Mental health disorders may begin in childhood or adolescence, and hospitalization is usually indicative of severity.

This study aimed to analyze hospitalizations for mental health disorders in pediatric population of Ecuador.

We examined eight years of nationwide data, focusing on sociodemographic factors, types of disorders, and length of hospital stays for each mental health disorder based on ICD-10 criteria. Data were obtained from the Ecuadorian National Institute of Statistics and Censuses. Logistic regression models were performed to calculate adjusted odds ratios (aOR).

Between 2015 and 2022, 15,521 hospitalizations for mental health disorders were recorded for pediatric population in Ecuador. The highest observed hospitalization rates were 7.69 per 100,000 inhabitants for psychoactive substance use disorders, 7.66 for depressive disorders and 2.75 for schizophrenia spectrum disorders. Hospitalizations for depressive disorders in the pediatric population peaked in 2022 with 15.44 hospitalizations per 100,000. Higher odds of hospitalization for depressive disorders were observed in females (aOR 2.54, 95 % CI 2.34-2.76). Males were more frequently hospitalized for mental and behavioral disorders due to psychoactive substance than females. Adolescents aged 15-19 years were more likely to be hospitalized for depressive or psychoactive substance use disorders. Mental and behavioral disorders related to psychoactive substance use were associated with shorter hospital stays, typically ≤2 days, while depressive disorders often required stays of >11 days.

Our results provide data for further research and development of more comprehensive mental health strategies in the pediatric population in low- and middle-income countries such as Ecuador.

Background: Early-life stress and dietary habits are key determinants of metabolic health. This study investigates the combined effects of maternal separation (MS) and a post-weaning high-fat diet (HFD) on liver morphology in male C57BL/6 mice. Methods: Male mice were subjected to MS during early postnatal life or kept unmanipulated (UM). After weaning, animals were assigned to either a control diet (CD) or an HFD, forming four groups: UM-CD, UM-HFD, MS-CD, and MS-HFD. Liver histology, collagen deposition, and both morphometric and stereological parameters were assessed following 16 weeks of dietary intervention. Results: MS and HFD independently altered liver structure, while the combination of both factors intensified these changes. The MS-HFD group exhibited pronounced steatosis, mixed inflammatory infiltrates, and hepatocellular ballooning, with a significantly higher NAFLD Activity Score (NAS). No significant differences were observed in liver fibrosis. Morphometric analysis revealed increased body mass in HFD-fed groups and elevated liver mass in MS-HFD. Liver volume was higher in MS-HFD, though not significantly. Liver stereology revealed reduced numerical density of hepatocytes (Nvhep) and increased surface density (Svhep) in MS groups, with the most pronounced effects in MS-HFD. Conclusions: Maternal separation amplifies the hepatic alterations induced by HFD, promoting early inflammatory and steatotic changes. These findings highlight the significance of early-life stress as a factor increasing susceptibility to diet-induced liver damage.

Early life stress (ELS) is a significant risk factor for the development of mood and metabolic disorders later in life, which are often in comorbidity. Although it is well known that not all the exposed individuals develop these conditions, the mechanisms leading to a vulnerable or a resilient phenotype for mood and metabolic disorders, as consequences of ELS exposure, are still not fully understood. In this study, we used a prenatal stress (PNS) model, mimicking perinatal adversities, to investigate the impact of ELS on metabolic function, stress-related and inflammatory markers in adult male and female offspring, with a particular focus on vulnerable or resilient phenotypes. PNS exposure was associated with a dysregulation of stress-related and metabolic markers both in the liver and also in the ventral hippocampus, with vulnerable males exhibiting increased insulin receptor levels and dysregulated expression of adipokine receptors (such as leptin and adiponectin). In contrast, female animals did not exhibit these changes. Additionally, PNS induced a pronounced neuroinflammatory response in the ventral hippocampus of vulnerable male rats, characterized by an upregulation of microglial activation markers. Interestingly, a similar pro-inflammatory status was observed in the liver of PNS-exposed males regardless of the pathologic phenotype; however, anti-inflammatory markers were upregulated only in resilient animals, suggesting an active mechanism of resilience. These findings suggest that specific metabolic and inflammatory changes underlie, with a sex-specific effect, the onset of a vulnerable phenotype to PNS and highlight the importance of targeting these pathways in the treatment of mood disorders and metabolic comorbidities.

Early life stress exposure exerts detrimental effects in adulthood and is a risk factor for psychiatric disorders. Studies addressing the molecular mechanisms of early life stress have primarily focused on hormones and stress circuits. However, little is known on how mitochondria and mitochondrial dynamics (i.e., the orchestration of mitochondrial fission, fusion, mitophagy, and biogenesis) modulate early life stress responses. Here, we used a maternal separation with early weaning (MSEW) paradigm to investigate the behavioral and molecular early life stress-elicited effects in male and female C57BL/6 mice in adulthood. We first applied a behavioral test battery to assess MSEW-driven, anxiety-related and stress-coping alterations. We then looked for MSEW-induced, mitochondria-centered changes in cingulate cortex, hippocampus and cerebellum, as well as in plasma by combining protein, mRNA, mitochondrial DNA copy number (mtDNAcn) and metabolomics analyses. We found that MSEW mice are more anxious, show decreased antioxidant capacity in the cingulate cortex and have higher mRNA levels of the fission regulator Fis1 and the mitophagy activator Pink1 in the hippocampus, indicating a shift towards mitochondrial degradation. Hippocampal mRNA level alterations of apoptotic markers further suggest an MSEW-driven activation of apoptosis accompanied by a dysregulation of purine catabolism in the cerebellum in MSEW mice. Sex-specific analysis revealed distinct MSEW-induced changes in male and female mice at the molecular level. Our work reveals a previously unexplored role of mitochondrial dynamics in regulating early life stress effects and highlights a mitochondria-centered dysregulation as a persistent outcome of early life stress in adulthood.

Mounting evidence suggests that mitochondria respond to psychosocial stress. Recent studies suggest mitochondrial DNA (mtDNA) deletions may be increased in some psychiatric disorders, but no studies have examined early-life stress (ELS) and mtDNA deletions. In this study, we assessed mtDNA deletions in peripheral blood mononuclear cells of medically healthy young adults with and without ELS.

Participants (n = 181; 69% female), ages 18 to 40 years, were recruited from the community. Participants with ELS (n = 108) had moderate to severe childhood maltreatment; 83 also had parental loss, and 59 had psychiatric disorders. Participants in the control group (n = 73) had no maltreatment, parental loss, or psychiatric disorders. Standardized interviews and self-report measures assessed demographic variables, stress, and mental health. mtDNA from peripheral blood mononuclear cells was amplified via long-range polymerase chain reaction; mtDNA deletions were quantified via Seq-Well, next-generation sequencing, and the Splice-Break pipeline. Linear regression models were used to assess relationships of mtDNA deletion metrics with ELS, adult stressors, psychiatric disorders, and demographics.

Participants with ELS had significantly greater rates of unique mtDNA deletion breakpoints per 10,000 coverage than participants without ELS (p < .001), correcting for age, sex, and sequencing depth. Cumulative mtDNA deletion read percentage was not significantly different between groups. Psychiatric disorders and adult stressors were associated with greater unique mtDNA deletion breakpoints (ps < .05) but did not account for associations of ELS with mtDNA deletions.

The increased number of unique mtDNA deletion breakpoints in participants with ELS suggests that mitochondrial genomes undergo observable alterations in the context of early stress. Future studies will examine mtDNA deletions with metabolic health measures.

We know more about the costs of chronic stress than the benefits of the acute stress response-an adaptive response that buffers organisms from life-threatening challenges. As yet, no primate study has empirically identified how the stress response adaptively affects evolutionary fitness. Here, we take advantage of a natural experiment-an El Niño drought-that produced unprecedented mortality for wild white-faced capuchins. Using a reaction norm approach, we provide evidence from primates that a more robust stress response to a challenge, measured using fecal glucocorticoids, predicts a greater likelihood of survival. We show that individuals with greater stress responsiveness to previous droughts later had higher survival across a severe El Niño drought. Evolutionary models need empirical data on how stress responsivity varies in adaptive ways. While we cannot buffer subjects from catastrophic events, we can use them to understand which aspects of the stress response help animals to "weather the storm."

Adverse experiences leading to physiological disruptions (stress) in early life produce cascade effects on various biological systems, including the endocrine and metabolic systems, which, in turn, shape the developing skeletal system. To evaluate the effects of stress on adipose and skeletal tissues, we examine the relationship between skeletal indicators of stress (porotic hyperostosis [PH] and cribra orbitalia [CO]), bone mineral density (BMD), vertebral neural canal (VNC) diameters, and adipose tissue distribution in a contemporary pediatric autopsy sample.

Data is from 702 (409 males, 293 females) individuals from a pediatric (0.5-20.9 years) autopsy sample from New Mexico who died between 2011 and 2022. Data includes visceral adipose tissue (VAT) in the abdomen, heart, and liver, CO/PH, VNC size of the fifth lumbar vertebra, and BMD.

We find that adipose tissue distribution and location are differentially associated with CO/PH, BMD, and VNC size; VNC size is smaller, and liver adiposity is higher in those with CO/PH. Further, increased VAT and small VNC size are associated with PH presence and low BMD. Body mass index categories do not correspond with porous cranial lesion presence.

This paper provides evidence for the complex relationship between skeletal markers of early-life stress (CO/PH, reduced VNC size, low BMD) and endocrine system function. VAT distribution and VNC size are partly shaped by stressors during gestation, likely through alterations of the HPA axis. It is possible that alterations of the HPA axis due to gestational stress also shape the expression of porous cranial lesions during exposure to childhood stressors.

Exercise can effectively prevent and treat depression and anxiety, with gut microbiota playing a crucial role in this process. Studies have shown that exercise can influence the diversity and composition of gut microbiota, which in turn affects depression through immune, endocrine, and neural pathways in the gut-brain axis. The effectiveness of exercise varies based on its type, intensity, and duration, largely due to the different changes in gut microbiota. This article summarizes the possible mechanisms by which exercise affects gut microbiota and how gut microbiota influences depression. Additionally, we reviewed literature on the effects of exercise on depression at different intensities, types, and durations to provide a reference for future exercise-based therapies for depression.

According to the World Health Organization, the number of people suffering from depressive disorders worldwide is approaching 350 million. The consequences of depressive disorders include considerable worsening of the quality of life, which frequently leads to social isolation. One of the key factors which may cause depression in adulthood is early life stress, in particular, insufficient maternal care during infancy. Studies performed with children raised in orphanages have shown that long-term complete absence of maternal care (chronic early life stress) leads to vulnerability to emotional disorders, including depression, in adulthood. All of the above dictates the need for a deep understanding of the mechanisms of the pathogenicity of stress in neurogenesis. Therefore, the consequences of stress experienced in the early stages of development are actively studied in animal models. A large body of evidence has accumulated indicating stress-induced changes in gene expression and behavioral disorders in adulthood. However, the connection between the molecular biology of neurons and complex behavior runs through the synaptic connections linking these neurons into complex neural networks. In turn, coordinated activity in neuronal ensembles, achieved by a balance of synaptic excitation and inhibition, is the basis of complex behavior. Unfortunately, the effect of stress on synaptic interactions of neurons remains poorly understood.

Depression and menstrual disturbance are common issues among female university students worldwide. Various studies in different countries have revealed a potential connection between depression and menstrual disturbance. However, no research specifically focusing on this relationship has been conducted with the Bangladeshi population. Thus, we aimed to investigate the prevalence of depression and its impact on menstrual disturbance among female university students in Bangladesh.

Data were collected from 470 female students of the University of Rajshahi in Bangladesh between September and November 2022. A multistage stratified random sampling method was employed to select a sample from the population. Depression severity was assessed using the nine-item Patient Health Questionnaire, categorising it as normal, depressive symptoms and probable depression. Two menstrual disturbances, irregular and painful menstruation, were considered. The factors associated with depression were examined using an ordinal logistic regression model.

The findings indicated that 45.5% of female university students exhibited depressive symptoms, while 30.9% have probable depression. Additionally, 71% experienced menstrual pain and 17.7% reported irregular menstruation. Factors significantly associated with probable depression (p<0.05) included being underweight; paternal occupation other than a farmer, having a job or being in business; low-income and middle-income family; and having a chronic disease. Furthermore, students with depressive symptoms and probable depression were found to be at higher risk of experiencing menstrual disturbances, particularly painful and irregular menstruation. Specifically, those with depressive symptoms and probable depression were more likely to report painful menstruation.

In this study, it was noted that a notable proportion of female students were experiencing probable depression, which was found to have an association with menstrual disturbance. It is advisable that healthcare providers and university authorities prioritise the mental and reproductive health of female students for their holistic well-being.

Early handling (EH), the brief separation of pups from their mother during early life, has been shown to exert beneficial effects. However, the impact of EH in a high anxiety background as well as the role of brain mitochondria in shaping EH-driven responses remain elusive.Here, we used a high (HAB) vs. normal (NAB) anxiety-related behavior mouse model to study how EH affects pup and dam behavior in divergent anxiety backgrounds. We also investigated EH-induced effects at the protein and mRNA levels in adult male HAB mice in the hypothalamus, the prefrontal cortex, and the hippocampus by examining the same mitochondrial/energy pathways and mitochondrial dynamics mechanisms (fission, fusion, biogenesis, and mitophagy) in all three brain regions.EH exerts anxiolytic effects in adult HAB but not NAB male mice and does not affect HAB or NAB maternal behavior, although basal HAB vs. NAB maternal behaviors differ. In adult HAB male mice, EH does not impact oxidative phosphorylation (OXPHOS) and oxidative stress in any of the brain regions studied but leads to increased protein expression of glycolysis enzymes and a correlation of anxiety-related behavior with Krebs cycle enzymes in HAB mice in the hypothalamus. Intriguingly, EH alters mitochondrial dynamics by increasing hypothalamic DRP1, OPA1, and PGC1a protein levels. At the mRNA level, we observe altered, EH-driven mitochondrial dynamics mRNA signatures which predominantly affect the prefrontal cortex.Taken together, our results show that EH exerts anxiolytic effects in adulthood in high anxiety and modulates mitochondrial dynamics pathways in a brain region-specific manner.

This study examined the relation between interparental conflict and cortisol recovery, with child temperamental negative affectivity as the moderator. Children (n = 118) ages 9 to 11 years observed an argument between their parents in the lab and provided saliva samples for cortisol assays. Children also reported levels of interparental conflict, and mothers reported their child's negative affectivity. Results showed that youths with high levels of negative affectivity experienced less cortisol recovery as interparental conflict levels increased. Further, demonstrating some support for differential susceptibility, youths with higher levels of negative affectivity exhibited less recovery at high levels of parental conflict but greater recovery at low levels of parental conflict, compared to peers with lower scores on negative affectivity. We also found that children with low levels of negative affectivity exhibited greater recovery as rates of interparental conflict increased. In summary, this study sheds light on sources of variability in cortisol recovery as it relates to interparental disharmony.

The experience of childhood trauma is known to predict health-relevant outcomes across the lifespan. Previous reviews summarize existing knowledge of the implications of childhood trauma for health in young adults and adults more generally. The current theoretical review aims to integrate the existing literature on the relationship between childhood trauma and health-relevant outcomes specifically in college students, consolidating findings across specific health domains. Further, the following theoretical review highlights the need for more research in this area and discusses how college campuses may use the knowledge in this area of work to develop targeted interventions aimed at improving the health of college students who experienced trauma in childhood.

Several studies in both animal models and in humans have provided substantial evidence that early life stress (ELS) induces long-term changes in behavior and brain function, making it a significant risk factor in the aetiology of various mental disorders, including anxiety and depression. In this study, we tested the hypothesis that ELS in male rats (i) leads to increased anxiety and depressive-like symptoms; and (ii) that these behavioral changes are associated with functional alterations in the endocannabinoid system of the medial prefrontal cortex (mPFC). We further assessed whether the predicted changes in the gene expression of two key components of the endocannabinoid system, cannabinoid receptor 1 (CB1R) and the fatty acid amide hydrolase (FAAH), are regulated by epigenetic mechanisms. Behavioral profiling revealed that the proportion of behaviorally affected animals was increased in ELS exposed male rats compared to control animals, specifically showing symptoms of anhedonia and impaired social behavior. On the molecular level we observed a decrease in CB1R and FAAH mRNA expression in the mPFC of adult ELS exposed animals. These gene expression changes were accompanied by reduced global histone 3 acetylation in the mPFC, while no significant changes in DNA methylation and no significant changes of histone-acetylation at the promoter regions of the analyzed genes were detected. Taken together, our data provide evidence that ELS induces a long-term reduction of CB1R and FAAH expression in the mPFC of adult male rats, which may partially contribute to the ELS-induced changes in adult socio-emotional behavior.

Glucocorticoids (GCs) are steroid hormones fundamental to the body's normal physiological functions and are pivotal in fetal growth and development. During gestation, the mother's cortisol concentration (active GCs) escalates to accommodate the requirements of fetal organ development and maturation. A natural placental GCs barrier, primarily facilitated by 11β hydroxysteroid dehydrogenase 2, exists between the mother and fetus. This enzyme transforms biologically active cortisol into biologically inactive corticosterone, thereby mitigating fetal GCs exposure. However, during pregnancy, the mother may be vulnerable to adverse factor exposures such as stress, hypoxia, caffeine, and synthetic GCs use. In these instances, maternal serum GCs levels may surge beyond the protective capacity of the placental GCs barrier. Moreover, these adverse factors could directly compromise the placental GCs barrier, resulting in excessive fetal exposure to GCs. It is well-documented that prenatal GCs exposure can detrimentally impact the offspring's cardiovascular system, particularly in relation to blood pressure, vascular function, and heart function. In this review, we succinctly delineate the alterations in GCs levels during pregnancy and the potential mechanisms driving these changes, and also analyze the possible causes of prenatal GCs exposure. Furthermore, we summarize the current advancements in understanding the adverse effects and mechanisms of prenatal GCs exposure on the offspring's cardiovascular system.

Due to the paucity of information on circus management effects on the welfare of horses, this study investigated the plasma concentrations of noradrenaline, dopamine and serotonin, known to be indices of mental status, as well as the reactive oxygen metabolites (d-Roms) and the biological antioxidant potential (BAP), likely to denote the oxidant/antioxidant equilibrium of organisms, in horses managed in different Italian circuses. For the study, 56 circus horses of different breeds and ages were enrolled and divided into six groups according to the horses' management (circus management, groups G1-G5; classic riding management representing the control group, CG). From each horse, blood samples were collected in order to assess the concentration of selected parameters. One-way ANOVA showed no differences (p > 0.05) in serotonin, dopamine, noradrenaline, d-Roms and BAP values between circus and control horses. No differences related to the breed of the horses enrolled in the study were found in the values of all investigated parameters (p > 0.05). Furthermore, neurotransmitters showed overlapping levels between the different age classes of investigated horses (p > 0.05); contrariwise, the age of the horse displayed a significant effect on BAP values, with the oldest horses (16-21 age class) exhibiting lower BAP values compared to 4-5, 6-10 and 11-15 age classes (p < 0.05), whereas the d-Roms showed similar values in horses of different age classes (p > 0.05). The results gathered in the present study suggest that the mental status of horses under circus management was not compromised; however, better attention and care in the management of older horses is advocated, as they showed a lower biological antioxidant potential than younger horses; thus, they could be more susceptible to oxidative stress.

Animal welfare has become an increasingly important concern regarding equids working as carriage animals. In the present study, the changes in the markers of stress and inflammatory responses as a result of the work performed by tourism carriage horses under real working conditions in Sicily (Italy) were investigated. Twenty-two Standardbreds performed a normal working day in the carriage tourism business during the months of May, June and July 2022, consisting of one day of work for each month. Blood samples were collected in the stables at rest before the tour route (Pre; 07.00 AM) and within 10 min after the end of the workday (Post; 05.00 PM). Haematological parameters, serum concentration of cortisol, total proteins together with the globulin fractions were investigated before and after the carriage work. Environmental temperature, relative humidity and temperature humidity index (THI) were also assessed. The direct erythrocyte indices increased after work compared to rest condition (P < 0.05). The values of cortisol, total proteins and globulins were not affected by carriage work (P > 0.05), while, higher cortisol, total proteins, α1- and α2-globulins values were observed in July compared to May and June (P < 0.05). These changes are probably due to the increase in THI values which showed mild stress in June and high stress in July. This study suggests that the tourism carriage horses herein investigated have adapted to their work activity, however, avoiding working horses during the hottest hours of the day in the summer months is advocated.

Research has identified fetal risk factors for adult diseases, forming the basis for the Developmental Origins of Health and Disease (DOHaD) hypothesis. DOHaD suggests that maternal insults during pregnancy cause structural and functional changes in fetal organs, increasing the risk of chronic diseases like type 2 diabetes mellitus (T2DM) in adulthood. It is proposed that altered maternal physiology, such as increased glucocorticoid (GC) levels associated with a dysregulated hypothalamic-pituitary-adrenal (HPA) axis in maternal stress and T2DM during pregnancy, exposes the fetus to excess GC. Prenatal glucocorticoid exposure reduces fetal growth and programs the fetal HPA axis, permanently altering its activity into adulthood. This programmed HPA axis is linked to increased risks of hypertension, cardiovascular diseases, and mental disorders in adulthood. With the global rise in T2DM, particularly among young adults of reproductive age, it is crucial to prevent its onset. T2DM is often preceded by a prediabetic state, a condition that does not show any symptoms, causing many to unknowingly progress to T2DM. Studying prediabetes is essential, as it is a reversible stage that may help prevent T2DM-related pregnancy complications. The existing literature focuses on HPA axis dysregulation in T2DM pregnancies and its link to fetal programming. However, the effects of prediabetes on HPA axis function, specifically glucocorticoid in pregnancy and fetal outcomes, are not well understood. This review consolidates research on T2DM during pregnancy, its impact on fetal programming via the HPA axis, and possible links with pregestational prediabetes.

Irregular menstrual cycle has negative health and psychosocial repercussions for women of reproductive age worldwide. However, there is no national data for policymakers and health planners in Ethiopia. Therefore, this review aimed to determine the overall burden of irregular menstrual cycle and predictors among reproductive-age women in Ethiopia.

International databases (SCOPUS, CINAHL, CAB Abstract, EMBASE, PubMed, Web of Science, Google, and Google Scholar) and lists of references were employed to search literature in Ethiopia. The random-effects model was used to calculate the odds ratios of the outcome variable using STATA version 18. The heterogeneity of the studies was measured by computing I 2 and p-values. In addition, sensitivity analysis and funnel plots were performed to test the stability of pooled data in the presence of outliers and publication bias.

The review includes 21 studies and 9109 populations. The overall burden of irregular menstrual cycles among reproductive-age women was 35% (95% CI: 30-41) with I 2 = 96.96%. Sleeping for <5 h a day (AOR: 2.49; 95% CI: 1.49-3.49) and a stressful life (AOR: 3.15; 95% CI: 1.44-4.85) were predictors of irregular menstrual cycles.

More than one in every three reproductive-age women in Ethiopia experience irregular menstrual cycles. Sleeping for <5 h a day and stress increase the likelihood of an irregular menstrual cycle, which can be modified by improving sleeping hours and decreasing stress stimulators through psychotherapy.

Social environments modulate endocrine function, yet it is unclear whether individuals can become like their social partners in how they physiologically respond to stressors. This social transmission of hypothalamic-pituitary-adrenal (HPA) axis reactivity could have long-term consequences for health and lifespan of individuals if their social partners react to stressors with an exaggerated HPA axis response. We tested whether glucocorticoid levels in response to stress of breeding partners changes after breeding depending on whether partners had similar or dissimilar postnatal conditions. We manipulated postnatal conditions by mimicking early life stress in zebra finch chicks (Taeniopygia guttata) via postnatal corticosterone exposure. When they reached adulthood, we created breeding pairs where the female and male had experienced either the same or different early life hormonal treatment (corticosterone or control). Before and after breeding, we obtained blood samples within 3 min and after 10 min or 30 min of restraint stress (baseline, cort10, cort30). We found that corticosterone levels of individuals in response to restraint were affected by their own and their partner's early life conditions, but did not change after breeding. However, across all pairs, partners became more similar in cort30 levels after breeding, although differences between partners in cort10 remained greater in pairs with a corticosterone-treated female. Thus, we show that HPA axis response to stressors in adulthood can be modulated by reproductive partners and that similarity between partners is reduced when females are postnatally exposed to elevated glucocorticoids.

Early life stress is linked to childhood obesity. As children enter adolescence, early life stress may be associated with increased rejection sensitivity, resulting in activation of behavioral and physiological changes that contribute to higher body mass index (BMI). Understanding the potential influence of rejection sensitivity on the association between early life stress and BMI is important to examine in female adolescents. For this secondary data analysis, we hypothesized that female adolescents with greater early life stress and greater rejection sensitivity would exhibit higher BMI-for-age 12 months later.

Seventy-eight adolescents (Mage = 13.1 years; 100% female sex; MBMI = 23.2 kg/m2) in the United States completed study procedures from 2012 to 2016. Among these procedures, the Psychosocial Schedule was used to assess cumulative early life stress and the Children's Rejection Sensitivity Questionnaire was used to assess anger and anxiety in response to rejection. Twelve months later, height and weight were measured to derive BMI-for-age.

Higher early life stress was associated with higher BMI-for-age among female adolescents with low rejection-provoked anger (1 SD below the mean). However, this association was not observed among female adolescents with high rejection-provoked anger (1 SD above the mean). Finally, there was no significant interaction between early life stress and rejection-provoked anxiety in predicting BMI-for-age.

Experiencing early life stress may interact with rejection-provoked anger, but not anxiety, to predict BMI-for-age. Findings inform a developmental perspective of how rejection sensitivity may influence the association between early life stress and early cardiometabolic risk.

Prenatal exposure to inflammation is related to the risk for cognitive impairment in offspring. However, mechanisms underlying the link between inflammatory cytokines at the maternal-fetal interface and human cognitive development are largely unknown. This study addressed this research gap by examining whether i) cytokines within the placenta are associated with different domains of neurocognitive development during infancy, and ii) if DHEA-S in cord blood mediates these associations. We also explored the role of early-life socioeconomic status (SES) in moderating the effect of fetal adrenal steroids on cognitive development in low- and middle-income country contexts. A cohort of 242 mother-infant dyads in Leyte, the Philippines participated in the study and all of them were followed from early pregnancy until 12-months. Concentrations of pro- and anti-inflammatory cytokines in the placenta, and DHEA-S in cord blood collected at delivery were evaluated. The multifactorial aspects of the infant's cognitive functioning were assessed based on the Bayley Scales of Infant Development, third edition (BSID-III). We used Structural Equation Modelling (SEM) with an orthogonal rotation to examine associated paths among latent variables of pro- and anti-inflammatory cytokines in the placenta, fetal neuroendocrine factors, and cognitive development. Pathway analyses showed that both pro- and anti-inflammatory cytokines in the placenta were indirectly related to cognitive (p < 0.05) and language developmental outcomes (p < 0.1) via DHEA-S in cord blood among the low SES group. Yet, we found no statistically significant indirect effect of pro- or anti-inflammatory cytokines on neurocognitive development among the high SES sub-sample. This study extends our understanding of how early-life socioeconomic conditions modify biological pathways underlying the relationship between prenatal factors and postpartum cognitive development.

Emerging epidemiological evidence indicates nature exposure could be associated with greater health benefits among groups in lower versus higher socioeconomic positions. One possible mechanism underpinning this evidence is described by our framework: (susceptibility) adults in low socioeconomic positions face higher exposure to persistent psychosocial stressors in early life, inducing a pro-inflammatory phenotype as a lifelong susceptibility to stress; (differential susceptibility) susceptible adults are more sensitive to the health risks of adverse (stress-promoting) environments, but also to the health benefits of protective (stress-buffering) environments.

Experimental investigation of a pro-inflammatory phenotype as a mechanism facilitating greater stress recovery from nature exposure.

We determined differences in stress recovery (via heart rate variability) caused by exposure to a nature or office virtual reality environment (10 min) after an acute stressor among 64 healthy college-age males with varying levels of susceptibility (socioeconomic status, early life stress, and a pro-inflammatory state [inflammatory reactivity and glucocorticoid resistance to an in vitro bacterial challenge]).

Findings for inflammatory reactivity and glucocorticoid resistance were modest but consistently trended towards better recovery in the nature condition. Differences in recovery were not observed for socioeconomic status or early life stress.

Among healthy college-age males, we observed expected trends according to their differential susceptibility when assessed as inflammatory reactivity and glucocorticoid resistance, suggesting these biological correlates of susceptibility could be more proximal indicators than self-reported assessments of socioeconomic status and early life stress. If future research in more diverse populations aligns with these trends, this could support an alternative conceptualization of susceptibility as increased environmental sensitivity, reflecting heightened responses to adverse, but also protective environments. With this knowledge, future investigators could examine how individual differences in environmental sensitivity could provide an opportunity for those who are the most susceptible to experience the greatest health benefits from nature exposure.

Mounting evidence supports the connections between exposure to environmental typologies(such as green and blue spaces)and human health. However, the mechanistic links that connect biodiversity (the variety of life) and human health, and the extent of supporting evidence remain less clear. Here, we undertook a scoping review to map the links between biodiversity and human health and summarise the levels of associated evidence using an established weight of evidence framework. Distinct from other reviews, we provide additional context regarding the environment-microbiome-health axis, evaluate the environmental buffering pathway (e.g., biodiversity impacts on air pollution), and provide examples of three under- or minimally-represented linkages. The examples are (1) biodiversity and Indigenous Peoples' health, (2) biodiversity and urban social equity, and (3) biodiversity and COVID-19. We observed a moderate level of evidence to support the environmental microbiota-human health pathway and a moderate-high level of evidence to support broader nature pathways (e.g., greenspace) to various health outcomes, from stress reduction to enhanced wellbeing and improved social cohesion. However, studies of broader nature pathways did not typically include specific biodiversity metrics, indicating clear research gaps. Further research is required to understand the connections and causative pathways between biodiversity (e.g., using metrics such as taxonomy, diversity/richness, structure, and function) and health outcomes. There are well-established frameworks to assess the effects of broad classifications of nature on human health. These can assist future research in linking biodiversity metrics to human health outcomes. Our examples of underrepresented linkages highlight the roles of biodiversity and its loss on urban lived experiences, infectious diseases, and Indigenous Peoples' sovereignty and livelihoods. More research and awareness of these socioecological interconnections are needed.

2020-2021 Healthy Minds Study, and used multivariable logistic regression to examine the associations between sexual minority status and psychotic experiences, adjusting for age, gender, and race/ethnicity. We then tested whether psychosocial factors accounted for the association. Sexual minority status was associated with 1.87 times greater odds of having psychotic experiences over the past 12 months (aOR: 1.87; 95% CI: 1.77-1.99; N = 110,551). Several factors mediated the association between sexual orientation and psychotic experiences such as loneliness (26.93%), anxiety (30.90%), depression (33.18%), and marijuana use (13.95%); all factors together accounted for 59.01% of the association between sexual minority status and psychotic experiences. Food insecurity, recent abuse, and discrimination did not significantly mediate the association. Findings should raise clinical awareness that psychotic experiences are more common among sexual minorities than among heterosexuals, which is largely explained by mental health factors, calling for targeted outreach and intervention.

Emerging evidence suggests that multiracial individuals are at high risk for mental health problems. Systematic and ongoing synthesis of literature is necessary to understand mental health among multiracial individuals.

We conducted a systematic review of scholarly articles published during the years 2016-2022. Studies must have focused explicitly on mental health outcomes of biracial/multiracial individuals using quantitative methods. A total of 22 articles met criteria for this review.

Studies were mainly from the United States, with one study from the United Kingdom and one from the Netherlands. Sample sizes ranged from 57 to 393,681. Findings revealed a complicated picture between multiracial identity and mental health, which may be a function of how multiracial identity is defined and empirically examined. Among studies comparing multiracial individuals with monoracial groups, multiracial individuals tended to have worse mental health, with notable exceptions depending on the multiracial subgroup, the mental health outcome, and the reference group. Among studies that only examined multiracial individuals, discrimination and ethno-racial identity emerged as complex explanatory factors that can shape mental health, though each of these constructs can be explored more deeply across social milieu.

The review focused on studies explicitly examining multiracial mental health, published during a limited time frame.

Multiracial individuals tended to have worse mental health outcomes compared to their monoracial counterparts, with variations depending on the outcomes, populations/subgroups, contexts, and reference groups. Racial discrimination and ethno-racial identity may shape mental health trajectories of multiracial people, calling for more research to inform targeted interventions.

Adversity during early life, a critical period for brain development, increases vulnerability and can have a lasting impact on the brain and behaviour of a child. However, the long-term effects of cumulative early-life stressors on brain and behaviour are not well known. We studied a 2-hit rat model of early-life adversity using maternal separation (MS) and immune activation (lipopolysaccharide (LPS)). Rat pups underwent MS for 15 (control) or 180 (MS) minutes per day from postnatal day (P)2-14 and were administered saline or LPS (intraperitoneal) on P3. Open-field (OFT) and object-place recognition tests were performed on rat offspring at P33-35 and P42-50, respectively. The pre-frontal cortex (PFC) and hippocampus were removed at the experimental endpoint (P52-55) for mRNA expression. MS induced anxiety-like behaviour in OFT in male and reduced locomotor activity in both male and female offspring. LPS induced a subtle decline in memory in the object-place recognition test in male offspring. MS increased glial fibrillary acidic protein (GFAP) and brain-derived neurotrophic factor expression in PFC and ionised calcium-binding adapter molecule-1 expression in male hippocampus. MS and LPS resulted in distinct behavioural phenotypes in a sex-specific manner. The combination of MS and LPS had a synergistic effect on the anxiety-like behaviour, locomotor activity, and GFAP mRNA expression outcomes.

Myocardial infarction is a major contributor to CVD-related mortality. T2DM is a risk factor for MI. Stress activates the HPA axis, SNS, and endogenous OPS. These POMC derivatives increase the blood glucose and cardiovascular response by inhibiting the PI3K/AkT insulin signaling pathway and increasing cardiac contraction. Opioids regulate the effect of the HPA axis and SNS and they are cardioprotective. The chronic activation of the stress response may lead to insulin resistance, cardiac dysfunction, and MI. Stress and T2DM, therefore, increase the risk of MI. T2DM is preceded by prediabetes. Studies have shown that prediabetes is associated with an increased risk of MI because of inflammation, hyperlipidemia, endothelial dysfunction, and hypertension. The HPA axis is reported to be dysregulated in prediabetes. However, the SNS and the OPS have not been explored during prediabetes. The effect of prediabetes on POMC derivatives has yet to be fully explored and understood. The impact of stress and prediabetes on the cardiovascular response needs to be investigated. This study sought to review the potential impact of prediabetes on the POMC derivatives and pathways that could lead to MI.

The normal stress response in humans is governed by the hypothalamic-pituitary-adrenal (HPA) axis through heightened mechanisms during stress, raising blood levels of the glucocorticoid hormone cortisol. Glucocorticoids are quintessential compounds that balance the proper functioning of numerous systems in the mammalian body. They are also generated synthetically and are the preeminent therapy for inflammatory diseases. They act by binding to the nuclear receptor transcription factor glucocorticoid receptor (GR), which has two main isoforms (GRα and GRβ). Our classical understanding of glucocorticoid signaling is from the GRα isoform, which binds the hormone, whereas GRβ has no known ligands. With glucocorticoids being involved in many physiological and cellular processes, even small disruptions in their release via the HPA axis, or changes in GR isoform expression, can have dire ramifications on health. Long-term chronic glucocorticoid therapy can lead to a glucocorticoid-resistant state, and we deliberate how this impacts disease treatment. Chronic glucocorticoid treatment can lead to noticeable side effects such as weight gain, adiposity, diabetes, and others that we discuss in detail. There are sexually dimorphic responses to glucocorticoids, and women tend to have a more hyperresponsive HPA axis than men. This review summarizes our understanding of glucocorticoids and critically analyzes the GR isoforms and their beneficial and deleterious mechanisms and the sexual differences that cause a dichotomy in responses. We also discuss the future of glucocorticoid therapy and propose a new concept of dual GR isoform agonist and postulate why activating both isoforms may prevent glucocorticoid resistance.

The commercial hatchery process is globally standardized and exposes billions of day-old layer chicks to stress every year. By alleviating this early stress, on-farm hatching is thought to improve animal welfare, yet little is known about its effects throughout production. This study compared welfare indicators and spatial behaviours during the laying period of hens hatched in an on-farm environment (OFH) to those hatched in a commercial hatchery and transferred at one day-old to a rearing barn (STAN). In particular, we assessed how OFH and TRAN hens differed in space-use and movement behaviours following the transfer to the laying barn at 17 weeks of age, a similar stressor encountered by STAN hens early in life, and determined whether effects aligned more with the 'silver-spoon' or 'environmental matching' hypothesis. We found that for the first three months post-transfer into the laying barn, OFH hens, on average, transitioned less between the aviary's tiers and spent less time on the littered floor. Because OFH hens became behaviourally more similar to STAN hens over time, these results suggest that OFH hens required a prolonged period to establish their daily behavioural patterns. Furthermore, OFH hens had more severe keel bone fractures throughout the laying period but similar feather damage and body mass to STAN hens. No differences were found in hen mortality or the number of eggs per live hen. These findings support the environmental matching hypothesis and suggest that early-life stressors may have prepared hens for later-life stressors, underscoring the importance of both early-life and adult environments in enhancing animal welfare throughout production.

Vesicular monoamine transporters (VMATs) are key regulators of neurotransmitter release responsible for controlling numerous physiological, cognitive, emotional, and behavioral functions. They represent important therapeutic targets for numerous pathological conditions. There are two isoforms of VMAT transporter proteins that function as secondary active transporters into the vesicle for storage and release via exocytosis: VMAT1 (SLC18A1) and VMAT2 (SLC18A2) which differ in their function, quantity, and regional expression. VMAT2 has gained considerable interest as a therapeutic target and diagnostic marker. Inhibitors of VMAT2 have been used as an effective therapy for a range of pathological conditions. Additionally, the functionality and phenotypic classification of classical and nonclassical catecholaminergic neurons are identified by the presence of VMAT2 in catecholaminergic neurons. Dysregulation of VMAT2 is also implicated in many neuropsychiatric diseases. Despite the complex role of VMAT2, many aspects of its function remain unclear. Therefore, our aim is to expand our knowledge of the role of VMAT with a special focus on VMAT2 in different systems and cellular pathways which may potentially facilitate development of novel, more specific therapeutic targets. The current review provides a summary demonstrating the mechanism of action of VMAT, its functional role, and its contribution to disease progression and utilization as therapeutic targets.

Consumption of a Western-type diet, high in fat and sugar, by mothers as well as maternal weight gain and obesity during gestation and lactation may impact offspring risk for mood and cognitive disorders. The objective of this study was to determine if ingestion of a high fat, high sucrose (HFS) diet by rat dams during gestation and lactation or by their pups after weaning impacted these behaviors and stress responsivity in young, adult offspring. To accomplish this, dams consumed either a 45% fat/high sucrose (HFS) diet or the AIN93G control diet during gestation and lactation. At weaning, pups from dams that consumed the HFS diet were weaned to the control diet. Pups from dams assigned to the control diet were weaned to either the control or HFS diet. Pup behavioral testing began at 10 weeks of age. Pups whose dams consumed the HFS diet during gestation and lactation exhibited increased depression-related behavior and baseline serum corticosterone levels, but no difference in peak levels in response to stress. Male pups of these dams displayed increased working memory during acquisition of the holeboard task and tended to exhibit more anxiety-related behavior in the elevated O-maze test. Regardless of when consumed, the HFS diet increased novelty reactivity in the open field test. These data indicate that diet but not maternal weight gain during gestation impacts offspring behavior and elevates stress hormone levels. Also, regardless of when consumed, the HFS diet increases novelty reactivity, a risk factor for depression and addiction.

Severe or chronic stress and trauma can have a detrimental impact on health. Evidence suggests that early-life adversity can become biologically embedded and has the potential to influence health outcomes decades later. Epigenetics is one mechanism that has been implicated in these long-lasting effects. Observational studies in humans indicate that the effects of stress could even persist across generations, although whether or not epigenetic mechanisms are involved remains under debate. Here, we provide an overview of studies in animals and humans that demonstrate the effects of early-life stress on DNA methylation, one of the most widely studied epigenetic mechanisms, and summarize findings from animal models demonstrating the involvement of epigenetics in the transmission of stress across generations. We then describe the results of a scoping review to determine the extent to which the terms intergenerational or transgenerational have been used in human studies investigating the transmission of trauma and stress via epigenetic mechanisms. We end with a discussion of key areas for future research to advance understanding of the role of epigenetics in the legacy effects of stress and trauma.

Cognitive function in humans depends on the complex and interplay between multiple body systems, including the hypothalamic-pituitary-adrenal (HPA) axis. The gut microbiota, which vastly outnumbers human cells and has a genetic potential that exceeds that of the human genome, plays a crucial role in this interplay. The microbiota-gut-brain (MGB) axis is a bidirectional signalling pathway that operates through neural, endocrine, immune, and metabolic pathways. One of the major neuroendocrine systems responding to stress is the HPA axis which produces glucocorticoids such as cortisol in humans and corticosterone in rodents. Appropriate concentrations of cortisol are essential for normal neurodevelopment and function, as well as cognitive processes such as learning and memory, and studies have shown that microbes modulate the HPA axis throughout life. Stress can significantly impact the MGB axis via the HPA axis and other pathways. Animal research has advanced our understanding of these mechanisms and pathways, leading to a paradigm shift in conceptual thinking about the influence of the microbiota on human health and disease. Preclinical and human trials are currently underway to determine how these animal models translate to humans. In this review article, we summarize the current knowledge of the relationship between the gut microbiota, HPA axis, and cognition, and provide an overview of the main findings and conclusions in this broad field.

Objective: Childhood maltreatment (CM) is associated with physical health problems throughout the lifespan, yet more research is needed regarding the trajectory of health problems (e.g., onset of health risk indicators) in young adults. The current study examined whether college students self-reporting higher levels of CM exhibited poorer physical health outcomes. Method: Young adults in college (N = 100) completed a physical health assessment (heart rate, body mass index (BMI), blood pressure, blood sugar, waist circumference), self-reported measures of health (symptoms of illness), and CM during spring semester 2018. Results: CM scores predicted higher heart rate and increased symptoms of illness. Females with maltreatment history presented higher levels of obesity and more metabolic syndrome conditions than their peers. Conclusions: Findings support the importance of examining the trajectory of CM to chronic disease, as health risk indicators are present in young adults.

Stress, inflammatory response, and their relationship were investigated in Simmental cows during the transition period (N = 8; 5 multiparous and 3 primiparous) and in their calves (N = 8; 5 heifers and 3 bulls). From cows, blood was collected at days -21 (±4), 0, +1, +7, and +21 days relative to calving. From calves, blood was collected after birth before colostrum intake (0) and then at 1, 7, and 15 days of age. Cortisol, Interleukin 6 (IL-6) and haptoglobin concentration was assessed by ELISA technique; white blood cells (WBC) were assessed using an ADVIA 2120 Hematology System machine. One-way ANOVA showed an effect of time for all the investigated parameters (P < 0.001) except for lymphocytes in peripartal cows. At calving and 1 d after, cortisol concentration was negatively correlated with levels of IL-6, WBC, and monocytes, whereas levels of IL-6 were positively correlated with WBC, neutrophils, and monocytes count. Cortisol, IL-6, haptoglobin, WBC and all leukocyte populations were affected by the age of neonatal calves (P < 0.001) except for neutrophils. A negative correlation between cortisol and IL-6, neutrophils, monocytes and haptoglobin was found at 15 days of age. A positive correlation between IL-6 and haptoglobin at day 15 of age, and with neutrophils and monocytes at days 7 and 15 of age was found. A positive correlation was obtained between cortisol levels measured in cows around calving and those obtained in calves after birth before colostrum intake (r = 0.83), and between IL-6 concentrations obtained from cows at calving and 1 d after and those obtained in calves at day 1 of age, after the colostrum intake (r = 0.93 and 0.79, respectively). The study suggests that immune function of peripartal cows is in an active state and that, in addition to other well-known factors driving the changes of parameters herein investigated, cortisol could have a role in the immune-modulatory adjustment during peripartum in cows. Furthermore, it can be hypothesized that cortisol is transferred from the cow to newborn calf through the placenta only and not through colostrum, whereas IL-6 levels in calves during the 24 h after birth seem to be influenced by IL-6 values measured in cows around calving due to its transfer through colostrum.

Higher maternal cortisol in pregnancy has been linked to childhood obesity. Much of the previous research has been limited in that cortisol in pregnancy is only measured at one time-point, precluding the ability to examine critical timing effects of prenatal maternal cortisol. To fill this gap, this longitudinal study measured maternal plasma cortisol at 15, 19, 25, and 31 weeks of pregnancy, and assessed infant body mass index percentile (BMIP)1 at birth, 3, 6, 12, and 24 months in 189 mother-infant pairs. Three distinct patterns of maternal cortisol in pregnancy (typical, steep, and flat trajectories) were identified using general growth mixture modeling (GGMM)2 and then used to predict child growth patterns using multilevel modeling. Infants of mothers who had flat cortisol trajectories, characterized by relatively high cortisol in early gestation that plateaus by mid-gestation, experienced more rapid increases in BMIP from birth to 6 months, and had higher BMIPs at 3 and 6 months, than infants whose mothers had the typical slow cortisol rise over gestation, or steep (rapidly accelerating) trajectories. These results suggest that it is not just the total amount of maternal cortisol in pregnancy that shapes early infant growth, but instead the timing and trajectory of prenatal cortisol exposure. To better understand the early origins of obesity risk, future research is needed to investigate the factors that shape mothers' prenatal cortisol trajectories.

Multiracial individuals appear to be at higher risk for mental health problems; however, more research is needed to confirm these racial disparities among young adult college populations.

We analyzed data from the Health Minds Study (N = 99728 young adult college students aged 18-34), collected online across 140 college campuses from September 2020 to June 2021. We used multivariable logistic regression to examine associations between multiracial identity and several mental health outcomes, including mental and behavioral health (depression, anxiety, languishing, perceived need, loneliness), self-injurious behaviors (non-suicidal self-injury, suicidal ideation, suicide plan, suicide attempt), and history of lifetime psychiatric disorders, adjusting for age and gender.

Almost a tenth of the weighted sample were multiracial. Multiracial students had greater odds of all mental and behavioral health outcomes, self-injurious behaviors (though only marginally significant for suicide attempt), and most lifetime psychiatric disorders.

Multiracial young adult college students were more likely to have mental health problems than their monoracial counterparts, calling for targeted preventive interventions on college campuses to address these mental health disparities.

Depression, substance use disorders, and other neuropsychiatric comorbidities are common in people with HIV (PWH), but the underlying mechanisms are not sufficiently understood. HIV-induced damage to the gastrointestinal tract potentiates residual immune dysregulation in PWH receiving effective antiretroviral therapy. However, few studies among PWH have examined the relevance of microbiome-gut-brain axis: bidirectional crosstalk between the gastrointestinal tract, immune system, and central nervous system.

A narrative review was conducted to integrate findings from 159 articles relevant to psychoneuroimmunology (PNI) and microbiome-gut-brain axis research in PWH.

Early PNI studies demonstrated that neuroendocrine signaling via the hypothalamic-pituitary-adrenal axis and autonomic nervous system could partially account for the associations of psychological factors with clinical HIV progression. This review highlights the need for PNI studies examining the mechanistic relevance of the gut microbiota for residual immune dysregulation, tryptophan catabolism, and oxytocin release as key biological determinants of neuropsychiatric comorbidities in PWH (i.e., body-to-mind pathways). It also underscores the continued relevance of neuroendocrine signaling via the hypothalamic-pituitary-adrenal axis, autonomic nervous system, and oxytocin release in modifying microbiome-gut-brain axis functioning (i.e., mind-to-body pathways).

Advancing our understanding of PNI and microbiome-gut-brain axis pathways relevant to depression, substance use disorders, and other neuropsychiatric comorbidities in PWH can guide the development of novel biobehavioral interventions to optimize health outcomes. Recommendations are provided for biobehavioral and neurobehavioral research investigating bidirectional PNI and microbiome-gut-brain axis pathways among PWH in the modern antiretroviral therapy era.

Changes in maternal weight affect the maternal and fetal hypothalamic-pituitary-adrenal axis, influencing birth weight and contributing to the fetal origin of adult diseases (Barker's hypothesis). This study primarily focused on cord blood cortisol levels and identified the association between maternal prepregnancy body mass index (pre-BMI) and birth weight. It also assessed cord blood lipid profile changes related to maternal pre-BMI, birth weight, and cord blood cortisol levels.

To study the mediation effect of cord blood cortisol level between maternal pre-BMI and birth weight and its correlation with cord blood lipid profile.

A total of 169 maternal-neonatal pairs were included at 2 tertiary care centers. Mediation analysis was used to estimate the extent of the association between maternal weight changes and birth weight.

For each unit increase in maternal pre-BMI, birth weight increased by 90.5 g; for every kilogram increase in gestational weight, birth weight increased by 128.44 g. No considerable mediation effect of cortisol was found between pre-BMI and gestational weight gain or between rate of weight gain and birth weight. Pre-BMI and birth weight had a significant negative correlation with high-density lipoprotein cholesterol (HDL-C) levels, i.e., HDL-C was decreased by 1.1 mg/dL for every unit increase in BMI (P=0.017) and for every 100-g increase in birth weight, HDL-C decreased by 0.6 mg/dL (P=0.046). A significant positive correlation was found between cord blood lipid profile and cortisol levels, especially HDL-C (P=0.041).

Cord blood cortisol levels did not mediate the association between maternal weight change and birth weight. A positive correlation was noted between cord blood cortisol levels and HDL-C level. Cord blood HDL-C level was negatively correlated with maternal pre-BMI and birth weight.