Psychoneuroendocrinology最新文献

Laboratory stress tests typically administer stress acutely, ranging from 3 to 15 minutes. However, everyday stressors usually last longer than ten minutes (e.g., examination stressors, work stressors, and social stressors. Moreover, in some studies, it may be relevant to induce stress for a longer period to affect certain psychological or physiological parameters. To this end, we developed a novel stress test that intends to induce psychosocial stress for 90 minutes. The Leuven Prolonged Acute Stress Test (L-PAST) combines physical (hand immersion in cold water), cognitive (mental arithmetic), and psychosocial (social evaluation and feelings of failure) stress elements of two well-known laboratory stress tests, the Maastricht Acute Stress Test (MAST) and the Montreal Imaging Stress Test (MIST). Fifty healthy women were subjected to both the L-PAST and a sham (control) test in a randomized and counterbalanced manner. The stress response was determined by salivary cortisol measurements and assessment of subjective stress ratings at regular time points during the time preceding the stress period (5 min), the stress period (90 min), and the recovery period (35 min). Cognitive reactivity to failure and subjective pain levels were also assessed at various time points. The childhood trauma questionnaire (CTQ) and the perceived stress scale (PSS) were administered prior to the testing phase. As expected, linear mixed models revealed that the stress response was significantly higher during the L-PAST as indicated by a significant time point by condition interaction effect for both the cortisol response (F_(10,450)=12.21, p < 0.0001, ηp²=0.11) and the subjective stress response (F_(13,637)=13.98, p < 0.0001, ηp² = 0.12). Moreover, there was a significant time point by condition interaction effect for cognitive reactivity to failure (F_(13,637) = 7.97, p < 0.0001, ηp² = 0.07) and subjective pain (F_(13,637) = 38.52, p < 0.0001, ηp² = 0.27), indicating that the levels were higher during the L-PAST at most stress induction time points. Lastly, higher CTQ scores were associated with higher subjective pain levels during the L-PAST (F_(1,44)=6.05, p = 0.02). Collectively, our results confirm the efficacy of the L-PAST in inducing a prolonged subjective as well as cortisol stress response.

Background

Adversity suffered in childhood may profoundly affect aging over the subsequent life cycle. The field of childhood adversity and aging has amassed a certain number of publications, but there are no bibliometric studies in this field.

Methods

Publications in 10 years on childhood adversity and aging were searched in the Web of Science Core Collection. Bibliometric tools were used to analyze and visualize these publications by country, institution, journal, author, keyword, research area, and co-citation.

Results

Four hundred thirty-five publications were retrieved from 2014 to September 21, 2023, with a 4.9% annual growth rate. The United States (251), University of California, San Francisco (59), Elissa S. Epel (11), and Psychoneuroendocrinology (29) were the countries, institutions, authors, and journals contributing the highest number of publications in this field, respectively. "Early-life stress" (87), "depression" (82), "childhood trauma" (69), and "aging" (60) were the keywords that appeared more frequently.

Conclusions

This is the first bibliometric study on childhood adversity and aging. The United States dominates the field regarding publication numbers, research institutions, and researchers. Publications in this field are interdisciplinary, covering several critical subject areas and having far-reaching impacts, with gerontology, neurosciences, psychology, and psychiatry at the core.

Background

Prenatal glucocorticoids are one of the most widely proposed prenatal programming mechanisms, yet few studies exist that measure fetal cortisol via neonatal hair. Neonatal hair provides a window into the fetal experience and represents cortisol accumulation in the third trimester of pregnancy. In the current study, we test the links between two types of anxiety over the course of gestation (pregnancy-related anxiety and general anxiety) with neonatal hair cortisol.

Method

Pregnant individuals (N = 107) and their neonates (59.8% female) participated in the current study. Prenatal pregnancy-related anxiety and general anxiety were measured using the Pregnancy Related Anxiety Scale (PRAS) and the State-Trait Anxiety Inventory (STAI), in each trimester of pregnancy. Hierarchical linear modeling was used to model the intercept and slope of each type of anxiety over gestation. Neonatal hair samples were collected shortly after birth (Median _days = 1.17, IQR = 0.75–2.00).

Results

Both higher pregnancy-related anxiety and general anxiety at the beginning of pregnancy and a flatter decline of pregnancy-related anxiety over gestation were associated with lower neonatal hair cortisol. After inclusion of gestational age at birth and parity as covariates, pregnancy-related anxiety (intercept: β = −0.614, p =.012; slope: β = −0.681, p =.006), but not general anxiety (intercept: β = −0.389, p =.114; slope: β = −0.302, p =.217) remained a significant predictor. Further, when both general and pregnancy-related anxiety were entered into the same model, only pregnancy-related anxiety (intercept and slope) were significant predictors of neonatal hair cortisol, indicating an association with pregnancy-related anxiety above and beyond general anxiety.

Conclusion

Cortisol plays a central role in maturation of fetal organ systems, and at the end of gestation, higher cortisol has beneficial effects such as promoting fetal lung maturation. Further, lower maternal cortisol is linked to less optimal cognitive development and altered brain development. As maternal higher anxiety in early pregnancy and a flatter decrease over time are both associated with lower neonatal hair cortisol, maternal pregnancy-related anxiety could be a target of future intervention efforts.

Harsh parenting has been shown to increase the risk of physical and mental health problems in later life. To improve our understanding of these risks and how they can be mitigated, we investigated associations of harsh parenting with a clinically relevant biomarker, epigenetic age deviation (EAD), using data from a randomized-control trial of the Incredible Years (IY) parenting program. This study included 281 children aged 4–8 years who were screened for heightened externalizing behavior and whose parents were randomly allocated to either IY or care-as-usual (CAU). Parents reported on their own parenting practices and their child’s externalizing behavior at baseline and at a follow-up assessment approximately three years later. Epigenetic age, based on the Pediatric Buccal Epigenetic (PedBE) clock, was estimated from child DNA methylation derived from saliva collected at the follow-up assessment. PedBE clock estimates were regressed on chronological age as a measure of EAD. Moderation analyses using multiple regression revealed that harsher parenting at baseline predicted epigenetic age deceleration in children that received CAU (b = −.21, 95% CI[-0.37, −0.05]), but no association was found in children whose parents were allocated to IY (b = −.02, 95% CI [-0.13, 0.19]). These results highlight a prospective association between harsh parenting and children’s EAD and indicate a potential ameliorating effect of preventive intervention. Future work is needed to replicate these findings and understand individual differences in children’s responses to harsh parenting in relation to epigenetic aging.

Background

Brain-derived neurotrophic factor (BDNF) has been implicated in the therapeutic action of antidepressants and possibly in the pathophysiology of Major Depressive Disorder (MDD). Clinical studies of peripheral blood levels of BDNF in MDD have provided conflicting results, and there are also conflicting reports regarding the predictive value of peripheral BDNF levels for antidepressant treatment response. The present study investigated the association between serum BDNF levels, the BDNF Val66Met polymorphism (rs6265), clinical characteristics and SSRI treatment response.

Methods

This open-label clinical trial included 99 physically healthy, unmedicated MDD participants and 70 healthy controls. Following a baseline assessment, 53 of the MDD participants completed an eight-week, open-label course of SSRI antidepressant treatment. Serum BDNF levels and Hamilton Rating Scale for Depression (HDRS) ratings were examined at baseline and after eight weeks of treatment. Antidepressant response was defined as a decrease in HDRS ratings of > 50% from baseline to the end-of-treatment. Finally, serum BDNF levels and SSRI treatment response were compared between MDD participants who were heterozygous or homozygous for the Met allele (“Met-carriers”) and individuals homozygous for the Val allele.

Results

Serum BDNF levels at baseline were significantly higher in the unmedicated MDD participants compared to healthy controls (15.90 ng/ml vs 13.75 ng/ml, t (167) = −2.041, p = 0.043). In a post-hoc analysis, this difference was seen in the female but not male participants (16.85 ng/ml vs 14.06 ng/ml, t (91) = −2.067, p = 0.042; 14.86 ng/ml vs 13.31 ng/ml, t (74) = −0.923, p = 0.359). Baseline serum BDNF levels were not associated with treatment responder status or with absolute change in depression ratings over the course of 8-week SSRI treatment (p = 0.599). In both Responders and Non-responders, no significant changes in serum BDNF levels were found over the 8-week period of SSRI-treatment (16.32 ng/ml vs 16.23 ng/ml, t (18) = 0.060, p = 0.953; 16.04 ng/ml vs 15.61 ng/ml, t (29) = 0.438, p = 0.665, respectively). Further, no differences were found in serum BDNF levels prior to treatment between MDD Met-carriers and MDD Val/Val homozygotes (15.32 ng/ml vs 16.36 ng/ml, t (85) = 0.747, p = 0.457), and no differences were found in post-treatment serum BDNF (F_1,42= 0.031, p = 0.862). However, MDD Val/Val homozygotes showed significantly greater antidepressant responses at week 8 than did MDD Met-carriers (F_1,46 = 4.366, p = 0.043).

Conclusion

Our results do not support sufficient reliability of using peripheral BDNF to characterize depression or to predict antidepressant response in clinical use.