Psychoneuroendocrinology最新文献

Empathic stress is the reproduction of psychological and physiological stress activation in an observer of a directly stressed target individual. It likely allows us to allocate the energy necessary to jointly alleviate a stressor at hand. The tendency to show such an empathic or "second-hand" stress response depends on the relationship between target and observer. Here, we investigated whether adolescents' empathic stress responses to their parents' acute stress experience were associated with the diurnal cortisol covariation the parent-adolescent dyad shared in everyday life. Fathers and mothers (N = 77) were confronted with a standardized laboratory stressor, the Trier Social Stress Test, while their adolescent children (13-16 years old) were watching. In the laboratory, parents and their adolescent children simultaneously provided multiple samples of salivary cortisol. On the weekend following the testing session, dyads provided diurnal cortisol samples over two days. These were used to gain a measure of the dyads' adrenocortical physiological attunement in everyday life. We found that the degree to which dyads covaried in their diurnal cortisol activity significantly increased adolescents' tendency for empathic stress responding in the laboratory. The amount of time that dyads spent together over the weekend, adolescents' attachment experiences, dyad type (father-daughter, mother-daughter, father-son, mother-son), and adolescents' puberty status did not significantly alter this relationship. Adolescent attachment avoidance, however, was negatively correlated with both adolescents' cortisol stress reactivity in the laboratory and the degree to which they covaried with their parents' diurnal cortisol release. We conclude that diurnal cortisol covariation between parents and adolescents is positively associated with stress resonance in the laboratory.

Heat stress (HS) triggers various pathophysiological responses in the brain, including neuroinflammation and cognitive impairments. The objective of this study was to examine the impact of HS by comparing the hippocampal transcriptomes of mice exposed to HS with those under control conditions. Our analysis revealed that HS exposure did not affect the number of SNP or InDel mutations in the mouse hippocampus, nor did it influence SNP functions, distribution, or types. However, HS did lead to differential gene expression in the hippocampus, with 210 differentially expressed genes (DEGs), including 72 upregulated and 138 downregulated genes. Gene Ontology (GO) analysis indicated that these DEGs are involved in hippocampal responses to various stimuli (chemical, oxygen-containing compounds, peptide hormones), metabolic processes (arachidonic acid, olefinic compound metabolism, lipid metabolism), and other functions. The regulation of these functions may be closely linked to specific DEGs, such as Card14, Ntrk1, Lcn2, Irs4, Cyp2c70, Hamp, Ambp, Gh, Mup19, and others, which exhibit the highest degree of differential variation. Furthermore, we observed that pre-treatment with taurine primarily modulated cognitive functions in the hippocampus following HS. Therefore, our study offers valuable insights for future research on heat stress-induced cognitive impairments and provides a theoretical foundation for developing taurine-based preventive strategies for high-risk populations.

In a variety of settings, cortisol and testosterone are positively "coupled." That is, within-person fluctuations of these hormones occur in parallel, with increases and decreases in one hormone corresponding to increases and decreases in the other. A dataset comprised of salivary cortisol and testosterone levels from varsity women athletes from six different Emory University sports teams (volleyball 2002, 2005, and 2008; softball 2004; tennis 2009; soccer 2013) was used to explore the relationship between coupling and hormone reactivity to athletic competition. In the majority of athletes, athletic competition was associated with increases in levels of salivary cortisol and testosterone occurring principally during the period between the start of warm-up and the end of competition. Athletes varied with respect to the degree that cortisol and testosterone were coupled. Athletes for whom these two hormones were strongly coupled showed substantially higher competition-related increases in cortisol and testosterone levels than athletes for whom these hormones were less strongly coupled. This heretofore undocumented relationship between hormone coupling and hormone reactivity in a sport setting is consonant with the idea that increases in cortisol and testosterone are parts of a coordinated and complementary response to the physical and/or psychological stress of athletic competition. Given that cortisol and testosterone, each in their own way(s) positively affect athletic performance, a singular benefit of cortisol/testosterone coupling may be an enhanced reactivity to competition, with a corresponding increase in the positive effects of each of these hormones on performance.

Anxiety is one of the most common mental disorders. Neurotensin (NT) is a neuropeptide widely distributed in the central nervous system, involved in the pathophysiology of many neural and psychiatric disorders such as anxiety. However, the neural substrates mediating NT's effect on the regulation of anxiety have not been fully identified. The medial septum (MS) is a crucial brain region in regulating anxiety and expresses neurotensin receptor 1 (NTS1). In the current study, we examined the role of NT/NTS1 in the MS on the anxiety-like behaviors of rats in non-stress and acute stress conditions. We reported that intra-MS infusion of NT produced remarkable anxiogenic effect in behavioral tests. The anxiogenic effect could be blocked by NTS1 antagonist SR48692 pretreatment. Microinjection of NTS1 antagonist to block endogenously released NT in the MS had no effect on anxiety-like behaviors in non-stressed rats, but significantly reduced anxiety in acute restraint stressed rats. Moreover, molecular knockdown of NTS1 in the MS ameliorated anxiety induced by acute restraint stress, also confirming the pharmacological results. Our study implicates NT and its receptors as potential targets for therapeutic interventions of psychiatric diseases, such as anxiety.

Background: Maternal stress can have short and long term adverse (mental) health effects for the mother and her child. Previous evidence suggests that the gut microbiota may be a potential mediator and moderator for the effects of stress via various pathways. This study explored the maternal microbiota trajectory during pregnancy as well as the association between pre- and postnatal maternal stress and features of the maternal and infant gut microbiota during and after pregnancy. In line with previous research, we hypothesized that maternal stress would be positively related to maternal and infant microbiota volatility and that infants of highly stressed mothers would show a relative increase in Proteobacteria and a relative decrease in Bifidobacterium.

Methods: We collected maternal stool samples at 18 and 32 weeks of pregnancy and 8 months postpartum. Infant stools samples were obtained at 2, 6 and 12 weeks and 8 months postpartum. All samples were analyzed using shotgun metagenome sequencing. We also collected several measures of maternal stress (self-reported depression, anxiety, and stress, and hair cortisol and cortisone), most at the same time points as the microbiota samples.

Results: Our data indicated that the maternal microbiota does not undergo drastic changes from the second to the third trimester of pregnancy but that the postpartum microbiota differs significantly from the prenatal microbiota. Furthermore, we identified associations between several stress measures and maternal and infant gut microbiota features at different time points including positive and negative associations with alpha diversity, beta diversity and individual microbial phyla and species relative abundances. Also, the maternal stress composite score, the perceived stress score and the log-ratio of hair cortisol and cortisone were all positively associated with infant microbiota volatility.

Conclusion: Our study provides evidence that maternal prenatal and postnatal stress is related to both the maternal and the infant microbiota. Collectively, this and previous studies indicate that maternal stress does not uniformly associate with most gut microbial features. Instead, the associations are highly time point specific. Regarding infant microbiota volatility, we have consistently found a positive association between stress and infant microbiota volatility. This warrants future research investigating this link in more depth.

Despite considerable social progress, transgender people still face multiple chronic stressors. This study evaluated the allostatic load index and assessed specific psychological characteristics between transgender and cisgender participants who were matched based on age and assigned-at-birth gender. Twenty-one transgender people (52.3 % transgender women, mean age 22.7 years) and 21 cisgender people (52.3 % cisgender women, mean age 23.1 years) participated. For both groups, allostatic load was assessed using circulating serum biomarkers, and psychological characteristics using a battery of self-reports on perceived stress, anxiety, depressive symptomatology, and quality of life. Mann Whitney U and chi square tests were performed. The allostatic load index of transgender people was significantly higher compared to their cisgender counterparts (U = 62.00, p < 0.001), and significantly correlated (p < 0.05) with the majority of the assessed psychological characteristics for both cohorts. Between-group comparisons revealed greater perceived stress, higher state and trait anxiety scores, increased depressive symptomatology, and lower quality of life in all dimensions assessed (p < 0.001), except for the environmental conditions (p = 0.561). The findings underscore the potential physiological and psychological burden experienced by transgender compared to cisgender individuals, emphasizing the need for targeted interventions and inclusive policies to address these disparities. Cohort studies with larger samples are necessary to increase clinicians' insight regarding the pathophysiological challenges of transgender people.

Background: It has been well-established that the allostatic load (AL) index, a cumulative score of multi-system dysregulation in response to chronic stress, is significantly increased at the time of a psychiatric diagnosis. However, no studies have investigated if there is an association between the AL index in childhood and the later development of mental health symptoms in young adults.

Methods: Using data from the Avon Longitudinal Study of Parents and Children (ALSPAC), a population cohort from Bristol, United Kingdom, we investigated the AL index at age 9 years and the risks for mental health symptoms at age 24 years. We used multinomial logistic regression analysis to investigate the association between AL threshold (categorised into bottom third: AL index ≤ 7, middle third: AL index = 7.1-9.9, and top third: AL index ≥ 10) and mental health symptoms while adjusting for sex, the age of mother at delivery, and social class. We used a relative risk ratio (RRR) and 95 % confidence interval(CI) for each variable. We further investigated the association between adverse childhood experiences (ACEs) and mental health symptoms.

Results: We identified a significant association between sex and mental health symptoms, with more females (59 % vs 41 %) showing mental health symptoms than males. We found no direct association between the AL index at age 9 and the later development of mental health symptoms. However, an RRR analysis showed that individuals in the middle and the top third of the AL index had an RRR of 1.99 and 2.20, respectively, to develop mental health symptoms if they were females. We found that individuals who experienced ACE had a much higher risk of developing mental health symptoms as young adults, with the adjusted RRR of 5.39 (95 % CI: 3.00;9.67), 6.79 (95 % CI: 2.55; 18.1), and 2.10 (95 % CI: 0.37;11.8) for neglect, physical and sexual abuse, respectively, in individuals with mood disorder symptoms. The adjusted RRR for neglect and physical and sexual abuse in individuals with psychotic symptoms was 0.99 (95 % CI: 0.37; 2.59), 2.92 (95 % CI: 0.35; 24.4), and 10.5 (95 % CI: 0.99; 112), respectively.

Conclusion: Although the AL index in childhood was not directly associated with the later development of psychotic and mood disorder symptoms in this cohort, females in the higher tertiles of the AL index measured at 9 years of age had an elevated risk of mental health symptoms as young adults. In line with previous work, a strong association was identified between childhood adversity and mental health symptoms in young adulthood. These results highlight the importance of considering the impact of early stress on biological embedding and the later emergence of mental health problems, especially in females.

Background: People with schizophrenia (SZ) and bipolar disorder (BD) show abnormalities in the biological stress system and low-grade inflammation. However, whether the hypothalamic-pituitary-adrenal (HPA) axis-immune regulation is disrupted in SZ and BD, is yet to be determined.

Methods: Cortisol and C-reactive protein (CRP) were measured in blood samples collected at or before 10 am in participants with SZ (N = 257), BD (N = 153), and healthy controls (N = 40). Cortisol/CRP ratio was calculated as an indicator of the balance between HPA axis activity and inflammatory activity, called HPA axis-immune regulation. Global functioning and symptom levels were obtained using the Global Assessment of Functioning (GAF) Scale and Positive and Negative Syndrome Scale (PANSS). Standardized neuropsychological tests were used to assess cognitive function. All analyses were adjusted for demographic variables (age and sex) and the time of blood sampling.

Results: Participants with a SZ or BD diagnosis had lower cortisol/CRP ratios (F=5.93, p = 0.003) compared to healthy controls. The difference was no longer statistically significant (p > 0.1) when BMI was added as a covariate to the model. Within patients, those on psychotropic treatment (n = 337) had lower cortisol/CRP ratio than those not taking psychotropic agents (n = 59) (F=4.72, p = 0.03). Compared to HC, only patients on regular psychotropic agents had lower cortisol/CRP ratio (p = 0.02). Within the SZ group, lower cortisol/CRP ratio was associated with having poorer general functioning as measured by GAF (ß=-0.18, p = 0.01), and more severe negative and general symptomatology as measured by PANSS (ß=0.19, p = 0.007 and ß=0.18, p = 0.01, respectively). In SZ, lower cortisol/CRP ratio was also associated with poorer verbal memory, learning, and processing speed (ß=-0.20 p = 0.007, ß=-0.19 p = 0.01, ß=-0.25, p > 0.001, respectively). No associations were observed between cortisol/CRP ratio and clinical and cognitive functioning in the BD group.

Conclusion: These findings may indicate HPA axis-immune dysregulation in SZ. Our study further indicates that disrupted HPA axis-immune regulation in people with SZ and BD is associated with psychotropic treatment and fat mass, highlighting the clinical importance of weight control and regular psychotropic treatment follow-ups within this group.

COVID-19 has significant long-term impacts, including a chronic syndrome known as long-COVID, characterized by persistent symptoms post-recovery. The inflammatory response during acute infection is hypothesized to influence long-term outcomes. This study aimed to identify inflammatory biomarkers predictive of functional outcomes one year after hospital discharge. A prospective cohort study was conducted with 213 COVID-19 patients admitted to ICUs in Southern Brazil between June and November 2020. After exclusions and follow-ups, 109 patients were evaluated for one-year post-discharge. Plasma levels of Th1 (TNF-α, INF-γ, IL-12), Th2 (IL-4, IL-5, IL-6, IL-10, IL-13), and Th17 (IL-17, IL-22) cytokines were measured. Functional outcomes in psychiatric, cognitive, general health, and health perception domains were assessed. Statistical analyses included multivariate regression, regularized partial correlation network analysis, and K-means clustering. We demonstrate that plasma levels of various cytokines, along with demographic and clinical characteristics, can predict four distinct domains of functional outcomes one year following hospital discharge due to COVID-19 and that an hyperinflammatory phenotype was associated with the occurrence of a worse in psychiatric, general health, and health perception domains. The network analysis highlighted complex interconnections among immune markers and clinical variables, elucidating their roles in long-term health. These findings support using biomarkers for patient stratification and indicate potential targets for therapeutic interventions.