicating that emotion and cognition, as well as their underlying neural networks, are in fact in close interaction. First, it turns out that emotion can serve cognition, as exemplified by its critical contribution to decision-making or to the enhancement of episodic memory. Second, it is also observed that reciprocally cognitive processes as reasoning, conscious appraisal or explicit representation of events can modulate emotional responses, like promoting or reducing fear. Third, neurobiological data indicate that reciprocal amygdalar-hippocampal influences underlie such mutual regulation of emotion and cognition. While supporting this view, the present review discusses experimental data, obtained in rodents, indicating that the hippocampal and amygdalar systems not only regulate each other and their functional outcomes, but also qualify specific emotional memory representations through specific activations and interactions. Specifically, we review consistent behavioral, electrophysiological, pharmacological, biochemical and imaging data unveiling a direct contribution of both the amygdala and hippocampal-septal system to the identification of the predictor of a threat in different situations of fear conditioning. Our suggestion is that these two brain systems and their interplay determine the selection of relevant emotional stimuli, thereby contributing to the adaptive value of emotional memory. Hence, beyond the mutual quantitative regulation of these two brain systems described so far, we develop the idea that different activations of the hippocampus and amygdala, leading to specific configurations of neural activity, qualitatively impact the formation of emotional memory representations, thereby producing either adaptive or maladaptive fear memories.
Abstract Ethnic minority groups across the world face a complex set of adverse social and psychological challenges linked to their minority status, often involving racial discrimination. Racial Discrimination is increasingly recognised as an important contributing factor to health disparities among non-dominant ethnic minorities. A growing body of literature has recognised these health disparities and has investigated the relationship between racial discrimination and poor health outcomes. Chronically elevated cortisol levels and a dysregulated hypothalamic-pituitary-adrenal (HPA) axis appear to mediate effects of racial discrimination on allostatic load and disease. Racial discrimination seems to converge on the anterior cingulate cortex (ACC) and may impair the function of the prefrontal cortex (PFC), hence showing substantial similarities to chronic social stress. This review provides a summary of recent literature on hormonal and neural effects of racial discrimination and a synthesis of potential neurobiological pathways by which discrimination affects mental health.
This study explored the association between the acute psychobiological stress response, chronic social overload and amniotic fluid corticotropin corticotropin-releasing hormone (CRH) and urocortin (UCN) in 34 healthy, second-trimester pregnant women undergoing amniocentesis. The study further examined the predictive value of second-trimester amniotic fluid CRH and UCN for fetal growth and neonatal birth outcome. The amniocentesis served as a naturalistic stressor, during which maternal state anxiety and salivary cortisol was measured repeatedly and an aliquot of amniotic fluid was collected. The pregnant women additionally completed a questionnaire on chronic social overload. Fetal growth parameters were obtained at amniocentesis using fetal ultrasound biometry and at birth from medical records. The statistical analyses revealed that the acute maternal psychobiological stress response was unassociated with the amniotic fluid peptides, but that maternal chronic overload and amniotic CRH were positively correlated. Moreover, amniotic CRH was negatively associated with fetal size at amniocentesis and positively with growth in size from amniocentesis to birth. Hardly any studies have previously explored whether acute maternal psychological stress influences fetoplacental CRH or UCN levels significantly. Our findings suggest that 1) chronic, but not acute maternal stress may affect fetoplacental CRH secretion and that 2) CRH is complexly involved in fetal growth processes as previously shown in animals.
Behavioural coping strategies represent a key means by which people regulate their stress levels. Attention has recently focused on the potential role in coping of ‘displacement behaviour’ - activities such as scratching, lip biting and face touching. Increased levels of displacement behaviour are associated with feelings of anxiety and stress; however, the extent to which displacement behaviour, as a short-term behavioural response to emotionally challenging stimuli, influences the subsequent experience of stress remains poorly understood. The aim of this study was to investigate the potential role of displacement behaviour in coping with stress. In a study population of 42 healthy adult men (mean age = 28.09 years, SD = 7.98), we quantified displacement behaviour during a Trier Social Stress Test (TSST), and used self-report questionnaires to assess trait and state anxiety before the TSST, and the experience of stress afterwards. We predicted displacement behaviour would diminish the negative impact of the stressful situation, and hence be associated with lower post-TSST stress levels. Furthermore, we predicted displacement behaviour would mediate the link between state and trait anxiety on the one hand and the experience of stress on the other. Results showed the rate of displacement behaviour was positively correlated with state anxiety but unrelated to trait anxiety, and negatively correlated with the self-reported experience of stress, in agreement with the idea that displacement behaviour has a crucial impact on regulation of stress. Moreover, serial mediation analyses using a bias-corrected bootstrapping approach indicated displacement behaviour mediated the relationship between state anxiety and the experience of stress, and that state anxiety and displacement behaviour - in combination, respectively - mediated the link between trait anxiety and experience of stress. These results shed important new light on the function of displacement behaviour, and highlight promising new avenues for research into emotional expression and stress regulation.
Numerous studies have demonstrated that acute psychological stress, induced by the Trier Social Stress Test (TSST) paradigm, affects salivary cortisol secretion and self-reported stress measures including anxiety. Allergy has been related to altered cortisol responsiveness and increased stress vulnerability. Here, we investigated acute stress responses and emotion regulation strategies in cohorts of allergic and healthy individuals. Groups of allergics and healthy individuals were subjected to the TSST and experienced levels of stress and anxiety as well as emotion regulation strategies were assessed. Cortisol and oxytocin concentrations were measured in saliva or plasma. The present findings confirm earlier results of altered stress responsiveness in allergic individuals. Acute stress by the TSST evoked higher physiological arousal in allergics by means of salivary cortisol secretion. Allergics also scored higher on emotion suppression. However, individuals who were more likely to use reappraisal recovered more efficiently from the cortisol increase. No such effect for reappraisal was found in the healthy population. No differences in self-reported anxiety and stress emerged between the groups. Plasma oxytocin levels prior to the TSST were significantly higher in allergics. Our data corroborate earlier findings on altered stress susceptibility in allergics. Moreover, we identified differences in emotion regulation and oxytocin secretion which should be further explored. Accounting for the emerging global prevalence of allergy, more in-depth research into the experience of stress, coping strategies and stress-related molecules in allergic people is warranted. Short summary: This study addressed stress experiences and emotion regulation in allergic and non-allergic adults. Allergics scored higher on emotion suppression, had higher pre-stress concentrations of plasma oxytocin and exhibited a stronger salivary cortisol response to stress than healthy people. The research outcomes indicate that allergic individuals cope less efficiently with acute stress but may benefit from adaptive emotion regulation strategies such as reappraisal.
Psychogenic non-epileptic seizures (PNES) is a conversion disorder that reflects underlying psychological distress. Female patients with PNES often present with a history of prolonged stressors, especially sexual abuse. In the current study, we studied the relationship between neuropeptide Y (NPY) and PNES symptoms in women with a history of sexual abuse. NPY has been associated with resilience to stress and we hypothesized that low levels would increase the extent and severity of PNES symptoms in this patient population. Serum levels of NPY, and related hormones were measured in fifteen female PNES patients and sixty female controls. PNES patients reported more severe abuse histories, feeling of abandonment, and decreased perception of quality of life than controls. Importantly, they also had lower NPY levels. Our analysis indicates that low levels of NPY in PNES may confer greater vulnerability to exhibit seizure-like symptoms and lower quality of life.