Psychoneuroendocrinology最新文献

Prenatal maternal psychological distress and physiological stress (hypothalamic-pituitary-adrenal [HPA] activity) can negative impact early child development. Research rarely examines the combined or interactive role of prenatal perceived stress and HPA activity on child outcomes. The current longitudinal study examined how prenatal distress and HPA activity impacted child socioemotional functioning from age 1-3. This sample (n=148) was followed from pregnancy, 15-, 24- and 35-months postpartum. During pregnancy, mothers reported their levels of perceived stress and hair samples were collected, reflecting cortisol secretion in the past 3 months. At each postpartum timepoint, mothers reported toddler socioemotional functioning using the Brief Infant-Toddler Social and Emotional Assessment. Multivariate regression results indicated that higher maternal perceived stress interacted with higher hair cortisol levels in association with greater socioemotional problems at 15 and 24 months. In addition, there was a main effect of higher prenatal perceived stress in relation to greater socioemotional problems at 36 months. Exploratory sex-specific moderation analyses indicated that sex interacted with hair cortisol, such that higher levels of prenatal cortisol were associated greater behaviour problems and lower socioemotional competence for females compared to males at 24-months. Findings indicated the importance of examining both physiological stress and psychological stress in pregnancy, as they interact to impact child socioemotional development. Findings also highlight sex-specific prenatal effects.

Objective: Pregnancy is often typified with a decrease in sleep quality, which for many women, progressively worsens across gestation and into the postpartum. A mechanism linking poor sleep with certain adverse pregnancy outcomes is dysregulation of the HPA axis resulting in atypically elevated cortisol production. While total cortisol output normally increases across pregnancy, the cortisol awakening response (CAR), a response to waking up, is influenced by factors such as stress and mood. It attenuates as pregnancy progresses, with normalization in the first weeks after delivery. The goals of the present study were to (1) assess the temporal relationship between sleep quality and cortisol indices across the perinatal period; (2) evaluate whether sleep quality was associated with postpartum mood; and (3) assess whether cortisol mediated these associations.

Method: Data were collected as part of the Healthy Babies Before Birth (HB3) study. Sleep quality, depressive and anxiety symptoms, and cortisol from four time-points (8-16 weeks gestation, 30-36 weeks gestation, 6 months postpartum, and 1-year postpartum) were assessed. Participants (N = 223) who had sleep quality (PSQI) and cortisol data from at least 1 of 4 time-points were included in analyses. Three salivary cortisol indices were calculated: cortisol awakening response (CAR), diurnal slope, and area under the curve (AUC). Multi-level models were run to predict cortisol parameters based on deviations and typical maternal sleep quality at each wave as well as mood outcomes.

Results: Multilevel (time, wave, and person) modeling indicated that sleep quality was not associated with any of the cortisol indices, and none significantly varied across time. However, when PSQI scores were higher than the woman's own mean sleep quality, the CAR slope was steeper (+1 point in PSQI, γ=0.18), and when PSQI scores were lower than mean, the CAR slope was flatter (-1 point, γ=0.11). Poorer sleep quality was associated with greater depression severity (γ = 0.367) and anxiety symptoms (γ = 0.120). Cortisol did not mediate the relationship between sleep quality and depression symptoms.

Discussion: Increases in PSQI scores, but not higher mean PSQI scores, were associated with a larger CAR. There was no association between sleep quality and the diurnal slope or AUC. These data suggest that variability in sleep quality is significantly associated with the amount of cortisol secreted upon awakening.

In the present study, we aimed to investigate how acute stress exerts its heterogeneous effects. Based on biophysical network models, we hypothesized that acute stress would improve occipital-mediated ultra-short-term and to a lesser degree affect occipital- and frontal-mediated short-term and working, and impairs hippocampal-mediated long-term memory processes and their respective behavioral measures. To test this, 111 healthy individuals (57 female) underwent both the Trier Social Stress Test (TSST) and a control test. Immediately afterward, participants' performance was measured in four memory tasks (Rapid Serial Visual Presentation, RSVP, Match-to-Sample, MTS, N-Back, NB and Free-Recall, FR tasks). TSST exposure seems to impair long-term memory (AC_FR; β = -1.50 ± 0.62; when free recall was tested approx. 80 minutes after initial encoding, immediately after the TSST), and working memory (AC_NB; β= -0.42 ± 0.20 %) but did not affect ultra-short-term (AC_RSVP; β = -0.03 ± 0.31 %) and short-term (AC_MTS; β=-0.18 ± 0.31 %) memory accuracies (ACs). Interestingly, TSST exposure increased the exploratory included measure of response times in MTS (RT_MTS; β =16.42 ± 7.18 msec) and impaired T1 detection in the RSVP (AC_T1; β=-0.48 ± 0.22 %) tasks. Contrary to the hypothesis, TSST exposure did not have the hypothesized effects on the memory processes. Instead, TSST exposure appeared to affect secondary behavioral indicators of motivation or task instruction adherence.