Psychoneuroendocrinology最新文献

Background

Diet quality during pregnancy is important for maternal health and offspring development. However, national dietary recommendations are not always met. A potential barrier for healthy food choices might be the experience of stress. Previous literature in non-pregnant populations suggests a negative effect of acute stress on diet quality. This preregistered study is the first to test whether an acute stressor leads to unhealthy food choices in pregnancy and examine the moderating role of stress, depressive and anxiety complaints in daily life.

Method

Pregnant women (N = 110, 3rd trimester) completed online self-reported surveys measuring stress, depressive and anxiety complaints in daily life. Hereafter, participants were invited for a laboratory visit, in which they were exposed to the Trier Social Stress Test or a control task. After this manipulation, self-reported and actual food choices and food intake were assessed. At the end of the visit, a hair sample was collected. Throughout the visit, visual analogue scales on negative affect were completed and saliva samples were collected.

Results

The stress group experienced significantly more psychological stress than the control group during the experimental manipulation. Main regression analyses showed that the acute laboratory stressor did not cause unhealthy food choices in the third trimester of pregnancy. In fact, the stress group chose fewer unhealthy foods and consumed fewer kilocalories compared to the control group. Additionally, the findings point at a moderating role of depressive and stress complaints in daily life on food choices within the control group: higher scores were related to more unhealthy food choices and more kilocalories consumed.

Discussion

As this was the first study to test the effect of an acute stressor on food choices in pregnant women, more research is needed to obtain a better understanding of stress-related eating in pregnancy. This knowledge may inform future interventions to support pregnant women in improving their diet quality.

Estrogen is a group of hormones that collaborate with the nervous system to impact the overall well-being of all genders. It influences many processes, including those occurring in the central nervous system, affecting learning and memory, and playing roles in neurodegenerative diseases and mental disorders. The hormone’s action is mediated by specific receptors. Significant roles of classical estrogen receptors, ERα and ERβ, in various diseases were known since many years, but after identifying a structurally and locationally distinct receptor, the G protein-coupled estrogen receptor (GPER), its role in human physiology and pathophysiology was investigated. This review compiles GPER-related information, highlighting its impact on homeostasis and diseases, while putting special attention on functions and dysfunctions of this receptor in neurobiology and biobehavioral processes. Understanding the receptor modulation possibilities is essential for therapy, as disruptions in receptors can lead to diseases or disorders, irrespective of correct estrogen levels. We conclude that studies on the GPER receptor have the potential to develop therapies that regulate estrogen and positively impact human health.

Objectives

We aimed to characterize the interplay between early life stress (ELS), metabolic syndrome (MetS), and plasminogen activator inhibitor-1 (PAI-1), a major inhibitor of the fibrinolytic system implicated in cardiometabolic diseases. We also examined the understudied intersection of ELS, physical activity and PAI-1.

Methods

Healthy young adults ages 18–40 (N=200; 68% female) were recruited from the community. Participants with ELS (N=118) experienced childhood maltreatment, and the majority (n=92) also experienced childhood parental loss. Control participants (N=82) had no history of childhood maltreatment or parental loss. Participants had no current cardiometabolic or thrombotic conditions. Fasting plasma samples were assessed for markers of metabolic risk and total PAI-1 using the Bio-Plex Pro Human Diabetes Panel (Bio-Rad Laboratories). A composite metabolic risk z-score (MetS risk) was computed from the mean standardized z-scores of waist-to-height ratio, systolic and diastolic blood pressure, triglycerides, total cholesterol, LDL and HLD cholesterol, fasting plasma glucose, and hemoglobin A1c.

Results

We found that a history of ELS was linked to both higher PAI-1 levels and a higher MetS risk score. ELS was associated with a higher MetS Z-score in adulthood via increased circulating PAI-1 levels (Average Causal Mediation Effect [ACME]= 0.07, p = 0.036). ELS was also linked to increased PAI-1 levels via greater MetS z-scores (ACME = 0.02, p < 0.001). There was a significant interaction effect of ELS and exercise on PAI-1 levels (p = 0.03), such that engaging in higher levels of daily exercise was linked to lower PAI-1 levels in individuals with ELS.

Conclusion

Healthy young adults with ELS have elevated PAI-1 levels and metabolic risk scores. Among individuals with ELS, exercise is linked to lower PAI-1 levels, suggesting a potential direction for early intervention.

Background

Frequent or prolonged exposure to stressors may jeopardize young children’s health. The onset of the COVID-19 pandemic, coupled with disruptions in daily routines and social isolation resulting from public health preventive measures, have raised concerns about its potential impact on children’ experienced stress, particularly for young children and vulnerable families. However, whether the pandemic was accompanied by changes in physiological stress remains unknown as perceived stress is not a good proxy of physiological stress. This study examined if preschoolers showed increasing hair steroid concentrations following the onset of the COVID-19 pandemic and whether family characteristics may have exacerbated or buffered these changes.

Methods

136 preschoolers (2–4 years) provided hair for steroid measurement (cortisol, dehydroepiandrosterone (DHEA), cortisone, cortisol-to-DHEA ratio, cortisol-to-cortisone ratio) in October-November 2019 (T0) and in July-August 2020 (T1). A 2-centimeter hair segment was analyzed, reflecting steroid production over the two months leading up to collection. Family income, conflict resolution and lack of cohesion, as well as parents’ COVID-19 stress were reported by parents. Linear mixed models for repeated measures and Bayes factors were used.

Results

No significant changes were noted from before to after the onset of the COVID-19 pandemic for most hair steroids. However, a moderating role of family conflict resolution was noted. Children living with parents with a better ability to resolve conflicts had lower levels of DHEA compared to those who had more difficulty managing conflicts. Additionally, lower levels of family cohesion and income were linked to some steroids, especially DHEA, suggesting that these factors may relate to children’s physiological stress. Finally, boys had higher DHEA levels than girls.

Conclusion

Our findings suggest that stress biomarkers were comparable from before to during the COVID-19 pandemic. This observation holds true despite the pandemic being perceived by many as a novel, unpredictable, and potentially threatening event. Findings further suggest that family characteristics are associated with hair steroid, especially DHEA, which deserves further investigation.

Roma living in marginalised communities are among the most disadvantaged groups in Slovakia. Socioeconomic disadvantage is associated with higher hair cortisol concentrations (HCC), including in parents. The aim of this study is therefore to assess differences in HCC, reflecting the levels of stress, between mothers living in MRCs and from the majority population, to assess the association of socioeconomic disadvantage with HCC, and whether disadvantage mediates the MRC/majority differences in HCC. Participants were mothers of children aged 15–18 months old living in MRCs (N=61) and from the Slovak majority population (N=90). During preventive paediatric visits, visits at community centres and home visits, hair samples and data by questionnaire were collected. HCC differed significantly between mothers living in MRCs and mothers from the majority population, with the mean HCC value being twice as high in mothers living in MRCs (22.98 (95% confidence interval, CI, 15.70–30.30) vs. 11.76 (8.34–15.20), p<0.05). HCC was significantly associated with education, household equipment and household overcrowding, but not with billing, socioeconomic stress and social support. The difference in HCC between mothers living in MRCs and mothers from the majority population was partially mediated by poor house equipment, such as no access to running water, no flushing toilet or no bathroom (the indirect effect of B=7.63 (95% CI: 2.12–13.92)). Practitioners and policymakers should be aware of high stress levels among mothers living in MRCs and aim at enhancing their living and housing conditions.

Disruptions in appetite-regulating hormones may contribute to the development and/or maintenance of avoidant/restrictive food intake disorder (ARFID). No study has previously assessed fasting levels of orexigenic ghrelin or anorexigenic peptide YY (PYY), nor their trajectory in response to food intake among youth with ARFID across the weight spectrum. We measured fasting and postprandial (30, 60, 120 minutes post-meal) levels of ghrelin and PYY among 127 males and females with full and subthreshold ARFID (n = 95) and healthy controls (HC; n = 32). We used latent growth curve analyses to examine differences in the trajectories of ghrelin and PYY between ARFID and HC. Fasting levels of ghrelin did not differ in ARFID compared to HC. Among ARFID, ghrelin levels declined more gradually than among HC in the first hour post meal (p =.005), but continued to decline between 60 and 120 minutes post meal, whereas HC plateaued (p =.005). Fasting and PYY trajectory did not differ by group. Findings did not change after adjusting for BMI percentile (M(SD)_ARFID = 37(35); M(SD)_HC = 53(26); p =.006) or calories consumed during the test meal (M(SD)_ARFID = 294(118); M(SD)_HC = 384 (48); p <.001). These data highlight a distinct trajectory of ghrelin following a test meal in youth with ARFID. Future research should examine ghrelin dysfunction as an etiological or maintenance factor of ARFID.

Oxytocin administration has demonstrated considerable promise for providing individualized support for autistic people. However, studies evaluating the effects of oxytocin administration on autistic characteristics have yielded inconsistent results. This systematic review and meta-analysis investigates the effect of oxytocin administration on social and routinized behaviors in autism using recently developed methods to accurately assess the potential impact of effect size dependency and publication bias. Our frequentist meta-analysis yielded a significant summary effect size estimate for the impact of oxytocin administration on social outcomes in autism (d = 0.22, p < 0.001). The summary effect size estimate for routinized behavior outcomes was not statistically significant (d = 0.14, p = 0.22), with a follow up test indicating that the effect size estimate was not either statistically equivalent (Z = −1.06, p = 0.2), assuming a smallest effect size of interest of 0.25. Frequentist and Bayesian assessments for publication bias, as well as results from Robust Bayesian meta-analysis of oxytocin effects on social outcomes in autism, indicated that summary effect sizes might be inflated due to publication bias. Future studies should aim to reduce bias by preregistering analysis plans and to increase precision with larger sample sizes.

Background

Cortisol typically peaks in the morning after waking up and declines throughout the day, reaching its lowest levels during nighttime sleep. Shift work can cause misalignment between cortisol levels and sleep-wake timing. We analyzed this misalignment in female shift workers focusing on the timing and extent of these changes.

Methods

We conducted a cross-sectional study involving 68 shift workers (aged 37 ± 10 years) and 21 non-shift workers (aged 45 ± 10 years) from a hospital. Shift workers were monitored through two day shifts and three night shifts, whereas non-shift workers were monitored during two day shifts. Each participant collected six to eight saliva samples (depending on their shift type) and provided sleep timing information, which was recorded via polysomnography and sleep diaries. Generalized additive mixed models were used to estimate shift-specific differences in cortisol smooth curves. Summary measures calculated for the cortisol smooth curves included cortisol awakening response, peak-to-bed slope, and total output.

Results

Between shift workers and non-shift workers, we observed similar diurnal cortisol profiles with a steep negative diurnal slope during day shifts. In shift workers on night shifts, a flattened U-shaped cortisol profile after the post-awakening maximum was observed, with a peak-to-bed slope close to zero. When comparing night to day shifts in the group of shift workers, mean cortisol levels were lower between 42 and 56 minutes and 1.8–11.9 hours after waking up, and higher between 14.9 and 22 hours after waking up.

Conclusion

Our findings indicate altered cortisol profiles in female hospital employees on night shifts. Specifically, cortisol levels were lower at night when higher levels would typically be necessary for work activities, and higher at bedtime after a night shift, when levels should normally be low.

Sleep deprivation and insulin resistance (IR) are two risk factors for Alzheimer's disease. As the population of people with IR increases and sleep restriction (SR) due to staying up late becomes the "new normal", it is necessary to investigate the effects and molecular pathogenesis of chronic SR on cognitive function in insulin resistance. In this study, 4-week-old mice were fed a high-fat diet (HFD) for 8 weeks to establish IR model, and then the mice were subjected to SR for 21 days, and related indicators were assessed, including cognitive capacity, apoptosis, oxidative stress, glial cell activation, inflammation, blood-brain barrier (BBB) permeability and adiponectin levels, for exploring the potential regulatory mechanisms. Compared with control group, IR mice showed impaired cognitive capacity, meanwhile, SR not only promoted Bax/Bcl2-induced hippocampal neuronal cell apoptosis and Nrf2/HO1- induced oxidative stress, but also increased microglia activation and inflammatory factor levels and BBB permeability, thus aggravating the cognitive impairment in IR mice. Consequently, changing bad living habits and ensuring sufficient sleep are important intervention strategies to moderate the aggravation of IR-induced cognitive impairment.

Positive and negative affect have been shown to have implications for hormones like cortisol but how moment to moment changes in affect (i.e., affect variability) influence cortisol secretion is less well understood. Additionally, context characteristics such as mean affect and stress may influence the association between affect variability and cortisol output. In the current study, we examined affect, stress, and cortisol data from 113 participants (age range = 25–63, M = 35.63, SD = 11.34; 29 % male; 42 % White/Caucasian, 37 % Asian or Pacific Islander, 13 % Hispanic/Latino, 4 % Black/African American, 1 % Native American, Eskimo, or Aleut, 4 % selected “other” for their race/ethnicity). Participants completed ecological momentary assessments assessing positive and negative affect and stress four times per day for five days and provided saliva samples at each time point. Saliva was assayed for cortisol, and area under the curve with respect to ground was computed. In a three-way interaction, both positive affect mean level and stress moderated the association between positive affect variability and cortisol (b = −1.55, t(100) = −3.29, SE = 0.47, p <.01, β = −4.05). When breaking down this three-way interaction, in the context of low stress and high mean positive affect, variability was positively related to total cortisol output. In contrast, in the context of high stress and high mean positive affect, variability was negatively related to total cortisol output. While greater positive affect variability is generally worse for health-relevant outcomes (as prior research has shown and as we show here at low levels of stress), at high levels of stress, fluctuation in affect may be adaptive. For someone experiencing a high stress week, having fluctuations in positive affect may mean that they are adaptively changing to meet their environmental needs especially when they typically report high mean positive affect levels. There were no associations between negative affect variability and cortisol secretion nor did mean negative affect or stress play a moderating role for negative affect variability. This study provides evidence that positive affect variability’s association with cortisol secretion throughout the day may vary based on stress and mean positive affect levels.