Psychoneuroendocrinology最新文献

Population-representative samples of hair-based cortisol have the potential to revolutionize studies of psychological stress. However, to integrate hair-based cortisol measurement into large-scale studies, it is crucial to understand the limitations and potential biases associated with self-collection. This study examines the associations between individual, household, and community characteristics, sample collection method, and hair cortisol concentration (HCC). We conducted a random-assignment experiment within a cohort design, comparing self-collection to professional-collection of hair samples among young adults. We attempted contact and hair collection among n = 1181 individuals and obtained hair samples from n = 617 individuals ages 18-22 participating in the Chitwan Valley Family Study in Nepal. The primary outcomes were the ability to provide an analyzable hair sample (defined by sufficient weight, length, and identification of the root-end) and HCC in the top quintile. There was no difference in the probability of providing a hair sample between the self-collection and professional-collection groups. However, self-collection decreased the odds of providing an analyzable sample (OR, 0.47; 95 % CI, 0.23-0.94). Women had higher odds of providing analyzable samples (OR, 9.86; 95 % CI, 3.94-24.72), while being married reduced sample suitability (OR, 0.36; 95 % CI, 0.14-0.92). Women also had decreased odds of high HCC (OR, 0.50; 95 % CI, 0.30-0.83). Our findings show that self-collection of hair samples is feasible for large-scale studies. However, gender influences successful self-collection and is also associated with HCC. Adjusting for gender related bias is both essential and feasible to fully realize the potential of large-scale hair cortisol measurement.

Background: Puberty is a critical developmental stage involving profound remodeling of neuroendocrine and neuromodulatory systems. While hormonal changes from a single system have been well studied, the systemic coordination across multiple systems and its sex-specific pattern remain unclear.

Methods: We recruited 449 healthy adolescents (226 males, 223 females) and constructed the network that encompasses nine hormones representative of the HPA and HPG axes, ECS, and melatonin system. The hormones were measured from hair with LC-MS/MS. Hormonal networks were estimated via Spearman correlations. Expected influence (EI), bridge expected influence (bridge EI), and global strength were calculated. Sex differences were examined in global strength, edge weight, EI and bridge EI using the Network Comparison Test.

Results: The pubertal network showed the strongest coupling between metabolically related hormone pairs (i.e., F - E, MEL - NAS and T - P) and antagonistic pairs with cross-system associations (i.e., DHEA - NAS and DHEA - AEA). Cortisol, testosterone and melatonin with the highest EI were identified as hubs where testosterone emerged as a puberty-specific central node, but 1-AG exerted negative influence as an inhibitor. The pubertal network exhibited high global strength. Males showed significantly stronger global strength than females, but weaker edgeweight at the F - DHEA, E - NAS and T - NAS edges. Significant sex differences also appeared in both EI and bridge EI at nodes NAS and 1-AG.

Conclusions: Puberty is marked by intensified neuroendocrine integration and sex-specific reorganization. Cortisol and melatonin consistently act as central hubs, testosterone and progesterone show sex-differentiated roles, and 1-AG emerges as a potential inhibitory hormone. These findings highlight systemic bases of pubertal sexual differentiation and demonstrate the value of network analysis for mapping complex hormonal interactions.

Background: A considerable proportion of life-time depression and anxiety emerges during childhood and adolescence. Some research has shown that pubertal maturity is associated with depression and anxiety. While most research has focused on gonadarche, the earlier phase of adrenarche remains less explored and understood. We aimed to examine the effects of timing and tempo of adrenarche on incidence and chronicity of depression and anxiety during adolescence.

Methods: Data were from the Child to Adult Transition Study (CATS), a longitudinal population-based cohort from Melbourne, Australia. CATS recruited Grade 3 students in 2012, who were followed up annually across adolescence. Adrenarchal timing was modelled as the level of adrenal hormones (DHEA, DHEAS, and testosterone) relative to peers at age 9 and tempo as the adrenal hormone progression rate relative to peers between 9 and 12. Incidence and chronicity of common mental disorders were defined using self-reported depressive and anxiety symptoms collected annually from age 12-18. G-computation was used to adjust for confounding. Missing data were handled via multiple imputation using chained equations.

Results: The study comprised 667 females and 572 males. Depression incidence (76 % females, 44 % males) and chronicity (34 % females, 7 % males) and anxiety incidence (69 % females, 36 % males) and chronicity (29 % females, 7 % males) were more common in female adolescents than males. Regardless of using DHEA, DHEAS, or testosterone as the index for adrenarche, the risk ratios for the association between timing and tempo of adrenarche and the incidence and chronicity of depression or anxiety were close to null and 95 % confidence intervals were inconclusive.

Conclusions: This study did not identify a meaningful effect of adrenarchal timing and tempo on depression and anxiety in adolescents, suggesting that individual differences in adrenarche may not influence risk for later significant mental health difficulties.

The maternal bond is a vital social connection that supports the survival and well-being of both the caregiver and offspring. Disruption of this bond, particularly following offspring loss, can result in profound trauma with long-lasting consequences. While considerable research has focused on the impact of maternal separation on offspring development, the biological effects of offspring loss on the mother remain largely unexplored. In this study, we examined the long-term effects of offspring loss on neuroplasticity, the oxytocin (OXT) and corticotropin-releasing factor (CRF) systems, and stress-coping behaviors in Sprague-Dawley rat mothers. We examined two groups of lactating mothers: (I) a control group, in which dams remained with their pups until natural weaning, and (II) a separated group, in which all offspring were removed on lactation day 1 and the mothers experienced offspring loss until the time corresponding to weaning (19 days). Our results reveal that pup removal increased oxytocin receptor binding-most prominently in the ventromedial hypothalamus (VMH)-and reduced dendritic spine density in this brain region, without altering estrogen receptor α or calbindin cell expression. Separated mothers additionally showed elevated plasma corticosterone levels and increased passive stress-coping behaviors in the forced swim test. Remarkably, passive stress-coping behavior was rescued by central CRF receptor blockade but not by central OXT treatment, indicating that the CRF system plays a critical role in the distress response to offspring loss. These findings establish a novel rat model to investigate the neurobiological consequences of maternal stress following offspring loss.

Early life adversity can have profound consequences that extend across generations, yet the epigenetic impact of paternal early life stress (ELS) on offspring neurodevelopment remains poorly understood. Here, we subjected F1 male rats to a maternal separation (MS) paradigm as a model of ELS and investigated the sex-specific transgenerational effects in their F2 offspring during adolescence (around 5 weeks of age), using behavioral tests and a transcriptomic profile of the medial prefrontal cortex (mPFC). Our findings revealed a female-biased vulnerability to paternal ELS. Specifically, female offspring of stressed fathers exhibited a range of deficits, including lower body weight and heightened anxiety-like behavior. This female-biased vulnerability extended to social behavior in a group setting; while sociability was impaired in both sexes, the deficit was more severe in females, who showed a greater reduction in social proximity. To elucidate the underlying neural mechanisms, we performed RNA sequencing on the mPFC, a key region for social behavior. This revealed a subtle but robust, female-specific transcriptomic signature, highlighted by the downregulation of the mitochondrial gene mt-Nd3 and pathways related to synaptic organization. In contrast, males showed no coherent transcriptomic alterations. Our findings demonstrate that paternal ELS induces a female-biased vulnerability to transgenerational deficits, potentially mediated by impaired mitochondrial function in the mPFC during a critical developmental window. This study underscores the critical role of paternal early-life history in shaping offspring neurodevelopmental trajectories in a sex-dependent manner.

Background: Cortisol is the principal glucocorticoid regulated by the hypothalamic-pituitary-adrenal (HPA) axis and plays a crucial role in maintaining pregnancy and promoting fetal growth and development. Renal function is a key determinant of cortisol exposure. Given that serum creatinine serves as a key biomarker of renal function, it is plausible that maternal creatinine levels contribute to the regulation of fetal cortisol exposure, although the underlying mechanisms remain to be fully elucidated.

Objective: This study was designed to (1) examine the association between maternal serum creatinine and umbilical cord blood cortisol levels, (2) assess the potential mediating role of maternal cortisol in this relationship, and (3) investigate corresponding changes in the protein expression of placental 11β-HSD1 and 11β-HSD2.

Methods: This study employed a paired maternal-fetal design. At delivery, maternal serum, umbilical cord blood, and placental tissue were collected simultaneously from 103 mother-newborn pairs. Cortisol and cortisone levels in maternal and cord blood were measured, and protein expression of 11β-HSD1 and 11β-HSD2 in placental tissue was analyzed. Correlation and mediation analyses were performed to assess the relationships among maternal serum creatinine, maternal cortisol, and cord blood cortisol.

Results: Each unit increase in maternal serum creatinine was associated with a significant decrease in cord blood cortisol levels. Maternal cortisol levels were positively correlated with cord blood cortisol. Mediation analysis showed that maternal cortisol mediated 31.75 % of the association between maternal creatinine and cord blood cortisol. In the high-creatinine conditions, placental expression of 11β-HSD1 was significantly decreased, while expression of 11β-HSD2 was increased.

Conclusion: Maternal cortisol showed evidence of partial mediation in the association between maternal renal function and fetal cortisol exposure. This observational finding highlights a potential link between maternal renal function and fetal glucocorticoid exposure and provides a basis for future studies to investigate the role of placental glucocorticoid regulation and fetal HPA axis development.